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

Major alterations in the glucose-mediated regulation of growth hormone are associated with sepsis; however, these alterations are not related to the rate of change in plasma glucose or changes in glucagon, epinephrine levels, or circulating levels of arginine. Alterations in the growth hormone regulatory mechanism occurred among septic patients who manifested severe glucose intolerance which was associated with suppression of insulin production. Inhibition of growth hormone release in these patients may have an adverse effect on amino acid movement, which lends further support to the concept that sustained hyperglycemia in the septic patient is undesirable.
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PMID:Glucose-dependent changes in growth hormone regulation associated with sepsis. 702 2

Hyperosmolality complicating the management of burned patients has multiple etiologies. Sepsis, hyperglycemia, renal failure, electrolyte disturbances, shock, and substances absorbed from the burn wound may be contributing factors. Chemicals, such as propylene glycol, within bacteriostatic topicals may also lead to hyperosmolality. This report describes a patient who developed severe hyperosmolality after 5% Betadine-glycerin therapy for a 60% partial-thickness burn. Status epilepticus developed 36 hours later, and triglycerides were 9,700 mg/dl. After Betadine-glycerin was stopped the central nervous system status slowly improved but pre-seizure function was never regained.
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PMID:Hyperosmolality caused by percutaneously absorbed glycerin in a burned patient. 706 13

Hypoglycemia is but one of a number of causes of hypothermia, but is important to keep in mind as a possible precipitating or concurrent event even in those cases in which there are other obvious explanations for decreased body temperature (exposure, alcoholism, starvation, sepsis or hypothyroidism). Hypoglycemia may occur in as many as 40 percent of very cold patients, and be clinically unrecognized because symptoms are masked by the hypothermia itself. Although serum glucose levels are depressed, a cold-induced renal tubular glycosuria may occur. Glucose in the urine, therefore, cannot be used as assurance of hyperglycemia in a hypothermic patient. And, although cold protects against serious end organ damage from hypoglycemia by decreasing tissue metabolic need for glucose, a serum specimen should be drawn for glucose determination in all hypothermic patients and a 50 percent glucose solution immediately given intravenously. If this is not done, serum glucose levels may plummet as the patient is rewarmed and begins to shiver.
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PMID:Hypoglycemia and accidental hypothermia in an alcoholic population. 723 90

Although it is known that hepatic failure occurs in late sepsis, it is not known whether there are alterations in hepatocellular function in early sepsis when hyperdynamic circulation exists in conjunction with hyperglycemia and hyperinsulinemia. To study this, indocyanine green (ICG) clearance and serum levels of hepatic enzymes were measured during early and late sepsis. Sepsis in rats was produced by cecal ligation and puncture (CLP). Ten hours following CLP (early sepsis) total hepatic blood flow (THBF) as measured by hydrogen polarography increased from 23.9 +/- 1.1 to 30.6 +/- 1.4 (ml/min/100 gm). ICG (5 mg/kg body weight--BW) was given intravenously and sequential blood samples taken to determine ICG clearance. ICG half-times (T/2) were 4.99 +/- 0.15 and 6.57 +/- 0.51 minutes for sham-operated and early sepsis rats, respectively (mean +/- S.E., P less than 0.01). SGOT and SGPT levels (IU/ml) increased from 38.1 +/- 0.6 to 69.8 +/- 2.6 and 9.9 +/- 0.4 to 25.6 +/- 1.5, respectively (P less than 0.001). Thus the T/2 of ICG as well as serum levels of liver enzymes increased significantly during early sepsis. Eight additional rats underwent CLP and were tested 16 hours later (late sepsis). THBF in late sepsis decreased to 15.5 +/- 0.5 ml/min/100 gm. ICG T/2 at that time was 8.2 +/- 0.48 min and SGOT and SGPT level were 132 +/- 14.5 and 42 +/- 3.4, respectively (P less than 0.001). These results indicate that heptocellular dysfunction occurs even in the early period of sepsis when THBF is increased. Progressive dysfunction occurs in late sepsis concomitant with a decrease in THBF.
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PMID:Hepatocellular dysfunction in early sepsis despite increased hepatic blood flow. 734 87

