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Ann Thorac Surg 2004;77:1309-1314
© 2004 The Society of Thoracic Surgeons

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Original article: cardiovascular

Management strategies for type A dissection complicated by peripheral vascular malperfusion

^a Department of Cardiothoracic Surgery, Weill Medical College of Cornell University, New York, New York, USA

Accepted for publication September 11, 2003.

^* Address reprint requests to Dr Girardi, Department of Cardiothoracic Surgery, 525 East 68^th St, M-424, New York, NY 10021, USA
e-mail: lngirard{at}mail.med.cornell.edu

	Abstract

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BACKGROUND: End-organ malperfusion is a dreaded complication of type A aortic dissections. Different strategies have been proposed to manage this complex cohort of patients. Ideal management includes the rapid restoration of organ perfusion while avoiding catastrophic rupture and tamponade. We present our experience with primary aortic repair as the optimal method of patient management.

METHODS: From July 1997 until April 2003, 101 patients underwent dissection repair and were assessed for malperfusion of the central nervous system, renal, visceral or extremity circulation. Patients with coronary artery malperfusion were analyzed separately. Aortic repair was performed expeditiously utilizing femoral bypass, circulatory arrest, and antegrade perfusion after completion of the distal anastomosis. Persistent malperfusion led to additional procedures. In-hospital morbidity, end-organ salvage, and mortality were determined. Chi-square analysis defined variables contributing significantly to outcome.

RESULTS: Twenty-three patients presented with malperfusion. The operative mortality for the entire cohort with malperfusion, 4.4% (n = 1), was not greater than those without it, 5.1% (n = 4). Five patients required additional procedures following aortic repair, a majority in patients with persistent extremity ischemia. All deficits resolved except for one patient with spinal ischemia and one with visceral ischemia. Visceral malperfusion was highly lethal with a mortality of 33% (n = 1). All other patients presenting with malperfusion survived to discharge.

CONCLUSIONS: Patients with malperfusion in the setting of acute type A dissection should undergo immediate aortic reconstruction as the primary means of reestablishing end-organ perfusion. Early postoperative intervention for persistent deficits leads to a gratifyingly high rate of end-organ salvage.

	Introduction

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Acute aortic dissection remains the most common lethal condition of the aorta, occurring nearly twice as often as a ruptured abdominal aortic aneurysm [1–3]. Greater than 60% of all aortic dissections are Stanford type A dissections [4]. The lethal nature of this catastrophic event is obvious with greater than 50% of patients dying in the first 48 hours following presentation, a majority from rupture into the pericardium, mediastinum, or pleural space [5]. Patients surviving the initial event may develop aortic branch vessel occlusion due to bulging of the false lumen into the ostium or extension of the dissection into the branch vessel proper [6]. End-organ malperfusion and ischemia resulting from this process occur in 16% to 30% of all cases of type A dissection and can dramatically reduce the chance of a successful outcome, particularly when the mesenteric circulation is compromised [7–10].

The surgical mortality for patients undergoing repair of acute type A aortic dissection has improved dramatically over the last decade [11, 12]. However a significant percentage of perioperative deaths continue to occur as complications of end-organ malperfusion [8, 11]. In one series, primary aortic dissection repair in the setting of malperfusion was associated with an 89% perioperative mortality [9]. This extraordinary increase in risk has generated interest in alternative methods to restore end-organ perfusion before primary aortic repair. Local vascular reconstruction, abdominal aortic fenestration, and interventional techniques such as angioplasty and stenting, have all been espoused as definitive means of restoring end-organ perfusion before dissection repair. This strategy has met with varying degrees of success [6, 10, 13, 14]. Others advocate peripheral intervention followed by delayed primary aortic repair after the malperfusion and reperfusion syndromes have been resolved [9]. These techniques, however, can dramatically prolong the interval between patient presentation and aortic repair. A percentage of the patients in this setting have gone on to die of rupture, myocardial infarction, or stroke while awaiting aortic reconstruction.

To avoid the added mortality associated with these delays, we established a practice of immediate central aortic repair with subsequent peripheral intervention for any malperfusion that remains following the reestablishment of flow to the true lumen. We sought to compare outcomes using this technique with the results from a previous era [8] to establish an algorithm for patients who present in this high-risk clinical setting.

