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.     

Thoracic aortic occlusion: somatosensory evoked potential monitoring and neurologic outcome in a canine model

Somatosensory evoked potentials (SEPs) were monitored in 17 canines during spinal cord ischemia induced by balloon occlusion of the thoracic aorta. Graded distal aortic hypotension to 40 mmHg in seven animals had no significant effect upon the evoked potential. A significant alteration in the SEP did result in 21 +/- 9.8 minutes when distal aortic pressures were reduced in a graded fashion below 30 mmHg. Acute occlusion of the thoracic aorta (10 animals, distal pressure 15-25 mmHg) was associated with a change in the SEP in 8.4 +/- 4.3 minutes. Continuation of aortic occlusion for 30 minutes beyond an evoked potential change resulted in a moderate to severe motor deficit in all cases. Somatosensory evoked potentials obtained 72-96 hours after the ischemic injury were closely correlated with sensory deficits, but were not predictive of motor examination. Histologic examination of the spinal cords demonstrated central gray necrosis of the lumbar region in all animals with a severe deficit, and a variable degree of neuronal loss in the intermediate and dorsal gray matter zones in animals with moderate deficits. This balloon occlusion method is relevant as a model of spinal cord injury during aortic occlusion, such as may occur during aortic surgery.     

Cold spinoplegia and transvertebral cooling pad reduce spinal cord injury during thoracoabdominal aortic surgery

OBJECTIVE: We examined the protective effects of the new selective spinal cord cooling by using cold saline infusion into the cross-clamped aorta and a transvertebral cooling pad placed over the lumbar vertebral column from paraplegia caused by ischemic spinal cord injury on thoracoabdominal aortic surgery. METHODS: Eighteen rabbits were divided into three groups: groups I, II, and III (n = 6 for each group). In group I (37 degrees C; 5 mL) and group II (3 degrees C; 5 mL), saline was infused into the isolated aortic segment twice, at 0 and 5 minutes after aortic cross clamping. In group III, a 3 degrees C saline solution plus cooling pads placed just after cross clamping were combined. The infrarenal aorta was then isolated proximally and distally by vascular clamps for 12 minutes. In our preliminary study, only the abdominal aorta just distal to the left renal artery was clamped. At 48 hours after reperfusion, the groups clamped for 12 and 15 minutes were all paraplegic. The time of clamping the aorta was set at 12 minutes as the critical point when paraplegia occurred upon simple clamping of the infrarenal aorta only. The spinal cord temperature was monitored at the L4 level continuously during the procedures in all three groups. At 8, 24, and 48 hours after the operation, hind limb function was estimated by using the Tarlov score, which is often used for evaluating motor function in animals. A histopathologic study using hematoxylin and eosin stains was also performed. RESULTS: At 48 hours after the operation, the Tarlov scores in groups I, II, and III were 0 +/- 0, 2.0 +/- 1.9, and 4.0 +/- 0 (mean +/- SD), respectively. The Tarlov score and histopathologic analysis in group III were significantly superior to those of groups I (P < .01) and II (P < .05). The spinal cord temperature in groups II and III decreased by -1.8 degrees C and -4.3 degrees C at its minimum. The rabbits in group III were also protected from paraplegia. CONCLUSIONS: Selective spinal cord cooling with cold saline infusion into the isolated aortic segment and transvertebral regional cooling can reduce the neurologic damage of spinal cord ischemia.     

Protection against ischemic spinal cord injury: One-shot perfusion cooling and percutaneous topical cooling

