Management of Abdominal Aortic AneurysmsJennifer M. Dehlin, BSGilbert R. Upchurch, Jr, MD*
Address*Section of Vascular Surgery, University of Michigan Health System, 2210 Taubman Health Care Center, 1500 East Medical Center Drive, Ann Arbor, MI 48109-0329, USA.E-mail: [email protected]
IntroductionIn this article, current treatment options for abdominalaortic aneurysms (AAAs) are described. This reviewfocuses on the infrarenal aorta, because this is the mostcommon aneurysm location. An AAA is defined as apermanent pathologic dilation of the aorta with adiameter greater than 1.5 times the expected anterior-posterior diameter of that segment, given the patient’sgender and body size [1]. For most individuals, this isapproximately 3 cm.
The most feared complication of an AAA is contin-ued expansion and rupture. When this occurs, manypatients die before reaching the hospital. Of thosewho survive to undergo surgery, operative mortalityis nearly 50% [2]. Brown and Powell [2] further docu-mented that only 11% of patients survive beyond30 days of rupture. In addition, rupture carries with itconsiderable morbidity and increased cost over electiverepair [3]. Thus, identifying patients with AAAs beforerupture is desirable.
The majority of AAAs are asymptomatic, with manyfound incidentally on abdominal or lumbosacral radio-graphs done for other reasons. Abdominal palpationduring physical examination has long been used todetect AAAs. However, a recent study suggested that thiswas only sensitive in thin patients with AAAs larger than5.0 cm [4]. For all patients tested, overall sensitivity andspecificity was poor at 68% and 75%, respectively [4].
Identifying risk factors for the development of AAAsfacilitates diagnosis in the asymptomatic patient. Therisk factor with the strongest association with AAAdevelopment is smoking [5,6]. Other independentlyassociated risk factors include increased height, coro-nary artery disease (CAD), hypertension, and a familyhistory [5]. AAAs are more than four times more preva-lent in men than in women, with prevalence increasingwith age [7]. Risk factors for the development of athero-sclerosis, such as low high density lipoprotein, seem tooverlap with risk factors for development of AAAs [7],
Opinion statementAbdominal aortic aneurysms (AAAs) are a lethal disease. Ultrasound is the modality of choice for screening patients for AAAs. It is reasonable to screen patients over age 60, particularly men, women with cardiovascular risk factors, smokers, and patients with a family history of AAAs. Patients with small (< 5.5 cm) AAAs should be followed with serial ultrasound. Medical management should focus on treating comorbidities, partic-ularly those that put patients at risk for other cardiovascular diseases. Smoking cessa-tion is mandatory in these patients. Patients with large or symptomatic AAAs should be evaluated for surgery; this includes careful imaging of the abdomen, aggressive treatment of comorbidities, and perioperative β blockade. Endovascular repair has lower short-term morbidity compared with conventional open repair. Trials assessing long-term results are in progress. Basic science and translational research focusing on the underlying pathogenesis of AAAs will likely pave the way for medical therapies in the future.
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but current research does not suggest that atherosclero-sis is directly causative [8].
Ultrasound is the modality of choice for screeningpatients for an AAA because of its excellent accuracy,low cost, patient acceptance, lack of radiation exposure,and wide availability [9]. In one study, even a 4-minute“quick screen” had nearly 100% accuracy in diagnosingAAAs [10].
There has been much discussion about developingguidelines for universal screening for AAAs. Afteranalyzing available data on cost and e ff icacy,Kent et al. [11] published a consensus statement onthe topic that recommended screening the followinggroups, when patients were deemed fit for possibleintervention: 1) a l l men aged 60 to 85 years ;2) women aged 60 to 85 years with cardiovascularrisk factors; and 3) men and women older than50 years with a family history of AAA.
Treatment options for patients with AAAs arediscussed below. Patients are categorized based on thesize of their aneurysm as found on initial screening.Treatment options for asymptomatic patients withsmall aneurysms (< 5.5 cm) are reviewed first. In thispatient population, the goal is to provide surveillance ofaneurysm size, while modifying risk factors for rupture.Operative management of patients with large or symp-tomatic aneurysms, including recommended preopera-tive assessment, is then discussed. Finally, managementof patients with ruptured aneurysms is reviewed.
