Aneurysm

Aneurysms are typically defined as vascular enlargements with a diameter ≥ 1.5 times that of a normal artery. True aneurysms are arterial enlargements in which all three layers of the vessel wall are weakened and form part of the aneurysmal wall. False aneurysms are extraarterial hematomas contained by surrounding tissues and/or the tunica adventitia that maintain persistent communication with the arterial lumen. Arterial dissections are vascular enlargements caused by the separation of arterial wall layers as blood enters the intima-media space through a tear in the tunica intima. Aneurysms are also differentiated according to their location. This article discusses the etiology and clinical features of cerebral, extracranial carotid, iliac, femoral, popliteal, and ventricular aneurysms. Symptoms generally depend on the location and size of the aneurysm. Management may be medical, surgical, or endovascular, depending on the type of aneurysm, symptoms, and associated complications.

For more specific information on individual types of aneurysms, see “Thoracic aortic aneurysm,” “Abdominal aortic aneurysm,” “Aortic dissection,” “Dissection of the carotid and the vertebral artery,” and “Subarachnoid hemorrhage.”

Categories of vascular enlargement

Abnormal vascular enlargement is often generically referred to as an aneurysm, but there are three distinct types of vascular enlargement with different etiologies and management strategies.

All three types of vascular enlargement can rupture and cause life-threatening hemorrhage.

Aneurysms by location ^[8]

Arterial dissections by location

Types

• Saccular aneurysm (Berry aneurysm) ^[12]
  • Round, saccular shape
  • Most common type of cerebral aneurysm
  • Typically occur at vessel junctions in the circle of Willis, most commonly between the anterior communicating artery and anterior cerebral artery
  • Account for ∼ 80% of cases of nontraumatic subarachnoid hemorrhage ^[13]
  • Risk factors ^[14][15][16]
    • Congenital conditions: autosomal-dominant polycystic kidney disease, Ehlers-Danlos syndrome, Marfan syndrome, aortic coarctation
    • Hypertension
    • Smoking
    • African-American race
    • Older age
    • Hyperlipidemia
    • Excessive alcohol consumption
    • Family history of aneurysms
    • Estrogen deficiency ^[17]
• Fusiform aneurysm ^[18][19]
  • Dilation of the entire circumference of the artery
  • Most frequently occur in the vertebrobasilar system
  • Associated with connective tissue diseases and atherosclerosis
• Mycotic aneurysm ^[20]
  • Mushroom-shaped dilation of infected vessel walls
  • Caused by septic emboli (mostly due to bacterial endocarditis)
  • Occur at small, peripheral segments of cerebral vessels and often involve the middle cerebral artery ^[21]
• Traumatic intracranial aneurysm ^[22]
  • Comprise < 1% of all intracranial aneurysms
  • Most commonly occur in the supraclinoid internal carotid artery and anterior cerebral artery
  • Have a high risk of rupture
• Charcot-Bouchard microaneurysm
  • Associated with hypertension and diabetes
  • Affect small lenticulostriate vessels in the basal ganglia and thalamus
  • Rupture may cause intracerebral hemorrhage.

Clinical features ^[23][24]

• Usually asymptomatic
• Headache ^[25]
• Signs and symptoms of TIA ^[26]
• Mass effects (symptoms depend on the affected vessel)
  • Anterior communicating artery: bitemporal hemianopia, visual acuity defects (optic nerve palsy from compression of CN II at the optic chiasm)
  • Posterior communicating artery: mydriasis (CN III palsy from compression of parasympathetic fibers); ptosis and ophthalmoplegia in severe compression
  • Intracavernous internal carotid artery: CN III palsy, CN IV palsy, CN V palsy, and CN VI palsy ^[27][28]
• Clinical features of SAH (if aneurysm ruptures)

Diagnostics ^[26][29]

Cerebral aneurysms are often found incidentally during the workup of suspected intracranial hemorrhage (e.g., SAH, ICH), ischemic stroke, or other CNS lesion.

