Perplexing bruises on the forearms

Abstract

CASEA 76-year-old man was referred to the dermatology clinic by primary care because of "frightful" bruising on both forearms, which had worsened over the past few years. He has a 50-pack-year history of smoking, and underwent coronary artery bypass grafting surgery 12 years ago after a myocardial infarction. He denied any new medications, history of liver disease, or signifi cant trauma. His family history was negative for clotting disorders. He takes simvastatin, allopurinol, low-dose aspirin, metoprolol, and occasionally naproxen. He had unsuccessfully attempted to treat the forearm bruises with self-prescribed diabetic skin lotion, antifungal creams, emu oil, and fabric bleach. He was particularly concerned that he might have Ebola, but he had not traveled to West Africa and had no constitutional symptoms. He asked if Agent Orange may have caused his bruising, commenting that he had seen similar skin on other Vietnam veterans.Physical examination revealed numerous actinic keratoses on the temples, ears, and bald scalp. His dorsal forearms were covered with overlapping 1-to 4-cm ecchymoses, brown discoloration, and streaky white scars (Figure 1). The volar forearms and areas covered by short sleeves and his watchband were spared. He had mild stasis dermatitis, and his toenails were thick and yellowed, but no other bruises were found. A 3-mm tender nodule suspicious for squamous cell carcinoma was found on the dorsal left hand. THE MOST LIKELY DIAGNOSIS IS• acquired von Willebrand disease • actinic purpura • antiplatelet drug reaction • metastatic squamous cell carcinoma • leukocytoclastic vasculitis DISCUSSIONThe patient's age, skin type, and the distribution of the bruises all support a diagnosis of actinic purpura. This condition, also known as senile purpura or solar purpura, is frequently encountered in a dermatology practice. Given this patient's typical physical appearance and history, biopsy and serologic testing were not indicated. Serologic studies would be unremarkable, and histopathology would show reduced dermal collagen, a fl attened and thin epidermis, and abnormal elastin. Similar fi ndings occur in patients with corticosteroid atrophy, whether from topical or systemic therapy, so this should be ruled out. In either case, the vessel walls are normal, but the lack of protective collagen leads to easily damaged veins, and minor trauma leads to rupture and extravasation of erythrocytes. The most convincing fi nding in this patient, as with most, is the photodistribution of the ecchymoses: sun-protected areas are without bruising. Stellate pseudoscars (Figures 2 and 3) are another typical fi nding, intermixed with other signs of photodamage. Hemosiderin deposition gives the dermis a characteristic brown color. The skin is rough in texture, and often covered in actinic and seborrheic keratoses. The loss of collagen and poor elasticity are apparent with palpation of crinkly, dry, thin skin. In contrast, the areas protected from UV radiation still appear in the patient's normal skin color and are smoo...