INDICATIONS FOR HOSPITALIZATIONIndications for hospitalization include the following:1) patients with a pulsatile abdominal mass andunexplained pain in the abdomen, back, testicles, orfemoral region, and 2) patients with hemodynamicinstability and suspected ruptured AAA.
Therapy for the asymptomatic patient with a small AAA
• To date, AAA is a disease cured by surgery. Therefore, when a patient is discovered to have an aneurysm, even if it is small, it is important to initiate discussion of possible surgery in the future. Two large, randomized, pro-spective trials, the ADAM (Aneurysm Detection and Management) Veterans Affairs Cooperative Study Group and the UKSAT (UK Small Aneurysm Trial), found no significant survival advantage in patients undergoing elective repair of aneurysms less than 5.5 cm in diameter [12,13••]. How-ever, recent results from long-term follow-up in the UKSAT showed a small long-term survival benefit in the early surgery cohort, which the researchers attributed to the increased rate of smoking cessation in this group [13••].
• Based on these studies, 5.5 cm should serve only as a guideline in discuss-ing surgical repair with patients. Other factors to consider include likeli-hood of adequate patient follow-up, fitness for intervention, and risk factors for rupture. One important risk factor to consider is gender. Women have a threefold higher risk of aneurysm rupture than men, but were the minority of study participants in both the ADAM and UKSAT. Aneurysms in women also tend to rupture at a smaller diameter. In the UKSAT, the mean diameter preceding rupture was 5.0 ± 0.8 cm for women versus 6.0 ± 1.4 cm for men (P = 0.001) [2]. Current smoking, lower forced expiratory volume in one second, presence of chronic obstructive pulmo-nary disease (COPD), and higher mean blood pressure are also significant risk factors for rupture [2].
• The natural history of the disease is one of continued expansion and rupture. However, expansion rates vary between patients, with the majority of patients dying from other causes with an intact aorta. In fact, approxi-mately 66% of patients with AAAs die from another cardiovascular cause [14]. The therapeutic goals for this treatment group are to 1) provide surveillance of aneurysm size to help surgical decision making; 2) attempt
Elective surgical repair
Medical management
Management of Abdominal Aortic Aneurysms Dehlin and Upchurch 121
to slow the growth of the aneurysm through controlling modifiable risk factors for expansion and rupture; and 3) provide aggressive management of the patient’s other cardiovascular disease.
Surveillance with serial ultrasound• Autopsy studies done beginning in the 1960s showed that rupture risk
increased with increasing AAA diameter. More sophisticated models have been used to show that aneurysm volume is actually a better predic-tor of rupture risk [15]. Presently, however, anterior-posterior diameter is still the parameter followed in clinical practice (Fig. 1). As discussed in the introduction, ultrasound is the modality of choice for this purpose. The safety of this strategy was verified during the ADAM and UKSAT discussed earlier.
• The surveillance interval for known AAAs varies, because there is no universally approved recommendation. Several groups have proposed general surveillance guidelines (Table 1) [11,16•]. Creating broad-based recommen-dations is difficult, because it depends on weighing a theoretic rupture risk over a given time period versus the risk of mortality associated with elective surgery. The latter varies significantly based on a number of variables, includ-ing surgeon training, surgeon volume of AAA repairs, hospital volume of AAA repairs, the condition of the patient, and the patient’s gender [17]. In a large retrospective study, women were 1.4 times more likely to die from intact AAA repair than men [18].
• In addition to absolute aneurysm size, it is also important to follow expansion rates. Some clinicians believe that expansion of 4 to 8 mm over 12 months suggests instability, and consider surgical intervention in these patients, even if their AAA is less than 5 cm. This practice is supported by data from Gadowski et al. [19], who found the average expansion rate in AAAs that eventually ruptured was 0.82 ± 0.74 versus 0.42 ± 0.41 cm/y in unruptured AAAs (P = 0.04).
Controlling modifiable risk factors for AAA expansion and rupture• Smoking cessation: The risk factor with the strongest association with
AAA is smoking [5,6]. It has been implicated in the development [6,20], expansion [21–23], and rupture [24] of AAAs. Current smokers are over seven times more likely to have an AAA than nonsmokers, with duration of smoking being the most important variable [6]. Each year of smoking
Figure 1. Duplex ultrasound showing anterior-posterior and transverse diameters of an abdominal aortic aneurysm.
