Butane-induced acute global myocardial ischemia without coronary artery pathology

ABSTRACT

The case report describes a case of acute myocardial ischemia precipitated by propane butane inhalation. The dependency of this substance around the world is still moderate but is increasing due to the easy availability of the substance and the facility with which the effects can be concealed. The toxicity of the substance is significant; affecting the heart, the brain and the liver. The most common outcome is sudden death. In this article, we describe a survivor after an episode of acute poisoning and his interesting cardiac pathology.

INTRODUCTION

Inhalant abuse represents a deliberate inhalation of a volatile substance in order to achieve an altered mental state. Such events are not usually reported to the spontaneous reporting systems [1]. Still, regardless of the lack of accurate epidemiological reports, inhalant abuse is a worldwide problem. Epidemiological studies indicate that a substantial number of children and adolescents worldwide experiment with volatile substances in order to achieve a euphoric state of mind [2]. According to the National Institute of Drug Abuse [3], the use of inhalants in the USA for the 8th and 10th graders declined from 21.6% in 1995 to 15.2% in 2002. During the same period, at least 17% of adolescents have experimented with inhalants [4]. Inhalants are pharmacologically diverse volatile products usually selected for their widespread availability, low cost, no legal restrictions and the ability to rapidly induce euphoria. According to a Nationwide survey in the USA, 1.1% of youth, aged 12–13 years, had used inhalants in the past month, and 66.3% of respondents, 12 years of age and older, were children when they first abused inhalants. In total, 10.7% of respondents reported inhalants as their first drug of abuse [5]. The abuse of solvents is mostly seen in disrupted families, economically disadvantaged groups and ethnic minorities [6]. The use of the substance is not gender-specific, still 90% of the dead are males [4].

Propane/butane is among the most commonly abused substances reported to US poison centers from 1996 to 2001 (6%) [7].

CASE REPORT

An 18-year-old male patient was brought into the emergency department of the hospital in Johannesburg, Republic of South Africa unconscious. His mother was not sure of what had happened. The family was watching TV in the lounge when they heard a sudden ‘thump’ from the first floor. They found the patient next to his bed, with a propane/butane refill canister next to him. The youngster was employed in a propane factory for gas canisters. He had developed the habit of sniffing the gas from a cigarette lighter when playing video games at night.

On arrival in emergency room the patient was not responding to noxious stimuli (Glasgow coma score was 5). His blood pressure was 90/60 mmHg, heart rate was 145 beats/min. Since the saturation was in the low 90s, the patient was intubated. The initial computed tomography did not reveal any brain pathology. An electrocardiography (ECG) performed later in intensive care unit (ICU) revealed a widespread ST elevation compatible with acute coronary ischemia (Fig 1a and b). The echocardiography on admission revealed hypercontractile myocardium with an ejection fraction of 80%. Repeated ECGs on the fourth and sixth hour after admission revealed widespread ST elevation. Initial management was conservative in view of the fragile hemodynamic state. Due to the frequent cardiac ectopy, he was started on an i.v. Amiodarone (Cordarone®)infusion. Maintenance therapy comprised a normal saline 120 ml/hour to provide diuresis.

Figure 1.

ECGs performed in ICU.

Echocardiography on the sixth hour after admission revealed widespread hypokinesia with an ejection fraction of 20%. Chest X-ray showed changes compatible with early pulmonary edema. Тhe patient was catheterized for diagnostic angiography. The latter revealed normal coronary arteries with global LV dysfunction and predominant hypokinesia of the inferior wall (Fig. 2a–c).

Figure 2.

Diagnostic angiography, showing normal coronary arteries (a and b) and global LV hypokinesia of the inferior wall (c).

Laboratory evaluations of blood samples are represented in Table 1.

Table 1.

Laboratory evaluations of blood samples

Result	Day 0	Day 1	Day 2
Hemoglobin	17.7 g/dl	17.7 g/dl	15.9 g/dl
Potassium	4.2 mmol/l	3.9 mmol/l	3.8 mmol/l
Creatinine	117 μmol/l		67 μmol/l
Gamma-glutamyl transpeptidase	144 IU/l	97 IU/l
ALT	149 IU/l	242 IU/l
AST	264 IU/l	755 IU/l
Myoglobin	3562 ng/ml	2163 ng/ml
Creatine kinase myocardial band	318 ng/ml	597 ng/ml
Trop T	0.29 ng/l	7.22 ng/l
Total Creatine kinase	581 IU/l	17 326 IU/l	3811 IU/l
WCC	16.3 x 109/l	24.34 x 109/l	22.2 x 109/l
Lactate dehydrogenase	505 U/l
CRP	4 mg/l		96 mg/l
Met hemoglobin	5%
Carboxyhemoglobin	200%
Sulfahemoglobin	Absent

ALT, alanine aminotransferase; AST, aspartate aminotransferase; WCC, white cell count; CRP, C-reactive protein.

