01 Pneumonia and its classifications.ppt

pneumonia and its types

1. Pneumonia

2. Definition

• Pneumonia is an
acute infection of the
parenchyma of the
lung(肺实质), caused by
bacteria, fungi(真菌）,
virus, parasite（寄生虫）
etc.
• Pneumonia may also be
caused by other factors
including X-ray,
chemical, allergen

3. Epidemiology
The morbidity and mortality of
pneumonia are high especially in old
people.

4. Etiology
There are two
factors involved in
the formation of
pneumonia ,
including pathogens
and host defenses.

6. Classification
Classification of anatomy
Classification of pathogen
Classification of acquired environment

7. Ⅰ.Classification by pathogen
Pathogen classification is the most
useful
to treat the patients by choosing
effective
antimicrobial agents

8. Bacterial pneumonia
(1) Aerobic Gram-positive bacteria,such
as streptococcus pneumoniae, staphy-
lococcus aureus, Group A hemolytic
streptococci
(2) Aerobic Gram-negative bacteria, such
as klebsiella pneumoniae, Hemophilus
influenzae, Escherichia coli
(3) Anaerobic bacteria

9. Atypical pneumonia
Including Legionnaies pneumonia ,
Mycoplasmal pneumonia ,chlamydia
pneumonia.

10. Fungal pneumonia
Fungal pneumonia is commonly
caused by candida(念珠菌) and
aspergilosis(曲菌).
pneumocystis jiroveci（肺孢子虫）

11. Viral pneumonia
Viral pneumonia may be caused by
adenoviruses, respiratory syncytial
virus, influenza, cytomegalovirus,
herpes simplex

12. Pneumonia caused by
other pathogen
Rickettsias (a fever rickettsia),
(立克次体）
parasites(寄生虫)
protozoa（原虫）

13. Ⅱ.Classification by anatomy
1. Lobar（大叶性） : Involvement of an
entire lobe
2. Lobular（小叶性） : Involvement of parts
of the lobe only, segmental or of alveoli
contiguous to bronchi
(bronchopneumonia).
3. Interstitial（间质性）

14. Lobar pneumonia

15. Lobular pneumonia

16. Interstitial pneumonia

17. Classification by acquired
environment
Community acquired pneumonia，CAP
（社区获得性肺炎）
Hospital acquired pneumonia，HAP ，NP
（医院获得性肺炎）
Nursing home acquired pneumonia,NHAP
 (护理院获得性肺炎）
Immunocompromised host pneumonia,(ICAP)
(免疫宿主低下肺炎）

18. Diagnosis（诊断步骤）
Give a definite diagnosis of pneumonia
To evaluate the degree of the
pneumonia
To definite the pathogen of the
pneumonia

19. Diagnosis
History and physical
examination(5W)
X-ray examination
Pathogen identification

20. Differentiation
Pulmonary tuberculosis
Lung cancer
Acute lung abecess
Pulmonary embolism
Noninfectious pulmonary infiltration

21. Pathogen identification
Sputum: More than 25 white blood cells
(WBCs) and less than 10 epithelial cells.
Nasotracheal suctioning
BAL, ETA, PSB, LA
Blood culture or pleural effusion culture
Serologic testing (immunological testing)
Molecular Techniques

22. The principal of therapy
Select antibiotics
According to guideline

23. Therapy
The therapy should always follow
confirmation of the diagnosis of
pneumonia and should always be
accompanied by a diligent effort to
identify an etiologic agent.
Empiric therapy,(4-8h)
Combined empiric therapy to target
therapy

24. It is important to evaluate the
severity degree of pneumonia
The critical management decision is
whether the patient will require hospital
admission. It is based on patient
characteristics, comorbid illness,
physical examinations, and basic
laboratory findings.

