The High Risk Newborn A Parthasarathy, MKC Nair, Naveen Jain, Srinivas Murki
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  1. Introduction to the High Risk Newborn2

Introduction to the High Risk Newborn1

MKC Nair,
Babu George,
Elsie Philip
Sustained global initiatives and efforts of local governments have improved child survival in most parts of the world and hence, now the focus should shift to quality of survival. Although the infant mortality in India has fallen significantly, the neonatal mortality is remaining by and large static and we do know that low birth weight is the major contributor.1 In the India CLEN multicentric neonatal health research initiative (NHRI) study, the causes of neonatal deaths as per verbal autopsy were respiratory distress syndrome (57%), low birth weight (51%), birth injury/asphyxia (42%), neonatal sepsis complex (36%), pre-maturity (29%), congenital malformations (13%), hypothermia (12%), jaundice (4%) neonatal tetanus (3%) and causes not known (3%).2 Poverty, illiteracy and poor environmental hygiene are factors detrimental to child survival and development, especially so for the marginalized and vulnerable groups.3 Parenting practices do play an important role in child survival and development. In a recent study on parenting practices, early child-care practices were reaching high standards, even in tribal and economically backward areas, probably explaining the better indicators observed in Kerala.4
Child development is a dynamic process of optimally utilizing the genetic potential of the baby, within the context of the environment made available, so as to enable him/her to achieve the full potential. Although a continuous process, the first one-year of life and pre-school years are the most critical period in the child's development. The difficult part is identifying babies at-risk for poor development. A risk factor is something that increases the likelihood of getting a disease or condition. The division of risk as mild, moderate and high is often arbitrary. Hence the concept of “at-risk” 4newborns may be replaced by the concept of “optimality”. Newborns with a low “optimality score” are considered highly likely to develop neurodevelopmental disabilities later in life. Which ‘high risk’ newborns require periodic screening, ideally needs to be determined locally, keeping in mind the feasibility and cost-effectiveness of any neonatal follow-up program. It must, however, be remembered that many babies not considered “at-risk” may also manifest developmental problems as they grow. These babies would obviously not be seen during “at-risk” focused follow-up screening.5
Risk factors for developmental deficits may be grouped under four categories; biological risk, genetic and metabolic disorders, environmental risk, and no apparent risk.6 Low birth weight babies form the single largest group of easily identifiable babies at-risk for poor development. Around two out of three babies weighing less than a kilogram at birth will suffer some degree of disability, usually as a result of lack of oxygen or brain hemorrhage.7 Half of surviving very preterm babies, grow up to be mentally or physically disabled.8 Although developmental delay is more likely to be found among babies with risk factors (at-risk concept), the large majority born with a risk factor are likely to develop normally. On the other hand cerebral palsy and mental retardation are also observed among the large group of babies born normally without any apparent risk. The concept of “double vulnerability” means that a baby with a biological risk factor like low birth weight is more likely to fare poorly if born into a family with poor child rearing capabilities as compared to one with a positive environment. This is very relevant in the Indian context.
In a follow-up study of graduates of level-II neonatal nursery, multiple regression analysis for Bayley scores at 1 and 2 years showed that after adjusting for the significant risk factors for development–birth weight, neonatal seizure, congenital anomaly, intrauterine infection, mother's education, type of baby, occupation of father and residence–the babies who had intervention had significantly higher Bayley scores compared to control babies. Also, the observation that for increase of every 500 grams, there was a significant and consistent increase in mean values of neurodevelopmental outcome indicators at 1 and 2 years and that in every birth weight group, the mean values were higher for the intervention group, suggest that early intervention is effective across the birth weight groups.9 Developmental follow-up of at-risk babies supported by early intervention therapy is the answer, as shown in the experience of the developed countries.10 Meta-analysis of early intervention efficacy 5studies done at Utah State University has shown that early intervention is effective in improving the developmental status, although there is still no uniform agreement as to whether the effects last long.11
A recent meta-analysis to review the effectiveness of early developmental intervention post-discharge from hospital for pre-term (less than 37 weeks) infants on motor or cognitive development concluded that intervention improved cognitive outcomes at infant age (0 to 2 years). However, there was significant heterogeneity between studies for cognitive outcomes at infant age.12 It has been shown that 40% reduction in poor performance could be achieved among low birth weight babies, by CDC model early stimulation.13,14 By early “Infant Stimulation” we mean early interventional therapy for babies at-risk for developmental delay and periodic developmental assessment. A team of professionals consisting of developmental pediatrician, developmental tester, developmental therapist and developmental teacher chalk out programmes of various activities including play, passive exercises and also teach the same to the mother, to help her to do the therapy at home. Improvement in one functional area helps the child to improve functions in other areas.
