AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• Mri
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

Background

Abdominal aortic aneurysms (AAAs) are segmental dilatations of the aortic wall that cause the vessel to be larger than 1.5 times its normal diameter or that cause the distal aorta to exceed 3 cm. These can continue to expand and rupture spontaneously, exsanguinate, and cause death.

AAA rupture is an important cause of unheralded deaths in people older than 55 years, claiming more than 15,000 lives annually in the United States alone.

Pathophysiology

A marked decrease in aortic elastin, an increase in collagen production and degradation, inflammatory changes, and imbalances of matrix metalloproteinases and their inhibitors have been noted in pathologic studies.^{1, 2, 3, 4, 5, 6, 7, 8, 9, 10} Atherosclerosis may be only a facilitating factor.

Genetic predisposition plays some role, especially in disorders such as Marfan disease and type IV Ehlers-Danlos syndrome. Familial clustering of cases also has been documented.¹¹

Clinical risk factors that predispose individuals to these degenerative changes in the arterial wall include smoking, advanced age, male sex, chronic obstructive pulmonary disease (COPD), hypertension, and family history.¹² Females, African-Americans, and persons with diabetes appear to have a lower prevalence of AAA.^{13, 14}

Larger aneurysms tend to enlarge at a higher rate, as noted by Bernstein.¹⁵

Table 1. Growth Rate of AAAs

The natural history of an individual case is difficult to predict, and AAAs can have intervals of stability and slow and rapid expansion. The general recommendation is to consider elective aneurysmorrhaphy for aneurysms with a diameter of 5 cm or greater or for small aneurysms that have an average growth rate of more than 0.5 cm/y.¹⁶ Approximately 20% of aneurysms expand faster than 0.4 mm/y; the rest do so at slower rates.

AAA rupture

In addition to the initial aneurysm diameter, independent predictors of rupture include current smoking, lower forced expiratory volume (FEV-1), and higher mean blood pressure, all risk factors possibly amenable to modification. Findings from various series have suggested that diabetes mellitus, elevated levels of serum markers such as amino-terminal type III procollagen propeptide (PIIINP), a rapid rate of AAA expansion, and unfavorable morphology and aortic wall compliance are also predictive of rupture.^{17, 18, 19, 20, 21, 22} Of note, the prevalence of diabetes in the population with AAAs is relatively low.

Attempts have been made to index the aneurysmal diameter to individual body size or anatomic points of reference (eg, body surface area, supraceliac aortic diameter, aneurysm length), but no feature has been found to be highly predictive of rupture. Rupture has been observed in some AAAs smaller than 5 cm in diameter but wider than the transverse dimension of the third lumbar vertebral body.²³

Findings from a few studies have suggested that most AAAs rupture into the left retroperitoneum. The retroperitoneum contains the leak by means of mechanisms that cause clotting or tamponade. This rupture can also cause abdominal, back, or flank pain; this symptom is related to impingement of the hematoma on adjacent structures.

Aneurysms that continue to leak or those that rupture into the peritoneal cavity can result in hemodynamic collapse and, often, death.

Frequency

United States

The estimated incidence of ruptured AAA in a population study from Sweden was 0.06 case per 1000 people.²⁴ This rate increased with age; the age-adjusted incidences were less than 0.01, 0.37, or 1.36 per 1000 people younger than age 60 years, those aged 70-79 years, and those older than 90 years, respectively.

The best-known predictor of rupture rate is the maximal aneurysm diameter. Simplified estimates for the annual rupture rates based on size are as follows:

Table 2. Annual Rupture Rates Based on Size

The annual rupture rate in the UK Small Aneurysm Trial (N = 2257, with about half in randomized arm and half in the registry) was 2.2% per year for the first 3 years of follow-up.²⁵ The initial aneurysm diameter was 3-6 cm, and the mean was approximately 4.4 cm.

