Acute Inhalation injuries

1. Acute Inhalation injuries Marc Francis PGY2 Emergency Medicine May 19th 2005

2. Overview • Background • Discuss mechanisms of toxicity • Analyze the anatomical sites involved and there differences • Historical and physical clues to diagnosis • Treatment options • Cases to put you to the test and discuss some specific toxins and exposures

3. In industrialized countries exposures to various toxicants are commonplace Acute injury is usually a sporadic event Often consequence of accidental release in workplace Smoke inhalation from residential fire Chemical disasters and widespread fire can magnify these injuries substantially Inhalational Injuries

4. Inhalational injuries • Interesting facts • In the aftermath of the World Trade Centre attacks in 2001 inhalation injury was the most common reason survivors sought attention • Although there is renewed interest in bioterrorism and chemical agents the most common toxicants are from industry, home and recreation sources • Wartime use of chemical agents (mustard gas) historically resulted in severe inhalation injuries, today’s soldiers are all trained and equipped for chemical exposure

5. Mechanisms of toxicity • Inhalation injuries produce a wide spectrum of clinical effects • The type of injury is a function of 1) Exposure level 2) Water solubility 3) Particle size 4) Cell injury and inflammation 5) Host Factors

6. Exposure Level • Major determinant of severity of damage • Exposure may be • Controlled – industrial process • Uncontrolled – explosion • Environment in which toxin released • Confined space vs outdoors • Canadian Centre for Occupational Health and Safety • Publishes exposure limits for chemical substances • www.ccohs.ca

7. Water Solubility • Key role in determining where inhaled agents deposit in the respiratory tract • The respiratory tract is lined with mucous in a watery solution • Gases can be classified as 1) Highly water soluble • Ammonia, Sulfur dioxide, Hydrogen Chloride 2) Intermediately water soluble • Chlorine 3) Less Water soluble • Phosgene, Ozone, Nitrogen oxides

8. High solubility Generally acute injury to mucous membranes Eyes, lining of nose, and upper airway Spare the lower resp tract Irritant and causes unpleasant symptoms which encourages pts to leave an exposure Low solubility Often no symptoms or ill effects in the upper airway Penetrate and cause irritation of bronchi, terminal bronchioles and alveoli Exposed individuals often remain in areas longer increasing risk of severe outcomes Water Solubility

9. Particle Size • Most particles that are smaller than 100 microns can enter the airway • Particles with diameter <10 microns can reach the lower respiratory tract • Particles smaller than 5 microns can deposit in lung parenchyma

10. Cell Injury and Inflammation • Substances that are irritants damage cells in a non-immunological fashion • Cell injury results from deposition or formation of • Acids • HCl, sulfur dioxide, hydrogen fluoride • Alkali • Ammonia, sodium hydroxide • Reactive O2 Species • Substances differ, but all mediated through lipid peroxidation • All of these can disrupt epithelial cell tight junctions

11. Cell Injury and Inflammation • Temperature • Inhaled substances can cause direct thermal injury to cells and tissues • Nasal passages and upper airway usually provide sufficient cooling to protect lower airways • Steam exposure can cause extensive thermal damage

12. Host factors • Older Individuals more susceptible • Pre-exisiting lung disease • Asthma • COPD • Risk of exacerbation of condition and increased risk for adverse outcomes

13. Anatomical sites of injury • Upper airway • Conducting airway • Lower respiratory tract • Systemic effects

14. Upper airway • Range from simple transient irritation to airway compromise!!! • Olfactory or irritant stimuli can provide warning • Upper airway defends against injury to lower resp tract • Reflex responses to irritants • Mucous secretion • Cough • Sneeze • Glottic closure • Apnea

15. Upper airway • Cell injury and inflammation occurs with destruction of epithelial tight juctions Nose • Nasal obstruction, epistaxis Mouth • Acute pharyngitis Larynx • Acute laryngitis with varying degrees of edema and spasm • Potential to compromise the airway

16. Conducting airways • Bronchoconstriction • By direct stimulation of parasympathetic nerve endings • By localized inflammation and release of mediators that exacerbate bronchoconstriction • Mild irritant effects include tracheitis and bronchitis • Irritation and inflammation exacerbate underlying reactive airways diseases • Airway obstruction may worsen over the first 24hours as inflammation develops

17. Lower Respiratory Tract • Substances <5 microns or low water solubility • Atelectasis may occur from disruption of the surfactant layer • Loss of tight junctions causes alveoli to fill with protein-rich fluid leading to pulmonary edema • Pneumonitis • Most common acute manifestation • Diffuse, bilateral process • Clinical features of cough, dyspnea, and hypoxemia • Usually self-limited • More severe injury can lead to severe pulmonary edema or ARDS

