The decision to treat an unruptured abdominal aortic aneurysm (AAA) is a complex one, based on operative risk, the risk of rupture, and the patient’s estimated life expectancy. Ruptured AAA is a life-threatening condition that requires emergent surgery. For other discussions on AAA, see Abdominal Aortic Aneurysm and Bedside Ultrasonography Evaluation of Abdominal Aortic Aneurysm.
History of the procedure
Vesalius described the first AAA in the 16th century. Before the development of a surgical intervention for the process, attempts at medical management failed. The initial attempts at surgical control used ligation of the aorta, with the expected consequences.
In 1923, Matas performed the first successful aortic ligation on a patient. Attempts were made to induce thrombosis by inserting intraluminal wires. In 1948, Rea wrapped reactive cellophane around the aneurysm in order to induce fibrosis and limit expansion. This technique was used on Albert Einstein in 1949, and he survived 6 years before succumbing to rupture. In 1951, Charles Dubost performed the first AAA repair using a homograft.
Prior to this, aortic aneurysms were treated using a variety of methods, including ligation, intraluminal wiring, and cellophane wrapping. Unfortunately, early homografts became aneurysmal because of preservation techniques. In 1953, Blakemore and Voorhees repaired a ruptured AAA using a Vinyon-N graft (ie, nylon). Later, these grafts were replaced by Dacron and GORE-TEX (ie, polytetrafluoroethylene [PTFE]) fabrics. The final advance was abandonment of silk sutures, which degenerate, in favor of braided Dacron, polyethylene, and PTFE (ie, GORE-TEX) sutures, all of which retain tensile strength.
Postoperative surgical mortality rates initially remained high (>25%) because the aneurysm sac generally was excised. Nearly simultaneously in 1962, Javid and Creech reported the technique of endoaneurysmorrhaphy (see the images below). This advancement dramatically reduced mortality. Today, operative mortality rates range from 1.8-5%.
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Aneurysm with retroperitoneal fibrosis and adhesion of the duodenum and fibrosis.
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Endoaneurysmorrhaphy.
In the late 1980s, Parodi et al described endovascular repair using a large Palmaz stent and unilateral aortofemoral and femorofemoral crossover Dacron grafts.[1] Currently, many devices are used for the endovascular treatment of AAA (see the image below).
Ruptured abdominal aortic aneurysm (AAA) causes an estimated 15,000 deaths per year. The frequency of rupture is 4.4 cases per 100,000 persons. The reported incidence of rupture varies from 1-21 cases per 100,000 person-years.
International statistics
The frequency of 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.
The prognosis is guarded in patients who suffer AAA rupture prehospital. More than 50% do not survive to the ED; of those who do, survival rate drops by about 1% per minute. However, survival rate is good in the subset of patients who are not in severe shock and who receive timely, expert surgical intervention.
In 1988, 40,000 surgical reconstructions for abdominal aortic aneurysm (AAA) were performed in the US, with substantial mortality differences between elective versus emergency operations. As elective aneurysm repair has a mortality rate drastically lower than that associated with rupture, the emphasis must be on early detection and repair free from complications.
The long-term prognosis is related to associated comorbidities. Long-term survival is shortened by chronic heart failure and chronic obstructive pulmonary disease. 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 aortic aneurysm repair is comparable to that of people in the age-matched population at large who have never had an aneurysm.[2, 3]
Aneurysm diameter is an important risk factor for rupture. In general, abdominal aortic aneurysms (AAAs) gradually enlarge (0.2-0.8 mm/y) and eventually rupture. Hemodynamics 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 factors have demonstrated that aneurysm volume is a better predictor of areas of peak wall stress than aneurysm diameter. This may have implications in 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 using the Laplace Law for wall tension: P × R/W, where P = mean arterial pressure (MAP), R = radius of the vessel, and W = wall thickness of the vessel.
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.
Persons with abdominal aortic aneurysms (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, or 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. At least 65% of patients with ruptured AAA die from sudden cardiovascular collapse before arriving at a hospital.
It is important to note progressive symptoms (eg, abdominal or back pain, vomiting, syncope, claudication). These should alert the clinician to the possibility of expansion with imminent rupture.
Peripheral emboli and claudication
Atheroemboli from small AAAs produce livedo reticularis of the feet or blue toe syndrome (see the image below). Occasionally, small AAAs thrombose, producing acute claudication.
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Atheroemboli from small abdominal aortic aneurysms produce livedo reticularis of the feet (ie, blue toe syndrome).
Aortocaval fistulae
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.
Aortoduodenal fistulae
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.
Even patients who do not have symptoms from their abdominal aortic aneurysms (AAAs) may eventually require surgical intervention because the result of medical management in this population is a mortality rate of 100% over time due to rupture. In addition, these patients have a high likelihood of limb loss from peripheral embolization.
