How Long to Feel Normal Again After Breathing in Natural Gas for Months
Tuberc Respir Dis (Seoul). 2013 Mar; 74(3): 120–123.
Acute Respiratory Distress Due to Methyl hydride Inhalation
Jun Yeon Jo, Grand.D.,1 Yong Sik Kwon, M.D.,1 Jin Wook Lee, Thousand.D.,1 Jae Seok Park, K.D.,1 Byung Hak Rho, M.D.,2 and Won-Il Choi, M.D., Ph.D. 
1
Jun Yeon Jo
oneSection of Internal Medicine, Keimyung Academy Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Korea.
Yong Sik Kwon
oneDepartment of Internal Medicine, Keimyung University Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Korea.
Jin Wook Lee
aneSection of Internal Medicine, Keimyung University Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Korea.
Jae Seok Park
aneSection of Internal Medicine, Keimyung University Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Korea.
Byung Hak Rho
2Section of Radiology, Keimyung Academy Schoolhouse of Medicine, Daegu, Korea.
Won-Il Choi
1Department of Internal Medicine, Keimyung Academy Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Korea.
Received 2012 May 27; Revised 2012 Jun 19; Accepted 2012 Aug xv.
Abstract
Inhalation of toxic gases can lead to pneumonitis. It has been known that methane gas intoxication causes loss of consciousness or asphyxia. There is, however, a paucity of information about acute pulmonary toxicity from marsh gas gas inhalation. A 21-yr-old man was presented with respiratory distress later an adventitious exposure to methane gas for one minute. He came in with a drowsy mentality and hypoxemia. Mechanical ventilation was applied immediately. The patient's symptoms and chest radiographic findings were consistent with acute pneumonitis. He recovered spontaneously and was discharged later 5 days without other specific treatment. His pulmonary function examination, 4 days afterward methane gas exposure, revealed a restrictive ventilatory defect. In decision, acute pulmonary injury can occur with a restrictive ventilator defect afterwards a short exposure to methane gas. The lung injury was spontaneously resolved without any significant sequela.
Keywords: Methane, Fume Inhalation Injury, Respiratory Insufficiency
Introduction
Methane is a component of natural gas, mainly used as a fuel source and chemical feedstock in industries. It is unremarkably harmless, however, at high concentrations, it may reduce the oxygen percentage in air, causing suffocation. It is likewise extremely combustible and can cause an explosion when its concentration reaches v% to 15% in air. Previous reports focused mainly on accidents involving workers in coal mines that related to asphyxia or methane gas explosions1-3. In this report, we described the first example of acute pulmonary toxicity from accidental inhalation of methane in a medical gas supply room.
Instance Report
A 21-year-quondam man, non-smoker, was admitted to the emergency department (ED) in a drowsy mentality subsequently exposure to methane gas. He had started working at a medical gas supply company 3 months agone. He had worked without any respiratory protective devices. While opening a methane gas tank, assuming information technology was a nitrogen tank, he was accidently exposed in a gas supply room, approximately 10×10 g. At that place was no window and the doors were kept closed in the room. When the methane tank was opened, gas escaped from the tank for about i minute. Immediately afterward exposure, he sought refuge in a room inside of the gas supply space and shortly lost consciousness. Approximately, 4.5 hours subsequently exposure he was admitted to the ED.
