toxic gases from fermentation - thaitox.orgthaitox.org/media/upload/file/nct2nd/toxic gas from...
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Toxic Gases from Fermentation
รศ.พญ.สุดา วรรณประสาทภาควิชาเภสัชวิทยา
หนวยเภสัชวิทยาและพิษวิทยาคลินิก ภาควิชาอายุรศาสตรคณะแพทยศาสตร มหาวิทยาลัยขอนแกน
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Confined space
HypoxiaSimple asphyxiants
Chemical
Asphyxiants
ชองวางหรือบริเวณปด ที่เกิดการสะสมของกาซพิษ ไอน้าํฝุน หรือภาวะออกซิเจนต่ํา โดยอาจเกิดจากการกอสราง ที่ตั้งหรือสภาพแวดลอมภายในเอง
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• Displace oxygen from ambient air
• Reduce fraction of oxygen in air or FIO2
(<21%)
• Have no pharmacological activity
• High concentration of asphyxiants in ambient air
• Working in confine spaces
Simple Asphyxiants
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FiO2 (%) Symptoms/signs
16-12 Tachypnea, hyperpnea, (resultant hypocapnia), tachycardia, reduced attention and alertness, euphoria, headache, mild incoordination
14-10 Altered judgment, incoordination, muscular
fatigue, cyanosis
10-6 Nausea, vomiting, lethargy, air hunger, severe incoordination, coma
<6 Gasping respiration, seizure, coma, death
Clinical Findings Associated with Reduction of Inspired Oxygen
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Specific agent
• Noble Gases: helium, neon, argon, xenon
• Short-chain aliphatic hydrocarbon gases:
methane, ethane, propane, butane
• Carbon dioxide (CO2)
• Nitrogen (N2) gas
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Treatment
• Immediate removal from exposure and ventilatory assistance
• Oxygen supplement
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Chemical asphyxants
• Cyanide
• Carbon monoxide
• Hydrogen sulfide
• Nitrogen oxide
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Hydrogen sulfide
Decaying organic matter
Sulfur containing proteins
Fish
Sewage
Manure
Hot, humid weather→ ↑microbial metabolism and gas production
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Rubber vulcanization
Synthetic fabric & paper production
Leather tanning
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potent inhibition of cytochrome oxidase
binds to ferric (Fe3+) moiety of
cytochrome a3 oxidase complex
higher affinity than cyanide
inhibition of oxidative phosphorylation
produces cellular hypoxia and anaerobic
metabolism
Mechanism of action
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Hydrogen sulfide, cyanide, carbon monoxide
Mechanism of action
Hydrogen sulfide
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Colorless gas
More dense than air
Irritating gas→ “rotten eggs” (low)
Olfactory nerve fatigue and paralysis (high)
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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 500Quickly unconscious; death without rescue 750Rapid collapse; respiratory paralysis 1,000
Immediate date 5,000
Effects of hydrogen sulfide gas on humans
Fuller DC.JOEM 2000;939
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When to suspect hydrogen sulfide poisoning
Person rapidly loses consciousness knocked downRotten eggs odorRescue from enclosed space, such as sewer or manure pitMultiple victims with sudden death syndromeCollapse of a previously healthy worker at work site
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Management
1. Supportive carePrehospital- 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
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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
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cytc2+ cytc3+
cyta3+ cyta2+
cyta32+ cyta3
3+
1/2O2+2H+ H2O
OxyHb
MetHb
SulMetHb
Sodium nitrite
H2S
OxyHb+SOX
Sodium nitrite
Sodium thiosulfate
OxyHb
MetHb
CyanoMetHb
Thiocyanate
Rhonanese
CN
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2. Antidote- Sodium nitrite (3%NaNO2) IV over 2-4 min 10 mL (300 mg)
Caution:HypotensionMethmoglobinemia
- Hyperbaric oxygen
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• Nitrogen oxides→ Oxidized nitrogenous compounds
• Irritant gas
• Low water solubility
• Heavier than air → collect just above silage
Nitrogen dioxide
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NO Nitric oxideNO2 Nitrogen dioxideN2O Nitrous oxideN2O2 Nitrogen Peroxide
N2O3 Dinitrogen trioxideN2O4 Dinitrogen tetroxide
N2O5 Dinitrogen Pentoxide
Nitrogen Oxides
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Crops
Silo
Fermentation
CO2, nitrogen oxide
NO, NO2, N2O4
Silo Filler’s disease
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NO2Low water solubility
No symptom in upper airway
Irritant effect in bronchi, terminal bronchioles and alveoli
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Pathophysiology
NO2
Free radical
Protein oxidationLipid peroxidation
Cell membrane damage
NO, HNO3, HNO2 Distal airway
Direct toxic effect
Type1 pneumocytes
ciliated airway cells
Delay onset ofchemical pneumonitis
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Clinical manifestration
• Depend on intensity and duration of exposure
• Lost of consciousness, Sudden death →Hypoxia
• Delay respiratory symptoms
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Acute Phase
• No upper respiratory irritation (low level)
• Upper respiratory symptom (high level)
• Methemoglobinemia
• CXR normal → do not rule out ALI
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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
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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
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Gurney JW. RidoGraphics 1991;625
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Management• Prehospital care
- 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
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Clinical feature and Management of H2S&NO2H2S
(manure pit)NO2
(silo)Property Rotten egg
irritantLow water soluble
Mechanism Inhibit cytochromeoxidase
Direct toxic alveolar cell, free radical
Signs & symptoms
Mucous membrane irritationRespiratory irritationCellular hypoxia
Laryngospasm, brochospasm, ARDSRespiratory arrest
Management Extrication/resuscitation/supportiveSodium nitrite
Bronchodilator, steroids
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“ขอบคุณคะ”