Toxic Gases from Fermentation

Transcription

1 Toxic Gases from Fermentation รศ.พญ.ส ดา วรรณประสาท ภาคว ชาเภส ชว ทยา หน วยเภส ชว ทยาและพ ษว ทยาคล น ก ภาคว ชาอาย รศาสตร คณะแพทยศาสตร มหาว ทยาล ยขอนแก น

2 Confined space Simple ช องว างหร อบร เวณป ด ท เก ดการสะสมของก าซพ asphyxiants ษ ไอน า ฝ น หร อภาวะออกซ เจนต า โดยอาจเก ดจากการก อสร าง Hypoxia ท ต งหร อสภาพแวดล อมภายในเอง Chemical s Asphyxiant

3 Simple Asphyxiants Displace oxygen from ambient air Reduce fraction of oxygen in air or FIO 2 (<21%) Have no pharmacological activity High concentration of asphyxiants in ambient air Working in confine spaces

4 Clinical Findings Associated with Reduction of Inspired Oxygen FiO 2 (%) Symptoms/signs Tachypnea, hyperpnea, (resultant hypocapnia), tachycardia, reduced attention and alertness, euphoria, headache, mild incoordination Altered judgment, incoordination, muscular fatigue, cyanosis 10-6 Nausea, vomiting, lethargy, air hunger, severe incoordination, coma <6 Gasping respiration, seizure, coma, death

5 Specific agent Noble Gases: helium, neon, argon, xenon Short-chain aliphatic hydrocarbon gases: methane, ethane, propane, butane Carbon dioxide (CO 2 ) Nitrogen (N 2 )gas

6 Treatment Immediate removal from exposure and ventilatory assistance Oxygen supplement

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8 Chemical asphyxants Cyanide Carbon monoxide Hydrogen sulfide Nitrogen oxide

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10 Hydrogen sulfide Decaying organic matter Fish Sulfur containing proteins Sewage Manure Hot, humid weather microbial metabolism and gas production

11 Leather tanning Rubber vulcanization Synthetic fabric & paper production

12 Mechanism of action potent inhibition of cytochrome oxidase binds to ferric (Fe 3+ ) moiety of cytochrome a 3 oxidase complex higher affinity than cyanide inhibition of oxidative phosphorylation produces cellular hypoxia and anaerobic metabolism

13 Mechanism of action Hydrogen sulfide, cyanide, Hydrogen carbon sulfide monoxide

14 Colorless gas More dense than air Irritating gas rotten eggs (low) Olfactory nerve fatigue and paralysis (high)

15 Effects of hydrogen sulfide gas on humans Effect Concentration (ppm) Detectable odor 0.2 Eye and respiratory irritation 50 Olfactory nerve paralysis 150 Exposure may cause pulmonary edema 250 Systemic symptom occur in ½ hr 500 Quickly unconscious; death without rescue 750 Rapid collapse; respiratory paralysis 1,000 Immediate date 5,000 Fuller DC.JOEM 2000;939

16 When to suspect hydrogen sulfide poisoning Person rapidly loses consciousness knocked down Rotten eggs odor Rescue from enclosed space, such as sewer or manure pit Multiple victims with sudden death syndrome Collapse of a previously healthy worker at work site

17 Management 1. Supportive care Prehospital - Attempt rescue only if using SCBA - Move victim to fresh air - Administer 100% oxygen - During extrication, consider traumatic injuries from falls - Apply ACLS protocols as indicated

18 Emergency department - Maximize ventilation and oxygenation - Consider PEEP for ALI - Treat acidosis based on arterial ph and serum bicarbonate analysis - Administer crystalloid and vasopressors for hypotension

19 Sodium nitrite OxyHb cytc 2+ cytc 3+ OxyHb Sodium nitrite MetHb CN cyta 3+ cyta2+ H 2 S MetHb CyanoMetHb cyta 3 2+ cyta 3 3+ SulMetHb Sodium thiosulfate Rhonanese 1/2O 2 +2H + H 2 O Thiocyanate OxyHb +SO X

20 2. Antidote - Sodium nitrite (3%NaNO 2 ) IV over 2-4 min 10 ml (300 mg) Caution: Hypotension Methmoglobinemia - Hyperbaric oxygen

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22 Nitrogen dioxide Nitrogen oxides Oxidized nitrogenous compounds Irritant gas Low water solubility Heavier than air collect just above silage

23 Nitrogen Oxides NO NO 2 N 2 O N 2 O 2 N 2 O 3 N 2 O 4 N 2 O 5 Nitric oxide Nitrogen dioxide Nitrous oxide Nitrogen Peroxide Dinitrogen trioxide Dinitrogen tetroxide Dinitrogen Pentoxide

24 Crops Silo Fermentation CO 2, nitrogen oxide NO, NO 2, N 2 O 4 Silo Filler s disease

25 NO 2 Low water solubility No symptom in upper airway Irritant effect in bronchi, terminal bronchioles and alveoli

26 Pathophysiology NO 2 NO, HNO 3, HNO 2 Distal airway Free radical Direct toxic effect Protein oxidation Lipid peroxidation Cell membrane damage Type1 pneumocytes ciliated airway cells Delay onset of chemical pneumonitis

27 Clinical manifestration Depend on intensity and duration of exposure Lost of consciousness, Sudden death Hypoxia Delay respiratory symptoms

28 Acute Phase No upper respiratory irritation (low level) Upper respiratory symptom (high level) Methemoglobinemia CXR normal do not rule out ALI

29 Delayed Phase Symptom free interval 3-24 hr follows acute phase Then develop chemical pneumonitis or ALI Dyspnea, tachycardia, hemoptysis, bronchospasm, rales and hypoxia CXR: perihilar infilatration progress to ALI

30 Subacute Phase Develop brochiolitis obliterans 2-4 wk after delay phase Acutely ill with fever and chills, cough, dyspnea, rales, wheezing, hypoxia CXR: ALI, multiple discrete nodule (miliary pattern) Pulmonary function test: obstructive and restrictive defects

31 Gurney JW. RidoGraphics 1991;625

32 Prehospital care Management - removal from source of exposure - supplement oxygen Emergency department care - supportive therapy to correct hypoxia, ventilatory failure, secondary infection - High dose steroid suggested in treatment of pulmonary manifestation - Methylene bule

33 Clinical feature and Management of H 2 S&NO 2 Property Mechanism Rotten egg irritant H 2 S (manure pit) Inhibit cytochrome oxidase NO 2 (silo) Low water soluble Direct toxic alveolar cell, free radical Signs & symptoms Mucous membrane irritation Respiratory irritation Cellular hypoxia Management Extrication/resuscitation/ supportive Sodium nitrite Laryngospasm, brochospasm, ARDS Respiratory arrest Bronchodilator, steroids

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