1. Complications (Gao et al., 2023)
1.1. Rupture
1.1.1. Aortic aneurysm rupture is the most severe and life-threatening coplication, where the aneurysm's weakened wall tears open, causing massive internal bleeding.
1.1.2. The rapid loss of blood can lead to hypovolemic shock, severe organ hypoperfusion, and cardiac arrest, with a high mortality rate if not treated immediately, often requiring emergency surgery to rapair the rupture.
1.2. Organ Damage
1.2.1. As the anuerysm enlarges, it can put pressure on surrounding structures, including vital organs, including the kidneys, lungs, and digestive tract.
1.2.1.1. This pressure can lead to renal ischemia (impaired kideney function).
1.2.1.2. Pulmonary dysfunction (due to compression of the trachea or lungs).
1.2.1.3. Gastrointestinal complications (such as mesenteric ischemia).
1.2.2. A rupture of dissection can disrupt blood flow to these organs, resulting in irreversible damage or organ failure without rapid medical intervention.
1.3. Embolism
1.3.1. Aortic aneurysms can lead to the formation of thrombi, blood clots, within the aneurysmal sac. These clots may break off and travel through the bloodstream, causing embolism to distant organs such as the brain, kidneys, or extremities.
1.3.2. Embolism to the brain can result in a stroke, while embolism to the limbs can cause ischemia and potential gangrene if not promptly treated.
1.4. Aortic Dissection
1.4.1. Aortic dissection occurs when there is a tear in the intimal layer of the aortic wall, allowing blood to flow between the layers of the aorta, creating a false lumen.
1.4.2. Can result in acute severe chest or back pain, cardivascular collapse, and organ ischemia due to the disruption of blood flow to vital organs.
1.4.3. Dissection are often life-threatening and require rapid surgical interventions to prevent rupture or further damage to the aorta and surrounding structures.
2. Diagnostic Tests and Labs
2.1. Initial Physical Assessment: Checking for a pulsating mass.
2.2. Imaging (Gao et al., 2023).
2.2.1. Ultrasound (Non-invasive, widely available, and cost-effective.)
2.2.1.1. Is a non-invasive, widely used first-line imaging test for abdominal aortic aneurysms (AAA). It is effective in detecting the size, location, and shape of the aneurysm. It is frequently used for screening in high-risk patients, such as men over 65 years with a history of smoking.
2.2.1.2. It is also used in monitoring the progression of smaller aneurysms (<5 cm) to determine if they require surgical intervention.
2.2.1.3. Less effective for thoracic aneurysms or detecting aneurysms in patients who are obese.
2.2.2. CT Angiography (CTA)
2.2.2.1. Provides detailed 3D imaging of the aorta, allowing precise measurement of the aneurysm's size and location and detailed images of the aneurysm's anatomy and associated complications.
2.2.2.2. Can be sued for both TAA and AAA.
2.2.2.3. Best for preoperative planning for surgical interventions and to assess how the aneurysm is afffecting nearby vascular structure.
2.2.2.4. Limitaiton is that there is exposure to contrast dye and radiation.
2.2.3. Magnetic Resonance Angiography (MRA)
2.2.3.1. Uses magnetic fields and radio waves to prodcue detailed images of blood vessels and provide excellent soft tissue contrast.
2.2.3.2. It can be useful in assessing TAA and can be used to evaluate the aortic arch and ascending aorta.
2.2.3.3. Limiations include limited availability, longer imaging time, and contraindicated in patients with pacemakers or metal implants.
2.2.4. Chest X-ray
2.2.4.1. May show signs of aortic dilation or widening of the mediastinum, which can suggest the presence of a thoracic aortic aneurysm.
2.2.4.2. Used as an initial screening tool or to assess post-surgical changes due to not being highly specific.
2.2.4.3. Does not provide definitive details of aneurysm size or location.
2.2.4.4. Is fast and inexpensive
2.2.5. Echocardiogram
2.2.5.1. Useful in detecting ascending aortic aneurysms and aortic root dilations, particularly in patients with bicuspid aortic valves or those with genetic connective tissue disorders like Marfan syndrome
2.2.5.2. Limited ability to visualize the descending aorta or abdominal aorta.
2.2.5.3. Non-invasive, provides real-time assessment of the aortic valve, aortic root, and the ascending aorta.
2.2.6. Conventional Angiography (usually through catheterrization)
2.2.6.1. Less commonly used today, but still may be used in emergent cases or for patients undergoing surgical repair.
2.2.6.2. Provides detailed images of the blood vessels and can identify dissections or ruptures.
2.3. Labs
2.3.1. Complete Blood Count (CBC) (Zhang et al., 2021)
2.3.1.1. Used to asses for anemia or signs of infection
2.3.1.2. Findings, such as low hemoglobin or hematocrit may indicate internal bleeding, indicating a rupture, or chronic blood loss.
