Abdominal Aortic Aneurysm 

Updated: Jan 08, 2019
Author: Saum A Rahimi, MD, FACS; Chief Editor: Vincent Lopez Rowe, MD 

Overview

Practice Essentials

Abdominal aortic aneurysms (AAAs) are relatively common and are potentially life-threatening. Patients at greatest risk for AAA are men who are older than 65 years and have peripheral atherosclerotic vascular disease. See the image below.

CT demonstrates abdominal aortic aneurysm (AAA). A CT demonstrates abdominal aortic aneurysm (AAA). Aneurysm was noted during workup for back pain, and CT was ordered after AAA was identified on radiography. No evidence of rupture is seen.

Signs and symptoms

AAAs are usually asymptomatic until they expand or rupture. An expanding AAA causes sudden, severe, and constant low back, flank, abdominal, or groin pain. Syncope may be the chief complaint, however, with pain less prominent.

Most clinically significant AAAs are palpable upon routine physical examination. The presence of a pulsatile abdominal mass is virtually diagnostic but is found in fewer than half of all cases.

Patients with a ruptured AAA may present in frank shock, as evidenced by cyanosis, mottling, altered mental status, tachycardia, and hypotension. Whereas abrupt onset of pain due to rupture of an AAA may be quite dramatic, associated physical findings may be very subtle. Patients may have normal vital signs in the presence of a ruptured AAA as a consequence of retroperitoneal containment of hematoma.

At least 65% of patients with a ruptured AAA die of sudden cardiovascular collapse before arriving at a hospital.

See Presentation for more detail.

Diagnosis

No specific laboratory studies can be used to diagnose AAA. The following imaging studies, however, can be employed diagnostically:

  • Ultrasonography - Standard imaging technique for AAA
  • Plain radiography - Using this method to evaluate patients with AAA is difficult because the only marginally specific finding, aortic wall calcification, is seen less than half of the time
  • Computed tomography (CT) and CT angiography (CTA) - This form of imaging is the main modality for defining and planning open or endovascular AAA repair; CT offers certain advantages over ultrasonography in defining aortic size, rostral-caudal extent, involvement of visceral arteries, and extension into the suprarenal aorta
  • Magnetic resonance imaging - This permits imaging of the aorta comparable to that obtained with CT and ultrasonography, without subjecting the patient to dye load or ionizing radiation
  • Angiography - With the fine resolution afforded by CTA, conventional angiography is rarely indicated to define the anatomy 

See Workup for more detail.

Management

AAAs are treated with surgical repair. When indicated, unruptured aneurysms can be addressed with elective surgery, whereas ruptured AAAs necessitate emergency repair. The primary methods of AAA repair are as follows:

  • Open - This requires direct access to the aorta via a transperitoneal or retroperitoneal approach
  • Endovascular - This involves gaining access to the lumen of the abdominal aorta, usually via small incisions over the femoral vessels; an endograft, typically a polyester or Gore-Tex graft with a stent exoskeleton, is placed within the lumen of the AAA, extending distally into the iliac arteries

See Treatment and Medication for more detail.

Background

Abdominal aortic aneurysms (AAAs) are relatively common and are potentially life-threatening. Aneurysms are defined as a focal dilatation in an artery, with at least a 50% increase over the vessel’s normal diameter. Thus, enlargement of the diameter of the abdominal aorta to 3 cm or more fits the definition.

AAA usually results from degeneration in the media of the arterial wall, leading to a slow and continuous dilatation of the lumen of the vessel (see Pathophysiology). Uncommon causes include infection, cystic medial necrosis, arteritis, trauma, inherited connective-tissue disorders, and anastomotic disruption. (See Etiology.)

AAAs generally affect elderly white men. Smoking appears to be the risk factor most strongly associated with AAA. In addition to increasing age and male sex, other factors include increased height, weight, body mass index, and body surface area. A familiar clustering has been noted in 15-25% of patients undergoing surgical repair of AAA. Female sex, African American race, and the presence of diabetes mellitus are negatively associated with AAA.[1, 2]

Most AAAs are asymptomatic, and many are detected as an incidental finding on diagnostic imaging obtained for other reasons. There is a wide spectrum of clinical presentations, and AAA should be considered in the differential diagnosis for a number of symptoms.

Ultrasonography is the standard imaging tool for AAA. Bedside emergency ultrasonography should be performed immediately if AAA is suspected. (See Workup and Bedside Ultrasonography Evaluation of Abdominal Aortic Aneurysm.)

Treatment of abdominal aortic aneurysms (AAAs) is with surgical repair. When indicated, unruptured aneurysms can undergo elective repair (see Treatment). The combination of ultrasonographic screening, reduced preoperative risk, and new minimally invasive techniques extend aortic aneurysm treatment into an increasingly elderly population. If an AAA ruptures, emergency surgical repair is required.

For patient education information, see the Circulatory Problems Center and the Cholesterol Center, as well as Aortic Aneurysm, High Cholesterol, and Cholesterol FAQs.

Anatomy

The abdominal aorta has three distinct tissue layers: intima, media, and adventitia. The intima is composed of the classic endothelial layer. The media comprises smooth muscle cells surrounded by elastin, collagen, and proteoglycans; to a great extent, this layer is responsible for the structural and elastic properties of the artery. The adventitia consists primarily of collagen but also contains a variety of cells (including fibroblasts and immunomodulatory cells), as well as adrenergic nerves.

The diameter of the aorta decreases from its thoracic portion to its abdominal and infrarenal portions. A normal aorta shows a reduction in medial elastin layers from the thoracic portion to the abdominal portion. Elastin content and collagen content are also reduced.

Most AAAs begin below the renal arteries and end above the iliac arteries. The size, shape, and extent of AAAs vary considerably. Like aneurysms of the thoracic aorta, AAAs may be broadly described as either fusiform (circumferential) or saccular (more localized). However, these descriptions represent two points on a continuum, and lesions that fall between the two points exist.

The important surgical and endovascular anatomic considerations include associated renal and visceral artery involvement (either occlusive disease or involved in the aneurysm process) and the iliac artery (either occlusive disease or aneurysms). The length of the infrarenal aortic neck is important in helping determine the surgical approach (ie, retroperitoneal or transabdominal) and the location of the aortic cross-clamp.

Consideration of hypogastric artery (internal iliac) outflow is important in planning surgical repair. Loss of blood flow from the hypogastric artery may result in impotence in males and sigmoid colon ischemia with necrosis.

Inflammatory aneurysms represent a subsegment of AAA and are characterized by a thick inflammatory peel. These aneurysms are associated with retroperitoneal fibrosis and adhesion of the duodenum and fibrosis (see the image below).

Aneurysm with retroperitoneal fibrosis and adhesio Aneurysm with retroperitoneal fibrosis and adhesion of duodenum.

Pathophysiology

AAAs arise as a result of a failure of the major structural proteins of the aorta (elastin and collagen). The inciting factors are not known, but a genetic predisposition clearly exists. Although aneurysms represent a dilatation in all layers of the vessel wall, AAAs develop after degeneration of the media. The degeneration ultimately may lead to widening of the vessel lumen and loss of structural integrity.

After age 50 years, the normal diameter of the infrarenal aorta is 1.5 cm in women and 1.7 cm in men. An infrarenal aorta that is 3 cm or more in diameter is considered an AAA, even if asymptomatic. Approximately 90% of AAAs are infrarenal.

A multidisciplinary research program supported by the US National Heart, Lung, and Blood Institute identified the following as mechanisms important in the development of AAA[3] :

  • Proteolytic degradation of aortic-wall connective tissue
  • Inflammation and immune responses
  • Biomechanical wall stress
  • Molecular genetics

Similarly, surgical specimens of AAA reveal the following (see the image below):

  • Inflammation, with infiltration by lymphocytes and macrophages
  • Thinning of the media
  • Marked loss of elastin
Inflammation, thinning of media, and marked loss o Inflammation, thinning of media, and marked loss of elastin.

Elastin

Elastin is the principal load-bearing element in the aorta. The aortic wall contains smooth muscle, elastin, and collagen arranged in concentric layers in order to withstand arterial pressure. The number of medial elastin layers is markedly reduced from the proximal thoracic aorta to the infrarenal aorta, with medial thinning and intimal thickening.

Elastin fragmentation and degeneration are observed in aneurysm walls. The decrease in content coupled with the histologic changes of this matrix protein in aneurysms may explain the propensity for aneurysm formation in the infrarenal aorta.

Proteolysis, metalloproteinases, and inflammation

In AAA, the aortic media appears to degrade by way of a proteolytic process. This implies an increase in the concentration of proteolytic enzymes relative to the concentration of their inhibitors in the abdominal aorta as the individual ages.

Some research has focused on the role of the metalloproteinases, a group of zinc-dependent enzymes responsible for tissue remodeling. Reports have documented increased expression and activity of matrix metalloproteinases (MMPs) in people with AAAs. MMPs and other proteases have been shown to be secreted into the extracellular matrix of AAAs by macrophages and aortic smooth-muscle cells.

MMPs and their inhibitors are present in normal aortic tissue and are responsible for vessel-wall remodeling. Aneurysmal tissue tends to demonstrate increased MMP activity and decreased inhibitor activity, which favor the degradation of elastin and collagen. The mechanism that tips the balance in favor of degradation of elastin and collagen in the aortic wall of AAAs by MMPs and other proteases is not yet known.

