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

At the present time, terms used to describe the clinical entity of sepsis are used inappropriately and interchangeably. The source and foci of infection are often unidentified, yet it is clear that some form of inflammatory episode is occurring. The following paper seeks to clarify the terminology used to describe 'sepsis' and link this with a non-bacteraemic source of this inflammatory response--the small intestine. The importance of accurately reflecting oxygen extraction and oxygen consumption by cells is addressed and a movement from the current emphasis on haemodynamic measurement to variables which reflect metabolic rate and lactic acidosis is discussed. Issues which are the concern of nurses working in intensive care are examined, in terms of primary prevention and secondary management.
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PMID:Intestinal barrier failure and the development of the systemic inflammatory response syndrome. 783 30

Familiarity with renal issues that can challenge the care of patients with human immunodeficiency virus (HIV) should expedite diagnosis and therapeutic interventions. Among the most common problems are electrolyte and acid-base imbalances from many opportunistic infections or their treatments, including hyponatremia, hyperkalemia, hypokalemia, and hypo- and hypercalcemia. Acid-base disturbances, simple or mixed, can be due to underlying sepsis, opportunistic infections, or the therapy thereof. A recent report of seven patients with HIV with type B lactic acidosis failed to identify a satisfactory etiology. Elevations in creatinine or diminishing urine output should alert the physician to the possibilities of prerenal azotemia or acute tubular necrosis, which can result from progression of prerenal azotemia or can occur secondary to administered nephrotoxins, such as certain antibiotics and radiocontrast agents. Agents associated with nephrotoxicity include aminoglycosides, antifungal, antiviral, and radiocontrast agents, and nonsteroidal anti-inflammatory pain medications. Although prerenal azotemia and acute tubular necrosis are the most frequent causes of acute renal failure, the differential diagnosis should include acute interstitial nephritis, obstructive nephropathy, and glomerulopathies such as hemolytic uremic syndrome, thrombotic thrombocytopenia purpura, the newly described IgA nephropathy, and, in certain populations, HIV nephropathy.
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PMID:The spectrum of kidney diseases in patients with human immunodeficiency virus infection. 792 95

Endotoxin and other bacterial products induce the release of mediators which alter the circulation and cellular metabolism. Recent evidence suggests nitric oxide (NO) is one such mediator. The proposed mechanism by which NO produces hypotension is the activation of guanylate cyclase with subsequent biosynthesis of 3':5' cyclic guanosine monophosphate (cGMP). We studied the production of cGMP during Escherichia coli-induced septic shock in two experiments; the first with sepsis alone and the second using NG-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of nitric oxide synthase. Animals in both experiments experienced significant bacteremia (P < 0.05), endotoxemia (P < 0.05), and lactic acidosis (P < 0.03). Mean arterial blood pressure decreased (P < 0.03) and heart rate increased (P < 0.05) within both groups but did not differ between groups. A significant increase in the production of circulating whole blood cGMP occurred at 3-5 h (P < 0.03). There was significantly less cGMP produced by the L-NMMA-treated animals (P < 0.01). These results demonstrate an elevation in cGMP during septic shock which is attenuated by the addition of L-NMMA. This suggests that NO may be present during gram-negative septic shock and its effects mediated through cGMP.
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PMID:Modulation of cyclic guanosine monophosphate production during Escherichia coli septic shock. 804 98

To study the molecular basis of ammonia toxicity, highly reproducible models of acute liver failure and acute hyperammonemia in the rabbit were developed. Acute liver failure was induced by two-stage liver devascularization, and acute hyperammonemia by prolonged ammonia infusion such that the plasma ammonia pattern found in acute liver failure was simulated. Clinical symptoms, spectral analysis of the EEG, biochemistry (blood gases, renal function, electrolytes and markers of hepatic injury) and the presence of cerebral edema were studied. During acute liver failure severe encephalopathy developed after 10.2 +/- 1.9 h (n = 6, mean +/- SEM). Other liver-failure-associated abnormalities were cerebral edema, lactic acidosis, renal dysfunction, hypothermia and septicemia. During acute hyperammonemia, severe encephalopathy developed after 18.2 +/- 0.4 h (n = 6, mean +/- SEM). Other abnormalities found were cerebral edema and lactic acidosis. In both animal models comparable EEG changes were observed (a decrease in mean dominant frequency and theta-activity, and an increase in delta activity). However, these changes were not statistically significant, and non-specific as they also occurred in control rabbits despite their clinical wellbeing. This study demonstrates in the rabbit the similarity between encephalopathy due to acute ischemic liver failure and that due to hyperammonemia. An observed difference in hyperammonemia-induced encephalopathy was pronounced ataxia, which did not occur during acute liver failure, whereas hypothermia, sepsis and renal failure occurred exclusively in acute liver failure. Our models appear satisfactory for the study of hepatic encephalopathy and ammonia toxicity.
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PMID:Encephalopathy from acute liver failure and from acute hyperammonemia in the rabbit. A clinical and biochemical study. 817 26

