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Mar 7, 2020 admin Uncategorized 0

Abdominal Aortic Aneurysm

  • Amit K. Jain, M.D.
  • Pranav M. Patel, M.D.

 Basic Information

Definition

An abdominal aortic aneurysm (AAA) is a focal full-thickness dilation of the abdominal aortic artery to at least 1.5 times the diameter measured at the level of the renal arteries, or exceeding the normal diameter of the abdominal aorta by 50%. The normal diameter at the renal arteries is 2 cm (range 1.4-3.0 cm), and a diameter 3 cm or larger is generally considered aneurysmal.

ICD-10CM CODES
I71.4 Abdominal aortic aneurysm, without rupture
I71.3 Abdominal aortic aneurysm, ruptured

Epidemiology & Demographics

1.Approximately 15,000 deaths/year in the United States are attributed to AAA.

2.AAA is predominantly a disease of older adults, affecting men more than women (4:1).

3.The prevalence rate ranges from 4% to 9% in men in developed countries.

4.Clinically important AAAs ≥4 cm are present in 1% of men between age 55 and 64; and the prevalence rate increases by 2% to 4% per decade thereafter.

5.The peak incidence is among men approximately 70 years old.

6.The frequency is much higher in smokers than in nonsmokers (8:1); and the risk decreases with smoking cessation.

7.Risk factors for AAA are similar to those for other atherosclerotic cardiovascular diseases. They include age, 8.Caucasian race, smoking, male gender, family history, hypertension, hyperlipidemia, peripheral vascular disease, and aneurysm of other large vessels.

9.AAA is two to four times more common in first-degree male relatives of known AAA patients.

10.A decreased risk of AAA is associated with female gender, non-Caucasian race, and diabetes.

11.Rupture of the AAA occurs in 1% to 3% of men age 65 or older.

12.Rupture is the 10th leading cause of death in men older than age 55.

13.Mortality from rupture is 70% to 95%.

14.Risk factors for rupture include cardiac or renal transplants, severe obstructive lung disease, uncontrolled blood pressure, female sex, and ongoing tobacco use.

15.A recent decline in incidence and prevalence of AAA and related mortality has been attributed to reductions in tobacco use.

Etiology

  1. •Exact etiology is unknown and is likely multifactorial.
    1. 1)

      Degenerative:

      1. a.Alterations in vascular wall biology leading to a loss of vascular structural proteins and wall strength.
      2. b.The most common association is atherosclerosis. It is uncertain whether atherosclerosis causes or results from AAAs.
      3. c.Tobacco use: >90% of people who develop an AAA have smoked at some point in their lives.
    2. 2)Inherited: Familial clusters are common. High familial prevalence rate is notable in male individuals. The nature of the genetic disorder is unclear but may be linked to alpha-1-antitrypsin deficiency or X-linked mutation. Connective tissue disorders, such as Marfan’s syndrome and Ehlers-Danlos syndrome, have also been strongly associated with AAA.
    3. 3)Inflammatory: AAA is a progressive inflammatory disease of the artery walls. Activated B lymphocytes promote AAA by producing immunoglobulins, cytokines, and matrix metalloproteinases (MMPs), resulting in the activation of macrophages, mast cells (MCs), and complement pathways that lead to the degradation of collagen and matrix proteins and to aortic wall remodeling.
    4. 4)Infection, mycotic: syphilis, Salmonella.

Natural History

1.AAAs tend to develop in the infrarenal aorta and to expand, on average, at a rate of 0.3 to 0.4 cm per year.

2.The risk of aneurysmal rupture is largely influenced by aneurysm size, rate of expansion, and sex. Other factors associated with increased risk for rupture include continued smoking, uncontrolled hypertension, and increased wall stress

3.Higher tension in the abdominal aorta (together with histopathologic changes such as accumulation of foam cells, cholesterol crystals, and matrix metalloproteinases) renders the abdominal aortic wall more susceptible to dilation and subsequent rupture

4.The 5-year rupture rate of asymptomatic AAAs is 25% to 40% for aneurysms >5.0 cm in diameter, 1% to 7% for AAAs 4.0 to 5.0 cm, and nearly 0% for AAAs <4.0 cm. The likelihood that an aneurysm will rupture is increased in aneurysms with a diameter >5.5 cm; this size also demonstrates a faster rate of expansion (>0.5 cm over 6 months) and is more likely to be found in those who continue to smoke and in females.

