Your activity: 90 p.v.
your limit has been reached. plz Donate us to allow your ip full access, Email:

Clinical features and diagnosis of abdominal aortic aneurysm

Clinical features and diagnosis of abdominal aortic aneurysm
Jeffrey Jim, MD, MPHS, FACS
Section Editors:
Joseph L Mills, Sr, MD
John F Eidt, MD
Mark A Creager, MD, FAHA, FACC, MSVM
Deputy Editor:
Kathryn A Collins, MD, PhD, FACS
Literature review current through: Dec 2022. | This topic last updated: Sep 01, 2022.

INTRODUCTION — Abdominal aortic aneurysm (AAA), which is an abnormal focal dilation of the abdominal aorta, is relatively common and has the potential for significant morbidity and mortality. Most patients with AAA are asymptomatic but come to medical attention by findings of a pulsatile mass on physical examination, as the result of other abdominal imaging studies, or through ultrasound screening programs for AAA [1]. When symptoms do occur, patients commonly present with abdominal, back, or flank pain, but thromboembolism can also occur, leading to symptoms of limb ischemia. Aneurysms that produce symptoms are at an increased risk for rupture, which is associated with high mortality rates.

A diagnosis of AAA generally requires imaging confirmation that an aneurysm is present, which is most often accomplished using abdominal ultrasound. However, in symptomatic patients, computed tomography of the abdomen provides additional information that can determine if the aneurysm has ruptured, is expanding rapidly, and, for those without signs of rupture, whether symptoms are likely to be related to the aneurysm or due to other abdominal pathology.

The clinical features and diagnosis of AAA will be reviewed here. The management of nonruptured and ruptured AAA is discussed elsewhere. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Introduction' and "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Introduction'.)

ANEURYSM DEFINITION AND ANATOMY — An aneurysm is defined as a segmental, full-thickness dilation of a blood vessel 50 percent greater than its normal diameter [2,3]. Although "normal" diameter varies with age, sex, and body habitus, the average diameter of the human infrarenal aorta is approximately 2.0 cm; the upper limit of normal is typically <3.0 cm [4]. Thus, for the majority of patients, an infrarenal aorta with a maximum diameter ≥3.0 cm is aneurysmal [2,4,5]. The normal diameter of the suprarenal aorta tends to be approximately 0.5 cm larger than the infrarenal aorta.

The aorta dilates with age, and the normal aortic diameter in older patients tends to be larger. In a population-based study using magnetic resonance imaging to obtain aortic diameters at various levels in 70-year-old patients, the average diameters were [6]:

Above the celiac artery – Men: 3.0 cm, women: 2.7 cm

Above the renal arteries – Men: 2.8 cm, women: 2.7 cm

Just below the renal arteries – Men: 2.4 cm, women: 2.2 cm

At aortic bifurcation – Men: 2.3 cm, women: 2.0 cm

The abdominal aorta (figure 1) is the most common anatomic site of arterial aneurysm [3]. Abdominal aortic aneurysms (AAAs) are described relative to the involvement of the renal or visceral vessels.

Infrarenal – The aneurysm originates below the renal arteries (image 1 and image 2).

Juxtarenal – The aneurysm originates at the level of the renal arteries, but the aorta at the renal arteries is normal.

Pararenal – The aneurysm involves the aorta at the level of the renal arteries (ie, the renal artery originates from an aneurysmal aorta (image 3)).

Suprarenal (visceral) – The aneurysm originates above the renal arteries.

Most AAAs are infrarenal (figure 2). Approximately 15 percent are juxtarenal [7]. Suprarenal aneurysms not also affecting the infrarenal, juxtarenal, or thoracic aorta are uncommon but may develop late following AAA repair [8].

RISK FACTORS — Risk factors associated with abdominal aortic aneurysms (AAAs) are listed here and are discussed in detail elsewhere. (See "Epidemiology, risk factors, pathogenesis, and natural history of abdominal aortic aneurysm".)

The following are associated with an increased risk of developing AAA [3,9-15]:


Male sex

Advancing age


Family history of AAA

Other arterial aneurysms (eg, iliac, femoral, popliteal, intracranial)

Connective tissue disorder (eg, Marfan, Ehlers-Danlos, Loeys-Dietz syndromes) or family history

Prior history of aortic dissection

Prior history of aortic surgery or instrumentation

The risk of aneurysm rupture is increased with:

Large initial aneurysm diameter (>5.5 cm)

Current smoking

Elevated blood pressure

Greater aortic expansion rate (>0.5 cm/year)

Female sex


Not being a White person and diabetes are associated with a decreased risk for AAA [12]. Although a smaller percentage of women have aneurysms (approximately 20 percent of all AAA diagnoses), women present with rupture more often than men [16].

CLINICAL PRESENTATIONS — Abdominal aortic aneurysm (AAA) presents clinically in a variety of ways. Most individuals with AAA have no symptoms. When symptoms do occur, pain is the most common complaint. Pain may or may not be associated with AAA rupture or other associated symptoms.

Asymptomatic AAA — An asymptomatic (occult) AAA may be discovered as a result of screening, on routine physical examination, or on imaging studies obtained to evaluate an unrelated condition.

Screening for AAA – Screening for AAA is performed in defined populations based upon risk. In some, but not all, countries, screening programs for AAA appear to have contributed to a reduced incidence of ruptured AAA [1,17,18]. Screening for AAA is discussed elsewhere. (See "Screening for abdominal aortic aneurysm".)

Pulsatile abdominal mass – Approximately 30 percent of asymptomatic AAAs may be suspected when a pulsatile abdominal mass is palpated on routine physical examination [19]. The ability to palpate and estimate the aortic diameter depends upon the patient's body habitus, the size of the aneurysm, and the clinical experience of the practitioner. (See 'Abdominal palpation' below.)

Incidental finding on radiography – AAA is frequently detected as an incidental finding on imaging studies performed for other purposes [20-23]. It is important to note that this information is often not passed on to the referring physician, and up to one-third of patients with aneurysms detected incidentally underwent no subsequent monitoring [20,24-26]. The following findings are illustrative [26]:

One review study identified AAA in 1 percent of 79,121 abdominal imaging studies, including computed tomography of the abdomen, ultrasound, and magnetic resonance imaging [20]. The mean aortic diameter was 4.0 cm. The presence of AAA was communicated to the family physician in only 15 percent of patients.

Another review identified delayed recognition or delayed communication of incidental findings on computed tomography in nearly two-thirds of patients, including eight patients who had AAA >5.5 cm, which represented 9 percent of newly diagnosed aortic dilations [24].

Associated arterial disease – AAA may also be detected during the clinical examination or workup for lower extremity symptoms (eg, claudication) thought to be due to peripheral artery disease, or evaluation related to another peripheral aneurysm (iliac, femoral, popliteal) (image 4). Iliac aneurysm commonly occurs in association with AAA. In a retrospective review of 10,038 patients with iliac aneurysm, 89 percent had a coexistent AAA [27]. Another study found a 14 percent incidence of femoral and/or popliteal artery aneurysms in association with AAA [28]. (See "Popliteal artery aneurysm" and "Iliac artery aneurysm".)

Symptomatic (nonruptured) AAA — Symptomatic AAA refers to any of a number of symptoms that can be attributed to the aneurysm. In surgical series, between 5 and 22 percent of AAA are symptomatic [29-34]. Because symptoms in association with a diagnosis of AAA increase the risk for rupture, symptoms that are not obviously attributable to another cause (eg, diverticulitis) should be presumed to be due to the aneurysm, until proven otherwise. (See 'Symptoms' below and "Management of asymptomatic abdominal aortic aneurysm", section on 'Aneurysm repair versus conservative management'.)

AAA can also present initially as a complication of instrumentation of the aorta (eg, arteriography, cardiac catheterization). As catheters are passed through the aorta, thrombus or atherosclerotic debris associated with the aneurysm can dislodge and embolize distally. Thromboembolism from thrombus within AAA has also been reported following abdominal trauma [35]. (See 'Limb ischemia' below.)

Ruptured AAA — Aortic rupture is due to the weakening of the aortic wall to the extent that it can no longer support the forces imposed upon it, leading to a full-thickness loss of tissue integrity that results in escape of blood outside the confines of the aorta, typically into the retroperitoneum, but occasionally free into the abdominal cavity. The AAA can also rupture into the adjacent vena cava (ie, aortocaval fistula), which can present with sudden onset of abdominal pain and/or shortness of breath. A loud abdominal bruit will be heard on physical examination, and the patient can present with signs of acute heart failure (jugular venous distention or leg swelling). (See 'Other manifestations' below.)

Whether aortic rupture is due to AAA or to another disease process (eg, penetrating aortic ulcer, aortic dissection) can only be ascertained though aortic imaging. (See 'Imaging symptomatic patients' below.)

The incidence of ruptured AAA in hospitalized patients underestimates the overall incidence of ruptured AAA because only approximately one-half of patients with ruptured AAA survive long enough for treatment, and not all patients with sudden death undergo autopsy to confirm the cause of death. (See "Epidemiology, risk factors, pathogenesis, and natural history of abdominal aortic aneurysm".)

