Reconstructive surgery in 59-year-old patient with coarctation of aorta under the monitoring of somatosensory evoked potential and spinal cord perfusion pressure]

Postoperative paraplegia is a relatively rare complication in reconstructive surgery for coarctation of the aorta and the operative treatment is usually performed without any adjuncts. A 59-year-old male patient underwent replacement of descending thoracic aorta with vascular prosthesis under the monitoring of SEP and spinal cord perfusion pressure (SCPP) [pressure difference between mean distal aortic pressure (MDAP) and the cerebrospinal fluid pressure (CSFP)]. During cross-clamping of the aorta, MDAP decreased from 61 to 40 mmHg and CSFP increased from 6 to 15 mmHg, SCPP was 25 mmHg, and the amplitude of the SEP waves rapidly decreased. As the ischemic changes of spinal cord were suspected, the aortic cross-clamping was released. The amplitude of SEP recovered to the preoperative level immediately after de-clamping. In order to prevent spinal cord ischemia, the partial cardio-pulmonary bypass was employed, and SCPP was maintained above 60 mmHg, so that SEP did not show any ischemic changes during cross-clamping of the aorta. The patient did not develop any neurological deficit postoperatively. The monitoring of SEP and SCPP appears to be useful for prevention of postoperative paraplegia in the surgical treatment for coarctation of the aorta.     

Prevention and detection of spinal cord injury during thoracic and thoracoabdominal aortic repairs

BACKGROUND: Spinal cord injury is a most dreaded and unpredictable complication. In this study, based on our experimental results in dogs and early clinical results, we reviewed the incidence of paraplegia and the detection of spinal cord injury. METHODS: Eighty-two patients who underwent elective surgical repair of the descending thoracic and thoracoabdominal aorta over 17 years were subjects for this study. Sixty-two patients were male and 20 were female. Their mean age was 61.6 years (range, 17 to 81 years). Monitoring somatosensory evoked potentials (SEP) and measurement of mean distal aortic pressure and cerebrospinal fluid pressure were performed perioperatively. RESULTS: Sixty patients had no ischemic change in SEP. In 17 patients with significant ischemic changes of SEP, SEP recovered by increasing spinal cord perfusion pressure to more than 40 mm Hg. Two patients with complete loss of SEP experienced paraplegia. One patient had delayed paraplegia. CONCLUSIONS: These results strongly suggest that SEP, mean distal aortic pressure, cerebrospinal fluid pressure should be monitored during aortic cross-clamping. Maintaining spinal cord perfusion pressure at more than 40 mm Hg by increasing mean distal aortic pressure or withdrawal of cerebrospinal fluid is valuable for preventing paraplegia.     

Somatosensory evoked potentials and spinal cord perfusion pressure are significant predictors of postoperative neurologic dysfunction

Paraplegia after thoracoabdominal aneurysm repair can occur in 3% to 40% of patients. This study investigated the efficacy of cerebrospinal fluid (CSF) drainage to protect the spinal cord during aortic cross-clamping (AXC) and the interrelationship between drainage, spinal cord perfusion pressure (SCPP), and changes in somatosensory evoked potentials (SEP) in a canine model of spinal cord ischemia. SCPP was defined as the mean distal aortic pressure minus the CSF pressure. In the experimental group, CSF was drained before AXC. SEP changes were quantitated as time to latency increase of 10% (L-10) and time to complete SEP loss. Drainage of CSF had no significant effect on the distal aortic pressure but significantly increased SCPP from 9.4 to 21.8 mm Hg and decreased the incidence of postoperative neurologic injury. Ischemic SEP changes were highly significant predictors of postoperative neurologic injury, occurring more than two times earlier in the paralyzed and paraparetic animals. Dogs without neurologic injury had significantly higher SCPP, delayed L-10 time, and delayed SEP loss.     

