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Ann Thorac Surg 2002;74:2034-2039
© 2002 The Society of Thoracic Surgeons


Original article: cardiovascular

Perioperative risk factors for mortality in patients with acute type a aortic dissection

Anil Z. Apaydin, MDa*, Suat Buket, MDa, Hakan Posacioglu, MDa, Fatih Islamoglu, MDa, Tanzer Calkavur, MDa, Tahir Yagdi, MDa, Mustafa Ozbaran, MDa, Munevver Yuksel, MDa

a Cardiovascular Surgery, Ege University Medical School, Izmir, Turkey

Accepted for publication July 22, 2002.

* Address reprint requests to Dr Apaydin, Department of Cardiovascular Surgery, Ege University Medical School, Bornova-Izmir, 35100 Turkey
e-mail: apaydina{at}efes.net.tr


    Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
BACKGROUND: This study was undertaken to identify the perioperative risk factors for death in patients with acute type A aortic dissection (AADA).

METHODS: Between 1993 and 2001, 108 consecutive patients (86 men; mean age, 53 years) underwent emergent operations for AADA. All patients but 2 underwent replacement of the ascending aorta with an open distal anastomosis during a period of hypothermic circulatory arrest. In addition, 22 patients had hemiarch and 5 had total arch replacement. Aortic root was replaced in 20 and repaired with gelatin-resorcinol-formaldehyde glue in 39 patients; aortic valve was separately replaced in 3, resuspended in 24, and remained untouched in 22 patients.

RESULTS: Overall in-hospital mortality was 25%. Mortality rate was significantly higher in patients with preoperative dissection complications than in those without (21/36 [58%] vs 6/72 [8%], p < 0.001). In multivariate analysis, predictors of mortality were presence of rupture, renal failure, and intestinal malperfusion, duration of cardiopulmonary bypass >=200 minutes, blood loss >=500 mL, and transfusion of blood >=4 units. Location of the intimal tear, extent of the replacement, type of the aortic root repair, and duration of hypothermic circulatory arrest did not emerge as predictors of mortality.

CONCLUSIONS: Major determinants of surgical mortality in patients with AADA are preoperative complications. Earlier diagnosis remains essential to improve the survival rate.


    Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Acute type A aortic dissection (AADA) is a catastrophic event that requires prompt surgical intervention. Despite the latest advances in diagnostic imaging, intraoperative techniques, and postoperative care, the surgical mortality rates in recent reports range between 15% and 26% [16]. Preoperative condition of the patient, surgical techniques and strategies, and perioperative complications may have a role on the mortality rates. This study was undertaken to identify the perioperative risk factors for death in a relatively large group of consecutive patients with AADA.


    Patients and methods
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Patients
Between 1993 and 2001, 108 consecutive patients (86 men; mean age, 53 years) underwent emergent operations for AADA. Patient information in our database was retrospectively reviewed. Postoperative follow-up was obtained by telephone communication or regular visits at our cardiology department. All patients were operated upon on an emergent basis after establishing the diagnosis of AADA. The onset of symptoms was hours to several days before admission.

Surgical technique
After median sternotomy and administration of systemic heparin, femoral artery and right atrium (or in patients with a bulging pericardium or a documented cardiac tamponade, the femoral vein) were initially cannulated. After the institution of cardiopulmonary bypass, patients were cooled to a rectal temperature of 15°C. Two cooling strategies were used upon surgeons’ preference. In one group, the ascending aorta was clamped and the proximal repair was accomplished during cooling. In the other group, the ascending aorta was not clamped initially and the distal repair was performed under hypothermic circulatory arrest (HCA). The proximal repair was performed during warming. To identify if these two different cooling strategies had any impact on the outcome, variables such as "placing the aortic cross-clamp first" and "duration of cooling" were also entered as factors in the analysis. Antegrade and retrograde cold blood cardioplegia was used for myocardial protection. The right superior pulmonary vein was used for venting. Indicators of adequate suppression of cerebral metabolism were electroencephalogram (EEG) silence in all, and obtaining jugular bulb venous oxygen saturation of higher than 95% in addition to EEG silence in patients operated upon in the last 18 months. All patients received 30 mg/kg of intravenous metylprednisolone 10 minutes before HCA as an adjunctive medication for brain protection. Aortic arch and proximal descending aorta were explored to identify the site of the intimal tear. All patients but 2 underwent replacement of the ascending aorta with an open distal anastomosis during a period of HCA. In these 2 patients, the dissection was limited to the ascending aorta only, which was replaced or repaired under cross-clamp after the exploration of the aortic arch during a brief period of HCA. Retrograde cerebral perfusion was used in 81 patients. Continuous perfusion of cold blood through the venous line at a rate of 600 to 800 mL/minute to achieve a central vein pressure of 20 mm Hg was administered.

