Abdominal Aortic Aneurysm (AAA) is a life-threatening condition that requires monitoring or treatment depending upon the size of the aneurysm and/or symptomatology. AAA may be detected incidentally or at the time of rupture. An arterial aneurysm is defined as a permanent localized dilatation of the vessel at least 150% compared to a relative normal adjacent diameter of that artery [rx].
Classification of Abdominal Aortic Aneurysm
- An aortic root aneurysm, or aneurysm of the sinus of Valsalva.
- Thoracic aortic aneurysms are found within the chest; these are further classified as ascending, aortic arch, or descending aneurysms.
- Abdominal aortic aneurysms, “AAA” or “Triple-A”, the most common form of aortic aneurysm, involve that segment of the aorta within the abdominal cavity. Thoracoabdominal aortic aneurysms involve both the thoracic and abdominal aorta.
- Thoracoabdominal aortic aneurysms comprise some or all of the aorta in both the chest and abdomen and have components of both thoracic and abdominal aortic aneurysms.
Causes of Abdominal Aortic Aneurysm
An abdominal aortic aneurysm may arise if the vessel wall becomes less elastic, for example as a normal part of aging. Other possible causes include smoking and too much pressure on the blood vessel, for instance, due to high blood pressure. If one part of the vessel wall starts bulging, it tends to continue to expand, and the aneurysm grows larger.
- Tobacco smoking – More than 90% of people who develop an AAA have smoked at some point in their lives.[21]
- Alcohol and hypertension – The inflammation caused by prolonged use of alcohol and hypertensive effects from abdominal edema which leads to hemorrhoids, esophageal varices, and other conditions, is also considered a long-term cause of AAA.
- Genetic conditions – including Marfan syndrome (In an IRAD review, Marfan syndrome was present in 50% of those under age 40, compared with only 2% of older patients), Ehlers-Danlos syndrome, Turner syndrome, and bicuspid aortic valve. In patients with Marfan syndrome, cystic medial necrosis is seen in the tissues
- Atherosclerosis – The AAA was long considered to be caused by atherosclerosis because the walls of the AAA frequently carry an atherosclerotic burden. However, this hypothesis cannot be used to explain the initial defect and the development of occlusion, which is observed in the process.[rx]
- Other causes of the development of AAA include – infection, trauma, arthritis, and cystic medial necrosis.[rx]
- Hypertension (occurs in 70% of patients with distal Standford type B AAD).
- An abrupt, transient, severe increase in blood pressure (e.g., strenuous weight lifting and use of sympathomimetic agents such as cocaine, ecstasy, or energy drinks).
- Pre-existing aortic aneurysm.
- Pregnancy and delivery (risk compounded in pregnant women with connective tissue disorders such as Marfan syndrome).
- Family history.
- Aortic instrumentation or surgery (coronary artery bypass, aortic or mitral valve replacement and percutaneous stenting or catheter insertion).
- Inflammatory or infectious diseases that cause vasculitis (syphilis, cocaine use)
- Risk factors for AAA include advanced age, tobacco use, hypertension, hypercholesterolemia, Chronic obstructive pulmonary disease, and male gender. Atherosclerosis is the most commonly associated pathology, but other causes such as cystic medial necrosis, dissection, syphilis, HIV and Ehlers-Danlos syndrome have been identified.
There are a number of factors that can increase someone’s risk of developing an abdominal aortic aneurysm.
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Sex: Abdominal aortic aneurysms are more common in men than in women.
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Age: The risk increases with age. Most people who have an abdominal aortic aneurysm are over 65 years old.
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Smoking: Smoking is the most important risk factor that you can influence yourself.
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Blood pressure: High blood pressure makes an abdominal aortic aneurysm more probable.
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Blood lipids: High levels of blood lipids (blood fats) increase the likelihood of an aneurysm developing.
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Genes: People who have white skin or close relatives who have had an abdominal aortic aneurysm are at greater risk.
Symptoms of Abdominal Aortic Aneurysm
Most abdominal aortic aneurysms don’t cause any symptoms and go unnoticed.
- Larger aneurysms may cause backache or abdominal pain, or pain in your sides. Then it may be discovered if a doctor looks for the source of the pain.
