GASTRO-INTESTINAL 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 Erosive gastritis 15-30%. Esophageal Varices 10-20%. 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 Aorto-duodenal fistula (rare)

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 H2-blockers 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 sitesnear/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 perfusionlower 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. Treatment- endoscopy / 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 Adolescents and young adults Adults to 55 y.o. Adults over 55 y.o. - Meckel’s diverticulum - Inflammatory bowel disease - Polyps Anorectal dis Inflammatory - Diverticulosis - Malignancy AVMs Diverticulosis

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 hydrationaccentuates 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 !