Upon histologic examination, AAAs demonstrate a chronic adventitial and medial inflammatory infiltrate. Infiltration of AAAs with lymphocytes and macrophages may trigger protease activation via various cytokines (eg, interleukin [IL]-1, IL-6, IL-8, and tumor necrosis factor [TNF]-α).

Immunoreactive proteins are found more conspicuously in the abdominal aorta, and this may contribute to the increased frequency of aneurysms in this location. Further study has defined a matrix protein that is immunoreactive with immunoglobulin G in the aneurysm wall. This autoantigen appears to be a collagen-associated microfibril. Certain infectious agents (eg, Chlamydia pneumoniae and Treponema pallidum) have been associated with the development of this protein; however, no direct cause-and-effect relation has been demonstrated.

Insights from molecular genetics

Through gene microarray analysis, various genes involved in extracellular matrix degradation, inflammation, and other processes observed in AAA formation have been shown to be upregulated, whereas others that may serve to prevent this occurrence are down-regulated. The combination of proteolytic degradation of aortic-wall connective tissue, inflammation and immune responses, biomechanical wall stress, and molecular genetics represents a dynamic process that leads to aneurysmal deterioration of aortic tissue.

Atherosclerosis

Most AAAs occur in individuals with advanced atherosclerosis. Atherosclerosis may induce AAA formation by causing mechanical weakening of the aortic wall with loss of elastic recoil, along with degenerative ischemic changes, through obstruction of the vasa vasorum.

Many patients with advanced atherosclerosis do not develop AAA, and some patients having no evidence of atherosclerosis do. The observed association between atherosclerosis and AAA probably is not causative; however, atherosclerosis may represent a nonspecific secondary response to vessel-wall injury that is induced by multiple factors.

Etiology

AAA is thought to be a degenerative process of the aorta, the cause of which remains unclear. It is often attributed to atherosclerosis because these changes are observed in the aneurysm at the time of surgery. However, a study by Blanchard et al found that the risk factors for AAA differ from those for atherosclerosis, with no association between cholesterol and AAA.[1] In addition, atherosclerosis fails to explain the development of occlusion, which is observed in the disease process.

Patients at greatest risk for AAA are men who are older than 65 years and have peripheral atherosclerotic vascular disease. A history of smoking often is elicited. Accordingly, in 2005, the US Preventive Services Task Force (USPSTF) recommended screening with ultrasonography in men aged 65-75 years who had ever smoked.[4] These recommendations were subsequently updated[5] on the basis of evidence from a 2014 study by Guirguis-Blake et al.[6]

A Swedish study showed that instances of AAA in elderly men have been decreasing, A phenomenon that can be attributed to a nationwide decline in smoking for the past 30 years, as well as the significantly improved longevity of the elderly population.[7] A one-time ultrasound scan is recommended for men once they reach age 65 years to detect and prevent possible occurrences of AAA.

Other risk factors for AAA include the following:

  • Chronic obstructive pulmonary disease (COPD)
  • Previous aneurysm repair or peripheral aneurysm (popliteal or femoral)
  • Hypertension (1-15% of cases)

Less frequent causes of AAA include Marfan syndrome, Ehlers-Danlos syndrome, and collagen-vascular diseases. In fewer than 5% of cases, AAA is caused by mycotic aneurysm of hematogenous origin. In these cases, local invasion of the intima and media gives rise to abscess formation and aneurysmal dilation of the vessel. Gram-positive organisms most commonly cause mycotic aneurysms. Other uncommon causes include cystic medial necrosis, arteritis, trauma, and anastomotic disruption producing pseudoaneurysms.

Persons who have first-degree relatives with AAA are at increased risk for AAA. The familial prevalence rate of AAA has been estimated at 15-25%. Studies by Majumder et al suggest that the genetic predisposition is isolated to a single dominant gene with low penetrance that increases with age.[8]

Tilson et al described the potential for an autoimmune basis for the development of AAA involving the DRB1 major histocompatibility locus.[9] This locus has been identified as a basis for inflammatory AAA.

In late 2018, the FDA issued a warning that fluoroquinolone use can increase the risk of aortic aneurysm and urged healthcare providers to avoid prescribing these antibiotics to patients with or at risk for an AA, such as those with peripheral atherosclerotic vascular disease, hypertension, or certain genetic conditions (eg, Marfan syndrome and Ehlers-Danlos syndrome), as well as the elderly.[10]

Risk factors for rupture

Aneurysm diameter is an important risk factor for rupture. In general, AAAs gradually enlarge (0.2-0.8 mm/year) and eventually rupture. Hemodynamic factors play an important role. Areas of high stress have been found in AAAs and appear to correlate with the site of rupture. Computer-generated geometric models have demonstrated that aneurysm volume is a better predictor of areas of peak wall stress than aneurysm diameter. This may have implications for determining which AAAs require surgical repair.

AAA rupture is believed to occur when the mechanical stress acting on the wall exceeds the strength of the wall tissue. Wall tension can be calculated by applying Laplace’s law, as follows:

  • P × R/W

where P is the mean arterial pressure (MAP), R is the radius of the vessel, and W is the thickness of the vessel wall. AAA wall tension is a significant predictor of pending rupture. The actual tension in the AAA wall appears to be a more sensitive predictor of rupture than aneurysm diameter alone. For these reasons, the clinician may wish to achieve acute blood pressure control in patients with AAA and elevated blood pressure.

Epidemiology

United States statistics

In autopsy studies, the frequency rate of AAA ranges from 0.5% to 3.2%. In a large US Veterans Affairs screening study, the prevalence was 1.4%.[2] The likelihood of development ranges from 3 to 117 cases per 100,000 person-years.

Ruptured AAA is the 13th-leading cause of death in the United States, causing an estimated 15,000 deaths per year. The frequency of rupture is 4.4 cases per 100,000 persons. The reported incidence of rupture ranges from 1 to 21 cases per 100,000 person-years. Despite increased survival following diagnosis, incidence and crude mortality seem to be increasing.

International statistics

The frequency rate of asymptomatic AAA is 8.2% in the United Kingdom, 8.8% in Italy, 4.2% in Denmark, and 8.5% in Sweden (in males only). The frequency rate of AAA in females is much lower, 0.6-1.4%. The frequency of AAA rupture is 6.9 cases per 100,000 persons in Sweden, 4.8 cases per 100,000 persons in Finland, and 13 cases per 100,000 persons in the United Kingdom.

Age-, sex-, and race-related demographics

The incidence of AAA begins to increase sharply after 50 years of age and peaks in the eighth decade of life (see the image below). In women, the onset is delayed and appears to begin at approximately age 60 years.

Age is risk factor for development of aneurysm. Age is risk factor for development of aneurysm.

The male-to-female incidence ratio in people younger than 80 years is 2:1. In those older than 80 years, the ratio is 1:1. White men have the highest incidence of AAA (~3.5 times that in African American men). AAAs are uncommon in African Americans, Asians, and persons of Hispanic heritage.

Prognosis

For patients who suffer rupture of an AAA before hospital arrival, the prognosis is guarded. More than 50% do not survive to reach the emergency department; for those who do, the survival rate drops by about 1% per minute. However, in the subset of patients who are not in severe shock and who receive timely, expert surgical intervention, the survival rate is good.

In 1988, 40,000 surgical reconstructions for AAA were performed in the United States, and substantial mortality differences between elective and emergency operations were noted. Because the mortality associated with elective aneurysm repair is drastically lower than that associated with repair of a ruptured AAA, the emphasis must be on early detection and repair free from complications.

In 2014, Ambler et al, in association with the Audit and Quality Improvement Committee of the Vascular Society of Great Britain and Ireland, used data collected during a 15-month period in the United Kingdom National Vascular Database to develop a model for assessing the risk of in-hospital mortality after AAA repair.[11]

The long-term prognosis is related to associated comorbidities. Long-term survival is shortened by chronic heart failure and COPD. Rupture of associated thoracic aneurysms is also an important cause of late death. Overall, AAA repair is very durable, with few long-term complications (< 5% false aneurysm). In general, the survival rate of patients with successful AAA repair is comparable to that of people in the age-matched population at large who have never had an aneurysm.[12, 13]

 

Presentation

History

As noted (see Etiology), patients at greatest risk for abdominal aortic aneurysms (AAAs) are those who are older than 65 years and have peripheral atherosclerotic vascular disease. Accordingly, a history of smoking, chronic obstructive pulmonary disease (COPD), and hypertension is often elicited. Less frequent causes include Marfan and Ehlers-Danlos syndromes, collagen vascular diseases, and mycotic aneurysm. Patients who have a first-degree relative with AAA are at increased risk.

AAAs are usually asymptomatic until they expand or rupture. Patients may experience unimpressive back, flank, abdominal, or groin pain for some time before rupture. Isolated groin pain is a particularly insidious presentation. This occurs with retroperitoneal expansion and pressure on either the right or left femoral nerve. This symptom may be present without any other associated findings, and a high index of suspicion is necessary to make the diagnosis.

At times, AAAs may cause symptoms from local compression, including early satiety, nausea, vomiting, urinary symptoms, or venous thrombosis from venous compression. Back pain can be caused by erosion of the AAA into adjacent vertebrae. Other symptoms include abdominal pain, groin pain, embolic phenomena affecting the toes (eg, livedo reticularis, or blue toe syndrome; see the image below), and fever. Occasionally, small AAAs thrombose, producing acute claudication.

