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Ann Thorac Surg 2005;80:1280-1289
© 2005 The Society of Thoracic Surgeons
a Department of Anesthesia, University of Pennsylvania, Philadelphia, Pennsylvania
b Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania
c Department of Surgery, University of Pennsylvania, Philadelphia, Pennsylvania
Accepted for publication April 21, 2005.
* Address reprint requests to Dr Cheung, University of Pennsylvania, Department of Anesthesia, 3400 Spruce St, Dulles 680, Philadelphia, PA 19104-4283 (Email: cheunga{at}uphs.upenn.edu).
Presented at the Forty-first Annual Meeting of The Society of Thoracic Surgeons, Tampa, FL, Jan 24–26, 2005.
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Abstract |
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 Top Abstract IntroductionPatients and MethodsResultsCommentDiscussionAcknowledgmentsReferences |
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METHODS: Patients in thoracic aortic aneurysm stent trials from 1999 to 2004 were analyzed for paraplegic complications. Lower extremity strength was assessed after anesthesia and in the intensive care unit. A loss of lower extremity somatosensory evoked potential or lower extremity strength was treated emergently to maintain a mean arterial pressure 90 mmHg or greater and a cerebrospinal fluid pressure 10 mm Hg or less.
RESULTS: Seventy-five patients (male = 49, female = 26, age = 75 ± 7.4 years) had descending thoracic aortic aneurysms repaired with endovascular stenting. Lumbar cerebrospinal fluid drainage (n = 23) and somatosensory evoked potential monitoring (n = 15) were performed selectively in patients with significant aneurysm extent or with prior abdominal aortic aneurysm repair (n = 17). Spinal cord ischemia occurred in 5 patients (6.6%); two had lower extremity somatosensory evoked potential loss after stent deployment and 4 developed delayed-onset paraplegia. Two had full recovery in response to arterial pressure augmentation alone. Two had full recovery and one had near-complete recovery in response to arterial pressure augmentation and cerebrospinal fluid drainage. Spinal cord ischemia was associated with retroperitoneal bleed (n = 1), prior abdominal aortic aneurysm repair (n = 2), iliac artery injury (n = 1), and atheroembolism (n = 1).
CONCLUSIONS: Early detection and intervention to augment spinal cord perfusion pressure was effective for decreasing the magnitude of injury or preventing permanent paraplegia from spinal cord ischemia after endovascular stent repair of descending thoracic aortic aneurysm. Routine somatosensory evoked potential monitoring, serial neurologic assessment, arterial pressure augmentation, and cerebrospinal fluid drainage may benefit patients at risk for paraplegia.
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Introduction |
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionAcknowledgmentsReferences |
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Initial success with a management algorithm designed to detect spinal cord ischemia and implement immediate therapeutic interventions to improve spinal cord perfusion prompted the application of this management strategy for patients undergoing endovascular stent graft repair of descending thoracic aortic aneurysms [6]. The effectiveness of this management strategy was assessed using the hypothesis that early detection of spinal cord ischemia, combined with interventions to augment spinal cord perfusion using arterial pressure augmentation and lumbar cerebrospinal fluid (CSF) drainage, were effective for the prevention and treatment of paraplegia after endovascular stent repair.
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Patients and Methods |
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionAcknowledgmentsReferences |
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The Gore endoprosthesis (WL Gore, Inc, Newark, DE) was delivered through a 20 to 24 French sheath and expanded with a trilobed balloon that did not occlude flow in the aorta. The Talent thoracic stent graft (Medtronic, Inc, Minneapolis, MN) was delivered using a 24 to 25 French system and also expanded with a balloon. All procedures were performed using standard endovascular techniques with fluoroscopy. Transfemoral access was usually by a groin cutdown. In some patients, a small retroperitoneal incision was performed to gain access to the common iliac artery. Angiographic access was through the contralateral femoral artery or brachial artery. The minimum amount of aorta was covered to exclude the aneurysm with an adequate seal. The extent of endovascular stent coverage of the descending thoracic aorta was classified into three groups: extent A was coverage from the origin of the left subclavian artery to the T6 vertebral level, extent B was coverage from T6 to the diaphragm, and extent C was coverage of the entire descending thoracic aorta from the left subclavian artery to the diaphragm [7, 8].
