Published on April 6, 2014
Dr.Vignesh.S Resident in Internal Medicine Guided by Prof.Dr.R.L.Meena RNT Medical college and Hospital
Upper GI Tract ◦ Proximal to the Ligament of Treitz ◦ 70% of GI Bleeds Lower GI Tract ◦ Distal to the Ligament of Treitz ◦ 30% of GI Bleeds
Initial Assessment and Resuscitation History and Physical Examination Assessment of the bleeding source Differential Diagnosis Investigations Management ◦ Conservative ◦ Therapeutic
Airway, Breathing and Circulation Vital Signs: ◦ Pulse, BP, Temperature, Respiratory Rate Fluid and Resuscitation Plan ◦ Co-morbidities
Estimated Fluid and Blood Losses in Shock Class 1 Class 2 Class 3 Class 4 Blood Loss, mL Up to 750 750-1500 1500-2000 >2000 Blood Loss,% blood volume Up to 15% 15-30% 30-40% >40% Pulse Rate, bpm <100 >100 >120 >140 Blood Pressure Normal Normal Decreased Decreased Respiratory Rate Normal or Increased Decreased Decreased Decreased Urine Output, mL/h 14-20 20-30 30-40 >35 CNS/Mental Status Slightly anxious Mildly anxious Anxious, confused Confused, lethargic Fluid Replacement, 3-for-1 rule Crystalloid Crystalloid Crystalloid and blood Crystalloid and blood Ref: Sleisinger and Fordtrans Gastrointestinal and Liver disease
Confirm the GI Bleed - Hemoptysis or Hemetemesis ??? Manner of Presentation of a GI Bleed ◦ Hemetemesis ◦ Malena ◦ Hematochezia ◦ Occult Blood loss ◦ Symptoms of Blood loss Is it only the GI Bleed ?? Assessment of the bleed ◦ Dizziness, Syncope, Chest Pain, SOB
Bleeding etiology Leading History Mallory-Weiss tear Multiple Emesis before hematemesis, alcoholism Esophageal ulcer Dysphagia, Odynophagia, GERD, Peptic ulcer Epigastric pain, NSAID or aspirin use Stress gastritis Patient in an ICU, gastrointestinal bleeding occurring after admission, respiratory failure, multiorgan failure Varices, portal gastropathy Alcoholism, Cirrhosis Gastric antral vascular ectasia Renal failure, cirrhosis Malignancy Recent involuntary weight loss, dysphagia, cachexia, early satiety Angiodysplasia Chronic renal failure, hereditary hemorrhagic telangiectasia Aortoenteric fistula Known aortic aneurysm, prior abdominal aortic aneurysm repair
Anticoagulation (warfarin/heparin) Use of Drugs NSAIDs,Steroids,Bisphosphonates Similar episodes before H/o Jaundice in past H/o Abdominal Surgery H/o Alcoholism H/o Smoking or Tobacco abuse H/o Cocaine abuse
Pt’s Consciousness, Orientation Pallor, Icterus, Clubbing, Pedal Edema Lymphadenopathy, JVP Signs of Liver Failure Systemic Examination ◦ Abdomen, CVS, RS, CNS
Alopecia, Pallor, Icterus, Fetor Hepaticus, Glossitis, Parotid Swelling Leukonychia, Clubbing, Palmar Erythema, Dupuytren’s Contracture, Asterexis Loss of Axillary hair, Spider naevi, Gynaecomastia, Ascitis, Spleenomegaly, Caput Medusae Testicular Atrophy, Loss of Pubic Hair Pedal Edema
Virchow’s node Palmar Tylosis Special Cases
