An Acute Case of Exogenous Lipoid Pneumonia Which Developed in Tent Sauna

Abstract

The aspiration or inhalation of lipid substances can cause lung injury, including chemical pneumonitis and exogenous lipoid pneumonia. We herein report a case of acute lung injury caused by kerosene inhalation in a tent sauna. A patient developed dyspnea with respiratory failure two hours after igniting a wood-burning stove with kerosene. High-resolution computed tomography revealed widespread ground-glass opacities, and bronchoalveolar lavage revealed lipid-laden macrophages. Systemic corticosteroid treatment led to a rapid improvement. Although kerosene is generally safe at room temperature, its vaporization in high-temperature environments may increase the risk of lung injury through inhalation.

Introduction

Sauna bathing is a traditional Finnish cultural practice with a history spanning thousands of years, and is widely recognized for its benefits in leisure, relaxation, and overall well-being (1). Its popularity expanded globally, particularly across Europe, after the 1930s (2), and public saunas were introduced to Japan in the 1950s (3). Since approximately 2022, Japan has been experiencing an unprecedented sauna boom, potentially driven by factors such as the adaptation of a sauna-themed book into a manga and television drama (4) as well as increased exposure through media and social networking platforms.

The recent surge in sauna popularity has also influenced sauna bathing styles. Notably, in response to coronavirus disease 2019 (COVID-19) prevention measures, private sauna experiences, including tent saunas, have gained traction as an outdoor recreational activity. A tent sauna employs a wood-burning stove as its primary heat source to elevate the internal temperature. Although the primary safety concerns associated with homemade saunas typically involve fire hazards and carbon monoxide poisoning, we encountered a case of acute lung injury associated with the use of kerosene as an accelerant for igniting a wood-burning stove in a tent sauna. Although acute lung injury caused by kerosene exposure is commonly attributed to ingestion or aspiration, cases resulting from inhalation have so far only rarely been reported. This highlights the potential dangers of kerosene use in enclosed high-temperature environments.

Case Report

A 46-year-old man with no underlying medical conditions presented to the emergency department with severe dyspnea. His medical history revealed that he had used 250 mL kerosene as an accelerator to ignite a wood-burning stove in his tent sauna (Fig. 1). Immediately after ignition, he perceived a strong volatile odor and subsequently developed nausea and dyspnea, accompanied by a cough. His symptoms progressively worsened over the next two hours, thus prompting him to call an ambulance.

Figure 1.

The wood-burning stove in the tent sauna that had actually been used in this case.

On physical examination, his vital signs were as follows: body temperature, 39.2°C, SpO₂ 100% while receiving 10 L/min of oxygen via a reservoir mask; respiratory rate, 18 breaths per minute; blood pressure, 92/57 mmHg; and heart rate, 87 beats per minute. Chest auscultation revealed no significant abnormalities. An arterial blood gas analysis, conducted under 10 L/min oxygen administration, demonstrated mild hypoxia, and carbon monoxide poisoning was ruled out (pH: 7.409; PaO₂: 209 Torr; PaCO₂: 36.5 Torr; HCO₃^-: 22.6 mmol/L; FCOHb: 1.9%). Laboratory blood tests revealed an elevated white blood cell count (8,620/μL), while procalcitonin (0.36 ng/mL), C-reactive protein (0.02 mg/dL), lactate dehydrogenase (193 IU/L), and krebs von den lungen-6 (176.8 U/mL) levels were within the normal ranges. The interleukin-6 level was elevated (8.969 pg/mL), suggesting severe inflammation. Rapid diagnostic tests for Mycoplasma, influenza, and COVID-19 yielded negative results. Tests for antibodies associated with collagen vascular diseases, including anti-cyclic citrullinated peptide, anti-aminoacyl-tRNA synthetase, anti-Scl-70, anti-ribonucleoprotein, anti-double-stranded DNA, anti-SS-A/Ro, proteinase-3 anti-neutrophil cytoplasmic, and myeloperoxidase anti-neutrophil cytoplasmic antibodies, were all negative.

Chest radiography revealed diffusely distributed ground-glass opacities (GGO) in both lungs (Fig. 2A). High-resolution computed tomography (HRCT) of the chest revealed diffuse areas of increased GGO with subpleural sparing in both the lungs. Additionally, focal areas of increased density were observed in the pulmonary panlobular regions along with band-like consolidations in the lower lobes of both lungs (Fig. 3A). No low-attenuation lesions, indicative of inhaled fat, were observed. Transthoracic echocardiography revealed no evidence of cardiac dysfunction or congestion. Based on the clinical presentation and characteristic chest imaging findings, acute exogenous lipoid pneumonia due to inhalation of evaporated kerosene (hydrocarbon components) was suspected.

