Nutrition
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The prevention of catheter sepsis lies in a sound understanding of the routes through which catheters get contaminated. The catheter hub has been recognized as a portal for microorganisms causing catheter sepsis, particularly in central venous catheters inserted for > 1 wk. Bacteria and fungi may reach the internal surface of the catheter connector during manipulation by hospital staff and then colonize the entire lumen of the catheter. ⋯ Needleless systems must be evaluated in terms of their safety in preventing endoluminal contamination. A new disinfecting catheter hub incorporating an antiseptic barrier has been developed and reduced hub-related catheter sepsis by more than 90%. The endoluminal route of intravascular catheter contamination must be taken into account when designing strategies for the diagnosis and prevention of catheter-related sepsis.
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Although intravascular devices have become indispensable tools in the care of seriously ill patients, the morbidity and mortality resulting from catheter-related infections and the high cost of managing such complications may offset the benefits derived from these devices. A scientific understanding of the pathogenesis, microbiology, and risk factors involved in catheter-related infection is the cornerstone of any effective preventive approach. ⋯ The first approach does not use antimicrobial agents and includes measures such as placement and maintenance of vascular catheters by a skilled infusion therapy team and use of maximal sterile barriers. The second approach uses antimicrobial agents and involves the application of topical disinfectants such as chlorhexidine, use of silver-impregnated subcutaneous cuffs (for short-term central venous catheters), flushing catheters with a combination of antimicrobial and antithrombotic agents, and coating of catheters with either antiseptic (chlorhexidine and silver sulfadiazine) or antimicrobial agents (minocycline and rifampin).
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The availability and widespread use of TPN enables physicians to help patients in a way that had not been possible in the past. However, in order to best utilize this modality, we must be aware of potential hazards and metabolic complications. Many patients receiving TPN, particularly those receiving perioperative TPN, are malnourished to various extents, and careful monitoring of glucose metabolism is warranted to avoid malnutrition-associated reactive hypoglycemia.
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Case Reports
Clinical and biochemical aspects of thiamine treatment for metabolic acidosis during total parenteral nutrition.
We encountered six cases of total parenteral nutrition (TPN)-associated lactic acidosis during the 6-y period of 1988-1993. The patients were characterized by severe disease of the digestive organs, minimal food intake before surgery, and postoperative TPN with no food intake and with no vitamin supplements. Within 4 wk of TPN, they developed hypotension (< or = 80/60 mmHg), Kussmaul's respiration, and clouding of consciousness, as well as abdominal pain not directly related to the underlying disease. ⋯ Thiamine replenishment at intravenous doses of 100 mg every 12 h resolved lactic acidosis and improved the clinical condition in 3 patients. This article includes a review of 11 relevant reports published from 1982-1992 and a discussion of the biochemical mechanism of onset of thiamine deficiency-associated lactic acidosis. We emphasize the needs (1) to supplement TPN with thiamine-containing vitamins for the patients whose food intake does not meet nutritional requirements; (2) to monitor the patients routinely measuring serum thiamine concentration and erythrocyte transketolase activity during TPN; and (3) to intravenously replenish using high-dose thiamine simultaneously with the manifestation of signs and symptoms of lactic acidosis.