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

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

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)

Smoke Inhalation Video Tape…

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

Toxic by-products of combustion

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

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

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

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

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

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

CO poisoning: pathophysiology CO affinity to hemoglobin is 240 times greater than Hgb- O 2 affinity CO-Hgb binding causes leftward shift in the oxyhemoglobin dissociation curve, impeding oxygen delivery to tissues CO binds to myoglobin, cytochromes a and a 3, and cytochrome c oxidase, impeding O 2 utilization and worsening cellular dysoxia

O 2 saturation in CO poisoning Pediatrics 1981; 68:218

CO exposure: neurologic symptoms

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

CO poisoning: Therapy Definitive therapy is 100% FiO 2 –reverses arterial hypoxemia –accelerates dissociation of CO from Hgb –maintain until carboxyhemoglobin level <5% Benefits of hyperbaric oxygen controversial Eucapneic hyperventilation with 100% FiO 2 Consider empiric concomitant treatment for cyanide toxicity

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

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

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