Reduction of neurologic injury after high-risk thoracoabdominal aortic operation. Cerebrospinal fluid drainage reduces paraplegia after thoracoabdominal aortic aneurysm repair: results of a randomized clinical trial. A prospective randomized study of cerebrospinal fluid drainage to prevent paraplegia after high-risk surgery on the thoracoabdominal aorta. Long-term clinical and neurophysiological effects of reconstructive vascular surgery for cerebral ischemia. Prediction and prevention of delayed ischemic dysfunction after aneurysmal subarachnoid hemorrhage and early operation. Randomized pilot trial of postoperative aspirin in subarachnoid hemorrhage. Hormonal effects of thoracic extradural analgesia for cardiac surgery. Can renal dysfunction after infra-renal aortic aneurysm repair be modified by multi-antioxidant supplementation? Failure of fibrinolytic endoventricular treatment to prevent neonatal post-haemorrhagic hydrocephalus. A case-control trial.
Of all aortic operations, thoracoabdominal aortic repairs have the highest risk of spinal cord neurologic injury, manifest by lower limb paraplegia or paraparesis. Cerebrospinal fluid drainage combined with intrathecal papaverine (CSFDr + IP) may reduce the risk and severity of neurologic injury. The objective of this study was to evaluate the effect of CSFDr + IP to prevent neurologic injury after high-risk thoracoabdominal aneurysm repairs.
                We screened 64 patients before operation with descending thoracic or thoracoabdominal aneurysms for possible inclusion in a prospective, randomized study. Thirty-three patients with high-risk type I and II thoracoabdominal aneurysms met inclusion criteria and 17 were randomly assigned to CSFDr + IP and 16 to the control group. The study was terminated early after interim analysis revealed a significant difference.
                Of 64 patients screened, 2 patients died after operation (3.1%, 2/64); both were in the randomized study (6%, 2/33), and neither had a neurologic injury. Neurologic injury developed in 2 CSFDr + IP patients and 7 control patients (p = 0.0392). Control patients also had lower postoperative motor strength scores (p = 0.0340). On multivariate analysis, risk factors for neurologic injury included (p < 0.05) longer cross-clamp time, failure to actively cool with bypass, and postoperative hypotension, whereas CSFDr + IP was protective. Logistic regression showed that CSFDr + IP and active cooling significantly reduced the risk of injury and that the two combined modalities were additive. Of 64 patients screened, only 2 (3%) had a permanent neurologic deficit preventing ambulation.
                For high-risk thoracoabdominal aneurysms, CSFDr + IP was effective in reducing the incidence and severity of neurologic injury. Active cooling may be further additive to CSFDr + IP protection, although this needs to be confirmed in a larger study. Despite the use of various strategies for the prevention of spinal cord ischemia, paraplegia and paraparesis continue to occur after thoracoabdominal aortic aneurysm (TAAA) repair. Although cerebrospinal fluid drainage (CSFD) is often used as an adjunct for spinal cord protection, its benefit remains unproven. The purpose of this randomized clinical trial was to evaluate the impact of CSFD on the incidence of spinal cord injury after extensive TAAA repair.
                After randomization, 145 patients underwent extent I or II TAAA repairs with a consistent strategy of moderate heparinization, permissive mild hypothermia, left heart bypass, and reattachment of patent critical intercostal arteries. The repairs were performed with CSFD (n = 76) or without CSFD (n = 69). In the former group, CSFD was initiated during the operation and continued for 48 hours after surgery. The target CSF pressure was 10 mm Hg or less.
                The two groups had similar risk factors for paraplegia. Aortic clamp time, left heart bypass time, and number of reattached intercostal arteries were also similar in both groups. Thirty-day mortality rates were 5.3% (four patients) and 2.9% (two patients) for CSFD and control groups, respectively (P =.68). Nine patients (13.0%) in the control group had paraplegia or paraparesis develop. In contrast, only two patients in the CSFD group (2.6%) had deficits develop (P =.03). No patients with CSFD had immediate paraplegia. Overall, CSFD resulted in an 80% reduction in the relative risk of postoperative deficits.
                Perioperative CSFD reduces the rate of paraplegia after repair of extent I and II TAAAs. This article is concerned with the study of the effect of several variables, principally that of cerebrospinal fluid drainage, on the incidence of neurologic deficit in a prospective randomized series of patients with extensive aneurysms of the descending thoracic and abdominal aorta (thoracoabdominal type I and II). Forty-six patients had cerebrospinal fluid drainage, and 52 were controls, with a total of 98 available for study. Cerebrospinal fluid pressure was continuously monitored in the former group and pressure maintained less than or equal to 10 mm Hg in 20, less than or equal to 15 mm Hg in 20, and greater than 15 mm Hg in 6 patients during period of aortic clamping. The method of treatment including reattachment of intercostal and lumbar arteries (p = 0.2), temporary atriofemoral bypass during aortic occlusion (p = 0.3), and spinal fluid drainage (p = 0.8) were not statistically significant in reducing the incidence of neurologic deficits. Thus cerebrospinal fluid drainage as we used it, was not beneficial in preventing paraplegia. On appropriate statistical analysis we found that the only significant predictor of delayed deficits was postoperative hypotension (p = 0.006). In a series of patients with unilateral supratentorial ischemia, clinical scores and parameters derived from computer analysis of the EEG and from measurement of the CBF were determined in the first several weeks after the stroke. Seventeen of these patients underwent a carotid-endarterectomy and 15 a STA-MCA bypass operation. Matched control patients were selected from the remaining cases. All patients, including the controls, were eligible for vascular surgery. The measurements were repeated respectively 3 months and 3 years after the first examination. Clinical improvement occurred in all groups. The degree of these clinical changes was similar for operated and non operated cases. EEG changes indicated more improvement in the cases without surgery. Finally, the CBF was remarkably stable in all patients. The overall effects of reconstructive vascular surgery on the recovery after cerebral ischemia appeared to be negligible. Mean hemispheric cerebral blood flow (CBF) was studied after the intravenous administration of xenon-133 in 20 anesthetized patients with aneurysmal subarachnoid hemorrhage. Before early aneurysm operation, repeated CBF measurements were made to evaluate the cerebral vascular reactivity to controlled hyperventilation. Thirteen individuals received intravenous treatment with the calcium channel blocker nimodipine, whereas the other seven patients did not receive such specific antiischemic treatment. Five of the latter patients had an impaired CO2 response, and three showed delayed ischemic deterioration (DID), whereas none of the seven nimodipine-treated patients with impaired CO2 response showed DID. One nimodipine-treated patient with a preserved CO2 response, in whom operation was complicated, developed DID. The observed findings indicate that DID after uncomplicated early aneurysm operation may be associated with an early disturbance of cerebral vasoreactivity. Treatment with nimodipine may counteract the development of DID in patients with an impaired CBF CO2 response. To assess the safety and feasibility of a clinical trial on the effectiveness of acetylsalicylic acid (ASA) in subarachnoid hemorrhage (SAH).
