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The inhalation of butane gas has been reported as a substance of abuse, often for the purpose of voice alteration or inducing euphoria. Butane gas belongs to the hydrocarbon group and can be found in common household items such as pocket lighters, deodorants, or natural gas used in homes. Unfortunately, it has been implicated in numerous tragic cases of death, primarily due to the development of refractory cardiac arrhythmias.
On a winter evening at 8:45 pm, a distressing incident occurred involving an 11-year-old boy with no known medical history.
He suddenly felt faint while in a supermarket parking lot and collapsed to the ground. Promptly, his friends alerted emergency services, who arrived at the scene. Upon arrival, they detected a strong odor of deodorant emanating from the child. Although he still had a pulse, he had stopped breathing, presenting with respiratory arrest. Tragically, at 9 pm, despite resuscitation efforts, the boy went into asystole. Advanced life support was administered for 45 minutes, but no further cardiac activity could be recorded.
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Subsequent investigation revealed that the boy, accompanied by one of his friends, had inhaled a deodorant aerosol after leaving school at approximately 5:30 pm. He briefly felt faint but seemed to recover. Encouraged by his friend to go home, the boy instead headed to the supermarket, where he inhaled another aerosol deodorant shortly before his fatal collapse. Near the location where the boy passed away, investigators discovered an empty aerosol deodorant can labeled "Narta_," and multiple other empty aerosol deodorants were scattered around the parking lot.
Examination of the body at the scene of death revealed a prepubescent boy with very pale skin, widespread mottling, moderate cyanosis, and no visible traumatic injuries. Sterile swabs were taken from the hands, face, nose, and throat, and these swabs were placed in individually sealed airtight glass tubes to preserve any potential gas content. Additionally, the boy's polo shirt was sealed in a similar glass tube to prevent gas evaporation, as it can occur through more porous plastic materials. The autopsy was conducted three days later and revealed findings of pulmonary edema, diffuse moderate congestion, and cerebral edema.
Pathological examination further revealed extensive eosinophilic and hemorrhagic pulmonary edema, with the bronchial epithelium showing marked hypercrinia and thickening of the basement membranes. The bronchial lumina contained widespread serohemorrhagic or mucinous material rich in macrophages. In one segmental bronchus of the right lung, refractive foreign bodies were observed, accompanied by an associated inflammatory response comprising neutrophils, eosinophils, and mastocytes. Examination of other organs revealed nonspecific lesions associated with circulatory failure, such as centrilobular hepatic congestion, low-flow subendocardial cardiomyocyte necrosis, and loss of Purkinje cells in the cerebellum. Perineuronal satellitosis lesions were also observed.
The toxicological analysis detected the presence of butane at concentrations of 22 mg/L in the peripheral blood, 97 mg/L in the gastric fluid, and 8 mg/Kg in the lungs. Isobutane was identified in the blood and in all the viscera. Limonene was detected in the gastric fluid, and decamethylcyclopentasiloxane was found in the gastric fluid and fatty tissue.
Swabs and clothing were directly analyzed by introducing the tip of the swab or a 1 g sample of cloth into a HS vial for analysis for volatile substances, similar to a blood sample analysis. For the analysis of decamethylcyclopentasiloxane, the swabs or clothing were incubated for 3 minutes in 1 mL of methanol in an ultrasonic bath, and two microliters of methanol were subsequently injected into the GCMS system.
The toxicological examination of the external samples taken from the young man revealed the presence of decamethylcyclopentasiloxane in three places: on his face, on the upper part of his clothing, and at the back of his throat. No decamethylcyclopentasiloxane was found on his hands or in his nose. Moreover, no butane, isobutane, or limonene was detected in any of the external samples, nor was any toxin found in the vitreous humor.
Additionally, toxicological analysis of another aerosol of the same brand of deodorant that was found near the victim’s body confirmed the presence of propellant gas containing butane and isobutane, along with decamethylcyclopentasiloxane and limonene. Forensic experts classified his death as isolated butane intoxication.
