11 Gastrointestinal disorders.pdfyjjgfghu
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May 14, 2025
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About This Presentation
Ppt
Slide Content
CHAPTER 11
GASTROINTESTINAL DISORDERS
Learning objectives
At the end of this lesson, the learner will able to;
1.Identify the etiology of GI disorders
2.Describe the pathophysiology of GI disorders
3.Identify the clinical features of GI disorders
4.Diagnose pediatric gastrointestinal disorders
5.Write the complication of GI disorders
6.Explain their nursing and medical management
1
GASTROINTESTINAL DISORDERS
Learning objectives
At the end of this lesson, the learner will able to;
1.Identify the etiology of GI disorders
2.Describe the pathophysiology of GI disorders
3.Identify the clinical features of GI disorders
4.Diagnose pediatric gastrointestinal disorders
5.Write the complication of GI disorders
6.Explain their nursing and medical management
1
Oral and Esophageal Lesions
Oropharyngeal candidiasis or oral thrush
• is infection of the oral cavity with C. albicans.
•it presents as white to gray patches that cover
the buccal mucosae, tongue, and gingivae.
2
Oropharyngeal candidiasis or oral thrush
• is infection of the oral cavity with C. albicans.
•it presents as white to gray patches that cover
the buccal mucosae, tongue, and gingivae.
2
oral thrush....
•is common in neonates from contact with the
organism in the birth canal or breast.
•The diagnosis is confirmed by direct
microscopic examination on potassium
hydroxide smears and culture of scrapings from
lesions.
•Usually self limited, most will resolve
spontaneously with in four to eight weeks
3
•is common in neonates from contact with the
organism in the birth canal or breast.
•The diagnosis is confirmed by direct
microscopic examination on potassium
hydroxide smears and culture of scrapings from
lesions.
•Usually self limited, most will resolve
spontaneously with in four to eight weeks
3
Oropharyngeal Candidiasis(OPC)…..
Treatement: nystatin, miconazole, or
- clotrimazole applied four times daily.
•topical application of nystatin to the oral cavity
of the baby and to the nipples of breast-feeding
mothers will hasten recovery.
•The use of oral rinses of 0.2% chlorhexidine
solution, plus systemic antifungals may be
effective in preventing OPC
4
Treatement: nystatin, miconazole, or
- clotrimazole applied four times daily.
•topical application of nystatin to the oral cavity
of the baby and to the nipples of breast-feeding
mothers will hasten recovery.
•The use of oral rinses of 0.2% chlorhexidine
solution, plus systemic antifungals may be
effective in preventing OPC
4
Infective Esophagitis
•Uncommon,
•Common in immunocompromised children,
•caused by fungal agents, such as Candida and
Torulopsis glabrata;
•viral agents, such as herpes simplex,
cytomegalovirus, HIV, and varicella zoster;
• rarely, bacterial infections, including
diphtheria and tuberculosis.
5
•Uncommon,
•Common in immunocompromised children,
•caused by fungal agents, such as Candida and
Torulopsis glabrata;
•viral agents, such as herpes simplex,
cytomegalovirus, HIV, and varicella zoster;
• rarely, bacterial infections, including
diphtheria and tuberculosis.
5
Infective Esophagitis….
The typical presenting signs and symptoms are;
• odynophagia (Painful on swallowing)
•dysphagia, and
• retrosternal pain;
•there may also be fever, nausea, and vomiting.
•Esophageal candidiasis manifests as concurrent
oropharyngeal infection in 11% of patients,
•occasionally progresses to esophageal stricture.
6
The typical presenting signs and symptoms are;
• odynophagia (Painful on swallowing)
•dysphagia, and
• retrosternal pain;
•there may also be fever, nausea, and vomiting.
•Esophageal candidiasis manifests as concurrent
oropharyngeal infection in 11% of patients,
•occasionally progresses to esophageal stricture.
6
Infective Esophagitis….
Diagnosis by ;
•endoscopy (ulcerations, exudates) and
•histopathologic examination;
•polymerase chain reaction,
• tissue-viral culture
Treatment is with appropriate antimicrobial
agents, analgesics, and antacids.
7
Diagnosis by ;
•endoscopy (ulcerations, exudates) and
•histopathologic examination;
•polymerase chain reaction,
• tissue-viral culture
Treatment is with appropriate antimicrobial
agents, analgesics, and antacids.
7
Esophageal varices
• Portal hypertension (PH): elevation of portal
venous pressure to levels 10-12 mmHg than SVC.
•PH +coronary vein in conjunction with the left
gastric veins gives rise to esophageal varices.
•Most esophageal varices are “uphill varices”;
•those that arise in the absence of portal
hypertension and with superior vena cava
obstruction are “downhill varices.”
• Hemorrhage from esophageal varices is the major
cause of morbidity and mortality due to portal
hypertension.
8
• Portal hypertension (PH): elevation of portal
venous pressure to levels 10-12 mmHg than SVC.
•PH +coronary vein in conjunction with the left
gastric veins gives rise to esophageal varices.
•Most esophageal varices are “uphill varices”;
•those that arise in the absence of portal
hypertension and with superior vena cava
obstruction are “downhill varices.”
• Hemorrhage from esophageal varices is the major
cause of morbidity and mortality due to portal
hypertension.
8
Esophageal varices…..
Clinical features
•Hematemesis, and melena(black stool);
•most patients have liver disease,
•some children with extrahepatic portal venous
thrombosis
•Any child with hematemesis and splenomegaly;
-should be presumed to have esophageal variceal
bleeding until proved otherwise.
9
Clinical features
•Hematemesis, and melena(black stool);
•most patients have liver disease,
•some children with extrahepatic portal venous
thrombosis
•Any child with hematemesis and splenomegaly;
-should be presumed to have esophageal variceal
bleeding until proved otherwise.
9
Esophageal varices….
Diagnosis
•upper endoscopy (definitive diagnosis)
•fluoroscopic barium contrast studies,
Treatments
•prophylactic sclerotherapy(inject into vein) or
Propranolol (to prevent variceal bleeding).
•Endoscopic variceal ligation
•Shunt surgery in refractory cases.
10
Diagnosis
•upper endoscopy (definitive diagnosis)
•fluoroscopic barium contrast studies,
Treatments
•prophylactic sclerotherapy(inject into vein) or
Propranolol (to prevent variceal bleeding).
•Endoscopic variceal ligation
•Shunt surgery in refractory cases.
10
Esophageal cancer
•Esophageal cancer is cancer of the esophagus.
• It is divided into two major types,
A. squamous cell carcinoma : arise in squamous
cells that line the esophagus.
•usually in upper & middle part of esophagus.
B. Adenocarcinomas :usually develop in the
glandular tissue in the lower part of the esophagus.
• If the cancer spreads outside the esophagus, it
often goes to the lymph nodes first.
11
•Esophageal cancer is cancer of the esophagus.
• It is divided into two major types,
A. squamous cell carcinoma : arise in squamous
cells that line the esophagus.
•usually in upper & middle part of esophagus.
B. Adenocarcinomas :usually develop in the
glandular tissue in the lower part of the esophagus.
• If the cancer spreads outside the esophagus, it
often goes to the lymph nodes first.
11
Esophageal cancer….
•Esophageal cancer can also spread to almost
any other part of the body, including the liver,
lungs, brain, and bones.
Cause of Esophageal cancer
The exact causes are not known.
Risk factors:
•Tobacco use,
•alcohol Use.
•Long-term irritation (gastric reflex)
•Had head and neck cancers
12
•Esophageal cancer can also spread to almost
any other part of the body, including the liver,
lungs, brain, and bones.
Cause of Esophageal cancer
The exact causes are not known.
Risk factors:
•Tobacco use,
•alcohol Use.
•Long-term irritation (gastric reflex)
•Had head and neck cancers
12
C/M of Esophageal cancer
•difficulty swallowing (dysphasia) and weight loss.
•Pain in the throat
•Hoarseness or chronic cough
•Vomiting
•Coughing up blood
DX:
•Clinically HX/PE
•Barium x-ray
•Endoscopy
•A biopsy
13
•difficulty swallowing (dysphasia) and weight loss.
•Pain in the throat
•Hoarseness or chronic cough
•Vomiting
•Coughing up blood
DX:
•Clinically HX/PE
•Barium x-ray
•Endoscopy
•A biopsy
13
four stages of esophageal cancer.
Stage I. only in the top layers of cells .
Stage II. involves deeper layers or
• it has spread to near by lymph nodes.
Stage III. more deeply into wall of esophagus
Stage IV. spread to other parts of the body.
14
Stage I. only in the top layers of cells .
Stage II. involves deeper layers or
• it has spread to near by lymph nodes.
Stage III. more deeply into wall of esophagus
Stage IV. spread to other parts of the body.
14
Treatments of esophageal cancer
•Surgery (most common)
•Radiation therapy
•Chemotherapy
•Laser therapy is the use of high-intensity light
to destroy tumor cells
•Provide adequate Nutrition
•Follow up care
15
•Surgery (most common)
•Radiation therapy
•Chemotherapy
•Laser therapy is the use of high-intensity light
to destroy tumor cells
•Provide adequate Nutrition
•Follow up care
15
Abdominal trauma
•Abdominal trauma is an injury to the abdomen.
•It may be blunt or penetrating
•injuries to the spleen, liver, pancreas,
gastrointestinal tract ……may occurred.
•trauma is leading cause of morbidity & mortality
•The abdomen is the third most commonly injured,
after the head and the extremities.
•have a mortality as high as 8.5%.
•8-10% of all trauma admissions to pediatric
hospitals.
16
•Abdominal trauma is an injury to the abdomen.
•It may be blunt or penetrating
•injuries to the spleen, liver, pancreas,
gastrointestinal tract ……may occurred.
•trauma is leading cause of morbidity & mortality
•The abdomen is the third most commonly injured,
after the head and the extremities.
•have a mortality as high as 8.5%.
•8-10% of all trauma admissions to pediatric
hospitals.
16
Etiology of Abdominal trauma
> 80% from blunt mechanisms;
• most commonly motor vehicle accidents.
falls or direct blows to the abdominal wall
stab wounds, dog bites, machinery …..
Signs and symptoms include;
• abdominal pain, tenderness, rigidity, and bruising
of the external abdomen.
DX: US, CT scan
Treatments: depend on affected part
•Fluid resuscitation
•Antipain
•Antibiotics
•Surgery
17
> 80% from blunt mechanisms;
• most commonly motor vehicle accidents.
falls or direct blows to the abdominal wall
stab wounds, dog bites, machinery …..
Signs and symptoms include;
• abdominal pain, tenderness, rigidity, and bruising
of the external abdomen.
DX: US, CT scan
Treatments: depend on affected part
•Fluid resuscitation
•Antipain
•Antibiotics
•Surgery
17
Appendicitis
• Appendicitis is inflammation and infection of the
vermiform appendix(5-10 cm in length).
•It arises from the cecum,
• mostly located in the right lower quadrant of the
abdomen.
•63 % in retrocaecal area, 33 % in pelvic
•Acute appendicitis is one of the most common
causes of abdominal pain.
18
• Appendicitis is inflammation and infection of the
vermiform appendix(5-10 cm in length).
•It arises from the cecum,
• mostly located in the right lower quadrant of the
abdomen.
•63 % in retrocaecal area, 33 % in pelvic
•Acute appendicitis is one of the most common
causes of abdominal pain.
18
Introduction .......
Positions of appendix
19
Positions of appendix
19
Epidemiology
•It is the most frequent condition leading to
emergent abdominal surgery in children.
•Annually a rate of 4/1,000 children < age 14 yr.
•It is rare less than 1 yrs old.
•The incidence peaking in adolescence
•The mean age is 6-10 years.
•The mortality rate is 0.1-1%.
•most patients perforate within 32 to 72 hours
•The risk of perforation in 1 to 4 yr (70-75%)
•But it is lowest in the adolescent (30-40%).
20
•It is the most frequent condition leading to
emergent abdominal surgery in children.
•Annually a rate of 4/1,000 children < age 14 yr.
•It is rare less than 1 yrs old.
•The incidence peaking in adolescence
•The mean age is 6-10 years.
•The mortality rate is 0.1-1%.
•most patients perforate within 32 to 72 hours
•The risk of perforation in 1 to 4 yr (70-75%)
•But it is lowest in the adolescent (30-40%).
20
Etiology of appendicitis
•obstruction of the lumen is the prime cause
common cause of obstruction in children are;
lymphoid hyperplasia of submucosal follicles &
fecalith (stool).
Rare causes include;
• foreign bodies, parasitic infections (eg, nematodes)
• inflammatory strictures, Crohn's disease
•primary or metastatic cancer and carcinoid syndrome.
