Appraisal of cerebrospinal fluid alterations during aortic surgery with intrathecal papaverine administration and cerebrospinal fluid drainage

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1 Appraisal of cerebrospinal fluid alterations during aortic surgery with intrathecal papaverine administration and cerebrospinal fluid drainage Lars G. Svensson, MB, PhD, Daniel F. Grum, MD, Marilyn Bednarski, RN, Delos M. Cosgrove III, MD, and Floyd D. Loop, MD, Cleveland, Ohio We have previously described a technique for intrathecal administration of papaverine and cerebrospinal fluid drainage to prevent paraplegia after aortic surgery. Herein we report the cerebrospinal fluid and hemodynamic alterations that occurred in 11 patients who had 30 mg of a specially prepared papaverine hydrochloride 10% dextrose solution injected before aortic cross-clamping and also had cerebrospinal fluid drainage. A mean of 26.6 ml (SD ml) was drained before and 34,6 ml (SD ml) was drained during aortic cross-clamping. The cerebrospinal fluid pressure increased significantly with anesthetic induction (p < 0.03), during the period between anesthetic induction and cerebrospinal fluid drainage (p < 0.005), and with aortic cross-clamping (p < 0.05). These cerebrospinal fluid pressure alterations were similar to central venous pressure increases with a significant linear correlation between cerebral spinal fluid pressure and central venous pressure before anesthetic induction (r 2 = 0.81, p < 0.005), and both before (r 2 = 0.94,p < 0.005) and after (~ = 0.74,p < 0.005) aortic cross-clamping. As expected, cerebrospinal fluid pressure was significantly reduced by cerebrospinal fluid drainage before aortic cross-clamping (p < 0.001). The admiuistration of intrathecal papaverine had no significant effect on mean arterial pressure, systemic vascular resistance, cerebrospinal fluid pressure, nor the ph of cerebrospinal fluid. Neither were there any complications noted related to the technique. All the patients survived, and no new immediate postoperative paraparesis or paraplegia occurred. The technique described may be used with other methods, such as distal aortic perfusion, in an attempt to protect the spinal cord against ischemie damage, and it may allow the surgeon a longer time to reanastomose critical segmental arteries to maintain spinal cord blood supply. (J VASC StatG 1990;11:423-9.) The protection of the spinal cord against ischemic injury when blood flow in the thoracic aorta is interrupted requires both, first, the provision of at least minimally adequate blood supply during the period of aortic interruption and, second, the restoration of normal blood flow to the spinal cord after the aortic circulation is restored by reattachment of critical segmental arteries.~,2 We have previously reported a new technique for protecting the spinal cord from prolonged ischemia during aortic surgery, which we began to use in humans in July ,3 The technique entailed the administration of intrathecal papaverine From the Departments of Thoracic and Cardiovascular Surgery, and Anesthesia, Cleveland Clinic Foundation. Reprint requests: Lars G. Svensson, MD, Department of Surgery, Baylor College of Medicine, One Baylor Plaza, Houston, TX /1/17246 combined with cerebrospinal fluid (CSF) drainage, ~ which we showed in nonhuman primates (Pupio ursinus) to cause both dilation of the anterior spinal artery and increased spinal cord blood flow thus preventing paraplegia? Similarly, in our recent report of studies in 11 humans) no immediate postoperative neurologic events occurred, although the sample size was small. In this study we report for the first time the hemodynamic and CSF alterations, including the changes in CSF ph and Po2 that occur with injection of intrathecal papaverine. The CSF pressure (CSFP) alterations that occur with CSF drainage during aortic cross-clamping in humans is also evaluated. Furthermore, we demonstrate and discuss the close relationship that exists between central venous pressure (CVP) and CSFP during the various periods of aortic surgery. Finally, the published reports of use of CSF 423

2 Svensson et al. Journalof VASCULAR SURGERY Table I. Alterations during aortic surgery using intrathecal papaverine and cerebrospinal fluid drainage (mean, _+ SD). Catheter Anesthetic Drainage Papaverine B A B A B A B A MAP CVP b 16 b CSFP d 16 <~ 20 'f 15 f CI h 3.3 h 3.1 SVR i 86 * 105 ABGpH 7.37 (0.11) CSFpH 7.28 (0.14) ABGPQ 223 (110) CSFPo2 125 (26) B, Before; A, after; 10, 15, 30, minutes; MAP, mean arterial pressure (ram Hg); CVP, central venous pressure (ram Hg); CSFP, cerebrospinal fluid pressure (nun Hg); CI, cardiac index (L/m2/min); SVR, systemic vascular resistance ( x 10 dyne/sec/cm-5); ABG, arterial blood gas; CSF, cerebrospinal fluid. Letters indicate comparisons and p values, (c,d,g,h, p < 0.05); (a,e,i,j,k, p < 0.01); (b,f, p < 0.001). drainage alone in animals are discussed in relation to our findings in humans. METHODS