ENMeningococcal infection in children ИНОСТР 2024.pdf

AHMEDAtif36 26 views 137 slides Oct 05, 2024
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About This Presentation

ENMeningococcal infection in children ИНОСТР 2024.pdf


Slide Content

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococca
l infection in
children

•Meningococcal
infection in
children
Loading…




Loading…








Meningococcus Of Wekselbaum
The causative agent of meningococcal infection is the
gram-positive diplococcus Neisseria meningitides,
belonging to the genus Neisseria of the family Neisseriacea
In the form of these pathogens resemble coffee beans.


Loading…



•Сolonies of Neisseria meningitidis on blood
agar. Colony mor

Сolonies of Neisseria
meningitidis on blood
agar. Colony mor











•There are light, moderate and severe forms
of the disease. The severity of
meningococcemia depends on the severity of
the symptoms of toxic phenomena, impaired
consciousness, the degree of fever, the
abundance and nature of hemorrhagic–
necrotic rash and changes in blood
circulation in the body.

•There is also a lightning-fast form of
meningococcemia (ultra-acute meningococcal
sepsis), which is very difficult. In this case, the
disease begins acutely with a sharp increase in body
temperature, chills, headaches with the appearance
of an abundant amount of hemorrhagic elements.
The rash quickly merges, forming extensive
hemorrhages.
•At first, blood pressure is kept at normal numbers,
then quickly decreases with the appearance of
circulatory insufficiency: increased heart rate, heart
tones are muted, the skin is pale, there is a cyanosis
of the fingertips.
• The skin is cold to the touch, covered with sticky
sweat, the facial features are sharpened. Young
children have vomiting, diarrhea, convulsions, loss
of consciousness due to the development of cerebral
edema (neurotoxicosis).












Meningococcal infection in children
•The causes and mechanisms of development
• of the Immune system
• Classification
•Clinical manifestations
• Principles of treatment
• Prevention
Diplococci – meningococci

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.

Meningococcal infection in children
•Meningococci can be located inside cells,
extracellularly, they do not form spores,
they do not have flagella. It quickly dies in
the environment, when boiled, it dies
quickly-within a few seconds, when exposed
to disinfectants-in a few hours.
Loading…

•Meningococcus is well grown in laboratory
conditions with high humidity, a slightly
alkaline reaction of the medium (pH 7.2–
7.4), a temperature of 37 ° C in media that
contain protein (blood, milk, yolk, etc.).
Pathogens are unstable in the external
environment: they die when temperature,
humidity, and sunlight intensity fluctuate.
Outside the human body, they continue
their vital activity for up to half an hour.

•Meningococcal infection is infected
and sick only people.
•The pathogen is released from the
mucous membrane of the
nasopharynx, from the cerebrospinal
fluid (CSF), blood, excreta (exudate)
of skin rashes.
•Meningococcus secretes allergenic
substances.


•The source of infection can only be a
sick person or a bacterial carrier. It is
most dangerous at the beginning of the
disease and especially in the presence of
catarrhal (inflammatory) phenomena in
the nasopharynx, and the disease occurs
in a common form (meningitis,
meningococcal sepsis,
meningoencephalitis).

•"Healthy" bacterial carriers without
acute inflammation in the
nasopharynx are less dangerous, but
the disease is widely spread through
the carrier.
•The duration of bacterial
transmission in meningococcal
infection is on average 2-3 weeks, in
some individuals-6 or more weeks
(in the presence of a chronic
inflammatory focus in the
nasopharynx).

•The infection is spread by airborne droplets
(aerosol) through infected droplets of mucus
released from the nasopharynx and upper
respiratory tract.
•Since meningococcus quickly dies in the external
environment, the duration of contact with a sick
child, the crowding of children in rooms (rooms),
especially in poorly ventilated public places, is
important for infection.
•Often, young children are infected from parents,
close relatives who are either carriers or patients
with a localized form of infection.
Сontagious index
•The susceptibility to the
disease is not very high
(the contagion index is
1-10-15 %).