5.Mortality rate after rupture can be as high as 90% because most patients do not reach the hospital in time for surgical repair. Of those who reach the hospital, the mortality rate is still 50%, compared with the 1% to 4% mortality rate for elective repair of a nonruptured AAA. The U.S. Preventive Services Task Force (USPSTF) also concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for AAA in women aged 65 to 75 who ever smoked and recommends against routine screening in women who never smoked (most recent update in June 2014).

Screening and Monitoring

1.The USPSTF recommends one-time screening for AAA by ultrasonography in men ages 65 to 75 who have a history of smoking, and in those 60 years of age or older with a history of AAA in a parent or sibling. These populations have been shown to have a higher prevalence of AAA, and selectively screening this group has been shown to decrease AAA-specific mortality.
2.The USPSTF has found little benefit in repeat screening in men with a negative ultrasound and has determined that men over the age of 75 are unlikely to benefit from screening. It was also concluded that the current evidence is insufficient to assess the balance of the harms and benefits of screening for AAA in women ages 65 to 75 who have ever smoked.
3.Monitoring by ultrasound or CT scan should be performed every 6 to 12 months for patients with AAAs measuring 4.0 to 5.4 cm in diameter and by ultrasound every 2 years for those with AAAs measuring <4 cm.

Physical Findings & Clinical Presentation

1.Most aneurysms are asymptomatic and incidentally discovered on imaging studies; however, symptomatic aneurysms are at an increased risk for rupture.
2.Physical examination has a sensitivity of 76% for detecting AAAs >5 cm and only 29% for AAAs 3.0-3.9 cm. The accuracy of the physical examination is markedly diminished by obese body habitus.
3.Symptomatic patients may present with abdominal, back, flank, or groin pain.
4.A pulsatile epigastric mass that may or may not be tender may be present.
5.Abdominal pain radiating to the back, flank, and groin.
6.Abdominal bruits can be present in case of renal or visceral arterial stenosis.
7.Common iliac arteries can be aneurysmal and palpable in the lower abdominal quadrants. In addition, prominent femoral and popliteal pulses warrant an abdominal ultrasound and lower extremity ultrasound.
8.Early satiety, nausea, and vomiting may be caused by compression of adjacent bowel.
9.Venous thrombosis or insufficiency may occur from iliocaval venous compression.
10.Thromboembolization can cause lower extremity pain and discoloration.
11.Ureteral obstruction and hydronephrosis can cause flank and groin pain and lead to obstructive renal failure.
12.Rupture classically presents as a triad of abdominal or back pain, hypotension, and a pulsatile abdominal mass in 50% of patients.
13.Acute blood loss may lead to myocardial infarction; arteriovenous fistulas may present as heart failure; aortoenteric fistulas may present as hematemesis or melena associated with abdominal and back pain.

Differential Diagnosis

Almost 75% of patients with AAA are asymptomatic, and the condition is discovered on routine examination or serendipitously when ordering studies for other symptoms. Diagnosis of AAA should be considered in the differential of the following symptoms: abdominal pain, back pain, and/or pulsatile abdominal mass.

Laboratory Tests

1.Not routinely indicated. For suspected infected or inflammatory aneurysms, WBC, ESR/CRP, and blood cultures can be considered. An elevated D-dimer may indicate a thrombus within the aneurysm. Fig. 1 describes an algorithm for the diagnosis and treatment of abdominal aortic aneurysms.