21
•obstruction of the lumen is the prime cause
common cause of obstruction in children are;
lymphoid hyperplasia of submucosal follicles &
fecalith (stool).
Rare causes include;
• foreign bodies, parasitic infections (eg, nematodes)
• inflammatory strictures, Crohn's disease
•primary or metastatic cancer and carcinoid syndrome.
21
pathophysiology of appendicitis
•Initially luminal obstruction, venous congestion
progresses to mucosal ischemia, necrosis, and
ulceration.
•Secondily, Bacterial invasion with inflammatory
infiltrate through all layers of appendiceal wall.
•Finally, necrosis of the wall results in perforation
and contamination of the peritoneum.
22
•Initially luminal obstruction, venous congestion
progresses to mucosal ischemia, necrosis, and
ulceration.
•Secondily, Bacterial invasion with inflammatory
infiltrate through all layers of appendiceal wall.
•Finally, necrosis of the wall results in perforation
and contamination of the peritoneum.
22
pathophysiology appendicitis.......
•Subsequent to perforation, the microbiologic
fecal contamination may be spread;
• to pelvis ,small bowel, or peritoneal cavity.
•Bacterial invasion of mesenteric veins result in ;
- portal vein sepsis (pylephlebitis) and
-subsequent liver abscess formation.
•perforation may lead to;
- intestinal obstruction or paralytic ileus.
23
•Subsequent to perforation, the microbiologic
fecal contamination may be spread;
• to pelvis ,small bowel, or peritoneal cavity.
•Bacterial invasion of mesenteric veins result in ;
- portal vein sepsis (pylephlebitis) and
-subsequent liver abscess formation.
•perforation may lead to;
- intestinal obstruction or paralytic ileus.
23
Pathophysiology
24
•pathway to acute appendicitis begins with
luminal obstruction Accumulation of mucoid
material increase the intraluminal pressure,
bacterial proliferation lymphatic and venous
congestion (obstructs venous drainage), edema
impaired arterial perfusion ischemia,
necrosis Gangrenous
perforationperitonitis.
24
•pathway to acute appendicitis begins with
luminal obstruction Accumulation of mucoid
material increase the intraluminal pressure,
bacterial proliferation lymphatic and venous
congestion (obstructs venous drainage), edema
impaired arterial perfusion ischemia,
necrosis Gangrenous
perforationperitonitis.
Sign and symptom of appendicitis
•The classic triad consists of abdominal pain,
nausea with vomiting, and fever.
•Fever is low grade unless perforation with
peritonitis has occurred.
•Anorexia is more common
•abdominal pain, initially central / periumbilical
but then localising to the right iliac fossa/RLQ.
•The sequence of symptoms with abdominal pain
preceding emesis and fever but not in AGE.
25
•The classic triad consists of abdominal pain,
nausea with vomiting, and fever.
•Fever is low grade unless perforation with
peritonitis has occurred.
•Anorexia is more common
•abdominal pain, initially central / periumbilical
but then localising to the right iliac fossa/RLQ.
•The sequence of symptoms with abdominal pain
preceding emesis and fever but not in AGE.
25
Sign and symptom of appendicitis.......
•Typically, maximal tenderness can be found at
the McBurney point in the RLQ.
•rebound tenderness
•Rovsing sign :pain in the RLQ in response to left-
sided palpation .
• psoas sign: place the child on the left side and
hyperextend the right leg at the hip, feel pain.
•obturator sign: by internally rotating the flexed
right thigh, feel pain .
26
•Typically, maximal tenderness can be found at
the McBurney point in the RLQ.
•rebound tenderness
•Rovsing sign :pain in the RLQ in response to left-
sided palpation .
• psoas sign: place the child on the left side and
hyperextend the right leg at the hip, feel pain.
•obturator sign: by internally rotating the flexed
right thigh, feel pain .
26
Sign and symptom of appendicitis.......
•irritation of the bladder(urinary symptoms).
•With perforation, the pain becomes generalized
• Palpation of an abdominal or rectal mass
indicates abscess formation.
27
•irritation of the bladder(urinary symptoms).
•With perforation, the pain becomes generalized
• Palpation of an abdominal or rectal mass
indicates abscess formation.
27
Complications of appendicitis
Complications occur in 25-30% of children with
appendicitis, primarily those with perforation.
•appendix mass, an abscess or perforation.
•peritonititis
•Sepsis
•Intra-abdominal abscess
•pylephlebitis ( portal vein sepsis)
•Liver abscess from portal vein sepsis
•Shock
•Bowel obstruction ,
•paralytic ileus
28
Complications occur in 25-30% of children with
appendicitis, primarily those with perforation.
•appendix mass, an abscess or perforation.
•peritonititis
•Sepsis
•Intra-abdominal abscess
•pylephlebitis ( portal vein sepsis)
•Liver abscess from portal vein sepsis
•Shock
•Bowel obstruction ,
•paralytic ileus
28
Diagnosis of appendicitis
History and physical examination
CBC-increased
WBC-increased, increased neutrophil
UA-small RBC and WBC
imaging studies –US(safe)
- MRI(more accurate)
-CT scan
- barium enema
29
History and physical examination
CBC-increased
WBC-increased, increased neutrophil
UA-small RBC and WBC
imaging studies –US(safe)
- MRI(more accurate)
-CT scan
- barium enema
29
30
Management of appendicitis
Symptomatic treatments
IV fluid
Antibiotics
Appendectomy
31
Symptomatic treatments
IV fluid
Antibiotics
Appendectomy
31
Management of appendicitis.....
ideally the emergency departement protocol for
managing the preoperative child should be;
Patients should be NPO
give IV Fluid
The administration of antibiotics,
nasogastric tubes,
urethral catheters,
antiemetic medicine,
antipyretic medicine,
analgesia (Antipain -0.5-.1 mg/kg of morphine)
32
ideally the emergency departement protocol for
managing the preoperative child should be;
Patients should be NPO
give IV Fluid
The administration of antibiotics,
nasogastric tubes,
urethral catheters,
antiemetic medicine,
antipyretic medicine,
analgesia (Antipain -0.5-.1 mg/kg of morphine)
32
Management of appendicitis.....
•Antibiotics are most effective when given
preoperatively and
•It decrease post-op infections and abscess
formation
•Post-op antibiotics indicated in perforation
•Appendicitis can be treated with antibiotics alone
•Antibiotics change from emergency to elective
surgery.
33
•Antibiotics are most effective when given
preoperatively and
•It decrease post-op infections and abscess
formation
•Post-op antibiotics indicated in perforation
•Appendicitis can be treated with antibiotics alone
•Antibiotics change from emergency to elective
surgery.
33
Management of appendicitis.....
Antibiotics; 1. Triple therapy;
•ampicillin (100 mg/kg/24 hr),
• gentamicin (5 mg/kg/24 hr), and
•clindamycin (25-40 mg/kg/24 hr) or
metronidazole (30 mg/kg/24 hr) OR
2. Ceftriaxone(50-100mg/kg/24 hr) and
metronidazole daily as effective as triples.
34
Antibiotics; 1. Triple therapy;
•ampicillin (100 mg/kg/24 hr),
• gentamicin (5 mg/kg/24 hr), and
•clindamycin (25-40 mg/kg/24 hr) or
metronidazole (30 mg/kg/24 hr) OR
2. Ceftriaxone(50-100mg/kg/24 hr) and
metronidazole daily as effective as triples.
34
Management of appendicitis.....
Surgical management- Appendectomy
•Appendectomy is the standard of care
•Acute appendicitis cured with surgery
•may be done as soon as possible to prevent
perforation and its complication.
•If there is a palpable mass in the right iliac fossa
and there are no signs of generalised peritonitis,
•appendicectomy performed after several weeks.
35
Surgical management- Appendectomy
•Appendectomy is the standard of care
•Acute appendicitis cured with surgery
•may be done as soon as possible to prevent
perforation and its complication.
•If there is a palpable mass in the right iliac fossa
and there are no signs of generalised peritonitis,
•appendicectomy performed after several weeks.
35
Prognosis of Appendicitis
•Generally, the prognosis is excellent.
• perforation is 80-100% for children < 3 years, BUT;
* 10-20% in children 10-17 yrs.
•Children with ruptured appendicitis are risk for
different complication-prolonged hospital stay.
•The mortality rate with appendicitis is 0.1-1%.
•Death is most common in neonates and infants
36
•Generally, the prognosis is excellent.
• perforation is 80-100% for children < 3 years, BUT;
* 10-20% in children 10-17 yrs.
•Children with ruptured appendicitis are risk for
different complication-prolonged hospital stay.
•The mortality rate with appendicitis is 0.1-1%.
•Death is most common in neonates and infants
36
Peritonitis
•Inflammation of the peritoneal lining of the
abdominal cavity .
Classification
•primary peritonitis, the source of infection
originates outside the abdomen
•Secondary peritonitis: arises from the
abdominal cavity itself .
•Tertiary peritonitis :recurrent diffuse or localized
disease and has poorer outcomes.
37
•Inflammation of the peritoneal lining of the
abdominal cavity .
Classification
•primary peritonitis, the source of infection
originates outside the abdomen
•Secondary peritonitis: arises from the
abdominal cavity itself .
•Tertiary peritonitis :recurrent diffuse or localized
disease and has poorer outcomes.
37
Acute Primary Peritonitis
•Most ascites from nephrotic syndrome or
cirrhosis.
•Infection can result from translocation of gut
bacteria as well as immune dysfunction.
• Rarely, occurs in previously healthy children.
•The sexes are affected equally
•most cases occur before 6 yr of age.
38
•Most ascites from nephrotic syndrome or
cirrhosis.
•Infection can result from translocation of gut
bacteria as well as immune dysfunction.
• Rarely, occurs in previously healthy children.
•The sexes are affected equally
•most cases occur before 6 yr of age.
38
Etiology; Acute Primary Peritonitis
•Pneumococci (most common),
• group A streptococci,
•enterococci, staphylococci, and
• gram-negative enteric bacteria especially
Escherichia coli and Klebsiella pneumoniae
•Rarely Mycobacterium tuberculosis and M. bovis
39
•Pneumococci (most common),
• group A streptococci,
•enterococci, staphylococci, and
• gram-negative enteric bacteria especially
Escherichia coli and Klebsiella pneumoniae
•Rarely Mycobacterium tuberculosis and M. bovis
39
Acute secondary peritonitis
•most often results from obstruction or infarction or
after rupture of an intra-abdominal visceral abscess.
•It most commonly follows perforation of appendix.
Other gastrointestinal (GI) causes include
•incarcerated hernias, rupture of a Meckel
diverticulum, midgut volvulus, intussusception,
•hemolytic uremic syndrome, peptic ulceration,
•inflammatory bowel disease,
• necrotizing cholecystitis, necrotizing enterocolitis,
•traumatic perforation.
40
•most often results from obstruction or infarction or
after rupture of an intra-abdominal visceral abscess.
•It most commonly follows perforation of appendix.
Other gastrointestinal (GI) causes include
•incarcerated hernias, rupture of a Meckel
diverticulum, midgut volvulus, intussusception,
•hemolytic uremic syndrome, peptic ulceration,
•inflammatory bowel disease,
• necrotizing cholecystitis, necrotizing enterocolitis,
•traumatic perforation.
40
Acute secondary peritonitis….
•Mostly in the neonatal period occurs as a
complication of necrotizing enterocolitis.
•The presence of a foreign body, such as a
ventriculoperitoneal catheter or peritoneal
dialysis catheter predispose for;
•Staphylococcus epidermidis, S. aureus, and
Candida albicans, contaminating the shunt.
•In postpubertal girls, Neisseria gonorrhoeae,
Chlamydia trachomatis
•direct toxic effects of bacteria as well as local and
systemic release of inflammatory mediators
41
•Mostly in the neonatal period occurs as a
complication of necrotizing enterocolitis.
•The presence of a foreign body, such as a
ventriculoperitoneal catheter or peritoneal
dialysis catheter predispose for;
•Staphylococcus epidermidis, S. aureus, and
Candida albicans, contaminating the shunt.
•In postpubertal girls, Neisseria gonorrhoeae,
Chlamydia trachomatis
•direct toxic effects of bacteria as well as local and
systemic release of inflammatory mediators
41
Clinical Manifestations of peritonitis
•Fever ,
•abdominal pain, nausea, and vomiting
•rebound tenderness, abdominal wall rigidity
•A toxic appearance, irritability, and restlessness
are common
•Decreased/absent bowel sounds( paralytic ileus)
•Hypotension /Shock
•acute respiratory distress
42
•Fever ,
•abdominal pain, nausea, and vomiting
•rebound tenderness, abdominal wall rigidity
•A toxic appearance, irritability, and restlessness
are common
•Decreased/absent bowel sounds( paralytic ileus)
•Hypotension /Shock
•acute respiratory distress
42
DX of peritonitis
•Clinically by HX/PE
•Increase WBC count >12,000 cells/mm
3
•
CT scan,
•
Abdominal x ray
peritoneal fluid analysis;
• pH gradient >0.1,
• elevated lactate,
•gram stain +ve,
•Rise WBC count of ≥250 cells/mm
3
, with >50%
polymorphonuclear cells.
