Portal Hypertension

Pathophysiology of portal hypertension and cirrhosis

  • Causes:  alcohol, viral hepatitis (B & C), hemachromatosis, gall stones, cystic fibrosis (biliary obstruction), right heart failure (CV), nonalcoholic steatohepatitis (NASH)
  • Cirrhosis is characterized by an irreversible alteration of the liver architecture (fibrosis followed by nodular degeneration)
    • Fibrosis near portal vein impedes blood flow causing portal HTN
      • Elevated portal pressure = hepatic venous pressure gradient of > 6 mm Hg
      • Highest risk of variceal bleeding at pressure gradient of > 12 mm Hg

Symptoms and complications associated with portal hypertension and cirrhosis

  • Complications:  hepatic encephalopathy, ascites, bacterial peritonitis (secondary to ascites), splenomegaly, bleeding esophageal or gastric varices
    • Hepatic encephalopathy (caused by excessive ammonia) = altered mental status due to liver impairment primarily due to the accumulation of toxic products not metabolized by the liver
      • Causes impaired consciousness, cognition, or motor abilities
  • Symptoms:  thrombotyopenia, encephalopathy, ascites

Agents used to treat and prevent portal hypertension and their complications

  • Hepatic encephalopathy treatment: lactulose (removes ammonia) + protein restriction with the goal is to lower blood ammonia levels to increase overall cognitive ability.  Limit to 20 g/day & increase by 5-10 grams every 5 days until tolerance established
    • Use vegetable sources over animal sources of protein due to the increased fiber content & fewer aromatic AAs
    • Lactulose (preferred treatment) is used 20-30 g TID-QID until 2-3 stools/day maintenance or 20-30 g q 1-2 h until bowel movement for an acute episode
    • Neomycin & metronidazole reduce ammonia-forming bacteria in the intestinal tract but are less favorable than lactulose
      • Lots of SE w/ long term use
      • Neomycin use should be cautioned in patients with renal insufficiency (metronidazole is metabolized by the liver, increased half-life in liver disease)
    • Flumazenil (benzo antidote) displaces benzo-like substance from GABA receptor which may be increased in patients with HE  (short term txt only)
  • Ascites treatment:  diuretics (not thiazides though), salt restriction (<2000mg/day)
    • **10:4 ratio spironolactone to furosemide**
      • Discontinue if severe hyponatremia or encephelaopathy despite fluid restriction or renal insufficiency
  • Spontaneous bacterial peritonitis (E. Coli, K. or S. pneumoniae) treatment:  cefotaxime (or 3rd gen cephalosporin) 2g Q 8h IV for 5-10 days, quinolone or Bactrim may be used as prophylaxis
  • Gastric/esophageal varices treatment:  prevention using (**non-selective) Beta-blockers (propanolol, nadolol, or timolol**) or  endoscopic band ligation (EBL) for patients for whom beta-blocker treatment is contraindicated
    • Treatment of acute variceal bleeds:
      • Octreotide** (50-100mcg bolus followed by 25-50 mcg/hr drip) which inhibits vasodilation of GI peptides & thus decreasing splanchnic blood flow & portal inflow
      • Intervention therapy:  EBL preferred to reduce episodes of rebleeding, EGD with EIS
      • Vasopressin (w or w/o nitro)–no longer 1st line therapy due to SE though
      • Prophylactic antibiotic therapy to prevent sepsis especially in the case of ascites
    • Secondary prevention (after the patient has survived an initial episode)
      • Nonselective beta-blocker  (used for primary & secondary txt of variceal bleeding)
        • Long-acting nitrate therapy (isosorbide mononitrate/dinitrate can be used in addition to a beta-blocker
      • A transjugular intrahepatic portosystemic shunt (TIPS) procedure may be performed
  • A liver transplant is the only cure for the complications of end stage liver disease (ESLD)

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