A Case of Pulmonary Edema due to Hydrogen Sulfide Poisoning

Dear Editor, A 23-year-old male patient experienced a sudden loss of balance, resulting in a backward fall while undertaking the task of drying a sludge tank. A staff member who was observing the incident performed chest compression. Following approximately ten times of chest compressions, the patient initiated movement. Subsequently, the same staff also fainted, prompting another employee to call an ambulance, which resulted in the rescue of both individuals. Approximately 30 min after the initial emergency medical technicians’ contact, a decline in percutaneous oxygen saturation levels (SpO2) was observed. The administration of oxygen was initiated. On-site inspection detected hydrogen sulfide (H2S). The patient’s vital signs on arrival were as follows: Glasgow Coma Scale E3V5M6, blood pressure 119/90 mmHg, pulse rate 90 beats per minute, respiratory rate 16 breaths per minute, and body temperature 36.4°C. A physical examination yielded no significant findings. A 12-lead electrocardiogram showed no changes in the ST segment. The arterial blood gas analysis under oxygen 15 L/min yielded the following results: pH 7.362, paCO2 41.5 mmHg, paO2 76.2 mmHg, HCO3– 23.0 mol/L, and base excess – 1.9 mmol/L. The diagnosis of pulmonary edema was made on computed tomography (CT) [Figure 1]. The patient was treated by hyperbaric oxygen (HBO) and methylprednisolone 1 mg/kg. On the 2nd day, the patient exhibited a paO2 level of 319 mmHg, with 10 L of oxygen per minute. Concurrently, the administration of oxygen and methylprednisolone was discontinued. He was discharged on the 5th day of his illness.Figure 1: Chest computed tomographic image (CT) on arrival. The diagnosis of pulmonary edema was made on the basis of diffuse frosted shadows in the bilateral lungs on the CTTo our knowledge, this is the first documented case of H2S-induced pulmonary edema with marked improvement without sequelae following combined HBO and steroid therapy. Exposure to H2S above a threshold value of 200–300 ppm is associated with the sudden onset of hemorrhagic pulmonary edema.[1] With regard to investigations on toxic mechanisms, a key tight junction protein in the vascular endothelium was found to be decreased.[2] Respiratory tract irritation constitutes an additional mechanism. It has been demonstrated that HBO therapy appears to result in the elimination of H2S from the mitochondrial cytochrome oxidase.[3] In addition, HBO has been observed to counteract the reduction in oxygen transport capacity caused by methemoglobinemia. Furthermore, the therapy has been shown to reduce cell edema.[4] Recently, for a case of H2S intoxication, nitrite was administered intravenously initially. However, the anticipated alleviation of symptoms did not materialize. Nevertheless, following HBO therapy, a marked alleviation of symptoms was immediately observed, similar to our case.[1] Conversely, the efficacy of corticosteroids in the treatment of pulmonary edema following human exposure to lung-damaging agents remains uncertain. However, experimental studies on animals have demonstrated the efficacy of steroids in addressing acute lung injury induced by H2S.[5] In this particular instance, it remains ambiguous whether the efficacy was attributable to HBO or to the administration of steroids alone, or whether the observed outcomes resulted from a synergistic effect. Consequently, further investigation is imperative as additional cases accrue in the future. Research quality and ethics statement The authors followed applicable EQUATOR Network (https://www.equator-network.org/) guidelines, notably the CARE guideline, during the conduct of this report. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understand that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed. Financial support and sponsorship This work was supported in part by a Grant-in-Aid for Special Research in Subsidies for ordinary expenses of private schools from The Promotion and Mutual Aid Corporation for Private Schools of Japan. Conflicts of interest There are no conflicts of interest.