How Long to Feel Normal Again After Breathing in Natural Gas for Months
Tuberc Respir Dis (Seoul). 2013 Mar; 74(3): 120–123.
Astute Respiratory Distress Due to Methane Inhalation
Jun Yeon Jo, Grand.D.,one Yong Sik Kwon, Thou.D.,1 Jin Wook Lee, M.D.,ane Jae Seok Park, M.D.,i Byung Hak Rho, One thousand.D.,2 and Won-Il Choi, M.D., Ph.D. 
1
Jun Yeon Jo
1Department of Internal Medicine, Keimyung University Dongsan Medical Middle, Keimyung Academy School of Medicine, Daegu, Korea.
Yong Sik Kwon
1Department of Internal Medicine, Keimyung University Dongsan Medical Center, Keimyung Academy School of Medicine, Daegu, Korea.
Jin Wook Lee
1Department of Internal Medicine, Keimyung University Dongsan Medical Middle, Keimyung University School of Medicine, Daegu, Korea.
Jae Seok Park
oneDepartment of Internal Medicine, Keimyung University Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Korea.
Byung Hak Rho
iiDepartment of Radiology, Keimyung Academy School of Medicine, Daegu, Korea.
Won-Il Choi
iDepartment of Internal Medicine, Keimyung University Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Korea.
Received 2012 May 27; Revised 2012 Jun 19; Accepted 2012 Aug 15.
Abstract
Inhalation of toxic gases can pb to pneumonitis. It has been known that methyl hydride gas intoxication causes loss of consciousness or asphyxia. There is, still, a paucity of information nigh acute pulmonary toxicity from marsh gas gas inhalation. A 21-yr-old human being was presented with respiratory distress after an adventitious exposure to marsh gas gas for ane infinitesimal. He came in with a drowsy mentality and hypoxemia. Mechanical ventilation was practical immediately. The patient'south symptoms and chest radiographic findings were consistent with acute pneumonitis. He recovered spontaneously and was discharged afterward v days without other specific handling. His pulmonary part test, four days after methane gas exposure, revealed a restrictive ventilatory defect. In conclusion, astute pulmonary injury tin can occur with a restrictive ventilator defect later a short exposure to methane gas. The lung injury was spontaneously resolved without whatsoever pregnant sequela.
Keywords: Methane, Smoke 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 usually harmless, however, at high concentrations, it may reduce the oxygen percentage in air, causing suffocation. It is also extremely flammable and can cause an explosion when its concentration reaches 5% 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 written report, we described the first case of acute pulmonary toxicity from accidental inhalation of methane in a medical gas supply room.
Case Study
A 21-yr-former man, non-smoker, was admitted to the emergency department (ED) in a drowsy mentality subsequently exposure to marsh gas gas. He had started working at a medical gas supply visitor 3 months agone. He had worked without any respiratory protective devices. While opening a marsh gas gas tank, assuming it was a nitrogen tank, he was accidently exposed in a gas supply room, approximately 10×10 yard. There was no window and the doors were kept airtight in the room. When the methane tank was opened, gas escaped from the tank for well-nigh one minute. Immediately after exposure, he sought refuge in a room inside of the gas supply space and soon lost consciousness. Approximately, four.five hours after exposure he was admitted to the ED.
