Gastroenterology

Acute gastroenteritis the most common cause

Presentation:
•Diffuse or localized
•Sharp, cramping, and colicky
•Nausea, vomiting, diarrhea and fever

Diagnostic tests:
•CBC, urine/stool analysis, serum analysis, CXR,
abdominal radiographs, CT scan of the abdomen,
pregnancy test if applicable
D/D
•In children less than 2 years of age,
trauma, intussusception, incarcerated hernia, volvulus,
and UTI
•In 2 – 5 years of age,
Sickle cell anemia, lower lobe pneumonia, and UTI
•Meckel diverticulum in infants and children
•Appendicitis in any older child or adolescent
•Mittelschmerz, ectopic pregnancy or pelvic
inflammatory disease in adolescent girls
•Other causes: pancreatitis, Henoch-Schonlein pupura
mesenteric adenitis, lead poisoning,
diabetic ketoacidosis, renal stones, and cholecystitis
Three or more episodes of abdominal pain, severe
enough to affect activities, occurring over a 3- month
period

Recurrent abdominal pain (RAP) occurs in about 10

15% of children between 5 and 15 years of age
Organic causes
•Constipation, lactose intolerance, parasites (Giardia
sp), IBD and PUD
Pancreatitis, cholelithiasis
•UTI, porphyria, sickle cell anemia, lead poisoning
Nonorgnaic causes
•Functional abdominal pain (IBS, nonulcer dyspepsia)
Presentation
•Patients with RAP have nonspecific symptoms
•Periumbilical pain
•Stressors such as school or exams
•Social factors such as family illness, sibling rivalry
•Irritable bowel syndrome: pallor, nausea, vomiting,
lethargy, and diarrhea
•30% have nocturnal enuresis, fears, and sleep
disturbances
•Abdominal pain
Recurrent abdominal pain features
•Characteristic presentation of chronic functional pain
•Onset >6 years old
•Midline paroxysmal pain
•Pain interrupts normal activity, but usually has with no
relationship to meals
•Typically relieved by passing stool
Features in organic causes:
•Onset <6 years old
•Fever
•Weight
•Weight loss
•Abnormal growth
•Joint symptoms
•Localized away from umbilicus
•Patient awakens from sleep
•Vomiting, diarrhea, blood in stool
Diagnostic tests
•History, Physical examination
•Stool studies, urine analysis, CBC, ESR, USG,
radiographic studies, breath hydrogen, and endoscopy

Treatment
Recurrent abdominal pain:
•Reassurance
•Biofeedback and relaxation techniques
An increased stool output, with excess loss of fluid and
electrolytes
Classified as acute or chronic

Mechanisms: secretory diarrhea, osmotic diarrhea,

motility disorders, mucosal inflammation

Secretory
•Secretogogue: binds to receptor on epithelium
•Watery, large volume
•Normal osmolarity: electrolyte loss
•Persists when no feeds given by mouth
•Cholera toxin, toxigenic E. coli, neuroblastoma, C.
difficile, cryptosporidiosis
Osmotic diarrhea
•Ingestion of poorly absorbed solute (laxatives) or one
not absorbed due to defect: lactase deficiency
•Lesser volume, decreases with fasting
•Increased osmolarity: FFA released from CHO
fermentation

Motility disorders
•Increased motility: decreased transit time
•Lose-to-normal appearing stool
•Irritable bowel, thyrotoxicosis, infection
Mucosal inflammation
•Decreased mucosal surface area and colonic
reabsorption, increased motility
•Blood and increased WBCs in stool (dysentery)
•Celiac disease, Salmonella, Shigella, amebiasis,
rotavirus
Causes of acute and chronic diarrhea are age
dependent
Acute diarrhea
•Almost always infectious
•Gastroenteritis the most common cause
•Food poisoning, systemic infections, parasitic
infections, antibiotics

Chronic diarrhea
•Commonly caused by lactase deficiency, IBS, IBD, and
parasitic infections
Presentation
•Rotavrus:
Causes watery diarrhea
Lasts for up to 7 – 10 days
May be accompanied by 3 – 4 days of vomiting
Fever may be present

•Enteropathogenic E. coli: seen in nurseries & day

care
•Enterotoxigenic E. coli: traveler’s diarrhea
•Enterohemorrhagic E. coli: hemorrhagic colitis & HUS