Atheroemboli from small abdominal aortic aneurysms Atheroemboli from small abdominal aortic aneurysms produce livedo reticularis of feet (ie, blue toe syndrome).

Patients may describe a pulse in the abdomen and may actually feel a pulsatile mass.

It is important to note progressive symptoms, which should alert the clinician to the possibility of expansion with imminent rupture. An expanding AAA commonly causes sudden, severe, and constant low back, flank, abdominal, or groin pain. Syncope may be the chief complaint, with pain less prominent.

Symptoms of ruptured AAA

Persons with AAAs that have ruptured may present in many ways. The most typical manifestation of rupture is abdominal or back pain with a pulsatile abdominal mass. However, the symptoms may be vague, and the abdominal mass may be missed. Symptoms may include groin pain, syncope, paralysis, and flank mass. The diagnosis may be confused with renal calculus, diverticulitis, incarcerated hernia, or lumbar spine disease.

Transient hypotension should prompt consideration of rupture because this finding can progress to frank shock over a period of hours. Temporary loss of consciousness is also a potential symptom of rupture.

Patients with a ruptured AAA may present in frank shock, as evidenced by cyanosis, mottling, altered mental status, tachycardia, and hypotension. As many as 65% of patients with ruptured AAAs die of sudden cardiovascular collapse before arriving at a hospital.

AAAs may rupture into the vena cava, producing large arteriovenous fistulae. In this case, symptoms include tachycardia, congestive heart failure (CHF), leg swelling, abdominal thrill, machinery-type abdominal bruit, renal failure, and peripheral ischemia. Finally, an AAA may rupture into the fourth portion of the duodenum. These patients may present with a herald upper gastrointestinal bleed followed by an exsanguinating hemorrhage.

Physical Examination

Most clinically significant AAAs are palpable upon routine physical examination; however, the sensitivity of palpation depends on the experience of the examiner, the size of the aneurysm, and the size of the patient. In one study, 38% of AAA cases were detected on the basis of physical examination findings, whereas 62% were detected incidentally on radiologic studies obtained for other reasons.

Abdominal examination includes palpation of the aorta and estimation of the size of the aneurysm. AAAs are palpated in the upper abdomen; the aorta bifurcates into the iliac arteries just above the umbilicus. The clinician need not be afraid of properly palpating the abdomen, because there is no evidence to indicate that aortic rupture can be precipitated by this maneuver.

Whereas the abrupt onset of pain due to rupture of an AAA may be quite dramatic, the associated physical findings may be very subtle. Patients may have normal vital signs in the presence of a ruptured AAA as a consequence of retroperitoneal containment of hematoma.

The presence of a pulsatile abdominal mass (see the image below) is virtually diagnostic of an AAA but is found in fewer than 50% of cases. It is more likely to be noted with a ruptured aneurysm. In an obese abdomen, an AAA is more difficult to palpate. Even in patients known to have an aneurysm, vascular surgeons are unable to palpate a pulsatile mass while preparing the patient for surgery in 25% of cases.

Pulsatile abdominal mass. Pulsatile abdominal mass.

Occasionally, an overlying mass (pancreas or stomach) may be mistaken for an AAA. An abdominal bruit is nonspecific for an unruptured aneurysm, but the presence of an abdominal bruit or the lateral propagation of the aortic pulse wave can offer subtle clues and may be more frequently found than a pulsatile mass. Bruits may also indicate the presence of renal or visceral artery stenosis; a thrill is possible with aortocaval fistulae. Patients with popliteal artery aneurysms frequently have AAAs (25-50% of cases).

Misdiagnosis is fairly common because the classic presentation of pain associated with hypotension, tachycardia, and a pulsatile abdominal mass is present in less than 30-50% of cases. The leading misdiagnosis is renal colic; dissection of the renal artery may produce flank pain and hematuria.

Normally, systolic blood pressures are higher in the thigh than in the arm. In patients with AAA, this relation may be reversed. Bilateral upper-extremity blood pressures should be measured in patients with AAAs. Upper-extremity blood pressures that differ from each other by more than 30 mm Hg indicate subclavian artery stenosis, and perioperative monitoring is important. Cervical bruits may indicate carotid artery stenosis. Hypertension may trigger a workup for renal artery stenosis.

Femoral/popliteal pulses and pedal (dorsalis pedis or posterior tibial) pulses should be palpated to determine if an associated aneurysm (femoral/popliteal) or occlusive disease exists. Flank ecchymosis (Grey Turner sign) represents retroperitoneal hemorrhage.

Complications

The following are potential complications of AAAs:

  • Death (1.8-5% mortality for elective open repair, < 1% for endovascular repair, and 50% if the AAA has ruptured, though studies are showing that this last figure is decreased with endovascular repair)
  • Pneumonia (5%)
  • Groin infection (< 5%)
  • Graft infection (< 1%)
  • Colon ischemia (< 1% for elective repair, 15-20% if the AAA has ruptured)
  • Renal failure related to preoperative creatinine level, intraoperative cholesterol embolization, and hypotension
  • Incisional hernia (10-20%)
  • Bowel obstruction
  • Amputation from major arterial occlusion
  • Blue toe syndrome and cholesterol embolization to feet
  • Impotence in males - Erectile dysfunction and retrograde ejaculation (>30%)
  • Paresthesias in thighs from femoral exposure (rare)
  • Lymphocele in groin (~2%)
  • Late graft enteric fistula
 

DDx

Diagnostic Considerations

Abdominal, back, or flank pain of sudden onset is characteristic of a rapidly expanding or ruptured abdominal aortic aneurysm (AAA). The diagnosis should be entertained whenever a patient older than 50 years presents with abdominal pain, particularly when pain is associated with syncope or signs of hemorrhagic shock.

Other problems to be considered in a patient with a possible AAA include the following:

  • Gastrointestinal (GI) bleed
  • Ischemic bowel
  • Nephrolithiasis
  • Musculoskeletal pain
  • Perforated GI ulcer
  • Pyelonephritis

Differential Diagnoses

 

Workup

Approach Considerations

More than 80% of patients with ruptured abdominal aortic aneurysm (AAA) present without a previous diagnosis of AAA, which contributes to an initial misdiagnosis rate of 24-42%. A rational approach to the diagnostic evaluation is predicated on a high degree of suspicion.

No specific laboratory studies exist that can be used to make the diagnosis of AAA. Laboratory testing may be used to aid in diagnosis of other pathology or associated medical disorders. Options for radiologic evaluation of AAA include ultrasonography (US), plain radiography, computed tomography (CT), magnetic resonance imaging (MRI), and angiography.

Laboratory Studies

A complete blood count (CBC) with differential is used to assess transfusion requirements and the possibility of infection. A metabolic panel (including kidney and liver function tests) is indicated for ascertaining the integrity of renal and hepatic function and thus help assess operative risk and guide postoperative management. Blood must be typed and crossmatched to prepare for the possibility of transfusion, including clotting factors and platelets.

Because synthetic material is used in the intervention, any potential foci of infection should be assessed and eliminated preoperatively with the aid of urinalysis.

The preoperative workup should also include assessment of pulmonary function to help evaluate operative risk and determine postoperative care. Patients who can climb a flight of stairs without excessive shortness of breath generally do well. If the patient’s pulmonary status is in question, blood gas measurement and pulmonary function tests are helpful.

Ultrasonography

US is the standard imaging tool for AAA (see the image below). When performed by trained personnel, it has a sensitivity of nearly 100% and a specificity approaching 96% for the detection of infrarenal AAA. US can also detect free peritoneal blood.

Ultrasonogram from patient with abdominal aortic a Ultrasonogram from patient with abdominal aortic aneurysm (AAA). This aneurysm was best visualized on transverse or axial image. Patient underwent conventional AAA repair.

US is noninvasive and may be performed at the bedside. Bedside emergency US should be performed immediately if AAA is suspected. Elderly patients with abdominal pain are prime candidates for bedside US screening. (See Bedside Ultrasonography Evaluation of Abdominal Aortic Aneurysm.)

Screening for AAA reduces the mortality from rupture and is cost-effective.[14] The US Preventive Services Task Force has recommended US screening in men aged 65-75 years who have smoked.[4, 6] Abdominal US can provide a preliminary determination of aneurysm presence, size, and extent. In addition, it is a cost-effective modality for monitoring patients whose aneurysms are too small for surgical intervention. It is also useful for follow-up after endovascular surgery to assess the durability of the repair.

Limitations of US in this setting are few but include inability to detect leakage, rupture, branch artery involvement, and suprarenal involvement. In addition, the ability to image the aorta is reduced in the presence of bowel gas or obesity.

Significant portions of the abdominal aorta (at least one third of its length) are not visualized on bedside emergency US in 8% of nonfasting patients.[15] This rate is higher than reported for fasting patients receiving elective US for evaluation of their aortas.

Plain Radiography

Plain radiography is often performed on patients with abdominal complaints before the diagnosis of AAA has been entertained. Using this method to evaluate patients with AAA is difficult because the only marginally specific finding, aortic wall calcification, is seen less than half of the time. Aortic-wall calcification (see the images below) may appear without aneurysm rim calcification, resulting in a high false-negative rate.