Metformin is a biguanide that can used alone or in combination with sulfonylureas or insulin in the treatment of non-insulin-dependent diabetes mellitus (NIDDM). Since biguanides do not increase pancreatic insulin secretion, they are referred to as antihyperglycemic agents, as opposed to hypoglycemic agents. Biguanides reduce hyperglycemia by increasing, insulin sensitivity, decreasing glucose absorption, and inhibiting hepatic gluconeogenesis. Advantages of metformin include achieving glycemic control without exacerbating weight gain or hyperinsulinemia and beneficially affecting serum cholesterol concentrations. Although metformin has the potential to cause lactic acidosis, the incidence is significantly lower compared with phenformin. Risk factors for lactic acidosis include renal serum creatinine > 1.5 mg/dL and cardiovascular, pulmonary, and hepatic disease. Metformin should be temporarily discontinued prior to surgery and before administration of radiologic intravenous contrast, and in patients with sepsis, severe gastrointestinal disease, trauma, and acute cardiovascular events.
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PMID:Metformin: a new treatment option for non-insulin-dependent diabetes mellitus. 865 73

1. The cardiovascular failure in sepsis may result from increased nitric oxide biosynthesis, through the diffuse expression of an inducible nitric oxide synthase. In such conditions, nitric oxide synthase inhibitors might be of therapeutic value, but detrimental side effects have been reported with their use, possibly related to the blockade of constitutive nitric oxide synthase. Therefore, the use of selective inhibitors of inducible nitric oxide synthase might be more suitable. The aim of this study was to evaluate the effects of L-canavanine, a potentially selective inhibitor of inducible nitric oxide synthase, in an animal model of septic shock. 2. Anaesthetized rats were challenged with 10 mg/kg lipopolysaccharide intravenously. One hour later, they randomly received a 5 h infusion of either L-canavanine (20 mg h-1 kg-1, n = 15), nitro-L-arginine methyl ester (5 mg h-1 kg-1, n = 13) or 0.9% NaCl (2 ml h-1 kg-1, n = 21). Lipopolysaccharide induced a progressive fall in blood pressure and cardiac index, accompanied by a significant lactic acidosis and a marked rise in plasma nitrate. All these changes were significantly attenuated by L-canavanine, which also improved the tolerance of endotoxaemic animals to acute episodes of hypovolaemia. In addition, L-canavanine significantly increased survival of mice challenged with a lethal dose of lipopolysaccharide. In contrast to L-canavanine, nitro-L-arginine methyl ester increased blood pressure at the expense of a severe fall in cardiac index, while largely enhancing lactic acidosis. This agent did not improve survival of endotoxaemic mice. In additional experiments, we found that the pressor effect of L-canavanine in advanced endotoxaemia (4 h) was reversed by L-arginine, confirming that it was related to nitric oxide synthase inhibition. In contrast, L-canavanine did not exert any influence on blood pressure in the very early stage (first hour) of endotoxaemia or in the absence of lipopolysaccharide exposure, indicating a lack of constitutive nitric oxide synthase inhibition by this agent. 3. In conclusion, L-canavanine produced beneficial haemodynamic and metabolic effects and improved survival in rodent endotoxic shock. The actions of L-canavanine were associated with a selective inhibition of inducible nitric oxide synthase and were in marked contrast to the deleterious consequences of nitro-L-arginine methyl ester, a non-selective nitric oxide synthase inhibitor, in similar conditions.
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PMID:Beneficial effects of L-canavanine, a selective inhibitor of inducible nitric oxide synthase, during rodent endotoxaemia. 866 74