The site of the tear was resected whenever possible. The location of the intimal tear was in the ascending aorta in 78%, in the arch in 16%, and in the descending aorta in 3% of patients. Three patients had no visible tears. In patients with reentry tear, the arterial cannula was inserted to the ascending aortic graft for antegrade flow. The mean duration of HCA, cardiac ischemia, and cardiopulmonary bypass was 34 ± 11, 101 ± 31, and 189 ± 46 minutes, respectively.

Procedures
Eighty patients had ascending aortic replacement only, and 1 patient underwent primary repair without any replacement. Twenty-two patients underwent hemiarch, and 5 underwent total arch replacement in addition to ascending aortic replacement. Either gelatin-precoated or collagen-impregnated Dacron graft material was used in all replacements. All aortic anastomoses were constructed with continuous 3-0 polypropylene suture, buttressed with a strip of Teflon felt. Aortic root was replaced in 20 and repaired with gelatin-resorcinol-formaldehyde (GRF) glue in 39 patients; aortic valve was separately replaced in 3, resuspended in 24, and remained untouched in 22 patients. Button-Bentall modification and composite grafts containing bileaflet mechanical valves were used in all root replacements. Patients undergoing root repair with GRF glue also had resuspension of the aortic valve commissures with pledgetted sutures.

Explanations about variables
Shock
This included cardiogenic shock associated with hypotension and severe metabolic acidosis, which develops secondary to severe aortic valve insufficiency, cardiac tamponade, or coronary malperfusion. Coronary malperfusion occurred in 4 patients. Therefore, it was not included in the analysis as a separate variable.

Acute renal failure
This is defined as low or no urine output associated with high or rising creatinine level. These patients required dialysis during the postoperative period.

Intestinal ischemia
This is defined as abdominal pain or distention with or without diarrhea causing signs of acute abdomen and severe metabolic acidosis. Six of the 8 patients underwent exploratory laparotomy, 1 before the aortic operation, which revealed dead or near-dead bowel. After the ascending aortic replacement, 1 patient underwent bowel resection and 1 had abdominal fenestration. In the remaining 2 patients who did not undergo laparotomy, findings of the abdominal CT were suggestive of an intestinal event in addition to physical signs and symptoms. None of these patients had preoperative mesenteric angiogram.

Limb ischemia
This is defined as new-onset loss of pulse associated with pain and neurological findings.

Rupture
This is defined as frank rupture of the aorta causing exsanguination when the pericardium was opened. Patients with rupture were in cardiac tamponade preoperatively. In 4 patients, rupture occurred in the intensive care unit (ICU) or on the operating table during preparation for operation. In these patients, operation was started while cardiopulmonary resuscitation was in progress.

Cardiac tamponade
This is defined as free blood in the pericardium causing tamponade physiology as documented by either preoperative echocardiography or intraoperative observation of a bulging pericardium with high cardiac filling pressures. Two of the patients with tamponade had undergone subxyphoidal drainage before being transported to our clinic.

New neurological symptoms
New-onset neurological symptoms that were present in our patients, such as confusion, dysorientation, dysartria, hemiplegia, and paraplegia other than the syncope, were evaluated under this category.

In-hospital mortality
This is defined as deaths occurring within 30 days after the operation or during initial hospitalization.

Criteria for blood transfusions
These were a hematocrit of less than 30% in a hemodynamically unstable patient requiring volume replacement or in a bleeding patient with a chest tube drainage of >=100 mL/hour. Autotransfusion system for reinfusion of the mediastinal shed blood was not used in any of the patients in the ICU.

