Phencyclidine-Associated Acute Rhabdomyolysis FREDERICK C. COGEN, M.D.; GERALD RIGG, M.D.; JERRY L SIMMONS, M.D.; and EDWARD F. DOMINO, M.D.; Ann Arbor, Michigan
Phencyclidine (PCP) is a dissociative veterinary anesthetic and tranquilizer that at present is being abused as a psychedelic and hallucinogenic agent with increasing frequency. The cases of two young patients suffering from phencyclidine toxicity are reported. In each, central nervous system depression was accompanied by an acute dystonic motor reaction resulting in acute rhabdomyolysis and myoglobinuria. Skeletal muscle injury was felt to be the result of excessive involuntary isometric motor activity rather than a direct effect of phencyclidine on skeletal muscle. Patients suffering from phencyclidine intoxication should be screened for acute rhabdomyolysis. Phencyclidine intoxication should be included in the differential of nontraumatic rhabdomyolysis and should be considered among the potential causes of acute myoglobinuric renal failure.
P H E N C Y C L I D I N E , a dissociative anesthetic used in veterinary medicine, is being abused by the psychedelic drug culture with ever-increasing frequency. K n o w n as the "Pea Cea Pill" (PCP), "Angel D u s t , " and " H o g " , it may be smoked, swallowed, "snorted," or injected parenterally. Phencyclidine is frequently found masquerading as other street drugs including 9-THC, LSD, and mescaline. It was detected in 184 out of 237 samples of illicit drugs in a recent survey (1). Clinical toxicity includes thought disorders, sympathetic dysfunction, and varying degrees of analgesia and anesthesia (2, 3). Acute rhabdomyolysis and myoglobinuria have been previously reported in patients abusing heroin (4, 5) and amphetamines (6). We report two cases in which phencyclidine abuse was associated with unusual muscular hyperactivity and profound rhabdomyolysis with myoglobinuria. Case Histories PATIENT 1
A 21-year-old male former heroin addict, maintained on daily methadone, developed abdominal cramps, vomiting, and then stupor after intravenous self-administration of "PCP." Within 2 h of the overdose, the patient became agitated and observers had to physically restrain him because of repeated episodes of writhing tonic movements of extremities accompanied by exaggerated myotonic contractions and opisthotonos. He was admitted to the Wayne County Hospital 20 h after the phencyclidine injection. On arrival at the hospital, the patient was semistuporous, • From the Section of Nephrology, Department of Medicine, Wayne County General Hospital; Eloise, Michigan; and the Department of Pharmacology, The University of Michigan; Ann Arbor, Michigan. 210
© 1978 American College of Physicians
Downloaded from https://annals.org by University of Otago user on 12/16/2018
dysarthric, and confused. Blood pressure was 150/80 m m Hg; pulse, 96; temperature, 38.3 °C; and abdominal examinations were unremarkable. Diffuse muscle tenderness was present without evidence of soft-tissue trauma. Horizontal nystagmus was observed, but pupillary reactions and cranial nerves were intact. Motor tone and power were normal, and reflex and sensory examinations were unremarkable. Urine was positive for both phencyclidine and methadone. Creatinine phosphokinase ( C P K ) was 210 000 U; serum glutamic oxalacetic transaminase (SGOT), 2200 U; lactic dehydrogenase ( L D H ) , more than 600 U; blood urea nitrogen (BUN), 22 m g / d l ; and creatinine, 1.5mg/dl. T h e urine was orthotolidine-positive, and the sediment contained several golden-brown casts and no erythrocytes. Urine was positive for myoglobin by the complement-fixation technique. Bilirubin was 0.9 m g / d l ; alkaline phosphatase, 80 U; Na, 145 meq/litre; K, 3.9 meq/litre; C 0 2 , 25 meq/litre; C I , 108 meq/litre; Ca, 9.8 m g / d l ; phosphate, 2.3 m g / d l ; uric acid, 7.4 m g / d l ; hemoglobin, 14 g/dl; leukocytes, 18 0 0 0 / m m 3 with a left shift; and glucose, 209 m g / dl. Chest roentgenogram, electrocardiogram, and arterial blood gases were normal. The patient was thought to have suffered acute muscle injury with myoglobinuria related to an intravenous overdose of phencyclidine. Vigorous diuresis was begun, and one dose of furosemide was given. N o further dystonic motor activity was observed in the hospital, and renal function remained normal; the patient was discharged home on the eighth hospital day. Quadriceps muscle biopsy was done on the second hospital day. Pathologic evaluation under light microscopy was normal, but electron microscopy showed scattered " Z - b a n d " smearing in myofilaments and lysozomal swelling. Histochemical stains also showed evidence of lysozomal abnormalities. These changes were nonspecific but consistent with diffuse muscle injury. PATIENT 2
