Hepatic Encephalopathy

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Basics

Description

Hepatic encephalopathy (HE) is characterized by changes in behavior and consciousness with motor disturbances, associated with hepatic insufficiency and the accumulation of substances normally metabolized by the liver. HE may result from a combination of:
  • Accumulation of ammonia (NH3) from:
    • Protein degradation by colonic enzymes and bacteria
    • Deamination of glutamine in small bowel, kidney, and muscle
    • Accumulated NH3 crosses the blood–brain barrier. Astrocytes uptake NH3 and metabolize it into glutamine which causes cellular swelling. Ultimately leads to cerebral edema and cerebral mitochondrial dysfunction
  • Accumulation of other neurotoxins:
    • Short-chain fatty acids
    • Manganese toxicity
    • Neurosteroids
    • Phenols
    • Mercaptans
    • Amino acids such as tryptophan
  • Increased levels of inhibitory neurotransmitters:
    • Benzodiazepines
    • γ-aminobutyric acid (GABA)
    • Serotonin
  • Decreased levels of excitatory neurotransmitters:
    • Glutamate
    • Dopamine
    • Aspartate
    • Catecholamines
  • Other contributing factors to HE:
    • Decreased cerebral blood flow and oxygen
    • Increased glucose consumption and possible hypoglycemia
    • Zinc deficiency
  • Genetics:
    • Inherited errors of the urea cycle

Etiology

  • Classification based on the eleventh World Congress of Gastroenterology:
    • Type A: HE associated with acute liver injury and fulminant hepatic failure (FHF)
    • Type B: HE associated with portosystemic bypass and no intrinsic liver disease
    • Type C: HE associated with cirrhosis and portal hypertension
  • Precipitating events:
    • GI bleeding (more common in elderly)
    • Hypokalemia and hyponatremia (diuretics)
    • Alkalosis decreases renal NH4 excretion
    • Sepsis (likely via inflammatory cytokines)
    • Spontaneous bacterial peritonitis (SBP) or other infections
    • Constipation
    • Noncompliance with treatment regimen in chronic liver failure
    • Hypoglycemia
    • Hypovolemia (e.g., post large-volume paracentesis)
    • Azotemia (e.g., diuretic or diarrhea induced)
    • Narcotics or sedatives, including alcohol
    • Zinc deficiency as multiple urea cycle enzymes are zinc dependent
    • Hepatocellular injury
    • Viral- or drug-induced hepatitis
    • Post portosystemic shunt placement
    • Recurrent encephalopathy can occur without precipitating factors

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Basics

Description

Hepatic encephalopathy (HE) is characterized by changes in behavior and consciousness with motor disturbances, associated with hepatic insufficiency and the accumulation of substances normally metabolized by the liver. HE may result from a combination of:
  • Accumulation of ammonia (NH3) from:
    • Protein degradation by colonic enzymes and bacteria
    • Deamination of glutamine in small bowel, kidney, and muscle
    • Accumulated NH3 crosses the blood–brain barrier. Astrocytes uptake NH3 and metabolize it into glutamine which causes cellular swelling. Ultimately leads to cerebral edema and cerebral mitochondrial dysfunction
  • Accumulation of other neurotoxins:
    • Short-chain fatty acids
    • Manganese toxicity
    • Neurosteroids
    • Phenols
    • Mercaptans
    • Amino acids such as tryptophan
  • Increased levels of inhibitory neurotransmitters:
    • Benzodiazepines
    • γ-aminobutyric acid (GABA)
    • Serotonin
  • Decreased levels of excitatory neurotransmitters:
    • Glutamate
    • Dopamine
    • Aspartate
    • Catecholamines
  • Other contributing factors to HE:
    • Decreased cerebral blood flow and oxygen
    • Increased glucose consumption and possible hypoglycemia
    • Zinc deficiency
  • Genetics:
    • Inherited errors of the urea cycle

Etiology

  • Classification based on the eleventh World Congress of Gastroenterology:
    • Type A: HE associated with acute liver injury and fulminant hepatic failure (FHF)
    • Type B: HE associated with portosystemic bypass and no intrinsic liver disease
    • Type C: HE associated with cirrhosis and portal hypertension
  • Precipitating events:
    • GI bleeding (more common in elderly)
    • Hypokalemia and hyponatremia (diuretics)
    • Alkalosis decreases renal NH4 excretion
    • Sepsis (likely via inflammatory cytokines)
    • Spontaneous bacterial peritonitis (SBP) or other infections
    • Constipation
    • Noncompliance with treatment regimen in chronic liver failure
    • Hypoglycemia
    • Hypovolemia (e.g., post large-volume paracentesis)
    • Azotemia (e.g., diuretic or diarrhea induced)
    • Narcotics or sedatives, including alcohol
    • Zinc deficiency as multiple urea cycle enzymes are zinc dependent
    • Hepatocellular injury
    • Viral- or drug-induced hepatitis
    • Post portosystemic shunt placement
    • Recurrent encephalopathy can occur without precipitating factors

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