Purpose: We investigated the protective effect of two methods of hypothermia against ischemic spinal cord injury: one-shot perfusion cooling and percutaneous topical cooling.Methods: Twenty-five rabbits were divided into five equal groups. The abdominal aorta was isolated proximally by a vascular clamp and distally by an inflated balloon catheter for 60 minutes. Group I served as control. In groups II (2.5 ml/min) and III (5.0 ml/min), hypothermic lactated Ringer's solution was infused for 3 minutes from the distal end of the catheter. Ice blocks were placed behind the backs of rabbits 30 minutes before ischemia in group IV. Group V underwent the procedures combined with those in groups II and IV (infusion of hypothermic solution plus placement of ice blocks). Another 15 rabbits underwent laminectomy at the L₂ or L₃ level. A temperature probe was inserted into the spinal cord to monitor cord temperature continuously during the procedures in all five groups (three rabbits per group).Results: Neurologic status on the second postoperative day in groups IV and V was significantly superior to that in group I (p < 0.01), but the neurologic status of groups II and III did not differ significantly from the neurologic status of group I. The spinal cord temperature in groups II and III dropped rapidly with the infusion, but it rose again quickly. In contrast, the spinal cord was kept sufficiently hypothermic during ischemia in groups IV and V.Conclusions: We concluded that the percutaneous cooling method can keep the spinal cord sufficiently hypothermic during ischemia to lead to a significantly superior neurologic outcome. (J VASC SURG 1994;19:882-7.)     

Effects of aortic occlusion on regional spinal cord blood flow and somatosensory evoked potentials in sheep

Somatosensory evoked potentials (SEPs) were recorded continuously during aortic occlusion in sheep, with simultaneous measurement of spinal cord blood flow (SCBF) by radiolabeled microspheres. Aortic occlusion was associated with disappearance of the SEPs in seven of nine sheep in 7.8 +/- 4.1 (SD) minutes. SCBF at the time of initial cross clamping and 30 minutes after the onset of ischemia revealed a severe reduction in white and gray matter flow in the thoracolumbar cord. Release of the aortic clamp was associated with reactive hyperemia in these ischemic regions. In two animals, the SEP persisted during aortic cross clamping. The total SCBF in the thoracic and lumbar regions of these two animals exceeded 20 ml/100 g/min after 30 minutes of ischemia and was significantly greater than the flow recorded in sheep whose evoked response disappeared. The relation between spinal cord ischemia and evoked potential alterations is discussed in detail.     

Prevention of paraplegia in pigs by selective segmental artery perfusion during aortic cross-clamping

PURPOSE: During thoracoabdominal aortic aneurysm repair, a prolonged interruption of the spinal cord blood supply can result in irreversible spinal cord damage. The aim of this study was to investigate whether selective segmental artery perfusion during aortic clamping could prevent paraplegia in pigs. METHODS: Specially designed segmental artery perfusion catheters, which could be attached to an extracorporeal bypass graft system, were used. In experiment I (n = 10), it was assessed whether selective segmental artery perfusion could reverse electrophysiologic evidence of spinal cord ischemia and maintain transcranial motor evoked potentials (tc-MEPs) during 60 minutes of aortic cross-clamping. The abdominal aorta, containing critical segmental arteries, was bypassed through use of an aortoaortic bypass graft system. After the disappearance of tc-MEPs, an aortotomy was followed by selective segmental artery perfusion. In experiment II (n = 10), the aim was to determine whether selective segmental artery perfusion could prevent paraplegia. In five animals (group A), aortic cross-clamping was followed by selective segmental artery perfusion; five control animals (group B) underwent segmental artery blockade only. Postoperative hind limb function and spinal cord histopathology were evaluated on the third postoperative day. RESULTS: In experiment I, tc-MEPs disappeared within 3.7 +/- 3.7 minutes after cross-clamping and returned in all animals in 8.5 +/- 5.3 minutes after selective perfusion. During the study period, tc-MEP amplitudes recovered to a median of 49% (range, 28%-113%) of baseline values. Total bypass graft flow was 880 +/- 294 mL/min, of which 184 +/- 54 mL/min was directed to the selective perfusion catheters. The flow in individual catheters was 52 +/- 13 mL/min. In experiment II, all perfused animals demonstrated normal hind limb function, whereas four of five control animals were paraplegic on day 3 (P =.04) In the perfused animals, histopathologic examination showed either no spinal cord damage or eosinophilic neurons only, whereas in paraplegic controls there was infarction in large areas of the cord (P <.0001). CONCLUSION: In pigs, selective segmental artery perfusion can provide sufficient spinal cord blood flow to prevent paraplegia resulting from 60 minutes of aortic clamping, as shown by clinical outcomes and histopathologic examination.     

