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

Eighty-five trauma patients between the ages of 18 and 55, with American College of Surgeon's (ACOS) trauma scores greater than or equal to 7 were entered into a double-blind, randomized, placebo-controlled study to assess the efficacy of prophylactic fibronectin (Fn) administration on clinical course, sepsis development, and septic mortality. Patients were randomized on admission to receive purified human virus-inactivated Fn or placebo control (human serum albumin, HSA). Fn or HSA was administered on a daily basis if and when the patient was Fn deficient (less than 75% normal). When a Fn deficiency was not evident, the patient received saline. Seventy one patients developed Fn deficiencies during their initial clinical course: 36 received Fn, 35 received HSA. Fourteen patients did not develop a Fn deficiency after trauma and thus received only saline. Analysis of admission data demonstrated no significant differences between the three groups with respect to extent of injury (injury severity score, ACOS trauma score) or physiologic assessments of organ function (serum creatinine, bilirubin, lactic acid). On day 1 after trauma, Fn levels were shown to correlate with other plasma proteins and cellular components (range of r values, 0.24 to 0.75; all p less than 0.05), but not with organ function parameters. Eighteen of 85 patients became septic as judged by clinical criteria. Ten of these patients had received Fn (10 of 36), five had received HSA (5 of 35), and three had received only saline (3 of 14) before the development of sepsis (differences not significant). When septic, nine of 17 patients developed Fn deficiencies. Six patients received Fn while septic, three received albumin, and eight received saline. Seven patients died: 5 of 6 Fn patients, 1 saline, and 1 HSA recipient. Our data suggest that exogenous Fn repletion in states of deficiency does not alter clinical course, the development of sepsis, or septic mortality.
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PMID:The influence of fibronectin administration on the incidence of sepsis and septic mortality in severely injured patients. The Medical College of Georgia Fibronectin Research Group. 250 98

The metabolic alterations, nutritional and metabolic assessment, and nutritional requirements of critically ill patients are discussed, and parenteral nutrition support therapies are reviewed. Physiological alterations in the metabolism of the injured or septic patient are mediated through the interactions of neuroendocrine, cardiovascular, toxic, and starvation responses. These responses cause mobilization of nutritional substrates in an effort to maintain vital organ function and immune defenses. A patient's nutritional status can be determined from anthropometric measurements, creatinine excretion rate, and evaluations of protein stores and immune reserves and function; body weight is a poor indicator. Nitrogen-balance calculations are also useful for determining the adequacy of nutritional intake and the degree of metabolic stress. Early assessments of nutritional status may assist in identifying those patients for whom nutritional support interventions are needed. Nutritional requirements are altered by the metabolic responses to injury and sepsis. Studies suggest that use of nutrient solutions enriched for branched-chain amino acids may enhance nitrogen retention and that energy expenditures in injured or septic patients are only moderately elevated. Most nonprotein calories in parenteral nutrient solutions are provided as glucose, but lipids are an important source of energy in the critically ill patient who has high energy requirements or carbohydrate intolerance; however, clearance of lipids may be decreased. Fluid, electrolyte, and mineral status must be evaluated frequently. Critically ill patients have unique nutritional requirements, and parenteral nutrition support therapies for these patients are being investigated and refined.
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PMID:Parenteral nutrition in the critically ill patient. 250 29

Rhabdomyolysis was evaluated by measurement of total creatine kinase (CK) and lactic dehydrogenase (LDH) in 19 patients with severe sepsis; 12 developed acute renal failure (Group B) and 7 did not (Group A). Results were compared to 7 patients with trauma (Group C) and 6 patients with chronic renal failure and minor infections (Group D). CK was higher (p less than 0.005) in Group B than in A. Results in Group C were similar to those in A. Elevation of CK correlated to increases in creatinine (r = 0.655, p less than 0.005). CK levels of Group D patients were lower than those of Group B. Blood pressure, lactate and pO2 were similar in both groups but thrombopenia was noted in Group B patients. Our results suggest that rhabdomyolysis and thrombopenia play a role in the development of renal failure in patients with severe sepsis.
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PMID:[Rhabdomyolysis caused by severe sepsis: discussion on its role in the development of acute renal failure]. 251 72

The Dialysis Centre at the Lagos University Teaching Hospital became operational in November 1981 and caters for acute haemodialysis, chronic maintenance haemodialysis and continuous arteriovenous haemofiltration. In the past 5 years, over 600 patients had presented out of whom 245 could be accommodated within the realities of available facilities and patients' financial status. Of the 245 patients, 25 were discharged against medical advice and five were transferred to hospitals abroad but did not survive. There were 117 patients in end-stage renal failure (ESRF), 75 males, 42 females, ratio M:F 1.8:1, age range 13-69 years, mean 37.5. There were 51 males and 47 females in acute renal failure (ARF), ratio 1.1:1, age range 13-76 years, mean age 32.3 (Table 1). All patients in ESRF had moderate to severe hypertension (diastolic pressure of greater than or equal to 120 mmHg or 22.1 kPa) and a creatinine clearance of less than or equal to 5 ml/min and about 75% had established cardiac decompensation. Full pertinent investigations were precluded or contra-indicated in most patients in ESRF because of late presentation. In only 13 patients was renal biopsy performed and the pathohistologies were end stage renal disease (8), chronic glomerulonephritis (4) and glomerulosclerosis (1). In ARF the cause of the renal damage was multifactorial in 66.7%, with sepsis being the direct cause of death in 60.0%. The commonest conditions were septicaemia (61.4%), nephrotoxin (17.2%), trauma (31.3%), septic abortion (33.3%) and toxaemia of pregnancy (29.0%) (Table 2). The dialysis associated complications which were encountered included shunt infection (7%), burst membrane (9%), suspected pyrogen reaction (5.6%) and femoral vein perforation (0.9%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Five years experience of haemodialysis at the Lagos University Teaching Hospital--November 1981 to November 1986. 255 Nov 60

