CASE REPORT chloral hydrate, status epilepticus
Chloral Hydrate in Intractable Status Epilepticus Five adult patients were admitted to the neurological department in a state of status epilepticus. All were treated unsuccessfully with IV diazepam and diphenylhydantoin. Administration of sodium valporate or phenobarbital also was ineffective. However, after treatment with intrarectal chloral hydrate, all seizures ceased. The excellent effect of this drug was proved both clinically and electrodiagnostically. Discussed is the possibility of using chloral hydrate to treat patients with status epilepticus in whom conventional treatment has failed. Lampl Y, Eshel Y, Gilad R, Sarova-Pinchas I: Chloral hydrate in intractable status epilepticus. Ann Emerg Med June 1990;19:674-676.] INTRODUCTION Chloral hydrate is a hypnotic drug often used clinically for sedation and sleep induction. Only a few reports, however, have described its use in treating status epilepticus in adults1, 2 and children. 3 Five patients suffering from status epilepticus were treated with chloral hydrate intrarectally after treatment with conventional medications had failed.
Yair Lampl, MD Yechiel Eshel, MD, MSc Ronit Gilad, MD Ida Sarova-Pinchas, MD Holon and Tel Aviv, Israel From the Department of Neurology, Edith Wolfson Medical Center, Holon, israel; and the Tel Aviv University Sackler Faculty of Medicine, Tel Aviv, Israel. Received for publication July 6, 1989. Revision received January 10, 1990. Accepted for publication January 30, 1990. Address for reprints: Yair Lampl, MD, Department of Neurology, Edith Wolfson Medical Center, Holon, Israel.
PATIENTS AND METHODS Five patients (four men and one woman aged 22 to 68 years) were hospitalized in a state of status epilepticus. The patients had five to 12 seizures within 30 minutes without returning to a normal alert state between the attacks. Patients' blood pressures ranged from 110/80 m m Hg to 185/100 m m Hg, and pulses ranged from 72 to 112. All five had spontaneous respirations at a rate of 12 to 38. Each patient was treated with 20 mg diazepam IV at a rate of 2 rag/rain combined with 20 mg/kg diphenylhydantoin at a rate that did not exceed 50 mg/min. The treatment failed in all cases. Thirty to 35 minutes after this treatment, three of the patients (2, 3, and 5) received an IV drip (5% glucose solution with 100 mg diazepam/500 mL) at 8 mg/hr. Two other patients (1 and 4) were given 20 mg/kg phenobarbital IV. Neither of the treatments stopped the seizures or reduced the number of convulsions. Diphenylhydantoin serum level was within effective range in each patient (Table). In two patients, a dose of 20 mg/kg intrarectal valporate proved unsuccessful. Four of the patients had been on anticonvulsive medication before admission (Table). In one patient (3), the treatment was discontinued a week before his admission. Another patient (2) had never suffered from any epileptic attacks before the present incident and had therefore not been treated. Comprehensive blood tests were carried out in all patients during their hospitalization. Lumbar puncture was done in four of five patients (1 through 4). No evidence of infectious disease of the central nervous system or subarachnoid hemorrhage was found. In patient 5, lumbar puncture was not done because a space-occupying lesion with a massive mass effect was found by computed tomography (CT). Repeated CT scan of the brain in all patients during the hospitalization demonstrated brain infarcts in two (1 and 2). The cerebral lesions were found in the right frontoparietal and temporal areas. In one patient (5),
19:6 June 1990
Annals of Emergency Medicine
674/91
CHLORAL HYDRATE Lampl et al
TABLE. Clinical patient characteristics
Patient No./ Age (yr)
Previous Diseases
1/62
2/57
Recurrent cerebrovascular accident
3/52
4/22
5/69
Tumor of lung with brain metastasis
Present Medical Treatment
Diazepam, DPH, phenobarbital, chloral hydrate Diazepam, DPH, sodium valporate, chloral hydrate Diazepam, DPH, sodium valporate Diazepam, DPH, phenobarbital chloral hydrate Diazepam, DPH, chloral hydrate
Type of Epileptic Attack and Time of Occurrence
