1. Hematemesis in Children- Beyond Infancy Dr. Divya Nair DNB Pediatrics Mahavir Hospital.

2. Gastrointestinal (GI) bleeding in children is a fairly common problem In the pediatric ICU population, 6-20% have upper GI bleeds. The incidence of lower GI bleeding has not been well established 10-20% of referrals to pediatric gastroenterologists

3. Upper gastrointestinal (UGI) bleeding originating from esophagus, stomach or duodenum-proximal to the ligament of Treitz (aka duodenojejunal ligament) Commonly presents with hematemesis (vomiting of blood or coffee ground-like material) and/or melena (black, tarry stools)

4. Etiology: A) Gastrointestinal causes B) Systemic causes C) Genetic causes D) Spurious causes

5. A) Gastrointestinal causes: 1) Esophagitis: GERD Hiatus Hernia  Infection: e.g. Candida, Aspergillus, CMV, HSV Medications: e.g. tetracycline, aspirin, NSAIDs, potassium chloride “ erosive esophagitis"

6. 2) Esophageal Rupture Mallory-Weiss Syndrome (located at LES)

7. 3) Gastritis: More common than ulcers Medications (e.g. NSAIDs, aspirin) Infections (e.g., Helicobacter pylori, CMV, herpes) Crohn’s disease 4) Gastric Erosions: Trauma, burn, shock or sepsis This is usually superficial and occurs mainly in the fundus of the stomach

8. 5) Peptic Ulcer Disease Zollinger-Ellison syndrome Gastrinoma Results in multiple diffuse GI/ small bowel ulcerations Ulcer with red spot

9. Bleeding Ulcer

10. 7)Portal hypertension: Esophagealvarices Gastricvarices Hypertensivegastropathy Cirrhosis due to congenital hepatitis, hepatic fibrosis, cystic fibrosis 8) Extra-hepatic portal vein obstruction Esophagealvarices

11. 9) Vascular malformations: Hemangiomas Aorto-esophageal/-enteric fistulas Dieulafoy ulcer (superficial defect of gastric mucosa which overlies an ectaticsubmucosal a.) Watermelon stomach (gastric antral vascular ectasia) Vasculitiseg: ITP

12. 10) Tumors: Polyps Lipomas, leiomyoma Adenocarcinoma Lymphoma Metastatic tumors, Kaposi’s sarcoma, Barrett’s esophagus Kasabach-Merritt synd (Hemangioma thrombocytopenia syndrome)

13. 11) Traumatic: Prolapsinggastropathy Foreign body ingestion Direct abdominal trauma Iatrogenic- throat/nose Sx, traumatic NG

14. 13) Miscellaneous: Hemobilia Hemosuccuspancreaticus Menetries’ Disease Eosinophilicenteropathy Munchausen by proxy syndrome Barrett’s ulcer secondary to GERD

15. B) Systemic Causes: Coagulopathy (congenital/acquired): Hemophilia, vWD 2) Sepsis, scarlet fever, malaria, leptospirosis 3) Burns, Sepsis ( Curling’s ulcer), Raised ICT, Head injury, Encephalitis ( Cushing’s ulcer) 4) HUS, HSP 5) Malignancy- Leukemia

16. 6) Poisonings- chemical, caustic 7) Drugs-aspirin, NSAIDS, anti-coagulants 8) Food (milk protein) allergy/ hypersensitivity 9) Idiopathic NSAID induced Ulcers

17. C) Genetic conditions: Turner syndrome Ehlers Danlos syndrome ( cutis hyperelastica) Pseudoxanthomaelasticum KlippelTrenaunay syndrome Osler-Rendu-Weber syndrome (hereditary hemorrhagic telangectesia) Blue rubber bleb naevus syndrome Hermansky-Pudlak syndrome

18. D) Spurious causes: I) Hematememis: Bleeding from nose (epistaxis), mouth, pharynx, hemoptysis II) Malena: Iron preparation, Bismuth, Lead, spinach, beets, blueberries

19. Grading of UGI Bleeds MILD: presents as nausea, vomiting, abdominal discomfort & small quantity of hematemesis/ malena MODERATE: significant blood loss, tachycardia, cold sweat, hypo- tension. No ongoing blood loss; recovers with blood transfusion SEVERE: more striking features of shock present, Hb falls to 8gm% or less. Requires multiple blood transfusions d/t ongoing blood loss Takes longer time to recover; very high mortality unless treated properly.

