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Prognostic factors. Total parenteral nutrition may cause more injury in infants small for gestational age or with bronchopulmonary dysplasia Pediatr Dev Pathol ; Fibrosis progresses with increased length of TPN use. Microscopic histologic description. Microscopic histologic images.
Contributed by Raul S. Raul S. Contributed by Anthony Chan, M. Sample pathology report. Other possibilities include fatty liver disease potentially alcoholic. Different policies of prevention were proposed to decrease the incidence and the severity of TPN AC, namely, shortened TPN course and early initiation of enteral feeding.
The components of TPN also contribute to the pathogenesis of TPN-AC, including taurine and carnitine deficiency, aluminum and manganese toxicity, and oxidant imbalance. Although previous studies reported the incidence of TPN-AC and described the potential contributing factors to its pathogenesis, very few tried to look at the predictive risk factors of TPN-AC for possible prevention.
Excluded were infants who had significant congenital malformations, died in the first 10 days of life or had other confirmed causes of cholestasis other than TPN-AC. The components of TPN were adjusted and individualized according to the patient's clinical condition. For the sake of analysis, the patients were divided into two groups: Cholestasis and noncholestasis groups, based on the value of direct serum bilirubin.
The possible risk factors collected were gestational age GA , birth weight Bwt , gender, Apgar score AS , TPN duration, age at initial feeding, age at full feeds, episodes of culture-confirmed sepsis, umbilical arterial and venous catheterization, bronchopulmonary dysplasia BPD , patent ductus arteriosus PDA , and necrotizing enterocolitis NEC. Bacterial sepsis was defined as positive blood, cerebrospinal fluid, or urine culture. The age at initial feeding was defined as the age of the first enteral feed.
Statistical analysis was performed using SPSS version Chi-square analysis was used to compare categorical variables, whereas independent sample t test was used to compare continuous variables among the two groups.
Multivariate logistic regression analysis was performed to calculate statistical significance of the risk factors as covariates. Receiver—operating characteristic ROC curve was used to determine optimal cutoff points for the significant risk factors and to calculate their sensitivity and specificity. Forty-two patients were excluded; 37 subjects expired in the first 10 days of life, 2 patients for missing charts and 3 neonates with significant congenital malformations.
The remaining patients were included and their medical records were reviewed. None of the infants with cholestasis developed end-stage liver disease. The potential risk factors for cholestasis in preterm infants with and without TPN-AC are shown in table 1. The mean GA was The potential risk factors were then fed into a multivariate logistic regression model.
Receiving TPN for more than the cutoff point of The incidence of cholestasis in the study population was found to be The incidence of cholestasis was also affected to a lesser extent by gestational age and AS [ Table 3 ]. These findings are supported by an earlier study, which has shown that the younger the gestational age, the higher is the direct bilirubin concentration. There are some limitations of our study. It is an uncontrolled retrospective study with all its known drawbacks.
Also, the study had been performed on a cohort of patients approximately 10 years old. Although no significant advances have been made in this period with regard to TPN-AC and its causation, it is difficult to rule out any possible time effects. Administering artificial nutrition in the first 24 hours after admission seems to have a protective effect. Artificial nutrition support is part of the standard of care in critically ill patients [ 1 ].
Some of these patients have sepsis or systemic inflammatory response syndrome, which produce hypermetabolism, accelerated lipolysis, insulin resistance, and protein catabolism.
These phenomena, associated with the lack of oral intake, can lead to malnutrition. Artificial nutrition usually does not reverse these metabolic derangements but can decrease the depletion of the lean body mass [ 2 ].
Hepatobiliary complications related to artificial nutrition have been widely reported, particularly in patients receiving total parenteral nutrition TPN , and less frequently in patients receiving enteral nutrition EN [ 3 ]. There are many potential causes of liver dysfunction LD related to artificial nutrition, but the etiology is unclear and there are few data on the prevalence in critically ill patients.