	Material and methods

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From July 1997 until April 2003, 101 consecutive patients were admitted to our hospital with acute type A aortic dissection. Patients presenting greater than 72 hours from the onset of their symptoms were considered subacute dissections and were not included in this analysis. Similarly, patients with chronic type A aortic dissections were excluded. Patients ranged in age from 20 to 91 years of age with a median age of 66 years old. There were 69 men and 20 women. Evidence of a connective tissue disorder was found in 17 patients, none of who developed a malperfusion syndrome (p < 0.01). The incidence of comorbidities for those patients with and without malperfusion is listed in Table 1.

Renal malperfusion was defined by an elevation of creatinine twice above baseline in the setting of oliguria or anuria, or a rising creatinine after admission. Patients with poor or absent renal enhancement on contrast CT evaluation were also included. Mesenteric malperfusion was diagnosed when a patient presented with abdominal pain, tenderness, or melena in the setting of metabolic acidosis. Peripheral malperfusion was diagnosed by the absence of pulses or lack of flow into the extremity by Doppler examination. Patients with coronary artery malperfusion had evidence of ongoing ischemia on their admission electrocardiogram. Coronary artery involvement was confirmed with intraoperative inspection of the main coronary arteries.

In patients having contrast CT scans, the vessel responsible for the malperfusion syndrome could usually be identified. Patients were not taken for angiography to further delineate the affected circulation. Preoperative interventional-based methods for reestablishing flow into organs subtended by the involved vessels were also not performed.

Pulmonary artery catheters, arterial lines, and transesophageal echocardiography were routinely used for intraoperative monitoring. Cardiopulmonary bypass was established by way of the femoral artery with bicaval venous cannulation in all cases. Axillary artery or left ventricular apical cannulation was not required. Patients were core cooled for a minimum of 30 minutes or until the bladder temperature was 18°C. Symmetric cerebral cooling was monitored with cerebral oxymetry (Somanetics Corp., Troy, MI). The ascending aorta was not cross-clamped during the period of cooling unless severe aortic insufficiency resulted in ventricular distention that could not be relieved with venting. Before the initiation of circulatory arrest 1 g of pentothal was administered. Ninety-four patients received full Hammersmith dose aprotonin. The 7 patients presenting with renal malperfusion were given amicar (30 g) as an antifibrinolytic. Activated clotting times were kept at greater than 480 seconds as measured by the Kaolin method.

The distal anastomosis was accomplished first during a period of profound hypothermic circulatory arrest (PHCA). Retrograde cerebral perfusion was delivered in all patients throughout the duration of this period as previously described [16]. Aortic arch tears were routinely resected with either a hemiarch or total arch replacement. After arch reconstruction, antegrade cardiopulmonary bypass was reestablished by directly cannulating the arch graft or by placing the aortic cannula into a sidebranch of the arch graft (Hemashield, Oakland, NJ). Repair of the aortic root, valve replacement or repair, and coronary artery bypass grafting were completed while systemic warming was performed (Table 2). Blood products were delivered as necessary to reverse the coagulopathy after protamine administration. Those patients with persistent malperfusion were then triaged for further intervention. In-hospital and 30-day mortality were recorded, as were all major postoperative complications. Data were also analyzed for patients with and without coronary malperfusion. Statistical analysis was performed using SPSS database version 10.0. Significance was determined through -square analysis with a p value of less than 0.05.

	Results

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Mean aortic cross-clamp time was 95 minutes (range: 28 to 182 minutes) and the mean time on cardiopulmonary bypass was 163 minutes (range: 98 to 288 minutes). The mean period of circulatory arrest was 26 minutes (range: 16 to 70 minutes). There was no significant difference in any of these operative times between groups.

Patients with malperfusion had a significantly higher (p < 0.02) need for reexploration for bleeding after the primary aortic procedure (5/23, 22%) when compared to those without malperfusion (4/78, 5.1%). Two of the five occurred in patients with mesenteric malperfusion who went on for abdominal explorations. However, when comparing those with malperfusion to those without it, there was no increased risk for stroke, hemodialysis dependant renal failure, respiratory failure/tracheostomy, or deep sternal wound infection (Table 3).

