Weeks Of Total Parenteral Nutrition Research Articles

Early predictors of liver injury in patients on parenteral nutrition.

Parenteral nutrition-associated liver disease (PNALD) is diagnosed after at least 2 weeks of total parenteral nutrition (PN). However, its symptoms may occur early during PN. The aim of this study was to determine the early biochemical predictors of PNALD. This cross-sectional retrospective study included 160 patients on total parenteral nutrition. The clinical and laboratory data collected during parenteral nutrition were analyzed. Patients were assessed before the onset, on the 2nd, 7th and on the 14th day of PN according to the definition of PNALD and in search for predominant liver function tests findings. Out of 160 patients, 21 fulfilled the laboratory criteria of PNALD on the 14th day of PN. In the group of patients with PNALD, 14 met these criteria on the 7th day of PN. In multivariate logistic analyses the laboratory criteria of PNALD met on the 7th day of PN (OR=5637; 95%Cl: 1.162-33.578; p-value=.039) were found to be of predictive value for PNALD on the 14th day. In PNALD group the 1.5-fold elevation of GGTP activity above upper limit of norm was the most prominent laboratory finding during the fourteen-day course of PN. The percentage of patients with 1.5-fold increased activity of GGTP varied in time from 76.2% to 95.2% on the 2nd and 14th day of PN, respectively. PNALD may be predicted by liver function monitoring after seven days of PN.

The Impact of Glucose-Based or Lipid-Based Total Parenteral Nutrition on the Free Fatty Acids Profile in Critically Ill Patients.

Introduction: Our study aim was to assess how the macronutrient intake during total parenteral nutrition (TPN) modulates plasma total free fatty acids (FFAs) levels and individual fatty acids in critically ill patients. Method: Adult patients aged 18–80, admitted to the intensive care unit (ICU), who were indicated for TPN, with an expected duration of more than three days, were included in the study. Isoenergetic and isonitrogenous TPN solutions were given with a major non-protein energy source, which was glucose (group G) or glucose and lipid emulsions (Smof lipid; group L). Blood samples were collected on days 0, 1, 3, 6, 9, 14, and 28. Results: A significant decrease (p < 0.001) in total FFAs occurred in both groups with a bigger decrease in group G (p < 0.001) from day 0 (0.41 ± 0.19 mmol∙L−1) to day 28 (0.10 ± 0.07 mmol∙L−1). Increased palmitooleic acid and decreased linoleic and docosahexaenoic acids, with a trend of increased mead acid to arachidonic acid ratio, on day 28 were observed in group G in comparison with group L. Group G had an insignificant increase in leptin with no differences in the concentrations of vitamin E, triacylglycerides, and plasminogen activator inhibitor-1. Conclusion: Decreased plasma FFA in critically ill patients who receive TPN may result from increased insulin sensitivity with a better effect in group G, owing to higher insulin and glucose dosing and no lipid emulsions. It is advisable to include a lipid emulsion at the latest from three weeks of TPN to prevent essential fatty acid deficiency.

Encapsulating peritoneal sclerosis

Would you recognize this condition?

Lebensbedrohliche Lactatacidosen bei totaler parenteraler Ernährung: Therapieerfolg mit Thiamin

Two patients, 37 and 44 years old, respectively, developed severe metabolic acidosis after abdominal surgery which was followed by three weeks of total parenteral nutrition. Septicaemia, peritonitis or hypoxia were excluded as possible causes. Both patients had very high serum lactate concentrations (24.3 and 22.8 mmol/l, respectively). Conventional treatment with buffer agents was unsuccessful. Because vitamin B1 deficiency was suspected, two doses of 400 mg thiamine were administered. In both patients the extreme lactic acidosis disappeared immediately after the injections. Both patients were later discharged without any symptoms.

