1 UGI BLEED Dr. KPP Abhilash Associate Professor Department of Emergency Medicine Christian Medical College, Vellore
2 Outline UGI bleed: etiology and presentation Management: Non variceal / variceal bleed Dilemma in management: Special situations
3 GI bleed Upper Esophageal Stomach Duodenum Hepatic Pancreatic Ligament of Trietz Lower Small bowel Colon Anus
4 GI Bleeding Upper GI bleeding 4x more common than lower GI bleeding Emergency resuscitation same for upper and lower GI bleeds
5 Upper GI bleed
6 Upper GI hemorrhage How do you know its upper? 85% of all GI hemorrhage is upper Hemetemesis is diagnostic Don t forget about nasal bleeding as possible source Melena Degradation of hemoglobin to hematin by acid Bowel bacteria and digestive enzymes also contribute Hematochezia 10% of patients with very rapid UGI source If bleeding very brisk and severe then can present with red blood PR!
7 History Aim of history and examination is 3 fold 1. Identify likely source upper vs lower and potential cause 2. Determine severity of bleeding 3. Identify precipitants (e.g. Drugs)
8 Physical examination Assess hemodynamic stability. Mild to moderate hypovolemia: Resting tachycardia Blood volume loss of at least 15 percent: Orthostatic hypotension Blood volume loss of at least 40 percent: Supine hypotension
9 Basic investigations to be sent CBC profile Electrolytes, Creatinine, LFT, BBVS rapid PT,PTT CXR ECG
10 Management Non variceal bleed Variceal bleed
11 First Fibroscope
12 Chain of events 1. Recognize severity 2. Establish access for resuscitation 3. Resuscitate 4. Identify source 5. Intervention
13 Peptic ulcer bleed-management Risk assessment scores PPI before scopy Timing of scopy
14 Risk Scores Rockall score Predicts the risk of rebreeding and death in hospitalized patients. Preendoscopic Rockall score (range, 0 7) uses only clinical data available immediately at presentation. Blatchford score Predicts the risk of intervention (transfusion and endoscopic or surgical therapy) and death in a population of patients presenting to hospital with UGIB. Blatchford score (range, 0 23) uses clinical data and laboratory available early after admission. Others Addenbrooke,AIMS65(inpatient mortality, Length of stay, increased cost)
15 Risk Stratification: Rockall Score Identifies patients at risk of adverse outcome following acute upper GI bleed Variable Score 0 Score 1 Score 2 Score 3 Age < >80 - Shock Nil HR >100 SBP <100 - Co-morbidity Nil major - IHD/CCF/major morbidity Diagnosis Endoscopic Findings Mallory Weiss tear All other diagnoses GI malignancy - None - Blood, adherent clot, spurting vessel Score <3 carries good prognosis Score >8 carries high risk of mortality Renal failure/liver failure -
16 Preendoscopic management- PPI before scopy Omeprazole before endoscopy in patients with gastrointestinal bleeding. (lau JY et al, N Engl J Med. 2007;356(16):1631.) Over a 17-month period, 638 patients were enrolled with 319 in each group The need for endoscopic treatment was lower in the omeprazole group than in the placebo group (60 of the 314 patients included in the analysis [19.1%]vs. 90 of 317 patients [28.4%], P=0.007). No significant differences between the two groups in the mean amount of blood transfused, number of patients who had recurrent bleeding, underwent emergency surgery,or who died within 30 days. Hospital stay was less than 3 days in 60.5% of patients in the omeprazole group, as compared with 49.2% in the placebo group (P=0.005). On endoscopy, omeprazole group had fewer actively bleeding ulcers (12 of 187, vs. 28 of 190 in the placebo group; P=0.01) and more ulcers with clean bases (120 vs. 90, P=0.001).
