This document provides information on gastroesophageal reflux disease (GERD) and acute gastroenteritis in children. It discusses the definition, epidemiology, risk factors, types, mechanisms, etiology and treatment of these conditions. For GERD, it describes the difference between physiologic and pathologic reflux. It also outlines diagnostic tests and treatment approaches including lifestyle changes, medications and surgery. For acute gastroenteritis, it defines the condition and discusses causative agents such as viruses, bacteria and parasites. It compares secretory and osmotic diarrhea and describes the pathogenesis of infectious diarrhea.

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Pediatrics
GIT
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Subject1: GERD
Gastroesophageal Reflux Disease GERD:
 GERD is defined as the effortless retrograde movement of gastric contents upward into
the esophagus.
 GERD is the most common esophageal disorder in children of all ages.
 Although occasional episodes of reflux are physiologic, exemplified by the
regurgitation of normal infants, the phenomenon becomes pathologic (GERD) in
children who have episodes that are more frequent or persistent, and thus produce
esophagitis or esophageal symptoms, or in those who have respiratory sequelae.
Physiologic GERD:
 Spitting up is normal in infants younger than 12
months old.
 Natural history:
o Reflux becomes evident in the 1st few
months of life, nearly half of all infants are
reported to spit up at 2 months of age.
o Peaks at ≈4 months.
o Resolves in most by 12 months and nearly all
by 24 months.
Criteria for physiologic GERD:
 Normal weight gain.
 Have no signs of respiratory or peptic complications.
 The absence of bloody or bilious vomiting.
Factors involved in physiologic GERD include:
 Liquid diet.
 Frequent, relatively large volume feedings.
 Horizontal body position.
 Short, narrow esophagus.
 Immature LES.
 Small, noncompliant stomach.

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As infants grow:
 They spend more time upright.
 Develop a longer and larger diameter esophagus.
 Have a larger and more compliant stomach.
 Eat more solid foods.
 Experience lower caloric needs per unit of body weight.
 As a result, most infants stop spitting up by 9 to 12 months of age.
Pathologic GERD:
 After 18 months of age or if there are complications in younger infants such as
o Esophagitis:
 This may present clinically as blood in the vomit or more insidiously with the
development of anemia or stricture.
 Older children may complain of heartburn with reflux.
 While smaller infants may develop feeding difficulties due to esophageal
discomfort.
o Respiratory symptoms:
 Wheezing, aspiration pneumonia, hoarse voice chronic cough, or apneic spells.
o Failure to thrive.
Diagnosis:
 A clinical diagnosis is often sufficient in children with classic effortless regurgitation
and no complications.
 Diagnostic studies are indicated for pathological GERD:
o Barium upper GI series  to exclude obstruction such as pyloric stenosis, hiatus
hernia, gastric antral web, duodenal stenosis, annular pancreas, and malrotation.
Because of the brief nature of the examination, a negative barium study does not
rule out GERD.
o 24-hour esophageal probe  Data typically are gathered for 24 hours, following
which the number and temporal pattern of acid reflux events are analyzed.
o Esophageal impedance monitoring  which records the migration of electrolyte
rich gastric fluid in the esophagus.
o Endoscopy  is useful to rule out esophagitis, esophageal stricture, and anatomic
abnormalities.

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Treatment of uncomplicated GERD:
 In otherwise healthy young infants ("well-nourished, happy spitters"), the mother
should be reassured and advised of simple measures to help with the problem.
 Positional therapy  supine upright in seat, elevate head of crib with head up is
helpful,
 Towel on caregiver's shoulder  cheap, effective, useful only for physiologic reflux.
 Thickened feedings  reduces number of episodes, enhances nutrition, thickening of
formula with a tablespoon of rice cereal per ounce of formula results in fewer
regurgitation episodes, greater caloric density (30kcal/oz), and reduced crying time.
 Smaller more frequent feedings  can help some, be careful not to underfeed child.
 Hypoallergenic  if there is a strong family history of atopy or signs of eczema.
Treatment of complicated GERD:
 Medical therapy:
o Proton-pump inhibitor PPIs  omeprazole, lansoprazole, pantoprazole,
rabeprazole, and esomeprazole, effective medical therapy for heartburn and
esophagitis.
o H2 receptor antagonist H2RAs  cimetidine, famotidine, nizatidine, and ranitidine,
reduces heartburn, less effective for healing esophagitis.
o Metoclopramide  enhances stomach emptying and LES tone, real benefit is often
minimal.
 Surgical therapy:
o For:
 Esophagitis unresponsive to medical therapy.
 Esophageal stricture.
 Apneic spells or chronic pulmonary disease unresponsive to 2–3 months of
medical therapy.
o Feeding jejunostomy  useful in child requiring tube feeds, delivering feeds
downstream eliminates GERD
o Nissen or other fundoplication procedure  for life-threatening or medically
unresponsive cases.
o Fundoplication procedures may be performed as open operations, by laparoscopy,
or by endoluminal (gastroplication) techniques.

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Subject2: Acute gastroenteritis
Introduction:
 The term gastroenteritis captures the bulk of infectious cases of diarrhea.
 The term diarrheal disorders is more commonly used to denote infectious diarrhea in
public health settings, although several noninfectious causes of gastrointestinal illness
with vomiting and/or diarrhea are well recognized.
 The term gastroenteritis denotes infections of the gastrointestinal tract caused by
bacterial, viral, or parasitic pathogens.
 Many of these infections are foodborne illnesses.
 The most common manifestations are diarrhea and vomiting, which can also be
associated with systemic features such as abdominal pain and fever.
Definition:
 Acute diarrhea is defined as the abrupt onset of 3 or more loose stools per day and
lasts no longer than 14 days.
 Increase frequency and/or liquidity of stool.
 Stool output >10 g/kg/24 hr, or more than the adult limit of 200 g/24 hr.
Epidemiology:
 Diarrheal disorders in childhood account for a large
proportion (18%) of childhood deaths.
 With an estimated 1.5 million deaths per year globally,
making it the second most common cause of child
deaths worldwide.
Risk factors for diarrhea:
 Lack of exclusive breastfeeding (0-5 mo).
 No breastfeeding (6-23 mo).
 Underweight, stunted, wasted (malnourished).
 Vitamin A deficiency.
 Zinc deficiency.
 Crowding (>8 persons/kitchen).
 Indoor air pollution.
 Unwashed hands.