Quilotórax neonatal: etiología, evolución y respuesta al tratamiento

To investigate the aetiology, clinical course and response to treatment of neonatal chylothorax.Prospective study over a 2-year period in a neonatal intensive care unit of a tertiary university hospital. All newborns followed a predefined therapeutic protocol that included the sequential administration of total parenteral nutrition (TPN), octreotide and surgery. The influence of aetiology on outcome and response to treatment was investigated.The study included 22 newborns. Surgery for congenital heart disease (CHD) (n = 14) and congenital diaphragmatic hernia (n = 4) were the most common aetiologies. The incidence of chylothorax in these aetiological groups was 11.2 % (95 % CI 5.7-16.8 %) and 26.6 % (95 % CI 4.3-40 %), respectively. Medical treatment was successful in 17 patients. Five of the 10 patients who did not respond to TPN were successfully treated with octreotide; none of the patients in whom octreotide failed responded to the subsequent 3 weeks of TPN. No side-effects were observed during octreotide administration. No significant association between aetiology and response to treatment was found, although all 4 patients who ultimately required surgery were in the CHD group. All patients had complications attributable to chylothorax. Five patients died during the 6 months of follow-up although mortality was never directly attributed to chylothorax.Most patients can be successfully managed with medical treatment but early surgery should be considered in patients who do not respond to medical treatment. Aetiology is the main determinant of mortality. Randomized controlled studies are needed to demonstrate the efficacy and adequate timing of application of each therapeutic intervention.

Successful Treatment of Congenital Chylous Ascites with Total Parenteral Nutrition

Congenital chylous ascites is a rare condition. It is predominantly idiopathic in etiology and presents a therapeutic challenge. A case of idiopathic congenital chylous ascites successfully treated with six weeks of total parenteral nutrition is described.

The effect of pre-operative total parenteral nutrition on energy-rich phosphates, electrolytes and free amino acids in skeletal muscle of malnourished patients with gastric carcinoma.

The effect of two weeks of total parenteral nutrition (TPN) on energy-rich phosphates, muscle water, electrolytes and free amino acids in skeletal muscle were determined in ten malnourished patients with gastric carcinoma. The total adenine nucleotide pool, phosphocreatine, creatine and glycogen were decreased before TPN, and only glycogen returned to normal after TPN compared with controls. Total muscle water and the intramuscular concentrations of sodium and chloride were initially increased and were not influenced by TPN. The total non-essential amino acids in muscle were decreased by 9 per cent, mainly due to a 15 per cent decrease in glutamine. The concentrations of free amino acids in muscle were not affected by two weeks of TPN. This study demonstrates disturbances in energy, water and amino acid metabolism in skeletal muscle of malnourished patients with gastric carcinoma, and that two weeks of TPN could not normalize these changes, except in the case of glycogen. The reason for this might be enzyme abnormalities due to adaptation to energy or protein deficit. A longer period of refeeding might therefore be necessary to improve peripheral metabolism in these patients.

Eating after mild pancreatitis

See article in J. Gastroenterol. Hepatol. 2005; 20: 1385‐1389. ‘Resting the pancreas’ has been a central dogma in the early management of acute pancreatitis. Every patient admitted with acute pancreatitis was made strictly ‘nil by mouth’ and had a naso-gastric tube to empty the stomach. When the patient was deemed to have severe pancreatitis, nutritional support was provided by total parenteral nutrition. Even a decade ago John Ranson reviewed the role of nutritional support in acute pancreatitis and underlined the primacy of parenteral feeding. 1 He stated that jejunal feeding was ‘not a therapeutic option early in the course of pancreatitis because of the associated paralytic ileus’. The avoidance of enteral feeding was also supported by the belief that stimulation of pancreatic exocrine secretion would exacerbate the severity of acute pancreatitis. How things have changed. In the absence of direct clinical evidence to support the concept of pancreatic rest, many patients are now allowed to drink limited clear fluids by mouth as soon as there is resolution of abdominal pain. There is no evidence to show that the naso-gastric tube alters the course of pancreatitis. Randomized trials have now defined best practice as the commencement of enteral nutrition (EN) in all patients with predicted moderate to severe acute pancreatitis and as soon as they are hemodynamically stable. 2 A naso-jejunal tube, often placed by the radiologist using fluoroscopic guidance, best delivers EN. Compared with total parental nutrition (TPN), the advantages of EN are safety, ease of administration, cost, and it is associated with lower markers of inflammation and pancreatitis severity. Parenteral nutrition is still sometimes required, but in a secondary role when the full calorie and protein requirements cannot be tolerated by the enteral route. It was no surprise to find that 2 weeks of total parenteral nutrition in patients with acute pancreatitis only managed to preserve body composition, and could only improve total body protein in the absence of sepsis or recent surgery. 3

