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Emergency And Acute Medicine – Purpura
Purpura refers to nonblanching skin lesions caused by extravasation of blood into the skin or subcutaneous tissue. These lesions do not completely blanch with pressure. Size-based terminology includes petechiae (≤4 mm), purpura (5-10 mm), and ecchymoses (>10 mm). Lesion color varies with depth and age: superficial and recent lesions appear red; deeper or evolving lesions may appear purple, brown, orange, or blue-green.
Purpura is categorized as nonpalpable or palpable. Nonpalpable purpura typically results from simple hemorrhage or microvascular occlusion and is usually associated with platelet disorders, including decreased production, increased destruction, abnormal function, or altered distribution. Palpable purpura most commonly reflects small-vessel vasculitis, often leukocytoclastic in nature, mediated by immune complex deposition in postcapillary venules with complement activation and neutrophil recruitment. Vessel wall damage leads to leakage of blood. In immunocompromised patients, vasculitic lesions may not be palpable.
Nonpalpable purpura may result from viral infections (e.g., echovirus, measles, parvovirus B19), medications (e.g., anticoagulants, NSAIDs, penicillins, sulfonamides, thiazides), nutritional deficiencies (vitamin C or K), bone marrow disorders, hypersplenism, idiopathic thrombocytopenic purpura (ITP), disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura, liver or renal insufficiency, thrombocytopenia (<50,000 />micro;L), extreme thrombocytosis, hemophilia, and solar purpura. Sudden increases in intravascular pressure from vomiting, coughing, or childbirth may also cause petechiae.
Palpable purpura may be triggered by infections (e.g., hepatitis B, streptococcal infection, meningococcus, gonococcus, Rocky Mountain spotted fever), medications, malignancies, autoimmune or connective tissue diseases, and septic emboli. Certain conditions produce characteristic patterns, including ecthyma gangrenosum from Pseudomonas infection, purpura fulminans associated with DIC and shock, cryoglobulinemia, Coumadin necrosis, and embolic phenomena. In children, important causes include Henoch–Schönlein purpura (HSP), hemolytic uremic syndrome, Kawasaki disease, neonatal protein C or S deficiency (purpura fulminans), maternal ITP, and Wiskott–Aldrich syndrome.
Clinical evaluation focuses on lesion characteristics and associated systemic findings. Lesions may be round (suggesting leukocytoclastic emboli) or irregular and retiform (suggesting infectious emboli or vascular occlusion). Distribution provides diagnostic clues: generalized purpura raises concern for DIC or meningococcemia; dependent purpura commonly affects the lower extremities; acral involvement may suggest vasculitis or embolic disease; mucosal involvement suggests platelet dysfunction such as ITP. Associated symptoms such as fever, hypotension, altered mental status, gingival bleeding, hematuria, arthralgias, or abdominal pain increase concern for systemic disease.
Specific syndromes have recognizable patterns. Meningococcemia may present with fever, headache, and retiform purpura involving palms, soles, and mucous membranes. Rocky Mountain spotted fever presents after several days of systemic symptoms with rash beginning on distal extremities including palms and soles, progressing to petechiae. Henoch–Schönlein purpura presents with palpable purpura on lower extremities and buttocks, often with abdominal pain, arthralgias, and hematuria. Disseminated gonococcal infection typically produces fewer than 10 purpuric papules or vesicopustules with fever and arthralgias. Levamisole-adulterated cocaine may cause necrotic retiform purpura involving ears and face with neutropenia.
Evaluation includes detailed history, including bleeding disorders, thromboembolic history, splenectomy, alcohol or drug use, family history, and medication review. Laboratory studies begin with platelet count (confirmed by peripheral smear), coagulation studies (PT/PTT), and DIC screen if the patient appears toxic. Basic chemistry including liver function tests, urinalysis, and rapid streptococcal testing may be indicated. Outpatient studies may include hepatitis serologies, antinuclear antibodies, complement levels, cryoglobulins, von Willebrand testing, and other hematologic or rheumatologic investigations depending on suspicion.
Emergency management depends on severity. Patients with fever, hypotension, altered mental status, or generalized ecchymoses require immediate stabilization with airway support, IV access, fluid resuscitation, and empiric IV antibiotics when infection is suspected. Ceftriaxone is recommended for suspected meningococcemia; doxycycline is first-line for suspected Rocky Mountain spotted fever (chloramphenicol in pregnancy). Early antibiotic administration is critical in suspected sepsis.
Admission is required for unstable vital signs, altered mental status, fever with concerning rash, or evidence of serious infection or critical thrombocytopenia. Discharge may be considered only after life-threatening causes have been excluded and the patient is stable, with close outpatient follow-up arranged. Patients should avoid contact sports or antiplatelet agents until cleared.
A key principle is to treat purpura as potentially life-threatening until proven otherwise. Empiric antibiotics should be strongly considered when there is any concern for meningococcemia, Rocky Mountain spotted fever, or sepsis. Early recognition and intervention can be lifesaving.
