Aneurysms and Dissection of Arteries

Authored by , Reviewed by Dr Adrian Bonsall | Last edited | Meets Patient’s editorial guidelines

This article is for Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Abdominal Aortic Aneurysm article more useful, or one of our other health articles.

Treatment of almost all medical conditions has been affected by the COVID-19 pandemic. NICE has issued rapid update guidelines in relation to many of these. This guidance is changing frequently. Please visit to see if there is temporary guidance issued by NICE in relation to the management of this condition, which may vary from the information given below.

See also the separate Abdominal Aortic Aneurysms, Thoracic Aortic Aneurysms, Ruptured Aortic Aneurysm and Aortic Dissection articles.

An arterial aneurysm is a localised abnormal dilatation of an artery due to a weakness in the arterial wall. The artery wall becomes weakened and balloons out. Arterial aneurysms can be classified as true or false aneurysms:

True aneurysms

  • True arterial aneurysms involve all three layers of the artery wall (intima, media and adventitia).
  • The artery wall can balloon out symmetrically to form a 'fusiform' aneurysm or there can be a local 'blow-out' to form a 'saccular' aneurysm.
  • Common sites are: abdominal aorta, iliac artery, popliteal artery, femoral artery.

False aneurysms

  • Represent a collection of blood, held around the vessel by a wall of connective tissue. The aneurysm does not involve the vessel wall.
  • May occur following trauma or there may be a slow leak of blood which is confined by surrounding tissues. False aneurysms may arise following angiogram, angioplasty or at the join between a graft and the artery.
  • Result in a slowly expanding blood-filled cavity, which will eventually rupture or lead to thrombosis.
  • Usually present as a pulsatile mass.
  • Atherosclerosis.
  • Vasculitis (eg, Kawasaki disease).
  • Syphilis.
  • Infective (may be due either to fungi or bacteria invading the vessel wall and may be due to distant spread from infective endocarditis or from localised spread from adjacent structures).
  • Penetrative or blunt trauma.
  • Congenital (eg, berry aneurysm).
  • Cocaine use has been associated with cerebral, aortic, visceral and peripheral aneurysms.

Risk factors

  • Aortic aneurysm:
    • Atherosclerosis.
  • Cerebral aneurysms:
    • Anomalous vessels.
    • Coarctation of the aorta.
    • Polycystic kidney disease.
    • Fibromuscular dysplasia.
    • Connective tissue disorders.
    • Vascular malformations and fistulae.

Cerebral aneurysms

See also the separate Subarachnoid Haemorrhage article.

  • Unruptured intracranial aneurysms occur in approximately 3% of the adult population and are increasingly detected due to more frequent cranial imaging[1].
  • The most common are saccular aneurysms, which are described as being berry-shaped swellings occurring at the bifurcation of arteries. Most aneurysms occur singly with the most frequent sites being the circle of Willis and the bifurcation of the middle cerebral artery. Cerebral aneurysms can be classified as:
    • Congenital saccular: arterial dilatations of less than 2.5 mm that appear in the bifurcation of the arteries of the circle of Willis.
    • Arteriosclerotic fusiform: caused by severe arteriosclerosis and arterial hypertension. The vessels of the circle of Willis are mainly affected. They are more frequent in the territory of the basilar and middle cerebral artery.
    • Mycotic: uncommon; caused by a septic degeneration of the elastic and muscular layer of the cerebral arteries.
    • Giant aneurysms: multifactorial origin with a diameter greater than 2.5 mm. They are more common in the vertebrobasilar system.
  • Usually present with subarachnoid haemorrhage at the age of 40-60 years (children make up fewer than 2% of cases).

Abdominal aortic aneurysms

  • These may be discovered incidentally as noticeable pulsation of the aorta.
  • In about 25% of cases, there is co-existing arterial occlusive disease in the renal or lower extremity arteries.

See the separate Abdominal Aortic Aneurysms article.

Thoracic aortic aneurysms (<10% of aortic aneurysms)

See the separate Thoracic Aortic Aneurysms article.

Peripheral and visceral aneurysms

Peripheral arterial aneurysms are uncommon. The choice of operative approach is determined on an individual patient basis. Some aneurysms (eg, femoral, subclavian and carotid) fare better with an open surgical first approach. Renal, splenic and some visceral artery aneurysms do better with an endovascular first approach[2].

Popliteal aneurysms

  • These account for about 70% of all peripheral aneurysms[3].
  • They are associated with aortic aneurysms and are often bilateral.
  • They cause symptoms from thrombosis, embolisation or compression of adjacent structures, causing venous thrombosis or neuropathy.

Femoral aneurysms

  • These are the second most common peripheral aneurysm.
  • Femoral pseudoaneurysms may complicate up to 8% of vascular interventional procedures[4].
  • Patients present with local pressure symptoms, thrombosis, or distal embolisation.
  • A pulsatile mass can be felt in the groin.

