PEDIATRIC GI EMERGENCIES

1. PEDIATRIC GI EMERGENCIES Kevin Levere Jan 16, 2003

2. Objectives • To appreciate differences from adults in • GI bleeds • Pancreatitis • Liver disease • To review common pediatric abdominal emergencies • IBD, toxic megacolon, metabolic disease, constipation, colic, and jaundice are not discussed

3. Pediatric GI Bleeds • Many etiologies similar to adult • Frequency differs significantly • Some uniquely pediatric causes • Mortality lower than adult counterparts • Fewer comorbidities • Relatively greater physiological flexibility • Division between upper and lower • Ligament of Treitz

4. Case • 4wo ex35wker girl, breast feeding. Spat up a shot-glass worth of red blood. • Apart from oral thrush, her exam is normal. • Hx: Got Vit K. No meds. Growing. No BRBPR. • FHx: No bleeding diatheses. Mom not on meds, but has mastitis. • Apt test turns yellow-brown

5. Case • 2yo boy passing several fairly large maroon coloured BMs, x12hrs. Painless. Normal BM Hx until then. • 37, 140, 90/70, 24, pale but playful. OB+. Hgb 60, rest of CBC normal. • Which is best course of action? • A) cross-match, radionuclide scan, IV bolus, surgery • B) cross-match, IV bolus, scan, surgery • C) cross-match, IV bolus, surgery, scan • D) IV bolus, 0- transfusion, surgery, forget the scan

7. Pediatric GI Bleeds • Hemorrhagic disease of the newborn • Early (<1wk) • Vitamin K deficiency • Rare now administration of vitamin K shortly after birth has become routine • Maternal anticoagulant and intrapartum antiepileptic drug use • Late onset (2-6mos) • Fat malabsorption

8. Pediatric GI Bleeds • Ingestion of maternal blood • Apt Downey test • 1:1 stool with tap water, spin • 5:1 supernatant with 1% NaOH • After 2 mins • Pink = fetal Hgb • Yellow = maternal Hgb

9. Pediatric UGI Bleeds • Upper GI Bleeds • No good epidemiologic data outside PICU • 6-25%, depending on prophylactic therapy • 0.4% considered significant • Commonest endoscopic findings • Gastritis • Esophagitis • Varices • Ulcers • Mallory-Weiss tears

10. Pediatric UGI Bleeds • Ulcers and Gastritis • Gastric acid production begins shortly after birth • Ulcers relatively rare • Most are associated with NSAIDs and stress • H. pylori infection • Diffuse nodular gastritis commonest presentation • Infection increases with age • <5yo rare • ~20-50% by 10yo (SES dependent) • 40-80% adults (SES dependent)

11. Pediatric UGI Bleeds • Esophagitis • Severe GERD • FB or chemical injury • Infection • Vascular anomalies • Hemangiomas • Hereditary telangiectasia • Aortoenteric fistulas • Congenital malformations • Duplications, obstructions • Predisposed to mechanical injury

12. Pediatric UGI Bleeds • Management • Similar to adults • ABC’s, history and physical • NG • Same dilemma as in adults, but no pediatric data • No longer use ice cold lavages • Diagnostics • CBC, PTT/INR, LFT’s, cross-match • Limited roles for imaging – CXR, U/S, angiography • Medications • Acid-suppressive +/- visceral vasoconstrictive • Limited but supportive data; dosing is the key difference

13. Pediatric UGI Bleeds • Management • Endoscopy • Indications less standardized than in adults • For severe or persistent/recurrent bleeding • Diagnostic • No data on risk of rebleeding based on findings • Interventional as in adults • Size the limiting factor for techniques • Safety similar to adult data • Complication rate 0.3% in retrospective study of 2026

14. Pediatric UGI Bleeds • Management • Surgery as back-up • Failed endoscopic therapy • Surgical lesion, e.g. Dieulafoy’s lesion • Take home point • Non-GI sources as common as GI sources in “pediatric UGI bleeds”

15. Pediatric LGI Bleeds • Lower GI Bleeds • 0.3% of ED visits • 50% <1yo • Allergic colitis, fissures commonest • >1yo • Infectious GE, fissure, polyps commonest • Ann Emerg Med, 1994

16. Pediatric LGI Bleeds • Diagnosis • Nature of bleeding helps localize origin • N.B. hematochezia unreliable in infants, with their faster GI transit times • History and physical • If doubt bleeding, or suspect false-pos guaiac • Immunodiffusion of fecal Hgb • Sensitivity and specificity ~70% each, as with guaiac • Fecal alpha-1-AT measurement • Sensitivity 88%, specificity 90% • Also elevated in protein-losing enteropathy???