25. The diagnostic standard of sever
pneumonia
Altered mental status
Pa02<60mmHg. PaO2/FiO2<300, needing MV
Respiratory rate>30/min
 Blood pressure<90/60mmHg
Chest X-ray shows that bilateral infiltration,
multilobar infiltration and the infiltrations
enlarge more than 50% within 48h.
Renal function: U<20ml/h, and <80ml/4h

26. CAP (社区获得性肺炎）
CAP refers to pneumonia acquired outside of
hospitals or extended-care facilities .
Streptococcus pneumoniae remains the most
commonly identified pathogen.
Other pathogens include Haemophilus influenzae,
mycoplasma pneumoniae, Chlamydophilia
pneumoniae, Moraxella catarrhalis and ects.
Drug resistance streptococcus
pneumoniae(DRSP)

27. Clinical manifestation
The onset is accute
Respiratory symptoms
Extrapulmonary symptoms

28. signs
Consolidation signs
Moist rales
Respiratory rate or heart rate

29. Laboratory examination
WBC
X-ray features

30. Diagnosis
Clinical diagnosis
Pathogen diagnosis
Evaluate the severity degree of
pneumonia

31. Therapy
Antiinfectious therapy(Combined
empiric therapy to target therapy)
Supportive therapy

32. Empiric therapy (1)
Outpatient<60 years
old and no comorbid
diseases
Common pathogens:
S pneumoniaes,
M pneumoniae,
C pneumoniae,
H influenzae and
viruses
A new generation
macrolide
A beta-lactam: the
first generation
cephlosporin
A fluoroquinolone

33. Empiric therapy (2)
Outpatient>65 years old or
having comorbid diseases
or antibiotic therapy within
last 3 months
Common pathogens: S
pneumoniae(drug-
resistant), M pneumoniae,
C pneumoniae, H
pneumoniae, H
influenzae, Viruses,
Gram-negative bacilli and
S aureus
A fluoroquinolone
A beta-lactam / beta-
lactamase inhibitor
The second generation
cephalosporin
or combination of a
macrolide

34. Empiric therapy (3)
Inpatient : Not
severely ill.
Common pathogen:S
pneumoniae, H
influenzae,
polymicrobial,
Anaerobes, S aureus,
C pneumoniae,
Gram-negative bacilli.
The second or third
generation
cephalosporin plus
A macrolide
A
beta-lactam/betalact
amase inhibitor.
A newer
fluoroquinolone

35. Empiric therapy (4)
Inpatient severely ill
Common pathogens:S
pneumoniae, Gram-
negative bacilli, M
pneumoniae, S aureus
and viruses
The second or third
generation
cephalosporin plus A
macrolide
A
beta-lactam/betalactam
ase inhibitor.
A newer
fluoroquinolone
Vancomycin

36. Empiric therapy (5)
Patients in ICU without
Pneudomonas
aeruginosa infection
The second or third
generation
cephalosporin plus A
macrolide
A
beta-lactam/betalactam
ase inhibitor.
A newer
fluoroquinolone
Vancomycin

37. Empiric therapy (6)
Patients in ICU with
Pneudomonas
aeruginosa infection
A antipneudomonas
aeruginosa beta-
lactam/betalactamas
e inhibitor plus
fluoroquinolone

38. prognosis
preventive

39. HAP（医院获得性肺炎）
HAP refers to pneumonia acquired in
the hospital setting.
Enteric Gram-negative organisms, S.
aureus, Pneudomonas aeruginosa,
ects.

40. The pathogen of HAP

Gram-negative bacteria (GNB) account
for 55% to 85% of HAP infections
 gram-positive cocci account for 20% to
30% and some other pathogens.

41. EPIDEMIOLOGY
General risk factors for
developing HAP include age
more than 70 years, serious
comorbidities, malnutrition,
impaired consciousness,
prolonged hospitalization, and
chronic obstructive pulmonary
diseases.

