La Revue du praticien
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La Revue du praticien · Jun 2006
Review[Complications of central venous and indwelling catheterization].
Complications on Hickman central venous catheter and venous access ports Hickman central venous catheter and venous access ports are widely used in patients with hematology or oncology disorders. However, these long-term venous access devices can be the source of several kinds of complications that may compromise the functional and/or vital patient's prognosis. ⋯ Extravasation of corrosive drugs represents a very serious complication of long-term venous access devices. The surgical technique that uses early subcutaneous wash-out in acute extravasation injuries is simple and safe; it helps to reduce the severe sequelae of highly toxic drug extravasation for the patient.
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Still today, as for the time of Charcot, multiple sclerosis is defined by pathology with the presence of inflammatory demyelinating foci ("plaques") disseminated in the white matter of the central nervous system (CNS). Each lesion follows its genuine course with an acute formation followed by a more or less complete regression whereas new lesions are forming elsewhere in the CNS throughout the disease duration. A permanent dynamics of the inflammatory activity, substratum of the lesional "dissemination in space and time" characteristic of the disease, is therefore operating. ⋯ During the progressive phase, be it secondary or primary, macroscopic atrophy and axonal loss, the main explanation of the irreversible neurological disability and the expression of the diffuse, chronic and progressive degeneration of the CNS, are emerging to the first place. Persisting controversies are many. Are there several distinct immunohistopathological patterns of the disease or do they correspond to different moments of the same disease? Is there a continuum between classic MS and pathological variants such as Marburg's disease, Balo's concentric sclerosis, Schilder's disease, and Devic's acute neuromyelitis optica or are there distinct nosological entities? As for autoimmunisation which leads to the selective destruction of myelin, is it primary or secondary to an oligodendrocytic apoptotic process?