43
•Clinically by HX/PE
•Increase WBC count >12,000 cells/mm
3
•
CT scan,
•
Abdominal x ray
peritoneal fluid analysis;
• pH gradient >0.1,
• elevated lactate,
•gram stain +ve,
•Rise WBC count of ≥250 cells/mm
3
, with >50%
polymorphonuclear cells.
43
Treatments of peritonitis
Parenteral antibiotic therapy :
•cefotaxime and an aminoglycoside or
•ampicillin, gentamicin, and clindamycin
•Therapy should be continued for 10-14 days.
•Treating the cause
44
Parenteral antibiotic therapy :
•cefotaxime and an aminoglycoside or
•ampicillin, gentamicin, and clindamycin
•Therapy should be continued for 10-14 days.
•Treating the cause
44
Intussusception
•It is telescoping of one portion of the intestine
into another
•The most common site in the ileocolonic,
• in which the ileum invaginates in to the cecum
and further in to the colon.
•most common in 3 months to 6 yrs of age.
•80% occur b/n 1 to 2 years old child.
•60% of patients are younger than 1 yrs
• it is rare in neonates.
•The incidence varies from 1 to 4/1,000 live births.
•The male: female ratio is 3:1.
45
•It is telescoping of one portion of the intestine
into another
•The most common site in the ileocolonic,
• in which the ileum invaginates in to the cecum
and further in to the colon.
•most common in 3 months to 6 yrs of age.
•80% occur b/n 1 to 2 years old child.
•60% of patients are younger than 1 yrs
• it is rare in neonates.
•The incidence varies from 1 to 4/1,000 live births.
•The male: female ratio is 3:1.
45
Pathophysiology of Intussusception
46
Invagination of the bowel
Infarction, perforation
If left untreated, FATAL
Obstruction resulting in compression of the vessels
and venous congestion and bowel wall edema
46
Invagination of the bowel
Infarction, perforation
If left untreated, FATAL
Obstruction resulting in compression of the vessels
and venous congestion and bowel wall edema
Causes of Intussusception
•Idiopathic (unknown) ( 90%)
•In less than 2 years old, nearly all are idiopathic.
•Viral-induced lymphoid hyperplasia may
produce a lead point in these children
•respiratory adenovirus (type C) infection
•change in the mucosa from another condition
such as cystic fibrosis, or hematoma; or post
operative)
47
•Idiopathic (unknown) ( 90%)
•In less than 2 years old, nearly all are idiopathic.
•Viral-induced lymphoid hyperplasia may
produce a lead point in these children
•respiratory adenovirus (type C) infection
•change in the mucosa from another condition
such as cystic fibrosis, or hematoma; or post
operative)
47
Clinical Manifestations of Intussusception
•sudden onset of crampy abdominal pain
occurring every 15 to 20 minutes
• absence of stools.
•bilious vomiting
•Abdominal distention
•bowel sound diminished, absent or high pitch.
•Sausage like mass palpable in RUQ/epigastrium
(Dance’s sign).
48
•sudden onset of crampy abdominal pain
occurring every 15 to 20 minutes
• absence of stools.
•bilious vomiting
•Abdominal distention
•bowel sound diminished, absent or high pitch.
•Sausage like mass palpable in RUQ/epigastrium
(Dance’s sign).
48
Clinical Manifestations of
Intussusception….
•Lethargic
•Blood in stool containing sloughed mucosa,
blood, and mucus(60%).
•Dehydration and fever
•Shock like state with rapid pulse, pallor, and
marked sweating
DDX: Gastroenteritis(diarhea)
•Enterocolitis (less pain, diarhea)
•Meckel diverticulum(painless rectal bleeding)
49
Intussusception….
•Lethargic
•Blood in stool containing sloughed mucosa,
blood, and mucus(60%).
•Dehydration and fever
•Shock like state with rapid pulse, pallor, and
marked sweating
DDX: Gastroenteritis(diarhea)
•Enterocolitis (less pain, diarhea)
•Meckel diverticulum(painless rectal bleeding)
49
Complications of Intussusception….
•if left untreated, most will lead to;
- intestinal infarction,
- intestinal perforation,
- - peritonitis
- shock
- death.
50
•if left untreated, most will lead to;
- intestinal infarction,
- intestinal perforation,
- - peritonitis
- shock
- death.
50
Diagnosis of Intussusception
•Ultrasonogram(best): may be done to locate
area of telescoped bowel.
•X-ray of abdomen: may show absence of gas or
mass in right upper quadrant.
•Barium enema
•CT scan
51
•Ultrasonogram(best): may be done to locate
area of telescoped bowel.
•X-ray of abdomen: may show absence of gas or
mass in right upper quadrant.
•Barium enema
•CT scan
51
Managements of intussusception
•Two approaches are used;
1.Non operative reduction
•resolved by gentle pressure exerted within the
intestine using barium or air enemas
•The success rate is 80-95%.
•But not if has complications,
2. Surgery with end-to-end anastomosis if:
• irreducible by enema
•necrotic intussusception
•long duration of sign/symptom
•Small bowel obstruction
•peritonitis or bowel infarction
52
•Two approaches are used;
1.Non operative reduction
•resolved by gentle pressure exerted within the
intestine using barium or air enemas
•The success rate is 80-95%.
•But not if has complications,
2. Surgery with end-to-end anastomosis if:
• irreducible by enema
•necrotic intussusception
•long duration of sign/symptom
•Small bowel obstruction
•peritonitis or bowel infarction
52
Managements of intussusception….
•intussusceptions reduce spontaneously(4-10%).
•Therapy must begin with placement of an IV
catheter and a nasogastric tube.
•fluid resuscitation to correct severe dehydration
53
•intussusceptions reduce spontaneously(4-10%).
•Therapy must begin with placement of an IV
catheter and a nasogastric tube.
•fluid resuscitation to correct severe dehydration
53
Nursing Intervention for intussusception
•Monitor intake and output
•Be alert for respiratory distress
•Monitor vital signs, pain, distention, and
• general behavior preoperatively and
postoperatively.
•Explain cause of pain to parents, and
•reassure them about purpose of diagnostic tests
and treatments.
•Administer analgesic as prescribed
54
•Monitor intake and output
•Be alert for respiratory distress
•Monitor vital signs, pain, distention, and
• general behavior preoperatively and
postoperatively.
•Explain cause of pain to parents, and
•reassure them about purpose of diagnostic tests
and treatments.
•Administer analgesic as prescribed
54
Nursing Intervention for intussusception….
•Maintain NPO status as ordered.
•Insert nasogastric tube if ordered to decompress
stomach.
•Continually reasses condition because increased
pain and bloody stools may indicate perforation.
•After reduction by hydrostatic enema, monitor
vital signs and general condition – especially
abdominal tenderness, bowel sounds, lethargy,
and tolerance to fluids – to watch recurrence.
•Encourage follow up care.
55
•Maintain NPO status as ordered.
•Insert nasogastric tube if ordered to decompress
stomach.
•Continually reasses condition because increased
pain and bloody stools may indicate perforation.
•After reduction by hydrostatic enema, monitor
vital signs and general condition – especially
abdominal tenderness, bowel sounds, lethargy,
and tolerance to fluids – to watch recurrence.
•Encourage follow up care.
55
Prognosis
•If Untreated in infants is usually fatal.
•Most infants recover if reduced in 1st 24 hrs.
The recurrence rate after :
•After reduction is about 10%,
•after surgical reduction it is 2-5%;
•none has recurred after surgical resection
56
•If Untreated in infants is usually fatal.
•Most infants recover if reduced in 1st 24 hrs.
The recurrence rate after :
•After reduction is about 10%,
•after surgical reduction it is 2-5%;
•none has recurred after surgical resection
56
Pyloric stenosis
•pylorus is a muscle that opens and closes to allow
food to pass through stomach into the intestine
Pyloric stenosis means a narrowed outlet
(pylorus) of the stomach
also called infantile hypertrophic pyloric stenosis
caused by an enlarged pylorus.
57
•pylorus is a muscle that opens and closes to allow
food to pass through stomach into the intestine
Pyloric stenosis means a narrowed outlet
(pylorus) of the stomach
also called infantile hypertrophic pyloric stenosis
caused by an enlarged pylorus.
57
58
Epidemiology, pyloric stenosis
It is one of the most common causes of intestinal
obstruction during infancy that requires surgery.
Presentation is usually between 3 and 5 weeks
of age, and
approximately 95% in those aged 3-12 weeks.
The incidence is increased with B &O blood
groups.
occurs in 1-3 /1,000 infants in the United States
more commonly seen in males(4:1).
Mortality is low
59
It is one of the most common causes of intestinal
obstruction during infancy that requires surgery.
Presentation is usually between 3 and 5 weeks
of age, and
approximately 95% in those aged 3-12 weeks.
The incidence is increased with B &O blood
groups.
occurs in 1-3 /1,000 infants in the United States
more commonly seen in males(4:1).
Mortality is low
59
Etiology of pyloric stenosis
The cause is unknown, but many risk factors
have been implicated.
•use of erythromycin in the first 2 weeks of life,
during pregnancy and breastfeeding.
•trisomy 18, more concordant in monozygotic
Abnormal muscle innervation,
elevated serum levels of prostaglandins,
Hyperacidity (repeated contraction of the
pylorus)
60
The cause is unknown, but many risk factors
have been implicated.
•use of erythromycin in the first 2 weeks of life,
during pregnancy and breastfeeding.
•trisomy 18, more concordant in monozygotic
Abnormal muscle innervation,
elevated serum levels of prostaglandins,
Hyperacidity (repeated contraction of the
pylorus)
60
Pathophysiology of PS
HPS occurs secondary to hypertrophy and
hyperplasia of the muscular layers of the
pylorus,
which cause a functional gastric outlet
obstruction.
In response to outflow obstruction and vigorous
peristalsis, stomach musculature becomes
uniformly hypertrophied and dilated.
Gastritis may occur after prolonged stasis.
Hematemesis is occasionally noted.
The patient may become dehydrated as a result
of vomiting
61
HPS occurs secondary to hypertrophy and
hyperplasia of the muscular layers of the
pylorus,
which cause a functional gastric outlet
obstruction.
In response to outflow obstruction and vigorous
peristalsis, stomach musculature becomes
uniformly hypertrophied and dilated.
Gastritis may occur after prolonged stasis.
Hematemesis is occasionally noted.
The patient may become dehydrated as a result
of vomiting
61
C/M of pyloric stenosis
Common main symptom is vomiting.
Non bilious forceful (“projectile”) vomiting
Emesis might follow each feeding
The vomiting usually starts after 3 wk of age
dehydration , malnutrition
potassium & sodium are lost through vomiting
As vomiting continues, a progressive loss of fluid,
hydrogen ion, and chloride leads to
hypochloremic metabolic alkalosis.
62
Common main symptom is vomiting.
Non bilious forceful (“projectile”) vomiting
Emesis might follow each feeding
The vomiting usually starts after 3 wk of age
dehydration , malnutrition
potassium & sodium are lost through vomiting
As vomiting continues, a progressive loss of fluid,
hydrogen ion, and chloride leads to
hypochloremic metabolic alkalosis.
62
C/M of pyloric stenosis ….
Visible peristaltic waves in the left upper part of
the abdomen
Hyperbilirubinemia (icteropyloric syndrome).
Constipation,
Fewer bowel movements
Weight loss
Lethargy (lack of energy)
63
Visible peristaltic waves in the left upper part of
the abdomen
Hyperbilirubinemia (icteropyloric syndrome).
Constipation,
Fewer bowel movements
Weight loss
Lethargy (lack of energy)
63
complication of PS
Sever dehydration
Electrolyte and acid -base imbalance
Unable to thrive
Malnutrition
Death (if not managed promptly)
Aspiration Pneumonia)
64
Sever dehydration
Electrolyte and acid -base imbalance
Unable to thrive
Malnutrition
Death (if not managed promptly)
Aspiration Pneumonia)
64
Differential diagnosis of PS
gastroesophageal reflux
Bowel Obstruction in the Newborn,
Duodenal Atresia
Gastroenteritis
Intestinal Malrotation.
65
gastroesophageal reflux
Bowel Obstruction in the Newborn,
Duodenal Atresia
Gastroenteritis
Intestinal Malrotation.
