Gastrointestinal tolerance and plasma status of carotenoids, EPA and DHA with a fiber-enriched tube feed in hospitalized patients initiated on tube nutrition: Randomized controlled trial.

BACKGROUND & AIMS: During the first days of tube feeding (TF) gastrointestinal (GI) complications are common and administration of sufficient nutrition is a challenge. Not all standard nutritionally complete formulas contain dietary fiber, fish oil or carotenoids, key dietary nutrients for health and wellbeing. The aim of this study was to investigate the effects of a fiber, fish oil and carotenoid enriched TF formula on diarrhea, constipation and nutrient bioavailability. METHODS: A multi-center randomized, double-blind, controlled, parallel trial compared the effects of a dietary fiber, fish oil and carotenoid-enriched TF formula (test) with an isocaloric non-enriched formula (control) in 51 patients requiring initiation of TF. Incidence of diarrhea and constipation (based on stool frequency and consistency) was recorded daily. Plasma status of EPA, DHA and carotenoids was measured after 7 days. RESULTS: The incidence of diarrhea was lower in patients receiving the test formula compared with the control group (19% vs. 48%, p = 0.034). EPA and DHA status (% of total plasma phospholipids) was higher after 7 days in test compared with control group (EPA: p = 0.002, DHA: p = 0.082). Plasma carotenoid levels were higher after 7 days in the test group compared with control group (lutein: p = 0.024, α-carotene: p = 0.005, lycopene: p = 0.020, ß-carotene: p = 0.054). CONCLUSIONS: This study suggests that the nutrient-enriched TF formula tested might have a positive effect on GI tolerance with less diarrhea incidence and significantly improved EPA, DHA and carotenoid plasma levels during the initiation of TF in hospitalized patients who are at risk of diarrhea and low nutrient status. CLINICAL TRIAL REGISTRATION: This trial was registered at trialregister.nl; registration number 2924.

Body fat loss achieved by stimulation of thermogenesis by a combination of bioactive food ingredients: a placebo-controlled, double-blind 8-week intervention in obese subjects.

BACKGROUND: A combination of tyrosine, capsaicin, catechines and caffeine may stimulate the sympathetic nervous system and promote satiety, lipolysis and thermogenesis. In addition, dietary calcium may increase fecal fat excretion. OBJECTIVE: To investigate the acute and subchronic effect of a supplement containing the above mentioned agents or placebo taken t.i.d on thermogenesis, body fat loss and fecal fat excretion. DESIGN: In total, 80 overweight-obese subjects ((body mass index) 31.2+/-2.5 kg/m(2), mean+/-s.d.) underwent an initial 4-week hypocaloric diet (3.4 MJ/day). Those who lost>4% body weight were instructed to consume a hypocaloric diet (-1.3 MJ/day) and were randomized to receive either placebo (n=23) or bioactive supplement (n=57) in a double-blind, 8-week intervention. The thermogenic effect of the compound was tested at the first and last day of intervention, and blood pressure, heart rate, body weight and composition were assessed. RESULTS: Weight loss during the induction phase was 6.8+/-1.9 kg. At the first exposure the thermogenic effect of the bioactive supplement exceeded that of placebo by 87.3 kJ/4 h (95%CI: 50.9;123.7, P=0.005) and after 8 weeks this effect was sustained (85.5 kJ/4 h (47.6;123.4), P=0.03). Body fat mass decreased more in the supplement group by 0.9 kg (0.5; 1.3) compared with placebo (P<0.05). The bioactive supplement had no effect on fecal fat excretion, blood pressure or heart rate. CONCLUSION: The bioactive supplement increased 4-h thermogenesis by 90 kJ more than placebo, and the effect was maintained after 8 weeks and accompanied by a slight reduction in fat mass. These bioactive components may support weight maintenance after a hypocaloric diet.

Introductory to the ESPEN Guidelines on Enteral Nutrition: Terminology, definitions and general topics.

The ESPEN guidelines on enteral nutrition are the first evidence-based European recommendations for enteral nutrition. They were established by European experts for a variety of disease groups. During guideline development it became evident that terms and definitions in clinical nutrition have been used inconsistently depending on medical disciplines as well as regional and personal preferences. Therefore, to increase explanatory accuracy it was necessary to unify them. In this chapter terms and definitions used throughout all guidelines are explained. Additionally answers to more general questions, which might be important in most indications are dealt with, i.e. use of fibre containing and diabetes formulae.