AAA rupture after stent-graft placement has been observed with specific devices, but device evolution and operator experience in both patient selection and device placement make it difficult to provide any stable estimates of the incidence at this time.^{26, 27, 28, 29}

Mortality/Morbidity

The mortality rate for ruptured AAA is substantial. As many as 2 of 3 patients with ruptured AAA die before arriving at the hospital.³⁰ Of those who reach the hospital, as many as one fifth of those who die do so before the operation, and the overall mortality rate still averages approximately 49%.

Multivariate analyses by Harris and coworkers revealed adverse predictors for early mortality, as shown in Table 3 below.³¹

Table 3. Predictors of Early Mortality

Note: For all comparisons, P <.05 unless otherwise noted. BP indicates blood pressure.

*P value <.10.

Deaths that occurred after the second postoperative day were predicted by variables shown in Table 4 below.

Table 4. Variables Predictive of Mortality

In the consecutive series of 180 patients with ruptured AAA,³² the following factors were independently related to the mortality rate: age; systolic BP less than 80 mm Hg; and a history of hypertension, angina, or myocardial infarction (MI). In patients who survived the surgery, the causes of death were as follows:

• Renal failure or multisystem failure (32%)



• Cardiac failure (29%)



• Respiratory failure, including pneumonia (17%)



• Coagulopathy (12%)



• GI hemorrhage (3%)



• Perforated duodenal ulcer (1.5%)



• Renal hemorrhage (1.5%)



• Hemorrhage from graft anastomosis (1.5%)



• Stroke (1.5%)



• Aspiration (1.5%)

Major postoperative complications observed in a series of 174 patients at the Mayo Clinic are shown in Table 5 below.

Table 5. Major Postoperative Complications

*CHF indicates congestive heart failure.

Other major postoperative morbidities reported in the literature include the following³³:

• Delayed hemorrhage from iatrogenic injuries



• GI or genitourinary tract injuries



• Pancreatitis



• Duodenal obstruction



• Prosthetic graft infection

One in 5 patients undergo a repeat operation. One half undergo repeat laparotomy, and the other half undergo a tracheostomy or vascular procedure.³¹

Late in-hospital deaths occur at a mean of 25 days ± 23.

The long-term outlook for patients is grim. Table 6 below shows survival statistics of the 147 patients with ruptured AAA (defined as blood outside the aortic wall) in the prospective Canadian Aneurysm Study.³⁴ Younger age and total intraoperative urine output were the only factors that were independently predictive of survival.

Table 6. Cumulative Survival of Ruptured AAA Patients, as Determined at Kaplan-Meier Analysis

Roughly 40% of early and late ( <5 y) deaths are attributable to coronary artery disease and its complications.³⁵

The availability of vascular surgeons, as opposed to general surgeons, was independently associated with a decreased 30-day mortality rate.²³

Sex

• In 2001, the National Center for Health Statistics reported that annual deaths attributable to AAA are almost 2-fold higher for males compared with females.



• An autopsy study revealed that the peak incidence of AAA was a decade later for women compared with men. Specifically, the peak incidence for women was at 90 years (4.5%) and 80 years in men (5.9%).³⁶



• Females were noted to have 3 times more ruptures than males in the UK Small Aneurysm Trial.³⁷ In addition, females who have ruptured AAA may have a higher mortality rate than that of their male counterparts.^{30, 24}

Age

• The incidence of AAA increases significantly after age 55 years in men and after age 70 years in women.³⁶



• The mean age of men with ruptured AAA is 70.6 years (range, 44-89 y) versus 77.3 years (range, 67-86 y) for women.³²



• Consequently, a number of competing comorbidities occur in this elderly cohort. These diminish the long-term survival rates even after successful AAA repair. On average, two thirds of postoperative patients died within the next 5 years, mostly due to causes related to cardiovascular disease.

Anatomy

Approximately one third of AAAs originate close to or at the level of the renal arteries, and suprarenal involvement has been reported in as many as 10% of patients.

