Abdominal compartment syndrome associated with endovascular and open repair of ruptured abdominal aortic aneurysms Chen Rubenstein, MD,a Gabriel Bietz, MBChB,b Daniel L. Davenport, PhD,c Michael Winkler, MD,c and Eric D. Endean, MD,d Jerusalem, Israel; San Antonio, Tex; and Lexington, Ky Background: Abdominal compartment syndrome (ACS) is a known complication of ruptured abdominal aortic aneurysm (rAAA) repair and can occur with either endovascular (EVAR) or open repair. We hypothesize that the underlying mechanism for the development of ACS may differ for patients treated with EVAR or open operation. Methods: All patients who presented with rAAA at a tertiary care medical center between January 2005 and December 2010 were included in the study. Demographic factors, type of repair (open vs EVAR), development of ACS, intraoperative and postoperative fluid requirements, estimated blood loss, length of stay, and morbidity and mortality were recorded. Student t-test and Fisher exact test were performed. A P value < .05 was considered significant. Results: Seventy-three patients, 62 men and 11 women with an average age of 70.5 years, were treated for rAAA. Fortyfour (60%) underwent open repair; 29 (40%) had EVAR. Overall mortality was 42% (31 of 73), with mortality being 31% (9 of 29) in EVAR and 48% (21 of 44) in open repair. ACS developed in 21 patients (29%), more frequently in open repair than in EVAR (15 of 44 [34%] vs 6 of 29 [21%]; P [ NS). Mortality was higher in patients who developed ACS compared with those without ACS (13 of 21 [62%] vs 17 of 52 [33%]; P [ .022). This finding was especially pronounced in the EVAR group, in which mortality in patients with ACS was 83% (5 of 6) compared with 17% (4 of 23) without ACS (P [ .005). Intraoperative fluid requirements were significantly higher in EVAR patients who developed ACS compared with those without ACS, including packed red blood cells (5600 mL vs 1100 mL; P < .0001), total blood products (9300 mL vs 1500 mL; P < .001), crystalloid (11,200 mL vs 4500 mL; P < .001), and estimated blood loss (5000 mL vs 660 mL; P [ .006). In patients treated with open repair, there were no significant differences in intraoperative fluid requirements between those who developed ACS and those without ACS. However, patients who developed ACS after open repair required significantly more crystalloid on the first and second postoperative days (first postoperative day, 8300 mL vs 5600 mL [P [ .01]; second postoperative day, 6500 mL vs 3800 mL [P [ .004]). Conclusions: This study demonstrates that the development of ACS after repair of rAAA is associated with increased mortality, especially in EVAR-treated patients. The higher intraoperative blood and blood product requirements associated with ACS in EVAR patients suggest that one potential cause of early ACS is continued hemorrhage from lumbar and inferior mesenteric vessels through the ruptured aneurysm sac. Hence, open ligation of such vessels should be considered in patients developing early ACS after EVAR for rAAA. (J Vasc Surg 2014;-:1-7.)