• Unruptured aneurysm (incidental finding on noncontrast neuroimaging or suspected clinically): Obtain neuroimaging with angiography. ^[26]
  • CTA head or MRA head: first-line option (high sensitivity, noninvasive)
  • Digital subtraction angiography (DSA): gold standard for accuracy , helpful for operative planning, invasive
• Suspected ruptured aneurysm or sentinel leak: Follow the “Diagnostic approach for SAH.”
• Confirmed SAH on plain CT head: Obtain CTA head or catheter arteriography. ^[29]
• Surveillance of known aneurysm: Options include CTA head, MRA head, and DSA. ^[26][29]
• High-risk asymptomatic individuals (e.g., strong family history, Ehlers-Danlos syndrome, polycystic kidney disease): Consider screening with CTA head or MRA head. ^[26][30][31]

Angiography (e.g., CTA, MRA, or DSA) helps determine the location, size, and morphology of most cerebral aneurysms, but visualization of Charcot-Bouchard microaneurysms may not be possible with standard techniques.

Differential diagnoses

• Other cerebrovascular lesion: e.g., arteriovenous malformations, fibromuscular dysplasia
• Brain tumor: e.g., pituitary adenoma, meningioma, intracranial metastasis
• Brain abscess
• Stroke: See “Overview of stroke.”
  • Ischemic stroke: See “Stroke symptoms by affected vessel.”
  • Hemorrhagic stroke: See “Differential diagnosis of intracranial hemorrhage.”
• Other causes of cranial nerve palsies
• Other causes of headache: See “Differential diagnosis of headache.”

Treatment

Unruptured intracranial aneurysms ^[26][32]

Treatment depends on the aneurysm size, location, growth rate, and the patient's perioperative risk assessment. ^[26]

• Interventional management ^[32]
  • Surgical clipping
  • Endovascular coiling
  • See “Intracranial aneurysm repair” for details.
• Conservative management
  • Primary prevention of ASCVD and surveillance imaging (e.g., CTA, MRA) ^[29][32]
  • Consider for low-risk lesions, older patients, and patients with comorbidities. ^[26][33]

Ruptured aneurysms

• Subarachnoid hemorrhage (most common): See “Management of SAH.”
• Intracerebral hemorrhage (rare): See “Intracerebral hemorrhage management.”

• Etiology: commonly atherosclerosis, trauma (iatrogenic or penetrating injury), infection (septic emboli)
• Clinical features
  • Pulsatile neck mass (below angle of mandible)
  • Associated bruit
  • Transient ischemic attacks (TIAs) or stroke
  • Mass effect on adjacent structures (veins and nerves) causes hoarseness, facial swelling, dysphagia
• Diagnosis
  • Ultrasound (initial): evidence of swirling blood with a thrombus
  • CT or MR angiography: determines the site and size of the aneurysm, excludes rupture or other pathologies
• Complications
  • Rupture: airway compression, pharyngeal hemorrhage, epistaxis
  • Neck infection: pain, fever
• Treatment: surgical repair, either in the form of an aneurysm excision and reconstruction or endovascular repair (grafting or stenting) ^[34]

Definition ^[10]

Ventricular aneurysm is a focal enlargement and/or bulge in the ventricle caused by thinning of the myocardium.

Etiology

• Myocardial infarction (most common) ^[35]
  • Occurs in < 5% of patients after MI ^[36]
  • Typically occurs within 2 weeks of MI but can occur months later ^[37]
• Risk factors include:
  • Occlusion of the left anterior descending coronary artery ^[10]
  • Female sex ^[38]

Clinical features

• Enlarged heart on percussion
• Diffuse and displaced apical pulse to the left midclavicular line
• 3^rd and 4^th heart sounds
• Systolic murmur (mitral regurgitation) ^[39]

Diagnosis

• ECG findings of LV aneurysm
  • Similar to ECG findings of STEMI or other causes of ST elevation
  • Features favoring the diagnosis of LV aneurysm
    • Persistent ST elevation (> 2 weeks), most often in the anterior precordial leads (classic finding) ^[40]
    • Combined T/QRS ratio of leads V1–V4 of < 0.22 ^[41]
    • Single T/QRS ratio of any one anterior precordial lead (V1, V2, V3, or V4) of ≤ 0.36 ^[42]
• CXR: cardiomegaly, bulge on the left side of the heart ^[37][43]
• Echocardiography: dyskinetic wall motion and diastolic deformity ^[10]
• Cardiac CT or cardiac MRI: can identify wall abnormalities not seen on echocardiography ^[43][44]
• Ventriculography: gold standard for distinguishing between LV aneurysm and LV pseudoaneurysm (invasive) ^[44]
• Cardiac biomarkers: Nonspecific elevations may be present. ^[37]

Treatment ^[36][45]

