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that a little bit further and examine exactly what the baby is getting with the fluids that were started and why it may be problematic that the baby was not initiated on early TPN. The fluids that were provided this baby, D10 in the UVC and D5W in the UAC, would provide about 22 cal/kg/day for this baby. That’s a very modest amount of energy and represents a glucose infusion rate of about 4 mg/kg/min. That means this baby would be catabolic because of the inadequacy of the energy provided. And in the absence of protein, as we see in both the Senterre article and the Radmacher articles that energy without protein will not place the baby in positive nitrogen balance. 1,2 So it is very important additionally to appreciate the relationship between early nutrition and severity of illness. In other words, because this baby was perceived as being so ill, the clinicians decided not to initiate the amino acids. This was a perception of illness, but as shown in the final paper that we reviewed, the paper from Ehrenkranz on how early nutrition mediates the influence of severity of illness on these babies, we learned that early nutrition, despite the baby being more ill, actually improves outcome, including prevention of morbidities and prevention of mortality. 3 MR. BUSKER: Doctor, let me ask you to speculate for us: is it possible that early TPN might have prevented both the nonoliguric hyperkalemia and the hyperglycemia in this infant? DR. ADAMKiN: It’s quite likely the answer to that is yes. We know that early amino acids have dramatically reduced the incidence of hyperglycemia and nonoliguric hyperkalemia in these extremely low birth weight infants. Early amino acids stimulate insulin activity and secretion of insulin to promote glucose tolerance. The insulin is necessary for transport of glucose into the cell and to prevent intracellular energy failure, which allows potassium to leak out of the cell. That is mediated through an enzyme called sodium potassium ATPase. This enzyme regulates the maintenance of potassium in the cell. When there is intracellular energy failure because insulin activity is decreased related to the absence of amino acids provided parenterally, then potassium will leak out of the cell as this enzyme activity decreases. MR. BUSKER: Thank you for that clarification, Dr. Adamkin. What happened next with this infant? DR. ADAMKiN: The next day, at 36 hours of age, this baby weighs 595 gm and that represents a 2.4% postnatal weight loss. The baby is now started on TPN, including 3 gm/kg/day of amino acids and 2 gm/kg/day of lipids. The infant, despite receiving two doses of surfactant, remains on 80 % oxygen, a rate of 60 on the ventilator, pressures of 20/4, and the x-ray demonstrates severe RDS. Labs done after being on this TPN for 16 hours include a BUN of 40mg/dL, a creatinine of .7mg/dL, and a triglyceride level of 220mg/dL. The urine output at 52 hours of age has been 4 ml/kg/hr for the last 24 hours MR. BUSKER: This elevation in the BUN — from 15 mg/dL to 40 mg/dL— what’s the significance of that? DR. ADAMKiN: This is a typical dilemma or conundrum for the clinician managing early TPN in babies receiving early amino acids. This was also addressed in the Radmacher paper reviewed in this issue of eNeonatal Review relating to early amino acid and the metabolic response of extremely low birth weight babies. 2 An elevated BUN of up to 40 mg/dL has been observed in neonates early in life with or without TPN. The concern is whether this represents excessive amino acid delivery with decreased utilization and subsequent oxidation, or more likely it means that the BUN is simply reflective of adequate utilization by the baby doing what the baby does metabolically in utero with amino acids and really is the principle of early amino acids asking the immature, extremely premature baby to use amino acids not only to make lean mass, but to burn as energy. In that same paper, the Radmacher paper, it was shown that there was no direct relationship between BUN and protein dose 2 The reason for that is BUN is also dependent on acuity of illness, on renal function and on fluid balance. Therefore, we shouldn’t make decisions about decreasing the protein in TPN simply with just one piece of information, a BUN that may be 40. Other factors need to be taken into account which include the creatinine for renal function, the urine output that the baby is having, and the clinical condition of the baby. eNeonatal Review Podcast <strong>Transcript</strong>, Volume 9: Issue 14 2