This report evaluates the subgroup of 11 patients who underwent thoracic or thoracoabdominal aortic surgery in the Department of Thoracic and Cardiovascular Surgery at the Cleveland Clinic Foundation between January 1987 and May One 57-yearold patient, who had a shunt inserted, had been included in our previous report.1 The study was approved by the Cleveland Clinic Institutional Review Board, and all patients received comprehensive information concerning the procedure and gave written consent. There were eight men and three women with a median age of 64 years (range 26 years to 75 years). Five patients had thoracoabdominal repairs from the left subclavian artery to varying extents of the abdominal aorta, and six had most of the descending thoracic aorta replaced. When distal aortic perfusion was used, either by a shunt or left atriofemoral bypass placement, the pulmonary artery mean pressure was maintained between 20 and 25 rnm Hg, which resulted in a monitored distal aortic pressure mostly above 60 mm Hg. It is important to note that in none of the patients were intercostal or lumbar arteries reattached. The technique and rationale for the use of CSF drainage and intrathecal papaverine injection has been presented before. La Briefly, the technique involved the insertion of a subarachnoid catheter under local anesthesia via L3-4 or L4-5 intervertebral spaces and the advancement of the catheter approximately 25 cm from the skin so that the tip would lie between T-10 and L-1. To direct the soft silicone rubber catheter cranially we used a flexible guide wire inside the catheter. When the pleural cavity was opened via a thoracic or thoracolumbar incision, 20 ml of CSF was withdrawn. Ten minutes before aortic crossclamping, 3 ml of a specially prepared 1% (30 rag) preservative-free papaverine hydrochloride in 10% dextrose water solution was instilled over a 5-minute interval to allow complete solubilization of the papaverine in the CSF. The ph of the papaverine solution, prepared at approximately monthly intervals, had been adjusted to a ph between 4 and 5 with 1N NaOH solution and was injected at body temperature. After injection of the papaverine the catheter was slowly flushed of remaining papaverine solutic~ over a 5-minute interval with 2 ml of either normal saline solution or CSF. The patient was then placed in a slight Trendelenberg position to allow the denser solution of papaverine, compared to CSF, to gravitate down alongside the spinal cord. During aortic cross-clamping, CSF was allowed to drain freely. More recently, however, we have monitored CSFP and kept it between 5 and 10 mm Hg and limited the total volume of drainage to 50 ml to reduce the risk of herniation of the brain stem and uncus. Systemic systolic, diastolic, mean arterial pressure (MAP), CVP, pulmonary artery pressures, and CSFP were continuously monitored on marquette pressure monitors (Marquette Company, Milwaukee, Wis.), and the data were recorded directly on computer for later recall. In addition, data were prospectively recorded by a trained research assistant (M,B.) at s W

3 Volume 11 Number 3 March 1990 Intrathecal papaverine and cerebrospinal fluid drainage 425 Clamped B A io " 20 c g 19 g I5 I i (0.10) 7.29 (0.08) 210 (177) 106 (37) Undamped B A 10 END 97 a 69 ~ I i 4.9 i k 67 k (0.09) 7.23 (0.13) 274 (166) 128 (36) cific stages and time intervals during the operation. T~';: pressure transducers were all on the same transducer bridge attached to the operating table and calibrated level with the right atrium. Cardiac output, cardiac index, and systemic vascular resistance were determined at the following intervals both before and after: intrathecal catheter placement, induction of anesthesia, CSF drainage, injection of papaverine, aortic cross-clamping, at regular intervals during crossclamping, unclamping, and at 10-minute and 30- minute intervals after unclamping. The CSF ph and CSF PO2 measurements were determined on the initial 20 ml of CSF withdrawn; approximately 10 minutes after papaverine injection during aortic cross-clamping; after unclamping; and at the end of the operation. All patients were evaluated both before and after ~xgery by a neurologist. After the patient arrived in the intensive care unit, radiography was used to check the position of the catheter tip before its removal. Data are expressed as mean _+ SD. Statistical comparisons of recorded data were made with the Mann-Whitney U test. For analyzing correlation between variables linear regression analysis was used for calculating the coefficient of determination (ra). RESULTS In evaluating the CSFP changes that occurred in the patients, we found that the CSFP progressively and significantly increased with the following (Table I): induction of general anesthesia and intnbation (p < 0.03); during the period between induction of anesthesia and CSF drainage (p < 0.005); and immediately after aortic cross-clamping (p < 0.05). However, as would be expected CSFP