STASIS DERMATITIS




PATIENT STORY



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A 55-year-old-woman was admitted to the hospital to rule out bilateral lower extremity cellulitis. She presented with lower extremity edema and sharply demarcated pretibial erythema that extended just above the medial malleolus bilaterally (Figure 60-1). She was afebrile, and complete blood count (CBC) was within normal limits. The patient was diagnosed with classic stasis dermatitis, a condition commonly misdiagnosed as bilateral lower extremity cellulitis.




FIGURE 60-1


Lower extremity edema and pretibial erythema consistent with stasis dermatitis. This is commonly misdiagnosed as bilateral lower extremity cellulitis.






EPIDEMIOLOGY



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  • The prevalence is estimated to be greater than 1% of the population.1



  • Slight female preponderance reported.1



  • Prevalence increases with age.




    • Estimated prevalence of 6% to 7% in patients older than 50 years.2





ETIOLOGY AND PATHOPHYSIOLOGY



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  • Stasis dermatitis likely occurs secondary to the chronic inflammation and microangiopathy that result from chronic venous insufficiency.1




    • Disruption in function of the venous valve system in the deep and perforating venous tributaries of the legs causes backflow into the superficial venous system, yielding venous hypertension.1




      • Valvular dysfunction results from increasing age or can be the result of specific events, including deep vein thrombosis, pregnancy, surgery, or history of a lower extremity injury.1



    • Venous hypertension decreases the flow of blood in the micro-vasculature and allows for an increase in the capillary permeability, resulting in the extravasation of erythrocytes and the passage of fluid and plasma proteins into the tissue, consequently leading to microangiopathy.1




      • Proteins, most commonly fibrin, are deposited perivascularly, forming a hyaline cuff and inhibiting oxygen diffusion.1,2



      • Decreased blood flow causes an upregulation of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule (VCAM-1), thus activating neutrophils and macrophages.1,2



      • Activated neutrophils release inflammatory mediators, free radicals, and proteases, causing pericapillary inflammation.1





DIAGNOSIS



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Clinical Features of Stasis Dermatitis





  • Often first manifests as lower extremity edema.



  • Scaling, xerosis, and pruritus are often present within the mid and distal medial calf (Figure 60-2). Less often, similar manifestations affect the lateral calf.



  • Hemosiderin deposition often leads to the classic brown discoloration seen in stasis dermatitis (Figure 60-3).



  • Erythema, scaling, and diffuse dermatitis can result in a weepy appearance with oozing and crusting (Figure 60-4).



  • When stasis dermatitis is present chronically, fibrosis of the underlying tissues progresses to lipodermatosclerosis.



  • A constricting band forms around the distal calf causing the classic “inverted wine bottle appearance” of the lower extremity (Figure 60-5).



  • Chronic stasis dermatitis can also present with violaceous papules, plaques, and nodules mimicking Kaposi sarcoma. This entity is known as pseudo-Kaposi sarcoma or acroangiodermatitis.2



Jan 13, 2019 | Posted by in CARDIOLOGY | Comments Off on STASIS DERMATITIS

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