Failure of motor evoked potentials to predict neurologic outcome in experimental thoracic aortic occlusion

Motor evoked potential monitoring was tested as an alternative to somatosensory evoked potential monitoring in evaluating spinal cord function during thoracic aortic occlusion in dogs. Twenty-seven animals underwent 60 minutes of cross-clamping of the proximal descending thoracic aorta with (n = 18) or without (n = 9) cerebrospinal fluid drainage. Spinal cord blood flow was measured with microspheres, and neurologic outcome was evaluated at 24 hours with Tarlov's scoring system. Cerebrospinal fluid drainage improved neurologic outcome (p less than 0.05). Motor evoked potentials recorded over the lumbar spinal cord were lost in 9 of 20 dogs with ischemic cord injury and were not lost in any of the 7 dogs that were neurologically normal. Somatosensory evoked potential were lost in 19 of 20 paraplegic/paraparetic dogs and lost in 3 of 7 normal dogs (p less than 0.01). After reperfusion, motor evoked potentials returned in all nine neurologically injured dogs that lost the potentials and were still present at 24 hours. Changes in amplitude, latency, or time until loss or return of motor evoked potentials or somatosensory evoked potentials did not predict neurologic injury. Loss of somatosensory evoked potentials had a high sensitivity (95%) but had low specificity (67%) because of peripheral nerve ischemia. Loss of motor evoked potentials recorded from the spinal cord had high specificity (100%) but a low sensitivity (46%) and was therefore not a reliable predictor of neurologic injury. Return of motor evoked potentials during reperfusion did not correlate with functional recovery. Motor evoked potentials stimulated in the cortex and recorded from the spinal cord had low overall accuracy (59%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Direct noninvasive monitoring of spinal cord motor function during thoracic aortic occlusion: use of motor evoked potentials

Spinal cord monitoring during thoracic aneurysmectomy by somatosensory evoked potentials has been criticized for its failure to measure anterior (motor) spinal cord function. We have developed a clinically applicable, noninvasive technique for intraoperative monitoring of motor evoked potentials (MEP), which allows direct functional assessment of spinal cord motor tracts during thoracic aortic occlusion. Twelve dogs underwent continuous intraoperative monitoring of MEP before, during, and after thoracic aortic cross-clamping. Motor tract response to noninvasive cord stimulation (5 to 10 mA, 0.02 msec, 4.3 H2) was recorded by subcutaneous electrodes placed along the length of the spine (T-10, L-1, and L-4). Six animals (group I) subjected to aortic cross-clamping alone demonstrated a characteristic time- and level-dependent deterioration and loss of MEP. Ischemic cord dysfunction (as determined by time from clamping to loss of MEP) progressed from the distal to the proximal cord (L-4 = 11.3 +/- 1.5 minutes; L-1 = 14.9 +/- 2.3 minutes; T-10 = 16.9 +/- 2.3 minutes; p less than 0.05 between all levels). Reperfusion of the distal aorta 20 minutes after clamping resulted in MEP return that progressed from the proximal (T-10) to distal (L-1 and L-4) cord. In another six animals (group II), distal perfusion (mean blood pressure = 95 mm Hg) was maintained for 1 hour after cross-clamping by left atrial-femoral artery bypass. Normal configuration and amplitude of MEP was maintained throughout the cross-clamping period. These data suggest that distinctive changes in MEP indicative of reversible ischemia of spinal cord motor tracts occur after aortic cross-clamping. Such ischemia begins in the most distal cord, exhibits upward progression with time, and can be prevented by maintenance of adequate distal aortic perfusion. Clinical use of MEP monitoring during thoracic aneurysmectomy may provide a method for intraoperative assessment of the adequacy of motor tract perfusion.     

