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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 non-toxic-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. 85–1). Laboratory tests are helpful, but a thorough history and physical examination can offer the most information to identify the cause. This section gives an overview of the main causes of petechiae and purpura in children.

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Figure 85-1.
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Differential diagnosis of petechiae and purpura.

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Etiology

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Purpura fulminans secondary to sepsis is a life-threatening condition characterized by hemorrhagic infarction of the skin and multiorgan dysfunction. It may be caused by acute severe gram-negative bacterial 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.1,2 Most cases of Staphylococcus aureus sepsis are reported as toxic shock syndrome. Outbreaks occur in semiclosed 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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Pathophysiology

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The septic lesions are thought to be initiated by local intradermal release of endotoxin leading to an inflammatory reaction and increased vascular permeability. The same endotoxin, 12 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 disseminated intravascular coagulation (DIC).1

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Recognition

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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 quickly progresses to petechiae within minutes to hours. The petechiae, which can be found anywhere on the body, will usually distribute acrally over the hands and feet. They then coalesce to form purpura (Fig. 85–2). Hemorrhagic infarction and subsequent skin necrosis can occur at this point without initiation of aggressive therapy. Frank skin necrosis and gangrene are associated with more than 50% morbidity and ...

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