1Kramp KH, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2018-224345

Case report

Cardiac arrest by inhalation of deodorant sprayKelvin Harvey Kramp, Mahdi salih, elsbeth thomeer, Martin Gardien

Unexpected outcome (positive or negative) including adverse drug reactions

To cite: Kramp KH, salih M, thomeer e, et al. BMJ Case Rep published online First: [please include Day Month Year]. doi:10.1136/bcr-2018-224345

Intensive Care, Maasstad Ziekenhuis, rotterdam, the Netherlands

Correspondence toDr Kelvin Harvey Kramp, k. h. kramp@ gmail. com

accepted 13 september 2018

© BMJ publishing Group Limited 2018. No commercial re-use. see rights and permissions. published by BMJ.

SummaryDrug abuse by inhalation of volatile household product substances is uncommon, however, it can have devastating consequences. this case report describes the fatal outcome of deodorant inhalation by a 19-year-old patient in a detoxification clinic who developed a cardiac arrest after inhaling butane from a deodorant spray. Despite initial successful resuscitation, he developed a postanoxic encephalopathy with a status epilepticus resistant to extensive treatment. Inhalant abuse can be a cause of death in young patients.

BaCkground Volatile substances in household products can be used in various ways as drugs to attain an altered mental state. Although the gross of medical personnel is largely unfamiliar with intoxication due to inhalant abuse, the consequences can be severe. Cardiac arrest appears to be caused by increased myocardial sensitivity to catecholamines, coronary spasms, depressed myocardium or a combination of these pathophysiological mechanisms. This case report describes a patient under treatment in a drug rehabilitation centre that relapsed in drug abuse by abusing butane, an inhalant readily available in household products. The aim of this paper is to emphasise that there might be an increased risk of inhalation-related cardiac deaths in isolated envi-ronments, such as detoxification clinics or prisons, because patients within these places are more inclined to abuse household products.

CaSe preSenTaTionA 19-year-old man was admitted to our hospital after a cardiac arrest. He had been admitted in a drug rehabilitation centre due to cannabis and ketamine abuse. The patient had a history of psychotic symptoms and was therefore placed on the atypical antipsychotic drug aripiprazole. During a hang out with other patients in the clinic, he had placed a towel over his head and inhaled deodorant spray. He became hyperactive jumping up and down and afterwards collapsed. The psychiatric nurses applied basic life support. On arrival of the paramedics, the patient had ventricular fibrillation and was therefore defibrillated. After six defibrilla-tions, there was a return of spontaneous circulation and ST changes were observed on the inferior leads of the ECG (figure 1).

On arrival at our emergency department, the patient was intubated. He had a pulse of 88, blood pressure of 133/76, breathing frequency of 20 and saturation of 96%. Physical examination showed

no signs of (self) strangulation or other physical trauma. Initial laboratory investigation showed a lactate acidosis (table 1).

Family history did not give any clues for a hered-itable cause that could have led to the cardiac arrest. The chest X-ray revealed broken ribs and a haemothorax, most likely the consequence of basic life support. Toxic substance screening of the urine was negative for amphetamine, cocaine, cannabis, 3,4-methyleendioxymethamfetamine (XTC) and phencyclidine.

At arrival on the intensive care unit, the patient was placed on dobutamine, enoximon and nitro-glycerine.1 He was sedated with midazolam and remifentanil and therapeutic hypothermia was initi-ated (33°C during a period of 24 hours) with cold infusion and a Blanketrol III (Cincinnati Sub-Zero Products).2 On day 2, after reaching normothermia, the ECG had normalised and troponin levels were decreasing.