Generalized grand real and petit mal since childhood No attacks before admission Generalized grand mal since age 22 years Generalized grand mal seizures since childhood Simple partial seizures for past two months
Previous Medical Treatment
Carbazepin 600 mg/ day, ethosuximid No therapy *DPH 300 mg/day; discontinued a week before present attack Carbazepin 600 mg/day DPH 300 mg/day
DPH Level In Blood Serum
19.5
Result of Brain CT Right temporal lesion
Right frontoparietal lesion No pathological findings
No pathological findings Metastasis in left parietotemporal region
Result of Chloral Hydrate Treatment
Seizure stopped after seven minutes Recurrent focal seizures after eight, 14, and 21 hours Seizure stopped after five minutes
21 Seizure stopped after five minutes 16 Seizure stopped after five minutes 17.5 17
Seizure stopped after 12 minutes Recurrent seizure after 18 hours
*DPH, diphenylhydantion. cerebral metastasis in the left parietotemporal region was found. The p r i m a r y site was diagnosed in the lung. In two patients (3 and 4), CT of the brain was normal. In patients 2, 3, and 4 EEG recording was done 20, 40, and 55 minutes, respectively, after the last chloral hydrate administration. All patients were treated with 30 mg/kg intrarectal chloral hydrate every two hours. Chloral hydrate treatm e n t was initiated in four patients within 50 minutes after onset of seizures and, in one patient, 60 minutes after onset of seizures. In three patients (2 through 4), the attacks corn92/675
pletely disappeared w i t h i n five to seven minutes. No new epileptic act i v i t y was recorded by electroencephalography. In one patient (1), three left focal seizures occurred eight, 14, and 21. hours after administration of chloral hydrate. In one patient (5), the attacks stopped after 12 minutes, but a single generalized seizure occurred more than 24 hours after treatment began. Six hours after the beginning of treatment, chloral hydrate was reduced to 20 mg/kg every four hours for a t o t a l t r e a t m e n t t i m e of 48 hours. Three of the patients (3 through 5) Annals of Emergency Medicine
regained full consciousness and were discharged after several days. One pat i e n t (2), who p r e v i o u s l y suffered from recurrent events of stroke, regained c o n s c i o u s n e s s and p a r t i a l functioning. After a week, there was a deterioration in his state of consciousness; on brain CT, an additional extensive parietal lesion was revealed. The p a t i e n t died a week later. During the ten days preceding his death, he did not develop new epileptic seizures. One patient (1) did not regain consciousness despite the disappearance of epileptic activity. She died three weeks after admission. An autopsy revealed a massive 19:6 June 1990
hemorrhagic infarct in the right temporal lobe. No evidence of severe hypoxemia was f o u n d i n repeated a n a l y s i s of blood gases during status epilepticus; therefore, no endotracheal i n t u b a t i o n or artifical r e s p i r a t i o n was needed. Also, no h e m o d y n a m i c , cardiovascular, or respiratory side effects were observed i n e i t h e r of the p a t i e n t s after chloral hydrate administration. DISCUSSION Chloral h y d r a t e is a widely used hypnotic drug. Its role as an anticonv u l s a n t is n o t clear, and only a few reports have proved its efficacy. Choral h y d r a t e has been used to treat t e t a n u s and eclampsia. Experim e n t a l research has indicated a suppressive effect i n a t t a c k s p r o d u c e d e x p e r i m e n t a l l y b y s t r i c h n i n e , pent y l e n e t e t r a z o l , or e l e c t r i c shock. 4 It also proved to be effective in cases of m y o c l o n i c epilepsy, s Very few r e p o r t s d e s c r i b e its e f f e c t i v e n e s s in treating status epilepticus in adultsl,2, 6 or children. 