|Year : 2014 | Volume
| Issue : 4 | Page : 195-199
Clinical profile and short-term outcome of hypoxic ischemic encephalopathy among birth asphyxiated babies in Katihar medical college hospital
Kumar Amritanshu1, Suruchi Smriti2, Vimal Kumar1, Apeksha Pathak1, Deba Prasad Banerjee1
1 Department of Paediatrics, Katihar Medical College, Katihar, Bihar, India
2 Department of Obstetrics and Gynecology, Katihar Medical College, Katihar, Bihar, India
|Date of Web Publication||14-Nov-2014|
Department of Paediatrics, Katihar Medical College, Katihar, Bihar
Source of Support: None, Conflict of Interest: None
Objectives: The aim was to determine the selected maternal and fetal risk factor for adverse short-term outcomes in babies with birth asphyxia. Materials and Methods: This was a prospective observational study, including all birth asphyxiated babies born between January 1, 2013 and December 1, 2013 who fulfill the inclusion criteria. Detailed maternal information and progress of babies were noted regularly until the time of death or discharge. Cord blood was collected after delivery for measurement of nucleated red blood cell/100 white blood cells (NRBC/100 WBC) for Katihar Medical College born babies only. Babies were categorized into different stages of hypoxic ischemic encephalopathy according to Sarnat and Sarnat staging. On the basis of outcome, they were divided into two groups, group one who survived and was discharged with stable sign and group two who died. Effects of risk factors on both groups were compared and result were expressed as (P < 0.05 was taken significant), using the Chi-square test. Results : During the study period, out of 5481 neonatal admissions 600 babies (10.94%) were asphyxiated. Of the total asphyxiated babies 60 babies (10%) expired. Maternal factors significantly associated with mortality included antenatal check-up, premature rupture of membranes, meconium stained liquor, parity and place of delivery. Birth injury, hypotension, hypothermia, hypoglycemia, hypoxemia, cord accidents and increased NRBC/100 WBC count were the baby factors. Conclusion : Early identification of high risk mothers and timely referral to tertiary care center can reduce the mortality. Furthermore, there is need to carefully evaluate and monitor the babies with low APGAR scores immediately after birth.
Keywords: Birth asphyxia, risk factors, short-term outcome
|How to cite this article:|
Amritanshu K, Smriti S, Kumar V, Pathak A, Banerjee DP. Clinical profile and short-term outcome of hypoxic ischemic encephalopathy among birth asphyxiated babies in Katihar medical college hospital. J Clin Neonatol 2014;3:195-9
|How to cite this URL:|
Amritanshu K, Smriti S, Kumar V, Pathak A, Banerjee DP. Clinical profile and short-term outcome of hypoxic ischemic encephalopathy among birth asphyxiated babies in Katihar medical college hospital. J Clin Neonatol [serial online] 2014 [cited 2019 Aug 18];3:195-9. Available from: http://www.jcnonweb.com/text.asp?2014/3/4/195/144749
| Introduction|| |
Birth asphyxia is defined as the failure to initiate and sustain breathing at birth. Globally, about one quarter of all neonatal death are caused by birth asphyxia.  According to World Health Organization estimates in the developing countries 3% of all infants (3.6 million) suffer from moderate to severe birth asphyxia of which 23% (840,000) die and approximately the same number develop serious sequel. 
Following improvement in primary and obstetric care in most industrialized countries, the incidence of birth asphyxia has reduced significantly and <0.1% newborn infants die from birth asphyxia. In developing countries, rates of birth asphyxia are several fold higher, ranging from 4.6/1000 in cape town to 26/1000 in Nigeria and case fatality rate may be 40% or higher. In the developing countries large proportion of births occurs in nonhospital setting. Due to limited availability of data, the figures are likely to underestimate the real proportion of mortality and morbidity due to birth asphyxia. 
Birth asphyxia can be caused by events that have their roots in either the antepartum, the intrapartum, or the postpartum periods or combination thereof. 
Despite of available information, there is only a handful of published studies  from developing countries, and none from Katihar, which is located on the Eastern Zone of Bihar, India. In order to implement preventative action, knowledge of risk factors leading to particular condition is essential; by identifying these risk factors we can aggressively manage the patient and may cut down the incidence of birth asphyxia.
| Materials and methods|| |
This prospective study was carried out at Neonatal Unit of Katihar Medical College and Hospital (KMCH) from January 1, 2013 to December 1, 2013. This study was approved by Ethical Committee of Katihar Medical College, Katihar.
