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.     

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.     

Somatosensory evoked potentials in the detection of spinal cord ischemia in aortic coarctation repair

Cortical somatosensory evoked potential (SEP) monitoring was used in 15 patients 2 to 50 years old undergoing repair of aortic coarctation to detect the onset of spinal cord ischemia during the cross-clamp period. Three different response patterns were observed. In 8 patients (53%), the SEP remained unchanged throughout the cross-clamping. This was designated a type 1 response. Six patients (40%) showed a gradual deterioration in the SEP after 15 minutes of cross-clamping (type 2 response). All SEPs returned to normal levels within 5 minutes of release of the clamp. One patient (7%) demonstrated a decline in SEP commencing prior to the application of the cross-clamp when an intercostal vessel was controlled with slings. The SEP completely disappeared within 5 minutes of cross-clamping, but after 19 minutes the repair was completed and the SEP returned within 3 minutes of reperfusion (type 3 response). No patient sustained neurological sequelae of repair. We believe that SEP monitoring offers the potential to identify the patient at risk of developing spinal cord ischemia intraoperatively before irreversible damage occurs. However, it is susceptible to deep halothane anesthesia, which abolishes all cortical responses and requires expert monitoring.     

Improvement in thoracic aortic pressure after proximal aortic cross-clamping by balloon occlusion of the distal aorta

Spinal cord hypoperfusion injury is a devastating complication of cross-clamping the proximal thoracic aorta. The collateral circulation around the cross-clamp is generally poorly developed, and the run-off is immense, resulting in extremely low thoracic aortic and spinal cord perfusion pressures. The authors postulated that balloon occlusion of the abdominal aorta might confine this reduced collateral flow around the cross-clamp to the thoracic aorta. In 8 of 16 dogs subjected to aortic cross-clamping of the aorta just beyond the arch vessels, the abdominal aorta was also occluded by a balloon. Thoracic aortic pressure and spinal cord perfusion pressure were significantly higher in the animals with aortic balloon occlusion than in those without balloon occlusion (77 +/- 8 mm Hg versus 26 +/- 1 mm Hg, p less than 0.01, and 67 +/- 8 mm Hg versus 18 +/- 2 mm Hg, p less than 0.01, at 10 minutes after cross-clamping). Abdominal aortic balloon occlusion increases thoracic aortic pressure after the aorta is cross-clamped proximally. Further studies are necessary in primates to assess the effect of this procedure in spinal cord perfusion and the rate of paraplegia.     

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)     

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.     

Epidural-evoked potentials: a more specific indicator of spinal cord ischemia

The purpose of this experimental study was to examine the differences between peripheral nerve stimulation and direct spinal stimulation in generating cortical somatosensory-evoked potential (SEP) responses for monitoring spinal cord ischemia during thoracic aorta cross-clamping. Adult mongrel dogs (n = 6) were placed under general anesthesia and a left thoracotomy was performed. A conventional stimulating electrode was placed over the posterior tibial nerve (PN-SEP), and a special bipolar electrode was placed epidurally over the spinal cord at L1-2 (SC-SEP). The aorta was cross-clamped proximal to the left subclavian artery. Stimulations were alternately performed through both electrodes, and SEP responses were continuously monitored. The cross-clamp was released after one hour and the animal was observed for another hour prior to sacrifice. Excellent SEPs were obtained with six stimuli over 3 sec via the SC-SEP stimulus in contrast to the 200 stimulations over 90 sec required for the PN-SEP stimulus. Aortic cross-clamping resulted in a significantly longer mean time to loss of SEPs for SC-SEP (mean +/- SEM, 13.7 +/- 1.0 min for SC-SEP vs 11.3 +/- 0.7 min for PN-SEP, P less than 0.05). Likewise, unclamping of the aorta consistently resulted in a shorter mean time to return of SEPs for SC-SEP compared with PN-SEP. These data indicate that direct epidural stimulation for evoked cortical responses is a more sensitive means of determining the adequacy of posterior spinal cord blood flow as reflected by posterior spinal cord function.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Longitudinal study of cerebral spinal fluid drainage in polyethylene glycol-conjugated superoxide dismutase in paraplegia associated with thoracic aortic cross-clamping