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increases the relative risk of developing AAA by 4% [6]. After cessation of smoking, there is a slow decline in the risk of occurrence of AAA [6]. As part of the UKSAT, investigators found that current smoking increased the rate of small AAA expansion [23].
• For some individuals, diagnosis with a cardiovascular illness, such as an AAA, can be a powerful motivator to quit smoking. However, degree of tobacco dependence is likely to be a stronger indicator of the ability to quit [25]. Numerous studies have investigated the efficacy of tools to help patients quit smoking, and the results have been analyzed in several Cochrane reviews. The following have all shown benefit: nico-tine replacement [26], nortriptyline and bupropion [27], and the combination of in-patient counseling coupled with at least 1 month of outpatient follow-up [25].
• Antihypertensive pharmacotherapy-� blockers: Factors that promote aortic wall degradation are an essential part of the pathogenesis of aneurysm for-mation, expansion, and rupture. In addition, aortic wall stress is believed to be important. Studies in animal models suggest that β blockers protect against aneurysm expansion and rupture, but the evidence in humans has been mixed [19,22,28–31].
• Regardless of the effect of � blockers on AAAs, they clearly decrease mortal-ity from other cardiovascular causes. As mentioned earlier, with as many as 66% of patients with AAAs dying from other cardiovascular causes, this is highly relevant to patients with AAAs [14].
Treatment of other cardiovascular illness• As part of the UKSAT, investigators found that age, sex, blood pressure,
cholesterol, body mass index, and history of treatment for hypertension or with aspirin did not affect the rate of small AAA expansion [23]. However, treating hypertension, hypercholesterolemia, and obesity are essential to maintaining overall cardiovascular health in this patient population.
• Histologically, the development of AAAs is characterized by destruction of collagen and elastin in the aortic media and adventitia, smooth muscle cell loss with thinning of the medial wall, infiltration of lymphocytes and macrophages, and neovascularization [8]. New medical therapies for AAA are targeted at halting this sequence of events. Specifically, four mechanisms relevant to AAA formation are being investigated: proteolytic degradation of aortic wall connective tissue, inflammation and immune response,
Table 1. Recommended screening interval for AAA based on the AP diameter at initial duplex ultrasound screening
Aneurysm AP diameter, cm
Recommended screening interval, moPowell and Brady [16•] Kent et al. [11]
Management of Abdominal Aortic Aneurysms Dehlin and Upchurch 123
biomechanical wall stress, and molecular genetics [8]. Work is being done in each area; however, few new therapies have been developed to the point of clinical trials.
• One of the most promising areas of research is the inhibition of matrix metalloproteinases (MMPs), which promote degradation of collagen and elastin and are integral to aneurysm formation [8]. In one study, oral doxy-cycline, a nonspecific inhibitor of MMPs, was safe and well tolerated for 6 months by 33 patients with small aneurysms [32]. At the end of the study period, plasma levels of MMP-9 were reduced; however, the study was not designed to detect differences in aneurysm expansion rate [32]. More recently, researchers have found promise in periaortic delivery of doxy-cycline as a transitional step in developing drug delivery or graft combina-tion products for endovascular repair [33].
AAAs greater than 5.5 cm and asymptomatic-elective repair
• Both the ADAM and UKSAT showed a survival advantage for patients undergoing elective repair once their aneurysms reached 5.5 cm. A distinct algorithm should be followed to assess the patient’s fitness for surgery, and to evaluate the anatomy of the aneurysm to determine the most appropri-ate surgical strategy.
• The purpose of perioperative assessment is to evaluate patients’ fitness for surgery, and to maximize their chances for a healthy outcome based on established risk factors for intraoperative and perioperative morbidity and mortality.
Cardiac risk stratify• Coronary artery disease is common in patients with AAAs. In one study,
coronary angiography was done on 100 patients scheduled for AAA repair, and nearly half were found to have a significant arterial lesion [34]. CAD is also the leading cause of early and late mortality after AAA repair [35]. The American College of Cardiology and American Heart Association Task Force on Practice Guidelines [36] and the American College of Physicians [37] both provide specific information for preoperative cardiac evaluation of patients undergoing noncardiac vascular surgery.