ESPEN Guidelines on Enteral Nutrition: Liver disease.

Enteral nutrition (EN) by means of oral nutritional supplements (ONS) and tube feeding (TF) offers the possibility to increase or to insure nutrient intake in case of insufficient oral food intake. The present guideline is intended to give evidence-based recommendations for the use of ONS and TF in patients with liver disease (LD). It was developed by an interdisciplinary expert group in accordance with officially accepted standards and is based on all relevant publications since 1985. The guideline was discussed and accepted in a consensus conference. EN by means of ONS is recommended for patients with chronic LD in whom undernutrition is very common. ONS improve nutritional status and survival in severely malnourished patients with alcoholic hepatitis. In patients with cirrhosis, TF improves nutritional status and liver function, reduces the rate of complications and prolongs survival. TF commenced early after liver transplantation can reduce complication rate and cost and is preferable to parenteral nutrition. In acute liver failure TF is feasible and used in the majority of patients.

[Diagnosing malnutrition in the elderly]. / Diagnostik der Mangelernährung des älteren Menschen. Ergebnisse eines internationalen Experten-Meetings der BANSS-Stiftung.

The concept of malnutrition in the geriatric population describes a deficient state of energy and nutrient intake with harmful clinical consequences. Despite of having a significant effect on morbidity and mortality, there are no generally accepted criteria for diagnosing malnutrition in the elderly. With increasing age the general recognition of the nutritional status becomes more important for the diagnosis of malnutrition than isolated parameters. Recording a patient"s history must include any weight loss and changes in appetite. Reasons for a diminished nutritional intake must be explored systematically as well. As part of physical examination one has to pay attention to clinical signs of malnutrition (general muscular atrophy, loss of subcutaneous fat) and to signs of micronutrient deficiencies. The documentation of oral intake can supply important evidence for deficient intake of energy and nutrients. Of special relevance among anthropometric values are a BMI of less than 20 kg/m and calf circumference of less than 31 cm. Individual follow-up data are superior to isolated measurements Laboratory diagnostic tests (for example albumin) are of minor importance for the diagnosis of malnutrition because of their low specificity. As a consequence of unsolved methodical problems, bioelectrical impedance analysis can currently be recommended only to those who are experienced with this method and its limitations. Screening and assessment tools like Mini Nutritional Assessment (MNA) and Nutritional Risk Screening(NRS) are helpful for a quick and simple identification of malnourished patients and those who are at risk. The MNA is especially applicable for people who live independently and for cooperative residents of nursing homes. The NRS is a valuable alternative for hospital patients and those unable to cooperate. Screening for malnutrition should be routine practice in the elderly population, especially for those at high risk for it like in hospitals and in nursing homes.

ESPEN guidelines for nutrition screening 2002.

AIM: To provide guidelines for nutrition risk screening applicable to different settings (community, hospital, elderly) based on published and validated evidence available until June 2002. NOTE: These guidelines deliberately make reference to the year 2002 in their title to indicate that this version is based on the evidence available until 2002 and that they need to be updated and adapted to current state of knowledge in the future. In order to reach this goal the Education and Clinical Practice Committee invites and welcomes all criticism and suggestions (button for mail to ECPC chairman).

Nutritional and clinical evaluation of a modified soy protein with covalently bound branched-chain amino acids in cirrhotic sprague-dawley rats.

Several studies suggested that branched-chain amino acids (BCAA) improve plasma amino acid imbalance as well as protein metabolism in patients with cirrhosis. However, commercial formulas supplemented with free BCAA have their limitations. We evaluated a modified soy protein diet with covalently bound BCAA (diet M) by comparing it with diets based on casein (diet C) or Hepatic Aid II (diet H; commercial formula) as protein sources. After 3 weeks of bile duct obstruction, 24 Sprague-Dawley rats divided into three groups received diets with 9% (w/w) protein/amino acids for 7 days. Nutritional and clinical parameters were determined. Nitrogen balance and weight gain (g)/protein intake (g) with diet M (0.19 +/- 0.31 and 1.33 +/- 1.43 g, respectively) were significantly higher (p < 0.05) than with diet H (-0.34 +/- 0.20 and -0.34 +/- 1.11 g), but comparable to those with diet C (0.04 +/- 0.38 and 0.20 +/- 0.93 g). Animals on diet M had a significantly (p < 0.05) increased plasma BCAA:aromatic amino acid ratio (1.8 +/- 0.3) as compared with those on diets H (1.3 +/- 0.1) and C (0.8 +/- 0.0). There were no significant differences in organ weight or liver function among the groups. We conclude that the BCAA-modified protein is an attractive option in the nutritional support of patients having cirrhosis.

