Henry Ford Hospital Medical Journal

Volume 38 Number 4 Article 14

12-1990

Passive Inhalation of Cocaine by Infants

Sabrina M. Heidemann

Mark G. Goetting

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Recommended Citation Heidemann, Sabrina M. and Goetting, Mark G. (1990) "Passive Inhalation of Cocaine by Infants," Henry Ford Hospital Medical Journal : Vol. 38 : No. 4 , 252-254. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol38/iss4/14

This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Original Contributions and Case Studies

Passive Inhalation of Cocaine by Infants

Sabrina M. Heidemann, MD,* and Mark G. Goetting, MD^

Cocaine abuse has increased gready in recent years, creating important medical, legal, and social problems. Urine drug testing is used to diagnose cocaine ingestion. The presence of the cocaine metabolite benzoylecgonlne (BZ) is commonly believed to be proof of recent cocaine intoxication. However, oral ingestion of even a minute quantity of cocaine can resull in a positive test resuh. BZ was delected in the urine of four nonbreast-fed infants aged 6 weeks to 14 months who were admitted with diagnoses unrelated to cocaine poisoning. These infants were exposed to cocaine hy passive inhalation of vapors generated by adult caretakers smoking "crack" cocaine. Two ofthe infants were retested 12 hours later and had no detectable BZ, strongly suggesting ingestion of a subpharmacologic amounl of cocaine. Because passive inhalation of cocaine can produce measurable urine BZ concentrations, a positive urine screen does nol necessarily indicate poisoning or intentional administration of the substance and therefore is not proof of child abuse or neglect. (Henry Ford Hosp Med J 1990;38:252-4)

ocaine use is widespread in our society. By 1986, 15% of raother's nipples before breast feeding (7). It has recentiy been Cthe United States population had used cocaine, with 40% of suggested that cocaine poisoning can occur by passive inhala­ those being between 25 and 30 years of age (1). Cocaine is avail­ tion of crack vapors (11). We report four children with urine co­ able as a hydrochloride salt which can be injected intravenously caine raetabolites present on admission to the hospital. All were or appUed to a raucous raerabrane, usuaUy intranasally (1,2). It unintentionally exposed to cocaine vapors in a room where is delivered raorerapidl y to the brain when smoked in its base crack was smoked. The erroneous belief that the detection of co­ forra called "crack" (1,3). Crack cocaine raore likely leads to ad- caine raetabolites in the urine proved intentional poisoning had dicrion because it is usually consuraed in doses three to six rimes profound social and legal iraplications. higher than cocaine hydrochloride and has a more rapid route of delivery (4). Unfortunately, crack cocaine has recently becorae Case Reports more available at a relatively low cost, precipitating an increase in the nuraber of cocaine addicts. The habitual use of cocaine by Case 1 parents and other caretakers can have profound effects on chil­ A formula fed, 3-month-old girl presented with status epileptii^"* dren. following several days of vomiting and diarrhea. After successful anti convulsant therapy she remained comatose. She appeared dehydra An increasing nuraber of infants are bom to women addicted and had severe diaper dermatitis with full-thickness ulcers. Her sera"' to cocaine (5,6). The adverse irapact on infant raorbidity and sodium was 162 mEq/L, and BUN 28 mg/dL. Cranial computed'"' mortality has been recentiy documented (5-9). Prenatal use of mography and cerebral angiography revealed a superior sagittal sim* cocaine is associated with spontaneous abortion, premature la­ thrombosis with extensive bilateral cerebral infarcts. Despite vigof bor, abruptio placentae, congenital malforraarions, low birth supportive care, she progressed to brain death. A urine toxico weight, cerebral infarction, and seizures (5-9). Neurobehavioral screen on admission showed benzoylecgonlne (BZ) by both radi abnorraalities have been noted in the neonatal period (5). The long-terra effects of cocaine exposure on the developing ner­ Submitted for publication: September 21.1990. Accepted for publication; December 20, 1990, ^fPe vous system are unknown. •Formerly Department of Pediatrics, Henry Ford Hospital. Currently Departme" In a review of 75 cases of child abuse by poisoning, none of diatrics, William Beaumont Hospital, Royal Oak, Ml. tDepartment of Pediatrics, Division of Critical Care Medicine, Henry ford ^''^^^^^H^ the children had cocaine poisoning (10). However, a case of Address correspondence to Dr. Goetting, Department of Pediatrics, Division accidental poisoning followed the application of cocaine to a Care Medicine, Henry Ford Hospital, 2799 W Grand Blvd, Detroil, Ml 48202. '2). Coc

