LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES Anesthetic Barbiturates in Refractory Status Epilepticus G.B. YOUNG, W.T. BLUME, C.F. BOLTON and K.G. WARREN SUMMARY: Two patients with previous INTRODUCTION hours). With intubation and respiratory cerebral damage and seizures and three Generalized status epilepticus is a support an intravenous bolus of 250 mgms. patients with acute inflammatory cerebral medical emergency requiring prompt thiopental was given, followed by 80-120 lesions developed status epilepticus. They mgm/hr. as a continuous infusion for four treatment to prevent cerebral damage days. The seizures stopped promptly. A were unresponsive to standard anticon­ or death. Rapidly acting anticonvuls­ vulsants, but anesthetic barbiturates right-sided hemiparesis resolved over the (thiopental and pentobarbital) stopped the ants such as diazepam, phenytoin or next week and he returned home without seizures promptly. paraldehyde are usually effective. additional neurologicaldeficit. Neurology texts, review articles and Case J. A 41 year old woman developed monographs on epilepsy occasionally measles a week prior to the onset of mention anesthesia for resistant cases. delirium and convulsions. Multi-focal RESUME: Deux patients souffrant pre- Anesthetic barbiturates are less com­ clonic or grand mal seizures continued for alablement de lesion cerebrate et d'epilepsie two days. These were refractory to et trois patients avec lesions cerebrates de monly specified and their effectiveness is not well documented. We present intravenous phenytoin (a loading dose of nature . inflammatoire aigue developpent 1000 mgm intravenously followed by 200 un status epilepticus. Les patients ne five cases successfully treated with mgm every twelve hours), phenobarbital repondent pas a la medication anticon­ anesthetic barbiturates after conven­ (200 mgm intravenous bolus and 60 mgm vulsive standard mais I'emploi de barbitur- tional anticonvulsants failed. every 6 hours), intravenous diazepam and iques anesthesiques (thiopental et pento­ rectal paraldehyde. Under respiratory barbital) s'avera d'un secours rapide. support intravenous pentobarbital infused CLINICAL MATERIAL at 100-150 mgms/hr. promptly stopped the Case /. A 19 year old girl with a seizures. Reduced dosage was associated congenital right hemiplegia and previous with recurrence of seizures and overall nine left hemispherectomy had a seizure disorder days of pentobarbital were required. She since age two years. A flurry of seizures recovered consciousness two days after occurred while she was toxic on phenytoin stopping the drug but showed a memory (serum level 50 meg/ ml. She had frequent deficit. This resolved completely over six grand mal seizures for five days becoming weeks but she has sporadic grand mal continuous for three hours. They failed to seizures. respond to repeated intravenous doses of Case 4. A 24 year old male developed a diazepam and phenobarbital, a reduced febrile illness with generalized and multi­ maintenance dose of phenytoin or rectal focal seizures. Herpes zoster was isolated paraldehyde. from a left temporal lobe biopsy. Seizures Artificial ventilation was used while she persisted for six days without intervening received pentobarbital 100-140 mgm/hr. consciousness. They were uncontrolled by intravenously. Seizures stopped instantly, intravenous phenytoin, phenobarbital, but when pentobarbital was discontinued diazepam and clonazepam; valproic acid two days later grand mal seizures returned. via nasogastric tube and rectal paraldehyde. Three more days of pentobarbital anesthesia With ventilatory assistance thiopental were required. She recovered conscious­ anesthesia controlled the attacks. Thirteen ness two days later and returning to her days of anesthesia were required. He previous state, was discharged home. recovered completely and had no neuro­ Case 2. A 62 year old man had meningitis logical deficits. twenty years ago with resulting mild Case 5. A 21 year old woman developed aphasia and recurrent right-sided and general malaise and fever followed one generalized convulsions. Continuous con­ week later by multi-focal and generalized Reprint requests to Dr. G.B. Young, University vulsions occurred four days prior to convulsions. Cerebrospinal fluid (CSF) Hospital, Saskatoon, Saskatchewan S7N 0X0 Canada. transfer to our unit, when serum phenytoin contained lymphocytic pleocytosis with From the University of Saskatchewan (Dr. Young), was 16.2 ugm/ ml. Seizures did not respond normal protein and glucose. A specific the University of Western Ontario (Drs. Blume and to intravenous phenobarbital (500 mgm. in viral or other agent was not identified Bolton) and the University of Alberta (Dr. Warren). 