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​Dermatology - Raynaud's phenomenon

2/7/2024

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​Dermatology - Raynaud's phenomenon
Raynaud phenomenon is a condition characterized by reduced blood flow to the fingers or toes, resulting in ischemia, which can be triggered by exposure to cold temperatures and/or mental stress. Vibration-induced injury can manifest in those who frequently utilize vibrating instruments, such as construction workers, butchers, typists, and pianists. Primary Raynaud phenomenon is characterized by the absence of an identifiable reason, whereas secondary Raynaud phenomenon is associated with an underlying disease as the causative factor. The causes of secondary Raynaud phenomenon include connective tissue diseases (such as scleroderma, lupus, dermatomyositis, vasculitis), atherosclerosis, thromboembolism, drugs and toxins including β-adrenergic blockers, ergotamines, and bleomycin, carpal tunnel syndrome, vibration injuries, cryoproteinemia, and cold agglutinins.

The fingers or toes exhibit blanching or cyanosis, which can be observed from the tip to different levels of the digits. The finger located beyond the area of reduced blood flow appears pale or cyanotic and has a lower temperature; the skin closer to the body looks rosy and has a higher temperature. Upon reheating the digits, the blanching may be substituted by cyanosis due to sluggish blood circulation. At the conclusion of the episode, the digits may regain their original color or exhibit a crimson hue, indicating the reactive hyperemic phase. Patients frequently have a continuous vasospasm instead of sporadic episodes. The skin undergoes trophic changes characterized by the development of tight, thin skin, pterygium formation, and clubbing and shortening of the terminal phalanges.

​Acrogangrene is a condition that is not commonly seen, but it is frequently observed in individuals with Raynaud phenomenon that is caused by scleroderma. In such cases, the terminal phalanges may become separated or gangrene may develop, which can result in the fingertips being self-amputated.
The diagnosis is primarily based on clinical evaluation, with the key focus being the identification of any underlying etiology, particularly scleroderma.

Calcium channel blockers, anti-adrenergic medications, intravenous prostacyclin, bosentan (an endothelin receptor antagonist), and local botox injections are effective in avoiding episodes.
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