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MMCTS (October 9, 2006). doi:10.1510/mmcts.2006.001933
Copyright © 2006 European Association for Cardio-thoracic Surgery

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Procedure


Adjuncts during surgery of the thoracoabdominal aorta and their impact on neurologic outcome: distal aortic perfusion and cerebrospinal fluid drainage

Anthony L. Estrera, Charles C. Miller, Ali Azizzadeh and Hazim J. Safi*

Department of Cardiothoracic and Vascular Surgery, The University of Texas at Houston Medical School, Memorial Hermann Heart and Vascular Institute, Houston, TX, USA

* Corresponding author: Department of Cardiothoracic and Vascular Surgery, The University of Texas Health Science Center, Memorial Hermann Hospital, 6410 Fannin, Ste. 450, Houston, TX 77030, USA Tel.: +1-713-500-5304; fax: +1-713-500-0647 E-mail: hazim.j.safi{at}uth.tmc.edu


   Summary
Top
 Summary
Introduction
 Surgical technique
 Results
 Conclusions
 Acknowledgements
 References
 
The adjunct (distal aortic perfusion, cerebrospinal fluid drainage, and moderate hypothermia) has been our mainstay in the prevention of paraplegia and paraparesis during repair of the descending thoracic and thoracoabdominal aorta.

Key Words: Aortic aneurysm • Thoracoabdominal aorta • Spinal cord protection • Neurologic


   Introduction
Top
 Summary
 Introduction
Surgical technique
 Results
 Conclusions
 Acknowledgements
 References
 
Neurologic deficit (paraplegia and paraparesis) is one of the most devastating complications that can occur during repair of the descending thoracic and thoracoabdominal aorta. During the clamp-and-sew era, aortic cross-clamp time was the principle predictor of immediate postoperative neurologic deficit. Analysis of Crawford's experience with 1509 patients revealed an overall incidence of paraplegia and paraparesis of 16.6% and an incidence of 31% in extent II cases. Incidence of neurologic deficit if clamp time exceeded 45 min was 50% [1]. The incidence of paraplegia in patients whose aortic cross-clamp time was <30 min was still significant at 8% [1]. We reported similar results using the clamp-and-sew technique [2]. Various methods to protect the spinal cord have been developed since the 1960s including passive shunts, distal aortic perfusion (left heart bypass), total cardiopulmonary bypass, profound hypothermic circulatory arrest, spinal cord cooling, and pharmacological agents, with varying success [1,3,4,5,6,7,8]. We have since adopted an adjunct technique, beginning in September 1992. Based on the work of Hollier et al. with cerebrospinal fluid drainage and Connolly's work with distal aortic perfusion [9,10], we theorized that decreasing cerebrospinal fluid pressure while increasing distal aortic perfusion pressure would provide superior protection to the spinal cord during cross-clamping of the aorta. After examining a model demonstrating its effectiveness, we adopted the adjunct of distal aortic perfusion and cerebrospinal fluid drainage along with passive moderate hypothermia [11]. This combination will be referred to as the adjunct for this presentation.

Anesthetic preparation
Following induction of general anesthesia, the patient is intubated with a double lumen endotracheal tube to permit right lung ventilation during surgery. Monitoring cardiac function, oxygenation, blood pressure, urine output, and coagulation is critical to the prevention of intraoperative and postoperative complications related to cardiac dysfunction, renal failure, paraplegia, pulmonary failure, and hemorrhage.

Electrodes attached to the scalp for electroencephalogram and along the spinal cord for motor and somatosensory evoked potential assess cerebral and spinal cord function, respectively (Schematic 1).


Figure 1
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  		Schematic 1 Brain function is monitored intraoperatively by electroencephalogram. Spinal cord function is monitored using somatosensory evoked potential (SSEP) and motor evoked potential (MEP).

 
A radial artery catheter checks arterial pressures. A Swan-Ganz catheter floated through another catheter placed in the internal jugular or subclavian vein monitors the central venous and pulmonary artery pressures. Probes placed in the patient's nasopharynx and bladder record temperatures. Large-bore central and peripheral venous lines are inserted for fluid and blood replacement therapy.

Rapid infusion system is often required for blood replacement therapy (Photo 1).


Figure 1
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  		Photo 1 The rapid infusion system.