Pathogenesis
•In the development of
meningococcal infection, the main
role is played by three factors:
meningococcus, endotoxin (a
substance contained inside the
microbe and released into the body
when it dies) and an allergenic
substance
The causative agent of
meningococcal infection is
transmitted only from person to
person. The infection is spread by
airborne droplets and enters the
body through the nasal mucosa,
oral cavity and pharynx
Introduction
of infection









•In some cases (1-2%), meningococcus
passes through local protective barriers
and enters the bloodstream by
lymphogenic route.
•This can be meningococcemia
(meningococcal sepsis) – with the blood
flow, infectious agents penetrate into
various organs and tissues: the skin,
joints, kidneys, adrenal glands, lungs, the
inner lining of the heart, and others.
• In some cases, meningococcus also
passes the blood-brain barrier, which
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis




•Hyperacute meningococcal sepsis, occurring
with infectious-toxic shock, develops as a
result of mass penetration of the pathogen
into the bloodstream and circulation of the
meningococcal toxin in the blood plasma.
•With the death of a large number of
pathogens, endotoxin is released, which,
acting on the inner lining of blood vessels
and the membranes of blood cells, leads to a
violation of blood circulation, especially to a
violation in the capillary network

•The presence of the toxin in the blood,
disorders in the capillary bed, DIC-
syndrome (intravascular blood clotting)
contribute to the occurrence of deep
metabolic disorders-acidosis (a shift in the
pH of the blood to the acidic side), a
disorder of the function of many organs
and systems.

•Acute adrenal, renal, and cardiovascular
insufficiency develops.

•As a result of the above changes, acute edema
may develop – swelling of the brain substance
(toxic brain edema).
•Clinically, these are convulsive phenomena, a
violation of consciousness, an increase in
intracranial pressure, the cerebellum is wedged
into the large occipital opening with compression
of the medulla oblongata, in which the centers of
regulation of vital systems are located.
• Death occurs due to paralysis of the respiratory
center of the medulla oblongata.

•With the penetration of meningococci in the shell
of the brain is the development of meningitis. The
inflammatory process is characterized by the
penetration of special cells-neutrophils into the
soft meninges.
•Substances with a strong destructive effect are
released from neutrophils.
•Under their action, the destruction of collagen and
elastic fibers, basal membranes, which are part of
the blood – brain barrier-the regulator of
metabolism between blood and nerve cells,
occurs.

•After a meningococcal infection or after a
long-term bacterial carrier, specific
antibodies begin to be produced in the
human body: agglutinins, bactericidal
antibodies, and precipitins.

•From the first days of the disease, the titer of
hemagglutinins begins to gradually
increase, reaching maximum figures by the
5th–7th day. After 3-4 weeks, the level of
antibodies decreases.

•Classification of meningococcal infection.
• 1. Localized forms:
•a) meningococcal carrier;
•b) acute nasopharyngitis.
•2. Generalized forms:
•a) meningococcemia (meningococcal sepsis);
• b) meningitis;
•c) meningoencephalitis.
•3. Mixed form: meningitis and meningococcemia.
•4. Rare forms:
• a) meningococcal endocarditis;
• b) pneumonia;
• c) iridocyclitis;
•d) arthritis, etc.

•The incubation period lasts from 2 to 10
days.

•Acute nasopharyngitis occurs in 80 % of
all meningococcal diseases.

• It occurs in three forms: mild, moderate
and severe.

•At the end of the first or beginning of the second day from the
beginning of the disease, a rash appears on the surface of the
skin. Meningococcal infection is characterized by a
hemorrhagic rash in the form of stars that have an irregular
shape. It is dense to the touch, rising above the surface of the
skin. It appears simultaneously on the entire skin, but more
massively on the lower parts of the arms, legs, buttocks, and
eyelids. In the case of a severe course, rashes appear on the
face, upper parts of the trunk. Elements of the rash-ranging in
size from spot to large hemorrhages with necrotic changes in
the center. Then the dead tissue is rejected with the formation
of defects and scars. In very severe and advanced cases,
gangrene of the nail phalanges, fingers, toes, and auricles
develops. The depth of necrotic processes can reach such a
size that the bones are exposed. At the same time, healing is
extremely slow.


Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Легкая форма.
•Usually, nasopharyngitis begins acutely (against
the background of complete health) with the
appearance of a body temperature of up to 38-38. 5
°C. There may be complaints of nasal congestion,
runny nose, headache, weakness. In some cases,
the body temperature does not change, the
condition is satisfactory. Inflammatory changes in
the nasopharynx are poorly expressed. In many
patients, there are no changes in the peripheral
blood, a moderate increase in the number of
neutrophils is possible









•In the blood of meningococcemia, there is an
increase in white blood cells to 15-25 x 10 9 /l,
an increase in the level of neutrophils, an
increase in ESR to 50-70 mm / h, but in
patients with mild forms of ESR may be within
the normal range.
Medium-heavy form
•Medium-heavy form. Increase in body temperature to
higher figures-38.5-39 °C. Complaints of weakness,
headache, dizziness, sore throat, pain when
swallowing, nasal congestion, runny nose. The sick
child is sluggish, sedentary. On examination, there is
redness and swelling of the posterior wall of the
pharynx, an increase in lymphoid follicles, swelling
of the lateral rollers, a small mucous discharge.

•Severe form.
•The body temperature rises to 40-40. 5 °C. The symptoms
characteristic of the moderate form are accompanied by
vomiting, convulsions, and abdominal pain.
•Is it possible to detect meningeal symptoms: stiffness of the
occipital muscles, while the child can not bend his head
forward, a symptom of Kernig (it is impossible to straighten
the bent leg) , etc. In the peripheral blood increased level of
leukocytes to 15 X 10 9 g/l, increased levels of neutrophils, a
shift of the leukocyte formula to the left, ESR increases to 20-
30 mm/h.
•Such conditions are often diagnosed as ARVI with convulsive
syndrome or viral meningitis. There is an increase in pressure
in the cerebrospinal fluid.
Meningococcemia
•Meningococcemia (bacteremia, meningococcal sepsis) is
a form of meningococcal infection in which the pathogen
penetrates and circulates in the blood.
•At the same time, in addition to general toxic
manifestations and skin lesions, there may be damage to
internal organs (spleen, lungs, kidneys, adrenal glands),
joints, and eyes. Usually the disease begins acutely,
against the background of good health, suddenly. In
some cases, parents can specify the hour of occurrence of
the disease.
•There is an increase in body temperature to high
numbers, chills, vomiting. At an early age, convulsive
seizures, a disorder of consciousness often develop.
Within 1-2 days, all clinical manifestations gradually
increase.




Meningococcal infection. Meningococcemia.
Zvezdocheta hemorrhagic rash with surface
necrosadisme


Meningococcal infection.
Meningococcemia. stellate
hemorrhagic rash with
surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme.
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme
Meningococcal infection. Meningococcemia. Zvezdocheta hemorrhagic rash
with surface necrosadisme














Meningococcal infection. Meningococcemia.
Stellate hemorrhagic rash with surface
necrosadisme






Кровоизлияния в надпочечники

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic position

Meningitis with meningoccemia
Meningococcal infection. Meningococcemia. Stellate hemorrhagic rash with
superficial necrosis.
Loading…
Meningococcemia, hemorrhages with necrosis in the center. The
beginning of epithelialization.












Менингококковый менингит.
•This form also begins acutely with an increase in
body temperature to 39-40 °C. Children complain of
chills, pronounced diffuse headache, which increases
when moving, turning the head, light, sound stimuli.
A sick child moans, holds his head, is restless, does
not sleep well and eats, does not play. Excitement can
turn into inhibition, indifference to the surrounding
environment. Increased pain even with a light touch
to the patient-hypersensitivity is one of the leading
symptoms of meningococcal meningitis. Often in the
first days of the disease, vomiting occurs, which is
not associated with food intake. An important sign of
meningitis is convulsions,



•. On the 2nd-3rd day, meningial symptoms occur: stiffness of
the occipital muscles, a symptom of Kernig, etc. In children
under one year of age, these signs are poorly expressed, but
often there is a symptom of Lessage (if you raise the child
holding his armpits, he bends his legs), trembling of the hands,
pulsation of the large fontanelle, throwing back the head. The
child takes a characteristic pose: the head is thrown back, the
legs are pulled up to the stomach and bent at the knees. With
the addition of cerebral edema, focal symptoms may appear;
rapidly passing damage to the cranial nerves (especially III,
VI, VII, VIII pairs) , etc. Herpes rashes are also often observed
on the skin.



