Postoperative Neurological Injury Research Articles

Stroke rate is markedly reduced after carotid endarterectomy by avoidance of protamine

Postoperative neurologic injury remains a significant risk of carotid endarterectomy. Mechanisms include embolization of debris and formation of thrombus on the newly endarterectomized surface. We hypothesized that the risk of postoperative neurologic injury would be lower in those patients who did not receive protamine for reversal of heparin anticoagulation. We reviewed 348 consecutive primary carotid endarterectomies performed since January 1, 1986, to determine the relationship between surgical outcomes and reversal of heparin anticoagulation. Patients undergoing additional simultaneous cardiovascular procedures were excluded. One hundred ninety-three patients received protamine after completion of the endarterectomy. The remaining 155 patients did not receive any protamine. All patients in both groups survived to discharge. There were no strokes in those patients who did not receive any protamine; however, the stroke rate in the protamine group was 2.6% (5 of 193), p < 0.045. The incidence of hematoma requiring reexploration was 1.0% (2 of 193) and 1.9% (3 of 155) in the protamine and no-protamine groups, respectively (p = NS). Intraoperative shunting was used more frequently in the no-protamine group (84% vs 67%, p < 0.001), and patch angioplasty was performed more frequently in the protamine group (35% vs 15%, p < 0.001). However, neither shunting nor patching significantly influenced stroke rates. We conclude that carotid endarterectomy without reversal of heparin anticoagulation is associated with a reduced postoperative stroke rate without a significant increase in morbidity rates.

Systemic gaseous microemboli during left atrial catheterization: A common occurrence?

Gaseous microemboli during cardiac surgery have been implicated as a potential cause of postoperative neurologic injury. Any monitoring technique that exposes the systemic circulation to atmospheric pressure could introduce gaseous microemboli, causing cerebral microembolization. The incidence of carotid artery gaseous microemboli was studied during left atrial catheter insertion. Prospective clinical study. Tertiary care university hospital. Twelve patients undergoing elective cardiac surgery. Perioperatively, a 5-MHz continuous wave Doppler probe was positioned over the left carotid artery to maximally record blood flow signals. The criteria used for detecting a gaseous microembolus were a sudden increase in the amplitude of the visual signal by 30% and a characteristic audible sound. Numbers of microemboli at three timepoints (before and during left atrial catheter insertion and during catheter flushing) were assessed using the Friedman test. No emboli were detected before left atrial catheter insertion. When compared with the preinsertion time period, statistically (p < 0.05) significant numbers of gaseous microemboli were found in six patients during catheter insertion (3 +/- 1 microemboli; range 1 to 7 microemboli) and in five patients during catheter flushing (5 +/- 2 microemboli; range 1 to 12 microemboli). There was a tendency for patients with lower filling pressures to entrain more microemboli during insertion (r = 0.44; p = 0.149). No patient showed evidence of gross neurologic dysfunction postoperatively, although sensitive neurologic testing was not performed. Left atrial catheter insertion and flushing can cause systemic gaseous microemboli in more than 50% of patients. Although the number of microemboli introduced is relatively small, extreme care should be used during left atrial catheter insertion.

Preoperative spinal artery localization and its relationship to postoperative neurologic complications.

To evaluate the risk of spinal cord revascularization and ascertain the relationship between preoperative spinal arteriography and the frequency of postoperative neurologic injury and overall morbidity and mortality in patients who require surgical repair of thoracoabdominal aortic aneurysms. Fifty patients scheduled for surgical repair of a thoracoabdominal aortic aneurysm underwent spinal arteriography. All patients were divided into a positive spinal artery group (in which the spinal artery was identified) or negative spinal artery group (in which the spinal artery was not identified) and further divided based on extent of disease. The complication rate of spinal arteriography was 4.6%; no patient had a permanent neurologic injury. No significant difference existed between the positive and negative spinal artery groups in occurrence of neurologic injury (P = .88) or combined morbidity and mortality (P = 51). Patients who require spinal cord revascularization do not have greater frequency of neurologic injury or overall morbidity and mortality than those without this requirement. Spinal arteriography enables definitive spinal cord revascularization and thereby reduces the risk of neurologic injury.

Neurological sequelae of regional anaesthesia

Postoperative neurological injury after regional anaesthesia is more often due to improper positioning or the surgical procedure itself rather than to the regional anaesthetic. Underlying disease processes (prolapsed intervertebral disc, spinal angioma, multiple sclerosis) can cause exacerbations after regional or general anaesthesia. When a postoperative deficit occurs, a systematic investigation is essential to determine the cause, initiate treatment and determine the prognosis. A detailed history of the patient's prior medical history and symptoms associated with underlying disease processes is important. Careful physical examinations to determine the neurological involvement and to assess daily improvement or worsening of symptoms is also necessary. Laboratory evaluations (glucose tolerance test, coagulation profile, complete blood count (CBC), lumbosacral spine films, computed tomography and EMG studies) should also be obtained as indicated. Knowledge of the regional anaesthetic techniques and of the local anaesthetic drugs used is essential for the patient's safety and for a smooth anaesthetic course.

Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta: I. Relationship of aortic cross-clamp duration, changes in somatosensory evoked potentials, and incidence of neurologic dysfunction

To determine if intraoperative monitoring of somatosensory evoked potentials detects spinal cord ischemia, we subjected 21 dogs to aortic cross-clamping distal to the left subclavian artery. Group I animals (short-term studies, n = 6) demonstrated decay and loss of somatosensory evoked potentials at 8.5 +/- 1.1 minutes after aortic cross-clamping. During loss of somatosensory evoked potentials, significant decreases in spinal cord blood flow occurred in cord segments below T6. Significant reactive hyperemia occurred without normalization of somatosensory evoked potentials after reperfusion. Fifteen Group II animals (long-term studies) were studied to determine the relationship between duration of spinal cord ischemia (evoked potential loss) and subsequent incidence of paraplegia. Extension of aortic cross-clamping for 5 minutes after loss of somatosensory evoked potentials in six dogs resulted in no paraplegia (mean cross-clamp time 12.7 +/- 0.6 minutes). Prolongation of aortic cross-clamping for 10 minutes after evoked potential loss in nine dogs (mean cross-clamp time 17.6 +/- 0.6 minutes) resulted in a 67% (6/9) incidence of paraplegia 7 days postoperatively (p = 0.02 versus 10 minutes of aortic cross-clamping). These findings demonstrate that simple aortic cross-clamping uniformly results in spinal cord ischemia and that such ischemia is detectable by monitoring of somatosensory evoked potentials. Duration of ischemia, as measured by the time of evoked potential loss during the cross-clamp interval, is related to the incidence of postoperative neurologic injury.