Figure 2.

The chest X-ray findings on admission shows ground-glass opacities predominantly in the right lung (A). A chest X-ray on the next morning after admission shows lung infiltration predominantly in the lower lung fields (B). A chest X-ray on day 3 shows improvement in infiltration (C). A chest X-ray on day 6 showed that the shadow had almost disappeared (D).

Figure 3.

HRCT on admission reveals diffuse areas of GGO with subpleural sparing in both lung fields and band-like consolidation in the lower lobes of both lungs (A). HRCT on day 6 reveals that the previously widespread GGO had almost completely resolved (B).

Following hospital admission, the patient's oxygen requirement was decreased to 1.5 L/min via a nasal cannula. Empirical antibiotic therapy with sulbactam/ampicillin (9 g/day) and levofloxacin (500 mg/day) was initiated. However, six hours after admission, his respiratory condition deteriorated, necessitating an increase in oxygen support with a high-flow nasal cannula set at an FiO₂ of 0.5 and a flow rate of 40 L/min. A follow-up chest radiograph revealed progression of pulmonary infiltrates, predominantly in the lower lung fields (Fig. 2B). Although no standardized treatment protocol exists for lipoid pneumonia, methylprednisolone (80 mg/day) was administered in accordance with the acute respiratory distress syndrome (ARDS) treatment guidelines (5). By the third day of hospitalization, the patient's oxygenation status had significantly improved and supplemental oxygen was no longer required. Chest radiography demonstrated a marked resolution of lung infiltrates (Fig. 2C). Consequently, the corticosteroids and levofloxacin were discontinued. On the fourth day, bronchoalveolar lavage (BAL) was performed via the right B3 bronchus to confirm a diagnosis of lipoid pneumonia. The BAL fluid recovery rate was 51.33% (77/150 mL) and the macroscopic appearance was blood-tinged. A cytological analysis revealed a total cell count of 3.3×10⁷/mL, with a predominance of macrophages (75% macrophages, 21.5% neutrophils, 0.5% lymphocytes, and 3% eosinophils). Oil Red O staining demonstrated the presence of lipid-laden foamy macrophages (Fig. 4), thus confirming the diagnosis of lipoid pneumonia. Chest radiography and HRCT on day 6 revealed that the previously widespread GGO had nearly completely resolved (Fig. 2D, 3B). The patient was discharged on day 8.

Figure 4.

BAL performed on day 4 detected lipid-laden foamy macrophages which were positive for Oil-Red-O staining.

Discussion

We herein report a case of acute-onset lipoid pneumonia caused by kerosene used to ignite a wood-burning stove in a tent sauna. The primary route of kerosene-induced lung injury is aspiration or inhalation (6), which can result in chemical pneumonia or ARDS, potentially leading to severe clinical outcomes (7). Kerosene-induced chemical pneumonia is pathologically characterized by exogenous lipoid pneumonia (8). Exogenous lipoid pneumonia occurs due to accidental ingestion, aspiration, or the inhalation of lipid materials, and it is classified into acute and chronic forms. Chronic exogenous lipoid pneumonia is typically associated with repeated episodes of aspiration or the inhalation of animal, mineral, or vegetable lipids found in various products, including foods, radiographic contrast agents, laxatives, petrolatum, and oil-based nasal sprays over an extended period (9,10). In contrast, acute exogenous lipoid pneumonia results from accidental exposure to a large quantity of lipid materials over a short duration, most commonly due to aspiration of significant amounts of petroleum-based products (11). Numerous cases of acute lung injury due to fire-eating (12-14) and diesel aspiration (15,16) have been reported, as well as cases linked to electronic cigarette use (17). Although several reports have been published on acute lung injury caused by kerosene (18-21), most are related to accidental ingestion or aspiration.

Acute exogenous lipoid pneumonia typically presents with clinical symptoms, such as fever, cough, and dyspnea, often necessitating oxygen therapy (22,23). The HRCT findings frequently revealed consolidation and GGO. Other radiological features may include interlobular septal thickening (crazy-paving pattern), nodules, or mass-like lesions that require differentiation from lung cancer, cavitary lesions, and pleural effusions (10-12,22,23). In some cases, fat attenuation regions may also be observed (9,24), but this was not observed in the present case. To date, no studies have compared differences in the exposure routes (i.e., aspiration versus inhalation) using HRCT findings. However, in cases of aspiration, imaging findings typically show predominance in the posterior segments of the lobes and lower lobes, which is consistent with the direction of gravitational deposition (9,11,23,24). In contrast, when exposure occurs via inhalation, findings may present GGO with subpleural sparing (17) or diffuse opacities (23). In this case, widespread GGO with subpleural sparing was observed, which was deemed to be consistent with inhalation-induced injury.

