Postinjury serum secretory phospholipase A2 correlates with hypoxemia and clinical status at 72 hours

Although trauma patients often suffer direct lung damage, an equally destructive mechanism of lung injury involves postinjury systemic inflammation. We postulate that secretory phospholipase A(2) (sPLA(2)) release induced by trauma relates to systemic inflammation that compromises both lung function and clinical status after injury. The objectives of this study were: to relate Injury Severity Score to postinjury sPLA(2); to determine whether circulating sPLA(2) relates to pulmonary oxygenation and compliance; and to determine whether early or persistent increases in sPLA(2) are associated with abnormal chest x-ray at 72 hours after injury.

The prospective cohort study comprised 54 consecutive intensive care admissions in patients with traumatic injury admitted over a 6-month period from November 1, 1996, to May 1, 1997.

Postinjury peak sPLA(2) values were associated with increased ISS (r = 0.49, r(2) = 0.24, p < 0.001). Patients with elevated sPLA(2) had poor oxygenation compared with those with normal sPLA(2) levels (Pa0(2)/Fi0(2) ratio 164 +/- 16 versus 260 +/- 26 mmHg [mean +/- SEM], p < 0.01) and also required additional PEEP (5.5 +/- 0.9 versus 2.5 +/- 0.4 cm H(2)O, p = 0.01). Secretory PLA(2) levels in patients with abnormal chest x-ray 72 hours after injury were higher (1.08 +/- 0.2 versus 0.34 +/- 0.1 activity units, p < 0.001) than levels seen in patients with normal x-rays.

Increasing injury magnitude is associated with elevated sPLA(2) levels, and increased sPLA(2) is related to postinjury hypoxemia and clinical status.