RESUMEN
Although neonates with severe birth asphyxia are known to be at increased risk of early-onset hypocalcaemia, the magnitude of the problem is not well documented. The objective of this study was to determine the prevalence of early-onset hypocalcaemia in severely asphyxiated neonates. In this case-control study, conducted at St Philomena Catholic Hospital (SPCH), Benin City, Nigeria, the total serum calcium concentrations of 31 full-term neonates with 1-minute Apgar score of 3 or less were measured using the O-cresulphthalein complexone method and the results were compared with those of their counterparts with 1-minute Apgar score of 7 and above. The total serum calcium concentration of severely asphyxiated neonates who received sodium bicarbonate therapy during resuscitation was compared with those of their counterparts who did not receive sodium bicarbonate therapy. All the study neonates (both the asphyxiated and the non-asphyxiated) were examined, at least, twice daily in the first 48 hours of life and their clinical findings were documented. Overall prevalence of early-onset neonatal hypocalcaemia (total serum calcium < 1.75 mmol/L) among asphyxiated neonates was 22.6%. Mean total serum calcium at the ages of 12, 24 and 48 hours were significantly lower among asphyxiated compared to non-asphyxiated neonates (p<0.001). The overall mean serum calcium concentrations were 1.68 + 0.06 mmol/L ( range 1.65 – 1.70 mmol/L) and 1.74 + 0.07 mmol /L(range 1.74 – 1.77 mmol/L) in neonates treated with bicarbonate and those without bicarbonate therapy respectively (p<0.01). Asphyxiated neonates with normal total serum calcium concentrations at the age of 12 and 24 hours maintained this normocalcaemia at the age of 48 hours. The commonest clinical finding among asphyxiated neonates with early-onset hypocalcaemia was convulsion (57.1%). Carpopedal spasm was not a prominent clinical manifestation. Hypocalcaemia was common in the first 48 hours of life in asphyxiated neonates, particularly if they received bicarbonate therapy during resuscitation. Asphyxiated neonates whose serum calcium concentration was normal at the age of 12 hours tended to maintain this normal level at the age of 48 hours.
RESUMEN
Background and objectives: This review focuses on three areas, basic acid-base physiology especially concerning hydrogen ion balance, development of acidosis in chronic kidney disease (CKD), and the consequences of acidosis. We highlight what is well established, what is less certain, and what is unknown. Method and results: The literature on acidosis in CKD were searched from 2004 to 2010 utilizing PubMed, Google Scholar, and Ovid to augment the classic work on acid base physiology over the past three decades. The original research in endogenous acid production and net acid excretion were reviewed. Touching upon the development of metabolic acidosis in CKD, we focused on the consequences of chronic metabolic acidosis on growth and other important variables. Finally, we recognize the significant issue of patients’ medical non-compliance and presented treatment strategy to counter this problem. Conclusion: The correction of acidosis in chronic kidney disease needs no advocacy. The case is made conclusively. Patient non-compliance because of the medication that needs to be taken several times a day is a problem, requiring due diligence.