was signifi- cantly reduced by CSF drainage before aortic crossclamping (p < 0.001). Central venous pressure increased progressively during the period after general anesthetic induction (p < 0.001) and aortic cross-clamping (p < 0.05). No consistent cardiac index changes nor systemic vascular resistance changes (p > 0.1) occurred with aortic cross-clamping. However, during the period between induction of anesthesia and aspiration of CSF, the cardiac index was increased (p < 0.05), and systemic vascular resistance was decreased (p < 0.01) by pharmacologic manipulation and administration of intravenous solutions, including mannitol. The significant increase (p < ) in the CVP during this period probably reflects the administration of fluid, including mannitol. As expected, MAP significantly fell with aortic unclamping (p < 0.01), as did systemic vascular resistance (p < 0.01), and cardiac index significantly increased (p < 0.01). The injection of intrathecal papaverine resulted in no significant measured effects on CSFP, CVP, MAP, cardiac index, systemic vascular resistance, CSF ph, nor CSF PQ (Table I). The CSFP correlated very significantly with the CVP before induction of general anesthesia (r 2 = 0.81, p < 0.005) and notably both before (r 2 = 0.94, p < 0.005) and after (r 2 = 0.74, p < 0.005) aortic cross-clamping. Immediately after unclamping of the aorta, no correlation between CVP and CSFP could be found, although, the CSFP tended to equilibrate over a period of time with the CVP. With the exception of a weak correlation between CSFP and MAP occurring sometime after CSF drainage, probably reflecting CSF secretion, first before injection of intrathecal,papaverine (r 2 = 0.34, p = 0.05) and

4 426 Svensson et al. Journal of VASCULAR SURGERY second 10 minutes after aortic undamping (r 2 = 0.45,p < 0.03), no other correlation could be found with MAPs. No other correlations were found between CSFP and cardiac index nor systemic vascular resistance (p > 0. i). The mean CSF volume drained before aortic cross-clamping, including spillage during catheter insertion, was 26.6 ml _+ 7.1 ml. The mean CSF volume drained during aortic cross-clamping was 34.6 ml _ ml. The mean CSF ph values after aspiration of 20 ml of CSF, after papavcrine injection (aspirated during aortic cross-clamping), after unclamping, and at completion of the operation were respectively: 7.28 _+ 0.14, , , and 7.26 _ Similarly, the respective CSF partial gas pressures of oxygen (Po2) were: 125 _+ 26, 106 _+ 37, 128 _ 36, and 114 _+ 31. Clearly,, neither thc ph nor Po2 changes in CSF were significantly altered (p > 0.1) by the presence of the injected papaverine nor by potential ischcmia of the spinal cord during aortic cross-clamping. The mean aortic cross-clamp time was 43 minutes _+ 20 minutes. In 10 patients the intrathecal catheter was directed cranially and lay anterior to the spinal cord. In one patient the catheter had turned caudally. One of the 11 patients in the postoperative period had a recurrence of a unilateral temporary paraparesis that he had previously suffered after a coronary artery bypass operation. Another patient, who initially had no neurologic dysfunction, on the third postoperative day suffered a respiratory arrest requiring reintubation and readmission to intensive care unit. He was found to have a temporary paraparesis, from which he recovered by the time of his discharge from the hospital. There were no postoperative deaths. No patients suffered any complications related to the papaverine injection nor postoperative headaches nor other complications related to the spinal catheter. DISCUSSION This study reports for the first time the CSF alterations that occur in humans with both intrathecal papaverine administration and also with CSF drainage during the course of aortic surgery. We found that neither hemodynamic nor CSFP alterations occurred with the injection of intrathecal papaverine, and therefore we believe that we can safely assume that the CSFP changes that occurred with aortic cross-clamping were not influenced by intrathecal papaverine. Thus it is of interest that CSFP increased progressively during the course of aortic surgery, and that these increascs correlated best with incrcascs in the CVP. Before the author's prospective use of intrathecal papaverine and CSF drainage in humans, which began in July 1985 and was reported in and then described in detail, 1,3 CSF drainage had only been described in two patients having aortic cross-clamping in 1958 and without compiication. Since we have as yet seen no harmful effects from the use of intrathecal papaverine with CSF drainage in 34 patients and no immediate postoperative paraplegia, we believe that intrathecal papaverine can be safely used intrathecally for its vasodilatory effect and other possible protective effects. 