Criteria for giving ffp
These were suspected coagulopathy after the administration of protamine despite adequate levels of ACT, elevated prothrombin time in the ICU, or transfusion of >=3 units blood in the operating room or in the ICU (for possible dilution of factors).

Surgeons
There were 7 surgeons and 2 attending surgeons in every operation, who assisted each other in different permutations. Some surgeons did more cases than the others; however, we did not see any variation in mortality among surgeons.

Statistical analysis
Statistical analyses were performed using the SPSS/PC+ (version 10.0) computer program (SSPS Inc, Chicago, IL). A p < 0.05 was considered significant. Frequency and percent values of categoric variables, and mean, average, and standard deviation values of continuous variables were determined. Patient characteristics and hospital outcomes were compared univariately by using t tests for continuous variables and {chi}2 or Fisher’s exact test for categoric variables. Patients were separated as having a particular variable or not. Therefore, patients with combined symptoms (eg, shock and intestinal malperfusion) have appeared in the analysis of both variables. Risk factors affecting mortality were analyzed by univariate analysis, which was followed by multivariate stepwise logistic regression analyses. Preoperative (dissection-related, patient-related), intraoperative, and postoperative factors were separately entered in the univariate analysis. The factors that reached significance were entered into the multivariate analysis. Postoperative survival was evaluated by Kaplan-Meier analysis.


    Results
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Eight patients died during surgery, and an additional 19 died within 30 days. In-hospital mortality was 25%. The causes of intraoperative deaths were cardiac failure in 3, uncontrollable bleeding in 3, and severe acidosis and coagulopathy due to intestinal necrosis in 2 patients. The causes of postoperative deaths were multiorgan failure in 11 (4 with severe visceral malperfusion and 1 with preoperative cirrhosis), cardiac failure in 3, renal failure in 2, stroke in 2, and rupture of the aortic arch in 1 patient. Hospital mortality rate was significantly higher in patients with preoperative dissection complications than in those without (21/36 [58%] vs 6/72 [8%], p < 0.001).

Univariate analysis revealed a number of preoperative, intraoperative, and postoperative factors that were associated with hospital death. The preoperative risk factors were shock, rupture, cardiac tamponade, acute renal failure, and intestinal ischemia (Tables 1, 2). Among the intraoperative factors, blood loss >=500 mL, transfusion of FFP >=3 units, and transfusion of blood >=4 units emerged as predictors of mortality (Table 3). Factors such as the location of the intimal tear, type of aortic root repair, extent of aortic replacement and duration of HCA did not emerge as predictors of mortality. Postoperative factors that were associated with death were renal failure, reoperation for bleeding, infection, cardiac failure, and gastrointestinal complications (bleeding or ischemia).


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Table 1. Univariate Analysis of Preoperative Dissection-Related Risk Factors for In-Hospital Mortality

 

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Table 2. Univariate Analysis of Preoperative Patient-Related Risk Factors for In-Hospital Mortality

 

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Table 3. Univariate Analysis of Intraoperative Risk Factors for In-Hospital Mortality

 
Multivariate analysis revealed that statistically significant independent preoperative predictors of hospital mortality were acute renal failure, intestinal ischemia, and rupture (Table 4). Among the operative variables, duration of CPB >=200 minutes, blood loss >=500 mL, and transfusion of blood >=4 units emerged as the predictors of adverse outcome (Table 5). Postoperative complications were not included in the multivariate analysis. Among the operative survivors, the incidence of stroke and temporary neurological dysfunction was 7.5% and 12%, respectively. The independent risk factor for stroke was the presence of new preoperative neurological symptoms (p < 0.001).


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Table 4. Multivariate Analysis of Preoperative Factors Responsible for Deaths

 

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Table 5. Multivariate Analysis of Intraoperative Factors Responsible for Deaths

 
Survival
The actuarial survival rates (including hospital deaths) were 68% at 3 years and 56% at 6 years (Fig 1).



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Fig 1. Actuarial (Kaplan-Meier) survival rate (including hospital mortality) of patients. The number of survivors is shown on the curve.

 

    Comment
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
There is a consensus that patients with AADA should undergo urgent surgical treatment, because the mortality rate is very high in those who were managed with medical treatment [7, 8]. However, the reported surgical mortality rate of AADA remains high, which is about 25%, even in the most recent studies [1, 5, 6]. The overall in-hospital mortality and mid-term survival rates in our study are comparable with those series [1, 2, 5, 6].

