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Interact CardioVasc Thorac Surg 2008;7:262-266. doi:10.1510/icvts.2007.164707
© 2008 European Association of Cardio-Thoracic Surgery
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ESCVS article - Experimental

Changes in cerebrospinal fluid and blood lactate concentrations after stent-graft implantation at critical aortic segment: a preliminary study{star},,{star}{star}

Abul Hasan Muhammad Bashara,*, Kazuya Suzukia, Teruhisa Kazuia, Mitsuo Yamaguchi Okadab, Takayasu Suzukia, Naoki Washiyamaa, Hitoshi Teradaa and Katsushi Yamashitaa

a First Department of Surgery, Hamamatsu University School of Medicine, 1-20-1, Handayama, Hamamatsu City, 431-3192, Japan
b Department of Neurosurgery, Hamamatsu University School of Medicine, Japan

Received 7 August 2007; received in revised form 26 December 2007; accepted 27 December 2007

{star} Presented at the 56th International Congress of the European Society for Cardiovascular Surgery, Venice, Italy, May 17–20, 2007. Back

{star}{star} Source of funding: The principal author (AHMB) is a post-doctoral fellow of the Japan Society for the Promotion of Science (JSPS) and the study was supported by an annual research grant from the JSPS.

*Corresponding author. Tel.: +81-53-435-2276; fax: +81-53-435-2272.

E-mail address: ahmbashar{at}yahoo.com (A.H.M. Bashar).


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 
Objectives: Obstruction of blood flow through the arteria radicularis magna (ARM) has been linked with ischemic spinal cord injury after conventional thoracic aortic repair. Whether or not endoluminal stent-grafts, deliberately positioned against this artery can cause similar damage to the spinal cord has not been comprehensively investigated. The purpose of this study was to assess the blood and cerebrospinal fluid (CSF) concentrations of lactate – a well-known biochemical marker of ischemic neurological injury, before and after stent-graft implantation against the ARM. Materials and methods: Endoluminal stent-grafting was performed in ten mongrel dogs. In five animals (experimental group), stent-grafts covered the fourth and fifth lumbar segmental arteries – which have been described as the canine equivalents to the ARM in humans. In the remaining five animals (control group), devices of similar length were placed in the lower thoracic aorta. CSF was obtained by cisternal puncture technique at the following time points; before stent-grafting, and 15, 30 and 60 min after stent-grafting. Parallel arterial blood samples were also obtained using a heparinized syringe. All samples were centrifuged and the supernatant analysed for lactate. Results: The mean preprocedural lactate concentration in the CSF was 1.7±0.3 mmol/l. Mean postprocedural levels in the experimental group at 15, 30 and 60 min were 3.1±1.9, 3.9±1.1 and 11.9±2.5 mmol/l, respectively (control values; 2.1±1.9, 2.7±1.1 and 1.9±1.5 mmol/l, respectively). Mean preprocedural blood lactate level was 1.8±0.6 mmol/l, while the mean postprocedural concentrations in the experimental group at 15, 30 and 60 min were 2.9±1.2, 3.4±1.7 and 3.9±2.0 mmol/l, respectively. Two out of the five animals in the experimental group suffered mild to moderate hind limb weakness. Conclusion: Selective placement of stent-grafts against the ARM in dogs resulted in a conspicuous increase in CSF and blood lactate concentrations 60 min after the procedure with or without physical signs of neurological deficits. Although the small sample size of this preliminary study does not allow any definitive conclusion, it may be worthwhile to confirm the findings in appropriately controlled larger studies.