42. EPIDEMIOLOGY
HAP is the most common infection occurring in
patients requiring care in an intensive care unit
(ICU), with incidence rates ranging from 6% up to
52%, much higher than the 0.5% to 2%
incidence reported for hospitalized patients as a
whole.
This increased incidence is due to the fact that
patients located in an ICU often require
mechanical ventilation, and mechanically
ventilated patients are 6 to 21 times more likely to
develop HAP than are nonventilated patients.
Mechanical ventilation is associated

43. PATHOGENESIS
 Aspiration :Microaspiration of
contaminated oropharyngeal secretions
seems to be the most important of
these factors, as it is the most common
cause of HAP.
Inhalation
Contamination

44. Clinical manifestations
The onset is acute or insidious
Respiratory symptoms
Physical signs

45. Laboratory examinations
Chest X-ray

46. diagnosis
Clinical diagnosis
Pathogen diagnosis
Evaluate the severity degree of
pneumonia

47. Treatment (1)
Antibiotic therapy: antimicrobial therapy begin
promptly because delays in administration of
antibiotics have been associated with worse
outcomes.
The initial selection of an antimicrobial agent
is almost always made on an empiric basis
and is based on factors such as severity of
infection, patient-specific risk factors, and
total number of days in hospital before onset.

48. Treatment (2)
All empiric treatment regimens should
include coverage for a group of core
organisms that includes aerobic gram
negative bacilli (Enterobacter spp,
Escherichia coli, Klebsiella spp, Proteus
spp, Serratia marcescens, and
Hemophilus influenzae) and gram-positive
organisms such as Streptococcus
pneumoniae and Staphylococcus aureus.

49. Treatment (3)
In patients with mild or moderate infections and
no specific risk factors for resistant or unusual
pathogens, monotherapy with a second-
generation cephalosporin such as cefuroxime; a
nonpseudomonal third-generation cephalosporin
such as ceftriaxone; or a beta-lactam/beta-
lactamase inhibitor such as
ampicillin/sulbactam, ticarcillin/clavulanate, or
piperacillin/tazobactam may be appropriate.
For patients in this low-risk category who have
an allergy to penicillin, it is appropriate to initially
use a fluoroquinolone

50. Treatment (4)

Patients with severe infections with specific risk
factors should have broadened empiric coverage.
Combination therapy should be employed in these
cases because of the high rate of acquired resistance
among these organisms.
Appropriate combinations for this group of patients
include an aminoglycoside or ciprofloxacin in addition
to a beta-lactam with antipseudomonal coverage.
Additionally, vancomycin should be considered if the
patient has risk factors that suggest methicillin-
resistant Staphylococcus aureus could be a pathogen.

51. Prevention
Release aspiration
Washing hands
vaccination

52. ICHP (免疫低下宿主肺炎 )
Pneumonia in an immunocompromised
host describes a lung infection that
occurs in
a person whose ability to fight infection
is greatly impaired.
(Non-HIV-ICH)

53. Causes, incidence, and risk
factors
Immunosuppression can be caused by HIV
infection, leukemia, organ transplantation,
bone marrow transplant, and medications to
treat cancer.
Microorganisms include all kinds of bacteria
and virus(CMV), candida(念珠菌) and
aspergilosis(曲菌).
pneumocystis carinii（PCP,卡氏肺孢子虫
）

54. Symptoms
The onset is incidous , but clinical
Symptoms are severe.
Fever
Nonproductive (dry) cough or cough with
mucus-like, greenish, or pus-like sputum
PCP
Fungal infection

55. Diagnosis
Earlier finding and diagnosis
 Pathogen diagnosis
Chest x-ray
Sputum gram stain, other special stains, and
culture
Arterial blood gases
Bronchoscopy
Chest CT scan,
Tissue diagnosis

56. Treatment
Antimicroorganism therapy
The goal of treatment is to get rid of the infection
with antibiotics or antifungal agents. The specific
drug used will depend on what kind of organism
is causing the problem. One drug may kill one
type of organism, but not another.
Respiratory treatments (to remove fluid and
mucus) and oxygen therapy are often needed.

57. Pneumococcal pneumonia

58. Abstraction
• Pneumococcal
pneumonia is
produced by
streptococcal
pneumoniae
• It is the most
commonly occurring
bacterial
pneumonia

59. Etiology
• Streptococcus pneumonia are
encapsulated,
gram-positive cocci that occur in
chains or
pairs
• The capsule which is a complex
polysaccharide
has specific antigenicity
• Type 3 is the most virulent,
usually causing
severe pneumonia in adults, but
type 6,14,19
and 23 are virulents is children

60. Bacteria are introduced into the
lungs by the four routes
Source Route Response Outcome
colonization aspiration
Air inhalation
Non-pulmonary blood lung pneu.
infection stream defenses
Contiguous direct
 infection extention

61. pathogenesis
Pneumococci usually
reach the lungs by
inhalation or
aspiration. They
lodge in the
bronchioles,
proliferation and
initiate an
inflammatory process.