17. Pediatric LGI Bleeds • Numerous laboratory and imaging options • Blood • Stool • Urine • Plain films, nuclear scans, endoscopy • Commonly used in painless bleeding • Non-barium contrast studies, U/S, CT, MRI, angiography • Dependent on suspected etiology

18. Pediatric LGI Bleeds • Management • Similar to adults • ABC’s, history and physical • NG • Aspirate can help identify if blood from UGI source • Diagnostics • CBC, PTT/INR, LFT’s, cross-match, etc • Medications • Visceral vasoconstrictive • Supportive data for role in LGI bleeds • Treat underlying cause

19. Pediatric LGI Bleeds • Neonatal • NEC • Risk factors • Prematurity (87% of cases) • Hypoxia • Sepsis • Acidosis • Early enteral feeds • Umbilical vascular catheter • PDA • Epidemics support infectious component

20. Pediatric LGI Bleeds • Neonatal • NEC • Onset • Typically <4wks of age; can be late as 3mos • Manifestation • Abdominal distention, gastric retention • Poor feeding, V/D, lethargy, apnea • Gross blood in stools in only 25% • Severe cases lead to SIRS

21. Pediatric LGI Bleeds • Pneumatosis intestinalis in 50-75% at diagnosis • Portal venous gas in severe disease

22. Pediatric LGI Bleeds • Neonatal • NEC • Complications • Mortality up to 5% • Strictures in 10% • Treatment • Supportive • Antibiotics, gut rest • Surgical back-up

23. Pediatric LGI Bleeds • Neonatal • Hirschsprung disease • Congenital aganglionic megacolon • Delayed (>48hr) passage of meconiom • History of (often progressive) constipation • 25% have blood in stool • Diagnosis • Contrast enema – proximal dilation = normal bowel • Rectal manometry • Biopsy with absent ganglion cells • Treatment is surgical resection

24. Pediatric LGI Bleeds • Infants • “Allergic” colitis • Intolerance to cow’s milk protein • 0.2-7.5% prevalence • Soy protein intolerance in 14-25% of these • Typically not IgE mediated • Resolves in most by 2yo • Treatment is dietary restriction • Volvulus • Intussusception

25. Pediatric LGI Bleeds • Children • Infectious enterocolitis • HUS, HSP, pseudomembranous colitis • IBD • Vascular malformations • Hemangiomas, telangiectias, varices, hemorrhoids • Polyps • Other tumors, e.g. colon cancer, are rare • Trauma • FB, NAT

26. Pediatric LGI Bleeds • Meckel’s diverticulum • Vitellointestinal duct remnant • 50% have gastric mucosa • Most important source of small bowel bleeding • Gastric mucosal ulceration vs intussusception • Rule of 2’s • 2% of population • 2:1 male:female • 2 feet from IC valve • Under 2yo commonest • Diagnosed by radionuclide scan • Treatment is surgical resection

27. Pediatric LGI Bleeds • Take home point • Think of NEC and Meckel’s • Both relatively common • Both potentially serious

28. Case • 13yo girl with 3days fever, despite Tylenol used round the clock. Also c/o N/V, anorexia, moderate epigastric pain. Today a bit jaundiced. Denies EtOH or other drug use. Her boyfriend has Mono. • 38.7, 100, 120/85, 22. Abdo tender, a bit distended, else exam normal.

29. Pancreatitis • Differential • Gastroenteritis • Ulcer • Hepatitis • Pneumonia • Biliary tract obstruction

30. Pancreatitis • Much less common than in adults • Pathogenesis • Cell injury (toxin or otherwise) sets off pancreatic autodigestion and inflammatory response

31. Pancreatitis • Acute • Interstitial edema • Usually resolves within 2-7 days – mortality 5% • Complications – rare • Pseudocyst – slow to mature and resolve (weeks) • Phlegmon, necrosis +/- hemorrhage • SIRS – 50-80%+ mortality • Chronic/recurring • Endocrine and exocrine insufficiencies • Calcification

32. Pancreatitis • Etiology – the key difference in pediatrics • Trauma • Blunt injury – commonest cause; think of NAT • Infection • Viral (not just mumps), et al • Multisystem disease • CF, collagen vascular disease, vasculitits, metabolic • Obstructive • Congenital anomalies, biliary microlithiasis • Drugs and Toxins • EtOH, acetaminophen • Hereditary – autosomal dominant • Idiopathic (25%)

33. Pancreatitis • Clinical Picture • Abdominal pain • Steady, epigastric, with tenderness, distention • Persistent vomiting • Proportional to abdominal pain • Fever • Associations in complicated picture • Mass, e.g. in 50% of cases with pseudocyst • Asictes, pleural effusions, hypocalcemia, hyperglycemia, jaundice • Grey Turner (flank) and Cullen (periumbilical) signs • MSOF and shock

