Presentation is loading. Please wait.

Presentation is loading. Please wait.

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

Similar presentations

Presentation on theme: "Acute Inhalation Injury By : ziba Loukzadeh, M.D Occupational Medicine department Yazd University of Medical Sciences."— Presentation transcript:

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

2 Types of inhaled substances  Aerosol  Fume  Mist  Gas  Vapor  Smoke  Dust

3 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

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

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

6 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

7 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

8 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

9 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

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

11 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

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

13 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

14 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

15 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

16 Copyright © 2007 by the American Roentgen Ray Society Pipavath, S. J. et al. Am. J. Roentgenol. 2005;185: Constrictive bronchiolitis pattern in 41-year-old male double lung transplant recipient with bronchiolitis obliterans syndrome

17 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

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

19 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

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

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

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

23 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

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

25 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

26 Systemic illness from inhaled toxins (inhalation fever)

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

28 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

29 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

30 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)

31 Polymer Fume Fever  Causes: pyrolysis (300 – 750 º C) 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

32 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)

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

34 Smoke inhalation (management)  O2  Evaluation of COHg & serum PH  Upper airway burn: endotracheal intubation  Significant smoke inhalation: 24h obseve

35 Thank you! Any Question?

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

Similar presentations

Ads by Google