AAA can present initially with rupture with no intervening symptoms. Although the signs and symptoms of ruptured AAA (rAAA) may be obvious (eg, patient with known AAA in shock), some presentations make ruptured AAA difficult to recognize. Patients with rupture into the retroperitoneum may attribute their symptoms to other causes and delay seeking medical attention. Even after presenting to a physician, a misdiagnosis of rAAA as ureteral colic, myocardial infarction, perforated viscus, diverticulitis, gastrointestinal hemorrhage, or ischemic bowel occurs approximately 30 percent of the time [36,37]. A systematic review noted that, although advanced cross-sectional imaging has become more widely available, the rate of initial misdiagnosis for patients with rAAA decreased only slightly from 42 percent for studies performed before 1990 to 32 percent for those performed later (four studies) [36].

An unsuspected AAA rupture can also be diagnosed on imaging studies obtained to evaluate symptoms presumed to be due to another diagnosis, or a diagnosis of ruptured AAA may only be learned upon autopsy after the patient's demise.

The clinical presentation of ruptured AAA in patients who have undergone prior endovascular aneurysm repair (EVAR) is similar to that of de novo rupture. Post-EVAR rupture, which is rare (<1 to 2 percent), is due to unresolved endoleak repressurizing the aneurysm sac and is most commonly seen in patients who have undergone EVAR with less than ideal anatomy or in those who have not been compliant with post-EVAR follow-up [38]. (See "Complications of endovascular abdominal aortic repair", section on 'Endoleak'.)


History — The medical history is useful for determining the patient's risk for developing abdominal aortic aneurysm (AAA) and, if AAA is present, the potential for rupture. (See 'Risk factors' above.)

In addition to assessing risk factors, the patient and his/her guardian should be asked:

Whether a diagnosis of AAA has been established in the past. Values of aortic diameter from prior imaging studies should be obtained for comparison. Whenever serial imaging studies are available, prior rates of aortic expansion (cm/year) should be obtained (or calculated) (image 5). This can be accomplished by taking the maximal aortic diameter from one year and subtracting the diameter from the prior year and dividing by the number of intervening years. As an example, if the aneurysm measured 3.5 cm one year and 5.25 cm two years later, the expansion rate is (5.25 cm - 3.5 cm)/2 years or 0.875 cm/year, which exceeds the average expansion rate of 0.5 cm/year and may increase the risk for rupture. (See 'Are symptoms related to AAA?' below and "Epidemiology, risk factors, pathogenesis, and natural history of abdominal aortic aneurysm", section on 'Expansion and rupture of AAA'.)

Whether prior AAA repair has been undertaken. Dilation of the suprarenal abdominal aorta can occur after open or endovascular AAA repair [39], or, in the case of prior endovascular repair, mechanical problems can lead to endoleak, which can pressurize the residual infrarenal aortic sac and potentially lead to rupture [40]. Following open AAA repair, late anastomotic failures can occur at the proximal or distal anastomosis with or without associated graft infection, leading to pseudoaneurysm. (See "Complications of endovascular abdominal aortic repair", section on 'Endoleak' and 'Are symptoms related to AAA?' below.)

The patient may or may not be aware of a diagnosis of AAA prior to clinical manifestations of rupture. Only 20 to 30 percent of patients who present to an emergency department with rupture have a known history of AAA [41,42].

In patients who present with symptoms, the history should also seek known disease processes that can cause abdominal/back or flank pain, as well as identify prior abdominal surgeries (eg, cholecystectomy, appendectomy). (See 'Differential diagnosis' below.)

Symptoms — Most individuals with AAA have no symptoms. Younger patients with AAA may be more likely to have symptoms compared with older patients [43]. When symptoms do occur, pain located in the abdomen, back, or flank is the most common clinical manifestation [3]. AAA can also present with limb ischemia, or with systemic manifestations related to an infected aneurysm or inflammatory aneurysm. These symptoms and other clinical manifestations may or may not be related to AAA rupture. The classic triad of severe acute pain, a pulsatile abdominal mass, and hypotension occurs in approximately 50 percent of patients with ruptured AAA [36,44-46].

Symptoms potentially related to AAA can mimic many other diseases; however, in patients known to have or subsequently shown to have AAA, symptoms are presumed to be due to the aneurysm until unequivocally proven otherwise. (See 'Differential diagnosis' below and 'Are symptoms related to AAA?' below.)

Pain — Patterns of pain referable to AAA vary widely related to the diameter and position of the aneurysm, whether the aneurysm is ruptured, and, if ruptured, the nature (contained or free) and the location of the rupture (proximal or distal aorta). However, a complaint of abdominal pain is relatively nonspecific and can be due to a variety of other conditions. The general approach and evaluation of patients with abdominal pain is discussed in detail elsewhere. (See "Evaluation of the adult with abdominal pain".)

Pain related to AAA is typically located in the abdomen, but back or flank pain, pelvic pain, or pain radiating to the groin or thigh are also described [47]. One retrospective review of 66 ruptured AAAs reported pain as a presenting symptom in 75 percent of patients; 45 percent had abdominal pain, 17 percent had flank/back pain, and 14 percent had both [46]. Abdominal pain was associated with nausea in 20 percent and syncope or a faint feeling in approximately 30 percent of patients. In a systematic review, the incidence of abdominal pain on presentation of a ruptured AAA was between 49 and 72 percent [36].

The location of the pain can usually be related to the position of the aneurysm, with aneurysms positioned more proximally producing upper abdominal/back pain and distal aneurysms producing lower abdominal/pelvic pain or radiculopathy. The pain is typically unaffected by position or movement.

Physiologically, the pain associated with AAA is related to [47-50]:

Compression and/or erosion of the aneurysm into surrounding structures (eg, spine, inferior vena cava), which typically does not occur unless the aneurysm is large (>5.5 cm).

Rapid expansion of the aneurysm (>0.5 cm/year), which can produce vague, nonspecific, abdominal discomfort or more focal pain.

Inflammation or infection of the aortic wall (eg, inflammatory aneurysm, infected aneurysm), which produces vague, nonspecific abdominal pain that may be associated with constitutional symptoms (eg, fever, weight loss).

Aneurysm rupture, which produces sudden-onset severe pain.

An indolent onset of pain that is vague and nonspecific is more typical of nonruptured AAA. The time course from the onset of pain to seeking medical attention is highly variable.

AAA rupture typically produces acute, severe abdominal pain and other manifestations that are determined by the location of the rupture and whether the rupture is contained, ruptures freely into the peritoneum, or ruptures into an adjacent venous structure causing a fistula (eg, aortocaval, aortoiliac) [47]. Autopsy studies have found that abdominal aortic aneurysm rupture occurs most commonly in the posterior wall of the aorta, which correlates to the levels of highest stress in mechanical modeling studies [51-53].

Proximal aortic rupture near the renal arteries leads to severe back/flank pain, whereas distal rupture near the iliac bifurcation causes low abdominal/pelvic pain and may cause pain that radiates to the groin or thigh due to lumbar nerve irritation.

Posterior aortic wall rupture is likely to be initially contained within the retroperitoneum leading to retroperitoneal hematoma. The initial rupture is associated with a severe, often focal, pain. If the hematoma stabilizes, the pain may subside. Patients with posterior rupture may attribute the initial pain to another cause and delay seeking medical attention.

Rupture of the anterior aortic wall may be contained for a brief period of time. The initial clinical manifestation will be abdominal pain, but rupture is likely to progress quickly to free intraperitoneal rupture with profound hemodynamic instability. Many of these patients succumb before they are able to be transported to the hospital.

Limb ischemia — AAA can present initially with symptoms of lower extremity ischemia due to embolism of thrombus or atherosclerotic debris from the aneurysm [35,54]. In association with abdominal/back/flank pain, distal embolism can be a sign of aneurysm rupture. Rarely, AAA can also present with acute aortic thrombosis leading to bilateral lower extremity ischemia, or rarely, spinal cord ischemia [55,56].

During AAA formation, thrombus builds up gradually along the wall as the aorta expands over time. This thrombus is typically laminated, well formed, and adherent to the wall of the aorta but may become disrupted as a result of more abrupt changes in aortic wall configuration (ie, rapid expansion), instrumentation, or trauma [35,54]. In some patients, aortic debris may be more friable and more prone to embolization. During AAA rupture, new thrombus may form in the region of the aortic tear, which can also embolize; however, distal embolization associated with AAA rupture may more often be related to aortic manipulation during open repair or instrumentation during endovascular repair [54]. (See "Complications of endovascular abdominal aortic repair", section on 'Extremity ischemia'.)

Distal embolization of atherothrombotic debris from the aneurysm as a source of symptoms of AAA is not well studied. In the available studies, up to one-third of the clinical manifestations associated with symptomatic AAA may be related to embolism, but the incidence varies widely [54]. This variability is likely due to the fact that AAA as the source for lower extremity ischemia is inferred from imaging studies that are typically obtained to evaluate progression of chronic lower extremity symptoms (eg, claudication, ischemic pain). In one retrospective review of 302 patients who underwent repair of AAA, 15 patients presented with distal embolization as the first manifestation of their AAA, which was limb-threatening in three patients [54]. In this study, the risk of embolization did not correlate with aneurysm diameter; 13 of 15 of the aneurysms that presented with embolization were <5.0 cm.

Thromboemboli from AAA can be single or multiple. The clinical manifestations of distal thromboembolism depend upon the size of the debris and number of embolic events. Clinical manifestations may not be apparent if smaller vessels are affected and arterial occlusion is well compensated, or the patients may present with chronic symptoms (eg, claudication). Alternatively, embolism may present acutely with painful, blue digits (blue toe syndrome) or with a painful, pulseless, cool extremity. The clinical manifestations of thromboembolic disease are discussed in detail elsewhere. (See "Thromboembolism from aortic plaque" and "Clinical features and diagnosis of acute lower extremity ischemia", section on 'Clinical presentations'.)

