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Ventricular fibrillation following butane gas inhalation
Resuscitation 37 (1998) 43 – 45
Case report
Ventricular fibrillation following butane gas inhalation D.R. Williams *, S.J. Cole Department of Anaesthesia and Intensi6e Care, Ninewells Hospital and Medical School, Dundee, Tayside DDI 9SY, UK Received 26 January 1998; accepted 11 March 1998
Abstract We report a case of out of hospital defibrillation in a 15-year-old schoolgirl who developed ventricular fibrillation (VF) in association with butane gas inhalation. Although defibrillation performed by an attending paramedic was successful in restoring a cardiac output, her clinical course was complicated by severe neurological impairment. Reports of successful resuscitation following volatile substance abuse are rare and we believe this is the first documented evidence of VF associated with butane gas. This case illustrates the tragedy of such abuse in fit young people and we briefly review the literature. © 1998 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Ventricular fibrillation; Butane gas inhalation
1. Case report A 15-year-old healthy school girl was persuaded by peers to try inhaling the contents of a butane gas lighter refill can for the first time. They found a secluded place near a riverbank and the girl began to inhale the contents by direct release into her mouth. Over a 2 h period of intermittent inhalation she was noticed by her peers to be giggling and staggering. Immediately after a final inhalation they were observed by two passing police officers. The group began running away and after a short distance, the schoolgirl was seen to collapse in an alleyway without any obvious external injury. The officers immediately attended the girl, who was noted to be cyanosed and totally unresponsive. One officer alerted the emergency services whilst the other placed her in the recovery position. After : 2 min, a pulse was checked for the first time and noted to be absent. Cardiac compressions were commenced, but mouth to mouth ventilation was not started until the chance arrival of a passing nurse with a pocket mask : 2 min later. Two person cardiopul* Corresponding author. Tel.: +44 1382 660111.
monary resuscitation at five chest compressions to one ventilation was continued for a further 8 min until the arrival of a paramedic ambulance crew who took over the resuscitation. The initial rhythm was coarse ventricular fibrillation. A single 200-J Direct Current shock changed the rhythm to asystole (Fig. 1). A few minutes later, following 1 mg of adrenaline intravenously, a palpable pulse returned and a sinus tachycardia was noted on the monitor. The patient’s trachea was intubated, she was ventilated with 100% oxygen and transferred to hospital. Cardiac status was stable throughout the transfer. On arrival at the accident and emergency department her Glasgow coma scale was three, there was a good cardiac output with a heart rate of 145/min and a blood pressure of 105/70 mmHg, but no spontaneous respiration. The electrocardiogram showed a sinus tachycardia with marked T wave inversion in the anterolateral leads. Arterial blood gases, full blood count and electrolytes were unremarkable. Blood and urine toxicology screens were positive for alcohol only. The working diagnosis at this point was ventricular fibrillation secondary to volatile substance inhalation with a global cerebral anoxic insult.
0300-9572/98/$19.00 © 1998 Elsevier Science Ireland Ltd. All rights reserved. PII S0300-9572(98)00030-6
44
D.R. Williams, S.J. Cole / Resuscitation 37 (1998) 43–55
She was admitted to the intensive care unit and sedated, paralysed and ventilated because of her neurological status. Paralysis and sedation were reduced unsuccessfully on day 3 because she developed clinical signs of raised intracranial pressure when gagging on the endotracheal tube. At this time no cortical function was observed. A CT scan showed a very tight swollen brain with complete compression of the lateral ventricles. Two boluses of mannitol 0.5 g/kg were given to try to improve the cerebral oedema and ventilation was continued for another 2 days. Over this period she remained cardiovascularly stable with persistent T-wave inversion on the ECG although cardiac enzymes and an echocardiogram were normal. Further CT scans demonstrated an improvement in ventricular size and on day 13 she was weaned from the ventilator with the aid of a tracheostomy. Multiple EEG tracings were consistent with diffuse cortical dysfunction. On day 18 she was transferred to the care of the neurologists for further assessment and rehabilitation.
