Thromboangiitis obliterans

Last updated: June 26, 2023

Summarytoggle arrow icon

Thromboangiitis obliterans (TAO), also known as Buerger disease, is an inflammatory, nonatherosclerotic, vasoocclusive disease affecting small and medium-sized vessels of the extremities. TAO most commonly affects adult males with a significant history of tobacco consumption (e.g., smoking, chewing, vaping). In susceptible individuals, tobacco exposure causes inflammation of the tunica intima, with the formation of a highly cellular thrombus that occludes the affected vessel. Patients frequently present with intermittent claudication, Raynaud phenomenon, and migratory superficial thrombophlebitis. Eventually, critical limb ischemia develops and the patient presents with rest pain, absent pulse in the extremities, and/or digital ulcerations. Angiography can determine the extent of the disease and differentiate TAO from other causes of peripheral vasculopathy. The most important therapeutic measure is the complete avoidance of tobacco exposure. Additionally, prostaglandin analogues (e.g., iloprost) may be used to improve ulcer healing and decrease rest pain. Patients with TAO who develop gangrene require amputation.

Epidemiologytoggle arrow icon

  • Prevalence: up to 20 cases per 100,000 individuals [1]
  • Sex: : > (3:1)
  • Age of onset: before the age of 45 years [2]

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

  • The exact etiology of TAO is unknown.
  • Tobacco consumption is the single most important risk factor for TAO. [3]

Pathophysiologytoggle arrow icon

TAO is an inflammatory, nonatherosclerotic, vasoocclusive disease affecting small and medium-sized vessels of the extremities.

Histopathological phases [4]

Clinical featurestoggle arrow icon

TAO affects the small and medium vessels of the extremities. Other systems are only very rarely involved.

Extremities [2][5]

TAO typically affects more than one limb. [2][6]

Upper extremity ischemia is often asymptomatic; perform an Allen test in all patients with TAO. [2][6]

Systemic symptoms [1][6]

Diagnosticstoggle arrow icon

General principles

Suspect TAO in a patient < 45–50 years old with signs of distal limb ischemia and a history of tobacco consumption.

Laboratory studies [2][3]

The following studies are normal in patients with TAO and should be obtained in all patients to rule out alternative diagnoses:

ESR and CRP remain within normal limits, which helps differentiate TAO from vasculitides.

Imaging studies [2][3]

An angiography is preferred over CTA and MRA because of its higher sensitivity for detecting small vessel disease in the extremities. [3]

Additional studies

Differential diagnosestoggle arrow icon

The following alternate diagnoses are typically investigated in a patient with suspected TAO. [2][3][5]

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon

General principles

  • There is no specific treatment for TAO.
  • Tobacco abstinence is the most important therapeutic measure.
  • Pharmacotherapy may improve ulcer healing.
  • Revascularization procedures are rarely performed.
  • Consult a vascular surgeon and/or a rheumatologist for all patients.

Prevention and supportive care [2][3]

  • Abstinence from tobacco in any form (e.g., smoking or chewing tobacco, nicotine patches or gum)
    • Most effective measure for reducing symptoms
    • Decreases the risk of amputation if started early in the disease course
  • Protection of fingers and toes from cold and mechanical injuries (e.g., wearing gloves and appropriate footwear)
  • Basic wound and skin hygiene (e.g., cleaning with soap and water, covering wounds with clean bandages) contributes to ulcer healing and prevents infections. [1]

Complete cessation of tobacco consumption in any form is the single most effective therapeutic measure. [1][3]

Even nicotine patches can reactivate TAO. Bupropion and varenicline are the preferred agents for assisting in tobacco cessation. [2][3]

Symptomatic therapy [2][6]

Surgical therapy [4][6]

Referencestoggle arrow icon

  1. Piazza G, Creager MA. Thromboangiitis Obliterans. Circulation. 2010; 121 (16): p.1858-1861.doi: 10.1161/circulationaha.110.942383 . | Open in Read by QxMD
  2. Perttu ET Arkkila. Thromboangiitis obliterans (Buerger's disease). Orphanet Journal of Rare Diseases. 2006.
  3. Jeffrey W. Olin. Thromboangiitis Obliterans (Buerger's Disease). N Engl J Med. 2000; 343 (12): p.864-869.doi: 10.1056/nejm200009213431207 . | Open in Read by QxMD
  4. Vijayakumar A, Tiwari R, Kumar Prabhuswamy V. Thromboangiitis Obliterans (Buerger’s Disease)—Current Practices. Int. J. Inflamm.. 2013; 2013: p.1-9.doi: 10.1155/2013/156905 . | Open in Read by QxMD
  5. Vanda Cristina Jorge, Ana Carolina Araújo, Manuel Vaz Riscado. Buerger’s disease (Thromboangiitis obliterans): a diagnostic challenge. BMJ Case Reports. 2011.
  6. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders ; 2014

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