Scott A. Buchanan

Prevention of spinal cord injury after repair of the thoracic or thoracoabdominal aorta

Spinal cord injury occurring as the result of surgical repair of thoracic and thoracoabdominal aortic disease remains a devastating complication. The incidence of postoperative neurologic deficits varies from 4% to 38%. Factors associated with a greater risk for injury include the presence of dissection or extensive thoracoabdominal disease, and a prolonged cross-clamp time. Spinal cord ischemia initiates a deleterious cascade of biochemical events that ultimately result in an increased intracellular calcium concentration. Calcium-activated proteases, lipases, and nucleases mediate the processes that cause cell injury. The accumulation of oxygen-derived free radicals and the occurrence of hyperemia during reperfusion are also contributing causes of spinal cord injury. Increasing the spinal cord blood flow with shunts, oxygenated bypass circuits, cerebrospinal fluid drainage, the intrathecal administration of vasodilators, and the reattachment of intercostal arteries has been tried in an effort to increase spinal cord perfusion. Pharmacologically based measures to prevent spinal cord injury have been pursued, and these have consisted of hypothermia, anesthetic agents, calcium channel blockers, free radical scavengers, and immune system modulation. However, no single technique has proved to be consistently effective in preventing ischemia-induced spinal cord injury.

Predicting survival after coronary revascularization for ischemic cardiomyopathy.

BACKGROUND The success of coronary revascularization for ischemic cardiomyopathy (left ventricular ejection fraction of 0.25 or less) has been unpredictable. We and others have demonstrated that the hospital operative mortality rate for these operations has been surprisingly low, particularly if evidence of ischemia is present. We subsequently liberalized our selection criteria based on our hypothesis that coronary artery bypass grafting is safe in this subset of patients regardless of the status of their distal coronary vasculature. METHODS To examine this hypothesis, we studied retrospectively our patients undergoing coronary artery bypass grafting from 1983 to 1993. Ninety-six patients with ejection fractions of 0.25 or lower underwent this operation, with 88 hospital survivors (mortality 8%). All of the patients had clinical symptoms of heart failure. The male to female ratio was 4.6:1. The average age was 63.1 +/- 0.9 years (mean +/- standard error of the mean). Patients were excluded if they had valvular heart disease other than mild to moderate mitral regurgitation, required resection of a ventricular aneurysm, or required an emergency operation for acute coronary occlusion. Possible predictors of death were examined retrospectively. The catheterization films were reviewed retrospectively by a cardiovascular surgeon who was blinded to patient outcome and was never involved in the clinical management of any of the patients. Vessel quality was described as good, fair, or poor. RESULTS Increased age and poor vessel quality were the only significant predictors of poor outcome. Sex, presence or absence of angina, preoperative angina, preoperative ejection fraction, preoperative arrhythmia disorder, aortic cross-clamp time, and the number of bypass grafts had no significant effect on outcome in the perioperative period. CONCLUSION These results demonstrate that poor vessel quality and older age are predictors of poor outcome in patients with low ejection fractions undergoing myocardial revascularization. We conclude that poor distal coronary vasculature is a contraindication to coronary artery bypass grafting in patients with an ejection fraction of 0.25 or less, even if angina is present.

Management of renal tumors involving the inferior vena cava

Abstract Purpose: We reviewed our experience of the resection of renal tumors involving the inferior vena cava (IVC) from 1987 to 1992 with the hypothesis that retrohepatic IVC involvement of renal tumors can be managed without cardiopulmonary bypass (CPB) and circulatory arrest with acceptable morbidity and mortality rates. Methods: We retrospectively reviewed our experience of radical nephrectomies for renal tumors from 1987 to 1992 ( n = 69). Of these, 13 had involvement of the IVC (19%). Three of the patients had right atrial extension requiring CPB with circulatory arrest. Three patients had retrohepatic involvement, and seven had infrahepatic involvement. All thirteen patients underwent operative removal of the tumor and tumor thrombus. Results: The patients with atrial extension who were treated with CPB and circulatory arrest had hospital and 1-year survival rates of 100% (three of three). The patients with retrohepatic extension treated without CPB and circulatory arrest had hospital and 1-year survival rates of 100% (three of three). The patients with infrahepatic extension treated without CPB and circulatory arrest had hospital and 1-year survival rates of 85% (six of seven) and 50% (three of six), respectively. There was no statistically significant difference between groups. The hospital death occurred in a patient who had a massive pulmonary embolism and disseminated intravascular coagulation before operation. The deaths that occurred before 1 year were due to metastatic disease and unresectable disease at the time of operation. Conclusion: CPB with circulatory arrest is not required in patients with retrohepatic IVC extension of renal tumors, and aggressive resection can be performed in these patients with acceptable morbidity and mortality rates. (J VASC SURG 1994;20:385-8.)