Key Words: Thoracic endografting; Arteria radicularis magna; Spinal cord ischemia; Lactate concentration


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Results
 4. Discussion
 References
 
Postoperative neurological deficit resulting from spinal cord ischemia is a dreadful complication of conventional thoracic and thoraco-abdominal aortic repair. Aortic cross-clamping is thought to be the principal reason [1] underlying this complication. Thoracic endovascular aortic repair (TEVAR) represents a notable departure from open thoracic aortic repair in the sense that no aortic cross-clamping is required in this technique. Thus, proximal hypertension and its harmful consequences on spinal cord perfusion are avoided. Distal aortic flow also remains largely uninterrupted ensuring continuous distal segmental artery perfusion. Additionally, there is no reperfusion injury as the segmental arteries are not reattached. It was therefore expected that TEVAR would dramatically reduce the incidence of paraplegia or paraparesis. Unfortunately, that expectation has not fully materialized and TEVAR is reported to have a paraplegia incidence ranging from 0 to 12% [1–4]. Like the conventional thoracic aortic repair, spinal cord ischemia in case of TEVAR is most likely multifactorial. Previous or concomitant abdominal aortic aneurysm (AAA) surgery which may result in a critical reduction of segmental arteries to jeopardize spinal cord perfusion has been described as an important precipitating factor [5].

Arteria radicularis magna (ARM), originating from one of the lower thoracic or lumbar segmental arteries constitutes a major source of blood supply to the thoracic and lumbar spinal cord [6, 7]. Numerous studies have suggested that obstruction of blood flow through this artery can give rise to ischemic spinal cord injury after conventional thoracic aortic repair [8, 9]. However, whether or not endoluminal stent-grafts, deliberately positioned against this artery can cause similar damage to the spinal cord has not been comprehensively investigated. We undertook this canine study to assess the blood and cerebrospinal fluid (CSF) concentrations of lactate – a well-known biochemical marker of ischemic neurological injury, before and after stent-graft implantation against the ARM in order to understand the true importance of this artery in the context of TEVAR.


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Results
 4. Discussion
 References
 
2.1. Animal preparation

A total of ten mongrel dogs of either sex weighing between 15 and 20 kg were used for this study. The study was approved by the Animal Care and Use Committee of Hamamatsu University School of Medicine. All animals received humane care in compliance with the ‘Guide for the Care and Use of Laboratory Animals’ published by the National Institutes of Hearth (NIH publication # 85-23, revised 1985) and the ‘Guidelines for Animal Experimentation’ formulated by Hamamatsu University School of Medicine (published 1987, revised 1991).

The animals were anesthetized with intravenous pentobarbital sodium (25 mg/kg) and ventilated with room air. Endoluminal stent-grafting was then performed through a transfemoral route under fluoroscopic monitoring. The animals were divided into two groups. In the experimental group (n=5), stent-grafts were positioned against the 4th and 5th lumbar segmental arteries – which have been described as the canine equivalents to the ARM in humans [10]. In the control group (n=5), the devices were positioned in the lower thoracic segment of the aorta. Aortogram was taken before and after the procedure to document precise device placement. Adjunctive balloon dilatation with a commercially available device (Cosmotec PTA balloon catheter, Cosmotec, Tokyo, Japan) was performed whenever postoperative aortogram showed incomplete device expansion. The endografts used in this study were all hand-made at our laboratory using biocompatible stainless steel wire (316L) and commercially available thin-walled woven Dacron fabric with a porosity of 150 ml/cm2/min (Fig. 1). Device dimensions were similar for both groups (6±0.5 cm in length and 12±0.2 mm in diameter).


Figure 1
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  		Fig. 1. Hand-made stent-graft devices used for the present study.

 
2.2. Sample collection

CSF was obtained by percutaneous cisternal puncture technique in the following way; first, the animal was placed in a squatting position with the front legs flexed at the knee. The head was held up in the midline with the help of a special device and the neck was kept partially flexed. A 23G needle was then vertically inserted at a point about 2.5 cm distal to the occipital protuberance. CSF was aspirated on reaching a depth of about 2.5 cm. The time points for CSF collection were as follows; before stent-grafting, and 15, 30 and 60 min after stent-grafting. Parallel arterial blood samples were also obtained using a heparinized syringe.

2.3. Neurological assessment

Neurological function of the animals was assessed before and after the stent-grafting procedure using the modified Tarlov scale, which is as follows; score 5: normal hop, score 4: weak hop, score 3: sit alone, score 2: sit with assistance, score 1: slight movement, score 0: no movement. The post-procedural assessment took place once the animals completely recovered from the influence of anesthesia.

