Search

Fatal intoxications with butane and/or propane are rare although the inhalation of such liquid gases in order to induce hallucinations is not uncommon amongst youngsters, the number of which is difficult to evaluate. Thus the possibility of gas intoxication should be taken into consideration in all cases of unclear death of youngsters, in which case the macroscopic and histological findings will be unspecific whereas the chemical-toxicological analyses, especially of the native brain, lung and liver tissue, lead to definite conclusions.

A case of suicide of a 26-year old woman by propane-butane inhalation is presented with a description of the circumstances, postmortem pathomorphological and toxicological findings. The literature relating to deaths due to inhalation of these gaseous substances was briefly reviewed.

This report describes a fully elaborated and validated method for quantitation of the hydrocarbons n-propane, iso-butane, and n-butane in blood samples. The newly developed analytical procedure is suitable for both emergency cases and forensic medicine investigations. Its practical applicability is illustrated with a forensic blood sample after acute inhalative intoxication with lighter fluid; case history and toxicological findings are included. Identification and quantitation of the analytes were performed using static headspace extraction combined with gas chromatography-mass spectrometry. In order to reconcile the large gas volumes injected (0.5 mL) with the narrowbore capillary column and thus achieve preconcentration, cold trapping on a Tenax sorbent followed by flash desorption was applied. Adequate retention and separation were achieved isothermally at 35 degrees C on a thick-film capillary column. Sample preparation was kept to a strict minimum and involved simply adding 2.5 microL of a liquid solution of 1,1,2-trichlorotrifluoroethane in t-butyl-methylether as an internal standard to aliquots of blood in a capped vial. Standards were created by volumetric dilution departing from a gravimetrically prepared calibration gas mixture composed of 0.3% of n-propane, 0.7% of iso-butane, and 0.8% of n-butane in nitrogen. In the forensic blood sample, the following concentrations were measured: 90.0 microg/L for n-propane, 246 microg/L for iso-butane, and 846 microg/L for n-butane.

Intentional hydrocarbon inhalation can be fatal. Death can be secondary to hydrocarbon's cardiopulmonary effects. We present a case of a patient who survived ventricular fibrillation after inhalation of Glade Air Freshener, which contains short chain aliphatic hydrocarbons (butane and isobutane). Unlike our case, myocardial sensitization and hypoxia are more commonly described with aromatic, halogenated or longer chain hydrocarbons.

Most cases of acute poisoning by butane and other volatile compounds occur in young people as a consequence of substance abuse by inhalation. Clinical symptoms are caused by asphyxia and mainly affect the cardiovascular, respiratory and central nervous system. There are also reported deaths from intoxication of butane inhalation, mostly by cardiac arrhythmia. We report the case of a healthy 14 year-old boy who inhaled butane gas from an aerosol can for refilling cigarette lighters. Despite successful resuscitation and defibrillation, he died two days later from multiple organ failure involving the central nervous system, cardiovascular system, pulmonary system and the liver. Although such incidents are rare in middle European countries, emergency and intensive care medicine staff should be instructed on the consequences and management of butane gas poisoning.

Resuscitation from cardiac arrest caused by volatile substance abuse is rarely successful. Large doses of catecholamines given during resuscitation, in the presence of butane, may cause recurrent ventricular fibrillation. We report a case of prolonged resuscitation in a young man who had inhaled butane. Cardiac output was restored 10 min after the administration of intravenous amiodarone. We suggest that antiarrhythmic agents should be used early during resuscitation to prevent recurrent arrhythmias.

A brief review of the causal and treatment literature relating to volatile substance dependency suggests the interaction between individual and system requires careful attention and understanding. A model is tentatively and provisionally adumbrated to help clarify the main factors involved from a dynamic biopsychosocial perspective. Ego boundary disturbances emerge from and reciprocally influence behaviour and social interactions. These disturbances can be avoided temporarily, although inevitably deepened in the long-term, by substance dependence. Two case examples, selected because they differ in many respects, including relative treatment effectiveness, illustrate this integrative perspective. The discussion focuses on explaining the differing outcomes in terms of the extent to which the inner-outer boundary is open to modification and how far it can be successfully negotiated and clarified. A major factor in differentiating between inside and outside is thought to be causal perceptions or "attributions." Successful differentiation tends to facilitate change, as opposed to reinforcing maladaptive homeostasis. Key issues for therapists overlap with addictions treatment in general, including emotional blocks or barriers in patients, difficulty engaging systems in a strategic manner, and countertransference problems. It is argued that these difficulties in therapy might respond to integrative psychotherapeutic responses, provided the differences in perspective are sufficiently understood.

