3 16 Brief cfinical and laboratory observations The Journal of Pediatrics Februa O' 1979 by administration of activated charcoal, however, may be more appropriate for patients ingesting unusually large doses. If both ipecac and charcoal are used, it is imperative that the emetic be given first, since ipecac is adsorbed by activated charcoal and thus rendered ineffective. Some sustained release theophylline preparations require 8 hours or longer to be completely absorbed," suggesting that the addition o f a nonadsorbed saline cathartic such as sodium sulfate be considered to decrease gut transit time. 16 E 14 -~, r x.._ \\\\\ 12 "~ o 10 _~ 6 ~ 4 ~ 2 X2 F~ ",j The authors wish to thank the nurses of the Clinical Research Center for their contribution to the study; Leon Burmeister, Ph.D., Department of Preventive Medicine and Environmental Health, University of Iowa, who reviewed the statistical analysis; and Barry H. Rumack, M.D., Director, Rocky Mountain Poison Center, Denver, Colorado, for his suggestions. REFERENCES co 0 I i i I I I 4 6 8 10 12 14 Time (hours) Figure. Mean _+SEM concentration-time curves for serum theophylline alone (.--.) and theophylline followed by activated charcoal (.__.) in five healthy adult volunteers. toxicity following ingestion of theophylline solutions, which are absorbed to a greater extent during the first 30 minutes than of the plain uncoated tablets used in the present study) In contrast, the absorption of delayed or sustained release products may be more completely inhibited. In addition, charcoal may be effective after a longer time interval with these slowly absorbed products. Although 30 gm of activated charcoal effectively inhibited the absorption of 500 to 600 mg of theophylline in this study, it is not possible to predict whether this amount would be adequate for larger doses. Initial treatment of acute theophylline ingestion should include prompt measures to reduce gastrointestinal absorption. The results of the present study suggest that the use of activated charcoal, if administered within the first half-hour after ingestion, may be an adequate therapeutic measure. Induction of emesis with ipecac followed 1. Chipps BE, Talamo RC, and Teets KC: Theophylline and the danger of differing absorption capabilities, J PEDIATR 91:346, 1977. 2. Vaucher Y, Lightner ES, and Walson PD: Theophylline poisoning, J PEDIATR90:827, 1977. 3. Corby DG, and Decker WJ: Management of acute poisoning with activated charcoal, Pediatrics 54:324, 1974. 4. Sintek C, Hendeles L, and Weinberger M: Activated charcoal adsorption of theophylline in vitro, Drug Intell Clin Pharm 12:158, 1978. 5. Orcutt J J, Kozak PP, Gillman SA, et al: Micro-scale method for theophylline in body fluids by reversed-phase, highpressure liquid chromatography, Clin Chem 23:599, 1977. 6. Gibaldi M, and Perrier D: Pharmacokinetics, New York, 1975, Marcel Dekker, Inc., p 149. 7. Gibaldi M, and Perrier D: Pharmacokinetics, New York, 1975, Marcel Dekker, Inc., pp 293-296. 8. Gibaldi M, and Perrier D: Pharmacokinetics, New York, 1975, Marcel Dekker, Inc., pp 150-151. 9. Hendeles U Weinberger M, and Bighley L: Absolute bioavailability of oral theophylline, Am J Hosp Pharm 34:525, 1977. 10. Dabbous IA, Bergman AB, and Robertson WO: The ineffectiveness of mechanically induced vomiting, J PEDIATR66:952, 1965. 11. Hendeles L, Weinberger M, and Bighley L: Absorption characteristics of various oral theophylline dosage forms, presented at the American Congress of Allergy and Immunology, New York City, March 30, 1977. Cerebrovascular complications in phencyclidine intoxication Carl J. Crosley, M.D.,* and Eugene F. Binet, M.D., Syracuse, N.Y. From the Departments of Neurology, Pediatrics and Radiology, SUNY, Upstate Medical Center. *Reprint address: Department of Neurology, SUNY Upstate Medical Center, 750 E. Adams St., Syracuse, NY 13210. Phencyclidine is a commercially available anesthetic agent used in veterinary medicine. It is a popular street drug and is sold as angel dust, "PeaCe Pill," and other pseudonyms. Intoxication in adults occurs, and the 0022-3476/79/200316+03500.30/0 9 1979 The C. V. Mosby Co. Volume 94 Number 2 Brief clinical and laboratory observations 3 17 surreptitious administration of PCP to children has been reported. 1 We have cared for a boy with PCP intoxication whose symptoms suggested a focal cerebrovascular lesion. Abbreviations used PCP: phencyclidine CT: computed tomography EEG: electroencephalogram CASE REPORT A 61A-year-old boy was found unresponsive at home. After school he had complained of nausea and had vomited; he was given a single Dristan tablet. Thirty minutes later, he became unresponsive and was brought to the hospital, where he had several left-sided clonic seizures. His vital signs included a temperature of 38.4~ pulse 124, respirations 28, and a blood pressure of 112/60. He was mute and unresponsive to commands. Tactile stimuli led to extreme agitation with abnormal posturing. His pupils were midposition; there was no nystagmus. Motor activity was constant, purposeless, and symmetrical. The deep tendon reflexes were brisk and symmetrical; plantar responses were equivocal. Laboratory values included a normal blood count, electrolytes, blood sugar, blood urea nitrogen, and blood aspartate amino transferase. The CSF was normal with a borderline protein level of 46 mg/dl. The blood salicylate level was 6.5 mg/dl. Urine screening for phenothiazines was faintly positive. The patient was given diphenhydramine without benefit. During the next 48 hours, he remained febrile and uncommunicative. He vomited intermittently and had several seizures that were usually of left focal origin and were controlled with diazepam and phenytoin. A right hemiparesis was noted on the first hospital day. An electroencephalogram performed that day showed generalized delta slowing with left hemispheric