20. Diagnosis: History Quantity, frequency, type of blood (bright red vs coffee ground) Nausea, vomiting, recurrent abdominal pain s/o PUD Dysphagia/ odynophagia, chest pain/burning, hematochezia, melena, bruising, bleeding, repeated retching f/b vomiting of blood Weight loss, early satiety s/o malignancy Psychiatric symptoms

21. Drug ingestion Bleeding sites- skin, mucosa, GUT, joints Recurrent epistaxis H/O Jaundice, stool color Severe and diffuse upper GI ulcerations with chronic diarrhea usually : Zollinger Ellison syndrome or gastrinoma Birth history: lines placed (umbilical lines can result in clotting of portal vein)

22.  Past history: History of liver disease, history of pancreatitis, GI surgeries  H/O Bleeding disorders in family Medications: NSAID use, aspirin use  Diet history: Formula intolerance, food allergies

23. Physical examination: Vitals:- Heart rate, respiratory rate, BP, capillary refill, orthostatic changes Pallor During examination of the head, ears, eyes, nose, and throat, look for causes such as: epistaxis, nasal polyps, and oropharyngeal erosions from caustics and other ingestions

24. Signs of Chronic Liver Disease: Jaundice, Clubbing, leukonychia, palmarerythema, spider nevi, gynecomastia, etc. Vascular malformations: hemangiomas, telangiectasias or purpura over skin Peutz- Jeghers syndrome: pigmented lips, palms, soles Pseudoxanthomaelasticum: “Plucked chicken appearance” of skin

25. Per Abdomen: Tenderness, Hyperactive bowel sounds Caput medusa with ascites, shrunken liver and splenomegalys/o Cirrhosis with Portal Hypertension Extra-hepatic PHT will have splenomegaly without hepatomegaly Spleen may contract following a massive bleed and may not be palpable (Smith Howard Syndrome)

26. Work up: CBP, PCV, RBS Coagulation studies LFT to r/o cirrhosis RFT Type and cross-match of several units of blood

27. Oesophago-gastro-duodenoscopy : If active bleeding, most sensitive and specific for diagnosis and provides therapeutic options Ultrasound with Doppler to assess liver disease and portal hypertension In episodic or obscure bleeding : nuclear medicine radionucleotide studies, arteriography, and wireless video capsule endoscopy are used to assist in identifying the site of blood loss

28. Special tests: Serum gastrin levels ( Zollinger Ellison syndrome) Peroxide based tests: Gastroccult for upper GI bleed Gastroccult : only test designed specifically for detecting gastric occult blood and determining gastric pH It includes a convenient pH comparison chart for the Clinically relevant range which is important in monitoring antacid prophylaxis Certain ingestions such as red meat, iron, and peroxidase-containing vegetables (eg: turnips, horseradish, broccoli, cauliflower, and cantaloupe), can give false-positive results

29. Imaging: Barium contrast studies- barium swallows, upper GI series, small bowel follow-throughs, or barium enemas : for non emergency bleeds, to point to foreign bodies, ulcers, IBD, or polyps

30. Endoscopy: Patients with severe upper GI bleeding should receive endoscopy within the first 12 hours of the hemorrhagic episode if they are sufficiently stable, because early endoscopy improves the diagnostic index The site of upper GI bleeding can be identified in 90% of cases when endoscopy is performed within 24 hours This modality is also beneficial in predicting the likelihood of continued bleeding

31. The Forress classification divides endoscopic findings into the following 3 categories: I - Active hemorrhage (Ia = bright-red bleeding, Ib = slow bleeding) II - Recent hemorrhage (IIa = non-bleeding visible vessel, IIb = adherent clot on base of lesion, IIc = flat pigmented spot) III - No evidence of bleeding

32. Arteriography : used to localize lesions when endoscopy has failed or when the patient cannot cooperate Detects vascular lesions in esophagus, stomach, hepatic aneurysms & pseudo- cysts of pancreas The modality can be helpful for bleeding that is distal to the ligament of Treitz

33. Management: Initial approach to ensure patient stability, to establish adequate oxygen delivery, to place intravenous access, to initiate fluid and blood resuscitation, to correct any underlying coagulopathies

34. Children at low risk for recurrent or life-threatening hemorrhage may be suitable for early hospital discharge or even outpatient care All patients with hemodynamic instability/ active bleeding should be admitted in ICU for resusitation and close observation ICU Requirements: Pediatric Intensivist, Pediatric Surgeon, Pediatric Gastroenterologist, Invasive monitors, Ventilators, Attached blood bank, Trained nursing staff

35. i) Big bore canula (IV/ IO) Hydration-NS/ RL SOS Transfusion ii) ICU care, invasive monitoring in unstable patients Cardiorespiratory monitor, intake- output chart, catheterization to monitor UO CVP monitoring helps to guide replacement therapy InjVit K 5mg to be given in case of hepatocellular failure, cholestatic jaundice.

36. iii) NG aspiration: Every ½ to 1 hourly for next 24 hours If significant blood loss estimated; as it ascertains fresh blood, decreases aspiration risk and aids in visualization via endoscope Gastric lavage with normal saline Iced saline does not stop bleeding and may even cause central hypothermia in a small child.