Incidence of nutritional risk and causes of inadequate nutritional care in hospitals.

BACKGROUND AND AIMS: Many patients in hospitals are undernourished and nutritional care is inadequate in most hospitals. The aim of this investigation was to gain insight into how this situation could be improved. METHODS: Seven hundred and fifty randomly selected patients were screened at admission in three hospitals and surveyed during their entire hospitalization. Each time a patient was not treated according to a clearly defined nutritional standard, the nurse responsible for the patient was interviewed about possible reasons according to preformed questionnaires. RESULTS: The investigators found that 22% of the patients were nutritionally at-risk, and that only 25% of these patients received an adequate amount of energy and protein. The departments had only screened for nutritional problems in 60% of the cases. Only 47% of the patients, who the departments judged to be at-risk patients, had a nutrition plan worked out, and only about 30% of the at-risk patients were monitored by the departments by recording of dietary intake and/or body weight. The main causes for inadequate nutritional care were lack of instructions to deal with these problems, and lack of basic knowledge with respect to dietary requirements and practical aspects of the hospital's food provision. Patient-related aspects and the system of food provision also contributed, but only to a small degree. CONCLUSIONS: These findings form the basis of the strategy to improve nutritional care in these hospitals.

Cerebral metabolism of ammonia and amino acids in patients with fulminant hepatic failure.

BACKGROUND & AIMS: High circulating levels of ammonia have been suggested to be involved in the development of cerebral edema and herniation in fulminant hepatic failure (FHF). The aim of this study was to measure cerebral metabolism of ammonia and amino acids, with special emphasis on glutamine metabolism. METHODS: The study consisted of patients with FHF (n = 16) or cirrhosis (n = 5), and healthy subjects (n = 8). Cerebral blood flow was measured by the 133Xe washout technique. Blood samples for determination of ammonia and amino acids were drawn simultaneously from the radial artery and the internal jugular bulb. RESULTS: A net cerebral ammonia uptake was only found in patients with FHF (1.62 +/- 0.79 micromol x 100 g(-1) x min(-1)). The cerebral glutamine efflux was higher in patients with FHF than in the healthy subjects and cirrhotics, -6.11 +/- 5.19 vs. -1.93 +/- 1.17 and -1.50 +/- 0.29 micromol x 100 g(-1) x min(-1), respectively (P < 0.05). Patients with FHF who subsequently died of cerebral herniation (n = 6) had higher arterial ammonia concentrations, higher cerebral ammonia uptake, and higher cerebral glutamine efflux than survivors. Intervention with short-term mechanical hyperventilation in FHF reduced the net cerebral glutamine efflux, despite an unchanged net cerebral ammonia uptake. CONCLUSIONS: Patients with FHF have an increased cerebral glutamine efflux, and short-term hyperventilation reduces this efflux. A high cerebral ammonia uptake and cerebral glutamine efflux in patients with FHF were associated with an increased risk of subsequent fatal intracranial hypertension.

Effects of high-volume plasmapheresis on ammonia, urea, and amino acids in patients with acute liver failure.

