ABSTRACT
OBJECTIVE: To compare the incidence of catheter colonization and catheter-related bloodstream infections between heparin-coated catheters and those coated with a synergistic combination of chlorhexidine and silver sulfadiazine. DESIGN: Randomized, controlled clinical trial. SETTING: A 20-bed medical-surgical intensive care unit. PATIENTS: A total of 180 patients requiring the insertion of a trilumen central venous catheter. INTERVENTIONS. Patients were randomized to receive either a trilumen heparin or chlorhexidine and silver sulfadiazine-coated catheter. MEASUREMENTS: Catheter colonization was defined by a semiquantitative catheter tip culture yielding 15 or more colony-forming units or quantitative culture of 1,000 or more colony-forming units/ml. Catheter-related bloodstream infection as the isolation of the same microorganism from a peripheral blood culture and catheter tip. RESULTS: A total of 260 catheters were cultured. Out of 132 heparin-coated catheters, 29 were colonized and out of 128 chlorhexidine and silver sulfadiazine-coated catheters, 13 were colonized ( p=0.03), relative risk RR=2.16 (1.18-3.97). This represents an incidence of 23.5 and 11.5 episodes of catheter colonization per 1,000 catheter-days, respectively ( p=0.0059), RR=2.04 (1.05-3.84). Microorganisms isolated in catheter colonization from heparin-coated catheters were gram-positive cocci 23, gram-negative bacilli 7, and Candida spp 4. In chlorhexidine and silver sulfadiazine-coated catheters were gram-positive cocci 6 and gram-negative bacilli 11 ( p=0.009). The incidence of catheter-related bloodstream infections per 1,000 catheter-days was 3.24 in heparin-coated catheters and 2.6 in chlorhexidine and silver sulfadiazine-coated catheters ( p=0.79), RR=1.22 (0.27-5.43). CONCLUSIONS: In critically ill patients the use of trilumen central venous catheters coated with chlorhexidine and silver sulfadiazine reduced the risk of catheter colonization due to prevention of gram-positive cocci and Candida spp.
Subject(s)
Anti-Infective Agents, Local/pharmacology , Catheterization, Central Venous/methods , Chlorhexidine/pharmacology , Critical Illness/therapy , Silver Sulfadiazine/pharmacology , Adult , Aged , Anticoagulants/pharmacology , Catheterization, Central Venous/adverse effects , Colony Count, Microbial , Critical Care , Female , Heparin/pharmacology , Humans , Male , Middle Aged , Staphylococcal Infections/blood , Staphylococcal Infections/etiology , Staphylococcal Infections/microbiology , Staphylococcus/drug effects , Staphylococcus/isolation & purificationABSTRACT
Warm ischemic (90 minutes) acute renal failure (ARF) was evaluated in the dog and found to cause polyuric ARF in the injured kidney if the opposite normal kidney was removed. In contrast, if the normal kidney were left intact, oliguric ARF was noted in the injured kidney. To further evaluate the mechanisms for oliguria and polyuria, chronic reinfusion of urine from a normal kidney into the inferior vena cava (ureterocaval anastomosis) resulted in polyuria in the opposite warm ischemic injured kidney; whereas chronic reinfusion of urine into the portal vein (ureteroportal anastomosis) resulted in profound oliguria in the opposite injured kidney. In separate additional experiments, urine acutely infused into the inferior vena cava at a rate of 0.38 ml/minute caused a significantly greater diuretic and renal hemodynamic response than seen with urine infused into the portal vein. Acute infusions of urea solution (0.38 ml/minute) with the same osmolality of urine were completely devoid of diuretic and renal hemodynamic effects. These studies reveal that urine contains a powerful hemodynamic and diuretic factor which appears to convert oliguric to polyuric ARF following warm ischemic renal injury in the dog. This factor is not urea and can be destroyed by the liver.