•Meningococcal meningoencephalitis is an inflammation of the
membranes and the brain itself. It develops more often in
young children. The disease is dominated by signs of brain
damage: impaired consciousness, motor arousal, convulsive
seizures, damage to the cranial nerves (III, IV, V, VIII pairs).
Possible development of hemiparesis-restriction of movement
in the extremities on the one hand; impaired movement,
decreased muscle tone.
•Sick children do not hold their heads, it is difficult for them to
sit and walk. Meningial symptoms are rare, most often the
most pronounced stiffness of the muscles of the back of the
head, a symptom of Kernig.















•For diagnosis, a spinal tap and the results of a
laboratory examination are of great
importance. Also used is bacterioscopic
examination of the sediment of spinal fluid and
blood smears; seeding on the nutrient media of
the cerebrospinal fluid, blood, mucus from the
nasopharynx.



•During bacteriological examination, 0.3–0.5 ml
of liquor and blood are sown on a special
medium, the answer is given on the fourth day.

•Enzyme immunoassay
(ELISA), PCR and
radioimmune research
methods are used in the
diagnosis of meningococcal
infection.

•Meningococcal infection in children of the first year of life. In
most cases, children under one year of age are dominated by
meningococcemia and its lightning-fast forms. Symptoms of
irritation of the meninges are less pronounced. Common
infectious symptoms are more typical: frequent vomiting,
general restlessness, weakness, changes in sensitivity,
trembling of the hands and chin, extensive convulsive seizures.
Children under one year of age with meningococcal meningitis
may experience unmotivated screaming, refusal to eat,
frequent repeated regurgitation, disturbed sleep, high body
temperature, increased muscle tone, but later it decreases,
severe lethargy and weakness. The most pronounced symptom
of hanging Lessage, stiffness of the occipital muscles,
followed by throwing back the head, which is why the child
occupies a characteristic positionoccupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.

occupies a characteristic position

•Purulent bacterial meningitis is characterized
by the presence of turbid liquor flowing under
high pressure, 1 ml contains more than 1000
cells with a predominance of neutrophils (60 %
or more), there is an increase in protein levels
and a decrease in glucose

•When establishing purulent bacterial meningitis, the
patient is prescribed antimicrobial therapy. When
choosing a drug, it is necessary to take into account
the age of the patient, the range of pathogens
common in this area, the resistance of circulating
strains of microorganisms, the permeability of drugs
through the blood-brain barrier
•1


Рекомендуемая терапия
0-4 Ампициллин (ампицид,
росциллин) + цефотаксим
(клафоран, клафотаксим) или
Ампициллин + аминогликозид
4-12
мес
Цефалоспорин третьего
поколения * + ампициллин
3-5 летЦефалоспорин третьего
поколения * + ампициллин

•Fight against brain edema.
•1. The regime of moderate hyperventilation (rSO 30-35 mm Hg) is the
main measure to combat brain edema, the transfer to a ventilator is
carried out at the first signs of a violation of consciousness, with normal
indicators of the gas composition of the blood.
•2. Dexazone at a dose of 0.15-0.25 mg / kg / day is recommended to be
administered no more than 3 days. It is used to prevent the progression of
cerebral edema against the background of the release of endotoxins, it is
very important to introduce hormones before the introduction of
antibiotics
•3. Lasix 0.5-1.0 mg/kg body weight.

• Regulation of external respiration
• 1. Airway sanitation, oxygen therapy
•2. Tracheal intubation, ventilator. Respiratory analeptics are
contraindicated.