FIG.1 

Algorithm for the diagnosis and treatment of abdominal aortic aneurysms (AAAs).
BP, Blood pressure; CT, computed tomography; MRI, magnetic resonance imaging; NS, normal saline; PRBCs, packed red blood cells; SBP, systolic blood pressure; US, ultrasonography.
From Adams JG et al.: Emergency medicine, clinical essentials, ed 2, Philadelphia, 2013, Elsevier.

Imaging Studies

2.Abdominal ultrasound (Fig. 2) has nearly 100% sensitivity and specificity in identifying an aneurysm and estimating the size to within 0.3 to 0.4 cm. It is not accurate in estimating the extension to the renal arteries or the iliac arteries.
FIG.2 

Transverse image of an abdominal aortic aneurysm.
Note the measurements of 3.33 × 3.85 cm. The inferior vena cava is seen to the patient’s right of the aorta, and the vertebral body is seen below the two vessels. Note also that there appears to be an echogenic flap within the aorta, possibly representing an aortic dissection.
From Adams JG et al.: Emergency medicine, clinical essentials, ed 2, Philadelphia, 2013, Elsevier.
3.Computed tomography (CT) (Fig. 3) scan is recommended for preoperative aneurysm imaging and estimates the size of the AAA to within 0.3 mm. There are no false-negative results, and the scan can localize the extent to renal vessels with more precision than ultrasound. It is the imaging modality of choice for symptomatic AAA. Intravenous contrast is not required to establish a diagnosis of ruptured AAA. CT can also detect the integrity of the wall (Fig. 4) and exclude rupture.
FIG.3 

Three-dimensional CT image illustrates the presence of an infrarenal abdominal aortic aneurysm.
An, Aneurysm; CIA, common iliac artery; EIA, external iliac artery; IIA, internal iliac artery; IN, infrarenal neck; LK, left kidney; RA, renal artery; RK, right kidney.
From Townsend CM et al. [eds]: Sabiston textbook of surgery, ed 17, Philadelphia, 2004, Saunders.
FIG.4 

Aneurysm of the abdominal aorta.
A large aortic aneurysm is evident. The aorta exceeds 5 cm in diameter. A large amount of thrombus (T) partially surrounds the contrast-enhanced patent lumen (L). Note the atherosclerotic calcification (arrowhead) in the wall of the aneurysm.
4.Magnetic resonance angiography (MRA) may also be used and is at least as accurate as CT.
5.Plain radiographs may show the outline of an aneurysm in calcified aortas. This is an insensitive test for diagnosing AAA.
6.Diagnostic aortography has essentially been replaced by other noninvasive imaging modalities such as CT or MR angiography. Intraoperative angiography is still used for determining treatment options and post-procedure efficacy (Fig. 5).
FIG.5 

A, Conventional catheter angiography with bilateral marked catheters in place demonstrates a large, lobulated, infrarenal aortic aneurysm (arrowhead) with a 4-cm proximal neck suitable for endovascular repair. B, An image after endovascular repair demonstrates complete exclusion of the aneurysm (arrowhead) with no endoleak and preservation of the renal and hypogastric arteries.
Soto JA, Lucey BC: Emergency radiology: the requisites, ed 2, Philadelphia, 2017, Elsevier.
7.Endovascular aneurysm repair (EVAR) needs a close and lifelong imaging surveillance for a timely detection of possible complications, including endoleaks, graft migration, fractures, and enlargement of aneurysm sac size with eventual rupture. Contrast-enhanced computed tomography (CTA) is considered the gold standard in EVAR follow-up, but it is accompanied with radiation burden and renal injury because of the use of contrast media. In the past 2 decades, several studies have shown the role of contrast-enhanced ultrasonography (CEUS) in post-EVAR surveillance, with very good diagnostic performance, absence of renal impairment, and no radiation, accompanied by low costs, in comparison with CTA. In numerous prospective studies and meta-analyses, the detection and characterization of endoleaks with CEUS is comparable to that of CTA imaging.