62. Pathology
Congestion
red hepatization
grey hepatization
resolution)

63. Pathology
Red hepatilization

64. ◆
All of the four main stages of the
inflammatory
reaction described above may be present at
the
same time
◆ In most cases, recovery is complete with
restoration of normal pulmonary anatomy

65. Clinical manifestations

66. Clinical manifestations (1)
• Many patients have had an upper respiratory
infection for several days before the onset of
pneumonia
• Onset usually is sudden, half cases with a
shaking chill
• The temperature rises during the first few
hours to 39-40
℃

67. Clinical manifestations (2)
Typically, patients have the symptoms
of high fever , shaking chill, sharp
chest pain, cough, dyspnea and
blood-flecked sputum.
But in some cases, especially those at
age extremes symptoms may be
more insidious.

68. • The pulse accelerates
• Sharp pain in the involved hemi thorax
• The cough is initially dry with pinkish or
blood-flecked sputum
• Gastrointestinal symptoms such as,
anorexia, nausea, vomiting abdominal
pain, diarrhea may be mistaken as acute
abdominal inflammation
Clinical manifestations (3)

69. Signs
1
• The acutely ill patient is tachypneic, and
may be observed to use accessory muscles
for respiration, and even to exhibit nasal
flaring
• Fever and tachycardia are present, frank
shock is unusual, except in the later stages
of infection or DIC

70. Signs 2
• Auscultation of the chest reveals
bronchovesicular or tubular breath
sounds and wet rales over the
involved lung
• A consolidation occurs, vocal and
tactile fremitus are increased

71. Laboratory examinations

72. Laboratory examinations (1)
• The peripheral white blood cell (WBC) count
• Before using antibiotic, the culture of blood and
of expectorated purulent sputum between 24-48
hours can be used to identify pneumococci
• Colony counts of bacteria from bronchoalveolar
lavage washings obtained during endoscopy
are
seldom available early in the course of illness
• Use of the PCR may amplify pneumococcal
DNA and improve potential for detection

73. X-ray examination
• Chest radiographs is more sensitive than

physical examination
• PA and lateral chest radiographs are
invaluable to detect pneumonia

74. X-ray examination
• Usually lobar or
segmental
consolidation
suggests a bacterial
cause for pneumonia
• If blunting of the
costophrenic angle is
noted, pleural
effusion may be
exist.

75. The features of CT
Air-bronchogram sign

76. Complications
In 5% to 10% of patients, infection may extend into the
pleural space and result in an empyema （脓胸）
In 15% to 20% of patients, bacteria may enter
the blood stream (bacteremia) via the lymphatics
and thoracic dust.
Invasion of the blood stream by pneumococci
may lead to serious metastatic disease at a
number of extra pulmonary sites (meningitis,
arthritis, pericarditis, endocarditis, peritonitis,
ostitis media etc).

77. Complications
sepsis （脓毒性休克）
lung abscess（肺脓疡） or
empyema
pleural effusion（胸腔积液）
pleuritis
ARDS（急性呼吸窘迫综合征）
ARF（急性呼吸衰竭）
pneumothorax（气胸）
Extrapulmonary infections

78. Diagnosis
According to history, the clinical signs ,
physical examinations, laboratory
examinations and radiographic
features
it is not difficult to make the diagnosis

79. Differential diagnosis
• pulmonary tuberculosis
• Other microbial pneumonias:
klebsiella pneumonia,
staphylococal pneumonia,
pneumonias due to G (-) bacilli,
viral and mycoplasmal
• Acute lung abscess
• Bronchogenic carcinoma
• Pulmomary infarction

80. Treatments
Antibiotics
Support therapy
Therapy of complications

81. Antibiotic therapy (1)
• All patients with suspected pneumococcal
pneumonia should be treated as promptly as

possible with penicillin G
• The dose and route of delivery may have to
be on the basis of patients status adverse
rea-
ction or complication that occur

