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Asian Cardiovasc Thorac Ann 1998;6:288-294
© 1998 Asia Publishing EXchange Pte Ltd

ORIGINAL CONTRIBUTION

Clinical Results of Retrograde Cerebral Perfusion in Treatment of Aortic Disease

Tanzer Çalkavur, MD, Yüksel Atay, MD, Tahir Yagdi, MD, Mustafa Çikirikçoglu, MD, Levent Can, MD1, Ugur Gürcün, MD, Mustafa Özbaran, MD, Önol Bilkay, MD, Suat Büket, MD

Department of Cardiovascular Surgery
1 Department of Cardiology Ege University Medical Faculty Izmir, Turkey
For reprint information contact: Suat Büket, MD Department of Cardiovascular Surgery Ege University Medical Faculty Bornova, Izmir 35100, Turkey Tel:90 232 388 2866 Fax:90 232 339 0002 Email:bukets{at}bornova.ege.edu.tr

   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Between 1993 and 1998, 106 adults underwent ascending aorta or aortic arch operations using deep-hypothermic circulatory arrest and retrograde cerebral perfusion via the superior vena cava. Aortic lesions were acute type I dissection in 44 (41.5%), chronic type I dissection in 12 (11.3%), acute type II dissection in 6 (5.7%), chronic type II dissection in 9 (8.5%), ascending aorta or aortic arch aneurysms in 34 (32.1%), and an aneurysm of the sinus of Valsalva with aortic arch aneurysm in 1 (0.9%). The overall neurologic dysfunction rate was 6.6%. Early mortality was 18.8%. By multivariate analysis, circulatory arrest longer than 60 minutes and chronic renal failure were significant predictors of neurological dysfunction. Female gender, preoperative hemodynamic instability, circulatory arrest longer than 60 minutes, preoperative neurological dysfunction, and preoperative organ malperfusion were significant predictors of early mortality. We concluded that retrograde cerebral perfusion minimized neurological complications by preventing debris and air emboli and by providing adequate metabolic support in patients who needed circulatory arrest for surgical treatment of aortic pathology.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Cerebral protection during surgical treatment of ascending aorta or transverse arch aneurysms and DeBakey type I and II acute aortic dissection is an issue of paramount importance. Deep-hypothermic circulatory arrest has been the most frequently used strategy for cerebral protection since its introduction in 1975.1 However, deep hypothermic circulatory arrest exceeding 45 minutes is associated with a higher incidence of neurologic dysfunction while longer than 65 minutes is associated with higher mortality.2 To extend the safe period of circulatory arrest and to avoid cerebral complications, retrograde cerebral perfusion via the superior vena cava was introduced as an adjunct to deep hypothermia.3 Clinical and experimental studies demonstrated that retrograde cerebral perfusion supports the metabolic demands of the brain, clears toxins, and prevents embolic events during circulatory arrest, thereby prolonging the safe period.4–6 This study retrospectively evaluated mortality and neurologic outcomes of continuous retrograde cerebral perfusion as an adjunct to deep-hypothermic circulatory arrest in the treatment of aortic lesions.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Between November 1993 and March 1998, 106 adult patients with aortic lesions involving the ascending aorta or aortic arch, underwent surgery using retrograde cerebral perfusion as an adjunct to deep-hypothermic circulatory arrest. Seventy-six patients were male and 30 were female. Ages ranged from 23 to 77 years with a mean age of 54.05 years. The clinical profile of the patients included: DeBakey acute type I dissection in 44 (41.5%), chronic type I dissection in 12 (11.3%), acute type II dissection in 6 (5.7%), chronic type II dissection in 9 (8.5%), ascending aorta or aortic arch aneurysms in 34 (32.1%), and aneurysm of the sinus of Valsalva with aortic arch aneurysm in 1 (0.9%). Chest and back pain was the most frequent presenting symptom. Two patients with acute DeBakey type I aortic dissection were in profound shock due to cardiac tamponade. The other presenting symptoms are listed in Table 1Go. The most commonly associated pathologic conditions were hypertension and aortic insufficiency, other associated pathologic conditions are shown in Table 2Go. Some patients had more than one of these associated conditions.