Total Parenteral Nutrition (TPN) via Peripheral Veins in Neonatal Surgical Patients

【Parenteral nutrition has been an essential part of postoperative care of neonates requiring major surgery who are unable to tolerate enteral feeding for long periods during the postoperative period. However, TPN via central venous catheters(central TPN), used in increasing trend, still presents significant morbidity. To find out whether TPN via peripheral veins(peripheral TPN) could be used as a viable alternative for postoperative parenteral nutrition in neonates, a clinical study was carried out by a retrospective analysis of 53 neonates subjected to peripheral TPN for more than 7 days after surgery. Operations consisted of procedures for esophageal atresia with tracheoesophageal fistula, gastroschisis and omphalocele. Surgery was performed at the Division of Pediatric Surgery, Department of Surgery, Hanyang University Hospitall, from 1983 to 1994. The mean total duration of TPN was 13.3 days (range; 7-58 days), the average daily total fluid intake was 117.6 ml/kg during TPN and 158.6 ml/kg during subsequent oral feeding. The average daily total calorie intake was 57.7 kcal/kg during full strength TPN and 101.3 kcal/kg during subsequent oral feeding. The mean urine output was maintained at 3.5 ml/kg/ hour during TPN and at 3.6 ml/kg/hour during subsequent oral feeding. The increment of body weight observed during TPN was 132 g in TEF, 53 g in gastroschisis and 3 g in omphalocele patients, while loss of body weight was not observed. The mortality rate was 5.7 %(3/53) and was related to the underlying congenital anomalies, not the TPN. The most common complication of peripheral TPN observed was laboratory findings suggestive of liver dysfunction in 23 cases(43.4 %) with no significant clinical symptom or signs in any case, transient pulmonary edema in one case, and generalized edema in one case. None of the major complications usually expected associated with central TPN were observed. The result of this study suggest that peripheral TPN can be used for adeguate postoperative nutritional support in neonates requiring 2 to 3 weeks of TPN.】

Long-term total parenteral nutrition and cholecystostomy tube in a rabbit model surgical procedure: management and preliminary results.

A rabbit model for long-term total parenteral nutrition (TPN), specially provided with cholecystostomy tube, was designed to investigate further aspects of TPN-associated cholestasis (TPN-AC). Modified surgical procedures concerning vascular access, cholecystostomy tube implantation and authors' original modalities for prolonged infusion management in the rabbit were used. Continuous TPN was performed in 30 young rabbits. Five animals died during the experiment (16.6%) and were excluded from final evaluation. Twenty-five rabbits were successfully maintained on continuous TPN for 28 days without restraint, having a cholecystostomy tube implanted 1 week after initiation of TPN. The collection of blood samples and daily parenteral administration of drugs were simply accomplished via a central venous catheter. At the same time the cholecystostomy tube enabled us to perform daily bile sampling. Saline irrigation of the biliary tree could be carried out in conscious animals maintained on TPN. A 4-week duration of TPN in this rabbit model made it possible for the first time to accomplish serial liver biopsies in order to verify the evolution of histologic changes in TPN-related hepatic dysfunction and possible effects of surgical and medical treatment. A preliminary analysis of operative findings and histology was carried out. An enlarged gallbladder containing hyperviscous bile was found in 80% of the animals 1 week after initiation of TPN. At this time it was possible to observe the first histologic changes consistent with TPN-associated hepatic disease, such as moderate to severe hepatocyte degeneration and portal inflammation. Biliary sludge was seen after 3 weeks of TPN in 70% of the rabbits, as well as a subsequent progression of TPN-associated histologic findings. Portal fibrosis and fatty liver degeneration occurred in 50% of the rabbits and bile duct proliferation in all animals. After 4 weeks of TPN (at autopsy) gallstones were found in 20% of TPN animals, as well as further progression of bile duct proliferation and fibrosis. Our first experiences with this model and preliminary results suggest that this concept offers new possibilities for further elucidation of TPN-associated hepatic dysfunction.