252 Henry Ford Hosp Med J—Vol 38, No 4. 1990 Passive Inhalation of Cocaine—Heidemann jjsay enzyme-multiplied immunoassay test (EMIT) meth- time administration (12). High dose, chronic cocaine admini­ Gas chromatography/mass spectrometry (GC/MS) confirmation stration has been associated in some cases with the presence of 0^^' gfformed. A repeat urine test 12 hours after admission was nega- BZ for 10 to 22 days after the last cocaine ingesrion (13). Con­ '^he baby's caretakers stated that crack was smoked daily around clusions conceming cocaine kinetics in terras of the last dose, ""^baby When questioned further, they stated that they would not route of adrainistration, and frequency of use have not been '''^ their cocaine on a baby. All denied the possibility of cocaine "ivaste , i„gestion by any other route. thoroughly studied (12). Routine urine toxicology screening for cocaine detects BZ by the EMIT raethod. A positive result is typically 300 ng/mL of BZ or greater (14). False-positive results are not known to oc­ /V l2-month-old boy presented with rhinorrhea, mild epistaxis, and cur (15,16). The urine BZ test is very sensitive. Recreational co­ •ver He was alert and behaved appropriately. He had distant heart unds and hepatomegaly. Chest radiography revealed enlargement of caine use can result in a positive test for two to three days fol­ ^ardioper'cardial silhouette. The blood and pericardial fluid yielded lowing ingestion (13). Clinically, even sraall amounts of co­ ''jiaetiiophilu^ influenzae. He was treated by pericardial drainage and caine can produce BZ detection. Ingestion of 50 rag of cocaine antibiotics, and completely recovered. For unclear reasons, the house is necessary for a pharmacological effect in adults. However, officer sent urine for toxicology screening on admission. BZ was de­ 25 rag of an oral dose of cocaine resulted in a positive test for lected by the EMIT method. The mother and child lived in a home 48 hours (17). When 12 volunteers received 20 mg of cocaine where cocaine was smoked and sold on a regular basis. Following this administered to their comeas, the urine BZ test was positive for adfflissi'"^' the mother voluntarily gave custody of her children to her 36 hours in the majority (18). The sarae authors found that oph- l ilherand subsequently entered a drug rehabilitation facility. She ques­ thalraic instillation of 8 mg of cocaine resulted in a positive tioned whether her child would suffer complications from the cocaine urine test for up to 36 hours (unpublished data). Even as little as but consistently denied that her child had ingested cocaine in any way 2.15 rag of cocaine in a cup of coca tea yielded a urine concen­ other than by passive inhalation. tration of BZ greater than 300 ng/raL for 17.5 hours after inges­ tion (19). Crack is coramonly smoked in doses of 300 rag or Case 3 raore. The araount inhaled by a nearby infant would vary de­ A botde fed. 6-week-old boy was admitted with depressed con­ pending on the quantity of cocaine released into the air, total sciousness, hypothermia, and severe dehydration. He had been feeding tirae of exposure, and the dimensions of the roora. Brief passive pooriy for at least two weeks and had diarrhea for several days. On ex­ sraoke exposure could result in cocaine metabolites in the urine. amination he was remarkably malnourished and dehydrated in appear­ ance with a temperature of 31.1 °C (87.9°F) rectally, a heart rate of 70 Cocaine poisoning by passive inhalation of cocaine smoke