2.3.1.3. An elevated white blood cell count could indicate an infection or inflammation in the case of a mycotic aneurysm
2.3.2. Renal Function Tests (Urbanek et al., 2020)
2.3.2.1. Since aortic aneurysms can sometimes affect renal perfusion, especially when there is aortic dissection, renal function tests (serum creatinine and BUN) are useful to monitor kidney health.
2.3.2.2. Important to monitor in patients undergoing contrast imaging or those with hypertension or diabetes.
2.3.3. Lipid Profile (Tian et al., 2025)
2.3.3.1. Can be used to address the patient's cardiovascualr health, since high cholesterol levels, especially LDL cholesterol, are a major contributor to the development of atherosclerosis, which can lead to aneurysm formation.
2.3.3.2. Important to use in patients with atherosclerotic aneurysms.
2.3.4. D-Dimer (Yao et al., 2021)
2.3.4.1. This testing is useful in the evaluation of aortic dissection. Elevated levels of D-dimer may indicate ongoing clot formation and fibrinolysis, a characteristic of aortic dissection or rupture.
2.3.4.2. Limitations of this testing is that although a positive D-dimer can support the idea of aortic dissection, it is not specific and must be interpreted in combination with imaging.
2.3.5. B-type natriuetic peptide (BNP) (Urbanek et al., 2020)
2.3.5.1. Can be used to help evaluate kidney function and electrolyte balance, particularly in patients who may need contrast imaging or are undergoing endovascular repairs.
2.3.5.2. Used to assess renal function, especially in patients with renal insufficiency who are at risk for contrast-induced nephropathy.
2.3.6. Procalcitonin (PCT) (Wu et al., 2024)
2.3.6.1. PCT may be used to detect bacterial infections, particularly in the case of mycotic aneurysms. Elevated procalcitonin levels could indicate a bacterial infection of the aneurysm wall.
2.3.6.2. Helps as a tool in diagnosing mycotic aneurysms associated with endocarditis or bacteremia.
3. Treatment Options
3.1. Observation and Monitoring (Small, asymptomatic aneurysms): Particularly those measuring less than 5 cm (for AAA) or 6 cm (for TAA), the treatment often involves regular monitoring with ultrasound or CT imaging. The goal is to track the aneurysm’s size and detect any signs of growth that may require more invasive treatment (Gao et al., 2023
3.1.1. Lifestyle Modifications: Patients are often advised to manage risk factors with smoking cessation, weight management, dietary modifications, and blood pressure control to slow the progression of the aneurysm.
3.2. Medication Management
3.2.1. Antihypertensive Medications (Gao et al., 2023).
3.2.1.1. Beta-Blockers (e.g., Labetalol, Metoprolol): These medications reduce the heart rate and the force of heart contractions, leading to a reduction in blood pressure and aortic wall stress
3.2.1.2. Angiotensin-Converting Enzyme (ACE) Inhibitors (e.g., Enalapril, Lisinopril): These medications block the renin-angiotensin-aldosterone system (RAAS), reducing blood pressure and potentially decreasing the formation of angiotensin II, which can contribute to vascular remodeling and weakening of the aortic wall.
3.2.1.3. Angiotensin II Receptor Blockers (ARBs) (e.g., Losartan, Valsartan): These work similarly to ACE inhibitors but block the action of angiotensin II at its receptor site
3.2.2. Statins (Tian et al., 2025).
3.2.2.1. Statins (e.g., Atorvastatin, Simvastatin) are commonly used to lower cholesterol levels, particularly LDL cholesterol.
3.2.2.2. Statins help stabilize the endothelial function (lining of blood vessels), reduce inflammation, and lower the activity of matrix metalloproteinases (MMPs), which degrade the extracellular matrix (including collagen and elastin), weakening the aortic wall. This reduction in MMP activity may slow the growth of the aneurysm.
