A 62-year-old woman with a 10-year history of varicose veins presents with chronic bilateral lower-leg erythema, scaling, and pruritus. Examination reveals reddish-brown pigmentation over the medial malleoli bilaterally, mild pitting edema, and no systemic signs of infection. The structure marked **A** in the diagram shows the characteristic findings of stasis dermatitis. Which of the following best explains the pathophysiologic mechanism underlying the hemosiderin pigmentation seen in this patient?

Explanation

## Why option 1 is correct Stasis dermatitis (marked **A**) is the cutaneous manifestation of chronic venous insufficiency (CVI) caused by valvular incompetence. The pathophysiology is well-established: failure of venous valves (from varicose veins, post-thrombotic syndrome, or calf-pump dysfunction) raises ambulatory venous pressure, dilating capillaries and increasing microvascular permeability. Plasma fibrinogen and red blood cells extravasate into the dermis. Resident macrophages phagocytose these extravasated RBCs, and the hemoglobin is metabolized to hemosiderin, which deposits in the dermis and imparts the characteristic reddish-brown pigmentation over the medial malleolus (the classic "gaiter area" location). This is CEAP stage C4a — pigmentation with eczema. The anchor fact directly links hemosiderin deposition to RBC extravasation from venous hypertension, not infection or arterial disease (Bolognia Dermatology 5e Ch 12). ## Why each distractor is wrong - **Option 2 (Acute bacterial infection)**: Cellulitis is the most commonly confused diagnosis with stasis dermatitis, but cellulitis is ACUTE, unilateral, accompanied by fever and leukocytosis, and does NOT produce hemosiderin pigmentation. The patient's chronic bilateral presentation with no systemic signs rules out infection. Iron deposition from bacterial siderophores is not a mechanism of cellulitis. - **Option 3 (Autoimmune melanocyte destruction)**: This describes vitiligo or other depigmenting disorders, not stasis dermatitis. Hemosiderin deposition is not a compensatory mechanism for melanocyte loss. Stasis dermatitis causes hyperpigmentation, not depigmentation. - **Option 4 (Chronic arterial insufficiency)**: Arterial insufficiency causes ischemic ulcers (typically on the toes or lateral malleolus, not medial), not stasis dermatitis. Arterial disease does not produce the venous hypertension-driven RBC extravasation and hemosiderin deposition seen in CVI. The patient's bilateral edema and medial-malleolar location are classic for venous, not arterial, pathology. **High-Yield:** Hemosiderin in stasis dermatitis = RBC extravasation from venous hypertension → macrophage phagocytosis; always check ABI ≥0.8 before applying compression to rule out arterial disease. [cite: Bolognia Dermatology 5e Ch 12; EVRA trial NEJM 2018]