Prevention of spinal cord injury after cross-clamping of the thoracic aorta

Paraplegia has been a devastating and unpredictable complication following cross-clamping of the thoracic aorta. In this study, the effect of the pressure gradient between the aortic pressure distal to occlusion and cerebrospinal fluid pressure (CSFP), defined as relative spinal cord perfusion pressure (RSPP), on the development of spinal cord injury was investigated. In 32 mongrel dogs, the thoracic aorta just distal to the left subclavian artery was cross-clamped. After a complete loss of somatosensory evoked potentials (SEP) had been confirmed, the dogs were divided into six groups by an additional cross-clamp interval and RSPP as follows: Group I (n = 6): 0 mmHg for 10 minutes; Group II (n = 8): 0 mmHg for 20 minutes; Group III (n = 3): 7.5 mmHg for 20 minutes; Group IV (n = 3): 7.5 mmHg for 40 minutes; Group V (n = 6): 15 mmHg for 40 minutes and Group VI (n = 6): 15 mmHg for 60 minutes. RSPP was adjusted by either withdrawal of cerebrospinal fluid or injection of normal saline solution into the subarachnoid space. SEP were generated by the stimulation of bilateral peroneal nerves. The incidence of postoperative paraplegia was 0% in Groups I and V, 33% in Group III, 50% in Group VI and 100% in Groups II and IV. This study showed that RSPP plays an important role in the development of spinal cord injury during cross-clamping of the thoracic aorta. Therefore, RSPP should be maintained at as high a level as possible in order to prevent spinal cord injury even if SEP disappear during aortic occlusion.     

Prevention of spinal cord injury after cross-clamping of the thoracic aorta

Paraplegia has been a devastating and unpredictable complication following surgical procedures involving temporary occlusion of the thoracic aorta. This study was undertaken to determine the effect of the pressure gradient between the aortic pressure distal to the occluding aortic clamp and cerebrospinal fluid pressure, defined as “Relative spinal cord perfusion pressure” (RSPP) on the development of the ischemic spinal cord injury. In twelve mongrel dogs, the thoracic aorta just distal to the left subclavian artery was cross-clamped. Somatosensory evoked potentials (SEP) were generated by peripheral stimulation of the bilateral peroneal nerves. After complete loss of SEP was evident, six dogs, Group 1, were subjected to occlusion of the descending thoracic aorta for a period of 20 minutes with maintenance of 0 mmHg of RSPP, by an injection of normal saline into the subarachnoid space. Six other dogs, Group 2, likewise underwent 40 minutes of aortic occlusion, keeping the RSPP at 15 mmHg by withdrawal ofcerebrospinal fluid. All the dogs in Group 1 developed paraplegia, whereas all the dogs in Group 2 demonstrated complete postoperative recovery without any neurological sequelae. Thus, RSPP is a most important factor in the development of the ischemic spinal cord injury during the temporary thoracic aortic occlusion.     

Effect of Cerebrospinal Fluid Drainage and/or PartiaI Exsanguination on Tolerance to Prolonged Aortic Cross-Clamping