In an old series by Rosch, 1 in 3 patients had accessory renal arteries, of which 7% arose from the AAA, and 1 in 5 patients had celiac or superior mesenteric artery stenosis.³⁸ As many as 30% of patients with AAA can have renal artery stenosis.³⁹ These are relevant findings because colon ischemia, as well as renal failure, can occur after aneurysmectomy.

A Japanese series of 97 cases of ruptured AAA revealed the following distribution of sites of rupture⁴⁰:

• Right lateral wall - 28%



• Pelvic arteries - 22%



• Posterior wall - 19%



• Left lateral wall - 17%



• Anterior wall - 10%



• Suprarenal - 4%

In a series of 226 AAAs in Italy, bleeding occurred into the following regions⁴¹:

• Retroperitoneal - 85.3%



• Peritoneal - 7.1%



• Inferior vena cava (IVC) or iliac vein - 5.8%



• Enteric - 1.8%

Although ruptures into the retroperitoneum typically originate from the left posterior aspect of the AAA, ruptures into the intestine tend to occur from the right anterior aspect.⁴²

Clinical Details

As many as three fourths of AAAs are initially asymptomatic.⁴³ Most aneurysms are incidentally discovered during routine physical examination, during a diagnostic imaging study, or during surgery for other abdominal pathology.

Hypotension, pulsatile abdominal mass, and flank or back pain constitute the classic triad for ruptured AAA. However, this triad may be incomplete in as many as 50% of patients. Cardiac arrest can be the clinical presentation in a fourth of patients.⁴⁴ In 1985, Donaldson et al described the presentation of their series of 81 patients that survived to undergo surgery for ruptured AAA.⁴⁵

Symptoms

• Abdominal pain - 58%



• Back pain - 70%



• Syncope - 30%



• Vomiting - 22%

Findings

• Mass - 91%



• Tenderness - 78%



• Systolic blood pressure less than 80 mm Hg - 42%



• White blood cell count greater than 10,000/µL - 79%



• Hematocrit less than 38-42%



• AAA apparent on abdominal plain film - 74%

Atypical presentations

• Pain radiating to the groin



• Back pain from AAA erosion into the vertebral body, with rare false aneurysm formation into the left psoas muscle



• Acute femoral neuropathy with or without thigh ecchymosis due to femoral nerve compression as blood dissects inferiorly between the iliacus and psoas muscles and the overlying fascial pockets



• Partial upper GI obstruction from AAA compression of the third portion of the duodenum



• Lower extremity ischemia and visceral thromboembolism caused by embolization of AAA mural thrombi



• Acute bilateral limb ischemia from aortic thrombosis



• GI bleeding secondary to aortoenteric fistula, usually involving the third part of the duodenum



• High output CHF, widened pulse pressure with machinery-like murmur, hematuria, rectal bleeding, priapism, or lower extremity swelling related to a fistula from the aorta to IVC or renal, lumbar, or common iliac vein

Preferred Examination

Intravenous access with 2 large-bore catheters should be established if a ruptured AAA is suspected. Blood should be drawn for stat determination of the CBC and kidney profile and for blood typing and screening. The vascular surgery team should be involved from the outset.

Ideally, in a hemodynamically stable patient, nonenhanced and enhanced helical or spiral CT of the thorax, abdomen, and pelvis should be expeditiously performed. This examination provides key information about the extent of aneurysmal disease, and it can be used to confirm and localize the site of rupture (see Image 1).

In the patient with an unstable presentation, an emergency operation is indicated. Time may permit only rapid bedside ultrasonography (US) and Doppler study of abdominal aorta and iliac arteries to confirm the presence of aneurysms.

The maximal aneurysm diameter is adequately assessed by using B-mode ultrasonography, CT scanning, and MRI. Aortography reveals only the lumen of the AAA because laminated clot obscures the outer limit of the aneurysm wall. Therefore, it often causes underestimation of the true aortic diameter.