Treatment

Nonpharmacologic Therapy

1.Despite lack of data substantiating reduction in expansion rate through treatment of cardiac risk factors, nonpharmacologic treatment continues to focus on risk factor modification (most importantly smoking cessation, diet, and exercise).
2.Serial studies have shown that expansion rates are faster in current smokers than in former smokers. Patients with known AAA or a family history of aneurysms should be advised to stop smoking and be offered smoking cessation interventions.
3.Definitive treatment depends on the size of the aneurysm (see “Chronic Rx”).

Acute General Rx

1.Acute symptomatic or ruptured AAA can be treated with open surgical or endovascular aneurysm repair (EVAR). The choice is determined by anatomic considerations, operative risks, and availability of regular patient follow-up for EVAR.
2.Emergent open repair has been the traditional method of treatment. However, multiple trials including Impact of Managed Pharmaceutical care on Resource utilization and Outcomes in Veterans affairs medical centers (IMPROVE) study have shown lower mortality and shorter hospital stay with EVAR. More centers are increasingly using endovascular repair for patients who fit certain anatomic and physiologic criteria.
3.However, a recent Cochrane meta-analysis for EVAR versus open repair for ruptured abdominal aortic aneurysm failed to show a difference in 30-day mortality between EVAR versus open repair. Further, long-term data on outcomes were lacking and should be the focus of future clinical trials.
4.The major limitations for EVAR include anatomical issues such as tortuosity or small caliber iliac arteries and inability to follow up patients to exclude late failure of stent-grafts and development of endoleaks.

Chronic Rx

1.Blood pressure and fasting lipids should be monitored and controlled as recommended for patients with atherosclerotic disease. Statins are associated with decreased mortality after successful AAA repair, and are recommended for those with known AAA to reduce the progression of atherosclerosis and overall cardiovascular risk.
2.The most commonly used predictor of rupture is the maximum diameter of the AAA.
3.Monitoring by ultrasound or CT scan should be performed every 6 to 12 months for patients with AAAs measuring 4.0 to 5.4 cm in diameter and by ultrasound every 2 years for those with AAAs measuring 3 to 4 cm and every 5 years for those with AAAs between 2.6 and 2.9 cm.
5.Long-term beta-blocker therapy has slowed the rate of aortic dilation and decreased the incidence of aortic complications in patients with Marfan’s syndrome. Several studies have also suggested that beta-blocker therapy may reduce the rate of expansion and risk of rupture; however, conclusive evidence is lacking.
6.A recent multicenter study of 5362 patients with AAA found no significant association between AAA progression and the use of statins, beta-blockers, angiotensin-converting enzyme inhibitors, or angiotensin II receptor blockers.
7.Antibiotics such as doxycycline and roxithromycin have been shown to limit the expansion of small AAAs.
8.Surgical repair to eliminate the risk for rupture should be performed for patients with infrarenal or juxtarenal AAA of approximately 5.5 cm or larger in diameter. All patients who are symptomatic should undergo repair, regardless of size. Timing of repair in symptomatic unruptured AAA is still under debate.
9.There is no clear advantage to early repair (open or endovascular) for small AAAs (less than 5.5 cm).
10.Percutaneous, endovascular, stent-anchored grafts placed with the patient under local anesthesia have provided an alternative approach (Fig. 6) for patients with favorable anatomy. In patients who have undergone endovascular repair, long-term surveillance is required to assess for an endoleak, stent migration, change in aneurysm size, and need for re-intervention.
FIG.6 