• Regulation of the functions of the cardiovascular system
•1. Correction of blood pressure.
•2. Correction of paroxysmal heart rhythm disorders
•3. Therapy of background heart disease

•Simultaneously with antibiotic therapy, it is advisable to use
measures aimed at combating toxic phenomena and normalizing
metabolism.
• In this case, patients are injected intravenously with hemodesis,
rheopolyglucine, 5-10% glucose solution, albumin, etc. But
excessive infusion therapy exacerbates the picture of brain edema.
•The total volume of intravenous fluid should not exceed 30-40,
maximum 50 ml / kg of the weight of a sick child. It is better to
inject the liquid in two doses – in the morning and in the evening.
At the same time, diuretics are administered in order to remove
excess fluid (lasix, furosemide).
•In severe forms and swelling of the brain, mannitol and urea can be
prescribed. In order to improve microcirculation, heparin (100-200
units / kg of body weight per day 4 times), trental, curantil are
administered.
•In meningoencephalitis with convulsive syndrome, prednisone is
used, 2-5 mg / kg or dexazone 0.2–0.5 mg / kg for 1-3 days. Also for
seizures – seduxen, GHB, phenobarbital, aminosine, promedol.
•to give an elevated position of the head (30 o), cold to
the head, to the carotid arteriesto assess the main
physiological parameterscatheterization of the
peripheral or central vein and infusion therapy, volume
of injected solutions: up to 1.5 liters for adults, up to 50
ml / kg for childrento determine arterial blood gases, if
necessary, ventilation - hyperventilation (pCO2 25-30to
assess the severity of the patient's condition on a scale
and the level of disorder of consciousness (SAPS scale,
Glasgow scale)dehydration of lasix 0.5-1.0 mg /kg
(repeated after 8-12 hours in the absence of
hypovolemia and cerebrospinal hypotension)general
blood test, fibrinogen, APTT, APTT, electrolytes,
glucose, blood biochemistry; general urine analysis;
blood culture for sterility (3 times a day) with
determination of antibiotic sensitivity; urine culture;
ECG; chest X-rayconsultation with an infectious disease
specialist, ENT, neurologist
АЛГОРИТМ ДЕЙСТВИЙ ПРИ ПОСТУПЛЕНИИ БОЛЬНОГО С ПОДОЗРЕНИЕМ НА ГНОЙНЫЙ
МЕНИНГИТ
consciousness is preserved,
there are no violations of
vital functions
consciousness is disturbed
consultation with
an infectious
disease
specialist,ENT,
neurologistgeneral
blood test,
urinechest X-
rayblood culture,
urineelectrolytes,
glucose
LUMBAR PUNCTURE *
* in the absence of a
violation of the functions of
vital organs, the first action
is a lumbar puncture


ПРОНИЦАЕМОСТЬ АНТИБАКТЕРИАЛЬНЫХ ПРЕПАРАТОВ В
СУБАРАХНОИДАЛЬНОЕ ПРОСТРАНСТВО
ХОРОШО
ПРОНИКАЮТ
ХОРОШО ПРИ
ВОСПАЛЕНИИ
ПЛОХО ИЛИ НЕ
ПРОНИКАЮТ ДАЖЕ
ПРИ ВОСПАЛЕНИИ
ко-тримаксозол, хлорамфеникол,
рифампицин, пефлоксацин,
тетрациклин, флуконазол
бензилпенициллин, ампициллин,
оксациллин, амоксициллин,
цефтриаксон, цефотаксим,
азтреонам, меропенем,
офлаксоцин, ципрофлоксацин,
ванкомицин, амикацин
карбенициллин,
аминогликозиды, макролиды,
линкозамиды, нитрофураны
Группы препаратов Лекарственные препараты
Пенициллины
Бензилпенициллин , ампициллин, оксациллин, метициллин,
пиперациллин
Цефалоспорины
Цефуроксим, цефтриаксон, цефотаксим, цефтазидим,
цефпиром
Карбапенемы Меропенем
Аминогликозиды Гентамицин, амикацин, тобрамицин
Гликопептиды Ванкомицин, тейкопланин
Пара-нитрофенилы (фениколы)Хлорамфеникол
Нитроимидазолы Метронидазол, тинидазол, орнидазол
Фторхинолоны
Пефлоксацин, ципрофлоксацин, офлоксацин, изучается –
тровафлоксацин
Сульфаниламиды +
диаминопиримидины
Ко-тримоксазол, сульфатон и аналоги
Сульфаниламиды
Сульфазин, сульфален, сульфамонометоксин и некоторые
другие
Ди-N-окси хиноксалина Диоксидин
Химиотерапевтические препараты, которые могут применяться для
лечения бактериальных менингитов и бактериальных инфекций ЦНС
http://www.rmj.ru/rmj/t6/n22/1.htm
Предраспологающий
фактор