Cholesterol embolization as a manifestation of AAA is less common and most often occurs after instrumentation (eg, arteriography, cardiac catheterization) or aneurysm repair (open or endovascular). (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)", section on 'Clinical manifestations'.)

Other manifestations — Other manifestations of AAA include constitutional or systemic symptoms that may indicate the presence of an infected or inflammatory aneurysm, disseminated intravascular coagulation, and other more unusual manifestations of AAA rupture.

Symptoms of fever, malaise, and other vague abdominal symptoms, which are often chronic, may indicate a primary aortic infection with aneurysm formation or secondary infection of an established AAA. The clinical manifestations of infected aneurysms are discussed elsewhere. (See "Overview of infected (mycotic) arterial aneurysm".)

Symptoms of chronic abdominal pain and weight loss in association with AAA are suggestive of an inflammatory aneurysm, which affects approximately 5 to 10 percent of patients with AAA [57-60]. When AAA initially presents in this manner, the diagnosis is frequently confounded and delayed. Patients with the inflammatory variant are younger and more often symptomatic than patients with noninflammatory AAA. Patients with inflammatory AAA also have abnormalities of serum inflammatory markers, such as the erythrocyte sedimentation rate. Ureteral displacement or symptoms of ureteral obstruction can also occur due to the retroperitoneal inflammatory reaction (image 6). The incidence of rupture in patients with inflammatory AAA may be lower than with noninflammatory aneurysm. In a review that included 180 patients, rupture occurred in 4 percent of patients with inflammatory aneurysm compared with 20 percent of those with noninflammatory aneurysms [61].

Large or extensive AAAs may be associated with clinical manifestations of disseminated intravascular coagulation (DIC) causing hemorrhagic or thrombotic complications. The incidence of DIC is reported to be as high as 4 percent [62,63]. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults".)

Other clinical manifestations that can be associated with ruptured AAA but are less commonly considered related include:

Myocardial infarction related to acute blood loss, which occurs in up to 25 percent of patients [42].

Heart failure due to arteriovenous fistula as a result of rupture of the aorta into a surrounding venous structure such as the inferior vena cava (aortocaval fistula (image 7) [64]), iliac vein, or left renal vein. Hematuria or massive leg swelling and lower extremity cyanosis without distal ischemia can also be signs of aortocaval fistula [65]. (See "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Physical examination' and "Causes and pathophysiology of high-output heart failure", section on 'Causes and their mechanisms'.)

Groin pain or the sudden appearance of groin hernia (even incarceration) can occur related to a sudden increase in intra-abdominal pressure [66].

Upper gastrointestinal bleeding may be due to an aortoduodenal fistula (image 8). Although more commonly related to aortic graft repair, aortoduodenal fistula has been reported in primary infected aortic aneurysm. (See "Aortoenteric fistula: Recognition and management".)

Physical examination — In patients with risk factors for and symptoms suggestive of AAA, the physical examination seeks to identify clinical signs that support a diagnosis of AAA, or possibly suggest an alternative diagnosis.

Vital signs in symptomatic patients may be normal or demonstrate sinus tachycardia or moderate-to-severe hypotension. The degree of hypotension in patients with a posterior aortic wall rupture is likely to be less severe upon initial clinical presentation compared with patients who suffer from anterior aortic wall rupture [47]. Fever associated with AAA may indicate an infected aneurysm.

Abdominal palpation — The sole use of abdominal palpation cannot be relied upon to diagnose or exclude AAA. Although abdominal examination may reliably diagnose a large AAA (>5.5 cm), AAA is identified on physical examination alone in fewer than 50 percent of asymptomatic patients [67]. However, in patients with ruptured AAA, a pulsatile abdominal mass is present in up to 62 percent of patients and is an important sign for making a correct initial diagnosis [36]. Most patients with ruptured AAA also have some degree of abdominal distention and tenderness.

An abdominal examination focused specifically on the diagnosis of AAA is more likely to identify an aneurysm than a nonfocused examination. AAA most often occurs in the segment of aorta below the renal arteries (figure 1) [3]. Thus, with the patient supine on the examination table and garments removed from the abdomen, palpation of the abdominal aorta is performed by gently but deeply palpating the abdomen between the xiphoid and umbilicus to identify a widened pulse that suggests the presence of an aneurysm [68]. Many patients will experience mild tenderness with deep palpation of the aneurysm. Patients with inflammatory or infected aneurysms may exhibit a greater degree of tenderness to palpation. This finding should not be used to brand the aneurysm as symptomatic in order to justify treatment. It is important to note that palpation of the abdomen to detect AAA is safe and has never been reported to precipitate aortic rupture [68].

Detection of an AAA by abdominal palpation is more likely when the aneurysm is large and when abdominal girth is small (waist <40 inches). The sensitivity and specificity of abdominal palpation for AAA as related to AAA diameter and girth are illustrated in the following studies:

A systematic review evaluated 15 studies involving patients not previously known to have an AAA and who were screened with both abdominal palpation and ultrasound [68]. The sensitivity of abdominal palpation was 29 percent for AAA 3.0 to 3.9 cm in diameter, 50 percent for AAA 4.0 to 4.9 cm, and 76 percent for AAA 5.0 cm or greater.

In a later study of 200 patients, the overall sensitivity of abdominal palpation for detecting AAA was 68 percent and the specificity was 75 percent [19]. Sensitivity significantly improved with increasing aneurysm diameter (61 percent, 3.0 to 3.9 cm; 69 percent, 4.0 to 4.9 cm; 72 percent, 4.0 cm or larger; 82 percent >5.0 cm). The patient's abdominal circumference also affected the examination with an overall sensitivity of 91 percent for patients with a waistline <40 inches (100 cm) versus 53 percent for >40 inches (100 cm). For a waistline of <40 inches, abdominal palpation was 100 percent sensitive for detecting AAA ≥5.0 cm.

A prominent but normal-sized aorta or a nonvascular mass overlying an easily transmitted, palpable aortic pulse can be mistaken as AAA, particularly in thin patients. Patients with hypertension, a wide pulse pressure, or a tortuous aorta can also have prominent aortic pulsation that may be mistaken for an AAA. For these reasons, it is important to confirm AAA suspected on the basis of abdominal palpation. (See 'Diagnosis' below.)

Ecchymosis — Extensive retroperitoneal hematoma from ruptured AAA may lead to extravasation of blood into the subcutaneous tissues to produce flank ecchymosis (Grey-Turner sign) (image 9), periumbilical ecchymosis (Cullen's sign) (picture 1), ecchymosis of the proximal thigh (Fox's sign), and, in males, discoloration of the scrotum (Bryant's sign) [69]. Although these signs are indicative of retroperitoneal hematoma and may suggest ruptured AAA in patients with positive risk factors for AAA and appropriate clinical symptoms and signs, they are not specific [69]. Other pathologies that may lead to ecchymosis at these sites include acute pancreatitis, ruptured ectopic pregnancy, ruptured hepatocellular hematoma, and perinephric hematoma.

Vascular examination — A complete peripheral arterial examination should be performed looking for evidence of distal embolization or ischemia. The identification of other peripheral artery aneurysms (femoral, popliteal) on physical examination supports a diagnosis of AAA [28].

On vascular examination, palpation of the carotid and the upper extremity pulses should be symmetric; asymmetry may indicate aortic pathology in the chest (eg, aortic dissection). Femoral and pedal pulses may or may not be palpable depending upon the patient's blood pressure, the presence of peripheral artery disease, or thromboembolism. If lower extremity pulses are not easily identified, a handheld continuous wave Doppler can be used to locate them. If palpable or Dopplerable pulses in the feet are identified (dorsalis pedis, posterior tibial), it is helpful to mark the vessels for later comparison.

Laboratory studies and biomarkers

Patients with symptoms — Most patients who present with acute abdominal complaints will undergo initial laboratory testing that includes a complete blood count, electrolytes, blood urea nitrogen, and creatinine. Those who present in shock will undergo additional studies, including liver function tests, coagulation parameters, fibrinogen, fibrin split products, arterial blood gases, a lactate level, cardiac enzymes, and toxicology studies.

Anemia and metabolic acidosis may point toward acute blood loss as the cause of shock related to a ruptured AAA.

An elevated white blood cell count may indicate aortic infection or inflammation in patients who present with systemic manifestations (eg, fever, weight loss). Additional studies such as blood cultures and an erythrocyte sedimentation rate may be useful for distinguishing infected or inflammatory AAA from more common aneurysms. The erythrocyte sedimentation rate (ESR) can be markedly elevated in patients with inflammatory AAA.

Although most patients with ruptured AAA have normal coagulation tests, some may have coagulopathy [70]. Laboratory evidence of disseminated intravascular coagulation may be related to a large or extensive aneurysm, such as a thoracoabdominal aneurysm (image 10) [62,63]. (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults", section on 'Diagnostic evaluation'.)

Patients with no symptoms — There are no laboratory studies or biomarkers that identify the presence of AAA or progression with certainty. Although hemostatic markers may be elevated in patients with AAA, these are nonspecific and can be abnormal in a variety of other thrombotic conditions, and some also increase with age [71-76]. We do not obtain such laboratories as a means to screen or diagnose AAA; however, in the future, such biomarkers may become useful for following asymptomatic aneurysm.