Two lethal poisonings by butane and propane are described, and the corresponding concentrations in the body fluids and organ tissues are evaluated. One case appeared to be an accident after deliberate inhalation for butane, one was a suicide. The mechanism of the inhalation could be reconstructed in both cases. The concentrations in the biological material agreed well with observations in similar cases.

Sudden death due to the inhalation of halogenated hydrocarbons is a well-documented phenomenon in the scientific and medical literature. Recently, there has been sporadic information suggesting that nonhalogenated hydrocarbons may cause potentially fatal cardiac arrhythmias. This report documents five sudden deaths due to inhalation of nonhalogenated hydrocarbons: n-butane, isobutane and propane. The hydrocarbons were identified by headspace gas chromatography in blood, brain, and lung tissue. Case histories, toxicological findings and analytical procedures are discussed.

A case of nonimmune hydrops fetalis resulting from fetal methemoglobinemia is presented. A woman with a pregnancy at 17 weeks' gestation was admitted after combustion gas intoxication. Although the mother totally recovered, the fetus showed signs of nonimmune hydrops fetalis at follow-up. Fetal methemoglobin levels were very high.

We report a case of hemiparesis resulting from acute intoxication following inhalation of butane gas from a canister in a 15 year-old boy.

The authors report on an acute compartment syndrome occurring symmetrically in the extensors of both forearms. The etiology of this unique compartment syndrome, not previously described, could be attributed to the inhalation of a propane-butane gas mixture, low in oxygen, while sleeping, in combination with external compression of both forearms, due to the patient's head lying on both forearms while sleeping. Ischemic damage to muscles was precisely located using non-invasive MRI (Magnetic Resonance Imaging). The extent of cellular damage due to ischemia after fasciotomy and healing by secondary intention was quantitatively assessed using non-invasive 31P-MRS (Phosphorus Magnetic Resonance Spectroscopy). The results correlate with the clinical and histological findings and indicate a bioenergetic regeneration of the ischemic skeletal muscle's cells.

Rapidly progressive bilateral pulmonary infiltrates occurred in a 19-year-old man following an unusual hydrocarbon abuse. The acute illness was the result of a "trick" known as "fire-breathing." Fire-breathing involves filling the oral cavity with butane gas, from an ordinary butane cigarette/cigar lighter, and exhalation of the volatile vapors over an open flame producing a flame-throwing effect. Because of the pulmonary toxic reaction, this activity could have a serious or even fatal outcome.

Four cases of cutaneous rash, clinically more or less similar to erythema multiforme have been observed in patient who either stayed in a room with an accidentally high content of fluorocarbons, or had a skin contact with butane or phenyl-azo-beta-naphthol. The cutaneous lesions appear to be secondary to absorption of the toxic product, and probably induced by inhalation rather than by percutaneous penetration. Arguments for the responsibility of the substances rely on anamnestic data.

A newborn infant who suffered intra-uterine anoxia is described, whose mother inhaled butane gas accidentally during the sixth month of pregnancy. The infant was born at 39 weeks. Ultrasonography and neuroradiological studies (CT scan and angiography) showed an almost complete absence of both cerebral hemispheres. The thalamus, brainstem and cerebellum were preserved. These findings were compatible with hydranencephaly. The authors believe that the malformation was due to intra-uterine anoxia occurring during fetal brain-development.

Postmortal changes of propane, butane and iso-butane concentration in the lung and fat of mice exposed to lethal intoxication with commercial liquid gas are studied. The hydrocarbon tissue concentrations after exposure were determined by gas liquid chromatography. The hydrocarbons progressively decreased in the lung and disappeared, depending on the degree of putrefaction; even in case of remarkable putrefaction, it was still possible to detect them in the fat tissue.