82. • For patients who are believed to be
allergic to penicillin, one may select the
first or second generation cephalosporin
or advanced macrolide+ β -lactam or
respiratory fluoroquinolone alone.
For patients with PRSP, one may select the
second and third generation
cephalosporin or advanced macrolide+ β -
lactam or respiratory fluoroquinolone
alone.
In some cases, vancomycin may be used.
Antibiotic therapy (2)

83. Antibiotic therapy
• Treatment with any effective agent
should be given for at least 5 to 7
day or after the patients have been
afebrile for 2-3 days

84. Supportive measure
Supportive measure are generally used in
the initial management of acute pneumo-
coccal pneumonia, such measures include
• Bed rest
• Monitoring vital signs and urine output
• Administering an occasional analgesic to
relieve pleuritic pain
• Replacing fluids, if the patient is dehydrated
• Correcting electrolytes
• Oxygen therapy

85. Treatment of complications
• Empyema develops in appoximately 5% of patients
with pneumococcal pneumonia, although pleural
effusion commonly develop in 10%- 20% patients
• Chest X-ray with lateral decubitus films are often
useful in the early recognition of pleural effusion,
pleural fluid that is removed should be subjected to
routing examination
• If pneumococcal bacteremia occurs, extra pulmonary
complications such as arthritis, endocarditis must be
excluded, because the therapy requires higher dosages
• Treatment of infections shock

86. Prognosis
Prognosis is much better
Any of the following factors makes the prognosis
less favorable and convalescence more prolonged
elderly
• involvement of 2 or more lobes
• underlying chronic diseases (heart lung
kidney) normal temperature and WBC
count <5000
• immunodeficiency with severe complication

87. Prevention
The most important
preventive tool available
is using a poly valent
pneumococcal vaccine
in those with chronic
lung diseases, chronic
liver diseases,
splenectomy, diabetes
mellitus
and aged

88. Staphylococcus pneumonia
• Staphylococcal
pneumonia is usually
caused by
staphylococcus
aureus
• It is often a
complication of influenza,
but may be
primary, particularly in
infants and the aged
•

89. It occurs in immunocompromissed patients such as
diabetes mellitus
hematologic disease ( leukemia, lymphoma,
leukopenia )
AIDS, liver disease, malnutrition, alcoholism
• Staphylococcal bacteremia complicating
infections at
other sites (furuncles, carbuncles) may cause
hematogenous pulmonary involvement (due to
blood
spread)

90. • Some or all of the symptoms of pneumococcal
pneumonia (high fever, shaking chill, pleural pain,
productive cough) may be present, sputum may be
copious and salmon-colored
• Prostration is often marked
• According the symptoms, signs of pneumonia,
leukocytosis and a positive sputum or blood
culture, the diagnosis can be made

91. • Gram stain of the
sputum provides
earliest
diagnostic clue
• Chest X-ray early in
the disease shows
many small round
areas of densities that
enlarge and coalesce
to from abscess, and
leave evidence of
multiple cavities

92. • Until the sensitivity results are know, a
penicillinase–resistant penicillin or a
cephalosporin should be given
• Therapy is continued for 2 weeks after
the patient has become afebrile and the
lungs have shown signs of clearing
• Vancomycin is the drug of choice for
patients allergic to penicillin and cepha-
losporin and for those not responding to
other antistaphylococcal drugs, mainly used in MRSA.