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  		Table 1. Signs and Symptoms in Patients with Proximal Aortic Lesions
 

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  		Table 2. Associated Pathologic Conditions in Patients with Proximal Aortic Lesions
 
Replacement of the ascending aorta by the open distal technique was carried out in 22 patients (2 had concomitant coronary bypass grafting). Replacement of the ascending aorta and proximal aortic arch was performed in 17 patients. Resuspension of the aortic valve and replacement of the ascending aorta was carried out in 20 patients of whom 2 had coronary artery bypass grafting (one needed a right coronary artery saphenous vein bypass graft because of an intimal tear in the right coronary ostium). Entire aortic arch replacement using the elephant trunk technique was performed in 14 patients. Composite graft replacement was carried out in 25, including 18 with a modified Bentall technique and 7 with the Cabrol technique. Separate aortic valve replacement and ascending aortic graft interposition was undertaken in 7 patients using the Wheat technique. Patch grafting of the aortic arch was carried out in one patient.

Patients were placed in the supine position and a bilateral radial artery cannula was inserted before induction of anesthesia. General anesthesia was induced with 10 µg·kg–1 fentanyl, 0.3 mg·kg–1 etomidate, and 0.1 mg·kg–1 pancuronium bromide, followed by continuous infusion of fentanyl (10 µg·kg–1 per hour) in combination with 0.2% to 2% enflurane and 100% oxygen. A double-lumen central line and a Swan-Ganz catheter were inserted. Nasopharyngeal and rectal temperatures were monitored. Five electroencephalographic leads were placed and the electroencephalograph was monitored continuously with a Life Scan brain activity monitor (Diatek Patient Management System, Inc., San Diego, CA, USA).

The chest and femoral region were prepared and draped in the usual fashion. After administration of heparin, the femoral artery was cannulated. In patients with acute DeBakey type I dissection or cardiac tamponade, the femoral vein was cannulated and cardiopulmonary bypass with cooling was begun immediately. After a median sternotomy, the superior vena cava was cannulated and connected to the bypass circuit via a Y-connector. In patients with aneurysms, acute dissection without cardiac tamponade, or chronic dissection, cardiopulmonary bypass was established via right-atrial bicaval cannulation. The superior vena cava was snared and the heart was vented through the right superior pulmonary vein. A bypass circuit between the arterial and venous line was instituted, which was clamped during cardiopulmonary bypass (Figure 1Go). The hematocrit was maintained at approximately 20% during cardiopulmonary bypass to prevent sludging during deep hypothermia. Alpha-stat strategy was used to maintain the acid-base balance.



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  		Figure 1. Cardiopulmonary bypass (CPB) and retrograde cerebral perfusion (RCP) circuit. Dotted arrows indicate blood flow during CPB. Solid arrows indicate blood flow during RCP. FA = femoral artery, FV = femoral vein, x = clamp during RCP.

 
Patients were cooled for a further 5 minutes after the electroencephalograph became flat and circulatory arrest was achieved. When the arterial and femoral venous or inferior vena caval lines were clamped, retrograde cerebral perfusion was instituted by releasing the clamp on the bypass circuit between the arterial and venous lines. Retrograde flow was adjusted to maintain an internal jugular vein pressure of 20 mm Hg throughout the circulatory arrest period. Back-bleeding from the carotid arteries into the aortic arch was aspirated. Myocardial protection was provided with combined intermittent antegrade selective perfusion of the left and right coronary arteries with cold blood cardioplegia and retrograde cold blood cardioplegia.