Radiograph shows calcification of abdominal aorta. Radiograph shows calcification of abdominal aorta. Left wall is clearly depicted and appears aneurysmal; however, right wall overlies spine.
On radiography, lateral view clearly shows calcifi On radiography, lateral view clearly shows calcification of both walls of abdominal aortic aneurysm, allowing diagnosis to be made with certainty.

Plain radiography should not, however, be ordered for the sole purpose of evaluating suspected AAA; because of its low diagnostic yield, its use can waste time, delay care, and place the patient at risk for aortic rupture and death.

Chest radiography may be employed to gain a preliminary assessment of the status of the heart and lungs. Concurrent pulmonary or cardiac disease may have to be addressed before the AAA is treated.

Computed Tomography

CT has a sensitivity of nearly 100% for detecting AAA, and it has certain advantages over US for defining aortic size, rostral-caudal extent, involvement of visceral arteries, and extension into the suprarenal aorta (see the image below). CT permits visualization of the retroperitoneum, is not limited by obesity or bowel gas, detects leakage, and allows concomitant evaluation of the kidneys. Spiral (helical) CT allows three-dimensional (3D) imaging of abdominal contents, facilitating detection of branch vessel and adjacent organ involvement.

CT demonstrates abdominal aortic aneurysm (AAA). A CT demonstrates abdominal aortic aneurysm (AAA). Aneurysm was noted during workup for back pain, and CT was ordered after AAA was identified on radiography. No evidence of rupture is seen.

Preoperative CT is helpful for more clearly defining the anatomy of the aneurysm and other intra-abdominal pathologic conditions. Nonenhanced CT is used to size aneurysms.[16] As important as sizing the aneurysm is determining the anatomic relations that are relevant to surgical repair. These include the location of the renal arteries, the length of the aortic neck, the condition of the iliac arteries, and the presence of anatomic variants such as a retroaortic left renal vein or a horseshoe kidney.

Enhanced spiral CT of the abdomen and pelvis with multiplanar reconstruction and CT angiography (CTA) is the modality of choice for preoperative evaluation for open and endovascular repair (see the image below).

Enhanced spiral CT scans with multiplanar reconstr Enhanced spiral CT scans with multiplanar reconstruction and CT angiogram.

In 10-20% of AAA cases, CT scans show focal outpouchings or blebs that are thought to contribute to the potential for rupture. The wall of the aneurysm becomes laminated with thrombus as the blebs enlarge. This process can yield the appearance of a relatively normal intraluminal diameter in spite of a large extraluminal size.

CT is the best modality for determining whether a patient is a candidate for endovascular aneurysm repair (EVAR). It can assess the aneurysm neck diameter, length, and angulation, as well as thrombus within the neck. The CT scan is also useful for assessing iliac vessel diameter, calcification, and tortuosity, which are important for determining whether the endovascular device can be advanced from the femoral artery.

Major disadvantages of CT include potential difficulties with technician availability, higher cost, longer study time, exposure to radiation and contrast material, and the need to send patients with possible rupture out of the emergency department for an extended period.

Magnetic Resonance Imaging

MRI permits imaging of the aorta comparable to that achievable with CT and US, but without subjecting the patient to a dye load or ionizing radiation (see the image below). It may offer better imaging of branch vessels than either CT or US does, but it is less valuable in assessing suprarenal extension and is not suitable in patients who are unstable. MRI may have a role in very stable patients with a severe dye allergy.

MRI of 77-year-old man with leg pain believed to b MRI of 77-year-old man with leg pain believed to be secondary to degenerative disk disease. During evaluation, abdominal aortic aneurysm was discovered.

Limitations of MRI in the assessment of AAA are the lack of widespread availability, the need for a stable patient, potential incompatibility with monitoring equipment, and high cost.

Angiography

Because of advances in CT imaging with 3D reconstruction capability, angiography (see the images below) currently is less often used in preoperative evaluation of AAA than it once was. Arteriography may miss an AAA if there is a lack of calcification because of the laminated thrombus within the AAA making a more normal-appearing aortic lumen. It is primarily used intraoperatively to facilitate endovascular repair.

Arteriography demonstrates infrarenal abdominal ao Arteriography demonstrates infrarenal abdominal aortic aneurysm. This arteriogram was obtained in preparation for endovascular repair of aneurysm.
Lateral arteriogram demonstrates infrarenal abdomi Lateral arteriogram demonstrates infrarenal abdominal aortic aneurysm. Demonstration of superior mesenteric artery, inferior mesenteric artery, and celiac artery on lateral arteriogram is important for complete evaluation of extent of aneurysm.

Limitations on the use of angiography include the invasiveness of the procedure, the cost, the potential lack of operator availability, the considerable time involved, and the risk of complications (eg, bleeding, perforation, and embolization). Routine use of angiography in the evaluation of AAA is not recommended.

Digital subtraction angiography (DSA) requires less time, uses less contrast material, and is less invasive than conventional angiography. However, DSA is not widely available and offers no real advantage over conventional CT.

Intra-aortic CTA (IA-CTA) has good sensitivity for locating the Adamkiewicz artery (AKA) in patients with thoracoabdominal aortic aneurysms. In one study, the AKA was visualized by IA-CTA in 27 of 30 cases (90%) before surgery for aneurysm or dissection of the thoracoabdominal aorta.[17] Continuity with the aorta was satisfactorily seen in 26 of 31 (84%) cases. Spinal angiography by selective catheterization confirmed the results of IA-CTA in 75% of cases in which the AKA was visualized.

In a number of centers, magnetic resonance angiography (MRA) is replacing traditional angiographic assessment of aneurysms. MRA provides excellent anatomic definition and 3D assessment of the problem. Gadolinium-enhanced MRA can provide excellent images, even though regional variations in quality are reported.

Echocardiography

Because of the fluid shift involved during the operative repair of AAA, cardiac function should be assessed by means of echocardiography. Ascertaining the ejection fraction of the patient facilitates planning of the operative intervention and institution of cardiac protective measures as needed. This study is particularly indicated in patients with a history of congestive heart failure or known cardiac enlargement.

Other Tests

Assessment of pulmonary function is of paramount importance in AAA patients. Because surgical intervention requires an abdominal incision, preoperative assessment of the patient’s pulmonary status allows postoperative care to be appropriately tailored to the patient’s condition.

Assessment of cardiac status is mandatory in all patients with vascular disease. If one vascular bed is involved with an atherosclerotic process, others may be involved as well. Electrocardiographic (ECG) findings provide a baseline assessment of cardiac rhythm and old disease processes. A stress test can be performed to uncover unsuspected cardiac ischemia. Significant coronary disease may have to be addressed before the AAA can be repaired.

On histologic examination, AAAs contain a chronic inflammatory infiltrate and neovascularity of varying degrees. Inflammatory AAAs may contain germinal centers.

 

Treatment

Approach Considerations

Treatment of abdominal aortic aneurysms (AAAs) consists of surgical repair. When indicated, an unruptured aneurysm can undergo elective surgical repair; a ruptured AAA calls for emergency repair.[18, 19] Possible approaches include the traditional open laparotomy, newer minimally invasive methodologies, and the placement of endovascular stents.

Surgical repair should be performed as expeditiously as possible by an experienced surgeon. An unstable patient with AAA should be transferred only if the sending facility is incapable of operative care. Personnel skilled at resuscitation should accompany the transfer. Consideration can be given to transferring stable asymptomatic patients after appropriate imaging studies have excluded rupture, expansion, or leak.

Treatment of Unruptured Aneurysms

Even patients who do not have symptoms from their AAAs may eventually require surgical intervention because the result of medical management in this population is a mortality of 100% over time as a consequence of rupture. In addition, these patients have a potential for limb loss from peripheral embolization.

The decision to treat an unruptured AAA is based on operative risk, the risk of rupture, and the patient’s estimated life expectancy. In 2009, the Society for Vascular Surgery (SVS) published a series of guidelines for the treatment of AAAs based on these principles[20] ; these were subsequently updated in 2018 (see Guidelines).[18, 19]

Operative risk is based on patients’ comorbidities and hospital factors (see Table 1 below). Patient characteristics, including age, sex, renal function, and cardiopulmonary disease are perhaps the most important factors. However, lower-volume hospitals and surgeons are associated with higher mortality.[21]

Table 1. Operative Mortality Risk With Open Repair of Abdominal Aortic Aneurysm (Open Table in a new window)

Lowest Risk

Moderate Risk

High Risk

Age < 70 y

Age 70-80 y

Age 80 y

Physically active

Active

Inactive, poor stamina

No clinically overt cardiac disease

Stable coronary disease; remote MI; LVEF >35%

Significant coronary disease; recent MI; frequent angina; CHF; LVEF < 25%

No significant comorbidities

Mild COPD

Limiting COPD; dyspnea at rest; O2 dependency; FEV1< 1 L/sec

...

Creatinine 2.0-3.0 mg/dL

...

Normal anatomy

Adverse anatomy or AAA characteristics

Creatinine >3 mg/dL

No adverse AAA characteristics

...

Liver disease (↑PT; albumin < 2 g/dL)

Anticipated operative mortality, 1-3%

Anticipated operative mortality, 3-7%

Anticipated operative mortality, at least 5-10%; each comorbid condition adds ~3-5% mortality risk

AAA = abdominal aortic aneurysm; CHF = chronic heart failure; COPD = chronic obstructive pulmonary disease; FEV1 = forced expiratory volume in 1 second; LVEF = left ventricular ejection fraction; MI = myocardial infarction; PT = prothrombin time.

