Myocardial dysfunction in septic shock: Part I. Clinical manifestation of cardiovascular dysfunction.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to C Haery.
Explore the source record for details and available documents.
Over the last decade, it has become clear that myocardial depression, like vascular dysfunction, is typical of human septic shock. Human septic myocardial depression is characterized by reversible biventricular dilatation, decreased ejection fraction, and decreased response to fluid resuscitation and catecholamine stimulation (in the presence of overall hyperdynamic circulation). A circulating myocardial depressant substance, not myocardial hypoperfusion, is responsible for this phenomenon. This substance has been shown to represent low concentrations of TNF-alpha and IL-1 beta acting in synergy on the myocardium through mechanisms that include NO and cGMP generation. Despite major advances in our understanding of the hemodynamics and pathogenesis of cardiac dysfunction in sepsis, successful attempts to modulate these mechanisms to improve clinical outcomes in human trials have not been demonstrated to date. For the moment, the therapeutic approach to the patient with cardiac dysfunction in distributive or septic shock must be primarily aimed at reestablishing adequate organ perfusion and oxygen delivery by vigorous fluid resuscitation and vasopressor or inotropic support. In the long term, however, only continued research regarding the cellular mechanisms of organ dysfunction, including septic myocardial depression, will lead to successful therapeutic strategies. These strategies will likely involve direct manipulation of intracellular signaling processes that lead to organ dysfunction as manifested by septic myocardial dysfunction and septic shock.
Explore the source record for details and available documents.
PURPOSE: To identify and characterize the MR findings of sarcoidosis when it involves the orbit and visual pathways. METHODS: The MR scans of 15 patients, 3 with presumed and 12 with proved orbital or optic pathway sarcoidosis were retrospectively reviewed. RESULTS: Eight patients had MR evidence of optic nerve involvement by sarcoid granuloma. Perineural enhancement was seen in four cases, optic atrophy in one. Three who had had unenhanced scans showed optic nerve enlargement. Nine patients had optic chiasmal involvement. One patient had increased T2 signal in the optic radiations. Three patients had orbital masses that had MR signal characteristics similar to pseudotumor. Five patients had periventricular white matter abnormalities closely resembling multiple sclerosis. CONCLUSIONS: Sarcoidosis should be considered in the differential diagnosis of optic nerve or nerve sheath enhancement on MR. Orbital sarcoidosis has MR characteristics very similar to pseudotumor.
Fibro-osseous lesions of the craniofacial structures are a group of pathologic conditions that are somewhat difficult to classify. Fibro-osseous lesions of the jaw may be divided into two categories: fibrous dysplasia, a developmental lesion characterized by the development of swelling, which consists of proliferating fibrous tissue that replaces normal bone; and those that have been postulated to originate from the periodontal ligament. This article describes the imaging characteristics of fibrous dysplasia and other fibro-osseous lesions of oral bones, including ossifying fibroma, periapical cemental dysplasia, cemento-ossifying fibroma, and florid osseous dysplasia.