Major causes Peptic ulcer disease Esophageal and gastric varices Hemorrhagic gastritis Esophagitis Duodenitis Mallory-Weiss tear Angiodysplasia Upper gastrointestinal malignancy Anastomotic ulcers (after bariatric surgery) Dieulafoy lesion
Minor causes Gastric antral vascular ectasia (watermelon stomach) Portal hypertensive gastropathy Gastric polyps Aortoenteric fistula Connective tissue disease Postprocedural: nasogastric tube erosions, endoscopic biopsy, endoscopic polypectomy, endoscopic sphincterotomy
Sources of Bleeding Proportions of Patients % Ulcers 31-67 Varices 6-39 Mallor Weiss Tears 2-8 Gastroduodenal Erosions 2-18 Erosive Oesophagitis 1-13 Neoplasm 2-8 Vascular ectasias 0-6 No source identified 5-14 Ref :Harrison Table 41-1
Massive bleeding cause significant risk for myocardial infarction from coronary artery hypoperfusion from hypovolemia. It is estimated that 16% who had severe gastrointestinal bleeding had ended up with myocardial infarction. Patients who have myocardial infarction consequent to massive bleeding often do not experience chest pain, or the chest pain may be misinterpreted as epigastric pain
Complete Blood count, ESR, Liver and Renal Function Tests, Electrolytes Prothrombin Time and INR BUN / Creatinine – ratio > 30 sensitivity of 68% and a specificity of 98% Stool Occult Blood Test Grouping and Cross Matching ECG, Cardiac enzymes(if essential) HIV, HbsAg, AntiHCV Markers
Explain NSP Nil by Mouth NG Tube insertion and Lavage Hemodynamically Unstable – Hypotension, Tachycardia, Postural Changes Urgent Endoscopy Hemodynamically Stable Plan Early Endoscopy IV PPI Therapy
A grossly bloody aspirate in the atraumatic NG intubation CONFIRMS a UGI Bleed The type of bleed Red blood - active bleeding Coffee ground - recently active bleeding. Continued aspiration of red blood - severe, active hemorrhage. Clears the field for endoscopic visualization Prevent aspiration of gastric content However, lavage may not be positive if bleeding has ceased or arises beyond a closed pylorus.
• PPI Infusion IV Omeperazole 80mg bolus then 8mg/hr infusion • Endoscopic Therapy Bipolar Coagulation, Heater Probe, Injection Therapy(Absolute Alcohol, 1:10,000 epinephrine), Hemoclips Medical Management ◦ Antacids, H2 receptor Antagonists, PPIs, ◦ Cytoprotective Agents - Bismuth Preparations, Prostaglandin Analogues ◦ H.Pylori Eradication Surgical Management ◦ Duodenal Ulcer ◦ Gastric Ulcer
Primary Prophylaxis – Beta Blockade Prevention of Rebleeding Medical Management ◦ Vasoconstricting Agents Baloon Tamponade – Sengstaken Blakemore Tube Endoscopic Management ◦ EVL, Sclerotherapy(CyanoAcrylate) Surgical Management ◦ TIPSS, Oesophageal Transection, Suguira Procedure ◦ Liver Transplantation
A transthoracoabdominal oesophageal transection, ◦ paraoesophageal devascularisation, oesophageal transection and reanastomosis, splenectomy, and pyloroplasty. The prognosis - liver function left at the time of operation but not on whether operation was done as an emergency, elective, or prophylactic measure.