 
A CSF catheter is placed in the 3rd or 4th lumbar space (Schematic 2 and Video 1). Cerebrospinal fluid pressure is monitored and kept below 10 mmHg throughout the procedure.


Figure 2
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  		Schematic 2 Placement of the lumbar catheter to provide cerebrospinal fluid (CSF) drainage and pressure monitoring.

 

Figure 1
Click on image to view video		 Video 1 The insertion of the cerebrospinal fluid drain into the Xth lumbar space.
 

   Surgical technique
Top
 Summary
 Introduction
 Surgical technique
Results
 Conclusions
 Acknowledgements
 References
 
The patient is placed in the right lateral decubitus position with the left hip flexed 45° for accessibility of the left and right groins. We tailor the chest incision to complement the extent of the aneurysm — a modified thoracoabdominal incision for the descending thoracic aorta and extent I or V thoracoabdominal aortic aneurysm, which taper to or just below the level of the celiac axis, and full thoracoabdominal exploration to the umbilicus for extent I and V that involve the superior mesenteric artery, and to the pubis for extent II, III, and IV aneurysms (Schematic 3).


Figure 3
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  		Schematic 3 Thoracoabdominal incisions tailored for extent of aneurysm.

 
The sixth rib is removed for all aneurysms except extent IV, and the left lung is collapsed. Taking care to avoid injury to the phrenic nerve, the aortic hiatus and the muscular portion of the diaphragm are cut for passage of the aortic graft (Video 2).


Figure 2
Click on image to view video		 Video 2 The patient is opened, and the sixth rib is exposed for removal. The phrenic nerve is identified and care is taken to avoid injuring it during the cutting of the aortic hiatus and muscular portion of the diaphragm.
 
The pericardium posterior to the left phrenic nerve is opened, and the left atrium cannulated through the left lower pulmonary vein or atrial appendage for distal aortic perfusion (Video 3). The perfusionist attaches a BioMedicus pump (Minneapolis, MN) with an in-line heat exchanger for postoperative rewarming to the cannula and arterial inflow is established through the left common femoral artery, the descending thoracic or abdominal aorta if the femoral artery is not accessible.


Figure 3
Click on image to view video		 Video 3 The pericardium is opened, exposing the left lower pulmonary vein, through which the left atrium is cannulated.
 
The left common femoral artery is preferred for cannulation (Video 4). In certain cases, such as the femoral artery being severely atheromatous, the contralateral common femoral artery may be used. Generally cannulation of the femoral artery will be performed using a 16–20 French cannula. After the patient is anticoagulated with heparin (1 mg/kg body weight), a transverse arteriotomy is performed and the cannula is secured using the umbilical tape. We monitor distal aortic perfusion pressure throughout the period of perfusion. Pressure is maintained between 60–80 mmHg and is managed by both the anesthesia and perfusion.


Figure 4
Click on image to view video		 Video 4 The left common femoral artery is exposed and cannulated.
 
The descending thoracic aorta is dissected from the level of the hilum of the lung, cephalad to the proximal descending thoracic aorta. We identify the ligamentum arteriosum and transect it, taking care to avoid injury to the left recurrent laryngeal nerve. We then initiate distal aortic perfusion.

The aorta is cross-clamped in sequential order to minimize organ ischemic time, beginning either proximal or distal to the left subclavian artery and then again at the mid-descending thoracic aorta (Video 5 and Schematic 4).


Figure 5
Click on image to view video		 Video 5 We clamp the aorta in a sequential fashion to reduce ischemic time.
 

Figure 4
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  		Schematic 4 We clamp the aorta in sequential segments in order to minimize ischemic time to the viscera.

 
Because of the danger of esophageal fistula, we no longer use the inclusion technique of wrapping the graft with the aneurysmal aortic wall in the proximal anastomosis. Instead, we completely transect the aorta to separate it from the underlying esophagus (Schematic 5 and Video 6).


Figure 5
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  		Schematic 5 The aorta is completely transected and separated from the esophagus.

 

Figure 6
Click on image to view video		 Video 6 The proximal aorta is transected, completely separating it from the esophagus.
 
We prefer a woven Dacron graft for aortic replacement. We suture the graft in an end-to-end fashion to the descending thoracic aorta, using a running 3-0 or 2-0 monofilament polypropylene suture. We check the anastomosis for bleeding and use pledgeted sutures for reinforcement, if necessary (Video 7).