A systematic review that compared hemostatic markers in patients with and without AAA found a significant association between AAA and elevated plasma levels of fibrinogen, D-dimer, and thrombin-antithrombin III complex [75]. These markers may reflect deposition and turnover of thrombus within the aneurysm sac (image 11). D-dimer concentration is strongly correlated with aneurysm diameter (r2 0.94). Serial D-dimer levels have been used to follow patients with known AAA [73,74]. In another study, myeloperoxidase and D-dimer independently correlated with AAA, which when combined yielded a diagnostic score that predicted rapid disease progression [71]. Elevated total homocysteine has also been associated with the presence of AAA in older men [77]. Similar to D-dimer, a positive correlation between increasing concentration and increasing aortic diameter has been identified. Other markers that have been studied include pro-brain natriuretic peptide (BNP) [78], interleukin 6 [79], and matrix metalloproteinase 9 [80].

In the Atherosclerosis Risk in Communities Study cohort, biomarkers of inflammation, hemostasis, thrombin generation, cardiac dysfunction, and vascular stiffness were measured in 15,411 individuals 45 to 64 years of age at risk for AAA [81]. Over a median of 22.5 years, 587 AAAs were identified with the majority occurring in smokers compared with never smokers (506 versus 71). The occurrence of AAA was determined through hospitalization records and, for those patients alive at the fifth and final visit, through abdominal ultrasound. White blood cell count, fibrinogen, D-dimer, troponin T, N-terminal pro-brain natriuretic peptide, and high-sensitivity C-reactive protein [CRP] were associated with an increase in incident AAA diagnosis during the follow-up period. After adjustment for other risk factors, the hazard ratios for AAA (smokers and nonsmokers) for 1, 2, 3, or 4 to 6 biomarkers compared with no biomarkers were 2.2, 3.3, 4.0, and 9.9, respectively, in the highest quartile of the six studied biomarkers. CRP was not associated with AAA in never smokers. There were no significant differences for men compared with women. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Aneurysm imaging'.)

DIAGNOSIS — Many patients with abdominal aortic aneurysm (AAA) and their physicians are unaware that an aneurysm is present. Because asymptomatic AAA can progress to rupture without any intervening symptoms, it is important that a diagnosis of AAA is considered in patients with the following:

No symptoms, but with risk factors for AAA. (See 'History' above.)

Physical examination consistent with AAA (eg, pulsatile abdominal mass) or other peripheral artery aneurysm (eg, femoral, popliteal). (See 'Physical examination' above.)

Clinical manifestations (eg, abdominal pain, thromboembolism, others) potentially representing a symptomatic AAA (nonruptured or ruptured). (See 'Symptoms' above.)

Although AAA may be suspected based upon these clinical features, a definitive diagnosis requires the demonstration of a focal, aortic dilation meeting the criteria for aneurysm (>1.5 times normal diameter) on imaging, or at the time of abdominal exploration. (See 'Aneurysm definition and anatomy' above.)

Although an imaging diagnosis is desirable, it is not an absolute requirement in the hemodynamically unstable patient with a known AAA who presents with classic symptoms and signs of rupture (abdominal/back/flank pain, hypotension, pulsatile mass). In this clinical scenario, patients who are candidates for repair are taken to the operating room for immediate management (intraoperative diagnosis). (See 'Imaging symptomatic patients' below.)

Any imaging study that demonstrates the focal dilation can be used to make a diagnosis, but abdominal ultrasound and computed tomography (CT) of the abdomen are the most useful. Each modality is sensitive and specific for establishing a diagnosis of AAA [82-84] but recommended under differing clinical circumstances (algorithm 1) depending upon the clinical presentation and the hemodynamic status of the patient. (See 'Imaging asymptomatic patients' below and 'Imaging symptomatic patients' below.)

Other imaging modalities (eg, magnetic resonance imaging) (image 12) are less often used in the initial evaluation of AAA but may play a role in selected patients, such as in the patient with known AAA (unrepaired or post-repair) who presents with new symptoms or in patients who cannot receive intravenous contrast [85,86]. Conventional arteriography, which demonstrates only the flow in the luminal channel often surrounded by luminal thrombus, is not accurate for determining the diameter of the aorta (image 13).

Imaging asymptomatic patients — For asymptomatic patients in whom a diagnosis of AAA is suspected on the basis of risk factors, abdominal palpation, or a prior imaging study suggesting AAA, abdominal ultrasound is recommended as the initial diagnostic modality (algorithm 1).

Ultrasound is noninvasive, inexpensive, and has a sensitivity of 98 percent and specificity of 99 percent for the diagnosis of AAA [82-84]. In prospective studies, ultrasound has been found to be a cost-effective screening tool for identifying small aneurysms (<4.0 cm) in patients with risk factors for AAA [87,88]. (See "Screening for abdominal aortic aneurysm".)

The routine sonographic evaluation of the aorta involves measuring the anteroposterior (AP), longitudinal (image 14), and transverse dimensions (image 15A-B) of the suprarenal, juxtarenal, pararenal, and infrarenal aorta. Given the correlation between AAA and iliac artery aneurysm, the examination should also include imaging of the iliac arteries. Patients are asked to fast prior to undergoing the examination to reduce the presence of overlying bowel gas that can obscure the aorta [89]. In approximately 1 to 2 percent of cases, the aorta cannot be adequately imaged because of technical difficulties (eg, bowel gas, aortic depth) [90].

The main limitation of abdominal ultrasound is that it is technician- and equipment-dependent [91]. If the ultrasound probe is not oriented perpendicular to the centerline, the AP diameter of the aorta may be overestimated [92]. There remains debate over the optimal method of measuring the diameter of the abdominal aorta (outer-to-outer, inner-to-inner, or leading-edge to leading-edge) [93-95]. A study that evaluated these measurement methods found that leading-edge measurements were the most reproducible, but all methods showed a high degree of variability [93]. The Society for Vascular Surgery (SVS) guidelines for the care of the patient with AAA suggest that the maximum aneurysm diameter should be based on an outer wall measurement perpendicular to the path of the aorta for CT scanning [96].

At times, ultrasound may not provide an accurate depiction of the iliac arteries, due to overlying loops of bowel [90]. If the ultrasound study is technically inadequate related to these factors, another imaging study should be obtained (typically computed tomography) (image 16).

In asymptomatic patients who have undergone a screening study or have been diagnosed with AAA incidentally as a result of another imaging study, it is important to determine if the aorta was adequately imaged. Some screening protocols provide only a limited evaluation of the aorta. If the abdominal aorta was not completely imaged, imaging did not include the iliac arteries, or the maximal AP diameter was not measured in a plane perpendicular to blood flow, a repeat study, typically another abdominal ultrasound, should be obtained.

Imaging symptomatic patients — Establishing a diagnosis of AAA in symptomatic patients is guided by the hemodynamic status of the patient (algorithm 1).

For hemodynamically unstable patients with a suspected rupture of a known AAA, imaging is highly desirable but is not absolutely required prior to intervention. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Initial management'.)

When ruptured AAA is suspected but the presence of an aneurysm is NOT known for certain, we suggest ultrasonography to confirm that an aneurysm exists, if immediately available. Ultrasound can be performed at the bedside or in the operating room while the patient is being resuscitated without causing an undue delay in care (algorithm 1). With routine use of the Focused Assessment with Sonography in Trauma (FAST) exam, many emergency department physicians are comfortable with the abdominal ultrasound exam and can quickly identify an abnormally enlarged aorta [25]. If the aneurysm is ruptured, retroperitoneal hematoma may also be seen, but the rupture site is not usually identified. When AAA is identified on ultrasound in a patient with hypotension and abdominal/flank/back pain, a presumptive diagnosis of ruptured AAA can be made.

For symptomatic patients suspected of having AAA who are hemodynamically stable, we recommend urgent abdominal CT, typically using intravenous contrast, rather than ultrasound (algorithm 1). If there is a concern for contrast-induced nephropathy, a noncontrast CT scan may be sufficient to provide additional anatomic details. Abdominal CT has the advantage of evaluating the abdomen in more detail, which is necessary for differentiating ruptured from nonruptured aneurysm, and CT is better than ultrasound for evaluating suprarenal aneurysms (image 17) [97-100]. Abdominal CT also readily identifies other abdominal pathologies as a potential cause of symptoms [97]. Abdominal CT defines the extent of the aneurysm (outer-wall-to-outer-wall measurement perpendicular to the path of the aneurysm), providing important anatomic information by which to plan urgent AAA repair, and determines whether the aneurysm is suited to endovascular aneurysm repair (EVAR) (image 18) [97-100]. Disadvantages of CT compared with ultrasonography are the potential to overestimate the aortic diameter, greater cost, the requirement for intravenous contrast (when CT arteriography is required), and the cumulative risk of radiation with repeated scans in patients with known AAA [85]. AAA diameter on CT scan should be measured perpendicular to the centerline of the aorta, to avoid overestimation, which can be obtained by using orthogonal measurements or facilitated with semi-automated software [101,102].

Intravenous contrast is generally not needed to establish a diagnosis of ruptured AAA (rAAA) [103]. However, many vascular centers use abdominal CT with intravenous contrast or CT angiography with three-dimensional reconstruction for suspected rAAA in anticipation of potential endovascular repair. However, in the setting of volume depletion, the risk for renal dysfunction is increased. (See "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management".)

