ANEURYSM OF THE ABDOMINAL AORTA

ANEURYSM OF THE ABDOMINAL AORTA - David H. Stubbs, MD
BASICS
DESCRIPTION
A permanent localized (i.e., focal) dilatation of the abdominal aorta having at least a 50% increase in diameter compared to the expected diameter of the artery. The clinical presentation of aneurysms relates to location, size, type, and comorbid factors affecting the patient. The majority of aneurysms are asymptomatic. Some present with rupture, others with embolism or thrombosis. The management and indications for surgical repair is dictated by the natural history of the aneurysm, the type, the consequences of repair, and the general status of the patient. There are two types, which are infrarenal (90%) and thoracoabdominal.
• System(s) Affected: Cardiovascular; Hemic/ Lymphatic/Immunologic
• Synonym(s): Aortic aneurysms; AAA
ALERT
Geriatric Considerations
Familial aggregations exist, but pathogenesis relates to interaction of genetic, environmental, and biochemical factors.
- Marfan syndrome
- Ehlers-Danlos syndrome
Pediatric Considerations
Etiology more likely infectious or collagen disorders
GENERAL PREVENTION
Screening: 1-time ultrasound screening for AAA in male patients, ages 65-75 who have ever smoked >100 cigarettes
EPIDEMIOLOGY
• Predominant age: Elderly
• Predominant sex: Male > Female (4:1)
Incidence
• >15,000 deaths per year
• 10th leading cause of death in males >55
- In men >60 years: 2-5%
- In men >65 years: 6%
- In men >75 years: 11%
• In women >65 years: 4%
• High risk groups
- Coronary disease: 5-9%
- Peripheral vascular disease: 10-15%
- 1st degree relative with AAA: 25%
- Males = 40% risk
- Females = 15% risk
- Obese patients >65 years
- Presence of peripheral aneurysms
RISK FACTORS
• Hypertension
• Nicotine
• COPD
• Familial: Siblings of patients with AAA
ETIOLOGY
• Atherosclerosis
• Inflammatory (5-10%)
• Traumatic
• Genetic predisposition (Marfan, Ehlers-Danlos)
ASSOCIATED CONDITIONS
• Marfan syndrome
• Ehlers-Danlos syndrome

DIAGNOSIS
SIGNS AND SYMPTOMS
Physical Exam
Majority of patients with abdominal aortic aneurysm (AAA) are asymptomatic. Many are discovered during radiologic procedures performed for other reasons.
• Pulsatile epigastric mass
• Vague abdominal pain
- May radiate to the back of flank
• Encroachment by aneurysm
- Vertebral body erosion
- Gastric outlet obstruction
- Ureteral obstruction
• Lower extremity ischemia secondary to microembolization or macroembolization of mural thrombus
• The triad of shock, pulsatile mass, and abdominal pain should always suggest rupture of AAA
- Shock may be absent if the rupture is contained.
- Palpable pulsatile mass may be absent in up to 50% of the patients with rupture.
- Pain may radiate to the back or into the groin.
- Rupture associated with 90% mortality rate.
• Unusual presentations
- Primary aortoenteric fistula: Erosion/rupture of AAA into duodenum
- Aortocaval fistula: Erosion/rupture of AAA into vena cava or left renal vein
- Inflammatory aneurysm: Encasement of aneurysm by thick inflammatory rind associated with chronic abdominal pain, weight loss, and elevated ESR
- Surrounding viscera are densely adherent.
ALERT
Geriatric Considerations
More common in this age group and may present atypically
TESTS
Lab
Evaluation for concomitant CAD
• Selective evaluation for CAD is appropriate prior to elective AAA repair (i.e., cardiac clearance).
• Patients with mild, stable cardiac symptoms should have a noninvasive cardiac stress study.
• Coronary revascularization should be performed when the CAD would merit intervention on its own.