17 Preendoscopic management PPI before scopy 1.Cochrane meta-analysis of six randomized trials ( N = 2,223) of pre-endoscopic PPI therapy no signifi cant differences between PPI and control in mortality (6.1 vs. 5.5 % ; odds ratio (OR) = 1.12, ), rebleeding (13.9 vs. 16.6%; OR = 0.81, ), or surgery (9.9 vs. 10.2%, OR = 0.96, ) -PPI therapy signifi cantly reduced the proportion of participants with higher risk stigmata of hemorrhage (active bleeding, non-bleeding visible vessel, and adherent clot) at index endoscopy (37.2 vs. 46.5%; OR = 0.67, ) and undergoing endoscopic therapy at index endoscopy (8.6 vs % ; OR = 0.68, ). 2.Cochrane meta-analysis of randomized trials of patients with UGIB who did not consistently receive endoscopic hemostatic therapy reported that PPI therapy was associated with reduced rebleeding (OR = 0.38, ; NNT = 10) and surgery (OR = 0.62, ; NNT = 17), but not mortality. Authors suggested that if endoscopy will be delayed or cannot be performed, PPI therapy may improve clinical outcomes. 1.Sreedharan A, et al. Proton pump inhibitor treatment initiated prior to endoscopic diagnosis in upper gastrointestinal bleeding. Cochrane Database Syst Rev 2010 (7): CD Leontiadis GI, et al. Proton pump inhibitor therapy for peptic ulcer bleeding: Cochrane collaboration meta-analysis of randomized controlled trials. Mayo Clin Proc 2007 ; 82 :
18 High-dose versus non-high-dose PPIs patients with actively bleeding ulcers or nonbleeding visible vessels High-dose IV PPIs (either omeprazole or pantoprazole given as a continuous infusion) Lower-dose IV PPI (omeprazole or pantoprazole given as a 40 mg intravenous bolus twice daily). - no differences with regard to recurrent bleeding (8 % in both groups), need for surgery (1 versus 0.4 %), mean units of blood transfused (1.7 versus 1.5 units), mortality (2 % in both groups). Fewer patients in the high-dose group had a hospital stay of less than five days (37 versus 47 %). High- versus low-dose proton pump inhibitors after endoscopic hemostasis in patients with peptic ulcer bleeding: a multicentre, randomized study. Andriulli A et al. Am J Gastroenterol. 2008;103(12):3011
19 High-dose versus non-high-dose PPIs 2. Meta-analysis that included seven randomized trials with 1157 patients who had received endoscopic treatment for a bleeding ulcer compared recurrent bleeding rates, the need for surgical intervention, and mortality between patients receiving high-dose omeprazole or pantoprazole (both given as an 80 mg bolus followed by 8 mg/h) and patients receiving nonhigh-dose omeprazole or pantoprazole (with oral doses ranging from 80 to 160 mg per day and IV doses ranging from 20 to 80 mg per day). - no differences in any of the outcomes between the two groups. 2.High-dose vs non-high-dose proton pump inhibitors after endoscopic treatment in patients with bleeding peptic ulcer: a systematic review and meta-analysis of randomized controlled trials.wang CH et al.arch Intern Med. 2010;170(9):751.
20 Timing of scopy Patients with UGIB should generally undergo endoscopy within 24 h of admission, following resuscitative efforts to optimize hemodynamic parameters and other medical problems. Studies of early endoscopy consistently show that patients undergoing endoscopy within 8 h of presentation have more high risk stigmata (active bleeding, visible vessels, or adherent clots) than those with later endoscopies, thereby increasing the proportion who requires endoscopic therapy. Spiegel BM, Vakil NB, Ofman JJ. Endoscopy for acute nonvariceal upper gastrointestinal tract hemorrhage: is sooner better? A systematic review. Arch Intern Med 2001 ; 161 : Observational studies do not document a benefit in clinical outcomes of endoscopy performed within 2 12 h of presentation Tsoi KKF, Ma TKW, Sung JJY. Endoscopy for upper gastrointestinal bleeding: How urgent is it? Nat Rev Gastroenterol Hepatol 2009 ; 6 :463 9.
21 Prevelance of SRH
22 Recommended endoscopic and medical management based on stigmata of hemorrhage in ulcer base ACG PRACTICE GUIDELINES 2012
24 Difficult situations A 60 yr old male with DM, HT, IHD on OHAs, anti HT, antiplatelets presents with 3 episodes of large volume hematemesis. Management prior to scopy?