65
Diagnostic methods, PS
•History and clinical
•Abdominal ultrasound: gold standard
Criteria to diagnose:
•Pyloric muscle thickness >4mm,
• pyloric muscle length >14 – 20mm and
•pyloric diameter >10-14mm is diagnostic in term
infants
66
•History and clinical
•Abdominal ultrasound: gold standard
Criteria to diagnose:
•Pyloric muscle thickness >4mm,
• pyloric muscle length >14 – 20mm and
•pyloric diameter >10-14mm is diagnostic in term
infants
66
Treatments, PS
•First fluids, electrolytes , naso-duodenal feeding
•Once this is done,the surgical procedure of choice
is pyloromyotomy (curative)
•surgery may proceed only when fluid balance,
acid-base status and electrolyte levels have been
restored to normal.
feedings can be initiated within 12-24 hr after
surgery
Over a 24- to 48-hour period, feedings are
gradually increased.
67
•First fluids, electrolytes , naso-duodenal feeding
•Once this is done,the surgical procedure of choice
is pyloromyotomy (curative)
•surgery may proceed only when fluid balance,
acid-base status and electrolyte levels have been
restored to normal.
feedings can be initiated within 12-24 hr after
surgery
Over a 24- to 48-hour period, feedings are
gradually increased.
67
Hernia
•A protrusion of tissue or viscus through a
weakness or abnormal opening.
•(hiatal, inguinal, Femoral, Umbilical, Incisional)
Clinical classification:
•Reducible hernia, Irreducible hernia, Sliding
hernia,
• Incarcerated hernia/Strangulated hernia
•Richter’s hernia: only part of bowel becomes
incarcerated or strangulated
•Littre’s hernia: incarcerated or strangulated part
is a diverticulum of the small intestine
68
•A protrusion of tissue or viscus through a
weakness or abnormal opening.
•(hiatal, inguinal, Femoral, Umbilical, Incisional)
Clinical classification:
•Reducible hernia, Irreducible hernia, Sliding
hernia,
• Incarcerated hernia/Strangulated hernia
•Richter’s hernia: only part of bowel becomes
incarcerated or strangulated
•Littre’s hernia: incarcerated or strangulated part
is a diverticulum of the small intestine
68
Inguinal hernia
•Inguinal hernia: protrusion through inguinal
canal (most common hernia )
majority of inguinal hernias in infants and
children are;
• congenital indirect hernias (99%) as a
consequence of a patent processus vaginalis.
The incidence is 10X higher in boys than in girls.
Other types of inguinal hernias include;
• direct or acquired (0.5-1.0%) & femoral (<0.5%).
69
•Inguinal hernia: protrusion through inguinal
canal (most common hernia )
majority of inguinal hernias in infants and
children are;
• congenital indirect hernias (99%) as a
consequence of a patent processus vaginalis.
The incidence is 10X higher in boys than in girls.
Other types of inguinal hernias include;
• direct or acquired (0.5-1.0%) & femoral (<0.5%).
69
Inguinal hernia….
• Approximately one half manifest clinically in the
1st year of life,
•most in the 1st 6 mo.
•Premature infants have an incidence of inguinal
hernia approaching 30%.
•The risk of incarceration and possible
strangulation is;
- greatest in the 1st year of life (30-40%)
70
• Approximately one half manifest clinically in the
1st year of life,
•most in the 1st 6 mo.
•Premature infants have an incidence of inguinal
hernia approaching 30%.
•The risk of incarceration and possible
strangulation is;
- greatest in the 1st year of life (30-40%)
70
Inguinal hernia….
Indirect inguinal hernias in infants and children
are congenital result from arrest of embryologic
development,
•failure of obliteration of the processus vaginalis,
relates to development of the gonads and
descent of the testis into the scrotum late in
gestation( 32-36 wk)
Closure of the processus vaginalis :
• ~40% close during the first months of life and
• ~20% of boys until 2 yr of age.
71
Indirect inguinal hernias in infants and children
are congenital result from arrest of embryologic
development,
•failure of obliteration of the processus vaginalis,
relates to development of the gonads and
descent of the testis into the scrotum late in
gestation( 32-36 wk)
Closure of the processus vaginalis :
• ~40% close during the first months of life and
• ~20% of boys until 2 yr of age.
71
Risk factor for inguinal hernia
The reasons for failure of closure of the
processus vaginalis are unknown
•Prematurity
•Cryptorchidism
•Exstrophy of the bladder or cloaca
•Hypospadius/epispadius
•Ascites
•Ventriculoperitoneal shunt
•Peritoneal dialysis catheter
•Increased intra-abdominal pressure
•Chronic respiratory disease (cystic fibrosis)
72
The reasons for failure of closure of the
processus vaginalis are unknown
•Prematurity
•Cryptorchidism
•Exstrophy of the bladder or cloaca
•Hypospadius/epispadius
•Ascites
•Ventriculoperitoneal shunt
•Peritoneal dialysis catheter
•Increased intra-abdominal pressure
•Chronic respiratory disease (cystic fibrosis)
72
Clinical Presentation inguinal hernia
•bulge in the inguinal region or extending
through the inguinal region into the scrotum.
• In girls, the mass typically occurs in the upper
portion of the labia majora.
The hallmark signs of an inguinal hernia;
• smooth, firm mass/bulge that emerges through
external inguinal ring that;
• enlarges with increased intra-abdominal
pressure (crying, straining, coughing).
73
•bulge in the inguinal region or extending
through the inguinal region into the scrotum.
• In girls, the mass typically occurs in the upper
portion of the labia majora.
The hallmark signs of an inguinal hernia;
• smooth, firm mass/bulge that emerges through
external inguinal ring that;
• enlarges with increased intra-abdominal
pressure (crying, straining, coughing).
73
Clinical Presentation inguinal hernia ...
•Valsalva maneuver : Older patients can be asked
to blowing up a balloon or coughing.
•examined while standing, after voiding
•“silk glove sign,” feeling of the layers of the
hernia sac (processus vaginalis) as they slide
over the spermatic cord structures, with rolling
of the spermatic cord beneath the index finger
at the pubic tubercle;
•retractile testes are common in infants and
young children , can mimic an inguinal hernia
74
•Valsalva maneuver : Older patients can be asked
to blowing up a balloon or coughing.
•examined while standing, after voiding
•“silk glove sign,” feeling of the layers of the
hernia sac (processus vaginalis) as they slide
over the spermatic cord structures, with rolling
of the spermatic cord beneath the index finger
at the pubic tubercle;
•retractile testes are common in infants and
young children , can mimic an inguinal hernia
74
Complication of inguinal hernia
A hydrocele
ischemic injury to the intestine, testis, or ovary
Injury to the Vas Deferens and Male Fertility
75
A hydrocele
ischemic injury to the intestine, testis, or ovary
Injury to the Vas Deferens and Male Fertility
75
Management of inguinal hernia-
•supportive,
•manual reduction (inguinal if acute),
• early surgery repair in the 1st 6-12 mo of life
•When the hernia cannot be reduced or is
strangulated, immediate operation is indicated .
76
•supportive,
•manual reduction (inguinal if acute),
• early surgery repair in the 1st 6-12 mo of life
•When the hernia cannot be reduced or is
strangulated, immediate operation is indicated .
76
Other hernia ….reading ast
•Umbilical hernia due to imperfect closure or weakness
of the umbilical ring.
•femoral hernia: protrusion through the femoral canal
on the medial aspect of the thigh.
•Haital hernia: Herniation of the stomach through the
esophageal hiatus
•Incisional hernia :at the site of a previous laparotomy
(uncommon)
•Diaphragmatic hernia :communication between the
abdominal and thoracic cavities
•Epigastric hernias: b/n xyphoid and umbilicus ,
77
•Umbilical hernia due to imperfect closure or weakness
of the umbilical ring.
•femoral hernia: protrusion through the femoral canal
on the medial aspect of the thigh.
•Haital hernia: Herniation of the stomach through the
esophageal hiatus
•Incisional hernia :at the site of a previous laparotomy
(uncommon)
•Diaphragmatic hernia :communication between the
abdominal and thoracic cavities
•Epigastric hernias: b/n xyphoid and umbilicus ,
77
Gastro esophageal reflux disease(GERD)
•It signifies the retrograde movement of gastric
contents into the esophagus.
•decreased lower esophageal sphincter tone
•Transient Lower relaxation of esophagus
physiologic : occasionally reflux (regurgitation of
normal infants),
•infant reflux :1
st
few months of life, peaks at ∼4 mo,
•resolves in up to 88% by 12 mo and
• nearly all resolves by 24 mo.
pathologic GERD :more frequent or persistent, and
thus produce esophagitis/respiratory sequelae.
78
•It signifies the retrograde movement of gastric
contents into the esophagus.
•decreased lower esophageal sphincter tone
•Transient Lower relaxation of esophagus
physiologic : occasionally reflux (regurgitation of
normal infants),
•infant reflux :1
st
few months of life, peaks at ∼4 mo,
•resolves in up to 88% by 12 mo and
• nearly all resolves by 24 mo.
pathologic GERD :more frequent or persistent, and
thus produce esophagitis/respiratory sequelae.
78
Cause of GERD
complex inheritance involving multiple genes and
environmental factors;
•genetic predispositions
• family clustering of GERD symptoms,
•esophagitis,
• hiatal hernia,
• esophagus adenocarcinoma
79
complex inheritance involving multiple genes and
environmental factors;
•genetic predispositions
• family clustering of GERD symptoms,
•esophagitis,
• hiatal hernia,
• esophagus adenocarcinoma
79
Clinical Manifestations , GERD
•regurgitation (especially after eating/feeding),
•signs of esophagitis (arching, choking, gagging,
feeding aversion)
•failure to thrive
•neck arching & turning of head-Sandifer syndrome.
•infants :obstructive apnea or stridor or
laryngomalacia or bronchopulmonary dysplasia.
•Otitis media, sinusitis, lymphoid hyperplasia,
hoarseness, vocal cord nodules, and laryngeal edema
•Airway manifestations in older children are more
commonly related to asthma or laryngitis or sinusitis.
80
•regurgitation (especially after eating/feeding),
•signs of esophagitis (arching, choking, gagging,
feeding aversion)
•failure to thrive
•neck arching & turning of head-Sandifer syndrome.
•infants :obstructive apnea or stridor or
laryngomalacia or bronchopulmonary dysplasia.
•Otitis media, sinusitis, lymphoid hyperplasia,
hoarseness, vocal cord nodules, and laryngeal edema
•Airway manifestations in older children are more
commonly related to asthma or laryngitis or sinusitis.
80
Diagnosis of GERD
•history and physical examination
•Contrast (usually barium) radiographic study of
the esophagus and upper gastrointestinal tract.
•esophageal pH monitoring
•Endoscopy : diagnosis of erosive esophagitis
81
•history and physical examination
•Contrast (usually barium) radiographic study of
the esophagus and upper gastrointestinal tract.
•esophageal pH monitoring
•Endoscopy : diagnosis of erosive esophagitis
81
Management of GERD
Conservative therapy and lifestyle modification
•avoid reflux-inducing foods (tomatoes, chocolate)
•Avoid beverages (juices, carbonated and
caffeinated drinks, alcohol).
•Weight reduction for obese patients
•elimination of smoke exposure
•Avoid Seated position
Pharmacotherapy: antacid, H2 receptor
antagonists , PPI
Surgery : Refractory , severe complication.
82
Conservative therapy and lifestyle modification
•avoid reflux-inducing foods (tomatoes, chocolate)
•Avoid beverages (juices, carbonated and
caffeinated drinks, alcohol).
•Weight reduction for obese patients
•elimination of smoke exposure
•Avoid Seated position
Pharmacotherapy: antacid, H2 receptor
antagonists , PPI
Surgery : Refractory , severe complication.
82
Inflammatory bowel diseases(IBD)
•represent 2 distinctive disorders of idiopathic chronic
intestinal inflammation:
1.Ulcerative colitis(UC) is limited to the colon and
rectum and extends only into the mucosa and
submucosa.
2. Crohn’s disease may involve any area of the
gastrointestinal tract and frequently is transmural
–Also known as regional enteritis,
–American Gastroenterologist: Burrill Bernard Crohn
83
•represent 2 distinctive disorders of idiopathic chronic
intestinal inflammation:
1.Ulcerative colitis(UC) is limited to the colon and
rectum and extends only into the mucosa and
submucosa.
2. Crohn’s disease may involve any area of the
gastrointestinal tract and frequently is transmural
–Also known as regional enteritis,
–American Gastroenterologist: Burrill Bernard Crohn
83
Epidemiology , IBD
•The annual incidence rates of
– 0.2-8.5 per100 000 for CD
– 0.5-4.3 per 100 000 for UC.
•indeterminate colitis: ∼10% of pediatric patients.
