Journal of Vascular Surgery
Volume 49, Issue 1 , Pages 29-35, January 2009

Complications of spinal fluid drainage in thoracoabdominal aortic aneurysm repair: A report of 486 patients treated from 1987 to 2008

Presented at the Society for Vascular Surgery meeting, San Diego, Calif, June 5-8, 2008.

University of Wisconsin School of Medicine and Public Health

Received 28 May 2008; accepted 25 July 2008. published online 28 October 2008.

Article Outline

Objective

Spinal fluid drainage reduces paraplegia risk in thoracic (TAA) and thoracoabdominal (TAAA) aortic aneurysm repair. There has not been a comprehensive study of the risks of spinal fluid drainage and how these risks can be reduced. Here we report complications of spinal fluid drainage in patients undergoing TAA/TAAA repair.

Methods

The study comprised 648 patients who had TAA or TAAA repair from 1987 to 2008. Spinal drains were used in 486 patients. Spinal fluid pressure was measured continuously, except when draining fluid, and was reduced to <6 mm Hg during thoracic aortic occlusion and reperfusion. After surgery, spinal fluid pressure was kept <10 mm Hg until patients were awake with normal leg lift. Drains were removed 48 hours after surgery. Spinal and head computed tomography (CT) scans were performed in patients with bloody spinal fluid or neurologic deficit. We studied the incidence of headache treated with epidural blood patch, infection, bloody spinal fluid, intracranial and spinal bleeding on CT, as well as the clinical consequences.

Results

Twenty-four patients (5%) had bloody spinal fluid. CT exams showed seven had no evidence of intracranial hemorrhage, 14 (2.9%) had intracranial blood without neurologic deficit, and three with intracranial bleeding and cerebral atrophy had neurologic deficits (1 died, 1 had permanent hemiparesis, and 1 with transient ataxia recovered fully). Two patients without bloody spinal fluid or neurologic deficit after surgery presented with neurologic deficits 5 days postoperatively and died from acute on chronic subdural hematoma. Neurologic deficits occurred after spinal fluid drainage in 5 of 482 patients (1%), and 3 died. The mortality from spinal fluid drainage complications was 0.6% (3 of 482). By univariate and multivariate analysis, larger volume of spinal fluid drainage (mean, 178 mL vs 124 mL, P < .0001) and higher central venous pressure before thoracic aortic occlusion (mean, 16 mm Hg vs 13 mm Hg, P < .0012) correlated with bloody spinal fluid.

Conclusion

Strategies that reduce the volume of spinal fluid drainage but still control spinal fluid pressure are helpful in reducing serious complications. Patients with cerebral atrophy are at increased risk for complications of spinal fluid drainage.

 

Spinal fluid drainage has become a standard intervention to reduce paraplegia risk in thoracic (TAA) and thoracoabdominal (TAAA) aortic aneurysm repair.1, 2, 3, 4 Complications associated with diagnostic lumbar puncture,5 neuraxial anesthesia,6 and spinal fluid drainage7, 8 have been reported. Although spinal fluid drainage has been used in TAAA repair for 20 years,9 there has not been a comprehensive study of the associated risks. Here we report a retrospective analysis of the complications of spinal fluid drainage in 486 patients.

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Methods 

A concurrently maintained, institutionally approved database was used to study 648 patients who had TAA or TAAA repair from 1987 to 2008. Surgery in all patients who had open repair with spinal fluid drainage was done without assisted circulation or heparinization. Since 2005, thoracic aneurysms have been treated with endografts. Endograft patients were heparinized to achieve an activated clotting time of 200 to 250 seconds.

Spinal drains were placed preoperatively by anesthesiologists in 486 patients. Drains were not placed in acute patients with hypotension, patients with known intracranial disease, or patients with abnormal results on coagulation studies. Elective patients stopped clopidogrel 7 days before surgery, but continued aspirin. If blood could be aspirated from the needle during drain insertion, elective surgery was postponed. From 1987 to 2000, a small (19-gauge) epidural catheter was placed using anatomic landmarks, with needle placement at L3-L4 or L2-L3 and the catheter advanced 10 cm after entering the dura. Because of an unacceptable number of drain failures and difficult drain insertions, after 2000 a larger (16-gauge) Silicone drain (Medtronic EMD lumbar drain, Goleta, Calif) was placed under fluoroscopy, with needle insertion at L3-L4 or L2-L3 and the catheter tip positioned at T9-T10.

