Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two regimens (A and B) for TPN were designed to meet the requirements of newborn infants for calories, amino acids, fatty acids, electrolytes, trace elements and vitamins. Both "A" and "B" included fat emulsion (Intralipid). "A" contained fructose and glucose, "B" glucose only. "A" provided amino acids (Vamin) in proportions similar to those of whole egg, "B" similar to those of human milk. All nutrients were given simultaneously into peripheral veins by constant infusion. Nineteen patients (11 newborns, 8 infants) were studied for 1-28 days. Twelve infants recovered, 7 died. In none could TPN be regarded as the cause of death. Treatment was complicated by sepsis in 5 infants. During the course of treatment, blood levels of substrates and insulin were measured before, during and 30 min after discontinuation of TPN. Highly raised concentrations of circulating substrates seen in 3 infants seemed to be related to a poor clinical condition rather than to the regimen used. Infants in good condition tolerated TPN well. Low levels of branch-chained amino acids and tendency to ketonemia, when infusion was stopped, suggested that minimal rather than optimal supply of energy and of amino acids in relation to energy was provided with both regimens. Low insulin levels associated with elevated blood levels of substrates suggested that insulin administration to selected cases might be indicated. Fructose (0.30 g/kg X hour-1) given with regimen A increased blood lactate concentrations. Homocystinaemia appeared in 2 cases; disappearance after excess vitamin B6 administration indicated increased B6 requirement.
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PMID:Total parenteral nutrition in infants. Blood levels of glucose, lactate, pyruvate, free fatty acids, glycerol, d-beta-hydroxybutyrate, triglycerides, free amino acids and insulin. 40 94

Four patients from a larger group of 18 patients receiving dextrose-free isotonic (3%) amino acid solution as nutritional support, form the basis of this report. An additional seven patients received intravenous isotonic (5%) dextrose as their sole support in the postoperative period following major elective surgery (average nitrogen balance = -12.3 +/- 2.7 g). All patients were well-nourished as determined by anthropometric measurements. The nonseptic patients receiving infusions of isotonic amino acids demonstrated an improvement in nitrogen balance (= delta 8.5 +2, P less than 0.001) when compared to the postoperative use of 100 to 150 g of glucose. However, sepsis produced a decreased net utilization of the infused crystalline amino acids such that nitrogen balance was similar to the intravenous glucose group (- 10.6 +/- 2.1). This septic response was associated with decreased plasma free fatty acid concentrations and the absence of starvation ketosis and ketonuria. While the nitrogen balance was not different in the septic and the dextrose control groups, deficiencies in plasma amino acid concentrations were observed in the group receiving intravenous infusion of glucose.
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PMID:Effect of deep surgical sepsis on protein-sparing therapies and nitrogen balance. 40 78

A new program of total parenteral nutrition (TPN) for surgical neonates has been described an investigated. The program is based on the use of fat emulsion as the major source of calories and infusion of large volumes of the solution via peripheral veins. This program has three main advantages over conventional hyperalimentation using a central venous catheter: (1) it avoids complications such as septicemia, thrombosis of large vessels, and metabolic complications such as hyperglycemia or osmotic diuresis; (2) it provides physiological nutritive elements containing a normal composition of glucose, protein, and fat; and (3) it is easy to start and manage the TPN using a peripheral vein. Thirty-four neonatal surgical patients with life-threatening gastrointestinal anomalies have been placed on this TPN program. Infusion of fat emulsion and large volumes of fluid were well tolerated and all patients gained weight during the period of observation.
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PMID:Total parenteral nutrition using peripheral veins in surgical neonates. 40 73

The importance of adhesion in regulating locomotion and accumulation of polymorphonuclear leukocytes (PMN) has remained vague. We found that the chemotaxis of human PMN resuspended in heat-inactivated plasma was maximal toward 1-10 nM N-formyl-met-leu-phe (f-Met-Leu-Phe), but fell below random motility toward >/= 100 nM. This impressive decrease of motility was paralleled by increased cell adherence on Petri dishes being minimal at 1 nM and maximal at >10 nM f-Met-Leu-Phe (6+/-1 and 37+/-2% [SE] adherent cells, respectively). Checked by phase-contrast microscopy, cells under stimulated adhesion lost the typical bipolar shape of moving PMN and became immobilized and highly flattened. PMN, preexposed to 250 nM f-Met-Leu-Phe and tested after washing, retained increased adhesiveness and showed extremely low random and chemotactic motility. In contrast, preexposure to 1 nM f-Met-Leu-Phe had no effect on chemotaxis. Supporting the concept that immobilizing hyperadhesiveness does not correspond to a general functional hyporesponsiveness of PMN, no depression of the initial ingestion rate was observed in the presence of 250 nM f-Met-Leu-Phe. Moreover, a close correlation was found between the induction of PMN adhesiveness and the stimulation of the hexose monophosphate pathway activity as well as of lysomal enzyme release (r >/= 0.98). Thus, "chemotactic deactivation" and "high-dose inhibition of chemotaxis" by N-formyl peptides is the consequence of increased cell adhesiveness. This phenomenon provides a mechanism for cell trapping at the inflammatory site. Conversely, if operative in circulating blood, e.g., in septicemia, it may impair PMN emigration to such sites.
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PMID:Modulating influence of chemotactic factor-induced cell adhesiveness on granulocyte function. 44 62