Conservative management

• Indication: small, asymptomatic aneurysms ^[46]
• Treatment
  • Monitor aneurysm size with serial imaging.
  • Manage heart failure if present.
  • Anticoagulation if LV thrombus is present ^[47]

Surgery ^[10][46]

• Indications
  • Large size or continued expansion
  • Refractory heart failure, arrhythmia, or thromboembolism
  • Pseudoaneurysm
• Technique: aneurysmectomy (often in conjunction with coronary artery revascularization)

Prevention ^[10][36]

• Early reperfusion (e.g., PCI) after acute MI
• Early administration of ACEIs or beta blockers after acute MI

Complications ^[48]

• Arrhythmias, e.g., sustained VT in patients with hypertrophic cardiomyopathy ^[49]
• Ventricular free wall rupture and cardiac tamponade
• LV thrombus formation → thromboembolism (e.g., stroke, mesenteric ischemia, renal infarction)
• Heart failure

LV aneurysm vs. LV pseudoaneurysm

Epidemiology ^[54][55]

• Prevalence: second most common aneurysm (after AAA), most common peripheral aneurysm
• ♂ > ♀
• Mean age: 65 years

Etiology

• Multifactorial (i.e., inflammatory, immune, genetic, and mechanical components)

Clinical features ^[54][55]

• Most patients present with an asymptomatic mass in the popliteal fossa (bilateral in 50% of cases).
• If symptomatic
  • Knee pain
  • 6 Ps of acute limb ischemia
  • Signs and/or symptoms of chronic peripheral artery disease

The symptoms of a popliteal artery aneurysm may be similar to those of atherosclerotic peripheral vascular disease. ^[55]

Diagnosis ^[54][55]

See also “Acute limb ischemia diagnostics” and “Peripheral artery disease diagnostics.”

• Duplex ultrasound: (initial test): can identify vascular enlargement, thrombus, and reduced patency; can exclude popliteal cysts
• CTA extremity or MRA extremity: helpful for preoperative assessment
• Digital subtraction angiography: may be required if acute limb ischemia is present ^[55]

Management ^[55]

• All patients
  • Screen for contralateral popliteal artery aneurysm and AAA.
  • Risk stratify for acute limb ischemia, e.g., using Rutherford grading.
  • Begin management of acute limb ischemia, e.g., anticoagulation, if present.
  • Optimize management of ASCVD.

• Surgery
  • The decision to repair is multifactorial and depends on aneurysm size, thromboembolic risk, perioperative risk assessment, and the patient's life expectancy.
  • Indications include:
    • Diameter ≥ 2 cm ^[55]
    • Presence of thrombus and/or suspicion of embolism
    • Distal arterial insufficiency
• Conservative management
  • Long-term clinical monitoring
  • Serial imaging

Complications ^[54][55]

• Acute limb ischemia and possible loss of limb
• Chronic thrombus and/or distal embolization, e.g., blue toe syndrome
• Rupture (rare)

Epidemiology ^[56][57]

• Iliac artery aneurysms accompany up to 50% of AAAs ^[58]
• Rarely occur in isolation

Etiology ^[56][57]

• Similar to AAAs: See “Risk factors for atherosclerosis.”
• Other causes: infection, collagen vascular disease, trauma, iatrogenic injury ^[59]

Clinical features ^[59]

• Unruptured IAA
  • Usually asymptomatic ^[60]
  • Palpable mass: pelvic, groin, or rectal
  • Mass effect caused by compression and/or erosion into adjacent vessels, nerves, or organs ^[58][59][60]
    • Pain: abdominal, rectal, flank, groin, hip, or leg
    • Clinical features of urinary obstruction, features of urosepsis or pyelonephritis
    • Constipation, tenesmus, clinical features of bowel obstruction
    • Features of acute limb ischemia (i.e., 6 Ps), swelling, and/or neuropathic pain in ipsilateral extremity
• Ruptured IAA ^[59][60]
  • Similar to clinical features of ruptured AAA
  • Hemorrhagic shock
  • Acute groin pain
  • GI bleeding or hematuria (if the aneurysm erodes into adjacent organs)

Diagnostics ^[59][60][61]

IAAs are often diagnosed incidentally during AAA screening or the workup of abdominal symptoms. ^[59]

• Abdominal ultrasound: used for screening, initial investigation in symptomatic patients, and surveillance
• CTA or MRA abdomen and pelvis: more accurate than ultrasound; usually required for operative planning

