Abdominal Aortic Aneurysm Clinical Presentation
- Author: Saum A Rahimi, MD, FACS; Chief Editor: Vincent Lopez Rowe, MD more...
As noted (see Overview, Etiology), patients at greatest risk for abdominal aortic aneurysms (AAAs) are those who are older than 65 years and have peripheral atherosclerotic vascular disease. Accordingly, a history of smoking, chronic obstructive pulmonary disease (COPD), and hypertension is often elicited. Less frequent causes include Marfan and Ehlers-Danlos syndromes, collagen vascular diseases, and mycotic aneurysm. Patients who have a first-degree relative with AAA are at increased risk.
AAAs are usually asymptomatic until they expand or rupture. Patients may experience unimpressive back, flank, abdominal, or groin pain for some time before rupture. Isolated groin pain is a particularly insidious presentation. This occurs with retroperitoneal expansion and pressure on either the right or left femoral nerve. This symptom may be present without any other associated findings, and a high index of suspicion is necessary to make the diagnosis.
At times, AAAs may cause symptoms from local compression, including early satiety, nausea, vomiting, urinary symptoms, or venous thrombosis from venous compression. Back pain can be caused by erosion of the AAA into adjacent vertebrae. Other symptoms include abdominal pain, groin pain, embolic phenomena affecting the toes (eg, livedo reticularis, or blue toe syndrome; see the image below), and fever. Occasionally, small AAAs thrombose, producing acute claudication.
Patients may describe a pulse in the abdomen and may actually feel a pulsatile mass.
It is important to note progressive symptoms, which should alert the clinician to the possibility of expansion with imminent rupture. An expanding AAA commonly causes sudden, severe, and constant low back, flank, abdominal, or groin pain. Syncope may be the chief complaint, with pain less prominent.
Symptoms of ruptured AAA
Persons with AAAs that have ruptured may present in many ways. The most typical manifestation of rupture is abdominal or back pain with a pulsatile abdominal mass. However, the symptoms may be vague, and the abdominal mass may be missed. Symptoms may include groin pain, syncope, paralysis, and flank mass. The diagnosis may be confused with renal calculus, diverticulitis, incarcerated hernia, or lumbar spine disease.
Transient hypotension should prompt consideration of rupture because this finding can progress to frank shock over a period of hours. Temporary loss of consciousness is also a potential symptom of rupture.
Patients with a ruptured AAA may present in frank shock, as evidenced by cyanosis, mottling, altered mental status, tachycardia, and hypotension. As many as 65% of patients with ruptured AAAs die of sudden cardiovascular collapse before arriving at a hospital.
AAAs may rupture into the vena cava, producing large arteriovenous fistulae. In this case, symptoms include tachycardia, congestive heart failure (CHF), leg swelling, abdominal thrill, machinery-type abdominal bruit, renal failure, and peripheral ischemia. Finally, an AAA may rupture into the fourth portion of the duodenum. These patients may present with a herald upper gastrointestinal bleed followed by an exsanguinating hemorrhage.
Most clinically significant AAAs are palpable upon routine physical examination; however, the sensitivity of palpation depends on the experience of the examiner, the size of the aneurysm, and the size of the patient. In one study, 38% of AAA cases were detected on the basis of physical examination findings, whereas 62% were detected incidentally on radiologic studies obtained for other reasons.
Abdominal examination includes palpation of the aorta and estimation of the size of the aneurysm. AAAs are palpated in the upper abdomen; the aorta bifurcates into the iliac arteries just above the umbilicus. The clinician need not be afraid of properly palpating the abdomen, because there is no evidence to indicate that aortic rupture can be precipitated by this maneuver.
Whereas the abrupt onset of pain due to rupture of an AAA may be quite dramatic, the associated physical findings may be very subtle. Patients may have normal vital signs in the presence of a ruptured AAA as a consequence of retroperitoneal containment of hematoma.
The presence of a pulsatile abdominal mass (see the image below) is virtually diagnostic of an AAA but is found in fewer than 50% of cases. It is more likely to be noted with a ruptured aneurysm. In an obese abdomen, an AAA is more difficult to palpate. Even in patients known to have an aneurysm, vascular surgeons are unable to palpate a pulsatile mass while preparing the patient for surgery in 25% of cases.
Occasionally, an overlying mass (pancreas or stomach) may be mistaken for an AAA. An abdominal bruit is nonspecific for an unruptured aneurysm, but the presence of an abdominal bruit or the lateral propagation of the aortic pulse wave can offer subtle clues and may be more frequently found than a pulsatile mass. Bruits may also indicate the presence of renal or visceral artery stenosis; a thrill is possible with aortocaval fistulae. Patients with popliteal artery aneurysms frequently have AAAs (25-50% of cases).
Misdiagnosis is fairly common because the classic presentation of pain associated with hypotension, tachycardia, and a pulsatile abdominal mass is present in less than 30-50% of cases. The leading misdiagnosis is renal colic; dissection of the renal artery may produce flank pain and hematuria.