Endovascular abdominal aortic aneurysm repair involves aneurysm exclusion with an endoluminal aortic stent-graft introduced remotely, usually through the femoral artery.
An endovascular graft extends from the infrarenal aorta to both common iliac arteries, preserving the flow to the internal iliac arteries. CIA, Common iliac artery; IIA, internal iliac artery; IN, infrarenal aortic neck; LK, left kidney; RK, right kidney; SA, suprarenal aorta.
From Townsend CM et al. [eds]: Sabiston textbook of surgery, ed 17, Philadelphia, 2004, Saunders.
11.Fenestrated endovascular repair is an alternative to open repair in the management of juxtarenal aortic aneurysms (JRAs) and short-neck abdominal aortic aneurysms. Contemporary literature shows that it is a safe and efficacious treatment, particularly for those deemed surgically high risk. Growing experience and innovation of stent-grafts are essential for the advancement of fenestrated grafting.
12.Randomized trials have shown that endovascular repair of AAA is associated with a significantly lower operative mortality than open surgical repair but it has increased rates of graft-related complications and reintervention, and is more costly. There are no differences between endovascular repair and open surgical repair in total mortality or aneurysm-related mortality at 7 years.
13.Compared with open aneurysm repair, EVAR is associated with better health-related quality of life up to 12 months postoperatively for unruptured aneurysms.
14.Most recent meta-analysis concludes that EVAR has lower rates of 30-day mortality, 30-day MI, and length of hospital stay in both elective and emergency AAA repair.
15.Based on current data, less than 2% of endovascular repairs require open conversion, and approximately half of all early endoleaks resolve spontaneously within a period of 30 days.
16.Open repair still represents a valuable solution for many patients with failed EVAR with relatively low mortality rates when performed electively.
17.Perioperative mortality is significantly less for EVAR compared with open repair (1.8% vs. 4.3%), whereas overall cumulative long-term mortality is similar (9.3 vs. 8.9 deaths) based upon the data obtained from the EVAR-1 trial.
18.In high-risk patients undergoing AAA repair, specifically those with coronary artery disease or those with more than one clinical risk factor based on the American Heart Association (AHA) guidelines, preoperative administration of beta-blockers titrated to a goal heart rate of 60 have been shown to decrease incidence of death from cardiac causes or nonfatal myocardial infarctions.
19.Patients with chronic obstructive pulmonary disease (COPD) are at higher risk for major clinical complications, particularly if the COPD is suboptimally managed or if it is present in conjunction with cardiac or renal disease. Smoking cessation for 2 months before surgery has also been shown to decrease pulmonary morbidity.
20.Renal dysfunction is a strong predictor of mortality, showing up to as high as 41% mortality in those with impaired renal function compared with 6% in those without renal dysfunction.

Referral

1.Vascular surgical referral should be made in asymptomatic patients with AAAs that are approximately 4.5 cm.
2.In patients with an expansion rate of 0.6-0.8 cm/year, it is reasonable to offer repair, although small studies have shown that using expansion as a criterion for surgical referral is of unclear benefit.
3.It is important to optimize any comorbid conditions before surgical referral.

Pearls & Considerations

1.Repairing asymptomatic AAAs smaller than 5.5 cm has not been shown to improve survival because the risk of rupture is lower than the risk of surgery.
2.The results from multiple trials to date demonstrate no advantage to immediate repair for small AAA (4.0-5.5 cm), regardless of whether open or endovascular repair is used and, at least for open repair, regardless of patient age and AAA diameter. Thus, neither immediate open nor immediate endovascular repair of small AAAs is supported by the currently available evidence.
3.Five-year survival remains poor after elective AAA repair despite advances in short-term outcomes and is associated with AAA diameter and patient age at the time of surgery. Research in this field should attempt to improve the life expectancy of patients with repaired AAA and to optimize patient selection.

Comments

1.Most AAAs are infrarenal.
2.Surgical risk is increased in patients with coexisting coronary artery disease, pulmonary disease, or chronic renal failure. Evaluation for ischemia and aggressive perioperative hemodynamic monitoring help identify high-risk patients and decrease postoperative complications.
3.It is estimated that AAAs at <5 cm expand at a rate of 0.3 to 0.4 cm/year.

Evidence

Abstract[1]

Comparative effectiveness of endovascular versus open repair of ruptured abdominal aortic aneurysm in the Medicare population.

OBJECTIVE

Endovascular aortic repair (EVAR) for abdominal aortic aneurysm (AAA) is increasingly used for emergent treatment of ruptured AAA (rAAA). We sought to compare the perioperative and long-term mortality, procedure-related complications, and rates of reintervention of EVAR vs open aortic repair of rAAA in Medicare beneficiaries.