34. Pancreatitis • Diagnosis • Serum lipase • sensitivity 86% to 99%; specificity of 50% to 99% • Elevated 1-2 weeks longer than amylase • Serum amylase • sensitivity 75% to 92%; specificity 20% to 60% • General lab evaluation • Urinary trypsin activation peptide (TAP) • Investigational prognosticator • Ranson and APACHE-II criteria • Not reliable in pediatrics

35. Pancreatitis • Diagnosis • Diagnostic imaging – 20% normal at first • Plain films • Pleural effusions, “sentinel loop”, “cut-off sign” • U/S • Biliary tract evaluation, or follow-up of cysts/abcesses • CT • Usually only if poor U/S visualization • ERCP/MRCP • Considered if recurrent/undiagnosed problems • For suspected stones

36. Acute pancreatitis Pseudocyst 5 months after acute episode Pancreatitis

37. Pancreatitis • Management • “Pancreatic rest” • NPO +/- NG • Pain control • Meperidine – opioid causing least enterobiliary pressure by contraction of Sphincter of Oddi • Fluid and electrolyte homeostasis • Surgical and antibiotic interventions rare • Abcess, infected pseudocyst, necrosis, hemorrhage • Address underlying cause if able

38. Pancreatitis • Take home point • Trauma, including non-accidental, is the commonest cause

39. Liver Failure • Fulminant hepatic failure • Acutely impaired hepatocyte function with • Encephalopathy within 8 weeks of initial symptoms, with a previously healthy liver, or • Encephalopathy within 2 weeks of jaundice, even if previously underlying liver dysfunction

40. Liver Failure • Cirrhosis • End-stage of acute or chronic disease • Fibrosis following injury from hepatitis, necrosis, or biliary obstruction • Restricts blood flow, creating portal hypertension, and ischemia further impairing heptocyte function • Biliary atresia • Commonest cause of liver failure in pediatrics

41. Fulminant Hepatic Failure • Etiology • Viral • HBV likely the commonest of these • TORCH • Toxins • Acetaminophen the most common toxin • Amanita phalloides, EtOH, PHT, VPA… • Vascular • Veno-occlusive disease, ischemia, thrombosis

42. Fulminant Hepatic Failure • Etiology • Metabolic • Wilson’s, neonatal iron storage disease, tyrosinemia, galactosemia, fatty acid oxidation defects, mitochondrial disease • Reye’s syndrome • Others • Malignancy, autoimmune, idiopathic (20-40%)

43. Fulminant Hepatic Failure • Clinical Picture • Jaundice • Fetor hepaticus • Fever • Anorexia • Vomiting • Abdominal pain • Encephalopathy • Grades I-IV = mild confusion to coma

44. Fulminant Hepatic Failure • Note about ALT • Most specific for hepatocellular toxicity, BUT… • Falls as exhaust hepatocyte supply • Markers of function • Bilirubin, albumin, INR, glucose, NH3

45. Fulminant Hepatic Failure • Complications • Cerebral edema • Renal failure • Coagulopathy • GIT commonest site of bleeding • Hypoglycemia • Metabolic instability • Infection • MSOF

46. Fulminant Hepatic Failure • Treatment in ED • Eliminate or treat cause if able • N-acetylcysteine, charcoal • Supportive therapy • ABC’s, then • Increased ICP • Mannitol or hyperventilation; no Dexamethasone • Bleeding • FFP; FVIIa being studied • H2 blocker > sucralfate; PPI role being studied

47. Fulminant Hepatic Failure • Treatment thereafter • Ongoing supportive care • Corticosteroids shown to worsen outcome • For encephalopathy • Lactulose • Neomycin • Low protein diet • Plasmapheresis • Specific therapies • Antivirals, TIPS, thrombolysis, transplant

48. Fulminant Hepatic Failure • Prognosis • 50% experience serious infection • Mortality with medical care ~70% • Worse prognosis if <10yo or >40yo • Transplant survival 50-80% • Spontaneous recovery • More likely with low grade encephalopathy • Viral and acetaminophen 50-60% • Wilson’s and some idiosyncratic reactions 10-20%

49. Liver Failure • Take home point • Infants with fulminant hepatic failure typically have congenital problems, i.e. underlying liver disease • They don’t strictly fit the definition for fulminance

50. Case • 5yo with 1day of vomiting and occasional diarrhea. Severe abdo pain on and off every 15 mins or so. No sick contacts. • 37.9, 120, 110/75, 22. Abdo diffusely tender, no peritonitis, no mass. CBC normal, OB+.