beats/min, gasping respirations, and blood pressure of 63/39 mm Hg. in infants and toddlers has been suggested in a recent report He was unresponsive to painful procedures. The remainder of his ex­ (11). While these four children had BZ in the urine, it is not amination was unremarkable. He responded to supportive treatment in­ clear whether intoxication occurred. One presented with exces­ duding volume resuscitation and mechanical ventilation and was dis­ sive drowsiness and another with a focal seizure during sleep. charged ten days later. Urine toxicology screening on admission was None were described as having signs of adrenergic overactiv­ positive for BZ, GC/MS confirmation was performed. The mother ad­ ity that typifies cocaine intoxication. It seeras plausible that at mitted that the baby was frequently exposed to crack cocaine smoke. least some of these patients were exposed to subpharmacologic amounts of cocaine, causing positive urine testing. In another Case 4 report, three infants had unexpected evidence of cocaine inges­ A 14-month-old boy, who had spent the day with his aunt, was re­ tion by toxicology testing (20). The proposed routes of admini­ lumed to his mother's care after developing a fever and ear pain. Two stration were intentional poisoning and passive transmission hours later, while eating in a high chair, he had a brief generalized sei­ through breast railk. Passive exposure to crack vapors was not zure. Fifteen minutes following the seizure, he was examined in the raentioned. It is unlikely that any of our patients had cocaine in­ emergency department. He was alert and responsive with a temperature toxication. While stroke is a reported complication of cocaine of 39.5°C (103. TF), and his right tympanic membrane was red and ''uiging. Twenty minutes after arrival, he had a second brief seizure. abuse (2), our first patient had a severe cerebral venous throm­ Laboratory values revealed a WBC count of 24.1 \tf/L (24,100/pL) bosis with extensive infarcts apparent immediately after her sei­ *ith 22% bands. BZ was pre.sent on urine toxicology screening. Repeat zures ceased. This thrombosis is not unexpected with serious de­ "••ine testing at 12 and 24 hours was negative. The mother stated that the hydration. Our fourth patient had two brief convulsions raost ''oy s aunt had smoked crack in his presence on the day of admission. consistent with febrile seizures. His raental status and vital signs The aunt felt that cocaine would not quiet an irritable child and stated before and after the seizures and his appetite iraraediately before 'hai she did not feed him cocaine. the first seizure are not consistent with cocaine poisoning. Also, neither of these infants had detectable BZ 12 hours after the ini­ tial urine test. Following pharmacologic doses of cocaine, BZ Discussion persists in the urine typically for several days (2,12,13). The ab­ Cocaine is metabolized to BZ and ecgonine methylester by sence of BZ 12 hours after the seizures is strong evidence P asma and liver cholinesterases (2). The half-life of cocaine is against acute intentional oral intoxication. Following extensive ^minutes, and BZ 6 to 8 hours (12,13). Infants have a longer investigation of parents and other caretakers by physicians, l^^caine half-life due to decreased plasraa cholinesterase activity nurses, and social and protective service workers, we believe • Cocaine kinetics are based on low dose, intravenous, one­ that these four children were not accidentally or intentionally