Abdominal compartment syndrome (ACS) develops as a result of increased intra-abdominal pressure and is often related to massive fluid resuscitation associated with either hemorrhage or splanchnic reperfusion. Increased intraabdominal pressure has deleterious effects on multiple organ systems. As intra-abdominal pressure rises, the inferior vena cava is compressed, resulting in a decrease in venous return that in turn leads to reduction in ventricular enddiastolic volume, stroke volume, and cardiac output and elevation of systemic vascular resistance. Elevated intraFrom the Department of Vascular Surgery, Hadassah Hebrew University, Jerusalema; Peripheral Vascular Associates, San Antoniob; and the Department of Radiologyc and Department of Surgery,d University of Kentucky College of Medicine, Lexington. Author conflict of interest: none. Reprint requests: Eric D. Endean, MD, Department of Surgery, C-215, 800 Rose St, Lexington, KY 40536 (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest. 0741-5214 Copyright Ó 2014 by the Society for Vascular Surgery. http://dx.doi.org/10.1016/j.jvs.2014.10.011
abdominal pressure also compresses the kidneys, and this along with the adverse effects on cardiac function causes a reduction in renal flow and a decrease in urine output. Simultaneously, increased intra-abdominal pressure compresses the diaphragm, raising intrathoracic pressure with an increase in airway pressures, pulmonary artery pressure, and central venous pressure and a decrease in pulmonary compliance. If ACS is left untreated, multiorgan failure develops. Treatment is directed at relieving the intraabdominal pressure, often requiring a decompressive laparotomy. Failure to relieve the pressure is almost uniformly fatal; surgical decompression demonstrates significant improvement in mortality.1 Patients with ruptured abdominal aortic aneurysm (rAAA) present with hemorrhagic shock. The hematoma that forms in the retroperitoneum is a space-occupying lesion that itself can contribute to a rise in intra-abdominal pressure. In the perioperative period, these patients have large fluid requirements from ongoing bleeding, coagulopathy, and third-space requirements that necessitate resuscitation with blood, blood products, and fluids. This resuscitation can lead to bowel edema and ascites that 1
2 Rubenstein et al
further increase intra-abdominal pressure and development of ACS. Indeed, the development of ACS has been documented after both open and endovascular repair of rAAA.2-7 We hypothesize that the underlying mechanisms for the development of ACS after repair of rAAA may be different for patients treated with an endovascular aneurysm repair (EVAR) technique compared with those with an open repair. METHODS A retrospective review of all patients treated for rAAA between January 2005 and December 2010 at the University of Kentucky Chandler Medical Center was conducted. The study was approved by the University of Kentucky Institutional Review Board (IRB approval No. 10-0011P1H). Patient consent was not needed. Patients were excluded if the aneurysm was an aortic dissection or if the aneurysm was symptomatic but not ruptured. The charts were reviewed to identify demographic information, aneurysm size, and comorbid medical conditions. Operative details, including type of repair (open vs endovascular), intraoperative fluid administration, operative time, aortic cross-clamp time (open aneurysms), and need for suprarenal clamp (open aneurysms), were recorded. Available preoperative computed tomography scans were reviewed by a vascular radiologist to identify the presence of patent lumbar and inferior mesenteric arteries arising from the aneurysm for patients treated with EVAR. Available intraoperative completion studies after endograft placement were reviewed for evidence of endoleaks. Postoperative fluid resuscitation and urine output were recorded. The diagnosis of ACS was made on the basis of a constellation of clinical findings including increased airway pressures, oliguria, and physical examination revealing a tense abdominal wall and (in some open cases) inability to close the abdomen due to bowel edema. The development of complications, including myocardial infarction, bowel ischemia, pneumonia, renal failure, need for dialysis, number of days on the ventilator, intensive care unit length of stay, total hospital length of stay, and sepsis, were recorded. Final outcome and disposition were noted. Descriptive data are presented as mean 6 standard error. Comparisons were made by the unpaired t-test. Categorical data was compared with Fisher exact test or the Mann-Whitney U test. P values of < .05 were considered to be significant. RESULTS Between January 2005 and December 2010, 73 patients, 62 men and 11 women, were treated for rAAA. The average age of patients was 70.5 years. Overall mortality for repair of rAAA was 31 of 73 (42%). ACS developed in 21 patients (29%). Twenty-nine patients (40%) had repair of rAAA with an endograft, whereas 44 (60%) underwent an open repair. Characteristics of patients undergoing EVAR or open repair were not statistically significant except that patients
