Abstracts

Rationale: Refractory status epilepticus (RSE) is commonly encountered in tertiary care settings, requiring intubation, anticonvulsant drips, and EEG monitoring. RSE is defined as SE unresponsive to two standard anticonvulsant medications. Some of these patients that present with SE have a negative seizure history. Goal is immediate cessation of seizures, and prevention of breakthrough seizures. Previous studies have focused on the management of RSE with continuous infusion of midazolam, propofol, or pentobarbital. There is scant data, however, on clinical neurological examination of patients in burst suppression, as most of the neurological examination is obscured by these medications. Andrefsky et al examined six patients on pentobarbital drip and found that ciliospinal reflex can be elicited in patients with reactive or unreactive pupils (J. Neurosurg 90:644-646, 1999). We wanted to determine the effect of pentobarbital on pupillary size and reactivity as we obseved a patient with pentobarbital induced coma and reversible pupillary changes. Methods: We studied eight consecutive patients who were placed in burst suppression from July, 2007 through April, 2008. All patients were directly examined, treated, and monitored with continuous EEG .Patient age ranged from three to 85. Six patients were treated for RSE; four patients had convulsive and nonconvulsive status epilepticus, while two had exclusively nonconvulsive status epilepticus. The etiology of refractory status epilepticus included stroke), encephalitis, tumor, and CNS degenerative disease . Two patients were placed in burst suppression for elevated intracranial pressure. All patients were placed in burst suppression or complete suppression. Six patients were treated with iv pentobarbital with or without midazolam, propofol, or fentanyl. Two patients were treated with propofol only. All patients also received routine anticonvulsant medications. Results: During burst suppression or complete suppression, 5/6 patients treated with pentobarbital demonstrated fixed, unreactive pupils at some point during their coma. Two patients who were in burst suppression with propofol alone had reactive pupils. Ancillary tests including funduscopic exam, radiological imaging, intracranial pressure monitoring demonstrated that the patients with fixed, unreactive pupils did not have cerebral herniation or elevated intracranial pressure to explain the pupillary findings. Conclusions: Pentobarbital may cause pupils to be fixed when patients are in burst suppression. This finding is not necessarily related to pentobarbital dosage or the underlying etiology of the status epilepticus. Upon pentobarbital withdrawl, the pupillary changes reverse. This finding has not been specifically described. When fixed, unreactive pupils are encountered in drug induced burst suppression ,pentobarbital induced pupillary changes should be considered. In the future, a multicenter trial of patients with pentobarbital induced burst suppression utilizing sophisticated infrared video pupillometry would be helpful in confirming our findings.