3.2.3. Anticoagulants and Antiplatelet Medications (Gao et al., 2023)
3.2.3.1. Anticoagulants and antiplatelet medications are used to prevent blood clots that can form within the aneurysmal sac and embolize to other organs, such as the brain, kidneys, or limbs, causing a stroke, organ ischemia, or limb ischemia.
3.2.3.1.1. Aspirin: This antiplatelet medication is often used to prevent blood clot formation by inhibiting platelet aggregation.
3.2.3.1.2. Warfarin: This is a vitamin K antagonist anticoagulant that may be prescribed in cases of aortic aneurysms with thrombus formation or if the aneurysm has been complicated by aortic dissection. Warfarin helps prevent clotting in the aneurysmal sac, reducing the risk of embolic events.
3.2.3.1.3. Direct Oral Anticoagulants (DOACs) (e.g., Apixaban, Rivaroxaban): These anticoagulants may be used for patients who require blood thinning but are considered more convenient than warfarin due to their more predictable pharmacokinetics and not requiring routine monitoring.
3.2.4. Pain Mangement (Gao et al., 2023)
3.2.4.1. Opioids (e.g., Morphine, Fentanyl): These are typically used for short-term, acute pain management in hospitalized patients.
3.2.4.2. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) (e.g., Ibuprofen, Aspirin): These medications are not commonly used in acute aortic aneurysm management due to the potential for increased bleeding risk but may be used for chronic pain or inflammation related to aneurysms in some cases
3.2.5. Vasodilators (Gao et al., 2023)
3.2.5.1. Vasodilators may be used in certain cases to reduce the pressure on the aorta by dilating blood vessels and lowering systemic vascular resistance.
3.2.5.1.1. Nitroprusside: This powerful vasodilator may be used in emergency situations to manage hypertensive crises, by rapidly lowering blood pressure and reducing stress on the aortic wall
3.2.5.1.2. Nitrates (e.g., Nitroglycerin): These are less commonly used in aortic aneurysm management but may be used to lower blood pressure and improve blood flow in certain clinical situations.
3.2.6. Antibiotics (Wu et al., 2024)
3.2.6.1. May be used if there is an associated infection or a specific infectious cause, such as infected aortic aneurysms or mycotic aneurysms. The choice of antibiotic depends on the pathogen responsible for the infection
3.2.6.2. Broad-spectrum antibiotics may be given before and after surgery to reduce the risk of surgical site infections (SSIs).
3.2.6.3. In cases where infective endocarditis (heart valve infection) causes emboli that lead to the formation of a mycotic aneurysm, antibiotic therapy is critical to treat the underlying infection.
3.3. Surgical Interventions (Gao et al., 2023)
3.3.1. Endovascular Aneurysm Repair (EVAR): stent grafting, minimally invasive, inovlves the insertion of a stent graft via a catheter through the groin.
3.3.2. Open Surgical Repair: For larger and complex aneurysms, or those not suited bor EVAR. Open surigical repair involves removing the aneurysm and replacing the affected segment of the aorta with a synthetic graft.
3.3.3. Trhoacoabdominal Aneurysm Repair: A more extensive surgery that may involve a combination of open repair, that could include aortic root replacement or valve-sparing surgery for patients with bicuspid aortic valave.
3.3.4. Emergency Surgery for Rupture or Dissection: Goal of this surgery is to repair the aorta and prevent further bleeding or organ damage. This type of surgery depends on the location and extend of damage.
3.4. Referrals (Gao et al., 2023)
3.4.1. Vascular Surgeon: Needed for open surgical repair or EVAR if the aneurysm needs surgical intervention. This specialist will manage the surgical aspect of treatment and preovide preoperative and postoperative care for patient.
3.4.2. Cardiologist: To assess the aneurysm and to determine whether surgical inervention is needed. These specialists will evaluate the size, location and groth rate of the aneurysm.
3.4.3. Genetic Counselor: If the aneurysm is thought to be related to a genetic condition. This counseling can help individual to make decisions in terms of screening and prevention.
3.4.4. Nutritionist/Dietitian: May be appropraite for patients who need help to manage modifiable risk factors such as weight managment, and help manage dietary factors, such as reducing sodium and cholesterol intake, and helping to improve overall cardiovascular health.