All patients had general anesthesia maintained at less than or equal to 0.5 minimum alveolar concentration for intraoperative somatosensory evoked potential (SEP) monitoring. Intraoperative SEP monitoring and lumbar CSF drainage were used in patients believed to be at increased risk of spinal cord ischemia. Arterial pressure was monitored with an intraarterial catheter. Lumbar CSF drainage was performed using a 0.7 mm internal diameter lumbar CSF drainage catheter inserted 7 cm to 12 cm into the subarachnoid space by a 14 g Tuohy needle at the L3-L4 vertebral interspace after the induction of general anesthesia. The CSF was drained for a lumbar CSF pressure 12 mm Hg or greater during operation. Epidural or subarachnoid narcotics or local anesthetics were not administered. The mean arterial pressure (MAP) was maintained at 75–85 mm Hg during general anesthesia.
Neurophysiologic monitoring consisted of upper and lower extremity SEP using the montages recommended by the American Clinical Neurophysiology Society. Lower extremity SEPs were recorded from the popliteal fossa, lumbar spine, cervical spine, and scalp to localize injury to the peripheral nerve, spinal cord, or brain [9]. Postoperative MAP was maintained using vasopressors or vasodilators at 75–85 mm Hg or at a MAP where SEP signals were intact. Lumbar CSF was drained in 10 mL aliquots to maintain CSF pressure 12 mm Hg or less. The lumbar CSF catheter was occluded at 24 hours and removed at 48 hours after operation in the absence of a neurologic deficit.
Postoperative neurologic assessments were performed on an hourly basis to detect lower extremity motor weakness until the patient was able to report symptoms of weakness or numbness. If a neurologic deficit was detected, a full neurologic examination was performed emergently by a neurologist. Subsequent examinations were performed serially and during any periods of improvement or decline in neurologic function. Special attention was directed toward diagnosing spinal cord ischemia to exclude brain ischemia or peripheral nerve injury as etiologies. Strength in each lower extremity proximal and distal muscle groups was assessed and the presence or absence of a sensory deficit was recorded. Paraparesis was defined as weakness in a lower extremity muscle group, incomplete paraplegia, or unilateral paraplegia.
In the event of spinal cord ischemia, the MAP was increased to 85–100 mm Hg using phenylephrine or norepinephrine. In patients with a functioning lumbar CSF drain, CSF was drained for CSF pressure 10 mm Hg or greater. In patients without a lumbar CSF drain, a lumbar CSF drain was inserted emergently if there was no immediate improvement in neurologic function after augmentation of the arterial pressure. If there was no neurologic recovery at a MAP of 90–95 mm Hg, the MAP was augmented further in 5 mm Hg increments until resolution or stabilization of the postoperative neurologic deficit. Glucocorticoid therapy was administered only to patients with persistent neurologic deficits that did not respond to increased spinal cord perfusion pressure.
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Results |
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionAcknowledgmentsReferences |
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Only one patient had an aneurysm associated with aortic dissection. The mean age was 75 ± 7 SD years with 28 (37%) patients being female. Fifty-two patients had Talent endovascular stent grafts (World Medical Corp, Sunrise, FL) and 23 had Gore endoprosthetic grafts (WL Gore). Lumbar CSF drainage and intraoperative SEP monitoring were used more often in patients with prior abdominal aortic aneurysm repair. Among the 17 patients with prior abdominal aortic aneurysm repair, 13 (76.5%) had lumbar CSF drainage during operation and 8 (47.1%) had intraoperative SEP monitoring. Among the 58 patients without prior abdominal aortic aneurysm repair, 10 (17.2%) had lumbar CSF drainage during operation and 7 (12.1%) had intraoperative SEP monitoring.