A 16-year-old girl, diagnosed with unregulated type 1 diabetes, experienced a grand mal seizure while watching a movie in her bedroom with a friend. Emergency services were promptly summoned to the scene. Her blood glucose level was measured at 3.68 g/L (normal serum glucose levels ranging from 0.70 to 1.10 g/L), which could not account for the occurrence of the grand mal seizure. Despite efforts at resuscitation, the attempt was unsuccessful.
Two days later, an autopsy was conducted, revealing extensive pulmonary edema with laryngeal regurgitation of food. Only routine samples were collected, including blood, stomach contents, and lung tissues, as the suspicion of butane intoxication had not arisen initially. Samples specific to butane intoxication, such as brain and fatty tissue, were not obtained.
Pathological examination unveiled significant eosinophilic and hemorrhagic pulmonary edema. Moreover, there were extensive and diffuse abrasions of the bronchial and bronchiolar epithelial lining. Clusters of bacteria were visible within the alveoli, devoid of any inflammatory response, suggesting a terminal inhalation mechanism. Additionally, foreign bodies in the form of crystalloid refractive material were noted focally, with no associated inflammatory infiltrate. The bronchial lumina contained substantial food debris and bacteria but lacked an inflammatory infiltrate. Examination of other organs revealed non-specific lesions linked to circulatory failure, including discrete dilation of the renal proximal convoluted tubule and low-flow cardiomyocyte necrosis. Hypoxic ischemic encephalopathy lesions were also observed, characterized by edema, marked scarcity of Purkinje cells, and stretched and pyknotic neurons.
The initial toxicological analysis only detected the presence of amiodarone, related to the medical treatment administered to the victim. Subsequently, when her friend admitted to her having inhaled deodorant, specific testing for volatile substances was conducted. Butane was identified at concentrations of 18.1 mg/L in the peripheral blood, 44.9 mg/L in the central blood, 27.3 mg/L in the gastric fluid, and less than 1 mg/Kg in the lungs. Isobutane and propane were not detected. Limonene was also found in the gastric fluid, while no other adjuvants like eugenol or geraniol were identified.
Various brands of aerosol deodorant were subsequently discovered in the victim’s bedroom trashcan. The presence of limonene and the absence of geraniol, eugenol, isobutane, and propane enabled the identification of a specific brand of aerosol deodorant. No other substances were identified. Her cause of death was attributed to isolated butane intoxication. Post-autopsy, the witness to the events was re-interviewed, and it was revealed that the victim had suffered the seizure after inhaling from a tissue soaked in deodorant.
A 19-year-old male patient experienced cardiopulmonary arrest after inhaling lighter gas and was transported to our emergency department by emergency ambulance services. Upon arrival, he was immediately admitted to the critical care room, where cardiopulmonary resuscitation (CPR) and intubation were performed. After 15 minutes of CPR, the patient's spontaneous circulation was successfully restored. Following the return of spontaneous circulation, the patient's vital signs were as follows: blood pressure 70/40 mmHg, heart rate 110 beats per minute, respiratory rate (intubated), temperature 36.6°C, and oxygen saturation at 97%. However, the Glasgow Coma Score indicated severe neurological impairment with a score of 3. Notably, his ECG revealed ST-segment elevations in leads D1-aVL and V4-V6.
In the complete blood count test, the white blood cell count was 11,900/mm3, and in the biochemical tests, the following results were obtained: glucose: 219 mg/dL, creatinine: 1.52 mg/dL, ALT: 135 U/L, AST: 140 U/L, LDH: 466 U/L, CPK: 1239 U/L, troponin: 0.007 ng/ml, and CK-MB: 13.8 U/L. The possibility of myocardial infarction was considered to be due to coronary vasospasm. While nitroglycerin could have been used to alleviate the vasospasm, it was not administered due to refractory hypotension. Consequently, the patient was transferred to another tertiary hospital for emergency cardiac catheterization and intensive care follow-up. The coronary angiogram, however, revealed normal epicardial coronary arteries but akinetic anterior and lateral walls. Tragically, on the second day, the patient suffered another cardiopulmonary arrest, ultimately resulting in his demise.
