Prevention of spinal cord ischaemia during descending thoracic and thoracoabdominal aortic surgery.

Surgery of the descending and thoracoabdominal aorta has been associated with post-operative paraparesis or paraplegia. Different strategies, which can be operative or non-operative, have been developed to minimise the incidence of neurological complications after aortic surgery. This review serves to summarise the current practice of spinal cord protection during surgery of the descending thoracoabdominal aortic surgery. The pathophysiology of spinal cord ischaemia will also be explained. The incidence of spinal cord ischaemia and subsequent neurological complications was associated with (1) the duration and severity of ischaemia, (2) failure to establish spinal cord supply and (3) reperfusion injury. The blood supply of the spinal cord has been extensively studied and the significance of the artery of Adamkiewicz (ASA) being recognised. This helps us to understand the pathophysiology of spinal cord ischaemia during descending and thoracoabdominal aortic operation. Techniques of monitoring of spinal cord function using evoked potential have been developed. Preoperative identification of ASA facilitates the identification of critical intercostal vessels for reimplantation, resulting in re-establishment of spinal cord blood flow. Different surgical techniques have been developed to reduce the duration of ischaemia and this includes the latest transluminal techniques. Severity of ischaemia can be minimised by the use of CSF drainage, hypothermia, partial bypass and the use of adjunctive pharmacological therapy. Reperfusion injury can be reduced with the use of anti-oxidant therapy. The aetiology of neurological complications after descending and thoracoabdominal aortic surgery has been well described and attempts have been made to minimise this incidence based on our knowledge of the pathophysiology of spinal cord ischaemia. However, our understanding of the development and prevention of these complications require further investigation in the clinical setting before surgery on descending and thoracoabdominal aorta to be performed with negligible occurrence of these disabling neurological problems.     

Current strategies for spinal cord protection during thoracic and thoracoabdominal aortic aneurysm repair

Surgery for thoracoabdominal aortic aneurysms remains challenging, with high mortality and morbidity rates despite overall improvements in the outcome of aortic surgery. Paraplegia and paraparesis remain devastating complications that severely restrict the chance of survival as well as the postoperative quality of life. Preventive measures vary considerably because the causes of spinal cord insufficiency are multifactorial. Here, we review measures to prevent paraplegia/paraparesis arising after surgery for thoracic and thoracoabdominal aortic aneurysms.     

Spinal cord protection during descending thoracic and thoracoabdominal aortic surgery

The incidence of postoperative paralysis after thoracic and thoracoabdominal aortic operations has decreased, but is still high in comparison with other operations. The analysis of the mechanism involved in the ischemic tolerance of the spinal cord could contribute to the protection of the spinal cord from ischemia. The identification of the Adamkiewicz artery and the predictive factors for postoperative paralysis in the preoperative period, the use of motor evoked potential, several adjuncts to keep the spinal cord circulation, the stabilization of the hemodynamics with good oxygenation, and hypothermia contribute to the prevention of the spinal cord ischemia. The anesthetics appropriate for the monitoring of the motor-evoked potential are propofol and fentanyl with or without ketamine. Among the anesthetic drugs, narcotics might exacerbate the motor function after the spinal cord ischemia. The analgesic drugs which do not aggravate the spinal cord dysfunction would be expected. Good cooperation of surgeons and anesthesiologists greatly contributes to the finding of the spinal cord ischemia during this operation.     

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.     