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Patient 1
A 73-year-old male with a contained rupture of a 4.5 cm thoracic aortic aneurysm underwent endovascular stent repair (Talent, extent B) through the right ileofemoral artery. Intraoperative transesophageal echocardiogram demonstrated grade IV (> 5 mm) mobile atheroma in the thoracic aorta. Intraoperative SEP monitoring detected complete loss of posterior tibial nerve SEP after stent deployment consistent with spinal cord ischemia. The patient had immediate-onset postoperative paraplegia that did not improve in response to lumbar CSF drainage, arterial blood pressure augmentation, or high-dose methylprednisolone. Atheroembolism also caused small bowel ischemia requiring exploratory laparotomy and small bowel resection and left leg ischemia. The patient died on postoperative day (POD) 36 from multisystem organ failure. Spinal cord infarction and multisystem failure was attributed to severe atheromatous disease of the aorta and atheroembolism during the procedure.
Patient 2
A 70-year-old female underwent endovascular stent graft repair of a 5.0 x 3.5 cm thoracic aortic aneurysm (Gore, extent C). The graft was deployed through a left retroperitoneal incision because a vascular sheath could not be inserted into the femoral artery. The procedure was complicated by thrombosis and dissection of the left femoral artery requiring thrombectomy, endarterectomy, angioplasty, and stenting of the left iliofemoral arteries. On POD 1, the patient developed acute bilateral lower extremity weakness and numbness associated with a decrease in blood pressure (100/60 mm Hg) and decrease in hemoglobin (8.3 g/dL). Neurologic examination demonstrated weakness of both psoas muscles and loss of sensation to the T12 level consistent with spinal cord ischemia. An abdominal computed tomographic scan demonstrated a left retroperitoneal hematoma. Lower extremity motor and sensory function recovered over the course of the next 48 hours in response to treatment with dopamine, blood transfusion, and volume expansion to maintain a systolic blood pressure greater than 140 mm Hg. The patient was discharged on POD 11, able to ambulate with minor assistance.
Patient 3
A 72-year-old male with prior abdominal aortic aneurysm repair underwent endovascular stent graft repair (Talent, extent C) of a 5.2 cm thoracic aortic aneurysm. A lumbar CSF drain was placed prior to operation and the lumbar CSF pressure was maintained at 10–12 mm Hg. The patient had bilateral lower extremity weakness immediately after emergence from general anesthesia. The neurologic examination revealed flaccid paralysis of the left lower extremity and weakness in all right lower extremity muscle groups with intact sensation. Phenylephrine was administered to maintain a MAP 100 mm Hg or greater. The lumbar CSF drain was replaced because it became occluded with blood-tinged CSF. Lower extremity motor strength improved gradually over the next 48 hours, but the right lower extremity remained weak. The lumbar CSF drain was removed at 36 hours after operation and the MAP remained greater than 100 mm Hg without phenylephrine. Magnetic resonance imaging of the spine showed a small amount of blood in the subarachnoid space without evidence of spinal cord infarction. Lower extremity motor strength continued to improve. On POD 6, the patient was able to ambulate with assistance, but continued to have residual 4/5 right leg motor weakness. The patient was discharged home on POD 8 with a residual neurologic deficit.
Patient 4
An 85-year-old male with a prior abdominal aortic aneurysm bifurcation graft underwent endovascular stent repair (Gore, extent C) of a 6.1 cm descending thoracic aorta aneurysm. Intraoperative SEP monitoring and lumbar CSF drainage were performed. After deployment of the endovascular stent, at a MAP of 77 mm Hg, an acute decrease in lower extremity SEP amplitude indicated spinal cord ischemia (Fig 1). Spinal cord perfusion pressure was augmented by drainage of CSF to achieve a lumbar CSF pressure 10 mm Hg or less and administration of epinephrine 2 mcg per min and norepinephrine 6–8 mcg per min to achieve a MAP of 115 mm Hg. The lower extremity SEP signals recovered in response to the increase in spinal cord perfusion pressure. The patient had normal strength and sensation in both lower extremities after emergence from general anesthesia. The lumbar CSF drain was occluded at 24 hours then removed at 48 hours after operation. Epinephrine and norepinephrine infusions were gradually discontinued over 48 hours. The patient was discharged home on POD 8 without neurologic deficits.