Stroke rate is markedly reduced after carotid endarterectomy by avoidance of protamine

PURPOSE Postoperative neurologic injury remains a significant risk of carotid endarterectomy. Mechanisms include embolization of debris and formation of thrombus on the newly endarterectomized surface. We hypothesized that the risk of postoperative neurologic injury would be lower in those patients who did not receive protamine for reversal of heparin anticoagulation. METHODS We reviewed 348 consecutive primary carotid endarterectomies performed since January 1, 1986, to determine the relationship between surgical outcomes and reversal of heparin anticoagulation. Patients undergoing additional simultaneous cardiovascular procedures were excluded. One hundred ninety-three patients received protamine after completion of the endarterectomy. The remaining 155 patients did not receive any protamine. RESULTS All patients in both groups survived to discharge. There were no strokes in those patients who did not receive any protamine; however, the stroke rate in the protamine group was 2.6% (5 of 193), p < 0.045. The incidence of hematoma requiring reexploration was 1.0% (2 of 193) and 1.9% (3 of 155) in the protamine and no-protamine groups, respectively (p = NS). Intraoperative shunting was used more frequently in the no-protamine group (84% vs 67%, p < 0.001), and patch angioplasty was performed more frequently in the protamine group (35% vs 15%, p < 0.001). However, neither shunting nor patching significantly influenced stroke rates. CONCLUSIONS We conclude that carotid endarterectomy without reversal of heparin anticoagulation is associated with a reduced postoperative stroke rate without a significant increase in morbidity rates.

Optimal timing of abdominal aortic aneurysm repair after coronary artery revascularization

ObjectiveThe authors ascertained the optimal timing of repair of an abdominal aortic aneurysm (AAA) after coronary artery revascularization. Summary Background DataCardiac events are the most common cause of death after elective repair of AAA. Preoperative coronary revascularization has significantly reduced postoperative cardiac complications after elective AAA repair. Currently, most patients undergo repair of asymptomatic AAA within 6 months after the coronary revascularization. MethodsThe authors performed a retrospective review of patients who underwent repair or scheduled repair of an asymptomatic AAA within 6 months after coronary artery bypass graft (CABG) between March 1988 and October 1993. ResultsThere was no mortality in the group of patients (n = 14) who underwent repair of AAA simultaneously or within 14 days of coronary revascularization. In contrast, there was a significantly increased mortality rate of 3 of 9 (33%) in patients scheduled to undergo repair of the AAA more than 2 weeks after coronary revascularization (p < 0.05). All nonsurvivors died between 16 and 29 days after CABG, and died as a result of ruptured AAA. ConclusionElective AAA repair should be undertaken simultaneously or within 2 weeks of coronary artery revascularization because of an increased risk of postoperative AAA rupture seen after this time period. In addition, simultaneous or early postoperative AAA repair does not increase the overall operative risk.