2.4. Sample analysis

Immediately after collection, all samples were kept in an ice box until the end of the experiment. They were then centrifuged and the supernatant fluid was stored in a freezer at –80° C, if a delay in the analysis was expected. Before analysis, the samples were allowed to thaw at room temperature. A two-way analysis of samples was carried out to measure the concentrations of lactate; first by a lactate measurement kit (Lactate Pro, Arkray Inc., Kyoto, Japan) followed by an automated blood gas analyzer (Stat Profile Ultra M; Nova Biomedical Corp, Tokyo, Japan).

2.5. Statistical analysis

Data are expressed as mean±S.D. For comparison between the corresponding values of control and experimental groups, Student's t-test was used. Due to the small sample size, differences were deemed statistically significant only when a P-value <0.005 was achieved.


   3. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
4. Discussion
 References
 
All stent-grafting procedures were technically successful (Fig. 2). Adjunctive balloon dilatation was required in three animals (two in the control, one in the experimental group) to ensure satisfactory device expansion. CSF sampling was also successful on all occasions except once in the experimental group 30 min after the procedure.


Figure 2
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  		Fig. 2. (a) Preprocedural aortogram showing relatively large 4th and 5th lumbar segmental arteries. (b) Postprocedural aortogram showing stent-graft placed against the L4 and L5 segmental arteries with absence of blood flow through them. Flow is seen through L6.

 
3.1. CSF and blood lactate concentrations

The two lactate measurement techniques showed excellent correlation. Concentrations of CSF lactate in the control and experimental groups at different time points are depicted in Fig. 3. The mean preprocedural lactate concentration in the CSF was 1.7±0.3 mmol/l. Mean postprocedural levels in the experimental group at 15, 30 and 60 min after stent-grafting were 3.1±1.9, 3.9±1.1 and 11.9±2.5 mmol/l, respectively (control values; 2.1±1.9, 2.7±1.1 and 1.9±1.5 mmol/l, respectively). Differences with the control group became statistically significant at 60 min after stent-grafting (P<0.001). A maximum 8-fold increase from baseline was noted in one animal of the experimental group 60 min after stent-grafting.


Figure 3
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  		Fig. 3. Graph showing changes in cerebrospinal fluid lactate concentrations before and after endoluminal stent-grafting. Post 1, Post 2, Post 3 represent 15, 30 and 60 min after stent-grafting, respectively.

 
Mean preprocedural blood lactate level was 1.8±0.6 mmol/l, while the mean postprocedural concentrations at 15, 30 and 60 min after the stent-grafting procedure were 2.9±1.2, 3.4±1.7 and 3.9±2.0 mmol/l, respectively (control values; 2.1±1.5, 2.0±0.8 and 2.1±1.6 mmol/l, respectively) (Fig. 4). Differences between the two groups were statistically significant at 60 min after stent-grafting (P<0.003).


Figure 4
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  		Fig. 4. Graph showing changes in blood lactate concentrations before and after endoluminal stent-grafting. Post 1, Post 2, Post 3 represent 15, 30 and 60 min after stent-grafting, respectively.

 
3.2. Neurological assessment

Animals of both groups had normal hind limb motor function before the induction of anesthesia. Two animals in the experimental group showed mild to moderate hind limb weakness (Tarlov scores 3 and 4) after the stent-grafting procedure, while there was no neurological deficit in the control group. In the experimental group, CSF lactate concentrations were higher in the two animals suffering neurological deficits (13.8 mmol/l and 12.1 mmol/l) compared with those neurologically intact. Postprocedural Tarlov scores for both control and experimental groups are depicted in Fig. 5.


Figure 5
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  		Fig. 5. Graph showing postprocedural neurological scores of the dogs in control and experimental groups according to the modified Tarlov scale.

