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

Insulin glucose therapy can correct hyponatraemia and renal sodium retention in burns, sepsis and circulatory failure. A case of fulminant hepatic failure (F.H.F.) is described in which the same effect was observed. Insulin was thought to have corrected abnormal cell membrane permeability. The actions of insulin are discussed in relation to its possible role in the management of F.H.F.
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PMID:The effects of insulin glucose administration in fulminant hepatic failure. 69 Mar 22

White blood cell counts and nitroblue tetrazolium dye tests were performed in three groups of dogs before and after the injection of Escherichia coli using colistimethate sodium and cephalothin sodium in the second and third groups, respectively, prior to the induction of sepsis. The response was a diminished white blood count and increased nitroblue tetrazolium dye test percentage in all groups. When antibiotic administration was performed prior to the induction of sepsis, the increase in the nitroblue tetrazolium reduction dye test was much more evident despite the overwhelming dose of bacteria given, suggesting that antibiotics given preoperatively will prevent the toxic effects of bacteria on the neutrophil and will enhance the phagocytic activity of the neutrophil.
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PMID:Effects of preventive antibiotics on neutrophil phagocytosis as measured by the nitroblue tetrazolium dye test. 77 47

The in vitro sensitivity to oxolinic acid shown by pathogenic gram-negative bacterial isolates from young calves with diarrhea, pneumonia, and septicemia was investigated by the bute dilution method. Minimal bactericidal concentrations of the drug for 65.5% of the isolates were less than or equal to 1.56 mug/ml and for 90%, less than or equal to 6.25 mug/ml. Cross resistance between oxolinic acid and chloramphenicol, streptomycin, neomycin, colistin, ampicillin, gentamicin, and oxytetracycline was not observed. Oxolinic acid was orally administered to a group of calves at dose levels of 12.5 to 57.0 mg/kg, and sodium oxolinate was intramuscularly injected in another group of calves at dose levels of 12.5 and 20 mg/kg. In the 1st group, oxolinic acid was detected in blood serum 15 minutes later; peak serum concentrations averaged 25 mug/ml at 10 hours after treatment with 50 mg of the drug/kg and 3 mug/ml at 7 hours, with 12.5 mg of the drug/kg. In the 2nd group, the dose level of 20 mg of sodium oxolinate/kg resulted in mean peak serum concentration of 4 mug/ml, observed 1 hour after the drug was injected. The half-life of the drugs in serum was approximately 3.5 hours after they were orally or intramuscularly given. These investigations indicate that oxolinic acid could be used in the treatment of the common calf diseases.
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PMID:Clinical pharmacology of oxolinic acid in young dairy calves. 77 48

Fifteen-hundred hospital blood cultures were made in duplicate, with and without 0.05% sodium polyanethol sulfonate in the broth medium. A significantly higher rate and speed of recovery of both gram-positive cocci and gram-negative bacilli was accomplished in sodium polyanethol sulfonate broth. The effect was independent of the content of 0.1% agar in the growth medium. In the cases of Neisseria meningitidis septicemia examined, however, a detrimental result on recoveries was observed. The addition of sodium polyanethol sulfonate also resulted in an increased frequency of recoveries of contaminating organisms.
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PMID:Effect of sodium polyanethol sulfonate in blood cultures. 80 66

Lactic acid is generated as the end product of anaerobic metabolism of glucose and is disposed by gluconeogenesis or oxidation. Changes in the lactate pyruvate ratio are not necessarily indicative of tissue hypoxia. The plasma lactate concentration is the result of lactate production and lactate removal (hepatic and renal gluconeogenesis; oxidation by muscle, liver and kidney). Lactic acidosis is defined as a state of metabolic acidosis (arterial pH less than 7.3) due to an increase in the blood concentration of lactate (greater than 2 mEq/l). Lactic acidosis may occur with evidence of tissue hypoxemia (type A) or in its absence (type B). Lactic acidosis has been described in association with phenformin therapy, hereditary enzymatic defects, hematological malignancy, prolonged fasting, shock with or without septicemia and occasionally without any underlying disease ("idiopathic" lactic acidosis). The therapy of lactic acidosis consists of administration of sodium bicarbonate and restoration of adequate tissue perfusion; hemodialysis may be helpful to control sodium excess and possibly to remove phenformin. The effectiveness of methylene blue, glucose and insulin are not yet established.
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PMID:Lactic acidosis. 87 61

The pathogenesis of experimental meningococcal septicemia and the efficacy of heparin sodium therapy were evaluated by inoculating rabbits intraperitoneally with type B meningococci in mucin. Half the rabbits died, and the respiratory distress and circulatory failure that occurred during the terminal phase of the disease were associated with diffuse pulmonary capillary and venular thrombosis and with renal glomerular fibrin deposition. Platelet and leukocyte counts and plasma fibrinogen levels decreased in all rabbits, and prothrombin and partial thromboplastin times were prolonged. Pretreatment with heparin sodium diminished intravascular fibrin deposition but failed to prevent the pulmonary microthrombi and did not either reduce the mortality or improve the survival time. We conclude that death in meningococcal septicemia is due to widespread thrombosis of the pulmonary microcirculation. The disease is complicated by diffuse intravascular coagulation, which can be controlled with heparin sodium but which is not immediately life-threatening.
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PMID:Experimental meningococcal septicemia. Effect of heparin therapy. 94 60