ouTCome and follow-upAfter stopping sedation the Glasgow Coma Score remained E1M1Vt. The patient showed persistent myoclonias despite treatment with propofol infusion and levetiracetam. This was accompa-nied by cerebral diabetes insipidus, suggested by increased urine production (maximum 1710 mL/hour), increased plasma sodium concentration and low urine osmolality (84 mOsm/L). Vasopressin was initiated with a consequent decrease in urine production. A brain CT-scan showed no signs of cerebral oedema or bleeding. Somatosensory evoked potential showed a bilateral present cortical negative peak at 20ms (N20) response, which did not predict a poor outcome per se. On day 3, the patient showed myoclonic jerks, for which leveti-racetam and propofol was started. On day 4, an electroencephalogram (EEG) showed spike and wave complexes with high index for which diph-antoine was added on. On day 5, the EEG showed generalised slow wave activity and excess of beta activity that was considered to be drug induced. Spike and wave complexes were still present but with a lower index compared with the day before. The patient had intermittent signs of an epileptic seizure for which valproate and midazolam were initiated along with the previously started propofol, levetiracetam and diphantoine. On day 7, the EEG showed an electrical status epilepticus. A barbitu-rate coma was induced with thiopental during two episodes of 24 hours with an initial reduction of epileptiform activity. On day 9, the second barbi-turate coma ended and the patient again showed rhythmic contractions of the eyebrows, knees and

2 Kramp KH, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2018-224345

unexpected outcome (positive or negative) including adverse drug reactions

repetitive swallowing. Considering the persistent Glasgow Coma Score (E1M1Vt) after stopping sedation and the recurrent signs of a status epilepticus on physical examination and EEG, unre-sponsive to treatment with propofol, levetiracetam, diphantoine and thiopental, further treatment was deemed futile. The patient was extubated and comfort care was given with morphine and midazolam. The patient died shortly thereafter.

diSCuSSionCardiac arrests after the inhalation of volatile substances have been reported for more than 40 years.3 The phenomenon

of sudden cardiac death after inhalant abuse has been named ‘sudden sniffing death’ after the epidemic of 110 cardiac arrests due to the rising popularity of glue sniffing in the 1960s among American youths.4 The first report of sudden cardiac death after butane intoxication due to the inhalation of deodorant spray was reported in 1975 by Kamm.5 There have been a large number of case reports afterwards describing cardiac arrests after deodorant inhalation, but only a few have described patients who survived after treatment.1 6

The misuse of volatile substances is one of the least known methods to attain an altered mental state by drugs. It is estimated that in the USA it causes 100–125 deaths per year.7 Inhalant abuse has a remarkable high prevalence in younger age groups, reaching its peak incidence between 15 and 19 years.7 8 The mean age of first use is 16.3 years, the youngest age of all drugs and the prevalence decreases sharply after the first few years after high school.7 9 The use of inhalants has been correlated with a low income, chaotic, fractured and abusive households.10 11 There is a 10-fold higher change of getting help from municipal care and the highest mortality is observed in urban populations.12

There is a long list of household products that can be used for inhalation.10 The substances can be categorised into: (1) volatile solutions such as lime, paint thinner and felt tip, (2) aerosols such as hairspray, deodorant and spray paint and (3) pressurised gasses such as from a lighter or camping gas.13 Inhalant abuse is usually categorised into three modalities: sniffing, huffing and bagging.14 Sniffing is the direct inhalation of volatile substances. Huffing is spraying the volatile substance on a piece of clothing and inhaling it through the nose or mouth. A piece of clothing can be soaked in a volatile substance, or as in our case, the substance can be sprayed through a clothing placed over the nose or mouth. Bagging is using a plastic bag or balloon to transfer the inhalant to outside of the original packing. A soaked clothing can be put into the plastic bag or the bag can be placed over the head. The latter carries the risk of hypoxia as a consequence of asphyxia next to inhalant intoxication, although getting unconscious would normally release the muscle tone needed to fixate the bag over the head. Which modality is used depends on the desired intensity and on the particular substance used. Often, there is a progression from sniffing to huffing and from huffing to bagging.15 Independent of the method of inhalation

figure 1 ECG after return of spontaneous circulation following defibrillation.

