OBJECTIVE: Delayed neurologic deficit after thoracoabdominal or thoracic aortic repair is an unusual complication. We previously examined the preoperative risk factors associated with immediate neurologic deficit to consider their relationship to delayed neurologic deficit. In the current study we wanted to determine whether postoperative events influence the likelihood of delayed neurologic deficit, independent of preoperative risk factors. METHODS: We studied postoperative hemodynamics and cerebrospinal fluid (CSF) drain function in patients who had delayed neurologic deficit (cases) and those who did not (controls). Our database contains data for 854 patients with descending thoracic and thoracoabdominal aortic aneurysm. Cases and controls were identified with a random number generator to select controls in an approximate 4:1 ratio. We identified 18 cases and 67 controls. Further data were obtained from medical records. RESULTS: We found no differences between the groups with regard to oxygen transport abnormalities, eg, pneumothorax, repeat intubation, cardiac arrest, atrial or ventricular dysrhythmia, or dialysis. Significant differences between the groups were present for CSF drain complications (eg, kinks, blood in CSF): 6 of 18 (33%) in the case group versus 3 of 67 (4.5%) in the control group (P <.003). Wide fluctuation in mean arterial pressure (MAP) was significant (P <.02), mainly because of very low MAP in the cases (P <.006). When odds ratio was adjusted for preoperative risk factors of extent II thoracoabdominal aortic aneurysm, acute aortic dissection, and chronic aortic dissection, MAP less than 60 mm Hg and CSF drain complications produced the highest odds of delayed neurologic deficit. CONCLUSION: No single risk factor explained the onset of delayed deficit. Rather, a combination of factors, especially lowest MAP and drain complications, produced the highest odds of deficit. Vigilant optimization of hemodynamics and immediate correction of CSF drain malfunction may prevent development of delayed neurologic deficit.
OBJECTIVE:Delayed neurologic deficit after thoracoabdominal or thoracic aortic repair is an unusual complication. We previously examined the preoperative risk factors associated with immediate neurologic deficit to consider their relationship to delayed neurologic deficit. In the current study we wanted to determine whether postoperative events influence the likelihood of delayed neurologic deficit, independent of preoperative risk factors. METHODS: We studied postoperative hemodynamics and cerebrospinal fluid (CSF) drain function in patients who had delayed neurologic deficit (cases) and those who did not (controls). Our database contains data for 854 patients with descending thoracic and thoracoabdominal aortic aneurysm. Cases and controls were identified with a random number generator to select controls in an approximate 4:1 ratio. We identified 18 cases and 67 controls. Further data were obtained from medical records. RESULTS: We found no differences between the groups with regard to oxygentransport abnormalities, eg, pneumothorax, repeat intubation, cardiac arrest, atrial or ventricular dysrhythmia, or dialysis. Significant differences between the groups were present for CSF drain complications (eg, kinks, blood in CSF): 6 of 18 (33%) in the case group versus 3 of 67 (4.5%) in the control group (P <.003). Wide fluctuation in mean arterial pressure (MAP) was significant (P <.02), mainly because of very low MAP in the cases (P <.006). When odds ratio was adjusted for preoperative risk factors of extent II thoracoabdominal aortic aneurysm, acute aortic dissection, and chronic aortic dissection, MAP less than 60 mm Hg and CSF drain complications produced the highest odds of delayed neurologic deficit. CONCLUSION: No single risk factor explained the onset of delayed deficit. Rather, a combination of factors, especially lowest MAP and drain complications, produced the highest odds of deficit. Vigilant optimization of hemodynamics and immediate correction of CSF drain malfunction may prevent development of delayed neurologic deficit.