OTA 1997 Posters - Trauma Issues

An Investigation of the Relative Effects of Pulmonary Contusion and Fat Embolism on Pulmonary Pathophysiology

Amr W. ElMaraghy, MD, Emil H. Schemitsch, MD, FRCS(C), Robin R. Richards, MD, FRCS(C), Robert J. Byrick, MD, FRCP(C)

St. Michael's Hospital, Univ. of Toronto, Toronto, Ontario, Canada

Purpose: To determine the individual and synergistic effects of direct lung injury with pulmonary contusion, and indirect lung injury with fat embolism, on pulmonary pathophysiology in a canine model of trauma.

Conclusion: Fat embolism by itself has greater detrimental effects on lung function than pulmonary contusion alone. The combination of pulmonary contusion and fat embolism leads to more severe pulmonary dysfunction than with either lung injury alone.

Significance: Pulmonary dysfunction in a trauma patient population may lead to respiratory failure and significant morbidity and mortality. There appears to be a subpopulation of trauma patients with both direct and indirect lung injury which develop severe respiratory dysfunction for whom early identification and support may be useful.

Summary of Method, Results, and Discussion: Multiply injured trauma patients may suffer pulmonary contusion and/or long bone fractures, which lead to fat embolism. Pulmonary contusion and fat embolism have detrimental effects on pulmonary pathophysiology. The synergistic effect of these forms of direct and indirect lung injury has not been previously investigated. Methods: After a standardized left thoracotomy, twenty-one skeletally mature cross-bred dogs (>25.0 kg) were randomly assigned to three groups; 1) pulmonary contusion (n=7), 2) pulmonary contusion + fat embolism (n=7), 3) fat embolism (n=7). Pulmonary contusion was produced by compressing the left lung in 5 standard locations using a c-clamp and uniform force as determined by piezoelectric force transducer. Fat embolism was produced by reaming the femur and tibia and pressurizing their intramedullary canals. The following outcome parameters were monitored; core body temperature (T), urinary output (UO), peak airway pressure (PawP), systemic blood pressure (BP), pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), arterial oxygen (PaO2), and arterial carbon dioxide (PaCO2). The following outcome parameters were calculated; total thoracic compliance (TTC), alveolar-arterial oxygen gradient (aA), and the ratio of PaO2/FiO2.

Results: Pulmonary contusion alone did not significantly affect PawP, systemic BP, PAP, PCWP, PaO2, PaCO2 or aA gradient. Fat embolism alone did not significantly affect PawP or PaCO2. Fat embolism significantly increased PAP (p=0.0017), PCWP (p=0.0372), and aA gradient (p=0.0022). The combination of pulmonary contusion followed by fat embolism significantly increased PawP (p=0.0187), and this effect persisted for 4 hours (p=0.0480). The largest decrease in PaO2 (p=0.0015), and systemic BP (p=0.0008) was noted with the combination of pulmonary contusion and fat embolism, and the hypotensive effect persisted for 1 hour. Pulmonary contusion and fat embolism significantly elevated PAP (p=0.0085), and this effect persisted for 4 hours (p=0.0201). The greatest elevation in PCWP (p=0.00142), and aA gradient (p=0.0012) was noted with pulmonary contusion and fat embolism. Only the combination of pulmonary contusion and fat embolism caused a significant increase in PCO2 (p=0.0042). TTC was decreased 11.6% by pulmonary contusion alone, 24.2% by fat embolism alone, and 34.6% (p=0.0245) by the combination of pulmonary contusion and fat embolism. PaO2/FiO2 was decreased 9.8% by pulmonary contusion alone, 49.7% by fat embolism alone (p=0.0022), and 61.4% (p=0.0009) by the combination of pulmonary contusion and fat embolism.