Emergency War Surgery NATO Handbook: Part II: Response of the Body to Wounding: Chapter X: Compensatory and Pathophysiological Responses to Trauma
United States Department of Defense
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Pulmonary vascular changes parallel the systemic circulatory response to trauma. The increase in pulmonary vascular resistance is proportionately greater and more persistent than that seen in systemic vascular beds. Although the etiology of the increase in pulmonary vascular resistance is not fully understood, studies of burn patients suggest that release of vasoactive agents, primarily thromboxane, may play an important role. There appears to be little, if any, change in pulmonary capillary permeability. As a component of the hypermetabolic response to injury, minute ventilation increases significantly as a result of increases in both tidal volume and the respiratory rate. This increase in minute ventilation results in a respiratory alkalosis. Post-injury respiratory alkalosis is appropriate under these circumstances and attempts should not be made to correct it pharmacologically or to suppress the respiratory drive. Hyperventilation can be further aggravated by post-traumatic fever, anemia, or sepsis.
Post-traumatic pulmonary insufficiency can result from penetrating or perforating pulmonary injury, pulmonary contusion secondary to blunt or blast trauma, and smoke inhalation. Aspiration of gastric content is another common cause, especially in the unconscious casualty. Aspiration can result in chemical and/or bacterial pneumonitis. Respiratory insufficiency may also result from the pulmonary edema of excessive fluid resuscitation. Massive blood transfusion, usually greater that ten units over 24 hours, also predisposes to pulmonary insufficiency. The common end result of these divergent pulmonary insults can be the adult respiratory distress syndrome (ARDS). Although the specific pathogenesis of ARDS remains undefined, it has been postulated that activation of the complement system via an alternative pathway causes aggregation and activation of neutrophils, which in turn damage the pulmonary microvasculature resulting in increased vascular permeability.
Clinically relevant ARDS manifests itself by tachypnea and an increased respiratory effort. Pulmonary secretions may be minimal and the breath sounds dry. Pulmonary compliance decreases and pulmonary arteriovenous shunting increases, with a resultant decrease in the PaO2. Characteristically, the decreased PaO2 is relatively unresponsive to increases in the inspired oxygen content (FIO2).
Chest X-ray changes may lag 12-24 hours behind pathophysiological changes. When they appear, one sees diffuse alveolar infiltrates, which commonly progress to complete consolidation.
ARDS therapy usually requires endotracheal intubation, mechanical ventilation, and the maintenance of positive end expiratory pressure (PEEP). Failure to respond to treatment is often related to pulmonary or remote infection. In those cases where treatment fails and the process progresses, the lungs become less compliant and more difficult to ventilate, even with inordinately high inspiratory pressures. In these casualties, the PaO2 progressively falls and the PaCO2 progressively rises, in spite of maximal FIO2 maximal levels of PEEP and maximal inspiratory pressures and rates. Ultimately, the hypoxemia, hypercarbia, and acidosis can result in death; however, the majority of these patients die of sepsis.
Because of the lethal problems associated with ARDS, efforts should be directed at preventing the development of the full-blown syndrome. Prophylactic pulmonary care should include avoidance of overly zealous fluid resuscitation, prevention of aspiration, and frequent pulmonary toilet. In the presence of progressively worsening ARDS requiring very high ventilatory pressures, the surgeon should consider the placement of prophylactic chest tubes. Prompt identification and treatment of both local and remote infections decreases the likelihood of sepsis-realted ARDS. It may be appropriate to choose a more appropriate or effective antibiotic in some cases. Humidification of inspired oxygen concentrations are also major considerations.
The early use of diuretics and parenteral albumin, may reduce pulmonary fluid.
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