Comparison of transcranial motor evoked potentials and somatosensory evoked potentials during thoracoabdominal aortic aneurysm repair

OBJECTIVE: To compare transcranial motor evoked potentials (tc-MEPs) and somatosensory evoked potentials (SSEPs) as indicators of spinal cord function during thoracoabdominal aortic aneurysm repair. SUMMARY BACKGROUND DATA: Somatosensory evoked potentials reflect conduction in dorsal columns. tc-MEPs represent anterior horn motor neuron function. This is the first study to compare the techniques directly during thoracoabdominal aortic aneurysm repair. METHODS: In 38 patients, thoracoabdominal aortic aneurysm repair (type I, n = 10, type II, n = 14, type III, n = 6, type IV, n = 8) was performed using left heart bypass and segmental artery reimplantation. tc-MEP amplitudes <25% and SSEP amplitudes <50% and/or latencies >110% were considered indicators of cord ischemia. The authors compared the response of both methods to interventions and correlated the responses at the end of surgery to neurologic outcomes. RESULTS: Ischemic tc-MEP changes occurred in 18/38 patients and could be restored by segmental artery reperfusion (n = 12) or by increasing blood pressure (n = 6). Significant SSEP changes accompanied these tc-MEP events in only 5/18 patients, with a delay of 2 to 34 minutes. SSEPs recovered in only two patients. In another 11 patients, SSEP amplitudes fell progressively to <50% of control without parallel tc-MEP changes or association with cross-clamp events or pressure decreases. At the end of the procedure, tc-MEP amplitudes were 84 +/- 46% of control. In contrast, SSEP amplitudes were <50% of control in 15 patients (39%). No paraplegia occurred. CONCLUSION: In all patients, tc-MEP events could be corrected by applying protective strategies. No patient awoke paraplegic. SSEPs showed delayed ischemia detection and a high rate of false-positive results.     

Spinal cord ischemia and reperfusion metabolism: The effect of hypothermia

Purpose: The metabolic and neurologic functional effects of regional hypothermia induced by cold (4° C) heparinized saline perfusion on spinal cord ischemia were evaluated in 35 rabbits.Methods: Spinal cord ischemia was induced for 20 minutes by infrarenal aortic occlusion in anesthetized animals. Regional spinal cord hypothermia was obtained by perfusing the lumbar arteries supplying the spinal cord through an infrarenal aortic catheter. The lumbar spinal cord was "snap frozen" in situ with liquid nitrogen and harvested immediately at the conclusion of the ischemic period or after 24 hours of normothermic reperfusion and neurologic observation. Spinal cord metabolic studies included determination of the energy charge and the intracellular concentrations of adenosine triphosphate, glucose, lactate, glutamate, and aspartate.Results: Postoperative neurologic function was normal in all but one animal treated with hypothermia, while normothermic ischemia resulted in paralysis in all animals ( p = 0.002). Spinal cord temperature during 20 minutes of ischemia and hypothermic perfusion decreased from 37.5° ± 0.43° C to 22.8° ± 0.00° C ( p = 0.0001) compared to a fall in systemic temperature from 38.8 to 36.1 ( p = 0.0001). Hypothermia reduced the decline in energy charge, adenosine triphosphate concentration and glucose concentration during ischemia but had no effect on markedly elevated levels of lactate acid. High-energy phosphates were restored after reperfusion in both normothermic and hypothermic animals and were not predictive of postoperative paraplegia. Intracellular glutamate and aspartate concentrations were unchanged during normothermic ischemia but decreased after reperfusion in all paralyzed animals. Intracellular glutamate and aspartate concentrations increased during hypothermic perfusion and remained elevated after reperfusion in animals with a normal or mildly abnormal neurologic examination result.Conclusions: We conclude that spinal cord hypothermia induced by cold heparinized saline perfusion is a simple technique that prevents paraplegia after 20 minutes of ischemia and preserves intracellular concentrations of important metabolites. (J VASC SURG 1994;19:332-40.)     

Establishment of a local cooling model against spinal cord ischemia representing prolonged induction of heat shock protein