METHODS

We examined perioperative and long-term mortality and complications after EVAR or open aortic repair performed for rAAA in all traditional Medicare beneficiaries discharged from a United States hospital from 2001 to 2008. Patients were matched by propensity score on baseline demographics, coexisting conditions, admission source, and hospital volume of rAAA repair. Sensitivity analyses were performed to evaluate the effect of bias that might have resulted from unmeasured confounders.

RESULTS

Of 10,998 patients with repaired rAAA, 1126 underwent EVAR and 9872 underwent open repair. Propensity score matching yielded 1099 patient pairs. The average age was 78 years, and 72.4% were male. Perioperative mortality was 33.8% for EVAR and 47.7% for open repair (P < 0.001), and this difference persisted for >4 years. At 36 months, EVAR patients had higher rates of AAA-related reinterventions than open repair patients (endovascular reintervention, 10.9% vs 1.5%; P < 0.001), whereas open patients had more laparotomy-related complications (incisional hernia repair, 1.8% vs 6.2%; P < 0.001; all surgical complications, 4.4% vs 9.1%; P < 0.001). Use of EVAR for rAAA increased from 6% of cases in 2001 to 31% in 2008, whereas during the same interval, overall 30-day mortality for admission for rAAA, regardless of treatment, decreased from 55.8% to 50.9%.

CONCLUSIONS

EVAR for rAAA is associated with lower perioperative and long-term mortality in Medicare beneficiaries. Increasing adoption of EVAR for rAAA is associated with an overall decrease in mortality of patients hospitalized for rAAA during the last decade. 

Abstract[2]

Survival following ruptured abdominal aortic aneurysm before and during the IMPROVE trial: a single-centre series.

OBJECTIVES

The first large-scale randomised trial (Immediate Management of the Patient with Rupture: Open Versus Endovascular repair [IMPROVE]) for endovascular repair of ruptured abdominal aortic aneurysm (rEVAR) has recently finished recruiting patients. The aim of this study was to examine the impact on survival after rEVAR when the IMPROVE protocol was initiated in a high volume abdominal aortic aneurysm (AAA) centre previously performing rEVAR.

METHODS

One hundred and sixty-nine patients requiring emergency infrarenal AAA repair from January 2006 to April 2013 were included. Eighty-four patients were treated before (38 rEVAR, 46 open) and 85 (31 rEVAR, 54 open) were treated during the trial period. A retrospective analysis was performed.

RESULTS

Before the trial, there was a significant survival benefit for rEVAR over open repair (90-day mortality 13% vs. 30%, p = 0.04, difference remained significant up to 2 years postoperatively). This survival benefit was lost after starting randomisation (90-day mortality 35% vs. 33%, p = 0.93). There was an increase in overall 30-day mortality from 15% to 31% (p = 0.02), while there was no change for open repair (p = 0.438). There was a significant decrease in general anaesthetic use (p = 0.002) for patients treated during the trial. Randomised patients had shorter hospital and intensive treatment unit stays (p = 0.006 and p = 0.03, respectively).

CONCLUSIONS

The change in survival seen during the IMPROVE trial highlights the need for randomised rather than cohort data to eliminate selection bias. These results from a single centre reinforce those recently reported in IMPROVE. 

Abstract[3]

EDITOR’S CHOICE

Five-year outcomes in men screened for abdominal aortic aneurysm at 65 years of age: a population-based cohort study.

OBJECTIVE

Acquiring contemporary data on prevalence and natural history of abdominal aortic aneurysms (AAA) is essential in the effort to optimise modern screening programmes. The primary aim of this study was to determine the fate of a 65-year-old male population 5 years following an invitation to an aortic ultrasound (US) examination.

METHODS

In this population-based cohort-study, men were invited to US examination at age 65, and were re-invited at age 70. Mortality, AAA repair, and risk factors were recorded. An AAA was defined as a diameter ≥30 mm, and a sub-aneurysmal aorta as 25–29 mm.