Paraplegia as a consequence of spinal cord ischemia associated with procedures on the thoracic and thoracoabdominai aorta has been linked to the interaction of proximal hypertension with elevated cerebrospinal fluid pressure (CSFP) during aortic cross-clamping (AXC). CSFP reduction via cerebrospinal fluid (CSF) drainage is thought to significantly prolong the cord's tolerance to AXC. Likewise, partial exsanguination is reported to effectively reduce ischemic injury by controlling proximal hypertension. To evaluate the individual and collective efficacy of both techniques, 18 mongrel dogs (25 to 35 kg), divided into three equal groups, underwent a fourth interspace left thoracotomy AXC. Baseline proximal arterial blood pressure (PABP), distal arterial blood pressure (DABP), and CSFP were established and monitored at 5-minute intervals during 120 minutes of AXC, and for 30 minutes thereafter. Group I animals were partially exsanguinated prior to AXC to maintain PABP at a mean of 115 to 120 mmHg. Group II animals had sufficient (16 ± 5 cc) CSF withdrawn to maintain a DABP-CSFP gradient, i.e., spinal cord perfusion pressure (SCPP) of 20 mmHg. Group III animals were treated with both CSF drainage and partial exsanguination in the same manner as groups I and II, respectively. Periop-erative somatosensory evoked potential (SEP) monitoring evaluated cord function. Postoperative neurological outcome was assessed with Tariov's criteria. SEPs degenerated approximately 22 minutes following AXC for groups II and III. In contrast, group I exhibited rapid (10 ± 7 min) SEP loss. All five surviving group I animals displayed paralysis 48 hours postopera-tively. Mean PABP was significantly higher in group II (155 ±18 mmHg) than in either group 1 (117 ± 9 mmHg) or Ill (120 ± 14 mmHg) (p < 0.001). CSFP was significantly higher in group I (14 ± 4 mmHg) than in either group II or III (5 ± 2 mmHg) (p < 0.0001). The only parameter associated with neurological injury was low SCPP, which inversely correlated with CSF dynamics. Group I animals, with a mean SCPP of 4.6 mmHg, exhibited paraplegia, while groups II and Ill, with SCPP values above 20 mmHg, were free of neurological injury. Proximal hypertension did not play a role in cord injury. This study underscores the potential of CSF drainage to protect the ischemic spinal cord. (J Card Surg 7994;9:637–637)     

Current strategies of spinal cord protection during thoracoabdominal aortic surgery

Despite improved survival rates after thoracoabdominal aortic aneurysm repairs, paraplegia remains a devastating complication with high incidence, ranging from 3 to 10%. Ischemic insults to the spinal cord are unavoidable during thoracoabdominal aortic aneurysm repairs. There is no single measure that can prevent paraplegia alone. A multimodality approach is required to minimize the ischemic insults during thoracoabdominal aortic aneurysm repairs and postoperative second hit to the spinal cord. Distal aortic perfusion is important to maintain the collateral network perfusion pressure, while cerebrospinal drainage allows to directly maintain the spinal cord perfusion. Reattachment of segmental arteries T8–T12 is encouraged to lower the incidence of both immediate and delayed paraplegia. Systemic arterial pressure should be maintained above 130 mmHg and cerebrospinal drainage should be continued until the second postoperative day, despite intact neurological status. In this article, we describe our current operative techniques and perioperative management in patients undergoing repairs of thoracoabdominal aortic aneurysm. A review of recent updates on spinal protection strategies is also reported.     

Prevention of spinal cord ischemia after thoracic aortic occlusion

Paraplegia has been a devastating and unpredictable complication following surgical procedures necessitating temporary occlusion of the thoracic aorta. This study was undertaken to investigate the effect of the pressure gradient between the aortic pressure distal to the occlusion and cerebrospinal fluid pressure (CSFP), defined as "Relative spinal cord perfusion pressure" (RSPP) on the development of ischemia to the spinal cord by using somatosensory evoked potentials (SEP). In 30 mongrel dogs, the thoracic aorta just distal to the left subclavian artery was occluded for either 30 or 120 minutes until SEP disappeared. RSPP was maintained at 20, 30 or 40 mmHg in each dog by adjusting the degree of occlusion of th aorta and/or changing CSFP by withdrawal of cerebrospinal fluid or injection of normal saline into the subarachnoid space. SEP were recorded as a cortical response to the electrical stimulation of bilateral peroneal nerves. SEP did not disappear for 30 or 120 minutes when RSPP was 40 mmHg. It would be concluded that 40 mmHg or higher of RSPP is necessary in order to prevent the spinal cord ischemia due to the temporary occlusion of the thoracic aorta.     

