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Midazolam coma for refractory status epilepticus in children
J Igartua1, P Silver, J Maytal
1Division of Critical Care Medicine, Schneider Children's Hospital, Long Island Jewish Medical Center, New Hyde Park, NY 11040, USA.
Insights
This study shows that a midazolam coma algorithm effectively treats refractory status epilepticus. The treatment is safe, with no cardiovascular instability observed, and often stops seizures before burst suppression is achieved on EEG.
Area of Science:
- Neurology
- Critical Care Medicine
- Pharmacology
Background:
- Refractory status epilepticus (RSE) is a life-threatening neurological emergency.
- Current treatment options for RSE can be limited and associated with significant side effects.
- Midazolam coma is a recognized treatment for RSE, but a standardized algorithm is needed.
Purpose of the Study:
- To implement and retrospectively evaluate a therapeutic algorithm for treating refractory status epilepticus using a midazolam-induced coma.
- To assess the efficacy and safety of this algorithm in a cohort of patients with RSE.
Main Methods:
- Eight consecutive patients with RSE were mechanically ventilated and continuously monitored via invasive arterial/central venous pressure and 16-channel video electroencephalogram (EEG).
- A standardized algorithm involving midazolam bolus and titration of continuous infusion was applied.
- Seizure cessation and/or EEG burst suppression determined the treatment endpoint and subsequent weaning protocol.
Main Results:
- The algorithm successfully terminated seizures in seven out of eight patients.
- Maximal midazolam doses ranged from 4-24 microg/kg/min (mean 14 +/- 6 microg/kg/min).
- Patients maintained stable cardiovascular function without requiring inotropic support, even at doses achieving burst suppression.
Conclusions:
- The described midazolam infusion algorithm is effective for terminating refractory status epilepticus.
- This therapeutic approach is not associated with cardiovascular instability.
- Seizure cessation is frequently achieved prior to reaching EEG burst suppression.
Objective:
To implement and retrospectively evaluate a therapeutic algorithm 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 patients were also continuously monitored by a 16-channel video electroencephalogram (EEG). A midazolam bolus of 0.15 mg/kg was administered, and a continuous infusion of 1-2 microg/kg/min was started. If seizures continued, the infusion was increased every 15 mins by 1-2 microg/kg/min. If seizures stopped and/or burst suppression was achieved, the patients continued to receive that dose for 48 hrs and were then weaned by decrements of 1-2 microg/kg/min every 15 mins.
Results:
The patients' ages ranged from 17 days to 16 yrs, and they had various underlying diseases. In five of the eight patients, cessation of seizures occurred before achieving burst suppression on EEG, in two patients, cessation occurred during burst suppression, and in one patient, no response before or during burst suppression was encountered. The maximal midazolam doses required to achieve cessation of seizures and/or burst suppression, whichever came first, ranged from 4-24 microg/kg/min, with a mean of 14 +/- 6 microg/kg/min. The patients maintained stable cardiovascular function while receiving the maximal dose of midazolam and did not require inotropic support.
Conclusion:
Midazolam infusion, as per our described algorithm, is effective in terminating refractory status epilepticus. This treatment is not associated with cardiovascular instability, even at doses resulting in burst suppression. In the majority of cases, cessation of seizures occur before burst suppression is achieved on EEG.