Rare but relevant: Hydrocarbons and sudden sniffing syndrome

Abstract

Inhaled hydrocarbon‐associated sudden collapse (IHASC), often referred to as ‘sudden sniffing death syndrome’ is a critical and often fatal event linked to the inhalation of volatile hydrocarbons, primarily occurring in adolescents and young adults. This syndrome manifests as sudden cardiac and/or respiratory arrest, typically occurring during or straight after inhalant use, almost always triggered by exertion or emotional distress. The prevalence is (likely) uncommon, but the syndrome concerning, given the young and vulnerable populations engaging in inhalant misuse. Those who collapse while alone are often found deceased, but those with a witnessed collapse and immediate bystander intervention with cardiopulmonary resuscitation (CPR) and defibrillation have good survival rates, far better than from cardiac arrest in general. Ultimately, death from IHASC is preventable with educational initiatives aimed at reducing inhalant misuse, preventative measures aimed at reducing access to commonly misused products, and educating lay people to provide immediate bystander CPR.

WHAT IS THE PROBLEM AND ITS CLINICAL PRESENTATION?

The term ‘sudden sniffing death syndrome’ was coined in the 1970s and refers to death associated with a sudden collapse while ‘sniffing’ hydrocarbon based aerosols [1]. The classical presentation involves an adolescent or young adult engaging in hydrocarbon inhalant use, more commonly referred to as ‘chroming’ to achieve a short term mood altering high [2, 3]. This hydrocarbon use is often concealed from parents or caregivers and frequently occurs in private settings such as bathrooms or bedrooms, behind sheds or in a park with friends, using easily accessible household products such as deodorant cans, air fresheners or spray paint cans [3, 4, 5, 6]. Collapse usually occurs in the context of a sudden shock or strenuous activity during the inhaled hydrocarbon use [1, 3, 7]. For example, the unexpected entrance of a parent triggering a fight‐or‐flight response, because of the fear of being caught. This physiological response results in a surge of catecholamines due to activation of the sympathetic nervous system [7]. Because of cardiac myocyte ‘sensitization’ from the inhaled hydrocarbons, this catecholamine surge leads to cardiac dysrhythmias, ultimately resulting in cardiac arrest and collapse [7, 8, 9]. Reports suggest that patients who have cardiac dysrhythmias and a subsequent unwitnessed cardiac arrest rarely survive long enough to present to a healthcare facility [1, 10]. In contrast, patients who receive immediate cardiopulmonary resuscitation (CPR) from a bystander or emergency services can have extremely good outcomes [11]. For this reason, the term sudden sniffing death syndrome is a misnomer and should be more correctly referred to as inhaled hydrocarbon associated sudden collapse (IHASC), because of the potential to survive.

Fortunately, IHASC is relatively uncommon, and the more typical emergency department presentation of patients with acute hydrocarbon inhalant use include central nervous system effects (confusion, seizures, loss of consciousness), respiratory symptoms (respiratory distress, pneumonitis) and/or electrolyte abnormalities (metabolic acidosis) [10, 12, 13].

INHALED HYDROCARBON USE

Hydrocarbons are carbon‐based organic compounds that exist in multiple forms—gaseous, liquid or solid—characterized by the arrangement and number of hydrogen and carbon atoms, along with the presence of additional elements or functional groups, particularly halogens [6, 9, 13, 14]. Because of their versatile structures, they are extensively used in various applications, such as fuels, solvents and aerosol propellants. For instance, propane and butane are widely used as fuel for domestic and industrial uses. One of the first uses of volatile hydrocarbons as propellant agents began during World War II, with the distribution of aerosolized insecticides to military personnel [15]. After this, the commercialization of aerosol sprays increased in the late 1940s to 1960s, with the introduction of cosmetic products such as hair spray [using chlorofluorocarbon (CFC) propellants], and adoption into other products including spray paint. CFCs remained the dominant propellant for these aerosol products until the late 1980s, when growing environmental concerns about their role in ozone layer depletion prompted significant regulatory changes [9, 15, 16]. This led to the introduction of alternative, less environmentally harmful propellants, such as hydrocarbons (e.g. propane and butane) and hydrofluorocarbons (HFCs) [15].

Recreational use of inhaled hydrocarbons paralleled the accessibility of aerosolised commercial products [17]. The inhalation of hydrocarbons is categorized under the broader umbrella of volatile substance misuse (VSM), which encompasses the intentional inhalation of fumes, vapors or gases to elicit psychoactive effects [18]. VSM also includes the inhalation of non‐hydrocarbon volatile gases such as amyl nitrite and nitrous oxide, which have different patterns of use and adverse effects to hydrocarbons [19]. The practice of inhaling hydrocarbon spray cans include various methods of inhalation such as huffing (inhaling vapors from a cloth soaked in the substance), bagging (inhaling vapors from a plastic bag containing the substance) and sniffing (direct inhalation from containers) [6]. Originally associated with chrome‐based spray paint, the term ‘chroming’ now encompasses a range of household or industrial product misuse such as deodorant and air freshener cans (containing the hydrocarbons butane and propane as propellants), paint thinners and glue (e.g. toluene), nail polish remover (e.g. acetone) and liquid lighter fuels and gas canisters (butane/propane) [3, 20].