Interleukin-2 (IL-2)-based immunotherapy is associated with profound reversible cholestasis and hyperbilirubinemia. We performed a nonrandomized retrospective and prospective analysis to determine the incidence, characteristics, clinical course, and nature of the IL-2-induced liver dysfunction in patients with cancer. Patients received IL-2 at a dose of 20,000 to 100,000 units (U)/kg thrice daily for up to 5 days. Fifty-one patients on adjuvant treatment protocols received a mean of 10.18 +/- 2.38 IL-2 doses and 11.67 +/- 4.16 doses were delivered to 210 patients with advanced disease during this period. Retrospective analysis of all patients receiving this therapy revealed increases in the following liver function tests expressed as median, 25th percentile, and 75th percentile (range): bilirubin (mg/dL) 4.5, 2.6, 6.5 (.4 to 38.5); alkaline phosphatase (U/L) 256, 179, 378 (56-1680); SGOT (U/L) 80, 52, 117 (18 to 483); SGPT (U/L) 91, 64, 132 (20-540); prothrombin time 13.4, 12.8, 14.5 (10.8 to 35.4); and albumin (g/dL) values decreased (trough) slightly 3.0, 2.8, 3.2 (2.3 to 3.8). Multiple regression analysis revealed several factors that were significantly associated with the increase in bilirubin when jointly considered (model P2 less than or equal to .001) including total IL-2 dosage, increase in creatinine, alkaline phosphatase, weight, and SGOT. Similar increases were noted in a prospectively evaluated group of 10 patients. A return to normal levels of bilirubin was noted within 5.6 days of stopping IL-2. Fasting serum cholylglycine increased from a mean of 32.3 +/- 1.6 to a peak of 1556.0 +/- 625.0 mg/mL. Although conventional ultrasound examinations were unrevealing, tissue ultrasound examinations revealed a mean scatterer spacing (MSS) increase compared to baseline of .10 +/- .04 (P less than .02) suggesting hepatic edema or an infiltrative process. Further, computerized hepatobiliary nuclear medicine scans revealed a delay in uptake (2.2 +/- 0.5 fold greater) and excretion (8.0 +/- 5.9 fold greater) of technetium-99m labeled disofenin. These findings support the development of profound reversible cholestasis as the primary basis for the elevated bilirubin in patients undergoing IL-2 treatment and may have implications for understanding the jaundice observed in some patients postoperatively as well as that associated with sepsis and other inflammatory disorders. Specifically, the release of IL-2 or the induction of other factors similarly induced by IL-2 may be responsible for these findings. Tissue ultrasound and computerized hepatobiliary scans provide additional noninvasive assessments of liver function and physiology.
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PMID:Interleukin-2 induces profound reversible cholestasis: a detailed analysis in treated cancer patients. 258 24

Recently, the association of granulocytic fragments on blood smear with leukoerythroblastosis in sepsis has been identified in nine patients. Granulocytic fragments were identified by both light and electron microscopy as well as cytochemistry. Leukoerythroblastosis is a poorly defined, uncommon syndrome with leukocytosis, left shift, and nucleated red blood cells (nRBCs) disproportionate to the degree of anemia, which may be associated with leukemia or neoplasia in the bone marrow, acute infection, hemolysis, myelofibrosis, or miscellaneous causes. Here a subgroup with high white blood cells (WBC) and acute infection was studied. The corrected WBC for nine patients was 40 x 10(9) per L with 33 nRBC per 100 WBC; serum C3 and C4 levels before and after the development of leukoerythroblastosis were 0.6 +/- 2 g per L; 0.18 +/- 0.04 g per L pre-leukoerythroblastosis and 0.7 +/- 0.46 g per L; 0.30 +/- 0.27 g per L post-leukoerythroblastosis, respectively, in four patients. The platelet count, prothrombin time (PT), and activated partial prothrombin time (aPTT) were 133 x 10(9) per L, 24.4 sec., and 53.5 sec., respectively, for nine patients. Multiphasic chemistries at the time of leukoerythroblastosis were measured in five patients; abnormal values included calcium of 2.0 +/- 0.4 mmol per L, creatinine of 336 +/- 130 mumol per L, total protein of 45 +/- 17 g per L, albumin of 27 +/- 11 g per L, total bilirubin of 421 +/- 362 mumol per L, uric acid of 499 +/- 264 mumol per L, triglycerides of 4.9 +/- 3.7 mmol per L, and alkaline phosphatase of 3.5 +/- 1.0 mu kat per L.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biochemical values, complement levels, and hemostatic data in septic leukoerythroblastosis. 260 78