The ascending aorta was opened longitudinally and the incision was extended towards the aortic arch if it was involved in the disease. In cases of aortic dissection, re-entry was checked by observing back-bleeding from the true or false lumen. The branches of the aortic arch were inspected carefully for atheromatous debris or dissection. End-to-end full thickness open anastomosis was carried out with a zero-porosity woven Dacron graft. After completion of the aortic reconstruction, air was evacuated while the blood drained in a retrograde manner from the open arch vessels, and retrograde flushing through the femoral artery was accomplished by releasing the clamp on the arterial line. During rewarming, the temperature gradient between the water bath and the blood was kept at less than 10°C to prevent gaseous microemboli. When the nasopharyngeal temperature reached 36°C, the patient was weaned from cardiopulmonary bypass and the chest was closed in the usual manner.

Statistical Analysis
The data were evaluated using SPSS version 6 for Windows software (SPSS, Inc., Chicago, IL, USA). The results were expressed as mean ± standard deviation. Univariate analysis was carried out with the chi-squared (Pearson) test. Variables that were likely to affect postoperative mortality and morbidity were entered for multivariate logistic regression analysis with stepwise addition of variables to determine odds ratios. A p value of less than 0.05 was considered significant.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Total circulatory arrest times ranged from 12 to 74 minutes (mean, 32.02 ± 14.31 minutes). Mean cardiac ischemia time was 83.6 ± 34.9 minutes (range, 20 to 180 minutes) and mean cardiopulmonary bypass time was 183.5 ± 48.5 minutes (range, 84 to 342 minutes). Just before the start of deep-hypothermic circulatory arrest, the mean rectal temperature was 16.3 ± 2.2°C.

Seven patients had postoperative neurologic dysfunction (6.6%). One of these (0.9%) had permanent neurologic dysfunction (quadriplegia). This patient had chronic type I dissection and the entire aortic arch was replaced using the elephant trunk technique. Temporary neurologic complications comprised confusion in 6 patients (5.7%). Two of these patients had preoperative chronic renal failure. Three patients who underwent entire aortic arch replacement had cord vocal paralysis due to surgical dissection near the left recurrent laryngeal nerve. Other postoperative complications included respiratory failure in 11 patients, atrial fibrillation in 11, sepsis and multiple organ failure in 10, renal failure in 5, excessive bleeding in 5, and low cardiac output in 4 patients.

The early mortality rate was 18.8% with 20 deaths, 5 of which occurred intraoperatively. The causes of death were sepsis and multiple organ failure in 10 patients, low cardiac output in 7, and excessive bleeding in 3. In the late postoperative period, there was one mortality because of cerebral embolism.

The preoperative and operative variables used to evaluate the risk of mortality and neurologic dysfunction were: sex, age greater than 65 years, preoperative hemodynamic instability, preoperative neurologic dysfunction, preoperative organ malperfusion, preoperative renal failure, aortic dissection, total circulatory arrest time longer than 60 minutes, cardiac ischemic time longer than 120 minutes, cardiopulmonary bypass time longer than 200 minutes, mean rectal temperature greater than 18°C, and the requirement of entire aortic arch replacement.

By multivariate analysis, preoperative and operative variables associated with increased risk of neurologic dysfunction were total circulatory arrest time longer than 60 minutes and preoperative chronic renal failure (Table 3Go). The significant predictors of early mortality by multivariate analysis are shown in Table 4Go. These comprised preoperative hemodynamic instability, female gender, total circulatory arrest time longer than 60 minutes, preoperative neurological dysfunction, and preoperative organ malperfusion.


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  		Table 3. Multivariate Analysis of Preoperative and Operative Risk Factors for Neurologic Dysfunction
 