Lymphocyte and granulocyte function in nutritionally depleted patients. The effect of 2 weeks of total parenteral nutrition

Parenteral nutrition has been reported to restore impaired immune function in nutritionally depleted patients. Lymphocyte and granulocyte function were studied before and after 2 weeks of total parenteral nutrition (TPN) in 9 depleted patients, 5 with gastrointestinal cancer and 4 with benign gastrointestinal disorders. The ability of purified blood lymphocytes to incorporate 14C-labelled thymidine spontaneously and following mitogenic and antigenic stimulation was studied. Before TPN spontaneous lymphocyte activity was significantly increased and mitogen and antigen responsiveness significantly decreased in comparison to healthy controls. These abnormalities were more pronounced in patients with malignant disorders while the remaining patients showed a moderate impairment. No improvement in lymphocyte capacity was observed following 2 weeks of TPN. Granulocyte function measured as chemotaxis, phagocytosis, NBT-reduction and bactericidal capacity did not differ significantly between patients and controls and no changes were seen following nutritional treatment. These findings support the concept that the underlying disease and/or other factors rather than the secondary nutritional depletion are the main reasons for immune impairment. Furthermore, no immunomodulating effects of lipid emulsions on lymphocyte and granulocyte function, under these experimental conditions, were apparent.

Chylous ascites: total parenteral nutrition as primary therapeutic modality

A female infant with Down syndrome and congenital chylous ascites presented at birth with respiratory distress secondary to marked abdominal distension. Total parenteral nutrition (TPN) and paracentesis were the primary therapeutic modality. On hyperalimentation, however, ascites initially recurred, requiring additional paracenteses to improve respiratory distress. The chylous ascites, lymphopenia and hypoalbuminemia were relieved after 10 weeks of TPN administration. We recommend a long-term course (10 weeks) of TPN before an exploratory laparatomy and possible surgical intervention are considered.

Energy Expenditure and Substrate Utilization in the Course of Renutrition of Malnourished Children

Energy expenditure (EE) and substrate utilization in the course of renutrition of malnourished children is not well understood in children receiving total parenteral nutrition (TPN). The aim of this study was to evaluate, during protein-glucose renutrition, EE and substrate utilization and the relationship between EE and growth and/or protein metabolism. Seven malnourished children were studied during the first 3 weeks of TPN. Weight-for-height = 81.4 +/- 8.0%, with an initial weight of 4.5 +/- 3.3 kg. Caloric support was progressively increased according to a preestablished protocol. Every 7 days the following were determined: (1) EE at 3 different 3-hour intervals per day using an open circuit indirect calorimetric system, (2) anthropometrically defined fat free mass (FFM), and (3) 24-hour urinary 3-methylhistidine (3-M-His) and protein balance. Compared to initial values, EE increased 13% at day 7 and 36% at day 14. A negative relationship was found between the amount of perfused glucose and lipid utilization (r = -0.82; p less than 0.0001). EE per kilogram of total body FFM changes during renutrition were more than EE changes per kilogram of total body weight. There was a relationship between EE and weight gain (r = 0.62; p less than 0.005) and a positive relationship between EE and protein gain (r = 0.48; p = 0.012) and 3-M-His excretion (r = 0.51; p less than 0.026).(ABSTRACT TRUNCATED AT 250 WORDS)

Total body potassium, fat and water during total parenteral nutrition in Crohn's disease