Table 4 outlines the interventions subsequently required to restore adequate end-organ perfusion. Three of 7 patients with extremity malperfusion required additional procedures to restore adequate blood flow to their legs. Two required femoral-femoral bypass grafting immediately following their aortic reconstruction. One of these had the need for a three-compartment fasciiotomy that subsequently was closed with a split thickness skin graft. One additional patient had a local femoral artery reconstruction to restore blood flow. All patients with extremity malperfusion recovered well without neurologic deficit. There was no need for amputation.

One patient had significant acidosis immediately following aortic repair and had a laparotomy at the completion of the case. She had complete bowel infarction and expired within 24 hours without further intervention.

The third patient cleared his acidosis and was extubated within 12 hours. However, he continued to complain of lower abdominal pain. A mesenteric angiogram was performed revealing chronic occlusion of his celiac axis, dissection of his superior mesenteric artery (SMA) out into the branch vessels, and prompt perfusion of a patent inferior mesenteric artery. His renal artery perfusion was intact. Aortic fenestration restored flow into the main SMA trunk and two stents in the proximal SMA restored flow to a majority of the vessel, including a large collateral to the common hepatic artery. Subsequent abdominal exploration revealed ischemic distal ileum and right colon requiring a right hemicolectomy with resection of the distal ileum. The remainder of the abdominal viscera were adequately perfused. A planned, second-look laparotomy 24-hours later confirmed adequate bowel perfusion and a primary anastomosis was performed. The patient made a full recovery with normal bowel function.

Table 5 summarizes the results when the 4 patients with coronary artery involvement are included in the cohort of patients with the malperfusion syndrome. Three of 4 patients presenting with this condition expired postoperatively with either right ventricular or biventricular failure. This significantly (p < 0.008) increases the mortality associated with malperfusion to 14.8% (4/27) when compared to patients with no major end-organ involvement where the mortality was 1.4% (1/74). This also significantly increases the incidence of major postoperative complications such as acute renal failure and postoperative hemorrhage requiring reexploration.

	Comment

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A majority of patients with malperfusion will have flow restored into the affected artery once the continuity of the true lumen is restored. A contemporary report summarized the results of endovascular stent-grafting in 19 patients with aortic dissections. Seventy-six percent had documented restoration of flow into the true lumen of the affected vessel once aortic continuity was reestablished [13]. An earlier report from Stanford also demonstrated that only a minority of patients with malperfusion will require additional procedures following central aortic repair. Only 8% of patients in this series required further intervention after ascending aortic replacement [8]. With this technique there was no significant difference in mortality for patients with (24%) or without (25%) malperfusion. This is quite consistent with our clinical experience where nearly 80% had complete resolution of their malperfusion syndrome with aortic repair alone.

The most expeditious means of restoring end-organ perfusion is rapid triage to the operating room. Once the diagnosis of type A dissection is confirmed, antegrade flow into the true lumen can be reestablished in less than 3 hours. This short period of warm ischemia is well tolerated and correction of any metabolic derangement is completed on cardiopulmonary bypass. The addition of aprotonin in this setting may also downregulate the inflammatory cascade and blunt the hemodynamic and coagulation abnormalities that may accompany reperfusion of ischemic organs. Minimizing the period of ischemia is particularly critical for those patients with central nervous system malperfusion where greater than 5% of patients may die of permanent neurologic deficits while awaiting correction of their metabolic values. Rapid central aortic repair also eliminates the risk of rupture and fatal tamponade that can be expected in approximately 5% of cases utilizing these alternative methods [9].

One difference between this series and those espousing delayed primary aortic repair is our exclusion of patients presenting with coronary malperfusion. Patients having type A dissection complicated by acute myocardial infarction will have a higher operative mortality. In the 1997 report by Deeb and coworkers [9], 3 of 8 patients had immediate aortic repair in the setting of acute myocardial malperfusion. All 3 patients expired of either left ventricular or biventricular failure. In addition, 1 of 3 patients with this syndrome who were managed with delayed repair also expired of postcardiotomy failure. Our experience with significant coronary malperfusion has also been dismal. Three of the deaths in our control cohort of type A dissection without malperfusion were due to prolonged myocardial ischemia that led to ventricular failure. Two had ventricular fibrillation and ongoing cardiopulmonary resuscitation on their way to the operating room, while one developed cardiogenic shock after a 3-day delay in the diagnosis of her dissection while being treated for a presumed acute right coronary occlusion. In the presence of acute infarction the diagnosis of acute dissection may be delayed until the patient is taken for cardiac catheterization. Should the patient progress to cardiogenic shock, one cannot expect a survival better than 50% regardless of any form of intervention [17].

