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Diagnosis and management of inhalation
Inhalation injury occurs when toxic gases or smoke are inhaled, potentially causing thermal or chemical damage to the upper and lower airways. This can lead to higher fluid needs, longer ventilation times, pneumonia risk, and acute respiratory distress syndrome. Diagnosis involves considering exposure history and examining for soot or burns, with tools like bronchoscopy and imaging. Management focuses on airway support through ventilation, suctioning, and bronchodilators to prevent obstruction. Targeted therapies aim to reduce inflammation and infection while systemic toxicology addresses issues like carbon monoxide poisoning.
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Diagnosis and management of inhalation
- 1. Diagnosis and managementof inhalation injury: an updated review Dr. Chamika Huruggamuwa Registrar In Anaesthesiology TH Kandy
- 3. Inhalation injury isdefined as the • “Aspiration of superheated gases, steam, hot liquids, or noxious products of incomplete combustion”
- 4. Inhalation injury canfeature • supraglottic thermal injury, • Chemical irritation of the respiratory tract, • systemic toxicity due to agents such as carbon monoxide (CO) and cyanide, • or a combination of these insults.
- 5. The resultant inflammatoryresponse may cause • higher fluid resuscitation volumes, progressive pulmonary dysfunction, • Prolonged ventilator days, • Increased risk of pneumonia, • Acute respiratory distress syndrome
- 6. Three distinct clinicalentities • Upper airway thermal injury (above larynx) • Lower airway thermal injury (below larynx) • Injury as a result of noxious gases
- 7. Pathophysiology • Inhalation injurycomplicates burns in approximately 10 to 20 % of patients and significantly increases morbidity and mortality. • Inhalation injury has also been found to be an independent predictor of mortality in burn patients and worsens survival even among patients with similar age and burn size
- 8. • The degreeof inhalation injury is variable and is dependent on several factors: • The gas components inhaled, • The presence of particulate matter (soot), • The magnitude of the exposure, and • Individual Host factors such as underlying lung disease and inability to flee the incident.
- 9. • Many productsof combustion, such as carbon • dioxide, function as simple asphyxiants by displacing • oxygen at the alveolar level. This is further exacerbated • by the hypoxic fire environment. • CO functions systemically as an asphyxiant by • (1) competitively displacing oxygen from hemoglobin and • (2) binding to cytochrome oxidase at the mitochondrial level. • By contrast, hydrogen cyanide binds only to cytochrome oxidase
- 10. • the chemicalinjury stimulates vasomotor and sensory nerve endings • to produce neuropeptides. Preclinical studies have shown these neuropeptides can induce an inflammatory response • Substance P and calcitonin gene-related peptide are two suggested neuropeptides inducing tissue injury after inhalation injury • These neuropeptides then induce bronchoconstriction and nitric oxide synthase (NOS) to generate reactive oxygen species (ROS
- 11. • these neuropeptidescan function as tachykinins, inducing a inflammatory response with the downstream effects of bronchoconstriction, increased vascular permeability, and vasodilation. • tachykinins like substance P and neurokinin A can modulate immune cells and stimulate neutrophil and eosinophil chemotaxis • Overall, these factors potentiate local cellular damage and the loss of hypoxic pulmonary vasoconstriction.
- 12. • These processes- • loss of hypoxic vasoconstriction, • increased blood flow to injured lung segments, • decreased ventilation of collapsed segments - contribute to ventilation-perfusion mismatch • as a primary mechanism of hypoxemia following the smoke inhalation injury
- 13. Diagnosis The diagnosis ofinhalation injury was subjective and made on the basis of clinical findings. first reviews the history and reported mechanism to determine the likelihood of an inhalation injury. • Pertinent information includes • exposure to flame, smoke, or chemicals (industrial and household), duration of exposure, exposure in an enclosed space, and loss of consciousness or disability. • Pertinent physical exam findings • include facial burns, singed facial or nasal hair, soot or carbonaceous material on the face or in the sputum, and signs of airway obstruction including stridor, edema, or mucosal damage [
- 14. • For confirminginhalation injury to include • fiberoptic bronchoscopy (FOB), • Chest computed tomography (CT), • carboxyhemoglobin measurement, • radionuclide imaging with 133Xenon, and • Pulmonary function testing
- 15. Management • Respiratory support •Aggressive pulmonary toilet and mechanical ventilation when indicated • As thermal injury increases airway edema and can lead to airway obstruction, early intubation is favored • One study suggests prophylactic intubation can decrease mortality related to pulmonary-related death in patients with inhalation injury
- 16. • Maintaining bronchialhygiene is paramount in patients who have suffered inhalation injury. • Early ambulation, • chest physiotherapy, • airway suctioning, and • Therapeutic bronchoscopy
- 17. • Mechanical ventilationmay be a significant contributor to mortality • in burn patients independent of inhalation injury. • He proposed increased intrathoracic pressure from positive pressure ventilation led to decreased venous return, followed by decreased cardiac and urine output. • The typical clinical reaction is to increase intravenous fluid administration, resulting in higher volumes of infused fluid, a known risk factor for adverse outcomes in burn patients
- 18. • lung-protective ventilationin patients with inhalation injury, nonconventional ventilator modes are employed. • High-frequency percussive ventilation (HFPV) • prone positioning and • Extracorporeal membrane oxygenation (ECMO
- 19. Targeted therapies • Bronchodilators-β2-adrenergic agonists, salbutamol/ epinephrine • Decrease airway pressure by smooth muscle relaxation and increase • PaO2/FiO2 ratio limiting the degree of bronchospasm. • In addition, epinephrine decreases blood flow to injured/obstructed airways, thus improving V/Q matching.
- 20. Mucolytic agents • N-acetylcysteine(NAC) is a powerful mucolytic
- 21. Anticoagulants • Inhaled anticoagulantshave been used to ameliorate the formation of fibrin casts, which contribute to airway obstruction following inhalation injury.
- 22.
- 23. Systemic toxicities • COhas an affinity for hemoglobin 200 to 250 times greater than oxygen and exposure results in hypoxia and ischemia. • CO displace oxygen from hemoglobin (forming carboxyhemoglobin (COHb)) and binds to cytochrome c oxidase. • COHb shifts the oxygen dissociation curve to the left, ultimately leading to decreased oxygen delivery at the tissue level and interfering with cellular respiration at the mitochondrial level.
- 24. Pneumonia • direct pulmonaryinjury, places the respiratory system at risk for infection • loss of ciliated cells impairs pulmonary immune function • Surfactant production impaired mucociliary transport secondary to damage to airway epithelium. • The development of respiratory tract infection is also effected by decreased function of pulmonary macrophages [
- 25. • Airway obstruction •Subglottic stenosis and other complications