Authors: Nobuhiko Tsukada, Yusuke Nakamura, Shohei Hara, Arata Honda, Azusa Tsukada, Majima Takaaki, Midori Tsuchiya, Koji Wake, Yasuo Shimizu, Seiji Niho
Categories: Case Report, Acetylene gas, Acute eosinophilic pneumonia, Corticosteroid, Occupational disease, Welding
Source: Respiratory Medicine Case Reports
A 58-year-old man who had inhaled acetylene while welding 2 and 4 days previously and subsequently developed cough, dyspnea, and fever was referred by his general practitioner. A computed tomography scan showed diffuse ground-glass opacities in both lungs, and bronchoalveolar lavage fluid showed an increased proportion of eosinophils (25 %). Acute eosinophilic pneumonia (AEP) was diagnosed. Inhalation of acetylene was considered to be the most likely cause of AEP. Respiratory symptoms improved rapidly with intravenous corticosteroids. This is a rare case of AEP caused by inhalation of acetylene.
Keywords: Welding, Acetylene gas, Acute eosinophilic pneumonia, Corticosteroid, Occupational disease
Acetylene, a commonly used industrial gas, is flammable and is mixed with oxygen for use in welding. Symptoms of acetylene inhalation include dizziness, headache, and nausea, and exposure to high concentrations of acetylene gas can be fatal [1]. Acute lung injury caused by inhalation of acetylene is rare, with only a few cases reported [2,3]. To our knowledge, only one case of acute eosinophilic pneumonia (AEP) caused by acetylene gas has been reported [3]. In this report, we present a rare case of AEP caused by inhalation of acetylene.
We experienced a 58-year-old man who had smoked 38 pack-years since the age of 20 and had a history of allergic rhinitis, as well as of testicular cancer surgery at age 20 years. No family or psychosocial history. Three weeks before visiting our hospital, he started taking the herbal medicine hachimijiogan for frequent urination. He worked in fusion cutting for car engine parts and wore a disposable face mask at work; the ventilation in the workplace was poor. One day, the acetylene gas hose became disconnected during fusion, and the patient inhaled leaking gas. This exposure was noticed because the gas had ignited from a leaking section of another pipe. About two hours after inhalation, he began to cough and have difficulty breathing, but he did not seek medical attention. Two days later, he inhaled leaking acetylene gas again, and his dyspnea worsened. He recognized acetylene inhalation because it was accompanied by a strange odor. The second exposure was due to inadequate ventilation resulting in the inhalation of acetylene used by colleague. The next day, he developed a fever of 39 °C and went to see his local doctor. His chest x-ray showed bilateral lung consolidation, and he was referred to our hospital.
On examination, he was conscious. His temperature was 37.7 °C; respiratory rate, 32/min; oxygen saturation, 97 % (with oxygen supply from a nasal cannula at a rate of 3 L/min); blood pressure, 124/70 mmHg; and pulse, 82/min. There were no significant lung sound abnormalities. Results of blood tests were as white blood cell count, 8100/μL (neutrophils, 76 %; eosinophils, 9 %); lactate dehydrogenase, 569 U/L; C-reactive protein, 17.2 mg/dL; surfactant protein A, 231 ng/mL; surfactant protein D, 373 ng/mL; immunoglobulin E, 123.1 IU/mL; B-type natriuretic peptide, 86.6 pg/mL; arterial blood gas pH, 7.42; partial pressure of carbon dioxide, 37.7 mmHg; partial pressure of oxygen, 90.4 mmHg (with oxygen supply from a nasal cannula at a rate of 2 L/min); and bicarbonate, 24.1 mEq/L. A chest computed tomography (CT) scan showed central and peri-bronchial alveolar opacities with air bronchograms and consolidation pattern (Fig. 1A and B). Electrocardiogram and transthoracic echocardiography results were both considered normal. Bronchoalveolar lavage fluid (BALF) showed a total cell count of 3.00 × 10^3^/μL, 25 % eosinophils, and 18 % neutrophils, and the patient was diagnosed with acute eosinophilic pneumonia (AEP). During bronchoscopy procedure, his respiratory status worsened, and he was intubated.
Fig. 1 Computed tomography imagesCentral and peri-bronchial alveolar opacities with air bronchograms and consolidation pattern were seen on admission (A, B). Improvement with treatment and residual ground glass opacities after 6 days of corticosteroid therapy (C, D).