Figure 7
Click on image to view video		 Video 7 The proximal anastomosis.
 
The lower clamp is then moved down to the distal thoracic aorta at the diaphragm level, and the remainder of the aneurysm is opened. For descending thoracic aortic aneurysms, the graft is cut in a beveled fashion and sewn to the distal thoracic aorta, using 3-0 or 2-0 monofilament polypropylene suture, incorporating the patent lower intercostal arteries that are in close proximity to the graft.

We reattach all patent lower intercostal arteries from T8 to T12, either together as a patch to a side hole made in the Dacron graft or individually (Video 8 and Schematic 6). Substantial back-bleeding from patent intercostal arteries can be minimized with temporary placement and inflation of balloon catheters (size 3F) prior to reimplantation. The upper intercostal arteries are generally ligated. However, if the lower intercostal arteries are occluded, any patent upper intercostal arteries are reimplanted instead, having assumed a more important role in supplying blood to the spinal cord. Once the intercostal arteries are reattached, forward pulsatile flow is restored to the spinal cord with the proximal clamp repositioned across the graft distal to the intercostal anastomosis.


Figure 8
Click on image to view video		 Video 8 Patent lower intercostal arteries are occluded to prevent back bleeding. An elliptical incision is made in the graft for reattachment of intercostal arteries.
 

Figure 6
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  		Schematic 6 The reattachment of patent lower intercostal arteries.

 
For thoracoabdominal aortic aneurysms, after reimplantation of the lower intercostal arteries the distal clamp is moved to the infrarenal abdominal aorta and the remainder of the aneurysm is opened (Video 9).


Figure 9
Click on image to view video		 Video 9 We perfuse the visceral and renal arteries via #9 or #12 French balloon perfusion catheters.
 
The celiac axis, superior mesenteric, right renal and left renal arteries are identified, cannulated with 9 or 12 French balloon perfusion catheters, perfused and cooled using either Ringer's lactate solution or blood at a flow rate of 300 to 600 ml/min (Schematic 7). Left renal artery pressure is monitored and maintained above 60 mmHg. At the same time, we maintain the patient's body temperature at about 33 °C by warming the lower circulation. If we are unable to warm the lower body we do not cool the viscera due to the risk of severe hypothermia (<30 °C core body temperature), and ventricular fibrillation.


Figure 7
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  		Schematic 7 Balloon-tipped catheters are inserted into the celiac, superior mesenteric, and renal arteries to permit perfusion. The kidneys and viscera are cooled using either Ringer's lactate solution or blood.

 
The visceral vessels must be evaluated intraoperatively before deciding how to proceed. If the celiac axis, superior mesenteric, and both renal arteries are in close proximity, they can be reimplanted as a single patch to a side hole made in the aortic graft, using running 3-0 or 2-0 monofilament polypropylene suture (Schematic 8). In a considerable number of patients, the left renal artery is more caudal and is instead reattached as a Carrell patch or using a short interposition bypass graft.


Figure 8
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  		Schematic 8 An elliptical hole is made in the graft for reimplantation of the visceral and renal arteries.

 
After completion of the visceral anastomosis the graft is clamped distal to the visceral vessel reattachment site and pulsatile flow is restored to the viscera (Schematic 9). The distal clamp is removed and the pump is stopped temporarily. The distal anastomosis is completed at the aortic bifurcation, using running 3-0 or 2-0 monofilament polypropylene suture.


Figure 9
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  		Schematic 9 Pulsatile flow is then restored to the visceral and renal arteries.

 
When the final anastomosis is completed pulsatile flow is restored to the legs and the pump is restarted to continue warming the patient to a nasopharyngeal temperature of 36 °C (Schematic 10).


Figure 10
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  		Schematic 10 The completion of the distal anastomosis.

 

   Results
Top
 Summary
 Introduction
 Surgical technique
 Results
Conclusions
 Acknowledgements
 References
 
The adjunct (distal aortic perfusion, CSF drainage, and moderate hypothermia) has reduced our overall incidence of immediate neurologic deficit to 2.4% [11] and in particular, 0.8% for descending thoracic aortic aneurysm repair [12] (Graph 1).


Figure 1
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  		Graph 1 Incidence of neurologic deficit based on quartile.