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 Poor water quality.
 Inappropriate excreta disposal.
 Immune deficiency.
 Measles.
Types of diarrhea:
 Acute watery diarrhea (<14 days).
 Dysentery (visible blood in stool).
 Persistent diarrhea (>14 days).
Mechanism of diarrhea:
 The basis for all diarrhea is disturbed intestinal solute transport.
 Water movement across intestinal membranes is passive and is determined by both
active and passive fluxes of solutes, particularly sodium, chloride, and glucose.
 The pathogenesis of most episodes of diarrhea can be explained by secretory, osmotic,
or motility abnormalities or a combination of these.
Secretory:
 Defect present:
o Increased secretion.
o Decreased absorption.
 Examples:
o Activation of cAMP: Cholera, toxinogenic E.coli (LT).
o Shigella, Salmonella, Campylobacter jejuni.
o Pseudomonas aeruginosa.
o Activation of cGMP: E. coli (ST), Yersinia enterocolitica toxin.
 Comments:
o Persists during fasting.
o No stool WBCs.
Osmotic:
 Defect present:
o Digestive enzyme deficiencies.
o Ingestion of unabsorbable solute.
 Examples:
o Malabsorption: Disaccharidase deficiencies (lactase), rota virus cause lactase
deficiency.
o Excessive intake of carbonated fluid.

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o Excessive intake of non-absorbable solute: Lactulose.
 Comments:
o Stop with fasting.
o No stool WBCs.
Osmotic Secretory
Stool volume Moderately increase <200ml/24h Large volume >200ml/24h
Stool Na < 70mEq/l >70
Fasting diarrhea stop Diarrhea continue
Ion gap >100mosm/kg < 100
Stool PH < 5 >6
Reducing substance +ve -ve
Note:
 The stool osmolality is indicated by the electrolytes and the ion gap is 100 mOsm/kg or
less.
 The ion gap is calculated by subtracting the concentration of electrolytes from total
osmolality.
 Ion gap = Stool osmolality – [ (stool Na + stool K) × 2]

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Pathogenesis of infectious diarrhea:
 Non-inflammatory diarrhea:
o Enterotoxin production by some bacteria.
o Destruction of villus (surface) cells by viruses.
o Adherence by parasites.
o Adherence and/or translocation by bacteria.
 Inflammatory diarrhea:
o Usually caused by bacteria that directly invade the intestine.
o Bacteria produce cytotoxins with consequent fluid, protein, and cells (erythrocytes,
leukocytes) that enter the intestinal lumen.
o Some enteropathogens possess more than one virulence property.
Etiology of diarrhea:
 Gastroenteritis is the result of infection acquired through the fecal-oral route or by
ingestion of contaminated food or water.
 General causes  poverty, poor environmental hygiene, and development indices.
 Viral gastroenteritis (“stomach flu”)  Rotavirus and the noroviruses are the most
common viral agents, followed by sapoviruses, enteric adenoviruses and astroviruses.
 Bacterial causes  Shigella, Salmonella, E. coli, Campylobacter.
 Parasitic causes  Giardia and Entamoeba histolytica.
Non-infectious diarrhea:
 Allergy to milk or its components.
 Malabsorption.
 Endocrinopathies.
 Poisoning.
 Neoplasia e.g.: neuroblastoma.
 IBD.
 Drugs / medications.
 Traveller’s Diarrhoea.
Infectious diarrhea:
1-Rotavirus infection:
 Typically begins after an incubation period of <48 hr with mild to moderate fever as
well as vomiting, followed by the onset of frequent, watery stools.

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 All 3 symptoms are present in about 50-60% of cases.
 Vomiting and fever typically abate during the 2nd day of illness, but diarrhea often
continues for 5-7 days.
 The stool is without gross blood or white blood cells.
 Dehydration may develop and progress rapidly, particularly in infants.
 Lead to secondary lactose intolerance so give lactose free milk.
 The most severe disease typically occurs among children 4-36 mo of age.
 Malnourished children and children with underlying intestinal disease, are particularly
likely to acquire severe rotavirus diarrhea.
2-Shigella:
 Four species of Shigella are responsible for bacillary dysentery:
o S. dysenteriae.
o S. flexneri.
o S. boydii.
o S. sonnei.
 It is most common in the 2nd and 3rd year of life, infection in the 1st 6 mo of life is
rare (may be due to Breast feeding).
 The colon is the target organ for shigellae.
 Symptoms:
o Generalized toxicity (high fever, sweating, shivering, nausea, fatigue).
o Urgency, and painful defecation characteristically occur.
o Watery  bloody mucoid stools (bed dysentery).
o Convulsions (due to toxin), headache, lethargy, confusion, nuchal rigidity, or
hallucinations may be present before or after the onset of diarrhea.
3-Salmonella
 Salmonella causes 2 clinical syndromes in humans: a GE that is usually self-limited, and
typhoid fever that is a relatively severe systemic illness classically caused by S. typhi.
 Nontyphoidal strains of Salmonella can also cause a severe bacteremic illness in some
circumstances.
 Clinical features  Acute Enteritis (mild to severe watery diarrhea, Bloody diarrhea).
4-Escherichia Coli:
 Gram-negative bacilli
 5 major groups of diarrheagenic E. coli:
o Enterotoxigenic E. coli (ETEC).
o Enteroinvasive E. coli (EIEC).
o Enteropathogenic E. coli (EPEC).

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o Shiga toxin–producing E. coli (STEC) known as enterohemorrhagic E. coli (EHEC).
o Enteroaggregative E. coli (EAEC).
5-Campylobacter:
 The organism invades the mucosa of the jejunum, ileum, and colon, producing
enterocolitis.
 Cause  Gastroenteritis, bacteremia, Guillain-Barré syndrome.
 Acute Gastroenteritis.
 Watery or bloody diarrhea.
 The abdominal pain is periumbilical; cramping but may mimic appendicitis or
intussusception.
6-Yersinia Enterocolitica:
 Infants & young children characteristically have a diarrheal disease.
 Older children usually have acute mesenteric lymphadenitis mimicking appendicitis or
Crohn disease.
 Arthritis, rash, and spondylopathy may develop.
7-Giardia Lamblia:
 It infects the duodenum and small intestine.
 There is usually no extraintestinal spread.
 Clinically:
o Asymptomatic.
o Acute infectious diarrhea  insidious onset of progressive anorexia, nausea,
gaseousness, abdominal distention, watery diarrhea.
o Chronic diarrhea  with persistent GIT signs and symptoms, including FTT and
abdominal pain or cramping.
o Others  malabsorption, -+ fever, gases.
o Not not not lead to bloody diarrhea.
8-Entamoeba histolytica:
 Clinical presentations asymptomatic cyst passage, amebic colitis, amebic dysentery,
ameboma, and extraintestinal disease as amebic liver disease.
 Amebic colitis:
o Gradual onset of colicky abdominal pains and frequent bowel movements (6–
8/day).
o Diarrhea is frequently associated with tenesmus.
o Stools are blood stained and contain a fair amount of mucus with few leukocytes.