It has been hoped that pharmacologic prophylaxis in thoracic aortic cross-clamping may avert the unpredictable complication of spinal cord paraplegia, may avoid the mechanical difficulties associated with shunts, partial bypass, or monitoring devices, and may serve as a substitute for or as an adjunct to cerebral spinal fluid drainage. Toward this end 21 mongrel dogs were studied in four groups and underwent 60 minutes of thoracic aortic cross-clamping: group I, five with thoracic aortic cross-clamping; group II, five with thoracic aortic cross-clamping and cerebral spinal fluid drainage; group III, five with thoracic aortic cross-clamping, cerebrospinal fluid drainage and intravenous administration of a single dose (5000 units/kg) of polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) given 15 to 20 minutes before thoracic aortic cross-clamping; and group IV, six with thoracic aortic cross-clamping and PEG-SOD. Paraplegia was graded by the Tarlov method at 24 hours and up to 5 days after thoracic aortic cross-clamping. The carotid and femoral artery pressures, the central venous pressure, and core temperature, taken during the experiment and at the time the dogs were killed, were found to be similar between groups. At 24 hours all dogs in group I were paraplegic; groups II and III had no paraplegic dogs (p less than 0.01), and group IV had fewer paraplegic dogs (two of six) than group I (p less than 0.05). Paraplegia was averted in all dogs treated with cerebral spinal fluid drainage, even 5 days after thoracic aortic cross-clamping.(ABSTRACT TRUNCATED AT 250 WORDS)     

Selective deep hypothermia of the spinal cord prevents paraplegia after aortic cross-clamping in the dog model.

We tested, in the dog, the hypothesis that selective deep hypothermia (19 degrees to 12 degrees C) of the spinal cord protects it from the ischemia that follows double aortic cross-clamping. The extracorporal perfusion system consisted of heat exchanger and a pump, infusing saline solution at 5 degrees C into the subarachnoid space (L-6) and draining it through the cisterna magna. After 30 minutes this system cools a normally perfused spinal cord to a stable temperature gradient of 13 degrees C (inflow) to 18 degrees C (outflow). Proximal and distal intrathecal, proximal and distal aortic, and central venous pressures were continuously recorded. Rectal temperature was maintained between 36.5 degrees C and 38.5 degrees C. Eight control dogs had cross-clamping of the aorta below the left subclavian artery and above the diaphragm without cord hypothermia. Nine experimental dogs had cord hypothermia initiated 50 minutes before systemic heparinization (100 U/kg) and double cross-clamping of the aorta. Cross-clamping was maintained for 45 minutes. The aorta was then unclamped, heparin was reversed, cord cooling was discontinued, and the dura was closed. Hindlimb function of animals was graded by use of Tarlov's scale at recovery and 24 hours later. The dogs were then killed, and the cords were removed and fixed for microscopy. All control animals were paraplegic and had histologic confirmation of spinal cord infarction. All experimental animals had intact hindlimb function and normal appearing cords on histologic examination. A two-tailed Fisher's exact test (chi square) shows this difference to be significant to p = 0.00004. In the dog selective deep hypothermia of the cord avoids the ischemic injury induced by aortic cross-clamping that results in paraplegia. The implications of these findings in thoracoabdominal aortic clamping in humans is discussed.     

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.     

Paraplegia after thoracic aortic occlusion: influence of cerebrospinal fluid drainage. Experimental and early clinical results

Paraplegia occurs in 6.5% to 40% of patients after repair of extensive thoracoabdominal aortic aneurysms requiring aortic clamping. This study aimed to determine whether drainage of cerebrospinal fluid (CSF) done before aortic cross-clamping could decrease the incidence of paraplegia in dogs. The descending thoracic aorta was clamped distal to the left subclavian artery for either 40 minutes (group I) or 60 minutes (group II). All control animals in group I (10) and group II (10) showed evidence of spinal cord injury with paraparesis or paraplegia. In contrast, 9 of 10 animals (90%) in group I and 7 of 10 animals (70%) in group II that had CSF drainage before aortic cross-clamping were neurologically normal (p less than 0.001 and p less than 0.01, respectively). Aortic pressure distal to the aortic cross clamp was the same in all groups; however, spinal cord perfusion pressure (distal aortic pressure minus CSF pressure) was significantly higher in neurologically normal animals (34 +/- 5 mm Hg, n = 15) compared with those with paraparesis (26 +/- 4 mm Hg, n = 8) or paraplegia (19 +/- 5 mm Hg, n = 8) (r = 0.871, p less than 0.001). This study demonstrates that drainage of CSF before thoracic aortic occlusion significantly increases spinal cord perfusion pressure and decreases the incidence of paraplegia. Limited early clinical experience suggests that CSF drainage may be a useful adjunct to prevent paraplegia in patients who are having repair of thoracoabdominal aortic aneurysms.     

