Acquired Purpura Fulminans

Francis, Robert B.

doi:10.1055/s-2007-1002684

Cited by 88 publications

(65 citation statements)

References 58 publications

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“…The hemorrhagic necrosis of the skin seen in meningococcal septicemia is histologically indistinguishable from the dermal Shwartzman reaction (3), suggesting that it may be due to an LSR-type reaction (4). Clinical observations in children with meningococcal septicemia indicate that peripheral ischemia can potentiate this type of hemorrhagic necrosis and suggest that a relatively brief period of ischemia, insufficient in itself to cause necrosis, may act in a similar manner to the second provocative dose of endotoxin given intravenously in the LSR.…”

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confidence: 99%

Local Shwartzman Reaction in the Rat Induced by Endotoxin and Ischemia: Potential Model for Skin Necrosis in Meningococcemia

et al. 2006

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ABSTRACT:The local Shwartzman reaction (LSR) is an inflammatory response in the skin that is considered a model for skin necrosis associated with meningococcemia. We tested the hypothesis that ischemia can act as the provocative agent to produce this response. In eight rats, bilateral inferior epigastric flaps were outlined. Within each flap, three injection sites were marked. Site 1 had 0.1 mL of endotoxin injected 24 h before surgery. The other two sites had either endotoxin or saline injected immediately before surgery. Both flaps were raised on their pedicle and one side rendered ischemic for 6 h and then reperfused. Animals were killed either 30 min or 48 h later and the tissue from each site examined. After 48 h of reperfusion, necrosis was grossly visible at the site of 24-h preischemia injection of endotoxin in three of four rats. No abnormalities were present at the other injection sites. Microscopically, all 24-h-delayed injection sites showed hemorrhage into all layers of the skin after both 30 min and 48 h of reperfusion. No hemorrhage was present at the other sites. These findings may serve as a potential model for the skin necrosis seen in meningococcemia.

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confidence: 99%

Local Shwartzman Reaction in the Rat Induced by Endotoxin and Ischemia: Potential Model for Skin Necrosis in Meningococcemia

et al. 2006

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“…In a 1990 review, Francis (1) reported the association of VZV and/or streptococcal infection in 30% of children with idiopathic purpura fulminans. Subsequently, acquired free PS deficiency was described in children and adults with acute VZV infection and PFϮTE (2)(3)(4)(5)(6)(7)(8).…”

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confidence: 99%

The Varicella-Autoantibody Syndrome

et al. 2001

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This cross-sectional study was conducted to determine the incidence of autoantibodies to phospholipids and coagulation proteins in children with acute varicella zoster virus (VZV) infection. Study groups included children with VZV alone or complicated by purpura fulminans and/or thromboembolism. VZV naïve children and children who had VZV Ͼ1 y before sample collection formed a control group. Blood was assayed for the following: free protein S (PS), protein C, antithrombin, and prothrombin; antibody binding to these proteins; lupus anticoagulant; anticardiolipin antibody; antiphospholipid antibodies; and prothrombin fragment 1ϩ2. Data regarding coinfections was collected. Forty-three VZV-infected children showed an increased frequency of lupus anticoagulant, anticardiolipin antibody, antiphospholipid antibodies, and autoantibodies to PS, protein C, prothrombin, and antithrombin in comparison to 52 children without acute VZV (p Ͻ 0.0001). Seventeen children with VZV and purpura fulminans and/or thromboembolism showed a statistically significant decrease in free PS, significantly increased PS IgG antibody, and significantly increased prothrombin fragment 1ϩ2 (p Ͻ 0.0001) compared with the group without acute VZV and the group with uncomplicated VZV. Twenty-six children with uncomplicated VZV showed In a 1990 review, Francis (1) reported the association of VZV and/or streptococcal infection in 30% of children with idiopathic purpura fulminans. Subsequently, acquired free PS deficiency was described in children and adults with acute VZV infection and PFϮTE (2-8). We reported the LA and free PS deficiency in seven previously healthy children with acute VZV infection complicated by PFϮTE (6). We previously found evidence suggestive of an autoimmune cause of acquired PS deficiency.We now report a cross-sectional study designed to determine the prevalence of autoantibodies directed against a variety of phospholipids and coagulation proteins in previously healthy children with VZV infection. The aim of this study was to compare results obtained on blood samples from children with uncomplicated acute VZV infection with samples from children with acute VZV complicated by symptomatic PFϮTE. It was hypothesized that coagulation abnormalities in the children with symptomatic PFϮTE would be more prevalent and more severe but not intrinsically different from those found in healthy children with uncomplicated VZV infection. METHODS Clinical MethodsThis cross-sectional study was performed with the approval of the Colorado Multi-Institutional Review Board and the Pediatric Clinical Research Center at The Children's Hospital of Denver. Informed consent and assent forms were signed before enrollment in the study.

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“…In addition to aggressive fluid resuscitation, prompt initiation of empirical broadspectrum antibiotics for underlying sepsis, correction of acid-base imbalance and electrolyte abnormalities, and the early administration of oxygen are also helpful [10,11]. Heparin may be administered to inhibit further thrombus formation, and may reverse the development of skin necrosis [12], Because the pathophysiology of purpura fulminans involves intravascular thrombosis. Fresh frozen plasma can be used to replete these coagulation factors.…”

Section: Discussionmentioning

confidence: 99%

Streptococcus pneumoniae induced purpura fulminans in a patient with splenic hypoplasia

Kojima¹,

Hiraoka²,

Ehara³

et al. 2017

IJCRI

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International Journal of Case Reports and Images (IJCRI) is an international, peer reviewed, monthly, open access, online journal, publishing high-quality, articles in all areas of basic medical sciences and clinical specialties.Aim of IJCRI is to encourage the publication of new information by providing a platform for reporting of unique, unusual and rare cases which enhance understanding of disease process, its diagnosis, management and clinico-pathologic correlations. Case Report: A 57-year-old male was presented to our emergency department in shock state with flu-like symptoms. Empirical broad-spectrum antibiotics and intensive care were started. His condition rapidly deteriorated with multiple organ failure. Blood culture grew up S. pneumoniae. Purpuric skin change developed in all extremities followed by ischemic gangrene, which required amputation. He did not have any history of immunosuppressive disease. His computed tomography scan of abdomen showed small size of spleen. Howell-Jolly bodies were recognized in peripheral blood smear. The patient was finally diagnosed with purpura fulminans with overwhelming pneumococcal sepsis. Although he had no history of immunodeficiency, he had evidence of Howell-Jolly bodies in peripheral blood smear, implying reduced splenic function, possibly due to splenic hypoplasia. To prevent this devastating condition, vaccination against S. pneumoniae may need to be considered for people with splenic hypoplasia. IJCRI publishes Conclusion:Since delay in therapy would lead to a poor outcome, clinicians should be alert to purpura fulminans in patients in shock state, even lacking typical skin manifestation initially. Splenic hypoplasia may be a risk factor of this condition.

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Acquired Purpura Fulminans

Cited by 88 publications

References 58 publications

Local Shwartzman Reaction in the Rat Induced by Endotoxin and Ischemia: Potential Model for Skin Necrosis in Meningococcemia

Local Shwartzman Reaction in the Rat Induced by Endotoxin and Ischemia: Potential Model for Skin Necrosis in Meningococcemia

The Varicella-Autoantibody Syndrome

Streptococcus pneumoniae induced purpura fulminans in a patient with splenic hypoplasia

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