Cerebrospinal fluid drainage and steroids provide better spinal cord protection during aortic cross-clamping than does either treatment alone

We investigated whether intravenous methylprednisolone (30 mg/kg) before 30 minutes of aortic cross-clamping and after 4 hours could enhance the effects of cerebrospinal fluid drainage on spinal cord perfusion pressure and postoperative paraplegia when proximal blood pressure was controlled with sodium nitroprusside and partial exsanguination. Dogs were randomized into three groups: group 1 (n = 6), control; group 2 (n = 7), steroids; and group 3 (n = 6), steroids with cerebrospinal fluid drainage. During aortic cross-clamping, blood pressure proximal to the clamp decreased significantly in each group compared with baseline (p less than 0.05), but did not differ among groups (group 1 = 82.2, group 2 = 82.1, group 3 = 86.6 mm Hg, p greater than 0.05). Mean distal pressure decreased from systemic values to 8.4, 8.5, and 3.7 mm Hg, respectively, after aortic cross-clamping (p less than 0.05); these values did not differ from one another (p greater than 0.05). During aortic cross-clamping, cerebrospinal fluid pressure in groups 1 and 2 did not differ significantly compared with baseline (12.2 versus 8.2, 14.2 versus 10.7 mm Hg, p greater than 0.05), whereas in group 3 the baseline cerebral spinal fluid pressure of 10.7 mm Hg decreased to 0.4 mm Hg (p less than 0.05). Spinal cord perfusion pressure in group 3 was significantly higher than in groups 1 and 2 (3.3 versus -3.9 and -5.7 mm Hg, p less than 0.05), but did not differ between groups 1 and 2 (p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

A study of spinal cord ischemia during aortic cross-clamp--evoked spinal cord potential and histological analysis of the spinal cord

The relationship between the evoked spinal cord potential (ESP) and the histological findings of the spinal cord after thoracic aortic cross-clamp was studied. Thoracic aorta was cross-clamped in 23 dogs and ESP was monitored before, during, and after cross-clamping. Incidence of paraplegia and histological findings were studied after the dogs recovered from the procedure. Aortic cross-clamp was maintained for 60 minutes in 20 dogs (Group A). And cross-clamp was released 10 minutes after the amplitude of ESP became lower than 20% of control in 3 dogs. (Group B). In group A, three types of ESP changes were detected; ESP became lower or lost during cross-clamping in type 1 response, ESP remained unchanged in type 2 response, and ESP returned after transient loss during cross-clamping in type 3 response. Four of five dogs with type 1, none of nine with type 2, two of five with type 3 response showed paraplegia. One of the dogs with type 2 response showed paraparesis. ESP could not detected in one dog, in which traumatic spinal cord injury during laminectomy caused paraplegia. In Group B, all dogs showed type 1 response and paraplegia. Characteristic histological finding of the spinal cords of the dogs with paraplegia was the ischemic necrosis mainly in the gray matter. Necrotic foci were limited in the posterior horn in mild, in the anterior and posterior horn in moderate changes. And neurons were lost in entire gray matter in severe histological changes. In the spinal cords of the dogs with spastic paraplegia, severe histological changes were limited in the lower lumbar region.(ABSTRACT TRUNCATED AT 250 WORDS)     

Development of spinal cord ischemia after clamping of noncritical segmental arteries in the pig.

BACKGROUND: Blood flow to the thoracolumbar spinal cord is thought to be critically dependent on the arteria radicularis magna. We investigated whether spinal cord blood supply becomes dependent on other, noncritical, segmental arteries if spinal cord perfusion pressure (SCPP) is decreased. The SCPP is equal to the mean arterial pressure (MAP) minus the cerebrospinal fluid (CSF) pressure (SCCP = MAP - CSF). METHODS: The thoracoabdominal aorta was exposed in 10 pigs. Functional integrity of spinal cord motor pathways was assessed with myogenic motor-evoked potentials after transcranial electrical stimulation (tc-MEPs). Using this technique, a group of segmental arteries not critical for spinal cord blood supply was identified. Before, during, and after clamping of the noncritical segmental arteries, spinal cord ischemia was produced by decreasing SCPP by means of increasing CSF pressure, and the SCPP threshold at which tc-MEPs showed evidence of spinal cord ischemia was determined. Ischemic SCPP thresholds, obtained during and after clamping of the noncritical segmental arteries, were compared with the ischemic threshold obtained before clamping (control value). RESULTS: Before noncritical segmental arteries were clamped, ischemic tc-MEP changes occurred when the SCPP was below 15 +/- 5 (SD) mm Hg. With a total of 9 +/- 3 (SD) segmental arteries clamped, the ischemic SCPP threshold was 48 +/- 14 mm Hg (p < 0.01). After the release of all clamps, ischemia occurred at a SCPP of 15 +/- 5 (SD) mm Hg. CONCLUSIONS: In this porcine experiment, clamping of originally noncritical segmental arteries significantly reduced the tolerance of the spinal cord to a decrease in SCPP.     

