Postgrad Med J: first published as 10.1136/pgmj.50.582.242 on 1 April 1974. Downloaded from

242 Case reports cases we report had blood lead values below 80 ,±g/ Aronsen, 1971). Their sensitivity is such that they 100 ml yet both cases were unequivocally suffering become abnormal at an early stage of lead intoxica- from lead poisoning. In addition, both cases had tion. Had our cases presented for routine occupa- normal haemoglobin concentrations and so would tional screening, both urinary coproporphyrin and have escaped detection by screening programmes amino laevulinic acid measurements would have based on the usual haemoglobin or blood lead recognized a state of lead poisoning; neither haemo- criteria. Similar cases have been reported (Waldron, globin nor blood lead measurements would have 1971; Gibson et al., 1968) and the latter authors recognized it. recommended that lead concentrations greater than ml Acknowledgments 60 ,ug/100 should prompt further investigation. Our thanks are due to Dr R. S. Savidge of Bury General Lead in the blood reflects absorption of the metal. Hospital and Professors W. R. Lee and S. W. Stanbury of Individuals vary in their susceptibility to intoxica- Manchester University for permission to report these cases. tion and in practice, indices of absorption do not Professor Lee and Dr P. H. Adams are responsible for many correlate with indices of intoxication improvements in the final manuscript. We are grateful to closely (Gibson Dr D. Walsh and the technicians of the Manchester Royal et al., 1968). It, therefore, seems logical to prefer Infirmary laboratories for the chemical estimations. evidence of intoxication to estimates of absorption both for occupational screening and for confirma- References GIBSON, S.L.M., MACKENZIE, J.C. & GOLDBERG, A. (1968) tion of clinical diagnoses. Of the investigations The diagnosis of industrial lead poisoning. British Journal tabulated for these patients, the measurement of ofIndustrial Medicine, 25, 40. erythrocyte protoporphyrin is too difficult and that HAEGER-ARONSEN, B. (1971) An assessment of the laboratory of 8-amino laevulinic acid dehydrogenase activity too tests used to monitor the exposure of lead workers. British Journal of Industrial Medicine, 28, 52. sensitive (Hernberg and Nikkanen, 1970) for routine HERNBERG, S. & NIKKANEN, J. (1970) Enzyme inhibition by use. Regular haemoglobin determinations in all lead under normal urban conditions. Lancet, i, 63. statutory lead workers are required by law (Ministry KING, E. & THOMPSON, A.R. (1961) The measurement of lead

of Labour, 1965). A decrement in haemoglobin con- absorption in industry. Annals of Occupational Hygiene,copyright. 3, 247. centration is evidence of significant lead poisoning, LANE, R.E., ETAL (1968) Diagnosis of inorganic lead poison- other causes having been excluded, but as shown in ing: a statement. British Medical Journal, 4, 501. this report, symptomatic poisoning may coincide MINISTRY OF LABOUR (1965) Annual Report of H.M. Chief with normal haemoglobin values. Measurements of Inspector ofFactories in Industrial Health, 1964. H.M.S.O, amino and London. urinary laevulinic acid urinary copropor- WALDRON, H.A. (1971) Correlation between some para- phyrins are useful in both the industrial and the meters of lead absorption and lead intoxication. British clinical context (Gibson et al., 1968; Haeger- Journal of Industrial Medicine, 28, 195. http://pmj.bmj.com/

Postgraduate Medical Journal (April 1974) 50, 242-244. Acute barbiturate poisoning in young epileptics

B. W. HANCOCK on September 24, 2021 by guest. Protected M.B., CH.B., D.C.H. Neurology Unit, Fulwood Annexe, Sheffield Summary COMA is a common presentation of the known Two young epileptic patients presenting in coma with epileptic patient to the acute medical unit. The focal neurological signs were found to be suffering following two cases are reported to emphasize the from unsuspected acute barbiturate overdose. There importance of excluding deliberate drug overdose in had been strenuous denial of any possibility of the young epileptic patient whose presenting coma is psychiatric disturbance or of self-poisoning in the in any way atypical or prolonged. history obtained from their parents at the time of admission. The importance of excluding deliberate Case 1 drug overdose in any young epileptic patient presenting A 12-year-old girl with a 2-year history of Grand with prolonged or atypical coma is re-emphasized. Mal epilepsy was admitted to the Neurology Unit Correspondence: B. W. Hancock, 42 Winchester Road, at midnight on 6 December 1972, after being seen at Sheffield S1O 4EE. home by her general practitioner. That evening she Postgrad Med J: first published as 10.1136/pgmj.50.582.242 on 1 April 1974. Downloaded from

