Despite recent advances in the treatment of status epilepticus (SE), the mortality and morbidity associated with this condition remains high. Although the reasons for this excessive mortality are not known, several factors are suspected, including cerebral ischemia, cardiovascular collapse, toxic stimulation by neurotransmitters and hormones, or toxic products of intermediary metabolism. Cerebral lactic acidosis can cause cortical injury and has been shown to occur with seizures in experimental animals and in a limited number of human studies. We determined cerebrospinal fluid (CSF) and plasma lactate in 29 patients with generalized SE of diverse etiology. CSF was obtained within 12 h of termination of clinical seizure activity. The mean CSF lactate for all SE patients was elevated (3.74 +/- 0.31 mM) as compared with that of normal controls (1.60 +/- 0.10 mM) from non-neurologic patients undergoing spinal anesthesia. In patients who died or had a poor neurologic recovery, CSF lactate level was 5.36 +/- 0.58 mM (9 patients), whereas in 20 patients who showed good recovery CSF lactate level was 3.01 +/- 0.22 mM (p less than 0.005). The results demonstrate that SE causes a significant increase in CSF lactate and suggest that the magnitude of lactate elevation may serve as a predictive indicator of morbidity and mortality.
Twenty-five patients with traumatic spinal cord injuries above T7 have been managed with low spinal anesthesia during endoscopic urologic procedures. The technique has been completely successful in preventing autonomic dysreflexia and has not been associated with hypotension.
Patients with high spinal cord injuries frequently will develop a syndrome of autonomic hyperreflexia when stimulated by urological instrumentation. Severe sustained hypertension is the most hazardous component encountered during this reaction. Herein we report a series of patients exhibiting this condition who were managed safely and successfully by the use of the ganglionic blocking agent, pentolinium.
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