Approach to upper GIT bleeding (UGIB)

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Approach to Upper GIT Bleeding (UGIB) Shaimaa Elkholy, M.D . Cairo University, Egypt

Transcript of Approach to upper GIT bleeding (UGIB)

Page 1: Approach to upper GIT bleeding (UGIB)

Approach to Upper GIT Bleeding (UGIB)

Shaimaa Elkholy, M.D .Cairo University, Egypt

Page 2: Approach to upper GIT bleeding (UGIB)

Shaimaa Elkholy, M.D. Cairo University

5 Q??

• Who ??• Why ??• How ??• When ??• What ??

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Shaimaa Elkholy, M.D. Cairo University

Agenda

• Definitions• Epidemiology • Aetiology• Initial Evaluation• General management• Risk stratification• Management of VGIB• Management of NVGIB• Take home message

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Shaimaa Elkholy, M.D. Cairo University

Definitions:

UGIB : bleeding from GIT above ligament of trietz.

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Shaimaa Elkholy, M.D. Cairo University

Definitions:

• Hematemsis: vomiting of blood or coffee-ground like material suggests bleeding proximal to the ligament of Treitz.

• Melena: black, tarry stools originates proximal to the ligament of Treitz (90 %), or from the small bowel or right colon.

• Hematochezia: red or maroon blood in the stool is usually due to lower GI bleeding. It can occur with massive upper GI bleeding.

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Epidemiology :

• Acute (UGIB) is a GIT emergency with a mortality of 4%-14% despite advances in critical care monitoring and support.

• Spontaneous cessation of bleeding occurs in 85% of cases.

• UGIB in the UK ranges between 84-172 per 100,000 per year, causing 50-70,000 hospital admissions per year.

• Major cases due to PUD.

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• UGIB in the United States is 160 hospital admissions per 100,000 population, which translates into more than 400,000 per year.

• 80 to 90% have NVGIB mainly PUD.• An increasing proportion related to the use of aspirin

/NSAIDs.• PUD bleed is seen predominantly among the elderly,

68% > 60 years/ 27% > 80 years.• Mortality remains high at 5-10%&medical costs for

the in-hospital care>$ 2 billion annually in US.

Epidemiology :

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Shaimaa Elkholy, M.D. Cairo University

Aetiology of UGIB:

• Peptic ulcer disease — 55 %• Oesphgealgasrtic varices — 14 %• A-V malformations — 6 %• Mallory-Weiss tears — 5 %• Tumors and erosions — 4 %• Dieulafoy's lesion — 1 %• Others 11 % .

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Shaimaa Elkholy, M.D. Cairo University

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Shaimaa Elkholy, M.D. Cairo University

Other rare cases:

• Idiopathic angiomas• Osler-Weber-Rendu syndrome• Radiation-induced telangiectasia• Traumatic or post-surgical• Foreign body ingestion• Post-surgical anastamosis• Aortoenteric fistula• Post gastric/duodenal polypectomy• Hemobilia• Hemosuccus pancreaticus

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EGYPTIAN scenario :• Variceal causes of bleeding were the most

common, representing 70.1% followed by non-variceal causes (26.1%) and obscure causes (3.8%).

• Gastric lesions were the most common causes of non variceal bleeding.

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VGIB:

• Variceal hemorrhage is the most common fatal complication of cirrhosis.

• At the time of diagnosis:30% of cirrhotic patients O.V.90% after approximately 10 years.• Bleeding ceases spontaneously in up to 40%

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• Correlation to the severity of liver disease:

Child–Pugh A patients: 40% have varices Child–Pugh C patients: 85% have varices

• Some patients may develop varices and hemorrhage early in the course of the disease, even in the absence of cirrhosis

• Patients with hepatitis C and bridging fibrosis: 16% have esophageal varices

VGIB:

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Prognosis:• Bleeding O.V. occurs 30 % in

the 1st year after diagnosis.• The mortality during the

attack: < 10% Child–Pugh grade A > 70% in advanced Child–

Pugh C cirrhotic stage. • Bleeding O.V. mortality rate

20% at 6 weeks.• The risk of re-bleeding is

high, reaching 80% within 1 year.

• High Portal venous pressure > 20 mmHg :

REBLEEDING : 1st week of admission

Failure to control bleeding (83% vs. 29%)

Higher 1-year mortality rate (64% vs. 20%).

