Random Dermatology MCQ - Vibration White Finger

A 45-year-old construction worker who has operated a jackhammer for 15 years presents with episodic, well-demarcated blanching of the fingertips of both hands, triggered by cold exposure or using vibrating tools. The episodes last 10-15 minutes and are followed by painful cyanosis and then erythema. He reports reduced grip strength and numbness in the fingers. The most likely diagnosis and the underlying pathophysiological mechanism is:

A. Primary Raynaud's phenomenon; idiopathic vasospasm without an underlying disease.
B. Vibration white finger (hand-arm vibration syndrome); chronic endothelial and nerve damage from segmental vibration leading to digital artery vasospasm and fibrosis.
C. Systemic sclerosis (scleroderma); autoimmune-mediated fibrosis and vasculopathy.
D. Thromboangiitis obliterans (Buerger's disease); inflammatory thrombosis of small and medium-sized vessels, strongly associated with smoking.
E. Acrocyanosis; persistent, painless cyanosis of the hands without the triphasic color change.

Correct Answer: B. Vibration white finger (hand-arm vibration syndrome); chronic endothelial and nerve damage from segmental vibration leading to digital artery vasospasm and fibrosis.

Answer and Explanation

The correct answer is B. This question describes the classic presentation of vibration white finger (VWF), the vascular component of hand-arm vibration syndrome (HAVS). The key clues are the long occupational history with high-frequency vibration tools (jackhammer), the triphasic (white-cyanotic-red) color change of the fingers, and the associated neurological symptoms (numbness, reduced grip). The pathophysiology involves chronic mechanical trauma from vibration, leading to endothelial damage, hypertrophy of the vascular intima and media, and perivascular fibrosis of the digital arteries. This causes increased vasomotor tone and a heightened vasospastic response (Raynaud's phenomenon), combined with direct nerve damage.

Why the Other Options are Incorrect:

• A. Primary Raynaud's phenomenon: This is idiopathic, typically affects young women, and is not associated with neurological symptoms or a specific occupational trigger. It is a diagnosis of exclusion.

• C. Systemic sclerosis (scleroderma): This autoimmune disease causes secondary Raynaud's phenomenon, but it is associated with other systemic features (skin thickening, telangiectasias, internal organ involvement) and specific autoantibodies (e.g., anti-centromere, anti-Scl-70), not a specific tool-use history.

• D. Thromboangiitis obliterans (Buerger's disease): This inflammatory, non-atherosclerotic occlusive disease presents with persistent pain, ulcers, and gangrene of the digits, strongly linked to tobacco use. It is not primarily vasospastic and triggered by cold/vibration.

• E. Acrocyanosis: This is a persistent, symmetric, bluish discoloration of the hands and feet that is not episodic or triphasic, and is not typically painful or associated with vibration exposure.

Additional High-Yield Information for Exams:

• Clinical Stages (Stockholm Workshop Scale): The vascular component is graded:

  • 0VT: No attacks.

  • 1VT: Occasional attacks affecting only the tips of one or more fingers.

  • 2VT: Occasional attacks affecting distal and middle phalanges of one or more fingers.

  • 3VT: Frequent attacks affecting all phalanges of most fingers.

  • 4VT: Very frequent attacks with trophic skin changes (ulceration, gangrene).

• Pathogenesis: Prolonged exposure to segmental vibration (especially in the 50-150 Hz range) causes:

  • Vascular: Endothelial dysfunction, smooth muscle hypertrophy, fibrosis of the tunica media, and eventual structural occlusion of digital arteries.

  • Neurological: Damage to myelinated sensory nerve fibers (causing numbness, tingling) and motor fibers (reducing grip strength and dexterity). This is the carpal tunnel syndrome-like component.

• Differential Diagnosis: The occupational history is the key differentiator from other causes of secondary Raynaud's phenomenon (CTDs, hematologic disorders, arterial obstruction).

• Associated Conditions & Prognosis:

  • Prognosis: Symptoms are often irreversible, even after cessation of exposure. Continued exposure leads to progression through the Stockholm stages, potentially to digital ulceration or gangrene.

  • Disability: Can lead to significant occupational disability and impaired quality of life.

• Management & Rationale:

  • Rationale: The cornerstone is primary prevention (engineering controls) and secondary prevention (early detection, removal from exposure). Treatment is symptomatic.

  • First-line/Preventive: Elimination or drastic reduction of vibration exposure is mandatory. This may require a change in work duties.

  • Engineering Controls: Use of anti-vibration gloves (limited efficacy), properly maintained tools with damping systems, and job rotation.

  • Medical Management: Smoking cessation is absolutely critical, as it is a powerful synergistic vasoconstrictor. Calcium channel blockers (e.g., nifedipine) can help reduce the frequency/severity of vasospastic attacks. Pentoxifylline or iloprost may be used in severe cases with trophic changes.

  • Occupational Health: Recognition as an occupational disease is key for worker's compensation and enforcing workplace safety regulations.