OBJECTIVE: In acute liver failure (ALF), urea production is severely impaired, and detoxification of ammonia by glutamine synthesis plays an important protective role. The aim of this study was to examine the effects of therapeutic high-volume plasmapheresis (HVP) on arterial concentrations and splanchnic exchange rates of ammonia, urea, and amino acids-in particular, glutamine. METHODS: A quantity of 8 L of plasma was exchanged over the course of 7 h in 11 patients with ALF after development of hepatic encephalopathy grade III-IV. Splanchnic exchange rates of ammonia, urea, and amino acids were measured by use of liver vein catheterization. RESULTS: HVP removed ammonia and glutamine at a rate of 1 micromol/min and 27 micromol/min, respectively. Arterial ammonia decreased from 160 +/- 65 to 114 +/- 50 micromol/L (p < 0.001). In contrast, arterial glutamine was only minimally changed from 1791 +/- 1655 to 1764 +/- 1875 micromol/L (NS). This implied that the rate of systemic glutamine synthesis was increased by 27 micromol/min. Splanchnic exchange rates (before vs after HVP) were as follows: for ammonia, -93 +/- 101 versus -70 +/- 80 micromol/min (NS); urea-nitrogen, 0.08 +/- 1.64 versus -0.31 +/- 0.45 mmol/min (NS); alanine, -73 +/- 151 versus 12 +/- 83 micromol/min (p < 0.05); and glutamine: 132 +/- 246 versus 186 +/- 285 micromol/min (NS), with negative values denoting release. CONCLUSIONS: Arterial ammonia decreased during HVP in patients with ALF. The data suggest that this effect of HVP could be explained by increased hepatic urea synthesis and possibly by increased glutamine synthesis in muscle tissue.

Splanchnic metabolism of fuel substrates in acute liver failure.

BACKGROUND/AIMS: This study aimed to characterize the exchange of fuel substrates in the splanchnic circulation in acute liver failure. METHODS: Liver vein catheterization was used in 22 patients with acute liver failure after development of hepatic encephalopathy grade III-IV Healthy controls, patients with cirrhosis and patients with acute on chronic liver disease were also studied. RESULTS: In acute liver failure there was splanchnic removal of glucose (0.21+/-0.44 mmol/min), release of lactate (0.34+/-0.37 mmol/min), pyruvate (0.08+/-0.06 mmol/min) and ketone bodies (0.04+/-0.02 mmol/min), while extraction of amino acids and free fatty acids was insignificant. In the acute liver failure group, a normal hepatic venous oxygen saturation (0.69+/-0.12) and normal pyruvate/lactate ratio suggested absence of hypoxia even though the acetoacetate/beta-hydroxybutyrate ratio was decreased. Only in the acute liver failure group did the measured splanchnic oxygen content difference exceed what could be accounted for even by hypothesizing complete oxidation of all extracted blood-borne fuel substrates; oxidation of endogenous substrates may be quantitatively important in this condition. CONCLUSION: Acute liver failure was associated with a state of accelerated glycolysis in the splanchnic region, leading to release of lactate in the absence of splanchnic hypoxia.

[Clinical nutrition in Danish hospitals. A questionnaire study among physicians and nurses]. / Klinisk ernaering på danske hospitaler. En spørgeskemaundersøgelse blandt laeger og sygeplejersker.

Specific nutrition standards have now been developed by the Joint Commission on Accreditation of Healthcare Organizations (JCAHO). We investigated the use of clinical nutrition in Danish hospitals and compared it with the standards of JCAHO by doing a questionnaire-based investigation among doctors and nurses randomly selected in 40 hospitals. Overall, 857 (43.4%) responded to the questionnaire (doctors: 395, nurses: 462). Forty percent found it difficult to identify risk-patients, and 52% needed specific screening tools. Eighty-four percent found that a nutrition plan should be described in the patient record, but 39% found it difficult to set up an individual plan, and 79% expressed a need for specific guidelines. The use of clinical nutrition in Danish hospitals did not fulfill the standards for nutrition support according to the criteria established by JCAHO. Special efforts should be aimed at education, specific screening tools and introduction of guidelines in clinical nutrition.

Splanchnic and leg exchange of amino acids and ammonia in acute liver failure.

BACKGROUND & AIMS: In patients with acute liver failure, hyperammonemia is associated with cerebral herniation. We examined the splanchnic and leg exchange of amino acids, urea, and ammonia in such patients. METHODS: Bedside liver vein catheterization was used in 22 patients after development of hepatic encephalopathy grades III-IV. Femoral venous blood was sampled in 7 of these patients. RESULTS: Arterial amino acid concentration (8.1 +/- 4.1 mmol/L) was increased 4-fold above normal. Glutamine (2.4 +/- 1.8 mmol/L) and alanine (0.57 +/- 0.35 mmol/L) were by far the predominant amino acids exchanged in the splanchnic and leg circulation. In the splanchnic circulation, there was a net uptake of glutamine (241 +/- 353 micromol/min) and ammonia and alanine were released in an almost 1:1 stoichiometry (r(2) = 0.47; P < 0.001). In the leg, ammonia and alanine were removed and glutamine released. The leg ammonia concentration difference was correlated to that of glutamine (r(2) = 0.80; P = 0.008) and alanine (r(2) = 0.67; P = 0.03). CONCLUSIONS: Splanchnic metabolism of glutamine in combination with decreased hepatic function was responsible for the splanchnic release of ammonia and alanine. These processes were reversed in skeletal muscle. Stimulation of skeletal muscle metabolism of ammonia could be a important target for future treatment of patients with acute liver failure.