1,4 However, strictly adhering to the precautions we have described in our methodology, induding attention to a totally sterile technique, adequate preinsertion intravenous fluid hydration, possible hemostasis abnormalities, and gentle insertion of the catheter we believe is crucial. We stress again that the papaverine and the catheter flushing solution must be at body temperature and be slowly injected as described. As with other spinal anesthetic techniques, the risk appears to be associated with the technique of catheter insertion and spinal anesthetics in general, such as severe hypotensive sympathetic responses, rather than the intrathecal administration of papaverine. 6"7 Our observations in humans suggest that the high CSFP values during aortic cross-clamping, also noted in animal studies, 8-~z are not solely due to aortic crossclamping, but that the induction of anesthesia and the subsequent period up to CSF drainage should be considered as additive factors that increase the CSFP. Of course, these alterations may have been different had we not drained CSF or pharmacologically manipulated the blood pressure during aortic cro~) clamping.13 Furthermore, we have noted that the use of distal aortic perfusion reduces the increase in CSFP that occurs with aortic cross-clamping? Despite drainage of 20 ml of CSF, the CSFP gradually returned to predrainage levels before cross-clamping, and this gradual rise in CSFP correlated with the mean arterial pressure (t a = 0.34, p < 0.05). We postulate that this was either because CSF was replenished (at the rate of approximately 25 ml an hour; a rate that is dependent on arterial pressure t4) or because the venous capacitance vessels surrounding the spinal cord had expanded to tal~e up the vacated space. We speculate that the possible reasons for the rapid rise in CSFP with aortic cross-clamping include the following: (1) The higher proximal MAP causing

5 Volume 11 Number 3 March 1990 Intrathecal papaverine and cerebrospinat fluid drainage 427 either dilation of intracranial arteries or expansion of nervous tissue volume. However, cerebral autoregulation would probably prevent any expansion of neural tissue or arterial vessel volume from occurring because of increased systemic arterial pressure or cerebral blood flow) 3as (2) Increased CSF secretion, possibly related to increased blood flow to the brain. However, previous experiments purporting to support this, which mimicked either rapid tumor expansion or intracranial hemorrhage, cannot, in the true sense, be considered to be analogous to aortic cross-clamping, where there is no forceful injection ofintrathecal fluid. 16,17 (3) The rise in CVP resulting in back pressure in the intracranial veins and venous sinuses. In our opinion, we tend to favor the third postulate. The classic Monro-Kellie hypothesis remains generally relevant, namely, that the total cranial and spinal columaa volumes remain constant within the closed space that the brain and spinal cord occupy. Any volume increase of the components (nervous tissue volume, blood volume, CSF volume) must therefore be at the expense of the other components. Normal CSFP will thus only be maintained until the compensatory mechanisms are exceeded. 18 However, with aortic cross-clamping, the one compensatory mechanism, namely compression of venous capacitance vessels (loss of blood volume together with the above), rather than compensating for any increases in the intracranial components, the venous capacitance vessels are the more likely cause of the increase in CSFP. Blaisddl and Cooley 8 have noted in dogs that CSFP increased with both anesthetic induction and cross-clamping, and in our own (unpublished data) and other animal experiments s,19 it has been found.nat CVP increased with aortic cross-clamping. It is known that a close relationship normally exists under physiologic conditions between subarachnoid, intracranial sinus, CVP, and the CSFP, 2 '21 and it is likely that spinal CSFP is similarly related to spinal venous pressures 2t including in Batson's plexus, the azygous vein (which drains segmental intercostal and lumbar veins), and in the superior vena cava. Since CVP tends to increase with induction of anesthesia and cross-clamping, the mechanism of increased CSFP is probably similar to that of the Queckenstedt test = or heart failure, 2a in that decreased venous return as a result of raised intrathoracic pressure or, heart failure, results in backpressure in the intracranial and perichordal capacitance vessels because of increased impedence to venous outflow. In addition, there may also be an increased volume of blood return from the upper body via the superior vena cava 24 because of increased shunting between the upper body arterial and venous systems as a result of pharmacologic vasodilators, further adding to the venous congestion. The significant linear correlation we noted between CSFP and CVP both before anesthetic induction, before cross-clamping, and with cross-clamping thus supports the concept that the increases in CSFP are probably due to increases in CVP. However, it should be noted that vasodilators themselves (nitroprusside, nitroglycerine, and trimethaphan) can cause an increased CSFPY,26 The implied or measured lumbar spinal cord CSFP, the site at which ischemia is maximal during aortic cross-clamping, 4,9,24,27 particularly without distal aortic perfusion, 27 is controversial. Dunbar et al. 2 found in dogs that CSFP in the lumbar spinal cord sac fell during aortic occlusion, whereas CSFP measured in the cisterna magna or intraventricularty increased. These pressure changes were reversed by terminating aortic occlusion. 