•Salmonella: contracted from infected animals and

contaminated foods such as eggs, mild, and poultry
•Shigella and Campylobacter: contracted by person-to-
person spread or from contaminated food
•Yersinia enterocolitica: transmitted by pets and
contaminated foods; arthritis and rash
•Clostridium difficile: H/O prior antibiotic use
Staphylococcus aureus food posioning: Onset within 12
h of ingestion and a common slource for the outbreak
•E. histolytica: infects colon; acute bloody diarrhea
•Giardia: causes anorexia, nausea, abdominal
distension, watery diarrhea, and weight loss; cysts are
from an infected individual or from contaminated food or
water
•Cryptosporidium: mild diarrhea in immunocomptetent;
severe diarrhea in AIDS patients
Diagnostic tests
•Recovering the organism from the stool
•Enzyme immunoassays detect rotavirus and enteric
adenovirus
•C. difficile toxin detected in the stool
•Giardia recovered from stool, duodenal aspirate or
small bowel biopsy

Treatment
•Viral diarrhea: supportive
•Salmonella: treatment indicated for ≤ 3 months of age,
a toxic patient, disseminated disease, or Salmonella
typhi
•Shigella: treated with trimethoprim/ sulfamethoxazole
Treatment (contd…)
•Campylobacter: usually self-limited; eythromycin
speeds recovery and reduces the carrier state;
recommended in severe disease or in dysentery
•Yersinia: usually does not require antibiotic;
amnoglycosides plus a 3rd generation cephalosporin for
infants ≤ 3 months of age, or culture-proven septicemia
•C. difficile: treated with metronidazole or vancomycin
along with discontinuation of other antibiotics
•Entamoeba: treated with metronidazole
•Giardia: treated with metronidazole, or furazolidone
Constipation: infrequent passage of hard, dry stools
Obstipation: absence of bowel movements
Definition depends on stool consistency, frequency, and
difficulty in passing

Risk factors/ etiology

•Functional constipation (volunatry withholding) the most
common cause outside of infancy
•Constipation occurs secondary to filling or emptying the
rectal vault
Other causes:
•Imperforate anus, cystic fibrosis with meconium ileus at
birth, an anteriorly displaced anus, and Hirschprung
disease, infantile botulism
Presentation
•Hard stools passed infrequently, sometimes after
several days and with difficulty
•Occasionally, liquid stool can pass around the
obstruction and give the false impression of diarrhea and
encopresis
•Constipation in the neonate should be considered
Hirschprung until proven otherwise
Aganglionic segment is in the colon, usually
rectosigmoid
Infants may have failure to thrive and abdominal
distension
In older children with Hirschsprung, the rectal vault is
empty of stool
Diagnostic tests:
•Hirschprung diagnosed by biopsy showing areas devoid
of ganglion cells
•Barium enema show a megacolon

Treatment
•Hirschsprung: surgical
•Functional constipation:
cleaning out,
Dietary manipulation, stool softeners, and counseling
Causes in children

•Neonates: GI obstruction secondary to congenital

malformations

•Infants: Gastroenteritis, gastroesophageal reflux, food

allergy, mild protein intolerance, overfeeding, inborn
errors of metabolism

•Children/ adolescents: Gastroenteritis, systemic

infections, toxic ingestions, appendicitis, ulcers,
pancreatitis
•An obstruction resulting from a failure of recanalization
of the duodenal lumen

•Occurs in 1/10,000 live births

•20 – 30% patients have trisomy 21

•Presents early usually in the first day of life

•Vomiting is bilious; history of polyhydramnios

•Abdominal film reveals “double bubble” of the stomach

and proximal duodenum

Treatment: Surgical correction

Patient should be evaluated for associated anomalies
•Lower esophageal sphincter (LES) pressure reduced, or
•Inappropriate LES relaxation, hiatal hernia, or delayed
gastric emptying

•Relatively common; usually minor & of no consequence

•More common in patients with developmental delay and
cerebal palsy
Presentation
•Patients have some form of spitting up and may have
forceful vomiting
•Chronic cough and wheezing may signal aspiration
•Poor weight gain, failure to thrive
•Sandifer syndrome: GER and opisthotonus to avoid
aspiration or decrease pain
Diagnostic tests
•pH probe
•Technetium scanning, barium swallow

