Hematemesis in children-Beyond Infancy


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Hematemesis in children-Beyond Infancy

  1. 1. Hematemesis in Children- Beyond Infancy<br />Dr. Divya Nair<br />DNB Pediatrics<br />Mahavir Hospital.<br />
  2. 2. Gastrointestinal (GI) bleeding in children is a fairly common problem<br />In the pediatric ICU population, 6-20% have upper GI bleeds. The incidence of lower GI bleeding has not been well established<br />10-20% of referrals to pediatric gastroenterologists<br />
  3. 3. Upper gastrointestinal (UGI) bleeding originating from esophagus, stomach or duodenum-proximal to the ligament of Treitz (aka duodenojejunal ligament)<br />Commonly presents with hematemesis (vomiting of blood or coffee ground-like material) and/or melena (black, tarry stools)<br />
  4. 4. Etiology:<br />A) Gastrointestinal causes<br />B) Systemic causes<br />C) Genetic causes<br />D) Spurious causes <br />
  5. 5. A) Gastrointestinal causes:<br />1) Esophagitis:<br /> GERD<br />Hiatus Hernia<br /> Infection: e.g. Candida, <br />Aspergillus, CMV, HSV <br />Medications: e.g. tetracycline,<br /> aspirin, NSAIDs, potassium chloride<br />“ erosive esophagitis"<br />
  6. 6. 2) Esophageal Rupture<br /> Mallory-Weiss Syndrome (located at LES)<br />
  7. 7. 3) Gastritis: 
More common than ulcers 
Medications (e.g. NSAIDs, aspirin) 
Infections (e.g., Helicobacter pylori, CMV, <br /> herpes) 
Crohn’s disease<br /> 4) Gastric Erosions:<br />Trauma, burn, shock or sepsis <br />This is usually superficial and occurs mainly in the <br />fundus of the stomach<br />
  8. 8. 5) Peptic Ulcer Disease<br />Zollinger-Ellison syndrome 
Results in multiple <br /> diffuse GI/ small bowel <br /> ulcerations<br />Ulcer with red spot<br />
  9. 9. Bleeding Ulcer<br />
  10. 10. 7)Portal hypertension: 
Hypertensivegastropathy<br /> Cirrhosis due to congenital <br /> hepatitis, hepatic fibrosis, <br /> cystic fibrosis<br />8) Extra-hepatic portal vein <br /> obstruction<br />Esophagealvarices<br />
  11. 11. 9) Vascular malformations: 
<br />Hemangiomas<br />Aorto-esophageal/-enteric fistulas<br />Dieulafoy ulcer (superficial defect of gastric mucosa which overlies an ectaticsubmucosal a.) <br />Watermelon stomach (gastric antral vascular ectasia) <br />Vasculitiseg: ITP<br />
  12. 12. 10) Tumors: <br />Polyps<br />Lipomas, leiomyoma<br />Adenocarcinoma<br />Lymphoma<br />Metastatic tumors,<br />Kaposi’s sarcoma, Barrett’s esophagus<br />Kasabach-Merritt synd (Hemangioma thrombocytopenia <br /> syndrome) <br />
  13. 13. 11) Traumatic:
Prolapsinggastropathy<br />Foreign body ingestion<br />Direct abdominal trauma<br />Iatrogenic- throat/nose Sx, <br /> traumatic NG<br />
  14. 14. 13) Miscellaneous: <br />Hemobilia<br />Hemosuccuspancreaticus<br />Menetries’ Disease<br />Eosinophilicenteropathy<br />Munchausen by proxy syndrome <br />Barrett’s ulcer secondary to GERD<br />
  15. 15. B) Systemic Causes:<br />Coagulopathy (congenital/acquired): Hemophilia, <br />vWD<br />2) Sepsis, scarlet fever, malaria, leptospirosis<br />3) Burns, Sepsis ( Curling’s ulcer),<br /> Raised ICT, Head injury, Encephalitis ( Cushing’s ulcer)<br />4) HUS, HSP<br />5) Malignancy- Leukemia <br />
  16. 16. 6) Poisonings- chemical, caustic<br />7) Drugs-aspirin, NSAIDS, anti-coagulants<br />8) Food (milk protein) allergy/ hypersensitivity<br />9) Idiopathic<br />NSAID induced Ulcers <br />
  17. 17. C) Genetic conditions:<br />Turner syndrome<br />Ehlers Danlos syndrome<br /> ( cutis hyperelastica)<br />Pseudoxanthomaelasticum<br />KlippelTrenaunay syndrome<br />Osler-Rendu-Weber syndrome<br /> (hereditary hemorrhagic telangectesia) <br />Blue rubber bleb naevus syndrome<br />Hermansky-Pudlak syndrome<br />
  18. 18. D) Spurious causes:<br />I) Hematememis: Bleeding from nose (epistaxis), <br /> mouth, pharynx, <br />hemoptysis<br />II) Malena: Iron preparation, Bismuth, Lead, <br /> spinach, beets, <br /> blueberries<br />