93. Pneumonia caused by klebsiella
Klebsiella pneumonia ( also named
Friedlander
pneumonia) is an acute lung infection, caused
by
Klebsiella pneumoniae 1, it occurs much more
in
aged, malnutrition, chronic alcoholism, and
in
whom with bronchial pulmonary disease

94. • This pneumonia is most likely to be found in
man with middle age, onset usually is
sudden,
with high fever, cough, pleuritic pain, abundant
sputum, cyanosis, tachycardia my be present,
half cases with a shaking chill
• Shock appears in early stage

95. • Clinical manifestations are similar to sever
pneumococcal pneumonia
• The sputum is viscid and “ropy”, and may be
“brick red” in color
• Chest X-ray shows a downward curve of the
horizontal interlobar fissure, if the right
upper lobe is involved
• Areas of increased radiance whithin dense
consolidation suggest cavitation
• It constitutes 2% of bacterial pneumonia,
but mortality may be as high as 30%

96. • When an elderly patient suffered from acute
pneumonia with sever toxic symptom, viscid
and “brick red”, sputum must consider this
disease
• The diagnosis is determined by bacterial
examination of sputum
• Early using antimicrobial therapy is im-
portant for patients with survivable ill-
illnesses, aminoglycoside (Kanamycin, Amikacin,
Gentamycin ) and the third generation cephalosporin are
often used.

97. Mycoplasmal pneumonia
• Mycoplasmal pneumonia is caused
by Mycoplasmal
pneumoniae
• Mycoplasmal pneumoniae is one
of the smallest
organisms 125-150 μm capable of
replication in
cell-free media
• Infection is spread form person
to person by
respiratory secretions expelled
during bouts of
coughing, causing epidemic or
sporadic occurance

98. • It commonly occurs in children, adolescent, mainly
in fall and winter
• It constitutes more than 1/3 of non bacterial
pneumonias, or 10% of pneumonias from all cause
• Cellular infiltrate around bronchioles, and in
alveolar interstitium, consists mostly of mono-
nuclear elements

99. Clinical findings
• The illness begins insidiously with
constitutional
symptomatology:
malaise, sore throat, cough, fever,
myalgia
• Half of cases have no symptom
•

100. Chest X-ray
Chest X-ray findings are
manifold
• Most patients have
unilateral lower lobe
segmental abnormalities
• The earliest signs are an
interstitial accentuation
of marking with
subsequent patch air
space
consolidation and
thickened bronchial
shadows

101. • The pneumonia may persist for 3-4 weeks
a slight leukocytosis is seen, with a normal
differential count
• The diagnosis is generally proved by a single
antibody titer of 1:32 or greater, a titer of
cold agglutinins of 1:32 or greater a single
Ig M determination
• The most promising in terms of speed,
sensitivity and specificity is PCR although
cost and lack of general availability limit its
routine use

102. Therapy
A definite clinical response
is seen to erythromycin and
some other newer macrolide

103. Legionnaies Pneumonia
Legionella can be an opportunistic
pathogen.
Patients with immunosuppression
are at increased risk for infection.
But sometimes outbreaks do occur
in previously healthy individuals.

104. Legionellae are small,
gram-negative,
obligately aerobic
baclli.
.

105. Legionnaires’ disease is
acquried by inhaling
aerosolized water
containing Legionella
organisms or possibly by
pulmonary aspiration of
contaminated water.
The contaminated water are
derived from humidifiers,
shower heads, respiratory
therapy equipment,
industrail cooling water.
Because of the frequently use
of air conditioner,
Legionnaies pneumonia is
also seen in CAP

106. Clinical manifestations
The onset of L.pneumonia is
sometimes severe.
High fever, rigors, and significant
hypoxemia are usually seen in
patients with L.pneumonia.
Failure to rapidly appropriate therapy
in these cases is likely to result in a
poor outcome.

107. Common signs include cough,
dyspnea, pleuritic chest pain,
gastrointestinal symptoms,
especially diarrhea or localized
abdominal pain, nausea, vomitting
are a prominent finding in 20% to
40% of patients with L.pneumonia.

108. Physical examination
Physical finding are often similar to
other pneumonias.
Rales are usually present over
involved areas
Pulse rate is not coincide to the body
temperate.

109. Chest X-ray
No diagnostic features on
the chest X-ray
distinguish it from other
pneumonia
Infiltrates can be
unilateral, bilateral,
patchy, or dense, and can
spread very quickly to
involve the entire lung,
pleural effusion, usually
small in volume occurs
Routine laboratory tests
also are nonspecific.

110. Laboratory examination
Serologic testing is the most often
used for establishing a diagnosis.
A fourfold or greater rise in antibody
is considered definitively exist for
Legionella.

