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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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. EEGs were classified into five groups: normal, excessive theta, predominant delta, triphasic waves, and suppression or burst suppression, in ascending order of severity. 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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PMID:The electroencephalogram in sepsis-associated encephalopathy. 155 2

Physicians and surgeons have long recognized that septic illness may be accompanied by abnormal brain functions; however, no systematic, comprehensive study has been done to define the clinical and laboratory features of the syndrome of sepsis-associated encephalopathy. We undertook such a prospective study in a tertiary care hospital and found that of 69 patients with fever and microbial cultures, 32 had marked brain dysfunction, 17 showed mild encephalopathy, and 20 were clinically nonencephalopathic. Severe cases showed obtundation and paratonic rigidity while milder cases showed confusion, inappropriate behavior, inattention, disorientation, and writing errors. There were no focal neurological deficits. The following factors correlated with the severity of brain dysfunction: adult respiratory distress syndrome; fatal outcome; certain types of EEG abnormality; axonal peripheral neuropathy; elevated peripheral white blood cell count; elevated serum levels of alkaline phosphatase, bilirubin, creatinine, phosphate, potassium, and urea; reduced blood pressure and reduced serum albumin level. Our data suggest that brain functions fail with dysfunction of other organs in septic illness. Pathogenetic mechanisms are discussed. The brain dysfunction should be regarded as potentially reversible, even in severely encephalopathic cases. Prompt control of the infection is the most important measure in controlling the encephalopathy and in preventing the increased mortality found with severely encephalopathic patients.
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PMID:The encephalopathy associated with septic illness. 207 9

Brain dysfunction is observed clinically in patients suffering from prolonged endotoxic shock. However, the etiology of brain dysfunction during sepsis is not clear. Certain researchers have reported that the decrease in brain catecholamines concentration during septic shock might be etiologically important in brain dysfunction. Therefore, we hypothesized that the beta-adrenergic receptor system undergoes a change during septic shock, and plays a role in the pathogenesis of septic encephalopathy. In this study, we examined two models of septic shock in rats, each of which has a different time course for the shock state. Male Wistar rats were divided into four groups: (1) Control--0.9% saline vehicle, (2) Lipopolysaccharide (LPS) i.v.-- Escherichia coli endotoxin 1.0 mg/ml i.v. bolus, (3) Sham-operated, and (4) Cecal ligation and puncture (CLP) model. The rats were killed by decapitation at 3, 12, or 24 hr after the treatments, and the brains were removed and subdivided into three areas: the forebrain, cerebellum, and brain stem. In the LPS i.v. group, the brain tissue norepinephrine (NE) concentration had decreased in the forebrain and brain stem and the tissue epinephrine (E) concentration had decreased in the brain stem by 3 hr after treatment. In the CLP group, the brain tissue NE concentration had decreased in the forebrain, cerebellum, and brain stem (P < 0.05), and the tissue E concentration had decreased in the forebrain and brain stem by 24 hr after treatment (P < 0.05). An alteration in beta-adrenergic receptor density in the forebrain was observed at 24 hr in the CLP group (control, 237.0 +/- 14.0 fmole/mg protein; LPS i.v., 233.2 +/- 3.0 fmole/mg protein; sham-operated, 236.0 +/- 3.0 fmole/mg protein; CLP, 177.0 +/- 4.2 fmole/mg protein). These alterations in transmitter concentrations and beta-adrenergic density in the forebrain may be an important factor in septic encephalopathy.
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PMID:Impairment of the brain beta-adrenergic system during experimental endotoxemia. 865 32

The use of cardiopulmonary bypass for surgical cardiac procedures is characterized by a whole-body inflammatory reaction due to the contact of blood through nonendothelialized surfaces; this stimulates the organism to recognize the cardiopulmonary bypass system as "nonself" and to activate specific (immune) and nonspecific (inflammatory) responses. These responses are then related with postoperative damage to many body systems, like pulmonary, renal or brain dysfunction, excessive bleeding and postoperative sepsis. In this paper, present knowledge on untoward responses of the patient to the use of cardiopulmonary bypass in cardiac surgery is reviewed and discussed, particularly focusing on the perturbation of the hemostasis and of the complement activation system.
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PMID:[Heart surgery, cardiopulmonary bypass and inflammatory response. I. Changes in hemostasis and complement]. 870 28