When he arrived at the ED, his vital signs were as follows: claret pressure, 160/100 mm Hg; heart rate, 130 beats/min; respiratory rate, 28 breaths/min; temperature, 36.2℃; and O2 saturation measured by pulse oxymeter (SpO2), 75% of room air. His oropharynx was institute to exist normal. There was a bilateral decrease in breathing sounds without wheezing, stridor or crackles on pulmonary auscultation. He was immediately intubated because he was cyanotic and in respiratory distress. Initial claret gas during intubation with 10 L/min oxygen supply showed pH 7.268, PCO2 34.v mm Hg, PO2 77.two mm Hg, HCO3 - 15.iii mmol/L, and SaO2 93.three%. Electrocardiography showed sinus tachycardia. Serum claret urea nitrogen, creatinine, and lactate were xi mg/dL, 0.8 mg/dL, and fourteen.0 mmol/50, respectively. Initial chest radiograph showed bilateral ill-defined air-space consolidations on both perihilar areas, which mimics pulmonary edema but heart and great vessels appeared unremarkable (Effigy 1A). A computed tomography (CT) browse of the chest showed bilateral symmetric air-space consolidation and footing glass opacity at the dependent portion of the lungs (Figure 1B). After mechanical ventilation (MV) with fraction of inspired oxygen (FiO2) of 0.6, his SpO2 increased to 98%. Four hours afterward MV he gained an alarm mentality. Subsequent blood gas analysis showed a pH 7.36, PCO2 34.5 mm Hg, PO2 77 mm Hg, HCO3 - 15.three mmol/Fifty, and SaOii 95.0% under MV (synchronized intermittent mandatory ventilation; SIMV; FiOii of 0.4). He received albuterol nebulizer treatment. Peripheral blood tests showed the post-obit: white claret cells, 14,550/mm3 (neutrophils, 36%; lymphocytes, 58%; and eosinophils, two%); hemoglobin, 15.9 g/dL; and platelets, 296,000/mm3. Four hours after arriving at the ED, he was weaned from MV to four L/min nasal cannula with SpOtwo 96%. The next solar day, a breast radiograph showed resolution of bilateral airspace consolidations (Effigy 1C). He was admitted to the intensive care unit for 24 hours and subsequently transferred to the general ward when oxygen was no longer required. A pulmonary part test was performed 4 days after exposure. The results were as follows: forced vital capacity (FVC), 3.3 50 (68% predicted); forced expiratory volume in one second (FEV1), 3.0 L (74% predicted); FEVi to FVC ratio, 90%; and total lung capacity, 4.2 Fifty (70% predicted). A single-breath carbon monoxide diffusing capacity (DLco) was 24.five mL/min/mm Hg (83% predicted). His symptoms resolved and he was discharged after 5 days without medication. Ten days later on discharge, the follow-up breast CT browse showed a consummate resolution of previous bilateral air-space consolidations (Figure 1D). The follow-upwards pulmonary function test showed recovery from the restrictive ventilatory defect.
Representative chest radiographs. (A) Chest radiograph: 4.5 hours following exposure. Initial chest radiograph shows bilateral ill-defined air-space consolidations at both perihilar areas. (B) Chest computed tomography (CT) scan at emergency section shows bilateral symmetric air-space consolidations and basis drinking glass opacities at dependent portion of both lungs. (C) Chest radiograph: 24 hours post-obit exposure. There is a rapid resolution of bilateral air-space consolidations on follow-up chest radiograph. (D) Follow-up breast CT scan shows no bilateral symmetric air-space consolidations and ground glass opacities without sequela.
Discussion
There are several reports focused on occupational methane gas exposure by asphyxia or burns1-iii. The first incidents happened accidently to coal mine workers and later to farmers after manure gas intoxication4,five. To the best of our noesis, this is the starting time reported case of acute pulmonary toxicity related to methyl hydride gas inhalation. In this case study, we highlight that even a brusk exposure time to a high concentration of methane gas can exist sufficient to crusade a serious problem.
Usually methane is not harmful; however, information technology can cause asphyxiation past reducing the percent of O2 in a sealed room. This may explicate the reason why the patient lost consciousness. The case exposed methane gas accidentally in a medical gas supply room. Fifty-fifty a 1-minute exposure to a high concentration of methane gas in a sealed room was enough to cause loss of consciousness. In that location was a case report that describes induced hypothermia used equally a treatment for comatose land in a patient with asphyxia caused gas intoxication including methane6. However, there was no established treatment for methane intoxication.
Acute restrictive ventilator defect with reduced DLco was found in a patient with heavy occupational exposure to fluorocarbon7. In the present example, we constitute a restrictive defect without changes in DLco on the fourth day afterward exposure. During recovery phase of lung injury, there is an increase in collagenous/elastic fibers causing restrictive ventilator pattern in the proper name of organizing pneumonia8. The restrictive pattern in pulmonary function test in the nowadays case supported the patient might have organizing pneumonia during recovery stage. Our patient is a young non-smoker without a history of lung disease. The real pathogenesis is not articulate; however, we suggest that marsh gas intoxication may develop reversible toxic alveolitis based on radiologic findings. However, direct pulmonary toxicity from inhalant abuse is rarely reported9.
This case demonstrates that acute lung injury can occur following short exposure to high concentrations of marsh gas gas in closed places. Acute pulmonary injury tin can occur with a restrictive ventilator defect. The lung injury tin can be spontaneously resolved without any meaning sequela.
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Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617131/
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