Complications to cerebrospinal fluid drainage and predictors of spinal cord ischemia in patients with aortic disease undergoing advanced endovascular therapy.

OBJECTIVE: To study the complications after cerebrospinal fluid (CSF) drainage and predictors of spinal cord ischemia (SCI) after advanced endovascular therapy with CSF drainage for complex aortic disease. METHODS: Between 2009 and 2012, 88 attempts of CSF drainage insertions/84 operations/83 patients, of the 658 operations for aortoiliac diseases, were performed. RESULTS: Indications for therapy were aortic dissection (n = 13) and aortic aneurysm (n = 70), of whom 38 had thoracoabdominal aortic aneurysm (TAAA). In all, 10 had ruptured aorta. The CSF drainages were inserted preoperatively (n = 75) and postoperatively (n = 9). In all, 14 CSF drainages were nonfunctioning. The SCI was present in 29 patients, transient/permanent in 12/17. Intraoperative circulatory instability (P = .001) and operation for TAAA, type II (P = .036), were associated with SCI. Meningitis (n = 1), epidural (n = 1), and subdural (n = 2) hematoma and needle-mediated paresis in 1 leg (n = 1) occurred after CSF drainage. CONCLUSIONS: Complication to CSF drainage occurred too frequently in this selected group of patients with high rate of SCI.

Subdural hematoma induced by cerebrospinal fluid drainage: potentially catastrophic complication of spinal cord protection after thoracoabdominal aneurysm repair.

A 50-year-old man underwent replacement of the descending thoracic aorta for a DeBakey type III-b chronic dissecting aortic aneurysm. During the surgery, lumbar cerebrospinal fluid (CSF) drainage with a 10 cm H2O pop-off pressure was used to protect against spinal cord ischemia. During cardiopulmonary bypass, the patient's pupils were isocoric, but anisocoric at end of the operation. As computed tomography of the brain showed right subdural hematoma, neurosurgical drainage was instituted emergently. Although some neurological deficit remained, the patient recovered well and was discharged. This case provides a strong reminder that CSF drainage for spinal cord protection against ischemia might induce subdural hematoma, which can be catastrophic during an operation for thoracoabdominal aortic aneurysm.

Cerebral spinal fluid drainage and distal aortic perfusion decrease the incidence of neurological deficit: the results of 343 descending and thoracoabdominal aortic aneurysm repairs.

OBJECTIVE: We reviewed our experience of 343 descending and thoracoabdominal aortic aneurysm repairs to determine the impact of the adjuncts distal aortic perfusion and cerebral spinal fluid drainage on neurological deficit and death. MATERIALS AND METHODS: Between January 1991 and March 1996, 104 (30%) patients were operated for thoracoabdominal aortic aneurysm type I, 118 (34%) for type II, 68 (20%) for type III or type IV, and 53 (15%) for descending thoracic type. Before September 1992, simple cross-clamp was used for 94 (27%) patients. After September 1992, adjuncts were used for 186 (54%) patients. RESULTS: Overall neurological deficit was 33/343 (10%). Neurological deficit for simple cross-clamp patients compared to adjunct patients was 15/94 (16%) vs. 12/186 (7%) (O.R. 0.36, p < 0.01). For types I and II the incidence was 11/52 (21%) vs. 12/141 (9%) (O.R. 0.35, p < 0.02) and for type II, nine out of 22 (41%) vs. 11/85 (13%) (O.R. 0.21, p < 0.003). Overall 30-day mortality was 43/343 (13%), including patients presenting with rupture. Excluding these patients, overall 30-day mortality was 33/322 (10%). CONCLUSION: Cerebral spinal fluid drainage and distal aortic perfusion decreased the incidence of neurological deficit and were particularly effective for patients at highest risk with type II thoracoabdominal aortic aneurysm.

A prospective randomized study of cerebrospinal fluid drainage to prevent paraplegia after high-risk surgery on the thoracoabdominal aorta.

This article is concerned with the study of the effect of several variables, principally that of cerebrospinal fluid drainage, on the incidence of neurologic deficit in a prospective randomized series of patients with extensive aneurysms of the descending thoracic and abdominal aorta (thoracoabdominal type I and II). Forty-six patients had cerebrospinal fluid drainage, and 52 were controls, with a total of 98 available for study. Cerebrospinal fluid pressure was continuously monitored in the former group and pressure maintained less than or equal to 10 mm Hg in 20, less than or equal to 15 mm Hg in 20, and greater than 15 mm Hg in 6 patients during period of aortic clamping. The method of treatment including reattachment of intercostal and lumbar arteries (p = 0.2), temporary atriofemoral bypass during aortic occlusion (p = 0.3), and spinal fluid drainage (p = 0.8) were not statistically significant in reducing the incidence of neurologic deficits. Thus cerebrospinal fluid drainage as we used it, was not beneficial in preventing paraplegia. On appropriate statistical analysis we found that the only significant predictor of delayed deficits was postoperative hypotension (p = 0.006).

Naloxone and spinal fluid drainage as adjuncts in the surgical treatment of thoracoabdominal and thoracic aneurysms.

Forty-seven patients who were treated for thoracoabdominal or thoracic aneurysms over a 5 1/2-year period were analyzed for neurologic deficit risk. Patients were divided into two groups for analysis. Twenty-four patients, who were treated from January 1984 to December 1986, did not undergo spinal fluid drainage or naloxone administration (group A). Twenty-three patients, who were treated from January 1987 to August 1989, had spinal fluid drainage (group B); 12 patients in this group also received naloxone as an intravenous drip at 1 microgram/kg/hr for 48 hours after surgery. Permanent neurologic deficits occurred in seven (29%) group A patients but in only one (4%) group B patient, who did not receive naloxone (p less than 0.03). The first two group B patients to receive naloxone showed complete reversal of neurologic deficits on waking from anesthesia. This significant reduction in neurologic deficit was associated with an increased 1-year survival rate (72% in group A, 91% in group B). We conclude that the use of naloxone and spinal fluid drainage reduces the incidence of neurologic deficit that is associated with repair of thoracoabdominal and thoracic aortic aneurysms. This reduction in neurologic deficit is associated with improved survival in the long term. The observed reversal of postoperative neurologic deficits with naloxone implicates opiates as a major factor in the pathophysiology of spinal cord ischemia.