Cardiac arrest following butane inhalation.

Butane is a commonly misused volatile agent, and a cause of intoxication. We present a case, who had a syncope and persistent ventricular fibrillation during the course of resuscitation. We discussed the management of this case in the intensive care unit and the accompanying difficulties in the light of the current literature.

INTRODUCTION

Hydrocarbons are abundant in many products such as gasoline, motor oils, dry-cleaning solutions, and solvents.[1] These products contain varying amounts and types of materials, which are difficult to identify. In the case of intoxication, correct diagnosis is severely delayed in the absence of correct information about the product and the route of exposure. Butane is such a product, commonly abused for its euphoric effect. Butane is easily obtainable in lighter refill cans and antiperspirants, and, therefore, is very popular among the youth.[2]

We present a case of cardiac arrest due to butane inhalation and discussed the intensive care management.

CASE REPORT

An 18-year-old male was brought to our emergency department by ambulance. The patient has been resuscitated for more than 30 min and was still in ventricular fibrillation. About an hour ago, the ambulance staff was called for a worker in a gas lighter factory. The patient was unconscious and breathing agonically when they arrived at the factory. He had no history of systemic disease, previous operation, drug use or known allergy. According to the witnesses, he was filling his pocket lighter with a butane bottle, and suddenly fell unconscious. The workers had been questioned for a possible leakage of gas, but no one confirmed this. The patient was transported to a nearby hospital, where he was intubated. During the intubation, cardiac arrest occurred, and he was resuscitated for 20 min. Upon the restoration of spontaneous circulation, he was transferred to our hospital, with frequent cardiac arrests during the transportation. At our emergency ward, the patient responded to defibrillation and resuscitation for another 10 min, was started on dopamine infusion at 10 μg/kg/min, and was transferred to the intensive care unit.

His medical history was unremarkable apart from tobacco smoking. His pupils were isocoric, myotic, and reactive to light on both sides. He was not responding to noxious stimuli (Glasgow coma score was: 7). His blood pressure was 130/100 mmHg, heart rate was 130 beats/min, body temperature was 36.5°C, and he was not spontaneously breathing. The computerized tomography of the brain and the plain chest radiography showed mild edema [Figure 1]. Transthoracic echocardiography showed global hypokinesia of the left ventricle (ejection fraction: 50%). He was started on prophylaxis for ventricular fibrillation (0.1% lidocaine infusion at a rate of 1/mg/kg/h), and intermittent mannitol infusion due to hypoxic convulsions (epilepsy was ruled out due to presence of the pupillary light reflexes). An arterial blood gas analysis after 2 h on volume-controlled ventilation (FiO2: 0.50, tidal volume: 550 ml, frequency: 12 beats/min, positive end-expiratory pressure: 5 cmH2O) was within normal levels.

Figure 1

(a) Axial computerized tomography of the brain shows mild cerebral edema with effacement of cerebral sulci. (b) Plain chest radiography of the patient shows mild congestion

While we were planning for further tests to rule out a channelopathy or cardiomyopathy, some of his co-workers mentioned that the patient sniffed the lighter fluid before he fell unconscious. The patient's status improved, and we gradually lowered the rate of the dopamine infusion. The next day, his Glasgow coma score was 13, and he was spontaneously breathing at a rate of 16 beats/min. He was put on assisted breathing support mode and extubated 8 h later.

On the 3rd day, he was still disoriented and uncooperative. Dopamine infusion and mannitol therapy were stopped, and the patient was started on enteral nutrition via a nasogastric tube. In the following days, his cooperation gradually improved, with frequent periods of agitation and disorientation. Cranial diffusion and venography magnetic resonance imaging studies showed two hyperintense-zones in diffusion and T1-weighted magnetic resonance image in both sides of the occipital lobe, about 1.5 cm in diameter, identified as subacute ischemic infarcts [Figure 2].

Figure 2

Axial magnetic resonance images show subacute ischemic infarction. (a) Long, black arrow shows the hyperintensity on T1-weighted image in left occipital lobe; short, white arrows show surrounding edema. (b) Black arrow shows almost homogenically hyperintense area on diffusion-weighted image in right occipital lobe

On the 6th day, the patient was fully cooperative, but still disoriented. His verbal response was limited to few meaningful words, yet no complete sentences. He could follow objects with his eyes, grab them and feed himself. He was discharged to the neurology ward, where he was treated for further 2 weeks. We were informed that after 3 months of rehabilitation, he started to work as a dozer operator.

DISCUSSION

We presented a case, where lighter refill gas was abused to near death. According to the information obtained from the factory, the refill canister contained 54% n-butane, 26% propane, and 20% isobutane. Most papers in the literature report that victims of butane intoxication died due to ventricular fibrillation and cardiovascular collapse within few minutes.[3] If that would be the case for our patient, he would most likely die at his working place, because he was not in ventricular fibrillation when the ambulance arrived at the scene.

These volatiles quickly vaporize and displace oxygen in the lungs, which leads to a transient hypoxia, which may explain why the patient fell unconscious. Following inhalation, these highly lipophilic volatiles quickly pass into the blood via the lungs and achieve high concentrations in lipid-rich organs such as brain and liver. Butane may cause direct toxicity in the brain and the myocardium while propane may cause an anesthetic effect on the central nervous system. However, more importantly, butane sensitizes the myocardium to the effects of catecholamines and predisposes the patient to life-threatening tachyarrhythmias. We do not know whether the patient was sufficiently anesthetized before the intubation. We believe that during the intubation, the catecholamine surge on the sensitized myocardium caused ventricular fibrillation.

We observed no prominent effects on the lungs, liver and kidneys. Hydrocarbons are known to cause inflammation, edema, or severe conditions such as pneumonitis in the lungs.[4] However, these conditions usually do not occur in the absence of aspiration. Similarly, hepatic toxicity usually occurs with carbon tetrachloride,[5] while renal toxicity occurs with chronic exposure to toluene.[6] The mild edema in the brain and the lungs of our patient may be attributed to the hypoxic injury and trauma due to the resuscitation.

There are similar reports in the literature. El-Menyar et al., reported a 14-year-old male sniffing 7 canisters of butane before cardiac arrest.[7] After reviewing some other case reports, they suggest that cardiac failure after butane inhalation may involve coronary artery spasm. We do not know whether this was the case for our patient because we did not perform cardiac catheterization. However, our patient had a much better left ventricular contractility compared to the previous cases, which suggests that transient hypoxia was the primary reason of syncope in our case.

Edwards and Wenstone reported a 17-year-old male with chronic misuse of butane.[8] They observed that the resuscitation was complicated with periods of ventricular fibrillation in rapid succession, particularly following administration of epinephrine. They emphasized that in such cases, the myocardium is sensitized to the effects of epinephrine, and anti-arrhythmic treatment should be initiated early.

Resuscitation of a case of butane intoxication requires a special treatment. Rapid collapse is common in these patients. Furthermore, threshold for ventricular fibrillation may be lowered by any of the fundamental practices of resuscitation like intubation or administering epinephrine. In the absence of witnesses or correct information, the efforts of the resuscitation team may become futile.