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Pathophysiology

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An inhalation injury from heat or chemicals causes the release of inflammatory mediators locally within the lung. These diffuse locally to increase:

  • airway resistance
  • bronchospasm
  • pulmonary artery blood flow
  • increase capillary transudation

The net result of these processes is a mismatch of perfusion and ventilation within the lungs. Interstitial oedema can progress to alveolar oedema. The lungs become stiff and this increases the work of breathing. Also, stiffness makes it harder to ventilate the patient with an increased likelihood of barotrauma.

The exudate is rich in fibrinogen and fibrin can form within the smaller airways. Fibrin casts plug the bronchioles and this predisposes to distal collapse and infection. After approximately three weeks, a pseudomembrane forms within the respiratory tree. Interstitial fibrosis may be the longterm sequel with a restrictive lung defect.


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