37. iv) Endoscopic therapy including: 1. Sclerotherapy (EST): The best Em/El procedure Acts by producing intimitis thrombosis  fibrosis of the vessels Sclerosants: Ethanolamine oleate 5% Sodium morrhuate 5% Sodium tetradecylsulphate 1.5% Cx: Esophageal ulceration, stricture, Broncho- esophageal fistula, thoracic duct damage, recurrance of varices, transient bacteremia

38. 2. Variceal banding: became popular b’cos of Cx of EST, but it is difficult in children Elastic band occludes the varix and it is necrosed & sloughed off in 5-10 days 3. Heater probe and bipolar coagulation for ulcers

39. v) Sengstaken Blakemore tube/ Minnesota tube: Mechanical Tamponade by balloons which compresses esophageal & gastric varices Has 3 lumens- for gastric and esophageal balloons & for aspiration of gastric contents Effectively controls acute bleeding, but assosiated with significant no. of Cx and rebleeding when tube is removed

40. vi) TransjugularIntrahepatic Porto-systemic Shunt (TIPSS): Percutaneous technique that creates a shunt in the liver between the portal & hepatic veins Indications: Refractory varicealh’age Refractory ascites Hepatorenal syndrome CI: Polycystic liver disease, Right Heart Failure, Systemic Infections, PV thrombosis, Biliary obstruction, severe hepatic encephalopathy Cx: Acute thrombosis or Delayed stenosis of shunt, Hepatic Encephalopathy

41. vii) Selective embolization viii) Laparoscopy/ Laparotomy Surgical repair rarely indicated: 1) Pt with EHPHT is from a remote area without facilities for EST/ blood transfusions 2) Pt continues to bleed from ectopic varices/ persistent esophageal varices, despite EST 3) Hypersplenism Surgeries done for PHT: Decompressive Shunts Devascularization Liver Transplantation

42. Pharmacotherapy: ix) Antacids: H2 blockers, Proton pump inhibitors: used as common causes of GI bleed are gastritis and peptic ulcer disease. Aluminium & Magnesium hydroxide x) Children known to have cirrhosis should receive Antibiotics, prefrebly before endoscopy, as bacterial infections are present in upto 20% of these patients Treat infections including triple therapy (antibiotics and proton pump inhibitor) for H. pylori Remove allergen in case of allergy

43. xi) Hormones/ hormone analogues (reduces splanchnic blood flow for variceal bleeding by vasoconstriction) : 1) Somatostatin- polypeptide, inhibits release of vasodialatory GI peptides eg glucagon, VIP & sustance P Dose: 250microgm IV bolus f/b 250microgm/hr infusion Disadvn: very short ½ life

44. 2) Octreotide-synthetic analogue of somatostatin, much longer ½ life & hence can be given as bolus or infusion Dose: 1microgm/kg IV infusion over 30min f/b 0.5microgm/kg/hour Disadvn: Exorbitant cost Nausea, flatulence, malabsorbtion (supresses GI motility & secretion) Bowel ischemia in high doses

45. 3) Vasopressin-non peptide, derived from posterior pituitary gland Splanchnic vasoconstriction, constricts lower esophageal sphincter Dose: 0.33unit/kg over 20min f/b IV infusion of 0.33units/kg/hour S/E: CVS-myocardial ischemia/infarction, VF (can be decreased by combining it with Nitroglycerine) Cerebral H’age, Respiratory arrest, Bowel ischemia & necrosis

46. 4) Terlipressin (Triglycyl-lysine vasopressin) Synthetic analogue of vasopressin Long duration of action & less cardiac S/E Dose: 2mg IV q6h until bleeding stops f/b 1mg q6h for next 24hrs 5) Miscellaneous Drugs: Clonidine (α2 agonist) Ketanserine & Ritanserine (5HT2 receptor antagonists) Molsidomine (venodialator)

47. Prophylaxis Against Bleed From Variceal Hemorrhage and Ulceration Primary prophylaxis is indicated because of high rate of bleeding from esophageal varices and the high mortality associated with bleeding Prophylactic Propranolol (most commonly used, 1-2mg/ kg) or Nadolol therapy are the only cost-effective ones No role of prophylactic EST/ EVL

48. Prophylaxis against stress ulcers are indicated in ICU patients with any of the following charecteristics: 1) Coagulopathy/ on anti-coagulants 2) Mechanical ventilation > 2 days 3) History of GI ulceration/ bleeding withinthe past year 4) Two or more of the following risk factors- sepsis, ICU admission lasting > 1 week, occult GI bleeding > 6 days, glucocorticoid therapy

49.  Effective identification and antibiotic treatment of H.Pylori infections is also crucial in preventing complications including upper GI bleeding  Prevention of NSAID related peptic ulcer disease and complicating UGI bleed in patients at high risk  In such patients COX-2 selective inhibitor/ non-selective NSAID + PPI/ Misoprostol is indicated

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