Case report
A 62-year-old man with no history of psychiatric or neurological problems came to hospital after 3 days of severe abdominal pain and constipation. Diagnosed with acute abdomen secondary to acute appendicitis perforation, he underwent an emergency operation anesthetized with sevoflurane, propofol, succinylcholine chloride and cis-atracurium. On the fourth day after, he began to show symptoms of delirium and agitation. He was given haloperidol (3 mg orally and then a 5-mg ampoule intramuscularly), with good results. Within a few hours he was mildly lethargic but confused, responding to verbal stimuli but not answering questions appropriately. He had diffuse rigidity. His baseline temperature climbed to 38°C and he developed persistent hypertension (180/100 mmHg), tachypnea (24 breaths/min) and tachycardia (110–140 beats/min). Neurological and physical examinations revealed no source of infection or intracranial pathology; results of cranial CT were normal. His leukocyte count rose from 11.4/mm3 to 14.2 (normal range 3.6–9.6/mm3), and other serum concentrations were high: creatinine phosphate 335 (normal 24–195) U/L, alanine aminotransferase 78 (normal 1–42) U/L and aspartate aminotransferase 64 (normal 1–37) U/L. Serum electrolyte results were normal.
We entertained a diagnosis of neuroleptic malignant syndrome (NMS) and administered bromocriptine (15 mg/d for 15 days). The patient’s confusion resolved, and his vital signs returned to normal.
Discussion
The cause of NMS is unknown. It is attributed by some to a primary dopamine-receptor blockade in the basal ganglia and hypothalamus, and to a disturbance of calcium uptake in skeletal muscle by others.1 The disease may be caused by a spectrum of inherited defects in genes responsible for a variety of calcium regulatory proteins within sympathetic neurons or the higher-order assemblies that regulate them.2
The clinical picture in NMS includes muscular rigidity, altered mental status and severe autonomic dysfunctions. It is associated with hyperthermia, elevated levels of plasma creatinine phosphate and leukocytosis.3
In recent years, there has been an increased awareness of the occurrence of NMS in surgical patients.1,4–6 Its causative factors include an interruption or alteration of the administration of neuroleptic drugs, the added use of narcotics, and physical stress such as infection, dehydration, malnutrition and tissue injury.4
In emergency surgical patients whose condition is associated with severe tissue injury and infection, NMS symptoms are easily attributed to a surgical complication when these patients had no psychiatric or neurological history. We recommend that surgeons bear the possibility of NMS in mind.
Footnotes
Competing interests: None declared.
- Accepted November 17, 2003.