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  		Table 4. Multivariate Analysis of Preoperative and Operative Risk Factors for Hospital Mortality
 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Deep hypothermia and cardiopulmonary bypass have been widely used as adjuncts in the treatment of proximal aortic lesions.7,8 They provide a dry and motionless operative field and avoid damp injury to the fragile aortic tissue. Minimal dissection and the absence of clamps are major advantages of deep-hypothermic circulatory arrest. Deep hypothermia also protects the brain and the other vital organs by reducing metabolic activity.9 Mills and Ochsner10 first described retrograde cerebral perfusion for preventing air embolization during operations on the aortic arch. Ueda and colleagues3 used retrograde perfusion of the brain during aortic arch replacement and there are several subsequent reports of good clinical results with this technique during operations on the aortic arch.11,12 After the report of open aortic anastomosis by Livesay and colleagues13 in 1982, most operations have been performed with the patient in the head-down position and without aortic clamping. Distortion of the aortic lumen, fragmentation of the fragile arterial wall, and further dissection are avoided using this technique. In acute aortic dissection, the false lumen can be safely and accurately obliterated with the distal suture line. However, with the patient placed head-down to prevent air induction into the aortic arch during open distal anastomosis without clamping, air may get into the descending aorta as it is higher than the open aortic arch. Air and debris in the descending aorta may be back-flushed by femoral arterial return after reestablishment of cardiopulmonary bypass. Ergin and colleagues14 also mentioned that a period of retrograde cerebral perfusion at the end of the arrest period might be a useful adjunct to wash out debris that may have escaped distally into the cerebral circulation. According to their report, the incidence of stroke significantly correlated with age, operation on the aortic arch, and descending aortic aneurysms containing clots and atheroma. In experimental embolization in pigs, recovery was improved by using deep hypothermia and retrograde cerebral perfusion.15 We have noted that particulate debris was frequently flushed out of the aortic arch vessels during retrograde cerebral perfusion. We feel strongly that the combination of retrograde cerebral perfusion followed by back-flushing of the femoral artery is essential for prevention of embolic events or stroke due to debris both in the cerebral vessels and in the descending aorta.

A major concern is the safety limit of circulatory arrest. Svensson and colleagues2 found that circulatory arrest times greater than 45 minutes were associated with a higher risk of stroke, whereas arrest times greater than 65 minutes were associated with a higher incidence of death. Safi and colleagues16 reported that a pump time greater than 60 minutes was associated with an increased risk of stroke and that retrograde cerebral perfusion decreased the incidence of stroke. In our study, total circulatory arrest time longer than 60 minutes was a strong predictor of neurologic dysfunction. However, longer times are required in some patients. We applied retrograde cerebral perfusion in a patient undergoing a Bentall procedure because of acute type I aortic dissection; the circulatory arrest time was 72 minutes and the patient was awake 4 hours after surgery.

There have been several circulation management techniques reported in other series. Ergin and colleagues14 reported a 19.3% temporary neurological dysfunction rate, a 9.6% rate of permanent stroke, and a 28.9% overall incidence of neurologic dysfunction in a series of 200 consecutive patients where they have used deep-hypothermic circulatory arrest alone. Alamanni and colleagues17 reported a 21% total neurologic dysfunction rate using deep-hypothermic circulatory arrest alone. A number of surgical groups have recently changed their circulation management to retrograde cerebral perfusion. Bavaria and colleagues18 demonstrated that the addition of retrograde cerebral perfusion to deep-hypothermic circulatory arrest reduced the incidence of stroke from 12% to 0%. Coselli and LeMaire19 found a lower mortality as well as reduced incidence of stroke when both of these techniques were employed, compared to using deep-hypothermic circulatory arrest alone.

The mortality rate in our series was 18.8%. Preoperative neurologic dysfunction, preoperative hemodynamic instability, female gender, organ malperfusion, and circulatory arrest time longer than 60 minutes were predictors of early mortality. The presence of hemodynamic instability has been reported to be a strong independent predictor of mortality.14 Svensson and colleagues2 found that the cardiopulmonary bypass time was a better predictor of early death than the circulatory arrest time.

