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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Septic encephalopathy is an early manifestation of sepsis. Changes in consciousness, focal or generalized seizures, multifocal myoclonus and/or varying hemiparesis are common clinical findings. All of these symptoms are reversible when sepsis has been successfully treated. Because there are no generally accepted criteria for the diagnosis of septic encephalopathy, it is a diagnosis of exclusion. We report the case of a 68-year-old patient who developed septic encephalopathy secondary to diarrhea and E. coli sepsis. In this case, symptoms of septic encephalopathy were fully reversed after the patient's E. coli sepsis had been adequately treated.
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PMID:[Diarrhea, coli infection, septic encephalopathy: escalation of a seemingly banal symptom]. 772 73

Septic encephalopathy (SE) is present in up to 70% of all patients with sepsis. In some cases, SE may proceed other parameters of sepsis. Loss of consciousness to a various extent is the leading symptom. CSF findings and CCT are usually unremarkable. EEG is a sensitive parameter to monitor SE. EEG-changes deteriorate in correspondence to the degree of SE. If sepsis can be treated successfully, clinical and electrophysiological signs are completely reversible. SE has a complex etiology. Bacterial endotoxins and other microbial products trigger the release of a multitude of mediators of sepsis. Due to liver dysfunction in sepsis, the brain neurotransmitter profile may be deranged. Other etiological factors include bacteriemia, liver or renal dysfunction, fluid and electrolyte imbalance, hypoglycemia and drug effects. Due to the prognostic significance of early adequate treatment, recognition of SE as a possible initial sign may be crucial for patients with sepsis.
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PMID:[Infection: impaired consciousness as the initial symptom. Clinical and pathophysiologic aspects of septic encephalopathy]. 946 47

Septic encephalopathy and critical illness polyneuropathy are two syndromes, appearing at different stages in critically ill patients. Their aetiology is unclear, but many arguments seem to associate them with respiratory insufficiency in a context of systemic inflammatory response syndrome (S.I.R.S.) and multiple organ dysfunction syndrome (M.O.D.S.). Septic encephalopathy appears early in the course of sepsis, diagnosis is based on clinical picture and electro-encephalogram. The exact pathogenesis is unclear. Prognosis is related to the underlying pathology, and treatment is supportive. Critical illness polyneuropathy is a predominantly motor axonal dysfunction, occurring in a setting of respiratory insufficiency, S.I.R.S., and M.O.D.S. A weaning problem often indicates the presence of critical illness polyneuropathy. Diagnosis is made on history, clinical picture and electromyographic studies. Indeed, motor and sensory conduction studies show a reduction of the amplitude of action potentials. In a later stage fibrillations and positive sharp waves emerge, with a further reduction of action potentials. Follow-up examinations reveal signs of axonal regeneration. The exact aetiology is unknown, but may be related to sepsis and M.O.D.S. Sepsis and M.O.D.S. are associated with the release of "mediator" substances, and somewhere in this cascade, there might be a toxin, influencing the nerve. A differential diagnosis with myopathy and neuromuscular transmission defects has to be made. Specific treatment is absent, and prognosis is related to the underlying pathology.
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PMID:Neurological complications in critically ill patients; septic encephalopathy, critical illness polyneuropathy. 963 46

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

Septic encephalopathy is associated with breakdown of the blood-brain barrier and cerebral oedema. These features are also common properties of brain tumours. Perimicrovessel oedema, disruption of associated astrocyte end feet and neuronal injury occur in a porcine model of acute septic encephalopathy. The adrenergic system has been implicated in the inflammatory response to sepsis and may play a role in controlling blood-brain barrier permeability, since the beta2-adrenoceptor agonist dopexamine inhibits perimicrovessel oedema formation whereas the alpha1-adrenoceptor agonist methoxamine provokes it. Electron microscopy revealed tight junction opening in high-grade astrocytoma microvessels. Expression of the tight junction protein occludin is reduced in these microvessels and this reduction is inversely correlated with the degree of cerebral oedema. Normal astrocytes secrete factors that induce barrier properties in endothelial cells, whereas high-grade astrocytomas secrete vascular endothelial growth factor, which stimulates angiogenesis, down regulates occludin and increases endothelial cell permeability. The water channel protein aquaporin-4 is normally expressed in astrocyte foot processes around cerebral microvessels. Its expression is massively up-regulated in high-grade astrocytoma and around metastatic adenocarcinoma. There is a significant correlation between aquaporin-4 expression and the degree of cerebral oedema, but it is not clear whether increased aquaporin-4 expression enhances oedema formation or clearance. These results suggest that the pathophysiology of brain oedema is multifactorial, but that there may be common processes operating regardless of the aetiology.
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PMID:Blood-brain barrier breakdown in septic encephalopathy and brain tumours. 1216 31