The use of cardiopulmonary bypass for surgical cardiac procedures is characterized by a whole-body inflammatory reaction due to the contact of blood through nonendothelialized surfaces; this stimulates the organism to recognize the cardiopulmonary bypass system as "nonself" and to activate specific (immune) and nonspecific (inflammatory) responses. These responses are then related with postoperative damage to many body systems of the body, like pulmonary, renal or brain dysfunction, excessive bleeding and postoperative sepsis. In this paper, present knowledge on untoward responses of the patient to cardiopulmonary bypass in cardiac surgery is reviewed and discussed, particularly focusing on the perturbation of the leukocytes, of the hormones and of the products of the arachidonic acid cascade.
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PMID:[Heart surgery, cardiopulmonary bypass, and organic inflammatory response. Part II: changes in leukocytes, arachidonic acid derivatives, and hormones]. 876 79

The pathophysiological processes of the nervous system observed in the reactions to aggressive external stresses like severe trauma, systemic infection and so on have been reviewed. As is generally understood, such stresses as tissue destruction lead to the metabolic changes via proprioceptive impulses to central nervous system and neuroendocrinological courses. Cytokines are well known to work to induce systemic inflammatory responses and also to be important components of sepsis syndrome, for example. In the early phase of septic encephalopathy without overt infection of the brain or the meninges, it is possible that cytokines cause capillary leakage with brain edema, interference with microcirculation and direct effects on tissue metabolism resulting in brain dysfunction. And besides, Interleukins are prove to be produced in a few hours post-injury in experimental model. In clinical settings, severe head injury patients, who are often complicated with respiratory or urinary infection and with bacterial translocation, can suffer not only from systemic inflammatory responses originated from the brain but also from septic encephalopathy mentioned above. Therefore multiply traumatized patients with damaged brain for instance might well have to be considered as the aggregation, or integration of the systemic insult from the aspect of aggressology.
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PMID:[The significance of neurological manifestations from the aspect of aggressology]. 894 Jun 84

Septic encephalopathy (SE) is a common term indicating the development of signs of progressing cerebral dysfunction and is associated with the presence of microorganisms and their toxins in the blood. Aim of this investigation was to analyze the frequency of this complication considering the consciousness disorders in quantitative sense and prognosis of the survival in patients with SE. The investigation comprised patients (n = 54) with positive hemoculture and signs of septic syndrome by the accepted criteria (fever, clinical signs of infection, respiratory frequency, heart rate, plasma lactate, oliguria). Patients with confirmed cerebral injury, hemorrhage or cerebral ischemia were excluded from the study. Lumbar punction and CT-scan of the brain were performed in all patients in order to exclude visible lesions of cerebral parenchyma and eventual presence of cerebral nervous system (CNS) infection as the causes of sepsis. Results of the investigation demonstrated that in 30 (55%) of patients existed mild consciousness disorder at the level of somnolescence, in 18 (33%) consciousness disorder at the level of sopor and in 6 (11%) consciousness disorder at the level of deep coma. Level of consciousness disorder was in positive correlation with the outcome of sepsis syndrome, which was additionally confirmed by the fact that only in the group of patients with deep coma lethal outcome was observed in 3 cases (50% of this subgroup) regardless of intensive antibiotic, metabolically active and symptomatic therapy. It can be concluded that SE syndrome has a favorable prognosis if macroscopic lesion and dissemination of microorganisms in CNS are not present, and simultaneously it represents changes in metabolic-electrolytic state with early presentation of consciousness disorders that represent clinically significant indicator for sepsis syndrome outcome.
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PMID:[Septic encephalopathy--prognostic value of the intensity of consciousness disorder to the outcome of sepsis]. 1147 68

