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CASE REPORTS
JOURNAL ARTICLE
REVIEW
Bowel Ischemia in Refractory Status Epilepticus: Report of Two Cases and Review of the Literature.
Neurocritical Care 2016 Februrary
BACKGROUND: Bowel ischemia is a rare life threatening complication seen in patients with refractory status epilepticus (RSE). The few reported cases of bowel ischemia in this setting have been associated with the use continuous barbiturate infusions. We report two patients with RSE in the absence of barbiturate infusion and without clear structural, infectious, anatomic, vascular, or autoimmune etiology. We review the clinical details of the cases and potential factors involved in the development of non-occlusive bowel ischemia in patients with RSE.
METHODS: The following is a retrospective review of two cases of non-occlusive mesenteric ischemia that occurred during the management of RSE. The clinical data and the details of pathological examination of the infarcted segments of bowel are presented in both cases.
RESULTS: In both cases, the bowel ischemia occurred in the absence of barbiturate infusion or evidence of clear thrombosis, infection, or autoimmune etiology. Case 1 had extensive ischemic necrosis of the small bowel with secondary pseudomembrane formation, and case 2 had full thickness infarction of both the large and small bowel.
CONCLUSIONS: The mechanism of bowel infarction in these cases is likely multifactorial and was not associated with barbiturate use. Likely contributors to ischemia include RSE itself, systemic hypotension, vasopressor use, general anesthesia, and abnormal cardiac function. During the management of RSE, every effort must be made to avoid the secondary complications such as bowel ischemia.
METHODS: The following is a retrospective review of two cases of non-occlusive mesenteric ischemia that occurred during the management of RSE. The clinical data and the details of pathological examination of the infarcted segments of bowel are presented in both cases.
RESULTS: In both cases, the bowel ischemia occurred in the absence of barbiturate infusion or evidence of clear thrombosis, infection, or autoimmune etiology. Case 1 had extensive ischemic necrosis of the small bowel with secondary pseudomembrane formation, and case 2 had full thickness infarction of both the large and small bowel.
CONCLUSIONS: The mechanism of bowel infarction in these cases is likely multifactorial and was not associated with barbiturate use. Likely contributors to ischemia include RSE itself, systemic hypotension, vasopressor use, general anesthesia, and abnormal cardiac function. During the management of RSE, every effort must be made to avoid the secondary complications such as bowel ischemia.
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