Once the presence of AAA is confirmed on CT, aortic anatomy must be carefully evaluated to determine if the aneurysm is ruptured or has signs of instability that may indicate impending rupture. The maximal aortic diameter should also be determined and compared with prior studies, if available, to identify patients who might have a rapidly expanding aneurysm (0.5 cm/year). In addition, the aortic wall should be evaluated to determine whether the aneurysm appears to be infected or is consistent with an inflammatory aneurysm. Lastly, for symptomatic patients in whom AAA is present but clearly not ruptured, a judgment must be made as to whether the aneurysm is the most likely cause for the symptoms in the context of other pathology that may be present on imaging. These issues are discussed more fully below.

Ruptured versus nonruptured AAA — Differentiating a symptomatic but nonruptured AAA from an aneurysm that is about to rupture or is in the process of rupturing is critical and is accomplished using CT of the abdomen, which is highly accurate [104]. Signs on CT associated with ruptured AAA and AAA that may be unstable and at risk for impending rupture are discussed below (table 1). Although rupture is unlikely in patients who have none of the features described, symptomatic patients with AAA, particularly in those with moderate- to large-sized aneurysm, are typically admitted and observed when another etiology cannot be determined. The AAA should be considered a "symptomatic AAA" until proven otherwise. The management of symptomatic, nonruptured AAA is discussed elsewhere. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Introduction'.)

In the setting of ruptured AAA, the risk for contrast-induced nephropathy is increased in the setting of volume depletion when intravenous contrast is used. (See 'Imaging asymptomatic patients' above and "Prevention of contrast-associated acute kidney injury related to angiography".)

In patients with acute symptoms lasting more than one hour, findings of AAA rupture on CT scan are usually obvious [105]. CT scan findings consistent with ruptured AAA include the following:

Retroperitoneal hematoma (image 19 and image 20)

Indistinct aortic wall (image 21)

Retroperitoneal stranding (image 21)

Loss of the fat plane between the aorta and surrounding tissue (image 22)

Extravasation of intravenous contrast outside the aorta (eg, into retroperitoneum, into a venous structure, into the bowel lumen) (image 23 and image 8 and image 7)

Some patients with AAA and abdominal pain have CT scans that fail to show signs of overt aortic rupture. Other findings on abdominal CT that may be associated with potentially unstable aneurysms or possible "impending rupture" include the following [97,106-110]:

A crescent sign of layering hematoma within the aorta (image 24)

Aortic blebs that bulge from the surface of the aorta (image 25)

"Draping" of the aorta over a vertebral body

Irregularity of the aortic wall

Breaks in the calcification of the aortic wall (image 20)

Localized areas of higher attenuation within mural thrombus (image 22)

These imaging abnormalities were initially described in a retrospective review of patients with ruptured AAA compared with nonruptured AAA. A later prospective study found only a 7 percent positive predictive value for subsequent AAA rupture using these findings [106]. Although there are no specific CT scan findings that definitively predict rupture, these signs of "impending rupture" in combination with an AAA of >5 cm may indicate an aneurysm that is rapidly changing anatomically [111]. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm", section on 'Impending rupture'.)

Are symptoms related to AAA? — In patients with symptomatic but clearly not ruptured AAA, the question always arises as to whether the aneurysm is the source of the symptoms. Imaging that demonstrates a pathology that is more consistent with the patient's symptoms (eg, renal colic) may indicate that the AAA is the incidental finding.

However, if the presenting symptoms are not typical for other pathologies identified on CT, or another etiology cannot be clearly determined, and the symptoms are consistent with those associated with AAA, then the patient is regarded as having a symptomatic AAA until proven otherwise. This determination usually requires admission to the hospital and observation, while undergoing further studies. In some patients with symptomatic, nonruptured AAA in the setting of hypertension, blood pressure control may sometimes alleviate pain. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Introduction'.)

For patients who present with lower extremity embolism, features of the aorta on CT that suggest that the aneurysm may be the source of embolism include an irregular luminal surface, multiple aortic lumens, heterogeneity of the aortic thrombus, calcification within the aortic thrombus, and fissures extending from the lumen into the aortic thrombus [54]. In addition, the presence of typical features of embolization in the distal vasculature in the absence of atherosclerotic peripheral artery disease in a patient with AAA and no other proximal source for embolus (eg, atrial fibrillation) suggests that the aneurysm is the source.

Infected versus inflammatory AAA — Inflammation is a common component of most aortic aneurysms, but the typical AAA must be distinguished from aneurysms that are infected, as well as a distinct clinical entity called an inflammatory aneurysm [5,58]. The management of these aneurysm subtypes differs from noninfected, noninflammatory AAAs.

Although clinical features of nonspecific abdominal pain associated with systemic symptoms (eg, fever, malaise) and a pulsatile abdominal mass may suggest a diagnosis of an infected or inflammatory AAA, specific features on CT imaging make the distinction.

Primary bacterial infection of the aortic wall, which can lead to rapid aortic expansion, is a rare cause of AAA. Preexisting AAA can also become secondarily infected [5,112]. Findings on CT (image 26) suggestive of an infected aneurysm include the following [113-119], while other clinical features and the diagnosis of infected aneurysm is discussed in detail elsewhere (see "Overview of infected (mycotic) arterial aneurysm"):

Saccular, eccentric, or multilobulated AAA

Soft tissue inflammation surrounding the aorta

AAA with intramural air, or air collection around the vessel

Perivascular fluid collection

Inflammatory abdominal aortic aneurysm (IAAA), which accounts for 2 to 10 percent of AAAs, is characterized by thickening of the adventitia due to marked inflammation [57,59,120-122]. Radiologically, an IAAA is defined as an AAA with a ≥1-cm thick inflammatory rind surrounding the aorta on abdominal CT (image 27) [57]. The periaortic soft tissue density may enhance when intravenous contrast is administered, and the retroperitoneal tissue planes between the aorta and retroperitoneum are indistinct. Other features consistent with IAAA are fibrosis of the adjacent retroperitoneum, adherence of the anterior aspect of the IAAA to adjacent structures (eg, duodenum, ureters), and medial deviation of the ureters (image 6). Inflammatory aneurysms are not associated with periaortic air or fluid, and, although inflamed, these aneurysms are not infected. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Introduction'.)

DIFFERENTIAL DIAGNOSIS — Aortic pathologies that can produce symptoms, particularly abdominal or flank pain, similar to abdominal aortic aneurysm (AAA) include aortic dissection and aortic pseudoaneurysm due to erosion of ulcerated plaque. The pain from aortic dissection is described as searing or tearing and often begins in the chest or back, migrating to the abdomen over time. Aortic dissection may affect arch vessels, leading to other symptoms (cerebral embolism, upper extremity ischemia) that will not be present in patients with AAA. In patients with ulcerated aortic plaque, the symptoms may be indistinguishable from those of ruptured AAA. Visceral aneurysm rupture may also mimic ruptured abdominal aortic aneurysm [123]. (See "Clinical features and diagnosis of acute aortic dissection".)

Aortic imaging will differentiate these etiologies from AAA; however, imaging protocols vary. Thus, if there is any question that aortic pathology may involve the thoracic aorta, simultaneous chest and abdominal imaging should be obtained rather than abdominal imaging alone. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Diagnosis' and "Clinical features and diagnosis of acute aortic dissection", section on 'Diagnosis'.)

The pain from symptomatic or ruptured AAA can mimic many other conditions such as renal colic, myocardial ischemia, diverticulitis, pancreatitis, mesenteric ischemia, and biliary tract disease, to name a few. The general approach to abdominal pain and the extensive differential diagnosis of abdominal pain are discussed elsewhere. (See 'Ruptured AAA' above and "Evaluation of the adult with abdominal pain" and "Causes of abdominal pain in adults".)

For patients with risk factors, abdominal symptoms, or a physical examination that in any way suggests AAA, the most practical approach is expedient abdominal imaging [41], even though the patient may have a history of another medical condition that could account for their symptoms. In a study of 152 patients, ruptured AAA was initially misdiagnosed as renal colic, perforated viscus, diverticulitis, gastrointestinal hemorrhage, or ischemic bowel in 30 percent of the patients, based upon clinical symptoms and signs alone [37]. With imaging, the absence of aortic dilation rules out AAA. If AAA is present but clearly not ruptured, a determination will need to be made whether or not the symptoms are due to the AAA. (See 'Are symptoms related to AAA?' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Aortic and other peripheral aneurysms".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Abdominal aortic aneurysm (The Basics)")

Beyond the Basics topics (see "Patient education: Abdominal aortic aneurysm (Beyond the Basics)")


Abdominal aortic aneurysm definition – Abdominal aortic aneurysm (AAA) is defined as a focal, full-thickness dilation of the aorta that is more than 50 percent greater than its normal diameter. The abdominal aorta below the renal arteries (infrarenal) is the most common site for aortic aneurysm. In the infrarenal aorta, a maximum diameter ≥3.0 cm is aneurysmal in the majority of patients. (See 'Aneurysm definition and anatomy' above.)

Medical history and risk factors – The patient's medical history identifies the risk factors for developing AAA and risk factors associated with rupture. The patient and any caregivers should be asked whether a diagnosis of AAA has been established in the past or if a prior AAA repair has been performed. The history may also help determine if clinical manifestations are likely related to a possible AAA versus another medical condition. Symptoms potentially related to AAA (eg, pain) can mimic those of many other diseases; however, in patients known to have or subsequently shown to have AAA, symptoms are presumed to be due to the aneurysm until unequivocally proven otherwise. (See 'History' above and 'Are symptoms related to AAA?' above.)