The SVS suggests that the Vascular Quality Initiative (VQI) mortality risk score be used preoperatively to assist patients in making informed decisions about proceeding with aneurysm repair.[19]

Abdominal ultrasonography (US) can provide a preliminary determination of the aneurysm’s presence, size, and extent. Rupture risk is in part indicated by the size of the aneurysm (see Table 2 below).

Table 2. Abdominal Aortic Aneurysm Size and Estimated Annual Risk of Rupture (Open Table in a new window)

AAA Diameter (cm)

Rupture Risk (%/y)

< 4

0

4-5

0.5-5

5-6

3-15

6-7

10-20

7-8

20-40

>8

30-50

AAA = abdominal aortic aneurysm.

In addition to aneurysm diameter, factors such as sex, aneurysm expansion rate, family history, and chronic obstructive pulmonary disease (COPD) also affect the risk of rupture (see Table 3 below).

Table 3. Factors Affecting Risk of Abdominal Aortic Aneurysm Rupture (Open Table in a new window)

Factor

Low Risk

Average Risk

High Risk

Diameter

< 5 cm

5-6 cm

>6 cm

Expansion

< 0.3 cm/y

0.3-0.6 cm/y

>0.6 cm/y

Smoking/COPD

None, mild

Moderate

Severe/steroids

Family history

No relatives

One relative

Numerous relatives

Hypertension

Normal blood pressure

Controlled

Poorly controlled

Shape

Fusiform

Saccular

Very eccentric

Wall stress

Low (35 N/cm2

Medium (40 N/cm2

High (45 N/cm2)

Sex

...

Male

Female

COPD = chronic obstructive pulmonary disease.

In patients with small AAAs, attempts should be made to reduce the expansion rate and rupture risk. Smoking cessation is of paramount importance.[19] Hypertension should be aggressively controlled. Beta-blocker therapy should be instituted to lower blood pressure and reduce stress on the artery wall. These agents can be administered safely unless the patient has a contraindication to their use (eg, COPD, allergy to the drug, bradycardia, or severe chronic heart failure).

Patients with an incidentally discovered AAA that is less than 3 cm in diameter require no further follow-up in the near term. If initial US screening identified an aortic diameter less than 3 cm but greater than 2.5 cm, rescreening after 10 years is suggested.[19]

According to the 2018 SVS guidelines, if the AAA is between 3.0 and 3.9 cm, surveillance imaging at 3-year intervals is suggested.[19] If the AAA is between 4.0 and 4.9 cm, surveillance imaging at 12-month intervals is suggested. If the AAA is between 5.0 and 5.4 cm, surveillance imaging at 6-month intervals is suggested. If there is any evidence of rapid growth (>1 cm in 1 year), the AAA should be repaired.

Patients with AAAs 5-6 cm in diameter may benefit from repair, especially if they have other contributing factors for rupture (eg, hypertension, continued smoking, or COPD). A study by Lederle et al found that with AAAs smaller than 5.5 cm, elective repair did not improve survival.[22] The 2018 SVS guidelines recommended elective repair for patients at low or acceptable surgical risk who have a fusiform AAA that is 5.5 cm or larger, as well as for patients who present with a saccular aneurysm.[19] AAAs are known to rupture at smaller diameters in women than in men; accordingly, the SVS guidelines suggested repair in women with an AAA between 5.0 cm and 5.4 cm.

Prospective studies suggest that following aneurysms larger than 5.5 cm with serial US or computed tomography (CT) is safe; this threshold may be lower for women.

For patients at higher risk, the threshold for repair may be a diameter of 6-7 cm, depending on their condition. At this size, the risk of rupture increases with age. These sizes apply to males of average height (170 cm); again, the threshold may be lower in women.

Thus, the decision to repair an AAA is a complex one in which the patient must play an important role. In many patients, the decision to operate is a balance between risks and benefits. In some very elderly patients or patients with limited life expectancy, aneurysm repair may not be appropriate. In these patients, the consequences of rupture should be frankly discussed. If rupture occurs, no intervention should be performed.

Although surgical repair may not be indicated in an elderly patient (>80 years) with significant comorbidities, the decision whether to intervene should not be based on age alone, even with rupture. The decision is best based on the patient’s overall physical status, including whether the patient has a positive attitude toward the surgical procedure and whether the patient is a candidate for endovascular aneurysm (or aortic) repair (EVAR).

Patients with known cancer that has an indolent course (eg, prostate cancer) may be suitable candidates for aneurysm repair if their estimated survival is 2 years or longer.

Contraindications for operative intervention of AAAs include severe COPD, severe cardiac disease, active infection, and medical problems that preclude operative intervention. These patients may be most likely to benefit from endovascular stenting of the aneurysm.

Initial Management

Prehospital care

Prehospital care of patients having symptoms compatible with or suggestive of AAA or aortic dissection consists of the following:

  • Ensuring adequate breathing
  • Maintaining oxygenation
  • Treating shock
  • Obtaining useful information concerning the history so as to expedite treatment on arrival at the emergency department (ED)

All patients with a suspected aortic aneurysm should receive 100% oxygen along with continuous electrocardiographic (ECG) and vital sign monitoring while en route to the hospital. Large-bore (14- or 16-gauge) intravenous (IV) lines should be inserted en route if possible.

Establishing the diagnosis in the field is usually difficult or impossible, but certain salient features of aortic aneurysm or dissection may be observed. Both can pose a threat to life if not quickly recognized and treated. Patients older than 50 years with sudden onset of abdominal pain should be presumed to have a ruptured AAA and should receive attentive airway management and vigorous fluid resuscitation, as indicated.

Patient presentation during the prehospital phase of care varies, depending on whether the aneurysm is acutely expanding or leaking or whether it involves the thoracic aorta or the abdominal aorta. Radio communication with the receiving hospital permits the medical control physician to direct care, and it facilitates selection of a capable destination hospital while permitting the ED to mobilize appropriate resources.

The physician directing prehospital care should request transport to a facility capable of operative treatment of an AAA in the rare event that the diagnosis can be suspected on the basis of information available for arrival at the hospital.

Use of military antishock trousers (MAST) to reverse shock due to ruptured AAA might seem beneficial, but it may actually be detrimental. Although the application of MAST theoretically offers temporary stabilization by compressing the leaking AAA and expanding hematoma, it can also lead to an undesirable reduction in cardiac output. Expeditious transport of unstable patients whose condition is deteriorating is a therapeutic imperative.

Emergency department care

The presence of a pulsatile abdominal mass in a patient suspected of having an AAA mandates immediate surgical intervention. Hemorrhagic shock is managed by means of fluid resuscitation, blood transfusion, and immediate surgical consultation. The concept of permissive hypotension, whereby aggressive fluid resuscitation is avoided so as not to aggravate bleeding by raising the blood pressure too much, should be taken into consideration. Treatment for coagulopathy may be initiated in the ED for patients who are receiving warfarin or heparin.

Elevated AAA wall tension is a significant predictor of impending rupture (see Etiology). Accordingly, the clinician may wish to achieve acute blood pressure control in patients with AAA and elevated blood pressure; agents commonly used include antihypertensive agents and analgesics. Fillinger et al reported that stress analysis, using three-dimensional (3D) computer models of AAAs reconstructed from CT data, offers a practical and feasible method for evaluating AAA rupture risk.[23]

Patients with leaking AAAs, if normotensive, do not require pharmacotherapy. In the setting of hypotension, reduction of blood pressure may be contraindicated.

Initial therapeutic goals include elimination of pain and reduction of systolic blood pressure to 100-120 mm Hg or to the lowest level consistent with adequate vital organ (cardiac, cerebral, or renal) perfusion. Whenever systolic hypertension is present, beta blockers can be used to reduce the rate of rise of the aortic pressure (dP/dt).

To prevent exacerbations in tachycardia and hypertension, patients should be treated with IV morphine sulfate. This reduces the force of cardiac contraction and the dP/dt and may thus delay rupture.

Patients who complain of back, flank, groin, or abdominal pain but have stable vital signs and do not appear ill present management challenges. They may be sent home or kept for extended periods in the ED while waiting for diagnostic testing for suspected ureterolithiasis or other benign abdominal conditions.

If the AAA ruptures and shock ensues, morbidity and mortality increase dramatically. Emergency physicians have been held liable for failure to diagnose AAA and obtain appropriate consultation in these situations. Therefore, a high index of suspicion is necessary if this medical-legal pitfall is to be avoided.

Patients should be admitted when they are unstable or symptomatic, when they have significant comorbid conditions, or when the diagnosis is uncertain. Elderly patients or those with preexisting conditions (eg, emphysema, hypertension, congestive heart failure, coronary artery disease, cerebrovascular disease, or renal insufficiency) may require stabilization before elective surgery.

Asymptomatic patients with inflammatory AAA or AAA that is associated with distal emboli, pain, or bowel obstruction require emergency repair regardless of the size of the aneurysm.

Options for Surgical Intervention

Choice of approach

There are two primary methods of AAA repair, open repair and EVAR. Open AAA repair requires direct access to the aorta via an abdominal or retroperitoneal approach. It is well established as definitive treatment, having been in use for over 50 years.