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o Generalized constitutional symptoms and signs are characteristically absent, with
fever documented in only ⅓ of patients.
 Others:
o Bloody diarrhea called (wet dysentery).
o Extraintestinal spread.
o Carrier (asymptomatic)  eradication.
Watery VS bloody diarrhea:
Causes of watery diarrhea:
 Viral enteritis.
 Enterotoxin producing bacteria:
o Escherichia coli.
o Klebsiella organisms.
o Clostridium perfringens.
o Vibrio species.
 Parasitic GE:
o Giardia.
o Cryptosporidium.
 Extraintestinal Infections:
o Parenteral Diarrhea e.g.: otitis media & urinary tract infection.
Causes of bloody diarrhea (real or apparent):
 In infants and children Infants aged <1 year:
o Intestinal infection  shigella, salmonella, E-coli, campylobacter, Yersinia,
E.histolytica.
o Infant colitis (Cow’s milk colitis)  non-specific allergic colitis.
o Rare causes  like Intussusception, Malrotation, volvulus.
 In infants aged >1 year:
o Intestinal infection.

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o Inflammatory bowel disease.
o Juvenile polyp.
o Rare causes  Intussusception, Malrotation, volvulus, Henoch-Schönlein purpura.
o Recent antibiotic use raises suspicion for antibiotic-associated colitis
and Clostridium difficile colitis.
Clinical evaluation of diarrhea:
1-Initial evaluation:
 Assessing the degree of dehydration and acidosis and provide rapid resuscitation and
rehydration with oral or intravenous fluids as required.
 Clinically determining the etiology of diarrhea for institution of prompt antibiotic
therapy.
2-History:
 Stool:
o Stool characteristics  consistency, color, volume, frequency.
o Presence of associated enteric symptoms  nausea, vomiting, fever, abdominal
pain.
o Use of child daycare  common pathogens: rotavirus, astrovirus, calicivirus,
Campylobacter, Shigella, Giardia, and Cryptosporidium species [spp].
o Food ingestion history  raw, contaminated foods, food poisoning.
o Water exposure  swimming pools, marine environment.
o Camping history  possible exposure to contaminated water sources.
o Travel history  common pathogens affect specific regions, also consider rotavirus
and Shigella, Salmonella, and Campylobacter spp regardless of specific travel
history, as these organisms are prevalent worldwide.
o Animal exposure  young dogs/cats: Campylobacter spp; turtles:Salmonella spp.
o Predisposing conditions  hospitalization, antibiotic use, immunocompromised
state.
 Although nausea and vomiting are nonspecific symptoms, they indicate infection in the
upper intestine.
 Fever suggests an inflammatory process (inflammatory diarrhea) but also occurs as a
result of dehydration or coinfection (e.g., urinary tract infection, otitis media) called
also parenteral diarrhea (etiology outside the G.I system).
 Severe abdominal pain, tenesmus and bloody diarrhea indicate involvement of the
large intestine and rectum.
 Features such as nausea and vomiting and absent or low-grade fever with mild to
moderate periumbilical pain and watery diarrhea indicate small intestine involvement
and also reduce the likelihood of a serious bacterial infection.

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 Extra intestinal: Fever, malaise, reactive arthritis, systemic spread of micro-organism,
GBS, HUS, hemolytic anemia.
3-Stool characteristics:
4-Investigations:
 Stool Examination:
o Microscopic examination of the stool  fecal leukocytes and RBC indicate bacterial
invasion of colonic mucosa, stool microscopy must include examination for
parasites causing diarrhea, such as G. lamblia and E. histolytica.
 Stool culture:
o Indications of stool culture in diarrhea:
 Signs of systemic toxicity (septic).
 Bloody diarrhea.
 Mucus in the stool.
 History of recent travel.
 Epidemic condition.
 Immunocompromised.
 Chronic diarrhea or 7 days diarrhea.
 Uncertain diagnosis.
o Time:
 Stool culture = 2 days.

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 Urine culture = 3 days.
 Blood culture = 10 days.
 Plasma electrolytes, urea, creatinine and glucose:
o Should be checked if intravenous fluids are required.
o Features suggestive of hypernatremia.
o Severe dehydration or shock.
o Children with severe malnutrition.
 Blood culture  if antibiotics are started, take blood culture.
 Urinalysis  to exclude UTI (parenteral diarrhea).
 Enzyme immunoassay  for rotavirus (ELISA) or adenovirus antigens.
 Specific:
o E. histolytica  identification of the organism in the stool, serologic tests are useful
for diagnosis of extraintestinal amebiasis, including amebic hepatic abscess.
o Giardiasis  identifying trophozoites or cysts in stool, less often a duodenal
aspirate or biopsy of the duodenum or upper jejunum is needed.
Complications: (Extra-intestinal manifestations of enteric infections)
 Focal infections from systemic spread of bacterial pathogens  gvulvovaginitis,
urinary tract infection, endocarditis, osteomyelitis, meningitis, pneumonia, hepatitis,
peritonitis, chorioamnionitis, soft-tissue infection, septic thrombophlebitis.
 Reactive arthritis.
 Guillain-Barré syndrome.
 Glomerulonephritis.
 Immunoglobulin A (IgA) nephropathy.
 Erythema nodosum.
 Hemolytic uremic syndrome: Escherichia coli O157:H7.
 Hemolytic anemia.
Prevention:
 Primary prevention (to reduce disease transmission):
o Rotavirus and measles vaccines.
o Handwashing with soap.
o Providing adequate and safe drinking water.
o Environmental sanitation.
 Secondary prevention (to reduce disease severity):
o Promote breastfeeding.
o Vitamin A supplementation.
o Treatment of episodes of AD with zinc.

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Zinc and diarrhoea:
 Zinc deficiency is common in developing countries and zinc is lost during diarrhea.
 Zinc deficiency is associated with impaired electrolyte and water absorption,
decreased brush border enzyme activity and impaired cellular and humoral immunity.
 Treatment with zinc reduces the duration and severity of AD and also reduces the
frequency of further episodes during the subsequent 2-3 months.
 WHO recommends that children from developing countries with diarrhea be given zinc
for 10-14 days:
o 10mg daily for children <6 months.
o 20 mg daily for children >6 months.
Conditions which can mimic gastroenteritis:

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Subject3: Chronic diarrhea
Definition:
 Chronic or persistent diarrhea is defined as an episode that lasts longer than 14 days.
 Four principle pathophysiologic mechanisms: osmotic, secretory, dysmotility
associated, and inflammatory.
Pathophysiologic mechanisms:
 Osmotic diarrhea:
o Caused by a failure to absorb a luminal solute, resulting in secretion of fluids and
net water retention across an osmotic gradient.
o Best exemplified by the common disorder of lactose malabsorption.
o Either because of dissacharidase deficiencies or because the absorptive capacity of
the intestine for that sugar may be overwhelmed by excessive consumption, e.g.
fructose and sorbitol.
o Such excessive intake may be seen in young children drinking fruit juices.
 Secretory diarrhea:
o Occurs when there is a net secretion of electrolyte and fluid from the intestine
without compensatory absorption.
o Children with a pure secretory diarrhea will therefore continue to experience
diarrhea even while fasting.
o Disease such as congenital chloride diarrhea.
 Chronic diarrhea associated with intestinal dysmotility:
o Typically occurs in the setting of intact absorptive abilities.
o Intestinal transit time is decreased, the time allowed for absorption is minimized,
and fluid is retained within the lumen.
o Disease such as diarrhea-predominant irritable bowel syndrome (IBS).
 Inflammatory diarrhea:
o May encompass all of the pathophysiologic mechanisms.
o Inflammation with resultant injury to the intestine may lead to malabsorption of
dietary macronutrients which, in turn, creates a luminal osmotic gradient.
o Additionally, particular infectious agents may induce secretion of fluid into the
lumen, and blood in the gut may alter intestinal motility.
o Diseases such as inflammatory bowel disease (IBD) and celiac disease.