•About 25% of people are diagnosed before age 20 years
•Crohn’s disease is common in older children
•UC is more common in children < 5 yrs
84
•The annual incidence rates of
– 0.2-8.5 per100 000 for CD
– 0.5-4.3 per 100 000 for UC.
•indeterminate colitis: ∼10% of pediatric patients.
•About 25% of people are diagnosed before age 20 years
•Crohn’s disease is common in older children
•UC is more common in children < 5 yrs
84
Etiopathogenesis of IBD
•The exact cause of IBD is unknown
•BUT results from a combination of :
–Genetic factors.
– Autoimmune disease.
–Environmental factors(Bacteria ,NSIDS, stress )
85
•The exact cause of IBD is unknown
•BUT results from a combination of :
–Genetic factors.
– Autoimmune disease.
–Environmental factors(Bacteria ,NSIDS, stress )
85
Clinical features
Crohn’s disease
•Abdominal pain and cramping
•Diarrhea
•Fever
•Weight Loss
•Bloating
•Anal pain or drainage
•Rectal abscess
86
Crohn’s disease
•Abdominal pain and cramping
•Diarrhea
•Fever
•Weight Loss
•Bloating
•Anal pain or drainage
•Rectal abscess
86
Clinical features, Ulcerative colitis
•Diarrhea, Rectal bleeding, Tenesmus
•Passage of mucus
•Crampy abdominal pain
•constipation
•Severe disease-liquid stools with blood , pus &
fecal matter.
•fulminant colitis: Fever, severe anemia,
•hypoalbuminemia, leukocytosis, and
•more than 5 bloody stools per day for 5 days
87
•Diarrhea, Rectal bleeding, Tenesmus
•Passage of mucus
•Crampy abdominal pain
•constipation
•Severe disease-liquid stools with blood , pus &
fecal matter.
•fulminant colitis: Fever, severe anemia,
•hypoalbuminemia, leukocytosis, and
•more than 5 bloody stools per day for 5 days
87
Diagnosis of IBD
•History – Physical Exam
•Laboratory
–CBC, ESR, CRP, albumin
–Stool culture
–Serology (antibodies )
Anti-Saccharomyces cerevisiae (ASCA)
Perinuclear antineutrophil antibody
(pANCA)
•Endoscopy and histopathology
•Imaging: Barium X-rays
88
•History – Physical Exam
•Laboratory
–CBC, ESR, CRP, albumin
–Stool culture
–Serology (antibodies )
Anti-Saccharomyces cerevisiae (ASCA)
Perinuclear antineutrophil antibody
(pANCA)
•Endoscopy and histopathology
•Imaging: Barium X-rays
88
Complications, IBD
•Hemorrhage
•Malabsorbtion
•Obstruction
•Possibility of malignant transformation
89
•Hemorrhage
•Malabsorbtion
•Obstruction
•Possibility of malignant transformation
89
Treatment of IBD
1.Anti-inflammatory drugs ( Asprin, predenslone)
2.Immune system suppressors (Azathioprine & 6-
mercaptopurine, the most extensive)
-Methotrexate ,Cyclosporine
3. Antibiotics (metronidazole)
4.Surgery
5.Parenteral nutrition (liquid diets containing amino
acids, simple carbohydrates, fats )
90
1.Anti-inflammatory drugs ( Asprin, predenslone)
2.Immune system suppressors (Azathioprine & 6-
mercaptopurine, the most extensive)
-Methotrexate ,Cyclosporine
3. Antibiotics (metronidazole)
4.Surgery
5.Parenteral nutrition (liquid diets containing amino
acids, simple carbohydrates, fats )
90
Surgery, IBD
For unresponsive to medical treatment,
•Bowel perforation,
•small bowel obstruction,
• intractable bleeding.
•Intra-abdominal or liver abscess.
Colectomy is performed for intractable disease.
Recurrence rate is high (>50% by 5 yr)
91
For unresponsive to medical treatment,
•Bowel perforation,
•small bowel obstruction,
• intractable bleeding.
•Intra-abdominal or liver abscess.
Colectomy is performed for intractable disease.
Recurrence rate is high (>50% by 5 yr)
91
Prognosis, IBD
•HAVE high morbidity but low mortality.
•The region of bowel involved often increases with
time,
•Beyond the 1st decade of disease, the risk of
development of colon cancer begins to increase
rapidly.
92
•HAVE high morbidity but low mortality.
•The region of bowel involved often increases with
time,
•Beyond the 1st decade of disease, the risk of
development of colon cancer begins to increase
rapidly.
92
Acute Gastroenteritis/
Acute Diarrheal diseases
•It is infections of the gastrointestinal (GI) tract
•It is inflammation of bowels and stomach.
•Many of these infections are foodborne illnesses
•Diarrhea :>= 3 loose or watery stools per 24 hrs.
•There are three clinical types of diarrhea:
1. Acute watery : lasts for less than 14 days
(commonest one-80-82%)
2. Dysentry – diarrhoea with blood in the stool.
3. Persistent diarrhea : lasts for 14 days or longer.
93
Acute Diarrheal diseases
•It is infections of the gastrointestinal (GI) tract
•It is inflammation of bowels and stomach.
•Many of these infections are foodborne illnesses
•Diarrhea :>= 3 loose or watery stools per 24 hrs.
•There are three clinical types of diarrhea:
1. Acute watery : lasts for less than 14 days
(commonest one-80-82%)
2. Dysentry – diarrhoea with blood in the stool.
3. Persistent diarrhea : lasts for 14 days or longer.
93
Types Greatest Danger
1. Acute watery
diarrhea (80% of cases)
Dehydration
K
+
loss
2. Bloody diarrhea
(Dysentry) 10% of
cases
Tissue damage
Toxemia(sepsis)
3. Persistent diarrhea(>
2 wks) 10% of cases
Malnutrition
4. Chronic diarrhea
(6wks or more)
Malnutrition
94
1. Acute watery
diarrhea (80% of cases)
Dehydration
K
+
loss
2. Bloody diarrhea
(Dysentry) 10% of
cases
Tissue damage
Toxemia(sepsis)
3. Persistent diarrhea(>
2 wks) 10% of cases
Malnutrition
4. Chronic diarrhea
(6wks or more)
Malnutrition
94
Acute Gastroenteritis…
•A young infant normally has ~5g/kg of stool
output per day.
•A small intestine absorb 10-11 L/day
•whereas the colon absorbs 0.5-1 L.
95
•A young infant normally has ~5g/kg of stool
output per day.
•A small intestine absorb 10-11 L/day
•whereas the colon absorbs 0.5-1 L.
95
Epidemiology of diarrheal disease
•account for 9 % of childhood deaths (2013),
•it the second most common cause of child
deaths worldwide.
•almost 2.5 billion episodes annually in children
<5 yr of age in developing countries
•about 3.6 episodes per child year
Now decline in diarrheal mortality b/c:
• rotavirus vaccination
• improved case management of diarrhea,
•improved nutrition of infants and children.
96
•account for 9 % of childhood deaths (2013),
•it the second most common cause of child
deaths worldwide.
•almost 2.5 billion episodes annually in children
<5 yr of age in developing countries
•about 3.6 episodes per child year
Now decline in diarrheal mortality b/c:
• rotavirus vaccination
• improved case management of diarrhea,
•improved nutrition of infants and children.
96
Epidemiology of diarrheal disease…
•Rotavirus most common
•Rota virus : 29% of all deaths due to diarrhea
among children <5 yr of age.
•Shigella dysenteriae type 1,
•most severe form ,
• almost 160,000 deaths annually.
• Enterotoxigenic Escherichia coli (ETEC) :
•300,000-500,000 deaths in <5 yrs annually.
97
•Rotavirus most common
•Rota virus : 29% of all deaths due to diarrhea
among children <5 yr of age.
•Shigella dysenteriae type 1,
•most severe form ,
• almost 160,000 deaths annually.
• Enterotoxigenic Escherichia coli (ETEC) :
•300,000-500,000 deaths in <5 yrs annually.
97
Risk factors for diarrhea/AGE
Behavioral:
Improper infant and young child feeding
Any uncooked food or
food contaminated by an ill food handler
Drinking contaminated water ,
Not washing hands properly ,
Not disposing of feces safely
poor hygiene during preparing food
Host factors:
-Malnutrition , zink & vit A deficiency
- Measles,
- young age
-Immunosuppression – like HIV/AIDS
98
Behavioral:
Improper infant and young child feeding
Any uncooked food or
food contaminated by an ill food handler
Drinking contaminated water ,
Not washing hands properly ,
Not disposing of feces safely
poor hygiene during preparing food
Host factors:
-Malnutrition , zink & vit A deficiency
- Measles,
- young age
-Immunosuppression – like HIV/AIDS
98
Etiology of AGE/diarhea
Etiology : virus ( >75%), bacteria( 10 -20%),
parasite ( < 5 %), malabsorbtion.....
•rota virus- common cause of acute watery
diarrhea
•others are escherichia coli, vibrio cholerae,
• giardia lamblia, cryptosporidiu, etc
•The common cause of dysentry is shigella
•Malabsorption
•Allergic enteritis
The transmission , through the fecal-oral route.
99
Etiology : virus ( >75%), bacteria( 10 -20%),
parasite ( < 5 %), malabsorbtion.....
•rota virus- common cause of acute watery
diarrhea
•others are escherichia coli, vibrio cholerae,
• giardia lamblia, cryptosporidiu, etc
•The common cause of dysentry is shigella
•Malabsorption
•Allergic enteritis
The transmission , through the fecal-oral route.
99
Causative agents of acute diarrhea
100
Viral Bacterial parasites
Rota virus Campaylobactor
jejuni
Giardia
Enteric
adenovirus
Closteridum defficil
and perfringens
E. histolitica
CMV E.coli cryptosporidium
HSV Shigella and
salmonella
Isospora belli
Vibro cholera strongloidosis
Staph.aureus Trichuris trichuria
Yersina
enterocolitica
100
Viral Bacterial parasites
Rota virus Campaylobactor
jejuni
Giardia
Enteric
adenovirus
Closteridum defficil
and perfringens
E. histolitica
CMV E.coli cryptosporidium
HSV Shigella and
salmonella
Isospora belli
Vibro cholera strongloidosis
Staph.aureus Trichuris trichuria
Yersina
enterocolitica
Pathogenesis of diarrhea
•The basis for all diarrhea is disturbed intestinal
solute transport.
• water movement across intestine membrane is
passive &
• is determined by both active & passive fluxes of
solutes, particularly Na+, Cl-, & glucose.
•The pathogenesis of most episodes of diarrhea
can be explained by secretory, osmotic, motility
problem, or a combination of these.
101
•The basis for all diarrhea is disturbed intestinal
solute transport.
• water movement across intestine membrane is
passive &
• is determined by both active & passive fluxes of
solutes, particularly Na+, Cl-, & glucose.
•The pathogenesis of most episodes of diarrhea
can be explained by secretory, osmotic, motility
problem, or a combination of these.
101
Mechanisms of Diarrhea
1.Osmotic diarrhea
- Digestive enzyme deficiencies
- Ingestion of unabsorbable solute
Examples:
Lactase deficiency
Milk , sucrose, coca cola
Laxative (mgso
4 ),
it stops during fasting,
No stool WBCs
102
1.Osmotic diarrhea
- Digestive enzyme deficiencies
- Ingestion of unabsorbable solute
Examples:
Lactase deficiency
Milk , sucrose, coca cola
Laxative (mgso
4 ),
it stops during fasting,
No stool WBCs
102
Mechanisms Cont…
2.Secretory Diarrhea: electrolyte and water fluxes
toward the intestinal lumen
Defect:
Increased secretion
Decreased absorption(virus villus damage)
Examples:
Cholera
Toxinogenic E.coli
Persists during fasting
No stool leukocytes
103
2.Secretory Diarrhea: electrolyte and water fluxes
toward the intestinal lumen
Defect:
Increased secretion
Decreased absorption(virus villus damage)
Examples:
Cholera
Toxinogenic E.coli
Persists during fasting
No stool leukocytes
103
Mechanisms of diarrhea…
3.Exudative Diarrhea:
Defects:
-Inflammation
-Decreased colonic reabsorption
-Increased motility
Examples: Bacterial enteritis
Blood, mucus and WBCs in stool
4.Increased motility: Decreased transit time
Example:
Irritable bowel syndrome, thyrotoxicosis,
5. Decreased motility:Defect in neurotransmiting
units results stasis (bacterial over growth)
104
3.Exudative Diarrhea:
Defects:
-Inflammation
-Decreased colonic reabsorption
-Increased motility
Examples: Bacterial enteritis
Blood, mucus and WBCs in stool
4.Increased motility: Decreased transit time
Example:
Irritable bowel syndrome, thyrotoxicosis,
5. Decreased motility:Defect in neurotransmiting
units results stasis (bacterial over growth)
104
C/M of AGE/diarheal disease
•The most common :diarrhea and vomiting;
•associated with abdominal pain and fever.