In the Indian context, it appears that reduction of low birth weight should be the centre point of our thoughts and actions, whether it is for reduction of mortality, morbidity, childhood disability and poor scholastic performance. In order to reduce the burden of low birth weight with the resultant consequences, it is important to understand the community attributable risk factors for low birth weight. In a large community study in India, reporting a 29% LBW incidence had described the following population attributable risks for LBW: Socioeconomic status (41.4%), severe anemia in pregnancy (34.5%), maternal height (29.5%) and maternal pre-pregnant weight (22.9%), highlighting the importance of improving pre-adolescent and adolescent girls' nutrition.15 However, it is to be appreciated that low birth weight has an intergenerational effect and interventions in one generation alone cannot address the issue fully.
Newborn encephalopathy represents the neurological manifestations of central nervous system injury due to any cause obvious or not so obvious, that occurs in the first few hours or days of life. The importance of intra-uterine asphyxia in the genesis of hypoxic-ischemic brain injury is well known. In a retrospective survey of 100 infants with hypoxic-ischemic 6encephalopathy there was evidence of intra-uterine hypoxia in 90% and only in 10% was the insult postnatal.16 Similarly, Brown et al in a series of 91 infants with hypoxic-ischemic encephalopathy reported intrauterine insult in 91% and postpartum insult in 9%.17 Two well conducted studies, a large prospective US national collaborative perinatal project (NCPP) and case control study in western Australia stand testimony to this.18,19
Newborn encephalopathy as described by Sarnat and later by Fenichel, particularly with seizures and recurrent apnoea has been demonstrated to be an important predictor of subsequent motor and cognitive handi-caps.20,21 Clinical presentation of birth asphyxia with severe newborn depression has demonstrated that most children who survived with sequelae had clinical signs of encephalopathy during the neonatal period.22 Hence prevention of perinatal asphyxia with better obstetric care, resuscitation using positive pressure ventilation, with or without oxygen and optimal brain protective immediate postnatal care would be the ideal solution. But in a vast country like India with extremes of perinatal care, abolishing post asphyxial encephalopathy would be a distant dream. Also it has been demonstrated that pyritinol, a widely used so-called neurotonic has no positive effect in improving the neurodevelopmental status of post asphyxial encephalopathy babies at one year of age and hence its use should be dissuaded.23
Severe forms of disability are not common and are often due to congenital, genetic, metabolic causes or intrauterine infections and need specific preventive strategies.24 Recurrent pregnancy wastage due to maternal infections transmissible in utero at various stage of gestation can be caused by a wide array of organisms which include the TORCH complex (toxoplasma gondii, rubella virus, cytomegalovirus, herpes simplex virus) and other agents like Chlamydia trachomatis, Treponema pallidum, Niesseria gonorrhoeae, HIV etc. Toxoplasmosis acquired during pregnancy may cause damage to the fetus.25 Seroepidemiological studies have shown that 10–20 percent of women in childbearing age in India are susceptible to Rubella infection.26 Infection with Rubella during pregnancy may lead to congenital malformation in 10–54 percent of cases.27 The infection caused by CMV in adult is usually asymptomatic but its significance is many times increased when it occurs during pregnancy. However, the rate of primary CMV infection is significantly higher for pregnant women from low socioeconomic group.28 The mother is the usual source of transmission of HSV to the fetus or newborn. Primary HSV infection during first half of pregnancy is associated with increased frequency of spontaneous abortion, still birth, and congenital malformation.297
Poverty, environmental deprivation and inadequacy of early stimulation are much more common and therefore need an integrated program of nutrition and developmental stimulation. Developmental research has clearly shown that both socioeconomic status (SES) and aspects of the home environment account for a significant proportion of the variance in cognitive functioning of both healthy and pre-term children. In addition, researchers have also established that the home environment may serve as a protective factor for children.30 It is suggested that early social environment plays a role in mediating establishment of neural networks that regulate a child's response to stress and capacity for self-control.31 Secure and stable relationships with caring adults assure that young children are adequately nourished and protected from dangerous illnesses, exposure to toxins, and hazards that can lead to preventable injuries. It also provides preventive health check-ups, protect from excessive stress and afford predictable daily routines that convey a sense of security. These influences contribute significantly to healthy brain development that depends upon the care and support provided by individuals in the community as well as in the family.32
In those parts of the country, where maternal education is poor, one of the strategies would be providing family counseling by regularly visiting families having specially identified persons such as pregnant mothers, post natal mothers, 0–2 months old (neonatal) babies, and 2–24 months old babies, observing and monitoring their parenting behavior, until such desirable changes are evident.33 Not withstanding the isolated centers of excellence, the overall quality of institutional neonatal care and postnatal follow-up care at home, remains unsatisfactory in India. It is in this context that the Indian Academy of Pediatrics and the National Neonatology Forum had resolved as early as 2004, to consolidate their ongoing partnership by looking at newer objectives and methods to improve the existing status of neonatal and child health in India.34 It is the same realization that necessitated provision of a group of community volunteers (ASHA) under national rural health mission (NRHM) and addition of the neonatal component in the integrated management of childhood illness (IMCI) in India.8