Limitations of Techniques

Although CT and MRI provide detailed information about the blood vessels and their surrounding structures, these examinations require time; therefore, they may be unsuitable for use in patients in unstable condition. When contrast material is used in conjunction with CT to delineate blood-filled structures, it poses a risk of acute renal failure, particularly in hypovolemic elderly patients who may already have baseline nephrosclerosis or diabetic nephropathy.

Sonography is a quick and convenient modality, but it is much less sensitive and specific for the diagnosis of aneurysmal rupture. The absence of sonographic evidence of rupture does not rule out this entity if clinical suspicion is high.

Patient Education: For excellent patient education resources, visit eMedicine's Circulatory Problems Center. Also, see eMedicine's patient education article Aortic Aneurysm.

DIFFERENTIALS

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Other Problems to be Considered

Nephrolithiasis or renal colic
Acute cholecystitis
Diverticulitis
Perforated gastric ulcer or peptic ulcer disease
Bowel infarction
GI hemorrhage
Musculoskeletal lower back pain
MI

RADIOGRAPH

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Findings

A curvilinear calcified rim often to the left of the midline is apparent on some plain abdominal radiographs. Lateral radiography can depict large AAAs on the basis of calcification in the wall. This finding can be seen in more than half of patients.

Degree of Confidence

The degree if confidence is low. Suspicious findings on the abdominal radiograph should be confirmed by using another imaging modality.

False Positives/Negatives

Mural calcification can be radiographically inapparent and lead to a false-negative finding in as many as half of small AAAs. Magnification errors are also possible, leading to over- or underestimation of AAA diameter.

CT SCAN

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Findings

General findings

Unlike angiography, CT and MRI provide information about the wall of the aorta, and they delineate the presence of thrombus.⁴⁶ They provide detail about surrounding abdominal structures and their relationship to the AAA (see Image 1). Perianeurysmal fibrosis, venous anomalies (eg, retroaortic left renal vein, circumaortic venous collar), and horseshoe kidney are reliably demonstrated. However, these modalities (particularly MRI) are currently time and labor intensive, and they are not suitable for use in patients in unstable condition.

Helical or spiral CT angiography (CTA) allows reasonable visualization of branches of the aorta in the context of surrounding structures. Postprocessing of images and 3-dimensional reconstruction are possible.

Magnetic resonance angiography (MRA) has the advantage of eliminating the need for potentially nephrotoxic contrast agents and ionizing radiation, but its acquisition speed, cost, and image quality still need to be improved. Ferromagnetic implants or severe claustrophobia also can preclude use of MRI and/or MRA.

Findings that indicate possible AAA rupture include soft tissue hyperintensity outside the aortic wall, an indistinct aortic wall, thinning or fracture of a calcified aortic wall segment, penetration of a hematoma into the leaves of the mesentery, or contrast extravasation into the psoas muscle or retroperitoneum.

The nonenhanced study shows a mass or collection that extends into the perirenal spaces, or, less commonly, into the pararenal spaces. The AAA is often obscured or anteriorly displaced. Other possible findings include a focally indistinct aortic margin (usually the site of rupture), enlargement or obscuration of the psoas muscle, and anterior displacement of the kidney.

CT-specific findings

Freshly extravasated blood typically has a high CT attenuation value, whereas an isoattenuating or hypoattenuating hematoma signifies that a leak that is days or weeks old.

The crescent sign is an enhancement within the AAA mural thrombus or wall that is thought to represent intramural hematoma.⁴⁷ This was found to be a sign of acute or impending rupture in a retrospective series, with a sensitivity, specificity, and positive predictive value of 77%, 93%, and 53%, respectively.⁴⁸

Periaortic fibrosis outside of the subintimal calcification is suggestive of inflammatory aneurysm.

Degree of Confidence

The degree of confidence is high.

False Positives/Negatives

Soft tissue attenuation outside of the abdominal aorta can be related to changes secondary to an inflammatory process. These findings may possibly be related to pathology from other abdominal viscera. The sensitivity and specificity for the detection of AAA rupture decreases if a nonenhanced study is performed.

