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Background/purpose: An increase in free radical activity has been observed in patients suffering from a variety of illnesses and has been correlated with disease severity. Free radical production is increased by the administration of total parenteral nutrition (TPN) and may be linked to its adverse effects. Some of the complications of TPN can be ameliorated by partial enteral feeding. The aim of this study was to investigate free radical activity during critical illness and during the administration of parenteral nutrition., Methods: Three groups of surgical infants were studied: (1) control infants (n = 8) before minor surgery, (2) stable infants on the ward recovering from a major operation (n = 24), (3) critically ill infants in the neonatal intensive care unit (NICU, n = 28). Fourteen patients in the ward and 17 patients in NICU were receiving parenteral nutrition. Of the 31 patients on TPN, 9 were also receiving minimal enteral feeding (3% to 24% of total calorie intake). Plasma malondialdehyde (MDA), an index of free radical activity, was measured in all 60 infants. The Paediatric Risk of Mortality (PRISM) score was obtained on NICU patients. The cytokines tumor necrosis factor (TNF-alpha) and interleukin 6 (IL-6) were measured in 25 patients., Results: Plasma MDA was significantly higher in (1) the stable patients on the ward compared with control patients (P < .001) and (2) patients in NICU compared with stable patients in the ward (P < .001). Parenteral nutrition was associated with higher levels of plasma MDA both in stable patients in the ward and critically ill infants in NICU. There was no correlation between the PRISM score and MDA. In patients not receiving TPN there is a correlation between MDA and TNF-alpha (r = 0.54, P = .02) and between MDA and IL-6 (r = 0.74, P = .001). The level of free radical activity in patients on TPN is not changed by partial enteral feeding., Conclusions: Critical illness causes a rise in free radical production. Parenteral nutrition causes a significant elevation in free radical activity in both stable infants in the ward and critically ill infants in NICU. The addition of minimal enteral feeding to parenteral nutrition does not reduce free radical activity. We hypothesize that the parenteral nutrition solution directly initiates free radical production.

Background/purpose: Increased oxygen-derived free radical activity has been reported during total parenteral nutrition (TPN) in infants and has been specifically linked to the fat infusion. The aim of this study was to test the hypothesis that during TPN, oxygen-derived free radical production can be reduced by increasing the utilisation of fat., Methods: In experiment A (17 patients) the fat infusion was kept constant (3 g/kg/d) and the carbohydrate infusion was changed from 18 g/kg/d on day 1 to 10 g/kg/d on day 2. In experiment B (six patients) the carbohydrate infusion remained constant and the fat infusion was changed from 3 g/kg/d on day 1 to 0 g/kg/d on day 2. Fat utilisation was measured by indirect calorimetry. Plasma malondialdehyde, an index of lipid peroxidation resulting from increased oxygen-derived free radical activity, was measured by a colorimetric assay., Results: In both experiments there was no significant change between the two study phases in oxygen consumption, carbon dioxide production, and resting energy expenditure demonstrating that the patients were metabolically stable. In experiment A there was a significant (P = .0005) increase in fat utilisation and a significant (P = .009) decrease in malondialdehyde (MDA) concentration between the two phases. In experiment B there was also a significant (P = .007) decrease in MDA concentration. The decrease in MDA concentration was similar between the two experiments., Conclusions: It is not necessary to stop the infusion of fat to reduce free radical production. Promoting fat utilisation by reducing the carbohydrate-fat ratio of the TPN reduces free radical activity to a similar extent as fat exclusion. These findings have important implications for the composition of TPN.

Pancreatic exocrine and endocrine function was assessed in seven patients 1 to 2 years after 95% pancreatectomy (group A) and three patients 9 to 11 years after 75% pancreatectomy (group B). In all cases surgery was undertaken for the treatment of hyperinsulinism and the histologic diagnosis was nesidioblastosis. The activities of pancreatic enzymes and bicarbonate concentrations were generally normal in group B, but were reduced in approximately half the children in group A. One child in group A had significant exocrine failure and poor weight gain. Blood glucose levels and fasting insulin levels were normal during a standard glucose tolerance test in all of the group B patients. One had a low fasting blood glucose level. In the group A patients three had low fasting glucose levels and one a frankly diabetic glucose tolerance test. C peptide and insulin levels were comparable but inappropriate insulin levels were noted in one patient, suggesting that the control of glucose-stimulated insulin release may remain abnormal. The results suggest that pancreatic function is not seriously impaired in the majority of patients 1 to 2 years after 95% pancreatectomy and that it is comparable to that noted in 75% pancreatectomy patients followed over a longer period of time.