•Nausea, abdominal cramps
•Effects of diarrhea include:
— Dehydration, metabolic acidosis,
—malnutrition, sepsis,
—hypokalemia, hyponatremia
105
•The most common :diarrhea and vomiting;
•associated with abdominal pain and fever.
•Nausea, abdominal cramps
•Effects of diarrhea include:
— Dehydration, metabolic acidosis,
—malnutrition, sepsis,
—hypokalemia, hyponatremia
105
Complications of acute diarhea
•Dehydration
• hypovolemic shock
•hypokalemia,
•hyponatremia
•Base deficit acidosis(HCO3)
•Hypoglycemia
•Malnutrition
•Dehydration(DHN) : loss of body fluid and
electrolytes mainly sodium.
106
•Dehydration
• hypovolemic shock
•hypokalemia,
•hyponatremia
•Base deficit acidosis(HCO3)
•Hypoglycemia
•Malnutrition
•Dehydration(DHN) : loss of body fluid and
electrolytes mainly sodium.
106
Types of DHN
•Three types of DHN based on tone/ serum
sodium levels:
•Isotonic DHN(isonatrimic)- loss of H2O =Na+
• it is common type of DHN( 70 -80%)
•Hypotonic (hyponatrimic)- loss of Na+ > H2O (10-15%)
•Hypertonic(Hypernatremic)- loss of H2O >Na+
107
•Three types of DHN based on tone/ serum
sodium levels:
•Isotonic DHN(isonatrimic)- loss of H2O =Na+
• it is common type of DHN( 70 -80%)
•Hypotonic (hyponatrimic)- loss of Na+ > H2O (10-15%)
•Hypertonic(Hypernatremic)- loss of H2O >Na+
107
Assessement and classification of DHN
Severe dehydration ( Two or more signs)- > 10% deficit
•Lethargic or coma
•Skin pinch goes very slowly(> 2second)
•Drinks poorly or not at all
•Very sunken eye balls
Some dehydration ( two or more)- 5-10% of TBW Deficit.
•Irritable
•Sunken eye balls
•Skin pinch goes slowly(< 2 second)
•Thirsty (drink water eagerly)
No DHN < 5 % fluid deficit: None of these signs
108
Severe dehydration ( Two or more signs)- > 10% deficit
•Lethargic or coma
•Skin pinch goes very slowly(> 2second)
•Drinks poorly or not at all
•Very sunken eye balls
Some dehydration ( two or more)- 5-10% of TBW Deficit.
•Irritable
•Sunken eye balls
•Skin pinch goes slowly(< 2 second)
•Thirsty (drink water eagerly)
No DHN < 5 % fluid deficit: None of these signs
108
DX of AGE/Diarrheal disease
•Clinical and stool examination
•Stool specimens should be examined for;
- mucus, blood, and leukocytes.
•Fecal leukocytes :bacterial invasion of colonic
mucosa
•S/E examined for parasite
• serum electrolytes
109
•Clinical and stool examination
•Stool specimens should be examined for;
- mucus, blood, and leukocytes.
•Fecal leukocytes :bacterial invasion of colonic
mucosa
•S/E examined for parasite
• serum electrolytes
109
Management of acute diarrhoea
Main principle in management of acute
diarrhea is;
Replace lost water and salts( ORS)
Continue to feed to prevent malnutrition.
Antibiotics & antiprotozoals when needed.
supplemental zinc :
–Reduce duration and severity of diarrhoea &
–Reduce the occurrence of future episodes
Prevention of diarrhea
110
Main principle in management of acute
diarrhea is;
Replace lost water and salts( ORS)
Continue to feed to prevent malnutrition.
Antibiotics & antiprotozoals when needed.
supplemental zinc :
–Reduce duration and severity of diarrhoea &
–Reduce the occurrence of future episodes
Prevention of diarrhea
110
Types of ORS
Solution Glu
g/dl
Na
mEq/L
K
meq/L
Cl
meq/L
WHO 2.0 90 20 80
Rehydralyte 2.5 75 20 65
Pedialyte 2.5 45 20 35
Infalyte 2.0 50 20 40
111
Solution Glu
g/dl
Na
mEq/L
K
meq/L
Cl
meq/L
WHO 2.0 90 20 80
Rehydralyte 2.5 75 20 65
Pedialyte 2.5 45 20 35
Infalyte 2.0 50 20 40
111
112
Antibiotics in acute diarrhea
• BACTERIA : give cotrimozazole.
•Dysentery -cotrimoxazole /Ciprofloxaccilin
• If cholera :Cotrimoxazole or erithromycin
•giardia, E. Histolytica :metronidazol/ tinidazole.
113
• BACTERIA : give cotrimozazole.
•Dysentery -cotrimoxazole /Ciprofloxaccilin
• If cholera :Cotrimoxazole or erithromycin
•giardia, E. Histolytica :metronidazol/ tinidazole.
113
Treatment plan A: Treat diarrhoea at home
for no DHN
•Counsel the mother on the 4 rules of home
treatment:
1.Give extra fluid,
2. continue feeding,
3.Zink supplimentation
4.when to return
114
for no DHN
•Counsel the mother on the 4 rules of home
treatment:
1.Give extra fluid,
2. continue feeding,
3.Zink supplimentation
4.when to return
114
Plan A…..
In addition to usual intake:
•Up to 2 years 50 to 100 ml after each loose stool
•2 years or more 100 to 200 ml after each loose
stool
•Tell the mother to:
- Give frequent small sips from cup.
- If the child vomits, wait 10 minutes
- Continue giving extra fluid until the diarrhea stops.
115
In addition to usual intake:
•Up to 2 years 50 to 100 ml after each loose stool
•2 years or more 100 to 200 ml after each loose
stool
•Tell the mother to:
- Give frequent small sips from cup.
- If the child vomits, wait 10 minutes
- Continue giving extra fluid until the diarrhea stops.
115
Home Fluids for Diarrhoea Must Be:
•Ideal home fluids contain:
–salts and nutrients (sodium, potassium,
chloride, and bicarbonate)
–calories to replenish diet
•Examples of home fluids:
–ORS solution
–salted soup
–salted drinks
116
•Ideal home fluids contain:
–salts and nutrients (sodium, potassium,
chloride, and bicarbonate)
–calories to replenish diet
•Examples of home fluids:
–ORS solution
–salted soup
–salted drinks
116
Unsuitable fluids
•Fluids which are sweetened with sugar
Examples:
•Commercial carbonated beverages
•soft drinks
•sweetened fruit drinks
•sweetened tea.
•Fluids which are stimulant, diuretic or purgative
effects eg,coffee
117
•Fluids which are sweetened with sugar
Examples:
•Commercial carbonated beverages
•soft drinks
•sweetened fruit drinks
•sweetened tea.
•Fluids which are stimulant, diuretic or purgative
effects eg,coffee
117
Treatment plan B, SOME DHN
give 75ml/kg over 4 hours ORS in clinic.
•If the child wants more ORS than shown, give
more.
• For infants under 6 months who are not
breastfed,
• also give 100-200 ml clean water during this
period.
118
give 75ml/kg over 4 hours ORS in clinic.
•If the child wants more ORS than shown, give
more.
• For infants under 6 months who are not
breastfed,
• also give 100-200 ml clean water during this
period.
118
Treatment plan B
AFTER 4 HOURS:
• Reassess the child and classify the child for
dehydration.
•Select the appropriate plan to continue treatment.
If the mother must leave before completing treatment:
• Show her how to prepare ORS solution at home.
• Show her how much ORS to give to finish 4-hour
treatment at home.
•Give her enough ORS packets to complete
rehydration.
• Also give her 2 packets as recommended in plan A.
119
AFTER 4 HOURS:
• Reassess the child and classify the child for
dehydration.
•Select the appropriate plan to continue treatment.
If the mother must leave before completing treatment:
• Show her how to prepare ORS solution at home.
• Show her how much ORS to give to finish 4-hour
treatment at home.
•Give her enough ORS packets to complete
rehydration.
• Also give her 2 packets as recommended in plan A.
119
Some DHN Plan B
•Fluid deficit 5-10%
•ORS 75ml/kg over 4-6 hrs.
•Reassess the degree of DHN
–If no sign of DHN home Rx with
replacement of on going losses(50-
100ml/bowel motion).
–If sign of some DHN repeat plan B
–If worse IV RX
120
•Fluid deficit 5-10%
•ORS 75ml/kg over 4-6 hrs.
•Reassess the degree of DHN
–If no sign of DHN home Rx with
replacement of on going losses(50-
100ml/bowel motion).
–If sign of some DHN repeat plan B
–If worse IV RX
120
121
Treatment plan C, SEVERE DHN
122
122
Treatment plan C……
•Reassess an infant after 6 hours and a child after
3 hours.
•Classify dehydration choose plan (A, B, or C) to
continue treatment.
•If no IV treatment, Refer urgently to hospital for
IV treatment.
- If the child can drink, provide the mother with
ORS solution(on trip).
•If (NG) tube , with ORS solution:
- give 20 ml/kg/hour for 6 hours .
123
•Reassess an infant after 6 hours and a child after
3 hours.
•Classify dehydration choose plan (A, B, or C) to
continue treatment.
•If no IV treatment, Refer urgently to hospital for
IV treatment.
- If the child can drink, provide the mother with
ORS solution(on trip).
•If (NG) tube , with ORS solution:
- give 20 ml/kg/hour for 6 hours .
123
Treatment of diarrhea Cont...
Treatment of DHN in malnourished pts
Whenever possible rehydration should be PO.
IV infusions are very dangerous and
not recommended unless there is severe shock
or loss of consciousness from confirmed DHN.
Malnourished patients tend to develop
electrolyte imbalance with a great excess of
sodium and deficit in potassium.
We use a special ORS for severely malnourished
,called ResoMal.
124
Treatment of DHN in malnourished pts
Whenever possible rehydration should be PO.
IV infusions are very dangerous and
not recommended unless there is severe shock
or loss of consciousness from confirmed DHN.
Malnourished patients tend to develop
electrolyte imbalance with a great excess of
sodium and deficit in potassium.
We use a special ORS for severely malnourished
,called ResoMal.
124
Local resomal solution preparation
1.WHO standard ORS : 1 sachet
2.Cooled boiled water: 2 litter
3.Sugar: 50gram(4TSP)
4.Mineral mix : 40ml
125
1.WHO standard ORS : 1 sachet
2.Cooled boiled water: 2 litter
3.Sugar: 50gram(4TSP)
4.Mineral mix : 40ml
125
Treatment of diarrhea Cont...
Give this amount over 12 hrs starting with:
- 5ml/kg every 30 minutes for 2 hours orally/NGT and
- then 5-10 ml/kg per hour .
For each watery stool give 30 ml of resomal soln.
Weigh the child each hour and assess the liver size,
RR and PR.
126
Give this amount over 12 hrs starting with:
- 5ml/kg every 30 minutes for 2 hours orally/NGT and
- then 5-10 ml/kg per hour .
For each watery stool give 30 ml of resomal soln.
Weigh the child each hour and assess the liver size,
RR and PR.
126
Treatment of diarrhea Cont...
•If the child is in shock and unconscious ,then use
IV fluids
- R/L with 5 % D/W or ½ N/S with 5 % D/W.
•Give 15 ml/kg over the 1
st
hour and if there is
improvement repeat the 15 ml/kg
•If no improvement assume as septic shock.
•As soon as the child regains consciousness stop
the drip and
• treat by orally or NGT with 10 ml/kg /hr of
resomal.
127
•If the child is in shock and unconscious ,then use
IV fluids
- R/L with 5 % D/W or ½ N/S with 5 % D/W.
•Give 15 ml/kg over the 1
st
hour and if there is
improvement repeat the 15 ml/kg
•If no improvement assume as septic shock.
•As soon as the child regains consciousness stop
the drip and
• treat by orally or NGT with 10 ml/kg /hr of
resomal.
127
Cause of Persistent diarrhea
Persistent diarrhea- ≥ 14 days, may be due to:
Less than 10 percent of all diarrhoea
but associated with 30 to 50 percent of diarrhoea
deaths.
Malnutrition greatly increases the risk of death.
any enteropathogen that infects an
immunocomp.host; or
residual symptoms due to the intestine by an
enteropathogen after an acute infection.
128
Persistent diarrhea- ≥ 14 days, may be due to:
Less than 10 percent of all diarrhoea
but associated with 30 to 50 percent of diarrhoea
deaths.
Malnutrition greatly increases the risk of death.
any enteropathogen that infects an
immunocomp.host; or
residual symptoms due to the intestine by an
enteropathogen after an acute infection.
