Midazolam coma for refractory status epilepticus in children

Objective: To implement and retrospectively evaluate a therapeutic algorith m for the treatment of refractory status epilepticus with midazolam coma. Methods: Eight consecutive patients with refractory status epilepticus were mechanically ventilated. Their arterial and central venous blood pressures were continuously monitored by indwelling vascular catheters, These patien ts were also continuously monitored by a 16-channel video electroencephalog ram (EEG), A midazolam bolus of 0.15 mg/kg was administered, and a continuo us infusion of 1-2 mu g/kg/min was started. If seizures continued, the infu sion was increased every 15 mins by 1-2 mu g/kg/min. If seizures stopped an d/or burst suppression was achieved, the patients continued to receive that dose for 48 hrs and were then weaned by decrements of 1-2 mu g/kg/min ever y 15 mins. Results: The patients' ages ranged from 17 days to 16 yrs, and they had var ious underlying diseases. In five of the eight patients, cessation of seizu res occurred before achieving burst suppression on EEG, in two patients, ce ssation occurred during burst suppression, and in one patient, no response before or during burst suppression was encountered, The maximal midazolam d oses required to achieve cessation of seizures and/or burst suppression, wh ichever came first, ranged from 4-24 mu g/kg/min, with a mean of 14 +/- 6 m u g/kg/min. The patients maintained stable cardiovascular function while re ceiving the maximal dose of midazolam and did not require inotropic support . Conclusion: Midazolam infusion, as per our described algorithm, is effectiv e in terminating refractory status epilepticus. This treatment is not assoc iated with cardiovascular instability, even at doses resulting in burst sup pression. In the majority of cases, cessation of seizures occur before burs t suppression is achieved on EEG.