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Medline ® Abstract for Reference 89

of 'Convulsive status epilepticus in adults: Treatment and prognosis'

89
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Refractory status epilepticus: effect of treatment aggressiveness on prognosis.
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Rossetti AO, Logroscino G, Bromfield EB
SO
Arch Neurol. 2005;62(11):1698.
 
BACKGROUND: Administration of antiepileptic drugs for coma induction in refractory status epilepticus (RSE) has not been widely studied. Moreover, the effect on outcome of electroencephalographic (EEG) burst suppression remains unclear.
OBJECTIVE: To investigate whether various coma-inducing options are associated with different prognoses after RSE.
DESIGN: Retrospectively assessed case series.
SETTING: Two tertiary referral hospitals in Boston, Mass.
PATIENTS: Among 127 consecutive episodes (107 patients) of status epilepticus, we identified episodes that were refractory to first-line and second-line antiepileptic drugs, needing induced coma with barbiturates, propofol, or midazolam for clinical management.
MAIN OUTCOME MEASURES: Short-term mortality and prevalence of return to functional baseline after the acute episode of status epilepticus were analyzed in relation to demographic and clinical variables and to treatment option (antiepileptic agents and EEG burst suppression).
RESULTS: Forty-nine episodes of RSE (47 patients) were found, occurring more frequently in incident than in recurrent episodes of status epilepticus (P = .06). Mortality was 23% for patients with RSE and 8% for those without RSE (P = .05). Return to baseline occurred more often in the non-RSE group (P = .04). In 20 (61%) of 33 monitored episodes, EEG burst suppression was achieved. Demographic data, clinical variables, and outcome did not differ significantly with the various coma-inducing agents or between episodes with and without EEG burst suppression.
CONCLUSIONS: Refractory status epilepticus is more prevalent in incident than in recurrent status epilepticus and is associated with higher mortality; clinical status is less likely to return to baseline than with non-RSE. Outcome was independent of the specific coma-inducing agents used and the extent of EEG burst suppression, suggesting that the underlying cause represents its main determinant.
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Department of Neurology, Division of Epilepsy and EEG, Brigham&Women's Hospital, Harvard Medical School, Boston, Mass 02115, USA.
PMID