Session IX - Femur
Sat, 10/9/04 Femur, Paper #52, 4:22 pm
Detection of Cerebral Fat Embolism in Patients with Femoral Diaphyseal Fractures
Purpose: We determined the role of an intracardiac shunt in the production of cerebral fat embolism in patients with femoral shaft fractures.
Methods: Forty-two adults with femoral shaft fractures admitted to our trauma center were entered into a prospective study. Exclusion criteria included: traumatic brain injury, inability to provide informed consent, and deep venous thrombosis. There were 34 men and 8 women, with a mean age of 29 years (range, 17 to 52). The mechanism of injury was a motor vehicle crash, 30; a fall, 6; gunshot wound, 4; and pedestrian accident, 2. Femoral fractures were classified as OTA 32A, 23; B, 17; and C, 4. Two patients had bilateral fractures, for a total of 44 fractures. Thirty-eight fractures were closed, and 6 were open: grade 1, 1; grade 2, 5. Associated fractures were present in 27 patients.
Transcranial Doppler (TCD) studies of the middle cerebral and basilar arteries were performed preoperatively, during intramedullary nailing of the femoral fracture, and postoperatively. Detection of an intracardiac shunt was performed with a contrasted TCD, with use of a micro bubble technique. All shunts were confirmed with echocardiography. Serial physical examination focused on the symptoms and signs of fat embolism, chest radiographs, and arterial blood gas analysis. Neurologic examination consisted of the NIH Stroke Scale and Folstein Mini-Mental Status administered pre- and postoperatively and repeated as necessary in patients who exhibited mental changes.
Results: The preoperative TCD showed cerebral fat emboli in 33 patients. The intraoperative TCD was positive for cerebral fat emboli in 38 patients, 8 of whom did not show emboli preoperatively. Intramedullary nailing was performed in all fractures. Postoperative TCD was positive in 30 patients. Initial arterial blood gas analysis yielded a mean PO2 = 82 mm, with a range from 35 to 115. Initial chest radiograph was positive in only one patient with a probable pulmonary contusion. Twenty patients developed pulmonary compromise and 7 had some form of central neurologic deficit. All of these patients had other signs consistent with fat embolism. Nineteen patients had positive postoperative TCD studies and pulmonary or neurologic changes. Fourteen patients had an intracardiac shunt, as detected by contrasted TCD; 9 of these had pulmonary compromise. Seven patients had evidence of neurologic changes. Statistical analysis was significant at P <0.0001, for the presence of an intracardiac shunt and neurologic changes. All patients survived with treatment, and gross neurologic recovery was achieved in all.
Discussion and Conclusion: In this study, we prospectively evaluated patients with femoral shaft fractures for cerebral fat embolism and the presence of an intracardiac shunt. Initially, cerebral fat emboli were seen in 33 of 42 patients (79%). The results indicated that these emboli occur soon after femoral fracture and may be produced during intramedullary nailing; 8 patients first developing the emboli intraoperatively. There was a close association between the presence of cerebral fat emboli as seen with TCD and the obvious manifestations of fat emboli syndrome. All neurologic changes were attributable to the fat emboli. Theoretically, an intracardiac shunt would predispose to "paradoxical" embolism because of the more direct route to the systemic circulation. The prevalence of a patent foramen ovale, the most common type of intracardiac shunt, in the general population is approximately 15%. Fourteen of our patients, 33%, were found to have an intracardiac shunt. The major risk factor for cerebral fat embolism is a femoral shaft fracture caused by blunt trauma. The prevalence could not be determined in this study, because not all patients with femoral shaft fractures were enrolled. It can be concluded that the majority of patients will have or develop cerebral fat embolism, and the presence of an intracardiac shunt is a strong predictor for neurologic deficit.