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GASTROINTESTINAL BLEEDING GIB • 1-2% of acute hospital admissions. • 5% mortality. • 90% cease spontaneously. Classification • Level of bleeding - Upper / Low. (above and below the ligament of Trietz). • Time - Acute / Chronic • Severity of blood loss Clinical Presentation • Hematemesis - bloody vomiting • Coffee Ground vomiting • Melena- dark/black stool.(degradation of hemoglobin). • Hematochezia-Rectal bleeding Evaluation of the bleeding patient -Patient assessment: anamnesis and hemodynamic status. -resusitation. -dignosis: bleeding source. -treatment. Medical history • Characteristics of bleeding ( melena, coffee ground, rectal bleeding). • Symptoms reflect severity of bleeding. (syncope, dizziness, onset and frequency). • Symptoms associate possible etiologies. Dyspepsia, abdominal pain, weight loss, early satiety, liver disease, alcohol abuse. Antececedent vomiting. Dysphagia and reflux. Cont• Constipation, bowel movements. • Medications: NSAIDS, coumadin. • Coagulopathy. • History of aortic surgery. • Previous episodes. • Comorbidities. (ability to respond to hemorrhage). Physical Examination • Determine degree of blood loss: - pale, cold extremeties, sweating. -pulse, BP, orthostatism. - consciousness. • Epigastric tenderness. Abdominal mass. • Signs of liver disease. (jaundices, ascites….) • Oropharynx (rare). Cont• Rectal examination – quality of stool. • Nasogastric tube. ( blood, coffee ground, bile, gastric fluids) Management and monitoring • Large bore IV lines (Haggen/Pousseleur low) • Fluids - Hartman’s solution (restoration of intravascular volume). • Oxygen (espicially in IHD pts). • Blood typing and cross matching . • Blood tests- CBC, PT PTT, LFT. Cont• Unstable pt- start packed cells, consider intubation(prevent aspiration in obtunded pts) . • Repair coagulation defects. • Consider central line cath (uaually not needed). • Urine output. Level of bleeding-Upper/Low Upper GI bleeding - the source is above the Treitz ligament • Lower GI bleeding – is below • Upper GI Bleeding Diagnosis Naso-gastric tube – blood or coffee ground • Melena in rectal exam • After stabilisation and primary treatment - upper GI endoscopy in first 12-24 hours • Specific treatment: medical, antibiotics, endoscopy, angiography, surgery. • Low GI Bleeding-diagnosis • • • • • Rectal bleeding – blood on rectal exam. Normal NGT contents. Melena with normal upper GI endoscopy After stabilization – rectoscopy , colonoscopy Proffuse bleeding – lateralisation of bleeding site by angio or bleeding scan Upper Gastrointestinal Bleeding Upper GI Bleeding • • • • • • • • • • Peptic disease – duodenal or gastric ulcer, 50%. Erosive gastritis 15-30%. Esophageal Varices 10-20%. Gastrinoma – Zollinger-Ellison synd. Mallory-Weiss tears 8-10%. Malignancy- 3%. Dieulafoy’s. Esophagitis. Osler weber rendu. Hypertrophic gastritis – Menetrier disease or Water-Melon Stomach Peptic disease • 5% - hemorrhage is presenting symptom. • 20%- develop bleeding at least once. • Hemorrhage is the most lethal form of complicated ulcer dis. Peptic disease- Pathogensis • Acid peptic erosions into submucosal or extraluminal vessels. • Helicobacter pylori. Most common etiology for duodenal ulcer. • NSAIDS. Damage to GI mucosa. - inhibition of prostaglandin synthysis--> inhibition of mucos and bicarbonate production. - delay ulcer healing. - epithlial acidification. - platelet dysfunction. • ZES. Gastrin secreting tumor. Peptic dis- prognostic factors • • • • • • Severity of bleeding, hemodynamic status. Persistent or recurrent. Transfusion requirements. Nasogastric aspirate, blood, coffee groud. Older pts. Comorbidities. Gastric ulcer- Classification • Type 1- distal lesser curvature. • Type 2- combined gastric and duodenal. High acid secretion. • Type 3- prepyloric. High acid secretion. • Type 4- proximal lesser curvature. • Type 5- secondary to NSAIDS. Gastric ulcer • 10% of gastric ulcers are malignant. • Most bleedind ulcers arise in incisura, antrum and distal body of stomach. Duodenal ulcer • 95% - secondary to Helicobacter pylori infection. • 10% of pts with HP develop ulcer. 