Treatment ^[56][62][63]

IAAs are usually repaired during treatment for concomitant AAAs. ^[61][64][65]

• Procedure: open surgical or endovascular repair
• Indications
  • Symptomatic aneurysm
  • Diameter ≥ 3.5 cm
  • Rapid expansion
  • Concomitant AAA repair planned

Complications

• Rupture
• Distal embolization, e.g., blue toe syndrome

Overview

Femoral artery aneurysm

Etiology ^[66][69]

• Atherosclerosis is the most common cause.
• Risk factors include ASCVD risk factors (especially male sex).
• Rare causes include vasculitis (e.g., Behcet disease) and trauma.

Clinical features ^[61][66][69]

• Unruptured
  • Asymptomatic in 30–40% of patients ^[69]
  • Thigh or groin pain
  • Palpable pulsatile mass in the thigh
  • Compressive and/or thromboembolic features, e.g.:
    • Nerve palsy
    • Acute limb ischemia
    • DVT, phlegmasia cerulea dolens
• Ruptured: severe pain, swelling, ecchymosis, clinical features of shock

Diagnostics ^[61][66]

Femoral artery aneurysm is often diagnosed incidentally during the workup of other aneurysms or vascular conditions. ^[61]

• Duplex ultrasonography
• CTA extremity
• MRA extremity

Treatment ^[61][69][70]

• All patients
  • Begin management of acute limb ischemia, e.g., anticoagulation, if present.
  • Optimize management of ASCVD.
  • Consider antiplatelet agents. ^[61][71]
• Interventional treatment ^[69]
  • Indications
    • Diameter > 2.5 cm
    • Symptomatic aneurysm of any size
  • Technique: open surgical repair (most common), endovascular stent placement

Complications ^[69]

• Rupture
• Thromboembolism and acute limb ischemia
• Infection

Femoral artery pseudoaneurysm

Etiology ^[1][68]

• Typically caused by femoral artery cannulation (e.g., for cardiac catheterization)
• Procedural risk factors include large sheath size, multiple punctures, and inadequate postprocedure compression.
• Patient risk factors include:
  • Female sex
  • Older age
  • PAD
  • Obesity
  • Hypertension
  • Use of antithrombotic agents

Clinical features ^[1]

• Postcannulation groin pain (especially pain out of proportion to physical findings)
• Swelling or palpable pulsatile mass
• Bruit or thrill
• Compressive symptoms, e.g.:
  • Peripheral neuropathy
  • DVT
  • Clinical features of PAD

Diagnostics

Usually obtained because of clinical suspicion after femoral artery cannulation

• Duplex ultrasonography (preferred initial study) ^[1][72]
• CTA extremity
• MRA extremity

Treatment ^{[1][68][70][73]}

• Observation with serial imaging: appropriate for uncomplicated pseudoaneurysms that are < 3 cm and asymptomatic ^[73]
• Ultrasound-guided thrombin injection: appropriate for uncomplicated pseudoaneurysms that are ≥ 3 cm or symptomatic, and patients taking anticoagulants ^[70]
  • Thrombin is injected directly into the cavity of the pseudoaneurysm under ultrasound guidance.
  • Thrombin initiates rapid thrombosis and hemostasis.
• Ultrasound-guided manual compression: Compression is applied directly on the neck of the aneurysm for ≥ 20 minutes. ^[73]
• Open surgical repair, endovascular repair, and/or embolization is indicated for: ^[2][73]
  • Rapidly expanding pseudoaneurysms
  • Complicated pseudoaneurysms, e.g., associated skin necrosis, cellulitis, acute limb ischemia, previous vascular surgery
  • Failure of less invasive therapy

Complications ^[68]

• Prolonged hospital stay
• Compression of adjacent structures
• Infection
• Rupture
• Thromboembolism

Prevention ^[1]

• The risk of developing a periprocedural femoral pseudoaneurysm can be reduced by:
  • Using fluoroscopy or ultrasound to guide arterial puncture
  • Appropriate length of arterial compression after needle or sheath removal, typically ≥ 10 minutes ^[74]
• Vascular closure devices reduce the risk of developing a large hematoma, but their effectiveness in preventing pseudoaneurysms is unclear. ^[75][76][77]

Apply manual pressure over the site of a femoral artery puncture for at least 10 minutes to reduce the risk of pseudoaneurysm formation.