Mild hypothermia protects the spinal cord from ischemic injury in a chronic porcine model.

OBJECTIVES: During thoracoabdominal aortic aneurysm repair, prolonged compromise of spinal cord blood supply can result in irreversible spinal cord injury. This study investigated the impact of mild hypothermia during aortic cross-clamping on postoperative paraplegia in a chronic porcine model. METHODS: The thoracic aorta was exposed and cross-clamped in 30 juvenile pigs (20-22 kg) for different intervals at normothermia (36.5 degrees C), and during mild hypothermia (32.0 degrees C). Three pigs were evaluated at each time and temperature. Myogenic motor-evoked potentials (MEPs) were monitored, and postoperative recovery evaluated using a modified Tarlov score. RESULTS: There were no significant hemodynamic or metabolic differences between individual animals, and the groups had equivalent arterial pressures (mean 64.3+/-3.6 mmHg). Time to recovery of MEPs correlated with severity of injury; all animals with irreversible MEP loss suffered postoperative paraplegia. At normothermia, animals with 20 min of aortic cross-clamping emerged with normal motor function, but those cross-clamped for 30 min suffered paraplegia. With mild hypothermia, animals tolerated 50 min of aortic cross-clamping without evidence of neurologic injury, but were all paraplegic after 70 min of ischemia. Animals appeared to recover normal motor function after 60 min of aortic cross-clamping at hypothermia initially, but exhibited delayed-onset paraplegia 36 h postoperatively. CONCLUSIONS: Our observations indicate that mild hypothermia dramatically increases the tolerance of the spinal cord to ischemia in the pig, and therefore suggests that cooling to 32.0 degrees C should be encouraged during surgery which may compromise spinal cord blood supply. An ischemic insult of borderline severity may result in delayed paraplegia.     

Assessment of spinal cord integrity during thoracoabdominal aortic aneurysm repair

BACKGROUND: Monitoring motor-evoked potentials (MEPs) is an accurate technique to assess spinal cord integrity during thoracoabdominal aortic aneurysm (TAAA) repair, guiding surgical strategies to prevent paraplegia. METHODS: In 210 consecutive patients with type I (n = 75), type II (n = 103), and type III (n = 32) TAAA surgical repair was performed using left heart bypass, cerebrospinal fluid drainage, and MEPs monitoring. RESULTS: Reliable MEPs were registered in all patients. The median total number of patent intercostal and lumbar arteries was five. After proximal aortic crossclamping, MEP decreased below 25% of base line in 72 patients (34%) indicating critical spinal cord ischemia, which could be corrected by increasing distal aortic pressure. By using sequential clamping it appeared that in 43% of type I and II cases spinal cord circulation was supplied between T5 and L1, and 57% between L1 and L5. In type II and III cases cord perfusion was dependent upon lower lumbar arteries in 16% and pelvic circulation in 8%, necessitating reattachment of these segmental arteries. In 9% of patients critical ischemic MEP changes occurred without visible arteries, requiring aortic endarterectomy and selective grafting. One patient suffered early paraplegia and 2 delayed, and 2 patients had temporary neurologic deficit (5 of 210; 2.4%). CONCLUSIONS: In patients with TAAA, blood supply to the spinal cord depends upon a highly variable collateral system. Monitoring MEPs is an accurate technique for detecting cord ischemia, guiding surgical tactics to reduce neurologic deficit (2.4%).     