A 19-year-old m a n developed abdominal pain and became stuporous after ingestion of 21 P C P tablets. When found unconscious by his parents, he had aimless hyperactive movements of all extremities. On admission to the Wayne County Hospital approximately 6 h after his ingestion, he was stuporous. Blood pressure was 140/90 m m Hg; pulse, 100; temperature, 38.3 °C; and respiration, 18. N o needle tracks were seen. Funduscopic, cardiac pulmonary, and abdominal examinations were normal. Repetitive dystonic flexor and extensor activity was observed in all extremities, and soft restraints were required. Contraction of facial muscles, grimacing, and opisthotonos were also noted. Reflex, cranial nerve, and gross sensory examinations were unremarkable. Gastric aspirate, serum, and urine were positive for phencyclidine. T h e C P K was 1900 U; SGOT, 90 U; L D H , 160 U; B U N 17 m g / d l ; and creatinine, 1.2 m g / d l . Urinalysis showed 1 + protein, orthotolidine positivity, golden-brown casts, and no erythrocytes. Urine was positive for myoglobin. Hemoglobin was 15.5 g/dl; leukocytes, 8900 mm 3 ; Na, 138 meq/litre; K, 4.1 meq/litre; C 0 2 , 24 meq/litre; C I , 102 meq/litre; bilirubin, 1.0 m g / d l ; alkaline phosphatase 55 U; Ca, 9.5 m g / d l ; phosphate, 4.2 m g / d l . Chest film, electrocardiogram, and results of lumbar Annals of Internal Medicine 88:210-212, 1978
puncture were unremarkable. Electroencephalogram was diffusely abnormal. Diagnosis of phencyclidine overdose was made, and assisted ventilation and vigorous diuresis were instituted. By the second day, myotonic activity against restraint was more pronounced despite large doses of diazepam. The CPK continued to rise to 40 000 U by the third day coincident with his continuing dystonic motor activity. Peripheral muscle blockade with pancuronium was then instituted to maintain the airway. The CPK level dropped to 9000 U within 24 h of pancuronium-induced motor paralysis. The remainder of the hospitalization was complicated by central nervous system depression, pulmonary infection, and complications of assisted ventilation. Renal function remained normal. By the 15th day, he was alert; however, transfer to ambulatory psychiatric service was necessary because of frank psychotic behavior.
Discussion
Certain similarities were noted in both young male patients suffering from phencyclidine intoxication, which was confirmed in each by direct chemical analysis of the urine by the gas chromatographic mass spectrometric technique (7). After self-administration of the drug, each patient suffered recurrent episodes of muscular hyperactivity accompanying prolonged central nervous system depression. Other known causes of nontraumatic rhabdomyolysis were not present. Grossman, Klawans, and Melyn (8) observed similar involuntary movements of the extremities accompanied by opisthotonus, torticollis, and facial grimacing in a young phencyclidine-intoxicated patient and termed this neuromuscular behavior an acute dystonic reaction. In each of our patients, exaggerated motor activity and agitation were countered with physical and mechanical restraint, both before arrival and during hospitalization. Thus, dystonic motor activity was accompanied by isometric muscle contraction. Evidence for acute and ongoing injury to skeletal muscle with resultant release of myoglobin was found on admission and seemed to correlate with the motor activity in these patients. Abolition of motor stress with intentional peripheral motor paralysis in one of the two patients resulted in dramatic reduction in levels of muscle enzymes. Early recognition of ongoing rhabdomyolysis