Septic encephalopathy is a complication of sepsis, and it is closely associated with the increased mortality of the sufferers. Pathophysiology of septic encephalopathy is not still completely understood. In an attempt to provide insight into the pathogenesis of septic encephalopathy, a light and electron microscopic investigation has been carried out in a rat model of intraperitoneal sepsis. Experimental fecal peritonitis was induced in Wistar rats which have been monitored for 6 h and sacrificed to harvest the samples of frontal cortex. Vital parameters and morphometric data obtained from investigation of the microvessels were then compared with the sham-operated and unoperated controls. In addition to the discernible drop in the blood pressure and in rectal temperature following initial increases, unstable but usually increased heart rate and marked respiratory failure were recorded. Estimation of the percentage of the microvessel area occupied by edema revealed the presence of significantly more perimicrovascular edema in the experimental fecal peritonitis group compared to both sham-operated and unoperated controls, while no significant difference was present between the latter two groups. Electron microscopic investigation confirmed the presence of distinctive perimicrovascular edema in the fecal peritonitis group although the endothelial cells were linked by tight junctions which appeared morphologically intact. Although it might be premature to draw any strict parallels between the septic encephalopathy in humans and the findings observed in the present model, the results may suggest that the edema observed around the microvessels would bare a role in the pathogenesis of the septic encephalopathy probably by affecting the exchange of oxygen and nutrients with carbon dioxide and waste products between the blood and brain parenchyma.
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PMID:Perimicrovascular edema in the frontal cortex in a rat model of intraperitoneal sepsis. 1642 49

Sepsis-associated encephalopathy (SAE) is a frequent but poorly understood neurological complication in sepsis that negatively influences survival. Here we present clinical and experimental evidence that this brain dysfunction may be related to altered neurotransmission produced by inflammatory mediators. Compared with septic patients, SAE patients had higher interleukin-1beta (IL-1beta) plasma levels; interestingly, these levels decreased once the encephalopathy was resolved. A putative IL-1beta effect on type A gamma-aminobutyric acid receptors (GABA(A)Rs), which mediate fast synaptic transmission in most cerebral inhibitory synapses in mammals, was investigated in cultured hippocampal neurons and in Xenopus oocytes expressing native or foreign rat brain GABA(A)Rs, respectively. Confocal images in both cell types revealed that IL-1beta increases recruitment of GABA(A)Rs to the cell surface. Moreover, brief applications of IL-1beta to voltage-clamped oocytes yielded a delayed potentiation of the GABA-elicited chloride currents (I(GABA)); this effect was suppressed by IL-1ra, the natural IL-1 receptor (IL-1RI) antagonist. Western blot analysis combined with I(GABA) recording and confocal images of GABA(A) Rs in oocytes showed that IL-1beta stimulates the IL-1RI-dependent phosphatidylinositol 3-kinase activation and the consequent facilitation of phospho-Akt-mediated insertion of GABA(A)Rs into the cell surface. The interruption of this signaling pathway by specific phosphatidylinositol 3-kinase or Akt inhibitors suppresses the cytokine-mediated effects on GABA(A)R, whereas activation of the conditionally active form of Akt1 (myr-Akt1.ER*) with 4-hydroxytamoxifen reproduces the effects. These findings point to a previously unrecognized signaling pathway that connects IL-1beta with increased "GABAergic tone." We propose that through this mechanism IL-1beta might alter synaptic strength at central GABAergic synapses and so contribute to the cognitive dysfunction observed in SAE.
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PMID:Interleukin-1beta enhances GABAA receptor cell-surface expression by a phosphatidylinositol 3-kinase/Akt pathway: relevance to sepsis-associated encephalopathy. 1656 7