3 C h l o r a l h y d r a t e is t h e h y d r a t e f o r m of chloral-(2,2,2,-trichloracetalaldehyde) a n d is rapidly reduced b y a l c o h o l d e h y d r o g e n a s e to trichlorethanol, w h i c h is most probably the effective central nervous system depressant substrate. In c o n t r a s t to chloral hydrate, trichlorethanol has a m u c h l o n g e r h a l f - t i m e (four to 12 hours). The m e c h a n i s m of chloral hydrate as an a n t i c o n v u l s i v e drug is unclear. Studies have reported changes i n the responsiveness of the central serotonergic n e u r o n s in feline dorsal raphae n u c l e u s after t r e a t m e n t w i t h chloral hydrate. 7 This report describes five adult patients in a state of status epilepticus who were treated w i t h 30 mg/kg intrarectal chloral hydrate. In all patients, chloral hydrate was administered after ineffective t r e a t m e n t w i t h c o n v e n t i o n a l d r u g s s u c h as diazepam, d i p h e n y l h y d a n t o i n , phenobarbital, and sodium valporate as a last a t t e m p t before i n d u c i n g barbiturate coma. A c o m b i n e d a d m i n i s t r a t i o n of diazepam and d i p h e n y l h y d a n t o i n , 7 or phenobarbital s is the drug t r e a t m e n t of choice for status epilepticus. The c o m b i n a t i o n of d i a z e p a m a n d dip h e n y l h y d a n t o i n has b e e n effective i n 88% of p a t i e n t s w i t h status epilepticus. 9 Some s t u d i e s describe s u c c e s s f u l 19:6 June 1990
trials w i t h s o d i u m valporate, lO-12 lorazepam, 13 clonazepam, 4 or midazolam. 14
Nevertheless, certain patients, especially those w i t h organic brain lesions, r e m a i n u n c o n t r o l l a b l e . Some authors r e c o m m e n d another trial of m o n o d r u g t h e r a p y - u s u a l l y lidoc a i n e or p a r a l d e h y d e ( a c e t a l h y d e polymer) - for 20 m i n u t e s after therapeutic failure. Is We used chloral hydrate i n patients w i t h r e s i s t a n t status epilepticus 50 to 60 m i n u t e s after failure of standard t h e r a p y as the last step before b a r b i t u r a t e coma. We chose chloral h y d r a t e b e c a u s e of its s a f e t y a n d lower risk of side effects compared with paraldehyde. Chloral hydrate and paraldehyde are closely related drugs t h a t c a u s e rapid s e d a t i o n by s i m i l a r m e c h a n i s m s . W h i l e paraldehyde m a y cause severe side effects s u c h as h y p o t e n s i o n , p u l m o n a r y hemorrhage and edema, venous thrombosis, kidney, a n d liver damage, 16 chloral hydrate is m u c h safer; the m o s t c o m m o n side effect of chloral hydrate is gastrointestinal irritation due to oral administration. R e s u l t s f r o m t r e a t m e n t of t h e a b o v e - m e n t i o n e d patients, who were successfully treated w i t h chloral hy&ate, raise the possibility of its use as an alternative drug i n treating patients w i t h intractable status epilepticus. It is w o r t h n o t i n g that no failure of chloral hydrate t r e a t m e n t or significant side effect could be demonstrated. It is i m p o s s i b l e t o d e t e r m i n e whether chloral hydrate acts alone or through p o t e n t i a t i o n of the previous drugs given to p a t i e n t s w i t h status epilepticus. This point m a y be elucidated by an initial trial of chloral hydrate as a first-choice drug i n treating patients w i t h status epilepticus. The excellent effect of intrarectal administration of chloral hydrate i n our series suggests the advantage of using chloral hydrate w h e n IV access cann o t be o b t a i n e d and i n p a t i e n t s i n w h o m s t a n d a r d t h e r a p y drugs are medically contraindicated. However, because of the l i m i t e d n u m b e r of patients i n our series, a control study to evaluate the efficacy of chloral hydrate as a s u p p l e m e n t is needed before it can be accepted as a r o u t i n e therapy.
SUMMARY Five patients with intractable staAnnals of Emergency Medicine
tus epilepticus, three of w h o m had o r g a n i c l e s i o n s , were t r e a t e d succ e s s f u l l y w i t h chloral h y d r a t e enemas. Epileptic activity ceased clinically and electroencephalographically w i t h i n a s h o r t period. No side effects were noted. The possibility of introducing this t r e a t m e n t for cases of epilepticus is raised considering its safety and efficacy.