HOW COMMON IS IT?

The prevalence of inhaled hydrocarbon use varies by country, region and demographic factors, but typically occurs in the young and vulnerable [6, 21, 22, 23, 24, 25]. Ease of access and relative cost (if any) to the availability of inhalable hydrocarbons are often cited as one of the leading contributions to use in such populations, as well as the likely lack of awareness of the associated risks of use [23, 24]. The majority of data regarding VSM derives from large‐scale drug use surveys, which predominantly target adolescents or young adults [10, 25, 26, 27, 28, 29]. These surveys, while informative, tend to overlook certain demographic groups, especially in developing regions and among minority populations in developed countries where VSM patterns may differ significantly [23, 24, 25, 30]. An important complication in accurately assessing the impacts and prevalence of VSM arises from the varied nature of products labelled as inhalants [17]. Many studies aggregate inhaled hydrocarbon misuse with other forms of VSM like amyl nitrite, which obscures specific usage patterns, particularly as there appears to be differing behaviours and motivations between those using spray cans and those using nitrous oxide for instance [19, 26].

In general, inhaled hydrocarbon misuse occurs globally and more frequently in the younger population, often with 10% to 20% of the adolescent population having used, and with many reports of use occurring around and below 12 years of age [5, 12, 28]. Recent Australian Poisons Centre data found that almost 50% of calls regarding inhaled hydrocarbon use involved patients 14 years or less [3]. More specifically, the prevalence of sudden collapse in the setting of inhalant misuse is more poorly defined, because of under‐reporting or under recognition and the reliance on coronial data, particularly since many fatal cases do not present to hospitals [3, 4].

Australian fatality data for deaths associated with inhalant misuse consistently identify a male predominance (70%–80%), with a median age varying between the early to mid‐20s [3, 4, 31]. Sudden collapse was noted in 29% of inhalant misuse related deaths in one report and was witnessed in almost half the cases [4]. Other studies often attribute cases with negative autopsy findings to sudden cardiac death, secondary to associated inhalant use, without definitive clinical evidence or toxicological confirmation. Other causes of death include respiratory arrest from asphyxia and anoxia [3, 4].

WHAT ARE THE PATHOLOGICAL MECHANISMS?

Inhaled hydrocarbons are rapidly absorbed in the lungs and are present at target organs such as the brain and heart within seconds [32]. This is what makes inhaled hydrocarbons (e.g. halothane) good anaesthetic agents and why with misuse a rapid onset ‘high’ occurs. Many inhaled hydrocarbons are removed unchanged via exhalation, whereas others, such as propane and butane, are primarily metabolised via the omega‐oxidation pathway and then via alcohol dehydrogenase [32, 33].

It was recognised early in the 20th century that cats anesthetized with chloroform, a classic halogenated hydrocarbon, exhibited heightened sensitivity to injections of adrenaline [9, 34, 35]. Administration of adrenaline led to short pauses on the electrocardiogram (ECG) trace, followed by tachycardia, which, if sustained, culminated in ventricular fibrillation [34, 36]. Over the following decades, the medical literature increasingly reported the risk of cardiac dysrhythmias in anesthetized patients, especially during induction with halogenated hydrocarbon anaesthetics [37]. Towards the end of the 1960s, deaths began being reported from sniffing aerosol propellants [38]. In 1970, Bass published 110 cases of sudden death after volatile agent misuse and coined the term ‘sudden sniffing death’ [1].

Halogenated hydrocarbons compounds have been shown to alter cardiac electrophysiology, leading to increased susceptibility to dysrhythmias [8, 39, 40]. The inhalation of these substances can affect cardiac potassium and calcium channels, which are crucial for cardiac repolarization [8, 41]. Disruption of these channels results in prolonged and heterogeneous (dispersion) cardiac action potentials, which appears as a prolonged QT interval on the ECG [40, 41, 42]. This ‘sensitisation’ is similar to the way that some drugs affect the delayed rectifier potassium channels (I _K ) in the heart, resulting in a prolonged QT interval and increased risk of dysrhythmia development, namely torsades de pointes [7]. The development of a dysrhythmia at this point still requires a secondary event to trigger the heart, usually an early after depolarisation [7, 8]. Rapid changes in heart rate by catecholamines release during stress may be such a trigger, via impact on cardiac calcium and sodium channels, altering the action potential refractory period and also via the activation of early depolarisations occuring on an incomplete action potential [7, 8].

WHAT IS THE PROGNOSIS AND TREATMENT?