JOURNAL OF VASCULAR SURGERY --- 2014
undergoing EVAR were older and more patients in the EVAR group had a history of cancer (Table I). Significantly more patients undergoing open repair required dialysis (P ¼ .009) than in the EVAR group. There was a trend for lower morality, length of stay, and intensive care unit length of stay in the EVAR group compared with the open repair group, but statistical significance was not reached. ACS developed in 21 patients, including 6 of 29 patients (21%) who had an EVAR and 15 of 44 patients (34%) who had an open repair. No differences were identified in patient characteristics whether or not they developed ACS in either the EVAR or open group (Table II). In patients who underwent open repair, there were nine deaths among the 15 patients who developed ACS (60%) compared with 13 deaths in 29 patients (45%) who did not develop ACS (P ¼ NS). However, in patients treated with EVAR, 5 of 6 patients (83%) who developed ACS died compared with four deaths among 23 patients (17%) who did not develop ACS (P ¼ .005). In patients who had an open repair, colon ischemia, multisystem organ failure, and sepsis were significantly higher in patients who developed ACS than in those without. No statistical significance was noted in these outcomes in the patients treated with EVAR. In patients who developed ACS, control of the aorta was obtained in a suprarenal position in 11, infrarenal in nine, and unknown in one. Patients who did not develop ACS had control of the aorta suprarenally in 17, infrarenally in 31, and unknown in four. In the entire study group, the location of aortic control was not significantly associated with the development of ACS. Similarly, in patients treated with an open repair, suprarenal control of the aorta was not associated with development of ACS. However, in EVAR patients, balloon control of the aorta was done in seven patients, whereas 20 did not have balloon control, and in one, it was unknown. In this subset of patients, ACS developed in six patients (five with balloon control, one unknown) and was found to be significantly associated with balloon control of the aorta (P < .001). Because fluid resuscitation can play a key role in the development of ACS, the amount and timing of fluids given patients were evaluated comparing groups who developed ACS and those who did not. In patients who developed ACS with EVAR, the amount of blood products (packed red blood cells, fresh frozen plasma, platelets, and cryoprecipitate), colloid, and crystalloid given intraoperatively was significantly higher than in those who did not develop ACS (Table III). Estimated blood loss was also significantly higher in patients who developed ACS. In comparison, in patients with an open approach, the only significant difference seen in intraoperative fluid administration between patients who developed ACS and those who did not was that significantly more fresh frozen plasma and platelets were given to patients who developed ACS. In comparing intraoperative fluid administration to patients who developed ACS between EVAR and open repair, significantly more blood products and crystalloid
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Rubenstein et al 3
Table I. Patient characteristics and outcome for the entire cohort of patients EVAR (n ¼ 29)
Open (n ¼ 44)
P value
73.7 23/29 (74) 11/29 (38) 8/29 (28) 10/29 (35) 5/29 (17) 15/29 (52) 1/29 (3) 1/29 (3) 4/29 (14) 4/29 (14) 27.8
68.4 39/44 (89) 18/44 (41) 12/44 (27) 14/44 (32) 11/44 (25) 25/44 (57) 7/44 (16) 5/44 (11) 0/44 0/44 28.1
.04 NS NS NS NS NS NS NS NS .022 .022 NS
7 (16) 9 (21) 1 (2) 13 (30) 9 (21) 7 (16) 8 (18) 4 (9.1) 22 (50) 17 9
NS NS NS NS .009 NS .078 .147 .148 .212 .051
Patient characteristics Age Gender (male) CAD Current smoking COPD DM Hypertension Hyperlipidemia History of CVA History of cancer CRF BMI Outcome MI Pneumonia CVA Renal failure Dialysis Sepsis Ischemic colon Multisystem organ failure Death Median hospital length of stay, days Median intensive care unit length of stay, days
3 8 1 9 0 3 1 0 9 9 5
(10) (28) (3) (31) (10) (3) (31)
BMI, Body mass index; CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CRF, chronic renal failure; CVA, cerebrovascular accident; DM, diabetes mellitus; EVAR, endovascular aneurysm repair; MI, myocardial infarction; NS, not significant. Fisher exact or Mann-Whitney U test as appropriate.