Treatment
•Majority of patients have resolution of symptoms
without any treatment
•Elevating the head of the bed and thickening of feeds
•Antacids, prokinetics, H2-receptor blockers, PPI
•Surgical correction with a Nissen fundoplication
A gastric outlet obstruction

•Occurs in about 3/1000live births

•Boys more frequently affected 4:1, especially first-born
males

Presentation
•Nonbilious projectile vomiting
•Vomiting begins after 3 weeks of age
•Baby remains hungry after the vomiting
•Lump palpable in the abdomen; peristaltic wave may be
seen
•Jaundice, weight loss, signs of dehydration may be
preset
Diagnostic tests
•Abdominal USG reveals a thickened, elongated pylorus
•Ba swallow shows a dilated stomach with elongated
pylorus (string sign)
•Lab tests: hypokalemic, hypochloremic metabolic
alkalosis

Treatment
•After fluid rehydration and correction of electrolyte
imbalance, surgical correction
GI bleeding can be described as:

•Hematemesis: bloodstained vomitus and indicates

bleeding proximal to the ligament of Treitz

•Melena: Soft, black, tarry stools and represent bleeding

anywhere from the oropharynx to the colon

•Hematochezia: Bright red stool and usually from the

colon but can reflect upper GI bleeding if the transit time
is fast enough
D/D of
GI
bleeding
•A portion of GI tract slips or telescopes into the portion
just distal to it
•Most intussusceptions are ileocolic

•Most occur between 6 and 24 months of age

•Associations with lymphoid hyperplasia, Meckel
diverticulum, lymphosarcoma, polyps, cystc fibrosis,
HSP, viral enteritis, rotavirus vaccine
Presentation
•Acute onset of cramping, colicky abdominal pain
•Vomiting, fever, lethargy
•Classic currant jelly stool a late finding
•Passing a stool may temporarily relieve pain
•A sausage-shaped mass palpated in the upper abdomen
•A shock like sate may occur

Diagnostic tests
•Ba enema both diagnostic and therapeutic
•A coil-spring sign as the Ba fills the obstruction
•Air enema
•USG
Treatment
•Reduction should be done as quickly as possible
•Hydrostatic reduction successful about 50% of the time
for symptoms >48 h and 75 – 80% for symptoms < 48 h
•Should not be done in the face of prolonged
intussusception, peritonitis, or perforation
•Surgery in those cases or after failure of hydrostatic
reduction

D/D
•Gastroenteritis
•Meckel diverticulum
•HSP
•The most frequent congenital anomaly of the GI tract
•A vestigial remnant of the omphalomesentric duct

Diasease of 2’s
•Occurs in 2% of infants
•Peak incidence by 2 years of age
•Contains 2 types of tissue (ectopic gastric mucosa)
•2 cm in size
•Located about 2 feet from the ileocecal valve
Presentation
•Painless rectal bleeding
•Sometimes currant jelly
•Occasionally, Meckel diverticulum can cause
obstruction or be the lead point for an intussusception
•It can be inflamed and mimic appendicitis, or it can
perforate and cause peritonitis

Diagnostic tests
•Technetium scan (Meckel scan)

Treatment
•Surgical removal
•An encephalopathy with fatty degeneration of the liver

•H/O recent viral URTI or varicella infection

•Concomitant use of aspirin also related to development
of Reye syndrome
•Peak age is 6 years with a range of 4 – 12 years

Presentation
•Patients typically recovered from a viral illness
•After 5-7 days present with abrupt onset of protracted
vomiting
•Delirium, combative behavior, stupor
•Seizures, coma, death
•Foal neurologic signs absent
Diagnostic tests
Lab tests:
•Ammonia, transaminases, ceratine kinase, LDH
markedly elevated
•Hypoglycema
•PT elevated
•Liver biopsy shows a diffuse noninflammatory fatty
infiltration with the mitochondria being the major site of
injury

Staged by symptoms
Treatment
•Supportive
•Intracranial pressure elevations to be treated
•Hypoglycemia should be avoided

D/D
•Encephalitis, toxic and drug encephalopathies, and
metabolic diseases
IBD includes:
•Crohn disease
•Ulcerative colitis

Characterized by exacerbations and remissions

Onset usually during adolescence
Specific etiology unknown