Pulmonary function after non—heart-beating lung donation in a survival model

BACKGROUND Lung procurement from recently deceased cadavers has been suggested to enlarge the limited donor pool. We hypothesized that lungs harvested from non-heart-beating donors (NHBD) would function as well as those harvested from heart-beating donors. METHODS Sixteen adult swine underwent left lung allotransplantation. Controls received lungs procured from heart-beating donors, NHBD pigs received lungs immediately harvested from donors after death from asphyxiation, and NHBD-15 and NHBD-30 pigs received lungs harvested after 15 and 30 minutes after asphyxiation. RESULTS After 1 week of survival, mean dynamic airway compliance (mL/cm H2O +/- standard error of the mean) was 16.3 +/- 0.7 in controls, and 17.3 +/- 1.0, 16.4 +/- 6.0, and 7.3 +/- 1.6 in the NHBD, NHBD-15, and NHBD-30 groups, respectively (p = 0.02, NHBD-30 versus others combined). No significant differences were noted in the pulmonary venous partial pressure of oxygen or pulmonary vascular hemodynamics compared with controls. CONCLUSIONS The decrease in airway compliance noted in the NHBD-30 group may reflect an exacerbation of reperfusion injury caused by 30 minutes of warm ischemia during organ retrieval. We conclude that posttransplantation lung function using an NHBD with up to 15 minutes of warm ischemia is equivalent to lung function after heart-beating harvest.

Non-heart-beating donors: A model of thoracic allograft injury

4ACKGROUND. Non-heart-beating donors (NHBDs) have been proposed for the critical shortage of donors for cardiac and pulmonary transplantation. We determined the effects of prearrest hypoxia and postarrest warm ischemia on cardiac and pulmonary allografts procured from NHBDs undergoing hypoxic arrest. METHODS. Rabbit hearts and lungs were procured from separate donors and placed on isolated blood perfusion circuits. Controls were excised and perfused without ischemia. Heart from NHBDs underwent either prearrest hypoxic perfusion alone or consecutive periods of prearrest hypoxic perfusion and 20 minutes of postarrest warm ischemia. A third group of hearts underwent 30 minutes of warm, global ischemia alone. Two groups of pulmonary allografts were studied using similar hypoxic perfusion/20-minute ischemia and 30-minute ischemia donors. RESULTS. Prearrest hypoxic perfusion clearly causes significant dysfunction of cardiac allografts from NHBDs compared with nonischemic controls. Prearrest hypoxic perfusion combined with postarrest ischemia results in an additive degree of dysfunction more severe than a similar period of warm ischemia alone. Both groups of experimental lungs displayed function similar to that of nonischemic controls in terms of pulmonary hemodynamics, airway resistance, and oxygenation potential. CONCLUSIONS. We conclude that prearrest hypoxic perfusion significantly contributes to the dysfunction of NHBD cardiac allografts. Pulmonary allografts may be more amenable to procurement of NHBDs.

Intratracheal Surfactant Administration Preserves Airway Compliance During Lung Reperfusion

BACKGROUND Decreased airway compliance after lung transplantation has been observed with severe ischemia-reperfusion injury. Further, it has been shown that the surfactant system is impaired after lung preservation and reperfusion. We hypothesized that surfactant replacement after allograft storage could preserve airway compliance during reperfusion. METHODS Rabbit lungs were harvested after flush with 50 mL/kg of cold saline solution. Immediate control lungs were studied with an isolated ventilation/perfusion apparatus using venous rabbit blood recirculated at 40 mL/min, room-air ventilation at 20 breaths/min, and constant airway pressure (n = 8). Twenty-four-hour control lungs were preserved at 4 degrees C for 24 hours and then similarly studied (n = 7). Surfactant lungs underwent similar harvest and preservation for 24 hours, but received 1.5 mL/kg of intratracheal surfactant 5 minutes before reperfusion (n = 10). Airway pressure and flow were recorded continuously during 30 minutes of reperfusion. Tidal volume and airway compliance were calculated at 30 minutes. RESULTS Tidal volume was 33.67 +/- 0.57, 15.75 +/- 5.72, and 29.83 +/- 1.07 mL in the immediate control, 24-hour control, and surfactant groups, respectively (p = 0.004, surfactant versus 24-hour control). Airway compliance was 1.94 +/- 0.27, 0.70 +/- 0.09, and 1.46 +/- 0.10 mL/mm Hg in the immediate control, 24-hour control, and surfactant groups, respectively (p = 0.002, surfactant versus 24-hour control). CONCLUSIONS We conclude that surfactant administration before reperfusion after 24 hours of cold storage preserves tidal volume and airway compliance in the isolated ventilated/perfused rabbit model of lung reperfusion injury.