The prognosis for inhaled hydrocarbon use associated sudden collapse is reportedly poor, with many cases resulting in death [1, 4, 43, 44]. While those who collapse alone are often found deceased, more recent evidence demonstrates that individuals who have a witnessed collapse and receive immediate bystander intervention, such as CPR and defibrillation, have significantly higher survival rates, much higher than those typically observed in other cardiac arrest scenarios [11]. These survival rates are likely because the patients have healthy hearts and that the hydrocarbon toxicity is short‐lived and reversible. A review of the epidemiology and survival outcomes of out‐of‐hospital cardiac arrests associated with inhaled hydrocarbon use in Queensland, Australia, reported survival rates of 69% at the time of arrest and 38% surviving to hospital discharge [11]. The critical factor influencing these outcomes was the time to CPR and defibrillation, because the time to return of perfusion to critical organs impacts the rates of complications such as multi‐organ failure or brain death secondary to the initial cardiac event [45].

The use of adrenaline in cardiac arrest secondary to hydrocarbon inhalation is contentious [46]. Some literature suggests minimizing adrenaline administration during advanced resuscitation following inhaled hydrocarbon sudden collapse because of its theoretical potential to worsen catecholamine‐induced dysrhythmias [11, 12, 46]. This concern arises predominantly from observational experience rather than definitive experimental evidence, using cases of repeated adrenaline administration associated with fatalities, to support causation between adrenaline use and death [11]. However, cases in which large or repeat doses of adrenaline have been used often reflect confounding factors, most importantly the severity and down time of such cases, rather than adrenaline causing the severe effects. The argument that because adrenaline sparked the dysrhythmia it should be avoided once there is a dysrhythmia is less valid and not supported by experimental evidence. In fact, increasing the heart rate, either by pharmacological (e.g. isoprenaline) or electrical pacing, is the standard treatment in patients having episodes of torsades de pointes secondary to drug induced QT interval prolongation [7, 47, 48]. Similarly in IHASC, once a dysrhythmia has been triggered by a catecholamine surge increasing heart rate, maintaining a faster heart rate with adrenaline is less likely to cause further dysrhythmias, but will act as a positive inotrope. This is supported by studies in dogs in which adrenaline readily induced ventricular arrhythmias under halothane anaesthesia and that atrial driving at a sufficient rate could prevent these arrhythmias [49].

The use of β‐adrenergic blockers has been suggested as a potential therapeutic intervention for managing arrhythmias associated with hydrocarbon inhalation, particularly in resistant ventricular fibrillation [10]. However, the autonomic response triggered by the fight or flight reaction during hydrocarbon exposure is likely to be a transient catecholamine surge that is unlikely to result in sustained adrenergic effects, in contrast to the prolonged sympathomimetic effects seen in cases with substances such as amphetamines. Current advanced life support (ALS) guidelines advocate for established resuscitation protocols focusing on immediate defibrillation and antiarrhythmic medications like lignocaine and amiodarone rather than β‐blockade [48]. Therefore, while some case reports indicate successes in other contexts, the application of β‐adrenergic antagonists for hydrocarbon‐induced dysrhythmias lacks sufficient clinical evidence and may not address the underlying pathophysiology effectively. Furthermore, it is essential to note that this approach aligns with the observation that most fatalities occur at the time of substance use, highlighting the urgency of effective interventions.

PREVENTION

IHASC should be preventable through educational initiatives aimed at reducing inhalant misuse, such as raising awareness about the dangers of inhalant misuse, implementing measures to limit access to commonly abused products and training lay persons to provide immediate bystander CPR. This is crucial for vulnerable populations such as adolescents and young adults. Studies have shown that increasing public knowledge about CPR and its significance in out‐of‐hospital cardiac arrest scenarios can lead to higher rates of bystander intervention [50].

Maclean and D'Abbs [51] emphasize the importance of both demand‐reduction measures, such as counselling and treatment services and supply reduction strategies, including regulations on the sale of commonly abused products. By limiting access to these substances and providing community‐based education, it is possible to reduce the incidence of inhalant misuse and its associated health risks, including IHASC [29, 51].

CONCLUSION

IHASC represents a significant public health challenge, particularly among adolescents and young adults who engage in volatile substance misuse. The acute nature of this syndrome, characterized by sudden cardiac and/or respiratory arrest, often unwitnessed and without early resuscitation, underscores the urgent need for effective prevention strategies. Treatment should focus on standard ALS protocols and should not exclude the use of adrenaline in patients in cardiac arrest.

AUTHOR CONTRIBUTIONS

IB and GIK drafted the manuscript, edited and proofread revisions.

DECLARATION OF INTERESTS

None.

Berling I, Isbister GK. Rare but relevant: Hydrocarbons and sudden sniffing syndrome. Addiction. 2025;120(9):1884–1888. 10.1111/add.70082

DATA AVAILABILITY STATEMENT

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.