Drug Therapy
Drug therapy may be necessary for patients with agitated delirium and
disruptive behavior. It is important to
avoid GABA-ergic drugs (e.g., benzo-
diazepines) for sedation in patients with hospital-acquired delirium
because
these drugs promote delirium (6).
DEXMEDETOMIDINE:
The most recent guidelines on sedation in the ICU
recommend dexmedetomidine for sedation of patients with hospital-
acquired delirium (16).
Dosage: Load with 1
μ
g/kg over 10 min, then infuse at 0.2–0.7
μ
g/kg/hr.
This drug can cause bradycardia and hypotension (see Chapter 51).
AlcoholWithdrawal Delirium
Alcohol withdrawal delirium, also known as
delirium tremens
or DTs, is
characterized by increased motor activity and increased activity on the elec-
troencephalogram (EEG). In contrast, hospital-acquired delirium is charac-
terized by decreased motor activity and slowing of the EEG activity (6).
Pathogenesis
The central nervous system depressant effects of ethanol are the result of
stimulation of GABA receptors (the major inhibitory pathway in
the brain) and inhibition of N-methyl-D-aspartate (NMDA) receptors
(the major excitatory pathway in the brain). When ethanol is withdrawn,
the resulting effects on both receptors results in central nervous system
excitation, which leads to the agitation, delirium, and seizures that are
characteristic features of alcohol withdrawal.
Clinical Features
The clinical features of alcohol withdrawal are shown in Table 44.2.
About 5% of patients who experience alcohol withdrawal symptoms will
develop DTs (17). Risk factors include a prolonged drinking history, prior
episodes of DTs, comorbid illness, and time since last drink. Signs of DTs
usually appear 2 – 3 days after the last drink, and include agitated deliri-
um, low-grade fever, tachycardia, hypertension, diaphoresis, nausea, and
vomiting. Associated conditions include dehydration, hypo-kalemia,
hypomagnesemia, and generalized seizures. The condition typically lasts
for 3 – 5 days (17), but severe cases can last for up to 2 weeks (personal
observation). The reported mortality is 5 – 15% (17).
WERNICKE’S ENCEPHALOPATHY:
Alcoholic patients who are admitted with
borderline thiamine stores and receive an intravenous glucose load can
develop acute Wernicke’s encephalopathy from thiamine deficiency
(because thiamine is a cofactor for enzymes involved in glucose metabo-
lism) (18). In this situation, the acute changes in mental status occur 2 – 3
days after admission, and can be confused with alcohol withdrawal
delirium. The presence of nystagmus or oculomotor palsies (e.g., lateral
gaze paralysis) will help to identify Wernicke’s encephalopathy. (For
more information on thiamine deficiency, see Chapter 47.)
804
Nervous System Disorders