A boy, aged 14 1/2 years, presented with Burkitt leukemia. His renal status was normal before treatment. Chemotherapy (SFOP LMB 86 protocol) was begun Oct. 9, 1986. After the first 2 courses of chemotherapy, the patient had Gram negative sepsis treated with cefotaxime, netilmycine, Vancomycin and ornidazole. During sepsis, nephrotic syndrome developed (albumin 25 g/l, non selective proteinuria 15 g/24 h), with moderately high blood pressure, functional renal failure (creatinine 141 mumols/l, U/P urea = 20), polyuria and tubular damage. Kidney ultrasonography was normal. Needle biopsy showed minimal glomerular lesions, acute tubular lesions, and no deposits in immunofluorescence. The nephrotic syndrome disappeared within 3 weeks, with treatment of leukemia. He is at present in complete remission with a follow-up of 25 months.
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PMID:[Nephrotic syndrome and B leukemia]. 262 44

A new reproducible animal model of sepsis was established to investigate interrelationship between disseminated intravascular coagulation (DIC) and multiple organ failure (MOF). Sepsis was induced by injecting fecal suspension into bile duct of rabbits, in which the amount of endotoxin in circulating blood was gradually increased and manifestations of sepsis were confirmed. During 9 hours' observation period, an occurrence of hypercoagulable state leading to DIC was evidenced by the abnormal hemostaseological parameters. Simultaneously the elevation of plasma bilirubin and creatinine levels was observed, indicating the presence of liver and kidney failure, which was confirmed by the histological examination. Thereby, the present sepsis model complicates DIC and MOF with high reproducibility, which is relevant to sepsis seen in clinical patients.
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PMID:Sepsis model with reproducible manifestations of multiple organ failure (MOF) and disseminated intravascular coagulation (DIC). 272 56

A 3-year-old girl is reported on who underwent laparotomy for ileocaecal intussusception elsewhere one week following severe gastroenteritis. Immediately after surgery, she developed haemolytic-uraemic syndrome with haemolytic anaemia, thrombocytopenia, increase of urea and creatinine and anuria as well as subsequent peritonitis, enterocolitis and sepsis. Following relaparotomy with establishment of ileostomy, peritoneal dialysis for several days was carried out for treatment of the haemolytic-uraemic syndrome. This case demonstrates that the haemolytic-uraemic syndrome can be treated effectively by peritoneal dialysis despite fresh bowel anastomoses, and that simultaneously occurring peritonitis can be managed by intraperitoneal administration of antibiotics via dialysis fluid.
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PMID:[Peritoneal dialysis in hemolytic-uremic syndrome following ileocecal resection for invagination in postoperative peritonitis]. 275 Mar 44

This retrospective study was conducted to identify the frequency of cytomegalovirus (CMV) disease in seronegative recipients of donor-specific transfusion (DST) and living-related donor (LRD) kidneys from seropositive donors. A total of 151 LRD transplants (TX) were performed at six transplant centers over a 3-year period. A total of 33 patients were identified as having been seronegative (pre-TX) for CMV, yet they had DST and a TX from a seropositive LRD. Of these patients, 12 (36.4%) seroconverted within the first 6 months post-TX and developed clinical CMV disease. Additional patients seroconverted, but did not have evidence of clinical disease and were not tested further. All TX centers, with the exception of one, had seronegative patients that became ill after receiving a seropositive DST/LRD TX. Six patients manifested their disease as a febrile illness with leukopenia and liver enzyme elevations, four had pneumonitis, and two developed CMV ulcerations of the colon (one of whom died from resultant sepsis). Of the 36 seronegative patients who received seronegative DST/LRD TX none became ill with CMV disease. Of the 72 seropositive patients who received DST/LRD TX, only 2 (2.8%) developed CMV illness (one, seropositive into seropositive, the other, seronegative into seropositive). Of the 33 seronegative patients receiving seropositive DST/LRD TX, 17 received antilymphocyte preparations (ALP), and 8 of these became ill (47.1%). Of 16 patients not receiving ALP, 5 (31.3%) developed clinical CMV illness. Of the 33 patients who were identified as having been seronegative for CMV yet received seropositive DST/LRD TX, the 12 who did develop CMV illness had two graft losses, one death, and a serum creatinine for the remaining 9 patients of 2.3 +/- 1.6 at last follow-up. The remaining 21 patients who developed no illness had a serum creatinine of 1.3 +/- 0.6 with no graft losses at the last follow-up. This evidence suggests that a prospective TX recipient who is seronegative for CMV who receives DST/LRD TX from a seropositive family member has a significant risk for developing morbidity related to clinical CMV illness.
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PMID:Incidence and morbidity of cytomegalovirus disease associated with a seronegative recipient receiving seropositive donor-specific transfusion and living-related donor transplantation. A multicenter evaluation. 282 52


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