An 18-year-old male was brought to our emergency department by ambulance after having been in ventricular fibrillation for more than 30 minutes. Approximately an hour prior, ambulance staff had been called to a gas lighter factory where they found the patient unconscious and in agonizing respiratory distress.
The patient had no history of systemic disease, previous operations, drug use, or known allergies. Witnesses at the scene reported that he had been filling his pocket lighter with a butane bottle when he suddenly lost consciousness. Despite questioning the workers at the factory, no one confirmed any gas leakage. The patient was initially transported to a nearby hospital, where he was intubated. However, during the intubation process, he experienced cardiac arrest and underwent resuscitation for 20 minutes. Once spontaneous circulation was restored, he was transferred to our hospital, experiencing frequent cardiac arrests during transport.
Upon arrival at our emergency ward, the patient was responsive to defibrillation and underwent resuscitation for another 10 minutes. He was started on a dopamine infusion at a rate of 10 mg/kg/min and subsequently transferred to the intensive care unit. His medical history was unremarkable except for tobacco smoking, and his physical examination showed myotic, isocoric pupils that were reactive to light bilaterally. He did not respond to noxious stimuli, with a Glasgow Coma Score of 7. His vital signs included a blood pressure of 130/100 mmHg, a heart rate of 130 beats per minute, a body temperature of 36.5°C, and no spontaneous breathing.
Brain computerized tomography and plain chest radiography revealed mild edema, while transthoracic echocardiography indicated global hypokinesia of the left ventricle with an ejection fraction of 50%. Prophylactic measures for ventricular fibrillation were initiated with a 0.1% lidocaine infusion at a rate of 1 mg/kg/h. Mannitol was intermittently administered due to hypoxic convulsions, with epilepsy being ruled out based on the presence of pupillary light reflexes. Arterial blood gas analysis, after 2 hours of volume-controlled ventilation, was within normal limits.
As further investigations were planned to rule out a channelopathy or cardiomyopathy, some of the patient's co-workers mentioned that he had sniffed lighter fluid before losing consciousness. The patient's condition gradually improved, allowing for the gradual reduction of the dopamine infusion rate.
On the next day, the patient's Glasgow Coma Score had improved to 13, and he exhibited spontaneous breathing at a rate of 16 breaths per minute. He was transitioned to assisted breathing support mode and was successfully extubated 8 hours later.
On the third day, the patient remained disoriented and uncooperative. Dopamine infusion and mannitol therapy were discontinued, and enteral nutrition was initiated through a nasogastric tube. In the following days, his cooperation gradually improved, although he still experienced periods of agitation and disorientation. Cranial diffusion and venography magnetic resonance imaging studies revealed two hyperintense zones in diffusion and T1-weighted magnetic resonance images on both sides of the occipital lobe, approximately 1.5 cm in diameter, indicative of subacute ischemic infarcts.
By the sixth day, the patient was fully cooperative but still disoriented, with limited verbal responses. He was able to follow objects with his eyes, grasp them, and feed himself. He was subsequently discharged to the neurology ward, where he received treatment for an additional 2 weeks. It was reported that after 3 months of rehabilitation, he resumed working as a dozer operator.
A 42-year-old man was exposed to butane leaking from a gas tube for six hours while sleeping and was brought to our emergency department by ambulance 30 minutes later. Upon arrival at the emergency room at 6 p.m., the patient exhibited tachypnea, agitation, and a Glasgow Coma Scale score of 10. Both pupils were isocoric and reacted to light. He presented with generalized edema and bilateral dorsum foot hypoesthesia without motor deficits, primarily in the lower limbs. Additionally, he was oligoanuric.