 
With adjuncts our rate of neurologic deficit for the most troublesome extent II thoracoabdominal aortic aneurysms has also declined and is now between 3% and 5% compared with rates between 30% and 40% in the era of clamp-and-sew [11] (Graph 2). Use of the adjunct has prevented approximately 1 in 20 cases of neurologic deficit in our overall population [13].


Figure 2
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  		Graph 2 Incidence of neurologic deficit for extent II TAAA based on quartile.

 
In the era of clamp-and-sew, clamp time was a significant predictor of neurologic deficit. Although clamp time has increased steadily every year since we have used the adjunct (34 s per year), neurologic deficit rates have decreased (Graph 3).


Figure 3
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  		Graph 3 Multiple logistic regression analysis according to risk of neurologic deficit and aortic cross-clamp time without (left) and with (right) adjunct use. The green area represents extent II thoracoabdominal aortic aneurysm (TAAA), and the yellow area represents all other extents.

 
Although other risk factors for neurologic deficit remain, cross-clamp time is no longer a significant predictor of neurologic deficit in our series [11].

Neurologic deficit
Immediate neurologic deficit is defined as paraplegia or paraparesis that occurs as the patient awakens from anesthesia. Delayed onset neurologic deficit refers to paraplegia or paraparesis that develops after a period of normal neurologic function. We have observed delayed neurologic deficit as early as 2 h and as late as 2 weeks following surgery (median, 2 days) in 2.4% of patients [14]. No single risk factor explains the onset of either deficit, but researchers have become increasingly interested in how a patient can emerge from surgery neurologically intact but later develop paraplegia. Using multivariable analysis, we found that acute dissection, extent II thoracoabdominal aortic aneurysm, and renal insufficiency were independent preoperative predictors [14]. In another study examining postoperative factors independent of preoperative risk factors, we found low postoperative mean arterial pressure (<60 mmHg) and CSF drain complications to be significant predictors [15]. We speculate that delayed neurologic deficit after thoracoabdominal aortic repair may result from a ‘second hit’ phenomenon. Although adjuncts may protect the spinal cord intraoperatively and reduce the incidence of immediate neurologic deficit, the spinal cord remains vulnerable during the early postoperative period. Additional ischemic insult caused by hemodynamic instability and CSF drainage catheter malfunction may constitute a ‘second hit,’ causing delayed neurologic deficit. Because postoperative factors associated with delayed neurologic deficit are likely related to arterial blood pressure and oxygen delivery, we keep mean arterial pressure above 90 mmHg to 100 mmHg, hemoglobin above 10mg/dl, and cardiac index >2.0 l/min.

If delayed neurologic deficit occurs while the CSF drain is in place, the patient is placed in the supine position, and CSF is drained freely until the CSF pressure drops below 10 mmHg. If the drain has been removed and delayed neurologic deficit occurs, the CSF drainage catheter is reinserted and drained for 72 h. With this protocol, we have observed partial recovery from neurologic deficit in more than 50% of patients and complete recovery in 40% [14] (Graph 4).


Figure 4
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  		Graph 4 Incidence and percent recovery of delayed neurologic deficit in patients with CSF drain in place, patients in whom the drain was replaced after onset of delayed neurologic deficit, and patients in whom the drain was not after onset.

 

   Conclusions
Top
 Summary
 Introduction
 Surgical technique
 Results
 Conclusions
Acknowledgements
 References
 
In conclusion, adjunct use during repairs of the thoracoabdominal aorta significantly reduced the risk of neurologic deficit, despite increasing aortic cross-clamp time. The use of the adjunct appears to blunt the affect of the aortic cross-clamp time and may provide the surgeon the ability to operate without being rushed. In our experience, because aortic cross-clamp time has been effectively eliminated as a risk factor with the use of the adjunct, using this variable to construct risk models becomes irrelevant.



   Acknowledgements
Top
 Summary
 Introduction
 Surgical technique
 Results
 Conclusions
 Acknowledgements
References
 
We thank Kirk Soodhalter for his editorial assistance and Chris Akers for medical illustrations and video editing.