The decision to treat an unruptured abdominal aortic aneurysm (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.[4] The operative risk is based on patients’ comorbidities and hospital factors.
Abdominal ultrasonography can provide a preliminary determination of aneurysm presence, size, and extent. Rupture risk is in part indicated by the size of the aneurysm (see Table 1, below).
Table 1. Abdominal Aortic Aneurysm Size and Estimated Annual Risk of Rupture
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See Table
In addition to aneurysm diameter, risk of rupture is also an expression of sex, aneurysm expansion rate, family history, and chronic obstructive pulmonary disease (COPD) (see Table 2, below).
Table 2. Risk of Abdominal Aortic Aneurysm Rupture
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See Table
The operative risk (see Table 3, below) is based on patients’ comorbidities and hospital factors. Patient characteristics, including age, sex, renal function, and cardiopulmonary disease are perhaps the most important. However, lower-volume hospitals and surgeons are associated with higher mortality.[5]
Table 3. Operative Mortality Risk of Open Repair of Abdominal Aortic Aneurysm
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See Table
With AAAs smaller than 5.5 cm, elective repair has not been shown to improve survival.[6]
Prospective studies have concluded that following aneurysms larger than 5.5 cm with serial ultrasounds or CT scans is safe. A slightly higher rupture rate in women exists, and this threshold may be lower.
Thus, the decision to repair an AAA is a complex one in which the patient must play an important role. 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.
Contraindications for operative intervention of abdominal aortic aneurysms (AAAs) include severe chronic obstructive pulmonary disease (COPD), severe cardiac disease, active infection, and medical problems that preclude operative intervention. These patients may benefit best from endovascular stenting of the aneurysm.
In many patients, the decision to operate is a balance between risks and benefits. In an elderly patient (>80 y) with significant comorbidities, surgical repair may not be indicated. However, the decision 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 a positive attitude toward the surgery.
Patients with known cancer that has an indolent course (eg, prostate cancer) may merit aneurysm repair if their estimated survival is 2 years or longer.
A complete blood count 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, in order to assess operative risk and guide postoperative management.
Type and crossmatch blood to prepare for the possibility of transfusion, including clotting factors and platelets.
Because synthetic material is used in the intervention, assess and eliminate potential foci of infection preoperatively by urinalysis.
Assessment of pulmonary function is part of the preoperative workup, to determine operative risk and 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.
Chest radiography
Chest radiography is used to gain a preliminary assessment of the status of the heart and lungs. Concurrent pulmonary or cardiac disease may need to be addressed prior to treating the aneurysm.
Computed tomography
Preoperative CT scanning helps more clearly define the anatomy of the aneurysm and other intra-abdominal pathologies. Nonenhanced CT scanning is used to size aneurysms.[7] Although sizing the aneurysm is important, the anatomic relationships important to surgery are also determined. These include the location of the renal arteries, length of the aortic neck, condition of the iliac arteries, and anatomic variants such as a retroaortic left renal vein or horseshoe kidney.
Enhanced spiral CT scanning of the abdomen and pelvis with multiplanar reconstruction and CT angiography is the test of choice for preoperative evaluation for open and endovascular repair (see the image below).
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Enhanced spiral CT scans with multiplanar reconstruction and a CT angiogram.
Of AAA cases, 10-20% have focal outpouchings or blebs visible on CT scans that are thought to contribute to the potential for rupture. The wall of the aneurysm becomes laminated with thrombus as the blebs enlarge. This can give the appearance of a relatively normal intraluminal diameter in spite of a large extraluminal size.
Magnetic resonance angiography
Magnetic resonance angiography (MRA) is quickly replacing the traditional angiographic assessment of aneurysms. The study provides excellent anatomical definition and 3-dimensional assessment of the problem. Gadolinium-enhanced MRA can provide excellent images, even though regional variations in quality are reported.
Conventional angiography
Angiography remains the criterion standard for the diagnosis of AAA, and it is indicated in the presence of associated renal or visceral involvement, peripheral occlusive disease, or aneurysmal disease. Angiography is also essential with any renal abnormality (eg, horseshoe kidney, pelvic kidney). (See the image below.)
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Angiography is used to diagnose the renal area. In this instance, an endoleak represented continued pressurization of the sac.
Echocardiography
Because of the fluid shift involved during the operative repair of AAA, cardiac function should be assessed using echocardiography. By ascertaining the ejection fraction of the patient, the operative intervention can be planned and cardiac protective measures can be instituted as needed. This study is particularly indicated in patients with a history of CHF or known cardiac enlargement.
Pulmonary assessment
Assessment of pulmonary function is of paramount importance in these patients. Because surgical intervention requires an abdominal incision, preoperative assessment of the patient's pulmonary status allows for tailored postoperative care.