Treatment was started with methylprednisolone 1000 mg/day for 3 days, ceftriaxone 2 g/day, and azithromycin 500 mg/day, after which respiratory failure rapidly improved, and the patient could be extubated on day 3. Eosinophils were almost absent after steroid pulse therapy. Prednisolone 1 mg/kg was administered from day 4 to day 7, and a chest x-ray was performed on day 1–5 (Fig. 2). On day 6, a CT scan showed almost complete improvement with only linear shadow (Fig. 1C and D). The patient was discharged on day 10. Since then, he has continued to improve.
Fig. 2 Chest x-rays on days 1–5 and summary of clinical courseChest x-rays on days 1–5 showed improvements shown by the x-rays. Respiratory status improved after corticosteroid treatment, and the patient was extubated on day 3. C-reactive protein levels decreased from day 2 onwards, and the fever resolved on day 2. Oxygen was withdrawn on day 6, and the patient was discharged on day 10. AZM, azithromycin; BT, body temperature; CRP, C-reactive protein; CTRX, ceftriaxone; mPSL, methylprednisolone; PSL, prednisolone; DIV, drip infusion in vein; PO, per os.
AEP causes acute respiratory failure and is characterized by pulmonary eosinophilia. It is thought to be a reaction to smoking, particulate matter, and inhaled antigens. The present patient was diagnosed with AEP because he presented with acute fever, bilateral pulmonary consolidations, type 1 respiratory failure, high proportion of eosinophils in BALF (25 %), and inhaled inducer exposure [4]. A possible mechanism of gas inhalation-induced AEP is the release of interleukin (IL)-33 from the injured airway epithelium, which may induce eosinophil infiltration via the immune pathway [5]. The present patient had a history of allergic rhinitis; therefore, it is highly likely that type 2 inflammation was present in the background, which may have been one of the reasons why this type of inflammation was easily activated. In addition to elevated eosinophils in the BALF, we also observed elevated neutrophils; the inflammatory pathway associated with IL-8 stimulation is thought to be involved also in inhalant gas injury, so a similar mechanism may have occurred in the present case [5].
Because acetylene gas is highly flammable, reports of industrial accidents often involve fires and explosions caused by ignition [6]. There have been reports of toxicity associated with the abuse of acetylene gas [1] and interstitial pneumonia due to acetylene gas [2]. Animal studies of acetylene inhalation showed that it causes alveolar fibrosis and necrosis by a non-immune mechanism involving oxidative and nitrosative stress, which is thought to be the pathogenesis of interstitial pneumonia [7]. AEP induced by acetylene gas are been rarely reported to date [3]. Similar to this case, accidental inhalation due to acetylene leakage has been the cause in previous cases [3], and leakage risk management is important when using acetylene gas.
In the present case, lung injury due to metal fume inhalation was also considered as a possible cause of AEP. The composition of the fused car engine parts is not known; however, copper-lead alloys and aluminum alloys are often used in the production of such parts. These alloys can produce fumes, so we cannot rule out the possibility that our patient inhaled such fumes. However, because he did not experience any symptoms during normal operations without acetylene gas leakage. Drug-induced pneumonia due to hachimijiogan can also be considered as another possible cause, but in the present case the course of disease onset was clear, and AEP due to gas injury was more likely than drug-induced lung injury. In addition, hachimijiogan-induced pneumonia is reported to be rare [8]. Parasitic infection can also cause AEP, but the patient had no history of such an infection [5]. Therefore, we concluded that the acetylene gas was the major inducer of AEP. He had never been inhaled acetylene before because of adequately ventilated. It seems that the ventilation was neglected due to the cold weather. This time the Labor Standards Inspection Office gave advice, because there were problems with the management system at the workplace.
We report a case of AEP induced by inhalation of acetylene. Acetylene gas should be considered as a potential cause of AEP.
Nobuhiko Tsukada: Investigation, Conceptualization. Yusuke Nakamura: Project administration, Investigation, Conceptualization. Shohei Hara: Investigation. Arata Honda: Investigation. Azusa Tsukada: Investigation. Majima Takaaki: Investigation. Midori Tsuchiya: Investigation. Koji Wake: Investigation. Yasuo Shimizu: Supervision, Project administration, Investigation. Seiji Niho: Supervision, Project administration, Investigation.
Written informed consent was obtained from the patient for publication of this case report, including any accompanying images.
The authors declare no competing financial interests.
IRB review is not required.
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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