2. Discussion Death from volatile substance abuse (VSA) is one of the leading causes of death in those under 18 years. At
Fig. 1. Initial rhythms of VF and asystole at the scene and sinus tachycardia on arrival at hospital.
age 15, 10% of all deaths and : 20% of deaths from accidents, violence and poisoning are due to VSA, making it the leading cause of death. This amounts to :100 deaths per year. Experimentation may have occurred in 3.5–10% of teenagers and 0.5–1% were regular abusers. The vast majority are male (90%). The largest number of deaths were attributable to butane gas cigarette lighter fluid (34.5%) followed by aerosols (26%). Other substances include solvents in glues (toluene), dry cleaning agents (trichloroethylene), typewriter correction fluid and inhalational anaesthetic agents [1]. In 51% of cases, death was attributed to the direct toxic effects (probably cardiac) of the substance abused, in 21%, to plastic bag asphyxia, in 18% to inhalation of stomach contents and in 11% to trauma [2]. VSA is a problem because it is not illegal, agents are easily available, cheap, and the effects are short lived allowing rapid return to school or home [1,2]. Although the ratio of deaths to non-fatal inhalation is low, the risk of sudden death in an unwitnessed environment means that resuscitation is seldom available or successful. Acute toxic effects of VSA include euphoria, disinhibition, hallucinations, tinnitus, ataxia, nausea, convulsions, coma, cardiac arrhythmias, respiratory depression and death. Death may ensue by direct cardiac toxicity (arrhythmias) or central nervous system toxicity (respiratory depression), or indirectly by hypoxia (bag over head), aspiration of vomit or trauma sustained in an inebriated state [3]. Chronic toxic effects include cardiomyopathy, renal and hepatic damage, and various neurological, psychiatric and metabolic syndromes. Little is known about the specific toxic effects of butane gas, which is a volatile hydrocarbon. Butane gas abuse has been followed by documented asystole in a previous case report [4]. In that case, because the collapse was unwitnessed, the possibilities included cerebral depression with associated anoxia, ventricular fibrillation deteriorating into asystole, or a direct effect of butane causing asystole. In our case, the most plausible mechanism is a direct effect of butane on the myocardium, as the witnessed events leading up to the collapse exclude respiratory depression and anoxia. There is substantial evidence to support sensitisation of the myocardium to the arrythmogenic effects of endogenous catecholamines in the presence of volatile hydrocarbons. Well controlled studies have shown the serious ventricular arrhythmias and asystole are precipitated by inhaling many different volatile hydrocarbons, especially in the presence of adrenaline and hypoxia [5,6]. Myocardial infarction and VF has been reported after toluene inhalation and coronary artery spasm proposed as the mechanism [7]. Another case of VF has followed inhalation of 1,1,1-trichloroethane in a child [8].
D.R. Williams, S.J. Cole / Resuscitation 37 (1998) 43–45
Sudden death associated with VSA has often occurred with intense sympathetic stimulation such as physical exertion (running) or various forms of auto erotic behaviour [9]. Hypoxia, hypercarbia, hypokalaemia and alcohol, further predispose to arrhythmias. Victims of VSA have often been seen running away in fear from the scene. Vivid hallucinations may be the cause and it is important to calm the victim to reduce further release of endogenous catecholamines which may increase the risk of serious ventricular arrythmias. In a previous review it has been suggested that the administration of adrenaline in cases of ventricular fibrillation secondary to VSA may be deleterious [10]. This case illustrates the sudden and devastating consequences of VSA, which should be considered as a possible cause of cardiac arrest in any young person found collapsed in the community. Observations at the scene suggest that this was a primary arrhythmia possibly due to a surge of endogenous adrenaline rather than a hypoxic arrest. Cardiac output was restored following the witnessed collapse, however, she sustained a severe global anoxic cerebral insult possibly due to a sub optimal resuscitation, which will probably result in a tragic neurological outcome. This emphasises the need for wider public and professional training in basic life support. Other conditions to be considered in any unknown cause of collapse or sudden death in adolescents are: hypertrophic cardiomyopathy, coronary artery abnormalities – congenital or acquired (premature arteriosclerosis, Kawasaki disease), aortic valve stenosis, aortic dissection secondary to Marfan’s syndrome, primary pulmonary hypertension or hereditary prolonged QT interval syndrome [11] Attempts have been made to reduce VSA deaths by health education campaigns and government legislation without success [12]. The British Adhesive Manufacturers Association founded Re-Solv in 1984, which is a national charity working to prevent VSA by broad educational campaigns. In 1985 there was legislation to
45
restrict the sale of glues and solvents, but not butane gas lighter refills. Thus ‘glue sniffing’ might shift towards the riskier practice of ‘gas sniffing’. It might be wise, as others have suggested, to withdraw butane gas lighter refills from the market and use disposable lighters. This of course might result in abuse of other more dangerous substances [12]. We require more educational projects aimed at teenagers to emphasise the dangers involved with VSA as this case demonstrates.
