GIT bleeding OUT LINES: - history and examination. - DDX . - Theoretical part . - OSCE cases . Mwf8een yaa raaab <3 Approach to GI bleeding GI bleeding is a common reason for referral from the emergency department. After initially ensuring that your patient is stable a reasonable approach would be to then try and determine the site of bleeding. This can be divided into: 1. Upper GI bleeding (above the ligament of Treitz) 2. Lower GI bleeding (below the ligament of Treitz) Upper GI Bleeding Upper GI blood loss can occur anywhere along the GI tract and the differential diagnosis reflect this. DDX: 1. Esophagus: • Esophageal varices • Esophagitis • Esophageal cancer • Mallory Weiss tear 2. Stomach • Gastric ulcer • Gastritis • Gastric cancer 3. Duodenum • Duodenal ulcer • Aortoenteric fistula (if previous aortic graft) 4. Coagulopathy (drugs, renal disease, liver disease) History: Adequate history taking may help identify the severity, duration, location and cause of the bleeding. GI bleeding may present with a wide spectrum of symptoms…if slow and chronic may only present with non-specific findings of anemia or fatigue. More acute serious bleeding however can present with things like hematemesis, chest pain and hemodynamic instability. Questions to consider include: 1- haematemesis: vomiting of blood -onset. -frequency. -amount. -nature (fresh or clotted , bright red or dark blood) 2- melena ( could be a symptom of upper or lower gi bleeding ) 3-abdominal pain :(onset "sudden or gradual " , site, duration ,severity , nature ,radiation , progression "increase , decrease or intermittent " , aggravating and relieving factors , The end of the pain " spontaneous or brought about by some action by the pt or doctor. 4-symptoms of the severity of bleeding : -loss of consciousness -postural drop -symptom of anemia : fatigue ,palpitation -chest pain -SOB 5-Other sites of bleeding: epistaxis or hemoptysis 6-risk factors : Esophageal varices ,PUD, heart burn , liver disease , blood transfusion ,contact with sick people ,IBD, blood disorders , cancer , smoking or alcohol consumption. hx of truma. 7- associated symptoms : Jaundice . weight loss , loss of appetite , fever, night sweats . 8- past HX : -Same episode -GIT surgery 9- drug HX: NSAID, steroid , anticoagulants . 10- family hx : - GIT cancer - blood disorders . Physical Exam/Investigations: The physical exam should confirm information found on the history. Things to look for include: 1. Vitals: • Tachycardia, hypotension, postural changes 2. Abdominal Exam • Distension, tenderness, masses • Evidence of chronic liver disease • Rectal – masses, Melena, bright red blood 3. Skin Exam • Jaundice, ecchymosis, telangectasia 4. Laboratory • CBC –HB, in rapid blood loss the initial Hct may not accurately reflect the amount of blood loss as equilibration of the extravascular fluid may take several hours • PTT, PT, INR, LFTs • BUN, Creatinine – ratio >10:1 suggestive of a UGIB. Occurs as a result of breakdown of blood proteins by bacteria to urea and re-uptake of this from the gut • Very important to repeat lab values in a couple hours to follow clinical course 5- Imaging : CXR "aspiration pneumonia , plural effusion , perforated esophagus" Erect supine abdominal X ray " perforated viscose" Endoscope: diagnostic and therapeutic tool . It is Contraindicated in acute MI and when pt is uncooperative . Management: The initial evaluation of a patient with an upper GI bleed involves an assessment of the hemodynamic stability and resuscitation if necessary. 1. ABC’s • 2 large bore IVs, patient should be placed in a monitored area • Fluid resuscitation – Ringers lactate or normal saline • Type and cross match pRBCs • Correct any Coagulopathy 2. Keep NPO – in case of sudden repeat bleed, may need urgent endoscopy or even intubation 3. EKG – looking for signs of ischemia or infarct 4. PPI – Losec PO if hemodynamically stable, IV pantoprozole for hemodynamically unstable UGIB 5. Endoscopy – attempts to identify the source of bleeding +/- therapeutic intervention to achieve hemostasis • Risks for rebelling include spurting or oozing, visible vessel or fibrin clot • UGI barium studies are contraindicated in the setting of an acute UGI bleed as it will interfere with