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Inhalational Injuries

Inhalational Injuries. Ping-Wei Chen PGY -2 Emergency Medicine. Special thanks to Dr. Chris Hall and Dr. Yael Moussadji. Clinical Pearl. Objectives. Mechanisms of injury Determinants of Toxicity Classes of Inhalational Toxins Simple Asphyxiants Pulmonary Irritants Cellular Poisons.

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Inhalational Injuries

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  1. Inhalational Injuries Ping-Wei Chen PGY -2 Emergency Medicine Special thanks to Dr. Chris Hall and Dr. Yael Moussadji

  2. Clinical Pearl

  3. Objectives • Mechanisms of injury • Determinants of Toxicity • Classes of Inhalational Toxins • Simple Asphyxiants • Pulmonary Irritants • Cellular Poisons

  4. Sources of Exposure • Industrial/Occupational • Home/Community • War/Chemical Weapons

  5. Mechanisms of Injury • Direct Pulmonary Toxicity • Alter air/lung interface by invoking irritant or inflammatory response • Dissolve to form acid/base • Oxygen free radicals • Systemic Toxicity • Reduce inspired fraction of O2 • Alter oxygen transport • Uncoupling of electron transport chain/oxidative phosphorylation

  6. Determinants of Injury • Exposure level • Water solubility • Particle size • Mixtures

  7. Exposure Level • Controlled vs Uncontrolled (explosion) • Confined vs Outdoors/Ventilated area • Duration of exposure

  8. Water Solubility • Determines level of respiratory tract involved and symptom onset • High water solublility • Mucous membranes • Upper airway • Rapid irritation • Poor water solubility • Lower airway • Delayed onset of symptoms • Intermediate water solubility • Mixed presentation upper/lower airway

  9. Particle Size • Determines level of respiratory tract involved • Particles ≥ 10 microns are filtered in the nose and/or deposited on the larynx • Particles ≤ 10 microns are deposited in the large airways • Particles ≤ 5 microns are deposited in the distal airways and alveoli

  10. Mixtures • Exposures commonly to mixture of substances • Synergistic toxics effects • Examples • Smoke • Mixture of household cleaning products

  11. Simple Asphyxiants • Mostly inert substances • Toxicity from displacement of O2 • Lowered FiO2 • Acute effects as result of hypoxia • Examples: • propane, butane, nitrogen • Mostly workplace related • Liquefied gases

  12. Simple Asphyxiants • Clinical symptoms due to hypoxia

  13. Simple Asphyxiants • Treatment • Removal from exposure • Supportive • Supplemental O2 preferred (room air suffices) • Disposition • Mild symptoms – brief observation; discharge • Significant symptoms/comorbidities • Admission for observation of post-hypoxic complications

  14. Case 1 • 37yo female • Cleaning her bathroom with a combination of bleach and disinfectants • Sudden onset of a strong odor • Developed marked irritation of eyes and burning sensation in nose and throat • Immediately left the bathroom • Feels nauseated and slightly dyspneic

  15. Pulmonary Irritants • Destruction of integrity of mucosal barrier of respiratory tract • Acid/Base reactions • Free radical generation • Host response • Neutrophil recruitment • Cytokine activation ACUTE LUNG INJURY

  16. Ammonia • High water solubility • Fertilizer, Cleaning agent, Refrigerant • Dissolves to form NH4(OH)

  17. Chloramines • High water solubility • Often from a mixture of ammonia and sodium hypochlorite bleach • Dissolves to form hypochlorous acid, ammonia, O2 free radicals

  18. Sulfur Dioxide • High water solubility • By-product of oil refining and smelting • Dissolves to form sulfuric acid • Cause of acid rain

  19. Chlorine • Intermediate water solubility • Mild initial symptoms • Prolonged exposure • Swimming pools, mixing acids with bleach • Dissolves to form HCL, hypochlorous acid, O2 free radicals

  20. Other Pulmonary Irritants • Hydrogen Fluoride • High water solubility • Gasoline, Glassware, Building Renovation, Semiconductor industries • Dissolves to form hydrofluoric acid • Systemic toxicity (hypocalcemia) • Phosgene • Low water solubility • Pesticide production • Dissolves to form HCl • “fresh hay” scent

  21. Management • Airway evaluation • Swelling can be rapid or delayed (water solubility) • Signs of upper airway dysfunction mandate visualization of the larynx ± airway stabilization • Symptomatic treatment • Bronchospasm: β-agonists • Chlorine/HCl: nebulized 2% NaHCO3 solution • ALI/ARDS: aggressive supportive care

  22. Supportive Care • Support airway patency • Pulmonary toilet – limit airway secretions • Maintain oxygenation • Ventilation Strategies: • Prone • Inverse ratio • PEEP • Low Tidal Volume • Currently, little to no evidence to support: • Cortisteroids (inhaled/systemic) • Antioxidants • Surfactant therapy

  23. Disposition • High Water Solubility Agents • Can be discharged if asymptomatic/improve with treatment • Intermediate/Poor Water Solubility Agents • Observe asymptomatic patients for several hours • Symptomatic/High Risk features (comorbidities, extremes of age, poor F/U) need to be observed for a minimum of 24 hours