We found six variables to be statistically significant risk factors for death in our patient population. Among these, three operative variables (long cardiopulmonary bypass duration, excessive blood loss, and transfusion) were typically present in patients who had developed cardiac failure or coagulopathy. Three preoperative dissection-related variables (acute renal failure, intestinal ischemia, and rupture) had a major impact on the mortality. This reflected as a high mortality rate in the cohort of patients who presented with any of the preoperative dissection complications (shock, cardiac tamponade, malperfusion, and rupture, but not aortic valve insufficiency). Six of the eight intraoperative deaths also presented with dissection complications. Therefore, we would like to discuss the impact of preoperative dissection complications on the outcome.

Several reports analyzing the effects of preoperative factors on the survival of patients with AADA have appeared in the literature [1, 4, 911]. Renal or visceral ischemia was reported to be an independent determinant of higher operative mortality [11]. A scoring system based on the preoperative variables has also been proposed for risk stratification in AADA [5]. Rupture and visceral malperfusion were the most common causes of hospital deaths in both acute type A and B dissections in the International Registry of Acute Aotic Dissection analysis [6]. Mortality in our patients with renal failure or intestinal malperfusion was very high, which is similar to the experience of others [12, 13]. These patients typically had severe acidosis and coagulopathy, and died of bleeding or multiple organ failure. Probably, they were the ones who had irreversible end-organ damage, making surgical interventions such as bowel resection or abdominal fenestration futile.

It seems that the detection and appropriate management of some of the dissection complications may decrease the mortality in AADA. However, this is not easy in practice. For example, by the time the clinical diagnosis of visceral malperfusion can be made with confidence, irreversible intestinal ischemia has often already occurred, as in most of our patients.

Management of these complications is another challenge. Rupture obviously requires an emergent aortic repair. Cardiac tamponade causing hemodynamic compromise also requires a prompt surgical intervention. Tan and associates reported that the preoperative drainage of pericardial tamponade by punction decreased the mortality rate significantly, and recommended this maneuver to gain time until the aortic repair [5].

There is no consensus regarding the timing of the management of renal or intestinal malperfusion. Retrospective analyses of small groups of patients with AADA and severe malperfusion treated with percutaneous fenestration or stenting before [15] or after [16] the definitive surgery have been reported. Deeb and associates advocated the percutaneous and medical treatment of malperfusion with delayed surgical repair of the ascending aorta [15]. However, the risk of rupture is a concern in patients undergoing delayed definitive operation. There are few reports regarding the natural course of patients undergoing delayed operation in the current era [15, 16]. Scholl and associates reported in a relatively small cohort with a possible selection bias that patients with AADA who underwent delayed surgery or medical treatment had acceptable early and short-term outcome, which was better than previously expected [16]. Because the outcome of our patients with severe visceral malperfusion has been dismal in spite of an intact ascending aortic repair, we believe that this group of patients should be an exception to the policy of replacing the ascending aorta emergently in all patients with AADA. We also believe that the risk of mortality from severe visceral malperfusion outweighs the risk of rupture. More data by means of prospective studies are required to define the management strategies based on objective data in patients who presented with severe visceral malperfusion.

It was encouraging to see in the analysis that the location of the intimal tear, extent of the replacement, and type of aortic root repair did not have any impact on the mortality rate. We attempted to limit the extent of aortic resection under these emergency conditions, but intraoperative circumstances, such as a dilated aortic root or transverse arch tear, mandated the replacement of the aortic root or the aortic arch. With current methods of cerebral and myocardial protection, we believe that it is safe to resect the intimal tear or perform adjunctive procedures when clinically indicated. We clamped the ascending aorta routinely, not only in case of a rupture, in a group of patients and did the proximal repair first. Clamping the ascending aorta during cooling, which was advocated to increase the mortality [3], did not emerge as a predictor of hospital mortality. Temporary neurological dysfunction, which was described by Ergin and associates [17] as a reflection of inadequate cerebral protection and subtle brain injury, occurred in patients who had HCA times longer than 30 minutes in this series. The duration of HCA was a risk factor for temporary neurological dysfunction (p < 0.0028), but not for hospital deaths or stroke. The presence of new preoperative neurological symptom was an independent predictor of postoperative stroke.