subsequent endoscopy or surgery if needed 80% of UGIB stop spontaneously. Mortality is approximately 10% Peptic Ulcer Disease Peptic ulcer disease is the most common cause of an upper GI bleed. An erosion (superficial to the muscularis mucosa) or ulcer (penetrates the mucosa) is a result of an imbalance between protective factors of the gut and things known to damage the lining of the gut. The two most common risk factors are H. Pylori and NSAID use. Others include smoking (increases risk and length of time to heal), alcohol, incompetent LES, stress, Zollinger-Ellison syndrome (gastrinomas). Reduction of these risk factors reduces ulcer recurrence and rebelling rates. Helicobacter Pylori • Common infection (20-40%), gram negative rod • Present in 90% of duodenal ulcers, 60% of gastric ulcers and 50% of nonulcerative dyspepsia • Most commonly acquired in childhood, presumably by fecal-oral route • The bacteria generally does not invade gastric tissue but instead disrupts the mucosal layer making it more susceptible to acid damage • Can be easily diagnosed either invasively on biopsy or non-invasively with a urea breath test or serology. A positive urea breath test indicates current active infection, however it is not useful to repeat serology after the patient has been treated as antibodies will remain positive for a long time after treatment Dyspepsia is the most common clinical presentation. Other things on history that suggest PUD include epigastric burning, pain that develops 1-3 hours after meals and is relieved by eating. Patients may also present with one of the complications of ulcers including bleeding (10%), perforation (2%), gastric outlet obstruction (2%), penetration (2%) – this may cause massive bleeding or pancreatitis. Diagnosis can be made with either endoscopy or UGI series. Endoscopy is the preferred method as it has higher accuracy (~90-95%), able to identify superficial gastritis, esophagitis or very small ulcerations, allows for biopsy of any suspicious looking lesion or ulcers in the stomach (“benign looking” gastric ulcers have a much higher rate of malignancy), allows for immediate treatment of bleeding ulcers or visible vessels, can biopsy for H.pylori. Treatment involves: 1. Stopping the offending agents • NSAIDs, smoking 2. Acid neutralization • Proton pump inhibitors - Irreversibly inhibits the parietal cell proton pump • H2-receptor antagonists 3. H. pylori eradication • Several treatment options – patients are treated for 1 week st • 1 line • PPI + clarithromycin (500mg OD) + amoxicillin (1000mg BID) or metronidazole (500mg) if patient has a penicillin allergy nd • 2 line • PPI + bismuth + metronidazole + tetracycline Mallory-Weiss Tears These are esophagogastric mucosal tears that occur in the region of the esophagogastric junction. They are often characterized by a history of retching or non-bloody vomiting (causing rapid increases in gastric pressure) followed by hematemesis. Bleeding occurs when the tear involves the underlying esophageal venous or arterial plexus. 90% of these bleeds stop spontaneously, however if persistent may need endoscopy with electrocaudery or surgical repair. Rebelling usually occurs in the first 24 hours, however is rare in the absence of portal hypertension or a Coagulopathy. Esophageal Varices Patients typically present with massive upper GI bleeding. Varices develop as a result of portal hypertension, the most common cause of this in the United States and Canada being alcoholic liver disease and chronic active hepatitis. Varices are also often found in the stomach and if found in isolation suggests obstruction of the splenic vein. Management depends on if the varices are actively bleeding. If there is no active bleeding then patients should be placed on a beta-blocker. Commonly used agents include propranolol or nadolol. These agents reduce portal hypertension by decreasing cardiac output and splachnic vasoconstriction. The addition of nitrates may also further lower portal pressures. If the patient has active bleeding then management must be directed at resuscitation and stabilization of the patient. IV fluids, blood products should be given to maintain blood pressure and any coagulation abnormalities should be corrected with