1. Inhalational injuries H.R.Sarreshtahdar, MD Occupational Medicine Specialist

2. Irritant lung reactions  Many gases, fumes, and aerosols are directly toxic to the respiratory tract  Site of effect is determined by: Water solubility  High solubility (ammonia): irritation of upper respiratory  Low solubility (O3): irritation of lower respiratory Particle size  Large particles (>10 μm): upper respiratory  Medium particles (3-10 μm): airways  Small particles (<3 μm): lung parenchyma

3. Irritant lung reactions  Examples of some irritants: Ammonia HCl SO2 NOx Phosgene O3  Clinical findings: Immediate irritation of upper respiratory tract to late pneumonitis and pulmonary edema

4. Management  Immediately obtain ABG + O2 therapy  Take a history (esp. attention to chemical asphyxiants)  Examine eyes, nose, pharynx for evidence of burns  Auscultate lungs  Baseline spirometry if subject is capable  Baseline CXray  Admit to hospital  Observe for 24-48h

5. Simple Asphyxiants  Gases: Methane, ethane, propane Ethylene, propylene, acethylene CO2 N2 NO  Effect: reduction of fractional inspiratory concentration of O2 → hypoxia  No toxic effects

6. Simple Asphyxiants  Exposure: typically in confined spaces (storage tanks, mines) For gases heavier than air any low-lying semi- closed space with little air movement is dangerous Methane (mining) CO2 (food preservation, manufacture of dry ice, … ) N2 (underwater work, mining, metallurgic operations, pressurizing oil wells)

7. Simple Asphyxiants  Clinical findings:  Related on: Asphyxiant concentration Level of physical activity Underlying medical status  Normal air O2: 21%  O2 (10-16%): tachycardia, tachypnea, exercise intolerance  O2 (6-10%): nausea, prostration, coma  O2 (<6%): rapid loss of consciousness

8. Simple Asphyxiants Treatment  Immediate removal from exposure  Supportive measures (esp. supplemental O2)

9. Toxic Asphyxiants Inhalation of asphyxiants which have toxicity to tissues  Carbon monoxide (CO)  Hydrogen cyanide (HCN)  Hydrogen sulfide (H2S)

10. CO  An odorless, colorless gas  CO intoxication: the leading cause of death from gas inhalation  Exposure: Incomplete combustion of fuels (vehicles, forklifts, generators, … esp. when used indoors)  Jobs: Firefighters, petroleum refinery workers, furnace operators, …

11. CO  Mechanism of action: Binding to Hgb (COHb):  ↓ O2 binding capacity  Leftward shift of O2 dissociation curve Binding to cytochrome oxidase:  Compromising cellular respiration  Clinical findings: Headache, nausea, vomiting, malaise, loss of consciousness, coma, death, cardiac ischemia  Lab data: ↑ COHb in cooximetry Routine ABG is not helpful EKG (MI without typical chest pain)

12. CO Treatment  Immediate removal from exposure  100% O2  Hyperbaric oxygen

13. HCN A colorless gas with bitter almond odor  Uses: metal plating, and extraction of silver and gold salts from ores  Exposure: thermolysis byproduct of many polymers  Jobs: Pesticide workers, printing, soldering, firefighting, photography, paper production, …  Mechanism of action: Binding to cytochrome oxidase  Clinical findings: Dyspnea, dizziness, headache, confusion, loss of consciousness, coma, death

14. HCN  Lab findings: Blood cyanide level (not available) Urine thiocyanate (not reliable)  Treatment: Removal of exposure Induction of metHgb (300 mg Na nitrite) Detoxification of cyanide (sodium thiosulfate) Supportive measures

15. H2S A colorless gas with rotten egg odor  Exposure:  Many jobs (petroleum production and refinery, farming, chemical laboratory, excavators, fish processing, sewage workers, …  Mechanism of action: Binding to cytochrome oxidase Irritant effect on mucous membranes

16. H2S  Clinical findings: Irritant findings: airway irritation, burning eyes Headache, dizziness, nausea and vomiting Dermatitis, pneumonitis, pulmonary edema loss of consciousness, coma, death  Lab data: Blood sulfide level  Treatment: Removal of exposure Induction of metHgb (300 mg Na nitrite) Supportive measures