4. Prevention Strategies (Gao et al., 2023)
4.1. Control Blood Pressure
4.2. Quit Smoking
4.3. Healthy Diet & Exercise
4.4. Routinue Screening (for those with risk factors)
4.5. Genetic Counseling (for those with family history)
5. An abnormal bulging or dilation of the aorta due to weakness in the aortic wall. Aneurysm refers to the abnormal growth of the aortic wall, which can result in the rupture of the inner layer of the aortic wall and the flow of blood into the surrounding layers (Liu et al., 2025).
6. Types
6.1. Abdominal Aortic Aneurysm (AAA): Occurs in the abdominal portion of the aorta (Rogers, 2023).
6.1.1. An abdominal aortic aneurysm (AAA) is a dilation of the abdominal portion of the aorta, which occurs when the wall of the aorta weakens and expands. The condition is typically defined as a dilation of the aorta by more than 50% of its normal diameter (Anagnostakos, & Lal, 2021). The normal diameter of the abdominal aorta is usually about 2 cm, with any enlargement above 3 cm being considered abnormal. An aneurysm is usually diagnosed when the abdominal aorta reaches 5 cm in diameter, though intervention is considered earlier if rapid growth occurs (Anagnostakos, & Lal, 2021).
6.2. Thoracic Aortic Aneurysm (TAA): Occurs in the chest portion of the aorta (Wang, & Desai, 2020).
6.2.1. A thoracic aortic aneurysm (TAA) is a dilation of the thoracic portion of the aorta, typically due to weakening of the aortic wall. This dilation is usually defined as an enlargement of the aorta by more than 50% of its normal diameter. The normal diameter of the thoracic aorta varies based on factors such as age, sex, and body surface area.
6.3. Thoracoabdominal Aneuysm: Involves both thoracic and abdominal parts (Wang, & Desai, 2020).
6.3.1. A thoracoabdominal aortic aneurysm (TAAA) is an aneurysm that involves both the thoracic and abdominal portions of the aorta. It is a more complex and rare type of aortic aneurysm that spans from the thoracic (chest) region to the abdominal region. It typically results from the progressive dilation of the aorta due to a variety of risk factors, including hypertension, atherosclerosis, and genetic conditions.
7. Risk Factors
7.1. Age: Risk increases with age, especially for indiduals over 65. Aortic wall weakens over time, increasing susceptiblity to aneurysms (Sterpetti et al., 2024).
7.2. Gender (more common in men) (Sterpetti et al., 2024).
7.3. Family History (Sterpetti et al., 2024).
7.4. Hypertension: Chronic high BP increases the pressure on the aortic wall, making it more prone to dilation and rupture (Sterpetti et al., 2024).
7.5. High Cholesterol: Elevated LDL cholesterol contibutes to atherosclerosis, which can weaken the aortic wall and increase risk of aneurysm formation (Tian et al., 2025).
7.6. Smoking: Accelerates atherosclerosis and damages the vessel walls (Sterpetti et al., 2024).
7.7. Alcohol: Chronic heavy drinking and alcohol abuse contibutes to hypertension, atherosclerosis and liver disease (Lionakis et al., 2023).
7.8. Diet: Diet high in sodium, saturated fats, refined sugars, and low in fiber can promote hypertention, atherosclerosis, and obeesity, which increase the changes of devleoping an aneurysm (Sterpetti et al., 2024).
7.9. Chronic Inflammation or Inflammatory Diseases: Conditions such as vascultitis can cause inflammation of the aortic wall, leading to weakened and dilated segments that can eventually form an aneurysm (e.g. Giant Cell Arteritis, Takayasu Arteritis) (Lionakis et al., 2023).
7.10. Chronic Infections: Can cause damage to the aortic wall, causing aneurysms to form (e.g. endocarditis, tuberulosis, syphilis) (Lionakis et al., 2023).
7.11. Aortic Valve Abnormalities: Conditions that predispose individuals to ascending aortic aneurysms due to the abnormal mechanical stress placed on the aortic wall (e.g. bicuspid aortic valve, aortic valve disease) (Lionakis et al., 2023).