MRI

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Findings

MRI is a valuable alternative to CT in patients with renal insufficiency in whom contrast material–induced nephropathy is a concern.⁴⁹ MRI is also helpful in further delineating the aorta in the context of a large retroperitoneal collection that obscures the borders between adjacent structures, as well as laminated clot or atherosclerotic debris on the aneurysmal wall (Lee, 1984).

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness withtroublemoving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

The degree of confidence is high.

False Positives/Negatives

Soft tissue intensity changes outside of the abdominal aorta can be related to changes secondary to an inflammatory process. These findings might actually be related to pathology from other abdominal viscera.

ULTRASOUND

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Findings

Unlike most other modalities (eg, aortography, CT, MRI), abdominal US can be performed expeditiously and at the bedside.²⁴

For partially encapsulated hematomas, a hypoechoic or anechoic para-aortic space-occupying lesion may be detected.

Color-flow Doppler can aid in detecting the site of leak or extravasation, although adjustment to low-velocity scales may be necessary to register leaks with low flow rates.

Degree of Confidence

The degree of confidence is high for the detection of AAA and low for the detection of AAA rupture.

Although duplex US is competitive with CT or MRI for the detection of an AAA (>95% sensitivity), the visualization of surrounding structures is poor, and the sensitivity and specificity for rupture are low.

False Positives/Negatives

Conditions that limit the detection and measurement of AAAs or its branches include excessive bowel gas, obesity, and recent abdominal surgery.

If a ruptured AAA is clinically suspected, other diagnostic modalities should be pursued even if the sonographic results are negative.

ANGIOGRAPHY

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Findings

Digital subtraction angiography (DSA) provides high-spatial-resolution images of the lumen of the vascular tree and permits the quantification of significant stenoses in renal, mesenteric, and iliofemoral arteries.³⁸ CT also depicts aberrant vessels well.

Angiographic findings of AAA rupture include the following:

• Contained rupture: Circumscribed extraluminal contrast enhancement is present. Additional views (oblique or lateral) may be required to detect this finding.



• Leaking aneurysm: Frank extravasation of contrast material with poor washout is observed. This is rarely demonstrated because the patients are typically in unstable condition and are transported directly to the operating room.



• Displacement of the visceral arteries or kidneys and ureters: Sometimes, this finding can be evident in larger collections of blood.



• Contrast enhancement: Contrast material may flow into these structures from the AAA in the rare circumstance of rupture into the GI tract or IVC.

Degree of Confidence

The degree of confidence is low.

Angiography is rarely used in the setting of suspected rupture and is relatively contraindicated except when endovascular stent grafting is planned because this is an experimental procedure. However, unusual manifestations of AAA rupture, such as into the IVC or GI tract (aortoenteric fistula) is demonstrated well with angiography.

False Positives/Negatives

The absence of extraluminal contrast cannot be used to totally rule out a small leak or stabilized rupture. If the degree of suspicion is high, a tomographic imaging modality should be performed.

Laminated or mural thrombus may give the false arteriographic impression that no AAA is present. A calcified aortic shell and the absence of lumbar arteries are clues to the presence of an aneurysm.

INTERVENTION

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In patients with AAA, initiate aggressive secondary prevention, including smoking cessation, dietary changes, and exercise. In addition, hypertension, hypercholesterolemia, and diabetes should be controlled.

AAA rupture, symptomatic expansion, or sentinel leak is a surgical emergency.⁵⁰ In the unstable patient, initial surgical proximal aortic control with the avoidance of perturbation of any tamponade effect provided by extra-aortic structures or hematoma is critical.

Large supplies of blood and blood products, including platelets and fresh-frozen plasma should be readily available.³² The availability of intraoperative autotransfusion can diminish this need.

Stent grafting with the option of proximal balloon occlusion for control of bleeding is an experimental approach that may prove to be an alternative in selected patients.⁵¹

Medical/Legal Pitfalls

• The failure to diagnose a ruptured AAA is a pitfall that can occur in as many as 30-64% of patients.²⁴ Marston catalogued the initial erroneous diagnosis in 46 of 152 retrospectively reviewed cases of ruptured AAA as shown in Table 7.

