Intravenous lipid emulsions are used both as a source of essential fatty acids and to provide concentrated calories to meet energy and growth requirements. Use of IV fat decreases the respiratory quotient and prevents essential fatty acid deficiency. It also avoids the fatty infiltration of the liver that may occur when only CHOs are given. Normal infant formulas have half of their calories as fat; however this is not true for TPN. With TPN, fat is < = 40% of NPCs. Never go above 60% as lipid, as this may lead to ketosis.
Lipids are usually started at 0.5-1 gm/kg/day and advanced daily up to a maximum of 3 gm/kg/d (can go up to 4 gm/kg/d in exceptional circumstances). To calculate the lipid grams, multiply the total NPCs by the fat percentage and divide by 9 Kcal/gm.
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Example: NPCs of 600, weight 30 kg, CHO:fat 70:30600 x 0.3 / 9 = 20 gm lipid OR 0.7 gm/kg/day |
Lipid emulsions come as either 10%, 20% or 30% solutions. Twice the amount of phospholipid is used to emulsify a gram of 10% lipid as compared to 20%. This excessive lipid content in the 10% solution has been associated with decreased lipid clearance because phospholipids produce lipoprotein-X-like substances that compete for hepatocyte binding sites. Therefore 20% lipid is more efficiently cleared by neonates and the use of 10% lipid should be avoided. 20% lipid is also the preferred solution for older children, although adolescents can be given the 30% solution as is used in adults.
Prematures are more susceptible to impaired lipid clearance resulting in hypertriglyceridemia. Triglyceride (TGL) levels are monitored closely and lipids are either not advanced, held at the same level or temporarily discontinued depending on the TGL level. Lipid deficiency can be seen after 1-2 days without fat in the premature, so even with elevated TGL levels, small amounts of IV fat (0.5 gm/kg/day) are usually still given to premies. Hypertriglyceridemia should be particularly avoided in the jaundiced neonate. This is due to the potential for high concentrations of plasma free fatty acids (FFAs) displacing bilirubin from albumin binding sites, leading to the deposition of unconjugated bilirubin in brain cells (kernicterus).
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