Case reports 243 had lapsed into coma after complaining for 2 hr of and electrolytes and blood sugar investigations were dizziness, slurred speech, double vision and un- all normal and a serum barbiturate level was found steadiness of gait. Her parents strenuously denied to be 2-4 mg%4 (consistent with regular medicinal that there was any possibility of tablet overdose, but doses of Phenobarbitone). The provisional diagnosis wondered if she could have injured herself whilst of prolonged post-ictal coma was made and the performing gymnastic exercises with her friends patient observed. There was no change in the earlier in the evening. They confirmed that the conscious state over the next 24 hr, but tendon patient had been taking regular anti-convulsant reflexes became difficult to elicit and the left plantar therapy of Phenytoin, 50 mg twice daily and Pheno- response became extensor. At this stage the patient barbitone, 30 mg twice daily and that in the months was transferred to the Neurology Unit for further prior to her admission she had been having only investigation. Echoencephalography and lumbar occasional convulsions. At the time of admission she puncture were normal but a repeat serum barbiturate was comatose but apyrexial. Examination of the estimation showed a level of 9-6 mg%4 (as Pheno- cardiovascular, respiratory and abdominal systems barbitone). By this time the patient's condition was was normal. Her fundi and pupil responses were slowly improving and he was treated expectantly. normal, there was no neck stiffness, the tendon re- On the following day the serum barbiturate level flexes were difficult to elicit, but the left plantar had fallen to 5-4 mg%0 and the patient was fully response was extensor. The history and findings were rousable, though still drowsy. When he had com- highly suggestive ofa brain stem catastrophe, possibly pletely recovered, the boy admitted to having vascular or traumatic, but a search for other ingested approximately thirty Phenobarbitone (30 remediable conditions was made. Echoencephalo- mg) tablets on the evening before admission. Psy- graphy, skull X-ray, blood sugar, serum urea and chiatric assessment confirmed reactive depression electrolytes and lumbar puncture were normal, but to problems at home and at work. the serum barbiturate level estimated 1 hr after admission was 8-2 mg%O. At this stage the child was Comments copyright. transferred to the Children's Hospital for intensive The usual causes for the known epileptic patient to care. An endo-tracheal airway was inserted, gastric be admitted to hospital in coma are status epilepticus, lavage performed and forced alkaline diuresis com- prolonged post-ictal unconsciousness and head menced and continued for the next 2 days. The serum injury occurring at the time of a convulsion. barbiturate level on the morning after admission was It is well recognized that epileptic patients may 9-8 mg%4 (as Phenobarbitone), and this gradually fell attempt suicide (Kessel, 1965) since they often have over the next 3 days to 4-4 mg%4, by which time the associated psychiatric disturbance (Scott, 1968), but patient was regaining consciousness. When she had in both of the above patients the possibilities of http://pmj.bmj.com/ fully recovered she willingly admitted to having psychiatric instability and of deliberate drug over- ingested more than twelve Phenobarbitone (30 mg) dose were discounted by the parents at the time of tablets and several Phenytoin (50 mg) capsules, admission. but would give no reason for her behaviour. Psychi- In Case 1, the presenting history and physical atric assessment showed her to be a depressed, with- findings indicated an acute neurological cause for drawn child with difficulties in adjusting to her the coma. Fortunately, a serum barbiturate level was epilepsy. requested and this revealed the true nature of the problem. This patient ingested an overdose of on September 24, 2021 by guest. Protected Case 2 Phenytoin as well as Phenobarbitone, and ataxia, A 15-year-old boy with a 2-year history of Grand vertigo and dysarthria (her presenting features) are Mal epilepsy was admitted to an acute medical unit recognized acute toxicity effects of both of these on the morning of 9 January 1973, with a history of drugs (Graham, 1962). unconsciousness following a convulsion. During the In Case 2, the history and examination at the time previous night he had been observed by his mother to of admission were consistent with post-ictal coma, have what she thought was a convulsion. He had but the period of unconsciousness following the remained unrousable throughout the night and next suspected single convulsion (usually no longer than morning. His regular anti-convulsant therapy had an hour, Elliott, 1964) was prolonged and late- been Phenytoin, 50 mg 8 hourly and Phenobarbitone developing signs once again suggested a neurological 60 mg at night. The parents gave no indication of cause. In this case, although a later estimation con- domestic problems and discounted any possibility of firmed the overdose, the initial serum barbiturate drug overdose. Examination at the time ofadmission, level (2-4 mg°o 12 hr after ingestion) was within the about 8 hr after the supposed convulsion, showed the limits normally accepted for epileptic patients taking patient to be unrousable but no other abnormali- regular Phenobarbitone therapy. Serum levels of ties were found. Skull X-ray, chest X-ray, serum urea between 1-5 and 3 5 mg%0 are normally accepted, Postgrad Med J: first published as 10.1136/pgmj.50.582.242 on 1 April 1974. Downloaded from

