Abstract
Neuroleptic malignant syndrome (NMS) is a potentially life threatening idiosyncratic reaction to the use of psychotropic medications. NMS has an incidence of 0.02–3% in patients in this population [1,2]. According to the DSM-IV, it is defined by severe muscle rigidity and elevated temperature as well as two or more other criteria [3]. Early identification plays a significant role in preventing significant morbidity and mortality. There are various recognized risk factors in developing NMS, including psychomotor agitation, prior occurrence of NMS and rapid antipsychotic titration or switching. Concomitant lithium use has also been implicated [4,5].
We are reporting a patient who presented with NMS during the course of her treatment and we intend to identify potential risk factors in this case.
A 31year old woman was admitted to our acute inpatient ward with mania in the context of 6 months of medication non-compliance on a background of bipolar disorder. This episode was characterized by religious delusions, disorganization, poor sleep, pressured speech, poor insight and judgement. She had a previous episode of NMS with risperidone one year prior.
She was started on lithium (450 mg bd) and quetiapine (600 mg daily). However, there was a significant prolongation of her QTc interval to 486 ms (baseline 420 ms), thus the quetiapine was ceased. Amisulpride was commenced with rapid dose escalation from 200 mg bd to 400 mg bd over three days. She was physically well, with no medication side effects, and was sent on weekend leave.
Whilst on leave she deteriorated physically, with mild confusion, tremor and blurred vision. She returned to the ward where on review she was diaphoretic, febrile, weak and mildly confused. She had significant muscle rigidity. Her vital signs were otherwise within normal limits.
Her White Cell Count (WCC) was 10.0 and Creatine Kinase (CK) was 924. QTc was 500 ms. A diagnosis of NMS was made, differentials at the time included lithium toxicity and infection. Lithium toxicity was excluded (level 0.5). We rapidly commenced stabilization measures including bromocriptine 2.5 mg tds and IV hydration. She was transferred for ongoing management to the medical ward where she improved over several days with improved CK (151) and mental state. She was started on sodium valproate monotherapy and discharged home.
There were several risk factors in this patient that are known to contribute to NMS, including switching of antipsychotic medications, rapid escalation of doses and the concomitant use of lithium. Rapid diagnosis and appropriate treatment in this case prevented the syndrome from progressing further.
This case highlights both the importance of being cautious in commencing antipsychotic medications in patients with a known history of NMS, and in being aware of its presence as a potential complication.