OBJECTIVES: Paraplegia is one of the serious complications of thoracoabdominal aortic operations. Regional hypothermia protects against spinal cord ischemia although the protective mechanism remains unknown. We attempted to create a simple model of local cooling under transient spinal cord ischemia and evaluated the effect using functional and histologic findings. METHODS: Male domesticated rabbits were divided into 3 groups: control, normothermic group (group N), and local hypothermic group (group H). A balloon catheter was used for spinal cord ischemia by abdominal aortic clamping. A cold pack attached to the lumbar region could lower the regional cord temperature initially. Neurologic function was evaluated by the Johnson score. Cell damage was analyzed by observing motor neurons with the use of hematoxylin and eosin staining, terminal deoxynucleotidyl transferase-mediated deoxy-uracil triphosphate biotin in situ nick end labeling (TUNEL), and immunoreactivity of heat shock protein. RESULTS: Physiologic estimation showed that local hypothermia improved the functional deficits (group N, 1.3 +/- 0.9; group H, 4.9 +/- 0.3; P =.0020). Seven days after reperfusion, there was a significant difference in the motor neuron numbers between groups N and H (group N, 7.2 +/- 1.9; group H, 20.4 +/- 3.2; P =.0090). The number of TUNEL-positive motor neurons was reduced significantly (group N, 7.2 +/- 2.4; group H, 1.0 +/- 0.7; P =.0082). Heat shock protein immunoreactivity was prolonged up to 2 days after reperfusion in the hypothermic group. CONCLUSIONS: These results suggest that local hypothermia extended the production of heat shock protein in spinal cord motor neurons after reperfusion and inhibited their apoptotic change.     

Somatosensory evoked potential monitoring of spinal cord ischemia during aortic operations

Somatosensory evoked potentials were monitored in 22 consecutive patients undergoing surgical correction of an aortic coarctation. Induction of spinal cord ischemia by cross clamping of the aorta elicited a change in the evoked potential in 9 patients (41%). These alterations occurred within 5 minutes of aortic clamping in 3 cases and after 18 to 21 minutes in the remaining 6 cases. Loss of the somatosensory evoked potential for more than 14 minutes was associated with postoperative neurological deficit. Alteration of the evoked potential within 5 minutes of aortic cross clamping was significantly related to poor collateral circulation shown on the preoperative aortogram. The pathophysiology of evoked potential changes in spinal ischemia is discussed in detail.     

Iloprost protects the spinal cord during aortic cross-clamping in a canine model

BACKGROUND: Surgical procedures on the thoracoabdominal part of the aorta make the spinal cord vulnerable to ischemia. Paraplegia is the most severe complication following thoracoabdominal operations. In this study, iloprost was used as an agent to decrease the severity of ischemia and reperfusion injury to the spinal cord during aortic occlusion and declamping. METHODS: Twelve adult mongrel dogs weighing 17+/-2 kg were used in this study. The animals were randomly assigned to either group I, which received saline solution (6 dogs), or group II, which received prostacyclin. Group I was referred to as the control group and group II as the iloprost group. After baseline measurements were completed, the aorta was cross-clamped for sixty minutes distal to the left subclavian artery. No pharmacologic agents were used to control blood pressure in group I. Proximal and distal mean arterial pressures (DMAP) were monitored continuously. DMAP were considered as diastolic pressure in preocclusion and reperfusion periods. Iloprost administration was started at a rate of 5 ng/kg/minute five minutes before the aortic occlusion. This dosage was increased to 25 ng/kg/minute during aortic occlusion. RESULTS: Mean proximal arterial pressure was 147+/-12 mmHg in the control group and 116+/-13 mmHg in the iloprost group at occlusion (p<0.01). Mean distal arterial pressure was 19+/-7 in the control group and 37+/-5 in the iloprost group during clamping (p<0.05). Functional outcome was evaluated according to Tarlov scores 24 hours after the study. Although none of the animals recovered completely from the control group, 4 animals from the iloprost group recovered (p<0.05). Following the neurologic assessment, animals were sacrificed and specimens were taken for the electron microscopic study. Electron microscopic changes documented that severe mitochondrial damage and vacuolisation occurred in the control group. However these changes were more subtle in the iloprost group. CONCLUSIONS: As a result of this study we concluded that iloprost infused before and during clamping of the thoracic aorta mitigates the spinal cord injury due to ischemia and reperfusion following unclamping.     

Motor and Somatosensory Evoked Potentials: Their Role in Predicting Spinal Cord Ischemia in Patients Undergoing Thoracoabdominal Aortic Aneurysm Repair with Regional Lumbar Epidural Cooling

Background: Paraplegia is a devastating complication for patients undergoing repair of thoracoabdominal aortic aneurysms. A monitor to detect spinal cord ischemia is necessary if anesthesiologists are to intervene to protect the spinal cord during aortic aneurysm clamping.