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Etiology:
 Enteric infections  are by far the most frequent cause of chronic diarrhea, both in
developing and industrialized countries.
 Lactose intolerance or carbohydrate malabsorption  may be caused by a brush-
border enzyme defect in lactase or other enzymes, more commonly, lactose
intolerance is secondary to lactase deficiency caused by intestinal mucosal damage.
 Allergy to cow’s milk protein  and other food proteins also may present during
infancy with chronic diarrhea, could lead to bloody diarrhea.
 Chronic diarrhea may be the manifestation of maldigestion  caused by exocrine
pancreatic disorders, in most patients with cystic fibrosis, exocrine pancreatic
insufficiency results in steatorrhea and protein malabsorption.
 The most benign etiology of chronic diarrhea is nonspecific diarrhea that encompasses
functional diarrhea (or toddler’s diarrhea)  in children younger than 4 years of age
and irritable bowel syndrome in those 5 years of age and older, the diseases fall under
the umbrella of functional disorders, in that in older children abdominal pain is often
associated with diarrhea alternating with constipation and growth and weight gain are
normal.
Note: Functional diarrhea in child less than 5 years is Toddlers diarrhea, and above 5 years is IBS.
 In older children and adolescents, inflammatory bowel diseases  including Crohn
disease, ulcerative colitis cause chronic diarrhea that is often associated with
abdominal pain, elevated inflammatory markers.
 Diarrhea may be the result from an excessive intake of fluid and carbohydrate (osmotic
diarrhea)  fruit juice, if the child’s fluid intake were >150 mL/kg/24 hr, fluid intake
should be reduced not to exceed 90 mL/kg/24 hr.
 A reduction of intestinal absorptive surface is responsible for diarrhea in celiac disease.
Etiology (summary):
 Infections:
o Enteric infections.
o Small intestinal bacterial overgrowth.
o Postenteritis syndrome.
 Diarrhea associated with exogenous substances:
o Excessive intake of laxatives containing lactulose
Note: Rota virus could lead
to chronic diarrhea (14 days)

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 Abnormal digestive processes:
o Cystic fibrosis.
o Chronic cholestasis.
 Nutrient malabsorption:
o Congenital or acquired lactase deficiency.
 Immune and inflammatory:
o Food allergy (cow's milk or soy proteins, others).
o Celiac disease.
 Structural defects:
o Microvillus inclusion disease.
o Lymphangiectasia.
 Defects of electrolyte and metabolite transport:
o Congenital chloride diarrhea.
o Congenital sodium diarrhea.
 Motility disorders:
o Hirschsprung disease.
o Thyrotoxicosis.
 Neoplastic diseases:
o Neuroendocrine hormone-secreting tumors (VIPoma).
 Chronic nonspecific diarrhea:
o Functional diarrhea (toddler's diarrhea).
o Irritable bowel syndrome.
Evaluation of Patients:
 History:
o Age.
o Personal & family history (congenital, allergy, inflammation).
o Previous episode of acute GE.
o Association with specific foods.
o Polyhydromnios.
o Specific amount of fluid ingested /day.
 General examination.
 Evaluation of nutritional status:
o Diatery history.
o Nutritional state, growth parameters, anthropometric evaluation → estimate the
severity of diarrhea
o Nutritional investigations.
o Biochemical markers  assist in grading malnutrition, the half-life of serum
proteins can differentiate between short & long term malnutrition.

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Stepwise diagnostic work-up for children with chronic diarrhea:
 Step1:
o Intestinal microbiology  GSE, microscopy for parasites, viruses, stool
cultures, stool electrolytes, pH & reducing substances, H2 breath test.
o Blood studies  CBC, ESR, electrolytes, blood urea, creatinine.
o Screening test for celiac disease.
o Noninvasive tests for  Intestinal function, pancreatic function and sweat test,
intestinal inflammation.
o Tests for food allergy  Prick/patch tests.
 Step2:
o Intestinal morphology.
o Standard jejunal/colonic histology.
o Morphometry.
 Step3:
o Special investigations.
o Intestinal immunohistochemistry.
o Hormonal studies.
o Autoantibodies.
o Brush border enzymatic activities.
o Others.
Treatment:
 Replacement of fluid and electrolyte.
 Empirical antibiotic therapy.
 Nutritional rehabilitation.
 Human immunoglobulins.
 Zinc supplement.
 Treatment of underlying cause.

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Lactose Intolerance:
Definition:
 Inability to digest significant amounts of lactose, which is the predominant sugar in
milk.
 A result of lactase insufficiency, the enzyme essential for the conversion of lactose into
glucose and galactose.
Types:
 Congenital  Very rare.
 Primary  Develops after 2 years of age.
 Secondary  Usually resolves in 1-2 weeks.
Clinical manifestation:
 Nausea, cramping, bloating, abdominal pain, gas, diarrhea, perianal excoriation.
Diagnosis:
 Stool pH < 5.5.
 Positive reducing substance in stool.
 Low lactase activity in jejunal mucosa.
 Increased H2 in expired air.
Treatment:
 Reduce lactose in diet.
 (SOY PROTEIN FORMULA) ISOMIL/Prosobee:
o 20 cal/oz.
o palm olein, soy, coconut, sunflower oil.
o Corn syrup/sucrose.
o Protein, 17 g/L.
o Soy isolate and L-MET.
o Iron 12mg/L.
o Vitamin D 405 IU/L.
o 200 mOsm/kg H2O.
o DHA and AA added (docosahexaenoic acid and arachidonic acid).
Cow’s milk allergy:
Definition:
 An abnormal immune system reaction to proteins in the cow’s milk.