  19. 19. Grading of UGI Bleeds<br />MILD: presents as nausea, vomiting, abdominal discomfort & small <br /> quantity of hematemesis/ malena<br />MODERATE: significant blood loss, tachycardia, cold sweat, hypo-<br /> tension.<br /> No ongoing blood loss; recovers with blood transfusion<br />SEVERE: more striking features of shock present, Hb falls to 8gm% <br /> or less.<br /> Requires multiple blood transfusions d/t ongoing blood loss<br /> Takes longer time to recover; very high mortality unless treated <br /> properly.<br />
  20. 20. Diagnosis:<br />History 
Quantity, frequency, type of blood <br /> (bright red vs coffee ground)<br />Nausea, vomiting, recurrent abdominal pain s/o PUD <br />Dysphagia/ odynophagia, chest pain/burning, <br />hematochezia, melena, bruising, bleeding, repeated retching f/b vomiting of <br /> blood <br />Weight loss, early satiety s/o malignancy<br />Psychiatric symptoms<br />
<br />
  21. 21. Drug ingestion <br />Bleeding sites- skin, mucosa, GUT, joints <br />Recurrent epistaxis<br />H/O Jaundice, stool color<br />Severe and diffuse upper GI ulcerations with chronic diarrhea usually : Zollinger Ellison syndrome or gastrinoma<br />Birth history: lines placed (umbilical lines can result in clotting of portal vein) <br />
  22. 22.  Past history: History of liver disease,<br /> history of pancreatitis, GI surgeries<br /> H/O Bleeding disorders in family 
<br />Medications: NSAID use, aspirin use 
<br /> Diet history: Formula intolerance, food <br /> allergies<br />
  23. 23. Physical examination:<br />Vitals:- Heart rate, respiratory rate, BP, capillary refill, orthostatic changes<br />Pallor<br />During examination of the head, ears, eyes, nose, and throat, look for causes such as: <br />epistaxis, nasal polyps, and oropharyngeal erosions from caustics and other ingestions<br />
  24. 24. Signs of Chronic Liver Disease: Jaundice, Clubbing, leukonychia, palmarerythema, spider nevi, gynecomastia, etc.<br />Vascular malformations: hemangiomas, telangiectasias or purpura over skin<br />Peutz- Jeghers syndrome: pigmented lips, palms, soles<br />Pseudoxanthomaelasticum: “Plucked chicken appearance” of skin<br />
  25. 25. Per Abdomen:<br />Tenderness, Hyperactive bowel sounds<br />Caput medusa with ascites, shrunken liver and <br />splenomegalys/o Cirrhosis with Portal Hypertension<br />Extra-hepatic PHT will have splenomegaly without hepatomegaly<br />Spleen may contract following<br /> a massive bleed and may <br /> not be palpable (Smith<br /> Howard Syndrome)<br />
  26. 26. Work up:<br />CBP, PCV, RBS <br />Coagulation studies <br />LFT to r/o cirrhosis <br />RFT<br />Type and cross-match of several units of blood <br />
  27. 27. Oesophago-gastro-duodenoscopy : If active bleeding, most sensitive and specific for diagnosis and provides therapeutic options<br />Ultrasound with Doppler to assess liver disease and portal hypertension <br />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<br />
  28. 28. Special tests:<br />Serum gastrin levels ( Zollinger Ellison syndrome)<br />Peroxide based tests: Gastroccult for upper GI bleed<br />Gastroccult : only test designed specifically for detecting gastric occult blood and determining gastric pH<br />It includes a convenient pH comparison chart for the Clinically relevant range which is important in monitoring antacid prophylaxis<br />Certain ingestions such as red meat, iron, and peroxidase-containing vegetables (eg: turnips, horseradish, broccoli, cauliflower, and cantaloupe), can give false-positive results<br />
  29. 29. Imaging:<br />Barium contrast studies- barium swallows, upper GI series, small bowel <br /> follow-throughs, or barium enemas : for non emergency bleeds, to <br /> point to foreign bodies, ulcers, IBD, or polyps<br />
  30. 30. Endoscopy:<br />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<br />The site of upper GI bleeding can be identified in 90% of cases when endoscopy is performed within 24 hours<br />This modality is also beneficial in predicting the likelihood of continued bleeding<br />
