Raynauds Disease

During the late nineteenth century Maurice Raynaud described digital vasospasm that seemed to be cold-induced. He believed that this phenomenon, now known as Raynaud's disease, was due to changes in the CNS control over vascular innervation. Raynaud's phenomenon is classically described in patients who develop extremity blanching and numbness with cold exposure, followed by cyanosis and then erythema on rewarming. The fingers are affected most commonly, but the toes and ears may also be involved.

Raynaud's disease has been divided into primary and secondary forms. Primary Raynaud's is more common than the secondary form, occurring in 3% to 16% of the general population.27 Secondary Raynaud's disease is far less common, developing in only 3% to 9% of patients; it is defined as Raynaud's phenomenon associated with the development of a connective tissue disease (most commonly scleroderma).

Evaluation of a patient in whom Raynaud's disease is suspected includes a thorough history and physical examination. Changes consistent with the disease can be reproduced in the office by immersing the patient's affected extremity in ice water. Antinuclear antibodies are positive in 17% to 26% of patients but do not predict disease progression.28

Investigations into the pathophysiology of Raynaud's disease have led to identification of a number of abnormalities, but the complete mechanism has not been fully established. Studies have shown that patients with this disorder have an abnormal adrenergic response. Neuropeptide release (possibly due to sensory nerve system damage) and endothelial factors have also been identified.27-29

It is important to discuss with patients the role of behavior modification. Conservative approaches to treatment include warm socks or mittens and cold avoidance. Patients are encouraged to stop smoking and to avoid vasoconstrictive drugs, such as amphetamines, cocaine, and over-the-counter decongestants. Caffeine may also exacerbate symptoms by causing a rebound vasoconstriction after an initial vasodilatation. In patients with vasospasm associated with emotional stress, relaxation and stress management strategies have also been helpful.

When conservative strategies fail, patients may respond to calcium channel blockers. Nifedipine has been the most widely studied at doses of 10 mg sublingually for immediate treatment of acute vasospasm or 30 to 60 mg of nifedipine taken on a chronic basis, although care must be taken to avoid symptomatic hypotension.

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