Hemodynamic instability despite vigorous resuscitation (>6 units transfusion) Failure of endoscopy Recurrent hemorrhage after initial stabilization Shock associated with recurrent hemorrhage Continued slow bleeding with a transfusion exceeding 3 units/day Oneofthecriteriausedtodeterminetheneedforsurgicalinterventionis thenumberofunitsoftransfusedbloodrequiredtoresuscitatethepatient. Themoreunitsrequired,thehigherthemortalityrate(Larson,1986). Operativeinterventionisindicatedoncethebloodtransfusionnumber reachesmorethan5units,asnotedinthefollowingtable(Larson,1986). NumberofUnits Transfused Needfor Surgery,% Mortality Rate,% 0 4 4 1-3 6 14 4-5 17 28 >5 57 43
Poor prognosis – 5yr survival rate 5% Surgical Resection –Oesophagectomy Radiotherapy – 5500 -6000 cGy for SCC Chemotherapy - 1or 2 drugs mostly cisplatin Palliative Gastrostomy, Jejunostomy Expansive Metal Stents Endoscopic Fulguration
Distal - Subtotal Gastrectomy Proximal – Near total Gastrectomy Radioresistant – RT only for palliation of Pain Chemotherapy ◦ 5FU + Leucovorin ◦ Cisplatin + Epirubicin/Docetaxel Debulking the primary – best Palliation
Mucosal lacerations at the gastroesophageal junction or in the cardia of the stomach A/w repeated retching or vomiting and are another important cause of nonvariceal UGIB in Alcoholics 2% to 8% of acute UGIB are secondary to Mallory-Weiss tears Some cases are self-limited and do not require endoscopic hemostasis Some cases could be severe enough to require blood transfusions, endoscopic hemostasis, surgery.
Vascular ectasia - Angiomas, AV malformations and Angiodysplasia Vascular ectasias 5% to 10% of cases and the severity - trivial to severe Vascular ectasias a/w – Congenital, CRF. The evidence for these associations is limited. Management is by endoscopic ligation, cauterisation and sclero therapy
Dieulafoy's lesion is a rare etiology in acute UGIB Dieulafoy's lesions are difficult to identify endoscopically because they often retract. Their histopathologic description is a “caliber-persistent artery” in the submucosal tissue On endoscopy, a Dieulafoy's lesion is akin to a visible vessel protruding from an ulcer, yet without an underlying ulcer.
Age > 60 yrs Comorbidities (Renal failure, Liver failure, CHF, Malignancy) Variceal bleeding (as compared with nonvariceal bleeding) Shock or hypotension on presentation Increasing number of units of blood transfused Active bleeding on Endoscopy Bleeding Ulcer of >2cm or a Spurting vessel Need for emergency surgery
No comorbid diseases Normal vital signs Normal or trace positive stool guaiac Negative gastric aspirate, if done No problem home support Proper understanding of signs and symptoms of significant bleeding Immediate access to emergent care if needed Follow-up arranged within 24 hr
Blood Urea(mg/dl) ◦ 6.5 - 8 2 ◦ 8 - 10 3 ◦ 10 - 25 4 ◦ ≥25 6 Haemoglobin (g/L) for men ◦ 12-13 1 ◦ 10-12 3 ◦ <10 6 Haemoglobin (g/L) for women ◦ 10-12 1 ◦ <10 6 Systolic BP (mm Hg) ◦ 100–109 1 ◦ 90–99 2 ◦ <90 3 •Other markers Pulse ≥100 (per min) 1 Presentation with melaena 1 Presentation with syncope 2 Hepatic disease 2 Cardiac failure 2 •scores ≥ 6 - 50% risk of needing an intervention. Score Score is"0" if : •Hemoglobin level >12.9 g(men) or >11.9 g(women) •Systolic blood pressure >109 mm Hg •Pulse <100/minute •BUN level <18.2 mg/dL •No melena or syncope •No liver disease or heart failure
Type Endoscopic Characteristics % of Bleeding % of Mortality 1 Active Bleeding 90 11 2a Non Bleeding Visible vessel 50 11 2b Adhereynt Clot 33 7 2c Flat Pigmentation 7 3 3 Clean Base 3 2
Various Endoscopic Modalities ◦ Inj.Epinephrine,Sclerosants,Thermal Cautery,Argon Plasma Coagulation, Electrocautery, Hemoclips, Bands, Fibrin Glue, Thrombin Endoscopic Sprays Post Endoscopic PPI therapy – lowers 30 day rebleeding rate Second Look Endoscopy – 16-24hrs Angioembolization – Gelatin Sponges, Polyvinyl Alcohol, Cyano Acrylic Glues, Coils.
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