Marino The ICU Book 4e, IE

804 Nervous System Disorders

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 When ethanol is withdrawn, the resulting effects on both receptors results in central nervous system excitation, which leads to the agitation, delirium, and seizures that are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.)