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Although purpura itself is not dangerous, it may be a sign of an underlying life-threatening illness that requires immediate attention.
Petechiae above the nipple line with a history of cough or vomiting may be benign and caused by increased venous pressure.
Purpura is present in almost all patients with Henoch–Schonlein purpura (HSP), but it may not always be the presenting sign. This can cause a delay in the diagnosis.
Think of idiopathic thrombocytopenic purpura (ITP) in a nontoxic-appearing child with absence of splenomegaly and a normal hemoglobin and white blood cell count.
Child abuse should be suspected if bruising occurs to nonbony prominences or in areas not normally subjected to injury, or if the history is not consistent with the physical findings.
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Purpura results from the extravasation of blood from vasculature into the skin or mucous membranes. A careful evaluation of a patient with a purpuric rash will help differentiate a benign illness from a life-threatening disorder (Fig. 89-1). Although laboratory tests are helpful, a thorough history and physical examination can offer the most information to identify the cause. This section provides an overview of the main causes of petechiae and purpura in children.
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Petechiae Caused by Sepsis
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Purpura fulminans due to sepsis is a hematologic emergency characterized by disseminated intravascular coagulation (DIC), skin necrosis, and multiorgan dysfunction.1 It may be caused by severe bacterial infection, most often gram-negative sepsis, or other infections. The organism most commonly implicated in pediatric patients is Neisseria meningitidis (>90%), followed by Streptococcus pneumoniae and group A and B streptococci.2,3 Most cases of Staphylococcus aureus sepsis are reported as toxic shock syndrome. Outbreaks occur in semi-closed communities, such as child care centers, college dormitories, and military bases. Transmission occurs by direct contact with secretions or fomites carrying the offending organism.
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The sepsis process is initiated by a local intradermal release of endotoxin leading to an inflammatory reaction and increased vascular permeability. The same endotoxin, up to 24 hours later, causes widespread microvascular thrombosis, hemorrhagic infarction of the skin, and necrotizing vasculitis. It does so by causing a disturbance in the anticoagulant and procoagulant pathways leading to DIC.2
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The sepsis-induced cutaneous lesions are similar regardless of the causative organism. The clinical course of skin necrosis begins with a region of dermal discomfort that develops into well-demarcated macules (petechiae) and evolves rapidly to purple–black necrotic lesions which are painful, dark, and raised (purpura)2 (Fig. 89-2). The progression of skin changes is rapid, occurring within minutes to hours. Distribution is usually acrally over the hands and feet. Although early lesions may be reversible with aggressive therapeutic intervention, lesions that progress to full thickness soft ...