Imaging
Screening: 1-time ultrasound screening for AAA in male patients, ages 65-75, who have ever smoked >100 cigarettes
Diagnostic Procedures/Surgery
• Clinical examination
• Ultrasonography is the preferred initial diagnostic tool in suspected AAA, but is not reliable for a diagnosis of a rupture.
• CT scans are the preferred preoperative study. Avoid contrast if the patient has significant renal insufficiency. CT scans assist in the diagnosis of an inflammatory aneurysm.
• MRI: Similar to CT and avoids contrast. MR angiography may replace arteriograms.
• Aortography: Does not define outside dimensions of aneurysms.
• Indications for aortography
- Associated renovascular hypertension
- Symptoms of visceral angina
- Significant iliofemoral occlusive disease
- Peripheral aneurysms
- Horseshoe or pelvic kidney
- Prior colectomy
DIFFERENTIAL DIAGNOSIS
• Abdominal masses transmitting aortic pulse
• Other causes of abdominal pain (e.g., peptic ulcer disease)
• Other causes of back pain (e.g., arthritis, metastatic disease)
TREATMENT
STABILIZATION
• The treatment of AAA is elective repair.
• The prevention of AAA is elective repair.
GENERAL MEASURES
• Control hypertension
• Treat atherosclerotic risk factors
• Stop smoking
SURGERY
• Repair when
- Rupture occurs
- Size >5.5 cm (or >6 cm in poor surgical risk patients)
- Expansion >0.5 cm/6 months
- Symptoms occur
• Poor surgical risk patients
- Class III-IV angina; LVEF 30%; recent CHF or MI; severe valve disease
- Serum creatinine >3 mg/dL
- PaO2 50 mm Hg; FEV1IL
- Cirrhosis with ascites
- Diffuse retroperitoneal fibrosis; hostile abdomen
- Physiologic age > chronological age
• Endovascular aneurysm repair
- There are currently 3 devices approved by the FDA for marketing. Late complications of these devices continue to occur.
- Long-term CT surveillance is required.
- Adequate iliac/femoral access
- Infrarenal non-aneurysmal neck length of at least 1 cm at the proximal and distal ends of the aneurysm
- Morphology suitable for endovascular repair
- One of the following: A diameter >5 cm, a diameter of 4-5 cm, and an increase in size by 0.5 cm in the past 6 months.
- Health status adequate to undergo the 2-hour plus implementation procedure
FOLLOW-UP
PROGNOSIS
• Aneurysms usually expand over time (Laplace's Law: T (wall tension) = Pressure  Radius. Wall tension is directly related to blood pressure and the radius of the artery.) When wall tension exceeds wall tensile strength, rupture occurs.
• Surgical Outcomes:Morbidity 32%; cardiac (MI) 11%; mortality 4.2%
• Risk of morbidity and mortality increase with age
• Operative mortality is inverse to surgeon volume, hospital volume, specialty (vascular vs general surgeon)
• Non-repair (natural history of AAA >5.5 cm); 57% mortality within 1.5 years
• Mean expansion is 0.4 cm per year
• Rupture risk is increased by:
- Diastolic hypertension
- Tobacco use
- Diameter >6 cm
- COPD
- Familial history
• Ruptured aneurysms
- 8% die before receiving definitive care and 50% of the remaining die during their treatment or hospitalization.
COMPLICATIONS
• Rupture
• Associated dissection
• Thrombosis
• Embolization distally
PATIENT MONITORING
• Hypertension control
• Lipid control
• Recurrent assessment of smoking status
• Perioperative complications
- MI: 5%
- Renal failure: 6%, chronic dialysis: 1%
- Pulmonary failure: 5-8%
- Microembolism (trash foot): 1-4%
- Ischemic colitis: 0.5-1%
- Wound infection: 2%
- Graft infection: 0.5%
- Stroke: 0.5-1%
- Paraplegia: 0.2%
• Postsurgical monitoring
- Anastomotic aneurysm
- Graft infections
- Aortoenteric fistula
- Graft limb occlusion
- Additional aneurysms: Thoracic, thoracoabdominal, femoral
REFERENCES
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