FFP. Emergent endoscopy should be preformed for rubber band ligation or injection of bleeding varices. IV octreotide or somatostatin should also be given. Somatostatin decreases splachnic blood flow by direct action on mesenteric smooth muscle and octreotide decreases portal blood flow through a direct vasoconstrictive effect and indirectly by inhibition of glucagon which normally increases portal blood flow. Bleeding stops spontaneously in more then 50% of patients, but mortality approached 70% in those with continued bleeding. Each bleed is associated with a 30% mortality and the risk of rebelling is high until the varices are obliterated. TIPSS (transjugular intrahepatic portal-systemic shunt) is a procedure that may be considered when the above measures are not effective in controlling recurrent varaceal bleeds. It is a radiological procedure in which a stent is inserted to connect the portal and systemic circulation, thus lowering portal pressures. It is however associated with a high rate of hepatic encephalopathy and stent occlusions . Lower GI Bleeding Lower GI bleeding occurs from a site distal to the Ligament of Treitz. As with a upper GIB the lesion can occur anywhere along the lower GI tract DDX: 1. Small Bowel • Neoplasm • Mocker’s diverticulum • Chron’s disease • Aortoenteric fistula • Vascular problems 2. Colon • Diverticuli • Angiodysplasia • Inflammatory bowel disease • Ischemic gut • Neoplasm • Infectious 3. Perianal • Hemorrhoid • Fissure • Fistula 4. Coagulopathy History : A well taken history can help determine the site of blood loss. As with the upper GI bleed it is very important to ask question regarding the severity of the bleeding (sx of hemodynamic instability – see above). These bleeding episodes are usually bright red as the blood is not first degraded in the gut. Other questions should be directed at the character of bleeding or other associated symptoms: Questions to consider include: 1-haematachezia: -onset. -frequency. -amount : Occult blood loss is associated with colon cancer. -mixed with feces, or on the surface of the feces "associated with hemorrhoids or fissures". -separated from the feces " after defecation or alone " -on toilet paper -nature (fresh or clotted , bright red or dark blood) 2- pain :(onset "sudden or gradual " , site, duration ,severity , nature ,radiation , progression "increase , decrease or intermittent " , aggravating and relieving factors , The end of the pain " spontaneous or brought about by some action by the pt or doctor). 3-symptoms of the severity of bleeding : -loss of consciousness -postural drop -symptoms of anemia : fatigue ,palpitation 4-Other sites of bleeding: epistaxis or hemoptysis Must always rule out a massive UGIB! Usually site is distal to the pylorus 5-per anal itching. 6- discharge :mucous , watery or purulent. 7-Palpable lump: analyze the lump , it appears only on defecation then disappears or it is persists after defecation. 8-bowel habit : tenesmus is a feeling of incomplete defecation. It is experienced as an inability or difficulty to empty the bowel at defecation , constipation , diarrhea . 9-risk factors : Polyps , liver disease , blood transfusion ,contact with sick people ,IBD, blood disorders , cancer , smoking or alcohol consumption. 10-incotinence:"sphinecter failure" 11- increase intra abdominal pressure : " cough , pregnancy , obesity , PPH , constipation. 12- hx of truma 13- associated symptoms : Jaundice . weight loss , loss of appetite , fever, night sweats . 14- past HX : -Same episode -GIT surgery -previous investigations. 15- drug HX: anticoagulants . 16- family hx : - GIT cancer - blood disorders . • Physical Exam See UGIB exam. The exam should evaluate signs of large volume loss, abdominal exam with rectal, skin exam looking for other systemic problems. Laboratory tests should include CBC, lytes, BUN, creatinine, PTT, PT, INR, LFTs. Management Volume resuscitation and management of ABC’s should be the first priority for these patients. If the patient is hemodynamically stable with low volume blood loss then the patient can be followed clinically with volume resuscitation and blood as needed. Once the bleeding has settled, the patient can be prepped for colonoscopy and the cause of bleeding