Factors Associated With Central Line-Associated Bloodstream Infections in a Cohort of Adult Home Parenteral Nutrition Patients.

BACKGROUND: Central line-associated bloodstream infection (CLABSI) is a potentially life-threatening complication in home parenteral nutrition (HPN) patients. We investigated potential predictors of CLABSI in a cohort of adult HPN patients METHODS: Patients managed by the HPN service at the Hospital of University of Pennsylvania on January 1, 2018, were included and followed through June 30, 2019, using existing medical records to collect demographic and clinical data. CLABSIs were adjudicated prospectively by infectious disease experts. Variables with P ≤ .2, when comparing patients with CLABSIs and those without, were included in logistic regression models. RESULTS: Among 114 patients, mean age was 54 ± 16 years, 78/114 were female, and BMI was 25 ± 5.6. Median experience with HPN was 516 days (range, 15-10,281), and 30 had prior CLABSI. Catheter types were peripherally inserted central catheters (83/114), tunneled (27), and implanted (4). The incidence of CLABSI was 0.89 per 1000 catheter days. One multivariate model identified ostomy/wound (odds ratio [OR], 22.0; 95% CI, 4.8-101.7), tunneled/implanted catheter (OR, 4.4; 95% CI, 1.4-13.9), and BMI < 18.5 (OR, 5.9; 95% CI, 1.4-24.2) as predictors of CLABSI. A second model identified patients with 2 potential predictors (OR, 22.9; 95% CI, 5.6-93.5) and tunneled/implanted catheter (OR, 6.7; 95% CI, 2.1-21.8) at high risk of CLABSI. Whether CLABSIrates might be reduced by more intense training in wound or catheter care (especially for those with multiple predictors), different types of catheters, or rapid treatment of malnutrition will require further study.

Preparing the Patient for Home Parenteral Nutrition and for a Successful Course of Therapy.

Preparing the patient for home parenteral nutrition (HPN) is a collaborative effort among many different clinicians. Identifying patients who will transition home with parenteral nutrition (PN) as early as possible allows for a thoughtful and safe approach. Communication regarding the HPN goals is critical to the patient's success, whether the requirement for PN is temporary or permanent. Management of these complex patients is best served by a multidisciplinary team with expertise in the area of nutrition support. Adherence to available guidelines that define best practice is imperative in all aspects of care for the patient on HPN.

A Patient With Parenteral Nutrition-Dependent Short Bowel Syndrome and Cardiovascular Disease With 4-Year Exposure to Teduglutide.

Clinical trials of the glucagon-like peptide 2 analogue teduglutide resulted in approval of the drug by the Food and Drug Administration in 2012 as a treatment for parenteral nutrition-dependent short bowel syndrome in adults. This report presents the case study of a man with short bowel syndrome caused by portal vein thrombosis who had 4 years exposure to the drug at the time of his death due to cardiovascular disease.

Clinical Management of Patients With Parenteral Nutrition-Dependent Short Bowel Syndrome During Teduglutide Therapy.

BACKGROUND: Patients with intestinal failure, who are dependent on parenteral nutrition (PN) to supplement their limited absorption of dietary nutrients, are subject to complications associated with long-term PN therapy. Medication therapy that results in improved dietary nutrient absorption may enable these patients to reduce or even become independent from PN therapy and its related complications. The glucagon-like peptide 2 (GLP-2) analogue teduglutide was approved for use in such patients by the U.S. Food and Drug Administration in 2012. PURPOSE: The purpose of this article is to describe the experience of 7 patients with PN-dependent intestinal failure who were treated with teduglutide by a single center that had been involved in the teduglutide clinical trials. RESULTS: Two patients who were treated during the clinical trials and 5 others who were treated since teduglutide came to market in the United States are described. Protocols used to prepare and monitor patients with this drug and PN weaning and adverse event outcomes are presented. CONCLUSIONS: While some patients had uncomplicated PN reduction, others experienced various complications. Careful monitoring of patients' clinical course is needed during drug therapy.

Choline and vitamin B12 deficiencies are interrelated in folate-replete long-term total parenteral nutrition patients.

BACKGROUND: Choline has recently been recognized as an essential nutrient, in part based on deficiency data in long-term home total parenteral nutrition (TPN) patients. Choline, a methyl donor in the metabolism of homocysteine, is intricately related to folate status, but little is known about choline and vitamin B12 status. Long-term TPN patients are also subject to vitamin B12 deficiency. OBJECTIVE: The objective of the study was to evaluate any interaction between choline, vitamin B12, and folate in patients with severe malabsorption syndromes, requiring long-term TPN. DESIGN: Plasma free choline, serum and red blood cell (RBC) folate, serum vitamin B12 methylmalonic acid, B6, and plasma total homocysteine concentrations were assayed by standard methods. Low choline was defined as values that fall 1 to < or =3 and marked low choline concentration as >3 SD below the control mean. RESULTS: Both low choline concentrations (52% were marked low, 33% low, 14% normal) and elevated methylmalonic acid concentrations (47%) were prevalent. Choline concentration was significantly lower and RBC folate higher in patients with elevated methylmalonic acid. Total homocysteine elevations were rare (3 of 21) and mild. CONCLUSIONS: These data suggest a strong interaction between vitamin B12 and choline deficiencies and folate status in this population, which may be due in part to variations in vitamin and choline delivery by TPN. Folate adequacy may increase B12 use for homocysteine metabolism, thus limiting B12 availability for methylmaIonic acid metabolism. Choline use may also increase, and choline deficiency may worsen if choline substitutes when the vitamin B12 side of the homocysteine metabolic pathway cannot be used.