References
[1] Esmail A, Meyer L, Pottier A, Wright S. Deaths from volatile substance abuse in those under 18 years: results from a national epidemiological study. Arch Dis Child 1993;69:356 – 60. [2] Anderson HR, Macnair RS, Ramsey JD. Deaths from abuse of volatile substances: a national epidemiological study. Br Med J 1985;8:304 – 7. [3] Shepherd RT. Mechanism of sudden death associated with volatile substance abuse. Hum Toxicol 1989;8(4):287 – 91. [4] Roberts MJ, McIvor RA, Adgey AA. Asystole following butane gas inhalation. Br J Hosp Med 1990;44(4):294. [5] Flowers NC, Horan LG. Nonanoxic aerosol arrhythmias. J Am Med Assoc 1972;219:33 – 7. [6] Reinhart CF, Azar A, Maxfield ME, Smith PE, Mullins LS. Cardiac arrythmias and aerosol sniffing. Arch Environ Health 1971;22:265 – 79. [7] Cunningham SR, Dalzell GWN, McGirr P, Khan MM. Myocardial infarction and primary ventricular fibrillation after glue sniffing. Br Med J 1987;294:739 – 40. [8] Nee PA, Llewellyn T, Pritty PE. Successful out of hospital defibrillation for ventricular fibrillation complicating solvent abuse. Arch Emerg Med 1990;7(3):220 – 2. [9] Bass M. Sudden sniffing death. J Am Med Assoc 1972;212:2075– 9. [10] Adgey AAJ, Johnston PW, McMechan S. Sudden cardiac death and substance abuse. Resuscitation 1995;29(3):219– 21. [11] Driscoll DJ, Jacobson SJ, Porter CJ, Wollan PC. Syncope in children and adolescents. J Am Coll Cardiol 1997;29(5):1039–45. [12] Esmail A, Anderson HR, Ramsey JD, Taylor J, Pottier A. Controlling deaths from volatile substance abuse in under 18s: the effects of legislation. Br Med J Sep 1992;305:692.
Case report
Ventricular fibrillation following butane gas inhalation D.R. Williams *, S.J. Cole Department of Anaesthesia and Intensi6e Care, Ninewells Hospital and Medical School, Dundee, Tayside DDI 9SY, UK Received 26 January 1998; accepted 11 March 1998
Abstract We report a case of out of hospital defibrillation in a 15-year-old schoolgirl who developed ventricular fibrillation (VF) in association with butane gas inhalation. Although defibrillation performed by an attending paramedic was successful in restoring a cardiac output, her clinical course was complicated by severe neurological impairment. Reports of successful resuscitation following volatile substance abuse are rare and we believe this is the first documented evidence of VF associated with butane gas. This case illustrates the tragedy of such abuse in fit young people and we briefly review the literature. © 1998 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Ventricular fibrillation; Butane gas inhalation
1. Case report A 15-year-old healthy school girl was persuaded by peers to try inhaling the contents of a butane gas lighter refill can for the first time. They found a secluded place near a riverbank and the girl began to inhale the contents by direct release into her mouth. Over a 2 h period of intermittent inhalation she was noticed by her peers to be giggling and staggering. Immediately after a final inhalation they were observed by two passing police officers. The group began running away and after a short distance, the schoolgirl was seen to collapse in an alleyway without any obvious external injury. The officers immediately attended the girl, who was noted to be cyanosed and totally unresponsive. One officer alerted the emergency services whilst the other placed her in the recovery position. After : 2 min, a pulse was checked for the first time and noted to be absent. Cardiac compressions were commenced, but mouth to mouth ventilation was not started until the chance arrival of a passing nurse with a pocket mask : 2 min later. Two person cardiopul* Corresponding author. Tel.: +44 1382 660111.
