Session VII - Polytrauma

Sat, 10/9/04 Polytrauma, Paper #36, 10:30 am

The Early Response to Major Trauma and Intramedullary Nailing

Tim O. White, MD (*); Edward Clutton (*);
Mike C. Robinson, MD (*); James Christie, MD (*);
Royal Infirmary of Edinburgh, Edinburgh, United Kingdom

Purpose: Major trauma causes fat embolism and activation of the coagulation and inflammatory cascades. This "stress response" may lead to adult respiratory distress syndrome and multiple organ dysfunction, with substantial morbidity and mortality. Previous studies that used animal models were based upon the instrumentation of intact or osteotomized bones. This approach both circumvents crucial steps in injury physiology and alters the biomechanical environment, and it may also invalidate the conclusions reached. We report the nature of the early stress response in an ovine model of high-energy injury which more closely replicates the clinical situation of major trauma. Our hypothesis was that the immediate stress response to trauma is characteristic, and its magnitude is governed by the initial injury and subsequent surgical management.

Methods: A novel model was developed centered on a pneumatic actuator that delivered an instantaneous thrust of 8500 N, creating severe injuries comprising comminuted long bone fractures with overlying soft tissue damage. Three groups of seven anesthetized sheep were studied. One group received comminuted fractures of both femora and tibiae. In the second group, sheep were subjected to the same injuries, and the fractures were then surgically stabilized by reamed intramedullary nailing. A third (control) group underwent anesthesia only. Invasive hemodynamic monitoring, transesophageal echocardiography, and repeated blood sampling were used to study the physiologic response.

Results: An immediate significant trophotropic (depressant) hemodynamic response was observed, with heart rate falling by a mean of 13 beats per minute and systolic blood pressure falling 8 mm Hg within 30 seconds of injury. Central venous and pulmonary arterial pressures fell 1.9 and 3.2 mm Hg, respectively, within 5 minutes of injury (all P <0.001), becoming progressively more depressed and remaining so for the remainder of the procedure. Fat embolism, seen on a transesophageal echocardiogram, was significantly greater at the time of injury than during subsequent reaming or nailing (P <0.01), and was no greater on pulmonary histologic examination after injury and nailing than after injury alone. Both inflammatory and coagulation systems were activated by injury, with significant decreases in the levels of fibrinogen and antithrombin III (by 35% and 40%, respectively, P <0.05) following fracture, with no significant additional activation by surgery.

Conclusion: We have developed the first large-animal model replicating the clinical situation of major orthopaedic trauma and have demonstrated that the initial response to severe injury is characteristic and consistent. It is unlike that reported by previous animal research in this field with use of uninjured models. Early surgical stabilization by intramedullary nailing did not result in significant further amplification of the stress response.

Significance: The safety of treating long bone fractures in the severely injured patient by intramedullary nailing has been questioned, and the role of "damage control" orthopaedic techniques is debated. Previous data based on animal models may be invalid because of methodologic weaknesses. A better understanding of the trophotropic response to trauma may have implications for the resuscitation of hypotensive patients.