Plaque hemorrhage

Coumarin/warfarin, given at a typical dosage of 4 to 5 mg/day, prevents the deleterious formation in the bloodstream of small blood clots and thus reduces the risk of heart attacks and strokes for individuals whose arteries contain sclerotic plaques. Taken in much larger doses, as for example in rodent poisons, Coumarin/warfarin can cause massive hemorrhages and death. 

Mastocytomas and diffuse cutaneous mastocytosis are further manifestations of cutaneous mastocytosis (CM) [9]. Solitary mastocytomas are common in children. Most are present at birth or develop in infancy. These lesions are flat or mildly elevated, well demarcated, solitary yellowish red-brown plaques or nodules, typically 2-5 cm in diameter. Diffuse cutaneous mastocytosis is a rare disorder characterized by diffuse mast cell infiltration of large areas of the skin that presents in infants in the first year of life. Severe edema and leathery indurations of the skin leads to accentuation of skin folds (pseudo-lichenified skin) and a peau-dbrange-like appearance. Systemic complications include hypotension and gastrointestinal hemorrhage. Infants and young children with considerable mast cell infiltration of the skin sometimes exhibit blister formation in the first 3 years of life. MPCM and other forms of CM have been classified in a consensus nomenclature (table 1) [10]. 

Janeway lesions are small, painless hemorrhagic macular plaques on the palms of the hands or soles of the feet due to septic emboli and more commonly associated with acute S. aureus IE (Fig. 71-3F). 

Virmani R, Kolodgie FD, Burke AP et al. Atherosclerotic plaque progression and vulnerability to rupture angiogenesis as a source of intraplaque hemorrhage. Arterioscler Thromb Vase Biol 2005 25 2054-2061. 

Superior to DSA, MRI can depict arterial flow or lumen as well as the vessel walls. Analysis of plaque morphology was improved in recent years by the development of specific MRI techniques. Plaques can now be characterized in vivo with regard to fibroid or lipid content or hemorrhagic lesions (Fig. 5.8). It can be expected that, in the future, plaque examination will influence stroke treatment protocols if the risk of plaque rupture can be reliably estimated (Cappendijk et al. 2005 Hayes et al. 1996 Trivedi et al. 2004 Yuan et al. 2001). Plaque examinations, however, are not yet clinical routine. Source images of TOF-MRA allow only limited assessment of vascular walls. 

A 70-year-old white man, with no significant preceding medical history, developed an acute painful rash, a fever (38.4° C), and severe arthralgia 5 days after starting to take diazepam 10 mg bd for lumbar muscular contracture due to hard physical exercise. He had taken no other medications. There were well-defined purple-red skin plaques, surmounted by vesicular and hemorrhagic blisters. He had a leukocytosis. Sweet s syndrome was confirmed by punch biopsy of a lesion. Diazepam was withdrawn, and prednisolone 30 mg/day was given for 2 weeks and then tapered. The patient improved quickly and the eruption cleared in 10 days. 

The complicated lesion is associated with occlusive disease the contents of the fibrous plaque become calcified and are altered as a result of hemorrhage, cell necrosis, and mural thrombosis. 

Janeway lesions. Hemorrhagic, painless plaques on the pahns of the hands or soles of the feet. These lesions are believed to be embolic in origin. 

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