Manage other comorbidities• In a recent study of patients identified as having an AAA through ultrasound
screening, 68% were found to have COPD when pulmonary function testing was done [38]. COPD is not a contraindication to AAA repair; however, extra care must be taken when considering AAA repair. A 2003 study evaluating morbidity and mortality after AAA repair in patients with COPD showed that the preoperative factors significantly associated with a poor outcome include 1) suboptimal COPD management, as evidenced by fewer inhalers used; 2) a lower preoperative hematocrit; 3) preoperative renal insufficiency; and 4) the presence of CAD [39]. For this reason, preoperative assessment normally includes arterial blood gas measurement and pulmonary function tests to evaluate the extent of the patient’s COPD.
Perioperative assessment
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Structural evaluation of the AAA• Computed tomography (CT) is the imaging modality of choice once an
intervention is planned (Fig. 2). In comparison to ultrasound, it provides 1) more precise definition of the proximal and distal extent of the aneur-ysm; 2) better delineation of the iliac artery anatomy; 3) the ability to evaluate AAA wall integrity, noting the location and amount of calcification within vessel walls; and 4) the ability to identify other intra-abdominal pathologic conditions and anomalies [40].
• Magnetic resonance angiography (MRA) is the preoperative study of choice if the iodinated contrast required for CT is contraindicated due to dye allergy or renal insufficiency [40].
• Aortography is used as an adjunct to other imaging modalities, and is indicated when 1) the extent of the aneurysm may include the juxtarenal or suprarenal aorta; 2) the clinical history is indicative of lower extremity
Figure 2. Three-dimensional computed tomography scan of a patient being considered for endovascular abdominal aortic aneurysm repair.
Management of Abdominal Aortic Aneurysms Dehlin and Upchurch 125
arterial occlusive disease; 3) renovascular disease may be present, as evi-denced by uncontrolled hypertension or azotemia; or 4) the patient has previously undergone arterial reconstruction [40].
Perioperative � blockadeA number of recent studies have shown that perioperative � blockade reduces the likelihood of cardiac events in noncardiac surgery. The results were analyzed in a literature review published in 2002 [41]. This practice is also advocated by the American College of Physicians [37]. Although the choice of agent is somewhat flexible, Fleisher and Eagle [42] recommend a short-acting agent, such as meto-prolol, so that dosing can be adjusted within a few days.
Standard dosage The recommended starting dose is 50 mg metoprolol orally twice a day; titrate to maintain heart rate less than 60 bpm prior to surgery [42].
Contraindications Hypersensitivity to drug/class/component, severe bradycardia, second- or third-degree atrioventricular block, cardiogenic shock, uncompensated heart failure, sick sinus syndrome without pacemaker. Avoid abrupt withdrawal. Caution if asthma or asthma history.
Main drug interactions Serious drug interactions include verapamil (the effects of both drugs may be increased) and clonidine (may cause life-threatening increases in blood pressure).
Main side effects Serious reactions include severe bradycardia, congestive heart failure, broncho-spasm, agranulocytosis, and hepatitis. Common reactions include fatigue, dizzi-ness, dyspnea, bradycardia, hypotension, bronchospasm, and dry mouth.
• The two types of operations available for AAA repair are conventional open repair and endovascular repair. The first step in determining which procedure is appropriate for the individual patient is to further characterize the aneurysm using the imaging modalities described earlier. Next, the risks, benefits, and possible complications of each procedure should be discussed with the patient. These are described next.
• A 2003 review of 22 nonrandomized controlled studies by Maher et al. [43] comparing endovascular aneurysm repair (EVAR) versus conventional open surgical treatment found that there were early benefits to endovascular repair. These included shorter hospital and intensive care stays, less blood loss, and fewer systemic complications. However, there were more local and vascular complications with endovascular repair, and more graft failures at mid- and long-term follow-up. Mortality rates were not signifi-cantly different. Maher et al. [43] concluded that until randomized con-trolled trials comparing the two treatments are completed, endovascular repair belongs only in select experienced centers. Randomized controlled trials are currently underway in the United Kingdom (UK EVAR [Endo-vascular Aneurysm Repair] trials) [24] and the Netherlands (DREAM [Dutch Randomised Endovascular Aneurysm Management] trial).
