Changing face of hepatic encephalopathy: Role of inflammation and oxidative stress

Table 1 Classification of hepatic encephalopathy[2]

Type	Definition
A	Acute and hyperacute liver failure
B	Portosystemic bypass without intrinsic hepatocellular disease
C	Cirrhosis and portal hypertension with portosystemic shunts

A: Acute; B: Bypass; C: Cirrhosis.

Table 2 Clinical presentation of hepatic encephalopathy[2]

Encephalopathy	Definition
Acute	Acute liver dysfunction
Recurrent or episodic	Episodes of mental alteration in a patient with cirrhosis, even in the absence of a known precipitating factor
Persistent	Neurological deficit that persists despite the reversal of liver injury, such as following liver transplantation or the removal of a precipitating factor
Minimal (previously known as subclinical)	No evidence of overt encephalopathy, but subtle cognitive deficits might be detected with a neuropsychological function test battery

Table 3 Factors precipitating hepatic encephalopathy[2]

Precipitating factors	Ammonia load e.g. upper gastrointestinal bleed or portocaval shunt
	Inflammation/oxidative stress
	Infection
	Dehydration
	Hyponatremia
	Sedative drugs e.g. benzodiazepines