approach to patients with upper gi bleeding

WELCOME TO THE SEMINAR

SESSION 2013-2014

Approach to a patient with UGI

Bleeding

Dr.Vignesh.SResident of Internal MedicineGuided 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

Sources of GI Bleeding

Ligament Of Treitz

Initial Assessment and Resuscitation History and Physical Examination Assessment of the bleeding source Differential Diagnosis Investigations Management

◦ Conservative◦ Therapeutic

Step wise Approach

Airway, Breathing and Circulation Vital Signs:

◦Pulse, BP, Temperature, Respiratory Rate

Fluid and Resuscitation Plan◦Co-morbidities

Initial Assessment and Resuscitation

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

History to be noted

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,BisphosphonatesSimilar episodes beforeH/o Jaundice in pastH/o Abdominal SurgeryH/o AlcoholismH/o Smoking or Tobacco abuseH/o Cocaine abuse

Other History

Pt’s Consciousness, OrientationPallor, Icterus, Clubbing, Pedal Edema

Lymphadenopathy, JVPSigns of Liver FailureSystemic Examination

◦ Abdomen, CVS, RS, CNS

Physical Examination

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

Hands and Nails

Spider naevi

Gynaecomastia Ascitis

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

Differential Diagnosis

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

Source of Bleeding in patients hospitalised for UGI Bleed

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

Gi bleed and cad

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

Initial Hct-misleading

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

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

Harisson’s Algorithm for UGI BLEED

Duodenal Ulcer

• 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

Varices

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

Sengstaken Blakemore Tube

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

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

Carcinoma Oesophagus

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

Gastric Carcinoma

GI Malignancy

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

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

Mallory Weiss Tear

Oesophagitis Angiodysplasia

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

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

ANGIOEMBOLIZATION

Injection Sclerotherapy

Bipolar Electrocoagulation

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

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

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

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

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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