Cardiac assessment
Assess cardiac status in all patients with vascular disease. If one vascular bed is involved with an atherosclerotic process, then consider that others also may be involved. Electrocardiography 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 need to be addressed before the AAA can be repaired.
Abdominal aortic aneurysms (AAAs) are typically repaired by an operative intervention. The possible approaches are the traditional open laparotomy, newer minimally invasive methodologies, or by the placement of endovascular stents.
Preoperative details
Preoperatively, obtain a careful history and perform a physical examination and laboratory assessment. These basic assessments provide the information for estimating perioperative risk and life expectancy after the proposed procedure.
Carefully consider 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 is made, identify comorbidities and risk factors that increase the operative risk or decrease survival. Ascertain the patient's activity level, stamina, and stability of health. Perform a thorough cardiac assessment tailored to the patient's history, symptoms, and results from preliminary screening tests such as the electrocardiogram and stress test.
Because COPD is an independent predictor of operative mortality, assess lung function by performing a 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.
Preoperative intravenous antibiotics (usually a cephalosporin) are administered to reduce the risk of infection. Arranging for appropriate intravenous accesses 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 to monitor ventricular volume and cardiac wall motion and to provide a guide with respect to fluid replacement and pressor use.
Prepare for blood replacement. The patient should have blood available for transfusion. Intraoperative Cell Saver use and preoperative autologous blood donation have become popular.
Maintain a normal body temperature during the operative intervention to prevent coagulopathy and maintain normal metabolic function. To prevent hypothermia, place a recirculating, warm forced-air blanket on the patient and warm any intravenous fluids and blood before administration.
In summary, the following are standard preoperatively:
Type and crossmatch blood
Administer prophylactic antibiotics (cefazolin, 1 g intravenous piggyback)
Insert a Foley catheter
Establish large-bore intravenous access
Monitor central venous pressure or establish Swan-Ganz catheterization (if indicated)
Prepare the skin from the nipples to the mid thigh
Administer general anesthesia (with or without epidural anesthesia)
Cell Saver use has become popular
Insert a nasogastric tube
Intraoperative details
The aorta may be approached either transabdominally or through the retroperitoneal space. Approach juxtarenal and suprarenal aortic aneurysms from the left retroperitoneal space.
Self-retaining retractors are used. Keep the bowel warm and, if possible, not exteriorized. The abdomen is explored for abnormalities (eg, gallstones, associated intestinal or pancreatic malignancy).
Depending on the patient's anatomy, the aorta can be reconstructed with a tube graft, an aortic iliac bifurcation graft, or an aortofemoral bypass.
For proximal infrarenal control, first identify the left renal vein. Occasionally (< 5% of cases), patients may have a retroaortic vein. In this situation, take care when placing the proximal clamp. Division of the left renal vein is usually required to clamp above the renal arteries.
Regarding pelvic outflow, in most instances, the inferior mesenteric artery is sacrificed. Therefore, to prevent colon ischemia, make every attempt to restore at least one hypogastric (internal iliac) artery perfusion. If the hypogastric arteries are sacrificed (associated aneurysms), reimplant the inferior mesenteric artery.
For supraceliac aortic control, first divide the ligaments to the left lateral segment of the liver and then retract the segment. The crura of the diaphragm are separated, and the aorta is bluntly dissected. Supraceliac control is recommended for inflammatory aneurysms.
The aorta is reconstructed from within using PTFE or Dacron. The aneurysm sac is closed, and the graft is put into the duodenum to prevent erosion.
Special considerations
Inflammatory aneurysms require supraceliac control, minimal dissection of the duodenum, and balloon occlusion of the iliac arteries. In patients with inflammatory aneurysms or large iliac artery aneurysms, identify the ureters; occasionally, ureteral stents are recommended in patients with inflammatory aneurysms.
Prevention of distal embolization
The patient is heparinized (5000 U intravenously) prior to aortic cross-clamping. If significant intraluminal debris, juxtarenal thrombus, or prior peripheral embolization is present, the distal arteries are clamped first, followed by aortic clamping.
Before restoring lower extremity blood flow, both forward flow (aortic) and back flow (iliac) are allowed to remove debris. The graft is also irrigated to flush out debris.
The colon is inspected prior to closure, and the femoral arteries are palpated. Before the patient leaves the operating room, determine lower extremity circulation. If a clot was dislodged at the time of aortic clamping, it can be removed with a Fogarty embolectomy catheter. Heparin reversal is not usually required.
Fluid shifts are common following 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. Monitor the patient in the surgical intensive care unit for hemodynamic stability, bleeding, urine output, and peripheral pulses. A postoperative electrocardiogram and chest radiograph are needed. Prophylactic antibiotics (eg, cefazolin at 1 g) are administered for 24 hours.