This study has several limitations. It is a retrospective analysis of a single institution. There are no angiographic imaging data for patients with malperfusion, and percutaneous stenting and fenestration techniques were not used. However, this is an unselected series of patients with AADA treated with immediate aortic repair by using widely accepted techniques.

In conclusion, major determinants of surgical mortality in patients with AADA are preoperative complications. Earlier diagnosis remains essential to improve the survival rate.[14]


    References
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 

  1. Fann J.I., Smith J.A., Miller D.C., et al. Surgical management of aortic dissection during a 30-year period. Circulation 1995;92(Suppl II):113-122.[Abstract/Free Full Text]
  2. Bachet J., Goudot B., Dreyfus G.D., et al. Surgery for acute type A aortic dissection: the Hopital Foch experience (1977–1998). Ann Thorac Surg 1999;67:2006-2009.[Abstract/Free Full Text]
  3. David T.E., Armstrong S., Ivanov J., Barnard S. Surgery for acute type A dissection. Ann Thorac Surg 1999;67:1999-2001.[Abstract/Free Full Text]
  4. Ehrlich M.P., Ergin M.A., McCullough J.N., et al. Results of immediate surgical treatment of all acute type A dissections. Circulation 2000;102(suppl III):248-252.
  5. Tan M.E., Kelder J.C., Morshuis W.J., Schepens M.A. Risk stratification in acute type A dissection: proposition for a new scoring system. Ann Thorac Surg 2001;72:2065-2069.[Abstract/Free Full Text]
  6. Hagan P.G., Nienaber C.A., Isselbacher E.M., et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000;283:897-903.[Abstract/Free Full Text]
  7. Anagnostopoulos C.E., Prabhakar M.J.J., Kittle C.F. Aortic dissections and dissecting aneurysms. Am J Cardiol 1972;30:263-273.[Medline]
  8. Debakey M.E., McCollum C.H., Crawford E.S., et al. Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery 1982;92:1118-1134.[Medline]
  9. Mehta R.H., Suzuki T., Hagan P.G., et al. Predicting death in patients with acute type A aortic dissection. Circulation 2002;105:200-206.[Abstract/Free Full Text]
  10. Bayegan K., Domanovits H., Schillinger M., Ehrlich M., Sodeck G., Laggner A.N. Acute type A aortic dissection: the prognostic impact of preoperative cardiac tamponade. Eur J Cardiothorac Surg 2001;20:1194-1198.[Abstract/Free Full Text]
  11. Miller D.C., Mitchell R.S., Oyer P.E., Stinson E.B., Jamieson S.W., Shumway N.E. Independent determinants of operative mortality for patients with aortic dissections. Circulation 1984;70(3 Pt 2):1153-1164.
  12. Fann J.I., Sarris G.E., Mitchell R.S., et al. Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg 1990;212:705-713.[Medline]
  13. Borst H.G., Laas J., Heinemann M. Type A aortic dissection: diagnosis and management of malperfusion. Sem Thorac Cardiovasc Surg 1991;3:238-241.[Medline]
  14. Deeb G.M., Williams D.M., Bolling S.F., et al. Surgical delay for acute type A dissection with malperfusion. Ann Thorac Surg 1997;64:1669-1677.[Abstract/Free Full Text]
  15. Slonim S.M., Miller D.C., Mitchell R.S., Semba C.P., Razavi M.K., Dake M.D. Percutaneous balloon fenestration and stenting for life-threatening ischemic complications in patients with acute aortic dissection. J Thorac Cardiovasc Surg 1999;117:1118-1127.[Abstract/Free Full Text]
  16. Scholl F.G., Coady M.A., Davies R., et al. Interval or permanent nonoperative management of acute type A aortic dissection. Arch Surg 1999;134:402-406.[Abstract/Free Full Text]
  17. Ergin M.A., Uysal S., Reich D.L., et al. Temporary neurological dysfunction after deep hypothermic circulatory arrest: a clinical marker of long-term functional deficit. Ann Thorac Surg 1999;67:1887-1890.[Abstract/Free Full Text]



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