18. Systemic Effects Certain inhaled substances cause systemic effects • Metal fume fever • A syndrome of flu-like symptoms associated with metal oxides (zinc, copper, Mg oxides) • Polymer fume fever • Fever, cough, chills and chest pains associated with inhalation of Teflon (tetrafluoroethylene) • Organic toxic dust syndrome • Agriculture workers after exposure to moldy grain • Flu-like syndrome with fever, cough, malaise, myalgias and fatigue • High dose hydrofluoric acid can produce severe hypocalcemia and hypomagnesemia

19. History A careful history of what was being done at the time of the exposure may provide details of substances involved and intensity or duration of the exposure

20. Historical components • Exact concentrations of solutions or liquids • Was there an odor? • Was there visible airborne substances? • Eye or upper airway irritation? • Occurrence of symptoms in co-workers? • Are material safety data sheets or containers available? • Past history of underlying lung and CVS disease

21. Symptoms • Determine respiratory symptoms and exact time of onset • Cough, sputum, wheezing, CP, SOB • Associated symptoms • Taste sensations • CNS symptoms • Systemic symptoms

22. Physical Examination • Vitals may initially be normal even in the setting of significant inhalation injury • Skin, hair, nares, oralpharynx should be examined for burns or chemical injury • Stridor signifies significant upper airway edema • Lung ausculation should focus on auditory wheezes or crackles • Other findings of significance • Cyanosis, confusion, tachycardia, pulsus paradoxus and fever

23. Laboratory • Routine • Pulse oximetry • ABG • EKG • CBC + Lytes • For pts with significant inhalations • If smoke inhalation suspected • Carboxyhemoglobin level • Elevated plasma lactate levels may indicated cyanide toxicity – and need for cyanide level • Particular toxin blood levels (mercury, cadmium) can be drawn if suspected

24. Chest Radiograph • Should be routine • May be normal in early course • Bilateral patchy infiltrates suggest pneumonitis • Air-trapping suggests obstruction

25. PFTS • In ED may be difficult to obtain full testing • Peak flow measurements +/- spirometry if available acutely • When acute resp distress resolves arrange full pulmonary function testing to determine new onset of restrictive or obstructive lung disease

26. Direct visualization • In selected cases where significant upper airway involvement suspected • Laryngoscopy or bronchoscopy • Significant findings on airway inspection • Deposits of soot or edema • Indicate potential need for intubation • Bronchoscopy helpful in acute setting in selected pts • Signs of lower resp tract injury often reflected in the upper airway exam

27. Soot and edema

28. Treatment • Predominantly supportive • Specific antidotes are rare • Initial management • O2 Ensure adequate oxygenation and displace CO from Hgb • Fluid resuscitation Particularly in smoke inhalation • Pulmonary Toilet For endobronchial cast formation • Intubation Significant airway compromise

29. Treatment • Antitussives • If cough is a significant symptom • Nasal Steroids • For significant rhinitis • Inhaled beta-adrenergics • added for bronchospasm

30. Steroids? • Controversial • Paucity of well designed clinical trials • Demonstrated to be of no benefit in smoke inhalation • Appropriate in cases where there is exacerbation of underlying reactive airways • All other cases • Evidence of reduced lung bacterial clearance and increased incidence of bacterial pneumonia • Outweighs any potential anti-inflammatory effects

31. Disposition • How long to observe? • Knowledge of the agent involved and intensity and duration of the exposure is critical • Usually prudent to observe for clinical deterioration for 4-6hrs • Certain agents (phosgene) can produce few initial symptoms yet go on to pulmonary edema, ARDS and respiratory failure within 12-24hrs • Indicators of poor prognosis 1) Progressive resp difficulties 2) Presence of rales 3) Burns to face 4) Hypoxemia 5) Altered mental status

32. 3 unique scenarios Household or Community Occupation and industry Chemical and biological weapons Cases and specific scenarios

33. Case 1 • 37yo mother of 3 • PMHx • Exercise induced asthma • HPI • Cleaning small bathroom with combination of bleach and multiple disinfectants • Sudden onset of strong odour • Marked irritation of eyes and burning in throat and nose • Immediately left the washroom and went outside for “some fresh air” • Felt nauseated and asked husband to drive her to ED

34. Case 1 • On examination • Vitals • HR 67, RR 25, BP 112/76, T 371, Sat 98% on RA • CVS = normal • Resp = diffuse wheezing heard throughout, no stridor • Abd = soft + non-tender • Derm = no rash • HEENT = mild conjunctivitis, marked rhinitis and normal oralpharynx

35. Investigations • CBC and Lytes • Normal • EKG • Normal sinus rhythm with no ST changes • CXR • No acute changes seen • Peak Flows • 60% of predicted

