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Acute Liver Failure .pdf


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Title: Acute Liver Failure
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Acute Liver Failure
Dr Indrajit Kumar Datta
FCPS(medicine),MD(Gastroenterology)
Assistant Professor
Dept. of GHPD
BIRDEM General Hospital and IMC.

Definition
Acute liver failure is defined as the rapid
development of hepatocellular dysfunction,
specifically coagulopathy and mental status
changes (encephalopathy) in a patient without
known prior liver disease. Acute liver failure is a
clinical syndrome that represents the final
common pathway of severe liver injury resulting
from numerous infectious, immunologic,
metabolic, vascular, and infiltrative disorders.

The syndrome was originally defined further as
occurring within 4 weeks of onset of the
precipitating illness, in the absence of evidence
of preexisting liver disease. This distinguishes it
from instances in which hepatic encephalopathy
represents a deterioration in chronic liver
disease.

Pathophysiology
Any cause of liver damage can produce acute liver
failure, provided it is sufficiently severe.
Acute viral hepatitis is the most common cause
worldwide, whereas paracetamol toxicity is the
most frequent cause in the UK. Acute liver failure
occurs occasionally with other drugs, or from
Amanita phalloides (mushroom) poisoning, in
pregnancy, in Wilson’s disease, following shock
and rarely, in extensive malignant disease of the
liver.

In 10% of cases the cause of acute liver failure
remains unknown and these patients are often
labeled as having ‘non-A–E viral hepatitis’ or
‘cryptogenic’ acute liver failure.

Clinical Feature
Cerebral disturbance (hepatic encephalopathy
and/or cerebral oedema) is the cardinal
manifestation of acute liver failure, but in the
early stages this can be mild and episodic and
so its absence does not exclude a significant
acute liver injury.

The initial clinical features are often subtle and
include reduced alertness and poor concentration,
progressing through behavioral abnormalities
such as restlessness and aggressive outbursts, to
drowsiness and coma. Cerebral oedema may
occur due to increased intracranial pressure,
causing unequal or abnormally reacting pupils,
fixed pupils, hypertensive episodes, bradycardia,
hyperventilation, profuse sweating, local or
general myoclonus, focal fits or decerebrate
posturing.


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