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Ann Thorac Surg 1999;67:1940-1942
© 1999 The Society of Thoracic Surgeons

Hypothermic cardiopulmonary bypass for spinal cord protection: rationale and clinical results

^a The Heart Center, Missouri Baptist Medical Center, St. Louis, Missouri, USA

Address reprint requests to Dr Kouchoukos, 3009 N. Ballas Rd, Suite 266C, St. Louis, MO 63131

Presented at the Aortic Surgery Symposium VI, April 30–May 1, 1998, New York, NY.

	Abstract

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Background. Hypothermic cardiopulmonary bypass with or without circulatory arrest has been used successfully for the treatment of complex aneurysms of the descending thoracic and thoracoabdominal aorta. Hypothermia has a protective effect on spinal cord function, and its use has been associated with a low incidence of paraplegia in traditionally high-risk patients. Experimentally, the protective effect of hypothermia has been related to amelioration of excitotoxic injury by reduction of neurotransmitter release and to inhibition of delayed apoptotic cell death.

Methods. During a 12-year period, 114 patients with descending thoracic or thoracoabdominal aortic disease underwent replacement of the involved aortic segments using hypothermic cardiopulmonary bypass and intervals of circulatory arrest.

Results. The hospital mortality was 8% (9 patients). Paraplegia occurred in 2 and paraparesis in 1 of the 108 patients whose lower limb function was assessed postoperatively (2.8%). None of 40 patients with aortic dissection and none of the last 81 patients in the series developed paralysis.

Conclusions. Our experience with hypothermic cardiopulmonary bypass and circulatory arrest confirms that hypothermia provides substantial protection against paraplegia, and it allows complex operations on the descending thoracic and thoracoabdominal aorta to be performed with acceptable mortality.

	Introduction

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Elective hypothermic cardiopulmonary bypass (CPB) with intervals of circulatory arrest has been used successfully for the treatment of complex disease involving the descending thoracic and thoracoabdominal aorta [1–4]. This technique is indicated when the presence of proximal aortic disease either makes clamping of the proximal aorta unsafe or mandates graft replacement of the arch, and when extensive thoracic or thoracoabdominal aortic disease is present and the risk of developing paraplegia is judged to be increased. The rationale for using hypothermic CPB with periods of profound hypothermic circulatory arrest and low flow is to increase the tolerable duration of spinal cord ischemia while resection and graft replacement of the involved aortic segment and reimplantation of critical intercostal and lumbar arteries is being performed.

	Material and methods

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Patients
Between January 1986 and April 1998, 114 patients with aortic disease involving the distal aortic arch, the descending thoracic aorta, or the thoracoabdominal aorta underwent resection and graft replacement of the diseased aortic segments using elective hypothermic CPB, usually in combination with a period of circulatory arrest. The patients ranged in age from 22 to 79 years (mean 60), and 67 (59%) were male. Fifteen patients (13%) had the clinical stigmata of Marfan syndrome. Sixty-four (56%) had symptoms associated with their aortic disease. The remaining patients had aneurysms that were more than twice the size of the adjacent normal aorta, or had evidence of progressive enlargement of the aorta. Fourteen patients (12%) underwent emergent operation for rupture of the aneurysm or because of acute dissection. Forty-six patients (40%) had had previous operations on the thoracic or thoracoabdominal aorta. Thirteen patients (11%) had undergone repair of an infrarenal abdominal aortic aneurysm.

Operative technique
Routine hemodynamic monitoring and double-lumen endotracheal intubation are performed. Electroencephalographic monitoring is used. The left common femoral artery and vein are exposed, and a 28F to 32F long cannula is inserted and positioned in the right atrium. Proper placement is verified with intraoperative transesophageal echocardiography. The femoral artery is cannulated with a 20F or 22F short cannula. The descending aorta is exposed through a left posterolateral thoracotomy incision through the bed of the resected fourth or fifth rib. If necessary, the incision is extended into the abdomen, and the diaphragm is incised circumferentially to minimize injury to the branches of the phrenic nerve. Cardiopulmonary bypass is established immediately after the chest is entered, and the patient is cooled until electroencephalographic silence is achieved, and nasopharyngeal temperatures of 12°C to 14°C and bladder temperature of 15°C to 19°C are reached. Methylprednisolone (7 mg/kg) and thiopental (10–15 mg/kg) are given during cooling. The left lung is collapsed, and the heart is vented through the apex or the left inferior pulmonary vein as soon as it fibrillates. The aorta distal to the diseased segment is isolated circumferentially. The remainder of the aorta is not dissected. When required, circulatory arrest is established. 1,000 to 1,500 mL of blood is drained into the venous reservoir, and the intracardiac vent is occluded.

Procedures confined to the distal aortic arch and proximal descending thoracic aorta
Resection and graft replacement are usually performed during a single period of circulatory arrest without placement of clamps proximally. Collagen-impregnated woven Dacron grafts (Hemashield; Meadox Medicals, Inc., Oakland, NJ) are used. Distally, the aorta is clamped or occluded intraluminally to minimize blood loss. As the distal anastomosis is being completed, the graft is clamped and arterial perfusion is reestablished through the femoral artery to evacuate the air. After completion of the anastomosis, the graft is deaired with an 18-gauge needle, the clamp is removed, and cardiopulmonary bypass and rewarming are initiated. The proximal anastomosis is then performed.