Moreover, these patients can present hepatic dysfunction as part of the multiple organ failure syndrome [ 4 ]. The aim of this study was to assess the prevalence of hepatobiliary complications related to artificial nutrition, the risk factors associated with these complications, and their influence on the prognosis in critically ill patients. This study was designed as a multicenter prospective cohort study of incidence of LD in patients admitted to any of the 40 participating intensive care units ICUs from tertiary hospitals in Spain between 1 March and 15 April Patients were enrolled consecutively when the treating physician expected them to need artificial nutrition for five days or more.
The protocol and definitions of LD were established previously in a meeting with the participants. The institutional review board of each participating hospital approved the study. Informed consent was waived according to these boards and Spanish law. Our funding sources had no role in the acquisition, analysis, or interpretation of data or in the submission of this report. Patients entered in the study were followed prospectively until hospital discharge or 28 days after ICU admission to check mortality at that time.
The diagnosis of sepsis or septic shock on admission was made according to previously published criteria [ 6 ]. Septic shock was defined as arterial hypotension induced by sepsis, which persists in spite of the adequate replacement of fluids and associated with hypoperfusion and organ dysfunction. Exclusion criteria were age of less than 18 years, expected survival of less than 24 hours, or previous cardiopulmonary resuscitation.
The clinician responsible for the patient chose the type of nutrition, the administration route, and the type of diet following the published recommendations [ 8 ].
The protocol was discussed in previous meetings with the researchers. The use of early artificial nutrition was encouraged to the participants. EN was recommended as the preferred route for feedings if the patient's gastrointestinal system was preserved.
Also, clinicians were allowed to administer EN for as long as the gastrointestinal function was recovered. In both cases, the amount of calories was limited to the planned caloric intake. TPN was administered through a central venous catheter, with the use of 'all in one' ternary mixtures, by means of a continuous pump infusion.
The TPN bag was replaced every 24 hours. EN was administered through a nasogastric or nasojejunal tube at the doctor's discretion and continuously through an infusion pump in accordance with a previously established protocol [ 9 ]. The systems used for EN administration were replaced at least once a day, and the feeding tube was flushed on a shift basis three times a day with 20 ml of distilled water. Malnutrition was assessed by means of the Subjective Global Assessment [ 10 ].
Enteral diets used in the EN group were always polymeric. Once the nutrition had been started, the following parameters were recorded: blood sugar and glucosuria every six hours; urea, creatinine, sodium, potassium, and chlorine every 24 hours; and a weekly analysis that included cholesterol, triglycerides, phosphorus, calcium, magnesium, and osmolarity.
Liver function tests total and direct bilirubin, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl-transferase, and alkaline phosphatase , prothrombin time, and international normalized ratio INR were recorded on admission and twice a week on Tuesday and Friday.
The withdrawal of artificial nutrition was defined as the definitive suppression of artificial nutrition, and suspension was defined as a temporary cancellation not longer than 24 hours. LD was diagnosed when any of the previously defined enzymatic alterations were present.
The diagnosis of acalculous cholecystitis was based on clinical criteria and ultrasound. Liver biopsies were not carried out in this study. The newly created database was centralized and managed by the main researchers.
Any doubts about application of the protocol were discussed with the participants, and the main researchers made the final decision. Once the time of the study was over, the database was closed down. The analysis was blind to the type of nutrition used. The quantitative values were analyzed for normality. The values with normal distribution were compared using the Student's t test, and the others using non-parametric tests Kruskall-Wallis test. Statistical significance was set at p less than 0.
The quantitative data were expressed as a median and interquartile IQ range, and the qualitative data were expressed in absolute values and percentages. The multivariate analysis for LD was carried out by means of a 'stepwise forward' logistical regression model with the most important demographic variables and those that reached statistical significance in the univariate analysis.
Time free of LD was analyzed using the Kaplan-Meyer test. Three thousand four hundred and nine patients were admitted during the study. Seven hundred and fifty-six patients received nutrition in some form, whether TPN or EN, but 31 were excluded and were studied Table 1. Four hundred and eighty-eight were men and were women. Three hundred and three patients Two hundred and eight patients had sepsis on admission; of these patients, had septic shock.
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