  31. 31. The Forress classification divides endoscopic findings into the following 3 categories:<br />I - Active hemorrhage (Ia = bright-red bleeding,<br />Ib = slow bleeding)<br />II - Recent hemorrhage (IIa = non-bleeding visible vessel, <br />IIb = adherent clot on base of lesion, <br />IIc = flat pigmented spot)<br />III - No evidence of bleeding<br />
  32. 32. Arteriography : <br /> used to localize lesions when endoscopy has failed <br /> or when the patient cannot cooperate<br /> Detects vascular lesions in esophagus, stomach, <br /> hepatic aneurysms & pseudo-<br /> cysts of pancreas <br /> The modality can be helpful <br /> for bleeding that is distal to <br /> the ligament of Treitz<br />
  33. 33. Management:<br />Initial approach<br />to ensure patient stability, <br />to establish adequate oxygen delivery, <br />to place intravenous access, <br />to initiate fluid and blood resuscitation, <br />to correct any underlying coagulopathies<br />
  34. 34. Children at low risk for recurrent or life-threatening hemorrhage may be suitable for early hospital discharge or even outpatient care<br /> All patients with hemodynamic instability/ active bleeding should be admitted in ICU for resusitation and close observation <br />ICU Requirements:<br /> Pediatric Intensivist, Pediatric Surgeon, Pediatric Gastroenterologist, <br /> Invasive monitors, Ventilators, Attached blood bank, Trained nursing <br /> staff<br />
  35. 35. i) Big bore canula (IV/ IO)<br />Hydration-NS/ RL<br />SOS Transfusion<br />ii) ICU care, invasive monitoring in unstable patients<br />Cardiorespiratory monitor, intake- output chart, <br /> catheterization to monitor UO<br />CVP monitoring helps to guide replacement therapy<br />InjVit K 5mg to be given in case of hepatocellular<br /> failure, cholestatic jaundice.<br />
  36. 36. iii) NG aspiration:<br /> Every ½ to 1 hourly for next 24 hours<br /> If significant blood loss estimated; as it ascertains fresh <br /> blood, decreases aspiration risk and aids in visualization via <br /> endoscope<br /> Gastric lavage with normal saline<br /> Iced saline does not stop bleeding and may even cause <br /> central hypothermia in a small child. <br />
  37. 37. iv) Endoscopic therapy including:<br /> 1. Sclerotherapy (EST): The best Em/El procedure<br /> Acts by producing intimitis thrombosis  fibrosis of <br /> the vessels<br />Sclerosants: Ethanolamine oleate 5%<br /> Sodium morrhuate 5%<br /> Sodium tetradecylsulphate 1.5% <br />Cx: Esophageal ulceration, stricture, Broncho- <br /> esophageal fistula, thoracic duct damage, <br />recurrance of varices, transient bacteremia<br />
  38. 38. 2. Variceal banding: became popular b’cos of Cx of <br /> EST, but it is difficult in children<br /> Elastic band occludes the varix and it is necrosed & <br /> sloughed off in 5-10 days<br />3. Heater probe and bipolar coagulation for ulcers<br />
  39. 39. v) Sengstaken Blakemore tube/ Minnesota tube:<br /> Mechanical Tamponade by balloons which <br /> compresses esophageal & gastric varices<br /> Has 3 lumens- for gastric and esophageal balloons<br /> & for aspiration of gastric contents<br /> Effectively controls acute bleeding, but assosiated<br /> with significant no. of Cx<br /> and rebleeding when tube <br /> is removed<br />
  40. 40. vi) TransjugularIntrahepatic Porto-systemic Shunt (TIPSS):<br />Percutaneous technique that creates a shunt in the <br /> liver between the portal & hepatic veins<br /> Indications: Refractory varicealh’age<br /> Refractory ascites<br />Hepatorenal syndrome<br /> CI: Polycystic liver disease, Right Heart Failure,<br /> Systemic Infections, PV thrombosis, Biliary obstruction, severe hepatic <br /> encephalopathy<br />Cx: Acute thrombosis or Delayed stenosis of shunt, Hepatic <br /> Encephalopathy<br />