Direct measurements of oxygen tension on the spinal cord surface of pigs after occlusion of the descending aorta

Spinal cord injury is the most dreaded complication of operative procedures on the descending aorta. Our previous experimental study on pigs indicated that an increase in the cerebrospinal fluid pressure after aortic cross-clamping did not influence the occurrence of spinal cord injury. We therefore concluded that the cause of spinal cord injury after aortic cross-clamping is due to primary oxygen deficiency in the spinal cord distal to the occlusion site, especially in the area supplied by the artery of Adamkiewicz. The aim of the present study is to examine the primary ischemic cause of spinal cord injury after aortic cross-clamping by directly measuring the oxygen tension on the spinal cord surface in pigs. During the occlusion phase, oxygen tension decreased significantly distal to the clamping site and especially in the areas supplied by the artery of Adamkiewicz both after occlusion of the high thoracic (Group I) and the lumbar aorta (Group II). The marked decrease in oxygen tension proves that hypoxia is the primary reason for spinal cord injury. The presence of a "steal phenomenon" should be discussed.     

Appraisal of cerebrospinal fluid alterations during aortic surgery with intrathecal papaverine administration and cerebrospinal fluid drainage

We have previously described a technique for intrathecal administration of papaverine and cerebrospinal fluid drainage to prevent paraplegia after aortic surgery. Herein we report the cerebrospinal fluid and hemodynamic alterations that occurred in 11 patients who had 30 mg of a specially prepared papaverine hydrochloride 10% dextrose solution injected before aortic cross-clamping and also had cerebrospinal fluid drainage. A mean of 26.6 ml (SD +/- 7.1 ml) was drained before and 34.6 ml (SD +/- 24.1 ml) was drained during aortic cross-clamping. The cerebrospinal fluid pressure increased significantly with anesthetic induction (p less than 0.03), during the period between anesthetic induction and cerebrospinal fluid drainage (p less than 0.005), and with aortic cross-clamping (p less than 0.05). These cerebrospinal fluid pressure alterations were similar to central venous pressure increases with a significant linear correlation between cerebral spinal fluid pressure and central venous pressure before anesthetic induction (r2 = 0.81, p less than 0.005), and both before (r2 = 0.94, p less than 0.005) and after (r2 = 0.74, p less than 0.005) aortic cross-clamping. As expected, cerebrospinal fluid pressure was significantly reduced by cerebrospinal fluid drainage before aortic cross-clamping (p less than 0.001). The administration of intrathecal papaverine had no significant effect on mean arterial pressure, systemic vascular resistance, cerebrospinal fluid pressure, nor the pH of cerebrospinal fluid. Neither were there any complications noted related to the technique. All the patients survived, and no new immediate postoperative paraparesis or paraplegia occurred.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prevention of Ischemic Spinal Cord Injury Following Aortic Cross-Clamping: Use of Corticosteroids