Возраст
Вероятные возбудители
0 – 4 нед
E.coli, L.monocytogenes, K. pneumoniae, Enterococcus spp.,
Salmonella spp.
4 – 12 нед
E.coli, L.monocytogenes, H. influenzae, S. pneumoniae,
N. meningitidis
3 мес – 5 лет H. influenzae, S. pneumoniae, N. meningitidis
5 – 50 лет N. meningitidis, S. pneumoniae
Старше 50 лет
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae
Иммуносупрессия
S. pneumoniae, N. meningitidis, L.monocytogenes,
Enterobacteriaceae, P. aeruginosa
Зависимость этиологии бактериального менингита от
возраста пациентов и преморбидного фона
Эмпирическая антимикробная терапия
бактериальных менингитов
Возраст Рекомендуемая терапия¹
0 – 4 нед
Ампициллин (ампицид, росциллин) + цефотаксим
(клафоран, клафотаксим) или ампициллин +
аминогликозид.
4 – 12 нед Ампициллин + цефалоспорин третьего поколения²
3 мес – 5 лет
Цефалоспорин третьего поколения² + ампициллин³
Ампициллин + хлорамфеникол.
5 – 50 лет Цефалоспорин третьего поколения² + ампициллин³
Старше 50 летЦефалоспорин третьего поколения² + ампициллин
¹ Ванкомицин должен быть добавлен к эмпирической терапии, если подозревается
высокая резистентность пневмококка к пенициллину или цефалоспоринам.

² Цефтриаксон (лендацин, офрамакс, роцепин) или цефотаксим

³ Добавить, если подозрение на менингит, вызванный листериями, например, у
пациентов с недостаточностью клеточно-опосредованного иммунитета.
Этиотропная антимикробная терапия при бактериальных
менингитах с идентифицированным агентом
ЭТИОЛОГИЯ ПРЕПАРАТЫ ВЫБОРА
АЛЬТЕРНАТИВНЫЕ
ПРЕПАРАТЫ¹
N meningitidis
Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Левомицетин -сукцинат
80-100 мг/кг/сут на 3
введения (не более 6,0 г)
Ципрофлоксацин 400 мг/
кг/сут в/в на 2 введения
S pneumoniae


Пенициллин 300-500 тыс.
ЕД/кг/сут в/в на 6
введений
Цефтриаксон 4,0 г/сут в/
в
Ампициллин 300 мг/кг/
сут в/в на 6 введений


Ванкомицин 2,0 г/сут., в/в
+ рифампицин 900-1200
мг/сут на 2 приема
Меропенем 3,0г/сут на 3
приема

H influenczae
Цефтриаксон 4,0 г/
сут в/в
Ампициллин 300 мг/
кг/сут в/в на 6
введений
Левомицетин -
сукцинат 80-100 мг/
кг/сут через 8 часов
Ципрофлоксацин 400
мг/кг/сут в/в на 2
введения
E coli¹
Цефтриаксон 4,0 г/
сут в/в
Ко-тримоксазол
20 мг/кг на 2
приема
Ципрофлоксацин
400 мг/кг/сут в/в
на 2 введения
Staphylococcus sp¹


Оксациллин 9,0-
12,0 г/сут в/в +
Ампициллин 300
мг/кг/сут в/в на 6
введений
Ванкомицин 2,0 г/
сут., в/в

Ванкомицин 2,0 г/
сут., в/в +
рифампицин 900-
1200 мг/сут на 2
приема
Меропенем 3,0г/сут
на 3 приема
Listeria¹
Ампициллин
300 мг/кг/сут в/в
на 6 введений

Ко-тримоксазол
20 мг/кг на 2
приема
Меропенем 3,0г/сут
на 3 приема
¹ Этиотропная терапия в зависимости от возбудителя по данным
бактериологического исследования
• cerebral edemade

