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upper gastrointestinal bleeding
This document discusses the approach to patients with upper gastrointestinal bleeding and its management. It covers the following key points in 3 sentences: The document outlines sources of GI bleeding, signs of blood loss severity, immediate assessment steps, diagnostic testing, endoscopic treatment options for variceal and non-variceal bleeding, risk stratification tools like the Rockall score, and angioembolization as a treatment option. Management involves fluid resuscitation, identifying the bleeding source, stopping active bleeding endoscopically, treating underlying causes, preventing rebleeding, and considering a second look endoscopy or other interventions based on risk stratification. Outpatient management may be appropriate for low risk patients while higher risk patients require intensive
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upper gastrointestinal bleeding
- 1. Approach to apatient of Upper G.I. Bleed & Its Management Dr Rahul Singh ADMO , LNM Rly Hospital , Gorakhpur
- 2. Sources of GIBleeding •Upper GITract • Proximal to the Ligament ofTreitz •80% of acute GI Bleeds •Lower GITract • Distal to the Ligament ofTreitz •20% of acute GI Bleeds
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- 4. Upper GI Bleeding UpperGI bleed : Lower GI bleed = 4:1 Incidence: 170 patients/ 100,000 population /year(usa data). 40% due to peptic ulcer(Most common). 80% are self-limited. Patients on anti platelet therapy has two fold increase in bleed as compared to normal ones .
- 5. Types Of UpperGI bleeds VARICEAL 20% of UGI Bleeds NON –VARICEAL 80 % of UGI Bleeds
- 7. OTHER CAUSES OFUGI BLEEDING Dieulafoy’s lesion Gastroesophageal reflux disease Trauma from foreign body Esophageal ulcer Cameron lesion Stress ulcer Drug induced erosions Angioma Watermelon stomach Portal hypertensive gastropathy Aorta-enteric Fistula Radiation telangiectasis/ Enteritis Benign tumours Malignant tumour Blue rubber bleb nevus syndrome Osler-Weber- Rendu syndrome Haemobilia Hemosuccus pancreatitis Infections(CMV,HSV) Stomal ulcer Zollinger-ellison syndrome
- 8. Approach in AcuteGI Bleed ImmediateAssessment & Resuscitation Stabilization of hemodynamic status Identify the source of bleeding Stopping the active bleeding Treat the underlying Prevent recurrent bleeding
- 9. Immediate Assessment &Resuscitation Assess airway , breathing and circulation ( ABCs) . Vital Signs: • Pulse, BP,Temperature, Respiratory Rate Assess magnitude of bleeding . Initiate appropriate monitoring . History and examination . Laboratory evaluation .
- 10. Estimated Fluid andBlood 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
- 11. History to benoted • 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
- 12. Features Hemoptysis Haematemesis DefinitionCoughing out of blood Vomiting out of blood Symptoms Symptoms of pulmonary and CVS disease Symptoms of upper GI tract diseases Content & colour Mixed with sputum & bright red in colour Mixed with food particles & coffee-ground in colour Premonitory symptoms Cough, salty sensation in throat Nausea , vomiting, retching, abdominal discomfort. Melaena Does not occur Usually followed by melaena the next day Amount Relatively less Huge in amount Reaction Alkaline(Blue litmus remain unchanged) Acidic(Blue litmus remains unchanged
- 13. Laboratory Evaluation •CBC •Bleeding &Coagulationprofile (BT, CT,PT, a PTT) •Liver FunctionTest •Complete S. Biochemistry •Relevant lab test for underlying disease
- 15. General Medical Management •FLUID RESUSCITATION • Vitals are monitored • Assessment of severity of blood loss :- An orthostatic decrease of 20 mm Hg in systolic blood pressure or increases in the pulse of 20 beats / min. indicate – 10% blood loss, if pt is pulsless and in shock- > 20% loss. • Order hemoglobin, hematocrit, BUN, grouping and cross matching of blood. • Insertion of central venous line may be beneficial to measure adequacy of fluid replacement and perfusion of vital organ . • Monitor urine output. • Fluid resuscitation is done by crystalloids such as normal saline or RL if hypoalbuminemia is detected use colloids. • Placing the patient in trendelenburg position to maintaine cerebral blood flow.
- 16. General Medical Management 1.Oxygensupport to prevent hypoxia of tissues 2.IV route - Crystalloid solution/Colloids | blood. 3. Blood transfusion: • maintain Hct at 30% in the elderly, esp. with comorbid diseases e.g.. CHF, CRF, IHD,COPD) • 20-25% in younger pt. • 25-28% in portal HTN • administration of vit k 4.In symptomatic thrombocytopenia (<50000 )infused platelets. 5.FFP-The transfusion of plasma should not be based solely on the patient’s abnormal INR and/or PTT. The decision to transfuse should be based on the patient’s clinical condition.
