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Pathogenesis of Metabolic Acidosis in Preterm Infants |
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| Correspondence
Address : C G A Aiken, 729 Frankley Road, New Plymouth 4371, New Zealand. Phone: +64 6 753 2950 Email: geoffaiken@xtra.co.nz |
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| Objective: To determine how the balance between mineral base, and carbonic and organic acids is altered to cause metabolic acidosis in preterm infants. Study Design: Mineral balance and arterial blood measurements of 3 groups of preterm infants given 5 different total parenteral nutrition (TPN) regimens were analyzed. Mineral base was measured as the difference between mineral cations and anions. Organic acid was measured as the difference between mineral base, bicarbonate and protein anion. Results: The degree of metabolic acidosis measured as base excess, was determined by deviation in both mineral base and organic acid from normal. Sodium minus chloride balance determined change in arterial blood mineral base. TPN containing more chloride than sodium caused mineral acidosis with low mineral base, whereas TPN containing more sodium than chloride caused mineral alkalosis with high mineral base. Lactic, organic and carbonic acidosis all increased mineral base. Arterial blood organic acid was determined by: 1. Glomerular filtration rate: Low rates after delivery caused high organic acid that fell as GFR improved. 2. TPN non metabolized organic acid content: Gluconate and sulphate caused organic acidosis by accumulating in blood and mineral acidosis by urine excretion resulting in mineral base loss. 3. Rate of protein catabolism: Increased protein catabolism from TPN providing only 25 kcal/g amino acids or from dexamethasone caused organic acidosis. Conclusion: Metabolic acidosis was caused by high organic acid, resulting from low glomerular filtration rates in the first 1-2 weeks, exacerbated by TPN containing gluconate or sulphate or only 25 kcal/g amino acids. Renal bicarbonate wasting could not account for metabolic acidosis. | ||||||
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