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HEPATIC ENCEPHALOPATHY - S.A.Center D.ACVIM phatophysiology and treatment 

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HEPATIC ENCEPHALOPATHY - S.A.Center D.ACVIM phatophysiology and treatment 

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Hepatic encephalopathy (HE) develops in liver disorders associated with portosystemic shunting, fulminant hepatic failure, or cirrhosis (acquired portosystemic shunts, reduced functional hepatic mass, intrahepatic shunting of blood around regenerative nodules). Clinical signs vary but involve disturbed sensorium ranging from mild dullness and an inability to respond to basic commands to overt abnormalities, including propulsive circling, head pressing, aimless wandering, weakness, ataxia, amaurosis (unexplained blindness), ptyalism, dementia, behavior change (eg, aggression), collapse, seizures, and coma. Although the pathophysiologic mechanisms of HE are not completely known, synergistic effects between the failure of the liver to detoxify ammonia and other endogenous substances, increased cerebral inflammatory cytokines, impaired brain perfusion, development of neuronal edema, hypoxia, mitochondrial dysfunction, neuroglycopenia, and oxidative injury are important interdependent mechanisms. Increased production of reactive oxygen and nitrogen oxide species are thought to trigger protein and RNA modifications that deleteriously influence brain function. The integrated concept of HE explains episodic variability and heterogeneous precipitating factors that correlate with diverse clinical scenarios.

Ammonia plays a key role in HE and is thought to sensitize the brain to numerous other precipitating factors/mediators. However, blood and cerebral ammonia concentrations are often discordant, disqualifying blood ammonia as a simplistic measure of HE. In healthy animals, most ammonia is removed by hepatocytes, converted into amino acids or urea, and excreted via kidneys in urine. In liver failure or portosystemic shunting, blood ammonia concentrations increase because of inadequate hepatic detoxification. In the circulation, ammonia can also be excreted by the kidneys (tubular secretion) and used for glutamine synthesis in skeletal muscle (temporary ammonia detoxification). This latter mechanism is why maintenance of lean body mass (muscle) is essential in animals with hepatic insufficiency that are susceptible to hyperammonemia and HE. A number of clinical scenarios and mechanisms can augment blood ammonia concentrations and precipitate HE, including dehydration (prerenal/renal azotemia), alkalemia, hypokalemia, hypoglycemia, catabolism, infection, PU/PD, anorexia, constipation, hemolysis, blood transfusion, GI hemorrhage, high dietary protein, and various drugs (eg, benzodiazepines, tetracyclines, antihistamines, methionine, barbiturates, organophosphates, phenothiazines, diuretics [overdosage], metronidazole (overdosage), and certain anesthetics).

Ammonia can influence multiple neurotransmitter systems directly (chemical influence) and indirectly (altered substrate availability for transmitters). There is substantial evidence that astrocytes play an important role in the pathogenesis of HE. Ammonia and other endogenous products, inflammatory cytokines, and hyponatremia (associated with portal hypertension) induce astrocyte swelling that can lead to brain edema and herniation most common in acute liver failure and acute severe HE.

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