12 hours), diazepam (repeated 10 to 20 serologically or by CSF culture. Phenytoin Presented at the XIV Congress of Neurological mgm. bolus doses) or rectal paraldehyde and phenobarbital intravenously and Sciences, Halifax, Nova Scotia. June 1979. (10 cc's with 10 cc's of mineral oil every four valproic acid by nasogastric tube failed to Vol. 7 No. 4 NOVEMBER 1980-291 Downloaded from https://www.cambridge.org/core. IP address: 170.106.202.126, on 25 Sep 2021 at 00:57:26, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0317167100022769 THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES control the seizures. Intravenous thiopental structures, even if the animals are CONCLUSIONS (30 mgm/kg bolus doses) controlled the paralyzed and adequately oxygenated. High dose anesthetic barbiturates seizures for the twelve days of its When status epilepticus is resistant to are effective in stopping generalized administration. She was left with impaired usually effective anticonvulsants we status epilepticus refractory to other intellect, ataxia and left hemiparesis. feel this risk outweighs the difficulties methods. Standard anticonvulsants The depth of anesthesia was assessed of anesthetic barbiturate administra­ should be tried first, in view of the electroencephalographically, clinically, and by serum barbiturate levels. A burst- tion. Early use of such drugs without necessity of ventilatory support and suppression electroencephalograph^ (EEG) intubation and ventilatory support the impairment of consciousness which pattern with a two to seven second was sometimes disastrous (Dundee occur with barbiturate anesthesia. The interburst interval stopped clinical and and Gray, 1967). With respiratory treatment may have to be continued electrographic seizures. The interburst support available in modern intensive for several days to prevent status interval was measured hourly in two care units, hazards are minimized. epilepticus from returning when the patients using a single channel (C, - 02 Neurological evaluation is difficult drug is stopped. This may apply derivation) at the bedside. Other patients with anesthesia but continued seizures especially to seizures due to inflam­ had standard recordings. The four patients treated with pentobarbital had twice daily confuse interpretation of clinical signs matory cerebral lesions. Skeletal muscle serum levels measured to help maintain a in the non-anesthetized patient. relaxants are not necessary when this serum barbiturate level of 2-4 mgm/dl as The anesthetic barbiturate pento­ treatment is used. suggested by Conn et al (1978) and barbital directly depresses neuronal Marshall et al (1975) in treating raised excitability by a gamma-amino butyric intracranial pressure. We found this level acid (GABA) mimetic action, an effect corresponded to a burst-suppression EEG not shown by phenobarbital, an anti­ pattern. Pupillary size was also helpful; in REFERENCES stages 3 and 4 of barbiturate anesthesia it convulsant, non-anesthetic barbiturate. ATKINSON, R.S., RUSHMAN, G.B. and returns to normal after constriction at Moreover, pentobarbital is more potent in augmenting GABA and LEE, A. (1977). Synopsis of Anesthesia, pp. lighter stages. (Atkinson, et al, 1977). 172-173. John Wright and Sons Publishers. Drugs given prior to anesthesia were decreasing glutamate responses Bristol. continued in maintenance doses by naso­ (Macdonald and Barber, 1979). These BLENNOW, G., BR1ERLEY, J.B., MELDRUM, gastric tube during anesthesia. Case 3, 4 properties of anesthetic barbiturates B.S. and SIESJO, B.K. (1978). Epileptic and 5 also received dexamethazone. Rectal likely account for their anesthetic brain damage: the role of systemic factors temperature dropped as low as 35.5°C. but action and also possibly for their that modify cerebral energy metabolism. controlled hypothermia was not instituted. potency against seizures. Brain 101: 687-700. All patients had ventilatory support but CONN, A.W., EDMONDS, J.F. and BARKER, Blennow et al (1978) suggest that B.A. (1978). Near drowning in cold water: none required skeletal muscle relaxants. brain damage due to seizures may be Muscle tone was flaccid, possibly because current treatment regimen. Canad. Anaesth. caused by the production of free Soc. J. 25: 259-265. of a depressant effect of anesthetic barbiturates on spinal motor neurons radicals with resultant lipid peroxida­ DEMOPOULOUS, H.B., FLAMMN, E.S., SEL1GMAN, M.L., JORGENSEN, E. and (Macdonald and Barber, 1979). tion and cell membrane or mito­ chondrial damage. Barbiturates may RANSHOFF, J. (1977). Antioxidant effects of barbiturates in model membranes under­ DISCUSSION decrease the suspectibility of these going free radical change. Acta Neurol. Our five cases with status epilepticus