were given intraoperatively to patients who had EVAR. A slightly higher estimated blood loss was recorded for EVAR patients compared with open repair patients who developed ACS (5000 mL vs 4400 mL; P ¼ .026). In making a similar comparison between patients who underwent EVAR and those who underwent open repair but did not develop ACS, the opposite trend was seen: patients who had EVAR had less blood, blood products, and crystalloid than did patients with an open repair. Less blood loss was observed in patients who did not develop ACS in those undergoing EVAR compared with those with open repair (660 mL vs 4000 mL; P < .0001). The amount of fluids administered on the first and second postoperative days was also evaluated (Table IV). Patients who had EVAR and developed ACS required more blood on postoperative day 1 (7200 mL vs 600 mL; P ¼ .017). This is in contrast to patients with ACS who had an open repair of the rAAA. These patients, compared with those who did not develop ACS, required significantly more crystalloid on postoperative day 1 (8300 mL vs 5600 mL; P ¼ .01) and day 2 (6500 mL vs 3800 mL; P ¼ .004), with a trend of requiring more blood on postoperative day 2. DISCUSSION In this retrospective review of patients undergoing repair of rAAA at one institution, the overall observed mortality of 42% is similar to that previously reported.7-11 Although it is not statistically significant in this report, there
was a trend for lower mortality when patients were treated with an endograft compared with an open repair, consistent with other reports.7-9,12-16 ACS developed in patients with both endograft repair and open repair. The incidence for the development of ACS is not known but is reported to occur on average in 10% of patients.17 A systematic review by Karkos et al8 reported that ACS occurred in 5.5% of patients treated with EVAR. A recent meta-analysis calculated the rate as being 8% but suggested that the true incidence could be >20% with increased awareness and vigilant monitoring.11 Interestingly, the occurrence of ACS in patients treated with EVAR in the current series was 21%. Not surprising, patients who develop ACS after repair of rAAA have a higher incidence of colon ischemia, sepsis, and multisystem organ failure. Treatment is directed at decreasing the intra-abdominal pressure, often needing a decompressive laparotomy.4,5 Failure to intervene can be fatal. Therefore, early diagnosis and treatment are essential. The death rate in patients who develop ACS after EVAR for rAAA has been reported to be as high as 57%.18 The current study confirms that patients who develop ACS after EVAR have a high mortality. It is of interest that the meta-analysis conducted by Karkos et al11 did not find a statistically significant association between ACS and mortality. Despite this lack of statistical significance, they stated that “the development of ACS after endovascular repair of RAAAs is an ominous scenario that has a significant negative effect on survival.clearly, the mortality rate is increased in patients with ACS.”11
JOURNAL OF VASCULAR SURGERY --- 2014
4 Rubenstein et al
Table II. Patient characteristics and outcome stratified by type of repair for ruptured abdominal aortic aneurysm (rAAA) and the presence or absence of abdominal compartment syndrome (ACS) EVAR
Gender (male) CAD Current smoking COPD DM Hypertension Hyperlipidemia History of CVA History of cancer CRF BMI Outcome MI Pneumonia CVA Renal failure Dialysis Sepsis Ischemic colon Multisystem organ failure Death Median hospital length of stay, days Median intensive care unit length of stay, days
Open
ACS (n ¼ 6)
No ACS (n ¼ 23)
P value
ACS (n ¼ 15)
No ACS (n ¼ 29)
P value
6/6 2/6 1/6 2/6 1/6 3/6 1/6 0/6 0/6 1/6 d
17/23 9/23 7/23 8/23 4/23 12/23 0/23 1/23 4/23 3/23 27.8
NS NS NS NS NS NS NS NS NS NS NS
13/15 4/15 2/15 7/15 5/15 9/15 3/15 1/15 0/15 0/15 26.5
26/29 14/29 10/29 7/29 6/29 16/29 4/29 4/29 0/29 0/29 28.9
NS NS NS NS NS NS NS NS NS NS NS
1/6 1/6 0/6 2/6 0/6 1/6 1/6 0/6 5/6 10, n ¼ 3 10, n ¼ 1
2/23 7/23 1/23 7/23 0/23 2/23 0/23 0/23 4/23 9, n ¼ 23 4.5, n ¼ 20
NS NS NS NS NS NS NS NS .005 .880 .571
3/15 3/15 0/15 5/15 3/15 5/15 6/15 4/15 9/15 8.5 11
4/29 6/29 1/29 8/29 6/29 2/29 2/29 0/29 13/29 19 8.5
NS NS NS NS NS .036 .013 .010 NS .117 .394
BMI, Body mass index; CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CRF, chronic renal failure; CVA, cerebrovascular accident; DM, diabetes mellitus; EVAR, endovascular aneurysm repair; MI, myocardial infarction; NS, not significant. Fisher exact or Mann-Whitney U test as appropriate.
