Diagnosis: Senile purpura
Our patient had senile purpura, a condition in which capillary bleeding results from chronic congestion and fragile blood-vessel walls. An increased tendency to hemorrhage from usually insignificant injury is seen with a wide variety of clinical disorders collectively called “hemorrhagic diatheses.” The hemorrhagic disorders may be acute or chronic and asymptomatic.
Senile purpura is characterized by hemorrhages on the extensor surfaces of the forearms and the dorsa of the hands; the lesions usually last one to three weeks. This form of purpura is similar to that seen in healthy women about the time of menstruation or in patients receiving systemic steroid therapy (which adversely affects extravascular tissues because of its hormonal anti-anabolic effects). Atrophy and loss of subcutaneous fat and elasticity render the skin susceptible to minor trauma, with the formation of petechiae and ecchymoses along the veins of the hands, forearm, legs, and feet.
Larger than petechiae but smaller than ecchymoses, purpura lesions may be tender and palpable. Local hemorrhages result from a combination of bleeding into the skin and impaired hemostasis. The colors through which a bruise passes reflect the transformation of released hemoglobin through a sequence of pigments into hemosiderin.
Primary hemostasis depends both on reflex vasoconstriction of the injured vessel and on development of a platelet plug. Chemical forces attract platelets to each other and to the denuded subendothelial collagen. On contact with collagen, the platelets swell and release vasoconstrictive amines. Larger hemorrhages require secondary hemostasis, which involves the cascade of coagulation factors and results in fibrin-clot reinforcement of the platelet plug. Whereas platelet problems are an important cause of purpuric skin lesions, defects or deficiency of a single procoagulant clotting factor is an uncommon case of cutaneous hemorrhage. A defect in clotting factors usually leads instead to soft-tissue hemorrhage, particularly into joints.
Pressure application with a glass slide or diascopy can reveal whether redness of the skin is due to purpura or to dilated vessels, such as those seen with inflammation and telangiectasias. The redness of purpura cannot be eliminated by pressure.
Purpura can have intravascular, vascular, and extravascular causes. Intravascular causes include platelet or coagulation-factor defects, while vascular causes consist of infection, hypergammaglobulinemia, cryopathies, emboli, inflammation, and increased fragility. Purpura can also have extravascular causes, such as connective tissue disease, trauma, and venom toxins.
Senile purpura does not routinely need laboratory workup; most clinicians consider the condition primarily a
cosmetic problem. When desired, laboratory tests that can be used to investigate the cause of purpura are peripheral blood-smear and bone-marrow examination, platelet count, bleeding times, capillary fragility, clot retraction, one-stage prothrombin time, partial thromboplastin time, thromboplastin-generation tests, and assays for protein C and S, fibrinogen, and fibrinolysis. Biopsy is indicated in patients with suspected vasculitis.
Our patient was told to minimize trauma to the skin of the extremities, prevent skin dryness with moisturizers, and use barrier protection, such as clothing, to protect his skin.