REFERENCES
1. SchulzH: On the treatment of status epilepticus. Psychiatr Neurol Med Psycho] (Leipzig) 1970;22:29-32. 2. BondarenkoES: Principlesof intensive therapy of status epilepticus in children. Zhurnal Nevropatologii I Psikhiatri 1979;79:1329-1334. 3. Powell TE, RosenblumL: The use of chloral hydrate for refractory childhood epilepsy. Dev Med Child Neurol 1983;25:524-526. 4. Rail TW, Schleifer LS: Drugs effective in the therapy of the epilepsies, in Gilman AG, Goodman L8, Rall TW, et al (eds): The Pharmacological Basis of Therapeutics, ed 7. New York, McMillan, 1985, p 470. 5. Hambert O, Peterson I: Clinical, electroencephalographical and neuropharmacological studies in syndromesof progressive myoclonus epilepsy. Acta Neurol Scand 1970;46:179-186. 6. Sahal Khalid M, Schulz H: The treatment and management of emergency status epilepticus. Epilepsy 1970;17:73-76. 7. Heym J, Steilffels EF, Jacobs BL: Chloral hydrate anesthesia alters the responsiveness of central serotonergic neurons in the cat. Brain Res 1984;291:63-72. 8. Leppik IE: Treatment of status epilepticus, in: Antiepileptic Drug Research: The Second Fifty Years. New York, Raven Press, 1987. 9. Treiman DM, Delgado Escuela AV: Status epilepticus, in Thompson RA, Green JR (eds): Critical Care of Neurological and Neurosurgical Emergencies. New York, Raven Press, 1980,
p 53-99. 10. Vajada FJF, SymingtonGR, Bladin PF: Rectal valporate in intractable status epilepticus. Lancet 1977;1:359. 11. VajadaFJF,Mihaly GW, Miles JL, et ah Rectal administration of sodium valporate in status epilepticus. Neurology 1978;28:897. 12. Snead OC, Miles MV: Treatment of status epilepticus in children with rectal sodium valporate. J Pediatr 1985;106:323-325. 13. Tinuper P, Aguglia V, Gastaut H: Use of clobazepam in certain forms of status epileptitus and in startle induced epileptic seizures. Epilepsy 1986;27:18-25. 14. Egli M, Albani C: Relief of status epileptitus after intramuscularadministrationof midazolam, in Katsuki 8, Tsubaki T, Tokoyura Y teds): World Congress of Neurology. New York, Excerpta Medica, 1982, p 44. 15. Delgado-EscuetaAV, WasterlainC, Treiman DM, et al: Current concepts in neurology Management of status epilepticus.N Engl J Med 1982;306:1137-1140. 16. Harvey SC: Hypnotics and sedatives, in Gilman AG, GoodmanLS, Rall TW, et al leds): The Pharmacological Basis of Therapeutics, ed 7. New York, MacMillan, 1985, p 366-367. 676/93
Chloral Hydrate in Intractable Status Epilepticus Five adult patients were admitted to the neurological department in a state of status epilepticus. All were treated unsuccessfully with IV diazepam and diphenylhydantoin. Administration of sodium valporate or phenobarbital also was ineffective. However, after treatment with intrarectal chloral hydrate, all seizures ceased. The excellent effect of this drug was proved both clinically and electrodiagnostically. Discussed is the possibility of using chloral hydrate to treat patients with status epilepticus in whom conventional treatment has failed. Lampl Y, Eshel Y, Gilad R, Sarova-Pinchas I: Chloral hydrate in intractable status epilepticus. Ann Emerg Med June 1990;19:674-676.] INTRODUCTION Chloral hydrate is a hypnotic drug often used clinically for sedation and sleep induction. Only a few reports, however, have described its use in treating status epilepticus in adults1, 2 and children. 3 Five patients suffering from status epilepticus were treated with chloral hydrate intrarectally after treatment with conventional medications had failed.
Yair Lampl, MD Yechiel Eshel, MD, MSc Ronit Gilad, MD Ida Sarova-Pinchas, MD Holon and Tel Aviv, Israel From the Department of Neurology, Edith Wolfson Medical Center, Holon, israel; and the Tel Aviv University Sackler Faculty of Medicine, Tel Aviv, Israel. Received for publication July 6, 1989. Revision received January 10, 1990. Accepted for publication January 30, 1990. Address for reprints: Yair Lampl, MD, Department of Neurology, Edith Wolfson Medical Center, Holon, Israel.