Surgery of the descending thoracic aorta: spinal cord protection with the Gott shunt

From July, 1974, to July, 1987, surgical treatment of descending thoracic aortic aneurysms was performed in 173 patients at l'H?pital du Sacré-Coeur de Montréal. The cause of the aneurysms was arteriosclerosis or medial degeneration in 83 patients, trauma in 50, dissection in 34, and a congenital malformation in 6. A single method of external shunting provided distal perfusion in all patients in the series. A 9-mm Gott aneurysm shunt was placed preferentially between the ascending aorta (67%) and the descending aorta (60%). Alternative sites of proximal cannulation (aortic arch, 9%; proximal descending aorta, 22%; left ventricle, 2%) and distal cannulation (abdominal aorta, 3%; left femoral artery, 37%) were chosen based on the location and the extent of the aortic aneurysm. No systemic heparinization was used. In the last 40 patients, a flowmeter adapted for use with the shunt allowed the recording of shunt flow (mean, 2,475 ml/min; range, 1,100 to 4,000 ml/min). Hospital mortality, including patients with ruptured aneurysms, was 15% (26/173). The mean aortic cross-clamp time was 37 minutes (range, 8 to 105 minutes). Of the 173 patients, 168 survived long enough to allow accurate clinical evaluation of the function of the spinal cord: no paraplegia or other spinal cord ischemic injury occurred. To date, our clinical experience has demonstrated the effectiveness of the 9-mm Gott shunt in preserving the functional integrity of the spinal cord during cross-clamping of the thoracic aorta.     

Prevention of spinal cord ischemia after cross-clamping of the thoracic aorta--monitoring of spinal cord perfusion pressure and somatosensory evoked potentials

The pressure difference between the mean distal aortic pressure (MDAP) and the cerebrospinal fluid pressure (CSFP), defined as the spinal cord perfusion pressure (SCPP), as well as somatosensory evoked potentials (SEP) were monitored intraoperatively to detect and prevent intraoperative spinal cord ischemia in 24 patients who required cross-clamping of the descending thoracic aorta. A temporary axillo-femoral shunt, utilizing a 10 mm woven Dacron tube graft, was employed in 10 patients and partial cardiopulmonary bypass was employed in fourteen. Ischemic SEP changes were seen in six patients. Two patients, whose SCPPs were 32 and 35 mmHg, showed a complete loss of SEP and subsequently developed paraplegia. In the other four cases, increase of the MDAP and/or withdrawal of cerebrospinal fluid were performed to increase the SCPP to more than 60 mmHg when ischemic SEP changes occurred. The SEP gradually recovered in two of these cases. The ischemic SEP changes seen in one patient, who had the longest aortic cross-clamping time, (175 minutes) returned to normal immediately after unclamping. In another case, who had a thoracoabdominal aortic aneurysm, the intercostal arteries were reimplanted since the ischemic SEP changes did not revert. These four patients recovered without any neurological deficit. In the other 18 cases without ischemic SEP change, SCPP was kept at more than 40 mmHg during aortic cross-clamping. We conclude that the SCPP should be maintained at more than 40 mmHg during aortic occlusion, and increased to more than 60 mmHg when ischemic SEP changes occur, by increasing MDAP and/or withdrawing cerebrospinal fluid in order to prevent postoperative paraplegia.     

Does prostaglandin E1 and superoxide dismutase prevent ischaemic spinal cord injury after thoracic aortic cross-clamping?

The beneficial use of prostaglandin E1 (PGE1) and superoxide dismutase (SOD) on the tolerance to ischaemia of the spinal cord was evaluated following thoracic aortic cross-clamping in dogs. Aside from spinally evoked somatosensory potential (SEP) by means of a bipolar epidural catheter, postoperative evaluation of motor deficits was used to determine the efficiency of pharmacological protection when compared with controls. The animals were divided into four groups. Group I (n = 12) served as controls. The dogs of Group II (n = 12) were treated with PGE1 (100 ng/kg/min) during clamping and the first hour after declamping. In the third group (n = 12) SOD was given as an intra-arterial bolus (1 mg/kg) prior to declamping which was followed by a continuous perfusion (0.4 mg/kg/min) into the carotid artery for 25 min. In Group IV (n = 12) the dogs were treated with a combination of PGE1 and SOD in the same manner as in Groups 3 and 4. Results after pharmacological protection were significantly better than controls. In Group I all animals but one (92%) were paraplegic, as were five in Group II (42%) and eight in Group III (67%). In contrast no dog in Group IV developed paraplegia. There was a close correlation of SEP and postoperative recovery. The group with combination therapy (PGE1 plus SOD) was characterised by a loss of the evoked potential for a mean of 15 min, the PGE1 group for 45.8 min and the SOD group for 58.5 min. While the control group was characterised by a loss of 72.7 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intrathecal perfusion of an oxygenated perfluorocarbon prevents paraplegia after aortic occlusion.