led to vigorous therapeutic measures directed at the prevention of myoglobinuric renal failure. Phencyclidine, which initially showed promise as a general anesthetic-analgesic, has been restricted to veterinary use primarily because of its hallucinogenic and schizophrenomimetic side-effects. Domino, Luby, and associates (2, 9) have described various neurologic and cognitive abnormalities as well as repetitive motor behavior in human volunteers given subanesthetic doses of phencyclidine. In some animal species treated with the drug, catatoniclike posturing or increased motor activity was observed (10, 11). There is no evidence that phencyclidine has direct toxic effects on either animal or human skeletal muscle. Kuncl and Meltzer (12) observed marked locomotor activity in rats injected with phencyclidine. Elevations of C P K 100 times normal were observed when phencyclidine-treated animals were restrained in immobilizing cages (12). The rise in C P K was highly correlated with
isometric muscle tension developed during the restraint periods. Muscle biopsy showed scattered necrosis of muscle fibers and myofibrillar disruption. These nonspecific myopathic changes did not occur in the restrained, phencyclidine-treated animal when the motor nerve to the biopsied area was previously interrupted. Likewise, rhabdomyolysis did not occur in the restrained untreated and in drug-treated, but unrestrained, animals. The prevention of morphologic pathology by previous denervation suggested that intense muscle activity against restraint, induced in some manner by toxic doses of phencyclidine, resulted in damage to skeletal muscle. Although routine hematoxylin and eosin sections from the muscle biopsy of our Patient 1 were essentially normal, myofibrillar changes seen under electronic microscopy Were strikingly similar to the myofibrillar changes reported from the hyperactive restrained muscle of KuncFs and Meltzer's rats. Tong and coworkers (13) have recently reported on the toxicity of phencyclidine in a group of patients from the San Francisco area. Although dyskinetic motor reactions were described, neither frank muscle injury nor renal failure was reported. Dandavino and colleagues (14), however, have recently reported a case of acute renal failure in a young man suffering from phencyclidine toxicity. They describe an agitated comatose patient with unusual exaggerated motor activity with associated elevations of C P K and other muscle enzymes and with a normal skeletal muscle biopsy. The authors attributed the acute renal failure to a vasculitis and treated their patient with steroids. We suspect that their patient was actually suffering from unrecognized myoglobinuric renal failure. Phencyclidine is recognized by those of the drug culture and by many unsuspecting young people as a readily available, rather inexpensive, and relatively safe psychedelic drug. Overdose with this agent is becoming a more serious and common medical problem in many localities (15). Moreover, the rising cost of marijuana may tempt more experimentation with PCP. Unfortunately, little publicity has been given to the potentially lethal manifestations of phencyclidine when taken in excess. We wish, therefore, to alert physicians who may be dealing with such patients to a newly recognized consequence of phencyclidine toxicity; that of an acute dystonic reaction with rhabdomyolysis and the potential of myoglobinuric renal failure. We would urge, therefore, that all patients under observation for documented or suspected phencyclidine overdose be screened for acute rhabdomyolysis. When this complication is diagnosed, prompt treatment to forestall myoglobinuric renal shutdown should be undertaken. From our recent experiences, we suggest that phencyclidine toxicity be included in the differential diagnosis of acute nontraumatic rhabdomyolysis with myoglobinuria and that this entity should be considered among the potential causes of acute myoglobinuric renal failure. ACKNOWLEDGMENTS: Received 28 September 1977; revision accepted 17 October 1977. • Requests for reprints should be addressed to E.F. Domino, M.D., MG322 Medical Science Building, University of Michigan, Ann Arbor, MI 48109. Cogenetal.
