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Myocardial calcification in an extremely low birth weight infant with chronic renal failure and secondary
R P Verma1, E M Smergel, K Chandrasekaran
1Department of Pediatrics, Hahnemann University Hospital, Philadelphia, PA 19102.
Insights
Myocardial calcification is a rare complication in preterm infants with renal failure. Maintaining calcium and phosphorus levels is crucial to prevent ectopic calcification in vulnerable infants.
Area of Science:
- Neonatalogy
- Pediatric Nephrology
- Cardiology
Background:
- Metastatic myocardial calcification is typically seen in adults with chronic renal failure.
- Myocardial calcification is rarely documented in premature infants, usually associated with specific conditions like coxsackievirus B1 infection.
Observation:
- A case of myocardial calcification in a preterm infant (680 gm) with prolonged renal failure and secondary hyperparathyroidism is presented.
- Subclinical myocardial injury was indicated by elevated serum creatine phosphokinase MB levels.
- Serum calcium and inorganic phosphorus product exceeded 75 mg x mg/100 ml, suggesting supersaturation and calcification risk.
Findings:
- This case highlights myocardial calcification as an unusual complication of renal immaturity in extremely low birth weight infants.
- The findings suggest intact parathyroid glandular function in these infants, contributing to mineral imbalances.
- Elevated calcium and phosphorus levels, exacerbated by secondary hyperparathyroidism, led to ectopic calcification.
Implications:
- Close monitoring of serum calcium and phosphorus levels is essential in preterm infants with renal failure to prevent myocardial and other ectopic calcifications.
- This case underscores the importance of managing mineral-electrolyte balance in neonatal intensive care to avoid severe complications.
- Understanding these risks is vital for optimizing care strategies for extremely low birth weight infants facing renal challenges.
Abstract:
Myocardial calcification has been rarely described in premature infants after myocardial infarction and myocarditis with coxsackievirus B1. In adults and older children, metastatic myocardial calcification has been reported in chronic renal failure. We report a case of myocardial calcification in a 680-gm preterm infant after a prolonged course of renal failure complicated by secondary hyperparathyroidism. Subclinical myocardial injury was evidenced by a high serum creatine phosphokinase MB band concentration, which probably provided a susceptible substrate for the deposition of calcium crystals, because the multiplication product of serum calcium and inorganic phosphorus levels transiently exceeded 75 mg x mg/100 ml, indicating serum saturation during the course of secondary hyperparathyroidism. We report this case as an unusual complication of renal immaturity in extremely low birth weight infants and an indication of a relatively intact parathyroid glandular function in them. Hypoxia, myocardial dysfunction, and renal failure are common complications in such infants, and in the presence of renal failure, the serum levels of calcium and inorganic phosphorus should be maintained below the pathologic level to avoid ectopic calcification of the tissues, including the myocardium.