Neuroleptic Malignant Syndrome

Published on 07/03/2015 by admin

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Chapter 82 Neuroleptic Malignant Syndrome

Jennifer M. Hall, DO , James L. Jacobson, MD

1 What is neuroleptic malignant syndrome (NMS)?

NMS is a rare, potentially fatal, idiosyncratic complication of antipsychotic medications. The usual presentation consists of four primary features:

Extreme generalized muscular rigidity

Autonomic instability

Altered mental status

These features generally appear 24 to 72 hours after the administration of an antipsychotic; however, NMS can also occur with chronic use. Altered mental status is the first presenting symptom in 80% of NMS cases. Mean recovery time after antipsychotic discontinuation is 7 to 10 days but may be prolonged when long-acting depot antipsychotics are implicated. For other common features of NMS, see Box 82-1.

2 How common is NMS?

Recent data suggest that the incidence of NMS in patients treated with antipsychotics ranges between 0.01% and 0.02%. Previous estimates were as high as 3%; however, because of increased awareness, judicious antipsychotic use, and rapid recognition and treatment the incidence of NMS has declined.

3 What is the mortality rate for NMS?

Despite the declining incidence of NMS, it remains a significant source of morbidity and mortality among patients receiving antipsychotics. The original description of NMS in 1968 estimated a mortality rate as high as 75%, which subsequently declined to 20% to 30% in the 1980s. More recently, the U.S. Agency for Healthcare Research and Quality reports that, of an estimated 2000 cases diagnosed annually in hospitals, mortality rates approximate 10%. Cause of death in NMS is usually a result of cardiac or respiratory arrest (cardiac failure, infarction, arrhythmia, aspiration pneumonia, or pulmonary emboli), myoglobinuric renal failure, or disseminated intravascular coagulation.

4 What is the pathogenesis of NMS?

Although the pathophysiology of NMS is poorly understood, dopamine receptor antagonism in the basal ganglia, hypothalamus, and postganglionic sympathetic neurons is hypothesized to be the primary culprit. Given the complexity of NMS, it is also hypothesized that other neurotransmitter systems involving γ-aminobutyric acid (GABA), serotonin, and glutamate have a contributing role in initiation and progression of NMS.

5 What are the diagnostic criteria for NMS?

The diagnosis of NMS is a clinical diagnosis of exclusion in which the administration of an antipsychotic medication has occurred (usually 24-72 hours) before the onset of the syndrome.

Research criteria in the American Psychiatric Association’s Diagnostic and Statistical Manual, fourth edition (DSM-IV-TR), include the following:

A. The development of severe muscle rigidity and elevated temperature associated with the use of neuroleptic medication.

B. Two or more of the following: diaphoresis, dysphagia, tremor, incontinence, changes in level of consciousness ranging from confusion to coma, mutism, tachycardia, elevated or labile blood pressure, leukocytosis, and laboratory evidence of muscle injury.

C. The symptoms in criteria A and B are not due to another substance or a neurologic or other general medical condition.

D. The symptoms in criteria A and B are not better accounted for by a mental disorder.

6 What is the differential diagnosis of NMS?

NMS is a clinical diagnosis of exclusion; therefore central, systemic, and toxic causes of hyperthermia, rigidity, rhabdomyolysis, and altered mental status must be excluded. See Box 82-2.

7 Are there specific laboratory findings for NMS?

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