Table 1 Laboratory evaluation at admission

plasma

parameter result unit normal range

CRP <1 mg/L <1

WBC 31.2 10E9/L 4.0–10.0

Potassium 2.9 mmol/L 3.5–5.0

Sodium 136 mmol/L 135–145

Creatinine 133 µmol/L 64–104

Urea 5.3 mmol/L 2.5–6.4

eGFR 66 mL/min/1.73 m2 >90

Corrected Calcium 2.33 mmol/L 2.20–2.65

ALAT 148 U/L 0–41

ASAT 140 U/L 0–37

LDH 356 U/L 0–250

Troponin 0.06 µg/L 0.00–0.04

Glucose 18.8 mmol/L 4.4–5.5

Arterial blood gas

pH 7.14 7.35–7.45

Partial pressure of carbon dioxide

40 mm Hg 35–48

HCO3 14 mmol/L 21–28

Partial pressure of oxygen

81 mm Hg 75–100

Lactate 14.1 mmol/L 0.5–2.2

ALAT, alanine aminotransferase; ASAT, aspartate aminotransferase; CRP, C reactive protein; eGFR, estimated Glomerular Filtration rate; HCO3, Bicarbonate; LDH, lactate dehydrogenase; WBC, White blood cells.

3Kramp KH, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2018-224345

unexpected outcome (positive or negative) including adverse drug reactions

and concentration of toxic substance inhaled, sudden death from inhalant abuse can result during a first single dose or during chronic use. It is reported that 43% of deaths are related to the first-time inhalant abuse.16 17

The main toxic substance in deodorant spray inhalation is butane. Butane is one of the hydrocarbons commonly used as propellants in sprayable household products. Hydrocarbons are lipophilic and therefore easily cross the air–blood and blood–brain barrier. It dissolves into tissues with a high fat content such as the nervous system, fat tissue, liver and kidneys. Elimination is through respiration.10 The longer the carbon chain inhaled the higher the lipophilicity and the lower the onset threshold for the desired experience.10 Raines et al18 conducted an electrophysi-ological study of the effects of butane on the gamma-aminobu-tyric acid (GABA) receptors and observed butane has the ability to enhance the effects of agonists on the GABA receptor.18 Thus, butane has similar neurological disinhibiting effect as alcohol. The intention of abusers is to experience feelings of euphoria and disinhibition. Symptoms that can reveal intoxication include slurred speech, ataxia, confusion, hallucinations and a loss of conscious at high blood concentration.14 19 Abusers can have a distinct smell on their clothing, skin or breath.

A review on the causes of death by inhalant abuse revealed that 77% of deaths could be attributed to direct effects of the inhalant, 18% by asphyxia due to the use of a plastic bag.7 Inhalants exert their potential lethal toxic effects primarily on the cardiovascular system. First, inhalants can sensitise the heart for adrenergic stimulation. Consequent physical activity due to hallucinations,20 sexual arousal21 and fright (eg, due to getting caught by a parent) may cause sympathic nervous system stim-ulation with cardiac ischaemia due to the increased sensitivity to adrenerge stimulation.21 Adgey et al therefore even propa-gate the advice to administer beta-adrenergic blocking agents to counteract the sympathic stimulation of the heart.8 Second, myocardial dysfunction might be involved in the pathophysio-logical process of sudden cardiac death as Harris has shown a depression of the myocardial contractility in response to inhalant administration in rats and monkeys.22 Lastly, coronary spasms have also been suggested as an explanation for sudden cardiac death. There are cases wherein the ECG demonstrated patterns of cardiac ischaemia with increased cardiac enzymes as in our case, but coronary angiography showed no evidence of coronary artery stenosis or thrombosis.23 24

As with many drugs that depress the nervous system, inhal-ants in high doses can cause central nervous system depression with respiratory failure,10 although there is only one report of respiratory arrest during inhalant abuse.25 Respiratory failure can also be caused by spraying directly into the pharynx. The

rapid decrease of the temperature of the fluids to −20˚C as a consequence of gas volume expansion can cause prolonged laryngospasm.26 Furthermore, the 1:100 increase in gas volume after spraying pressurised deodorant can cause alveolar hypoxia leading to cardiac arrest.

In conclusion, our case describes the fatal outcome of deodorant inhalation and subsequent cardiac arrest in a detox-ification clinic. Medical personnel should be cautioned on the dangers of inhalant abuse in this population.

Contributors KHK was part of the medical care during admittance of the patient and wrote case presentation, outcome, follow-up and discussion of the paper. Ms was and part of the medical care during follow-up and wrote case presentation, outcome, follow-up and discussion of the patient. et took part in the neurological examination and follow-up of the patient and reviewed the final version of the article. MG supervised the medical treatment and reviewed the final version of the article.

funding the authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

Competing interests None declared.

patient consent parental/guardian consent obtained.

provenance and peer review Not commissioned; externally peer reviewed.