20% of pts with ulcer and HP bleed. • Bleeding DU, usually located on the posterior duodenal wall. Peptic dis- Treatment • • • • • • • • NPO. Fluids. Stop NSAIDS. Antisecretory agent. H2-rec blockers or proton pump inhibitors. PPI may reduce rebleeding. Endoscopy- diagnostic and therapeutic. within 12-24 hours. Anti H pylori treatment. Not immediatly. Massive bleeding- consider emergent endoscopoy. The Role of Adjunctive Pharmacological Therapy • Clot stabilization: at a pH of above 6.0 pepsin is inactivated and cannot lyse clots • Effective clotting may not occur at pH<6. • Antacids, iced saline gastric lavage and H2blockers and other interventions are ineffective in reducing rebleeding. • PPI decreases the incidence of rebleeding. Peptic dis- Endoscopy • Rebleeding 10-20%. Consider re-endoscopy • Prognostic endoscopic findings for rebleed: 1) appearence -small clean ulcer base. 0% - flat, pigmented 10% - adherent clot. 20% - visible vessel. 40% - active bleeding. 2) size > 2cm. Peptic Ulcer • Endoscopic manipulation - Coagulation - Injection of sclerosant or vasoconstricting agent. - Clip. Peptic Ulcer Endoscopy Endocliping of Bleeding Ulcer Angiography- embolization • To consider in: - high risk pts. - rec bleeding. Duodenum: gastroduodenal art. Angioembolization of bleeding duodenal ulcer Surgical therapy • Indications: -active bleeding not responsive to endoscopic treatment. - significant rec bleeding after endoscopic treatment. -ongoing transfusion requirment. 6 pc/d. • The goal of surgery: to control hemorrhage. • Acid reducing procedure is secondary, but important. Surgery for bleeding ulcer • DU: Suturing of bleeding ulcer +/vagotomy with or without drainage. Rebleeding<10%. • GU: Partial gastrectomy or wedge resection. • Antrectomy+truncal vagotomy Vagotomy Drainage Procedure Gastrectomy Bleeding ulcer in pts with HP • Eradication of HP decrease the incidence of rebleeding. • Only 0.2 % of ulcer pts with HP infection need surgery for bleeding peptic ulcer. Erosive Gastritis • common source of bleeding in critically ill pts, elderly and NSAIDS treated pts. • Lesions distributed throught the gastric mucosa. • Pathogenesis- acid peptic injury and mucosal ischemia d/t hypoperfusion Erosive gastritis • in critically ill pts- prophylaxis H2 rec antagonist is recommended. • Treatment- conservative+ treat the underlying dis. • PPI • In profuse bleeding : - angiography- embolization. - surgery- rarely indicated, if single bleeding site gastrotomy, suturing of and vagotomy. if multiple sitesnear/total gastrectomy Esophageal varices • Dilated submucosal veins that communicate portocollateral circulation and the systemic venous system secondary to Liver cirrhosis or portal hypertension. • 25-30% develop hemorrhage. • 70% rebleeding. Esophageal varices • Pathogenesis: elevated portal venous pressure. Hepatic pressure gradient>12 mmHg varices. • Risk for hemorrhage: size. red color signs on endoscopy. poor liver function. active alcohol use. Primary treatment • B-blockers. • Nitrate. Less common. • Endoscopy. Band ligation , sclerotherapy. Treatment of acute hemorrhage • Vasoactive drugs:Vasopressin IV, empiric Somatostatin IV. effective 80-90%. • Emergent Endoscopy-ligation or sclerotherapy. - Rule out other etiologies. - decrease rebleeding and mortality. Esophageal Varices Endoscopy Endoscopic Ligation of Varices Varices – acute hemorrhage • Blackmore tube insertion- massive bleeding Varices-Treatment of rec bleeding • B-blocker. Decrease rebleed- 30%. • Repeated endoscopy. • TIPS: - nonselective shunt. decrease hepatic flow may induce encephlopathy. - rebleeding-20%. - thrombosis- 30-40%. - useful in acute hemorrhage. -definitive or temporary treatment. • Surgical shunt. • Liver Tx. Surgical porto-systemic shunt • High mortality rate as emergency procedures. • Nonselective- more effective in reduce hemorrhage. - greater risk for encephalopathy. - effective for ascites. • Selective- selective decompressing of left side portal system and esophageal varices. -allow hepatic perfusionlower rate of encephlopathy. • Procedure of choice- distal splenorenal shunt. • Devascularization procedure- if shunt procedure not possible. Mallory-Weiss Tears • Tear in the gastric mucosa near GEJ. • Characterized by antecedent history of vomiting,retching or coughing. • Common- associated alcoholism, nsaids, hiatal hernia, age>60. Mallory-Wiess treatment • 90% stop spontaneously. • Endoscopy for diagnosis and treatment. • Rebleeding:pts with active bleeding in initial endoscopy, or pts with coagulation disorders. • Surgery rarely needed.