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
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PMID:Hypophosphatemia in hospitalized patients. 44 90

Glucose intolerance occurs in patients with sepsis, and resistance to insulin has been thought to be part of this process. To study this phenomenon, peritonitis was produced in rats by cecal ligation and puncture. One group was killed ten hours later (early sepsis). A second group of rats was killed 16 to 24 hours after ligation, just prior to their expected death (late sepsis). Insulin stimulated glucose uptake to the same extent in muscles from rats in early sepsis, late sepsis, and from control rats. Even at an insulin concentration that produced submaximal stimulation of glucose uptake, no difference in glucose uptake between the three groups of muscles was observed. Thus, there was no resistance to the stimulatory action of insulin on glucose uptake by skeletal muscle during early and late sepsis. However, basal glucose uptake by isolated soleus muscle from animals in late sepsis was significantly increased compared with controls when these muscles were incubated in an aerobic environment. Under anaerobic conditions, glucose uptake in these two groups of muscles increased to the same level. This indicates that there is some stimulus that increases glucose uptake in late peritonitis and may explain the hypoglycemia of late experimental or untreated sepsis. This stimulus could be hypoxia or some other factor resulting from decreased blood flow and increased anaerobic metabolism.
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PMID:Studies of peripheral glucose uptake during sepsis. 45 60

Six insulin-dependent diabetics were studied on their conventional insulin treatment and during continuous, dual-rate, subcutaneous insulin infusion for periods of up to 4 days. Dabetic control, as assessed by mean plasma glucose, range of plasma glucose values, M-value or range of M-values was improved significantly in 5 patients (mean +/- SD plasma glucose concentration on final infusion day 6.9 +/- 1.3 mmol/l, versus 11.3 +/- 3.2 mmol/l on conventional treatment). Once a suitable insulin dose was established blood glucose control could be maintained by continuous subcutaneous insulin infusion using the same daily infusion rate without frequent adjustment. In some case this was less than the daily dose on the conventional treatment. However, glycaemic control in one "brittle" diabetic, with unpredictable swings in blood glucose on her normal regimen, was not improved by continuous subcutaneous insulin infusion. During the period tested there was no sepsis at the cannula implantation site and patients did not find the system uncomfortable or unduly inconvenient.
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PMID:Continuous subcutaneous insulin infusion:good blood glucose control for up to 4 days. 46 48

Simultaneous longitudinal hormonometabolic-physiologic (cardiopulmonary) profiles were measured in 14 nonseptic trauma/general surgery (T/GS) patients and in ten patients with Gram-negative abdominal surgical sepsis. The physiologic state classification system was used as the frame of reference. There were no response differences between the T and GS groups: they had A State responses. The sepsis (S) patients initially had exaggerated A State responses with significant changes in glucose, fat, amino acid, and glucagon plasma levels relative to T/GS. The S patients who survived (four) demonstrated profiles as in T/GS. The S patients who expired (six) progressively evolved an unbalanced, hyperdynamic B State response with progressive elevations of glucose, lactate, aromatic and branched-chain amino acids and glucagon, and low ketone bodies. There is definite correlation over time between metabolic and physiologic responses; the physiologic responses reflect the metabolic responses; the metabolic responses are consistent with a peripheral energy-fuel deficit.
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PMID:Correlations between metabolic and cardiopulmonary measurements in patients after trauma, general surgery, and sepsis. 46 74

Glucose intolerance has been commonly observed in sepsis and has been attributed to a multitude of endocrine and metabolic disorders. From 1977 to 1978, 19 patients were studied using intravenous glucose tolerance tests to evaluate this phenomenon; 15 patients presented with ongoing sepsis and four patients served as stress controls. Glucose intolerance was found to be a significant finding in less than 40% of the septic group. This state of intolerance was noted to be associated with a high mortality rate (60%), whereas glucose tolerance in sepsis was associated with a much improved mortality rate (10%). Hormone levels were correlated with glucose tolerance curves using the parameters of insulin, glucagon, growth hormone, cortisol, and epinephrine levels. Glucose intolerance and a high mortality rate were linked to sustained hyperglucagonemia, which was unresponsive to glucose challenge, and to marked suppression of growth hormone. This apparently represents a decompensated peripheral metabolic energy deficit, which results in the increased mortality rate.
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PMID:The sepsis-glucose intolerance riddle: a hormonal explanation. 47 28

Both acute and chronic hepatic insufficiency can result in lactate accumulation and lactic acidosis; data from both types of patients were compared. In the chronic group, an acute precipitating event was identified in seven of nine subjects. Four had sepsis and three had gastrointestinal hemorrhage. In these patients, results from most tests of hepatic function were not altered dramatically. There were no long-term survivors in this group. In contrast, patients with acute hepatic failure had striking alterations in their results of hepatic function tests. Notable prolongation of the prothrombin time was always present initially and antedated other abnormalities of hepatic function. Three of seven patients in this group survived. Hypoglycemia was seen in both groups and in two subjects with acute hepatic insufficiency, glucose administration alone resulted in rapid lowering of lactate levels.
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PMID:Lactic acidosis and liver disease. 50 18


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