Patient 5
A 78-year-old female had endovascular stent repair (Talent, extent C) of a 6.5 cm saccular aneurysm of the descending thoracic aorta. Endovascular stent graft deployment through the right external iliac artery was complicated by avulsion of the right common iliac artery requiring blood transfusion, right common iliac artery angioplasty, and right ileofemoral artery bypass grafting. At 9 hours after operation, the arterial pressure decreased from 140/70 mm Hg to a low of 70/48 mm Hg (Fig 2). The decrease in arterial pressure was followed by the acute onset of flaccid paralysis of the left leg without sensory loss. The was no evidence of bleeding and MAP was increased to 85–100 mm Hg with phenylephrine and norepinephrine. The increase in MAP was followed by complete recovery of left lower extremity motor strength (Fig 2). Norepinephrine was tapered off over 12 hours and phenylephrine infusion was discontinued at 24 hours. After discontinuation of phenylephrine, a second episode of flaccid paralysis of the left leg occurred on POD 2 that again recovered in response to resuming phenylephrine to maintain a MAP of 90–100 mm Hg (Fig 2). Phenylephrine infusion was tapered off again over the next 48 hours as the arterial pressure improved. The patient had no further episodes of leg weakness and was discharged on POD 14 without neurologic dysfunction.
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Comment |
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionAcknowledgmentsReferences |
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Factors that may have contributed to spinal cord ischemia after endovascular stent repair of thoracic aortic aneurysms were previous abdominal aortic aneurysm repair, hypotension associated with an occult retroperitoneal bleed, severe atherosclerosis of the thoracic aorta, injury to the external iliac artery, and the extent of the descending thoracic aorta covered by graft. Published series [1–4] also have reported that prior abdominal aortic aneurysm repair and the length of the stent graft were risk factors for spinal cord ischemia. The risk of spinal cord ischemia in patients with extent B or C coverage of the descending thoracic aorta may be explained by the exclusion of critical intercostal arteries at the T6 to T12 vertebral levels that supply the anterior spinal artery. The risk of spinal cord ischemia in patients with prior abdominal aortic aneurysm repair may be explained by compromise of pelvic and hypogastric collaterals that supply the anterior spinal artery [11]. Similarly, injury to the external iliac artery from stent delivery may have contributed to spinal cord ischemia because anterior spinal artery collaterals originating from the iliac arteries may have been compromised [12]. Hypotension associated with an occult retroperitoneal hemorrhage was temporally related to the onset of paraplegia in one patient. In this case, the decrease in spinal cord perfusion pressure associated with hypotension was the triggering event for spinal cord ischemia. Other reports have also described retroperitoneal hematoma combined with external iliac artery injury as a cause of spinal cord ischemia after endovascular stent repair [13, 14]. In another patient, hypotension preceding the onset of two distinct episodes of postoperative paraparesis may have been caused by autonomic dysfunction, and represented an early manifestation of spinal cord ischemia [6]. Systemic atheroembolism as a cause for spinal cord ischemia after endovascular instrumentation during stent deployment occurred in a patient who had severe atheromatous disease and mobile atheroma in the thoracic aorta, and has been reported as a cause of paraplegia after endovascular stent repair of abdominal aortic aneurysm [15].