In our study, retrograde cerebral perfusion was regulated to maintain a pressure of 20 mm Hg in the internal jugular vein. However, the optimal perfusion pressure during deep hypothermia is controversial. Nojima and colleagues20 stated that 20 mm Hg is most appropriate for retrograde cerebral perfusion. Venous hypertension is an additional factor that may contribute to morbidity and mortality in retrograde cerebral perfusion. With a central venous pressure higher than 25 to 35 mm Hg, cerebral edema may develop. We did not exceed this pressure so as to avoid complications. Although there are risks of edema of the brain and venous bleeding, we consider that the retrograde cerebral perfusion pressure we used was not hazardous. There was no arterial antegrade perfusion during circulatory arrest so that the pressure gradient was 20 mm Hg between the venous side and the open aorta. The early awakening and mental alertness of our patients after the operation indicated that there was no cerebral edema due to venous hypertension. In 1995, de Brux and colleagues21 showed that a liquid injected into the superior vena cava reached the brain through the azygos vein system even if the valves in the internal jugular vein were competent. It was demonstrated by using a technetium-99m-labeled brain perfusion agent that the human brain was adequately perfused during retrograde cerebral perfusion and deep-hypothermic circulatory arrest.22 A safe period of circulatory arrest with retrograde cerebral perfusion has not been established but it is considered to be between 80 and 90 minutes at 19°C according to a Japanese multicenter survey of 228 patients.23

It was shown that retrograde cerebral perfusion provides metabolic substrates including oxygen to the cerebral tissues.24 We demonstrated that blood pH, glucose levels, and O2 saturation in back-bleeding from the carotid arteries during retrograde cerebral perfusion were lower than that measured in samples taken simultaneously from oxygenated blood perfused through the superior vena caval cannula.25 Retrograde cerebral perfusion also maintains brain temperature at an optimal level during circulatory arrest.

Although flow dynamics and details of brain metabolism during retrograde cerebral perfusion have not yet been determined in humans, we believe that this technique extends the time limit for brain protection during hypothermic circulatory arrest. It also offers the advantage of exclusion of air, particulate, and atheromatous debris from the aorta.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Griepp RB, Stinson EB, Hollingsworth JF, Buehler D. Prosthetic replacement of the aortic arch. J Thorac Cardiovasc Surg 1975;70:1051–63.[Abstract]

  2. Svensson LG, Crawford ES, Hess KR, Coselli JS, Raskin S, Sheneq SA, et al. Deep hypothermia with circulatory arrest: determinant of stroke and early mortality in 656 patients. J Thorac Cardiovsc Surg 1993;106:19–31.[Abstract]

  3. Ueda U, Miki S, Kusuhara K, Okita Y, Tahata Y, Yamanaka K. Surgical treatment of the aneurysm or dissection involving the ascending aorta and aortic arch, utilizing circulatory arrest and retrograde cerebral perfusion. J Cardiovasc Surg 1990;31:553–8.[Medline]

  4. Ergin A, Griepp EB, Lansman SL, Galla JD, Levy M, Griepp RB. Hypothermic circulatory arrest and other methods of cerebral protection during operations on the thoracic aorta. J Cardiac Surg 1994;9:525–37.[Medline]

  5. Midulla PS, Gandsas A, Sadeghi AM, Mezrow CK, Yerlioglu ME, Wang W, et al. Comparison of retrograde cerebral perfusion to antegrade cerebral perfusion and hypothermic circulatory arrest in a chronic porcine model. J Cardiac Surg 1994;9:560–75.[Medline]

  6. Usui A, Hotta T, Hiroura M, Murase M, Maeda M, Koyama T, et al. Retrograde cerebral perfusion through a superior vena caval cannula protects the brain. Ann Thorac Surg 1992;53:47–53.[Abstract]

  7. Cooley DA. Experience with hypothermic circulatory arrest and the treatment of aneurysms of the ascending aorta. Semin Thorac Cardiovasc Surg 1991;3:166–70.[Medline]

  8. Crawford ES, Svensson LG, Coselli JS, Safi HJ, Hess KR. Surgical treatment of aneurysms and/or dissection of the ascending aorta and transverse aortic arch. Factors influencing survival in 717 patients. J Thorac Cardiovasc Surg 1989;98:659–74.[Abstract]

  9. Griepp RB, Ergin MA, Lansman SL, Galla JD, Pogo G. The physiology of hypothermic circulatory arrest. Semin Thorac Cardiovasc Surg 1991;3:188–93.[Medline]