Downloaded from https://annals.org by University of Otago user on 12/16/2018
• Phencyclidine and Rhabdomyolysis
211
References 1. H A R T JB, M C C H E S N E Y JC, G R I E F M: Composition of illicit drugs and the use of drug analysis and abuse abatement. J Psychedelic Drugs 5:8388, 1972 2. D O M I N O EF, LUBY ED: Abnormal mental states induced by phencyclidine as a model of schizophrenia, in Psychopathology and Psychopharmacology, edited by C O L E JO, FREEDMAN AM, FRIEDHOFF AJ. Proceedings of the 62nd Meeting of American Psychopathic Association. Baltimore, Johns Hopkins Press, 1973, pp. 37-50 3. RAINEY JM, C R O W D E R MK: Prevalence of phencyclidine in street drug preparations. N Engl J Med 290:466-467, 1974 4. R I C H L E R RW, C H A L L E N O R YB, P E A R S O N J, K A G E N LJ, H A M I L T O N
LL, RAMSEY WH: Acute myoglobinuria associated with heroin addiction. JAMA 216:1172-1176, 1971 5. K L O C K J, SEXTON M: Rhabdomyolysis and acute myoglobinuric renal failure following heroin use. Calif Med 119:5-8, 1973 6. G R O S S M A N RA, H A M I L T O N RW, M O R S E BM, P E N N AS, G O L D B E R G
M: Nontraumatic rhabdomyolysis and acute renal failure. N Engl J Med 291:807-811, 1974 7. D O M I N O EF, WILSON AE: Effects of urine acidification on plasma and urine phencyclidine levels in overdosage. Clin Pharmacol Ther, in press
212
8. GROSSMAN HJ, K L A W A N S HL, M E L Y N MA: Considerations in the
drug treatment of drug-induced and other acute dyskinesias. / Pediatr 85:142, 1974 9. L U B Y ED, C O H E N BD, R O S E N B A U M G, G O T T L I E B JS, K E L L Y R: Study
of a new schizophrenomimetic drug—Sernyl. Arch Neurol Psychiatry 81:363-372, 1959 10. D O M I N O EF: Neurobiology of phencyclidine. Int Rev Neurobiol 6:303347, 1964 11. C H E N G, E N S O R C, R U S S E L L D, B O H N E R B: The pharmacology of 1-(1-
phencyclohexyl) piperidine-HCl. J Pharmacol Exp Ther 127:241-250, 1959 12. K U N C L RW, M E L T Z E R HY: Pathologic effect of phencyclidine and restraint on rat skeletal muscle: prevention by prior denervation. Exp Neurol 45:387-402, 1974 13. T O N G TG, B E N O W I T Z NL, B E C K E R CE, F O R N I PJ, B O E R N E R U: Phen-
cyclidine poisoning. JAMA
ication aigue a la phencyclidine avec atteinte musculaire importante et insufficance renale aigue. Union Med Can 104:57-60, 1975 15. L I D E N CB, LOVEJOY FH, COSTELLO CE: Phencyclidine. nine cases of poisoning. JAMA 234:513-516, 1975
February 1978 • Annals of Internal Medicine • Volume 88 • Number 2
Downloaded from https://annals.org by University of Otago user on 12/16/2018
234:512-513, 1975
14. D A N D A V I N O R, FRIBORG J, B E A U D R Y C, L A P L A N L E L: Un cas d'intox-
Phencyclidine (PCP) is a dissociative veterinary anesthetic and tranquilizer that at present is being abused as a psychedelic and hallucinogenic agent with increasing frequency. The cases of two young patients suffering from phencyclidine toxicity are reported. In each, central nervous system depression was accompanied by an acute dystonic motor reaction resulting in acute rhabdomyolysis and myoglobinuria. Skeletal muscle injury was felt to be the result of excessive involuntary isometric motor activity rather than a direct effect of phencyclidine on skeletal muscle. Patients suffering from phencyclidine intoxication should be screened for acute rhabdomyolysis. Phencyclidine intoxication should be included in the differential of nontraumatic rhabdomyolysis and should be considered among the potential causes of acute myoglobinuric renal failure.