Laboratory examination revealed several abnormalities, including metabolic acidosis (pH: 7.26, HCO3 12 mmol/L), lactate levels of 2.7 mmol/L, CPK levels of 32,800 U/L, blood urea levels of 18 mmol/L, creatinine levels of 182.2 mmol/L, and hyperkalemia at 6.6 mmol/L. Brain computed tomography did not reveal any abnormalities.
Following oxygen administration, the patient was transferred to the intensive care unit at 8:30 p.m. To address his hyperkalemia, treatment included intravenous calcium gluconate, alkaline diuresis, and dextroinsulin infusion. By day 3, anuria, hyperkalemia, and severe metabolic acidosis persisted, along with an increase in CPK levels (80,000 U/I). Multiple sessions of hemodialysis were performed, and on day 13 of hospitalization, he was discharged to the renal unit. On day 40, the patient was finally discharged after the normalization of laboratory values, particularly with creatinine levels at 75 mmol/L.
This case involves an 18-year-old male smoker with no significant medical or surgical history. He inhaled butane gas from a pocket lighter with the intention of altering his voice, while in the company of a friend. Suddenly, he collapsed and became unresponsive at home, witnessed by family members. He was promptly transported to a nearby hospital, which was approximately 10 minutes away from his residence.
Upon arrival at the hospital, the patient was found to be pulseless, leading to the initiation of CPR following Standard Advanced Cardiac Life Support (ACLS) guidelines. The patient was diagnosed with ventricular fibrillation and received two unsynchronized shocks of 200 joules each. Return of spontaneous circulation was successfully achieved, and the patient was subsequently intubated using Rapid Sequence Intubation (RSI).
Various diagnostic tests, including chest X-ray, brain computed tomography (CT), and echocardiography, were conducted, all of which showed no abnormal findings. Blood investigations, apart from metabolic acidosis, yielded normal results.
After six hours from the return of spontaneous circulation (ROSC), the patient was extubated in the Intensive Care Unit (ICU) as he regained consciousness. However, he exhibited neurological symptoms of disorientation and confusion, prompting his referral to our facility, a tertiary care hospital.
Upon presentation at our hospital, the patient displayed confusion and disorientation regarding time and place, along with short-term memory loss. His vital signs were stable in the Emergency Department. Multiple ECGs were performed, revealing some abnormalities. A repeat CT scan of the brain showed no acute brain insult, and overall, blood investigations remained unremarkable.
The patient was admitted under cardiology care in the Cardiac Care Unit (CCU) for rhythm monitoring and further workup. A multidisciplinary team was involved in his care. On the following day, a detailed neurological examination was conducted, which was largely unremarkable except for disorientation, short-term memory loss, and ataxia. Subsequently, MRI and EEG were ordered to rule out hypoxic or toxic brain injury.
By the third day of his hospitalization, the patient showed improvement. He was conscious, oriented, and his memory was gradually improving. He was mobilizing with assistance, and no further cardiac or neurological events were observed. Consequently, he was discharged home with a follow-up appointment for EEG, MRI of the brain, and a neurology clinic evaluation.
A 30-year-old male was brought to the Emergency Department (ED) by Emergency Medical Services (EMS) while unconscious and in a seizure state that had lasted for more than 30 minutes.
Upon arrival at the ED, the patient was unconscious but breathing normally as reported by EMS. The patient had no prior history of systemic diseases, surgeries, medications, or known allergies. According to witnesses, the patient was alone in a coffee shop, and next to him was a lighter refill canister containing 250 ml of extra purified butane gas. He suddenly collapsed and experienced a seizure. Fluid infusion was initiated, but tachycardia persisted despite the administration of 2 liters of fluids. Consequently, the patient was intubated to secure the airway, placed on mechanical ventilation (volume-control mode, FiO2: 0.50, Tidal volume: 550 ml, frequency: 12 beats/min, positive end-expiratory pressure: 5 cm H2O), and had a central line inserted. Sedation was provided using midazolam and fentanyl infusions.