244 Case reports but levels of up to 6 mg%0 have been recorded Acknowledgments (Lous, 1954). I am grateful to Dr E. W. J. Gumpert for his encourage- Undoubtedly, acute barbiturate toxicity is associ- ment and to Dr Gumpert and Dr J. Carson for allowing me ated with the development ofneurological signs, such to report details of their patients. as depressed tendon reflexes and extensor plantar responses (Carroll, 1969) but it is of interest that both References patients showed these changes without gross CARROLL, B.J. (1969) Barbiturate overdosage-presentation with focal neurological signs. Medical Journal ofAustralia, respiratory or cardiovascular depression. 1, 1133. Following recovery from coma, both patients ELLIOTT, F.A. (1964) Clinical Neurology. Ist Edition, p. 64. admitted taking an overdose of drugs and both were Philadelphia: Saunders. found to be psychiatrically disturbed, much to the GRAHAM, J.D.P. (1962) The Diagnosis and Treatment of Acute Poisoning, pp. 107, 137. London: Oxford Uni- surprise and chagrin of their parents who, at the versity Press. time of admission, had unwittingly misled the KESSEL, N. (1965) Self poisoning. British Medical Journal, 2, attendant medical staff. 1265. Acute barbiturate poisoning should therefore be Lous, P. (1954) Blood serum and cerebrospinal fluid levels and renal clearance of phenobarbitone in treated epileptics. considered in any epileptic patient presenting with Acta Pharmacologica et Toxicologica, 10, 166. atypical coma, even when there is no evidence of SCOTT, D.F. (1968) Psychiatric aspects of epilepsy. Post- possible overdose or of psychiatric instability. graduate Medical Journal, 44, 319.

Postgraduate Medical Journal (April 1974) 50, 244-246. copyright. Ergotamine-induced venous thrombosis

U. MINTZ S. BAR-MEIR M.D. M.D. A. DE VRIES M.D., PH.D. http://pmj.bmj.com/

Tel-Aviv University Medical School, Department of Medicine D, Beilinson Hospital, Petah Tikva, Israel

Summary earlier she had severe migraine and took 5 g of A patient is described who developed venous throm- aspirin instead of the ergotamine tartrate tablets she bosis in the leg following an intramuscular injection of was wont to use but which were out of stock. The on September 24, 2021 by guest. Protected ergotamine tartrate. next morning, on the expected day, her menstruation started, this time, however, with excessive blood loss Introduction to an extent she had never experienced before. The Ergotamine poisoning in the human classically severe menorrhagia continued for 3 days until at manifests as arterial spasm and arterial thrombosis, 10.30 a.m. on the day of admission she received an sometimes leading to gangrene of the extremities. intragluteal injection of 0.5 mg ergotamine tartrate. We wish to report a rare vascular complication of Three quarters of an hour later she felt a cramp in ergotamine treatment, venous leg thrombosis which the neck muscles and a sensation of severe burning appeared in a woman following an intragluteal pain radiating along both thighs downward. On injection of ergotamine tartrate given for menor- lying down the burning pain disappeared but when rhagia. she tried to rise at 13.00 p.m. she felt a sharp pain in the left calf preventing her from standing. Since Case report the pain continued unabated she was admitted at The patient, a female teacher, aged 38 years, 18.30 p.m. Noteworthy in her history are frequent mother of two healthy children, was admitted with attacks of severe migraine of many years duration the complaint of pain in her left calf. Four days for which she had been taking various analgesics,