Table III. Intraoperative fluid administration and estimated blood loss for open vs endovascular aneurysm repair (EVAR) EVAR
Intraoperative fluids/blood loss (volumes in milliliters) PRBC FFP Platelets Cryoprecipitate Total blood products Colloid Crystalloid Estimated blood loss
Open
ACS
No ACS
P value
ACS
No ACS
P value
ACS EVAR vs open, P value
5600 27 730 280 9300 1500 11,000 5000
1100 220 70 15 1500 650 4500 660
Abdominal compartment syndrome (ACS) develops as a result of increased intra-abdominal pressure and is often related to massive fluid resuscitation associated with either hemorrhage or splanchnic reperfusion. Increased intraabdominal pressure has deleterious effects on multiple organ systems. As intra-abdominal pressure rises, the inferior vena cava is compressed, resulting in a decrease in venous return that in turn leads to reduction in ventricular enddiastolic volume, stroke volume, and cardiac output and elevation of systemic vascular resistance. Elevated intraFrom the Department of Vascular Surgery, Hadassah Hebrew University, Jerusalema; Peripheral Vascular Associates, San Antoniob; and the Department of Radiologyc and Department of Surgery,d University of Kentucky College of Medicine, Lexington. Author conflict of interest: none. Reprint requests: Eric D. Endean, MD, Department of Surgery, C-215, 800 Rose St, Lexington, KY 40536 (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest. 0741-5214 Copyright Ó 2014 by the Society for Vascular Surgery. http://dx.doi.org/10.1016/j.jvs.2014.10.011
abdominal pressure also compresses the kidneys, and this along with the adverse effects on cardiac function causes a reduction in renal flow and a decrease in urine output. Simultaneously, increased intra-abdominal pressure compresses the diaphragm, raising intrathoracic pressure with an increase in airway pressures, pulmonary artery pressure, and central venous pressure and a decrease in pulmonary compliance. If ACS is left untreated, multiorgan failure develops. Treatment is directed at relieving the intraabdominal pressure, often requiring a decompressive laparotomy. Failure to relieve the pressure is almost uniformly fatal; surgical decompression demonstrates significant improvement in mortality.1 Patients with ruptured abdominal aortic aneurysm (rAAA) present with hemorrhagic shock. The hematoma that forms in the retroperitoneum is a space-occupying lesion that itself can contribute to a rise in intra-abdominal pressure. In the perioperative period, these patients have large fluid requirements from ongoing bleeding, coagulopathy, and third-space requirements that necessitate resuscitation with blood, blood products, and fluids. This resuscitation can lead to bowel edema and ascites that 1
2 Rubenstein et al
further increase intra-abdominal pressure and development of ACS. Indeed, the development of ACS has been documented after both open and endovascular repair of rAAA.2-7 We hypothesize that the underlying mechanisms for the development of ACS after repair of rAAA may be different for patients treated with an endovascular aneurysm repair (EVAR) technique compared with those with an open repair. METHODS A retrospective review of all patients treated for rAAA between January 2005 and December 2010 at the University of Kentucky Chandler Medical Center was conducted. The study was approved by the University of Kentucky Institutional Review Board (IRB approval No. 10-0011P1H). Patient consent was not needed. Patients were excluded if the aneurysm was an aortic dissection or if the aneurysm was symptomatic but not ruptured. The charts were reviewed to identify demographic information, aneurysm size, and comorbid medical conditions. Operative details, including type of repair (open