voltage depression and right frontal spike activity. Computed tomography of the brain demonstrated an area of decreased density in the left parieto-occipital area which was mildly enhanced following the intravenous injection of contrast agent. Multiple linear densities resembling enlarged arteries and veins supplying an arteriovenous malformation were identified (Fig. 1) suggesting an arteriovenous malformation in the distribution of the left middle cerebral artery. The flow study from a technetium99 m radionuclide brain scan showed an area of increased perfusion in the left posterior hemisphere lasting only 3 seconds (Fig. 2, A). The delayed study was normal (Fig. 2, B). Although the CT suggested an arteriovenous malformation, the radionuclide study did not support that contention, and cerebral angiography was deferred. During the next three days, the patient became more responsive. His right hemiparesis completely resolved by the fourth hospital day. Repeat CT and repeat radionuclide study at that time were normal. Qualitative gas chromatography and mass spectrometry of his urine showed the presence of phencyclidine but not phenothiazines. Subsequently, the parents ascertained that the boy had been given a small white pill by an older child at school. His EEG after two weeks showed less posterior slowing, and one month later his physical examination was normal. Fig. 1. Computed tomography study following contrast enhancement. Multiple linear densities suggesting enlarged arteries and veins possibly supplying an arterio-venous malformation. DISCUSSION Phencyclidine ingestion has been characterized as low, moderate, or high dose intoxication. 2 Nausea and agitation are often seen in the low-dose state; persons who have knowingly ingested the drug report disturbances of body image, perception, and feelings of isolation. These individuals are mute and unresponsive and nystagmus is usually present. In the moderate-dose state the eyes remain open, the patient is nonresponsive and has midposition pupils, but there is no respiratory depression. Repetitive and r a n d o m motor motions and even dystonic postures have been noted; vomiting, hypersalivation, and intermittent variable hypertension are c o m m o n l y seen. Opisthotonus, generalized seizure activity, and fever mark the progression to high-dose intoxication, Recovery is marked by several days of alternating periods of sleep, waking, and sensory distortion. The presentation of our patient is fairly typical of an individual who has passed into the high-dose state. However, several aspects of his clinical and radiologic presentation are unusual and have not been reported previously. 3 18 Brief clinical and laboratory observations The Journal of Pediatrics February 1979 Fig. 2. Technetium 99m cerebral imaging study. A, Posterior flow study shows area of increased perfusion in left parieto-occipital area. B, Delayed study is normal. Focal seizures in infants and children (under 3 or 4 years of age) may be a consequence of generalized disorders? While the focal seizures in our patient may represent a variation in maturation, they were sufficient cause for the consideration of focal structural abnormalities. Seizures described in PCP intoxication occurring in adults and adolescents have been generalized and have included one episode of fatal status epilepticus. '.~ In younger children with high-dose intoxication, involuntary movements including opisthotonus, but not seizures, have been described. No EEG correlation has been reported in these cases to clarify the potential epileptic nature of the reported movements?.'~ Our patient's course strongly suggests that the focal seizures were a direct action of the drug. The hemiparesis is a rather unique occurrence. It (and perhaps the other focal phenomena) may be explained by the vascular effects of PCP. The pressor effects of PCP are well known and hypertension may occur both early and late in the course of intoxication? 7 The drug can cause marked vasoconstriction, which may be secondary to the enhancement of the action of catecholamines and serotonin.~ To place these documented sympathomimetic mechanisms in the context of this patient, it may be postulated that the area of decreased density on CT represents an area of vasoconstriction and cerebral ischemia. The subsequent enhancement of this area and the transiently prominent vascular pattern seen on CT and brain scan may represent luxury perfusion. ~ This case documents several very atypical aspects of intoxication with phencyclidine and suggests that sympathomimetic effects may account for striking abnormalities with potentially permanent focal neurologic deficits. The recognition that with phencycline intoxication can present with focal neurologic signs will raise a note of caution before individual patients are subjected to needless procedures. REFERENCES 1. Liden CB, Lovejoy FH, and Costello CE: Phencyclidinenine cases of poisoning, JAMA 234:513, 1975. 2. Burns RS, Lerner SE: Perspectives: acute phencyclidine intoxication, Clin Toxicol 9:477, 1976. 3. Gamstorp I: Pediatric neurology, New York, 1970 Appleton-Century Crofts, p 69. 4. Rainey JM, and Crowder MK: Prolonged psychosis attributed to phencyclidine: report of three cases. Am J Psychiatry 132:1076, 1975. 5. KesslerGF, Demers LM, and Brennan RW: Phencyclidine and fatal status epilepticus, N Engl J Med 291:979. 1974. 6. Dorand RD: Phencyclidine ingestion: therapy review, South Med J 70:117, 1977. 7. Eastman JW: Hypertensive crises and death associated with phencyclidine poisoning, JAMA 231:1270, 1975. 8. Ilett KF, Jarrott B, O'Donnell SR, Wanstall JC: Mechanism of cardiovascular actions of l-(1-phencyclohexyl)piperidine hydrochloride (phencyclidine), Br J Pharmacol 28:73, 1966. 9. TavarasJM, Wood EH: Diagnostic neuroradiology, Baltimore, 1976, The Williams & Wilkins Company, p 650.