RESULTS

In 2006–2007, 3,268 65-year-old men were invited, and 2,736 (83.7%) were examined. After 5 years, 24 had completed AAA repair (6 died within 0–4 years), an additional 239 had died, and 194 had moved. Thus, 2,811 70-year-old men were re-invited, and 2,247 (79.9%) were examined. The AAA prevalence increased from 1.5% at 65 to 2.4% (95% CI: 1.8 to 3.0) at 70, and of sub-aneurysmal aortas from 1.7% at 65 to 2.6% (2.0 to 3.3), at 70. Of 2,041 with <25 mm at 65, 0.7% had an AAA at 70. Of 40 with a sub-aneurysmal aorta at 65, 52.5% progressed to AAA at 70. In a Cox regression analysis, subaneurysmal aorta at 65 (hazard ratio [HR] 59.78) and smoking (HR 2.78) were independent risk factors for AAA formation. Among 44 with AAA at 65, 22 completed AAA repair with no 30-day mortality.

CONCLUSIONS

AAA screening in a contemporary setting was safe at 5 years, with a single AAA rupture observed among non-attenders. Men with a screening detected AAA had a high repair rate and high non-AAA related mortality. AAA-formation was common among men with sub-aneurysmal dilatation, indicating a possible need for surveillance of this group. 

Abstract[4]

A review of current reporting of abdominal aortic aneurysm mortality and prevalence in the literature.

BACKGROUND

It is common for authors to introduce a paper by demonstrating the importance of the clinical condition being addressed, usually by quoting data such as mortality and prevalence rates. Abdominal aortic aneurysm (AAA) epidemiology is changing, and therefore such figures for AAA are subject to error. The aim of this study was to analyze the accuracy of AAA prevalence and mortality citations in the contemporaneous literature.

METHODS

Two separate literature searches were performed using PubMed to identify studies reporting either aneurysm prevalence or mortality. The first 40 articles or those published over the last 2 years were included in each search to provide a snapshot of current trends. For a prevalence citation to be appropriate, a paper had to cite an original article publishing its own prevalence of AAA or a national report. In addition, the cited prevalence should match that published within the referenced article. These reported statistics were compared with the most recent data on aneurysm-related mortality.

RESULTS

The prevalence of AAA was reported to be as low as 1% and as high as 12.7% (mean 5.7%, median 5%). Only 47.5% of studies had referenced original articles, national reports or NICE, and only 32.4% of cited prevalences matched those from the referenced article. In total 5/40 studies were completely accurate. 80% of studies cited aneurysm mortality in the USA, with the majority stating 15,000 deaths per year (range 9,000 to 30,000). Current USA crude AAA mortality is 6,289 (2010).

CONCLUSION

References for AAA mortality and prevalence reported in the current literature are often inaccurate. This study highlights the importance of accurately reporting mortality and prevalence data and using up-to-date citations.

Evidence-Based References

  • 1S.T. Edwards, M.L. Schermerhorn, A.J. O’Malley, et al.: Comparative effectiveness of endovascular versus open repair of ruptured abdominal aortic aneurysm in the Medicare population. J Vasc Surg. 59:575–582 2014 24342064 

  • 2G.K. Ambler, C.P. Twine, J. Shak, et al.: Survival following ruptured abdominal aortic aneurysm before and during the IMPROVE Trial: a single-centre series. Eur J Vasc Endovasc Surg. 47:388–393 2014 24534638 

  • 3S. Svensjö, M. Björck, A. Wanhainen: Five-year outcomes in men screened for abdominal aortic aneurysm at 65 years of age: a population-based cohort study. Eur J Vasc Endovasc Surg. 47:37–44 2014 24262320

  • 4P.W. Stather, D.A. Sidloff, I.A. Rhema, et al.: A review of current reporting of abdominal aortic aneurysm mortality and prevalence in the literature. Eur J Vasc Endovasc Surg. 47:240–242 2014 24368205

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