Abstract

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Objective: To study the correlation of clinical perinatal asphyxia with counts of nRBC/100 WBC in cord blood.
Method: This is a prospective comparative study conducted from July 2008 to June 2009. It comprised of two groups, cases and controls. The case group consisted of 50 newborns with perinatal asphyxia and the control group had 50 non asphyxiated newborns. The cord blood was collected immediately after birth for Hb%, TLC, pH and nRBC/100WBC count determination. Early neonatal outcome of both the groups was also evaluated. Statistical analysis was done using SPSS software and application of chi square and Pearson’s correlation (sigma 2-tailed) tests.
Results: The mean nRBC/100 WBC count for control group was 5.7 (+2.33212) and for case group was 10.34 (+3.87883). This difference was statistically significant (p
Conclusion: The nRBC/100 WBC count correlates well with perinatal asphyxia and associated early neonatal outcome.

Introduction

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Perinatal asphyxia still remains a significant cause of perinatal mortality and is known to complicate 5-10% of all deliveries. There is no universally accepted definition of asphyxia, a term that should be exclusively used to indicate those infants who have metabolic acidosis and hypoxia at birth. Recently evidence has been accumulating rapidly that FHR (fetal heart rate) changes and blood acid base status of the fetus /neonate and Apgar scores are very poor predictors of long term outcome. It is now being suggested that birth asphyxia should only be diagnosed when the baby goes on to develop HIE which has shown to be a much more reliable indicator of long term handicap than any other perinatal markers. In situations where facilities for cord blood analysis are not available it would be very useful to have another surrogate marker for fetal asphyxia .Considering the hematopoietic response to hypoxia inutero the elevated nRBC/100 WBC count is being hailed as the marker for not only perinatal asphyxia but also the chances of the neonate to go on to developing neurological sequelae[1].
The present study was undertaken to assess the nRBC /100 WBC count as a marker of perinatal asphyxia in conjunction with other clinical markers and its ability to predict immediate neonatal prognosis in cases of asphyxia.

Method

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This prospective comparative study was conducted from July 2008 to June 2009. It included 50 women each in case and control groups who were in labour between 38 and 42 weeks of gestation with term singleton pregnancies. They were observed during labour for development of signs of irregular FHS, meconium staining of liquor, APGAR at 1 min < 6 and umbilical cord arterial blood pH < 7.1 were taken as case group. For the control group the criteria were reassuring FHS pattern , clear liquor , APGAR at 1min > 6 and pH >7.1 .Pregnancies associated with elevated nRBC count in fetal/ neonatal blood , Rh isoimmunisation , maternal anemia , diabetes mellitus , multiple pregnancy and preterm deliveries were excluded from the study. Immediately after the birth of the placenta , 1 ml of blood was collected in a pre heparinised syringe from a doubly clamped segment of the umbilical cord for pH estimation by Combiline analyser and another 2 ml was collected in an EDTA vial from which haemoglobin , total leucocyte count and a thin blood film was prepared .The film was stained by Leishman’s stain and nRBC / 100 WBC were counted at 40X magnification .The data was analysed using SPSS 11.5 software and chi square or Pearson’s correlation ( sigma 2 tailed) were applied as appropriate.

Observation and Discussion

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Both the case and control groups were comparable in terms of maternal age, parity, period of gestation, birth weight and sex of the neonate (Table 1). The mean nRBC/100 WBC count for case group was 10.3400+3.87883 and for the control group was 5.7000+2.33212. This difference was highly significant (p Previous authors have concluded that intra uterine hypoxia causes release of erythropoietin leading to increased mitosis of erythroid precursors and their release in the fetal circulation. This holds true for both acute as well as chronic hypoxia though the exact mechanism of increased peripheral NRBC still remains elusive.
Fanaroff (2) concluded that normoblasts could enter the bloodstream within 30 minutes of a severe hypoxic injury. Korst et al (3) and Phelan et al (4) found increased nRBCs after acute catastrophic intrapartum events. The duration of these catastrophic events was undoubtedly less than one hour in most cases. Although it is now reasonable to conclude that it is less than 60 minutes and perhaps as short as 20-30 minutes. Phelan et el(4) found the mean nRBC/100 WBC count of 3.4+3.0 in non asphyxiated neonates and the count was 34.5+6.83 in asphyxiated neonates . In this study the mean nRBC /100 WBC count in cases of perinatal asphyxia was 10.34+3.88 in comparison the mean value for controls was 5.7+2.33.
Spencer et al (5) have observed that nRBC count is a better marker of fetal metabolic acidosis than MSAF, non reassuring FHR, low APGAR scores. Hanon-Lundberg and Kirby (6) found that nRBC counts increased with progressive increase in cord acidosis and progressive decreases in APGAR scores. In this study a very strong and negative correlation was present between nRBC values and APGAR scores at 1 min and umbilical artery pH.
Bunocore et al (7), Ghosh et al (8) and Ferns et al (9) concluded that nRBC count at birth not only reflects a haematological response of infant to perinatal asphyxia but is also a reliable marker of perinatal brain damage .This study shows a very strong significance between nRBC counts of group with early neonatal mortality and group without neonatal mortality (p)

Conclusion

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The clinical diagnosis of perinatal asphyxia is based on several criteria, the two main ones being evidence of cardiorespiratory and neurological depression (defined as an Apgar score remaining less than 7 at 5 minutes after birth) and evidence of acute hypoxic compromise with acidaemia (defined as an arterial blood pH of less than 7.1 or base excess greater than 12 mmol/L). In many settings, especially resource-poor countries, it may be impossible to assess fetal or neonatal acidaemia. Hence nRBC count can be a useful part of the obstetrician’s armamentarium for the evaluation of perinatal asphyxia where facilities of pH sampling are not available and can serve as are liable, inexpensive and easily available marker of perinatal asphyxia.

References

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1. Saracoglu F, Sahin I, Eser E, et al. Nucleated red blood cell as a marker of fetal hypoxia. International J Obstetric and Gynecology 2000; 71:113-8.
2. Jones G, Steketee RW, Black RE, et al. How many child deaths can we prevent this year? Lancet 2003; 362:65–71.
3. Korst LM, Phelan JP, Ahn MO, et al. Nucleated red blood cells: An update on the marker for fetal asphyxia. Am J Obstet Gynecol 1996; 175:843-846.
4. Phelan JP, Korst LM, Ahn MO, et al. Neonatal nucleated red blood cell and lymphocyte counts in fetal brain injury. Obstet Gynecol 1998; 91:485-489.
5. Blackwell SC, Refuerzo JS, Wolfe HM, et al. The relationship between nucleated red blood cell counts and early-onset neonatal seizures. Am J Obstet Gynecol 2000; 182:1452-1457.
6. Hanlon-Lundberg KM, Kirby RS. Nucleated red blood cells as a marker of acidemia in term neonates. Am J Obstet Gynecol 1999; 181:196-201.
7. Buonocore G, Perrone S, Gioia D, et al. Nucleated red blood cell count at birth as an index of perinatal brain damage. Am J Obstet Gynecol 1999; 181:1500-1505.
8. Ghosh B, Mittal S, Kumar S, Dadhwal V. Prediction of perinatal asphyxia with nucleated red blood cells in cord blood of newborns. International Journal of Gynecology and Obstetrics 2003; 8:267-71.
9. Ferns SJ, Bhat BV, Basu D. Value of nucleated red blood cells in predicting severity and outcome of perinatal asphyxia Indian J Pathol Microbiol 2004 Oct; 47(4):503-5.

Source(s) of Funding

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No funds required

Competing Interests

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No competing interests

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