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Acute Inhalation Injury
By : ziba Loukzadeh, M.D Occupational Medicine department Yazd University of Medical Sciences
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Types of inhaled substances
Aerosol Fume Mist Gas Vapor Smoke Dust
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Properties of inhalants
Gas (water solubility) High water solubility: ammonia, SO2,HCL Immediate injury to upper airway person quickly leave area low water solubility: Phosgene, ozone, NOX Injury of terminal bronchiole & alveolus person remain in area Intermediate water solubility: chlorine
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Properties of inhalants
Particle (size) : >10µm :upper airway 2.5-10µm :lower air way <2.5µm :lung parenchyma
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Acid (chlorine, HCL,SO2, NOX, phosgene) Alkali (ammonia)
coagulation Alkali (ammonia) liquefaction Reactive o2 species(ozone, NOX, chlorine) Lipid peroxidation
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Pathophysiology Direct contact & tissue damage
Direct smooth muscle contraction Stimulation of neuronal receptors Influx of inflammatory cells & mediators Leakage of interstitial fluid & edema Decrease epithelium’s barrier function
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Classification of injury
Acute (1-2 days of exposure) Laryngeal edema Airflow obx- asthma & bronchitis Pneumonitis, pulmonary edema ARDS Persistent sequelae( weeks to months) COPD RADS (Reactive Airway Dysfunction Syndrome) Bronchitis Bronchiolitis obliterans BOOP
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Upper airway injury- presentation
Burn of skin, eyes, nasal & throat Rhinitis Conjunctivitis lacrimation Sputum production Coughing & sneezing Airway obx tissue edema, thick secretion, sloughed cells Laryngospasm hoarseness ,stridor
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Conductive airway Acute Hospitalization for observation
Tracheobronchitis & bronchorrhea Hospitalization for observation Asymptomatic person+ objective evidence of respiratory compromise Airflow O2sat Abnormal CXR Asymptomatic person+ history of intense exposure With respiratory symptoms
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Conductive airway Baseline spirometry repeat after 24-48h
Significant decrement: FEV1≤80% Decrease ≥ 10% from baseline
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Conductive airway Symptomatic person without decrement in airflow
Inhaled steroid +bronchodilator Symptomatic person with airflow obx Short course of systemic steroids AND
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Conductive airway( chronic injury )
COPD (chlorine, SO2) Intensity of exposure Smoking Pre-existing pulmonary dx Rx Smoking cessation Bronchodilator Steroids O2
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Conductive airway( chronic injury)
RADS (sulfuric acid, chlorine, ammonia, smoke, household cleaner) Persistence of airway reactivity after inhalational injury Single, acute, high intensity exposure Previous exposure: - Pre-existing respiratory dx: - Rx Steroids bronchodilators
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Lung parenchyma (acute injury )
Exposure Low water soluble Massive high/intermediate water soluble Pneumonitis dyspnea, cough Hypoxemia Mild restriction Diffuse bilateral infiltration Rx:o2 +/- mechanical ventilation Pulmonary edema , ARDS
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Lung parenchyma (chronic injury)
Bronchiolitis obliterans (ammonia, mercury, NOx, SO2) Survivors of acute lung injury asymptomatic period irreversible obx (after 1-3 wks) PH/EX: early inspiratory crackles CXR: NL or hyperinflation Infiltration: generally – PFT: Obx +/- restriction Rx: 6-month trial of steroids
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--Constrictive bronchiolitis pattern in 41-year-old male double lung transplant recipient with bronchiolitis obliterans syndrome Pipavath, S. J. et al. Am. J. Roentgenol. 2005;185: Copyright © 2007 by the American Roentgen Ray Society
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Lung parenchyma (chronic injury)
BOOP (ammonia, mercury, SO2) Proliferative bronchiolitis Like Community acquired pneumonia: Non-productive cough, DOE, Malaise, fever, weigh loss, …. PH/EX: NL or late respiratory crackle CXR: Bilateral, most peripheral patchy opacity start as focal lesions, wax & wane PFT: NL or restrictive Rx: at least 6-month steroid Dramatically response