  10. Mills NL, Ochsner JL. Massive air embolism during cardiopulmonary bypass: causes, prevention, and management. J Thorac Cardiovasc Surg 1980;80:708–17.[Abstract]

  11. Coselli JS, Büket S, Djukanovic B. Aortic arch surgery: current treatment and results. Ann Thorac Surg 1995;59: 19–27.[Abstract/Free Full Text]

  12. Deeb GM, Jenkins E, Bolling SF, Brunsting LA, Williams DM, Quint LE, et al. Retrograde cerebral perfusion during hypothermic circulatory arrest reduces neurological morbidity. J Thorac Cardiovasc Surg 1995;109:259–68.[Abstract/Free Full Text]

  13. Livesay JJ, Cooley DA, Duncan JM, Ott DA, Walker WE, Reul GJ. Open aortic anastomosis: improved results in the treatment of aneurysms of the aortic arch. Circulation 1982;66(Suppl I):I-122–7.

  14. Ergin MA, Galla JD, Lansman SL, Quintana C, Bodian C, Griepp RB. Hypothermic circulatory arrest in operations on the thoracic aorta. Determinants of operative mortality and neurologic outcome. J Thorac Cardiovasc Surg 1994; 107:788–99.[Abstract/Free Full Text]

  15. Yerlioglu ME, Wolfe D, Mezrow CK, Weisz DJ, Midulla PS, Zhung N, et al. The effect of retrograde cerebral perfusion after particulate embolization to the brain. J Thorac Cardiovasc Surg 1995;110:1470–85.[Abstract/Free Full Text]

  16. Safi HJ, Brien HW, Winter JN, Thomas AC, Maulsby RL, Doerr HK, et al. Brain protection via cerebral retrograde perfusion during aortic arch aneurysm repair. Ann Thorac Surg 1993;56:270–6.[Abstract]

  17. Alamanni F, Agrifoglio M, Pompilio G, Spirito R, Sala A, Arena V, et al. Aortic arch surgery: pros and cons of selective cerebral perfusion. A multivariate analysis for cerebral injury during hypothermic circulatory arrest. J Cardiovasc Surg 1995;36:31–7.[Medline]

  18. Bavaria JE, Woo YJ, Hall RA, Carpenter JP, Gardner TJ. Retrograde cerebral and distal aortic perfusion during ascending and thoracoabdominal aortic operations. Ann Thorac Surg 1995;60:345–53.[Abstract/Free Full Text]

  19. Coselli JS, LeMaire SA. Experience with retrograde cerebral perfusion during proximal aortic surgery in 290 patients. J Cardiac Surg 1997;12:322–5.[Medline]

  20. Nojima T, Magara T, Nakajima Y, Waterida S, Onoe M, Sugita T, et al. Optimal perfusion pressure for experimental retrograde cerebral perfusion. J Cardiac Surg 1994;9:548–59.[Medline]

  21. de Brux J-L, Subayi J-B, Pegis J-D, Pillet J. Retrograde cerebral perfusion: anatomic study of the distribution of blood to the brain. Ann Thorac Surg 1995;60:1294–8.[Abstract/Free Full Text]

  22. Pagano D, Boivin CM, Faroqui MH, Bonser RS. Retrograde perfusion through the superior vena cava perfuses the brain in human beings. Thorac Cardiovasc Surg1996; 111:270–2.

  23. Usui A, Abe T, Murase M. Early clinical results of retrograde cerebral perfusion for aortic arch operations in Japan. Ann Thorac Surg 1996;62:94–104.[Abstract/Free Full Text]

  24. Coselli JS. Retrograde cerebral perfusion via a superior vena caval cannula for aortic arch aneurysm operations. Ann Thorac Surg 1994;57:1668–9.[Abstract]

  25. Büket S, Alayunt A, Disçigil B, Apaydin A, Yüksel M, Durmaz I. Continuous retrograde cerebral perfusion supplies substrates for brain metabolism during hypothermic circulatory arrest. Perfusion 1995;10:237–44.[Abstract/Free Full Text]





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