EXCLUSION of a thoracic aortic aneurysm (TAA) by endoluminal deployment of a stent graft appears to be effective therapy. Complications of endovascular graft placement include the technical problems associated with graft insertion, systemic effects of anesthesia and surgery, and specific problems related to the device reliability during follow-up. 1Acute-onset paraplegia is an uncommon yet devastating complication of endovascular TAA repair.

The patient was a 77-yr-old man with a descending thoracic aortic aneurysm (6 cm), infrarenal aortic aneurysm (3 cm), and left common iliac artery aneurysm (2.5 cm). He had a history of bilateral carotid artery stenosis, transient ischemic attacks, ischemic cardiomyopathy, mitral and aortic insufficiencies, hypertension, orthopnea, pulmonary emphysema resulting in dyspnea at rest, and gastroduodenal peptic ulcer. His poor physical status resulted in a decision to treat his TAA via  an endoluminal approach.

The patient underwent transfemoral insertion of an endovascular stent-graft (Excluder 40 × 20; W.L. Gore & Associates, Inc., Flagstaff, AZ) that extended from a point just distal to the left subclavian artery to the level of the tenth thoracic vertebra. This was performed under general anesthesia with etomidate, fentanyl, vecuronium and O2–air–isoflurane. The patient was hemodynamically stable throughout the procedure. There were no hypertensive or hypotensive episodes. He was extubated in the operating room, but showed acute onset of paraplegia, and was transported directly to the intensive care unit. The neurologist immediately evaluated the patient. She diagnosed flaccid paraplegia with total absence of sensation below the level of T4, accompanied by loss of movement, deep tendon reflexes, vibration, and joint-position sense in the lower limbs. Spinal cord ischemia was considered the most probable cause. No imaging of the spinal cord was performed. Conservative therapy was selected. The neurologist began anticoagulation with sodium heparin in order to limit neurologic deficit extension. Intravenous methylprednisolone (500 mg every 8 h), ranitidine (50 mg every 12 h) and N-acetyl-cysteine (2,000 mg every 8 h) were also given. The symptomatology did not improve in 1 h, so an urgent lumbar intrathecal catheter was inserted. Sodium heparin infusion was stopped at the moment of the catheter insertion. There were no difficulties during the placement of the intrathecal catheter despite of anticoagulation. The initial cerebrospinal fluid (CSF) pressure was greater than 25 mmHg. Immediate improvement was seen upon catheter insertion and commencement of drainage, which was continued in an effort to maintain CSF pressure of 12 mmHg. Immediate improvement was seen upon catheter insertion and commencement of drainage, which was continued in an effort to maintain CSF pressure lower than 12 mmHg. The patient began to recover sensitivity in 1 h and motor function in 3 h (in the left toes and foot at the beginning, extending afterwards to the rest of the lower limbs in 4 h).

The neurologic deficit resolved progressively. Recovery of sensory function was complete after 3 days, although motor function in the lower limbs continued to improve, extending to complete recovery after 13 days. CSF drainage was removed the third day due to fever, despite mild weakness of the right leg. Drug therapy was maintained 6 days. The patient was discharged with no neurologic deficit 15 days after surgery.

The standard technique for the treatment of descending TAAs is elective open surgical repair with graft interposition. 1Endoluminal approaches are becoming more common. Endoluminal therapy is restricted in our hospital to patients with aneurysms that contain proximal and distal stent graft landing zones whose coexisting diseases may preclude open surgical repair. This was believed to be most appropriate for the patient described.

Spinal cord ischemia may occur in 1–11% of operations involving open TAA repair. Acute-onset paraplegia after endoluminal TAA repair had not been reported previously. The etiology is multifactorial, involving a series of progressive interdependent events that include perioperative hypotension, increase in CSF pressure, inadequate perfusion to critical intercostal or lumbar vessels, oxygen radical–mediated lipid peroxidation and the extent of the aortic pathology.

The high cardiopulmonary risk of this patient resulted in a decision to treat his new deficit conservatively, so the therapy was focused on improving the etiologic factors. There was no perioperative hypotension, so cardiovascular drugs to maintain blood pressure were not needed. Second, oxygen radical–mediated lipid peroxidation has been suggested increasingly to be a therapeutic target for acute pharmacologic neuroprotection, 2so N-acetyl-cysteine was administered to the patient (2,000 mg every 8 h). Methylprednisolone has been also shown to possess significant antioxidant efficacy. 2This drug, in combination with CSF drainage, produces a synergistic benefit of extending the time interval of safe aortic cross-clamping 3and improves neurologic outcome after normothermic spinal cord ischemia. 4This patient received methylprednisolone (500 mg every 8 h), although the utility of steroids with CSF drainage had not been reported yet in acute paraplegia after TAA repair. Greater doses of steroids (such as those used in spinal cord section) were avoided because of the patient’s gastroduodenal peptic ulcer. Ranitidine (50 mg every 12 h) was also administered.

Third, prompt CSF decompression was performed to reduce the CSF pressure and improve spinal cord perfusion pressure. 3Cerebrospinal fluid drainage was useful previously in treating three cases of delayed paraparesis at 13, 512, 6and 6 h 7after aortic aneurysm repair, but this technique had not been employed before in acute-onset paraplegia. A CSF pressure of 12 mmHg was established as the critical point of drainage because this patient had acute paraplegia instead of delayed paraparesis (Khong et al.  5reported 15 mmHg). We avoided CSF overdrainage, because it can cause complications that result in neurologic deterioration (such as acute pneumocephalus, brain collapse, Chiari II–like syndrome with vocal cord paralysis and life-threatening aspiration, or temporal downward herniation with kinking of the posterior cerebral artery and acute brain infarction) or even in the death of the patient. 8Intermittent CSF drainage with a closed circuit (because of deficient flow throughout the catheter) and daily biochemical and microbiological CSF monitoring (to avoid infections) were established. Intrathecal catheter was removed the third day because of fever peak. CSF monitoring maintained negative all days. Neurologic recovery continued on after catheter removal, so we did not consider it necessary to insert a new one.

Finally, the extent of the aortic pathology is also important. Attachment of the endovascular stent graft to aortic wall could result in the stent crossing the ostia of critical intercostal vessels or even Adamkiewicz’s artery (usually originated at T9–T12), leading to inadequate perfusion and spinal cord ischemia. The mechanisms involved in the improvement of the patient’s neurologic deficit remain poor defined. Urgent CSF decompression could permit adequate spinal cord perfusion throughout collateral vessels, and pharmacologic therapy could have limited neurologic deterioration.

In conclusion, this case demonstrates the potential therapeutic role for prompt cerebrospinal fluid spinal decompression in combination with methyl-prednisolone and N-acetyl-cysteine administration to reduce the complications of acute paraplegia after endovascular thoracic aortic aneurysms repair.

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