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1/8. Acute infantile hemorrhagic oedema.

    Acute infantile hemorrhagic oedema (AIHO) was first described in 1913 but, despite frequent reports in the European literature, it is not well recognized in the English language literature. It is considered by many to be a variant of Henoch Schonlein Purpura (HSP) because of similarities in cause and histopathology. However, because of the benign nature of this condition and frequent absence of IgA associated with HSP, it may be sensible to consider this as a distinct variety of cutaneous small vessel vasculitis (CSVV). We report this case to highlight the condition and emphasize its benign nature.
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2/8. Free-tissue transfer for limb salvage in purpura fulminans.

    A series of 13 patients is described to demonstrate the experience of the authors with free-tissue transfer for limb salvage in patients with purpura fulminans. A total of seven free-flap procedures were performed, with a loss of flap in one patient. The flaps were used for lower-extremity salvage in six patients and for upper-extremity salvage in one. purpura fulminans is a devastating illness caused by endotoxin-producing bacteria such as meningococcus and pneumococcus. Clotting derangements and systemic vasculitis often lead to widespread tissue necrosis in the extremities. Local tissue is usually not available to cover vital structures in these complex wounds. In these situations, free-tissue transfer is necessary to achieve limb salvage. Microsurgical reconstruction in patients with purpura fulminans is a formidable challenge. Because of high platelet counts and systemic vasculitis, successful microvascular anastomosis is difficult. Abnormally high platelet counts persist well into the subacute and chronic phases of the illness. Pretreatment with antiplatelet agents before microvascular surgery may be beneficial. The systemic nature of the vascular injury does not permit microvascular anastomosis to be performed outside the "zone of injury." Extensive vascular exposure, even at a great distance from the wound, does not reveal a disease-free vessel. The friable intima is difficult to manage with a standard end-to-side anastomosis, but conversion to end-to-end anastomosis may salvage free-tissue transfers in cases in which intimal damage is too severe to sustain a patent anastomosis. patients often have peripheral neuropathies caused by the underlying disease; however, this resolves with time and is not a contraindication to limb salvage.
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3/8. Idiopathic purpura fulminans and varicella gangrenosa of both hands, toes and integument in a child.

    Chicken pox is a common childhood illness and, though a vaccine is readily available, it is not routinely included in the vaccination schedule of most countries owing to its mild clinical nature. However, varicella gangrenosa is a rare complication of this disease, infrequently reported in the literature. We report the case of a child who developed purpura fulminans in the convalescent phase of chicken pox and subsequently presented with peripheral gangrene of both hands and the toes of the right foot, and skin gangrene. To our knowledge, bilateral gangrene of the hands has rarely been reported, and we present this case to highlight the serious nature of complications following varicella infection.
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4/8. The pressure-dependent nature of the rash in Henoch Schonlein purpura.

    A 10 month old girl with Henoch-Schonlein purpura (HSP) developed a rash predominantly on the anterior aspect of the knees. The authors speculate that this distribution of the rash was due to the pressure effects consequent to crawling and propose that the distribution of the rash in HSP should be described as pressure-dependent rather than merely gravity-dependent. The therapeutic implications of pressure-dependency in HSP are discussed.
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5/8. Henoch-Schonlein purpura after intravesical administration of bacillus Calmette-Guerin.

    The administration of intravesical bacille Calmette-Guerin (BCG) in early stages of bladder cancer is usually a safe therapy. Side-effects of BCG immunotherapy can be of both local and systemic nature. We report the first case of Henoch-Schonlein purpura following intravesical administration of BCG.
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6/8. IgA anticardiolipin antibodies associated with Henoch-Schonlein purpura.

    Henoch-Schonlein purpura is associated with the deposition of immune complexes containing IgA. The nature of the antigen in these immune complexes is uncertain but in some reported cases has included autoantigens such as IgA rheumatoid factor and IgA antineutrophil cytoplasmic antibody. We report the finding of an IgA class anticardiolipin antibody in a 51-year-old patient with Henoch-Schonlein purpura. A potential role for IgA autoantibodies in Henoch-Schonlein purpura needs to be further explored.
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7/8. Group A beta-haemolytic streptococcal infection and Henoch-Schonlein purpura with cardiac, renal and neurological complications.

    A 6-year-old girl had a group A beta-haemolytic streptococcal (GABS) throat infection and Henoch-Schonlein purpura (HSP). The clinical course was complicated by nephrotic syndrome due to crescentic glomerulonephritis, transient neurological symptoms due to focal ischaemia of the brain, and congestive cardiac failure due to myocarditis. The clinical presentation highlights the diversity of systemic involvement in HSP, the transient nature of apparently serious central nervous system involvement, and a possible role of GABS in its aetiology.
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8/8. Encephalopathy complicating Henoch-Schonlein purpura: reversible MRI changes.

    A 10-year-old boy with Henoch-Schonlein purpura complicated by encephalopathy, transient cortical blindness, and a secondary generalized seizure is reported. Reversible changes in the posterior white and gray matter were seen on magnetic resonance imaging. Our patient illustrates uncommon neurologic manifestations of Henoch-Schonlein purpura. The nature and location of the lesions and the normalization of the patient's magnetic resonance imaging is consistent with a posterior predominant parieto-occipital encephalopathy and suggests that cerebral edema from blood-brain barrier breakdown may play a central role in the pathophysiology of the central nervous system symptomatology in some patients.
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