Spinal fluid pressure (SFP) was measured immediately after drain insertion, continuously during surgery except when fluid was drained to gravity in 5-mL increments, and for 48 hours after surgery. In open repairs spinal fluid was drained to achieve a SFP of <6 mm Hg during surgery. Beginning in 2003, spinal fluid was drained to achieve a SFP of <6 mm Hg only during thoracic aortic occlusion and reperfusion, focusing on controlling SFP during critical periods of the surgery by draining the smallest volume of spinal fluid possible. In thoracic endograft procedures, SFP was reduced to <10 mm Hg before device deployment.

The total volume of spinal fluid drained during surgery was measured. Drain failure was defined as being unable to drain enough fluid to control SFP during thoracic aortic occlusion. After surgery, spinal fluid was drained to keep the SFP <10 mm Hg only until patients were awake with normal leg lift. After normal leg lift was observed, SFP was monitored, and fluid was not drained unless weakness occurred. Drains were removed 48 hours after open repairs and 24 hours after endograft procedures.

Drainage was stopped if the fluid became bloody. Spinal and head computed tomography (CT) scans were performed in patients with bloody spinal fluid and in all patients with abnormal neurologic signs. Postoperative postural headache was treated with epidural blood patch.

Patients were followed up for 12 months after surgery. We studied the incidence of epidural blood patch, postoperative neurologic deficit, infection, bloody spinal fluid, presence of spinal and intracranial bleeding on CT, and the resulting clinical consequences. The Fisher exact test and multivariate analysis were done to analyze factors associated with complications.

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Results 

The mean age was 67 years, and 54% of patients were men. There were 72 patients (15%) with TAA, and 25 (34%) were treated with endografts. There were 414 patients with TAAAs, consisting of Crawford category type 1 in 73 (18%), type 2 in 139 (34%), type 3 in 89 (21%), and type 4 in 113 (27%). There were 135 acute patients (28%), with rupture, acute dissection, aortitis, or trauma. The 30-day mortality was 3.8% in elective patients and 13.3% in those presenting acutely. A total of 311patients (64%) had a small drain, and 175 (36%) had a large drain. Four acute patients died intraoperatively and could not be analyzed for drain complications. Twenty-three patients (4.8%) were paralyzed, and six of these had delayed paralysis.

There was no difference in mean volume of fluid drained in small drain (127 mL) and large drain (128 mL) patients, or in mean volume of fluid drained in patients treated from 1987 to 2003 (130 mL) and those treated from 2003 to 2008 (120 mL; P = .074). Drain failure occurred in 24 of 308 patients (7.8%) with small drains and in three of 174 patients (1.7%) with large drains placed using fluoroscopy; this difference was significant (P = .0054). Since using fluoroscopy, we were technically unable to place a drain in only one patient and did not aspirate blood during drain placement in any patient. Two small-drain patients (0.6%) and four large-drain patients (2.3%) had postural headaches that were treated with epidural blood patch; this difference was not significant. There were no spinal drain infections.

Bloody spinal fluid was noted in 24 patients (5.0%), and they underwent spinal and head CT scans. No patient had spinal hematoma on CT. Seven of the 24 had no CT evidence of an intracranial hemorrhage. Head CT scans showed intracranial bleeding in 17 patients (3.5%): 10 patients had small, five had moderate, and two had large subdural, subarachnoid, or intraparenchymal hemorrhages. Six patients had small or moderate intraparenchymal bleeding only, without an accompanying subarachnoid or subdural hematoma. No epidural hematomas were found.

Of the 17 patients with intracranial blood on CT, 14 did not have neurologic deficits (Table I). In three of the 14 patients without deficits, small acute hemorrhages were superimposed on an existing undiagnosed intracranial lesion: one patient had new hemorrhage at the site of an old subdural hematoma, one had bleeding near a small meningioma, and one had new hemorrhage at the site of an old cerebellar infarct.

Table I. Location of hemorrhage on computed tomography scan in patients with bloody spinal fluid
YearSubarachnoidIntraparenchymalSubduralVentricleSizeNeurologic deficit
1994 R cerebralYesLrgBrain herniation/death
1997L frontalL frontalFalx/tentoriumYesS
1997 L cerebellarTentoriumYesS
1997Inferior falxL parietalInferior falx S
1997 R/L cerebellar M
1998Posterior fossa Tentorium Lrg
1998 R temporal S
1999R parietal, R/L sulci M
1999 R temporal/parietal S
2001 Posterior falx S
2002 TentoriumYesS
2002 R cerebellar YesMAtaxia that resolved
2002 L cerebellarL tentorium S
2003R lateral fissure Tentorium S
2003 L cerebellar YesM
2003R frontal/parietal R frontal/parietal ML hemiplegia, ambulatory
2006 L cerebellar S

L, left; Lrg, Large; M, moderate; R, right; S, small.