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Small varices Large varicesNo varices

7-8%/year 7-8%/year

Varices Increase in Diameter Progressively

Merli et al. J Hepatol 2003;38:266

VARICES INCREASE IN DIAMETER PROGRESSIVELY

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I. Dilated venes (< 5mm) still at the level of the surrounding tissue

II. Dilated, straight venes (> 5 mm) protruding into the esophageal lumen but not obstructing it

Grades of O.V:.

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III. Large, tense and winding venes already obstructing the esophageal lumen considerably

IV. Near complete obstruction of the esophageal lumen with impending danger of hemorrhage (cherry red spots)

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NVGIB :

Peptic ulcer disease: • The mortality associated with acute bleeding from a

peptic ulcer remains high (5 to 10%). • 4 risk factors:H. pylori infectionNSAIDsStressGastric acidAlcoholism

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FORREST - classification of upper gastrointestinal hemorrhageAcute hemorrhageForrest IA Active spurting hemorrhageForrest IB Oozing hemorrhageSigns of recent hemorrhageForrest IIA Non-bleeding visible vesselForrest IIB Adherent clotForrest IIC Hematin on ulcer baseLesions without active bleedingForrest III Clean-base ulcers

Bleeding PUD

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Endoscopic Stigmata of Bleeding Peptic Ulcer, Classified as High Risk or Low Risk

Spurt blood (grade IA) Ooze blood (grade IB) Nonbleeding visible vessel (grade IIA)

Adherent clot (grade IIB) Flat, pigmented spot (grade IIC)

Clean base (grade III)

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DIEULAFOY'S LESION:

• Dilated aberrant submucosal vessel which erodes the overlying epithelium in the absence of a primary ulcer.

• It’s caliber 1 to 3 mm, 10-times the normal caliber of mucosal capillaries.

• Usually on lesser curve below the cardia, may be found any where.

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DIEULAFOY'S LESION:

• unknown, but may be congenital. • Events triggering bleeding are also not well-

understood(?? NSAIDs).• Male patients with comorbidities including

cardiovascular disease, hypertension, CKD , diabetes, or alcohol abuse.

• Bleeding is usually self limited but it may be severe.

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Mallory-Weiss syndrome:• longitudinal mucosal lacerations

s in the distal esophagus and proximal stomach, which are usually associated with forceful retching.

• secondary to a sudden increase in intraabdominal pressure e.g. vomiting, straining or lifting, coughing, epileptic convulsions, hiccups under anesthesia, closed-chest massage, blunt abdominal injury.

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• Precipitating factors:

hiatus hernia, chronic alcoholismincreasing age

Mallory-Weiss syndrome:

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GAVE & P.H.G:

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Tumors:BenignLeiomyomaLipomaPolyp (hyperplastic, adenomatous, hamartomatous)

MalignantAdenocarcinomaMesenchymal neoplasmLymphomaKaposi's sarcomaCarcinoidMelanomaMetastatic tumor

Page 29: Approach to upper GIT bleeding (UGIB)

Shaimaa Elkholy, M.D. Cairo University Pathway last updated: 22 February 2013

Copyright © NICE 2013. All rights reserved

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Resuscitation and initial management:

Initial evaluation: “QUICK” Triage. General support. Fluid resuscitation. Blood transfusions. Nasogastric lavage.

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General management:• Triage: “QUICK” ICU admission Hemodynamic instability (shock, orthostatic

hypotension).Active bleeding (manifested by hematemesis,

bright red blood per nasogastric tube, or hematochezia).

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General management:• Support : oxygen by nasal cannula. NPO. Two large caliber (16-18 gauge) peripheral I.V. Catheters. Central venous line if possible. Pulmonary artery catheter should be considered in

patients with hemodynamic instability or who need close monitoring during resuscitation.

Elective endotracheal intubation in patients with ongoing hematemesis with altered respiratory or mental status.

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General management:• Fluid resuscitation: resuscitation and stabilization is essential prior to

endoscopy Patients with active bleeding should receive

intravenous fluids (crystalloids or colloids) while being typed and cross-matched for blood

transfusion. Patients at risk of fluid overload may require intensive

monitoring with a pulmonary artery catheter.

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General management:• Indications of blood transfusion: • Hb below 7mg/dl (low risk).• High risk patients (old or comorbid) 10mg/dl.• Active (fresh) bleeding & Hypovolemea even with normal HB.• Indications of platelet & FFP transfusion:• low platelet count (<50,000/microL) OR INR > 1.5.• life-threatening bleeding receiving antiplatelet or anti coagulation.• Patients receiving massive blood transfusion due to dilutional

coagulopathy.• Over-transfuse patients with suspected variceal bleeding can precipitate

worsening of bleeding (10 mg/dl).

