Gastroenterology

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-toperson 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