Neurologic deficits were present in three patients with intracranial bleeding on CT: one died from brain herniation caused by mass effect, one sustained permanent left hemiparesis but was ambulatory; and one recovered fully from transient ataxia. Both the patient who died and the patient with hemiparesis had large right-sided cerebral subdural hematomas. The patient with transient ataxia had a moderate-sized left cerebellar intraparenchymal hemorrhage (Table I). All three patients had pre-existing, but unknown, cerebral atrophy with brain volume loss.

Two patients who did not have bloody spinal fluid or neurologic deficit after surgery developed neurologic deficits on postoperative day 5 (3 days after spinal drain removal) after receiving enoxaparin for deep venous thrombosis and heparin for pulmonary embolus. Both had acute cerebral subdural hematomas at the site of an undiagnosed chronic subdural hematoma on CT and died despite neurosurgical evacuation of the hematoma.

Neurologic deficits occurred in five of 482 patients (1%) after spinal fluid drainage, and three of these patients died. The mortality from spinal drain complications was 0.6% (3 of 482). By univariate and multivariate analysis, higher central venous pressure before aortic occlusion (mean, 16 vs 13 mm Hg, P < .0012) and volume of spinal fluid drained intraoperatively (mean, 178 vs 124 mL, P < .0001) correlated with bloody spinal fluid (Table II, Table III, Table IV). Age, gender, drain type, SFP, acuity, blood replacement, Crawford aneurysm type, renal ischemia time, preoperative renal function, arterial blood pressure, and other hemodynamic variables were not significant. No patient presented with a new neurologic deficit after discharge.

Table II. Univariate Analysis for Intracranial Bleeding
VariableMeanBleed Y/NP
Age, years67.76Y.933
66.99N
SF drained, mL178.46Y<.0001a
124.09N
SFP-1, mm Hg16.92Y.613
16.28N
SFP-2, mm Hg6.2Y.741
5.95N
SFP change, mm Hg−11.08Y.575
−10.29N
CVP-1, mm Hg16.61Y.0012a
13.11N
CVP-2, mm Hg21.25Y.0034
17.34N
CVP-3, mm Hg21.6Y.0178
18.01N
MAP-1, mm Hg88.84Y.2363
84.98N
MAP-2, mm Hg98.33Y.3971
95.51N
MAP-3, mm Hg82.87Y.5291
81.09N
Blood replacement, L6.31Y.0735
4.93N
Pre-op creatinine, mg/dL1.44Y.5527
1.33N

1, Preclamp; 2, during clamp; 3, unclamped; CVP, central venous pressure; MAP, mean arterial pressure; PAP, pulmonary artery pressure; SFP, spinal fluid pressure.

aVolume of spinal fluid drainage and higher CVP were significant for bleeding on univariate analysis.

Table III. Univariate analysis for intracranial bleedinga
VariableBleedingTotal No.%P
Drain
Large drain121597.56.1235
Small drain122944.23
Acute
Yes71275.22.9022
No173265.51
Gender
Female142056.82.2158
Male102484.25

aAge, gender, and acuity were not significant.

Table IV. Multivariate analysis
VariableProbabilityOR95% CI
Spinal fluid removed0.00010.0053−0.0255−0.0085
CVP-10.03860.0356−0.01883−0.00648
CVP-20.37470.2727−0.117990.04584
Blood replacement0.67420.4875−0.00011−0.00009

1, Preclamp; 2, during clamp; CI, confidence interval; CVP, central venous pressure; OR, odds ratio.

CVP before aortic occlusion and volume of spinal fluid drained remained significant on multivariate analysis.