Conventional surgical treatment
Standard procedure A transabdominal or retroperitoneal approach is used. Normal aorta, proximal and distal to the aneurismal segment is isolated. The patient is systemically heparin-ized and clamps are applied distally, followed by proximally. The aneurysm is open longitudinally and the aortic thrombus is removed. All backbleeding lumbar arter-ies are oversewn. A Dacron or polytetrafluoroethylene graft is sewn in place proxi-
Pharmacologic treatment
Surgery
126 Vascular Disease
mally and distally. Flow is re-established in the pelvis and lower extremities. Hemostasis is attained. The aneurysm is closed over the graft, and then the retro-peritoneum is closed.
Contraindications In patients considered to have a high risk of operative mortality, surgery is gener-ally delayed until theoretic risk of rupture exceeds the estimated risk of operative mortality. Rupture risk increases markedly as AAAs enlarge. In a study of nearly 200 veterans in whom repair was delayed due to medical contraindication or patient refusal, the 1-year incidence of rupture by initial AAA diameter was 9.4% for AAAs 5.5 to 5.9 cm, 10.2% for AAAs 6.0 to 6.9 cm (19.1% for the subgroup of 6.5 to 6.9 cm), and 32.5% for AAAs larger than 7.0 cm. Once AAAs reached 8 cm, 25.7% ruptured within 6 months [44].
Complications In a 1989 study of 666 patients undergoing conventional repair, 15% of patients experienced postoperative cardiac events [45]. This accounted for 62.5% of deaths. Other complications included pulmonary insufficiency (8%), renal insuffi-ciency (6%), bleeding (4%), embolization (3%), wound infection (2%), graft infection (1%), and aortoenteric fistula (1%). The latter become evident after 3 to 5 years [45].
Special points The transperitoneal approach is preferred when there is a need to revascularize the right kidney or the aneurysm extends into the right iliac artery. Relative indications for the retroperitoneal approach include obesity, as well as multiple prior laparotomies, creating a hostile abdomen.
Cost/cost-effectiveness In a 2000 multicenter trial, average total inpatient hospital cost of conventional surgical repair of AAA was approximately $12,000 [46]. See below for a comparison with endovascular repair.
Endovascular repair
Standard procedure Access to the aorta is typically gained via bilateral femoral artery exposure. Bifur-cated modular endografts are currently the standard of care and are deployed over a wire. Aortography is then used to assess for endoleaks.
Contraindications Endovascular repair can only be offered to patients who fit anatomic requirements, when the proper graft and a qualified operator are available.
Complications The most common complication is an endoleak, defined as persistent blood flow in the aneurysm after placement of the graft. Lifelong surveillance with serial CT is currently recommended to identify when endoleaks occur. Secondary procedures, including open repair, may be necessary. Other complications are similar to those encountered with conventional repair, and include postoperative cardiac events, pulmonary or renal insufficiency, bleeding, embolization, wound or graft infection, and aortoenteric fistula.
Cost/cost-effectiveness Endovascular repair is more expensive to perform than conventional surgical repair, primarily because of increased endograft costs [43]. In 2000, the cost of a conven-tional graft was $600 versus approximately $10,000 for an AneuRx (Medtronic AVE, Santa Rosa, CA) endovascular device [46]. Overall cost-effectiveness has not been established, because data are lacking on the cost of follow-up imaging, and of possible repeat interventions for patients undergoing endovascular repair. These costs are partially offset by reduced operating room time, and shorter hospital stays for patients undergoing endovascular repair [43].
Symptomatic or ruptured AAAs: urgent repair
• Pain or tenderness of an AAA has long been thought to indicate acute expansion or imminent rupture. Patients may experience pain in the back, abdomen, flank, or groin. The pain is often described as gnawing, and it can last from a few hours to days.
• Differential diagnosis for symptomatic AAA includes diverticulitis, renal colic, irritable bowel syndrome, inflammatory bowel disease, ovarian torsion, or appendicitis.
Management of Abdominal Aortic Aneurysms Dehlin and Upchurch 127
• In the stable patient, if the patient’s aneurysm is less than 5.5 cm and they do not have risk factors for rupture, other causes for pain besides AAA should be quickly sought. If none are identified, the next step is CT or MRA, based on the patient’s ability to tolerate iodinated contrast (see imaging section of evaluation for elective repair earlier). CT or MRA is the first step in evaluating those patients with symptomatic AAAs greater than 5.5 cm. If the patient becomes hemodynamically unstable at any time, or if retro-peritoneal blood is noted, the studies should be stopped and the patient transported immediately to the operating room for repair.