vs endovascular), intraoperative fluid administration, operative time, aortic cross-clamp time (open aneurysms), and need for suprarenal clamp (open aneurysms), were recorded. Available preoperative computed tomography scans were reviewed by a vascular radiologist to identify the presence of patent lumbar and inferior mesenteric arteries arising from the aneurysm for patients treated with EVAR. Available intraoperative completion studies after endograft placement were reviewed for evidence of endoleaks. Postoperative fluid resuscitation and urine output were recorded. The diagnosis of ACS was made on the basis of a constellation of clinical findings including increased airway pressures, oliguria, and physical examination revealing a tense abdominal wall and (in some open cases) inability to close the abdomen due to bowel edema. The development of complications, including myocardial infarction, bowel ischemia, pneumonia, renal failure, need for dialysis, number of days on the ventilator, intensive care unit length of stay, total hospital length of stay, and sepsis, were recorded. Final outcome and disposition were noted. Descriptive data are presented as mean 6 standard error. Comparisons were made by the unpaired t-test. Categorical data was compared with Fisher exact test or the Mann-Whitney U test. P values of < .05 were considered to be significant. RESULTS Between January 2005 and December 2010, 73 patients, 62 men and 11 women, were treated for rAAA. The average age of patients was 70.5 years. Overall mortality for repair of rAAA was 31 of 73 (42%). ACS developed in 21 patients (29%). Twenty-nine patients (40%) had repair of rAAA with an endograft, whereas 44 (60%) underwent an open repair. Characteristics of patients undergoing EVAR or open repair were not statistically significant except that patients
JOURNAL OF VASCULAR SURGERY --- 2014
undergoing EVAR were older and more patients in the EVAR group had a history of cancer (Table I). Significantly more patients undergoing open repair required dialysis (P ¼ .009) than in the EVAR group. There was a trend for lower morality, length of stay, and intensive care unit length of stay in the EVAR group compared with the open repair group, but statistical significance was not reached. ACS developed in 21 patients, including 6 of 29 patients (21%) who had an EVAR and 15 of 44 patients (34%) who had an open repair. No differences were identified in patient characteristics whether or not they developed ACS in either the EVAR or open group (Table II). In patients who underwent open repair, there were nine deaths among the 15 patients who developed ACS (60%) compared with 13 deaths in 29 patients (45%) who did not develop ACS (P ¼ NS). However, in patients treated with EVAR, 5 of 6 patients (83%) who developed ACS died compared with four deaths among 23 patients (17%) who did not develop ACS (P ¼ .005). In patients who had an open repair, colon ischemia, multisystem organ failure, and sepsis were significantly higher in patients who developed ACS than in those without. No statistical significance was noted in these outcomes in the patients treated with EVAR. In patients who developed ACS, control of the aorta was obtained in a suprarenal position in 11, infrarenal in nine, and unknown in one. Patients who did not develop ACS had control of the aorta suprarenally in 17, infrarenally in 31, and unknown in four. In the entire study group, the location of aortic control was not significantly associated with the development of ACS. Similarly, in patients treated with an open repair, suprarenal control of the aorta was not associated with development of ACS. However, in EVAR patients, balloon control of the aorta was done in seven patients, whereas 