So in this particular case, a BUN of 40 with a normal creatinine, normal urine output, normal postnatal weight loss, would not appear to represent any problem with the early initiation of amino acids. The second issue that needs to be addressed is that when amino acids are used for energy, per our discussion just a moment ago, the amino acids are converted to carbon dioxide and ammonia. The ammonia is converted to urea. That’s why there is an elevated BUN and it does not represent toxicity, it simply represents adequate utilization of the amino acid solution. MR. BUSKER: As you described, this baby’s triglyceride level is 220mg/dL. What’s the reason for that elevated level? DR. ADAMKiN: The elevated triglyceride levels in this patient probably represent low enzyme activity for lipoprotein lipase, which is the enzyme that breaks down or hydrolyzes the intravenous fat solution. We know that the extremely low birth weight infant and, in particular, small for gestational age infants, have the lowest levels of this particular enzyme and are at the greatest risk to develop hypertriglyceridemia. This baby is both an ELBW baby and is also an SGA infant. The triglyceride levels probably should be kept below 200 or perhaps even less than 150 mg/dL in these patients. We know that when babies have significant elevations of triglyceride, then some of the fat can end up in cells lining the intestine and also theoretically in the lung. There is a simple way to prevent hypertriglyceridemia in the majority of babies. It has to do with what I call the lipid infusion rate. We know that if we don’t exceed a rate of 0.12 gm/kg/hr of lipids, then the majority of babies that we treat with intravenous lipids will not develop hypertriglyceridemia. However, in this particular case, the baby was receiving 2 grams per kilogram per day of lipid infused over 24 hours, and that comes out to .08 grams per kilogram per hour, which is certainly below the .12 grams per kilogram per hour that we recommended. However, again, what’s unique about this baby is the fact that the baby was born growth restricted or SGA. For the majority of babies, again, if we don’t exceed the .12 grams per kilogram per hour, these babies will not develop hypertriglyceridemia. Therefore, the maximum dose of lipid recommended by the Committee of Nutrition of the Academy of Pediatrics is 3 gm/kg/day of lipids. When we infuse that dose over 24 hours, it comes out to 0.12 gm/kg/hr which is the rate of infusion that we recommend. Therefore, the simplest strategy is to infuse babies over 24 hours with whatever their lipid dose is so that we know at the maximum dose we won’t exceed the .12 gm/kg/hr. MR. BUSKER: You also noted that this baby has severe RDS and requires a high concentration of oxygen. Is it safe to administer lipids to an infant with these problems? And overall, what can you tell us about the implications of hypertriglyceridemia on lung disease? DR. ADAMKiN: This is also a controversial area in the management of the extremely low birth weight baby. A potential hazard of hyperlipidemia resulting from the failure to clear the infused lipid in the system is an adverse effect on gas exchange in the lungs. In particular, significant concerns have been raised about the high polyunsaturated fatty acid content of the lipid emulsions that we use in the United States that have a very high content of an omega-6 fatty acid called linoleic acid. The solutions in the United States contain over 50% of the fatty acids come from linoleic acid. Why is that important? Linoleic acid is an 18-carbon-2-doublebond omega-6 fatty acid and it is the essential fatty acid. It is converted to a 20-carbon-4-double-bond omega-6 compound, which is called arachidonic acid. Here’s where things become important. Arachidonic acid is converted into vasoactive mediators that may cause pulmonary vasoconstriction or decrease the ability of the baby to oxygenate. These compounds include eicosanoids, prostaglandins, thromboxanes, and leukotrienes, and all of these increase vasomotor tone. Therefore, we recommend that for late preterm babies or term babies who have persistent pulmonary hypertension, the clinician be very judicious with the use of lipids in those babies, restricting them to even no lipids during the height of their illness or a very modest dose, and the extension to the babies that we’re talking about today, the extremely low birth weight baby like this one with surfactant deficiency that one may want to be conservative with dosing lipids 1 gm/kg/day to 2 gm/kg/day in babies who have severe lung disease, and once they’re recovering we can increase the dose to the maximum of 3 gm/kg/day. eNeonatal Review Podcast <strong>Transcript</strong>, Volume 9: Issue 14 3
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