Acute Inhalation Injury By : ziba Loukzadeh, M.D Occupational Medicine department Yazd University of Medical Sciences

Types of inhaled substances Aerosol Fume Mist Gas Vapor Smoke Dust

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

Properties of inhalants Particle (size) : >10µm :upper airway 2.5-10µm :lower air way <2.5µm :lung parenchyma

Acid (chlorine, HCL,SO2, NOX, phosgene) Alkali (ammonia) coagulation Alkali (ammonia) liquefaction Reactive o2 species(ozone, NOX, chlorine) Lipid peroxidation

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

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

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

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

Conductive airway Baseline spirometry repeat after 24-48h Significant decrement: FEV1≤80% Decrease ≥ 10% from baseline

Conductive airway Symptomatic person without decrement in airflow Inhaled steroid +bronchodilator Symptomatic person with airflow obx Short course of systemic steroids AND

Conductive airway( chronic injury ) COPD (chlorine, SO2) Intensity of exposure Smoking Pre-existing pulmonary dx Rx Smoking cessation Bronchodilator Steroids O2

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

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

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

--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;185:354-363 Copyright © 2007 by the American Roentgen Ray Society

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

Evaluation ABG CXR PFT (spirometry, peak flowmetry) Methacholine challenge Lung Bx 24h observation for low water soluble inhalants

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

Prevention Engineering controls Regular maintenance Worker training Plan to handle accident Evacuation plan Availability of emergency provision (o2, shower, respirator)

Ammonia Manufacturing industry Chemical industry Agricultural industry Manufacture of explosives, cyanide, synthetic fiber, plastic Chemical industry Petroleum refining Agricultural industry Soil fertilizer

Ammonia Highly water soluble Injury: Thermal burn Alkali burn Irritation of eye, skin & upper & conductive airway Parenchymal injury in high exposure Biphasic pattern

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

NOx Exposure Low water soluble Mining Acetylene welding explosive manufacturing In closed area with engines Agricultural worker ( silo fillers dx) Low water soluble

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

Systemic illness from inhaled toxins (inhalation fever)

Background Various causes Similar features Flu-like symptoms Self-limited Important differential diagnosis - Inhalational lung injury - HP - Infections

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

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

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)

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

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)

Significant smoke inhalation Steam exposure Closed space Exposure to plastic fumes Burn of facial hair Altered consciousness Respiratory symptoms Lactic acidosis COHg>20%

Smoke inhalation (management) Evaluation of COHg & serum PH Upper airway burn: endotracheal intubation Significant smoke inhalation: 24h obseve

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