Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, varices, Mallory-Weiss tears, or esophagitis. It typically presents as hematemesis, melena, or maroon stools. Evaluation involves stabilizing the patient, assessing vitals, performing lab tests, and using nasogastric lavage to help locate the source of bleeding. Treatment consists of fluid resuscitation, coagulation factor replacement if needed, endoscopy for diagnosis and potential intervention, and surgery in some cases of severe or recurrent bleeding.
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Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, varices, Mallory-Weiss tears, or esophagitis. It typically presents as hematemesis, melena, or maroon stools. Evaluation involves stabilizing the patient, assessing vitals, performing lab tests, and using nasogastric lavage to help locate the source of bleeding. Treatment consists of fluid resuscitation, coagulation factor replacement if needed, endoscopy for diagnosis and potential intervention, and surgery in some cases of severe or recurrent bleeding.
Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, varices, Mallory-Weiss tears, or esophagitis. It typically presents as hematemesis, melena, or maroon stools. Evaluation involves stabilizing the patient, assessing vitals, performing lab tests, and using nasogastric lavage to help locate the source of bleeding. Treatment consists of fluid resuscitation, coagulation factor replacement if needed, endoscopy for diagnosis and potential intervention, and surgery in some cases of severe or recurrent bleeding.
Copyright:
Attribution Non-Commercial (BY-NC)
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Download as PPT, PDF, TXT or read online from Scribd
Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, varices, Mallory-Weiss tears, or esophagitis. It typically presents as hematemesis, melena, or maroon stools. Evaluation involves stabilizing the patient, assessing vitals, performing lab tests, and using nasogastric lavage to help locate the source of bleeding. Treatment consists of fluid resuscitation, coagulation factor replacement if needed, endoscopy for diagnosis and potential intervention, and surgery in some cases of severe or recurrent bleeding.
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Upper Gastrointestinal Bleeding
27 may 2009
Sathaporn Kunnathum M.D.
Overview • Cause of Gastrointestinal bleeding • Clinical Presentation • Evaluation • Treatment Introduction • Causes depend on site – UGI = proximal to ligament of Treitz – LGI = distal to ligament of Treitz Causes of Significant GI Bleeding Upper Percentage Lower Percentage Peptic ulcer dz 45 Diverticulosis 18-43
Gastric Angiodysplasia 20-40
erosions 23 Unknown 11-32 Varices 10 Cancer/polyps 9-33 Mallory-Weiss 7 Rectal disease 8-9 Esophagitis 6 IBD 1-7 Duodenitis 6 Clinical Presentation • Most common = hematemesis, melena, hematochezia or black stools – Hematemesis associated with bleeding proximal to lig of treitz – Melena usually proximal to jejunum with greater than 4 hrs transit time • requires blood 50-100 mL Clinical Presentation – Hematochezia usually due to colonic source BUT UGIB > 1000 mL and less than 4 hours transit may be red or maroon • UGIB: 71% have melena, 56% hematemesis, 21% maroon stool Evaluation • First priority is ABCs • Intubation occasionally necessary for overwhelming UGIB • Aggressive fluid resuscitate if hemodynamic unstable = Mandatory to have 2 Large Bore I.V. or central access • While stabilizing, get initial history, place on monitor and start O2 Evaluation • History: – Duration, quantity, color of blood, associated symptoms ,precipitating factor, history of GIB, alcohol, drugs use, underlying disease Evaluation • Physical Exam Vital signs – PR, BP, RR – Hypothermia with significant volume depletion Others – General appearance: pale?jaundice? conscious? – Skin: turgor, capillary refill, petechiae/purpura – Lungs/Heart – Abdominal exam – PR Evaluation • Laboratory – Hct – CBC,plt – PT/PTT for correctable coagulopathy – Cross match – Blood chemistry for azotemia/ARF/Acidosis – LFT – ABG if indicated Treatment • NPO • Always start with ABCs • O2 • 2 Large bore IVs • Monitor • NG tube • Foley cath • ET tube ? Treatment • NG lavage – Essential to differentiate UGI vs. LGI – 10-15% of pts with hematochezia have UGIB Treatment • NG lavage, cont. – 79% sensitive for ACTIVE UGIB – Useful to assess for ongoing hemorrhage – Not therapeutic – Not harmful in varices or MW tear Treatment • NG lavage, additional notes – Must confirm placement of tube prior to lavage – Sterile lavage fluid not necessary – Lavage until clear Treatment • Fluid resuscitation – Crystalloid initially – PRC,Fresh whole blood, FFP, plt conc • Critical to monitor Treatment
• Coagulation Defects - consider FFP, Vit K
• Thrombocytopenic (<50,000 and bleeding) transfuse platelets • For severe bleeds - consult GI early as well as general surgery Treatment • Additional options – Empiric acid-suppressive therapy : PPI and H2 receptor antagonist – Octreotide - Besson in NEJM 1995 showed decreased rebleeding in varices after Octreotide - no change in mortality, however (50 mcg bolus, then 25-50/hr) Treatment • Sengstaken-Blakemore Tube – Generally not used except in dire circumstance – High rate of complications and death (14%, 3%) including aspiration, esophageal and gastric rupture, mucosal and nasal necrosis – Attempt only after failure of Octreotide as a bridge to endoscopy in pts exsanguinating from known varices – Need to be intubated prior to placement Treatment • Endoscopy – Most accurate tool for evaluating source of bleeding – Not usually necessary in first 12 hrs • no increase in diagnostic accuracy if done earlier – May be necessary if bleeding is ongoing, unresponsive to resuscitation or recurrent to dictate therapy • Intervention angiography Treatment • Surgery – 15-34% of patients with GIB require surgery – Mortality for emergency surgery is 23% • Thank you for your attention