Clinical features  

Asymptomatic AAA – Most patients with AAA do not have any symptoms. Asymptomatic AAA may be discovered because of screening in patients with risk factors for AAA, on routine physical examination, or on imaging studies to evaluate an unrelated complaint. (See 'Asymptomatic AAA' above.)

Symptomatic AAA – Symptoms from AAA may occur if the aneurysm is expanding rapidly, has become large enough to compress surrounding structures, is an inflammatory or infectious aneurysm, or has ruptured. Patients with symptomatic AAA most commonly present with abdominal, back, or flank pain, which may or may not be associated with AAA rupture. The classic triad of acute abdominal pain, abdominal distention, and hemodynamic instability is present in approximately 50 percent of patients with ruptured AAA. AAA can also present with other clinical manifestations such as limb ischemia (acute or chronic), or other systemic manifestations (fever, malaise). (See 'Symptomatic (nonruptured) AAA' above and 'Ruptured AAA' above and 'Symptoms' above.)

Diagnosis – Although AAA may be suspected based upon risk factors and clinical features, including abdominal palpation or other physical examination findings, a definitive diagnosis requires abdominal imaging studies that demonstrate a focal, aortic dilation meeting the criteria for aneurysm (>1.5 times normal diameter). Sole use of abdominal palpation cannot be relied upon to diagnose or exclude AAA and is affected by the abdominal girth of the patient. (See 'Abdominal palpation' above and 'Diagnosis' above.)

Abdominal imaging – Abdominal ultrasound and computed tomography of the abdomen are both highly sensitive and specific for diagnosing AAA but are recommended under differing clinical circumstances (algorithm 1) depending upon the presence of symptoms and the hemodynamic status of the patient.

Asymptomatic AAA – For most asymptomatic patients, we recommend abdominal ultrasound as the initial diagnostic modality. Ultrasound is noninvasive and cost effective for diagnosing AAA in asymptomatic patients. (See 'Imaging asymptomatic patients' above.)

Symptomatic AAA

-Hemodynamically stable – For most symptomatic patients who are hemodynamically stable, we recommend computed tomography (CT) of the abdomen as the initial diagnostic modality. Abdominal CT provides additional anatomic detail that identifies ruptured aneurysm, infected aneurysm, inflammatory aneurysm, and other features that are important in the subsequent management of symptomatic AAA. Abdominal CT may also identify other pathologies that may be the source of symptoms. (See 'Imaging symptomatic patients' above.)

-Hemodynamically unstable – For symptomatic patients who are hemodynamically unstable and suspected of having ruptured AAA, where a diagnosis of AAA is NOT previously known, we suggest a focused ultrasonography exam (bedside, operating room) to confirm that an aneurysm exists prior to exploration, provided it is immediately available. Patients with a known AAA, who present with classic symptoms and signs of rupture, are generally taken for repair without preoperative imaging. (See 'Imaging symptomatic patients' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge Emile R Mohler, III, MD, now deceased, who contributed to an earlier version of this topic review. UpToDate also acknowledges Dr. Mohler's work as our Section Editor for Vascular Medicine.

The editorial staff also acknowledge Robert W Thompson, MD, who contributed to an earlier version of this topic.

