W ith unrelieved pressure, tissue ischemia develops, and metabolic wastes accumulate in the interstitial tissue, resulting in anoxia and cellular death.¹ This pressure-induced ischemia also leads to excessive tissue hypoxia, further promoting bacterial proliferation and tissue destruction.² In clinical settings, some pressure-induced ischemic wounds are caused by support surfaces, and some lower-limb diabetic pressure ulcers are caused by footwear. Infection of these wounds considerably impairs the healing process. For example, with pressure ulcers, the prevalence of inf

M any diseases show a chronic course, and among them, chronic venous insufficiency is considered to be the most common disorder of venous origin.^1,2 Chronic venous insufficiency refers to a set of physical alterations that occur on the skin and in subcutaneous tissue, mainly affecting the lower limbs, and manifest as edema, hyperpigmentation, eczema, and lipodermatosclerosis.³ These manifestations are the result of long-term venous hypertension caused by valvular insufficiency and/or venous obstruction with skin ulceration as a complication.^1,3–6 Ulcers of v

Presentation

A 63-year-old white woman presented with a rash on all extremities and the face, conjunctivitis, and painful perioral and oral mucosal erosions. She denied pharyngeal or esophageal dysphagia. The patient was afebrile and denied weakness, malaise, or other constitutional symptoms. Her past medical history was significant for lung cancer, diagnosed 1 year prior to presentation, which was currently in remission. The patient also had a past medical history of dry eye syndrome and hypertension. She underwent initial chemotherapy followed by maintenance therapy with gefitinib (Iress