Purpura fulminans

Seven children with purpura fulminans are reported. All were very sick and had extensive purpuric and ecchymotic skin lesions. Five of them had septicemia, one had meningitis and one had viral respiratory tract infection. The bacteria cultured were Staphylococcus aureus (1), Hemophilus influenzae (1), Pseudomonas aeroginosa (1), Klebsiella pneumoniae (1) and Neisseria meningitidis (2). Consumptive coagulopathy was present in all. Three of the seven children survived. Of the remaining four, two had fulminant meningococcemia and died within 4–5 hours of admission as also a third child with Kleb. pneumoniae septicemia. Two of the three survivors had received heparin as well as steroids apart from treatment of the infection.     

Neonatale Purpura fulminans

Congenital homozygous or compound heterozygous protein C deficiency is a rare autosomal recessive inherited disorder. In most cases it becomes manifest as purpura fulminans in the neonatal period. Patients develop disseminated intravascular coagulation as a consequence of accelerated microvascular thrombogenesis. The characteristic clinical picture and a decreased protein C plasma concentration function as diagnostic criteria. Untreated, the disease takes a lethal course. We report on a newborn with purpura fulminans due to congenital homozygous protein C deficiency.     

Purpura fulminans associated with Streptococcus pneumoniae infection in a child.

BACKGROUND: Neisseria meningitidis is the most frequent isolate associated with purpura fulminans in children. Although Streptococcus pneumoniae infection has been associated with purpura fulminans, with the exception of one adult, it has only been reported in immunocompromised hosts. PURPOSE: We report an apparently previously healthy child who presented with purpura fulminans associated with pneumococcal meningitis. METHODS: Case report and review of the medical literature from September 1966 to June 1997, using a MEDLINE search. CONCLUSION: While systemic pneumococcal infection is common in childhood, progression to purpura fulminans does not typically occur in overtly healthy children. Our patient illustrates that invasive pneumococcal infection should be considered and empirically treated in a child who presents with purpura fulminans, even in the absence of preexisting functional or anatomic asplenia.     

Purpura fulminans in a Chinese boy with congenital protein C deficiency

Severe and recurrent purpura fulminans developed in a Chinese boy at one day of age. Results of coagulation studies performed on the patient during attacks were compatible with the diagnosis of disseminated intravascular coagulation. Subsequent investigations have revealed that the patient is homozygous and that his parents are heterozygous for protein C deficiency. Cryoprecipitate and fresh frozen plasma induced a remission, and administration of warfarin has been successful in preventing recurrence of attacks for as long as 8 months without infusion of any plasma components. None of the family members who are heterozygous for protein C deficiency have had thrombotic episodes.     

Purpura fulminans in a case of protein C deficiency

We report a case of protein C deficiency which presented with purpura fulminans. The inheritance of protein C deficiency is discussed and the importance of warfarin (Coumadin) treatment in this condition is emphasized.Abbreviations DIC disseminated intravascular coagulation - PT prothrombin time     

Purpura fulminans bei einem 19 monatigen Kinde

Zusammenfassung Ein Kind mit positivem Wassermann starb innerhalb von 2 Tagen an einer Purpura fulminans.Mit 2 Textabbildungen.