Inclusion and exclusion criteria
All babies with clinical diagnosis of birth asphyxia (newborn with history of delayed cry or APGAR score <7 in 5 min were included in the study). Babies with gross congenital malformation, still birth, Rh incompatibility were excluded.
Although APGAR score does not exactly predict the neuro developmental outcome, but is still most feasible and practical to perform. Therefore 5 min APGAR score is still the valid index for assessing the effectiveness of resuscitation and validity of new born. 
Informed consent was obtained from mothers of all recruited newborns. The purpose of handling and intended mode of handling was explained to the working group which included resident medical doctors and nurses. KMCH babies were resuscitated who failed to develop spontaneous breathing. The duration of resuscitation was measured from the delivery until the infant had spontaneous breathing with a heart rate >100 beats, and resuscitation was withdrawn after 20 min if spontaneous breathing had not been established as suggested by American Heart Association.  After initial stabilization and resuscitation, babies maintaining the APGAR score >7 at 5 min were kept in postnatal ward for observation and essential newborn care for 12 h and then discharged. While those who had APGAR score of <7 at 5 min were shifted to neonatal intensive care unit for further management.
For KMCH as well as out born babies, detailed maternal history was taken from available maternal and hospital record and attendant for enrolled cases in a pretested questionnaire. Referral notes were also consulted. The babies were examined in detail and the progress was noted till the time of discharge or death and categorized into stages of hypoxic ischemic encephalopathy (HIE) according to Sarnat and Sarnat staging.  Outcome was noted and on the basis of outcome, two groups were formed, a group who survived and a second group of babies who expired. Factors ([maternal age, educational status, occupation, antenatal check-up [ANC], premature rupture of membranes [PROM], meconium stained liquor, parity, place of delivery], [babies: birth injury, hypotension, hypothermia, hypoglycemia, hypoxemia, cord accidents, sex, nucleated red blood cells/100 white blood cells [NRBC/100 WBC]) affecting both groups were compared. Group of survivors included babies who were discharged successfully, were taking feed and had stable vital signs. Correlation of cord blood NRBC/100 WBC count with different stages of HIE was done during hospital management for KMCH born babies only. For this immediately after the birth of the baby, 2 ml of blood was collected in a heparinized syringe and sent to our college central laboratory for examination. Chi-square test was applied and P values were calculated for risk factor and outcome of babies.
| Results|| |
The frequency of birth asphyxia at neonatal unit was 10.94% (600/5481) neonatal admission). Of the total asphyxiated babies 60 babies (10%) expired. Males were (n = 333, [55.5%]) and (n = 267, [44.5%]) were female among birth asphyxiated babies. At admission 488 (81.33%) were in Stage I HIE, 85 (14.16%) were in Stage II HIE and 27 (4.5%) were in Stage III HIE. The outcome in terms of mortality in Stages I, II and III were 2 (3.3%), 35 (41.17%) and 23 (85.18%), respectively [Table 1]. The background sociodemographic characteristics of the mothers of the babies such as age, educational status and occupation were not statistically significant (P < 0.001).
|Table 1: Number of neonates with birth asphyxia and relation of NRBC/100 WBC with different stages of HIE |
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Among statistically significant identified risk factors were ANC (P = 0.021), PROM (P = 0.003), meconium stained liquor (P = 0.004), parity (P = 0.003) and place of delivery (P < 0.001) [Table 2]. In our study, 272 (45.3%) were home delivery, 98 (16.33%) delivered at private clinic or maternity home and 230 (38.33%) were delivered at KMCH. Regarding mode of delivery (n = 193, 32.16%) were born by C-section (includes done at both private clinic or maternity home and KMCH), while (n = 407, 67.83) were born by normal vaginal delivery. There was no statistical significant difference in the outcome of babies where they died or discharged (P = 0.097).