Methods: The medical records of 60 patients who underwent thoracoabdominal aortic aneurysm repair with regional lumbar epidural cooling with evoked potential monitoring were reviewed. The authors analyzed latency and amplitude of motor evoked potentials, somatosensory evoked potentials, and H reflexes before cooling and clamping, after cooling and before clamping, during clamping, and after release of aortic cross clamp.

Results: Twenty minutes after the aortic cross clamp was placed, motor evoked potentials had 88% sensitivity and 65% specificity in predicting spinal cord ischemia. The negative predictive value of motor evoked potentials at 20 min after aortic cross clamping was 96%.     

Reappraisal of the role of motor and somatosensory evoked potentials during open distal aortic repair

ObjectiveIntraoperative motor and somatosensory evoked potentials have been applied to monitor spinal cord ischemia during repair. However, their predictive values remain controversial. The purpose of this study was to evaluate the impact of motor evoked potentials and somatosensory evoked potentials on spinal cord ischemia during open distal aortic repair.MethodsOur group began routine use of both somatosensory evoked potentials and motor evoked potentials at the end of 2004. This study used a historical cohort design, using risk factor and outcome data from our department's prospective registry. Univariate and multivariable statistics for risk-adjusted effects of motor evoked potentials and somatosensory evoked potentials on neurologic outcome and model discrimination were assessed with receiver operating characteristic curves.ResultsBoth somatosensory evoked potentials and motor evoked potentials were measured in 822 patients undergoing open distal aortic repair between December 2004 and December 2019. Both motor evoked potentials and somatosensory evoked potentials were intact for the duration of surgery in 348 patients (42%). Isolated motor evoked potential loss was observed in 283 patients (34%), isolated somatosensory evoked potential loss was observed in 18 patients (3%), and both motor evoked potential and somatosensory evoked potential loss were observed in 173 patients (21%). No spinal cord ischemia occurred in the 18 cases with isolated somatosensory evoked potential loss. When both signals were lost, signal loss happened in the order of motor evoked potentials and then somatosensory evoked potentials. Immediate spinal cord ischemia occurred in none of those without signal loss, 4 of 283 (1%) with isolated motor evoked potential loss, and 15 of 173 (9%) with motor evoked potential plus somatosensory evoked potential loss. Delayed spinal cord ischemia occurred in 12 of 348 patients (3%) with intact evoked potentials, 24 of 283 patients (8%) with isolated motor evoked potentials loss, and 27 of 173 patients (15%) with motor evoked potentials + somatosensory evoked potentials loss (P < .001). Motor evoked potentials and somatosensory evoked potentials loss were each independently associated with spinal cord ischemia. For immediate spinal cord ischemia, no return of motor evoked potential signals at the conclusion of the surgery had the highest odds ratio of 15.87, with a receiver operating characteristic area under the curve of 0.936, whereas motor evoked potential loss had the highest odds ratio of 3.72 with an area under the curve of 0.638 for delayed spinal cord ischemia.ConclusionsSomatosensory evoked potentials and motor evoked potentials are both important monitoring measures to predict and prevent spinal cord ischemia during and after open distal aortic repairs. Intraoperative motor evoked potential loss is a risk for immediate and delayed spinal cord ischemia after open distal aortic repair, and somatosensory evoked potential loss further adds predictive value to the motor evoked potential.     

Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta. IV. Clinical observations and results