2 Others 81m6 have measured the cisterna magna pressure in dogs during aortic cross-clamping and have confirmed, as noted by Dunbar et al.,20 that CSFP in the cisterna magna increases. However, it has been implied from these pressure changes measured in the cisterna magna that lumbar spinal cord pressures also increase. Indeed, we did find that CSFP, measured alongside the lumbar spinal cord, increases with aortic cross-clamping from a mean of i5 mm Hg to i9 mm Hg, but not as markedly when compared to the increase from 13 mm Hg before induction of anesthesia to 20 mm Hg before CSF drainage. It is clear from the above discussion that CSFP measured in the cisterna magna may not accurately reflect the CSFP alterations in the lumbar spinal cord vicinity. Furthermore, Killen et al.28 reported that the distal aortic pressure did not reflect the spinal cord arteriolar (nor capillary) blood pressure, but that the higher segmental intercostal or lumbar artery end pressures were a closer approximation. Therefore by implication, the double assumption by Miyamoto et al. s of "relative spinal cord perfusion pressure" being equal to distal aortic pressure minus the cistema magna pressure probably does not hold true. Moreover, Griffiths et al. 21 have shown that perfusion pressure is a far greater determinant of blood flow than the possible inhibitory effect of a raised CSFP. They concluded that "spinal cord blood flow can accomodate any fluctuations in CSFP." There are even reports of increased cerebral blood flow with an increased intracranial pressure, la It should be

6 428 Svensson et al. Journal of VASCULAR SURGERY noted that the resistance to reabsorption of CSF in dogs is 17 times greater than that of man, 14 and thus any increases in CSFP in man may be more quickly compensated for. Whether CSF drainage alone will reduce the incidence of paraplegia after aortic cross-clamping in humans is an unanswered question, although apparently good results have been reported by McCullough et al.10 in 24 patients, 10 of whom were low Crawford type III thoracoabdominal aortic aneurysms and six type IV (total or near total abdominal aneurysm) with an expected paraparesis or paraplegia rate of 3.2% or 2.1% 29, respectively. Experiments in dogs, draining CSF from the cisterna magna, have shown discrepant results. Blaisdell and Cooley 8 in 1962 and more recent studies by others 9"11,16 report the incidence of postocclusion neurologic dysfunction is reduced. Nevertheless, it is of note that Blaisdell, despite his earlier work, does not believe that "we can provide any protection by modifying spinal fluid pressure." (Commentary on Bower et al.9) Furthermore, Killen et al.28 in a similar dog model were tmable to show a protective effect by draining CSF from the cisterna magna. Similarly, Wadouh et al?9 used a porcine model, and in our own nonhuman primate model, CSF drainage by a limited lumbar laminectomy failed to reduce the incidence of paraplegia. ~ In conclusion, it would appear that the acute changes in CSFP are primarily a function of increased intracranial and intraspinal venous blood volume, which is determined by venous back pressure during anesthetic induction, intravenous fluid administration and aortic cross-clamping. Whether CSF drainage alone will reduce the incidence of postoperative paraplegia is not proved and can only be evaluated by a prospective randomized study. Thus it would appear to us that the best method of preventing paraplegia, with its multifactorial causes, is to use intrathecal papaverine with CSF drainage to prolong the safe period of aortic cross-clamping, reanastomose identified critical segemental arteries by a technique that has been presented by the author, s and use distal aortic perfusion in selected complex situations, such as aortic dissection. 2 However, distal aortic perfusion has not proved to be a panacea in preventing either paraplegia because of spinal cord anatomic reasons 27 or acute renal failure. 2,3t Robert W. Stewart, MD, and Bruce W. Lyric, MD, allowed their patients to be entered into the study and gave valuable advice. The preoperative and postoperative neurologic assessments were performed by Antonio Salgado, MD, and Anthony Furlan, MD, from the Department ot Neurology, and Marion Robinson, PhD, performed the statistical analyses. REFERENCES 1. Svensson LG, Stewart RW, Cosgrove DM, et al. 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