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
References
 
ARM has been an issue of much contention in the recent years among investigators working in the area of open thoracic and thoracoabdominal aortic repair. Some authorities claim that the artery has a crucial role in the maintenance of spinal cord circulation and that it should be preoperatively identified and its flow carefully preserved during any thoracic aortic intervention [11, 12]. Others are less convinced and some actually question the very existence of any such artery in the spinal cord circulation [13]. Elaborating on what they termed the ‘collateral network concept’, Griepp et al. have recently foreseen routine sacrifice of all intercostal and lumbar arteries without any negative impact on the neurological outcome [14]. While the issue continues to evolve in the area of conventional thoracic and thoracoabdominal aortic surgery, there is a relative lack of efforts in this regard in the area of TEVAR. To the best of our knowledge, ours is the first study to deal with it in an animal experiment setting. Earlier clinical studies indicated that obliteration of crucial intercostal arteries can produce spinal cord ischemia during TEVAR [15, 16]. The elevated serum and CSF lactate levels that were found in the present study after endograft placement against the ARM may be supporting this notion.

Vulnerability of an individual patient to spinal cord ischemia during thoracic and thoracoabdominal aortic endografting is determined by a number of factors. Jacobs et al. have observed that in patients with thoracoabdominal aortic aneurysm (TAAA), most intercostal and lumbar arteries are occluded and spinal cord perfusion depends on an eminent collateral network, which includes lumbar arteries and pelvic circulation [17]. In the present study, stent-grafting was performed in healthy aortas with all side branches patent. It is quite remarkable that despite the relative resistance of the canine species to spinal cord ischemia [10], all experimental animals showed increased lactate concentrations. However, the elevated lactate concentrations translated into obvious neurological deficit in only two animals which is interesting. While there is no known explanation for this difference, it can be speculated that individual variation in the pattern of spinal cord circulation, in other words, differences in the ability to collateralize under ischemic stress, might have been responsible. Parker has described such variation in dogs [18]. Does similar variation also exist in humans? If so, it would be worthwhile to preoperatively map out the vascular anatomy of the spinal cord including the ARM in each patient to determine individual patient vulnerability to spinal cord ischemia. Nijenhuis et al. in a recent clinical study have documented the feasibility and usefulness of this strategy [19].

A number of techniques are available to document intraoperative spinal cord ischemia. Notable among them are motor evoked potential, somatosensory evoked potential, and various biological markers. Lactate has been a well-known biomarker of ischemic neurological injury. It is produced in the cellular cytosol from pyruvate in the glycolytic pathway as a result of anerobic metabolism during the ischemic insult. Nagy et al. have reported elevated CSF and serum lactate levels after thoracic cross-clamping in dogs [20]. Earlier, Drenger et al. showed elevated levels of blood and CSF lactate in a small series of patients undergoing TAAA surgery [21]. In their study, the rise in CSF lactate concentrations was more pronounced in patients suffering paraplegia than in those having no neurological deficits. In our study too, the highest lactate level was found in an animal that suffered moderate hind limb paresis. Thus, our data support the existing view that measurement of CSF and serum lactate can be a reliable means of evaluating ischemic neurological damage. Although the use of other biomarkers such as alkalaine phosphatase, glutamate, neurone specific enolase, S-100, glial fibrillary acidic protein etc. have also been reported [22, 23], none has been as consistent a marker of ischemic neurologic injury as lactate. However, it is important to note that lactate may rise even without obvious neurological deficit [23].

Although the present study brings into focus a number of important aspects about ischemic spinal cord injury during TEVAR, its limitations are obvious. First, we carried out the study in dogs, which has been described as a poor model for ischemic spinal cord injury in humans [10] on the premise that spinal cord circulation in humans is different from that in dogs. Human spinal circulation is highly de-segmented, while dogs have a more segmental arterial supply [24]. Thus, dogs are thought to be relatively resistant to spinal cord ischemia [10]. However, using selective spinal angiography, latex injections, and corrosion castings, Bower et al. showed that the anterior spinal artery in dogs was indeed continuous, like in human and claimed that the dog was certainly a good model for studying spinal ischemia [25]. Second, we did not perform selective lumbar arteriography to precisely identify the ARM. Third, we assessed only a single biochemical marker of neural ischemia, whereas a more detailed evaluation would have given a clearer picture. Finally, the study does not take into account the possible influence of factors like previous or concomitant AAA surgery, co-morbid conditions, perioperative hypotension etc. on the outcome. Therefore, our results might not be directly applicable to the clinical field.