Patients with diabetes mellitus are at a higher risk to undergo surgical intervention compared with the non-diabetic population, and additionally, they have an increased perioperative morbidity and mortality. Insulin deficiency and insulin resistance are aggravated by surgery and anaesthesia. The consequences of hyperglycemia are glycosuria, volume depletion from osmotic diuresis, impairment of wound healing and leucocyte function and exacerbation of ischemic brain damage. Depending on the extent of hypoinsulinemia, lipolysis and ketogenesis are enhanced which may result in metabolic acidosis with subsequent electrolyte disturbances. Protein catabolism is increased because of increased breakdown and decreased synthesis. Insulin administration reverts or overcomes most of these disturbances. The preoperative assessment includes the diagnoses of the long-term complications to judge the intraoperative risks. Long-acting insulins, such as ultralente of animal origin should be stopped preoperatively and substituted by protamine and lente insulins. In type-2-diabetic patients, long-acting sulfonylurea drugs such as chlorpropamide should be stopped and substituted by short-acting agents. Metformin must always be stopped. Type-2-diabetic patients with marked hyperglycemia under oral treatment should be switched to insulin before operation. The insulin requirements in diabetic patients during surgery vary from 0.25-0.40 U per gram glucose in normal weight patients, 0.4-0.8 U per gram glucose in case of obesity, liver disease, steroid therapy or sepsis, to 0.8-1.2 U per gram glucose in patients undergoing cardiopulmonary bypass surgery. Therefore, the appropriate dose has to be determined individually. The regimen nowadays preferred by most authors is based on variable rate insulin infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Perioperative management of the diabetic patient. 758 26

The aim of this work was to evaluate the use of 1 m2 Cuprophan hollow fiber filters for continuous arteriovenous hemodialysis procedures. Thirty one critically ill patients (18 male) aged between 20 and 80 years old, subjected to 35 hemodialysis procedures were studied. Sixteen patients had acute renal failure (10 of these had multiorgan failures) and 15 terminal chronic renal failure. Femoral vessels were used for vascular access and isotonic peritoneal dialysis solution flowing at 16.6 ml/seg as dialyzing solution. No extracorporeal pump assistance was used. Mean procedure time was 76 +/- 69.7 h, filter consumption was 2.8 +/- 2.1 filters/procedure, ultrafiltration rate was 168 ml/min and urea clearance was 19.9 +/- 4.4 ml/min. No replacement solutions were required and good electrolyte and circulating volume control was achieved with excellent hemodynamic stability. Blood urea fell from 116.9 +/- 49.1 to 64 +/- 27.2 mg/dl after the procedure (p < 0.001). Hyperglycemia was observed in eight procedures, six patients developed non infectious vascular access complications and two patients catheter related sepsis. We conclude that continuous arteriovenous hemodialysis using cuprophan membranes is a good renal substitution technique for critically ill patients.
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PMID:[Continuous hemodialysis with cuprophan membranes in critical patients]. 780 33

L-asparaginase is a valuable chemotherapeutic agent used in the induction of remission and improvement of long term survival in patients with acute lymphoblastic leukemia. Hyperglycemia is a well known side effect of L-asparaginase. Fourteen patients developed hyperglycemia during induction therapy of acute lymphoblastic leukemia with L-asparaginase, prednisolone, vincristine and daunorubicin. Hyperglycemia was observed after a mean of five doses of L-asparaginase (range 2-10). Seven of fourteen patients had neutropenic related infective episodes. Hyperglycemia resolved in all patients within 12 days (range 4-25) and two patients died of neutropenic septicemia. During reinduction therapy with the same drugs, only one out of ten patients developed hyperglycemia E-coli-L-asparaginase was replaced by Erwinia asparaginase in two patients one of who had recrudescence on further therapy. Close monitoring during L-asparaginase therapy for hyperglycemia will enable prompt recognition and early correction and prevent delay in therapy of acute lymphoblastic leukemia.
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PMID:L-asparaginase related hyperglycemia. 822 80

