Hepatic Failure

Overview
  • Liver failure is a syndrome which occurs when the liver can no longer meet the functional requirements of the body. Hepatic failure may manifest slowly or acutely and often comes to clinical attention during an acute illness or surgery when functional demands on the liver are increased.
Etiology and Pathogenesis
  • Liver failure is the final-common end point of a wide variety of insults to the liver. Often, but not always, these etiologies first proceed through a general morphological precursor, which if not corrected ends in hepatic failure. Fulminant hepatitis and cirrhosis are the two classic morphological precursors which can progress to hepatic failure. Regardless of the etiology, the ultimate cause of hepatic failure is one of insufficient total hepatic function whose specific contribution to physiology is discussed in hepatic physiology.
Clinical Consequences
  • Hepatic Encephalopathy
    • Characterized by alterations in mental status, behavioral changes, and cerebral edema (see page).
  • Hepatorenal Syndrome
    • Characterized by initiation of Acute Renal Failure (see page).
  • Jaundice
    • Reduced hepatic functionality results in insufficient secretion of bilirubin resulting in hyperbilirubinemia and eventually signs of jaundice.
  • Generalized Edema
    • Reduced hepatic synthesis of albumin results in hypoalbuminemia. This reduces the plasma oncotic pressure which in turn allows increased ultrafiltration of plasma into the ECF as discussed in microcirculatory physiology.
  • Hyperammonemia
    • Due to reduced urea cycle function in the liver.
  • Elevated Estrogen
    • The cause of elevated estrogen in hepatic failure is not well-understood but is thought to be responsible for palmar erythema and spider telangiectasias of the skin. In men hyperestrinism can cause gynecomastia and testicular atrophy.
  • Bleeding Disorder
    • Presents with lower GI bleeding as a result of reduced hepatic synthesis of plasma coagulation factors. When failure is a result of chronic cirrhosis, secondary splenomegaly and resultant sequestration of platelets can result in severe thrombocytopenia, yielding mucocutaneous bleeding, petechiae and ecchymoses.