PATIENTS AND METHODS Five patients (four men and one woman aged 22 to 68 years) were hospitalized in a state of status epilepticus. The patients had five to 12 seizures within 30 minutes without returning to a normal alert state between the attacks. Patients' blood pressures ranged from 110/80 m m Hg to 185/100 m m Hg, and pulses ranged from 72 to 112. All five had spontaneous respirations at a rate of 12 to 38. Each patient was treated with 20 mg diazepam IV at a rate of 2 rag/rain combined with 20 mg/kg diphenylhydantoin at a rate that did not exceed 50 mg/min. The treatment failed in all cases. Thirty to 35 minutes after this treatment, three of the patients (2, 3, and 5) received an IV drip (5% glucose solution with 100 mg diazepam/500 mL) at 8 mg/hr. Two other patients (1 and 4) were given 20 mg/kg phenobarbital IV. Neither of the treatments stopped the seizures or reduced the number of convulsions. Diphenylhydantoin serum level was within effective range in each patient (Table). In two patients, a dose of 20 mg/kg intrarectal valporate proved unsuccessful. Four of the patients had been on anticonvulsive medication before admission (Table). In one patient (3), the treatment was discontinued a week before his admission. Another patient (2) had never suffered from any epileptic attacks before the present incident and had therefore not been treated. Comprehensive blood tests were carried out in all patients during their hospitalization. Lumbar puncture was done in four of five patients (1 through 4). No evidence of infectious disease of the central nervous system or subarachnoid hemorrhage was found. In patient 5, lumbar puncture was not done because a space-occupying lesion with a massive mass effect was found by computed tomography (CT). Repeated CT scan of the brain in all patients during the hospitalization demonstrated brain infarcts in two (1 and 2). The cerebral lesions were found in the right frontoparietal and temporal areas. In one patient (5),
19:6 June 1990
Annals of Emergency Medicine
674/91
CHLORAL HYDRATE Lampl et al
TABLE. Clinical patient characteristics
Patient No./ Age (yr)
Previous Diseases
1/62
2/57
Recurrent cerebrovascular accident
3/52
4/22
5/69
Tumor of lung with brain metastasis
Present Medical Treatment
Diazepam, DPH, phenobarbital, chloral hydrate Diazepam, DPH, sodium valporate, chloral hydrate Diazepam, DPH, sodium valporate Diazepam, DPH, phenobarbital chloral hydrate Diazepam, DPH, chloral hydrate
Type of Epileptic Attack and Time of Occurrence
Generalized grand real and petit mal since childhood No attacks before admission Generalized grand mal since age 22 years Generalized grand mal seizures since childhood Simple partial seizures for past two months
Previous Medical Treatment
Carbazepin 600 mg/ day, ethosuximid No therapy *DPH 300 mg/day; discontinued a week before present attack Carbazepin 600 mg/day DPH 300 mg/day
DPH Level In Blood Serum
19.5
Result of Brain CT Right temporal lesion
Right frontoparietal lesion No pathological findings
No pathological findings Metastasis in left parietotemporal region
Result of Chloral Hydrate Treatment
Seizure stopped after seven minutes Recurrent focal seizures after eight, 14, and 21 hours Seizure stopped after five minutes
21 Seizure stopped after five minutes 16 Seizure stopped after five minutes 17.5 17
Seizure stopped after 12 minutes Recurrent seizure after 18 hours
*DPH, diphenylhydantion. cerebral metastasis in the left parietotemporal region was found. The p r i m a r y site was diagnosed in the lung. In two patients (3 and 4), CT of the brain was normal. In patients 2, 3, and 4 EEG recording was done 20, 40, and 55 minutes, respectively, after the last chloral hydrate administration. All patients were treated with 30 mg/kg intrarectal chloral hydrate every two hours. Chloral hydrate treatm e n t was initiated in four patients within 50 minutes after onset of seizures and, in one patient, 60 minutes after onset of seizures. In three patients (2 through 4), the attacks corn92/675