128
Cause of Persistent diarrhea
–Secondary disaccharidase deficiency
–Salmonella sp.
–Shigella sp.
–Enteroadherent E. coli
–Cryptosporidium
–G.lamblia
129
–Secondary disaccharidase deficiency
–Salmonella sp.
–Shigella sp.
–Enteroadherent E. coli
–Cryptosporidium
–G.lamblia
129
Etiology of Chronic Diarrhea
130
130
Persistent Diarrhea
•Contributing Factors
–Protein energy malnutrition
–Micronutrient deficiencies
–Immunodeficiency
•Refer those who have persistent diarrhoea AND
who are also dehydrated to hospital
–mortality is 8 to 10 times higher than that with
acute diarrhoea
–may need nutritional rehabilitation
–may need investigation for immune deficiencies
and/or resistant bacteria 131
•Contributing Factors
–Protein energy malnutrition
–Micronutrient deficiencies
–Immunodeficiency
•Refer those who have persistent diarrhoea AND
who are also dehydrated to hospital
–mortality is 8 to 10 times higher than that with
acute diarrhoea
–may need nutritional rehabilitation
–may need investigation for immune deficiencies
and/or resistant bacteria 131
Risk factors for Persistent
Diarrhea
•Age of baby < 1 yr.
•Malnutrition
•Recent introduction of animal milk
•Recent acute diarrhea
•Previous persistent diarrhea
N.B Important cause of mortality
132
Diarrhea
•Age of baby < 1 yr.
•Malnutrition
•Recent introduction of animal milk
•Recent acute diarrhea
•Previous persistent diarrhea
N.B Important cause of mortality
132
Treatment of persistent
diarrhea
•Correct Dehydration
•Correct Nutritional Problems
–Reduce disaccharides
–Increase energy intake
–Supplement micronutrients (Vit A)
•Give Antibiotics for Dysentery
•Avoid These Therapies
–Antibiotics for watery diarrhoea
–Anti-motility agents
–Diluted feeds
133
diarrhea
•Correct Dehydration
•Correct Nutritional Problems
–Reduce disaccharides
–Increase energy intake
–Supplement micronutrients (Vit A)
•Give Antibiotics for Dysentery
•Avoid These Therapies
–Antibiotics for watery diarrhoea
–Anti-motility agents
–Diluted feeds
133
Prevention of diarrheal disease
Wash your hands frequently, especially after using the
toilet, changing diapers.
Wash your hands before and after preparing food.
Adequate Nutrition,
Hygienic food preparation,
Vaccination (rotavirus, measles………)
Promotion of Exclusive Breast-feeding
Improved Complementary Feeding Practices
Improved Water and Sanitary Facilities
Promotion of Personal and Domestic Hygiene
Improved Case Management of Diarrhea
134
Wash your hands frequently, especially after using the
toilet, changing diapers.
Wash your hands before and after preparing food.
Adequate Nutrition,
Hygienic food preparation,
Vaccination (rotavirus, measles………)
Promotion of Exclusive Breast-feeding
Improved Complementary Feeding Practices
Improved Water and Sanitary Facilities
Promotion of Personal and Domestic Hygiene
Improved Case Management of Diarrhea
134
Intestinal parasitosis
•Most common infection worldwide.
•Nematodes
–Roundworm: Ascaris Lumbricoides
–Whipworm: Trichuris trichuria
–Hookworms: N. Americanus, Acylostoma Duodenale
–E. vermicularis
–Strongyloides Stercoralis
•Trematodes – Schistosomiasis
•Cestodes - Taeniasis/ cyctcrecosis
-Hymenolepisis nana
135
•Most common infection worldwide.
•Nematodes
–Roundworm: Ascaris Lumbricoides
–Whipworm: Trichuris trichuria
–Hookworms: N. Americanus, Acylostoma Duodenale
–E. vermicularis
–Strongyloides Stercoralis
•Trematodes – Schistosomiasis
•Cestodes - Taeniasis/ cyctcrecosis
-Hymenolepisis nana
135
Intestinal parasitosis….
•Giardia lamblia, Entamoeba histolytica
•Cryptosporidium hominis and parvum
•Isospora belli
•Cyclospora cayetanensis(in decreased immunity)
•Leishmania
136
•Giardia lamblia, Entamoeba histolytica
•Cryptosporidium hominis and parvum
•Isospora belli
•Cyclospora cayetanensis(in decreased immunity)
•Leishmania
136
Mode of transmission and predisposing
factors for worm infection:
•Contaminated food and water
•Through piercing the skin (Hookworms)
•Habits like eating mud in children (“Pica”)
•Vectors transmission
•Feco - oral transmission
•Unsanitary conditions
•Malnutrition
•Improperly cooked meals
•Improper hygiene practices
137
factors for worm infection:
•Contaminated food and water
•Through piercing the skin (Hookworms)
•Habits like eating mud in children (“Pica”)
•Vectors transmission
•Feco - oral transmission
•Unsanitary conditions
•Malnutrition
•Improperly cooked meals
•Improper hygiene practices
137
Clinical features of Intestinal parastosis
•Mostly; - abdominal pain, vomiting,
- diarrhea , abdominal cramping,
•Giardia :Stools initially may be profuse and
watery and later become greasy and foul smelling
, abdominal pain , Abdominal cramps
•Amoeba : tenesmus.
» Almost all stool is heme-positive.
138
•Mostly; - abdominal pain, vomiting,
- diarrhea , abdominal cramping,
•Giardia :Stools initially may be profuse and
watery and later become greasy and foul smelling
, abdominal pain , Abdominal cramps
•Amoeba : tenesmus.
» Almost all stool is heme-positive.
138
Clinical features of Intestinal parastosis….
•hook worm : respiratory symptom(cough) ,
- malnutrition, anemia ,edema
•Trichuria : rectal prolapsed
•E.vermicularis,stronglodiasis: anal itching
•schistosomiasis :
• -Complain of frequency, dysuria, and hematuria
• -epilepsy ,encephalitis, Hepatosplenomegaly
•Leishmania: few papular, nodular, plaquelike or
ulcerative lesions
139
•hook worm : respiratory symptom(cough) ,
- malnutrition, anemia ,edema
•Trichuria : rectal prolapsed
•E.vermicularis,stronglodiasis: anal itching
•schistosomiasis :
• -Complain of frequency, dysuria, and hematuria
• -epilepsy ,encephalitis, Hepatosplenomegaly
•Leishmania: few papular, nodular, plaquelike or
ulcerative lesions
139
Diagnosis I.parastosis
• S/E ,
•CBC(Hgb, RBC,WBC…..) ,
•urine test,
• liver function test
• imaging
140
• S/E ,
•CBC(Hgb, RBC,WBC…..) ,
•urine test,
• liver function test
• imaging
140
Treatement of I.parastosis
•most of them RX by Albendazole or mebendazole
–Roundworm: Ascaris Lumbricoides
–Whipworm: Trichuris trichuria
–Hookworms: N. Americanus, Acylostoma
Duodenale
–E. vermicularis
Strongyloides Stercoralis (RX-Ivermectin)
•Trematodes – Schistosomiasis(RX- Praziquantel)
141
•most of them RX by Albendazole or mebendazole
–Roundworm: Ascaris Lumbricoides
–Whipworm: Trichuris trichuria
–Hookworms: N. Americanus, Acylostoma
Duodenale
–E. vermicularis
Strongyloides Stercoralis (RX-Ivermectin)
•Trematodes – Schistosomiasis(RX- Praziquantel)
141
Treatement of I.parastosis
• Taeniasis/ cyctcrecosis - Praziquantel)
•-Hymenolepis nana- niclosimide /praziquantel
Giardia, ameoba : metronidazole/tinidazole
Leishmania: sodium stibogluconate
•cryptosporidiosis is self-limited
Prevention of I. Parastosis;
•Deworming by albendazole/mebendazole(2-5yrs)
•prevent the Mode of transmission and
•Reduce predisposing factors.
142
• Taeniasis/ cyctcrecosis - Praziquantel)
•-Hymenolepis nana- niclosimide /praziquantel
Giardia, ameoba : metronidazole/tinidazole
Leishmania: sodium stibogluconate
•cryptosporidiosis is self-limited
Prevention of I. Parastosis;
•Deworming by albendazole/mebendazole(2-5yrs)
•prevent the Mode of transmission and
•Reduce predisposing factors.
142
Acute Pancreatitis
•The most common pancreatic disorder in children
•At least 30-50 cases in major pediatric centers per
year.
most common etiologies are;
blunt abdominal injuries,
biliary stones
drug toxicity (6-mercaptopurine ,asparginase)
•infections, metabolic disorders,
•mutations in susceptibility genes
•Less than 5% of cases are idiopathic
143
•The most common pancreatic disorder in children
•At least 30-50 cases in major pediatric centers per
year.
most common etiologies are;
blunt abdominal injuries,
biliary stones
drug toxicity (6-mercaptopurine ,asparginase)
•infections, metabolic disorders,
•mutations in susceptibility genes
•Less than 5% of cases are idiopathic
143
C/M acute pancreatitis…
Mild
•severe abdominal pain,
•persistent vomiting, and possibly fever.
•The pain is epigastric or in upper quadrant
Severe: Shock, high fever, jaundice, ascites,
hypocalcemia, and pleural effusions can occur.
•A bluish discoloration on umbilicus (Cullen sign)
or in the flanks (Grey Turner sign).
144
Mild
•severe abdominal pain,
•persistent vomiting, and possibly fever.
•The pain is epigastric or in upper quadrant
Severe: Shock, high fever, jaundice, ascites,
hypocalcemia, and pleural effusions can occur.
•A bluish discoloration on umbilicus (Cullen sign)
or in the flanks (Grey Turner sign).
144
C/M acute pancreatitis…
•The pancreas is necrotic and can be transformed
into an inflammatory hemorrhagic mass.
•multiple organ dysfunction, shock, renal failure,
•acute respiratory distress syndrome,
•disseminated intravascular coagulation,
•massive gastrointestinal bleeding, and
•systemic or intra-abdominal infection.
145
•The pancreas is necrotic and can be transformed
into an inflammatory hemorrhagic mass.
•multiple organ dysfunction, shock, renal failure,
•acute respiratory distress syndrome,
•disseminated intravascular coagulation,
•massive gastrointestinal bleeding, and
•systemic or intra-abdominal infection.
145
DX of acute pancreatitis
•Measure serum lipase and amylase (increase)
•hemoconcentration, coagulopathy,
•leukocytosis, hyperglycemia, glucosuria,
•hypocalcemia, hyperbilirubinemia.
•Abdominal x-ray
•Acdominal US
•CT scanning (good)
146
•Measure serum lipase and amylase (increase)
•hemoconcentration, coagulopathy,
•leukocytosis, hyperglycemia, glucosuria,
•hypocalcemia, hyperbilirubinemia.
•Abdominal x-ray
•Acdominal US
•CT scanning (good)
146
Treatments of pancreatitis
•Aim :relieve pain & restore metabolic homeostasis
•Fluid, electrolyte, and mineral
•If severe, prophylactic antibiotics, NG tube
•drainage of necrotic material or abscess
Prognosis
•If uncomplicated recover within 4-5 days.
147
•Aim :relieve pain & restore metabolic homeostasis
•Fluid, electrolyte, and mineral
•If severe, prophylactic antibiotics, NG tube
•drainage of necrotic material or abscess
Prognosis
•If uncomplicated recover within 4-5 days.
147
Hepatitis
•Hepatitis is an inflammation of the liver
• can result in liver cell damage and destruction.
Cause of Hepatitis:
Virus :Hepatitis viruses(hepatitis A, B, C, D, and E),
•Cytomegalovirus (CMV), Epstein-Barr virus (EBV),
•Herpes simplex virus (HSV),
• Varicella zoster virus(VZV),
•Rubella, Adenovirus, Entero viruses(coxsackie
viruses and echoviruses) and Parvovirus.
Autoimmune liver disease.
148
•Hepatitis is an inflammation of the liver
• can result in liver cell damage and destruction.
Cause of Hepatitis:
Virus :Hepatitis viruses(hepatitis A, B, C, D, and E),
•Cytomegalovirus (CMV), Epstein-Barr virus (EBV),
•Herpes simplex virus (HSV),
• Varicella zoster virus(VZV),
•Rubella, Adenovirus, Entero viruses(coxsackie
viruses and echoviruses) and Parvovirus.
Autoimmune liver disease.
148
Hepatitis A & E :
•usually spread by fecal-oral contact
•They do not cause chronic infection
Hepatitis B(HBV)
• It can be mild,
• it may cause chronic hepatitis
•risk for chronic liver disease and liver failure.