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Discussion 

The choroid plexus and walls of the ventricles produce cerebrospinal fluid at a rate that varies in a diurnal rhythm from 0.2 to 0.7 mL/min, producing a total of 400 to 600 mL of fluid each 24 hours.10 Cerebrospinal fluid circulates continuously from the brain to the spinal canal and back to the brain, where it is reabsorbed in the venous sinuses. The total volume of circulating fluid is about 140 mL in an adult, and the ventricles hold an additional 25 mL.10

Changes in spinal fluid volume and pressure affect intracranial mechanics and can produce deleterious clinical effects. When spinal fluid is removed, SFP drops, producing intracranial hypotension. Headache is a well-known result of procedures that reduce spinal fluid volume and pressure, such as lumbar puncture, spinal anesthesia, myelography, and ventricular shunts.11 The mechanism of headache is thought to be tension on the sensory receptors of the dural sinuses.12, 13 Headache requiring treatment with epidural blood patch was a complication of spinal fluid drainage during TAAA repair. CT and magnetic resonance scans done after spinal fluid removal in diagnostic lumbar puncture show caudal displacement of the brain, with cerebellar tonsillar sagging, a decrease in ventricular size, and dilated veins.14 These findings correlate with decreased SFP.15 Venous engorgement after lumbar puncture may cushion the displacement of the brain caused by spinal fluid removal.

Intracranial hypotension can cause acute intracranial bleeding. This complication has been documented after diagnostic lumbar puncture,11 spinal anesthesia,6 ventriculoperitoneal shunt placement, myelography,13 spinal fluid drainage during neurosurgery or thoracic aortic surgery,7, 8 and dural leak after spine surgery.13 Some series have reported subdural hematomas in 10% of cases of intracranial hypotension, regardless of the cause.11

Loss of spinal fluid reduces intracranial pressure, leading to an enlargement of the dural venous sinuses.16 Caudal brain displacement from lower intracranial pressure creates tension on enlarged venous sinuses that predisposes to venous tears.12 Intracranial hypotension can stretch and rupture large cortical veins crossing the subdural space.17 Reflex vasodilatation in response to pressure on the dura, veins, and dural sinuses by the caudally displaced brain may increase the risk of subdural bleeding.18

Bleeding can occur in the posterior fossa under the tentorium cerebellum as the cerebellum sags onto the foramen magnum, above the tentorium as the cerebrum sags in a caudal fashion onto the cerebellum, and in the temporal and parietal lobes as the cerebrum sags onto the cranium. If the sag is slow, there may be no bleeding at all; but if the brain deforms rapidly, the resulting tension may tear subdural veins, producing bleeding. Intracranial hypotension can also produce subarachnoid hemorrhage.13 Patients with a history of head trauma, chronic subdural hematoma, cerebral atrophy, cranial vault abnormalities, arteriovenous malformations, abnormalities of coagulation, or cerebral aneurysms may be at increased risk for hemorrhagic complications of intracranial hypotension.12

SFP normally approximates central venous pressure,19 and spinal cord perfusion pressure is the difference between mean arterial pressure and SFP. Thoracic aortic clamping produces an acute rise in both central venous pressure and SFP. This increase in SFP decreases spinal cord blood flow.20, 21 Animal experiments using thoracic aortic occlusion models show that draining spinal fluid during aortic occlusion reduces SFP, improves spinal cord perfusion, and reduces paralysis.22, 23 Spinal fluid drainage has also been shown to reduce paralysis in randomized trials of patients having TAAA repair.24, 25 Although there are proven benefits to spinal fluid drainage, less is known about the risks.

Whether neuraxial bleeding occurs from spinal fluid drainage during TAAA repair and whether it results in neurologic deficit probably depends on factors such as traumatic drain placement, volume and rate of spinal fluid drainage, extent of venous engorgement, size of the veins that rupture, pre-existing intracranial pathology, and the presence of coagulopathy. The most serious complication of spinal fluid drainage was intracranial bleeding, and not intraspinal, spinal subarachnoid, epidural or subdural bleeding at the site of needle insertion or catheter placement, although others have reported intraspinal bleeding.26 In our experience the appearance of blood in the spinal fluid was a very sensitive indication of intracranial bleeding, even in the absence of clinical neurologic signs. Bloody spinal fluid occurred with both small and large drains and correlated with draining a larger volume of fluid during surgery. Higher central venous pressure before thoracic aortic occlusion also correlated with bloody spinal fluid. Arterial hypertension did not.

Subdural27, 28 and intraparenchymal29 intracranial hematoma are recognized complications of spinal fluid drainage after TAAA repair. In the series of 230 patients reported by Dardik et al,28 draining a larger volume of fluid (690 vs 359 mL) in the perioperative period increased the risk that a subdural hematoma would develop.28 These totals included significant drainage after surgery.