- If the abdominal aorta ruptures, it causes sudden back pain that radiates to the sides or groin. A large amount of blood is lost through the rupture, causing dizziness, loss of consciousness, and eventually circulatory collapse.
Diagnosis of Abdominal Aortic Aneurysm
A physical examination can prove useful diagnostically, but should not delay the above emergency investigations. It should include:
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measurement of the BP in both arms (unequal BP is a sign, though not a reliable sign)
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documentation of all peripheral pulses (lack of peripheral pulses may be the only sign if the dissection spares the ascending aorta)
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close attention to heart sounds (aortic regurgitation and tamponade are possible with proximal extension)
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neurologic examination (hemiplegia or paraplegia can result from occlusion of the carotid arteries and anterior spinal arteries, respectively)
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assessment of renal function, including urine microscopy and catheterization for accurate measurement of renal output
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a chest x-ray, which often shows a distended aorta or generalized widening of the mediastinum
Treatment of Abdominal Aortic Aneurysm
All patients with small abdominal aortic aneurysms who do not undergo repair need periodic follow up with an ultrasound every 6 to 12 months to ensure that the aneurysm is not expanding[rx].
One RCT examined the effect of roxithromycin on aneurysm growth.[rx] patients with small aneurysms were given either roxithromycin or placebo for four weeks and subsequently followed up for a mean of 1.5 years. Once adjustments had been made for smoking, blood pressure, and IgA, there was a significant difference in aneurysm growth between treatment and placebo groups.
Matrix metalloproteinase (MMP) inhibition
Tetracyclines have long been known to prevent connective tissue breakdown by their inhibitory effect on MMPs and several experimental studies have suggested that doxycycline reduced the growth of degenerative aneurysms and suppressed MMP-9 production in the rat elastase model. In a clinical trial, preoperative treatment with doxycycline caused a reduction in both the expression of macrophage MMP-9 mRNA and the activity of MMP-2 in aneurysm tissue.7
Drugs Acting on the Renin/Angiotensin Axis
In 1998 a French group reported the effects of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II antagonists in a strain of rat prone to rupture of the internal elastic lamina of the aorta. To ensure any beneficial effects were not due to the antihypertensive properties of the drugs, they were compared to hydralazine and two calcium channel antagonists. Both ACE inhibitor and angiotensin II antagonists prevented a rupture of the internal elastic lamina, suggesting this was due to the effect on angiotensin II and not on another part of the renin/angiotensin system
Anti-chlamydial therapy
SVS Guidelines on Management of Patients With Abdominal Aortic Aneurysms
The Society for Vascular Surgery (SVS) issued updated guidelines on the care of patients with abdominal aortic aneurysms that include the following:
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Yearly surveillance imaging in patients with an AAA of 4.0 to 4.9 cm in diameter.
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Assessment of distal leg pulses at each clinic visit.
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For unruptured AAA, endovascular aneurysm repair (EVAR) is recommended.
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Endovascular procedure should only be done in a hospital that has performed at least 10 cases every year and has a conversion rate to open of less than 2%
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Elective AAA open surgery should be done in hospitals with a mortality of less than 5% and that performs at least 10 open cases a year
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For ruptured AAA, a facility with door to intervention time of less than 90 minutes is preferred.
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Recommend treatment of type I and III endoleaks as well as of type II endoleaks with aneurysm expansion.
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Antibiotic prophylaxis is not recommended before respiratory tract procedures, genitourinary, dermatologic, gastrointestinal or orthopedic procedures unless there is a potential for infection as in an immunocompromised patient.
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Color duplex ultrasonography should be used for postoperative surveillance after Endovascular surgery.
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A preoperative 12-lead electrocardiogram is recommended in all patients undergoing EVAR or open surgical repair within 4 weeks of the elective surgery.
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If the patient just had a drug-eluting stent placed, then open aneurysm surgery should be delayed for at least 6 months; or one can perform endovascular surgery while the patient is on dual antiplatelet therapy.
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Only transfuse blood perioperatively if hemoglobin is less than 7 g/dL.
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Elective repair should be recommended in patients at low risk when the AAA is 5.5 cm.
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The open surgery should be done under general anesthesia.
