Articles: sepsis.
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Pulmonary arterial hypertension, defined as a mean pulmonary artery pressure exceeding 20 mmHg has been observed both in experimental animal and human sepsis, even before development of the adult respiratory distress syndrome. In this article we review several mechanisms that have been invoked for the pulmonary arterial hypertension associated with sepsis (and the adult respiratory distress syndrome): obstruction of the pulmonary microcirculation with microthrombi composed of platelets and leukocytes, and active pulmonary vasoconstriction induced by the autonomous nervous system, hypoxia or vasoactive humoral factors ("mediators"). Some of these mediators, in particular serotonin and arachidonic acid metabolites have been the subject of substantial research and therapeutic manipulation. Since pulmonary arterial hypertension imposes an increased afterload to the right ventricle and because right ventricular dysfunction appears to be a major determinant of the outcome of sepsis, the study of the mechanisms involved in pulmonary arterial hypertension may lead to improved management of sepsis and septic shock.
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To define the EEG and associated clinical features of septic encephalopathy, we studied 62 patients with positive blood cultures. Patients were divided into three clinical groups: nonencephalopathic (NE), mildly encephalopathic (ME), and severely encephalopathic (SE); the latter two groups had diffuse cerebral dysfunction. ⋯ The EEG (1) was more sensitive than our clinical criteria for encephalopathy, (2) showed features that were, when considered with clinical and laboratory characteristics, compatible with a potentially reversible encephalopathy, and (3) had well-defined categories that correlated with percent mortality, even within a single clinical group. We conclude that the EEG is a sensitive index of brain function in septic encephalopathy and that it is especially useful in the intensive care monitoring of patients with sepsis.
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Klinische Wochenschrift · Dec 1991
ReviewOxygen radicals--an important mediator of sepsis and septic shock.
There is considerable evidence to implicate aggressive species of oxygen in the pathogenesis of organ dysfunction consequent to sepsis and septic shock. The inflammatory process appears to participate ubiquitously in this setting. A characteristic of inflammation is the involvement of activated neutrophils and their generation of aggressive oxygen species. ⋯ For those reasons, the potential for antioxidants as therapy should include consideration of the volume of distribution of such substances. It is probably important that antioxidants access excluded spaces including cell interiors in order to have their maximum effect in this setting. We have studied ina preliminary way the effects of n-acetyl-cysteine, a highly permeable free radical scavenger and anti-oxidant, in patients with established ARDS.(ABSTRACT TRUNCATED AT 250 WORDS)
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Dtsch. Med. Wochenschr. · Dec 1991
Case Reports[Atraumatic Clostridium septicum infection in granulocytopenia].
A fatal Clostridium septicum infection occurred in three patients. Case 1. A 55-year-old man died of septicaemia resulting from granulocytopenia of uncertain aetiology; it was associated with perforation of ileal mucosal ulcers. ⋯ Myonecrosis of the left arm, caused by Clostridium septicum, developed without external cause in a 12-year-old girl with congenital neutropenia. Despite aggressive surgical intervention she died of toxic shock. Autopsy revealed caecal mucosal ulcers as the portal of entry of Clostridium septicum.