  41. 41. vii) Selective embolization<br /> viii) Laparoscopy/ Laparotomy<br />Surgical repair rarely indicated:<br /> 1) Pt with EHPHT is from a remote area without facilities for EST/ <br /> blood transfusions<br /> 2) Pt continues to bleed from ectopic varices/ persistent esophageal <br />varices, despite EST<br /> 3) Hypersplenism<br />Surgeries done for PHT: Decompressive Shunts<br />Devascularization<br /> Liver Transplantation <br />
  42. 42. Pharmacotherapy:<br />ix) Antacids:<br />H2 blockers, Proton pump inhibitors: used as common causes of GI bleed <br /> are gastritis and peptic ulcer disease. <br />Aluminium & Magnesium hydroxide<br />x) Children known to have cirrhosis should receive Antibiotics, <br />prefrebly before endoscopy, as bacterial infections are present <br /> in upto 20% of these patients<br />Treat infections including triple therapy (antibiotics and proton pump <br /> inhibitor) for H. pylori<br />Remove allergen in case of allergy<br />
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  43. 43. xi) Hormones/ hormone analogues (reduces splanchnic blood <br /> flow for variceal bleeding by vasoconstriction) :<br />1) Somatostatin- polypeptide,<br /> inhibits release of vasodialatory GI peptides<br />eg glucagon, VIP & sustance P<br /> Dose: 250microgm IV bolus f/b 250microgm/hr <br /> infusion<br />Disadvn: very short ½ life <br />
  44. 44. 2) Octreotide-synthetic analogue of somatostatin, <br /> much longer ½ life & hence can be given as bolus or <br /> infusion<br /> Dose: 1microgm/kg IV infusion over 30min f/b<br /> 0.5microgm/kg/hour<br />Disadvn: Exorbitant cost<br /> Nausea, flatulence, malabsorbtion (supresses GI <br /> motility & secretion)<br /> Bowel ischemia in high doses <br />
  45. 45. 3) Vasopressin-non peptide, derived from posterior pituitary gland<br />Splanchnic vasoconstriction, constricts lower <br /> esophageal sphincter<br /> Dose: 0.33unit/kg over 20min f/b IV infusion of <br /> 0.33units/kg/hour<br /> S/E: CVS-myocardial ischemia/infarction, VF (can <br /> be decreased by combining it with Nitroglycerine)<br /> Cerebral H’age, Respiratory arrest, <br /> Bowel ischemia & necrosis<br />
  46. 46. 4) Terlipressin (Triglycyl-lysine vasopressin)<br /> Synthetic analogue of vasopressin<br /> Long duration of action & less cardiac S/E<br /> Dose: 2mg IV q6h until bleeding stops f/b 1mg q6h for next <br /> 24hrs<br />5) Miscellaneous Drugs:<br />Clonidine (α2 agonist)<br />Ketanserine & Ritanserine (5HT2 receptor antagonists)<br />Molsidomine (venodialator)<br />
  47. 47. Prophylaxis Against Bleed From Variceal Hemorrhage and Ulceration<br />Primary prophylaxis is indicated because of high rate of <br /> bleeding from esophageal varices and the high mortality <br /> associated with bleeding<br />Prophylactic Propranolol (most commonly used, 1-2mg/<br /> kg) or Nadolol therapy are the only cost-effective ones<br /> No role of prophylactic EST/ EVL<br />
  48. 48. Prophylaxis against stress ulcers are indicated in ICU patients with any of the following charecteristics: <br /> 1) Coagulopathy/ on anti-coagulants <br /> 2) Mechanical ventilation > 2 days <br /> 3) History of GI ulceration/ bleeding withinthe <br /> past year <br /> 4) Two or more of the following risk factors- <br /> sepsis, ICU admission lasting > 1 week, occult <br /> GI bleeding > 6 days, glucocorticoid therapy <br />
  49. 49.  Effective identification and antibiotic treatment of <br />H.Pylori infections is also crucial in preventing <br /> complications including upper GI bleeding <br /> Prevention of NSAID related peptic ulcer disease and <br /> complicating UGI bleed in patients at high risk<br /> In such patients COX-2 selective inhibitor/ non-selective <br /> NSAID + PPI/ Misoprostol is indicated <br />
  50. 50. <ul><li>Patients with history of uncomplicated/ complicated </li></ul> PUD should be tested for H.pylori prior to beginning a <br /> NSAID/ low dose aspirin <br /> If H.pylori present it should be treated with appropriate <br /> therapy, even if it is believed that PU was due to NSAIDs<br />
  51. 51. THANK YOU<br />