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Smoke Inhalation

Smoke Inhalation. Burn Symposium STATION 4. Jon Marinaro, MD Trauma-Surgical ICU Director UNM Burn Center: adult & pediatric injury. from tragedy… hope!. Respiratory Dysfunction… Burns. Cutaneous Burns. Smoke Inhalation. Respiratory Dysfunction. Wound Infection. Pneumonia. Sepsis.

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Smoke Inhalation

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  1. Smoke Inhalation Burn Symposium STATION 4 Jon Marinaro, MD Trauma-Surgical ICU Director UNM Burn Center: adult & pediatric injury from tragedy… hope!

  2. Respiratory Dysfunction… Burns Cutaneous Burns Smoke Inhalation Respiratory Dysfunction Wound Infection Pneumonia Sepsis

  3. Inhalation Injury • Involves any or all of the following: • Thermal Injury • Chemical Injury • Particulate-induced Inflammatory Alveolitis • Asphyxial Injury (secondary to hypoxia, or CO poisoning)

  4. Smoke Inhalation Video Tape…

  5. Inhalation Injury -- Thermal • Largely limited to upper airway • e.g., above vocal cords • Direct thermal injury to the lungs is rare unless steam is inhaled • Early recognition of upper airway burns is crucial--massive edema can rapidly evolve

  6. Toxic by-products of combustion

  7. Tracheobronchial Injury Chemicals in Smoke Chemotaxin release Epithelial Cell Injury Alveolar M Activation PMN activation Phospholipase activation O-2 Species Bronchoconstriction Exudative Injury

  8. Inhalation Injury--Time Course • Phase 1: first 12 hours • respiratory distress, lung consolidation, bronchospasm, tracheobronchial obstruction • Phase 2: 6 to 72 hours post-exposure • characterized by pulmonary edema • Phase 3: begins 24 hours post-exposure • risk of pneumonitis and/or bronchopneumonia • S. aureus early, P. aeruginosa later

  9. Pulmonary Dysfunction • Delayed Onset (days to weeks): • Pulmonary Embolism • immobilization and/or compartment syndrome resulting in altered flow • hypercoaguable state secondary to SIRS • Atelectasis/lobar collapse • thoracic pump dysfunction/intercostal atrophy • Restrictive lung disease • eschar formation and/or restrictive dressings

  10. Smoke Inhalation: Diagnostics • Carboxyhemoglobin level, ?Cyanide level • ABGs, Pulse oximetry • Chest X-Ray • WNL early; insensitive indicator of lung injury • exclude other injury, provide baseline • Upper endoscopy / bronchoscopy • PFTs, or flow-volume loops

  11. Inhalation Injury: Therapy and Airway Management • Humidified Oxygen • Bronchodilators (IV or nebulized) • Mucolytics and/or expectorants • Intubation, mechanical ventilation • PEEP may be required (bi-vent) • Pulmonary edema: role of fluid therapy • Antibiotics: gram+ versus gram- coverage • Corticosteroids controversial

  12. Carbon Monoxide Poisoning • Lethal concentration of carboxyhemoglobin found in 50% of autopsied fire victims • Higher metabolic rate of children, resulting in more rapid uptake of CO, puts pediatric patients at greater risk

  13. CO poisoning: pathophysiology • CO affinity to hemoglobin is 240 times greater than Hgb-O2 affinity • CO-Hgb binding causes leftward shift in the oxyhemoglobin dissociation curve, impeding oxygen delivery to tissues • CO binds to myoglobin, cytochromes a and a3, and cytochrome c oxidase, impeding O2 utilization and worsening cellular dysoxia

  14. O2 saturation in CO poisoning Pediatrics 1981; 68:218

  15. CO exposure: neurologic symptoms

  16. CO poisoning: Therapy • If comatose or hypercapneic, intubate • Treat cerebral edema with hyperventilation, mannitol, and fluid restriction • Optimize hemodynamics/blood pressure • Pharmacologic correction of mild acidosis discouraged--acidosis shifts oxyhemoglobin dissociation curve to the right, facilitating improved oxygen delivery

  17. CO poisoning: Therapy • Definitive therapy is 100% FiO2 • reverses arterial hypoxemia • accelerates dissociation of CO from Hgb • maintain until carboxyhemoglobin level <5% • Benefits of hyperbaric oxygen controversial • Eucapneic hyperventilation with 100% FiO2 • Consider empiric concomitant treatment for cyanide toxicity

  18. Half-life of Carboxyhemoglobin • JAMA 1976; 236:1503 Many centers believe in the “4-hour washout”

  19. CO exposure: Prognostic Factors • Acidosis on admission reported to be a negative prognostic sign • Reversal of coma within 48 hours associated with some degree of recovery • Correlation between LOC on admission and later neuropsychiatric sequellae • High rate of late neuropsychiatric sequellae in pts who appear completely recovered

  20. Questions… one child burned, is one child too many! Jon Marinaro, MD UNM Burn Center Adults & Pediatrics from tragedy… hope!

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