Arterial blood pressure augmentation to improve spinal cord perfusion pressure was effective for the treatment of spinal cord ischemia complicating endovascular stent repair. Restoration of arterial blood pressure by volume expansion and vasopressor therapy was effective for the treatment of paraplegia caused by hypotension from an occult retroperitoneal hemorrhage. Vasopressor therapy to treat hypotension associated with spinal cord ischemia was effective for the treatment of two separate episodes of paraparesis in an individual patient. The immediate administration of vasopressor agents to augment arterial pressure after intraoperative spinal cord ischemia detected by SEP monitoring restored lower extremity SEP signals and may have prevented paraplegia or paraparesis in one patient. Arterial pressure augmentation in combination with lumbar CSF drainage contributed to the improvement, though incomplete recovery from spinal cord ischemia in a patient who had paraparesis upon emergence from general anesthesia. Arterial pressure augmentation was ineffective for the treatment of paraplegia caused by spinal cord infarction from atheroembolization in the patient with severe atherosclerotic disease of the thoracic aorta. The efficacy of arterial pressure augmentation for the treatment of spinal cord ischemia after endovascular repair was consistent with the demonstrated efficacy of this intervention for the treatment of delayed-onset spinal cord ischemia after open thoracoabdominal aortic aneurysm repair [6, 11, 16, 17]. Other published reports [1, 12] have also described the application of arterial pressure augmentation to treat paraparesis after endovascular stent repair. In general, arterial pressure was augmented to maintain a spinal cord perfusion pressure (MAP-lumbar CSF pressure) of at least 70 mm Hg at all times and vasopressor agents were administered to increase the MAP further in response to clinical evidence of spinal cord ischemia. Although no complications were associated with arterial pressure augmentation, the risk of hemorrhage as a consequence of arterial pressure augmentation may be less after endovascular repair when there are no major vascular anastomoses. Arterial pressure augmentation may be particularly important for the treatment of autonomic dysfunction or neurogenic shock associated with spinal cord ischemia [6, 11].
Lumbar CSF drainage is an established technique to decrease the risk of spinal cord ischemia after open thoracoabdominal aortic aneurysm repair [18]. Reports also support the use of lumbar CSF drainage for the prevention or treatment of spinal cord ischemia after endovascular stent repair of aortic aneurysms and dissections [1, 5, 12, 13, 19–21]. In our series, the efficacy of lumbar CSF drainage for the prevention and treatment of spinal cord ischemia after endovascular stent repair was more difficult to establish. Two patients in the series with clinical evidence of spinal cord ischemia recovered without need for lumbar CSF drainage. Prophylactic use of lumbar CSF drainage may have contributed to partial recovery in one patient with spinal cord ischemia detected upon emergence from anesthesia and in another patient with evidence of intraoperative spinal cord ischemia detected by SEP monitoring, but lumbar CSF drainage was not effective for the treatment of paraplegia in the patient with atheroembolic spinal cord infarction. Prophylactic lumbar CSF drainage was used more frequently in patients with prior abdominal aortic aneurysm repair when the risk of spinal cord ischemia was perceived to be greater. This practice was consistent with the practice described by Ellozy and colleagues [5], but it was not possible to determine if lumbar CSF drainage decreased the frequency or severity of spinal cord ischemia in that subgroup. Lumbar CSF pressures did not increase after endovascular stent deployment, but differences in CSF hemodynamics in response to endovascular compared with open repair of thoracic aortic aneurysms remain to be studied. No complications related to the use of lumbar CSF drainage were observed, but patients with lumbar CSF drainage required a longer intensive care unit length of stay for management and removal of the lumbar CSF catheter.
Intraoperative neurophysiologic monitoring is a recognized technique for detecting spinal cord ischemia during open repair of thoracoabdominal aortic aneurysm [9], but only limited experience has been reported for its use in endovascular repairs [22, 23]. In our series, intraoperative SEP monitoring was used, if available, for patients with prior abdominal aortic aneurysm repair or if there was a perceived risk of spinal cord ischemia. Intraoperative monitoring of lower extremity SEP during endovascular stenting in 15 cases detected two spinal cord ischemic events. In one patient, intraoperative spinal cord ischemia was verified by postoperative paraplegia. In the other patient, prompt intervention to augment spinal cord perfusion pressure was associated with recovery of lower extremity SEP and the absence of any postoperative neurologic deficits. Although it was not possible to verify that intraoperative SEP changes in the absence of postoperative neurologic deficits were caused by spinal cord ischemia, the onset of bilateral SEP changes isolated to the lower extremities at the time of stent deployment and recovery of SEP amplitudes in response to increased spinal cord perfusion pressure were consistent with a spinal cord ischemic event. In the patient with incomplete recovery from intraoperative spinal cord ischemia, it was tempting to speculate whether use of intraoperative SEP monitoring would have improved outcome by enabling earlier detection and treatment of spinal cord ischemia. Monitoring motor-evoked potentials during operation may have also increased the sensitivity of detecting spinal cord ischemic events causing only motor neuron dysfunction, but was not tested. Although additional experience will be necessary to justify the routine use of neurophysiologic monitoring for endovascular stent procedures, the preliminary experience supported the ability of intraoperative SEP monitoring to detect spinal cord ischemia.