7.12. Connective Tissue Disorders:: Certiann conditoins increase the chance of devleoping aneurysms due to defects in collagen and elastin (e.g. Marfan syndrome, Ehlers-Danlos syndorme, Loeys-Dietz syndrome) (Lionakis et al., 2023).
8. Pathophysiology at the Cellular Level (Gao et al., 2023)
8.1. Elastin and Collagen Degredation
8.1.1. The loss of elastin and collagen leads to a weakened aortic wall that is less able to resist mechanical stress and prone to dilation, eventually leading to aneurysm formation
8.2. Smooth Muscle Apoptosis
8.2.1. The loss of smooth muscle cells (SMCs) reduces the aortic wall’s ability to produce essential extracellular matrix (ECM) components, further weakening the vessel and contributing to aneurysm formation.
8.3. Immune cells infiltrate the aortic wall, releasing cytokines and proteases that exacerbate ECM degradation and smooth muscle dysfunction, contributing to aneurysm progression.
8.4. Chronic Inflammation
8.5. These combined processes lead to progressive aortic dilation, weakening the vessel wall and increasing the risk of rupture, the most dangerous complication of an aortic aneurysm (Liu et al., 2025).
9. Causes
9.1. Atherosclerosis (main cause in U.S.): Hardening of the arteries due to plaque buildup (Lionakis et al., 2023).
9.1.1. Atherosclerotic lesions occur mostly at sites of low shear stress (decreased blood flow velocity), inducing aneurysm formation as a result of endothelial damage.
9.1.2. Overexpression of certain enzymes in the atherosclerotic process (e.g., angiotensin-converting enzyme) leads to enhanced inflammatory response and further induces proteolysis of extracellular matrix proteins.
9.2. Kawasaki disease is the main cause in the Eastern societies (Lionakis et al., 2023).
9.2.1. Kawasaki disease (acute, self-limited vasculitis) which occurs in childhood, may lead to development of coronary artery aneurysms in 15-25% of untreated children
9.2.2. The autoimmune/inflammatory process in Kawasaki disease activates a series of pathophysiological mechanisms that causes endothelial injury and providing vulnerable vessel sites for the creation of aneurysms.
9.3. Hypertension: High blood pressure, which stresses the aortic walls, leading to the dialtion and weakening of the aorta (Rogers, 2023).
9.4. Genetic Influences, mutations, congenital defects (e.g. Marfan syndrome, Ehlers-Danlos, Loeys-Dietz syndrome, Alport syndeorme, Bicuspid aortic valve) (Rogers, 2023).
9.5. Trauma: Direct injury to the aorta, e.g. accidents or penetrating wounds), can cause localized damage that results in the formation of an aneurysm (Rogers, 2023).
9.6. Infections: Bacterial infections can weaken the aortic wall, causing aneurysms, (e.g. from endocarditis or bacteremia) (Zhang et al., 2021).
9.7. Cocaine Use (Gao et al., 2023).
10. Signs & Symptoms (Gao et al., 2023)
10.1. Adonminal Aortic Aneurysm (AAA)
10.1.1. Pulsatile abdonimal mass, pain
10.1.2. Often asynptomatic until rupture
10.1.3. Nausea, vomiting, back/flank pain
10.2. Thoracic Aortic Aneurysm (TAA)
10.2.1. Chest pain, back pain, difficulty swallowing
10.2.2. Shortness of breath, hoarseness
10.3. Rupture
10.3.1. Suddent, severe pain (chest or abodmen), Hypotension, shock could indicate rupture
11. Impact on Other Systems (Gao et al., 2023)
11.1. Cardiovascualr
11.1.1. Aneurysms can lead to aortic valve insufficiency, increased stroke risk, and hypovolemic shock if ruptured.
11.2. Renal
11.2.1. Renal ischemia, acute kidney injury, and chronic kidney disease can occur due to reduced renal perfusion.
11.3. Neurological
11.3.1. Embolic events can lead to stroke or transient ischemic attacks (TIAs); aortic dissection may lead to neurological deficits and spinal cord ischemia.
11.4. Respiratory
11.4.1. Compression of the trachea or bronchi, pulmonary edema, and respiratory failure are possible complications.
11.5. Gastrointestinal
11.5.1. Mesenteric ischemia, compression of abdominal organs, and gastrointestinal bleeding are important concerns, especially in abdominal aneurysms.