Gastroesophageal Varices and Hemorrhage

H. Anh Nguyen

Background

  • Varices form due to portosystemic collaterals in the setting of portal HTN
  • Gastroesophageal varices are present in approximately 50% of patients with cirrhosis and their presence correlates with severity of liver disease
  • The risk of mortality with esophageal variceal hemorrhage (EVH) can be up to 15-20%
  • Recurrence occurs in over 60% of patients within 1-2 years of the index event
  • The most important predictor of hemorrhage is the size of the varices. Other predictors include decompensated cirrhosis (Child B/C) and endoscopic presence of red wale marks or red spots
  • Variceal Screening:
    • Regular screening not required in all patients with cirrhosis though initial EGD at time of cirrhosis diagnosis is recommended. Screening can be omitted in patients without evidence of clinically significant portal hypertension (low liver stiffness on elastography [LSM <20 and platelets >150], repeated TE annually) and in patients at low risk of bleed on NSBB.
    • Compensated cirrhosis without varices: EGD q3yr
    • Compensated cirrhosis with small varices that have not bled: EGD q2yr (unless on NSBB, then no need for follow-up EGD)
    • Decompensated cirrhosis: EGD at time of decompensated and then q1yr
    • Medium/large varices that have not bled: NSBB if tolerated (follow up surveillance EGD unnecessary) or EVL, repeated until obliterated with first surveillance EGD 1-3 months after and q 6-12 months to check for recurrence
  • In general, most patients with cirrhosis should be on propranolol or carvedilol (preferred due to intrinsic anti-alpha-1-adrenergic activity and facilitates the release of nitric oxide, induces intrahepatic vasodilation further reducing portal pressure), per new guidelines. Always check with the hep attendings if BB needs to be started.

Management (Non-Bleeding Varices)

  • Primary ppx with either NSBB (preferred if tolerated; see table below) or endoscopic variceal ligation (EVL). EVL indicated in patients with high risk of bleeding (medium/large varices, small varices with red wale sign, or decompensated patients with varices of any size).
    • Carvedilol has greater reduction in portal pressures and is preferred if tolerated (goal 6.25mg BID)
    • Nadolol (given nightly as portal pressures are highest at night) or propranolol (BID)
    • For secondary ppx, initiate ~72hr after acute bleed has resolved and octreotide discontinued
  • Discontinue if: hypotension (SBP <90), AKI-HRS, SBP, or hyponatremia with refractory ascites
  • Secondary ppx with both NSBB and EVL
    • NSBB are associated with reduced mortality, while EVL is not
  • Of note, in patients with clinically significant portal HTN but are without varices, there is no evidence to support the use of NSBB to prevent varices formation, but high-level evidence does support use of NSBB (strongest evidence for Carvedilol) in prevention of any decompensation (ascites, variceal hemorrhage, HE) and has a mortality benefit (likely driven by significant reduction in ascites development)

Management (Bleeding Varices)

  • Place two large-bore IVs (18G or larger), resuscitate with blood products and albumin. Activate massive transfusion protocol if needed.
  • Consider intubation if need for emergent EGD, change in mental status, ongoing hematemesis, or inability to protect airway
  • Start octreotide 50 mcg IV bolus followed by continuous infusion of 50 mcg/h, to be continued for at 2-5 days should EVH be confirmed on endoscopy
  • Ceftriaxone 1g IV q24h for SBP prophylaxis (reduced mortality), then transition to PO ciprofloxacin for total 7-day course
  • Consult GI for upper endoscopy for possible EVL vs sclerotherapy. EGD should be performed within 12 hours of admission.
  • Consider balloon tamponade with Blakemore as temporizing measure before definitive management. Patient must be intubated before placement, and preferably GI should be made aware prior to placement.
  • No role for the correction of INR, even in the presence of bleeding as excessive blood products and FFP can increase portal pressures and cause worsening bleeding
    • Vitamin K can be given w/ ↑ INR, though is unlikely to help in the acute setting
    • Check TEG and fibrinogen and transfuse based on results
    • AASLD does not recommend specific platelet targets during variceal hemorrhage
  • Administer blood products in balanced ratio to avoid transfusion related coagulopathy

Therapy

MOA

Starting dose

Titration

Max dose

Goal
Propranolol Decreased cardiac output; caused by decreased heart rate and contractility from beta-1 adrenergic blockade 20–40 mg twice daily Increase the dose every 2–3 d until treatment goal Without ascites: 320 mg/day; with ascites: 160 mg/day HR of 55–60 bpm if tolerated; SBP should be maintained ≥90 mm Hg
Nadolol Above plus Splanchnic arterial vasoconstriction; caused by beta-2 blockade leading to unopposed alfa-adrenergic vasoconstriction 20–40 mg at bedtime Increase the dose every 2–3 d until treatment goal Without ascites: 160 mg/day; with ascites: 80 mg/day HR of 55–60 bpm if tolerated; SBP should be maintained ≥90 mm Hg
Carvedilol Above plus decreased intrahepatic vascular resistance; caused by anti-alpha-adrenergic activity 6.25 mg once daily Increase to 6.25 mg twice daily after 3 d 12.5 mg/day (higher doses could be considered for non-hepatic indications) No HR goal; SBP should be maintained ≥90 mm Hg
Last updated on