  Table 7. Misdiagnosis of AAA

  Initial Diagnosis	Misdiagnosed Cases, %	Average Delay, h
  Renal colic	24	15
  Diverticulitis	13	79
  GI hemorrhage	13	17
  Acute MI	8.7	13
  Back pain	8.7	18
  Motor vehicle accident	6.5	1.5
  Sepsis	6.5	26
  Other GI problem	6.5	4
  Other/no diagnosis	13	18






• In one study, the mean delay to correctly make the diagnosis of ruptured AAA was 24.4 hours.⁵² Of note, a high degree of suspicion as well as careful attention to the abdominal examination may help minimize missing this diagnosis. In patients with a misdiagnosis, the vascular specialist was able to detect a pulsatile mass in 71%, compared with only 25% during the initial examination.⁵²



• In an analysis published in 1984, Hiatt found the following determinants of failure in the treatment of ruptured AAA:
• • Failure to perform elective aneurysmectomy in patients with known AAA
  
  
  
  • Initial misdiagnosis leading to delayed surgery
  
  
  
  • Undue delays in induction of anesthesia
  
  
  
  • Intraoperative technical errors, most commonly venous injuries (eg, renal, iliac, or lumbar vein hemorrhage, which can be difficult to control)
  
  
  

Special Concerns

• Factors that portend an 80% or higher mortality rate include the following^{32, 24}:
• • Patient aged 80 years or older
  
  
  
  • Shock presentation with free intraperitoneal rupture (in contrast to a mortality rate of approximately 20% in stable patients with a small contained rupture)
  
  
  
  • Persistent preoperative hypotension despite aggressive fluid and blood replacement
  
  
  
  • Preoperative cardiac arrest
  
  
  
  • Admission hematocrit level less than 25%
  
  
  
• More results of recent series from select centers indicate possible improvements in surgical survival, and investigators advocate a continued aggressive approach for these patient subgroups.⁴⁴



• Because the average age of patients with AAA is high, comorbidities requiring unrelated surgeries are not uncommon in patients being followed up for AAA.³² Findings from several small series suggest an elevated risk of rupture after other surgical procedures.
• • The observed rate of rupture in association with open-heart surgery is 0-14%.^{35, 53, 54}
  
  
  
  • Of the 13 patients who underwent open biliary procedures in the series by Fry and Fry, 1 patient had a thoracoabdominal aneurysm that ruptured 8 days after cholecystectomy.⁵⁵ Conversely, an estimated 5% of patients with AAA also have gallstones and are considered at risk for cholecystitis after aneurysmectomy.
  
  
  
  • The observed prevalence of colon cancer is approximately 2% in the population with AAA. Nora and coworkers noted 3 (11%) AAA ruptures in 27 patients; all occurred within 3 days of surgery for intra-abdominal malignancy.⁵⁶
  
  
  
  • Coexistent disease claims as many lives over time as do ruptures in patients with AAA. Therefore, preventive therapy to reduce the risk of atherosclerosis and its sequelae is mandated.
  
  
  
  • Special attention should be paid to the detection of inflammatory aneurysms because of the associated higher operative morbidity and mortality rates. Patients with these types of aneurysms account for 3-10% of those with AAAs, but as many as half of their aneurysms may go unrecognized before surgery. Abdominal or back pain is common, and significant weight loss is observed in as many as 25% (Pennell, 1985). The inflammatory process can also cause adhesions, ureteric obstruction with secondary hydronephrosis or pyelonephritis; renal failure; and, rarely, duodenal obstruction.
  
  
  
• Acknowledgments: The authors would like to thank the staff of the Hopwood Library at UPMC Shadyside and Christopher Tan for their support and assistance.