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Evaluation ABG CXR PFT (spirometry, peak flowmetry)
Methacholine challenge Lung Bx 24h observation for low water soluble inhalants
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Management Removal from exposure Irrigation with large amount of water
Suction of secretion Airway obx Inhaled epinephrine Endotracheal intubation Tracheotomy O2 if hypoxemia Bronchodilator Corticosteroids No influence Extensive edema: suggested Prophylactic Antibiotic: NO Management of Skin & mucosal surface burns Ophthalmologic consultation
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Prevention Engineering controls Regular maintenance Worker training
Plan to handle accident Evacuation plan Availability of emergency provision (o2, shower, respirator)
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Ammonia Manufacturing industry Chemical industry Agricultural industry
Manufacture of explosives, cyanide, synthetic fiber, plastic Chemical industry Petroleum refining Agricultural industry Soil fertilizer
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Ammonia Highly water soluble Injury:
Thermal burn Alkali burn Irritation of eye, skin & upper & conductive airway Parenchymal injury in high exposure Biphasic pattern
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Chlorine (CL2) Use: Intermediate water solubility
Bleaching agent (textile & paper industry) Water purification (swimming pool & sewage treatment) Intermediate water solubility Mixing of chlorine compound & other substance: Chlorine + ammonia: chloramine gas Household bleach+ phosphoric acid : CL2 gas
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NOx Exposure Low water soluble Mining Acetylene welding
explosive manufacturing In closed area with engines Agricultural worker ( silo fillers dx) Low water soluble
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Phosgene (low water soluble)
Used to catalysis reactions Polyurethane resin TDI Pesticide Dye Produced via heat decomposition of Solvents Paint remover Dry cleaning fluid Methylene chloride
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Systemic illness from inhaled toxins
(inhalation fever)
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Background Various causes Similar features Flu-like symptoms
Self-limited Important differential diagnosis - Inhalational lung injury - HP - Infections
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Characteristics Symptoms: fever, chills, headache, cough, chest tightness, minimal dyspnea, malaise, myalgia Signs: fever, tachycardia, tachypnea, occasionally crackles Develop 4-8 h after exposure Lab data: leukocytosis CXR : NL PFT : NL Self-limiting: 24-48h
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Metal fume fever Causes: - Zinc oxide
- Other metals: Mg, Cu, Cr, Ir, Ni, Ag, Al, Hg - Cd: acute lung injury - ZnCl2: acute lung injury Jobs: Brass foundry, Welding or Flame-cutting of galvanized metal Constitutional symptoms + metallic taste
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Organic Dust Toxic Syndrome (ODTS)
Causes: moldy or damp silage, hay, moldy wood chips Silo unloader’s syndrome (Vs. silo filler’s disease) /atypical farmer’s lung Summer and fall Atopy a risk factor DD: farmer’s lung (HP)
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Polymer Fume Fever Causes: pyrolysis (300 –750ºC) products of polytetrafluoroethylene resins (Teflon) Jobs: welding or flame-cutting of metals coated with PTFE, molding or extruding machines, cigarette smoking No tolearnace DD: acute lung injury
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Smoke inhalation In fire exposed person Smoke
Thermal content: supraglotic region Chemical content: vary from fire to fire Irritants Acrolein Ammonia Chloride HCL SO2 phosgene Chemical asphyxiants CO (incomplete combustion) Cyanide (combustion of acrylic, nylon, polyurethane)
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Significant smoke inhalation
Steam exposure Closed space Exposure to plastic fumes Burn of facial hair Altered consciousness Respiratory symptoms Lactic acidosis COHg>20%
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Smoke inhalation (management)
Evaluation of COHg & serum PH Upper airway burn: endotracheal intubation Significant smoke inhalation: 24h obseve
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Thank you! Any Question?
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