The body composition was studied by measurement of body weight (BW) and total body potassium (TBK), fat and water in 13 patients with Crohn's disease (CD), who were given altogether 18 courses of total parenteral nutrition (TPN) with nil by mouth each lasting at least 3 weeks. At the start of TPN, one group of steroid-free patients displayed intracellular potassium depletion, as reflected by the ratio TBK/lean body mass (LBM) (group 1). Another group of steroid-free patients showed no depletion of intracellular potassium (group 2). The patients given prednisolone all showed intracellular potassium depletion and were assigned to a separate group (group 3). During the initial 19–44 days of TPN, TBK, LBM and BW increased in group 1. All patients with intracellular potassium depletion (groups 1 + 3) showed an increase in TBK and TBK/LBM during the initial 19–51 days of TPN. For steroid-free patients (groups 1 + 2) there were linear relationships between the rate of energy supply per kg LBM and the 24 h change in BW during the third and fourth weeks of TPN ( r = 0.79) and between the 24 h change inBW and LBM during the first 19–44 days of TPN ( r = 0.59). A steady state in BW was found on administering 53 kcal/kg LBM/24 h. It is concluded that CD patients with intracellular potassium depletion are likely to be improved in terms of TBK and TBK/LBM by at least 3 weeks of TPN as given in the present study. Steroid-free CD patients with intracellular potassium depletion are, moreover, likely to show an improvement in LBM by at least 3 weeks of TPN, and an increase in their BW during the initial 3–6 weeks of TPN will probably reflect an increase in LBM. The pre-TPN TBK/LBM ratio may be a predictor of the repletion rate of the LBM compartment during TPN of steroid-free wasted CD patients.

Therapeutic and diagnostic implications of acquired choledochal obstruction in infancy: Spontaneous resolution in three infants

Three infants aged 2 days to 11 weeks with conjugated hyperbilirubinenemia, had sonographically documented dilated common hepatic bile ducts, and echogenic material in the gallbladder. A 2-day-old infant, born to a diabetic mother, had none of the classic predisposing factors for cholelithiasis, and two infants had received total parenteral nutrition (TPN) and TPN plus furosemide. The first infant after receiving 4 1 2 weeks of TPN and furosemide, developed common duct obstruction with increasing bilirubin and hepatic duct caliber over a 12-day period. An operation was scheduled; however, on the following day the bilirubin dropped abruptly and surgery was canceled. The experience with this infant encouraged conservative management in two subsequent infants with similar clinical and sonographic findings. Spontaneous resolution occurred 9 days after the onset of common duct obstruction in one infant and after 16 days in the other.

The effect of metronidazole on TPN-associated liver dysfunction in neonates

The effect of metronidazole (MNZ) on hepatic dysfunction associated with total parenteral nutrition (TPN) in neonates was investigated. Neonates receiving TPN for more than 2 weeks were divided into three groups. In group 1, TPN was given alone, in group 2, 25 mg/kg/d of MNZ was administered intravenously for the first 2 weeks of TPN, and in group 3, 50 mg/kg/d of MNZ was given for the first 3 weeks of TPN. Several parameters of liver function tests (LFTs) during the first 4 weeks of TPN were compared among these three groups. There was no significant difference of these parameters between group 1 and group 2. Although there was no significant difference of alkaline phosphatase, γ-glutamyl transpeptidase, direct bilirubin, and total bile acid between groups 1 and 3, transaminase (glutamic oxaloacetic, glutamic pyruvic) of group 3 remained significantly lower than those of group 1. In conclusion, the administration of MNZ 50 mg/kg/d for 3 weeks, at least, prevented the elevation of transaminase during TPN in neonates, suggesting the possible involvement of intestinal anaerobic flora in the pathogenesis of TPN-associated liver dysfunction.

Serum cobalamins and cobalamin-binding proteins during total parenteral nutrition.

Levels of serum cobalamin and both saturated and unsaturated serum cobalamin-binding proteins (transcobalamin II and R-binders) were determined prospectively in 43 patients before and after 2 weeks of total parenteral nutrition (TPN). Nine patients showed subnormal serum levels of cobalamin but none of them had clinical signs of cobalamin deficiency. Serum cobalamin levels significantly declined after 2 weeks of TPN as did both saturated and unsaturated R-binder levels whereas transcobalamin II levels remained constant. Since cobalamin in serum is entirely bound to proteins, of which R-binders comprise 80-90%, the changes in R-binder levels will markedly influence serum cobalamin levels, in fact they adequately explain the short time fluctuations of serum cobalamin levels observed. It is argued that the changes in serum cobalamin levels may reflect a changed distribution of cobalamins over the various body compartments rather than decreased or increased body stores. Moreover, only cobalamin bound to transcobalamin II is delivered to the tissues. Therefore, serum cobalamin levels alone may inadequately reflect cobalamin availability in patients receiving TPN.