Procedures on most of the descending or the thoracoabdominal aorta
Circulatory arrest is established, the distal aorta is occluded, and the proximal aorta is transected at the appropriate level. After completion of the proximal anastomosis, the graft is cannulated and connected to a second arterial cannula. Selective flow is adjusted with the help of a line occluder and an accurate flow meter (HT 109; Transonic Systems Inc., Ithaca, NY) attached to the second arterial line. This line is used to de-air the aortic arch. Retrograde venous perfusion is occasionally used to assist in de-airing. The aortic graft is then occluded distal to the proximal arterial line, and flow into the upper aorta is reestablished. One-third of the total arterial flow is directed through the proximal arterial line, and two-thirds through the distal line. During the period of hypothermic low flow, the anastomoses between the aortic graft and the lower intercostal, lumbar, visceral, renal arteries, and distal aorta are completed. An attempt is made to reimplant all patent intercostal and lumbar arteries below the level of the sixth intercostal space. Whenever possible, the clamp is repositioned below the intercostal artery-to-graft anastomoses before the lower anastomoses are performed to permit perfusion of the implanted intercostal and lumbar arteries, and rewarming is then initiated. During rewarming, spontaneous defibrillation usually occurs when the nasopharyngeal temperature reaches 26°C to 28°C. When normothermia is reached, the left ventricular venting catheter is removed and CPB is discontinued.

	Results

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The hospital and 30-day mortalities were 8% (9 patients). It was 38% (3 patients) for the 8 patients who received aprotinin and 6% (6 patients) for the remaining 106 patients (p < 0.01).

Lower intercostal and lumbar arteries were preserved or attached separately to the aortic graft in 83 of the 95 patients (87%) who had replacement of the distal descending thoracic or thoracoabdominal aorta. Paraplegia occurred in 2, and paraparesis in 1 of the 108 patients whose lower limb function was assessed postoperatively (2.8%). Among the 59 operative survivors with thoracoabdominal aortic disease, paraplegia occurred in 1 of 23 with Crawford type I, none of 29 with type II, and 1 of 12 with type III disease. None of the 40 patients with aortic dissection, and none of the last 81 patients in the series developed paraplegia. There have been no patients with delayed ischemic spinal cord injury.

Among the 109 operative survivors, renal failure requiring dialysis occurred in 1 patient (1%, aprotinin group). Eight patients (7.3%) had low cardiac output requiring prolonged inotropic support, 7 (6.4%) required reoperation for bleeding, 3 (2.8%) sustained a stroke, 22 (20%) required mechanical ventilation for longer than 48 h, and 8 (7.3%) required tracheostomy. No patient who did not receive aprotinin developed multiple organ system failure.

	Comment

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In the management of disease of the descending thoracic or thoracoabdominal aorta, hypothermic circulatory arrest offers certain advantages over other techniques, such as simple aortic clamping or use of distal perfusion with atriofemoral or femoral-femoral bypass. These include minimal dissection of the aorta, elimination of the need for proximal aortic clamping, access to the proximal aortic arch and ascending aorta, and a bloodless field. The profound hypothermia provides effective protection of the brain, spinal cord, kidneys, and the abdominal viscera.

Numerous experimental studies have established that hypothermia has a protective effect on spinal cord function during periods of aortic occlusion [5–9]. In a primate study employing proximal and distal hypothermic perfusion with circulatory arrest, hypothermia adequately protected spinal cord function after double-aortic cross-clamping for 60 min [10]. The protective effect of hypothermia on spinal cord function has also been established clinically [4, 11, 12].

The precise mechanism by which hypothermia exerts its protective effect on neural tissue is not known. Hypothermic protection is related to a reduction in oxygen demand, which results in increased ischemic tolerance [13–15]. However, the degree of protection is not proportional to metabolic rate reduction [16, 17]. Recent evidence implicating the inhibition of the release of excitatory neurotransmitters makes simple metabolic depression an unlikely sole mechanism for the protective effect of hypothermia [18–20]. Specifically, neurotransmitter release has been implicated in the pathogenesis of hypoxic ischemic injury in the spinal cord [21–23], and more specifically in injury caused by aortic crossclamping [24]. Hypothermia inhibits the biosynthesis, release, and uptake of these excitotoxic neurotransmitters, and via this mechanism may affect the outcome of the ischemic insult [25, 26]. We showed in a clinically relevant model of spinal cord ischemia that deep hypothermia prevented the release of amino acids in the extracellular space, and that glutamate levels remained depressed even after rewarming to normothermia [27].

We have not encountered delayed ischemic spinal cord injury in this patient series. It has been suggested that delayed paraplegia represents delayed cell death by the mechanism of apoptosis, which may have a protracted course when compared with necrosis [28, 29]. Hypothermia may prevent delayed ischemic spinal cord injury by conferring adequate intraoperative protection to neuronal cells that would otherwise proceed to fail functionally later by the mechanism of apoptotic cell death. In other words, delayed paraplegia may reflect damage programmed into the spinal cord at the time of the operation, and may not be related to postoperative impairment of spinal cord perfusion.

Hypothermic CPB with circulatory arrest allows complex and extensive operations on the descending thoracic and thoracoabdominal aorta to be performed with acceptable mortality, a low incidence of paralysis, and an incidence of other complications that does not exceed that reported with other techniques. This technique is particularly useful in patients at highest risk for development of paraplegia: those with Crawford type II aneurysms and aneurysms associated with dissection. Further advances in neurophysiology and pharmacology may better define the multifactorial nature and reduce the incidence of spinal cord ischemic injury.

	References

Top Abstract Introduction Material and methods Results Comment References

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Nicholas T. Kouchoukos Chris K. Rokkas Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kouchoukos, N. T. Articles by Rokkas, C. K. Search for Related Content PubMed PubMed Citation Articles by Kouchoukos, N. T. Articles by Rokkas, C. K.