P H E N C Y C L I D I N E , a dissociative anesthetic used in veterinary medicine, is being abused by the psychedelic drug culture with ever-increasing frequency. K n o w n as the "Pea Cea Pill" (PCP), "Angel D u s t , " and " H o g " , it may be smoked, swallowed, "snorted," or injected parenterally. Phencyclidine is frequently found masquerading as other street drugs including 9-THC, LSD, and mescaline. It was detected in 184 out of 237 samples of illicit drugs in a recent survey (1). Clinical toxicity includes thought disorders, sympathetic dysfunction, and varying degrees of analgesia and anesthesia (2, 3). Acute rhabdomyolysis and myoglobinuria have been previously reported in patients abusing heroin (4, 5) and amphetamines (6). We report two cases in which phencyclidine abuse was associated with unusual muscular hyperactivity and profound rhabdomyolysis with myoglobinuria. Case Histories PATIENT 1
A 21-year-old male former heroin addict, maintained on daily methadone, developed abdominal cramps, vomiting, and then stupor after intravenous self-administration of "PCP." Within 2 h of the overdose, the patient became agitated and observers had to physically restrain him because of repeated episodes of writhing tonic movements of extremities accompanied by exaggerated myotonic contractions and opisthotonos. He was admitted to the Wayne County Hospital 20 h after the phencyclidine injection. On arrival at the hospital, the patient was semistuporous, • From the Section of Nephrology, Department of Medicine, Wayne County General Hospital; Eloise, Michigan; and the Department of Pharmacology, The University of Michigan; Ann Arbor, Michigan. 210
© 1978 American College of Physicians
Downloaded from https://annals.org by University of Otago user on 12/16/2018
dysarthric, and confused. Blood pressure was 150/80 m m Hg; pulse, 96; temperature, 38.3 °C; and abdominal examinations were unremarkable. Diffuse muscle tenderness was present without evidence of soft-tissue trauma. Horizontal nystagmus was observed, but pupillary reactions and cranial nerves were intact. Motor tone and power were normal, and reflex and sensory examinations were unremarkable. Urine was positive for both phencyclidine and methadone. Creatinine phosphokinase ( C P K ) was 210 000 U; serum glutamic oxalacetic transaminase (SGOT), 2200 U; lactic dehydrogenase ( L D H ) , more than 600 U; blood urea nitrogen (BUN), 22 m g / d l ; and creatinine, 1.5mg/dl. T h e urine was orthotolidine-positive, and the sediment contained several golden-brown casts and no erythrocytes. Urine was positive for myoglobin by the complement-fixation technique. Bilirubin was 0.9 m g / d l ; alkaline phosphatase, 80 U; Na, 145 meq/litre; K, 3.9 meq/litre; C 0 2 , 25 meq/litre; C I , 108 meq/litre; Ca, 9.8 m g / d l ; phosphate, 2.3 m g / d l ; uric acid, 7.4 m g / d l ; hemoglobin, 14 g/dl; leukocytes, 18 0 0 0 / m m 3 with a left shift; and glucose, 209 m g / dl. Chest roentgenogram, electrocardiogram, and arterial blood gases were normal. The patient was thought to have suffered acute muscle injury with myoglobinuria related to an intravenous overdose of phencyclidine. Vigorous diuresis was begun, and one dose of furosemide was given. N o further dystonic motor activity was observed in the hospital, and renal function remained normal; the patient was discharged home on the eighth hospital day. Quadriceps muscle biopsy was done on the second hospital day. Pathologic evaluation under light microscopy was normal, but electron microscopy showed scattered " Z - b a n d " smearing in myofilaments and lysozomal swelling. Histochemical stains also showed evidence of lysozomal abnormalities. These changes were nonspecific but consistent with diffuse muscle injury. PATIENT 2
A 19-year-old m a n developed abdominal pain and became stuporous after ingestion of 21 P C P tablets. When found unconscious by his parents, he had aimless hyperactive movements of all extremities. On admission to the Wayne County Hospital approximately 6 h after his ingestion, he was stuporous. Blood pressure was 140/90 m m Hg; pulse, 100; temperature, 38.3 °C; and respiration, 18. N o needle tracks were seen. Funduscopic, cardiac pulmonary, and abdominal examinations were normal. Repetitive dystonic flexor and extensor activity was observed in all extremities, and soft restraints were required. Contraction of facial muscles, grimacing, and opisthotonos were also noted. Reflex, cranial nerve, and gross sensory examinations were unremarkable. Gastric aspirate, serum, and urine were positive for phencyclidine. T h e C P K was 1900 U; SGOT, 90 U; L D H , 160 U; B U N 17 m g / d l ; and creatinine, 1.2 m g / d l . Urinalysis showed 1 + protein, orthotolidine positivity, golden-brown casts, and no erythrocytes. Urine was positive for myoglobin. Hemoglobin was 15.5 g/dl; leukocytes, 8900 mm 3 ; Na, 138 meq/litre; K, 4.1 meq/litre; C 0 2 , 24 meq/litre; C I , 102 meq/litre; bilirubin, 1.0 m g / d l ; alkaline phosphatase 55 U; Ca, 9.5 m g / d l ; phosphate, 4.2 m g / d l . Chest film, electrocardiogram, and results of lumbar Annals of Internal Medicine 88:210-212, 1978
puncture were unremarkable. Electroencephalogram was diffusely abnormal. Diagnosis of phencyclidine overdose was made, and assisted ventilation and vigorous diuresis were instituted. By the second day, myotonic activity against restraint was more pronounced despite large doses of diazepam. The CPK continued to rise to 40 000 U by the third day coincident with his continuing dystonic motor activity. Peripheral muscle blockade with pancuronium was then instituted to maintain the airway. The CPK level dropped to 9000 U within 24 h of pancuronium-induced motor paralysis. The remainder of the hospitalization was complicated by central nervous system depression, pulmonary infection, and complications of assisted ventilation. Renal function remained normal. By the 15th day, he was alert; however, transfer to ambulatory psychiatric service was necessary because of frank psychotic behavior.