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 Triggered by a combination of genetically inherited factors and early introduction of
cow’s milk or soy protein into an infant’s diet.
Symptoms:
 An immune system reaction.
 Gastrointestinal Manifestations  vomiting, diarrhea, malabsorption, protein-losing
enteropathy, colic, GIT bleeding, FTT.
 Systemic Manifestations  anaphylaxis, rhinitis, wheezing, pulmonary
hemosiderosis, peripheral eosinophilia, IDA secondary to GIT bleeding.
Diagnosis:
 Mainly clinical.
 Symptoms disappear after withdrawal of cow’s milk.
 Very cautious CHALLENGE with few CC of cow’s milk produces the symptoms again.
Treatment:
 SOY PROTEIN (30-50%) are also allergic to soy protein.
 HYDROLYSED MILK FORMULA (pregestemile).
Protein Hydrolysate Formulas
 Alimentum Advance.
 Pregestimil/Pregestimil Lipil.
 Nutramigen Lipil:
o Protein Casein hyrolysate + free AA’s.
o Fat (Alimentum and Pregestimil) Medium chain + Long chain triglycerides;
(Nutramigen) Long chain triglycerides.
o Carbohydrate: Lactose free.
Prognosis:
 Most cases recover spontaneously within 1-2 years.
Toddlers diarrhea:
 A pattern of intermittent loose stools, occurs commonly between 1 and 3 yr of age.
 These otherwise healthy growing children often drink excessive carbohydrate-
containing beverages.
 The stools typically occur during the day and not overnight.
 The volume of fluid intake is often excessive; limiting sugar-containing beverages and
increasing fat in the diet often leads to resolution of the pattern of loose stools.

22. 22
Irritable bowel syndrome:
 This disorder, also common in adults, is associated with altered gastrointestinal
motility and an abnormal sensation of intra-abdominal events.
 Symptoms may occur following a gastrointestinal infection.
 Studies of pressure changes within the small intestine of children with irritable bowel
syndrome suggest that abnormally forceful contractions occur.
 It has also been shown that affected adults experience pain on inflation of balloons in
the intestine at substantially lower volumes than do controls.
 There is therefore an interplay between these two factors, both of which are
modulated by psychosocial factors such as stress and anxiety.
 There is often a positive family history and a characteristic set of symptoms, although
not all patients experience every symptom:
o Abdominal pain, often worse before or relieved by defecation.
o Explosive, loose or mucousy stools.
o Bloating.
o Feeling of incomplete defecation.
o Constipation (often alternating with normal or loose stools).

23. 23
Subject4: Celiac disease
Celiac disease (Gluten Sensitive Enteropathy):
 Is an immune mediated enteropathy caused by permanent sensitivity to gluten in
genetically susceptible individuals.
Pathogenesis:
 Celiac disease develops only after dietary exposure to the protein gluten, which is
found in wheat, rye, and barley.
 The activity of gluten resides in the gliadin fraction, that lead to sensitization of lamina
propria lymphocytes.
 The inflammatory response results in villus atrophy, crypt hyperplasia, and damage to
the
surface epithelium in the small bowel.
 The injury is greatest in the proximal small bowel and extends distally for a variable
distance.
 Celiac disease results in a decrease in the absorptive and digestive capacity of the small
intestinal surface area and a relative increase in immature epithelial cells.
Causes:

24. 24
Genetic predisposition:
 Concordance in monozygotic twins approaching 100%.
 Two to 5% of first-degree relatives have symptomatic gluten-sensitive enteropathy,
and as many as 10% of first-degree relatives have asymptomatic damage to small
bowel mucosa consistent with this disorder.
 Celiac disease is associated with  (HLA) types (DQ8 and DQ2), down syndrome, type
1 diabetes, viruses.
Clinical presentation:
 The typical presentation  diarrhea, abdominal distention, FTT, appear in toddler (6-
24 mo.) after introduction of gliadin containing diet.
 The stools are characteristically pale, loose, and offensive.
 Neurologic symptoms  many children are emotionally withdrawn, irritable, fretful.
 Other Manifestations  smooth tongue, oral ulcers, excessive bruising, finger
clubbing, peripheral edema.
 Non-Intestinal Manifestations.
Association of Celiac disease:
 Osteopenia/osteoporosis.
 Short stature & delayed puberty.
 IDA not responding to oral iron therapy.
 Hepatitis.
 Arthritis.
 Epilepsy.
 Ataxia.
 Autoimmunity: DM1, thyroiditis, 1 ry biliary cirrhosis, addison disease & dermatitis
herpetiformis.
 Syndromes: Turner, Down.
 Malignancy.
Differential diagnosis:
 Giardiasis.
 Malnutrition.
 Cow’s milk protein allergy.

25. 25
Investigations:
 Anemia usually IDA but dimorphic anemia may occur.
 Hypoproteinaemia.
 Hypoprothrombinaemia.
 ↑fecal fat estimation.
Serologic tests:
 Serologic tests such as anti-endomysium IgA antibody test (EMA), anti-tissue
transglutaminase IgA antibody test (TTG), and HLA DQ2 or DQ8 genotype testing are
useful for evaluation of asymptomatic subjects with diabetes mellitus, thyroiditis,
Down syndrome, Turner syndrome, William syndrome, or IgA deficiency who have a
higher incidence of celiac disease, and first-degree relatives of patients with celiac
disease (CD).
 The anti-endomysium IgA antibody and anti-tissue transglutaminase IgA antibody
tests are highly sensitive and specific in identifying individuals with celiac disease.
 Some 10% of patients whose disease is diagnosed earlier than 2 years of age show
absence of IgA anti-TG2. For them, the measurement of serum antigliadin antibodies is
generally advised.
 Antibodies against gliadinderived deamidated peptides (D-AGA) have been assessed.
 Compared with conventional AGA, the peptide antibodies (IgG and IgA) have a greater
sensitivity and specificity.
 A problem with serology is represented by the association of celiac disease with IgA
deficiency (10-fold increase compared to the general population).
 Serum IgA should always be checked, and in the case of IgA deficiency, D-AGA, IgG
anti-endomysium, or TG2 should be sought.
 Negative serology should not preclude a biopsy examination when the clinical
suspicion is strong.

26. 26
Genetic tests:
 Have an increasing role in the diagnosis.
 Less than 2% of celiac patients lack both HLA specificities; at the same time,
approximately one third of the “normal” population has one or the other marker.
 That means that the measurement of HLA DQ2 and/or DQ8 has a strong negative
predictive value but a very weak positive predictive value for the diagnosis of celiac
disease.
Small Intestinal Biopsy:
 Definitive diagnosis of celiac disease requires small intestinal biopsy, as none of the
available serologic tests are 100% reliable.
 The characteristic histologic changes  partial or total villous atrophy, crypt
elongation and decreased villous/crypt ratio, increased number of intraepithelial
lymphocytes.
 The mucosal involvement can be patchy, so multiple biopsies must be obtained.
ESPGHAN current criteria:
 The 2 requirements mandatory for the diagnosis of celiac disease are:
 Characteristic histologic features.
 Full clinical remission after withdrawal of gluten from the diet.
 Reversal of positive serologic tests after gluten withdrawal is considered supportive
evidence.
 In children <2 years of age, milk protein-sensitive enteropathy can produce changes
similar to celiac disease, confirmation of diagnosis after a gluten challenge is
sometimes required.
 This necessitates three biopsies: an initial biopsy at presentation, the 2nd to document
healing with gluten withdrawal, and the 3rd to show recurrent damage with
reintroduction of gluten.
 Gluten challenge is not considered mandatory except in situations where there is
doubt about the initial diagnosis.
Treatment:
 The only treatment for celiac disease is lifelong exclusion of gluten.
 This requires a wheat-,barley-, and rye-free diet.
 After gluten withdrawal, there is rapid remission of symptoms, improved bone
mineralization, and reversal of growth failure and nutritional deficiencies.
 It is recommended that children with celiac disease be monitored with periodic visits
for assessment of symptoms, growth, physical examination, and adherence to the
gluten-free diet.

