Download - Approach to patients with upper gi bleeding
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WELCOME TO THE SEMINAR
SESSION 2013-2014
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Approach to a patient with UGI
Bleeding
Dr.Vignesh.SResident of Internal MedicineGuided by Prof.Dr.R.L.Meena
RNT Medical college and Hospital
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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
Sources of GI Bleeding
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Ligament Of Treitz
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Initial Assessment and Resuscitation History and Physical Examination Assessment of the bleeding source Differential Diagnosis Investigations Management
◦ Conservative◦ Therapeutic
Step wise Approach
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Airway, Breathing and Circulation Vital Signs:
◦Pulse, BP, Temperature, Respiratory Rate
Fluid and Resuscitation Plan◦Co-morbidities
Initial Assessment and Resuscitation
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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
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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
History to be noted
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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
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Anticoagulation (warfarin/heparin)Use of Drugs
NSAIDs,Steroids,BisphosphonatesSimilar episodes beforeH/o Jaundice in pastH/o Abdominal SurgeryH/o AlcoholismH/o Smoking or Tobacco abuseH/o Cocaine abuse
Other History
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Pt’s Consciousness, OrientationPallor, Icterus, Clubbing, Pedal Edema
Lymphadenopathy, JVPSigns of Liver FailureSystemic Examination
◦ Abdomen, CVS, RS, CNS
Physical Examination
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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
Look for Signs of Liver Cell Failure
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Hands and Nails
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Spider naevi
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Gynaecomastia Ascitis
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Virchow’s node Palmar Tylosis
Special Cases
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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
Differential Diagnosis
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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
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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
Source of Bleeding in patients hospitalised for UGI Bleed
Ref :Harrison Table 41-1
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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
Gi bleed and cad
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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
Investigation Panel
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Initial Hct-misleading
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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
Management
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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.
Role of NG Tube and Lavage
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Harisson’s Algorithm for UGI BLEED
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Duodenal Ulcer
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• 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
Peptic Ulcer Disease
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Varices
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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
Oesophageal Varices
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Sengstaken Blakemore Tube
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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.
Surgical Alternative - Sugiura Procedure
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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
One of the criteria used to determine the need for surgical intervention is the number of units of transfused blood required to resuscitate the patient. The more units required, the higher the mortality rate (Larson, 1986). Operative intervention is indicated once the blood transfusion number reaches more than 5 units, as noted in the following table (Larson, 1986).
Number of Units Transfused
Need for Surgery, %
Mortality Rate, %
0 4 4
1-3 6 14
4-5 17 28
>5 57 43
Indications for Surgery in Gastrointestinal Hemorrhage
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Carcinoma Oesophagus
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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
Carcinoma Oesophagus
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Gastric Carcinoma
GI Malignancy
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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
Adenocarcinoma Stomach
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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.
Mallory Weiss TEAR
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Mallory Weiss Tear
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Oesophagitis Angiodysplasia
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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
VASCULAR ECTASIA
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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.
Dieulafoy's lesion
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ANGIOEMBOLIZATION
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Injection Sclerotherapy
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Bipolar Electrocoagulation
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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
Adverse Prognostic Variables in Patients with Acute UGI BLEED
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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
Very-Low-Risk Criteria for Patients Complaining of
Gastrointestinal Bleeding Who Can Be Discharged Home
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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
Glasgow-Blatchford Score
•Other markersPulse ≥100 (per min) 1Presentation with melaena 1Presentation with syncope 2Hepatic disease 2Cardiac failure 2
•scores ≥ 6 - 50% risk of needing an intervention.ScoreScore 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
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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
Forrest and Finlayson’s Version
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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.
Medicine Update 2013
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Thank You