Discussion
Certain similarities were noted in both young male patients suffering from phencyclidine intoxication, which was confirmed in each by direct chemical analysis of the urine by the gas chromatographic mass spectrometric technique (7). After self-administration of the drug, each patient suffered recurrent episodes of muscular hyperactivity accompanying prolonged central nervous system depression. Other known causes of nontraumatic rhabdomyolysis were not present. Grossman, Klawans, and Melyn (8) observed similar involuntary movements of the extremities accompanied by opisthotonus, torticollis, and facial grimacing in a young phencyclidine-intoxicated patient and termed this neuromuscular behavior an acute dystonic reaction. In each of our patients, exaggerated motor activity and agitation were countered with physical and mechanical restraint, both before arrival and during hospitalization. Thus, dystonic motor activity was accompanied by isometric muscle contraction. Evidence for acute and ongoing injury to skeletal muscle with resultant release of myoglobin was found on admission and seemed to correlate with the motor activity in these patients. Abolition of motor stress with intentional peripheral motor paralysis in one of the two patients resulted in dramatic reduction in levels of muscle enzymes. Early recognition of ongoing rhabdomyolysis led to vigorous therapeutic measures directed at the prevention of myoglobinuric renal failure. Phencyclidine, which initially showed promise as a general anesthetic-analgesic, has been restricted to veterinary use primarily because of its hallucinogenic and schizophrenomimetic side-effects. Domino, Luby, and associates (2, 9) have described various neurologic and cognitive abnormalities as well as repetitive motor behavior in human volunteers given subanesthetic doses of phencyclidine. In some animal species treated with the drug, catatoniclike posturing or increased motor activity was observed (10, 11). There is no evidence that phencyclidine has direct toxic effects on either animal or human skeletal muscle. Kuncl and Meltzer (12) observed marked locomotor activity in rats injected with phencyclidine. Elevations of C P K 100 times normal were observed when phencyclidine-treated animals were restrained in immobilizing cages (12). The rise in C P K was highly correlated with
isometric muscle tension developed during the restraint periods. Muscle biopsy showed scattered necrosis of muscle fibers and myofibrillar disruption. These nonspecific myopathic changes did not occur in the restrained, phencyclidine-treated animal when the motor nerve to the biopsied area was previously interrupted. Likewise, rhabdomyolysis did not occur in the restrained untreated and in drug-treated, but unrestrained, animals. The prevention of morphologic pathology by previous denervation suggested that intense muscle activity against restraint, induced in some manner by toxic doses of phencyclidine, resulted in damage to skeletal muscle. Although routine hematoxylin and eosin sections from the muscle biopsy of our Patient 1 were essentially normal, myofibrillar changes seen under electronic microscopy Were strikingly similar to the myofibrillar changes reported from the hyperactive restrained muscle of KuncFs and Meltzer's rats. Tong and coworkers (13) have recently reported on the toxicity of phencyclidine in a group of patients from the San Francisco area. Although dyskinetic motor reactions were described, neither frank muscle injury nor renal failure was reported. Dandavino and colleagues (14), however, have recently reported a case of acute renal failure in a young man suffering from phencyclidine toxicity. They describe an agitated comatose patient with unusual exaggerated motor activity with associated elevations of C P K and other muscle enzymes and with a normal skeletal muscle biopsy. The authors attributed the acute renal failure to a vasculitis and treated their patient with steroids. We suspect that their patient was actually suffering from unrecognized myoglobinuric renal failure. Phencyclidine is recognized by those of the drug culture and by many unsuspecting young people as a readily available, rather inexpensive, and relatively safe psychedelic drug. Overdose with this agent is becoming a more serious and common medical problem in many localities (15). Moreover, the rising cost of marijuana may tempt more experimentation with PCP. Unfortunately, little publicity has been given to the potentially lethal manifestations of phencyclidine when taken in excess. We wish, therefore, to alert physicians who may be dealing with such patients to a newly recognized consequence of phencyclidine toxicity; that of an acute dystonic reaction with rhabdomyolysis and the potential of myoglobinuric renal failure. We would urge, therefore, that all patients under observation for documented or suspected phencyclidine overdose be screened for acute rhabdomyolysis. When this complication is diagnosed, prompt treatment to forestall myoglobinuric renal shutdown should be undertaken. From our recent experiences, we suggest that phencyclidine toxicity be included in the differential diagnosis of acute nontraumatic rhabdomyolysis with myoglobinuria and that this entity should be considered among the potential causes of acute myoglobinuric renal failure. ACKNOWLEDGMENTS: Received 28 September 1977; revision accepted 17 October 1977. • Requests for reprints should be addressed to E.F. Domino, M.D., MG322 Medical Science Building, University of Michigan, Ann Arbor, MI 48109. Cogenetal.