Factor associated with dying of babies during first 72 h of birth are birth injury (P < 0.001), hypotension (P < 0.001), hypothermia (P = 0.002), hypoglycemia (P = 0.001), hypoxemia (P < 0.001) and cord accidents (P = 0.036). Sex of the babies were not found to be significant risk factor (P = 0.0935) [Table 3]. Mean NRBC/100 WBC count correlated with stage of HIE was found to be 16.22 in Stage I HIE, 47.5 in Stage II HIE, and 78.13 in Stage III HIE was also statistically significant (P < 0.001). The NRBC/100 WBC count was significantly higher in babies who expired as compared to those who were discharged [Table 4]a and b.
| Discussion|| |
This study was on analysis of risk factors and short-term outcome of birth asphyxiated babies admitted in Neonatal Unit of KMCH. The frequency of birth asphyxia was 10.94% in our study, while it varies from 9%  to 13%  in different studies. This variation was due to different operational definition of birth asphyxia adopted by different researchers, APGAR score at 1 min and 5 min, duration of resuscitation, breathing effort at 1 min etc. 
Mortality in our study is mainly contributed by Stages III and II of HIE. In this study maternal age did not show any association with mortality among asphyxiated babies. This finding was consistent with Bhuinyan  and Crawford.  They also found that maternal age is an isolated event and cannot be considered as a risk factor for birth asphyxia. No association was found among the various educational and occupational levels of the mothers of discharged and expired.
In our study, 8% of babies expired whose mothers had regular ANC as compared to 14% whose mother did not have their ANC done. This reflects the low awareness for ANC in our society, irrespective of social class and educational background.
Among all the women of birth asphyxiated babies 180 (30%) had PROM, out of which 15.55% of babies expired, when compared to 7.6% whose mother had no history of PROM. Thus, PROM appears to be a significant risk factor. In this study largest number of babies affected by birth asphyxia who were delivered at home expired (14.7%) when compared to KMCH born babies (3.47%). The better survival rate among asphyxiated in-born babies may be reflection of the advantage of quality, immediate postdelivery neonatal care available to them. Such relatively better outcome among in-born with asphyxia had earlier been reported. 
In this study, other important maternal risk factors affecting mortality include meconium stained liquor and primipara mothers. 32.16% of the cases in our data are emergency caesarean deliveries. This makes our study different from another hospital based study  where only 53% of the deliveries were cesarean deliveries. Itoo et al. from Madinah  found that deliveries by emergency caesarean section were significantly higher in their study group. However, this factor was not found to be significant for mortality among asphyxiated babies.
Birth injury and cord-accidents were found to be significantly associated with mortality due to birth asphyxia (P ≤ 0.001 and P = 0.036 respectively). Consistent with other study which also found cord accidents (prolapse, entanglement, cord presentation, tight cord round neck) to be significant risk factors. , Cord accidents often lead to reduced blood flow form placenta to the fetus causing impaired gaseous exchange and babies are usually born asphyxiated. 
Cardiovascular complication such as hypotension were present and have been observed by other workers  also. Other clinical complications present in babies who died included hypothermia, hypoglycemia and hypoxemia. Sex of the babies is not significant risk factor affecting outcome.
Studies on hematological variation in asphyxiated neonates as a predictor of neonatal asphyxia have suggested that NRBC in cord blood of asphyxiated neonates help in identifying birth asphyxia. The number of NRBC/100 WBCs (NRBC/100 WBC) is quite variable, but is rarely >10. Considering the hematopoietic response to hypoxia in utero, the elevated NRBC/100 WBC count is being hailed as the marker for not only prenatal asphyxia, but also the chances of the neonates to develop neurological squeale. ,,,,, In our study, NRBC/100 WBC count was significantly higher in babies who expired as compared to those who survived.
Majority of death occurred in Stages II and III of HIE, showing that once severe hypoxia occurs, treatment cannot be very effective, so more attention needs to pay to early assessment and intervention, during which intervention might be efficacious in reducing severity of brain damage. Additional, dilemma relates to the probability that infants with the greatest hypoxic-ischemic brain damage will benefit least by any specific intervention, while those with only mild to moderate damage will benefit most with the therapy. The clinical management of neonates with hypoxic ischemic damage is limited to supportive medical care.
| Conclusion|| |
The study demonstrates multiple risk factors affecting mortality of birth asphyxiated infants. Early identification of high risk mothers and timely referral to tertiary care center can reduce the mortality. Furthermore, there is need to carefully evaluate and monitor the babies with low APGAR scores immediately after birth.