Generally, EVAR has been advocated for patients who are at increased risk with open repair, but to date, patient preference has commonly been the strongest determinant in deciding between endovascular and open approaches. For EVAR to be considered, the following anatomic criteria should be met[24] :

  • Iliofemoral access vessels that will allow safe insertion and deployment of the device, adequate seal, and sufficient length to provide axial support for the graft
  • Infrarenal aortic neck of adequate length, limited angulation, and appropriate diameter

The 2018 SVS guidelines recommended EVAR as the preferred treatment for ruptured AAAs, if it is anatomically feasible.[19]

Outcome data

In a randomized study of 1252 patients (EVAR-1 UK trial) with large AAAs (5.5 cm in diameter), EVAR was associated with a significantly lower perioperative mortality than open surgical repair was.[25]  However, no long-term differences in total mortality or aneurysm-related mortality were reported. EVAR was associated with increased rates of graft-related complications and reinterventions and was more costly. The 15-year follow-up data from EVAR-1, published in late 2016, also did not show significant differences in mortality.[26]

In a study of more than 2200 patients with small AAAs (4-5.4 cm), no significant survival difference was observed between patients who underwent immediate open repair for these lesions and those for whom surveillance, rather than surgery, served as first-line treatment.[27]

In a randomized trial involving 404 patients who were physically ineligible for open repair, endovascular repair of AAA was associated with a significantly lower rate of aneurysm-related mortality than no repair was.[28]  However, endovascular repair was not associated with a reduction in the rate of death from any cause. The rates of graft-related complications and reinterventions were higher with endovascular repair, and this approach was more costly.

In a 6-year, multicenter, randomized, controlled trial (DREAM trial) involving 351 patients with an AAA at least 5 cm in diameter who were considered suitable candidates for both open repair and EVAR, the two techniques were found to yield similar survival rates.[29]  The primary outcomes were mortality from any cause and rate of reintervention. The rate of secondary interventions was significantly higher for EVAR.

In a study of 106 patients with ruptured AAAs (75 treated with open repair and 31 with EVAR), minimally invasive EVAR was associated with significantly better aneurysm-related survival at 30 days than open surgical repair was (70% vs 33%).[30]  EVAR was also associated with a shorter hospital stay, fewer complications and interventions, less pneumonia, and fewer transfusions. At 5 years, however, mortalities in EVAR and open surgical repair were similar, with death occurring primarily from cardiovascular complications.

In a study by Mehta et al involving 136 patients undergoing EVAR for ruptured AAAs, mortality was greater in those with hemodynamic instability.[31]  The 136 patients were divided into two groups: (1) hemodynamically stable (systolic blood pressure ≥80 mm Hg; n = 92 [68%]) and (2) hemodynamically unstable (systolic blood pressure < 80 mm Hg for >10 min; n = 44 [32%]). The 30-day mortality, postoperative complications, need for secondary reinterventions, and midterm mortality were recorded.

The two groups were found to be similar with respect to comorbid conditions, mean maximum AAA diameter (6.6 cm vs 6.4 cm), need for on-the-table conversion to open repair (3% vs 7%), and incidence of nonfatal complications (43% vs 38%) and secondary interventions (23% vs 25%).[31]  Intraoperative need for aortic occlusion balloon, mean estimated blood loss, incidence of abdominal compartment syndrome, and mortality were all increased in the hemodynamically unstable group (40% vs 6%, 744 vs 363 mL, 29% vs 4%, and 33% vs 18%, respectively).

Perioperative use of beta blockers is associated with an overall reduction in postoperative cardiac events in patients undergoing infrarenal aortic reconstruction. In most patients with low perioperative bleeding, beta-blockers are protective; however, patients with severe bleeding who are treated with perioperative beta blockers have higher mortality and an increased risk of multiple organ dysfunction syndrome (MODS).[32]

Endovascular methods are used in the majority of infrarenal AAA repairs performed in the United States. Preoperative baseline aortoiliac anatomic characteristics were reviewed for each patient in a study by Schanzer et al, for which the primary outcome was post-EVAR AAA sac enlargement.[33]  The study results suggested that adherence to EVAR device guidelines was considered low and that post-EVAR aneurysm sac enlargement was high; this raises concerns regarding the long-term risk of aneurysm rupture.

In conclusion, when outcomes after open repair are compared with those after EVAR, perioperative mortality (30 days or inpatient) is significantly lower for EVAR. Outcome at 2 years also favors EVAR, but the difference between the two approaches is not statistically significant.[34]

A 2012 Cochrane review indicated that in comparison with systemic opioid-based drugs, epidural analgesia provided better pain relief and reduced tracheal tube use after abdominal aortic surgery.[35]

Open Repair

Open repair of AAAs and thoracic aortic aneurysms (TAAs) has a mortality of about 4%, with myocardial infarction (MI) being a frequent cause of death.[14]  Preoperative reduction of cardiac risk by means of cardiac investigations and beta blockade may lower mortality. Autologous transfusion techniques (eg, acute normovolemic hemodilution and intraoperative cell salvage) reduce the need for allogeneic blood and the complications associated with open surgery.

Preparation for surgery

Before the procedure, it is important to obtain a careful history and perform a physical examination and laboratory assessment. These basic evaluations provide the information that allows the treating physician to estimate perioperative risk and life expectancy after the proposed procedure.

Careful consideration should be given to the issue of whether the patient’s current quality of life is sufficient to justify the operative intervention. In the case of elderly persons who may be debilitated or may have mental deterioration, this decision is made in conjunction with the patient and family.

Once the decision in favor of surgical treatment is made, the next step is to identify any comorbid conditions or risk factors that may increase operative risk or decrease the chances of survival. To this end, the patient’s activity level, stamina, and stability of health are evaluated, and a thorough cardiac assessment is performed that is tailored to the patient’s history, symptoms, and results from preliminary screening tests (eg, ECG and stress testing).

Because COPD is an independent predictor of operative mortality, lung function should be assessed by performing room-air arterial blood gas measurement and pulmonary function tests. In patients with abnormal test results, preoperative intervention in the form of bronchodilators and pulmonary toilet often can reduce operative risks and postoperative complications.

Antibiotics (usually a cephalosporin, such as cefazolin, 1 g IV piggyback) are administered to reduce the risk of infection. Arranging for appropriate IV access to accommodate blood loss, arterial pressure monitoring through an arterial line, and Foley catheter placement to monitor urine output are routine preparations for surgery.

For patients at high risk because of cardiac compromise, a Swan-Ganz catheter is placed to assist with cardiac monitoring and volume assessment. Transesophageal echocardiography (TEE) can be useful for monitoring ventricular volume and cardiac wall motion and for helping guide fluid replacement and pressor use.

Preparations are made for blood replacement. The patient should have blood available for transfusion. Intraoperative use of a cell salvage machine and preoperative autologous blood donation have become popular.

The patient’s body temperature should be kept at a normal level during the operative intervention to prevent coagulopathy and maintain normal metabolic function. To prevent hypothermia, a recirculating, warm forced-air blanket should be placed on the patient, and any IV fluids and blood should be warmed before being administered.

The skin is prepared from the nipples to the midthigh. General anesthesia is administered, with or without epidural anesthesia.

Operative details

The aorta may be approached either transabdominally or through the retroperitoneal space. Juxtarenal and suprarenal aortic aneurysms are approached from the left retroperitoneal space. Self-retaining retractors are used. The bowel is kept warm and, if possible, is not exteriorized. The abdomen is explored for abnormalities (eg, gallstones or associated intestinal or pancreatic malignancy). Depending on the anatomy, the aorta can be reconstructed with a tube graft, an aortic iliac bifurcation graft, or an aortofemoral bypass.

For proximal infrarenal control, the first step is to identify the left renal vein. Occasionally (< 5% of cases), patients may have a retroaortic vein. In this situation, care must be taken in placing the proximal clamp. Division of the left renal vein is usually required for clamping above the renal arteries.

Before aortic cross-clamping, the patient is heparinized (5000 U IV). If significant intraluminal debris, juxtarenal thrombus, or prior peripheral embolization is present, the distal arteries are clamped first, followed by aortic clamping.

With respect to pelvic outflow, the inferior mesenteric artery is sacrificed in most instances. Therefore, to prevent colon ischemia, every attempt must be made to restore perfusion from at least one hypogastric (internal iliac) artery. If the hypogastric arteries are sacrificed (eg, because of associated aneurysms), the inferior mesenteric artery should be reimplanted.

For supraceliac aortic control, the ligaments are first divided to the left lateral section of the liver, which is then retracted. The crura of the diaphragm are separated, and the aorta is bluntly dissected.

Supraceliac control is recommended for inflammatory aneurysms, along with minimal dissection of the duodenum and balloon occlusion of the iliac arteries. In patients with inflammatory aneurysms or large iliac artery aneurysms, the ureters should be identified; occasionally, ureteral stents are recommended in patients with inflammatory aneurysms.

The aorta is reconstructed from within by using a polytetrafluoroethylene (PTFE) or Dacron graft. The aneurysm sac is closed, and the graft is put into the duodenum to prevent erosion. Before restoration of lower-extremity blood flow, both forward flow (aortic) and backflow (iliac) are allowed to remove debris. The graft is also irrigated to flush out debris.

Before closure, the colon is inspected, and the femoral arteries are palpated. Before the patient leaves the operating room, the status of the lower-extremity circulation must be determined. If a clot was dislodged at the time of aortic clamping, it can be removed with a Fogarty embolectomy catheter. Heparin reversal usually is not required.