pletely disappeared w i t h i n five to seven minutes. No new epileptic act i v i t y was recorded by electroencephalography. In one patient (1), three left focal seizures occurred eight, 14, and 21. hours after administration of chloral hydrate. In one patient (5), the attacks stopped after 12 minutes, but a single generalized seizure occurred more than 24 hours after treatment began. Six hours after the beginning of treatment, chloral hydrate was reduced to 20 mg/kg every four hours for a t o t a l t r e a t m e n t t i m e of 48 hours. Three of the patients (3 through 5) Annals of Emergency Medicine
regained full consciousness and were discharged after several days. One pat i e n t (2), who p r e v i o u s l y suffered from recurrent events of stroke, regained c o n s c i o u s n e s s and p a r t i a l functioning. After a week, there was a deterioration in his state of consciousness; on brain CT, an additional extensive parietal lesion was revealed. The p a t i e n t died a week later. During the ten days preceding his death, he did not develop new epileptic seizures. One patient (1) did not regain consciousness despite the disappearance of epileptic activity. She died three weeks after admission. An autopsy revealed a massive 19:6 June 1990
hemorrhagic infarct in the right temporal lobe. No evidence of severe hypoxemia was f o u n d i n repeated a n a l y s i s of blood gases during status epilepticus; therefore, no endotracheal i n t u b a t i o n or artifical r e s p i r a t i o n was needed. Also, no h e m o d y n a m i c , cardiovascular, or respiratory side effects were observed i n e i t h e r of the p a t i e n t s after chloral hydrate administration. DISCUSSION Chloral h y d r a t e is a widely used hypnotic drug. Its role as an anticonv u l s a n t is n o t clear, and only a few reports have proved its efficacy. Choral h y d r a t e has been used to treat t e t a n u s and eclampsia. Experim e n t a l research has indicated a suppressive effect i n a t t a c k s p r o d u c e d e x p e r i m e n t a l l y b y s t r i c h n i n e , pent y l e n e t e t r a z o l , or e l e c t r i c shock. 4 It also proved to be effective in cases of m y o c l o n i c epilepsy, s Very few r e p o r t s d e s c r i b e its e f f e c t i v e n e s s in treating status epilepticus in adultsl,2, 6 or children. 3 C h l o r a l h y d r a t e is t h e h y d r a t e f o r m of chloral-(2,2,2,-trichloracetalaldehyde) a n d is rapidly reduced b y a l c o h o l d e h y d r o g e n a s e to trichlorethanol, w h i c h is most probably the effective central nervous system depressant substrate. In c o n t r a s t to chloral hydrate, trichlorethanol has a m u c h l o n g e r h a l f - t i m e (four to 12 hours). The m e c h a n i s m of chloral hydrate as an a n t i c o n v u l s i v e drug is unclear. Studies have reported changes i n the responsiveness of the central serotonergic n e u r o n s in feline dorsal raphae n u c l e u s after t r e a t m e n t w i t h chloral hydrate. 7 This report describes five adult patients in a state of status epilepticus who were treated w i t h 30 mg/kg intrarectal chloral hydrate. In all patients, chloral hydrate was administered after ineffective t r e a t m e n t w i t h c o n v e n t i o n a l d r u g s s u c h as diazepam, d i p h e n y l h y d a n t o i n , phenobarbital, and sodium valporate as a last a t t e m p t before i n d u c i n g barbiturate coma. A c o m b i n e d a d m i n i s t r a t i o n of diazepam and d i p h e n y l h y d a n t o i n , 7 or phenobarbital s is the drug t r e a t m e n t of choice for status epilepticus. The c o m b i n a t i o n of d i a z e p a m a n d dip h e n y l h y d a n t o i n has b e e n effective i n 88% of p a t i e n t s w i t h status epilepticus. 9 Some s t u d i e s describe s u c c e s s f u l 19:6 June 1990
trials w i t h s o d i u m valporate, lO-12 lorazepam, 13 clonazepam, 4 or midazolam. 14
