Pathophysiology of Buerger’s Disease


Smoking is very closely related to Buerger’s disease and smoking history is one of the critera for diagnosing the disease. In general if the patient absolutely abandons smoking the course of the disease will be invariably benign, but if smoking continues any treatment will ultimately be futile. Though “passive smoking” has adverse effect on cardiovascular system, non smokers should never develop the disease. Active smokers can be identified by measuring levels of nicotine, the major metabolite of nicotine in urine. Since all smokers do not develop the disease an immunopathogenesis is considered probable. It has been proposed in Japanese that presence of a gene linked to some HLA antigens might control the susceptibility to the disease (

Most patients with Buerger’s are heavy smokers, but some cases occur in patients who smoke “moderately”; others have been reported in users of smokeless tobacco. It has been postulated that Buerger’s Disease is an “autoimmune” reaction (one in which the body’s immune system attacks the body’s own tissues) triggered by some constituent of tobacco (

Mogotlane (2005) said that nicotine in cigarette acts as a vasoconstrictor so there will be less oxygen supply to the extremities, and in addition, is thought to alter the surface properties of platelets so that they become more stick, increasing the risk of clots formation causing further damage.

Although this condition is different from atherosclerosis, Buerger’s disease in older patients may also be followed by atherosclerosis of the larger vessels after involvement of the smaller vessels. The patient’s ability to walk may be severely limited. Patients are at higher risk for non healing wounds because of impaired circulation (Smeltzer and Bare, 2004).

Onset of the disease is gradual and first occurs in the feet or hands. Inflammation occurs in small and medium-sized arteries and veins near the surface of the limb. In advanced cases, blood vessels in other parts of the body may be affected. There is a progressive decrease in the blood flow to the affected areas. The pulse in arteries of the feet is weak or undetectable. The lack of blood flow can lead to gangrene, which is decay of tissue due to restricted blood supply (Zhang, 2008).

Symptoms. The thromboangiitis obliterans (Buerger’s disease presents with a triad of symptoms and signs: digital arteries occlusion, Raynaud’s phenomenon, and migrating superficial vein thrombophlebitis (Lilly, 2007).
Early symptoms include decrease in the blood supply (arterial ischemia) and superficial (near the skin surface) phlebitis. The main symptom is pain in the affected areas is the outstanding manifestation. A cold sensitivity in the hands with color changes, similar to that seen in Raynaud’s disease, can develop and may be another early manifestation. In this case, the hands turn color–white, blue, and then intense rubor or reddish blue discoloration (Zhang, 2008; Smeltzer and Bare, 2004).

Claudication type of pain is common with pain in the arch of the foot. Various types of paresthesias may occur. Pulsations in the posterior tibial and dorsalis pedis arteries are weak or absent. In advance cases, the extremities may be abnormally red or cyanotic, particularly when dependent (Black and Hawks, 2005).


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