Inhalation injury Causes and pathophysiology Smoke Heat Particulates Systemic toxins -> CO and CN Respiratory irritants: Ammonia HCl Oxides of nitrogen Phosgene Aldehydes Thermal injury Oropharyngeal airway Local airway affected if steam, volatile gases, explosive gasses or hot liquid inhalation. MetHb Heat denaturation of Hb, oxides produced in fire and nitrates -> decreased O2 carrying capacity. Combustion uses O2 Low FiO2 -> hypoxemia. CO tissue hypoxemia. CN Poisoning of electron transport chain -> lactic acidosis. Impacts on the pulmonary function: Direct issue injury. Acute bronchospasm. Activation of inflammatory cascade. Oxygen radicals and proteolytic enzymes. Mucosa damage Bronchitis. Mucus plugging. Pulmonary edema. Bronchospasm. Bronchorrhea. Hypoxemia -> raises A-a gradient. SIRS. Clinical features Burns around the face. Especially nose and mouth. Singed nasal hair. Carbonaceous sputum. Nasal deposits. Soot, charring, mucosal erythema, oedema, blistering and necrosis. Voice changes and hoarseness. Respiratory distress syndrome: Hypoxemia. Elevated A-a gradient Stridor Wheeze Tachypnoea Dyspnoea High CO levels -> may look cherry red. CN -> bitter almond odour. CO and CN toxicity Lactic acidosis SvO2 Mental confusion Hypotension Diagnostics and investigations Inhalation injury should be suspected when any of the following are present: History of being in a confined space. Facial burns, singed eyebrows, and/or nose hair, evidence of soot on the face or in the airway. Stridor Dyspnoea Extensive burns. In suspected inhalation injury the following tests should be performed: Bedside respiratory function To rule out airway obstruction. Chest x-ray -> to rule out ADRS Carboxyhaemoglobin levels. End-tidal CO2 Serum lactate Flexible fibreoptic bronchoscopy May show mucosal erythema, edema and blistering, ulceration and/or soot deposits. Flexible fibreoptic laryngoscopy May show laryngeal edema. Treatment and Management Intubation and high flow oxygen therapy. Carbon dioxide toxicity: 100% oxygen therapy. Rapid transport to a hyperbaric centre. Cyanide toxicity: Sodium thiosulphate Produces metHb -> bonds to CN -> allows metabolism by liver enzymes. Vitamin B12 -> actively binds to CN -> allows renal elimination.