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Abdominal Aortic Aneurysms

  1. An AAA is an increase in aortic diameter by greater than 50% of normal (aortic diameter of greater than 3 cm diameter).
  2. More prevalent in elderly men. Male : female ratio is 4:1
  3. Risk factors – hypertension, peripheral vascular disease, family history (15-25%)
  4. Other causes of aortic aneurysms include:
    1. Genetic: There is a familial tendency to aortic aneurysms. Connective tissue disorders such as Ehlers-
    2. Danlos syndrome and Marfan's syndrome.
    3. Post-traumatic:
    4. Arteritis, e.g.Takayasu disease, giant cell arteritis, and polychondritis.
    5. Congenital malformation of the aorta (aneurysms tend to develop just beyond the narrowing of a coarctation of the aorta).
    6. End-stage (tertiary) syphilis, which tends to affect the ascending aorta and arch of the aorta. Q
    7. Mycotic: infective (immunodeficiency, IV drug abuse, valve surgery).
  5. Degenerative aneurysms account for more than 90% of all infrarenal AAAs.Q
  6. Most cases of AAA begin below the renal arteries and end above the iliac arteries.
  7. They generally are spindle shaped (fusiform) 

Risk Factors for Rupture of Abdominal Aortic Aneurysm






<5 cm

5-6 cm

>6 cm


<0.3 cm/yr

0.3-0.6 cm/yr

>0.6 cm/yr

Smoking, COPD

None, mild



Family history

No relatives

One relative

Numerous relatives


Normal blood pressure


Poorly controlled




Very eccentric






Ref: Sabiston Textbook of Surgery, 18th Edition Ch 65

  1. Natural history
    1. In general, AAAs gradually enlarges (0.2-0.8 mm/y) and eventually rupture.
    2. 5 year risk of rupture:
      1. 5.0 – 5.9 cm = 25%
      2. 6.0 – 6.9 cm = 35%
      3. More than 7 cm = 75% 
  2. Pathophysiology:
    1. The aortic wall contains smooth muscle, elastin, and collagen arranged in concentric layers.
    2. The number of medial elastin layers from the proximal thoracic aorta to the infrarenal aorta is markedly reduced, with medial thinning and intimal thickening.
    3. Elastin is the principal load-bearing element in the aorta Q. Elastin fragmentation and degeneration are observed in aneurysm walls.
    4. It is coupled with the histological changes of this matrix protein in aneurysms. 
  3. Clinical features: 75% are asymptomatic
    1. Possible symptoms include
      1. Epigastric pain
      2. Back pain
      3. Malaise and weight loss (with inflammatory aneurysms)
    2. Rupture presents with
      1. Sudden onset abdominal pain
      2. Hypovolaemic shock
      3. Pulsatile epigastric mass
    3. Rare presentations include
      1. Distal embolic features: may cause livedo reticularis (blue toe syndrome)
      2. Acute aortic occlusion: Occasionally, small AAAs thrombosis, producing acute claudication.
      3. Aorto-caval fistula (symptoms include tachycardia, congestive heart failure (CHF), leg swelling, abdominal thrill, machinery-type abdominal bruit, renal failure, and peripheral ischemia).
      4. Primary aorto-intestinal fistula (AAA may rupture into the fourth portion of the duodenum and present with a herald upper gastrointestinal bleed). Q 

Indications for operationQ

  • Rupture
  • Symptomatic aneurysm; any size.
  • Rapid expansion
  • Asymptomatic > 6 cm – exact lower limit controversial. 
  1. Contraindications:
    1. COPD/ severe cardiac disease/ active infection/ and medical problems that preclude operative intervention. Q
    2. These patients may benefit best from endovascular stenting of the aneurysm. 
      Severe life-threatening comorbidities include advanced cancer, end-stage lung disease, or cardiac disease. 
  2. Approach:
    1. Monitor patients if AAA is smaller than 4 cm with ultrasound every 6 months, offer surgical intervention if the aneurysm expands or becomes symptomatic. Q
    2. Patients with an AAA of 5-6 cm in diameter benefit from repair, especially if they have other contributing factors like hypertension, continued smoking, or COPD.
    3. For patients at higher risk, the threshold for repair may be 6-7 cm in diameter.  
  3. Pre-operative investigationQ
    1. Need to determine
      1. Extent of aneurysm
      2. Fitness for operation
    2. Ultrasound, conventional CT and more recently spiral CT
    3. Determines – aneurysm size, relation to renal arteries, involvement of iliac vessels
    4. Angiography: It is indicated only(not in all cases) when associated renal or visceral involvement, peripheral occlusive disease, or aneurysmal disease exists. Q
    5. Most significant post op morbidity and mortality related to cardiac disease
    6. Cardiac revascularisation required in up to 10% of patients.