Cerebral dysfunction in sepsis is common in critically ill adults. However, little is known of the effects of sepsis on cerebral haemodynamics. We studied 12 sedated and ventilated patients in whom sepsis had been established for > 24 h. Transcranial Doppler measurements of the middle cerebral artery flow velocity were made at normocapnia, then hypocapnia (-1 kPa) and hypercapnia (+1 kPa). From these data, cerebrovascular reactivity to carbon dioxide was calculated. Variables indicating disease severity, systemic cardiovascular status and outcome were also recorded. We found significant changes in cerebrovascular reactivity to carbon dioxide. Only three of 12 patients had a cerebrovascular reactivity to carbon dioxide in the normal range; seven patients had a reduced cerebrovascular reactivity to carbon dioxide, whereas in two patients it was raised. In this smaD sample, we could not find any trend of association between altered cerebrovascular reactivity to carbon dioxide and severity of illness, cardiovascular status or outcome. This study suggests that established sepsis profoundly affects the vascular tone and reactivity, not only of the systemic circulation, but also of the cerebral vasculature.
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PMID:Cerebrovascular reactivity to carbon dioxide in sepsis syndrome. 1263 65

Systemic sepsis commonly produces brain dysfunction, sepsis-associated encephalopathy, which can vary from a transient, reversible encephalopathy to irreversible brain damage. The encephalopathy in the acute phase clinically resembles many metabolic encephalopathies: a diffuse disturbance in cerebral function with sparing of the brain stem. The severity of the encephalopathy, as reflected in progressive EEG abnormalities, often precedes then parallels dysfunction in other organs. Recent research has revealed a number of potentially important, non-mutually exclusive, mechanisms that have therapeutic implications.
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PMID:Progress in clinical neurosciences: sepsis-associated encephalopathy: evolving concepts. 1277 48

The objective of the trial is to evaluate the efficacy of capecitabine in patients with metastatic hormone-resistant prostate carcinoma (HRPC), in terms of prostate-specific antigen (PSA) response and clinical benefit (decrease of pain or analgesic score) and its safety profile. In all, 25 patients with HRPC were enrolled on a phase II trial of capecitabine (Xeloda) at a dose of 1250 mg m(-2) orally twice daily on days 1-14 every 21 days. The inclusion criteria were PSA serum levels >3 x upper limit of normal, a WHO performance status 0-2, age <85 years and adequate bone marrow, liver and renal function. In patients with grade 2 or higher haematological toxicity on day 1 of the treatment cycle, therapy was first delayed, and then continued at a lower dose. Trial end points were PSA response and clinical benefit defined by quality of life (QL) data and analgesic consumption. The median age of patients was 70 years (range 54-85 years). A median of three cycles of capecitabine was administered (range 1-8). PSA response was observed in three patients (12%, 95% CI 3-31%), with times to tumour progression of 18, 21 and 35 weeks, respectively. In these patients, the response durations were 12, 17 and 32 weeks, respectively. Minor PSA regression was also seen in two further patients. The median time to tumour progression of all patients was 12 weeks (95% CI 9-15 weeks). Haematological toxicity was minor, with leukopenia grade 3 observed in one patient. There were three deaths during trial treatment, respectively, due to sepsis following mucositis and leukopenia, presumed sepsis with mucositis induced by chemotherapy and concomitant radiotherapy and cerebral dysfunction progressing to coma. Hand-foot syndrome grades 2 and 3 were observed in four patients each. Clinical benefit was observed in five patients (20%, CI 7-41%). Based on toxicity data, we recommend a lower starting dose of 1000 mg x m(-2) orally twice daily. While capecitabine has some activity in HRPC, as suggested by observed PSA responses, we conclude that it is not worthwhile to investigate capecitabine monotherapy in a phase III trial. Combinations of capecitabine with other agents, such as vinorelbine or docetaxel, may prove to be more effective.
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PMID:Capecitabine in hormone-resistant metastatic prostatic carcinoma - a phase II trial. 1505 47


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