111. Diagnosis
According to history, clinical signs,
X-ray features and serologic testing,
we can diagnose it.

112. Therapy
Erythromycin is considered the drug
of choice.It should be given until
clinical improvement is seen.It
usually lasts 2-3 weeks.

113. Candidiasis
Candidiasis is an opportunistic
disease, it is caused by candida.

114. Clinical signs
Respiratory signs: fever,cough, sputum
production, dyspnea.
X-ray shows no specific.It is similar to
acute pneumonia.

115. diagnosis
Mainly according to sputum culture or
biopsy of lung.

116. Therapy
Nystatin or various azole drugs

117. Aspergillosis
Aspergillosis refers to infection with any
of species of the genus Aspergillus

118. Clinical signs
The disease generally occurs in
immunosuppressed and anticancer
therapy patients.
There are four types of pulmonary
aspergillosis.

119. Clinical signs of Pulmonary
aspergillosis
Presents as chronic productive cough,
hemoptysis, dyspnea, weight loss, fatigue,
chest pain, or fever
Sometimes patients with pulmonary
aspergillosis accompany with prior chronic
lung disease.
Typical picture of an aspergilloma is a
fungus ball in a cavity in an upper lobe
The sputum culture is positive in most
patients.

120. Diagnosis
The repeated isolation of Aspergillus
from sputum or the demonstration of
hyphae in sputum or BALF suggests
endobronchial infection.

121. Treatment
With intravenous amphotericin B (1.0
to 1.5 mg/kg daily)
Patients with severe hemoptysis due
to fungus ball of lung may benefit
from lobectomy

122. Therapy to Infectious Shock
Treatment in intensive care units
cardiac rhythm, blood pressure, cardiac performance, oxygen
delivery, and metabolic derangements can be monitored
Adequate oxygenation and ventilatory support
(sometimes mechanical ventilation)
Effective antibiotic therapy
Maintain blood pressure, including maintain
circulation blood volume, use of dopamine

123. Summary
1.肺炎的定义
2.肺炎的分类
3.CAP和HAP的定义和常见的病原体
4.肺炎球菌肺炎的典型的临床表现和影
象特点及其治疗原则
5.各种病原体肺炎的治疗原则
6.感染性休克的治疗原则

124. Questions
1.What is the differences between CAP
and HAP?
2.What is the standard of sever
pneumonia?
3.what are the principals of antibiotic
therapy of various of pneumonias?

125. Case report
患者,男性,32岁
主诉:发热伴咳嗽 6天
现病史:患者于6天前劳累后出现发热 ,体温
最高达39 ,
℃
稍有畏寒 ,自服退热药后热退 ,之
后体温又上升 ,达38 ,
℃
伴有咳嗽 ,痰为白色黏
液样,偶呈黄脓性 ,遂于我院就诊 ,胸部X线
显示:左下肺片状高密度影 ,外周血白细胞
6.0*10
9
/L,N66.2%,在门诊予与亚星和左克抗
感染3天,体温不退 ,行胸部CT检查示:左下
肺片状密度增高影。故收入院进一步诊治。

126. 入院体检
神清，一般可， T：38
℃
，P90次/分
，R18次/分，BP110/70mmHg，口
唇无紫绀，全身浅表淋巴结未及肿大，
颈软，两肺呼吸音粗，未及干湿罗音，
腹软，无压痛，双下肢无浮肿， NS(-)

127. 辅助检查
血支原体抗体 IgM１：160
胸片
胸部CT

128. 胸片

129. 胸部CT

130. case2
患者，男性， 50岁
主诉:咳嗽伴咳黄痰二十余天
现病史:患者于入院前二十余天开始无明显诱因下出现
咳嗽,咳黄脓痰 ,量中,无咯血,胸痛和呼吸困难等其他
呼吸系统症状。四天后出现发热一次，体温未测，自服
安乃近后热平，但一直有夜间出汗较多伴乏力，遂于当
地医院就诊，胸片示两肺多发阴影，拟肺炎后于次日来
我院行CT（见CT结果），为进一步诊治入院。
追问病史患者于入院约半年前
确诊天疱仓，遂开始服 用
强
地松片
30mg/d,后因病
情反复增加用量，并于入院前
２月加用硫唑嘌呤２
片／
d

