Gastroesophageal (GE) Varices and Hemorrhage

Matei Caleap

Background

  • Ceftriaxone 1g QD in patients with UGIB 
  • Portal HTN → portosystemic collaterals → GE varices , especially at GE junction 
    • Varices usually appear when portal hepatic vein gradient >10mmHg; bleeding risk rises when once >12 mmHg
    • GE Varices are present in ~50% of patients with cirrhosis; only 1/3 will bleed. 
    • Rebleeding occurs in ~70% of patients within 1 year of the index event. 
    • Per episode mortality up to 20%

Higher Bleed Risk

  • Location: GE junction (thinnest layer)>gastric fundus>elsewhere 
    • Larger varices, red wale marks 
    • Child-Pugh B or C 
    • Hx of previous variceal bleed 
    • Variceal pressure (>12 mmHg increases risk, w/ >16mmHg ~72% chance of incidence)

Variceal Screening and Primary Prophylaxis

  • Compensated, no varices: EGD q3yr 
  • Compensated cirrhosis with small varices (no prior bleed): EGD q2yr 
  • Decompensated cirrhosis: EGD at decompensation and then q1yr 
    • Management of non-bleeding varices HEPATOLOGY 239 
  • Primary ppx with either NSBB (preferred, ideally with carvedilol) or EVL (endoscopic variceal ligation). EVL indicated in patients with high risk of bleeding (medium/large varices, small varices with red wale sign, or decompensated
  • Medium/large varices or high-risk small varices (red whale sign or any varix in decompensation pt) 
    • Start NSBB if tolerated or do EVL 
    • If EVL, repeat until obliterated, then surveillance EGD 1–3 months after, then q6–12 months. 
  • No NSBB if: hypotension (SBP <90), AKI-HRS, SBP, hyponatremia (Na<130) , diuretic- resistant ascites 

*In patients with clinically significant portal HTN (i.e. portosystemic collaterals on imaging OR high risk features on fibrosis testing such as elastography) but no decompensation, evidence does support use of NSBB in prevention of any decompensation (ascites, variceal hemorrhage, HE) and has a mortality benefit.

Therapy

MOA

Starting dose

Titration

Max dose

Goal
Propranolol (preferred in decompensated cirrhosis ppx) Decreased cardiac output; caused by decreased heart rate and contractility from beta-1 adrenergic blockade 10–20 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
Nadolol (preferred in decompensated cirrhosis ppx) Above plus Splanchnic arterial vasoconstriction; caused by beta-2 blockade leading to unopposed alfa-adrenergic vasoconstriction 20 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
Carvedilol (preferred in patients w/ compensated cirrhosis) Above plus decreased intrahepatic vascular resistance; caused by anti-alpha 1-adrenergic activity 3.125 mg BID Increase to 6.25 mg BID after 3 d 6.25 mg BID (higher doses could be considered for non-hepatic indications) Dose goal is 6.25mg BID regardless of BP/HR (makes easier to titrate than others)

NSBB should be held or stopped of Systolic BP consistently <100, HR <55 or patient symptomatic.

Management of active bleeding varices 

  • Place two large-bore IVs (16G 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/hr, to be continued for at 2-5 days should EVH be confirmed on endoscopy 
    • Start Ceftriaxone 1g IV q24h for SBP prophylaxis (reduced mortality), then transition to PO ciprofloxacin 500mg BID for total 7-day course 
    • Consult GI for upper endoscopy for possible EVL vs sclerotherapy. EGD should be performed within 12 hours.
    • 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 (unless patient iatrogenically anticoagulated), 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 
    • TEG based repletion/correction is currently thought to be most effective guide to optimize coagulopathy in these patients with active bleeding.

Secondary Prophylaxis

  • After an EV bleeding episode, once bleeding controlled and octreotide stopped (~day 5): 
    • Start NSBB if no contraindication: Both NSBB and EVL is standard for secondary prevention and should be in place before discharge when possible.
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