36. Chlorine Gas • A greenish-yellow gas • Important component of many industrial processes • Inadvertent mixing of household chemicals can lead to exposure • Sodium hypochlorite bleach + phosphoric acid cleaning powders = intermittent Cl2 gas exposure • Intermediate water solubility • Irritant effects vary from rhinitis and tracheobronchitis to pneumonitis and pulmonary edema

37. Case 2 • 49yo M accountant • PMHx • Smoker • Hyperlipidemia • HPI • Pt was working in his garage cleaning multiple paint brushes • Insidious onset of persistent headache and dizziness • Patient left the closed garage and felt unsteady on his feet almost falling over • Called 911 when he developed persistent and severe abdominal pains and some confusion • Onset of some vague chest discomfort on arrival to ED

38. Case 2 • On Examination • Vitals • HR102, RR 20, BP 131/68, T 373, Sat 96% RA • Neuro • Alert and oriented, unsteady gait with wide stance • CVS • Normal HS, normal pulse • Resp • Tachypneic, but in no apparent distress • Abd • Soft but tender diffusely to palpation

39. Investigations • CBC • Normal • Lytes • Normal • EKG • 1mm of ST segment ↓ in the lateral leads • ABG • HbCO 16%

40. Methylene Chloride • Halogenated hydrocarbon solvent found in paint removers and other solvents • Pulmonary absorption is principle source of systemic toxicity • Symptoms include • Dizziness, HA, ataxia, abd pain, coma, apnea • Is metabolized to CO • HbCO levels increase gradually and can contribute to cardiac ischemia/infarct • Treated using the same approach as CO inhalation as clinical and cellular effects are the same • CO production can continue despite efforts at ongoing elimination

41. Case 3 • 68yo F retired • PMHx • COPD • Stable Angina • HPI • Patient involved in mutli-level residential fire after leaving burner on overnight • Pt “trapped” in upper floor of the building with prolonged extracation by fire dept • Extensive smoke and flames in pts apartment • Patient was disoriented but conscious at the scene • Now complaining of CP and SOB

42. Case 3 • On examination • Vitals • HR 94, RR 24, BP 110/60, Sat 94% on 10L O2 by mask • CVS • Normal heart sounds • RESP • Coughing and some mild wheezing throughout • Dark black sputum noted • HEENT • Singed nasal and facial hair noted • Some 2nd degree burns to forehead and face • Derm • Combination 2nd and 3rd degree burns to upper extremities

43. Case 3

44. Case 3 • Investigations • CBC + Lytes • Hgb 104, WBC 20.1, Plt 432 • Electrolytes Normal • EKG • Inferior ischemic changes with marked ST depression • CXR • normal • ABG • Mild metabolic acidosis • Serum Lactate of 13mmol/L

45. Smoke Inhalation • The single most likely cause of acute inhalation injury in ED setting • Leading cause of death from structure fires • Mortality rates of 5-8% • Represents a combination of • Direct pulmonary injury • Systemic toxicities • Metabolic toxicities

46. Smoke Inhalation • The composition of smoke is variable and unpredictable • Gas phase constituents of smoke include: • CO, hydrogen cyanide, acid and aldehyde gases, and oxidant • All are mucosal irritants • Smoke also contains particulates • Predominate in the 3-5µm range • These particles adhere to the mucosa and keep adsorbed toxicants in contact with the mucosa • Direct mucosal injury compromises the mucociliary escalator

47. Early diagnosis based largely on clinical suspicion History of disorientation or unconscious at scene Can reflect smoke inhalation May indicated prolonged smoke exposure Respiratory symptoms may be delayed Clinical clues of smoke inhalation syndrome Carbonaceous sputum Singed nasal or facial hairs Facial burn Cough or wheezing Diagnosis and Early Resuscitation

48. Investigations • Initial investigations often normal • CXR • Frequently normal early on as injury to airways not lung parenchyma • ABG • Metabolic acidosis from CO • Decrease in measured SaO2 • Blood lactate level greater than 10mmol/L refractory to therapy is a surrogate marker of cyanide toxicity

49. Hydrogen Cyanide • Combustion product of natural and synthetic materials • Absorbed across alveolar membrane • Contribution of toxicity in acute smoke inhalation is debated • Binds mitochondrial cytochromes decreasing ATP production • CNS and myocardium are most sensitive • Coma, seizure, ↓CO, and metabolic acidosis can all occur • Detoxified in tissue especially the liver by sulfur transferase to thiocyanate and the excreted by the kidneys

50. Nitrates Inhalation (amylnitrite) IV (sodium nitrite) Induces methemoglobin Facilitates transport of cyanide from mitochondria to hepatocytes Sulfur IV sodium thiosulfate Aids in conversion of cyanide to thiocyanate by sulfur transferase When O2 transport is already compromised (CO) sodium thiosulfate can be administered alone Cyanide Antidote Kit