Internal Medicine

0521779407-09 CUNY1086/Karliner 0 521 77940 7 June 4, 2007 21:12

678 Hepatic Encephalopathy

■elevated blood ammonia level

➣arterial specimen is the only accurate assay

➣diagnosis or treatment response should not be based on ammo-

nia

■psychometric tests: sensitive for subclinical HE when neurological

examination is otherwise normal, e.g., Reitan or trail-making tests

■electroencephalogram (not used routinely): high-frequency, low-

voltage waves

■cerebrospinal fluid (not used routinely): elevated glutamine level

differential diagnosis

■subcategories of HE

■Type A: acute liver failure-associated hepatic encephalopathy

■Type B: major portosystemic shunting without cirrhosis

■Type C: cirrhosis, with 5 major subtypes of presentations

➣subclinical HE

➣single or recurrent episodes of overt HE

➣chronic overt HE

➣acquired hepatocerebral degeneration

➣spastic paresis

■non-hepatic causes of encephalopathy or CNS dysfunction: hypoxia,

hypoglycemia, electrolytic disturbances, uremia, diabetic coma,

drugs, infection, CNS structural lesion

■combined hepatic and non-hepatic encephalopathy

management

What to Do First

■systematic neurologic and mini-mental examination

■panculture, including diagnostic paracentesis

■digital rectal exam to exclude gastrointestinal bleed

General Measures

■altered mental status in a patient with known or suspected cirrhosis

should be considered HE until proven otherwise

■four-pronged simultaneous approach:

➣supportive measures for a patient with altered mental status

aspiration precaution, pressure sore prevention, toilet care;

maintenance of fluid, electrolyte, and nutrition

➣exclude other causes of encephalopathy

➣identify and treat correctable precipitating factors

➣initiate empirical treatment