  1. Shreibati JB, Baker LC, Hlatky MA, Mell MW. Impact of the Screening Abdominal Aortic Aneurysms Very Efficiently (SAAAVE) Act on abdominal ultrasonography use among Medicare beneficiaries. Arch Intern Med 2012; 172:1456.
  2. Johnston KW, Rutherford RB, Tilson MD, et al. Suggested standards for reporting on arterial aneurysms. Subcommittee on Reporting Standards for Arterial Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and North American Chapter, International Society for Cardiovascular Surgery. J Vasc Surg 1991; 13:452.
  3. Chaikof EL, Brewster DC, Dalman RL, et al. The care of patients with an abdominal aortic aneurysm: the Society for Vascular Surgery practice guidelines. J Vasc Surg 2009; 50:S2.
  4. Wanhainen A. How to define an abdominal aortic aneurysm--influence on epidemiology and clinical practice. Scand J Surg 2008; 97:105.
  5. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006; 113:e463.
  6. Wanhainen A, Themudo R, Ahlström H, et al. Thoracic and abdominal aortic dimension in 70-year-old men and women--a population-based whole-body magnetic resonance imaging (MRI) study. J Vasc Surg 2008; 47:504.
  7. Jongkind V, Yeung KK, Akkersdijk GJ, et al. Juxtarenal aortic aneurysm repair. J Vasc Surg 2010; 52:760.
  8. Martin GH, O'Hara PJ, Hertzer NR, et al. Surgical repair of aneurysms involving the suprarenal, visceral, and lower thoracic aortic segments: early results and late outcome. J Vasc Surg 2000; 31:851.
  9. Altobelli E, Rapacchietta L, Profeta VF, Fagnano R. Risk Factors for Abdominal Aortic Aneurysm in Population-Based Studies: A Systematic Review and Meta-Analysis. Int J Environ Res Public Health 2018; 15.
  10. Singh K, Bønaa KH, Jacobsen BK, et al. Prevalence of and risk factors for abdominal aortic aneurysms in a population-based study : The Tromsø Study. Am J Epidemiol 2001; 154:236.
  11. Forsdahl SH, Singh K, Solberg S, Jacobsen BK. Risk factors for abdominal aortic aneurysms: a 7-year prospective study: the Tromsø Study, 1994-2001. Circulation 2009; 119:2202.
  12. Kent KC, Zwolak RM, Egorova NN, et al. Analysis of risk factors for abdominal aortic aneurysm in a cohort of more than 3 million individuals. J Vasc Surg 2010; 52:539.
  13. Joergensen TM, Houlind K, Green A, Lindholt JS. Abdominal aortic diameter is increased in males with a family history of abdominal aortic aneurysms: results from the Danish VIVA-trial. Eur J Vasc Endovasc Surg 2014; 48:669.
  14. Norrgård O, Angqvist KA, Fodstad H, et al. Co-existence of abdominal aortic aneurysms and intracranial aneurysms. Acta Neurochir (Wien) 1987; 87:34.
  15. Kim DH, Van Ginhoven G, Milewicz DM. Familial aggregation of both aortic and cerebral aneurysms: evidence for a common genetic basis in a subset of families. Neurosurgery 2005; 56:655.
  16. Dillavou ED, Muluk SC, Makaroun MS. A decade of change in abdominal aortic aneurysm repair in the United States: Have we improved outcomes equally between men and women? J Vasc Surg 2006; 43:230.
  17. Giles KA, Pomposelli F, Hamdan A, et al. Decrease in total aneurysm-related deaths in the era of endovascular aneurysm repair. J Vasc Surg 2009; 49:543.
  18. Guirguis-Blake JM, Beil TL, Senger CA, Whitlock EP. Ultrasonography screening for abdominal aortic aneurysms: a systematic evidence review for the U.S. Preventive Services Task Force. Ann Intern Med 2014; 160:321.
  19. Fink HA, Lederle FA, Roth CS, et al. The accuracy of physical examination to detect abdominal aortic aneurysm. Arch Intern Med 2000; 160:833.
  20. van Walraven C, Wong J, Morant K, et al. Incidence, follow-up, and outcomes of incidental abdominal aortic aneurysms. J Vasc Surg 2010; 52:282.
  21. van Walraven C, Wong J, Morant K, et al. The influence of incidental abdominal aortic aneurysm monitoring on patient outcomes. J Vasc Surg 2011; 54:1290.
  22. Muzaffar R, Kudva G, Nguyen NC, Osman MM. Incidental diagnosis of thrombus within an aneurysm on 18F-FDG PET/CT: frequency in 926 patients. J Nucl Med 2011; 52:1408.
  23. Lanitis S, Zacharioudakis C, Zafeiriadou P, et al. Incidental findings in trauma patients during focused assessment with sonography for trauma. Am Surg 2012; 78:366.
  24. Gordon JR, Wahls T, Carlos RC, et al. Failure to recognize newly identified aortic dilations in a health care system with an advanced electronic medical record. Ann Intern Med 2009; 151:21.
  25. Lee SI, Mueller PR, Thrall JH. Re: "managing incidental findings on abdominal CT: White Paper of the ACR Incidental Findings Committee". J Am Coll Radiol 2011; 8:e3.
  26. van Walraven C, Wong J, Morant K, et al. Radiographic monitoring of incidental abdominal aortic aneurysms: a retrospective population-based cohort study. Open Med 2011; 5:e67.
  27. Lawrence PF, Gazak C, Bhirangi L, et al. The epidemiology of surgically repaired aneurysms in the United States. J Vasc Surg 1999; 30:632.
  28. Diwan A, Sarkar R, Stanley JC, et al. Incidence of femoral and popliteal artery aneurysms in patients with abdominal aortic aneurysms. J Vasc Surg 2000; 31:863.
  29. Sullivan CA, Rohrer MJ, Cutler BS. Clinical management of the symptomatic but unruptured abdominal aortic aneurysm. J Vasc Surg 1990; 11:799.
  30. Nevala T, Perälä J, Aho P, et al. Outcome of symptomatic, unruptured abdominal aortic aneurysms after endovascular repair with the Zenith stent-graft system. Scand Cardiovasc J 2008; 42:178.
  31. Franks S, Lloyd G, Fishwick G, et al. Endovascular treatment of ruptured and symptomatic abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 2006; 31:345.
  32. Antonello M, Lepidi S, Kechagias A, et al. Glasgow aneurysm score predicts the outcome after emergency open repair of symptomatic, unruptured abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 2007; 33:272.
  33. Shifrin EG, Pizov R, Perel A, et al. Urgent abdominal aortic aneurysm repair in patients over the age 80. J Cardiovasc Surg (Torino) 1987; 28:167.
  34. Cambria RA, Gloviczki P, Stanson AW, et al. Symptomatic, nonruptured abdominal aortic aneurysms: are emergent operations necessary? Ann Vasc Surg 1994; 8:121.
  35. Nigro G, Giovannacci L, Engelberger S, et al. The challenge of posttraumatic thrombus embolization from abdominal aortic aneurysm causing acute limb ischemia. J Vasc Surg 2011; 54:840.
  36. Azhar B, Patel SR, Holt PJ, et al. Misdiagnosis of ruptured abdominal aortic aneurysm: systematic review and meta-analysis. J Endovasc Ther 2014; 21:568.
  37. Marston WA, Ahlquist R, Johnson G Jr, Meyer AA. Misdiagnosis of ruptured abdominal aortic aneurysms. J Vasc Surg 1992; 16:17.
  38. Powell JT, Brown LC, Greenhalgh RM, Thompson SG. The rupture rate of large abdominal aortic aneurysms: is this modified by anatomical suitability for endovascular repair? Ann Surg 2008; 247:173.
  39. Hallett JW Jr, Marshall DM, Petterson TM, et al. Graft-related complications after abdominal aortic aneurysm repair: reassurance from a 36-year population-based experience. J Vasc Surg 1997; 25:277.
  40. Jones JE, Atkins MD, Brewster DC, et al. Persistent type 2 endoleak after endovascular repair of abdominal aortic aneurysm is associated with adverse late outcomes. J Vasc Surg 2007; 46:1.
  41. Akkersdijk GJ, van Bockel JH. Ruptured abdominal aortic aneurysm: initial misdiagnosis and the effect on treatment. Eur J Surg 1998; 164:29.
  42. Gloviczki P, Pairolero PC, Mucha P Jr, et al. Ruptured abdominal aortic aneurysms: repair should not be denied. J Vasc Surg 1992; 15:851.
  43. Muluk SC, Gertler JP, Brewster DC, et al. Presentation and patterns of aortic aneurysms in young patients. J Vasc Surg 1994; 20:880.
  44. Kiell CS, Ernst CB. Advances in management of abdominal aortic aneurysm. Adv Surg 1993; 26:73.
  45. Tsai YW, Blodgett JB, Wilson GS, et al. Ruptured abdominal aortic aneurysm. Pathognomonic triad. Vasc Surg 1973; 7:232.
  46. Rinckenbach S, Albertini JN, Thaveau F, et al. Prehospital treatment of infrarenal ruptured abdominal aortic aneurysms: a multicentric analysis. Ann Vasc Surg 2010; 24:308.
  47. Assar AN, Zarins CK. Ruptured abdominal aortic aneurysm: a surgical emergency with many clinical presentations. Postgrad Med J 2009; 85:268.
  48. Robertson GS, Macpherson DS. Aortic aneurysm presenting as deep venous thrombosis. Lancet 1988; 1:877.
  49. Moore RD, Rutter ED, Zapko DR, et al. Abdominal aortic aneurysm with inferior vena cava compression in association with deep venous thrombosis. Am J Med Sci 2013; 346:521.
  50. Singla V, Virmani V, Modi M, et al. Chronic rupture of abdominal aortic aneurysm with vertebral erosion: an uncommon but important cause of back pain. Ann Vasc Surg 2014; 28:1931.e1.
  51. Erhart P, Grond-Ginsbach C, Hakimi M, et al. Finite element analysis of abdominal aortic aneurysms: predicted rupture risk correlates with aortic wall histology in individual patients. J Endovasc Ther 2014; 21:556.
  52. Fillinger MF, Marra SP, Raghavan ML, Kennedy FE. Prediction of rupture risk in abdominal aortic aneurysm during observation: wall stress versus diameter. J Vasc Surg 2003; 37:724.
  53. Vorp DA, Raghavan ML, Webster MW. Mechanical wall stress in abdominal aortic aneurysm: influence of diameter and asymmetry. J Vasc Surg 1998; 27:632.
  54. Baxter BT, McGee GS, Flinn WR, et al. Distal embolization as a presenting symptom of aortic aneurysms. Am J Surg 1990; 160:197.
  55. Hirose H, Takagi M, Hashiyada H, et al. Acute occlusion of an abdominal aortic aneurysm--case report and review of the literature. Angiology 2000; 51:515.
  56. Wong SS, Roche-Nagle G, Oreopoulos G. Acute thrombosis of an abdominal aortic aneurysm presenting as cauda equina syndrome. J Vasc Surg 2013; 57:218.
  57. Pennell RC, Hollier LH, Lie JT, et al. Inflammatory abdominal aortic aneurysms: a thirty-year review. J Vasc Surg 1985; 2:859.
  58. Rasmussen TE, Hallett JW Jr. Inflammatory aortic aneurysms. A clinical review with new perspectives in pathogenesis. Ann Surg 1997; 225:155.
  59. Cavallaro A, Sapienza P, di Marzo L, et al. [Inflammatory aneurysm of the abdominal aorta. Study of 355 patients with aortic aneurysm]. Recenti Prog Med 2001; 92:269.
  60. Hellmann DB, Grand DJ, Freischlag JA. Inflammatory abdominal aortic aneurysm. JAMA 2007; 297:395.
  61. Lindblad B, Almgren B, Bergqvist D, et al. Abdominal aortic aneurysm with perianeurysmal fibrosis: experience from 11 Swedish vascular centers. J Vasc Surg 1991; 13:231.
  62. Aboulafia DM, Aboulafia ED. Aortic aneurysm-induced disseminated intravascular coagulation. Ann Vasc Surg 1996; 10:396.
  63. Fisher DF Jr, Yawn DH, Crawford ES. Preoperative disseminated intravascular coagulation associated with aortic aneurysms. A prospective study of 76 cases. Arch Surg 1983; 118:1252.