Downloaded from https://annals.org by University of Otago user on 12/16/2018
• Phencyclidine and Rhabdomyolysis
211
References 1. H A R T JB, M C C H E S N E Y JC, G R I E F M: Composition of illicit drugs and the use of drug analysis and abuse abatement. J Psychedelic Drugs 5:8388, 1972 2. D O M I N O EF, LUBY ED: Abnormal mental states induced by phencyclidine as a model of schizophrenia, in Psychopathology and Psychopharmacology, edited by C O L E JO, FREEDMAN AM, FRIEDHOFF AJ. Proceedings of the 62nd Meeting of American Psychopathic Association. Baltimore, Johns Hopkins Press, 1973, pp. 37-50 3. RAINEY JM, C R O W D E R MK: Prevalence of phencyclidine in street drug preparations. N Engl J Med 290:466-467, 1974 4. R I C H L E R RW, C H A L L E N O R YB, P E A R S O N J, K A G E N LJ, H A M I L T O N
LL, RAMSEY WH: Acute myoglobinuria associated with heroin addiction. JAMA 216:1172-1176, 1971 5. K L O C K J, SEXTON M: Rhabdomyolysis and acute myoglobinuric renal failure following heroin use. Calif Med 119:5-8, 1973 6. G R O S S M A N RA, H A M I L T O N RW, M O R S E BM, P E N N AS, G O L D B E R G
M: Nontraumatic rhabdomyolysis and acute renal failure. N Engl J Med 291:807-811, 1974 7. D O M I N O EF, WILSON AE: Effects of urine acidification on plasma and urine phencyclidine levels in overdosage. Clin Pharmacol Ther, in press
212
8. GROSSMAN HJ, K L A W A N S HL, M E L Y N MA: Considerations in the
drug treatment of drug-induced and other acute dyskinesias. / Pediatr 85:142, 1974 9. L U B Y ED, C O H E N BD, R O S E N B A U M G, G O T T L I E B JS, K E L L Y R: Study
of a new schizophrenomimetic drug—Sernyl. Arch Neurol Psychiatry 81:363-372, 1959 10. D O M I N O EF: Neurobiology of phencyclidine. Int Rev Neurobiol 6:303347, 1964 11. C H E N G, E N S O R C, R U S S E L L D, B O H N E R B: The pharmacology of 1-(1-
phencyclohexyl) piperidine-HCl. J Pharmacol Exp Ther 127:241-250, 1959 12. K U N C L RW, M E L T Z E R HY: Pathologic effect of phencyclidine and restraint on rat skeletal muscle: prevention by prior denervation. Exp Neurol 45:387-402, 1974 13. T O N G TG, B E N O W I T Z NL, B E C K E R CE, F O R N I PJ, B O E R N E R U: Phen-
cyclidine poisoning. JAMA
ication aigue a la phencyclidine avec atteinte musculaire importante et insufficance renale aigue. Union Med Can 104:57-60, 1975 15. L I D E N CB, LOVEJOY FH, COSTELLO CE: Phencyclidine. nine cases of poisoning. JAMA 234:513-516, 1975
February 1978 • Annals of Internal Medicine • Volume 88 • Number 2
Downloaded from https://annals.org by University of Otago user on 12/16/2018
234:512-513, 1975
14. D A N D A V I N O R, FRIBORG J, B E A U D R Y C, L A P L A N L E L: Un cas d'intox-