(gastrotomy and oversewing of the mucosal tear). Esophageal sources • • • • • • • Esophagitis GERD. Barrett’s Malignancy. Medications. Radiation. IBD. Rare Source - Dieulafoy Aberrant submucosal vessel m/p in the lesser curv. • Treatmentendoscopy / surgery. • Endoscopic diagnosis is difficult, no ulcerated lesion. • Rebleeding is common. • Hypertrophic Gastritis • Water-melon stomach or Menetrier syndrome Zollinger-Ellison Syndrome • Bleeding from ulcers – duodenal and postbulbar origin • CT and EUS are diagnostic tools • Operation with complete resection or at least debulking is treatment of choice Lower GI Tract Bleeding LGIB • • • • • • • Bleeding below ligament of Trietz. 97% colon 3% small bowel. Incidence increases with age. Slow bleeding may present as melena. Shock is less common than in UGIB. Usually intermittent. LGIB- Etiology • • • • • • • • Diverticulosis of the colon AV malformation or angiodysplasia Colon Cancer IBD-Ulcerative colitis/Crohn’s Hemorrhoides and anorectal diseases. Ischemic colitis. Radiation injury.(proctitis) Meckle’s diverticulum, or other small bowel diverticula. Etiology by age group, in order of frequency Adults over 55 y.o. - Diverticulosis - AVMs - Polyps - Malignancy Adults to 55 y.o. Adolescents and young adults -Anorectal dis - Inflammatory bowel disease - Diverticulosis - Polyps - Malignancy - AVMs - Meckel’s diverticulum - Inflammatory bowel disease - Polyps Diagnostic procedures • • • • • Rigid proctoscopy- in the ER, for all pts. Colonoscopy. Nuclear scintigraphy. Angiography. Operative intervention. proctoscopy • Rule out anorectal disease. Colonoscopy • Useful in evaluating patients with: - occult chronic GI bleeding -Acute self limited hemorrhage that has stopped bleeding.(test of choice). • Use in patients with massive ongoing bleeding remains controversial. • PROS :Diagnostic and therapeutic tool.(laser, coagulation, Injection). • CONS:-Technical difficulty in not prepared pts. -Complications, Perforation. Nuclear scintigraphy • Bleeding scan- detect intraluminal extravasation of blood, utilize technetium sulfur colloid or technetium 99m-labeled red blood cells. • PROS:-Noninvasive. -Detects bleeding as slow as 0.1 mL/min. - repeated scans are possible up to 24h, it can detect intermittent bleeding. • CONS:-not therapeutic. - delay in diagnosis. -lateralization lt or rt , but not localization of bleeding. Red blood cells bleeding scan Angiography • Selective catheterization of mesenteric vessels and injection of contrast – Looking for extravasation and pooling of media within intestinal lumen – In absence of preangiographic localization catheterize SMA IMA Celiac. – Once site of hemorrhage found intra-arterial infusion of vasopressin arterial, venous, and bowel contraction promotes thrombosis at bleeding site --If patient an operative risk, transcatheter embolization with gel foam, wire coils, or autologous blot clots.(may be complicated with bowel infarction). Angiography • PROS:- localization of bleeding. - visualize nonbleeding vascular malformations, neoplasms and other lesions. - Detects bleeding as slow as 0.5 mL/min. - therapeutic - recently superselective embolization is optional . - 85% effectiveness – identify and control hemorrhage. • CONS: - achieves temporary control before definitive surgical resection. - Invasive. - Complications: cardiac, visceral, and peripheral ishchemia (relative contraindication) - Chance of rebleeding. Angiography Diverticulosis • Diverticular bleeding is the most common source of LGIB, 40-50%. • Diverticulosis Present in > 50% of population > 60 y.o. • Risk of bleeding 5% of pts. • Hemorrhage is not associated with diverticulitis. Diverticulosis • Hemorrhage d/t weakening and erosion/rupture of vasa recta/branches of the marginal arteries,at the dome or the neck of the diverticulum, with decompression into bowel lumen. • Luminal traumatic factors lead to hemorrhage . • Hemorrhage tends to be massive d/t arterial source • The most common source of massive LGIB, from the lt colon. Diverticulosis • Most cases stop spontaneously. – Risk of rebleeding 25% at 4 years. – 50% risk if patient has suffered two prior episodes of diverticular bleeding • 10-20% bleeding continues in absence of intervention. • Colonoscopy- diagnostic and therapeutic. • Consider surgery for recurrent episodes. Endoscopy of