27. 27
Prognosis:
 The clinical response to a gluten-free diet usually results in improvement of mood,
appetite, and lessening of the diarrhea within a week.
 Reduced bone mineral density also improves with gluten exclusion.
 No long-term complications from a gluten-free diet have been recognized.
 Celiac disease is associated with intestinal lymphoma and other forms of cancer,
especially adenocarcinoma of the small intestine, of the pharynx, and of the
esophagus.
 Several follow-up studies suggest that a gluten-free diet protects from cancer
development, especially if started in the 1st years of life.
 Therefore, early diagnosis and strict dietary restrictions appear to be the only
possibility of preventing risk for rare but very aggressive forms of cancer associated
with celiac disease.

28. 28
Subject5: Cystic fibrosis
Definition:
 A multisystem disease.
 Autosomal recessive inheritance.
 Commonest lethal genetic condition affecting caucasian people.
 Defect in chloride transport in epithelial tissue.
 This result in relative dehydration of airway secretions.
Genetics:
 CF is inherited as an autosomal recessive trait.
 Let C= normal CFTR.
 Let c= mutant CFTR.
 If mom and dad are both carriers then:
C c
 With mom and dad carriers, then:
o 50% chance of having child who is a carrier
o 25% chance of child being affected
o 25% of child with no mutant copies of CFTR
Cystic fibrosis transmembrane conductance regulator (CFTR) gene:
 The CF gene codes for a protein of 1,480 amino acids called the CF transmembrane
regulator (CFTR).
 CFTR is expressed largely in epithelial cells of airways, the gastrointestinal tract
(including the pancreas and biliary system), the sweat glands, and the genitourinary
system.
 The most common CFTR gene is located on the long arm of chromosome 7.
 There are >1500 mutations in CFTR.

29. 29
 Commonest mutation is Δ F508-- -70% CF alleles in Caucasians (deletion of a single
phenylalanine residue at amino acid 508).
 A Cl- channeh
 2 sets of 6 transmembrane domains
 2 “ATP-binding cassettes” (thus “ABC
transport protein”)
 ATP
 ATP
 What’s wrong with DF508?
The most common mutation (70% of mutants): A
phenylalanine (F) is deleted at position 508 in ATP-
binding cassette #1
Pathogenesis:
 Four long-standing observations are of fundamental pathophysiologic importance.
 Failure to clear mucous secretions a paucity of water in mucous secretions an elevated
salt content of sweat and other serous secretions chronic infection limited to the
respiratory tract.
CFTR helps to control bulk water flow across epithelia:
 Na+ channels are usually open, but extensive Na+ flux
requires a counterion.
 If CFTR is open, Clbecomes the counterion.
 Therefore NaCl flows across the membrane.
 Water then flows around the cells to maintain osmotic
pressure.
 Result: isotonic NaCl solution flows from the blood to
the lumen (or vice-versa)
CFTR and Airway Surface Liquid 

30. 30
Clinical features of CF:
 Chronic sino-pulmonary disease (like bronchiectasis).
 Nutritional deficiency/GI abnormality.
 Obstructive Azoospermia.
 Electrolyte abnormality.
 CF in a first degree relative.
 Others  Bronchiectasis, Nasal Polyps, Digital Clubbing, Meconium ileus.
Diagnostic methods:
 Sweat chloride:
o Chemical that stimulates sweating placed under electrode pad; saline under other
electrode pad on arm.
o Mild electric current is passed between electrodes.
o Sweat collected Positive Sweat chloride: > 60 meq/L.
 Genetic testing:
o DNA Testing for most common CFTR mutations
 Other diagnostic tests:
o Increased potential differences across nasal epithelium.
o Prenatal diagnosis  Amniotic fluid or Chorionic villous sampling.
 Newborn Screening for CF:
o Immunoreactive trypsinogen usually first followed by either sweat or DNA testing.
Diagnostic criteria for Cystic Fibrosis:
Treatment:
 Multidisciplinary  Pulmonary Therapy, Infection, Nutrition, Gastrointestinal,
Infertility, Social Issues.
 Nutrition:
o High calorie supplemental.
o Vitamin supplementation.
o Pancreatic enzymes.

31. 31
Subject6: Malabsorption
Introduction:
 Disorders affecting the digestion or absorption of nutrients.
 Approximately a quarter of patients present in childhood or adolescence.
 Crohn disease can affect any part of the gastrointestinal tract from mouth to anus.
 In ulcerative colitis the inflammation is confined to the colon.
Manifest as:
 Abnormal stools  the true malabsorption stool is difficult to flush down the toilet
and has an odor which pervades the whole house, pale, bulky, creasy, oily.
 Failure to thrive or poor growth in most but not all cases.
 Specific nutrient deficiencies, either singly or in combination.
 UC and CD  lead to chronic diarrhea.
 UC  diarrhea and malignancy.
 CD  FTT, abdominal pain and mass, aphthus ulcer, fistula, perianal lesion.
Causes:

32. 32
Clinical presentation:
Ulcerative colitis:
 Diagnosis:
o Made on endoscopy (upper and ileocolonoscopy) and on the histological features,
after exclusion of infective causes of colitis.
o In contrast to adults, in whom the colitis is usually confined to the distal colon, 90%
of children have a pancolitis.
 Treatment:
o In mild disease, aminosalicylates (balsalazide and mesalazine) are used for
induction and maintenance therapy.
o Disease confined to the rectum and sigmoid colon may be managed with topical
steroids.
o More aggressive or extensive disease requires systemic steroids for acute
exacerbations and immunomodulatory therapy, e.g. azathioprine to maintain
remission alone or in combination with low-dose corticosteroid therapy.
Crohn disease:
 Diagnosis:
o Based on endoscopic and histological findings on biopsy.
o Upper gastrointestinal endoscopy, ileocolonoscopy and small bowel imaging.
 Treatment:
o Remission is induced with nutritional therapy, the normal diet is replaced by whole
protein modular feeds (polymeric diet) for 6–8 weeks, effective in 75% of cases.
o Systemic steroids are required if ineffective.

