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Early recognition and treatment of post‐traumatic pulmonary microembolism

There is a special form of pulmonary dysfunction which most often occurs following massive tissue damage, such as major fractures accompanied by hypovolemia. This syndrome may be appropriately called post-traumatic pulmonary microembolism to distinguish it from other causes of respiratory failure. We believe that pathophysiology is initiated at the time of trauma and consists of platelet aggregation and fibrin deposition in the pulmonary microcirculation caused by release of tissue-thromboplastin products. Whether this acute traumatic pulmonary microembolism will progress to a fully developed post-traumatic pulmonary microembolism with respiratory symptoms depends upon the magnitude and duration of tissue-thromboplastin release and the efficiency of the fibrinolytic system to clear the lungs. The early microembolic effects on the lungs consist mainly of ventilatory derangements with a low ventilation/perfusion ratio; not until a later stage does true shunting of mixed venous blood across fluid-filled alveoli and small airways occur. Frequently determinations of Pao2 and AaDO2 during air breathing (“air-test”) to reveal a low ventilation/perfusion ratio is, therefore, preferable to true shunt determinations in patients who may develop this syndrome; caution must be exercised in giving room air to critically ill patients. These ventilatory variables, combined with frequent platelet counts, allow early recognition of post-traumatic pulmonary microembolism.