Prior to proximal aortic cross-clamping, baseline measurements of spinal cord blood flow and function were done. Blood flow was evaluated with radioactive microspheres and function determined by assessment of somatosensory evoked potential (SEP). Group 1 (N = 6) animals had aortic cross-clamping for 5 minutes after ischemic spinal cord dysfunction (SEP loss) was documented. Group 2 (N = 9) underwent aortic cross-clamping for 10 minutes after loss of SEP. Group 3 (N = 6) also underwent 10 minutes of cross-clamping after initial SEP loss, but were treated intravenously with methylprednisolone (30 mg per kilogram of body weight) 10 minutes prior to cross-clamping and again 4 hours postoperatively. After release of the cross-clamp, the animals were allowed to recover and serial evaluations of spinal cord blood flow and neurological status were carried out for seven days. Group 1 animals recovered uneventfully without evidence of neurological injury. Group 2 animals sustained a 67% incidence of permanent spastic paraplegia (p = 0.02 versus Group 1). In contrast, methylprednisolone-treated animals sustained no clinically detectable neurological injury (p = 0.02 versus Group 2). Measurements of spinal cord blood flow at the time of SEP loss revealed similar degrees of spinal cord ischemia in all groups. No significant differences were observed in the duration of aortic cross-clamping prior to SEP loss among the three groups. The data indicate that short periods of cross-clamping (5 minutes) following SEP loss are well tolerated, whereas longer periods (10 minutes) are associated with a high incidence of paraplegia. This injury can be prevented if an adequate dose of methylprednisolone is given before and after cross-clamping. Beneficial effects of steroid administration do not appear to be related to changes in spinal cord blood flow, but may be related to protective effects on cellular and subcellular components. Clinical investigations employing this regimen of corticosteroid protection during surgical procedures on the thoracoabdominal aorta appear to be indicated.     

Thoracic and thoracoabdominal aortic aneurysm repair: Use of evoked potential monitoring in 118 patients

PURPOSE: Paraplegia is the most dreaded and severe complication of surgery on the descending thoracic aorta (TAA) and thoracoabdominal aorta (TAAA). The functional integrity of the spinal cord can be monitored by means of intraoperative recording of myogenic-evoked responses after transcranial electrical stimulation (tcMEP) and somatosensory-evoked potential (SEP) monitoring. In this study, we evaluated the results of evoked potential monitoring and the adequacy of the strategy followed. METHOD: The spinal cord of 118 patients (78 men; age, 65 +/- 12 years; 79 TAAAs, 39 TAAs) undergoing surgery on the TAA or TAAA was monitored with tcMEP and SEP. Spinal cord protection was achieved by means of a multimodality approach: moderate hypothermia (32 degrees C rectal temperature), continuous cerebrospinal fluid drainage to keep the pressure less than 10 mm Hg, reimplantation of intercostal arteries, left ventricular bypass grafting, and staged clamping. In the case of evoked potential changes more than 50% of baseline, the strategy was adjusted: reattachment of more segmental arteries when technically feasible, higher distal and proximal perfusion pressures, and enhanced cerebrospinal fluid drainage. RESULTS: Forty-two of 118 patients (35.6%) had a more than 50% of baseline tcMEP reduction during cross-clamping. At this point, only 5 of those 42 cases were also associated with SEP reduction of more than 50% of baseline. On the basis of the tcMEP findings, the strategy was adjusted. Five patients had postoperative paraplegia (4.2%). CONCLUSION: tcMEP monitoring seems to be a useful adjunct of the protective techniques and may cause substantial adjustments in strategy, reducing the incidence of postoperative paraplegia.     

Immediate ischemic preconditioning based on somatosensory evoked potentials seems to prevent spinal cord injury following descending thoracic aorta cross-clamping.

OBJECTIve: Delayed ischemic preconditioning has demonstrated neuroprotective effects in spinal cord ischemia. We investigated the effects of immediate ischemic preconditioning based on somatosensory evoked potentials monitoring in a model of spinal cord injury due descending thoracic aorta occlusion in dogs. METHODS: Twenty-one dogs were submitted to spinal cord ischemia induced by descending thoracic aorta cross-clamping for 45 min. Control group underwent only the aortic cross-clamping (n=7), group A underwent one cycle of ischemic preconditioning (n=7) and group B underwent three equal cycles of ischemic preconditioning (n=7), immediately before the aortic cross-clamping. Ischemic preconditioning cycles were determined by somatosensory evoked potentials monitoring. Neurologic evaluation was performed according to the Tarlov score at 72 h of follow-up. The animals were then sacrificed and the spinal cord harvested for histopathology. RESULTS: Aortic pressures before and after the occluded segment were similar in the three groups. Ischemic preconditioning periods corresponded to a mean ischemic time of 3+/-1 min and a mean recovery time of 7+/-2 min. Severe paraplegia was observed in three animals in Control group, in four in group A and in none in group B. Tarlov scores of group B were significantly better in comparison to the Control group (P=0.036). Histopathologic examination showed severe neuronal necrosis in the thoracic and lumbar gray matter in animals who presented paraplegia. CONCLUSIONS: Immediate repetitive ischemic preconditioning based on somatosensory evoked potentials monitoring seems to protect spinal cord during descending aorta cross-clamping, reducing paraplegia incidence.     

