Abstracts

Rationale: The propofol infusion syndrome (PRIS) is known to be found in status epilepticus (SE) patient treated with propofol. PRIS is defined as a syndrome which has more than one feature such as metabolic acidosis, cardiac dysfunction, rhabdomyolysis, lipidemia, hepatic dysfunction, death, arrhythmia, or renal dysfunction. But there is still controversy whether PRIS is caused by propofol itself or by status epileptics per se. Our aim is to investigate whether propofol treatment may change the course of SE and cause the features of PRIS in SE. Methods: We enrolled 32 patients who were diagnosed as SE from Jan 2005 to Jan 2009. After dividing them into SE group with propofol (SE , N=13) and SE without propofol (SE-, N=19) we analyzed and compared the demographic factors, previous medical history, seizure semiology, etiology of SE, the kinds and dosage of antiepileptic drug, duration of hospital stay, neurologic status at discharge, and clinical components of PRIS between two groups. Results: In SE group (mean age 29.9 13.4 yrs), mean dosage of propofol was 77.2 63.3 mg as bolus, mean infusion rate was 4.9 3.0 mg/kg/hr, and the peak infusion rate was 7.3 4.8 mg/kg/hr. Mean duration of propofol infusion was 153.3 151.6 hours. Among them, 12 patients (92%) could be diagnosed as PRIS: hypotension was found in 12, dyslipidemia in 3, and metabolic acidosis in 4, cardiac dysfunction in 4, rhabdomyolysis in 6, hepatic dysfunction in 6, death in 5, cardiac arrhythmia in 5, and renal dysfunction in 3 patients. However, there was no significant difference in the frequency of acidosis, cardiac dysfunction, rhabdomyolysis, hepatic dysfunction, dyslipidemia, death, arrhythmia, and renal dysfunction, the duration of hospital days, and the seizure outcome between SE and SE-. The incidence of hypotension or dyslipidemia was definitely higher in SE group, but that did not influence on the overall prognosis of SE. Conclusions: Propofol treatment frequently caused hypotension and dyslipidemia in patients with SE, which were components of PRIS. However, the incidence of PRIS was not related to propofol dosage/infusion rate but to SE itself. Our findings suggest that the presence of PRIS did not influence of the prognosis of SE.