Thirty-three patients undergoing operations on the descending thoracic or thoracoabdominal aorta were monitored to evaluate causes and effects of spinal cord ischemia as manifested by changes in somatosensory evoked potentials. Maintenance of distal aortic perfusion pressure (greater than 60 mm Hg) by either shunt or bypass techniques in 17 patients resulted in preservation of somatosensory evoked potentials and a normal postoperative neurologic status, irrespective of the interval of thoracic cross-clamping (range 23 to 105 minutes). In 16 other patients in whom cross-clamp time ranged from 16 to 124 minutes, evoked potential loss was observed because of failure to provide distal perfusion (n = 8), inadequate maintenance of distal perfusion pressure (less than 60 mm Hg) despite shunt/bypass (n = 6), or interruption of critical intercostal arteries (n = 2). Incidence of paraplegia in the entire group was 15.1% (5/33) and was limited to only those patients in whom evoked potential loss occurred (5/16, 31.2%) (p = 0.02). Loss of somatosensory evoked potentials for more than 30 minutes resulted in a 71.2% (5/7) incidence of paraplegia, whereas no neurologic deficit was noted in patients (0/26) in whom evoked potential loss was either prevented or limited in duration to 30 minutes (p less than 0.001 versus loss for more than 30 minutes). Intraoperative monitoring of somatosensory evoked potentials is a sensitive indicator of spinal cord ischemia. Simple aortic cross-clamping, failure to maintain distal perfusion pressure above 60 mm Hg, and inability to reimplant critical intercostals in a timely fashion result in a high rate of paraplegia if duration of spinal cord ischemia as measured by somatosensory evoked potentials exceeds 30 minutes. Routine evoked potential monitoring during thoracoabdominal procedures appears useful in assessing the adequacy of spinal cord perfusion. Furthermore, it can alert the surgeon to the necessity for critical intercostal artery reimplantation as well as the need for adjustment or regulation of distal aortic perfusion.     

Clinical outcome of the operation using deep hypothermic cardiopulmonary bypass with intervals of circulatory arrest in thoracoabdominal aortic aneurysm

Deep hypothermic cardiopulmonary bypass with intervals of circulatory arrest has been used for protection of the spinal cord during operations for thoracoabdominal aortic aneurysm (TAAA) in our hospital. We examined the effect of this adjunct this time. We studied 15 patients who were operated using deep hypothermic cardiopulmonary bypass with intervals of circulatory arrest among 19 patients with the TAAA who we performed the operations from 1995 through 2003. The patients ranged in age from 21 to 80 (an average of 65 +/- 14 SD) years. We used deep hypothermic cardiopulmonary bypass with intervals of circulatory arrest between 16 and 20 degrees C for the adjunct but did not use a monitor of evoked spinal cord potentials or cerebrospinal fluid drainage. Operation time was an average of 805 +/- 168 minutes. Cardiopulmonary bypass time was an average of 403 +/- 73 minutes. Deep hypothermic cardiopulmonary bypass time was an average of 215 +/- 67.5 SD minutes. Duration of spinal cord ischemia to the intercostal arteries were reconstructed was from 25 to 104 (50.5 +/- 24) minutes. We recognized nerve disorder in 6 cases in progress after operation, and respiratory organs management period and a hospitalization period became long, but the hospitalization death was 3 cases, and, as for the paraplegia was no case, 12 patients were discharged in good condition. The deep hypothermic cardiopulmonary bypass with intervals of circulatory arrest was regarded as a useful adjunct for prevention of the paraplegia.     

Spinal cord ischemia after endovascular repair of the descending thoracic aorta in a sheep model.

OBJECTIVES: Spinal cord ischemia remains a devastating complication after thoracic aortic surgery. The aim of this study was to investigate the pathophysiology of spinal cord ischemia after thoracic aortic endografting and the role of intercostal artery blood supply for the spinal cord in a standardized animal model. METHODS: Female merino sheep were randomized to either I, open thoracotomy with cross-clamping of the descending aorta for 50 min (n=7), II, endograft implantation (TAG, WL Gore & Ass.), (n=6) or III open thoracotomy with clipping of all intercostal arteries (n=5) . CT-angiography was used to assess completion of surgical protocol and assess the fate of intercostal arteries. Tarloy score was used for daily neurological examination for up to 7 days post-operatively. Histological cross sections of the lumbar, thoracic and cervical spinal cords were scored for ischemic damage after stained with Hematoxylin-Eosin, Klüver-Barrrera and antibodies. Exact Kruskall-Wallis-Test was used for statistical assessment (p<0.05). RESULTS: Incidence of paraplegia was 100% in group I and 0% in group II (p=0.0004). When compared to the endovascular group, there was a higher rate of histological changes associated with spinal cord ischemia in the animals of the control group (p=0.0096). Group III animals showed no permanent neurological deficit and only 20% infarction rate (p=0.0318 compared to group I). CONCLUSIONS: In sheep, incidence of histological and clinical ischemic injury of the spinal cord following endografting was very low. Complete thoracic aortic stent-grafting was feasible without permanent neurologic deficit. Following endovascular coverage or clipping of their origins, there is retrograde filling of the intercostal arteries which remain patent.     

Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta. II. Use of somatosensory evoked potentials to assess adequacy of distal aortic bypass and perfusion after thoracic aortic cross-clamping

Pulsatile left atrial-femoral artery bypass was instituted after aortic cross-clamping distal to the left subclavian artery in a canine experimental model to determine the relationship of distal aortic perfusion pressure with spinal cord blood flow and somatosensory evoked potentials. In six animals (Group I) distal aortic perfusion pressure was maintained at 100 mm Hg throughout a 1 hour interval of aortic cross-clamping. During this period, somatosensory evoked potentials and spinal cord blood flow (radioactive microspheres) showed no significant change from baseline. In six other dogs (Group II) distal aortic perfusion pressure was initially maintained at 100 mm Hg after aortic cross-clamping and then progressively decreased to 70, 40, and 25 mm Hg. Somatosensory evoked potentials and spinal cord blood flow were preserved at baseline levels for all distal perfusion pressures greater than 70 mm Hg. At 40 mm Hg, abnormalities in amplitude of the somatosensory evoked potentials were noted in all animals with progression to complete loss of evoked potential activity at lower perfusion pressures. Maintenance of adequate somatosensory spinal cord conduction after thoracic aortic cross-clamping is dependent on a critical level of distal aortic perfusion that can be accomplished by use of an adjunct such as pulsatile left atrial-femoral artery bypass. The critical level of distal aortic perfusion pressure to maintain normal somatosensory evoked potentials and spinal cord blood flow in this canine experimental study was 70 mm Hg or greater. Because inadequate distal aortic perfusion can be easily detected by monitoring of somatosensory evoked potentials, these techniques should prove helpful in evaluating the effectiveness of distal perfusion techniques during clinical aortic cross-clamping for procedures on the thoracoabdominal aorta.     

Does ischemic preconditioning reduce spinal cord injury because of descending thoracic aortic occlusion?

OBJECTIVE: Ischemic preconditioning has been found to protect various organs from a subsequent longer ischemic insult. We investigated whether the late phase of ischemic preconditioning reduces spinal cord injury from occlusion of the descending thoracic aorta. METHODS: Twenty-four pigs (27 to 30 kg) were randomly divided in four groups: group I (n = 4) underwent a sham operation, group II (n = 4) underwent aortic occlusion for 20 minutes, group III (n = 8) underwent aortic occlusion for 35 minutes, and group IV (n = 8) underwent aortic occlusion for 20 minutes and, 48 hours later, aortic occlusion for 35 minutes. Aortic occlusion was accomplished with two balloon occlusion catheters placed fluoroscopically at T(6) to T(8) above the diaphragm and at the aortic bifurcation. Neurologic evaluation was performed by an independent observer according to Tarlov's scale (0 to 4, with 4 as normal). The lower thoracic and lumbar spinal cords were harvested at 120 hours and examined histologically with hematoxylin and eosin stain. Histologic results (number of neurons and grade of inflammation) were scored 0 to 4 (4, intact spinal cord; 0, no neurons and high inflammation) and were similarly analyzed. Results were expressed as the mean +/- the standard error of the mean, and statistical analysis used the Kruskal-Wallis test. RESULTS: Group IV had a better neurologic outcome at 24, 48, and 120 hours in comparison with group III (P <.001), although 120 hours after the end of the experiment, the neurologic outcome in group IV was worse than at 24 hours (P =.014). The histologic changes were proportional to the neurologic test scores, with the more severe and extensive gray matter damage in the animals of group III (number of neurons, P <.001; and grade of inflammation, P <.001). CONCLUSION: Ischemic preconditioning (late phase, 48 hours after the first occlusion) reduces spinal cord injury after aortic occlusion, as estimated with Tarlov's score and histopathology.