Senile Purpura: Differential Diagnosis and Clinical Features

Clinical Terminology and Morphological Classification

Senile purpura denotes red blood cell (RBC) extravasation into the mucous membrane or skin. As a result, purpuric lesions do not blanch upon pressing with a finger or glass slide (diascopy). The condition has a broad differential diagnosis that may be narrowed down through classification based on morphology and other laboratory and clinical findings (Soutor & Hordinsky, 2013). Associated clinical terminologies include the following:

Petechiae: Flat lesions no more than 4 mm in dimension; usually bright red at first, subsequently fading and acquiring a rusty color.

Ecchymosis: Also flat lesions, greater than 5 mm in diameter; usually purple or red at first, subsequently fading and acquiring a green, yellow, or brown color.

Palpable purpura: Oval or round, elevated, occasionally barely noticeable purple or red plaques or papules.

Retiform purpura: Branching or stellate lesions with geometric or angular borders, occurring both as non-palpable patches and as clear plaques (Soutor & Hordinsky, 2013).

Causes and Associated Conditions of Senile Purpura

Senile purpura (also known as blood spots, purpura senilis, or skin hemorrhages) widely occurs among older individuals who have a tendency to develop bruises, particularly on the legs and forearms. These bruises are not caused by mineral or vitamin deficiencies or bleeding disorders. As individuals age, the skin and its blood vessels become fragile and thin, causing bruises that initially appear purplish-red in color. Large purpuric lesions are termed ecchymoses, while extremely small spots are termed petechiae (PHC, 2018).

Common causes include the natural weakening of connective tissues and thinning of the skin with age, overuse of steroids, aspirin, and other blood thinners, diabetes or vascular ailments, and thrombocytopenic purpura emerging from meningococcemia and similar infections or medications that prevent platelet formation or disturb platelet functioning.

Meningococcal septicaemia, diphtheria, and streptococcal septicaemia are examples of bacterial infections that cause purpuric rashes. A number of serious viral infections — including Ebola viral fever, Lassa fever, Rift Valley viral fever, chickenpox, smallpox, measles, and parvovirus B19 — also result in purpuric rashes (Imm, 2015).

Henoch-Schönlein purpura (HSP) represents one commonly occurring condition caused by blood vessel wall infiltration and swelling as an anaphylactic response to various chemical and physical stimuli, such as infections. Upper respiratory tract infections triggered by β-haemolytic streptococcal infection typically precede it. It may occur as an epidemic among children, characterized by a fever and a slightly raised purpuric rash (Saulsbury, 2010), normally affecting the buttocks and the front of the legs. Acute arthritis, nephritis with proteinuria, and gastrointestinal pain may occur in association. The rash can continue forming over many weeks, with major complications including bleeding in the central nervous system, acute kidney injury, or acute intussusception. The condition is generally self-limiting, though potentially responsive to steroids. A Cochrane review failed to produce any evidence of benefit from short prednisolone courses in the prevention of acute kidney illness in Henoch-Schönlein purpura (Hahn, Hodson, Willis, et al., 2015).

Disseminated intravascular coagulation (DIC) is marked by major ecchymosis with an erythematous halo and irregular, sharp, purple-colored boundaries. The condition may aggravate and give rise to blue-black gangrene and haemorrhagic bullae, appearing as symmetrical multiple lesions involving pressure areas, distal extremities, and the lips, nose, trunk, and ears (Imm, 2015).

Continued consumption of potent steroids may result in widespread bruising and purpura, commonly on the extensor surfaces of the arms, thighs, and hands, caused by atrophy of collagen fibers that support skin blood vessels. This presentation appears similar to senile purpura (Imm, 2015).

Serious thrombocytopenia occurring between 5 and 12 days after receiving any platelet-containing blood product is rare and is normally limited to multiparous females (Shtalrid, Shvidel, Vorst, et al., 2006). This occurs because of the development of an antibody against a specific platelet antigen typically absent in the patient. Although normal recovery takes 1 to 3 weeks, the condition may prove lethal and may require treatment with intravenous immunoglobulins or plasmapheresis.

These represent a group of diseases whose characteristic feature is erythrocyte extravasation, especially in the lower legs, linked to haemosiderin deposition (Imm, 2015).

Both primary and secondary amyloid may lead to "pinch" purpura, so named because it usually appears on the individual's cheeks (Crookston et al., 2010).

This diagnosis may be considered in cases of unexplainable episodes of bruising or bleeding. Such episodes can represent acute psychiatric or emotional disturbance or may even signify abuse (Yamada, Sakurai, Shibata, et al., 2009).

References

Crookston, K., et al. (2010). Acquired bleeding disorders. Amyloidosis. PathologyOutlines.com.

Hahn, D., Hodson, E. M., Willis, N. S., et al. (2015). Interventions for preventing and treating kidney disease in Henoch-Schonlein Purpura (HSP). Cochrane Database of Systematic Reviews. doi:10.1002/14651858.CD005128.pub3.

Imm, N. (2015). Purpuric rashes. Patient Platform Limited.

PHC. (2018). Senile purpura. Prime Health Channel.

Saulsbury, F. T. (2010). Henoch-Schonlein purpura. Current Opinion in Rheumatology, 598–602.

Shtalrid, M., Shvidel, L., Vorst, E., et al. (2006). Post-transfusion purpura: A challenging diagnosis. Israel Medical Association Journal, 672–674.

Soutor, C., & Hordinsky, M. (2013). Clinical Dermatology. New York: McGraw-Hill Professional.

Yamada, K., Sakurai, Y., Shibata, M., et al. (2009). Factitious purpura in a 10-year-old girl. Pediatric Dermatology, 597–600.