Upon presentation, the following vital signs were recorded by the ED physicians: heart rate: 170 beats per minute, body temperature: 37.80°C, oxygen saturation: 90% on room air, and an electrocardiogram revealed sinus tachycardia.
The timeline of the case, starting from spotting the patient to admission, and including different stages of interventions, is illustrated below:
Laboratory investigations indicated acute renal failure, elevated levels of creatinine kinase (1700 U/L), suggesting tissue damage, particularly in the myocardium and muscle tissue. A computed tomography scan of the brain revealed mild brain edema.
Tachycardia persisted even after 3 hours, followed by a drop in blood pressure to 70/50 mm Hg. Inotropic agents were initiated by the physician, but 6 hours later, the patient developed ventricular fibrillation. Despite attempts at amiodarone infusion, followed by 4 instances of defibrillation and cardioversion, the patient succumbed after 45 minutes of resuscitation efforts.
Butane gas has been reported as a cause of death over the years, primarily due to its effect of sensitizing the heart to catecholamines, which may lead to refractory arrhythmias (6). Neurological, renal, or pulmonary symptoms are also attributed to the toxic effects of butane gas, as it can permeate various tissues in the body, as confirmed by autopsy reports in the brain, lungs, heart, and liver (1)(7).
In Table 1 we summarize the outcomes of butane gas poisoning:
| Age | Outcome | Reference |
|---|---|---|
| 11 y/o | Cardiac arrest and death | Alunni V. et al, J Forensic Sci, January 2018, Vol. 63, No. 1 |
| 16 y/o | Seizures, cardiac arrest, and death | Corbacioglu, Seref et al, Journal of Academic Emergency Medicine, (2015), 6, 16-18 |
| 19 y/o | Cardiac arrest and death | Corbacioglu, Seref et al, Journal of Academic Emergency Medicine, (2015), 6, 16-18 |
| 18 y/o | Arrhythmia, alive | Sen A et al, Anesth Essays Res 2015;9:273-5 |
| 42 y/o | Rhabdomyolysis and acute kidney disease | Mohamed Fekih Hassen et al, Trends in Anaesthesia and Critical Care 18 (2018) 10e11 |
| 18 y/o | Arrhythmia, cardiac arrest, ataxia, memory loss, alive | Sen A et al, Anesth Essays Res 2015;9:273-5 |
| 30 y/o | Arrhythmia, cardiac arrest, and death | Khalid N. Almulhim, Saudi Med J 2017; Vol. 38 (12): 1250-1254 |
The cases presented in this study provide a sobering insight into the dangers associated with butane gas inhalation. Butane, a commonly found hydrocarbon gas in various household products, has been linked to a range of severe medical consequences, including cardiac arrest, seizures, rhabdomyolysis, acute kidney disease, and even death.
The outcomes observed in these cases emphasize the critical need for public awareness and education regarding the risks of butane gas abuse. Adolescents and young adults appear to be particularly vulnerable, with several cases demonstrating fatal consequences after inhalation.
Furthermore, the varied clinical presentations, including cardiac arrhythmias, neurological symptoms, and renal dysfunction, underscore the complexity of butane gas toxicity. This complexity requires healthcare providers to remain vigilant and consider butane exposure as a potential cause when faced with unexplained medical emergencies.
It is essential for healthcare professionals, educators, and parents to work together to raise awareness about the hazards of butane gas misuse and to promote responsible use of household products. Additionally, further research and epidemiological studies are warranted to gain a deeper understanding of the long-term effects and prevalence of butane gas abuse.
Ultimately, the cases discussed in this report highlight the urgent need for preventive measures and early intervention to mitigate the devastating consequences associated with butane gas inhalation.
Research Report: Butane Gas Inhalation Case Study. (2024, Jan 24). Retrieved from https://studymoose.com/document/research-report-butane-gas-inhalation-case-study
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