• If the aneurysm is unruptured, repair should be undertaken within 24 hours. Before surgery, comorbid diseases should be optimized medically, and � blockade should be instituted as described earlier.
EVAR
Standard procedure Surgical options are the same as those provided to patients undergoing elective repair. As mentioned earlier, several large randomized trials are underway that may provide guidance as to whether EVAR should be recommended in these cases.
Contraindications Endovascular aneurysm repair can only be offered to patients who fit anatomic requirements, and the proper graft and qualified operator must be available. Conventional treatment can be offered to all patients. However, clinicians should also discuss the option of comfort care with patients and their family members when the risk of operative mortality is extremely high.
Complications Recent studies show promising results for patients with symptomatic AAAs treated with EVAR. This includes a lower first-month mortality [47]. This improvement is welcome, because morbidity and mortality after precipitous repair have historically been poorer than elective repair. A 1990 study showed that patients undergoing precipitous conventional repair of symptomatic, but unruptured, AAAs had consid-erable morbidity, with a 37% risk of pulmonary failure, a 31% incidence of acute renal failure, a 21% incidence of myocardial infarction, and a 10% incidence of stroke [48]. These results were not significantly different from those for patients undergoing repair of ruptured AAAs [48]. In this study, the mortality rate associ-ated with repair of symptomatic AAAs was nearly equal to that of ruptured AAAs, and was five times the rate of elective repair [48].
Ruptured AAAs: emergent repair
• The classic presentation for ruptured AAA is the triad of hypotension, back or abdominal pain, and a pulsatile abdominal mass. However, all three signs and symptoms are only present in approximately one half of patients [40].
• A ruptured AAA can be mistaken for other serious conditions (Table 2).
Conventional open repair
Standard procedure Repair of ruptured AAAs is performed similar to standard conventional open AAA repair. Differences include 1) the expedited nature of prepping the patient prior to the induction of anesthesia in case of hemodynamic collapse; 2) obtaining supraceliac aortic control prior to entering the retroperitoneal hematoma; and 3) managing the complications of having a large retroperitoneal hematoma induc-ing an abdominal compartment syndrome.
Surgery
Surgery
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Contraindications The consensus is that repair should not be denied, even in patient groups with high morbidity and mortality [40]. There are those that disagree, and have worked to identify those at highest risk for a poor outcome. In a 2004 study by Sultan et al. [49], no one parameter strongly predicted outcome; however, the constellation of male gender, age greater than 70 years, hypovolemic shock, and low preoperative hemoglobin taken together predicted a very poor outcome. Additionally, no patient with a preoperative cardiac arrest survived more than 24 hours after aortic surgery. The authors admitted that the influence of gender in their study may be questionable due to a low number of female participants.
Complications Intraoperative mortality from conventional repair of ruptured AAAs is nearly 50% [2]. There is also considerable morbidity associated with the procedure, including cardiac events, mesenteric ischemia, renal failure requiring dialysis, bleeding, infection, and multisystem organ failure.
Cost/cost-effectiveness Although the cost of surgical repair of ruptured AAAs is high, data show that it is cost-effective in comparison with no intervention as long as operative mortality does not exceed 88%, or initial hospitalization costs exceed $195,000 [50].
• Lee et al. [51] reported favorable results following the addition of endo-vascular AAA repair as a treatment option for ruptured AAAs. This study compared outcomes during an early time period when conventional open surgery was used exclusively, versus a later time period when endovascular AAA repair was performed in the majority of patients (76%) and conven-tional repair was reserved for patients with hemodynamic instability or unfavorable aortic anatomy. Perioperative mortality in the early versus late periods was 37% and 12%, respectively, but this difference did not reach statistical significance. Results that did reach statistical significance were the following: decreased median procedure times in the late time period (275 vs 149 minutes, P < 0.01), decreased blood loss (3800 vs 138 mL, P < 0.0001), and decreased length of stay (18 vs 6 days, P < 0.05). These results suggest that endovascular AAA repair may serve an important role in the future in the treatment of ruptured AAAs.
Table 2. Conditions sometimes mistaken for ruptured AAA
Management of Abdominal Aortic Aneurysms Dehlin and Upchurch 129
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