Prepared by:

Dr. Mohammad Shaikhani

MBChB/CABM/FRCP

Introduction:

• Variceal hemorrhage is a lethal complication of cirrhosis, particularly with clinical decompensation (i.e., ascites, encephalopathy,a previous episode of hemorrhage, or jaundice).

• Lines of management:• Primary prophylaxis to prevent a first episode of VH. • Treatment of the acute bleeding episode• Secondary prophylaxis (prevention of recurrent VH).

Small varicesSmall varices Large varicesLarge varicesNo varicesNo varices

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

Varices Increase in Diameter ProgressivelyVarices Increase in Diameter Progressively

Merli et al. J Hepatol 2003;38:266Merli et al. J Hepatol 2003;38:266

VARICES INCREASE IN DIAMETER PROGRESSIVELY

Predictors of hemorrhage: Variceal size

Red signs Child B/C

Predictors of hemorrhage: Variceal size

Red signs Child B/C

NIEC. N Engl J Med 1988; 319:983NIEC. N Engl J Med 1988; 319:983

Variceal hemorrhageVariceal hemorrhage Varix with red signsVarix with red signs

PROGNOSTIC INDICATORS OF FIRST VARICEAL HEMORRHAGE

Natural history:• GE varices are present in 50% of patients with cirrhosis at the

time of diagnosis, with the highest rate among patients with Child–Turcotte–Pugh class B or C disease

• Development/growth of GE varices each occur at a rate of 7% /year.

• The 1-year rate of a first variceal hemorrhage depends on• 1.Size: 12% (5% for small , 15% for large varices).• 2.Red wale marks on varices • 3.Stage: advanced liver disease (Child class B or C) identify

patients at a high risk for variceal hemorrhage.• The 1-year rate of recurrent variceal hemorrhage is 60%.• The 6-week mortality with each episode of variceal hemorrhage is

15-20%; 0% with Child class A disease to 30% with Child class C.

Risk Stratification for Portal Hypertension• 1. Compensated or decompensated cirrhosis.• Compensated cirrhosis (No ascites, variceal hemorrhage,

encephalopathy, or jaundice)• 2. Presence GE varices usually by OGD have a higher rate of

death/ decompensation than those without.• Less invasive methods as capsule endoscopy its accuracy in

evaluating the presence of varices, red wale marks, variceal size is still suboptimal.

• 3.A ratio of platelet(per cubic millimeter) to spleen size (the maximum bipolar diameter in millimeters by US) above 909 has a high negative predictive value,but requires further validation.

Capsule Endoscopy for Screening for Varcies

Grade 3 Varices Grade 1 Varices

Risk Stratification for Portal Hypertension• 4. The presence of varices (or collaterals on imaging studies)

indicates clinically significant portal hypertension • 5.Child class or its lab components (bilirubin,albumin ,INR)

correlate roughly with clin sign portal HT& can be used to stratify risk in both compensated& decompensated cirrhosis; Child class C associated with HVPG> 20 mmHg& poor outcome.

• 6.The Model for End-Stage Liver Disease score, which is used for organ allocation in liver transplantation,predict the development of decompensation in patients without varices&6-week mortality after variceal hemorrhag.

Risk Stratification for Portal Hypertension

• 7.Measurement of liver stiffness, a noninvasive,correlates reasonably well with the HVPG, particularly at HVPG values below 10 mm Hg, useful in identifying the presence of clinically significant portal hypertension.

Risk Stratification for Portal Hypertension

• 8. HVPG In patients without varices & with variceal hemorrhage, HVPG is the best method to risk stratification.

• Portal hypertension is present when the HVPG is > 5 mm Hg.• In patients without varices HVPG is considered clinically significant

when > 10 mm Hg, because, this pressure is the strongest predictor of the development of varices, clinical decompensation,hepatocellular carcinoma.

• In patients with variceal hemorrhage, an HVPG of > 20 mm Hg (within 24 hours after admission) is the best predictor of a poor outcome.

• A reduction in the HVPG to < 12 mm Hg or a reduction of > 20% from the baseline value is associated with a decreased risk of variceal hemorrhage / improved survival.

• The HVPG is obtained by catheterization of a hepatic vein with a balloon catheter through a jugular or femoral vein.

• It is invasive & its use is not widespread.

Portal Hypertensive Gastropathy• A portal hypertension–related GI mucosal lesion characterized by

ectatic gastric mucosal vessels mostly in the fundus & body of the stomach.

• The presence of GE varices&Child class are predictive of its presence, whereas its development or its progression from mild to severe correlates only with the Child class.

• Although the prevalence of portal hypertensive gastropathy is higher among patients who have undergone endoscopic therapy (sclerotherapy or endoscopic variceal ligation) thanamong those who have not, the clinical course is the same.

• The most common presentation, occurring mainly in patients with severe portal hypertensive gastropathy, is chronic, slow hemorrhage resulting in anemia.

• The initial management consists of iron supp, use of nonselective BB;also effective in preventing recurrent hemorrhage.

• If hemorrhage continues& the patient requires frequent transfusions, shunt therapy (either TIPS shunt or shunt surgery) considered.

Associated Portal-Vein Thrombosis

• The development of portal-vein thrombosis is an important event in the natural history of advanced cirrhosis.

• It is associated with worsening liver function, ascites, variceal hemorrhage.

• The incidence is 16%/year in patients with advanced liver disease.• Treatment (e.g., with anticoagulation, thrombolysis,or TIPS) is

currently determined on a caseby-case basis.