Acute Inhalation Injury

By : ziba Loukzadeh, M.DBy : ziba Loukzadeh, M.D

Occupational Medicine departmentOccupational Medicine department

Yazd University of Medical SciencesYazd 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) 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

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 Inhaled steroid +bronchodilator

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

Copyright © 2007 by the American Roentgen Ray Society

Pipavath, S. J. et al. Am. J. Roentgenol. 2005;185:354-363

--Constrictive bronchiolitis pattern in 41-year-old male double lung transplant recipient with bronchiolitis obliterans syndrome

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 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: 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

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)

O2 Evaluation of COHg & serum PH Upper airway burn: endotracheal

intubation Significant smoke inhalation: 24h obseve

Thank you!

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