A canine model was used to evaluate the effects of continuous intrathecal perfusion of an oxygenated perfluorocarbon emulsion on systemic and cerebral hemodynamics and neurologic outcome after 70 minutes of normothermic aortic occlusion. Twelve mongrel dogs were instrumented to monitor proximal and distal arterial blood pressure, cerebrospinal fluid pressure, spinal cord perfusion pressure, and somatosensory evoked potentials. The intrathecal perfusion apparatus consisted of two perfusing catheters, placed in the intrathecal space through a laminectomy, and a draining catheter percutaneously inserted in the cisterna cerebellomedullaris. The aorta was cross-clamped just distal to the left subclavian artery for 70 minutes. Animals were randomized into two groups: group 1 (n = 6) animals were treated with intrathecal perfusion of saline solution, whereas group 2 (n = 6) animals received oxygenated Fluosol-DA 20%. Data were acquired at baseline, during the cross-clamp period, and after reperfusion. Normothermic Fluosol or saline solution was infused at a rate of 15 mL/min beginning 15 minutes before cross-clamping and continued throughout the ischemic interval. There was no difference in proximal arterial blood pressure (97.2 versus 95.4 mm Hg; p > 0.05) or distal arterial blood pressure (14.6 versus 15.0; p > 0.05) between the two groups throughout the cross-clamp interval. Cerebrospinal fluid pressure rose significantly in both groups with the onset of intrathecal perfusion of either saline solution or Fluosol (7 +/- 1 versus 24 +/- 5 and 8 +/- 1 versus 40 +/- 4 mm Hg, respectively; p < 0.05). The rise in cerebrospinal fluid pressure was sustained throughout the perfusion interval in both groups.(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.     

Ultrastructural and cytochemical correlates of myocardial protection by cardiac hypothermia in man

We report observations on ultrastructural and cytochemical changes in the myocardium after hypothermic protection in 21 patients who underwent cardiac operation. Two general categories of hypothermic protection were studied. (1) topical cooling during anoxic arrest and moderate general hypothermia (10 patients with aortic valve replacement, Group 1) and (2) intermittent perfusion during moderate general hypothermia combined with topical cooling (11 patients with multiple valve replacement, Group II). Transmural left ventricular biopsies were taken at the start of the cardiopulmonary bypass and shortly after the end of aortic cross-clamping. In Group I (cross-clamp time, 51 +/- 12 minutes) only minor pathologic changes of the myocardial fine structure were found, with no differences among the left ventricular layers. In most mitochondria, structure remained intact but the mitochondrial granules disappeared. Cytochrome-c-oxidase activity was unchanged. In Group II (total cross-clamp time, 83 +/- 16 minutes) the subendocardium was well preserved. Slight subcellular damage comparable with that of resulting from topical cooling was seen in all hearts even after a total cross-clamp period of 106 minutes. Cytochrome-c-oxidase activity was unchanged. In the subepicardium, however, a positive correlation was found between the severity of ultrastructural damage and total cross-clamp time (p less than 0.05). Matrix clearing, damage to the cristae and the mitochondrial membranes, and nuclear abnormalities occurred when the aorta was cross-clamped for morethan 60 minutes. Cytochrome-c-oxidase activities decreased in these samples. It is concluded that: (1) no significant subcellular injury was found in hearts cooled topically during 1 hour of anoxic arrest; and (2) in hearts protected by intermittent perfusion during moderate general hypothermia and additional external cooling, the subendocardium was well preserved for anoxic periods of up to 106 minutes. However, after 60 minutes of aortic cross-clamping subcellular damage increased progressively in the subepicardium.     

Further Experience with Exsanguination for Descending Thoracic Aneurysms

Resection and graft replacement of descending thoracic aortic aneurysms is associated with potential ischemic sequelae related to aortic cross-clamping. Such complications are minimized when the ischemic period is shorter than 30 minutes. We have devised a technique in which a single aortic cross-clamp is applied proximal to the lesion, and the distal anastomosis is performed in “open” fashion, with limited distal aortic dissection. This technique depends upon continuous autotransfusion, which allows distal aortic decompression by means of partial exsanguination through the open distal aorta and segmental spinal arteries. In addition, the period of cord ischemia from aortic clamping is minimized. From April 1989 to October 1993, we used this approach in 71 consecutive patients (50 men and 21 women), 8 (11.3%) of whom died during the early postoperative period. Complications included 6 cases of spinal cord dysfunction (8.5%) and 4 cases of renal failure (5.6%). Our success with this approach may contradict more accepted concepts of spinal cord protection from ischemic injury. (J Card Surg 1994;9:625–630)