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General management:• Nasogastric lavage:• Its use before endoscopy in the ER remains controversial. • Benefits: To confirm an UGI source of bleeding(can still miss up to

15%) Prognostic index for identifying high-risk lesions as

presence fresh red blood in the NGT aspirate. May exclude false hematemsis. To facilitate lavage of the upper GI tract to improve

mucosal views at subsequent endoscopy.

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Risk assessment :• Blatchford score at first assessment.• Rockall score after endoscopy.

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ScoreLow risk defined as score of <=24.3% rebleeding0.1% mortality

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Medications (pre- endoscopy):

• Acid suppression.• Prokinetics. • Somatostatin and its analogs in VUGIB.• Antibiotics for patients with cirrhosis.

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• Acid suppression:• starte empirically on an I.V. PPI &continued

until confirmation of the cause of bleeding. • I.V. of a PPI significantly reduces the rate of

rebleeding compared& hospital stay in comparison to H2 blockers.

• 80 mg bolus followed by 8 mg/hr infusion for 72 days then switched to oral.

Medications (pre- endoscopy):

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• Prokinetics: erythromycin & metchlopromide.• Somatostatin, or its analog Octreotide

splanchnic vasoconstriction and decreased portal inflow

50 mcg bolus followed by a continuous infusion of 50 mcg per hour and is continued for 3-5 days.

Medications (pre- endoscopy):

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• Antibiotics for patients with cirrhosis:• The AASLD guidelines : (max.7 days)Oral norfloxacin (400 mg twice daily) or

intravenous ciprofloxacinIn patients with advanced cirrhosis, I.V.

ceftriaxone (1 g/day) & with a high prevalence of quinolone-resistant organisms.

Medications (pre- endoscopy):

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:Timing of endoscopy

• Patients with UGIB should generally undergo endoscopy within 24 h of admission, following resuscitative efforts to optimize hemodynamic parameters and other medical problems

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Timing of endoscopy

• Patients who are hemodynamically stable and without serious comorbidities:

Endoscopy as soon as possible in a non-emergent setting to identify the substantial proportion of patients with low-risk endoscopic findings who can be safely discharged

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Timing of endoscopy

• Patients with higher risk clinical features endoscopy within 12 h may be considered to potentially improve clinical outcomes

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Endoscopic management VUGIB:• EIS ( endoscopic injection

sclerotherapy)

Sclerosing materials : ethanolamin oleate(E/O) cyanoacrylate (H/A).

• Local complications : Ulceration Bleeding stricture formation portal hypertensive gastropathy• Regional complications esophageal perforation and

mediastinitis.• Systemic complications sepsis and aspiration with

ventilation perfusion mismatch and hypoxemia

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Endoscopic management VUGIB:

Video 1

Video 2

Video 3

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Shaimaa Elkholy, M.D. Cairo University

• EVL: endoscopic variceal ligation

• Less complications e.g. ulcers, stricture (rare).

• Less sessions.

Endoscopic management VUGIB:

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• Endoscopic therapy should be provided to patients with Forrest grade IA, IB, or IIA.

• Endoscopic therapy may be considered for patients with an adherent clot resistant to vigorous irrigation.

• Endoscopic therapy should not be provided to patients who have an ulcer with a clean base or a flat pigmented spot (Forrest grade IIC, or III).

Endoscopic management NVUGIB:

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Endoscopic Stigmata of Bleeding Peptic Ulcer, Classified as High Risk or Low Risk

Spurt blood (grade IA) Ooze blood (grade IB) Nonbleeding visible vessel (grade IIA)

Adherent clot (grade IIB) Flat, pigmented spot (grade IIC)

Clean base (grade III)

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• Mechanical method (for example, clips) with or without adrenaline

• Thermal coagulation with adrenaline• Fibrin or thrombin with adrenaline• No single method of endoscopic thermal

coaptive therapy is superior to another

Endoscopic management NVUGIB:

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Take home messeges • Patient with UGIB is critically ill patient with different presentations.• PUD is the commonest cause world wide.• VUGIB is commonest cause in Egypt.• Stepped approach to UGIB has to be known.• Resuscitation is essential prior to endoscopy.• Indications of blood , platelets & FFP transfusion differs from one

patient to another.• Target HB differs according to the patient.• Risk assessment is essential in those patients by different scoring

systems.• Forrest classification is essential to determine the line of management.• EVL is much preferred than injection sclerotherapy.

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Thank you