Purpura refers to nonblanching skin lesions caused by extravasation of blood into the skin or subcutaneous tissue. These lesions do not completely blanch with pressure. Size-based terminology includes petechiae (≤4 mm), purpura (5-10 mm), and ecchymoses (>10 mm). Lesion color varies with depth and age: superficial and recent lesions appear red; deeper or evolving lesions may appear purple, brown, orange, or blue-green.
Purpura is categorized as nonpalpable or palpable. Nonpalpable purpura typically results from simple hemorrhage or microvascular occlusion and is usually associated with platelet disorders, including decreased production, increased destruction, abnormal function, or altered distribution. Palpable purpura most commonly reflects small-vessel vasculitis, often leukocytoclastic in nature, mediated by immune complex deposition in postcapillary venules with complement activation and neutrophil recruitment. Vessel wall damage leads to leakage of blood. In immunocompromised patients, vasculitic lesions may not be palpable.
Nonpalpable purpura may result from viral infections (e.g., echovirus, measles, parvovirus B19), medications (e.g., anticoagulants, NSAIDs, penicillins, sulfonamides, thiazides), nutritional deficiencies (vitamin C or K), bone marrow disorders, hypersplenism, idiopathic thrombocytopenic purpura (ITP), disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura, liver or renal insufficiency, thrombocytopenia (<50,000 />micro;L), extreme thrombocytosis, hemophilia, and solar purpura. Sudden increases in intravascular pressure from vomiting, coughing, or childbirth may also cause petechiae.
Palpable purpura may be triggered by infections (e.g., hepatitis B, streptococcal infection, meningococcus, gonococcus, Rocky Mountain spotted fever), medications, malignancies, autoimmune or connective tissue diseases, and septic emboli. Certain conditions produce characteristic patterns, including ecthyma gangrenosum from Pseudomonas infection, purpura fulminans associated with DIC and shock, cryoglobulinemia, Coumadin necrosis, and embolic phenomena. In children, important causes include Henoch–Schönlein purpura (HSP), hemolytic uremic syndrome, Kawasaki disease, neonatal protein C or S deficiency (purpura fulminans), maternal ITP, and Wiskott–Aldrich syndrome.
Clinical evaluation focuses on lesion characteristics and associated systemic findings. Lesions may be round (suggesting leukocytoclastic emboli) or irregular and retiform (suggesting infectious emboli or vascular occlusion). Distribution provides diagnostic clues: generalized purpura raises concern for DIC or meningococcemia; dependent purpura commonly affects the lower extremities; acral involvement may suggest vasculitis or embolic disease; mucosal involvement suggests platelet dysfunction such as ITP. Associated symptoms such as fever, hypotension, altered mental status, gingival bleeding, hematuria, arthralgias, or abdominal pain increase concern for systemic disease.
Specific syndromes have recognizable patterns. Meningococcemia may present with fever, headache, and retiform purpura involving palms, soles, and mucous membranes. Rocky Mountain spotted fever presents after several days of systemic symptoms with rash beginning on distal extremities including palms and soles, progressing to petechiae. Henoch–Schönlein purpura presents with palpable purpura on lower extremities and buttocks, often with abdominal pain, arthralgias, and hematuria. Disseminated gonococcal infection typically produces fewer than 10 purpuric papules or vesicopustules with fever and arthralgias. Levamisole-adulterated cocaine may cause necrotic retiform purpura involving ears and face with neutropenia.
Evaluation includes detailed history, including bleeding disorders, thromboembolic history, splenectomy, alcohol or drug use, family history, and medication review. Laboratory studies begin with platelet count (confirmed by peripheral smear), coagulation studies (PT/PTT), and DIC screen if the patient appears toxic. Basic chemistry including liver function tests, urinalysis, and rapid streptococcal testing may be indicated. Outpatient studies may include hepatitis serologies, antinuclear antibodies, complement levels, cryoglobulins, von Willebrand testing, and other hematologic or rheumatologic investigations depending on suspicion.
Emergency management depends on severity. Patients with fever, hypotension, altered mental status, or generalized ecchymoses require immediate stabilization with airway support, IV access, fluid resuscitation, and empiric IV antibiotics when infection is suspected. Ceftriaxone is recommended for suspected meningococcemia; doxycycline is first-line for suspected Rocky Mountain spotted fever (chloramphenicol in pregnancy). Early antibiotic administration is critical in suspected sepsis.
Admission is required for unstable vital signs, altered mental status, fever with concerning rash, or evidence of serious infection or critical thrombocytopenia. Discharge may be considered only after life-threatening causes have been excluded and the patient is stable, with close outpatient follow-up arranged. Patients should avoid contact sports or antiplatelet agents until cleared.
A key principle is to treat purpura as potentially life-threatening until proven otherwise. Empiric antibiotics should be strongly considered when there is any concern for meningococcemia, Rocky Mountain spotted fever, or sepsis. Early recognition and intervention can be lifesaving.
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