The acute onset of oliguria and azotemia in the postoperative setting may be caused by pre-renal causes or intrinsic renal damage. The first step in arriving at a diagnosis is to review the history as noted above for clues regarding fluid balance, treatment with nephrotoxins, etc. The typical patient with prerenal azotemia will present with evidence of the recent onset of worsening of pre-existing cardiac disease, renal or gastrointestinal fluid loss, or the accumulation of acites, edema, or retroperitoneal fluid. In the absence of very recent diuretic therapy, he will be excreting a scant amount of concentrated (greater than 400 mOsm per L) sodium free (less than 10 to 20 mEq per L) urine. The serumBUN/Cr ratio is often greater than 15 to 20:1, and their urinary sediment will be bland. In an occasional patient in whom these studies give equivocal results, additional help may be obtained with measurements of central venous pressure (CVP) or pulmonary wedge pressure (PWP) and by noting their response to intravenous fluid loading. A rising CVP or PWP in the face of salt loading is, of course, evidence against prerenal azotemia. Patients with obstructive uropathies may be oligoanuric or polyuric-occasionally a characteristic alternating polyuria and oliguria is found (due to displacement of a stone or relief of edema). When oliguric their urine typically contains substantial amounts of sodium (greater than 20 mEq per L), is isotonic, and their OsmU:OsmP is les s than or equal to 1.2. Their urinary sediment will reflect the cause of their obstruction as noted above. A renal scan, ultrasound study, or infusion IVP are mandatory to rule out the possibility of obstructive uropathy. If these nonivasive studies are equivocal, one must consider doing a unilateral retrograde. The development of ATN usually occurs in the setting of hypotension, sepsis, dehydration, and with exposure to nephrotoxins. Most patients with be excreting scant amounts of isotonic urine containing more than 20 to 30 mEq per L of sodium. Their CrU:CrP is less than or equal to 20:1 and their urinary sediment reveals many epithelial cells and casts. Those patients with nonoliguric ATN have urine outputs which may exceed 2 liters per day. Despite this output they demonstrate a stepwise increase in serum urea and creatinine. Urine sodium and osmolality are not very helpful in this setting. Many such patients do have low (less than 20 mEg per L) urine sodium concentration and excrete isotonic urine.
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PMID:Pre- and postoperative renal failure. 96 Mar 14

Hospital nursery A has used chloramphenicol and nursery B has used the combination of penicillin G sodium and kanamycin sulfate routinely in the treatment of neonatal sepsis and other bacterial infections. A hypothesis was formulated that these different antibiotic pressures would select out a substantial number of populations of resistant bacteria in each of the two nurseries. This was tested by periodic sampling of the skin, mouth, and rectal flora of babies and the permanent personnel in these nurseries. These bacteria were studied for susceptibility to a number of antibiotics. The population of resistant strains selected out was correlated with the antibiotics used in each nursery. There is a need for continuing surveillance of hospital nursery strains of bacteria for in vitro susceptibilities to commonly prescribed antimicrobials.
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PMID:Susceptibilities of bacteria to different antibiotic regimens. Study in two nursery populations. 109 52

To determine the source of pyococci causing attacks of sepsis in infantile eczema 20 patients with continuing eczema were followed up for one year, regular swabs being taken from the skin, nose, throat, and family contacts. The staphylococci were phage typed and the streptococci serologically typed. Staphylococci of the same phage type in most cases remained in reservoir sites on the skin and coincidently in the nose. Staphylococci causing attacks of clinical sepsis arose from these persistently colonized sites. Staphylococci of the same phage type were also common in family contacts. Streptococci of the same group in most cases did not remain on the skin. Streptococci causing attacks of clinical sepsis arose as new infections from external sources, sometimes from throat infections in the patient or family contacts. Strains of streptococci which are known to be associated with glomerulonephritis were isolated. It has been confirmed that staphylococci resistant to neomycin and sodium fusidate quickly emerge after the topical use of these antibiotics. Streptococci are highly resistant to neomycin and gentamicin, and moderately resistant to sodium fusidate, so the use of these antibiotics in topical steroid preparations will have little effect in preventing further attacks of clinical sepsis in these patients.
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PMID:Pyogenic cocci in infantile eczema throughout one year. 114 31

Proteins from four fish rhabdoviruses have been studied by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The viruses were: trout viral hemorrhagic septicemia (VHS), infectious hematopoietic necrosis virus (IHN), spring viremia virus of carp (SVC), and the pike fry rhabdovirus (PFR). For the two salmonid viruses (VHS-IHN), gel electrophoresis indicated the proteins, with molecular weights estimated to be 190,000, 80,000, 38,000, 25,000, and 19,000, respectively. The electrophoretic profile of the two other viruses (SVC-PFR) revealed four major proteins with molecular weights of 190,000 80,000 42,000 and 21,000, respectively. In this case a minor component with 50,000 daltons was found. For each virus only one protein was found to be glycosylated, i.e., the one with a molecular weight of 80,000. A major protein (molecular weight between 38,000 and 42,000) was found to be associated with the nucleocapsid. All these results revealed marked similarities in protein structure between the four fish rhabdoviruses and the previously well-characterized members of rhabdovirus group. However, one can distinguish two groups of viruses: the first one is composed of salmonid viruses (VHS and IHN) with a protein structure comparable to that of rabies virus and potato yellow dwarf virus; the second one is composed of carp and pike viruses, having a protein structure very similar to that of vesicular stomatitis virus.
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PMID:Fish rhabdoviruses: comparative study of protein structure. 117 Dec 63


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