20 did not have balloon control, and in one, it was unknown. In this subset of patients, ACS developed in six patients (five with balloon control, one unknown) and was found to be significantly associated with balloon control of the aorta (P < .001). Because fluid resuscitation can play a key role in the development of ACS, the amount and timing of fluids given patients were evaluated comparing groups who developed ACS and those who did not. In patients who developed ACS with EVAR, the amount of blood products (packed red blood cells, fresh frozen plasma, platelets, and cryoprecipitate), colloid, and crystalloid given intraoperatively was significantly higher than in those who did not develop ACS (Table III). Estimated blood loss was also significantly higher in patients who developed ACS. In comparison, in patients with an open approach, the only significant difference seen in intraoperative fluid administration between patients who developed ACS and those who did not was that significantly more fresh frozen plasma and platelets were given to patients who developed ACS. In comparing intraoperative fluid administration to patients who developed ACS between EVAR and open repair, significantly more blood products and crystalloid
JOURNAL OF VASCULAR SURGERY Volume -, Number -
Rubenstein et al 3
Table I. Patient characteristics and outcome for the entire cohort of patients EVAR (n ¼ 29)
Open (n ¼ 44)
P value
73.7 23/29 (74) 11/29 (38) 8/29 (28) 10/29 (35) 5/29 (17) 15/29 (52) 1/29 (3) 1/29 (3) 4/29 (14) 4/29 (14) 27.8
68.4 39/44 (89) 18/44 (41) 12/44 (27) 14/44 (32) 11/44 (25) 25/44 (57) 7/44 (16) 5/44 (11) 0/44 0/44 28.1
.04 NS NS NS NS NS NS NS NS .022 .022 NS
7 (16) 9 (21) 1 (2) 13 (30) 9 (21) 7 (16) 8 (18) 4 (9.1) 22 (50) 17 9
NS NS NS NS .009 NS .078 .147 .148 .212 .051
Patient characteristics Age Gender (male) CAD Current smoking COPD DM Hypertension Hyperlipidemia History of CVA History of cancer CRF BMI Outcome MI Pneumonia CVA Renal failure Dialysis Sepsis Ischemic colon Multisystem organ failure Death Median hospital length of stay, days Median intensive care unit length of stay, days
3 8 1 9 0 3 1 0 9 9 5
(10) (28) (3) (31) (10) (3) (31)
BMI, Body mass index; CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CRF, chronic renal failure; CVA, cerebrovascular accident; DM, diabetes mellitus; EVAR, endovascular aneurysm repair; MI, myocardial infarction; NS, not significant. Fisher exact or Mann-Whitney U test as appropriate.
were given intraoperatively to patients who had EVAR. A slightly higher estimated blood loss was recorded for EVAR patients compared with open repair patients who developed ACS (5000 mL vs 4400 mL; P ¼ .026). In making a similar comparison between patients who underwent EVAR and those who underwent open repair but did not develop ACS, the opposite trend was seen: patients who had EVAR had less blood, blood products, and crystalloid than did patients with an open repair. Less blood loss was observed in patients who did not develop ACS in those undergoing EVAR compared with those with open repair (660 mL vs 4000 mL; P < .0001). The amount of fluids administered on the first and second postoperative days was also evaluated (Table IV). Patients who had EVAR and developed ACS required more blood on postoperative day 1 (7200 mL vs 600 mL; P ¼ .017). This is in contrast to patients with ACS who had an open repair of the rAAA. These patients, compared with those who did not develop ACS, required significantly more crystalloid on postoperative day 1 (8300 mL vs 5600 mL; P ¼ .01) and day 2 (6500 mL vs 3800 mL; P ¼ .004), with a trend of requiring more blood on postoperative day 2. DISCUSSION In this retrospective review of patients undergoing repair of rAAA at one institution, the overall observed mortality of 42% is similar to that previously reported.7-11 Although it is not statistically significant in this report, there
