Coma before and Following Status Epilepticus
Abstract number :
2.132
Submission category :
Year :
2001
Submission ID :
2196
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
L.K. Garnett, RN, MSHA, Neurology, Virginia Commonwealth University, Richmond, VA; L.D. Morton, M.D., Neurology, Virginia Commonwealth University, Richmond, VA; A.R. Towne, M.D., Neurology, Virginia Commonwealth University, Richmond, VA; E.J. Waterhouse,
RATIONALE: To explore the occurence of coma prior to and following Status Epilepticus (SE), and to examine the relationships between coma, SE etiology and outcome.
METHODS: Data was obtained from the NIH Greater Richmond Metropolitan Area Status Epilepticus Database. Cases were divided into three groups: patients with Glasgow Coma scores consistent with coma prior to SE (coma prior); patients who had no post-ictal coma after SE (no coma); and patients who had a post-ictal coma after SE (post SE coma). Coma duration, SE etiologies and outcome were examined; there were multiple etiologies for some cases.
RESULTS: A total of 972 cases were included in this study. There were 109 adult and 58 pediatric cases in the coma prior group (n=167, or 17%), 86 adult and 35 pediatric cases in the no coma group (n=121 or 13%), and 491 adult and 193 pediatric cases in the post SE coma group (n=684, or 70%). Pediatric mortality was 10.3% in the coma prior group, 5.7% in the no coma group, and 5% in the post SE coma group. Adult mortality was 65% in the coma prior group, 16.3% in the no coma group (of these, 4 cases died during SE and were excluded from further analysis), and 26.5% in the post SE coma group. Mortality for the coma prior group was 46%, and by etiology within this group was 26.6% for CNS acute, 37.2% Hypoxia/anoxia, 29.5% for NonCNS acute, 5.7% for Remote and 1% for Withdraw. Mortality in the no coma group was 8%, and by etiology within this group was 61.5% for CNS acute, 7.7% for Hypoxia/anoxia, 15.4% for NonCNS acute, 15.4% for Remote and 0% for Withdraw. Mortality in the post SE coma group was 20.5%, and by etiology within this group was 37.3% for CNS acute, 26.4% for Hypoxia/anoxia, 16.1% for NonCNS acute, 9.8% for Remote, 9.4% for Withdraw, and 1% Other. Length of coma in relation to age groups, mortality and etiolgy will be presented.
CONCLUSIONS: Presence of coma prior to the onset of SE was associated with the highest mortality rate (65% in adult and 10.3% in pediatric cases). Absence of coma was associated with the lowest mortality overall (16.3% in adult and 5.7% in pediatric cases). Coma following SE represented the largest group and overall had an intermediate mortality (26.5% in adult and 5% in pediatric cases). In all cases, mortality was higher in the adult population. In all coma categories, mortality tended to be highest in the CNS acute, Hypoxia/anoxia and NonCNS acute etiology categories. Patients in coma prior to SE represent a particularly vulnerable population with the highest mortality; further studies are necessary to ellucidate the relationship between coma and mortality.
Support: NIH P50NS25630.