determined. If patients are hemodynamically unstable with rapid rates of blood loss other investigations can be arranged. Colonoscopy is not useful in the setting of ongoing bleeding so there is no urgent indication. Barium enemas may detect proximal lesions not detected by colonoscopy, but interferes with subsequent angiography and colonoscopy, thus there is no indication for urgent use 1. Tagged red blood cell scan • Non-invasive, but only localized bleeding to areas of the abdomen. Accuracy ranges from 24-91% • Can be positive with 0.1cc/min but diagnostic in less then 50% • Once tagged can be easily rescanned 2. Angiography • Needs blood flow of 0.5cc/min to be positive • Identifies site in 60% of bleeds, 50-80% are a result of bleeding from the superior mesenteric artery • Allows for therapeutic intervention 3. Surgery • Consider in patients with ongoing bleeding and hemodynamic instability but with failure of other therapeutic maneuvers. . Diverticulosis • Most common cause of lower GI bleeds. Occurs in ~33% of LGIB although only 15% of patients with diverticulosis will develop significant bleeding • A diverticulum is a sac-like protrusion of the colonic wall. • Prevalence is age dependent - <5% at 40yrs, 30% at 60yrs and 65% at 85 yrs • 75% of the diverticular occur on the left side of the colon, however 50-90% of diverticular bleeding is from right sided diverticuli • May be massive since they often form at sites of arterial vascular penetration • Bleeding is usually painless • Bleeding usually stops spontaneously, however rebelling occurs in up to 25% of medically patients • Risk factors for development include: • Lack of dietary fiber, aspirin and NSAID use, advanced age and constipation Angiodysplasia Angiodysplasia refers to dilated tortuous submucosal vessels. The walls are composed of endothelial cells which lack smooth muscle. Much less uncommon, accounting for 8% of lower GI bleeds. The risk does however increase with age and the incidence of bleeding increases with time due to degeneration of vessel walls. Angiodysplasia occurs throughout the colon but bleeding usually originates from the cecum or the ascending colon. As with diverticular disease this bleeding is also usually self-limited. Blood loss is also usually painless but because this is venous blood loss, not arterial, it is often lower volume blood loss. On colonoscopy lesions appear as cheery red spots on the mucosa. Endoscopic caudery or injection sclerotherapy often achieves coagulation. Colon Cancer Cancer is a relatively rare cause of hematochezia, it usually presents with occult blood loss. Bleeding occurs when there is overlying erosion or ulceration. It is usually low volume and recurrent. Bright red blood is associated with left sided colon lesions. Right sided malignancies present with maroon stools or Melena Colitis Colitis is mucosal inflammation of the bowel wall from any number of acute processes. All result in activation of the immune system and inflammatory cascade. It’s important to differentiate between them as therapy is very different. Patients present with abdominal pain, hematochezia +/- diarrhea, fever and dehydration. On colonoscopy the bowel appears edematous, friable, erythematous and ulcerated. The differential includes: 1. Infectious • Clostridium difficile should be considered in patients with a history of antibiotic use or recently hospitalized • Others include E.coli 0157:H7, Campylobacter jejuni or Entamoeba histolytica 2. Ischemic • Seen with patients with hypoperfusion and vasoconstriction, usually elderly patients. • Lactate levels would be elevated • Therapy should be aimed at correcting the underlying cause and volume repletion 3. Inflammatory bowel disease Inflammatory Bowel Disease Chron’s disease: • Transmural inflammation with skip lesions. Linear ulcers lead to typical “cobble-stone” pattern on colonoscopy • Bimodal distribution – before 30 years or after 60 years • May affect any part of the GI tract from mouth to anus – 35% small bowel only, 45% large and small bowel, 20% large bowel only • Usually presents with recurrent episodes of diarrhea, abdominal pain and fever Ulcerative colitis • Diffuse inflammation confined to the mucosa • Always involves the rectum, lesions