•Transmission of HBV- blood contact
Hepatitis D
•only occur in the presence of hepatitis B.
•Transmission - blood contact
•the transmission from mother to baby is less
common than Hepatitis B
149
•usually spread by fecal-oral contact
•They do not cause chronic infection
Hepatitis B(HBV)
• It can be mild,
• it may cause chronic hepatitis
•risk for chronic liver disease and liver failure.
•Transmission of HBV- blood contact
Hepatitis D
•only occur in the presence of hepatitis B.
•Transmission - blood contact
•the transmission from mother to baby is less
common than Hepatitis B
149
Hepatitis C
•Hepatitis C: usually mild and gradual.
•Children often show no symptoms at all
•Transmission of HCV- infected blood,
•There is no vaccine for hepatitis C.
• People who are at risk should be checked
regularly for hepatitis C.
•People who have hepatitis C should be ;
•monitored closely for signs of chronic hepatitis
and liver failure.
150
•Hepatitis C: usually mild and gradual.
•Children often show no symptoms at all
•Transmission of HCV- infected blood,
•There is no vaccine for hepatitis C.
• People who are at risk should be checked
regularly for hepatitis C.
•People who have hepatitis C should be ;
•monitored closely for signs of chronic hepatitis
and liver failure.
150
Clinical features of hepatitis
•Most are asymtomatic.
•that are symptomatic present in three forms:
1.Anicteric form -The symptoms are non specific.
- Patients present with vomiting, fever and malaise.
•The diagnosis is suspected if a child has;
• history of contact with hepatitis or
• if the liver enzymes (SGOT, SGPT) are elevated
151
•Most are asymtomatic.
•that are symptomatic present in three forms:
1.Anicteric form -The symptoms are non specific.
- Patients present with vomiting, fever and malaise.
•The diagnosis is suspected if a child has;
• history of contact with hepatitis or
• if the liver enzymes (SGOT, SGPT) are elevated
151
Clinical features of hepatitis…..
2. Icteric form -The patients present with fever,
nausea, vomiting, abdominal discomfort,
jaundice and tender and enlarged liver.
3. Fulminant form –
•This is due to massive hepatic necrosis.
•deep jaundice,
• impaired mental status that progress to
coma, and death.
•The prognosis is poor.
152
2. Icteric form -The patients present with fever,
nausea, vomiting, abdominal discomfort,
jaundice and tender and enlarged liver.
3. Fulminant form –
•This is due to massive hepatic necrosis.
•deep jaundice,
• impaired mental status that progress to
coma, and death.
•The prognosis is poor.
152
Clinical features of hepatitis…..
•Jaundice
•Decreased appetite,
•Fever ,
• Nausea and/or vomiting,
• Abdominal pain or discomfort,
• Diarrhea,
• Clay-colored stools and Dark urine
153
•Jaundice
•Decreased appetite,
•Fever ,
• Nausea and/or vomiting,
• Abdominal pain or discomfort,
• Diarrhea,
• Clay-colored stools and Dark urine
153
Diagnosis of hepatitis
• Liver function studies,
•Increased serum bilirubin ,
•Antibody and polymerase chain reaction studies ,
•Cellular blood counts,
•Computed tomography scan (CT scan),
• Magnetic resonance imaging (MRI) and
•Liver biopsy.
154
• Liver function studies,
•Increased serum bilirubin ,
•Antibody and polymerase chain reaction studies ,
•Cellular blood counts,
•Computed tomography scan (CT scan),
• Magnetic resonance imaging (MRI) and
•Liver biopsy.
154
Treatment of hepatitis
•supportive ( diet ,rest ),
•treat associated symptom,
•antiviral ,
•Maintaining adequate growth and development,
•Avoiding alcohol and drugs,
•Preventing the spread of the disease
•Hospitalization (severe cases),
• Liver transplantation
Preventions:
•Proper hygiene,
•Vaccinations ( for hepatitis A and B)
•Antibody preparation If exposed to A or B virus
• Blood transfusions are routinely screened
155
•supportive ( diet ,rest ),
•treat associated symptom,
•antiviral ,
•Maintaining adequate growth and development,
•Avoiding alcohol and drugs,
•Preventing the spread of the disease
•Hospitalization (severe cases),
• Liver transplantation
Preventions:
•Proper hygiene,
•Vaccinations ( for hepatitis A and B)
•Antibody preparation If exposed to A or B virus
• Blood transfusions are routinely screened
155
Hemorrhoid
•often related to a-diet deficient in fiber and
- poor hydration.
•Clinical Manifestations of hemorroid
External hemorrhoids occur below dentate line
•extreme pain and itching, often due to acute
thrombosis.
Internal hemorrhoids are located above the
dentate line
•bleeding, prolapse, and occasional incarceration.
156
•often related to a-diet deficient in fiber and
- poor hydration.
•Clinical Manifestations of hemorroid
External hemorrhoids occur below dentate line
•extreme pain and itching, often due to acute
thrombosis.
Internal hemorrhoids are located above the
dentate line
•bleeding, prolapse, and occasional incarceration.
156
Treatments of hemorrhoid
•dietary modification,
•decreased straining,
•avoidance of prolonged time sitting on toilet
•topical analgesics or anti-inflammatories
•sitz baths
•thrombectomy
•Surgical treatment is reserved for patients failing
conservative management
157
•dietary modification,
•decreased straining,
•avoidance of prolonged time sitting on toilet
•topical analgesics or anti-inflammatories
•sitz baths
•thrombectomy
•Surgical treatment is reserved for patients failing
conservative management
157
Hirschsprung disease or
congenital aganglionic megacolon
•it is neurocristopathy of enteric nervous system,
• characterized by the absence of ganglion cells in
the submucosal and myenteric plexus.
• It is the most common cause of lower intestinal
obstruction in neonates,
•overall incidence of 1 in 5,000 live births.
158
congenital aganglionic megacolon
•it is neurocristopathy of enteric nervous system,
• characterized by the absence of ganglion cells in
the submucosal and myenteric plexus.
• It is the most common cause of lower intestinal
obstruction in neonates,
•overall incidence of 1 in 5,000 live births.
158
Hirschsprung disease...
•The male:female ratio is 4 : 1
•Nearly all children DX during the first 2 yrs of life.
•one half are DX before they are aged 1 year.
•The overall mortality of Hirschsprung
enterocolitis is 25-30%,
•Cause of HD: inheritance & Genetic defects
159
•The male:female ratio is 4 : 1
•Nearly all children DX during the first 2 yrs of life.
•one half are DX before they are aged 1 year.
•The overall mortality of Hirschsprung
enterocolitis is 25-30%,
•Cause of HD: inheritance & Genetic defects
159
Pathophysiology ,Hirschsprung disease
1.absence of parasympathetic ganglion cells in
the myenteric and submucosal plexus of the
rectum and/or colon.
2.arrest of neuroblast migration from the
proximal to distal bowel
3.inadequate relaxation of the bowel wall and
bowel wall hypertonicity
4.lead to intestinal obstruction.
160
1.absence of parasympathetic ganglion cells in
the myenteric and submucosal plexus of the
rectum and/or colon.
2.arrest of neuroblast migration from the
proximal to distal bowel
3.inadequate relaxation of the bowel wall and
bowel wall hypertonicity
4.lead to intestinal obstruction.
160
HD can be classified as follows:
•Classical HD (80% of cases): Rectosegmoid
•Long segment HD -proximal to sigmoid colon ( 10-15% )
•Total colonic aganglionosis (5% )
•rare variants include the following:
–Total intestinal aganglionosis
–Ultra-short-segment HD (involving the distal
rectum below the pelvic floor and the anus)
161
•Classical HD (80% of cases): Rectosegmoid
•Long segment HD -proximal to sigmoid colon ( 10-15% )
•Total colonic aganglionosis (5% )
•rare variants include the following:
–Total intestinal aganglionosis
–Ultra-short-segment HD (involving the distal
rectum below the pelvic floor and the anus)
161
Clinical presentation of HD
•Newborns :
–Failure to pass meconium within the first 48
hours of life
99% meconium is passed within 48 hrs of birth.
–Abdominal distension that is relieved by
rectal stimulation or enemas
–Vomiting
–Neonatal enterocolitis
162
•Newborns :
–Failure to pass meconium within the first 48
hours of life
99% meconium is passed within 48 hrs of birth.
–Abdominal distension that is relieved by
rectal stimulation or enemas
–Vomiting
–Neonatal enterocolitis
162
Clinical presentation of HD…
Symptoms in older children;
–Severe constipation
–Abdominal distension
–Bilious vomiting
–Failure to thrive
In HD Assosciated enterocolitis;
•abdominal distension,
•explosive diarrhea,
•vomiting, fever, lethargy,
•rectal bleeding, or shock
163
Symptoms in older children;
–Severe constipation
–Abdominal distension
–Bilious vomiting
–Failure to thrive
In HD Assosciated enterocolitis;
•abdominal distension,
•explosive diarrhea,
•vomiting, fever, lethargy,
•rectal bleeding, or shock
163
diagnostic workup for HD
•Rectal Biopsy: best (presence of ganglion cells)
•Plain abdominal radiography
•Contrast enema
•Anorectal manometry measures the pressure of
the internal anal sphincter while a balloon is
distended in the rectum.
164
•Rectal Biopsy: best (presence of ganglion cells)
•Plain abdominal radiography
•Contrast enema
•Anorectal manometry measures the pressure of
the internal anal sphincter while a balloon is
distended in the rectum.
164
Treatment of HD
•Frist colostomy
•The treatment is surgical removal or bypass of
the aganglionic bowel
•definitive surgery is when child is older
•Treat complication
165
•Frist colostomy
•The treatment is surgical removal or bypass of
the aganglionic bowel
•definitive surgery is when child is older
•Treat complication
165
Short bowel syndrome
•It is a condition that occurs when part of the
small intestine is missing or has been removed.
can result in symptoms of;
• generalized malabsorption disorder or
• nutrient deficiencies,
At birth,
• the length of small bowel is 200-250 cm;
• by adulthood, it grows to 300-800 cm.
166
•It is a condition that occurs when part of the
small intestine is missing or has been removed.
can result in symptoms of;
• generalized malabsorption disorder or
• nutrient deficiencies,
At birth,
• the length of small bowel is 200-250 cm;
• by adulthood, it grows to 300-800 cm.
166
Short bowel syndrome
•An infant with as little as 15 cm of bowel with an
ileocecal valve, or 20 cm without,
•has the potential to survive by total parenteral
nutrition (TPN).
Cause: Most cases are acquired,
•Some congenital (atresia, gastroischisis).
• Risk factors :diseases that may require surgery:
such as Crohn's disease , Hirschsprung disease
necrotizing enterocolitis
Other; Volvulus, tumor/injury to small intestine.
167
•An infant with as little as 15 cm of bowel with an
ileocecal valve, or 20 cm without,
•has the potential to survive by total parenteral
nutrition (TPN).
Cause: Most cases are acquired,
•Some congenital (atresia, gastroischisis).
• Risk factors :diseases that may require surgery:
such as Crohn's disease , Hirschsprung disease
necrotizing enterocolitis
Other; Volvulus, tumor/injury to small intestine.
167
Short bowel syndrome
Clinical Manifestations :
•The major clinical manifestations are ;
- malabsorption and diarrhea
•Abdominal pain, Diarrhea and steatorrhea
•Fluid depletion,
•Weight loss and malnutrition,
•Fatigue
•Vit & mineral deficiencies
• anemia
•muscle spasms and bone pain.
168
Clinical Manifestations :
•The major clinical manifestations are ;
- malabsorption and diarrhea
•Abdominal pain, Diarrhea and steatorrhea
•Fluid depletion,
•Weight loss and malnutrition,
•Fatigue
•Vit & mineral deficiencies
• anemia
•muscle spasms and bone pain.
168
complications of Short bowel syndrome
Related to parenteral nutrition:
•central catheter infection, thrombosis, hepatic
cholestasis and cirrhosis, and gallstones.
vitamin B
12, folate, iron deficiency
fat-soluble vitamins deficiency,
Renal stones
169
Related to parenteral nutrition:
•central catheter infection, thrombosis, hepatic
cholestasis and cirrhosis, and gallstones.
vitamin B
12, folate, iron deficiency
fat-soluble vitamins deficiency,
Renal stones
169
Short bowel syndrome
Treatement:
•More than 90% survive.
•Fluid and electrolyte replacements
• The use of parenteral nutrition
•antibiotics (metronidazole….)
•Surgical
There is no cure for short bowel syndrome
except transplant.
170
Treatement:
•More than 90% survive.
•Fluid and electrolyte replacements
• The use of parenteral nutrition
•antibiotics (metronidazole….)
•Surgical
There is no cure for short bowel syndrome
except transplant.
170
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