Postoperative care

Fluid shifts are common after aortic surgery. Fluid requirements may be high in the first 12 hours, depending on the amount of blood loss and fluid resuscitation in the operating room. The patient should be monitored in the surgical intensive care unit for hemodynamic stability, bleeding, urine output, and peripheral pulses. Postoperative ECG and chest radiography are indicated. Prophylactic antibiotics (eg, cefazolin 1 g) are administered for 24 hours. The patient is seen in 1-2 weeks for suture or skin staple removal, then yearly thereafter.

Endovascular Repair

EVAR (see the image below) first became practical in the 1990s, as performed by Parodi et al,[36]  and has since become an established and increasingly popular alternative to open repair. In 2006, EVAR overtook open repair, with 21,725 procedures performed.[14, 37, 33]  The combination of screening, reduced preoperative risk, and advances in minimally invasive endovascular techniques has extended AAA treatment to an increasingly elderly population.

Arteriogram after successful endovascular repair o Arteriogram after successful endovascular repair of abdominal aortic aneurysm.

Endovascular repair of an AAA involves gaining access to the lumen of the abdominal aorta, usually via small incisions over the femoral vessels. An endograft, typically a polyester or Gore-Tex graft with a stent exoskeleton, is placed within the lumen of the AAA, extending distally into the iliac arteries. Several such grafts have been approved for use in the United States.[38]

The graft serves to contain aortic flow and decrease the pressure on the aortic wall, leading to a reduction in AAA size over time and a decrease in the risk of aortic rupture. Whereas EVAR repair has less operative morbidity than open repair does, it is more likely to necessitate secondary intervention, which increases cost.[25, 28, 29]

In some instances, EVAR can result in endoleaks, which represent continued pressurization of the sac (see the image below). Aneurysm sacs may also demonstrate elevated pressure despite the absence of a demonstrable endoleak. This phenomenon has been referred to as endotension.

Angiography is used to diagnose renal area. In thi Angiography is used to diagnose renal area. In this instance, endoleak represented continued pressurization of sac.

Persistently elevated aneurysm sac pressure, whether secondary to endoleak or to endotension, is worrisome because it may progress to AAA expansion and rupture. Early data demonstrated a need for secondary interventions, via endovascular techniques, in as many as 30% of patients over a 6-year period, compared with 10% over a comparable period for open repair. Improvement has been made in the rate of secondary interventions after EVAR, but long-term durability has yet to be determined.

Endoleaks can be classified into four different types, as follows[39] :

  • Type I - Blood flow into the aneurysm sac due to incomplete seal or ineffective seal at the end of the graft; this type of endoleak usually occurs in the early course of treatment but may also occur later
  • Type II - Blood flow into the aneurysm sac due to backflow from collateral vessels (eg, lumbar or inferior mesenteric arteries)
  • Type III - Blood flow into the aneurysm sac due to inadequate or ineffective sealing of overlapping graft joints or rupture of the graft fabric; again, this type of endoleak usually occurs early after treatment, as a consequence of technical problems, or later, as a result of device breakdown
  • Type IV - Blood flow into the aneurysm sac due to the porosity of the graft fabric itself, causing blood to pass through from the graft and into the aneurysm sac

Patients should be informed about the potential problems before a graft is implanted. In addition, patients with endografts require follow-up evaluation with serial CT on a schedule that demands more office visits than are required for patients who receive conventional grafts (eg, at 1, 6, and 12 months, then annually thereafter to confirm that the graft is effective).

Consultations

The urgency of consultation is dictated by the stability of the patient. In patients who are stable and without symptoms, the diagnostic workup takes precedence. Consideration should be given to consulting a radiologist to determine whether US, CT, or magnetic resonance imaging (MRI) would be the most appropriate study.

Follow-up with a vascular surgeon is warranted if the diameter of the abdominal aorta exceeds 3 cm or if the diameter of any segment of the aorta is more than 1.5 times the diameter of an adjacent segment.

Patients who have an AAA less than 4 cm in diameter require serial US twice per year. If the diameter increases by more than 0.5 cm over 6 months or comes to exceed 4 cm, surgical repair usually is warranted.

For patients with an AAA who are symptomatic, immediate consultation with a surgeon is indicated. If the patient is hemodynamically stable, imaging modalities may be considered after discussion with the surgical consultant.

Immediate surgical consultation is also mandatory for cases involving unstable patients, followed by notification of anesthesia and operating room personnel. Bedside US may be obtained while the patient awaits definitive treatment; however, it should not be allowed to delay surgery. CT is not appropriate in patients who are unstable.

 

Guidelines

SVS Guidelines on Care of Patients With Abdominal Aortic Aneurysms

In January 2018, the Society for Vascular Surgery (SVS) issued updated guidelines on the care of patients with abdominal aortic aneurysms (AAAs).[18, 19]  These guidelines included the following recommendations:

  • Surveillance imaging at 12-month intervals is recommended for patients with an AAA of 4.0 to 4.9 cm in diameter.
  • Recommend performing physical examination that includes an assessment of femoral and popliteal arteries.
  • Endovascular aneurysm repair (EVAR) is recommended as the preferred method of treatment for ruptured aneurysms.
  • To incorporate knowledge gained through the Vascular Quality Initiative (VQI) and other regional quality collaboratives, it is suggested that the VQI mortality risk score be used for mutual decision-making with patients considering aneurysm repair.
  • It is suggested that elective EVAR be limited to hospitals with a documented mortality and conversion rate to open surgical repair of 2% or less and that perform at least 10 EVAR cases each year.
  • It is suggested that elective open aneurysm repair be limited to hospitals with a documented mortality of 5% or less and that perform at least 10 open aortic operations of any type each year.
  • To encourage the development of effective systems of care that would lead to improved outcomes for those patients undergoing emergency repair, a door-to-intervention time of < 90 minutes, based on a framework of 30-30-30 minutes, is suggested for the management of the patient with a ruptured aneurysm.
  • Recommend treatment of type I and III endoleaks as well as of type II endoleaks with aneurysm expansion but recommend continued surveillance of type II endoleaks not associated with aneurysm expansion.
  • Whereas antibiotic prophylaxis is recommended for patients with an aortic prosthesis before any dental procedure involving the manipulation of the gingival or periapical region of teeth or perforation of the oral mucosa, antibiotic prophylaxis is not recommended before respiratory tract procedures, gastrointestinal or genitourinary procedures, and dermatologic or musculoskeletal procedures unless the potential for infection exists or the patient is immunocompromised.
  • Increased utilization of color duplex ultrasonography is suggested for postoperative surveillance after EVAR in the absence of endoleak or aneurysm expansion.
  • Recommend a preoperative resting 12-lead electrocardiogram (ECG) in all patients undergoing EVAR or open surgical repair within 30 days of planned treatment.
  • Suggest deferring open aneurysm repair for at least 6 months after drug-eluting coronary stent placement or, alternatively, performing EVAR with continuation of dual antiplatelet therapy.
  • Perioperative transfusion of packed red blood cells recommended if the hemoglobin level is < 7 g/dL.
  • Recommend elective repair for the patient at low or acceptable surgical risk with a fusiform AAA that is ≥5.5 cm.
  • General endotracheal anesthesia is recommended for patients undergoing open aneurysm repair.
 

Medication

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Antihypertensive agents are used to reduce tension on the vessel wall in patients with abdominal aortic aneurysms (AAAs) who have elevated blood pressure (BP). Analgesics are also an important element of care.

Antihypertensives

Class Summary

Antihypertensives are used to reduce the rate of rise of the aortic pressure (dP/dt). For acute reduction of arterial pressure, the potent vasodilator sodium nitroprusside is very effective. To reduce dP/dt acutely, administer a beta blocker intravenously (IV) in incremental doses until a heart rate of 60-80 beats/min is attained. When beta blockers are contraindicated, as in second- or third-degree atrioventricular block, consider using calcium-channel blockers.

Esmolol (Brevibloc)

An ultrashort-acting beta1 blocker, esmolol is particularly useful in patients with elevated arterial pressure, especially if surgery is planned. It can be discontinued abruptly if necessary. This agent is normally used in conjunction with nitroprusside. It may be useful as a means of testing beta-blocker safety and tolerance in patients with a history of obstructive pulmonary disease who are at uncertain risk for bronchospasm from beta blockade. The elimination half-life of esmolol is 9 minutes.

Labetalol (Trandate)

Labetalol blocks alpha1-, beta1-, and beta2-adrenergic receptor sites, decreasing blood pressure.

Propranolol (Inderal LA, InnoPran XL)

A class II antiarrhythmic nonselective beta-adrenergic receptor blocker, propranolol has membrane-stabilizing activity and decreases the automaticity of contractions. It is not suitable for emergency treatment of hypertension; it should not be administered IV in hypertensive emergencies.

Metoprolol (Lopressor, Toprol-XL)

Metoprolol is a selective beta 1-adrenergic receptor blocker that decreases the automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and electrocardiograms. When considering conversion from IV to oral (PO) dosage forms, use the ratio of 2.5 mg PO to 1 mg IV.

Nitroprusside (Nitropress)

Nitroprusside causes peripheral vasodilation by acting directly on venous and arteriolar smooth muscle, thus reducing peripheral resistance. This agent is commonly used IV because of its rapid onset and short duration of action. It is easily titrated to the desired effect.