Strategy for spinal cord protection during thoracoabdominal aortic surgery

INTRODUCTION: Our basic strategy for spinal cord protection during thoracoabdominal aortic surgery has been established since August 1994 such as: 1) distal aortic perfusion using partial cardiopulmonary bypass (32-34 degrees C), 2) multi-segmental sequential clamping, 3) deep hypothermic circulatory arrest when sequential clamping is impossible, 4) evoked spinal cord potential-guided reconstruction of the critical intercostal arteries (preoperative evaluation using multi-detector row computed tomography), 5) cerebrospinal fluid drainage, and 6) administration of naloxone hydrochloride and methylprednisolone. In this paper, we analyzed clinical outcome of thoracoabdominal aortic surgery according to this strategy. MATERIALS AND METHODS: We have performed thoracoabdominal aortic surgery for 84 patients (52 male, mean 62 +/- 12 years old) during 1991-2003. Their etiology was 34 dissection, 44 non-dissection degenerative disease, 3 pseudo-aneurysm, and 3 infection. Ten operations were performed urgently and 8 emergently. Crawford's classification (type I/II/III/IV/V) was 17/28/17/13/9 for each type. We used partial cardiopulmonary bypass for 67 cases and deep hypothermic circulatory arrest for 14. RESULTS: For overall/elective cases (n = 84/66), we experienced 13.1/12.1% of incidence of spinal cord injury (paraplegia/paraparesis) and 8.3/4.5% of in-hospital mortality. Within 65 cases (55 elective) operated after August 1994, they decreased up to 7.7/5.5% (0% in type II) and 4.6/1.8%, respectively. Paraplegia was experienced in 2 patients before and 2 patients (emergent operations due to infective aneurysm) after August 1994 (4.8%). Thus, we have experienced no paraplegia in elective cases after establishment of our strategy. CONCLUSIONS: Our strategy for spinal cord protection during thoracoabdominal aortic surgery could provide acceptable clinical outcome and seemed justified.     

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.     

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%).     

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.     

Intraoperative spinal cord monitoring during descending thoracic and thoracoabdominal aneurysm surgery

BACKGROUND: Postoperative paraplegia is one of the most dreaded complications after descending thoracic and thoracoabdominal aneurysm surgery. In this study, intraoperative monitoring was applied during resection of descending thoracic and thoracoabdominal aneurysms to detect spinal cord ischemia and help prevent paraplegia. METHODS: Fifty-six patients (descending thoracic, 25; thoracoabdominal, 31) were monitored intraoperatively with both motor- (MEP) and somatosensory- (SSEP) evoked potentials. MEPs were elicited with transcranial electrical stimulation and recorded from the spinal epidural space (D wave) or peripheral muscles (myogenic MEP). SSEPs were obtained with median and tibial nerve stimulation. RESULTS: A total of 16 patients (28.6%) showed MEP evidence of spinal cord ischemia, only 4 of whom had delayed congruent SSEP changes. In 13 patients (23.2%), ischemic changes in MEPs were reversed by reimplanting segmental arteries or increasing blood flow or blood pressure. None of these 13 patients suffered acute paraplegia regardless of the status of SSEP at the end of the procedure, but 1 of them developed delayed postoperative paraplegia after multisystem failure. Three patients (5.4%) who had persistent loss of MEPs despite of recovery of SSEPs awoke paraplegic. CONCLUSIONS: The results demonstrate that compared with SSEP, MEP, especially myogenic MEP, is more sensitive and specific in detection of spinal cord ischemia, and that intraoperative monitoring can indeed help prevent paraplegia.     

Fighting spinal cord complication during surgery for thoracoabdominal aortic disease

Paraplegia or paraparesis after otherwise successful thoracic or thoracoabdominal aortic reconstruction is a devastating complication for both patient and physician. Various strategies have been developed to minimize the incidence of neurological complications after aortic surgery. The incidence of spinal cord ischemia and subsequent neurological complications has been correlated with (1) the duration and severity of ischemia, (2) failure to establish a spinal cord blood supply, and (3) reperfusion injury. Preoperative identification of the arteria radicularis magna, the artery of Adamkiewicz, facilitates identification of critical intercostal vessels for reimplantation, resulting in reestablishing spinal cord blood flow. Techniques for monitoring spinal cord function using evoked potentials have been developed, and surgical techniques have evolved to reduce the duration of ischemia. Furthermore, sequentially sacrificing all the intercostal arteries while maintaining collateral circulation to the cord has produced good outcomes. The severity of ischemia can be minimized by using cerebrospinal fluid drainage, hypothermia, distal bypass, managing the blood pressure, and adjunctive pharmacological therapy. Reperfusion injury can be reduced with the use of antioxidant therapy. Recent advances in endovascular stentgrafting have reduced the incidence of postoperative spinal complications, especially among high-risk patients.     