Normally, systolic blood pressures are higher in the thigh than in the arm. In patients with AAA, this relation may be reversed. Bilateral upper-extremity blood pressures should be measured in patients with AAAs. Upper-extremity blood pressures that differ from each other by more than 30 mm Hg indicate subclavian artery stenosis, and perioperative monitoring is important. Cervical bruits may indicate carotid artery stenosis. Hypertension may trigger a workup for renal artery stenosis.
Femoral/popliteal pulses and pedal (dorsalis pedis or posterior tibial) pulses should be palpated to determine if an associated aneurysm (femoral/popliteal) or occlusive disease exists. Flank ecchymosis (Grey Turner sign) represents retroperitoneal hemorrhage.
The following are potential complications of AAAs:
Death (1.8-5% mortality for elective open repair, <1% for endovascular repair, and 50% if the AAA has ruptured, though studies are showing that this last figure is decreased with endovascular repair)
Myocardial infarction (2-5%)
Groin infection (<5%)
Graft infection (<1%)
Colon ischemia (<1% for elective repair, 15-20% if the AAA has ruptured)
Renal failure related to preoperative creatinine level, intraoperative cholesterol embolization, and hypotension
Incisional hernia (10-20%)
Amputation from major arterial occlusion
Blue toe syndrome and cholesterol embolization to feet
Impotence in males - Erectile dysfunction and retrograde ejaculation (>30%)
Paresthesias in thighs from femoral exposure (rare)
Lymphocele in groin (~2%)
Late graft enteric fistula
Blanchard JF, Armenian HK, Friesen PP. Risk factors for abdominal aortic aneurysm: results of a case-control study. Am J Epidemiol. 2000 Mar 15. 151(6):575-83. [Medline].
Lederle FA, Johnson GR, Wilson SE, Chute EP, Littooy FN, Bandyk D, et al. Prevalence and associations of abdominal aortic aneurysm detected through screening. Aneurysm Detection and Management (ADAM) Veterans Affairs Cooperative Study Group. Ann Intern Med. 1997 Mar 15. 126(6):441-9. [Medline].
Wassef M, Baxter BT, Chisholm RL, Dalman RL, Fillinger MF, Heinecke J, et al. Pathogenesis of abdominal aortic aneurysms: a multidisciplinary research program supported by the National Heart, Lung, and Blood Institute. J Vasc Surg. 2001 Oct. 34(4):730-8. [Medline].
Guirguis-Blake JM, Beil TL, Senger CA, Whitlock EP. Ultrasonography screening for abdominal aortic aneurysms: a systematic evidence review for the U.S. Preventive Services Task Force. Ann Intern Med. 2014 Mar 4. 160(5):321-9. [Medline].
Svensjö S, Björck M, Gürtelschmid M, Djavani Gidlund K, Hellberg A, Wanhainen A. Low prevalence of abdominal aortic aneurysm among 65-year-old Swedish men indicates a change in the epidemiology of the disease. Circulation. 2011 Sep 6. 124(10):1118-23. [Medline].
Tilson MD, Ozsvath KJ, Hirose H, Xia S. A genetic basis for autoimmune manifestations in the abdominal aortic aneurysm resides in the MHC class II locus DR-beta-1. Ann N Y Acad Sci. 1996 Nov 18. 800:208-15. [Medline].
Ambler GK, Gohel MS, Mitchell DC, Loftus IM, Boyle JR. The Abdominal Aortic Aneurysm Statistically Corrected Operative Risk Evaluation (AAA SCORE) for predicting mortality after open and endovascular interventions. J Vasc Surg. 2014 Jun 28. [Medline].
Von Allmen RS, Powell JT. The management of ruptured abdominal aortic aneurysms: screening for abdominal aortic aneurysm and incidence of rupture. J Cardiovasc Surg (Torino). 2012 Feb. 53(1):69-76. [Medline].
Anjum A, von Allmen R, Greenhalgh R, Powell JT. Explaining the decrease in mortality from abdominal aortic aneurysm rupture. Br J Surg. 2012 May. 99(5):637-45. [Medline].
Daly KJ, Torella F, Ashleigh R, McCollum CN. Screening, diagnosis and advances in aortic aneurysm surgery. Gerontology. 2004 Nov-Dec. 50(6):349-59. [Medline].
Blaivas M, Theodoro D. Frequency of incomplete abdominal aorta visualization by emergency department bedside ultrasound. Acad Emerg Med. 2004 Jan. 11(1):103-5. [Medline].
Bobadilla JL, Suwanabol PA, Reeder SB, Pozniak MA, Bley TA, Tefera G. Clinical implications of non-contrast-enhanced computed tomography for follow-up after endovascular abdominal aortic aneurysm repair. Ann Vasc Surg. 2013 Nov. 27(8):1042-8. [Medline].