| References|| |
|1.||World health organization. Basic Newborn Resuscitation Guidelines. http:\\www.who.int/maternal-child-adloscent/en. [Last accessed on 2013 Oct 27]. |
|2.||State of the World Children. UNICEF, 2009. Maternal and newborn health. http://www.unicef.org/scowc09/report/report.php. [Last accessed on 2014 Feb 20]. |
|3.||Azra Haider B, Bhutta ZA. Birth asphyxia in developing countries: Current status and public health implications. Curr Probl Pediatr Adolesc Health Care 2006;36:178-88. |
|4.||Ondoa-Onama C, Tumwine JK. Immediate outcome of babies with low Apgar score in Mulago Hospital, Uganda. East Afr Med J 2003;80:22-9. |
|5.||Black RE, Kelley L. Reducing Perinatal and Neonatal Mortality. Child Health Research Project. Special Report; 1999. p. 1-48. |
|6.||Mare DB, Sehexnayder SM, Chameides L, Terry M, Donorhue A, Hickey RW, et al. Special report-Pediatric Basic life suppot: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Pediatrics 2010;126:e1345. |
|7.||Sarnat HB, Sarnat MS. Neonatal encephalopathy following fetal distress. A clinical and electroencephalographic study. Arch Neurol 1976;33:696-705. |
|8.||Shrestha M, Shrestha L, Shrestha PS. Profile of asphyxiated babies at Tribhuvan University Teaching Hospital. J Nepal Pediatr Soc 2009;29:3-5. |
|9.||Thornberg E, Thiringer K, Odeback A, Milsom I. Birth asphyxia: Incidence, clinical course and outcome in a Swedish population. Acta Paediatr 1995;84:927-32. |
|10.||Bhuiyan SJ. Incidence, risk factors and immediate outcome of asphyxia neonatorum in hospitalized neonates. Department of Paediatrics IPGMR [Dessertation]. Dhaka: BCPS; 1996. |
|11.||Crawford JS. Maternal age as an isolated factor in the incidence of perinatal asphyxia. Am J Obstet Gynecol 1966;95:569-71. |
|12.||Owa JA, Osinaike AI. Neonatal morbidity and mortality in Nigeria. Indian J Pediatr 1998;65:441-9. |
|13.||Lodé N, Chabernaud JL, Chouakri O, Casadevall I, Maury I, Lagrue E, et al. Newborn asphyxia at term during delivery. J Gynecol Obstet Biol Reprod (Paris) 2003;32 1 Suppl: 1S98-105. |
|14.||Itoo BA, Al-Hawsawi ZM, Khan AH. Hypoxic ischemic encephalopathy. Incidence and risk factors in North Western Saudi Arabia. Saudi Med J 2003;24:147-53. |
|15.||Derham RJ, Matthews TG, Clarke TA. Early seizures indicate quality of perinatal care. Arch Dis Child 1985;60:809-13. |
|16.||MacDonald HM, Mulligan JC, Allen AC, Taylor PM. Neonatal asphyxia. I. Relationship of obstetric and neonatal complications to neonatal mortality in 38,405 consecutive deliveries. J Pediatr 1980;96:898-902. |
|17.||WHO. Basic Newborn Resuscitation. A Practice Guide. ?? WHO Report; 1997. p. 2, 3.Mother and reproductive health/Safe mother hood unit.Division of reproductive health (Technical support) World Health Organization, Geneva. |
|18.||De Souza SW, Richards B. Neurological sequelae in newborn babies after perinatal asphyxia. Arch Dis Child 1978;53:564-9. |
|19.||Green DW, Mimouni F. Nucleated erythrocytes in healthy infants and in infants of diabetic mothers. J Pediatr 1990;116:129-31. |
|20.||Phelan JP, Ahn MO, Korst LM, Martin GI. Nucleated red blood cells: a marker for fetal asphyxia? Am J Obstet Gynecol 1995;173:1380-4. |
|21.||Philip AG, Tito AM. Increased nucleated red blood cell counts in small for gestational age infants with very low birth weight. Am J Dis Child 1989;143:164-9. |
|22.||McCarthy JM, Capullari T, Thompson Z, Zhu Y, Spellacy WN. Umbilical cord nucleated red blood cell counts: Normal values and the effect of labor. J Perinatol 2006;26:89-92. |
|23.||Ghosh B, Mittal S, Kumar S, Dadhwal V. Prediction of perinatal asphyxia with nucleated red blood cells in cord blood of newborns. Int J Gynaecol Obstet 2003;81:267-71. |
|24.||Hermansen MC. Nucleated red blood cells in the fetus and newborn. Arch Dis Child Fetal Neonatal Ed 2001;84:F211-5. |
[Table 1], [Table 2], [Table 3], [Table 4]