Total parenteral nutrition-related infections: Prospective epidemiologic study using semiquantitative methods

Studies of total patenterai nutrition-related infection have incorrectly relied on positive results on culture of the cannula tip to confirm the source. We undertook a prospective study of total parenteral nutrition-related infections in adult patients by obtaining blood from all total parenteral nutrition lines for pour-plate culture twice weekly and culturing intravascular line segments by the technique of Maki. Twelve of 100 courses of total parenteral nutrition (12 percent) in 69 patients resulted in infections—five (5.0 percent) had sepsis, and seven (7.0 percent) had local infection. In five of these 12, pour-plate culture gave positive results (five of 38 pour plates) with counts of 8 colony-forming units per ml (cfu/ml) for Candida tropicalis, and 25 to more than 1,000 for bacterial isolates. In nine of 12, culture of the intravascular line segment gave positive results with more than 50 cfu/ml. Pathogens isolated from intravascular line segments included Staphylococcus epidermidls (three cases), Candida species (three cases), Staphylococcus aureus (two cases), Serratia marcescens (one case) and mixed bacterial pathogens (one case). In contrast, pour-plate culture gave positive results in only seven of 88 uninfected (control) courses (318 pour plates), and culture of intravascular line segments gave positive results in two of 65 uninfected courses (p < 0.001). No differences existed among patients with and without infection with regard to age, underlying disease, surgery, systemic antibiotic usage, or the presence of other infections. The duration of total parenteral nutrition was longer in courses without infection than in courses with infection (14.7 ± 9.4 days versus 11.0 ± 4.0 days; p < 0.02). In six of 12 courses with infection, the line had been violated compared with 22 of 88 courses without infection (p < 0.001). T-connectors for the central administration of intralipid were associated with infection (p < 0.02). The value of routine pour-plate culture was illustrated in three courses in which the positive pour-plate culture results antedated positive blood culture results or line removal.     

Total parenteral nutrition and cholestasis

Hepatobiliary dysfunction is recognized as a major adverse effect of total parenteral nutrition (TPN). It is unknown if this is caused by a deficiency or toxicity of the TPN solution or the underlying pathophysiology of disease processes that require TPN therapy. This article presents algorithms for evaluating abnormal liver tests in patients on TPN and discusses treatment options and the current status of intestinal transplantation.     

Hepatic complications of total parenteral nutrition

Total parenteral nutrition is now widely used in the treatment of nutritional depletion. Among problems that persist in the use of this technique, the development of hepatic abnormalities has received increasing attention. In this review, the current understanding of the pathogenesis and management of liver injury during short-term total parenteral nutrition is summarized. These complications include fatty liver, cholestasis, and nonspecific triaditis. The experience with hepatic complications during long-term total parenteral nutrition is also reviewed. Evidence that progressive liver injury develops in some patients requiring lifelong total parenteral nutrition raises a serious dilemma for both patients and physicians. Better understanding of the pathogenesis is required before appropriate treatment can be prescribed.     

Total parenteral nutrition in Crohn's disease

The effect of total parenteral nutrition on 19 patients suffering from severe active Crohn's disease was studied. Total parenteral nutrition was effective as primary therapy in 56 per cent. In the remaining patients, it was highly effective as supportive therapy, enabling them to undergo uneventful major surgery.     

Metabolic and catheter complications of parenteral nutrition

Since its introduction in the 1960s, total parenteral nutrition (TPN) has played a vital role in improving clinical outcomes for patients with acute and chronic illnesses. The evolution of TPN solutions and vascular access techniques, combined with an increased awareness and better understanding of the physiology of TPN, have improved the safety of this therapy. Nevertheless, complications are not uncommon and can be life threatening. This article provides an updated review on the metabolic and catheter complications associated with TPN.     

全胃肠外营养与非酒精性脂肪性肝病

全胃肠外营养（total parenteral nutrition,TPN）始于20世纪60年代末,由美国外科医师Dudrick首先在动物实验中获得成功并应用于临床,此方法能维持机体基本生理功能并促进生长,现已成为处理危重患者的常规手段。然而,TPN会导致很多并发症,其中非酒精性脂肪性肝病（nonalcoholic fatty liver disease,NAFLD）受到越来越多的关注。虽然随着TPN配方的改进,如增加脂肪含量、降低葡萄糖含量、氨基酸制剂的改进、脂肪乳剂等,NAFLD的发病率有所下降,但其仍是TPN最突出的问题。     

Management of complications in patients receiving home parenteral nutrition

Patients receiving long-term home parenteral nutrition tend to fall under the care of adult and pediatric gastroenterologists. This article reviews the management of potential infectious, mechanical and metabolic complications and describes common psychosocial issues related to the therapy. The point at which to refer the patient to an intestinal failure program offering autologous bowel reconstruction and small bowel transplantation is discussed.     

Total parenteral nutrition-associated changes in mouse intestinal intraepithelial lymphocytes

Intraepithelial lymphocytes (IEL) play a major role in mucosal defense mechanisms against intraluminal foreign antigens. To address the role luminal nutrients have on the phenotype and function of the IEL, we administered total parenteral nutrition (TPN) to mice, with the absence of enteral intake. We hypothesized that administration of TPN would result in changes in the phenotype and function of the IEL. For this, we utilized a mouse model of TPN. A significant decline in the CD4⁺ IEL population occurred with TPN. Additionally, the CD8⁺,CD44⁺ IEL subset showed a 65% decline (P < 0.05), and the CD4⁺,CD44⁺ subset declined by 55% with TPN (P < 0.05). The CD8⁺ population (a marker of thymic-dependence) also declined by 92% (P < 0.01) with TPN. IEL in the TPN group showed a significantly lower degree of in vitro proliferation. In conclusion, the IEL showed significant phenotypic changes with TPN including the loss of the thymic-derived population. Functionally, the IEL showed a significant decline in proliferation. Such changes demonstrate the important role luminal nutrients have on IEL phenotype and function.     

Total parenteral nutrition after surgery rapidly increases serum leptin levels

OBJECTIVE: In humans, leptin is regulated by long-term changes in energy intake. However, short-term regulation of serum leptin by nutrients has been difficult to show. The aim of this study was to investigate whether short periods of fasting and stress sensitise the leptin response to nutrients. SUBJECTS AND EXPERIMENTAL PROTOCOL: Fourteen patients of normal weight undergoing elective open cholecystectomy were randomised into two groups. One group received saline infusion during surgery and for 24 h postoperatively. The other group also received saline during the surgical procedure, but total parenteral nutrition (TPN) was started immediately after surgery. Blood samples were drawn before as well as 2, 4, 8, 16, and 24 h after the start of surgery to determine the serum levels of leptin and other hormones. RESULTS: Postoperative TPN induced a significant rise in serum leptin within 6 h, reaching a more than fourfold increase within 14 h (P<0.001). Serum glucose and insulin levels increased within 2 h. Growth hormone and IGF-1 serum levels also increased significantly in the group receiving TPN. Serum cortisol levels increased postoperatively in both groups, which may explain why no significant reduction in serum leptin was observed in the group receiving saline. Free tri-iodothyronine (T3) decreased in both groups, while catecholamines were similar in the groups. CONCLUSION: During fasting and surgical stress, nutrients rapidly increased the serum leptin levels in humans in a manner similar to that previously reported in rodents. This may be mediated by increases in serum glucose, insulin and cortisol.