33. 33
Subject7: Some points about abdominal pain
Causes of acute abdominal pain:
Acute appendicitis:
 Information:
o Acute appendicitis is the commonest cause of abdominal pain in childhood
requiring surgical intervention.
o Although it may occur at any age, it is very uncommon in children <3 years old.
 Symptoms:
o Anorexia.
o Vomiting (usually only a few times).
o Abdominal pain  initially central and colicky (appendicular midgut colic), but then
localizing to the right iliac fossa (from localised peritoneal inflammation).
 Signs:
o Flushed face with oral fetor.
o Low-grade fever 37.2–38°C.
o Abdominal pain aggravated by movement, e.g. on walking, coughing, jumping,
bumps on the road during a car journey.
o Persistent tenderness with guarding in the right iliac fossa (McBurney’s point).
 In preschool children:
o The diagnosis is more difficult, particularly early in the disease.
o Fecoliths are more common and can be seen on a plain abdominal X-ray.
o Perforation may be rapid, as the omentum is less well developed and fails to
surround the appendix, and the signs are easy to underestimate at this age.

34. 34
 With a retrocaecal appendix:
o Localised guarding may be absent, and in a pelvic appendix there may be few
abdominal signs.
 Diagnosis:
o Appendicitis is a progressive condition and so repeated observation and clinical
review every few hours are key to making the correct diagnosis, avoiding delay on
the one hand and unnecessary laparotomy on the other.
o No laboratory investigation or imaging is consistently helpful in making the
diagnosis.
o Neutrophilia  not always present on a full blood count.
o White blood cells or organisms in the urine  are not uncommon in appendicitis as
the inflamed appendix may be adjacent to the ureter or bladder.
o Ultrasound  is no substitute for regular clinical review, it may support the clinical
diagnosis (thickened, noncompressible appendix with increased blood flow);
demonstrate associated complications such as abscess, perforation or appendix
mass; and exclude other pathology causing the symptoms.
o Laparoscopy  is available to see whether or not the appendix is inflamed.
 Treatment:
o Appendicectomy is straightforward in uncomplicated appendicitis.
o Complicated appendicitis includes the presence of an appendix mass, an abscess or
perforation.
o If there is generalized guarding consistent with perforation, fluid resuscitation and
intravenous antibiotics are given prior to laparotomy.
o If there is a palpable mass in the right iliac fossa and there are no signs of
generalized peritonitis, it may be reasonable to elect for conservative management
with intravenous antibiotics, with appendicectomy being performed after several
weeks.
o If symptoms progress, laparotomy is indicated.
Meckel diverticulum:
 Around 2% of individuals have an ileal remnant of the vitello-intestinal duct, a Meckel
diverticulum, which contains ectopic gastric mucosa or pancreatic tissue.
 Most are asymptomatic but they may present with severe rectal bleeding, which is
classically neither bright red nor true melena.
 Other forms of presentation include intussusception, volvulus around a band, or
diverticulitis which mimics appendicitis.
 A technetium scan will demonstrate increased uptake by ectopic gastric mucosa in 70%
of cases.
 Treatment is by surgical resection.

35. 35
Malrotation:
 During rotation of the small bowel in fetal life, if the mesentery is not fixed at the
duodenojejunal flexure or in the ileocaecal region, its base is shorter than normal, and
is predisposed to volvulus.
 Ladd bands may cross the duodenum, contributing to bowel obstruction.
 There are two presentations:
o Obstruction.
o Obstruction with a compromised blood supply.
 Obstruction with bilious vomiting is the usual presentation in the first few days of life
but can be seen at a later age.
 Any child with dark green vomiting needs an urgent upper gastrointestinal contrast
study to assess intestinal rotation, unless signs of vascular compromise are present,
when an urgent laparotomy is needed.
 Treatment:
o At operation, the volvulus is untwisted, the duodenum mobilized and the bowel
placed in the non-rotated position with the duodenojejunal flexure on the right and
the caecum and appendix on the left.
o The malrotation is not ‘corrected’, but the mesentery broadened.
o The appendix is generally removed to avoid diagnostic confusion in the event the
child subsequently has symptoms suggestive of appendicitis.
Causes and assessment of the child with recurrent abdominal pain:

36. 36
Hirschsprung disease:
 The absence of ganglion cells from the myenteric and submucosal plexuses of part of
the large bowel results in a narrow, contracted segment.
 The abnormal bowel extends from the rectum for a variable distance proximally,
ending in a normally innervated, dilated colon.
 In 75% of cases, the lesion is confined to the rectosigmoid, but in 10% the entire colon
is involved.
 Clinical presentation:
o Presentation is usually in the neonatal period with intestinal obstruction heralded
by failure to pass meconium within the first 24 h of life.
o Abdominal distension and later bile-stained vomiting develop.
o Rectal examination may reveal a narrowed segment and withdrawal of the
examining finger often releases a gush of liquid stool and flatus.
o Temporary improvement in the obstruction following the dilatation caused by the
rectal examination can lead to a delay in diagnosis.
o Occasionally, infants present with severe, life threatening Hirschsprung
enterocolitis during the first few weeks of life, sometimes due to Clostridium
difficile infection.
o In later childhood, presentation is with chronic constipation, usually profound, and
associated with abdominal distension but usually without soiling.
o Growth failure may also be present.
 Diagnosis:
o Diagnosis is made by demonstrating the absence of ganglion cells, together with
the presence of large, acetylcholinesterase-positive nerve trunks on a suction rectal
biopsy.
o Anorectal manometry or barium studies may be useful in giving the surgeon an idea
of the length of the aganglionic segment but are unreliable for diagnostic purposes.
 Management is surgical and usually involves an initial colostomy followed by
anastomosing normally innervated bowel to the anus.

37. 37
Subject8: Pyloric stenosis
Definition:
 Pyloric stenosis is an acquired condition
caused by hypertrophy and spasm of the
pyloric muscle, resulting in gastric outlet
obstruction.
Epidemiology:
 It occurs in 6 to 8 per 1000 live births.
 5:1 male predominance.
 More common in first-born children.
Clinical manifestations:
 Vomiting:
o Non-bilious vomiting usually begins between ages 2 and 4 weeks and rapidly
becomes projectile after every feeding or it may be intermittent.
o Vomiting in pyloric stenosis differs from spitting up (gastroesophageal reflux)
because of its extremely forceful and often projectile nature.
o The vomited material never contains bile because the gastric outlet obstruction is
proximal to the duodenum, this feature differentiates pyloric stenosis from most
other obstructive lesions of early childhood.
o After vomiting the infant is hungry and wants to feed again.
o Affected infants are ravenously hungry early in the course of the illness, but
become more lethargic with increasing malnutrition and dehydration.
o As vomiting continues a progressive loss of fluid, hydrogen ion, and chloride leads
to hypochloremic metabolic alkalosis.
 Constipation:
o Usually occur.
 Jaundice:
o Associated with a decreased level of glucuronyl transferase is seen in approximately
5% of affected infants.
o The indirect hyperbilirubinemia usually resolves promptly after relief of the
obstruction.

