Status Epilepticus

Figure 77.1. EEG burst suppression pattern (HF 70 Hz, LF 1 Hz SEN 5 μV/mm) [54].

Burst suppression pattern is used as a clinical tool to avoid over-medicating when the neurologic exam is obliterated by anesthetic medications. This EEG pattern has often been suggested as a goal for therapy in refractory SE, but achieving burst-suppression is neither necessary nor sufficient for the control of SE. Therefore, the goal should be seizure suppression; this is usually maintained for 12 to 24 hours, and then decreased by some arbitrary degree, such as 50%, for several hours while observing for seizure recurrence. Simultaneously, an anticonvulsant or an appropriate combination is added, with the goal of maintaining a seizure free state once barbiturate is cleared. Continuous EEG monitoring is required during this weaning process, as recurrence of seizure activity prompts a return to the previous dose with adjustments in doses or types of the other anticonvulsants [21].

Figure 77.2. Management of status epilepticus.

Midazolam infusion in the setting of refractory SE offers a favorable pharmacokinetic profile [40]. One small study showed rapid control of seizure that had failed multiple medications, including diazepam, lorazepam, phenytoin, with or without phenobarbital, with minimal hypotension [41]. In critically ill patients, midazolam can accumulate, especially as increasingly higher doses of midazolam are usually required to maintain burst suppression. Some studies have shown that there may be lower mortality in a select group of patients treated with a midazolam infusion compared to those treated with a propofol infusion [42].

Propofol has a very short half life in comparison to the alternatives discussed for refractory SE treatment. Additionally it is highly lipid soluble and therefore fast acting in CNS. Several studies and reviews have demonstrated its effectiveness in treating refractory GCSE and NCSE [43-46]. Some recent studies have suggested an increased mortality associated with propofol infusion [41], but others have not supported this trend when compared to pentobarbital or midalozam at anesthetic doses for the treatment of SE [46]. Care must be taken to not discontinue propofol abruptly, as this may be associated with recurrent seizures. Hypotension is more common with propofol than with midazolam. Triglyceride levels must be monitored during prolonged infusion as development of hypertriglyceridemia may prompt discontinuation of propofol infusion. The clinician should observe carefully for development of the the propofol infusion syndrome, which may manifest as either a metabolic acidosis or rhabdomyolysis. If either of these occur, propofol should be discontinued and another agent substituted.

77.7 Conclusions

In the ICU, mortality associated with SE is high, and irreversible brain damage ensues quickly. The detection and diagnosis of SE, along with identification of its etiology, is crucial for clinicians at all stages of this condition, as the goal must be termination of seizure as soon as possible. A systematic yet aggressive approach to the treatment of SE is recommended. The clinician must be prepared to escalate rapidly to more potent anesthetic medications while providing basic life support measures, until either clinical or electrographic end of seizure is apparent.

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