Hepatic encephalopathy is aggravated by all except
Pathophysiology Hepatic encephalopathy is thought to be due to a disturbance of brain function provoked by circulating neurotoxins that are normally metabolised by the liver. Accordingly, most affected patients have evidence of liver failure and poosystemic shunting of blood, but the balance between these varies from individual to individual. Some degree of liver failure is a key factor, as poosystemic shunting of blood alone hardly ever causes encephalopathy. The 'neurotoxins' causing encephalopathy are unknown but are thought to be mainly nitrogenous substances produced in the gut, at least in pa by bacterial action. These substances are normally metabolised by the healthy liver and excluded from the systemic circulation. Ammonia has traditionally been considered an impoant factor. Recent interest has focused on g-aminobutyric acid (GABA) as a mediator, along with octopamine, amino acids, mercaptans and fatty acids that can act as neurotransmitters. The brain in cirrhosis may also be sensitised to other factors, such as drugs that can precipitate hepatic encephalopathy . Disruption of the function of the blood-brain barrier is a feature of acute hepatic failure and may lead to cerebral oedema.Hepatic encephalopathy may be aggravated during hyperkalemia . Ref Davidson edition23rd pg865
Hyperkalemia
Anaemia
Hypehyroidism
Barbiturates
G.I.T