38. 38
Diagnosis:
 The diagnosis can be established clinically 60–80% of the time by an experienced
examiner.
o Palpating the pyloric mass:
 The mass is firm, movable, approximately 2 cm in length, olive shaped, hard,
best palpated from the left side, and located above and to the right of the
umbilicus in the mid epigastrium beneath the liver edge.
 After the infant vomits, the abdominal musculature is more relaxed and the
“olive” easier to palpate.
o Peristaltic wave:
 After feeding, there may be a visible gastric peristaltic wave that progresses
across the abdomen.
 Ultrasound examination:
o Confirms the diagnosis in the majority of cases, allowing an earlier diagnosis.
o Pyloric thickness greater than 4 mm or overall pyloric length greater than 14 mm.
o Ultrasonography has a sensitivity of approximately 95%.
 Barium studies:
o Elongated pyloric channel.
o Shoulder sign  a bulge of the pyloric muscle into the antrum.
o Double tract sign  parallel streaks of barium seen in the narrowed channel.
The preoperative treatment:
 Correction of dehydration and hypochloremic alkalosis  generally with an initial
normal saline fluid bolus followed by infusions of half-normal saline containing 5%
dextrose and potassium chloride when urine output is observed.
 Fluid therapy should be continued until the infant is rehydrated and the serum
bicarbonate concentration is <30 mEq/dL, which implies that the alkalosis has been
corrected.
 Correction of the alkalosis is essential to prevent postoperative apnea, which may be
associated with anesthesia.
Surgical management:
 The surgical procedure of choice is the ramstedt pyloromyotomy.
 The procedure is performed through a short transverse incision or laparoscopically.
 The underlying pyloric mass is split without cutting the mucosa, and the incision is
closed.
 The surgical treatment of pyloric stenosis is curative, with an operative mortality of 0-
0.5%.

39. 39
Subject9: Intussusception
Definition:
 Intussusception is the "telescoping" of a segment of proximal bowel (intussusceptum)
into downstream bowel (intussuscipiens).
Epidemiology:
 It is the most common cause of intestinal obstruction between 3 months and 6 years
of age.
 Sixty percent of patients are younger than 1 years, and 80% of the cases occur before
24 months; it is rare in neonates.
 The incidence varies from 1-4 in 1,000 live births.
 The male:female ratio is 4:1.
Etiology:
 Viral-induced lymphoid hyperplasia may produce a lead point in these children.
 In infants the lead point is presumed to be an enlarged Peyer’s patch, the lymphoid
tissue presumably responding to a viral stimulant.
 This becomes the apex of the intussusception which then proceeds for a variable
distance into the colon.
 Correlation with adenovirus infections has been noted.
 The condition may complicate otitis media, gastroenteritis, Henoch-Schönlein purpura,
or upper respiratory tract infections.
 In older children (> 2years) the proportion of cases of patients caused by a pathologic
lead point increases, the lead point may be:
o Intestinal polyp.
o Meckel diverticulum.
o Neurofibroma.
o Hemangioma, or malignant conditions such as lymphoma.
o Intussusception may complicate mucosal hemorrhage as in henoch-schönlein
purpura or hemophilia.
Pathology:
 Intussusceptions are most often ileocolic, less commonly cecocolic, and rarely
exclusively ileal.
 Very rarely, the appendix forms the apex of an intussusception.
 The upper portion of bowel, the intussusceptum, invaginates into the lower, the
intussuscipiens, pulling its mesentery along with it into the enveloping loop.

40. 40
 Constriction of the mesentery obstructs venous return; engorgement of the
intussusceptum follows, with edema, and bleeding from the mucosa leads to a bloody
stool, sometimes containing mucus.
 Most intussusceptions do not strangulate the bowel within the 1st 24 hr but may later
eventuate in intestinal gangrene and shock.
Clinical manifestations:
 Pain:
o In typical cases there is sudden onset, in a previously well child, of severe
paroxysmal colicky pain that recurs at frequent intervals, with legs and knees flexed
and loud cries.
o Pallor with a colicky pattern occurring every 15 to 20 minutes.
o The infant may initially be comfortable and play normally between the paroxysms
of pain, but if the intussusception is not reduced, the infant becomes progressively
weaker and lethargic.
o Eventually a shock like state may develop with fever.
 Vital signs:
o The pulse becomes weak and thread.
o The respirations become shallow and grunting.
o The pain may be manifested only by moaning sounds.
 Vomiting:
o Vomiting occurs in most cases and is usually more frequent early.
o In the later phase, the vomitus becomes bile stained.
 Stool:
o Stools of normal appearance may be evacuated during the first few hours of
symptoms.
o After this time, fecal excretions are small or more often do not occur and little or no
flatus is passed.
o Blood generally is passed in the first 12hr but at times not for 1–2 days and
infrequently not at all, 60% of infants pass a stool containing red blood and mucus,
the currant jelly stool.
 Abdominal examination:
o Palpation of the abdomen usually reveals a slightly tender sausage-shaped mass,
sometimes ill defined, most often in the right upper abdomen.
o About 30% of patients do not have a palpable mass.
o P.R: The presence of bloody mucus on the finger as it is withdrawn after rectal
examination supports the diagnosis of intussusception.
o Abdominal distention and tenderness develop as intestinal obstruction becomes
more acute.
o On rare occasions, the advancing intestine prolapses through the anus.

41. 41
Diagnosis:
 The clinical history and physical findings are usually sufficiently typical for diagnosis.
 Laboratory and Imaging Studies:
o Plain abdominal radiographs  density in the area of the intussusception.
o Ultrasonography  sensitive diagnostic tool in the diagnosis of intussusception.
o Barium enema  coiled-spring sign.
Treatment:
 Admission:
o Therapy must begin with placement of an IV fluid and a nasogastric tube.
o Surgical consultation should be obtained early.
 Reduction:
o Reduction of an acute intussusception is an emergency procedure and performed
immediately after diagnosis with preparation for possible surgery.
o Reduction in the theater either by:
 Non-operative reduction.
 Pneumatic reduction.
 Hydrostatic reduction.
o If reduction is not complete, emergency surgery is required.
 Surgery:
o The surgeon attempts gentle manual reduction.
o But may need to resect the involved bowel after failed reduction because of severe
edema, perforation, pathologic lead point (polyp, Meckel diverticulum), necrosis.
Prognosis:
 Untreated intussusception in infants is almost always fatal.
 The chances of recovery are directly related to the duration of intussusception before
reduction.
 Spontaneous reduction during preparation for operation is not uncommon.
 The recurrence rate after reduction of intussusceptions is ≈10%, and after surgical
reduction it is 2–5%, none has recurred after surgical resection.
 Corticosteroids may reduce the frequency of recurrent intussusception.
Ibnlatef Notes Pediatric – GIT