Ruptured Abdominal Aortic Aneurysm: The state of play

Abdominal aortic aneurysm (AAA) is a dilatation of the aorta as it passes through the abdomen. 11 697 patients with an asymptomatic, unruptured AAA (ICD-10 code I71.4) were treated in German hospitals in the year 2000; the corresponding figure for 2010 was 13 586 patients, of whom 13% were women. Over the same interval, the number of patients treated for ruptured AAA (rAAA, ICD-10 code I71.3) rose from 1899 to 2410, of whom 19% were women. In 2010, 1251 persons died of rAAA in Germany, including 891 men and 360 women. (Source for all data: Federal Health Monitoring [Gesundheitsberichterstattung des Bundes].)

Ruptured abdominal aortic aneurysm (rAAA) is characterized by the presence of blood outside the adventitia of the dilated aortic wall. Free rupture, with egress of blood into the peritoneal cavity, is distinct from covered rupture, in which there is less blood loss because the periaortic hematoma is enclosed by retroperitoneal tissue (Figure 1).

Figure 1

Covered rupture of an abdominal aortic aneurysm

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There can also be retroperitoneal perforation into neighboring structures, including the inferior vena cava (aortocaval fistula) and the small or large intestine (aortoenteric fistula). An unruptured abdominal aortic aneurysm can produce symptoms resembling those of an rAAA, ranging from a mild feeling of tension to maximally intense pain with a feeling of impending doom; the defining difference between the two is the presence or absence of blood outside the adventitia (Figure 2).

Figure 2

Contrast-enhanced CT scan of a symptomatic, unruptured abdominal aortic aneurysm

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Pain is caused by expansion of the aortic wall and bleeding into the intravascular thrombotic edge. The differential diagnosis of pain resembling that of an rAAA includes other abdominal conditions such as cholecystitis, diverticulitis, and pancreatitis.

The incidence of asymptomatic abdominal aortic aneurysm is estimated variably in the literature from 3.0 to 117.2 per 100 000 persons per year; the reported incidence of rAAA varies from 1 to 21 per 100 000 persons per year (2). The documented risk factors for abdominal aortic aneurysm are advanced age, male sex (sex ratio ranging from 1 : 3 to 1 : 8), positive family history, hypertension, cigarette smoking, and hypercholesterolemia (2).

The classic clinical triad of rAAA consists of

• pain in the abdomen and/or back,
• hypotension, and
• a pulsatile abdominal mass

in a patient over age 50.

Methods

In this article, we survey the current state of knowledge of the treatment of rAAA by selectively reviewing pertinent literature retrieved by an electronic search in the PubMed, Web of Science, and Cochrane Library databases with the keywords “abdominal aortic aneurysm,” “ruptured,” “open repair,” and “endovascular.” We consider articles that were published in English or German up to and including March 2012 and pay special attention to the current Clinical Practice Guidelines of the European Society for Vascular Surgery (1).

Initial treatment

An important question in the initial treatment of patients with rAAA by the emergency medical services is whether they should be transported to the nearest hospital or to a specialized center that may be farther away (i.e., preferential referral to a high-volume hospital or high-volume vascular surgeon). Studies from the U.S.A., Canada, and the United Kingdom have shown that the latter is indeed associated with a significant lowering of mortality (p = 0.001) (3). In Finland, the centralized care of patients with rAAA lowered the mortality of this condition by 20% from 1996 to 2004 (4).

When a patient arrives at the hospital with a suspected rAAA, an emergency ultrasound examination is performed in the resuscitation room to confirm the diagnosis (or to determine the true cause if no rAAA is found). If possible, permissive hypotension (target systolic blood pressure, 50 to 80 mmHg; see below) should be maintained while the patient undergoes abdominal computed tomography (CT) with contrast medium. CT yields a definitive diagnosis in cases where the ultrasound findings are ambiguous (5) and provides reliable information about individual anatomy, which serve in turn as the basis for the decision whether to operate or perform an endovascular procedure. A minority of authors prefer to proceed to treatment immediately, without a CT scan, once the rAAA has been diagnosed by ultrasound; they point out that, if endovascular treatment is intended, diameters and lengths for the selection of the optimally configured stent prosthesis can be measured intraprocedurally (6).

Permissive hypotension

The concept of permissive hypotension is based on laboratory animal studies of acute hemorrhagic shock and has been successfully applied in the routine clinical management of multiple trauma (7). Animals resuscitated with permissive hypotension, rather than with restoration of normotension, survived at a significantly higher rate (8). The applicability of this concept to the treatment of rAAA has been demonstrated (9). Avoiding normal or supranormal systolic pressures is thought to make thrombus dislocation and recurrent hemorrhage (“clot popping”) less likely, thereby lowering retroperitoneal blood loss (9); at the same time, infusing a lower amount of fluid lessens the harmful effects of hemodilution and the resulting hypothermia and coagulopathy (10). In a review of pertinent literature from 1990 to 2009, it was concluded that the early administration of fresh-frozen plasma (FFP) along with platelets and erythrocyte concentrate significantly lowers mortality in patients with hemorrhagic shock (11, e1).

