Which of the following is not a precipitating factor for hepatic encephalopathy in patients with chronic liver disease -
Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver disease. As it progresses, delirium is followed by coma. Simple delirium needs to be differentiated from delirium tremens and Wernicke's encephalopathy, and coma from subdural haematoma, which can occur in alcoholics after a fall . Features include changes of intellect, personality, emotions and consciousness, with or without neurological signs. The degree of encephalopathy can be graded from 1 to 4, depending on these features, and this is useful in assessing response to therapy . When an episode develops acutely, a precipitating factor may be found . The earliest features are very mild and easily overlooked, but as the condition becomes more severe, apathy, inability to concentrate, delirium, disorientation, drowsiness, slurring of speech and eventually coma develop. Convulsions sometimes occur. Examination usually shows a flapping tremor (asterixis), inability to perform simple mental arithmetic tasks or to draw objects such as a star (constructional apraxia;), and, as the condition progresses, hyper-reflexia and bilateral extensor plantar responses. Hepatic encephalopathy rarely causes focal neurological signs; if these are present, other causes must be sought. Fetor hepaticus, a sweet musty odour to the breath, is usually present but is more a sign of liver failure and poosystemic shunting than of hepatic encephalopathy. Rarely, chronic hepatic encephalopathy (hepatocerebral degeneration) gives rise to variable combinations of cerebellar dysfunction, Parkinsonian syndromes, spastic paraplegia and dementia. Pathophysiology Hepatic encephalopathy is thought to be due to a disturbance of brain function provoked by circulating neurotoxins that are normally 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. Ref Davidson edition23rd pg 865
Hypokalemia
Hyponatremia
Hypoxia
Metabolic acidosis
G.I.T