   References
Top
 Summary
 Introduction
 Surgical technique
 Results
 Conclusions
 Acknowledgements
 References
 

  1. Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HJ. Experience with 1509 patients undergoing thoracoabdominal aortic operations.J Vasc Surg 1993;17:357–368; discussion 368 –70.[CrossRef][Medline]
  2. Safi HJ, Bartoli S, Hess KR, Shenaq SS, Viets JR, Butt GR, Sheinbaum R, Doerr HK, Maulsby R, Rivera VM. Neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysms: the role of cerebral spinal fluid drainage and distal aortic perfusion. J Vasc Surg 1994;20:434–444; discussion 442–43.[Medline]
  3. Miyamoto K, Ueno A, Wada T, Kimoto S. A new and simple method of preventing spinal cord damage following temporary occlusion of the thoracic aorta by draining the cerebrospinal fluid. J Cardiovasc Surg (Torino) 1960;1:188–197.[Medline]
  4. Acher CW, Wynn MM, Archibald J. Naloxone and spinal fluid drainage as adjuncts in the surgical treatment of thoracoabdominal and thoracic aneurysms. Surgery 1990;108:755–761; discussion 761–62.[Medline]
  5. Safi HJ. Role of the BioMedicus pump and distal aortic perfusion in thoracoabdominal aortic aneurysm repair. Artif Organs 1996;20:694–699.[Medline]
  6. Safi HJ, Hess KR, Randel M, Iliopoulos DC, Baldwin JC, Mootha RK, Shenaq SS, Sheinbaum R, Greene T. Cerebrospinal fluid drainage and distal aortic perfusion: reducing neurologic complications in repair of thoracoabdominal aortic aneurysm types I and II. J Vasc Surg 1996;23:223–228 discussion 229.[CrossRef][Medline]
  7. Rokkas CK, Kouchoukos NT. Profound hypothermia for spinal cord protection in operations on the descending thoracic and thoracoabdominal aorta. Semin Thorac Cardiovasc Surg 1998;10:57–60.[Medline]
  8. Svensson LG. An approach to spinal cord protection during descending or thoracoabdominal aortic repairs. Ann Thorac Surg1999;67:1935–1936; discussion 1953–58.[Abstract/Free Full Text]
  9. Hollier LH, Money SR, Naslund TC, Proctor CD Sr, Buhrman WC, Marino RJ, Harmon DE, Kazmier FJ. Risk of spinal cord dysfunction in patients undergoing thoracoabdominal aortic replacement. Am J Surg 1992;164:210–213; discussion 213–4.[CrossRef][Medline]
  10. Connolly JE, Wakabayashi A, German JC, Stemmer EA and Serres EJ. Clinical experience with pulsatile left heart bypass without anti-coagulation for thoracic aneurysms. J Thorac Cardiovasc Surg 1971;62:568–576.[Medline]
  11. Safi HJ, Estrera AL, Miller CC, Huynh TT, Porat EE, Azizzadeh A, Meada R, Goodrick JS. Evolution of risk for neurologic deficit after descending and thoracoabdominal aortic repair. Ann Thorac Surg 2005;80:2173–2179; discussion 2179.[Abstract/Free Full Text]
  12. Estrera AL, Miller CC 3rd, Chen EP, Meada R, Torres RH, Porat EE, Huynh TT, Azizzadeh A, Safi HJ. Descending thoracic aortic aneurysm repair: 12-year experience using distal aortic perfusion and cerebrospinal fluid drainage. Ann Thorac Surg 2005;80:1290–1296; discussion 1296.[Abstract/Free Full Text]
  13. Safi HJ, Miller CC 3rd, Huynh TT, Estrera AL, Porat EE, Winnerkvist AN, Allen BS, Hassoun HT, Moore FA. Distal aortic perfusion and cerebrospinal fluid drainage for thoracoabdominal and descending thoracic aortic repair: ten years of organ protection. Ann Surg 2003;238:372–380; discussion 380–81.[Medline]
  14. Estrera AL, Miller CC 3rd, Huynh TT, Azizzadeh A, Porat EE, Vinnerkvist A, Ignacio C, Sheinbaum R, Safi HJ. Preoperative and operative predictors of delayed neurologic deficit following repair of thoracoabdominal aortic aneurysm. J Thorac Cardiovasc Surg 2003;126:1288–1294.[Abstract/Free Full Text]
  15. Azizzadeh A, Huynh TT, Miller CC 3rd, Estrera AL, Porat EE, Sheinbaum R and Safi HJ. Postoperative risk factors for delayed neurologic deficit after thoracic and thoracoabdominal aortic aneurysm repair: a case-control study. J Vasc Surg 2003;37:750–754.[CrossRef][Medline]



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