Surgical management

Permissive hypotension is maintained and the patient is transferred to the operating room, preferably a so-called hybrid OR that also contains the radiological equipment needed for endovascular treatment. The patient is then positioned on a warmed surface (to prevent hypothermia), and an arterial line for invasive blood pressure measurement, a nasogastric tube, a central venous catheter, and wide-bore catheters for peripheral venous access are inserted, if not already done in the resuscitation room.

If an open surgical approach has been chosen, general endotracheal anesthesia should not be initiated until the operative field has been sterilely prepped and draped, just before the skin incision. General anesthesia relaxes the muscles of the abdominal wall; sudden reduction of the abdominal pressure can convert a retroperitoneal perforation into an intraperitoneal hemorrhage, immediately causing shock (12). There are a number of different approaches and techniques for achieving the primary goal of surgery— safe, rapid, and effective cross-clamping of the aorta. A prospective, randomized trial showed the transperitoneal and left extraperitoneal approaches to be equally safe and effective (13); the operating surgeon decides which to use in the individual case depending on personal experience. Some prefer to cross-clamp the aorta below the renal arteries, as in elective aneurysm surgery, while others think it advantageous to cross-clamp above the celiac artery (to avoid venous injury when a peri-aortic hematoma obscures surgical visibility). Some perform intraoperative hemostasis with transfemoral or transbrachial balloon occlusion, a technique borrowed from the endovascular treatment of aneurysms (14, e2). Intraoperative volume substitution with an autotransfusion system (“cell saver”) has been shown to lessen the need for allogeneic blood transfusion (15). Mortality is also lowered by the balanced administration of FFP and erythrocyte concentrate (11).

Postoperative course

Patients with rAAA have a high postoperative morbidity (Table).

Table

Perioperative complications and their associated mortality

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Intra- and postoperative bleeding is a major problem, exacerbated by coagulopathy. The latter can be prevented by timely surgery and by the administration of FFP, prothrombin concentrate (PPSB), and antifibrinolytic drugs (16). If a diffuse, intractable bleeding tendency nonetheless persists after the aneurysm has been repaired, intra-abdominal packing (tamponade of the retroperitoneum with closely packed, sterile abdominal compresses) may help as a last resort but confers a high risk of intra-abdominal infection in both the early and the late phases (13% and 18%, respectively) (17).

Postoperative renal failure arises in 26% to 42% of patients with rAAA; 11% to 40% of these patients need dialysis, of whom 76% to 89% die (18). Renal failure is associated with supraceliac cross-clamping, cross-clamping for more than 30 minutes, pre-existing renal dysfunction, age > 80 and the central hypovolemia syndrome (“declamping shock”). The overall etiology is multifactorial, and even infrarenal cross-clamping lowers renal blood flow, with consequent lowering of the glomerular filtration rate and of urine production. Stimulation of renin production by way of the renin-angiotensin system and the sympathetic nervous system seems to play a causal role (12, 19). None of the putatively protective measures tested so far have been found useful, except optimization of volume status. Multiple drugs—mannitol, furosemide, fenoldopam, dopamine, popexamine, calcium-channel blockers, natriuretic peptide—have been tested without any clear finding that they lower the risk of postoperative renal failure (12).

Postoperative colonic ischemia ranges from purely mucosal involvement to transmural tissue loss; if resection is needed, the mortality is high (73%–100%). This problem is more likely in the setting of perioperative hypotension, retroperitoneal hematoma, transection of the inferior mesenteric artery, and altered collateralization from the superior mesenteric artery and/or internal iliac artery. If colonic ischemia is suspected, postoperative colonoscopy can reveal it in timely fashion so that resective surgery can be performed (20). Abdominal compartment syndrome is defined as an intravesically measured abdominal pressure over 20 mmHg together with organ dysfunction (renal failure, rising ventilatory pressure) (21, 22); it must be treated with abdominal decompression (23, 24). Some authorsseven recommend temporary abdominal wall closure (either mesh closure, or vacuum-assisted closure) for primary closure after open surgical rAAA repair (24).

About half of all persons with rAAA die before reaching a hospital, 25% of those who do reach a hospital alive die before treatment, and 40% of those who undergo surgery die; thus, the overall mortality of rAAA is roughly 80% (25). The past five decades have seen only scant improvement (lowering of perioperative mortality by 3.5% per decade) (26). Men with rAAA are about 10% more likely to survive than women (27).