monary resuscitation at five chest compressions to one ventilation was continued for a further 8 min until the arrival of a paramedic ambulance crew who took over the resuscitation. The initial rhythm was coarse ventricular fibrillation. A single 200-J Direct Current shock changed the rhythm to asystole (Fig. 1). A few minutes later, following 1 mg of adrenaline intravenously, a palpable pulse returned and a sinus tachycardia was noted on the monitor. The patient’s trachea was intubated, she was ventilated with 100% oxygen and transferred to hospital. Cardiac status was stable throughout the transfer. On arrival at the accident and emergency department her Glasgow coma scale was three, there was a good cardiac output with a heart rate of 145/min and a blood pressure of 105/70 mmHg, but no spontaneous respiration. The electrocardiogram showed a sinus tachycardia with marked T wave inversion in the anterolateral leads. Arterial blood gases, full blood count and electrolytes were unremarkable. Blood and urine toxicology screens were positive for alcohol only. The working diagnosis at this point was ventricular fibrillation secondary to volatile substance inhalation with a global cerebral anoxic insult.
0300-9572/98/$19.00 © 1998 Elsevier Science Ireland Ltd. All rights reserved. PII S0300-9572(98)00030-6
44
D.R. Williams, S.J. Cole / Resuscitation 37 (1998) 43–55
She was admitted to the intensive care unit and sedated, paralysed and ventilated because of her neurological status. Paralysis and sedation were reduced unsuccessfully on day 3 because she developed clinical signs of raised intracranial pressure when gagging on the endotracheal tube. At this time no cortical function was observed. A CT scan showed a very tight swollen brain with complete compression of the lateral ventricles. Two boluses of mannitol 0.5 g/kg were given to try to improve the cerebral oedema and ventilation was continued for another 2 days. Over this period she remained cardiovascularly stable with persistent T-wave inversion on the ECG although cardiac enzymes and an echocardiogram were normal. Further CT scans demonstrated an improvement in ventricular size and on day 13 she was weaned from the ventilator with the aid of a tracheostomy. Multiple EEG tracings were consistent with diffuse cortical dysfunction. On day 18 she was transferred to the care of the neurologists for further assessment and rehabilitation.
2. Discussion Death from volatile substance abuse (VSA) is one of the leading causes of death in those under 18 years. At
Fig. 1. Initial rhythms of VF and asystole at the scene and sinus tachycardia on arrival at hospital.
age 15, 10% of all deaths and : 20% of deaths from accidents, violence and poisoning are due to VSA, making it the leading cause of death. This amounts to :100 deaths per year. Experimentation may have occurred in 3.5–10% of teenagers and 0.5–1% were regular abusers. The vast majority are male (90%). The largest number of deaths were attributable to butane gas cigarette lighter fluid (34.5%) followed by aerosols (26%). Other substances include solvents in glues (toluene), dry cleaning agents (trichloroethylene), typewriter correction fluid and inhalational anaesthetic agents [1]. In 51% of cases, death was attributed to the direct toxic effects (probably cardiac) of the substance abused, in 21%, to plastic bag asphyxia, in 18% to inhalation of stomach contents and in 11% to trauma [2]. VSA is a problem because it is not illegal, agents are easily available, cheap, and the effects are short lived allowing rapid return to school or home [1,2]. Although the ratio of deaths to non-fatal inhalation is low, the risk of sudden death in an unwitnessed environment means that resuscitation is seldom available or successful. Acute toxic effects of VSA include euphoria, disinhibition, hallucinations, tinnitus, ataxia, nausea, convulsions, coma, cardiac arrhythmias, respiratory depression and death. Death may ensue by direct cardiac toxicity (arrhythmias) or central nervous system toxicity (respiratory depression), or indirectly by hypoxia (bag over head), aspiration of vomit or trauma sustained in an inebriated state [3]. Chronic toxic effects include cardiomyopathy, renal and hepatic damage, and various neurological, psychiatric and metabolic syndromes. Little is known about the specific toxic effects of butane gas, which is a volatile hydrocarbon. Butane gas abuse has been followed by documented asystole in a previous case report [4]. In that case, because the collapse was unwitnessed, the possibilities included cerebral depression with associated anoxia, ventricular fibrillation deteriorating into asystole, or a direct effect of butane causing asystole. In our case, the most plausible mechanism is a direct effect of butane on the myocardium, as the witnessed events leading up to the collapse exclude respiratory depression and anoxia. There is substantial evidence to support sensitisation of the myocardium to the arrythmogenic effects of endogenous catecholamines in the presence of volatile hydrocarbons. Well controlled studies have shown the serious ventricular arrhythmias and asystole are precipitated by inhaling many different volatile hydrocarbons, especially in the presence of adrenaline and hypoxia [5,6]. Myocardial infarction and VF has been reported after toluene inhalation and coronary artery spasm proposed as the mechanism [7]. Another case of VF has followed inhalation of 1,1,1-trichloroethane in a child [8].