  64. Nakazawa S, Mohara J, Takahashi T, et al. Aortocaval fistula associated with ruptured abdominal aortic aneurysm. Ann Vasc Surg 2014; 28:1793.e5.
  65. Salo JA, Verkkala KA, Ala-Kulju KV, et al. Hematuria is an indication of rupture of an abdominal aortic aneurysm into the vena cava. J Vasc Surg 1990; 12:41.
  66. Khaw H, Sottiurai VS, Craighead CC, Batson RC. Ruptured abdominal aortic aneurysm presenting as symptomatic inguinal mass: report of six cases. J Vasc Surg 1986; 4:384.
  67. Lederle FA, Johnson GR, Wilson SE, et al. Yield of repeated screening for abdominal aortic aneurysm after a 4-year interval. Aneurysm Detection and Management Veterans Affairs Cooperative Study Investigators. Arch Intern Med 2000; 160:1117.
  68. Lederle FA, Simel DL. The rational clinical examination. Does this patient have abdominal aortic aneurysm? . JAMA 1999; 281:77.
  69. David M, Pelberg J, Kuntz C. Grey Turner's sign. QJM 2013; 106:481.
  70. Kordzadeh A, Parsa AD, Askari A, et al. Presenting Baseline Coagulation of Infra Renal Ruptured Abdominal Aortic Aneurysm: A Systematic Review and Pooled Analysis. Eur J Vasc Endovasc Surg 2016; 51:682.
  71. Zagrapan B, Eilenberg W, Prausmueller S, et al. A Novel Diagnostic and Prognostic Score for Abdominal Aortic Aneurysms Based on D-Dimer and a Comprehensive Analysis of Myeloid Cell Parameters. Thromb Haemost 2019; 119:807.
  72. Isaia G, Greppi F, Ausiello L, et al. D-dimer plasma concentrations in an older hospitalized population. J Am Geriatr Soc 2011; 59:2385.
  73. Diehm N, Baumgartner I. D-dimer measurement: a useful prognostic marker in surveillance of patients with abdominal aortic aneurysm? Eur Heart J 2011; 32:258.
  74. Golledge J, Muller R, Clancy P, et al. Evaluation of the diagnostic and prognostic value of plasma D-dimer for abdominal aortic aneurysm. Eur Heart J 2011; 32:354.
  75. Sidloff DA, Stather PW, Choke E, et al. A systematic review and meta-analysis of the association between markers of hemostasis and abdominal aortic aneurysm presence and size. J Vasc Surg 2014; 59:528.
  76. Stather PW, Sidloff DA, Dattani N, et al. Meta-analysis and meta-regression analysis of biomarkers for abdominal aortic aneurysm. Br J Surg 2014; 101:1358.
  77. Wong YY, Golledge J, Flicker L, et al. Plasma total homocysteine is associated with abdominal aortic aneurysm and aortic diameter in older men. J Vasc Surg 2013; 58:364.
  78. Acosta S, Gottsäter A, Engström G, et al. B-type natriuretic peptide for prediction of incident clinically significant abdominal aortic aneurysm: A population-based prospective study. Vasc Med 2018; 23:46.
  79. Takagi H, Watanabe T, Mizuno Y, et al. Circulating interleukin-6 levels are associated with abdominal aortic aneurysm presence: a meta-analysis and meta-regression of case-control studies. Ann Vasc Surg 2014; 28:1913.
  80. Li T, Jiang B, Li X, et al. Serum matrix metalloproteinase-9 is a valuable biomarker for identification of abdominal and thoracic aortic aneurysm: a case-control study. BMC Cardiovasc Disord 2018; 18:202.
  81. Folsom AR, Yao L, Alonso A, et al. Circulating Biomarkers and Abdominal Aortic Aneurysm Incidence: The Atherosclerosis Risk in Communities (ARIC) Study. Circulation 2015; 132:578.
  82. LaRoy LL, Cormier PJ, Matalon TA, et al. Imaging of abdominal aortic aneurysms. AJR Am J Roentgenol 1989; 152:785.
  83. American College of Cardiology Foundation (ACCF), American College of Radiology (ACR), American Institute of Ultrasound in Medicine (AIUM), et al. ACCF/ACR/AIUM/ASE/ASN/ICAVL/SCAI/SCCT/SIR/SVM/SVS/SVU [corrected] 2012 appropriate use criteria for peripheral vascular ultrasound and physiological testing part I: arterial ultrasound and physiological testing: a report of the American College of Cardiology Foundation appropriate use criteria task force, American College of Radiology, American Institute of Ultrasound in Medicine, American Society of Echocardiography, American Society of Nephrology, Intersocietal Commission for the Accreditation of Vascular Laboratories, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, Society for Interventional Radiology, Society for Vascular Medicine, Society for Vascular Surgery, [corrected] and Society for Vascular Ultrasound. [corrected]. J Am Coll Cardiol 2012; 60:242.
  84. Lederle FA, Johnson GR, Wilson SE, et al. Relationship of age, gender, race, and body size to infrarenal aortic diameter. The Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Investigators. J Vasc Surg 1997; 26:595.
  85. Ernst CB. Abdominal aortic aneurysm. N Engl J Med 1993; 328:1167.
  86. Petersen MJ, Cambria RP, Kaufman JA, et al. Magnetic resonance angiography in the preoperative evaluation of abdominal aortic aneurysms. J Vasc Surg 1995; 21:891.
  87. Ashton HA, Buxton MJ, Day NE, et al. The Multicentre Aneurysm Screening Study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial. Lancet 2002; 360:1531.
  88. Lee TY, Korn P, Heller JA, et al. The cost-effectiveness of a "quick-screen" program for abdominal aortic aneurysms. Surgery 2002; 132:399.
  89. Scott RA, Ashton HA, Kay DN. Abdominal aortic aneurysm in 4237 screened patients: prevalence, development and management over 6 years. Br J Surg 1991; 78:1122.
  90. Beales L, Wolstenhulme S, Evans JA, et al. Reproducibility of ultrasound measurement of the abdominal aorta. Br J Surg 2011; 98:1517.
  91. Chiu KW, Ling L, Tripathi V, et al. Ultrasound measurement for abdominal aortic aneurysm screening: a direct comparison of the three leading methods. Eur J Vasc Endovasc Surg 2014; 47:367.
  92. Schermerhorn M. A 66-year-old man with an abdominal aortic aneurysm: review of screening and treatment. JAMA 2009; 302:2015.
  93. Gürtelschmid M, Björck M, Wanhainen A. Comparison of three ultrasound methods of measuring the diameter of the abdominal aorta. Br J Surg 2014; 101:633.
  94. Hartshorne TC, McCollum CN, Earnshaw JJ, et al. Ultrasound measurement of aortic diameter in a national screening programme. Eur J Vasc Endovasc Surg 2011; 42:195.
  95. Meecham L, Evans R, Buxton P, et al. Abdominal Aortic Aneurysm Diameters: A Study on the Discrepancy between Inner to Inner and Outer to Outer Measurements. Eur J Vasc Endovasc Surg 2015; 49:28.
  96. Chaikof EL, Dalman RL, Eskandari MK, et al. The Society for Vascular Surgery practice guidelines on the care of patients with an abdominal aortic aneurysm. J Vasc Surg 2018; 67:2.
  97. Siegel CL, Cohan RH, Korobkin M, et al. Abdominal aortic aneurysm morphology: CT features in patients with ruptured and nonruptured aneurysms. AJR Am J Roentgenol 1994; 163:1123.
  98. Isselbacher EM. Thoracic and abdominal aortic aneurysms. Circulation 2005; 111:816.
  99. Litmanovich D, Bankier AA, Cantin L, et al. CT and MRI in diseases of the aorta. AJR Am J Roentgenol 2009; 193:928.
  100. Ten Bosch JA, Teijink JA, Willigendael EM, Prins MH. Endovascular aneurysm repair is superior to open surgery for ruptured abdominal aortic aneurysms in EVAR-suitable patients. J Vasc Surg 2010; 52:13.
  101. Kontopodis N, Metaxa E, Gionis M, et al. Discrepancies in determination of abdominal aortic aneurysms maximum diameter and growth rate, using axial and orhtogonal computed tomography measurements. Eur J Radiol 2013; 82:1398.
  102. Mora C, Marcus C, Barbe C, et al. Measurement of maximum diameter of native abdominal aortic aneurysm by angio-CT: reproducibility is better with the semi-automated method. Eur J Vasc Endovasc Surg 2014; 47:139.
  103. Mehta M, Taggert J, Darling RC 3rd, et al. Establishing a protocol for endovascular treatment of ruptured abdominal aortic aneurysms: outcomes of a prospective analysis. J Vasc Surg 2006; 44:1.
  104. Biancari F, Paone R, Venermo M, et al. Diagnostic accuracy of computed tomography in patients with suspected abdominal aortic aneurysm rupture. Eur J Vasc Endovasc Surg 2013; 45:227.
  105. Chien DK, Chang WH, Yeh YH. Radiographic findings of a ruptured abdominal aortic aneurysm. Circulation 2010; 122:1880.
  106. Boules TN, Compton CN, Stanziale SF, et al. Can computed tomography scan findings predict "impending'' aneurysm rupture? Vasc Endovascular Surg 2006; 40:41.
  107. Arita T, Matsunaga N, Takano K, et al. Abdominal aortic aneurysm: rupture associated with the high-attenuating crescent sign. Radiology 1997; 204:765.
  108. Mehard WB, Heiken JP, Sicard GA. High-attenuating crescent in abdominal aortic aneurysm wall at CT: a sign of acute or impending rupture. Radiology 1994; 192:359.
  109. Roy J, Labruto F, Beckman MO, et al. Bleeding into the intraluminal thrombus in abdominal aortic aneurysms is associated with rupture. J Vasc Surg 2008; 48:1108.
  110. Wiernicki I, Szumilowicz P, Kazimierczak A, et al. The blood flow channel index as novel predictor of abdominal aortic aneurysm impending rupture based on the intraluminal thrombus angio-CT study. Eur J Radiol 2015; 84:662.
  111. Thammaroj J, Vungtal S, Srinakarin J. Predictive CT features in ruptured abdominal aortic aneurysm. J Med Assoc Thai 2006; 89:434.
  112. Oderich GS, Panneton JM, Bower TC, et al. Infected aortic aneurysms: aggressive presentation, complicated early outcome, but durable results. J Vasc Surg 2001; 34:900.
  113. Vogelzang RL, Sohaey R. Infected aortic aneurysms: CT appearance. J Comput Assist Tomogr 1988; 12:109.
  114. Ou P, Sidi D, Bonnet D, Brunelle F. Infected pulmonary artery aneurysms: CT imaging findings. Eur J Cardiothorac Surg 2006; 29:248.
  115. Gomes MN, Choyke PL. Infected aortic aneurysms: CT diagnosis. J Cardiovasc Surg (Torino) 1992; 33:684.
  116. Lee MH, Chan P, Chiou HJ, Cheung WK. Diagnostic imaging of Salmonella-related mycotic aneurysm of aorta by CT. Clin Imaging 1996; 20:26.
  117. Rozenblit A, Bennett J, Suggs W. Evolution of the infected abdominal aortic aneurysm: CT observation of early aortitis. Abdom Imaging 1996; 21:512.
  118. Lee WK, Mossop PJ, Little AF, et al. Infected (mycotic) aneurysms: spectrum of imaging appearances and management. Radiographics 2008; 28:1853.
  119. Shang EK, Nathan DP, Boonn WW, et al. A modern experience with saccular aortic aneurysms. J Vasc Surg 2013; 57:84.
  120. Paravastu SC, Murray D, Ghosh J, et al. Inflammatory abdominal aortic aneurysms (IAAA): past and present. Vasc Endovascular Surg 2009; 43:360.
  121. Stone WM, Fankhauser GT, Bower TC, et al. Comparison of open and endovascular repair of inflammatory aortic aneurysms. J Vasc Surg 2012; 56:951.
  122. Dalainas I, Nano G, Ranucci M, et al. Inflammatory abdominal aortic aneurysms. A 20-year experience. J Cardiovasc Surg (Torino) 2007; 48:305.
  123. Wiseman D, Harris K, Ehmann J. Spontaneous rupture of a rare adrenal artery aneurysm mimicking a ruptured abdominal aortic aneurysm. Vasc Endovascular Surg 2013; 47:159.
Topic 15229 Version 38.0