Winner of the ESVS prize 1989. Microcirculation of the spinal cord during proximal aortic cross-clamping

The relationship between the cerebrospinal fluid pressure (CSFP) and the microcirculation of the spinal cord was studied during cross-clamping (XC) of the thoracic aorta in pigs. CSFP was recorded via an intrathecal catheter. The microcirculation was measured by the laser Doppler technique using a needle probe inserted percutaneously into the spinal cord. A left thoracotomy was performed, and the thoracic aorta was cross-clamped for 30 minutes distal to the left subclavian artery. Prior to XC a pulsatile flux recording from the spinal cord (SCF) was observed. Following cross-clamping of the aorta SCF was dramatically reduced (P less than 0.001), then stabilised at 40% of base-line values. During XC, variations in CSFP were observed but these changes were not statistically significant. CSFP gradually increased to pre cross-clamp levels following release of XC (P less than 0.05). SCF increased 51% following removal of 1 ml of cerebrospinal fluid (P less than 0.05). By injection of 0.9% saline at body temperature SCF was totally inhibited at CSFP above 15 mmHg. Occlusion of the azygos vein increased CSFP 1.3 mmHg (P less than 0.05) whereby SCF decreased 58% (P less than 0.01). Following release of XC of a hyperaemic period of the SCF was demonstrated in ten out of 13 animals. In conclusion, SCF was significantly influenced by changes in CSFP during XC of the thoracic aorta. The findings support the theory that removal of spinal fluid during XC of the thoracic aorta may increase the perfusion pressure to the spinal cord, thereby improving its blood supply.     

Effects of exsanguination and sodium nitroprusside on compliance of the spinal canal during aortic occlusion.

To evaluate the effects of sodium nitroprusside (SNP) and partial exsanguination (EXS) on systemic hemodynamics and cerebrospinal fluid dynamics, we monitored proximal and distal blood pressure (BP), cerebrospinal fluid pressure (CSFP), spinal cord perfusion pressure (SCPP), and compliance of the spinal canal (CSC) in 10 mongrel dogs during aortic cross-clamping of the descending thoracic aorta. CSC was measured by serial injections of 2 ml of saline solution into the cisterna cerebellomedullaris via a percutaneously placed catheter with simultaneous measurements of CSFP. Data were acquired at baseline (BL), during aortic cross-clamping with proximal hypertension (AXC), and after control of proximal hypertension with EXS and SNP. During the cross-clamp interval, mean proximal aortic pressure (PxBP) rose from 114 +/- 6 to 150 +/- 3 mm Hg (P less than 0.001), whereas mean blood pressure decreased to 88 +/- 5 and 82 +/- 4 mm Hg during the SNP and EXS intervals, respectively (P less than 0.05 vs BL). EXS and SNP were equally effective in controlling PxBP (82 +/- 4 vs 88 +/- 5 mm Hg, P greater than 0.05). Mean distal aortic pressure (DsBP) decreased from systemic values to 21.5 +/- 1.9 mm Hg during AXC, and to 12.4 +/- 1.0 and to 8 +/- 0.8 mm Hg during EXS and SNP, respectively (P less than 0.05 AXC vs EXS and SNP). SNP lowered DsBP significantly more than EXS, 8 +/- 0.8 vs 12.4 +/- 1.0 mm Hg (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)