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following inhalation of butane gas. Ned Tijdschr Geneeskd 2011;155:a3443. 2 schenone aL, Cohen a, patarroyo G, et al. therapeutic hypothermia after cardiac

arrest: a systematic review/meta-analysis exploring the impact of expanded criteria and targeted temperature. Resuscitation 2016;108:102–10.

3 reinhardt CF, azar a, Maxfield Me, et al. Cardiac arrhythmias and aerosol "sniffing". Arch Environ Health 1971;22:265–79.

4 Bass M. sudden sniffing death. JAMA 1970;212:2075–9. 5 Kamm rC. Fatal arrhythmia following deodorant inhalation: case report. Forensic Sci

1975;5:91–3. 6 Woods Dt, perry aW, solomou s. the neuropsychological sequelae of a 14-year-old girl

following successful resuscitation from ventricular fibrillation and collapse secondary to butane gas inhalation. Resuscitation 2012;83:e214–e215.

7 Bowen se, Daniel J, Balster rL. Deaths associated with inhalant abuse in Virginia from 1987 to 1996. Drug Alcohol Depend 1999;53:239–45.

8 adgey aa, Johnston pW, McMechan s. sudden cardiac death and substance abuse. Resuscitation 1995;29:219–21.

9 Butler J. 2010 National survey on drug use and health, 2011. 10 Dinwiddie sH. abuse of inhalants: a review. Addiction 1994;89:925–39. 11 oetting er, edwards rW, Beauvais F. social and psychological factors underlying

inhalant abuse. NIDA Res Monogr 1988;85:172–203. 12 anderson Hr, Macnair rs, ramsey JD. Deaths from abuse of volatile substances: a

national epidemiological study. Br Med J 1985;290:304–7. 13 Lubman DI, Yücel M, Lawrence aJ. Inhalant abuse among adolescents: neurobiological

considerations. Br J Pharmacol 2008;154:316–26. 14 Baydala L. Inhalant abuse. Paediatr Child Health 2010;15:443–8. 15 Henretig F. Inhalant abuse in children and adolescents. Pediatr Ann 1996;25:47–52. 16 Field-smith Me, Butland BK, ramsey JD, et al. Trends in death associated with abuse

of volatile substances. Department of Community Health Sciences. St George's Hospital Medical School (June 2006) Report, (19), 2005.

17 Harris D, Mirza Z. Butane encephalopathy. Emerg Med J 2005;22:676–7. 18 raines De, Claycomb rJ, Forman sa. Modulation of GaBa(a) receptor function by

nonhalogenated alkane anesthetics: the effects on agonist enhancement, direct activation, and inhibition. Anesth Analg 2003;96:112–8.

19 Flanagan rJ, Ives rJ. Volatile substance abuse. Bull Narc 1994;46:49–78. 20 Kurtzman tL, otsuka KN, Wahl ra. Inhalant abuse by adolescents. J Adolesc Health

2001;28:170–80. 21 Cordner sM. an unusual case of sudden death associated with masturbation. Med Sci

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1973;131:162–6. 23 Godlewski K, Werner B, sterliński M, et al. Myocardial infarction after butane

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25 Fitzgerald rL, Fishel Ce, Bush LL. Fatality due to recreational use of chlorodifluoromethane and chloropentafluoroethane. J Forensic Sci 1993;38:13431J–83.

learning points

► The abuse of volatile substances in everyday household products as inhalants is popular among youngsters in puberty and adolescents and has the highest prevalence among children from troubled households.

► Medical personnel unfamiliar with inhalant abuse can be confronted with their dramatic consequences such as asphyxia, trauma, aspiration during unconsciousness and cardiac arrest.

► Patients with a history of substance abuse who reside in an isolated environment, such as a drug rehabilitation centre or prison, may be at increased risk for using inhalants.

4 Kramp KH, et al. BMJ Case Rep 2018. doi:10.1136/bcr-2018-224345

unexpected outcome (positive or negative) including adverse drug reactions

26 ramsey J, anderson Hr, Bloor K, et al. an introduction to the practice, prevalence and chemical toxicology of volatile substance abuse. Hum Toxicol 1989;8:261–9.

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