Visceral artery aneurysms[5, 6]

  • The prevalence of visceral artery aneurysms is reported to be 0.1-2% but the number of undetected visceral artery aneurysms may be much higher.
  • Hepatic artery aneurysms are the most common visceral artery aneurysms. They are often caused by medial degeneration of the hepatic artery but also by trauma.
  • Splenic artery aneurysms are less common but are four times more common in women than in men.
  • Renal artery aneurysms are rare and usually asymptomatic. Associated clinical features may include pain, haematuria, refractory hypertension, thromboembolism, dissection and rupture[7].

A tear in the tunica intima results in blood splitting the tunica media. This produces a false lumen that can progress in an antegrade or retrograde direction. Rupture may occur back into the lumen or externally. The two most common types of dissection are aortic dissection and carotid dissection. See the separate Aortic Dissection article.

Carotid dissection[8]

  • The majority (75%) occur extracranially in the internal carotid artery and together with vertebral artery dissection are a significant cause of stroke in younger patients.
  • The extracranial vertebral artery is the second most common site, accounting for 15% of cases.
  • Carotid dissection is associated with migraines, hypertension, pregnancy and oral contraceptives.
  • Carotid dissection may present with headache, neck and facial pain ipsilateral to dissection, which precede development of a stroke. Episodes of transient blindness, syncope, swelling neck and pulsating tinnitus may also occur.
  • Examination may reveal neurological deficits, Horner's syndrome (half of cases), hemiparesis, carotid bruit.
  • Investigations include duplex carotid ultrasonography, CT scan of the brain and/or MRI scan, both with and without angiography[9]. The latter has a high specificity and sensitivity and thus is preferred over CT scanning.
  • Management is aimed at prevention of infarction and, on the whole, is similar to the treatment of an acute CVA. Thus, presentation within three hours may meet the requirement for thrombolysis and, outside of this window, antithrombotic therapy or anticoagulation is indicated.
  • It remains unclear as to whether treatment with antiplatelet agents or anticoagulation is superior and decisions are based on risk/benefit calculation for the individual patient.
  • Ongoing ischaemia may require surgical intervention and/or endovascular stenting. Endovascular stenting has been shown to be safe and effective in selected patients[10].

See relevant articles for details.

See the separate Primary Prevention of Cardiovascular Disease and Cardiovascular Risk Assessment articles.

Further reading and references

  1. Etminan N, Brown RD Jr, Beseoglu K, et al; The unruptured intracranial aneurysm treatment score: a multidisciplinary consensus. Neurology. 2015 Sep 885(10):881-9. doi: 10.1212/WNL.0000000000001891. Epub 2015 Aug 14.

  2. Mohan IV, Stephen MS; Peripheral arterial aneurysms: open or endovascular surgery? Prog Cardiovasc Dis. 2013 Jul-Aug56(1):36-56. doi: 10.1016/j.pcad.2013.06.001. Epub 2013 Jul 23.

  3. Trinidad-Hernandez M, Ricotta JJ 2nd, Gloviczki P, et al; Results of elective and emergency endovascular repairs of popliteal artery aneurysms. J Vasc Surg. 2013 May57(5):1299-305. doi: 10.1016/j.jvs.2012.10.112. Epub 2013 Feb 1.

  4. Tisi PV, Callam MJ; Treatment for femoral pseudoaneurysms. Cochrane Database Syst Rev. 2013 Nov 2911:CD004981. doi: 10.1002/14651858.CD004981.pub4.

  5. Pitton MB, Dappa E, Jungmann F, et al; Visceral artery aneurysms: Incidence, management, and outcome analysis in a tertiary care center over one decade. Eur Radiol. 2015 Jul25(7):2004-14. doi: 10.1007/s00330-015-3599-1. Epub 2015 Feb 19.

  6. Hemp JH, Sabri SS; Endovascular management of visceral arterial aneurysms. Tech Vasc Interv Radiol. 2015 Mar18(1):14-23. doi: 10.1053/j.tvir.2014.12.003. Epub 2014 Dec 29.

  7. Coleman DM, Stanley JC; Renal artery aneurysms. J Vasc Surg. 2015 Sep62(3):779-85. doi: 10.1016/j.jvs.2015.05.034. Epub 2015 Jul 26.

  8. Costello F; Carotid artery dissection and vertebrobasilar insufficiency. Int Ophthalmol Clin. 2009 Summer49(3):1-14.

  9. Rao AS, Makaroun MS, Marone LK, et al; Long-term outcomes of internal carotid artery dissection. J Vasc Surg. 2011 Aug54(2):370-4

  10. Ohta H, Natarajan SK, Hauck EF, et al; Endovascular stent therapy for extracranial and intracranial carotid artery dissection: single-center experience. J Neurosurg. 2011 Jul115(1):91-100. Epub 2011 Mar 18.