Although the cause is unknown, several theories account for the reduced digital blood flow: intrinsic vascular wall hyperactivity to cold, increased vasomotor tone due to sympathetic stimulation, and antigen-antibody immune response (the most likely theory because abnormal immunologic test results accompany Raynaud’s phenomenon). Risk factors include associated diseases (Buerger’s disease, atherosclerosis, rheumatoid arthritis, scleroderma, and SLE) and smoking.

This disorder affects women more often than men.

After exposure to cold or stress, the skin on the fingers typically blanches and then becomes cyanotic before changing to red and before changing from cold to normal temperature. Numbness and tingling may also occur. These symptoms are relieved by warmth. In longstanding disease, trophic changes, such as sclerodactyly, ulcerations, or chronic paronychia, may result. Although it’s extremely uncommon, minimal cutaneous gangrene necessitates amputation of one or more phalanges.

• Clinical criteria that establish Raynaud’s disease include skin color changes induced by cold or stress; bilateral involvement; absence of gangrene or, if present, minimal cutaneous gangrene; normal arterial pulses; and a history of clinical symptoms of longer than 2 years’ duration.

• Diagnosis must also rule out secondary disease processes, such as chronic arterial occlusive or connective tissue disease.

• Antinuclear antibody (ANA) titer is used to identify autoimmune disease as an underlying cause of Raynaud’s phenomenon. Further testing must be performed if ANA titer is positive.

• Arteriography rules out arterial occlusive disease.

• Doppler ultrasonography may show reduced blood flow if symptoms result from arterial occlusive disease.

• A cold-stimulation test measures the temperature of each finger after
they are placed in an ice-water bath. Raynaud’s phenomenon may be diagnosed if the finger temperature takes greater than 20 minutes to return to pre-bath temperature.

• Nailfold capillaroscopy is useful to determine the presence of a connective tissue disorder.

Initially, treatment includes avoidance of cold, mechanical, or chemical injury; cessation of smoking; and reassurance that symptoms are benign. Because adverse drug effects, especially from vasodilators, may be more bothersome than the disease itself, drug therapy is reserved for unusually severe symptoms. Sympathectomy may be helpful when conservative treatment fails to prevent ischemic ulcers; it becomes necessary in less than 25% of patients.

• Warn the patient to avoid exposure to the cold. Tell him to wear mittens or gloves in cold weather or when handling cold items or defrosting the freezer.

• Advise the patient to avoid stressful situations and to stop smoking.

• Instruct the patient to inspect the skin often and to seek immediate care for signs of skin breakdown or infection.

• Teach the patient about drugs, their use, and their adverse effects.

• Provide psychological support and reassurance to allay the patient’s fear of amputation and disfigurement.

Stenosis or occlusion of the renal artery stimulates the affected kidney to release the enzyme renin, which converts angiotensinogen—a plasma protein—to angiotensin I. As angiotensin I circulates through the lungs and liver, it converts to angiotensin II, which causes peripheral vasoconstriction, increased arterial
pressure and aldosterone secretion and, eventually, hypertension.

Atherosclerosis (especially in older men) and fibromuscular diseases of the renal artery wall layers—such as medial fibroplasia and, less commonly, intimal and subadventitial fibroplasias—are the primary causes in 95% of patients with renovascular hypertension. Other causes include arteritis, anomalies of the renal arteries, embolism, trauma, tumor, and dissecting aneurysm. Less than 5% of patients with high blood pressure have renovascular hypertension; it’s most common in those younger than age 30 or older than age 50.

In addition to elevated systemic blood pressure, renovascular hypertension usually produces symptoms common to hypertensive states, such as headache, palpitations, tachycardia, anxiety, light-headedness, decreased tolerance of temperature extremes, retinopathy, and mental sluggishness. An altered level of consciousness and pitting edema may occur if renal failure ensues.