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Abdominal Aortic Aneurysm Treatment & Management

  • Author: Saum A Rahimi, MD, FACS; Chief Editor: Vincent Lopez Rowe, MD  more...
 
Updated: Sep 28, 2015
 

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. 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.

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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 2003, the Society for Vascular Surgery (SVS) published a series of guidelines for the treatment of AAAs based on these principles.[16]

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.[17]

Table 1. Operative Mortality Risk of 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.

Abdominal ultrasonography 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)

  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. 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. If the AAA is 3-4 cm in diameter, annual ultrasound imaging should be used to monitor for further dilatation. AAAs 4-4.5 cm in diameter should be evaluated with ultrasonography every 6 months, and patients with AAAs greater than 4.5 cm in diameter should be referred to a vascular surgeon.

With AAAs 4-5 cm in diameter, elective repair may be of benefit for patients who are young, have a low operative risk, and have a good life expectancy. Additionally, AAAs are known to rupture at smaller diameters in women than in men; therefore, a threshold of 4.5 cm for elective repair has been advocated in women. 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.[18] Prospective studies suggest that following aneurysms larger than 5.5 cm with serial ultrasonography 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.

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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.[19]

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.

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Surgical Intervention

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 is advocated for patients who are at increased risk with open repair, but until results from randomized controlled trials are available, patient preference is the strongest determinant in deciding between endovascular and open approaches.

Open repair

Open repair of thoracic and abdominal aortic aneurysms has a mortality of about 4%, with myocardial infarction being a frequent cause of death.[12] 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 operation

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, electrocardiography [ECG] and stress testing).

Because chronic obstructive pulmonary disease (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 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.

Surgical procedure

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,[20] and has since become an established and increasingly popular alternative to open repair. In 2006, EVAR overtook open repair, with 21,725 procedures performed.[12, 21, 22] 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.[23]

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.[24, 25, 26]

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[27] :

  • 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).

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.[24] 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.

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.[28]

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.[25] 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.[26] 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%).[29] 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.[30] The 136 patients were divided into 2 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 minutes; n = 44 [32%]). The 30-day mortality, postoperative complications, need for secondary reinterventions, and midterm mortality were recorded.

The 2 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%).[30] 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.[31]

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.[22] 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 endovascular repair, but the difference between the two approaches is not statistically significant.[32]

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.[33]

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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 ultrasonography, 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 ultrasonography 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 ultrasonography 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.

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Contributor Information and Disclosures
Author

Saum A Rahimi, MD, FACS Interim Chief, Assistant Professor of Surgery, Division of Vascular Surgery, Rutgers Robert Wood Johnson Medical School

Saum A Rahimi, MD, FACS is a member of the following medical societies: American College of Surgeons, Society for Vascular Surgery, Eastern Vascular Society, Vascular Society of New Jersey

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Society for Vascular Surgery, Vascular and Endovascular Surgery Society, Society for Clinical Vascular Surgery, Pacific Coast Surgical Association, Western Vascular Society

Disclosure: Nothing to disclose.

Acknowledgements

Suman Annambhotla, MD Fellow in Vascular Surgery, Northwestern University, The Feinberg School of Medicine

Suman Annambhotla, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, Association for Academic Surgery, and Society for Vascular Surgery

Disclosure: Nothing to disclose.

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: lippincott Royalty textbook royalty; wiley Royalty textbook royalty

Jeffrey Lawrence Kaufman, MD Associate Professor, Department of Surgery, Division of Vascular Surgery, Tufts University School of Medicine

Jeffrey Lawrence Kaufman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Society for Artificial Internal Organs, Association for Academic Surgery, Association for Surgical Education, Massachusetts Medical Society, Phi Beta Kappa, and Society for Vascular Surgery

Disclosure: Nothing to disclose.

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

William H Pearce, MD Chief, Division of Vascular Surgery, Violet and Charles Baldwin Professor of Vascular Surgery, Department of Surgery, Northwestern University, The Feinberg School of Medicine

William H Pearce, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, American Surgical Association, Association for Academic Surgery, Association of VA Surgeons, Central Surgical Association, New York Academy of Sciences, Society for Vascular Surgery, Society of Critical Care Medicine, Society of University Surgeons, andWestern Surgical Association

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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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 calcification of both walls of abdominal aortic aneurysm, allowing diagnosis to be made with certainty.
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.
Arteriography demonstrates infrarenal abdominal aortic aneurysm. This arteriogram was obtained in preparation for endovascular repair of aneurysm.
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.
Arteriogram after successful endovascular repair of abdominal aortic aneurysm.
Ultrasonogram from patient with abdominal aortic aneurysm (AAA). This aneurysm was best visualized on transverse or axial image. Patient underwent conventional AAA repair.
MRI of 77-year-old man with leg pain believed to be secondary to degenerative disk disease. During evaluation, abdominal aortic aneurysm was discovered.
Age is risk factor for development of aneurysm.
Inflammation, thinning of media, and marked loss of elastin.
Pulsatile abdominal mass.
Aneurysm with retroperitoneal fibrosis and adhesion of duodenum.
Aortic endoprosthesis (Cook aortic and aortobi-iliac endograft).
Endoaneurysmorrhaphy
Endovascular grafts.
Atheroemboli from small abdominal aortic aneurysms produce livedo reticularis of feet (ie, blue toe syndrome).
Enhanced spiral CT scans with multiplanar reconstruction and CT angiogram.
Angiography is used to diagnose renal area. In this instance, endoleak represented continued pressurization of sac.
Table 1. Operative Mortality Risk of Open Repair of Abdominal Aortic Aneurysm
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.
Table 2. Abdominal Aortic Aneurysm Size and Estimated Annual Risk of Rupture
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.
Table 3. Factors Affecting Risk of Abdominal Aortic Aneurysm Rupture
  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.
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