When Can we Feed after a Gastrointestinal Bleed?

PURPOSE OF REVIEW: Gastrointestinal (GI) bleeding can carry minimal or significant risk for recurrent hemorrhage. Timing of feeding after GI bleeding remains an area of debate, and here we review the evidence supporting recommendations. RECENT FINDINGS: Improved understanding of the pathophysiology of GI bleeding and the evolution of treatment strategies has significantly altered the management of GI bleeding and the associated propensity for rebleeding. Early feeding following peptic ulcer bleeding remains ill-advised for high risk lesions while early initiation of liquid diets following cessation of esophageal variceal bleeding is appropriate and shortens hospital stays. Time to feeding following GI bleeding is inherently based on the disease etiology, severity, and risk of recurrent hemorrhage. With evolving standards of care, rates of rebleeding following endoscopic hemostasis are decreasing. Some evidence exists for early feeding however, larger multi-center trials are needed to help optimize timing of feeding in higher risk lesions.

Optimizing the nutrition support care model: Analysis of survey data.

BACKGROUND: Malnutrition is underrecognized and underdiagnosed, despite high prevalence rates and associated poor clinical outcomes. The involvement of clinical nutrition experts, especially physicians, in the care of high-risk patients with malnutrition remains low despite evidence demonstrating lower complication rates with nutrition support team (NST) management. To facilitate solutions, a survey was designed to elucidate the nature of NSTs and physician involvement and identify needs for novel nutrition support care models. METHODS: This survey assessed demographics of NSTs, factors contributing to the success of NSTs, elements of nutrition education, and other barriers to professional growth. RESULTS: Of 255 respondents, 235 complete surveys were analyzed. The geographic distribution of respondents correlated with population concentrations of the United States (r = 90.8%, p < .0001). Most responding physicians (46/57; 80.7%) reported being a member of NSTs, compared with 56.5% (88/156) of dietitians. Of those not practicing in NSTs (N = 81/235, 34.4%), 12.3% (10/81) reported an NST was previously present at their institution but had been disbanded. Regarding NSTs, financial concerns were common (115/235; 48.9%), followed by leadership (72/235; 30.6%), and healthcare professional (HCP) interest (55/235; 23.4%). A majority (173/235; 73.6%) of all respondents wanted additional training in nutrition but reported insufficient protected time, ability to travel, or support from administrators or other HCPs. CONCLUSION: Core actions resulting from this survey focused on formalizing physician roles, increasing interdisciplinary nutrition support expertise, utilizing cost-effective screening for malnutrition, and implementing intervention protocols. Additional actions included increasing funding for clinical practice, education, and research, all within an expanded portfolio of pragmatic nutrition support care models.

Ketogenic Diet: from the Historical Records to Use in Elite Athletes.

PURPOSE OF REVIEW: To review the available literature/evidence on low carbohydrate/high fat (LCHF) and low carbohydrate ketogenic (LCKD) diets' effects on human athletic performance and to provide a brief review of the physiology and history of energy systems of exercise. RECENT FINDINGS: Multiple studies have been conducted in an attempt to answer this question, many within the last 3-5 years. Studies are heterogenous in design, intervention, and outcome measures. Current available data show that LCHF and LCKD do not significantly enhance or impair performance in endurance or strength activities. However, there is a trend towards improved body composition (greater percent lean body mass) across multiple studies. While this may not translate to enhanced performance in the primarily laboratory conditions in the reviewed studies, there could be a benefit in sports in which an athlete's strength-to-weight ratio is a significant determinant of outcome.

Mechanisms of liver disease in patients infected with HIV.

OBJECTIVE: To describe the various mechanisms of liver disease in patients with HIV infection, and to link these mechanisms to disease states which may utilise them. BACKGROUND: Non-AIDS causes of morbidity and mortality are becoming increasingly common in patients chronically infected with HIV. In particular, liver-related diseases have risen to become one of the leading causes of non-AIDS-related death. A thorough understanding of the mechanisms driving the development of liver disease in these patients is essential when evaluating and caring for these patients. METHODS: The literature regarding mechanisms of liver disease by which different disease entities may cause hepatic injury and fibrosis was reviewed and synthesised. RESULTS: A number of discrete mechanisms of injury were identified, to include: oxidative stress, mitochondrial injury, lipotoxicity, immune-mediated injury, cytotoxicity, toxic metabolite accumulation, gut microbial translocation, systemic inflammation, senescence and nodular regenerative hyperplasia. Disease states may use any number of these mechanisms to exert their effect on the liver. CONCLUSIONS: The mechanisms by which liver injury may occur in patients with HIV infection are numerous. Most disease states use multiple mechanisms to cause hepatic injury and fibrosis.

Hyperbilirubinaemia in HIV-HCV co-infected patients on antiretroviral therapy: drug effect or liver disease severity?

OBJECTIVE: Hyperbilirubinaemia (HB) is common in HIV and hepatitis C virus (HIV-HCV) co-infected patients and poses a unique challenge in management as it may be due to medications such as the protease inhibitors (PIs) or to hepatic dysfunction. There are no data on the relationship of HB to liver histology and PI use in this population. Clinicians caring for these patients are faced with the difficult task of determining whether increasing serum bilirubin is due to drug effects or progression of liver disease. METHODS: To address this gap in knowledge, we performed a retrospective analysis of 344 consecutive HIV-HCV co-infected patients undergoing liver biopsy to identify factors associated with HB. Demographic, clinical, laboratory data were collected. Advanced fibrosis was defined as bridging fibrosis or cirrhosis. Those with hepatitis B virus, hepatic decompensation or hepatocellular carcinoma were excluded. RESULTS: The prevalence of HB (range 1.3-9.4) was 33% and more common in those on a PI (46%) than those who were not (10%; p≤0.001) and mostly in those on indinavir (40%) or atazanavir (46%). Of the patients on these PIs, HB was not associated with fibrosis grade, demographics, or other clinical variables. Conversely, in those not on a PI, HB was associated with fibrosis grade (p≤0.0001) after adjusting for other clinical and demographic variables. CONCLUSIONS: In the setting of indinavir or atazanavir use, HB is common and unrelated to underlying disease severity and the medications can be continued safely. Conversely, HB in HIV-HCV co-infected patients not on a PI is due to their underlying liver disease and suggests these patients require closer monitoring.