Gram-negative sepsis/septic shock in the newborn continues to be a major medical problem, causing high mortality. Hyperglycemia followed by hypoglycemia is a common symptom in endotoxic shock. However, the mechanism of newborn glucoregulatory response to endotoxin has not been well understood. Paradoxically, monocyte-phagocytes can contribute to shock by overwhelming secretion of cytokines and also host defense by detoxifying endotoxin. Since monocyte-phagocyte function is immature in the newborn, this study was performed to evaluate Kupffer cell's role in liver glycogenolysis during endotoxic shock. Endotoxin (LPS) induced hyperglycemia in 10-day-old rats, and increased net glucose output in the isolated perfused liver. 1) Cytarabine decreased Kupffer cell function (decreased hepatic colloid carbon uptake) and blunted LPS-increased liver net glucose output in the Cytarabine + LPS-treated group (104 +/- 4 vs. 146 +/- 3 micrograms/min/g wet liver in the LPS-treated group: P < .001). 2) Indomethacin (IND) suppressed LPS-induced liver net glucose output in the LPS + IND-treated group (133 +/- 5 vs. 146 +/- 3 micrograms/min/g wet liver, P < .05). Thus, prostaglandins were suggested to contribute to glycogenolysis in the 10-day-old rat liver. 3) Phorbol 12-myristate 13-acetate (PMA) increased liver net glucose output (166 +/- 4 micrograms/min/g wet liver), and H-7, a protein kinase C inhibitor, blunted PMA-induced liver glucose output (140 +/- 2 micrograms/min/g wet liver, P < .05). H-7 enhanced LPS-induced liver net glucose output (196 +/- 9 micrograms/min/g wet liver, P < .01). Therefore, protein kinase C may not be the dominant cell signaling system for LPS stimulation in suckling rat Kupffer cells.
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PMID:Lipopolysaccharide alters suckling rat liver glycogenolysis. 832 90

Nutritional support for critically ill patients with diabetes mellitus will be successful when nutrition meets the patient's metabolic needs; blood glucose levels are maintained between 100 and 200 mg/dL; complications of hyperglycemia, sepsis, and hypoglycemia are prevented; insulin dosages take basal metabolic needs, stress level, pharmacologic therapy, and the degree of illness into account; and nutritional support is provided in the least invasive manner possible. Providing nutritional support without adequate glycemic control and appropriate insulin administration is counterproductive for the patient. Careful monitoring of blood glucose and blood chemistries, along with the physical assessment of patients receiving nutritional support, are essential to successful treatment. Further research is necessary to define better which levels of glycemic control are most beneficial for providing optimal nutritional support for critically ill patients with diabetes mellitus.
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PMID:Nutritional support for the patient with diabetes. 844 2

Increased hepatic glucose production and glucose utilization involving multiple tissues occur in response to administration of bacterial lipopolysaccharide (LPS) and are metabolic hallmarks of hypermetabolic sepsis. As a proximal mediator in the host response to infection-like challenges, tumor necrosis factor (TNF) may enhance glucose metabolism by directly interacting with cells or by initiating a cascade of events leading to changes in glucose production and utilization. To determine if endogenous TNF is an important mediator in LPS- or sepsis-induced changes in glucose metabolism, rats were pretreated with a neutralizing goat anti-TNF IgG antibody prior to intravenous LPS or subcutaneous live Escherichia coli administration. Whereas high levels of plasma TNF were observed in rats not pretreated with anti-TNF, TNF was not detected 90 min after LPS in rats receiving the antibody. Pretreatment with anti-TNF attenuated the increase in plasma lactate and glucagon levels in LPS-challenged rats but failed to ameliorate the LPS-induced hyperglycemia and increase in glucose rate of appearance (Ra). The LPS-stimulated increase of in vivo glucose metabolic rate (Rg) of examined tissues, measured with [14C]-2-deoxyglucose, was not altered by anti-TNF. Likewise, rats treated with anti-TNF prior to induction of hypermetabolic infection exhibited usual increases in whole-body glucose Ra and metabolic clearance rate. Although neutralizing TNF failed to prevent the sepsis-induced augmentation of Rg in any tissue examined, it reduced the increase in the lung (P < 0.05) and tended to decrease it in other barrier tissues as well as in the spleen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of glucose metabolism after endotoxin and during infection is largely independent of endogenous tumor necrosis factor. 845 46


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