was a trend for lower mortality when patients were treated with an endograft compared with an open repair, consistent with other reports.7-9,12-16 ACS developed in patients with both endograft repair and open repair. The incidence for the development of ACS is not known but is reported to occur on average in 10% of patients.17 A systematic review by Karkos et al8 reported that ACS occurred in 5.5% of patients treated with EVAR. A recent meta-analysis calculated the rate as being 8% but suggested that the true incidence could be >20% with increased awareness and vigilant monitoring.11 Interestingly, the occurrence of ACS in patients treated with EVAR in the current series was 21%. Not surprising, patients who develop ACS after repair of rAAA have a higher incidence of colon ischemia, sepsis, and multisystem organ failure. Treatment is directed at decreasing the intra-abdominal pressure, often needing a decompressive laparotomy.4,5 Failure to intervene can be fatal. Therefore, early diagnosis and treatment are essential. The death rate in patients who develop ACS after EVAR for rAAA has been reported to be as high as 57%.18 The current study confirms that patients who develop ACS after EVAR have a high mortality. It is of interest that the meta-analysis conducted by Karkos et al11 did not find a statistically significant association between ACS and mortality. Despite this lack of statistical significance, they stated that “the development of ACS after endovascular repair of RAAAs is an ominous scenario that has a significant negative effect on survival.clearly, the mortality rate is increased in patients with ACS.”11
JOURNAL OF VASCULAR SURGERY --- 2014
4 Rubenstein et al
Table II. Patient characteristics and outcome stratified by type of repair for ruptured abdominal aortic aneurysm (rAAA) and the presence or absence of abdominal compartment syndrome (ACS) EVAR
Gender (male) CAD Current smoking COPD DM Hypertension Hyperlipidemia History of CVA History of cancer CRF BMI Outcome MI Pneumonia CVA Renal failure Dialysis Sepsis Ischemic colon Multisystem organ failure Death Median hospital length of stay, days Median intensive care unit length of stay, days
Open
ACS (n ¼ 6)
No ACS (n ¼ 23)
P value
ACS (n ¼ 15)
No ACS (n ¼ 29)
P value
6/6 2/6 1/6 2/6 1/6 3/6 1/6 0/6 0/6 1/6 d
17/23 9/23 7/23 8/23 4/23 12/23 0/23 1/23 4/23 3/23 27.8
NS NS NS NS NS NS NS NS NS NS NS
13/15 4/15 2/15 7/15 5/15 9/15 3/15 1/15 0/15 0/15 26.5
26/29 14/29 10/29 7/29 6/29 16/29 4/29 4/29 0/29 0/29 28.9
NS NS NS NS NS NS NS NS NS NS NS
1/6 1/6 0/6 2/6 0/6 1/6 1/6 0/6 5/6 10, n ¼ 3 10, n ¼ 1
2/23 7/23 1/23 7/23 0/23 2/23 0/23 0/23 4/23 9, n ¼ 23 4.5, n ¼ 20
NS NS NS NS NS NS NS NS .005 .880 .571
3/15 3/15 0/15 5/15 3/15 5/15 6/15 4/15 9/15 8.5 11
4/29 6/29 1/29 8/29 6/29 2/29 2/29 0/29 13/29 19 8.5
NS NS NS NS NS .036 .013 .010 NS .117 .394
BMI, Body mass index; CAD, coronary artery disease; COPD, chronic obstructive pulmonary disease; CRF, chronic renal failure; CVA, cerebrovascular accident; DM, diabetes mellitus; EVAR, endovascular aneurysm repair; MI, myocardial infarction; NS, not significant. Fisher exact or Mann-Whitney U test as appropriate.
Table III. Intraoperative fluid administration and estimated blood loss for open vs endovascular aneurysm repair (EVAR) EVAR
Intraoperative fluids/blood loss (volumes in milliliters) PRBC FFP Platelets Cryoprecipitate Total blood products Colloid Crystalloid Estimated blood loss
Open
ACS
No ACS
P value
ACS
No ACS
P value
ACS EVAR vs open, P value
5600 27 730 280 9300 1500 11,000 5000
1100 220 70 15 1500 650 4500 660