We do not believe that postoperative drainage is necessary or desirable as long as patients have normal leg strength. Because we let SFP return to baseline as soon as patients are awake, our patients had very little postoperative fluid drainage. However, draining a larger volume of fluid intraoperatively (178 vs 124 mL) was a significant risk factor for intracranial bleeding. Whether the pressure threshold for drainage should be 12, 10, 5, or 0 cm H2O or mm Hg (cm H2O/1.3 = mm Hg), groups choose different target pressures somewhat arbitrarily because there is no evidence to prove which pressure has better outcomes.

Because most of the patients in the Dardik et al study with subdural hematomas were drained to a pressure of 5 cm H2O (3.8 mm Hg), they recommended draining only to a pressure of 10 cm H2O (7.7 mm Hg).28 However, our patients all had spinal fluid drainage to <6 mm Hg, and lower SFP was not a risk factor in intracranial bleeding. Dardik reported that only two of eight subdural hematomas appeared in the first week, and two were diagnosed 1.5 and 5 months after surgery.28 We did not have any late subdural hematomas. All patients were monitored for 1 year after discharge, and no patient presented with neurologic deficit or clinical signs of subdural hematoma >5 days after surgery.

Moderately small amounts of subdural, subarachnoid, or intraparenchymal blood did not result in neurologic deficit. Each of the three patients that presented with immediate neurologic deficits had a large intracranial hemorrhage on CT. These patients also had unknown cerebral atrophy, with loss of brain volume, that may have affected the size of the initial hemorrhage or, in the case of subdural hematoma, whether it became large enough to cause neurologic deficit or death from intracranial mass effect. The two patients who did not have bloody spinal fluid or neurologic deficit after surgery that developed delayed neurologic deficits on postoperative day 5 after being anticoagulated both had an acute subdural cerebral hematoma at the site of an undiagnosed old subdural hematoma on CT. In these patients, 115 and 120 mL of spinal fluid was removed without immediate complications, and we believe anticoagulation in the presence of an old subdural hematoma also played a role in their hemorrhages.

Epidemiologic studies report the incidence of chronic subdural hematoma as 7.35 to 13/100,000 population in persons aged >65 years and up to 58/100,000 in persons >70 years.30, 31 These estimates were extrapolated from neurosurgical procedures in elderly populations and may actually underestimate the incidence of asymptomatic subdural hematomas. Patients with pre-existing intracranial disease that produces loss of brain volume, those with hydrocephalus, and those with old subdural hematoma may be at more risk of intracranial bleeding complications from spinal fluid drainage during TAAA repair. Although we believe patients with pre-existing intracranial abnormalities are more likely to have serious neurologic deficits from intracranial bleeding after spinal fluid drainage, it is not always possible to identify them before surgery. However, elective patients with abnormal neurologic findings, alcoholism, and previous head injury or neurosurgery now undergo preoperative head CT scanning.

It is important to note that although most patients with bloody spinal fluid had CT evidence of intracranial hemorrhage, most patients with CT evidence of bleeding did not have neurologic deficits. If spinal fluid became bloody, we stopped draining fluid immediately and corrected any coagulopathy that could increase the size of the hematoma and the likelihood it would produce neurologic deficit. Early diagnosis and proactive management of coagulopathy are important measures in reducing neurologic morbidity and mortality from spinal fluid drainage complications.

Controlling SFP with the minimum volume of spinal fluid drainage probably reduces intracranial bleeding complications. The total amount of fluid drained depends in part on the duration of surgery and aortic occlusion. However, timing spinal fluid drainage so that the SFP is not reduced too early in surgery has allowed us to decrease the volume of fluid drained and still control spinal fluid pressure at critical times during surgery. We suspect that using this strategy in the last 5 years has helped to reduce the occurrence of large intracranial bleeds from spinal fluid drainage that cause neurologic deficits; however, this difference in practice over time was not significant on analysis.

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Conclusion 

Using strategies to decrease the volume of spinal fluid drained, but still control SFP, may reduce serious complications of spinal fluid drainage during TAAA repair. Patients with cerebral atrophy or unrecognized chronic subdural hematoma may be at increased risk for serious neurologic complications after spinal fluid drainage.

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Author contributions 


Conception and design: MW, GT, JH

Analysis and interpretation: MW, CA, MM

Data collection: MW, CA

Writing the article: MW, CA

Critical revision of the article: MW, CA

Final approval of the article: MW, CA, MM, GT, JH

Statistical analysis: CA

Obtained funding: Not applicable

Overall responsibility: MW

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 Competition of interest: none.

PII: S0741-5214(08)01283-4

doi:10.1016/j.jvs.2008.07.076

Journal of Vascular Surgery
Volume 49, Issue 1 , Pages 29-35, January 2009

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