Because nitroprusside is light-sensitive, both bottle and tubing should be wrapped in aluminum foil. Before initiating nitroprusside therapy, administer a beta blocker to counteract the physiologic response of reflex tachycardia that occurs when nitroprusside is used alone. This physiologic response will increase the shear forces against the aortic wall, thus increasing dP/dt. The objective is to keep the heart rate between 60 and 80 beats/min.

Analgesics

Class Summary

Pain control is essential to quality patient care. It ensures patient comfort, promotes pulmonary toilet, and prevents exacerbation of tachycardia and hypertension.

Morphine sulfate (Astramorph, Infumorph, Duramorph)

Morphine is the drug of choice for narcotic analgesia because of its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Like fentanyl, morphine sulfate is easily titrated to the desired level of pain control. Morphine sulfate administered IV may be dosed in a number of ways. It is commonly titrated until the desired effect is obtained.

Fentanyl citrate

Fentanyl citrate is a synthetic opioid that has 75-200 times more potency of and a much shorter half-life than morphine sulfate. It has fewer hypotensive effects than morphine and is safer in patients with hyperactive airway disease because of minimal or no associated histamine release. By itself, fentanyl citrate causes little cardiovascular compromise, although the addition of benzodiazepines or other sedatives may result in decreased cardiac output and blood pressure.

Fentanyl citrate is highly lipophilic and protein-bound. Prolonged exposure to it leads to accumulation of the drug in fat and delays the weaning process. Consider continuous infusion because of the medication's short half-life.

 

Questions & Answers

Overview

Which group is at highest risk for abdominal aortic aneurysms (AAAs)?

What are the signs and symptoms of abdominal aortic aneurysms (AAAs)?

How are abdominal aortic aneurysm (AAA) diagnosed?

What is the role of surgical intervention in the treatment of abdominal aortic aneurysm (AAA)?

How are abdominal aortic aneurysms (AAAs) defined?

What are possible causes of an abdominal aortic aneurysm (AAA)?

What are the risk factors for abdominal aortic aneurysm (AAA)?

How are most abdominal aortic aneurysms (AAAs) detected?

What is the role of ultrasonography in the workup of abdominal aortic aneurysm (AAA)?

What are the treatment options for abdominal aortic aneurysms (AAAs)?

Where is patient information for abdominal aortic aneurysm (AAA) available?

What is the anatomy of the abdominal aorta?

Where in the body are most abdominal aortic aneurysms (AAAs) located?

What anatomic considerations should be addressed when planning surgical repair of abdominal aortic aneurysm (AAA)?

What are inflammatory abdominal aortic aneurysms (IAAAs)?

What is the pathogenesis of abdominal aortic aneurysms (AAAs)?

At what diameter is an infrarenal aorta considered an abdominal aortic aneurysm (AAA)?

Which mechanisms are involved in the pathogenesis of abdominal aortic aneurysm (AAA)?

What do surgical specimens of abdominal aortic aneurysm (AAA) reveal?

What is the role of elastin in the pathogenesis of abdominal aortic aneurysm (AAA) present?

What is the role of matrix metalloproteinases (MMPs) in the pathogenesis of abdominal aortic aneurysm (AAA)?

What factors may trigger protease activation in the pathogenesis of abdominal aortic aneurysms (AAAs)?

What is the role of immunoreactive proteins in the pathogenesis of abdominal aortic aneurysm (AAA)?

What is the role of genetics in the pathogenesis of abdominal aortic aneurysm (AAA)?

What is the role of atherosclerosis in the pathogenesis of abdominal aortic aneurysm (AAA)?

Which risk factors are common to abdominal aortic aneurysm (AAA) and atherosclerosis?

What are the USPSTF recommendations for abdominal aortic aneurysms (AAAs) screening?

What are risk factors for abdominal aortic aneurysm (AAA)?

What are the less common causes of abdominal aortic aneurysm (AAA)?

What are the genetic etiologic factors of abdominal aortic aneurysm (AAA)?

What are the risk factors for rupture of abdominal aortic aneurysm (AAA)?

What is the prevalence of abdominal aortic aneurysm (AAA) in the US?

What is the global prevalence of abdominal aortic aneurysm (AAA)?

How does the incidence of abdominal aortic aneurysm (AAA) vary between males and females and among races?

What is the survival rate of abdominal aortic aneurysm (AAA) rupture?

What is the difference in mortality rates between elective and emergency repair of abdominal aortic aneurysm (AAA)?

Which factors influence the long-term prognosis of abdominal aortic aneurysm (AAA)?

Presentation

What should be the focus of history in suspected abdominal aortic aneurysms (AAAs)?

What are the signs and symptoms of abdominal aortic aneurysm (AAA)?

What are the symptoms of a ruptured abdominal aortic aneurysm (AAA)?

Which physical findings suggest aortic aneurysm (AAA)?

What does the presence of an abdominal bruit suggest in suspected abdominal aortic aneurysm (AAA)?

How frequently is a classic presentation of abdominal aortic aneurysm (AAA) seen?

What is the role of blood pressure in the diagnosis of abdominal aortic aneurysm (AAA)?

What are potential complications of abdominal aortic aneurysms (AAAs)?

DDX

Which conditions should be included in the differential diagnoses of abdominal aortic aneurysm (AAA)?

What are the differential diagnoses for Abdominal Aortic Aneurysm?

Workup

How should the workup of abdominal aortic aneurysm (AAA) be approached?

What is the role of lab testing in the workup of abdominal aortic aneurysm (AAA)?

What is the role of ultrasonography in the workup of abdominal aortic aneurysm (AAA)?

What is the role of radiography in the workup of abdominal aortic aneurysm (AAA)?

What is the role of CT scanning in the diagnostic and preoperative evaluation of aortic aneurysm (AAA)?

How prevalent is a finding of focal outpouching on CT scan for abdominal aortic aneurysm (AAA)?

What is the preoperative use for CT scanning in abdominal aortic aneurysm (AAA)?

What are the limitations of CT scanning in the workup of abdominal aortic aneurysm (AAA)?

What is the role of MRI in the workup of abdominal aortic aneurysm (AAA)?

What are limitations of MRI in the workup of abdominal aortic aneurysm (AAA)?

What is the role of angiography in the workup of abdominal aortic aneurysm (AAA)?

What are the limitations of angiography in the workup of abdominal aortic aneurysm (AAA)?

What is the role of DSA in the workup of abdominal aortic aneurysm (AAA)?

What is the role of IA-CTA in the workup of abdominal aortic aneurysm (AAA)?

What is the role of MRA in the workup of abdominal aortic aneurysm (AAA)?

What is the role of echocardiography in the workup of abdominal aortic aneurysm (AAA)?

Which supplemental studies may be useful in the workup of abdominal aortic aneurysm (AAA)?

Treatment

What are the treatment options for abdominal aortic aneurysm (AAA)?

What are the SVS treatment guidelines for unruptured abdominal aortic aneurysm (AAA)?

What are treatment options for small abdominal aortic aneurysms (AAAs)?

How do treatment options vary based on the size of an abdominal aortic aneurysm (AAA)?

What factors are considered when deciding whether to repair an abdominal aortic aneurysm (AAA)?

What are the contraindications for surgical intervention of abdominal aortic aneurysms (AAAs)?

What is the prehospital for a patient with a ruptured abdominal aortic aneurysm (AAA)?

What is the treatment of suspected abdominal aortic aneurysm (AAA) when a pulsatile abdominal mass is present?

What is the significance of elevated abdominal aortic aneurysm (AAA) wall tension?

What is the role of drug treatment in normotensive leaking abdominal aortic aneurysm (AAA)?

What are the initial goals for treatment of abdominal aortic aneurysm (AAA)?

How are exacerbations in tachycardia and hypertension prevented in the initial treatment of abdominal aortic aneurysm (AAA)?

What treatment should be given for suspected abdominal aortic aneurysm (AAA) with pain but stable vital signs in the ED?

What are the possible liability factors for ED physicians treating abdominal aortic aneurysm (AAA)?

When should patients be admitted for inpatient treatment of abdominal aortic aneurysm (AAA)?

When is emergency repair indicated in abdominal aortic aneurysm (AAA)?

What are the primary methods of abdominal aortic aneurysm (AAA) surgical repair?

How do the outcomes of open and EVAR repair of abdominal aortic aneurysm (AAA) compare?

What is the mortality rate of open surgical repair of abdominal aortic aneurysm (AAA)?

How are patients prepared for open surgery repair of abdominal aortic aneurysm (AAA)?

How is open surgery performed on a patient with abdominal aortic aneurysm (AAA)?

What is the postoperative care for abdominal aortic aneurysm (AAA)?

How commonly is endovascular repair (EVAR) of abdominal aortic aneurysm (AAA) performed?

How is endovascular repair (EVAR) performed for abdominal aortic aneurysm (AAA)?

What are endoleaks from EVAR for abdominal aortic aneurysm (AAA)?

What monitoring is required for endografts following repair of abdominal aortic aneurysm (AAA)?

What specialist consultations should are needed for abdominal aortic aneurysm (AAA)?

Medications

What are the goals of drug treatment for abdominal aortic aneurysm (AAA)?

Which medications in the drug class Analgesics are used in the treatment of Abdominal Aortic Aneurysm?

Which medications in the drug class Antihypertensives are used in the treatment of Abdominal Aortic Aneurysm?