Sepsis-associated encephalopathy is a global cerebral dysfunction induced by the systemic response to inflammation and infection, without a liver or renal injury. Alteration of consciousness, from confusion to coma, is the main clinical symptom. This encephalopathy is associated with an increase in mortality due to sepsis. Its physiopathology is unknown. There is frequently an increased permeability of the blood-brain barrier, which might explain a role of endotoxins on cerebral metabolism. Changes in neurotransmitter release or concentrations (norepinephrine, serotonin, dopamine, GABA) have been reported. There is not any specific treatment of septic encephalopathy. In most cases, this syndrome is rapidly reversible after the treatment of sepsis.
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PMID:[Brain injury during severe sepsis]. 1669 Feb 46

In this study, we demonstrate that mice deficient in TNFR1 (TNFR1(-/-)) were resistant to LPS-induced encephalopathy. Systemic administration of lipopolysaccharide (LPS) induces a widespread inflammatory response similar to that observed in sepsis. Following LPS administration TNFR1(-/-) mice had less caspase-dependent apoptosis in brain cells and fewer neutrophils infiltrating the brain (p<0.039), compared to control C57Bl6 (TNFR1(+/+)) mice. TNFR1-dependent increase in aquaporin (AQP)-4 mRNA and protein expression was observed with a concomitant increase in water content, in brain (18% increase in C57Bl6 mice treated with LPS versus those treated with saline), similar to cerebral edema observed in sepsis. Furthermore, absence of TNFR1 partially but significantly reduced the activation of astrocytes, as shown by immunofluorescence and markedly inhibited iNOS mRNA expression (p<0.01). Septic encephalopathy is a devastating complication of sepsis. Although, considerable work has been done to identify the mechanism causing the pathological alterations in this setting, the culprit still remains an enigma. Our results demonstrate for the first time that endotoxemia leads to inflammation in brain, with alteration in blood-brain barrier, up-regulation of AQP4 and associated edema, neutrophil infiltration, astrocytosis, as well as apoptotic cellular death, all of which appear to be mediated by TNF-alpha signaling through TNFR1.
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PMID:TNF is a key mediator of septic encephalopathy acting through its receptor, TNF receptor-1. 1788 56

Sepsis-associated encephalopathy is an early manifestation of sepsis, resulting in a diffuse dysfunction of the brain. Recently, nitric oxide (NO) has been proposed to be one of the key molecules involved in the modulation of inflammatory responses in the brain. The aim of this study was to assess the role of NO in cerebrovascular endothelial cell activation/dysfunction during the early onsets of sepsis. To this end, we employed an in vitro model of sepsis in which cultured mouse cerebrovascular endothelial cells (MCVEC) were challenged with blood plasma (20% vol/vol) obtained from sham or septic (feces-induced peritonitis, FIP; 6 h) mice. Exposing MCVEC to FIP plasma for 1 h resulted in increased production of reactive oxygen species and NO as assessed by intracellular oxidation of oxidant-sensitive fluorochrome, dihydrorhodamine 123 (DHR 123), and nitrosation of NO-specific probe, DAF-FM, respectively. The latter events were accompanied by dissociation of tight junction protein, occludin, from MCVEC cytoskeletal framework and a subsequent increase in FITC-dextran (3-kDa mol mass) flux across MCVEC grown on the permeable cell culture supports, whereas Evans blue-BSA (65-kDa mol mass) or FITC-dextran (10-kDa mol mass) flux were not affected. FIP plasma-induced oxidant stress, occludin rearrangement, and MCVEC permeability were effectively attenuated by antioxidant, 1-pyrrolidinecarbodithioic acid (PDTC; 0.5 mM), or interfering with nitric oxide synthase (NOS) activity [0.1 mM nitro-L-arginine methyl ester (L-NAME) or endothelial NOS (eNOS)-deficient MCVEC]. However, treatment of MCVEC with PDTC failed to interfere with NO production, suggesting that septic plasma-induced oxidant stress in MCVEC is primarily a NO-dependent event. Taken together, these data indicate that during early sepsis, eNOS-derived NO exhibits proinflammatory characteristics and contributes to the activation and dysfunction of cerebrovascular endothelial cells.
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PMID:Role of endothelial nitric oxide synthase-derived nitric oxide in activation and dysfunction of cerebrovascular endothelial cells during early onsets of sepsis. 1872 68


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