How to prevent spinal cord injury during endovascular repair of thoracic aortic disease

The incidence of spinal cord injury in thoracic endovascular aortic repair (TEVAR) has been 3–5 % from recent major papers where sacrifice of the critical intercostal arteries is inevitable by a stent graft. Hemodynamic stability, which depends on a network of blood vessels around the cord is most important not only during but also after stent-graft deployment. High risk factors of spinal cord injury during endovascular aortic repair are (1) coverage of the left subclavian artery, (2) extensive coverage of long segments of the thoracic aorta, (3) prior downstream aortic repair, (4) compromising important intercostal (T8–L1), vertebral, pelvic and hypogastric collaterals, and (5) shaggy aorta. Preoperative, intraoperative, and postoperative managements have been required to prevent spinal cord injury with TEVAR. For imaging assessment of blood supply to spinal cord including Adamkiewicz artery, prophylactic cerebrospinal fluid drainage is mandatory, and monitoring motor-evoked potential is recommended for high risk factors of spinal cord injury. Mean arterial pressure should be maintained over 90 mmHg after stent-graft placement for a while to prevent delayed spinal cord ischemia in high-risk patients of spinal cord ischemia. Finally, because spinal cord injury during TEVAR is not rare and negligible, perioperative care during TEVAR should be strictly performed according to the protocol proposed by each cardiovascular team.     

Spinal cord ischemia after thoracic and thoracoabdominal aortic aneurysm repair

In this paper, the author reviews the problematic around the spinal cord ischemic disfunction that sometimes occurs following the surgical management of thoracic and thoracoabdominal aortic aneurysm. After an anatomical review of the spinal cord vascularization, the diverse pathogenic mechanisms involved are described together with its importance and clinical significance, as well as the multiple procedures, techniques and pharmacotherapy employed nowadays aimed at lowering the occurrence of this most dramatic complication of thoracic and thoracoabdominal aortic aneurysm repair.     

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.     

胸腹主动脉瘤修复术后脊髓缺血损伤的发生机制及其防治

胸腹主动脉瘤修复术因其高病死率和高并发症率,一直是心血管外科极具挑战的手术。目前临床上常用于治疗胸腹主动脉瘤的手术方式有传统开放手术、杂交手术、腔内修复术。术后主要的并发症脊髓缺血损伤可导致患者截瘫,严重影响患者远期生存率和生活质量。本文主要针对胸腹主动脉瘤修复术后脊髓缺血损伤的发病机制、危险因素、防治措施进行总结和思考。     

Gastrointestinal complications after descending thoracic and thoracoabdominal aortic repairs: a 14-year experience

OBJECTIVE: There is a paucity of data regarding gastrointestinal (GI) complications after descending thoracic and thoracoabdominal aortic (DTA/TAA) surgical repairs. We examined our 14-year experience with these repairs to determine the incidence, outcomes, and risk factors for postoperative GI complications. METHODS: Between February 1991 and February 2005, we repaired 1,159 DTA/TAA. Data were prospectively collected. The mean patient age was 68 years and 36% were women. Complications were classified as biliary disease, hepatic dysfunction, pancreatitis, GI bleeding, peptic ulcer disease, bowel ischemia, and ileus. Risk factors for the occurrence of GI complications were ascertained by univariate and multivariable analysis. RESULTS: Of the 1,159 patients, 81 had 109 GI complications, for a 7% incidence. The mortality associated with GI complications was 39.5% compared with 13.5% (P < .0001) in patients without GI complications. The incidences of complications were bowel ischemia, 2.5% with 62% mortality; biliary disease, 0.3% with 75% mortality; hepatic dysfunction, 1.6% with 38% mortality; acute pancreatitis, 0.3% with 20% mortality; GI bleeding, 1.5% with 29% mortality; peptic ulcer disease, 0.9% with 30% mortality; and ileus, 2.2% with 26% mortality. Postoperative biliary disease (odds ratio [OR], 16.58; P = .001), hepatic dysfunction (OR, 3.58; P = .006), and bowel ischemia (OR, 10.03; P = .0001) were significantly associated with an increased postoperative mortality. Risk factors for the occurrence of GI complications were visceral involvement of the aortic repair (TAA extent II, III, and IV) (OR, 2.08; P = .002) and low preoperative glomerular filtration rate (OR, .98; P = .0002). CONCLUSION: Biliary disease, hepatic dysfunction, and bowel ischemia after DTA/TAA surgical repairs were associated with an increased mortality. Visceral involvement and preoperative renal insufficiency were risk factors for the occurrence of GI complications.