•hydrationthe

•use of corticosteroids
THE REASONS FOR THE DECREASE IN THE
CLINICAL EFFECTIVENESS OF ANTIMICROBIAL
DRUGS
БАЗИСНАЯ ТЕРАПИЯ ГНОЙНЫХ МЕНИНГИТОВ , ТЯЖЕЛОЕ ТЕЧЕНИЕ
ЭТИОТРОПНАЯ
ТЕРАПИЯ
БОРЬБА С ОТЕКОМ МОЗГА И
ПРОФИЛАКТИКА ПОВЫШЕНИЯ
ВНУТРИЧЕРЕПНОГО ДАВЛЕНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
ВНЕШНЕГО ДЫХАНИЯ
РЕГУЛЯЦИЯ ФУНКЦИИ
СЕРДЕЧНО-СОСУДИСТОЙ
СИСТЕМЫ
РЕГУЛЯЦИЯ ВОДНО-СОЛЕВОГО
И КИСЛОТНО-ОСНОВНОГО
СОСТОЯНИЯ
Антимикробная терапия схема №1 и №2
ИВЛ в режиме умеренной гипервентиляции
Предпочтительно дексазон 0,15-0,25 мг/кг/сутки в/в не
более 3 сут.
Лазикс 0,5-1,0 мг/кг (повторно через 8-12 часов)
Санация дыхательных путей, установка
воздухопровода, оксигенотерапия
Интубация трахеи, при необходимости ИВЛ
Дыхательные аналептики противопоказаны
Коррекция АД
Коррекция пароксизмальных нарушений
сердечного ритма
Терапия сопутствующей патологии
сердца
Инфузионная терапия под контролем: КЩС,
осмолярности мочи и крови, электролитов крови,
уровня белка,альбуминов, ЦВД, пробы на
гидрофильность в режиме нормоволемии
при
необходимости
наблюдение
кардиологом
ПРОТИВОСУДОРОЖНАЯ
ТЕРАПИЯ
ПРЕПАРАТЫ
МЕТАБОЛИЧЕСКОГО
ДЕЙСТВИЯ
по показаниям реланиум,, гексенал,
тиопентал, пропофол, ГОМК
Рибоксин 2% - 20,0 в/в капельно
Актовегин 10,0 в/в или Неотон 1-6 г в/в

Объем парентеральной жидкости – не более 50% от
суточной дозы или равной площади поверхности тела (до 1,
7 л). Кристаллоидные растворы (квартасоль, глюкозо-
калиевая смесь) и коллоидные растворы (криоплазма,
альбумин, инфукол 6%, реополиглюкин) в соотношении 3 : 1
Объем определяется с учетом жидкости, вводимой в
желудок, под контролем почечных и внепочечных потерь
ИНФУЗИОННАЯ ТЕРАПИЯ
НЕЙРОПРОТЕКТОРНАЯ
ТЕРАПИЯ
Витамин Е 2,0 мл 3 раза в/м, Мексидол по схеме в/в капельно,
Витамин С 5% 60 мл в сутки в/в –первые 3-4 суток, далее – в
обычной дозировке, Глицин 1 г х 1 р. сублингвально , Глиатилин
1000 мг в/в 10
УЛУЧШЕНИЕ ПЕРФУЗИИ
ТКАНИ МОЗГА
УХОД ЗА БОЛЬНЫМ,
ПРОФИЛАКТИКА
ОСЛОЖНЕНИЙ
Трентал 5 – 10 мл 2 раза в/в
Эуфиллин 2,4% 7,0 мл 2 раза в/в
Профилактика гипостатической пневмонии,
тромбоэмболии легочной артерии, пролежней,
гнойной язвы роговицы, ранних контрактур

•Наиболее часто выделяют следующие
микроорганизмы:
•1) при гнойных менингитах: менингококк,
пневмококк,стафилококк золотистый, стрептококки
групп А, В, D, Н, бактерии коли, протеус,псевдомонос и
др.;
•2) при асептических менингитах: туберкулезная
палочка,возбудитель лептоспироза, токсоплазмоза,
вирусы.