290 Emergency Medicine
(a and b)These are both antipsychotic medications that can worsen the
symptoms of NMS and should not be administered. (d)Diphenhydramine,
an anticholinergic, should be avoided as it is ineffective and may worsen the
reaction by interfering with temperature regulation. (e)Acetaminophen, an
antipyretic, may help in lowering the temperature. However, NMS is a cen-
trally mediated process. External cooling is more effective.
266.The answer is a.(Tintinalli, p 1015.)This patient exhibits the classic
triad of Wernicke encephalopathy (WE): confusion, ataxia, and oph-
thalmoplegia.WE is a result of thiamine deficiencyleading to decreased
glucose metabolism and neuronal destruction, primarily in the cerebellum,
hypothalamus, vestibular system, and memory. It is typically found in
chronic alcoholicscaused by nutritional deficiency, but can also occur in
other malnutrition states, pregnancy, persistent vomiting, or dialysis. WE
can mimic acute stroke symptoms and can lead to permanent nystagmus
and ataxia. It carries 10% to 20% mortality if untreated.
Eye examination findings in WE include horizontal nystagmus, vertical
gaze palsy, or cranial nerve VII palsy. Cerebellar destruction presents with
ataxic, wide-based gait. WE is a clinical diagnosis. Thiamine deficiency can
also lead to the development of high-output cardiac failure and Korsakoff
syndrome. The treatment is parenteral thiamine supplementation.
Korsakoff syndrome (b)is another sign of thiamine deficiency and
involves disorientation and confabulation. Normal pressure hydrocephalus
(c)presents with dementia, ataxic gait, and urinary incontinence. Head CT
shows large ventricles. Central vertigo (d)is caused by lesions in the brain-
stem or cerebellum. It is associated with vertical or rotary nystagmus and
nausea and vomiting. Alcohol withdrawal (e)typically presents with sym-
pathetic and CNS overactivity.
267.The answer is b. (Tintinalli, p 1113.)The patient has cocaine-
induced autonomic and CNS hyperactivitycausing agitation, paranoia,
and a hyperadrenergic state. More severe CNS manifestations of cocaine
poisoning include hyperthermia, intracranial hemorrhage, seizures, spinal
cord infarctions, and acute dystonic reactions. The CNS effects of cocaine
are managed with benzodiazepines,which decrease sympathetic tone and
prevent hyperthermia and seizures.
(a)β-Adrenergic receptor blockers decrease HR and BP. In this case,
however, metoprolol administration does not address the underlying cause
of the adrenergic hyperactivity. More importantly, β-adrenergic receptor