THE first successful resection of a descending aortic aneurysm was performed by Lam and Aram in 1951, which was also the first reported complication of partial paraplegia after thoracic aneurysm repair. 1Since then, investigators have been encouraged to explore adjuncts to attempt to lower the risk for spinal cord ischemia, which varies between 3% and 26%. 2
Cerebrospinal fluid drainage (CSFD) first implemented in 1988 is an often used adjunct for thoracoabdominal aortic aneurysm repair (TAAA) repair that restores blood flow in an edema-compromised spinal cord. 1,3–6Although the improvements in operative technique such as sequential aortic clamping and left heart bypass have led to a reduction of immediate neurologic deficit, the mechanism that causes delayed deficits still remains to be elucidated.
Herein, we report two cases of complete reversal of delayed onset of paraplegia with the immediate resumption of CSFD after TAAA repair. The findings in our case report further support the evidence for immediate initiation of CSFD therapy in delayed neurologic deficits occurring after TAAA surgery.
A 60-year-old woman underwent elective surgery for a Crawford extent II aneurysm in March 2002 after a replacement of the ascending thoracic aorta was accomplished in January 2002. Beyond a history of hypertension, no other co-morbidities were present. Standard intraoperative management included distal aortic perfusion with left heart bypass (left heart bypass time: 52 min); visceral perfusion of the celiac trunk and the superior and inferior mesenteric arteries as well as both renal arteries (perfusion time: 36 min); and CSFD. The operative technique is described in detail elsewhere. 7A CSFD (Cordis lumbar drain kit; Cordis, Miami, FL) was implemented between L3 and L4 by introducing a 14-gauge Tuohy needle in the intervertebral space until free-flow of liquid from the needle was achieved. Thereafter, the catheter was adjusted to maintain cerebrospinal fluid (CSF) pressure at 10 mmHg. During operation (duration 360 min), 400 ml were drained. After an uneventful intraoperative course, the patient was transferred to the intensive care unit in a hemodynamic stable condition. No difficulties were encountered on awakening from sedation, and extubation was performed on postoperative day 1. Aside from delirium, the patient was in a stable condition. However, after 48 hours and a 250 ml drainage amount, the CSF drain was accidentally removed. Because the protocol in our department recommends duration of CSFD between 48 and 72 hours, no reinsertion of a new CSFD was attempted. One hour after removal, the patient reported weakness of the lower extremity. Neurologic status was assessed by scoring the deficit as described by Crawford et al. 8. Two hours later, the patient was unable to move her legs (score 0). A new CSFD was subsequently inserted. Liquid pressure after insertion was 20 mmHg, and 150 ml of fluid were drained to adjust the target pressure to 10 mmHg. No additional pharmacologic therapy was administered. There were no significant changes in systolic blood pressure before or during the period of neurologic deficit, with average systolic values between 120 and 150 mmHg. During the next 8 hours, the patient was again able to move her legs (score 1). The CSFD was removed after 72 hours, and the total drained volume was 610 ml. At this time, the patient had a score of 2. Complete motor function was regained during the next 2 weeks, and she could was discharged with minimal residual deficit (score 5).
A 69-year-old woman with chronic renal insufficiency who was otherwise healthy was admitted for TAAA repair for a Crawford extent I aneurysm with a maximum diameter of 9 cm. She successfully underwent surgery on April 2002 (left heart bypass time: 45 min, visceral perfusion time: 19 min). For operative details, refer to reference. 7A CSFD (Cordis lumbar drain; Cordis) was initiated preoperatively and was allowed to drain by gravity whenever the liquid pressure exceeds 10 mmHg. During the operation (duration: 300 min) 306 ml was drained. The patient was extubated 8 hours after surgery and was transferred to the ward on postoperative day 2. After 72 hours, the CSF catheter was removed, and the total drained volume was 550 ml. Two hours thereafter, the patient reported first signs of bilateral lower extremity weakness (score 2) and exhibited full paraparesis during the next 4 hours (score 0) until CSFD therapy was resumed with insertion of a new CSFD. Slight fluctuations in systolic blood pressure were noted before the onset of the neurologic deficit. However, systolic blood pressure was maintained above 130 mmHg. At 1 hour after reinsertion of the CSF catheter, slight improvements were noted by the patient (score 1). She was able to move her legs and could raise them after 24 hours. The drainage was left in place for 96 hours, during which 800 ml of liquid were drained. Standing up (score 3) was possible after removal of the CSF catheter after 4 days. She was discharged after 54 days with a score of 5 and showed no remaining deficits at a follow-up visit 4 months after surgery.
The technique of CSFD was introduced by Miyamoto et al. in 1960 with experiments of spinal cord protection in dogs. However, the use of CSFD remained dormant until 1988 when McCullough and Hollier revived it. 2,3
The effect of CSFD is based on the hypothesis that lowering CSF pressure increases spinal cord pressure and therefore ensures spinal cord perfusion. By draining excess liquid, spinal cord compression is released and perfusion is enhanced. Furthermore, through the use of distal aortic perfusion, the distal aortic pressure is elevated and further increases spinal cord perfusion. 9–11The consensus regarding the target CSF pressure is that it should not exceed 10 mmHg. 9
Although several studies advocate the use of CSFD, none provides recommendations regarding the duration of CSFD. After intensive literature review, we found durations between 40 hours 12and 120 hours, 13with 72 hours as the most common. 6,9–11,14–17
Immediate reinsertion of a CSFD after recognition of delayed neurologic deficit is an established treatment method with acceptable success rates. 13,18,19Safi et al. reviewed their experience in managing patients with delayed neurologic deficit after TAAA repair. 18A spinal cord compartment syndrome triggered by unstable blood pressure and increased CSF pressure possibly caused by spinal cord edema is suggested as the primary reason for the development of delayed neurologic deficit. 19
However, the possibility of epidural hematoma formation has also been considered in a patient with new onset of paraparesis after TAAA repair. Brain computed tomography is recommended for identifying this rare but serious complication that necessitates neurosurgical intervention. 20
The present cases and those in the literature 13,18,19indicate that 72 hours is too short to effectively prevent the development of delayed neurologic deficit, because increased CSF pressure to reperfusion edema persists for more than 72 hours. The amount of drained CSF with 550 ml and 610 ml, respectively, in our two cases further supports this hypothesis. As a consequence of these findings, we leave CSFD in place for at least 96 hours, and a drainage volume of less than 100 ml in 24 hours is required before removal of the CSFD. The last three patients treated with this regimen produced an average of 1,700 ml of liquid during CSFD duration of 120 hours, which represents a sevenfold increase in the normal 24-hour production of 250 ml liquid. We observed an increased daily volume between days 2 and 4, which let us assume that spinal cord edema persists for more than 2 days.
Nevertheless, further studies addressing the optimal drainage duration must be conducted to elucidate this still underinvestigated field of TAAA repair. Despite such recognized adjuncts such as CSFD, left heart bypass, distal aortic perfusion, and reattachment of critical intercostals arteries, paraplegia still occurs with an incidence of 3% to 15% in experienced centers, which underlines the need for continuing research for this most feared complication after thoracoabdominal aortic aneurysm repair. 3,14