131. 入院体检、辅助检查
体检无特
殊阳性体征
胸部
ＣＴ检查

132. How do we
diagnose?

133. 选择题
1．
男性，
58 岁，有
慢性咳嗽、咯痰史
15
年，1 周来高热
、咯红砖色胶冻样痰，伴气急
紫绀，
谵妄，本 例可能性最大的诊断 是：
B
A、
肺炎球菌肺炎
B、
克雷白杆菌肺炎

C、浸润
型肺结核
D、
病毒性肺炎
E、
支原体肺炎

134. 2．
男性，
35 岁，发热
、寒颤
3 天，体温
39 度，胸片示
右上肺大片阴影，痰 涂片见较
多
革兰氏阳性成对 或短链状球菌，这时治疗首
选
？
C
A、头
孢唑啉
B、丁胺
卡那霉素
C、青霉素

D、氟哌酸

E、红霉素

135. 3．
肺炎球菌肺炎在病 变消散后肺组织结
构
：
E
A、纤维组织
增生
B、
有小空洞残留
C、
肺泡壁水肿
D、局
部支气管扩张
E、
肺泡壁无损坏

136. 4．
男，
20 岁，低热
咽痛，咳嗽半 月入院，咳嗽 甚剧
，为
刺激性干咳，体检：
T37.8 度，
咽充血，心肺无
阳
性体征，化验：
WBC：8＊10^9/L，中性 70％
，X 线胸片示
右下肺间质性炎 变，间有小片状阴影，
以
下哪 项检查对明确诊断意义较大？
E
A、
痰细菌培养
B、咽拭
子细菌培养
C、
痰查抗酸杆菌
D、
结核菌素试验
E、冷凝集试验

137. 5．
患者，
25 岁，
女性，咽痛，咳嗽，乏力，四肢 肌
肉疼
痛，中等发热，双肺呼吸音稍粗，未 闻罗音，白
细胞 9.6＊10^9/L，中性 86％
，胸片示：左下肺部
斑
片状浸润阴影，血清 冷凝集试验 ：
1：64 阳
性，
最
好 应选择的治疗药物是：
E
A、
抗结核药
B、青霉素

C、头
孢菌素
D、氨基甙
类抗生素
E、红霉素

138. 6.军团
菌肺炎首选的抗生素是
:A
A.红霉素
B.青霉素
C.头
孢菌素
D.丁胺
卡那霉素
E.氯霉素

139. 7．
肺炎球菌 致病力的主 要因素是
E
A．
肺炎球菌 内毒素
B．
肺炎球菌外毒 素
C．
肺炎球菌菌体 蛋白质
D. 肺炎球菌
迅速繁殖
E．
肺炎球菌 含高分子多 糖体荚膜对组
织
的侵袭力

140. 8．
治疗肺炎球菌肺炎 首选抗生素是
B
A 红霉素

B．青霉素
C．丁胺
卡那霉素
D．氯霉素
E．羧苄青霉素

141. 9．
男性，
25岁，因
受凉后突起畏寒、发热
(39.2度)。左
侧
胸痛伴咳嗽，咯 少量铁锈色痰，胸部
X线
摄
片见左下肺
野大片淡薄阴影。其最可 能的诊断
是
：
C
A.金
黄色葡萄球菌肺炎
B．
结核性胸膜炎
C．
肺炎球菌肺炎
D原发性支气
管肺癌合并阻塞性肺炎
E．
急性原发性肺脓疡

142. 9．
肺炎球菌肺炎患者在抗生 素治疗下体
温
接近正常后反又升高，白细胞增高，
首先考虑
：
E
A．
细菌产生耐药
B．
抗生素用量不足
C．
药物热
D．加用
退热药
E．
出现并发症

143. 10.肺炎球菌肺炎的炎症发
展最高峰是：
A
A.灰
色肝样变期
B.消散期
C.红
色肝样变期
D.病
变组织的机化
E.充
血期