MULTIMEDIA

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Media file 1:  Contrast-enhanced abdominal CT in an elderly patient who presented with severe back pain but was hemodynamically stable. CT reveals an abdominal aortic aneurysm (AAA) with eccentric mural thrombus. A disruption of the calcific rim of the AAA toward the left quadrant appears with adjacent isoattenuating soft tissue anterior to the left psoas muscle. Clinical and radiologic findings are consistent with a diagnosis of contained AAA rupture with left retroperitoneal hematoma.
	View Full Size Image
Media type:  CT

REFERENCES

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1. Busuttil RW, Abou-Zamzam AM, Machleder HI. Collagenase activity of the human aorta. A comparison of patients with and without abdominal aortic aneurysms. Arch Surg. Nov 1980;115(11):1373-8. [Medline].
2. Dobrin PB, Baker WH, Gley WC. Elastolytic and collagenolytic studies of arteries. Implications for the mechanical properties of aneurysms. Arch Surg. Apr 1984;119(4):405-9. [Medline].
3. Campa JS, Greenhalgh RM, Powell JT. Elastin degradation in abdominal aortic aneurysms. Atherosclerosis. May 1987;65(1-2):13-21. [Medline].
4. Baxter BT, McGee GS, Shively VP, et al. Elastin content, cross-links, and mRNA in normal and aneurysmal human aorta. J Vasc Surg. Aug 1992;16(2):192-200. [Medline].
5. Baxter BT, Davis VA, Minion DJ, et al. Abdominal aortic aneurysms are associated with altered matrix proteins of the nonaneurysmal aortic segments. J Vasc Surg. May 1994;19(5):797-802; discussion 803. [Medline].
6. Thompson RW, Parks WC. Role of matrix metalloproteinases in abdominal aortic aneurysms. Ann N Y Acad Sci. Nov 18 1996;800:157-74. [Medline].
7. Knox JB, Sukhova GK, Whittemore AD, Libby P. Evidence for altered balance between matrix metalloproteinases and their inhibitors in human aortic diseases. Circulation. Jan 7 1997;95(1):205-12. [Medline].
8. McMillan WD, Pearce WH. Inflammation and cytokine signaling in aneurysms. Ann Vasc Surg. Sep 1997;11(5):540-5. [Medline].
9. Tamarina NA, McMillan WD, Shively VP, Pearce WH. Expression of matrix metalloproteinases and their inhibitors in aneurysms and normal aorta. Surgery. Aug 1997;122(2):264-71; discussion 271-2. [Medline].
10. Davis V, Persidskaia R, Baca-Regen L, et al. Matrix metalloproteinase-2 production and its binding to the matrix are increased in abdominal aortic aneurysms. Arterioscler Thromb Vasc Biol. Oct 1998;18(10):1625-33. [Medline].
11. Tilson MD, Seashore MR. Fifty families with abdominal aortic aneurysms in two or more first- order relatives. Am J Surg. Apr 1984;147(4):551-3. [Medline].
12. Tilson MD. Aortic aneurysms and atherosclerosis. Circulation. Jan 1992;85(1):378-9. [Medline].
13. Sonesson B, Lanne T, Vernersson E, Hansen F. Sex difference in the mechanical properties of the abdominal aorta in human beings. J Vasc Surg. Dec 1994;20(6):959-69. [Medline].
14. Lederle FA, Johnson GR, Wilson SE, et al. The aneurysm detection and management study screening program: validation cohort and final results. Aneurysm Detection and Management Veterans Affairs Cooperative Study Investigators. Arch Intern Med. May 22 2000;160(10):1425-30. [Medline].
15. Bernstein EF, Chan EL. Abdominal aortic aneurysm in high-risk patients. Outcome of selective management based on size and expansion rate. Ann Surg. Sep 1984;200(3):255-63. [Medline].
16. Hollier LH, Taylor LM, Ochsner J. Recommended indications for operative treatment of abdominal aortic aneurysms. Report of a subcommittee of the Joint Council of the Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular Surgery. J Vasc Surg. Jun 1992;15(6):1046-56. [Medline].
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Article Last Updated: Mar 23, 2007