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Thromboangiitis Obliterans

*Thromboangiitis obliterans*

For medical students2 min readUpdated 2026-10-10

Thromboangiitis obliterans (also known as Buerger disease) is a segmental acute and chronic inflammatory disease of the arteries and veins of the extremities. The pathology is invariably accompanied by thrombosis, subsequent connective tissue proliferation (sclerosis), and complete obliteration of the vascular lumen.

At-risk groupThe disease occurs almost exclusively in male smokers around 35 years of age.
LocalizationThe pathological process primarily involves small- and medium-sized arteries.
SpecificsInflammation initiates within the thrombus itself and subsequently spreads to the vessel wall.
ComplicationsThe end-stage of circulatory disorders is gangrene of the affected extremities.

Epidemiology and Clinical Presentation

Thromboangiitis obliterans presents with a very specific and recognizable patient profile. Epidemiological data indicate that the pathology occurs almost exclusively in male smokers. The onset of the disease typically occurs in young to middle adulthood—around the age of 35. In clinical practice, the development of this condition is very frequently combined with manifestations of superficial migrating thrombophlebitis, which further worsens the state of the vascular bed.

The symptoms of the disease directly stem from progressive peripheral circulatory disorders in the affected areas. Patients regularly report intense pain in the extremities. A classic clinical marker of ischemia in this pathology is intermittent claudication—a specific pain syndrome that forces a person to periodically stop while walking due to an acute lack of tissue perfusion.

Etiology and Pathogenesis

Despite being studied for a long time, the exact cause of thromboangiitis obliterans remains unknown. The scientific community actively discusses the hypothesis of a potential infectious agent acting as the primary trigger, though exact confirmations have yet to be found.

The pathogenesis of the disease is characterized by a unique sequence of events. It is generally accepted that the inflammatory process initially originates not within the vessel wall tissues, but directly inside the formed thrombi. Only afterwards does the aggressive inflammation spread by contact to the vascular wall.

The main targets of the pathology are medium- and small-sized arteries. Large vascular trunks are involved only in rare cases. As the disease progresses, inflammation is not limited exclusively to the arterial bed; it steadily spreads to accompanying veins and adjacent nerve trunks. The outcome of such extensive involvement is the development of pronounced fibrosis in all surrounding tissues.

Morphological Findings and Complications

Macroscopic and microscopic examination of the affected tissues reveals frequent thrombus formation within the vascular lumen. A key morphological feature of Buerger disease is the presence of specific microabscesses within these thrombi.

The structure of such a microabscess has clear boundaries. Peripherally, it is surrounded by a dense cellular wall consisting of epithelioid cells and fibroblasts. Among them, Langhans giant cells are prominent, and their presence serves as an important diagnostic sign.

During the natural organization of the thrombus, these microabscesses do not remain unchanged—they are gradually replaced by newly formed granulation tissue, ultimately leading to sclerosis and persistent luminal obliteration.

It is important to emphasize a critical differential diagnostic criterion: necrosis of the vessel wall itself and damage to the internal elastic lamina are not characteristic of thromboangiitis obliterans. The disease itself is characterized by a remitting course. This means that histological examination can simultaneously reveal completely different stages of the pathological process in various segments of the vascular bed—from fresh thrombi to areas of dense fibrosis.

The main and most formidable complication of long-standing thromboangiitis obliterans is the development of gangrene of the extremities, which is associated with a critical drop in blood flow due to complete vascular obliteration.

Mnemonic

BUERGER: Bain in extremities (Pain), Under 35 years old (Young males), Episodic (Remitting course), Recurrent superficial thrombophlebitis, Gangrene, Everyday smoking, Reduction of small artery lumen.

Frequently asked questions

What arterial diseases require differential diagnosis with thromboangiitis obliterans?

Differential diagnosis of thromboangiitis obliterans is performed with other diseases causing chronic arterial insufficiency of the extremities. The main pathologies include:

  • Obliterating endarteritis — the clinical picture is virtually identical, but Buerger disease is additionally accompanied by migratory thrombophlebitis.
  • Raynaud's disease — differs by predominantly affecting the upper extremities.
  • Atherosclerosis obliterans — based on an atherosclerotic process with narrowing and occlusion of the vascular lumen.
What pathological changes develop in nerve trunks during the progression of Buerger disease?

As Buerger disease progresses, the pathological process gradually extends to surrounding tissues, including nerve fibers. Inflammation directly spreads from the affected arteries to accompanying veins and adjacent nerve trunks. Ultimately, this specific involvement leads to pronounced fibrosis within the nerve trunks.

What macroscopic signs are characteristic of extremity gangrene in Buerger disease?

Buerger disease often leads to wet gangrene of the extremities, characterized by specific macroscopic changes. The main features include:

  • Tissues turn black due to the formation of iron sulfide.
  • Liquefactive (wet) necrosis develops: the affected tissue becomes flaccid and contains a lot of fluid.
  • The tissue swells, becomes edematous, with a characteristic foul odor and myomalacia (softening).
  • A demarcation line is not defined because there is no tendency to wall off the necrotic process from healthy tissues.
Which vessels are the primary targets in Buerger disease?

Small- and medium-sized arteries are primarily affected. Large arteries are extremely rarely involved in the pathological process.

Does destruction of the vessel wall occur in thromboangiitis obliterans?

No, necrosis of the vessel wall and damage to the internal elastic lamina are not characteristic of this disease.

What happens to microabscesses over time?

As the thrombus organizes, the microabscesses are gradually replaced by granulation tissue, leading to further sclerosis and obliteration.

What is the characteristic pattern of the inflammatory process?

The disease follows a remitting course. Different stages of inflammation and thrombosis can be found simultaneously in various vascular segments.

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