Nevertheless, certain patients, especially those w i t h organic brain lesions, r e m a i n u n c o n t r o l l a b l e . Some authors r e c o m m e n d another trial of m o n o d r u g t h e r a p y - u s u a l l y lidoc a i n e or p a r a l d e h y d e ( a c e t a l h y d e polymer) - for 20 m i n u t e s after therapeutic failure. Is We used chloral hydrate i n patients w i t h r e s i s t a n t status epilepticus 50 to 60 m i n u t e s after failure of standard t h e r a p y as the last step before b a r b i t u r a t e coma. We chose chloral h y d r a t e b e c a u s e of its s a f e t y a n d lower risk of side effects compared with paraldehyde. Chloral hydrate and paraldehyde are closely related drugs t h a t c a u s e rapid s e d a t i o n by s i m i l a r m e c h a n i s m s . W h i l e paraldehyde m a y cause severe side effects s u c h as h y p o t e n s i o n , p u l m o n a r y hemorrhage and edema, venous thrombosis, kidney, a n d liver damage, 16 chloral hydrate is m u c h safer; the m o s t c o m m o n side effect of chloral hydrate is gastrointestinal irritation due to oral administration. R e s u l t s f r o m t r e a t m e n t of t h e a b o v e - m e n t i o n e d patients, who were successfully treated w i t h chloral hy&ate, raise the possibility of its use as an alternative drug i n treating patients w i t h intractable status epilepticus. It is w o r t h n o t i n g that no failure of chloral hydrate t r e a t m e n t or significant side effect could be demonstrated. It is i m p o s s i b l e t o d e t e r m i n e whether chloral hydrate acts alone or through p o t e n t i a t i o n of the previous drugs given to p a t i e n t s w i t h status epilepticus. This point m a y be elucidated by an initial trial of chloral hydrate as a first-choice drug i n treating patients w i t h status epilepticus. The excellent effect of intrarectal administration of chloral hydrate i n our series suggests the advantage of using chloral hydrate w h e n IV access cann o t be o b t a i n e d and i n p a t i e n t s i n w h o m s t a n d a r d t h e r a p y drugs are medically contraindicated. However, because of the l i m i t e d n u m b e r of patients i n our series, a control study to evaluate the efficacy of chloral hydrate as a s u p p l e m e n t is needed before it can be accepted as a r o u t i n e therapy.
SUMMARY Five patients with intractable staAnnals of Emergency Medicine
tus epilepticus, three of w h o m had o r g a n i c l e s i o n s , were t r e a t e d succ e s s f u l l y w i t h chloral h y d r a t e enemas. Epileptic activity ceased clinically and electroencephalographically w i t h i n a s h o r t period. No side effects were noted. The possibility of introducing this t r e a t m e n t for cases of epilepticus is raised considering its safety and efficacy.
REFERENCES
1. SchulzH: On the treatment of status epilepticus. Psychiatr Neurol Med Psycho] (Leipzig) 1970;22:29-32. 2. BondarenkoES: Principlesof intensive therapy of status epilepticus in children. Zhurnal Nevropatologii I Psikhiatri 1979;79:1329-1334. 3. Powell TE, RosenblumL: The use of chloral hydrate for refractory childhood epilepsy. Dev Med Child Neurol 1983;25:524-526. 4. Rail TW, Schleifer LS: Drugs effective in the therapy of the epilepsies, in Gilman AG, Goodman L8, Rall TW, et al (eds): The Pharmacological Basis of Therapeutics, ed 7. New York, McMillan, 1985, p 470. 5. Hambert O, Peterson I: Clinical, electroencephalographical and neuropharmacological studies in syndromesof progressive myoclonus epilepsy. Acta Neurol Scand 1970;46:179-186. 6. Sahal Khalid M, Schulz H: The treatment and management of emergency status epilepticus. Epilepsy 1970;17:73-76. 7. Heym J, Steilffels EF, Jacobs BL: Chloral hydrate anesthesia alters the responsiveness of central serotonergic neurons in the cat. Brain Res 1984;291:63-72. 8. Leppik IE: Treatment of status epilepticus, in: Antiepileptic Drug Research: The Second Fifty Years. New York, Raven Press, 1987. 9. Treiman DM, Delgado Escuela AV: Status epilepticus, in Thompson RA, Green JR (eds): Critical Care of Neurological and Neurosurgical Emergencies. New York, Raven Press, 1980,
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