When he arrived at the ED, his vital signs were every bit follows: claret pressure level, 160/100 mm Hg; heart charge per unit, 130 beats/min; respiratory rate, 28 breaths/min; temperature, 36.2℃; and Oii saturation measured by pulse oxymeter (SpOii), 75% of room air. His oropharynx was found to be normal. There was a bilateral subtract in breathing sounds without wheezing, stridor or crackles on pulmonary auscultation. He was immediately intubated because he was cyanotic and in respiratory distress. Initial blood gas during intubation with 10 L/min oxygen supply showed pH 7.268, PCO2 34.5 mm Hg, PO2 77.2 mm Hg, HCOiii - xv.3 mmol/50, and SaOii 93.3%. Electrocardiography showed sinus tachycardia. Serum blood urea nitrogen, creatinine, and lactate were xi mg/dL, 0.8 mg/dL, and 14.0 mmol/L, respectively. Initial chest radiograph showed bilateral ill-defined air-infinite consolidations on both perihilar areas, which mimics pulmonary edema but heart and great vessels appeared unremarkable (Figure 1A). A computed tomography (CT) scan of the breast showed bilateral symmetric air-space consolidation and ground glass opacity at the dependent portion of the lungs (Figure 1B). After mechanical ventilation (MV) with fraction of inspired oxygen (FiO2) of 0.half-dozen, his SpO2 increased to 98%. Four hours after MV he gained an alert mentality. Subsequent blood gas analysis showed a pH vii.36, PCOtwo 34.v mm Hg, PO2 77 mm Hg, HCOthree - 15.3 mmol/L, and SaOtwo 95.0% nether MV (synchronized intermittent mandatory ventilation; SIMV; FiO2 of 0.4). He received albuterol nebulizer handling. Peripheral blood tests showed the following: white blood cells, xiv,550/mm3 (neutrophils, 36%; lymphocytes, 58%; and eosinophils, ii%); hemoglobin, 15.9 g/dL; and platelets, 296,000/mmiii. Four hours later on arriving at the ED, he was weaned from MV to iv Fifty/min nasal cannula with SpOii 96%. The adjacent day, a chest radiograph showed resolution of bilateral airspace consolidations (Effigy 1C). He was admitted to the intensive care unit of measurement for 24 hours and subsequently transferred to the general ward when oxygen was no longer required. A pulmonary role test was performed 4 days after exposure. The results were as follows: forced vital capacity (FVC), 3.3 L (68% predicted); forced expiratory volume in one second (FEV1), 3.0 L (74% predicted); FEV1 to FVC ratio, xc%; and total lung capacity, four.2 L (70% predicted). A single-jiff carbon monoxide diffusing chapters (DLco) was 24.5 mL/min/mm Hg (83% predicted). His symptoms resolved and he was discharged later on 5 days without medication. Ten days subsequently discharge, the follow-upwardly chest CT scan showed a complete resolution of previous bilateral air-space consolidations (Figure 1D). The follow-up pulmonary function test showed recovery from the restrictive ventilatory defect.
Representative breast radiographs. (A) Chest radiograph: 4.5 hours post-obit exposure. Initial chest radiograph shows bilateral ill-defined air-infinite consolidations at both perihilar areas. (B) Chest computed tomography (CT) browse at emergency department shows bilateral symmetric air-infinite consolidations and ground glass opacities at dependent portion of both lungs. (C) Breast radiograph: 24 hours following exposure. At that place 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-infinite consolidations and ground drinking glass opacities without sequela.
Discussion
There are several reports focused on occupational methane gas exposure past asphyxia or burns1-iii. The start incidents happened accidently to coal mine workers and later on to farmers afterwards manure gas intoxication4,5. To the all-time of our noesis, this is the beginning reported instance of astute pulmonary toxicity related to methane gas inhalation. In this instance report, nosotros highlight that even a curt exposure fourth dimension to a high concentration of methane gas can exist sufficient to crusade a serious problem.
Unremarkably methyl hydride is not harmful; still, it can cause asphyxiation by reducing the per centum 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. Even a 1-infinitesimal exposure to a loftier concentration of methane gas in a sealed room was enough to cause loss of consciousness. At that place was a instance report that describes induced hypothermia used every bit a handling for comatose country in a patient with asphyxia caused gas intoxication including methane6. Still, at that place was no established handling for methyl hydride intoxication.
Acute restrictive ventilator defect with reduced DLco was found in a patient with heavy occupational exposure to fluorocarbon7. In the present case, we plant a restrictive defect without changes in DLco on the fourth twenty-four hour period after exposure. During recovery stage of lung injury, there is an increase in collagenous/elastic fibers causing restrictive ventilator blueprint in the name of organizing pneumonia8. The restrictive design in pulmonary function exam in the present case supported the patient might take organizing pneumonia during recovery phase. Our patient is a immature non-smoker without a history of lung disease. The real pathogenesis is non clear; withal, we suggest that methyl hydride 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 methane gas in closed places. Astute pulmonary injury can occur with a restrictive ventilator defect. The lung injury can exist spontaneously resolved without any meaning sequela.
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Articles from Tuberculosis and Respiratory Diseases are provided here courtesy of The Korean Academy of Tuberculosis and Respiratory Diseases
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617131/
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