A global hypoxia resulting in an oxygen debt is assumed to be present in patients who suffer from the different stages and degrees of sepsis including septic shock and ARDS. As a consequence, the therapeutic concept of optimal values for cardiac output and oxygen delivery for these patients was proposed. This article reviews the literature with the objective of determining whether investigations dealing with oxygen delivery and consumption and with the plasma lactate concentration support the idea of the global hypoxia in septic patients. The finding of a pathologic oxygen supply dependency and an increase in plasma lactate concentration were taken as evidence for a global hypoxia. Between 1983 and 1991, oxygen supply dependency in septic patients was reported in an increasing number of publications. The increase in plasma lactate concentration was interpreted as lactic acidosis without presentation of plasma pH values and taken as evidence of global hypoxia and oxygen debt. From 1989 on, the number of publications that failed to show oxygen supply dependency even in the presence of an increased plasma lactate concentration increased. The problem in the method of determination of oxygen supply dependency became evident. Deducing both oxygen consumption and oxygen delivery from cardiac output from a common shared variable subject to measurement error may produce errors in the calculation of the regression between oxygen delivery and consumption. Oxygen supply dependency was not demonstrated in most investigations in which oxygen delivery and consumption were measured independently of each other. No decrease in mortality could be shown in prospective randomized studies for patients with sepsis and septic shock who were treated according to the concept of the optimal values. The lactate plasma concentration was below 5 mmol/l in most studies, which represents the borderline value for a clinically significant lactic acidosis. The term acidosis is not justified without a decrease in plasma pH or a decrease in the bicarbonate plasma concentration. An increased lactate plasma concentration can be merely the result of a hypermetabolism which is often found in septic patients. There is no proven evidence for global tissue hypoxia in septic patients from the investigations of oxygen delivery and consumption. This is also true for patients in septic shock after plasma volume expansion. The dogmatic proposal to increase cardiac output and oxygen delivery to certain levels cannot be sustained. However, regional hypoperfusion (e.g., of the splanchnic vascular bed) cannot be excluded. New approaches like gastric mucosal tonometry, measurement of splanchnic blood flow, and determination of regional metabolism are currently under investigation.
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PMID:[Is infection and septic shock caused by a global oxygen deficiency? An overview in 2 parts. 1: Infection and correlation between DO2 and VO2]. 867 14

Hemodynamic and oxygen-kinetic data of 16 burn patients with sepsis were analysed to explore relationship between oxygen transport pattern and clinical outcome after dopamine and dobutamine therapy. Two patterns of oxygen transport were shown in the 16 patients. Of them, ten (62.5%) had optimal DO2 and VO2 values (model I), and six (37.5%) had lower DO2 and VO2 values than the optimal (model II). All of 6 patients with model II developed lactic acidosis, septic shock and MOF and died. Two of 10 patients in model I developed MOF, only one died. The results indicate that, in burn patient with sepsis, the decreased response of DO2 and VO2 to inotropic therapy suggests failure of tissue perfusion, oxygen extraction and utilization, and may possibly predict the outcome.
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PMID:[Oxygen transport pattern in burned patient with sepsis under inotropic support]. 873 4

A rat grading model of chronic sepsis was developed by inoculation of a small (0.8 ml) or a large (1.5 ml) fecal pellet consisting of sterile rat feces, agar and a known number and strain of bacteria. A uniform spherical abscess containing Escherichia coli and Bacteroides fragilis was formed in 100% of the animals that survived the initial peritonitis stage. The effects of a large biclonal abscess were compared with those of a small abscess and of a sham operation. The peritonitis stage with high mortality was followed by an abscess stage. In rats with a large abscess, net body weight did not increase and there was 16% mortality during the abscess stage. On the 7th day, severe hepatic energy deficiency and lactic acidosis occurred in the septic liver with B. fragilis bacteremia. Rats with small abscesses showed mild metabolic disturbances with no mortality. Standardization of rat models with chronic graded septic abscess is possible by controlling the size of the fecal pellet and the species and number of inoculated bacteria.
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PMID:Manipulation of the size and clone of an intra-abdominal abscess in rats. 873 1

A patient with paroxysmal nocturnal hemoglobinuria developed lactic acidosis associated with severe anemia. The lactic acidosis corrected after blood transfusion. In the absence of shock, sepsis, or other identifiable causes of lactic acidosis, the severe anemia (hemoglobin 1.2 g/dl) appeared to be the primary etiologic factor.
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PMID:Lactic acidosis secondary to severe anemia in a patient with paroxysmal nocturnal hemoglobinuria. 920 7


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