In conclusion, we found in this preliminary study that selective placement of stent-grafts against the ARM in dogs resulted in a conspicuous increase in CSF and blood lactate concentrations. However, the elevated lactate concentrations were not always associated with obvious physical signs of neurological deficit. Although our small sample size precludes any definitive conclusion, the findings are highly clinically relevant and merit confirmation in appropriately controlled larger studies.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 

  1. Weigang E, Hartert M, Siegenthaler MP, Beckmann NA, Sircar R, Szabò G, Etz CD, Luehr M, von Samson P, Beyersdorf F. Perioperative management to improve neurologic outcome in thoracic or thoracoabdominal aortic stent-grafting. Ann Thorac Surg 2006;82:1679–1687.[Abstract/Free Full Text]
  2. Criado FJ, Abul-Khoudoud OR, Domer GS, McKendrick C, Zuzga M, Clark NS, Monaghan K, Barnatan MF. Endovascular repair of the thoracic aorta: lessons learned. Ann Thorac Surg 2005;80:857–863.[Abstract/Free Full Text]
  3. Chiesa R, Melissano G, Marocco-Trischitta MM, Civilini E, Setacci F. Spinal cord ischemia after elective repair of the thoracic aorta. J Vasc Surg 2005;42:11–17.[CrossRef][Medline]
  4. Dake MD, Miller DC, Mitchell RS, Semba CP, Moore KA, Sakai T. The "first generation" of endovascular stent-grafts for patients with aneurysms of the descending thoracic aorta. J Thorac Cardiovasc Surg 1998;116:689–704.[Abstract/Free Full Text]
  5. Baril DT, Carroccio A, Ellozy SH, Palchik E, Addis MD, Jacobs TS, Teodorescu V, Marin ML. Endovascular thoracic aortic repair and previous or concomitant abdominal aortic repair: is the increased risk of spinal cord ischemia real? Ann Vasc Surg 2006;20:188–194.[CrossRef][Medline]
  6. Dommisse GF. The blood supply of the spinal cord: a critical vascular zone in spinal surgery. J Bone Joint Surg 1975;56B:225–235.
  7. Svensson LG, Klepp P, Hinder RA. Spinal cord anatomy of the baboon —comparison with man and implications for spinal cord blood flow during thoracic aortic cross-clamping. S Afr J Surg 1986;24:32–34.[Medline]
  8. Kieffer E, Richard T, Chiras J, Godet G, Cormier E. Preoperative spinal cord arteriography in aneurysmal disease of the descending thoracic and thoracoabdominal aorta: preliminary results in 45 patients. Ann Vasc Surg 1989;3:34–46.[Medline]
  9. Crawford ES, Crawford JL, Safi HJ, Coselli JS, Hess KR, Brooks B, Norton HJ, Glaeser DH. Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining immediate and long-tem results of operations in 605 patients. J Vasc Surg 1986;3:389–404.[CrossRef][Medline]
  10. Doppman JL, Ramsey R. Selective arteriography of the lumbar spinal cord in dogs. Neuroradiology 1971;3:64–67.[CrossRef][Medline]
  11. Kawaharada N, Morishita K, Hyodoh H, Fujisawa Y, Fukada J, Hachiro Y, Kurimoto Y, Abe T. Magnetic resonance angiographic localization of the artery of Adamkiewicz for spinal cord blood supply. Ann Thorac Surg 2004;78:846–851.[Abstract/Free Full Text]
  12. Hyodoh H, Kawaharada N, Akiba H, Tamakawa M, Hyodoh K, Fukada J, Morishita K, Hareyama M. Usefulness of preoperative detection of artery of Adamkiewicz with dynamic contrast-enhanced MR angiography. Radiology 2005;236:1004–1009.[Abstract/Free Full Text]
