Neuroleptic Malignant Syndrome: Severe Hyperthermia Treated with Endovascular Cooling

Abstract

A 30-year-old man with a long-standing psychotic disorder treated with olanzapine, diazepam and lofepramine was admitted to hospital after being found collapsed at home. There was some evidence of head trauma possibly related to falling out of bed. His mother reported that he was normally withdrawn but had not demonstrated any recent change in behaviour or shown signs of physical illness. There had been no recent changes to his medication.He presented to the emergency department with a reduced level of consciousness and a Glasgow Coma Score (GCS) of 6 (E4, V1, M1). However, he seemed aware of his environment despite a lack of speech and motor response. Pupils were normal size and reactive. On physical examination, he was pyrexial with an axillary temperature of 40°C. His muscle tone and reflexes were normal. He was tachycardic with a pulse of 110 beats per minute (bpm), and normotensive.Salient laboratory results were: serum glucose 78 mmol/L, white cell count 15 x 10 9 /L, creatinine 279 μmol/L, CRP 11 mg/L, corrected (for glucose) serum sodium 166 mmol/L and creatine kinase 4,000 IU/L. Urinalysis was positive for glucose and protein but negative for ketones. A venous blood gas showed a normal pH with lactate of 2.7 mmol/L.The initial diagnosis in the emergency department was recorded as collapse secondary to diabetic ketoacidosis (DKA) and possible head injury. Cerebral infection was also considered and ceftriaxone plus acyclovir were started. He was resuscitated with an infusion of normal saline and insulin commenced at 6 IU/h. A CT scan of the brain was normal. He was transferred to the acute medical admissions unit without referral to critical care. Over the next 10 hours, his serum glucose concentration fell from 78 to 34 mmol/L and the corrected serum sodium rose from 164 to 175 mmol/L.His raised serum osmolality (400 mosm/L) and abnormal electrolytes were subsequently managed with appropriate fluid resuscitation.A consultant physician reviewed him at this time (11 hours post admission) and considered hyperosmolar hyperglycaemic non-ketotic state to be more likely than DKA. He also raised the possibility of neuroleptic malignant syndrome (NMS) and referred the patient to critical care.At review by the critical care team, he was noted to have a sinus tachycardia of 150 beats per minute and persistent pyrexia of 39.2°C. His GCS had improved to 11 (E 4, M 6, V 1) and he was moving limbs occasionally to command. The plantar reflexes were normal and muscle tone was not increased. There was no evidence of a compartment syndrome. He was transferred urgently to the intensive care unit (ICU) where he was resuscitated with cold intravenous fluids and surface cooling. Further blood tests revealed a significantly elevated creatine kinase at 14,570 IU/L, evidence of hepatic injury (AST peaked at 2,000 IU/L) and deranged clotting studies (INR 2.0, APTR 3.3). A 12-lead ECG confirmed a sinus tachycardia with no QT prolongation. The diagnosis at this stage remained uncertain, but acute drug poisoning by agents known to ca...

Atypical neuroleptic malignant syndrome. “Doing more harm than gain”

“…Every class of neuroleptic drugs has been implicated, including the newer 'atypical' antipsychotics. 1 A number of diagnostic criteria are currently in use, however there is no consensus of opinion and fever, muscle rigidity and altered level of consciousness are the most common and classical features of this syndrome. 2 When the above typical features are lacking , the patients may be treated for an exacerbation of a their primary psychiatric disorder, suspected neurological infections or adverse drug effects hence delaying the diagnosis of a rare but life threatening condition.…”