Risk assessment

In theory, reliable preoperative risk assessment would let us predict how likely a patient is to survive and could be used to select surgical candidates. Expensive operative treatment could be dispensed with for patients with absolutely no chance of survival, who would instead receive humane palliative care. Although such an approach would clearly save money, it would just as clearly have ethical and legal implications that are beyond the scope of this article, which deals exclusively with medical considerations. Univariate studies have revealed a small number of risk factors associated with death after rAAA repair, which, in turn, have been incorporated into risk-scoring systems. No fewer than 18 risk scores and subsequent modifications have been evaluated for their usefulness in assessing individual risk (28). The published findings are inconsistent; in any case, no score seems capable of predicting the fate of an individual patient reliably enough to permit therapeutic decision-making on the basis of the score alone. Some scores do, however, seem to be useful for comparing groups of patients in different treatment centers and for comparing the results of different types of treatment (28).

Discussion

The current treatment of patients with rAAA still has unsatisfactory results, and the question arises how it might be improved. Two approaches seem to be promising:

• Screening might shift some patients toward elective AAA repair who would otherwise have an rAAA at some later time, thereby improving the overall outcome (e3).
• Endovascular techniques that have been applied successfully in the elective treatment of asymptomatic AAA might conceivably be used with advantage in the treatment of rAAA as well.

In a recent review article in Deutsches Ärzteblatt International, Eckstein and colleagues concluded that screening for AAA would be beneficial (29). They analyzed studies from the United Kingdom, Australia, and Denmark and determined that the systematic ultrasonographic screening of men over age 65 would significantly lower the rate of AAA-associated death in the medium (3–5 years) and in the long term (7–15 years), while raising the rate of elective surgery and lowering the rate of emergency surgery for AAA (29–31). The number of persons needed to screen (NNS) to prevent one death from AAA was markedly lower than the NNS for mammography (1000–2000), colonoscopy (862), or a fecal occult-blood test (808) (32).

After the initial publication of endovascular treatment techniques for abdominal aortic aneurysms (e4–e6), further studies documented their success in the elective treatment of asymptomatic AAA (33–35). Endovascular treatment was first used for rAAA in 1994; the subsequent literature contains increasing evidence that its use for rAAA may be advantageous (36). For anatomical reasons, however, only about 60% (range in published series, 18%–83%) of patients with rAAA can be treated with an endovascular approach (1). Further limitations of endovascular treatment are its xdifficulty and the specialized staff and apparatus that it requires, but these can be overcome by the local implementation of a multidisciplinary, interprofessional rAAA protocol (37).

Permissive hypotension is used in the endovascular treatment of patients with rAAA just as it is in their open surgical treatment. If necessary, hemostasis can be obtained early on with a wide-lumen aortic balloon inserted either transfemorally or transbrachially. Moreover, endovascular transfemoral aneurysm repair with stent prostheses can be performed under local anesthesia. The use of uni-iliac stent prostheses seems to yield comparable results to the use of bifurcated systems (1). Multiple literature reviews have arrived at the conclusion that the endovascular method is superior to open surgery for rAAA (38), but bias probably pervades the published clinical series (e7–e11, 39): in many, patient selection (rather than randomization) seems to have taken place, and the percentage of patients given only palliative treatment ranged from 10% to 30%. Moreover, multiple studies have shown that, for anatomical reasons, endovascular treatment is feasible for only 30% to 80% of patients. There was also marked variation from one study to another in the accompanying parameters of the treated patients: “hemodynamic stability,” for example, was variably defined as a minimum systolic blood pressure of anywhere from 50 to 100 mmHg. More reliable information on this subject is likely to be obtained from the prospective, randomized trials that are currently in progress, one each in the Netherlands (AJAX), France (RCAR), and the United Kingdom (IMPROVE) (e12–e14).

Ruptured abdominal aortic aneurysm thus remains a challenging problem. Its treatment is still fraught with high mortality and high perioperative morbidity, and improvement is needed. The findings presented here imply that patients would do better if the treatment was centralized and if systematic screening was performed. Future studies will show whether endovascular treatment with stent prostheses improves outcomes.

Conflict of interest statement

The authors declare that no conflict of interest exists.

Manuscript submitted on 7 March 2012, revised version accepted on 6 June 2012.

Translated from the original German by Ethan Taub, M.D.

Corresponding author
Prof. Dr. med. Michael Gawenda
Leitender Oberarzt der Klinik für Gefäßchirurgie
Herzzentrum, Uniklinik Köln
Universität zu Köln
Kerpener Str. 62
50937 Köln, Germany
michael.gawenda@uk-koeln.de

@For eReferences please refer to:
www.aerzteblatt-international.de/ref4312