Repair of isolated descending thoracic aortic aneurysms with endovascular stent grafts may compromise the vascular supply to the spinal cord and cause spinal cord ischemia or infarction in susceptible patients. Based on this clinical experience, an algorithm has been proposed to manage the risk of spinal cord ischemia in patients undergoing endovascular stent repair of isolated descending thoracic aortic aneurysms (Fig 3). Patients requiring extent B or C graft coverage of the descending thoracic aorta, with a compromised pelvic hypogastric collateral supply to the spinal cord from prior abdominal aortic aneurysm repair or external iliac artery injury, appear to be at increased risk of spinal cord ischemia after endovascular stent graft repair. Events such as hemorrhage or autonomic dysfunction causing hypotension may also trigger spinal cord ischemia after endovascular stent repair. Immediate detection of spinal cord ischemia by intraoperative SEP monitoring or neurologic examination combined with interventions that increased spinal cord perfusion were effective in treating paraplegia or paraparesis during and after endovascular stent repair.
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Discussion |
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionAcknowledgmentsReferences |
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My first question is regarding the patients in your study that had a prior abdominal aortic aneurysm repair. Did this subset of patients in your study have an endovascular repair or open repair? Secondly, we have found in our experience at the Arizona Heart Institute that there is a difference in spinal cord ischemia when there is a temporal delay between the AAA (abdominal aortic aneurysm) repair and the thoracic aneurysm repair. If we wait more than a month between procedures, we found that the incidence of spinal cord ischemia following thoracic aorta endoluminal grafting has declined. We aren't sure of the mechanism involved yet, but it may be related to the development of collaterals. Did you by chance identify any such temporal effects in your patients regarding the interval between a previous AAA repair and the time that these patients had their thoracic aortic aneurysm repaired?
DR CHEUNG: That is an excellent question. In the contemporary series published by Moon and others from the Stanford group, combined abdominal aortic aneurysm and thoracic aortic endovascular stenting at the same time was also associated with a higher rate of spinal cord ischemia that was consistent with your experience.
The patients in our study who had prior abdominal aortic aneurysm repairs, all had open repairs that were performed remotely in their history. However, we did observe that the patients who had prior abdominal aortic bifurcation grafts seemed to have a higher risk of spinal cord ischemia after thoracic aortic stenting, possibly because the middle sacral artery was sacrificed or that femoral iliac collaterals were compromised from the earlier operation. I would speculate, although we do not have data to support this, that prior endovascular stent repair of abdominal aortic aneurysm with a bifurcation graft, in comparison to prior open repair of abdominal aortic aneurysm, may pose a higher risk for spinal cord ischemia after thoracic aortic stenting.
DR WHEATLEY: Thank you.
DR HAZIM J. SAFI (Houston, TX): I need to congratulate you on really analyzing your data without trying to sell us the stent. I am considered a dinosaur when it comes to stented grafts, but this is a landmark paper; everybody should read it.
I had a patient who came to me with an aneurysm involving the intercostal artery patch, and he was an older man. We decided to use a stent. Before we began, we used a balloon to occlude the thoracic aorta and we used motor evoked potential, all of which disappeared. So we did the open repair. Are you going to monitor all such patients with motor evoked potential?
And my other question is why do you use the CSF (cerebrospinal fluid) drainage only for patients with infrarenal? It is not a big deal; your anesthesiologist can insert it and leave it there. And how long are you going to follow the patients with the drainage? Is it one day or two days or three days? Really, this is a great paper and congratulations.
DR CHEUNG: Thank you, Dr Safi. In response to your first question, there has been actually one published study by Midorikawa and others in the Japanese literature using sensory evoked potentials and monitoring sensory evoked potentials during test occlusion of the aorta prior to stent deployment to predict the risk of spinal cord ischemia prior to thoracic endovascular stenting.