  24. Metal Fume Fever • Metal oxide fumes • Onset hours post-exposure • Welding, galvanizing, smelting • Recurrent influenza-like illness • fever/chills (38-39oC) • cough/dyspnea/CP • Headache • Myalgias • Metallic taste • Immunologic/toxic etiology • 48hr natural history • Tx: Analgesic/antipyretics

  25. Case 2 • 55 yo male construction worker • Involved in explosion, thrown backward 10 feet • Second and third degree burns to face, neck, torso, arms and legs • Comes in with EMS on backboard in collar, alert and screaming in pain • VSS

  26. Case 2

  27. Smoke Inhalation • Multiple etiologies of injury • Irritant • Combusted carbonaceous material increases exposure to adsorbed toxins • Simple asphyxiant • Fire consume O2 • Chemical asphyxiant • Multiple substances involved • Cyanide • Carbon monoxide

  28. Smoke Inhalation • Mortality rates of combined major burn injury and inhalation injury exceed that of either alone • Inhalation injury is a predictor of prolonged ventilator dependence and death • Twenty percent of those requiring admission to a burn unit carry a diagnosis of inhalation injury

  29. Management • Evaluate airway patency early!! • Airway Compromise • Edema (exacerbated by fluid resuscitation) • Intraluminal debris (soot) • Bronchospasm • Diagnostic Tests • ABGs (beware pulse oximeters – CO) • Serum lactate > 10mmol/L – suspect cyanide/CO poisoning • CXRay – baseline study

  30. Clinical Course • Early resuscitation phase • acute pulmonary insufficiency +/- critical airway narrowing that can progress over 18-24 hours • Post-resuscitation phase (2-5 days) • characterized by mucosal necrosis, secretions, distal airway obstruction, atelectasis, pulmonary interstitial edema, and bronchopneumonia • Inflammatory-infection phase (5 days and beyond) • continues until there is lung healing and burn wound closure; no role for prophylactic antibiotics

  31. Chemical Asphyxiants Oxygen Transport Oxygen Utilization Carbon Monoxide Cyanide Hydrogen Sulfide • Carbon Monoxide

  32. Carbon Monoxide • Generated by incomplete combustion of carbon containing material • CO binds to Hgb to form carboxyhemoglobin • Slowly reversible reaction

  33. Carbon Monoxide • Uncouples oxidative phosphorylation/electron transport chain • Inhibits final cytochrome complex

  34. Clinical Presentation • Signs/Symptoms consistent with asphyxia • CNS: mild to severe • headache, N/V, dizziness, confusion • Altered LOC, seizures, coma • CV: • Hypotension, dysrhythmias, cardiovascular collapse • “Cherry-Red skin” is a post-mortem finding! • Delayed neurological sequelae • Appears after 2 – 40 days • Neurologic syndromes • Psychiatric/Cognitive findings

  35. Treatment • Prevention of delayed neurological sequelae • Severity of poisoning may not correlate with COHb levels • Oxygen is the mainstay of treatment • Achieve sufficient PO2 to sustain life in absence of normal Hgb • Shorten half-life of CO

  36. Hyperbaric Oxygen Therapy • Controversial • Cognitive sequelae less at 6 weeks and 12 months with HBOT (3 sessions) • 25% versus 46.1% • Other studies: mixed/no benefit • Cochrane Review (2005) • “No evidence to support use of hyperbaric oxygen for treatment of patients with carbon monoxide poisoning”

  37. To HBOT or not HBOT • Considerations: • Neurologic abnormality • Cardiovascular instability • COHb > 25% • Pregnant and COHb >15%

  38. Cyanide • Photography, Metallurgy, Synthetic manufacture, Fumigation • “bitter almond” smell • Rapid absorption after inhalation • Uncouples oxidative phosphorylation/electron transport

  39. Hydrogen Sulfide • Petroleum, Natural Gas, Waste Management • Irritant + Systemic Toxicity • Uncouples oxidative phosphorylation/electron transport chain • Intermediate water solubility • “rotten egg” smell

  40. Clinical Presentation • Signs/Symptoms consistent with asphyxia • CNS: mild to severe • headache, N/V, dizziness, confusion • Altered LOC, seizures, coma • CV: • Hypotension, dysrhythmias, cardiovascular collapse • May have persistent or delayed onset neurologic sequelae

  41. Treatment Hydrogen Cyanide Hydrogen Sulfide Removal from exposure Supportive Care If severe toxicity Inhaled amyl nitrite IV sodium nitrite • Re-activate cytochrome oxidase system • Cyanide Antidote Kit: • Create MetHb to bind cyanide • Inhaled amyl nitrite • IV sodium nitrite • NOT with CO poisoning (MetHb + COHb = BAD) • Enhance metabolism/elimination • Sodium thiosulfate • Hydroxocobalamin • Cyanide binds to form Vit B12

  42. Don’t forget to warn others who are exposed!!

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