are continuous • 2/3 of cases before the age of 30 • Hematochezia is more commonly seen with ulcerative colitis then chron’s • Presents with diarrhea, rectal bleeding, abdominal pain and tenesmus • Systemic features of fever, weight loss & fatigue also common Complications/Other Manifestations • General: Growth retardation, severe wasting due to malabsorption • Head & neck: Uveitis, chorioretinitis, iridocyclitis • Renal: Urinary calculi • GI: Cirrhosis, sclerosing cholangitis, fatty liver, cholelithiasis, vitamin deficiencies, iron deficiency, obstruction, perforation, toxic megacolon, strictures, fistulas, perianal abscesses, cancer • MSK: Erythema nodosum, erythema multiforme, pyoderma gangrenosum, arthritis, ankylosing spondylitis, migratory thrombophlebitis • Iatrogenic – steroids, blood transfusions, surgery • Patients with UC have more liver problems (esp. sclerosing cholangitis) and an increased risk of colorectal cancer. Suggest yearly screening and bx in patients with pancoloitis for >10 years Diagnosis • Sigmoidoscopy without prep for diagnosis • Colonoscopy and barium enema to determine the length of bowel involved – both contra-indicated in acute severe flares • Stool cultures to exclude infection Management • 5-ASA – used to treat mild-moderate disease and maintains remissions • Steroids – used to remit acute flares – not maintenance, may mask intraabdominal sepsis • Immunosuppressive agents • Metronidazole/Cipro – decreases disease activity and improves perianal disease in Chron’s patients • Surgical – indicated for toxic megacolon, pre-malignant changes, obstruction, abscess, perforation and bleeding. Cure is only possible in UC patients. Bleeding Problems 1. A 35 year old developmentally delayed patient is brought in by his health care worker because of a 3 day history of diarrhea and 1 day history of vomiting dark colored liquid. She is concerned about Norwalk virus. Past medical history includes a seizure disorder and daily headaches. BP is 120/80, P 80 with no postural changes. Initial Hg was 130. While in the emergency department he has a dark, tarry bowel movement. What is your differential diagnosis? What else would you like to know on history? How are you going to manage this patient? 2. A 83 year old female presents with a one day history of bright red blood per rectum. She has had 4-5 episodes of painless bleeding. She feels lightheaded when walking but denies any syncope, chest pain or SOB. Her past medical history includes HTN, chronic atrial fibrillation and colon polyps. Her blood pressure is 130/80, P 80 lying and 110/50, P110 standing. Abdominal exam is diffusely tender but no rebound or guarding. Rectal shows bright red blood with clots. What else do you want to know on history? What investigations will you order? What is your differential diagnosis? How will you manage the patient? 3. A 56 year old male presents to the emergency department complaining of vomiting blood. He has a past history of alcohol abuse and IV drug use. The emergency department is very busy and so asks you help in managing the patient soon after arrival. His blood pressure is 90/60, pulse is 120, afebrile, sats 96% on room air. How are you going to initially manage the patient? What else are you looking for on history? What are you looking for on physical exam? What investigations will you order? What is the differential diagnosis? What will be your admission orders? • What are the other sites of porto-systemic anastamosis? Region Name portal circulation systemic circulation Esophageal esophageal varices left gastric vein Esophageal Vein Rectal hemorrhoids superior rectal vein middle rectal veins and inferior rectal veins Paraumbilical caput medusae paraumbilical veins Retroperitoneal (no clinical name) right colic vein, renal vein, suprarenal middle colic vein, left vein, paravertebral vein, colic vein and gonadal vein Patent ductus venosus (no clinical name) - rare Left branch of portal vein superficial epigastric vein inferior vena cava It can be one of the conditions caused by portal hypertension. A useful mnemonic is that portal hypertension causes problems in the butt, the gut, and caput. A dilated inferior mesenteric vein may or may not be related to portal hypertension.