If the risk of rupture is high, surgery is the only preventive measure. There are two types of surgery for a large aneurysm:
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Open surgery through an abdominal incision (cut): The aneurysm is opened, and replaced by an artificial vessel (graft).
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The endovascular procedure through a small incision in the groin: A small tube (stent) is put into the artery, pushed along to where the aneurysm is, and implanted in the aneurysm.
Both of these procedures are associated with risks. Determining whether a surgical procedure is a good idea is a very personal decision: On the one hand there are risks, but on the other there is the possible danger of the aneurysm rupturing.
Complications
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Bleeding
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Limb ischemia
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Delayed rupture secondary to endoleak
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Abdominal compartment syndrome
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Myocardial infarction
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Pneumonia
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Graft infection
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Colon ischemia
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Renal failure
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Bowel obstruction
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Blue toe syndrome
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Amputation
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Impotence
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Lymphocele
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Death
Postoperative and Rehabilitation Care
After repair, it is essential that the patient discontinue smoking, eat a healthy diet, and maintain a healthy weight. Physical and/or occupational therapy may be necessary.
Other Issues
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Patients with abdominal aortic aneurysms should quit smoking is to reduce the risk of enlargement.
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Medical optimization of hypertension, hyperlipidemia, diabetes, and other atherosclerotic risk factors.
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Moderate exercise does not cause rupture or AAA expansion [21].
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The Society for Vascular Surgery Guidelines recommends ultrasound screening for all men and woman 65 years of age or older who have smoked or have a family history of AAA(20).
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Surveillance Guidelines for AAA per the Society for Vascular Surgery using duplex US are the following:
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3-year intervals for patients with an AAA between 3.0 and 3.9 cm
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12-month intervals for patients with an AAA of 4.0 to 4.9 cm in diameter.
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6-month intervals for patients with an AAA between 5.0 and 5.4 cm in diameter
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Those patients with an initial aortic diameter <3 cm have a low risk for rupture. At this time there are no recommendations for surveillance; however, it should be noted that gradual expansion in these patients has been noted over time.
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Patients presenting with asymptomatic AAA should be considered for urgent repair.
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Asymptomatic patients with AAA demonstrating an aortic diameter > 5.4 cm or those with the rapid expansion of small AAA should be evaluated for repair.
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The goal of AAA repair is to increase survival. Consideration of quality of life after the repair is important; particularly in those with shortened life expectancy due to medical co-morbidities or cancer.
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Endovascular repair may offer fewer complications and better quality of life in those at high risk for open repair up to 1-year post-intervention [rx].
Factors that increase the operative risk for abdominal aortic aneurysm repair include:
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Severe heart disease.
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Severe chronic obstructive pulmonary disease.
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Poor renal function
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Comorbidities such as stroke, diabetes, hypertension, and advanced age can increase open surgical risk. These individuals should be considered for endovascular stenting of the aneurysm if the aortic anatomy permits.
References
- https://www.ncbi.nlm.nih.gov/books/NBK470237/
- https://www.ncbi.nlm.nih.gov/books/NBK459176/
- https://www.ncbi.nlm.nih.gov/books/NBK534278/
- https://www.ncbi.nlm.nih.gov/books/NBK534278/
- https://www.ncbi.nlm.nih.gov/books/NBK441574/
- https://www.ncbi.nlm.nih.gov/books/NBK2210/
- https://www.ncbi.nlm.nih.gov/books/NBK554567/
- https://www.ncbi.nlm.nih.gov/books/NBK430752/
- https://www.ncbi.nlm.nih.gov/books/NBK554573/
- https://www.ncbi.nlm.nih.gov/books/NBK441963/
- https://www.ncbi.nlm.nih.gov/books/NBK534270/
- https://www.ncbi.nlm.nih.gov/books/NBK286056/
- https://www.ncbi.nlm.nih.gov/books/NBK538140/
- https://www.ncbi.nlm.nih.gov/books/NBK537339/
- https://www.ncbi.nlm.nih.gov/books/NBK448198/
- https://en.wikipedia.org/wiki/Aortic_aneurysm
- https://en.wikipedia.org/wiki/Abdominal_aortic_aneurysm
- https://en.wikipedia.org/wiki/Aortic_aneurysm