Clarençon F, Di Maria F, Cormier E, Gaudric J, Sourour N, Gabrieli J, et al. Comparison of intra-aortic computed tomography angiography to conventional angiography in the presurgical visualization of the Adamkiewicz artery: first results in patients with thoracoabdominal aortic aneurysms. Neuroradiology. 2013 Oct 2. [Medline].
Brewster DC, Cronenwett JL, Hallett JW Jr, Johnston KW, Krupski WC, Matsumura JS. Guidelines for the treatment of abdominal aortic aneurysms. Report of a subcommittee of the Joint Council of the American Association for Vascular Surgery and Society for Vascular Surgery. J Vasc Surg. 2003 May. 37(5):1106-17. [Medline].
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.
Lederle FA, Wilson SE, Johnson GR, Reinke DB, Littooy FN, Acher CW, et al. Immediate repair compared with surveillance of small abdominal aortic aneurysms. N Engl J Med. 2002 May 9. 346(19):1437-44. [Medline].
Fillinger MF, Raghavan ML, Marra SP, Cronenwett JL, Kennedy FE. In vivo analysis of mechanical wall stress and abdominal aortic aneurysm rupture risk. J Vasc Surg. 2002 Sep. 36(3):589-97. [Medline]. [Full Text].
Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg. 1991 Nov. 5(6):491-9. [Medline].
Reichart M, Geelkerken RH, Huisman AB, van Det RJ, de Smit P, Volker EP. Ruptured abdominal aortic aneurysm: endovascular repair is feasible in 40% of patients. Eur J Vasc Endovasc Surg. 2003 Nov. 26(5):479-86. [Medline].
Schanzer A, Greenberg RK, Hevelone N, et al. Predictors of abdominal aortic aneurysm sac enlargement after endovascular repair. Circulation. 2011 Jun 21. 123(24):2848-55. [Medline].
Tan JW, Yeo KK, Laird JR. Food and Drug Administration-approved endovascular repair devices for abdominal aortic aneurysms: a review. J Vasc Interv Radiol. 2008 Jun. 19(6 Suppl):S9-S17. [Medline].
United Kingdom EVAR Trial Investigators. Greenhalgh RM, Brown LC, Powell JT, Thompson SG, Epstein D, Sculpher MJ. Endovascular versus open repair of abdominal aortic aneurysm. N Engl J Med. 2010 May 20. 362(20):1863-71. [Medline].
United Kingdom EVAR Trial Investigators, Greenhalgh RM, Brown LC, Powell JT, Thompson SG, Epstein D. Endovascular repair of aortic aneurysm in patients physically ineligible for open repair. N Engl J Med. 2010 May 20. 362(20):1872-80. [Medline].
De Bruin JL, Baas AF, Buth J, Prinssen M, Verhoeven EL, Cuypers PW, et al. Long-term outcome of open or endovascular repair of abdominal aortic aneurysm. N Engl J Med. 2010 May 20. 362(20):1881-9. [Medline].
White GH, Yu W, May J. Endoleak--a proposed new terminology to describe incomplete aneurysm exclusion by an endoluminal graft. J Endovasc Surg. 1996 Feb. 3(1):124-5. [Medline].
Filardo G, Lederle FA, Ballard DJ, et al. Immediate open repair vs surveillance in patients with small abdominal aortic aneurysms: survival differences by aneurysm size. Mayo Clin Proc. 2013 Sep. 88(9):910-9. [Medline].
O’Riordan M. EVAR Improves Aneurysm-Related Survival Over Surgery. Medscape Medical News. Available at http://www.medscape.com/viewarticle/778123. Accessed: February 6, 2013.
Mehta M, Paty PS, Byrne J, Roddy SP, Taggert JB, Sternbach Y, et al. The impact of hemodynamic status on outcomes of endovascular abdominal aortic aneurysm repair for rupture. J Vasc Surg. 2013 May. 57(5):1255-60. [Medline].
Le Manach Y, Collins GS, Ibanez C, Goarin JP, Coriat P, Gaudric J, et al. Impact of Perioperative Bleeding on the Protective Effect of ß-Blockers during Infrarenal Aortic Reconstruction. Anesthesiology. 2012 May 30. [Medline].
Lederle FA, Freischlag JA, Kyriakides TC, Padberg FT Jr, Matsumura JS, et al. Outcomes following endovascular vs open repair of abdominal aortic aneurysm: a randomized trial. JAMA. 2009 Oct 14. 302(14):1535-42. [Medline].
Nishimori M, Low JH, Zheng H, Ballantyne JC. Epidural pain relief versus systemic opioid-based pain relief for abdominal aortic surgery. Cochrane Database Syst Rev. 2012 Jul 11. 7:CD005059. [Medline].
|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.|
|AAA Diameter (cm)||Rupture Risk (%/y)|
|AAA—abdominal aortic aneurysm.|
|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|
|Family history||No relatives||One relative||Numerous relatives|
|Hypertension||Normal blood pressure||Controlled||Poorly controlled|
|Wall stress||Low (35 N/cm2||Medium (40 N/cm2||High (45 N/cm2)|
|COPD—chronic obstructive pulmonary disease.|