Clinical nutrition in danish hospitals: a questionnaire-based investigation among doctors and nurses.

Specific nutrition standards are now developed by the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) in order to improve the nutritional status in hospitalized patients. We investigated the use of clinical nutrition in Danish hospitals and compared it with the standards of JCAHO by doing a questionnaire-based investigation among doctors and nurses randomly selected in 40 hospitals including internal medicine, gastroenterology, oncology, orthopedic departments and intensive care units (ICU).Overall, 857 (43.4%) responded to the questionnaire (doctors: 395, nurses: 462). Seventy-seven percent stated that nutritional assessment ought to be performed on admission, but only 24% stated that it was a routine procedure. Forty percent found it difficult to identify risk-patients, and 52% needed specific screening tools. Twenty-two percent registered body weight in all patients, and 18% registered nutrient intake routinely. Eighty-four percent found that a nutrition plan should be described in the patient record, but 39% found it difficult to set up an individual plan, and 79% expressed a need for specific guidelines. Eighty-four percent would only accept a patient being on isotonic glucose and/or electrolyte infusion for < 5 days (42% for < 2 days), and 33% would only accept a weight loss of 5% before active nutrition was initiated. About 50% would be restrictive in supplying enteral or parenteral nutrition to patients with impaired liver or kidney function. Twenty-seven percent did not use active nutritional therapy at all. Seventy-six percent found that nutritional assessment should be performed during hospital stays, but only 23% monitored the nutritional status. Sixty-eight percent stated that responsibility should be assigned to one or more persons, but this was the case in only 20%The use of clinical nutrition in Danish hospitals did not fulfill the standards for nutrition support according to the criteria established by JCAHO. Special efforts should be aimed at education, specific screening tools and introduction of guidelines in clinical nutrition.

Cerebral herniation in patients with acute liver failure is correlated with arterial ammonia concentration.

Cerebral edema leading to cerebral herniation (CH) is a common cause of death in acute liver failure (ALF). Animal studies have related ammonia with this complication. During liver failure, hepatic ammonia removal can be expected to determine the arterial ammonia level. In patients with ALF, we examined the hypotheses that high arterial ammonia is related to later death by CH, and that impaired removal in the hepatic circulation is related to high arterial ammonia. Twenty-two patients with ALF were studied retrospectively. In addition, prospective studies with liver vein catheterization were performed after development of hepatic encephalopathy (HE) in 22 patients with ALF and 9 with acute on chronic liver disease (AOCLD). Cerebral arterial-venous ammonia difference was studied in 13 patients with ALF. In all patients with ALF (n = 44), those who developed CH (n = 14) had higher arterial plasma ammonia than the non-CH (n = 30) patients (230 +/- 58 vs. 118 +/- 48 micromol/L; P <. 001). In contrast, galactose elimination capacity, bilirubin, creatinine, and prothrombin time were not different (NS). Cerebral arterial-venous differences increased with increasing arterial ammonia (P <.001). Arterial plasma ammonia was lower than hepatic venous in ALF (148 +/- 73 vs. 203 +/- 108 micromol/L; P <.001). In contrast, arterial plasma ammonia was higher than hepatic venous in patients with AOCLD (91 +/- 26 vs. 66 +/- 18 micromol/L; P <.05). Net ammonia release from the hepatic-splanchnic region was 6.5 +/- 6. 4 mmol/h in ALF, and arterial ammonia increased with increasing release. In contrast, there was a net hepatic-splanchnic removal of ammonia (2.8 +/- 3.3 mmol/h) in patients with AOCLD. We interpret these data that in ALF in humans, vast amounts of ammonia escape hepatic metabolism, leading to high arterial ammonia concentrations, which in turn is associated with increased cerebral ammonia uptake and CH.