Both blood and crystalloid-based extracellular solutions are superior to intracellular solutions for lung preservation☆☆☆★★★♢♢♢

OBJECTIVE Lung transplantation remains limited by donor organ ischemic time, inadequate graft preservation, and reperfusion injury. We evaluated lung preservation with use of an extracellular solution, with or without the addition of blood, as compared with preservation with the intracellular Euro-Collins solution. METHODS With use of an isolated, whole blood perfused/ventilated rabbit lung model, we studied three groups of animals. Lungs were flushed with Euro-Collins, low-potassium dextran, or 20% blood-low-potassium dextran solution. Lungs were harvested en bloc, stored inflated at 4 degrees C for 18 hours, and then reperfused at 60 ml/min with whole blood. Continuous measurements of pulmonary artery pressure, pulmonary vascular resistance, and dynamic airway compliance were obtained. Fresh, nonrecirculated venous blood was used to determine the single-pass pulmonary venous-arterial oxygen gradient. RESULTS Lungs preserved with Euro-Collins solution demonstrated elevated pulmonary artery pressure and pulmonary vascular resistance when compared with those preserved with low-potassium dextran and 20% blood-low-potassium dextran solutions (pulmonary artery pressure: 40.8 +/- 2.2 mm Hg vs 28.9 +/- 2.4 mm Hg and 28.3 +/- 1.5 mm Hg, respectively, p < 0.001; pulmonary vascular resistance: 46.0 +/- 3.1 x 10(3) dynes x sec x cm(-5) vs 29.0 +/- 4.2 x 10(3) dynes x sec x cm(-5) and 28.8 +/- 2.3 x 10(3) dynes x sec x cm(-5), respectively, p < 0.001). Euro-Collins solution-preserved lungs demonstrated a significant drop in compliance when compared with those preserved with low-potassium dextran and 20% blood-low-potassium dextran (-21.9% +/- 4.7% vs 1.8% +/- 3.3% and 1.4% +/- 6.2%, respectively; p = 0.002). Oxygenation was improved with low-potassium dextran and 20% blood-low-potassium dextran solutions as compared with that with Euro-Collins solution (296.3 +/- 54.6 mm Hg and 290.2 +/- 66.4 mm Hg, respectively, vs 37.2 +/- 4.6 mm Hg; p = 0.001). CONCLUSIONS Extracellular solutions provided superior preservation of pulmonary function in this rabbit lung model of ischemia-reperfusion. However, the addition of blood does not confer any demonstrable advantage over low-potassium dextran solution alone with use of an 18-hour period of cold ischemia.

Thromboxane receptor blockade improves oxygenation in an experimental model of acute lung injury

BACKGROUND Adult respiratory distress syndrome remains a major cause of morbidity and mortality. We investigated the role of thromboxane receptor antagonism in an experimental model of acute lung injury that mimics adult respiratory distress syndrome. METHODS Three groups of rabbit heart-lung preparations were studied for 30 minutes in an ex vivo blood perfusion/ventilation system. Saline control (SC) lungs received saline solution during the first 20 minutes of study. Injury control (IC) lungs received an oleic acid-ethanol solution during the first 20 minutes. Thromboxane receptor blockade (TRB) lungs received the same injury as IC lungs, but a thromboxane receptor antagonist (SQ30741) was added to the blood perfusate just prior to study. Blood gases were obtained at 10-minute intervals, and tidal volume, pulmonary artery pressure, and lung weight were continuously recorded. Oxygenation was assessed by measuring the percent change in oxygen tension over the 30-minute study period. Tissue samples were collected from all lungs for histologic evaluation. RESULTS Significant differences were found between SC and IC lungs as well as TRB and IC lungs when comparing pulmonary artery pressure (SC = 33.1 +/- 2.2 mm Hg, TRB = 35.4 +/- 2.1 mm Hg, IC = 60.4 +/- 11.1 mm Hg; p < 0.02) and percent change in oxygenation (SC = -20.6% +/- 10.3%, TRB = -24.2% +/- 9.5%, IC = -57.1% +/- 6.2%; p < 0.03). None of the other variables demonstrated significant differences. CONCLUSIONS Thromboxane receptor blockade prevents the pulmonary hypertension and the decline in oxygenation seen in an experimental model of acute lung injury that mimics adult respiratory distress syndrome.