In our experience, the inclusion of this high-risk population into an analysis of patients with peripheral vascular malperfusion increased the in-hospital mortality tenfold, and potentially obscures the excellent outcomes with immediate aortic repair. While we wish to exclude this cohort of patients from our analysis of patients with peripheral vascular malperfusion, we do continue to advocate surgical salvage for patients with coronary malperfusion. There are no alternative means to restore coronary blood flow and a low, but gratifying, rate of salvage may be achieved with aggressive attempts to reestablish the coronary circulation with aortic repair and perhaps coronary bypass grafting.

Patients presenting with mesenteric malperfusion in the setting of acute type A dissection continue to have a poor prognosis. Daily and associates [15], reported an 80% mortality for those patients with this complication who required laparotomy following repair of their aortic dissection. Lauterbach and colleagues [10] were able to substantially reduce the mortality for this subset of patients to 50%. They espouse an alternative approach utilizing interventional techniques to reestablish gut perfusion before proceeding with aortic repair [10]. Although our mortality for this group of patients is not significantly better, 33%, a majority of our patients did improve with central aortic repair as their first intervention. Mesenteric angiography should be performed if there is any clinical or laboratory evidence of persistent bowel ischemia following aortic reconstruction. Interventional fenestration, angioplasty, or stenting may improve the circulation further and should always be followed by abdominal exploration to resect any bowel that still has inadequate blood flow. Regardless of the approach, patients with aortic dissection complicated by mesenteric malperfusion will continue to have a high perioperative mortality. We will continue this aggressive surgical approach and hope that future pharmacologic support for patients with inflammatory syndromes may reduce the mortality even further.

Finally, we agree with Westaby and associates [12], that conservative aortic root and arch reconstruction will yield consistently low operative mortality for repair of acute type A dissection with or without malperfusion. Proponents of surgical delay report an 89% operative mortality for immediate surgery when dissection is complicated by malperfusion. However, 7 of 9 patients (78%) in this group had complete root reconstruction with prolonged periods of cardiopulmonary bypass (CPB; mean 243 minutes). Only 1 patient survived. In addition, extended periods of PHCA (mean PHCA time, 40 minutes) were required for complex arch and great vessel reconstruction. A majority of the deaths were attributed to multiple organ failure and the adult respiratory distress syndrome. Myocardial injury and ventricular failure were also responsible for significant operative mortality.

We agree with the authors of this report that prolonged periods of CPB and large volume blood product resuscitation will contribute to a severe capillary leak and end-organ damage. However, we disagree that these patients were the victims of an inflammatory process primarily attributed to the malperfusion syndrome. Utilizing a more conservative approach, we avoided complex root reconstruction in all but 17% of our patients, reserving this technique for those patients with total root destruction or an obvious connective tissue disorder. Similarly, only 1 patient required total arch replacement. We believe the improved results with immediate aortic repair are reflective of shorter periods of CPB (mean 163 minutes) and PHCA (mean 26 minutes) afforded when conservative aortic repair is utilized. Antegrade end-organ perfusion is reestablished more rapidly and the organ system in jeopardy can be assessed and, if necessary, treated in a more timely fashion. A majority of patients with acute type A dissection and malperfusion will improve with these methods and the 15% mortality associated with surgical delay can be avoided.

	References

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This Article Abstract Full Text (PDF) Online Discussion 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): Leonard N. Girardi Karl H. Krieger Leonard Y. Lee Charles A. Mack Anthony J. Tortolani O. Wayne Isom Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Girardi, L. N. Articles by Isom, O. W. Search for Related Content PubMed PubMed Citation Articles by Girardi, L. N. Articles by Isom, O. W. Related Collections Great vessels