  1. Medical therapy: Smoking cessation/ aggressively control hypertension. Q
  2. Surgical therapy: Operative approach is through the traditional open laparotomy approach or, by the placement of endovascular stents.
    Prevention of distal embolization: The patient is heparinized prior to aortic cross clamping. If significant intraluminal debris, juxtarenal thrombus, or prior peripheral embolization exists, the distal arteries are clamped first, followed by aortic clamping. Q 
  3. Endovascular aneurysm repair Q
    1. Morbidity of conventional open aneurysm surgery related to:
      1. Exposure of infra-renal aorta/ Cross clamping of aorta
    2. Endovascular repair achieved by transfemoral or transiliac placement of prosthetic graft
    3. Proximal and distal cuffs / stents anchor graft
    4. Exclude aneurysm from circulation
    5. Only ~40% of aneurysms suitable for this type of repair
    6. Major problem related to placement and leakage around stent  
  4. Complications
    1. Graft migration/ Endovascular leak/ Graft kinking/ Graft occlusion
    2. One of the principle reasons for endograft failure is the presence of endoleak. Endoleak is defined as persistence of blood flow outside of the graft and within the aneurysm sac. 
  • Aortic dissection
    1. Commonest aortic emergency Q
    2. Incidence is twice that of ruptured abdominal aortic aneurysm
    3. Most commonly seen between 50 and 70 years
    4. Associated with hypertension, Marfan's syndrome, bicuspid aortic valve  
  1. Pathology
    1. Intimal tear results in blood splitting the aortic media
    2. Rupture can occur back into the lumen or externally in pericardium/ mediastinum
    3. External rupture often results in fatal pericardial tamponade
    4. Commonest site of intimal tear is within 2-3 cm of aortic valve Q
    5. Dissection can result in occlusion of aortic branches
    6. Most commonly involved are renal, spinal, coronary or iliac arteries  
  2. Stanfard ClassificationQ
    1. Type A: involves the ascending aorta (with or without the transverse and decending thora ic aorta.
    2. Type B: involves decending aorta (and thoracoabdominal aorta.
  3. Clinical features
    1. Chest pain occur in anterior chest.
    2. Back pain with dissection of the aorta occurs in about one-third of the patients.
    3. Another characteristic of the pain is tendency to migrate into different areas as dissection extends distally.
    4. Pain may radiate to the neck, the arm, the epigastrium or the leg.
    5. A myocardial infarction by contrast may gradually develop pain of increasing severity over several minutes.
    6. Syncope occurs in 10-20 % of the cases.
    7. Stroke develops in 3-5% of the cases.
    8. Hypertension occurs in 75-85% of the cases.
    9. An aortic diastolic murmur appears in 20-30 % of the cases.
    10. On chest radiograph a widened mediastinum or a left pleural effusion from extravasation of the blood.
    11. 2-D echography is the diagnostic investigation.
    12. Usually presents with tearing chest pain radiating to back associated with collapse
    13. Examination may show
      1. Reduced or absent peripheral pulsed
      2. Soft early diastolic murmur
    14. Chest x-ray usually shows a widened mediastinum.
    15. If aortic branches occluded there may clinical evidence of
      1. Acute renal failure
      2. Paraplegia
      3. Acute limb ischaemia       
      4. Cerebrovascular accident
      5. Inferior myocardial infarction  
  4. Complications of Aortic Dissection
    1. Aortic valve insufficiency
    2. Coronary malperfusion
    3. Pericardial tamponade
    4. Subclavian or iliofemoral artery malperfusion
    5. Carotid artery malperfusion
    6. Spinal malperfusion
    7. Mesenteric malperfusion
    8. Renal malperfusion 
  5. Management
    1. All patients require urgent management of associated hypertension
    2. Type A dissections usually require surgical intervention Q
    3. Dissection excised and aorta replaced with graft
    4. Aortic valve is preserved if possible
    5. An evolving CVA or established renal failure are contraindications to surgery
    6. Type B dissections may be treated without surgery Q
    7. Requires fastidious blood pressure control
    8. Surgery should be considered if evidence of aortic expansion.
    9. Surgery for Type B dissections is associated with significant risk of paraplegia
    10. Without operation the prognosis for Type A dissections is poor
    11. 40% die within 24 hours and 80% die within 2 weeks  
  • Popliteal artery aneurysms
    1. Defined as a popliteal artery diameter greater than 2 cm
    2. Account for 80% of all peripheral aneurysms (AIIMS Nov 08)
    3. 50% are bilateral. 50% are associated with an abdominal aortic aneurysm. 50% are asymptomatic
    4. Symptomatic aneurysms present with features of:
      1. Compression of adjacent structures (veins or nerves)
      2. Rupture
      3. Limb iscahemia due to emboli or acute thrombosis
    5. Treatment is by proximal and distal ligation Q
    6. Revascularisation of the leg with a femoropopliteal bypass
    7. With a symptomatic popliteal aneurysm 20% patients will undergo an amputation

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