PULMONARY PROBLEMS (RESUSCITATION PHASE 0 - 48 hours) Continued

Mediator Activity:

A vast array of mediators are likely involved.  As described, oxidants and oxidant-activated eicosanoid and leukotriene production are known to be present.^31-35   The release of neutrophil proteases may well be involved in the mucosal slough itself.  A group of agents that are described generally as the neuropeptides are also involved.  The neuropeptides produced in the submucosa after airway injury are potent bronchoconstrictors and can increase blood flow and alter permeability.^38-41  The mucosal production of endopeptidases is responsible for neutralizing these agents.  Loss of these agents from mucosal damage by smoke may well lead to an accentuated neuropeptide response. ^38-41  This mechanism is the likely reason for the persistent, sometimes permanent increase in airways irritability and bronchospasm.

TNF, tumor necrosis factor; IL, interleukin

The role of injury to the alveolar capillary membrane remains unclear.^42,43   There is an increase in lung water.⁴²  Retrograde filling of alveoli from an airway edema is a likely explanation, as opposed to an alveolar capillary leak.  This concept is best corroborated by the fact that alveolar edema in humans is not commonly seen in the initial 24 to 36 hr resuscitation period, when large quantities of fluid are infused, especially in the presence of a burn.  It is more likely that a second insult 2 to 3 days post-injury will cause activation of the inflamed lung with a later alveolar capillary leak.  Certainly, clearance of excess parenchymal fluid is impaired due to injured lymphatics in the interstitium from the airway injury.  The lung is therefore more prone to fluid accumulation. 

Alveolar injury leading to atelectasis occurs with severe injury, likely due to altered surfactant.

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