Serum concentration of folates during total parenteral nutrition in Crohn's disease

Folate status as evidenced by the fasting serum (S-) concentration of folates was determined in a consecutive series of 15 patients with Crohn's disease (CD) given total parenteral nutrition (TPN)—nil per os—for between 23 and 97 days (mean, 56 days). At introduction of TPN three patients displayed sub-normal S-folate levels—below 4.0 nmol/1—(group 1), whereas 12 patients recorded S-folates above 4.0 nmol/l (group 2). During the TPN each patient received one ampoule of water-soluble vitamins, including 0.2 mg of folic acia per 24 h. S-folates were normalised during the TPN in group 1 and maintained a level near the middle of the reference range (4–23 nmol/l) in group 2. It would thus appear that during 6–8 weeks of TPN the vitamin regimen studied, including 0.2 mg of folic acid per 24 h, is able to maintain the S-folate concentration within the reference range in CD patients with no evidence of folate deficiency and to prevent signs of folate deficiency in CD patients with an initially sub-normal S-folate concentration.

Urinary excretion of 3-methylhistidine as an index of protein nutrition in total parenteral nutrition.

In 39 healthy adult volunteers and nine patients receiving total parenteral nutrition (TPN), determinations were made of the urinary excretion of 3-methylhistidine (3-Mehis) to estimate the degree to which the urinary output of 3-Mehis reflects the status of protein nutrition. In 19 males and 10 females of the former group, measurements were made of the amount of 3-Mehis and of creatinine (Cr) in 24-hr urine samples. The urinary output of 3-Mehis was also measured in two subgroups of five healthy adult male subjects who were fed one of the two different diets prescribed: meat (M) and meat-free (F) diet. Furthermore, in one of these subgroups which was fed on F diet, the urinary output of 3-Mehis was measured both while the subject was kept at bed rest and while the subject was allowed to live a normal life. From these measurements the standard value was determined for the urine 3-Mehis level and the 3-Mehis/Cr ratio in 24-hr urine in healthy adult human subjects of both sexes. In nine patients maintained on TPN these indices of nutritional status were measured before and at 4 weeks of TPN. The time course of the indices was also investigated. The results obtained suggest that both the urinary output of 3-Mehis and the 3-Mehis/Cr ratio can provide a sensitive index of the status of protein nutrition.

Carnitine levels in skeletal muscle of malnourished patients before and after total parenteral nutrition

Carnitine is necessary for the transport of long-chain fatty acids across the mitochondrial membrane and it is derived from the diet and from endogenous synthesis from lysine and methionine. Of the body's carnitine pool, about 98% is located in skeletal muscle tissue. Skeletal muscle carnitine levels were determined in two groups of malnourished patients, eight patients with anorexia nervosa with a weight loss of 32.4% ± 1.8 (mean ± SEM) and six surgical patients with major gastrointestinal disorders and a weight loss of 15.2% ± 2.7. Their hepatic and kidney functions were normal. On admission, the muscle carnitine levels were 16.9 ± 4.0 μmol/g dry weight (mean ± SD) for the surgical patients and 20.8 ± 5.0 μmol/g dry weight for the anorexia nervosa patients, which corresponded to carnitine levels seen in healthy subjects. No statistical significance was found between the two groups. Total parenteral nutrition was given to the surgical patients for 2 weeks and to the anorexia nervosa patients for 3–5 weeks. No statistical difference in muscle carnitine levels was found in either group after nutritional support. These malnourished patients had no decreased muscle carnitine levels on admission and maintained them during several weeks of total parenteral nutrition.