D.R. Williams, S.J. Cole / Resuscitation 37 (1998) 43–45
Sudden death associated with VSA has often occurred with intense sympathetic stimulation such as physical exertion (running) or various forms of auto erotic behaviour [9]. Hypoxia, hypercarbia, hypokalaemia and alcohol, further predispose to arrhythmias. Victims of VSA have often been seen running away in fear from the scene. Vivid hallucinations may be the cause and it is important to calm the victim to reduce further release of endogenous catecholamines which may increase the risk of serious ventricular arrythmias. In a previous review it has been suggested that the administration of adrenaline in cases of ventricular fibrillation secondary to VSA may be deleterious [10]. This case illustrates the sudden and devastating consequences of VSA, which should be considered as a possible cause of cardiac arrest in any young person found collapsed in the community. Observations at the scene suggest that this was a primary arrhythmia possibly due to a surge of endogenous adrenaline rather than a hypoxic arrest. Cardiac output was restored following the witnessed collapse, however, she sustained a severe global anoxic cerebral insult possibly due to a sub optimal resuscitation, which will probably result in a tragic neurological outcome. This emphasises the need for wider public and professional training in basic life support. Other conditions to be considered in any unknown cause of collapse or sudden death in adolescents are: hypertrophic cardiomyopathy, coronary artery abnormalities – congenital or acquired (premature arteriosclerosis, Kawasaki disease), aortic valve stenosis, aortic dissection secondary to Marfan’s syndrome, primary pulmonary hypertension or hereditary prolonged QT interval syndrome [11] Attempts have been made to reduce VSA deaths by health education campaigns and government legislation without success [12]. The British Adhesive Manufacturers Association founded Re-Solv in 1984, which is a national charity working to prevent VSA by broad educational campaigns. In 1985 there was legislation to
45
restrict the sale of glues and solvents, but not butane gas lighter refills. Thus ‘glue sniffing’ might shift towards the riskier practice of ‘gas sniffing’. It might be wise, as others have suggested, to withdraw butane gas lighter refills from the market and use disposable lighters. This of course might result in abuse of other more dangerous substances [12]. We require more educational projects aimed at teenagers to emphasise the dangers involved with VSA as this case demonstrates.
References
[1] Esmail A, Meyer L, Pottier A, Wright S. Deaths from volatile substance abuse in those under 18 years: results from a national epidemiological study. Arch Dis Child 1993;69:356 – 60. [2] Anderson HR, Macnair RS, Ramsey JD. Deaths from abuse of volatile substances: a national epidemiological study. Br Med J 1985;8:304 – 7. [3] Shepherd RT. Mechanism of sudden death associated with volatile substance abuse. Hum Toxicol 1989;8(4):287 – 91. [4] Roberts MJ, McIvor RA, Adgey AA. Asystole following butane gas inhalation. Br J Hosp Med 1990;44(4):294. [5] Flowers NC, Horan LG. Nonanoxic aerosol arrhythmias. J Am Med Assoc 1972;219:33 – 7. [6] Reinhart CF, Azar A, Maxfield ME, Smith PE, Mullins LS. Cardiac arrythmias and aerosol sniffing. Arch Environ Health 1971;22:265 – 79. [7] Cunningham SR, Dalzell GWN, McGirr P, Khan MM. Myocardial infarction and primary ventricular fibrillation after glue sniffing. Br Med J 1987;294:739 – 40. [8] Nee PA, Llewellyn T, Pritty PE. Successful out of hospital defibrillation for ventricular fibrillation complicating solvent abuse. Arch Emerg Med 1990;7(3):220 – 2. [9] Bass M. Sudden sniffing death. J Am Med Assoc 1972;212:2075– 9. [10] Adgey AAJ, Johnston PW, McMechan S. Sudden cardiac death and substance abuse. Resuscitation 1995;29(3):219– 21. [11] Driscoll DJ, Jacobson SJ, Porter CJ, Wollan PC. Syncope in children and adolescents. J Am Coll Cardiol 1997;29(5):1039–45. [12] Esmail A, Anderson HR, Ramsey JD, Taylor J, Pottier A. Controlling deaths from volatile substance abuse in under 18s: the effects of legislation. Br Med J Sep 1992;305:692.