I am not surprised that you saw loss of motor evoked potentials with balloon occlusion, because balloon occlusion of the aorta abolishes distal flow. Unless distal aortic perfusion is provided, there will be eventual loss of both lower extremity sensory and motor evoked potentials. For that reason, I am not so sure that loss of sensory or motor evoked in response to temporary balloon occlusion of the aorta would necessarily predict paraplegia after stent deployment. I also agree with you that thoracic endovascular stenting may be a perfect setting to use motor evoked potentials in the operating room. As you know, it is very difficult to provide anesthesia to monitor motor evoked potentials during open repairs because of the need to avoid neuromuscular blockade, but it may be much more feasible for cases of endovascular stent repair. So hopefully that is going to be in the future.
In response to the use of lumbar CSF drainage, we use it selectively in patients, because we believe that if the patients just have coverage of the thoracic aorta, the risk of paraplegia is relatively low. The low risk of paraplegia in patients with isolated thoracic aortic aneurysms was also demonstrated in your series of open repairs, and actually the incidence of spinal cord ischemia in your series was similar to that observed after endovascular stent repairs. However, for patients who have had a previous AAA repair, I believe that situation is the physiologic equivalent to a Crawford Extent II or a Crawford Extent III thoracoabdominal aortic aneurysm, and these are the high risk patients that we would like to target with CSF drainage. CSF drainage, although it is a safe technique in experienced centers, it does require an increased ICU (intensive care unit) length of stay.
We drain CSF for the first 24 hours, then cap the lumbar drain for 24 hours, and pull the lumbar drainage catheter on the third day. Using a lumbar CSF drain requires a 48-hour ICU length of stay after operation, and that may not be necessary for patients undergoing uncomplicated primary stent repair for a descending thoracic aneurysm. But that is an important point.
DR DAVID SPIELVOGEL (Valhalla, NY): I want to congratulate you and this is a wonderful series and this is very important work as we are all seeing a small but definite incidence of paraplegia after these devices. We have not seen any acute paraplegias.
All of the paraplegias that we have seen have been delayed; delayed as long as six weeks after implantation. The patients were perfectly stable and they began to have neurologic deficits at home. So I was just curious, do you have any ideas if there are two different mechanisms here? One is the acute coverage of a whole series of intercostals and then perhaps the delayed events or perhaps embolization from a type II endoleak, maybe perfusion of the sac and subsequent embolization, and if you have any comments related to that.
I also would like to echo Dr Safi's comments regarding motor evoked potentials because I think that is a very, very good way to know within a very short period of time if you have spinal cord ischemia. Thank you.
DR CHEUNG: Thank you for mentioning the problem. I am not sure how to define the syndrome of delayed onset paraplegia six weeks or maybe even months after the operation nor can I speculate on the mechanism leading to this problem. Certainly, as we get better at getting patients through the initial period of the operation and treating early onset delayed paraplegia, the syndrome of very delayed-onset paraplegia is guaranteed to arise. Unfortunately, we have very little clinical experience to guide how to treat those patients.
Our approach has been to titrate antihypertensive therapy and not get too aggressive with antihypertensive therapy in the early postoperative period. The objective is to ensure adequate spinal cord perfusion pressure during the period of risk until collaterals have a chance to develop. But certainly there are some patients, and we have had some of those, who develop late onset spinal cord ischemia as a recurrent problem and that is a very difficult condition to treat. Maybe some neuroprotective drugs will become available that will help us in the future for treating this condition.
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TopAbstractIntroductionPatients and MethodsResultsCommentDiscussionAcknowledgmentsReferences |
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J. J. Appoo, W. G. Moser, R. M. Fairman, K. F. Cornelius, A. Pochettino, E. Y. Woo, J. E. Kurichi, J. P. Carpenter, and J. E. Bavaria Thoracic aortic stent grafting: Improving results with newer generation investigational devices J. Thorac. Cardiovasc. Surg., May 1, 2006; 131(5): 1087 - 1094. [Abstract] [Full Text] [PDF]
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