'"fy Ford Hosp Mod Vol 38, No 4, 1990 Passive Inhalation of Cocaine—Heidemann & Goetting 253 poisoned but had a positive drug screen frora passively inhaling 4, Siegel RK, Cocaine smoking (Letter). N Engl J Med I979;.300:373, cocaine vapors. 5, Chasnoff U, Bums WJ, Schnoll SH, Bums KA, Cocaine use in pregnancj,, NEngI JMed 1985;313:666-9, Few would disagree that cocaine addicts generally raake poor 6, Chasnoff IJ, Bussey ME, Savich R, Slack CM, Perinatal cerebral intarctioj parents. However, in the city of Detroit, parental use of cocaine and matemal cocaine use, J Pediatr 1986;108;456-9, alone does not constitute child neglect or abuse. Intentional poi­ 7, Chaney NE, Franke J, Wadlington WB, Cocaine convulsions in a breast, soning of a child would result in legal action. Recently, the fo­ feeding baby. J Pediatr 1988;112:134-5, rensic raedicalopinio n supplied to the police and child protec­ 8, Bingol N, Fuchs M, Diaz V, Slone RK. Gromisch DS. Teratogenicity of jj, caine in humans. J Pediatr 1987; 110:93-6, tion services was that cocaine raetabolitesi n the urine are proof 9, Chasnoff IJ, Lewis DE, Squires L, Cocaine intoxication in a breast-fed ij. of abuse or neglect. In case 1, the raother was charged with mur­ fant. Pediatrics 1987;80:836-8. der. Positive drug screens aided in removing the child from the 10, Tenenbein M, Pediatric toxicology: Currenl controversies and receni ad. horae in cases 2 and 3. vances. Curr ProbI Pediatr 1986;16:185-233. In conclusion, our cases suggest that cocaine metabolites raay 11, Bateman DA, Heagarly MC, Passive freebase cocaine ("crack") inhala. tion by infants and toddlers. Am J Dis Child 1989;143:25-7. be present in the urine after passive inhalarion of cocaine vapors. 12, Ambre J. The urinary excretion of cocaine and metabolites in humans; A Infants who reside in crack houses are chronically exposed to kinetic analysis of published dala, J Anal Toxicol 1985;9:241-5. cocaine sraoke and are probably at high risk for a posirive co­ 13, Weiss RD, Gawin FH. Protracted elimination of cocaine metabolites ij caine urine test. Medical and developmental effects of this situa­ long-term, high-dose cocaine abusers. Am J Med l988;85;879-80. tion are unknown. Legal implications are significant. Controlled 14, Joem WA. Routine detection of benzoylecgonlne in urine at a sensihvity of 35 ng/mL by a combination of EMIT and gas chromatography/mass spec­ laboratory studies may be necessary to establish the association trometry. J Anal Toxicol 1987; 11:110-2. of cocaine vapors by passive inhalation and cocaine metabolites 15, Allen LV Jr, Stiles ML. Specificity of the EMIT drug abuse urine assay in the urine. methods. Clin Toxicol 1981;18;l043-65, 16, Mikkelsen SL, Ash KO. Adulterants causing false negatives in illicit drug testing, Clin Chem 1988;34;2333-6, References 17, Basell RC, Chang R, Urinary excretion of cocaine and benzoylecgonine 1. Gawin FH, EUinwood EH Jr. Cocaine and olher stimulants; Actions, abuse, following oral ingestion in a single subjecl. J Anal Toxicol 1987; 11:81-2, and treatment. N Engl J Med 1988;318:1173-82. 18, Bralliar BB. Skarf B. Owens JB. Ophthalmic use of cocaine and the urine 2. Cregler LL, Mark H. Medical complications of cocaine abuse. N Engl J test for benzoylecgonine (Letter), N Engl J Med 1989:320:1757-8, Med 1986;315:1495-5(X), 19, elSohly MA, Stanford DF, elSohly HN, Coca lea and urinalysis for co­ 3. Jekel JF, Allen DF, Podlew.ski H, Clarke N, Dean-Patterson S, Cartwright caine metabolites (Leiler), J Anal Toxicol 1986; 10:256, P, Epidemic free-base cocaine abuse. Case study from the Bahamas, Lancet 20, Shannon M, Lacoulure PG. Roa J. Woolf A, Cocaine exposure among 1986;1:459-62. children .seen al a pediatric ho.spital. Pediatrics 1989:83:337-42.

254 Henry Ford Hosp Med J—Vol 38, No 4, 1990 Passive Inhalation of Cocaine—Heidemann