                Several studies have indicated that increased platelet activity might be involved in the pathogenesis of delayed cerebral ischemia (DCI) after SAH.
                Fifty patients who had early surgery (< or =4 days) for a ruptured aneurysm were enrolled in this randomized, double-blind, placebo-controlled trial. Trial medication, consisting of suppositories with 100 mg ASA versus placebo, was started immediately after surgical clipping of the aneurysm and continued for 21 days. End points were functional outcome and quality of life at 4 months, clinical deterioration after operation, development of DCI, hypodense lesion on postoperative CT, and hemorrhagic complications.
                One-third of all patients with aneurysmal SAH were eligible for the trial. Fifteen of 26 patients receiving placebo deteriorated clinically versus 10 of 24 patients receiving ASA; 4 patients in each group deteriorated from DCI. Postoperative hypodensities on CT were observed in 27 patients, distributed equally in both groups. Functional outcome and quality-of-life scores were slightly in favor of patients who had received ASA, but not to a significant degree (p = 0.22). Two patients in the ASA group had an asymptomatic hemorrhagic complication, and one patient in the placebo group had a fatal and another a symptomatic hemorrhagic complication.
                This pilot study shows that a clinical trial of acetylsalicylic acid (ASA) in subarachnoid hemorrhage (SAH) is feasible and probably safe. The effectiveness of ASA on functional outcome and delayed cerebral ischemia has to be studied in a larger trial. We have investigated the hormonal and metabolic effects of thoracic extradural analgesia with bupivacaine in addition to sufentanil 20 micrograms kg-1 in nine patients undergoing coronary artery bypass surgery. A control group received general anaesthesia alone. The catecholamine response was inhibited for 24 h after surgery in patients who had received extradural analgesia, and the cortisol response was suppressed during cardiopulmonary bypass. Blood glucose values were unchanged until 24 h after surgery in the extradural group. There were no significant differences in cardiac index between the two groups of patients, although heart rate and mean arterial pressure decreased before surgery in patients who received extradural analgesia. The benefits of this technique in terms of a reduction in postoperative morbidity remain to be determined. Renal failure after lower torso ischemia is a serious problem, partly caused by hypotension and indirect reperfusion injury. This injury is partly due to the formation of oxygen free radicals by activated neutrophils. This injury results in albuminuria and renal function impairment. There are indications that free radical damage in indirect reperfusion injury can be diminished by administering extra antioxidants before and during reperfusion.
                In this prospective randomised study we have looked at the influence of a multi-antioxidant supplementation on renal function in patients undergoing an elective open infrarenal abdominal aneurysm repair. The patients received either standard treatment (n=22) or standard treatment with additional antioxidants perioperatively (Allopurinol, vitamin E and C, N-acetylcysteine and mannitol). For renal function we have looked at the albumin/creatinine ratio in urine and 24 hr creatinine clearance.
                Despite significantly increased serum total antioxidant capacity, the group receiving extra antioxidants showed no decrease in the albumin/creatinine ratio in urine. There was however a significantly higher creatinine clearance in this group at day 2.
                The results indicate that the diminished renal function after infrarenal aneurysm repair may be influenced by antioxidant therapy. Post-haemorrhagic hydrocephalus is assumed to result from obstruction of the cerebrospinal fluid (CSF) pathways by blood clots and subsequent chronic infiltration with collagen. The aim of this work was to evaluate the possibility of preventing permanent shunt dependence by enhancing the endoventricular fibrinolysis by means of an endoventricular streptokinase infusion in babies affected by posthaemorrhagic ventricular dilation. A case-control trial was carried out in 12 neonates affected by intraventricular haemorrhage and subsequent progressive ventriculomegaly. Six of them were treated with 20,000 U/day of streptokinase infused over 96 h through a percutaneous ventricular catheter. Our results show that the percentage of shunted babies was identical in treated and control patients despite the enhancement of endoventricular fibrinolysis obtained in all treated patients. On the basis of our results we do not recommend intraventricular streptokinase infusion for routine use in post-haemorrhagic ventricular dilatation.
There are limited data supporting the role of CSFD in thoracic and thoracoabdominal aneurysm surgery for prevention of neurological injury. Further clinical and experimental studies are indicated.