25 Difficult situations A 30 yr old female with RHD and AF on anticoagulants presents with 3 episodes of large volume hematemesis. Management prior to scopy?
26 Any anticoagulant and antiplatelet treatment should be discontinued to help stopping the acute bleeding On the other hand, discontinuing this type of therapy can significantly increase the risk for cardiovascular or cerebrovascular complications because of the underlying disease.
27 The relative risk for upper GI bleeding increases up to 10% in patients being treated with these therapies In a population-based observational cohort study of elderly patients who survived MI, the rate of GIB was 1.5% per year with aspirin alone and 4.6% per year with aspirin plus clopidogrel or ticlopidine Buresly K, Eisenberg MJ, Zhang X, Pilote L. Bleeding complications associated with combinations of aspirin, thienopyridine derivatives, and warfarin in elderly patients following acute myocardial infarction. Arch Intern Med 2005; 165:
28 Thienopyridines (Clopidogrel) affect the ADP pathway by irreversibly blocking the ADP receptor P2Y12 Aspirin irreversibly inhibits cyclooxygenase-1
29 Management Platelet transfusion FFP transfusion Active bleeding Hemodynamically unstable
30 When to restart antiplatelets and anticoagulants patient-specific approach Balance risk with benefits For cases where the short-term benefit of anticoagulant or antiplatelet therapy outweighs the immediate risk, the appropriate agent can be restarted within four to five days of achieving hemostasis.
31 Variceal bleeds management
32 Medical management before scopy
33 Management of Variceal bleeds Emergency resuscitation as already described Drugs Endoscopy Somatostatin/octreotide vasoconstricts splanchnic circulation and reduces pressure in portal system Terlipressin vasoconstricts splanchnic circulation and reduces pressure in portal system Propanolol used only in context of primary prevention (in those found to have varices to reduce risk of first bleed) Band ligation Injection sclerotherapy Radiological procedure used if failed medical/endoscopic Mx Surgical Selective catheterisation and embolisation of vessels feeding the varices TIPSS procedure: transjugular intrahepatic porto-systemic shunt shunt between hepatic vein and portal vein branch to reduce portal pressure and bleeding from varices): performed if failed medical and endoscopic management Can worsen hepatic encephalopathy Surgical porto-systemic shunts (often spleno-renal) Liver transplantation (patients often given TIPP/surgical shunt whilst awaiting this)
34 Sengstaken-Blakemore Tube TIPSS
37 Take Home Points Obtain a good history to identify potential sources of the upper GI bleed and assess the severity of the bleed Emergent management includes ABCs, two large caliber IVs, fluid resuscitation, possible transfusion All patients should be treated initially with PPI. If you suspect variceal bleed, add somatostatin analogue and empiric antibiotics
38 Lower GI bleeding
39 Lower GI bleed Etiology Diverticulosis 40-55% Right sided lesions > left 90% stop spontaneously 10% rebleed in 1 st year and 25% at 4 years Angiodysplasia 3-20% Most common cause of SB bleeding in >50 y/o >50% are in right colon Neoplasia Typically bleed slowly Inflammatory conditions 15% of UC patients, 1% of chron s patients Radiation, infectious, AIDS rarely Vascular Hemorrhoids >50% have hemorrhoids, but only 2% of bleeding attributed to them Others
40 Management Emergency resuscitation as already described Pharmacological Stop NSAIDS/anti-platelets/anti-coagulants if safe Tranexamic acid Endoscopic OGD (15% of patients with severe acute PR bleeding will have an upper GI source!) Colonoscopy diagnostic and therepeutic (injection, diathermy, clipping)
41 Take Home Points Obtain a good history to identify potential sources of the upper GI bleed and assess the severity of the bleed Emergent management includes ABCs, two large caliber IVs, fluid resuscitation, possible transfusion All patients should be treated initially with PPI. If you suspect variceal bleed, add somatostatin analogue and empiric antibiotics
43 Copyright of this educational material rests with the author and Christian Medical College, Vellore. Duplication, revision and redistribution are not permitted. For any further clarification please contact the concerned author reserved to author and Christian Medical College, Vellore
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