  13. Griepp RB, Ergin MA, Galla JD, Lansman S, Quintana C, McCollough J, Bodian C. Looking for the artery of Adamkiewicz: a quest to minimize paraplegia after operations for aneurysms of the descending thoracic and thoracoabdominal aorta. J Thorac Vardiovasc Surg 1996;112:1202–1213.[CrossRef]
  14. Griepp RB, Griepp EB. Spinal cord perfusion and protection during descending thoracic and thoracoabdominal aortic surgery: the collateral network concept. Ann Thorac Surg 2007;83:S865–869.[Abstract/Free Full Text]
  15. Greenberg R, Resch T, Nyman U, Lindh M, Brunkwall J, Brunkwall P, Malina M, Koul B, Lindblad B, Ivancev K. Endovascular repair of descending thoracic aortic aneurysms: an early experience with intermediate-term follow-up. J Vasc Surg 2000;31:147–156.[CrossRef][Medline]
  16. Makaroun MS, Dillavou ED, Kee ST, Sicard G, Chaikof E, Bavaria J, Williams D, Cambria RP, Mitchell RS. Endovascular treatment of thoracic aortic aneurysms: results of the phase II multicenter trial of the GORE TAG thoracic endoprosthesis. J Vasc Surg 2005;41:1–9.[CrossRef][Medline]
  17. Jacobs MJ, de Mol BA, Elenbaas T, Mess WH, Kalkman CJ, Schurink GW, Mochtar B. Spinal cord blood supply in patients with thoracoabdominal aortic aneurysms. J Vasc Surg 2002;35:30–37.[Medline]
  18. Parker AJ. Distribution of spinal branches of the thoracolumbar segmental arteries in dogs. Am J Vet Res 1973;34:1351–1353.[Medline]
  19. Nijenhuis RJ, Jacobs MJ, Schurink GW, Kessels AG, van Engelshoven JM, Backes WH. Magnetic resonance angiography and neuromonitoring to assess spinal cord blood supply in thoracic and thoracoabdominal aortic aneurysm surgery. J Vasc Surg 2007;45:71–77.[CrossRef][Medline]
  20. Nagy G, Dzsinich C, Selmeci L, Sepa G, Dzsinich M, Kekesi V, Juhasz-Nagy A. Biochemical alterations in cerebrospinal fluid during thoracoabdominal aortic cross-clamping in dogs. Ann Vasc Surg 2002;16:436–441.[CrossRef][Medline]
  21. Drenger B, Parker SD, Frank SM, Beattie C. Changes in cerebrospinal fluid pressure and lactate concentrations during thoracoabdominal aortic aneurysm surgery. Anesthesiology 1997;86:41–47.[CrossRef][Medline]
  22. van Dongen EP, ter Beek HT, Schepens MA, Morshuis WJ, Haas FJ, de Boer A, Boezeman EH, Aarts LP. The relationship between evoked potentials and measurements of S-100 protein in cerebrospinal fluid during and after thoracoabdominal aortic aneurysm surgery. J Vasc Surg 1999;30:293–300.[CrossRef][Medline]
  23. Anderson RE, Winnerkvist A, Hansson LO, Nilsson O, Rosengren L, Settergren G, Vaage J. Biochemical markers of cerebrospinal ischemia after repair of aneurysms of the descending and thoracoabdominal aorta. J Cardiothorac Vasc Anesth 2003;17:598–603.[CrossRef][Medline]
  24. Caulkins SE, Purinton PT, Oliver JE Jr. Arterial supply to the spinal cord of dogs and cats. Am J Vet Res 1989;50:425–430.[Medline]
  25. Bower TC, Murray MJ, Gloviczki P, Yaksh TL, Hollier LH, Pairolero PC. Effects of thoracic aortic occlusion and cerebrospinal fluid drainage on regional spinal cord blood flow in dogs: correlation with neurologic outcome. J Vasc Surg 1988;9:135–144.[CrossRef]




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