Diverticulosis Angiodysplasia=AVM • Small ectatic vessels in the submucosa, arteriovenous malformation. • common in old cardiac pts, CRF, AS. • 5-20% of LGIB. • The most common cause of hemorrhage from SB. • The most common cause of massive LGIB from rt colon. Endoscopy of angiodyspasia AVM- diagnosis • Occur primarily in cecum and ascending colon of elderly patients> 50%. • Recurrent intermittent bleeding. • Colonoscopy-most sensitive tool. - diagnostic and therapeutic. • Angiographic criteria for identification of AVM – 1) early and prolonged filling of draining vein – 2) clusters of small arteries – 3) visualization of vascular tufts Colon Cancer • Most common after AVM and diverticulosis. • 5-10%. • Colonoscopy and biopsy is essential • massive bleeding uncommon. Endoscopy of Colon Cancer COLON CANCER • Proximal colonic tumors have high propensity for occult bleeding • Rectosigmoid tumors easily confused with hemorrhoidal bleeding – Treatment of hemorrhoids should be preceded by flexible sigmoidoscopy in patients > 40-50 y.o. Inflammatory Bowel Disease • bleeding more common in ulcerative colitis IBD- UC • Minor and hemodynamically insignificant bleeding conservative treatment directed at inflammatory disease • Hemodynamically significant bleeding surgery – total abdominal colectomy – End ileostomy + Hartmann’s pouch Anorectal disease • Small amounts of bright red blood on surface of stool and toilet tissue, hemodynamically insignificant – Precipitated by strained passage of hard stool • Hemorrhoids – Engorgement of venous plexi of rectum/anus with protrusion of mucosa • Anal Fissure – Tear in anal epithelium Internal hemorrhoids Colitis Infectious • Ischemic • Obscure GI bleeding • Intermittent GI bleeding for which no source has been determined, despite rigorous endoscopic (gastroscopy+colonoscopy) and radiologic investigation. • Almost all are from small bowel. Bleeding from obscure source • • • • • Angiodysplasia of small bowel, most common. 40%. Acquired lesions, may recur . Polyps and neoplasms. Meckel’s Diverticulum. Most common in young. Submucosal lesion – lymphoma, stromal cell tumor etc. Others. Obscure GIB- Diagnostic modalities -Enteroclysis or CT enterography: Able to detect SB tumors (80%), but poor modality for superficial mucosal lesions as AVM. – Enteroscopy : can visualize through to the jejunum. – Arteriography: special attention to evidence of angiodysplasia. 60% sen – Meckel’s scan. Initial evaluation in young pts. – GI capsule- camera. – Laparotomy and intraopertive enteroscopy. (70%sen) – Provocative testing: arteriography + heparin or thrombolytics to precipitate acute bleeding Obscure GI bleeding (cont.) • Operative exploration – Exploratory laparotomy with examination from GE junction to intraperitoneal rectum followed by: • Transillumination of bowel wall with fiberoptic light source • Intraoperative endoscopy • Vigorous hydrationaccentuates thin walled veins that constitute most AVMs – Treatment = resection of segment of SB or LB containing the offending lesion Meckel’s Diverticulum • Rare, true diverticulum. • Gastric, pancreatic mucosa. • The origin of bleeding is ulceration of small bowel mucosa distally to the diverticulum. • Treatment: excision of diverticulum and segment of ileum to assure inclusion of adjacent ulceration. Submucosal lesions Lymphoma of small bowel – rare disease • Stromal cell tumor - GIST may be a reason of mucosal erosions and bleeding. • Operative intervention in massive unidentified bleeding source • Exploratory laparotomy : – Thorough examination of entire GI tract • Initial step: determine visually location of blood within GI tract • Next: careful inspection and gentle palpation of entire GI tract • Intraoperative upper endoscopy in absence of obvious bleeding source. Operative intervention (cont.) • If bleeding site localized preoperatively: – Segmental bowel resection that includes offending lesion – Usually safe to perform primary anastomosis – End stoma + mucous fistula if patient hemodynamically unstable, malnourished Operative intervention (cont.) • If bleeding site not localized preoperatively: – intraoperative colonoscopy followed by segmental colectomy. – if bleeding site still not identified: “blind” total colectomy is indicated. • repeat proctoscopy to definitely rule out rectal source of bleeding. • 5% mortality rate. Thank You !