The patient is seen in 1-2 weeks for suture or skin staple removal, then yearly thereafter.
For patient education information, see the Circulatory Problems Center and Cholesterol Center, as well as Aortic Aneurysm, High Cholesterol, and Cholesterol FAQs.
Endovascular stent grafts for the treatment of abdominal aortic aneurysm (AAA) are a less invasive form of treatment. Patients are discharged 1-2 days following surgery. The graft is placed through 2 small incisions. In September 2000, 2 grafts were approved by the US Food and Drug Administration (FDA). Since then, several more devices have received FDA approval.[8] Recently, the FDA has recommended careful follow-up because of persistent endoleaks and late ruptures.
In some instances, endoleaks represent continued pressurization of the sac (see image below). Aneurysm sacs may also demonstrate elevated pressure despite the absence of a demonstrable endoleak. This has been described as "endotension."
Persistently elevated aneurysm sac pressure, whether secondary to endoleak or endotension, is worrisome because it may progress to AAA rupture. Early data demonstrated a need for secondary interventions, via endovascular techniques, in as many as 10% of patients per year following endovascular aneurysm repair, compared with 2% in the first 5 years for open repair. Improvement has been made in the rate of secondary interventions following endovascular repair, but long-term durability has yet to be determined.
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Angiography is used to diagnose the renal area. In this instance, an endoleak represented continued pressurization of the sac.
Informing the patient about these potential problems is important prior to implanting these grafts. In addition, patients with endografts require follow-up evaluation with serial CT scanning on a schedule that demands more office visits than are required for patients who receive conventional grafts.
Currently, endovascular repair is advocated for patients at increased risk for open aneurysm repair, but until results from randomized controlled trials are available, patient preference is the strongest determinant in deciding between endovascular and open aneurysm repair.
Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Disclosure: Nothing to disclose.
Specialty Editors
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
Disclosure: Nothing to disclose.
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
Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other
Chief Editor
David FM Brown, MD, Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
The UK Small Aneurysm Trial Participants. Mortality results for randomized controlled trial of early elective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms. Lancet. 1998;353:1649-55.
Aneurysm with retroperitoneal fibrosis and adhesion of the duodenum and fibrosis.
Endoaneurysmorrhaphy.
Endovascular grafts.
Atheroemboli from small abdominal aortic aneurysms produce livedo reticularis of the feet (ie, blue toe syndrome).
Enhanced spiral CT scans with multiplanar reconstruction and a CT angiogram.
Angiography is used to diagnose the renal area. In this instance, an endoleak represented continued pressurization of the sac.
Angiography is used to diagnose the renal area. In this instance, an endoleak represented continued pressurization of the sac.
Endoaneurysmorrhaphy.
Endovascular grafts.
Atheroemboli from small abdominal aortic aneurysms produce livedo reticularis of the feet (ie, blue toe syndrome).
Aneurysm with retroperitoneal fibrosis and adhesion of the duodenum and fibrosis.
Enhanced spiral CT scans with multiplanar reconstruction and a CT angiogram.
Angiography is used to diagnose the renal area. In this instance, an endoleak represented continued pressurization of the sac.
Table 2. Estimated annual rupture risk.
Table 3. Rupture risk.
Table 1. Operative mortality risk of open AAA repair.
Radiograph shows calcification of the abdominal aorta. The left wall is clearly depicted and appears aneurysmal; however, the right wall overlies the spine.
The lateral view clearly shows calcification of both walls. Abdominal aortic aneurysm can be diagnosed with certainty.
CT demonstrates an abdominal aortic aneurysm. The aneurysm was noted during workup for back pain, and CT was ordered after the abdominal aortic aneurysm was identified on radiographs. No evidence of rupture is seen.
Arteriogram demonstrates an infrarenal abdominal aortic aneurysm. This arteriogram was obtained in preparation of an endovascular repair of the aneurysm.
Lateral arteriogram demonstrates an infrarenal abdominal aortic aneurysm. Demonstration of the superior mesenteric artery, inferior mesenteric artery, and celiac artery on the lateral arteriogram in important to completely evaluate the extent of the aneurysm.
Arteriogram after successful endovascular repair of an abdominal aortic aneurysm.
Ultrasonogram of a patient with an abdominal aortic aneurysm. This aneurysm was best visualized on a transverse or axial image. This patient underwent a conventional abdominal aortic aneurysm repair.
MRI of a 77-year-old man with leg pain believed to be secondary to degenerative disk disease. During evaluation, an abdominal aortic aneurysm was discovered.
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
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
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
CHF – chronic heart failure; COPD – chronic obstructive pulmonary disease; LVEF – left ventricular ejection fraction; MI – myocardial infarction; PT – prothrombin time
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