Pathologically, exogenous lipoid pneumonia is believed to result from a foreign-body reaction to lipid substances within the alveoli. Although alveolar macrophages absorb these lipids, they are unable to metabolize them, leading to alveolar infiltration by lipid-laden macrophages during the acute phase (24,25). It is thought that the GGO observed on imaging corresponds to alveolar filling and inflammation caused by macrophages (24). BAL is considered useful for diagnosing exogenous lipoid pneumonia in conjunction with a history of lipid substance exposure and radiological findings (10,23,25). In the BAL fluid, in addition to the macroscopic appearance being informative (10,23), the presence of lipid-laden macrophages and extracellular oil droplets serves as diagnostic evidence (10,26).

Empirical antibiotic therapy is commonly administered to manage secondary infections (12,13,18,20,21,26). Corticosteroids are also considered to be effective treatment options (10,12,13,20,21,23,25). However, due to the limited number of reported cases, no systematic clinical trials have been conducted to evaluate the efficacy of corticosteroids, and an optimal treatment protocol has not been established, even for severe cases that meet the definition of ARDS. In this case, a clinical improvement was observed following the administration of antibiotics and corticosteroids. However, the extent to which these treatments contributed to the patient's recovery remains unclear. Additionally, BAL has been reported to have potential efficacy in removing lipid substances, lipid-laden macrophages, and inflammatory mediators from the lungs (26,27). However, there is still insufficient evidence to support this treatment.

Kerosene consists of hydrocarbons containing approximately 6-16 carbon atoms and it has a flash point of 38°C or higher (6). Kerosene is relatively safe to store and handle because its flash point exceeds normal room temperature, thus making it a common household fuel. However, its low viscosity and surface tension allow it to easily enter the lungs, causing inflammation, surfactant loss, and pulmonary toxicity, including lipoid pneumonia (6). In typical tent saunas, an ignition agent is used to light the wood-burning stove, thereby increasing the internal temperature. However, in this case, the patient did not have any ignition agent on that day and instead used kerosene for the first time. The ignition agent (Bunka Takitsuke^Ⓡ, Marumi Fujiya Shoten, Sapporo, Japan), which had normally been used by this patient, also contained kerosene. However, the amount of kerosene in the ignition agent used for one sauna session was estimated to be approximately 60-70 mL, whereas he had used kerosene of 250 mL on the day of the accident.

Vapor pressure, defined as the pressure exerted by a vapor in equilibrium with its liquid phase, depends on the temperature and generally increases as the temperature increases (28). Kerosene is a mixture of various substances (6) and its vapor pressure varies depending on its composition, making it difficult to define a specific vapor pressure. However, the vapor pressure increases with increasing temperature. Therefore, it is presumed that the increase in temperature inside the tent accelerated the vaporization of the portion of kerosene applied to the firewood that was not involved in combustion, thus leading to the accumulation of vaporized kerosene within the tent and ultimately resulting in the observed lung injury.

In general, fire hazards and the generation of harmful gases such as carbon monoxide are major concerns in tent saunas, and the use of kerosene is no exception. Tents specifically designed for saunas are equipped with ventilation openings and a chimney connected to the stove. When wood burns inside a stove, an updraft is generated, which vents smoke and harmful gases outside the tent, thereby ensuring safe usage. In this case, a specialized tent with an appropriate ventilation and chimney system was used to prevent carbon monoxide poisoning. However, kerosene has a high vapor density of 4.5 (29), which likely causes the vapor to accumulate in the lower parts of the tent, leading to inadequate ventilation. This suggests that the standard ventilation and exhaust systems designed to prevent carbon monoxide poisoning may be insufficient to prevent the inhalation of kerosene vapor.

In conclusion, this case highlights the potential for developing acute lung injury associated with kerosene vapor inhalation, particularly in enclosed and high-temperature environments, such as tent saunas. This underscores the importance of understanding the physicochemical properties of kerosene to mitigate the risk of pulmonary toxicity and to promote the safe and healthy use of saunas. The use of a large amount of kerosene to ignite a stove in a closed environment should therefore not be widely used by tent sauna users.

The Institutional Ethics Committee of the Oita University Faculty of Medicine waived the requirement for approval as this was a case report without identifiable personal information.

The authors state that they have no Conflict of Interest (COI).