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- 20. Effective control aftervariceal banding
- 21. Variceal Bleeding Patients withvariceal hemorrhage have poorer outcomes than patients with other sources of UGIB . Ligation is the endoscopic therapy of choice for esophageal varices Primary Prophylaxis Non-selective beta blockers Chronic therapy with beta blockers plus endoscopic ligation is recommended for prevention of recurrent esophageal variceal bleeding. Endoscopic Management • EVL, Sclerotherapy( CyanoAcrylate , Na morrhuate , ethanolamine ,etc) Surgical Management • TIPSS,OesophagealTransection, Suguira Procedure • LiverTransplantation
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- 24. Surgical Alternative -Sugiura Procedure • A transthoracoabdominal oesophageal transection • paraoesophageal devascularisation, oesophageal transection and reanastomosis, splenectomy, and pyloroplasty.
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- 27. Approach to non-varicealUGI Bleed
- 28. Approach to pepticulcer bleeding
- 30. ENDOSCOPIC MODALITIES AVAILABLEFORTHE MANAGEMENT OF U.G.I. BLEED • INJECTION • Adrenalin • Fibrin glue • HumanThrombin • Sclerosants • Alcohol • THERMAL • Heater Probe • Bicap Probe • Gold Probe • Argon plasma coagulation • Laser therapy • MECHANICAL • Haemoclips • Banding • Endoloops • Staples • Sutures
- 32. SECOND LOOK ENDOSCOPY Routinesecond-look endoscopy is not recommended for most patients with peptic ulcer bleeding. Typically done 24 hours after the initial endoscopy. Any persistent stigmata of haemorrhage are treated. It is beneficial in certain circumstances, especially after injection monotherapy.
- 35. Gastric antral ulcerwith a clean base
- 36. Duodenal ulcer withflat pigmented spots
- 37. Duodenal ulcer witha dense adherent clot
- 38. Duodenal ulcer withactive spurting (arrow)
- 39. MALLORY WEISS SYNDROME/TEARS • Mucosal lacerations at the gastroesophageal junction or in the cardia of the stomach • Patients generally present with hematemesis or coffee-ground emesis after alcohol intake • Typically have a history of recent nonbloody vomiting with excessive retching followed by hematemesis • Endoscopy usually reveals a single tear that begins at the gastroesophageal junction and extends several millimeters distally into a hiatal hernia sac/within cardiac portion of stomach.
- 40. Mallory-Weiss tear atthe gastroesophageal junction
- 41. • Occasionally, morethan one tear is seen. • The bleeding stigmata of Mallory-Weiss tears can include a clean base, oozing, or active spurting. • Bleeding stop spontaneously in 80 – 90% of the patients and mucosa often heals within 72 hours . In 0 – 5% of the patient bleeding recurs Endoscopic electro-coagulation of the tears Angiography therapy with intra arterial infusion of vasopressin or embolisation. Operative therapy with oversewing of tear.
- 42. RISK FACTORS ANDRISK STRATIFICATION • To identify patients with nonvariceal UGI bleeding at greatest risk for mortality and rebleeding. • Pts may be categorised as low, intermediate and high risk .
- 43. Most patients needintervention if their score is 6 or higher.
- 44. ROCKALL SCORING SYSTEM VariablePoints 0 1 2 3 Age(yr) <60 60-79 >80 - Pulse rate <100 >100 - - Systolic BP Normal >100 <100 - Comorbidity None - IHD, Cardiac failure. Renal failure, hepatic failure , metastatic cancer. Diagnosis MalloryWeiss tear or no lesion observed All other diagnosis Malignant lesions - Endoscopic stigmata No stigmata or dark spot in ulcer base - Blood in UGI tract , visible vessel etc -
- 45. Risk category: High (>5) Intermediate (3–5) Low (0–2) Total score Mortality rate(%) Rebleeding rate(% 0 0 4.9 1 0 3.4 2 0.2 5.3 3 2.9 11.2 4 5.3 14.1 5 10.8 24.1 6 17.3 32.9 7 27.0 43.8 ≥8 41.1 41.8
- 46. Management as perrisk • 1- Low risk(0-2)-Usually 80 % of the pt recovers spontaneously with medicalTt( PPI)+ Hospitalisation for 24 hrs and may be discharge if uneventful. • 2-Intermediate risk(3-5)- sameTt + Hospitilisation for at least 72 hrs. • 3- High risk(>5%)- SameTt+ Hospitilisation in I.C.U.
- 47. Angioembolization – GelatinSponges, Polyvinyl Alcohol, Cyano Acrylic Glues, Coils.
- 48. TAKE HOME MESSAGE •Early Resuscitation. • Nasogastric wash + look forGH. • High dose PPI therapy for at least 72 hrs. • Urgent Endoscopic therapy for mod to severe UGI bleeding. • Combination therapy preferred along with medical management. • Relook endoscopy should be preffered only for mod to severe bleeding. • Pt should also be treated for specific cause/disease.
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