The patient was tested for cocaine, barbiturates, opiates, benzodiazepines, amphetamines, cannabinoids, LSD, methaqualone, phencyclidine, propoxyphene, ecstasy, methcathinone, tricyclic antidepressants, paracetamol, salicylates, which were all negative. No testing could be performed for propane/butane.

In total, 8–12 hours later the ECG changes started to settle. For the next 24 hours, the patient improved hemodynamically with the heart rate stabilizing ~120 beats/min and no more ectopies. Cordarone therapy was discontinued. Maintenance management continued with a saline infusion at a rate of 120 ml/hour with small boluses of furosemide to keep the urine output. On the 24th hour, piperacillin/tazobactam (Tazocin) was initiated since white cell count climbed to 24 000.

Neurologically, the patient improved slightly as mild orientational responses to painful stimuli appeared. Perfusion and diffusion magnetic resonance imaging still did not reveal any pathology. The ECG continued to settle with fairly quick involution of the hyperacute changes (Fig. 3). In total, 48 hours later echocardiography was repeated revealing well contractile myocardium with full resolution of the hypokinesia.

Figure 3.

ECG performed during the second day of hospitalization, showing involution of the hyperacute changes.

DISCUSSION

There are many clinical reports about propane/butane refill abusion almost or even leading to death. However, in the case presented, there are two particular points that are worth noting.

The first one is the absence of myocardial infarction. Several clinical cases are available in literature revealing no changes in coronary arteries, but still myocardial infarction development [8, 9]. In the present case there is no sign of ischemic necrosis. Yet, the extremely high troponin T and creatinine kinase levels were suggestive for some myocardial damage. Myocardial ischemia and hypoperfusion were hypothesized being the cause for the cardiac complications. According to literature, coronary vasospasm causing ischemia after butane inhalation remains at the base of the suggestions [4, 10]. From a pathophysiological point of view, along with acute coronary spasm, inhaled substances could damage cardiac microcirculation resulting in myocardial toxicity. Decreased contractility could be the manifestation of myocardial ‘stunning’ followed 48 hours later by improvement. The heart seems to be the most often affected with anterior chest pain, agitation, collapse and cardiac arrhythmia [11].

Even in the absence of ischemic necrosis of the myocardium, the extremely high Creatine phosphokinase level and elevated myoglobin may indicate rhabdomyolysis.

The second point worth mentioning is the hyperdynamic state first witnessed in echocardiography. Myocardial sensitization to catecholamines (their bathmotropic effect—consistent with the frequent cardiac ectopy described above) could accomplish for that finding. Stimulation of the vagal nerve following spraying of propellants in the mouth eventually led to inhibition of the heart and subsequent widespread hypokinesia with decreased ejection fraction. Cardiac arrest is described as the most common cause of sudden death in volatile substance abuse [4], along with respiratory depression (hypoxia), asphyxia, vagal inhibition and cardiac arrhythmia [3].

The psychotropic effects depend on the amount of inhaled substance, its concentration and the duration of inhalation [12]. Excitation is usually first observed (ranging from euphoria to delusions, hallucinations and seizures) followed by a depressive effect on the nervous system and eventually coma [13, 14]. Even though few fatal cases have been described, sudden death is not impossible [15].

There are no trials on groups of survivals after butane poisoning. Still, the possibility of butane intoxication should be taken in consideration in cases of sudden loss of consciousness, especially in young patients. Butane can be determined in blood—thus, samples should be sent for assessment.

CONCLUSION

The low price, the ease of acquisition and concealment of inhalation agents are factors that make them desirable substances of abuse in adolescents. Till now they are relatively rarely used as a tool to achieve euphoria, but an increase in abuse is also possible in the future. Fatal outcomes, still rare, are a possible sequel. Unraveling a possible case of inhalants abuse will allow undertaking a proper therapeutic approach to patients in order to prevent future episodes and possible complications.

Conflict of interest statement. None declared

ETHICAL APPROVAL

No ethical approval was required for this report.

CONSENT

Written informed consent was obtained from the patient for publication of this case report and accompanying images.

GUARANTOR

Evgeni Grigorov