  1. Nair MKC, Jana AK, Niswade AK. Editorial. Neonatal Survival and Beyond. Indian Pediatr 2005;42:985–8.
  1. Niswade AK, Zodpey SP, Ughade SN, et al. Neonatal Health Research Initiative - Phase-I Report, Clinical Epidemiology Unit, Government Medical College,  Nagpur,  2004.
  1. Nair MKC, Rekha Radhakrishnan S. Early Childhood Development in Deprived Urban Settlements. Indian Pediatr 2004;41:227–237.
  1. Nair MKC, Sumaraj L, Padmamohan J, Radhakrishnan R, Rajasenan Nair V, George B, Suresh Kumar G. Parenting practices in Kerala : A cross-sectional study. Vulnerable children and Youth Studies 2007;2(1):71–7.
  1. Prahbhjot Malhi, ‘Screening Young Children for Delayed Development, Indian Pediatr 1999;36:569–577.
  1. Nair MKC. Editorial. Simplified developmental assessment. Indian Pediatr 1991; 28:837–40.
  1. Disability risk for early babies.
  1. Nair MKC, Elsie Philip, Jeyaseelan L, Babu George, Suja Mathews, Padma K. Effect of CDC Model Early Stimulation among At-risk Babies – A Randomized Controlled. Trial Ph.D Thesis, submitted to University of Kerala  1997.
  1. Nair MKC. Editorial. Symposium: Early Interventional Therapy. Indian J Pediatr 1992;59:657–9.
  1. White K, Casto G. An integrative review of early intervention efficacy studies with at risk children: Implications for the handicapped. Analysis and Intervention in Developmental Disabilities 1985;5:7–31.
  1. Spittle AJ, Orton J, Doyle LW, Boyd R. Early developmental intervention programs post hospital discharge to prevent motor and cognitive impairments in preterm infants. Cochrane Database Syst Rev. 2007; 2: CD005495.
  1. Nair MKC. Early Child Development – Kerala Model. Global Forum for Health Research, Forum-3,  Geneva, Switzerland,  1999.
  1. Nair MKC, Early stimulation CDC Trivandrum Model. Indian J Pediatr. 1992;59: 663–7.
  1. Hive SS, Genetra. Determinants of Low Birth Weight: A Community based prospective Cohort study. Indian Pediatr 1994;31:1221–5.
  1. Volpe JJ. Observing the infant in the early hours after asphyxia. In: Gluk L (Ed.) Intrauterine asphyxia and the developing fetal brain. Year Book Publishing Company  Chicago:  1977:263–83.
  1. Brown JK, Purvis RJ, Farfar JO, et al. Neurological aspects of perinatal asphyxia. Dev Med Child Neurol 1974;16:567–80.
  1. Nelson KB, Ellenberg H. Antecedents of cerebral palsy: multivariate analysis of risk. N Engl J Med 1986;315:81–6.
  1. Blair E, Stanley FJ. Intrapartum asphyxia: A rare cause of cerebral palsy. J Pediatr 1988;112:519.
  1. Nelson KB. Ellenberg JH. Neonatal signs as predictors of cerebral palsy. Pediatrics 1979;64:225–32.
  1. Low JA, Galbraith RS, Muir DW, et al. The predictive significance of biological riskfactors for deficits in children of higher risk population. Am J Obstet Gynecol 1983;145:1059.9
  1. Scott. Out come of severe birth asphyxia. Arch Dis Child 1976;51:712–16.
  1. Nair MKC, Babu George, Jeyaseelan L. Pyritinol in Term Post Asphyxial Encephalopathy Babies - A Randomized Controlled Double Blind Trial. M.Med.Sc. Thesis Submitted to University of Newcastle,  Australia,  1994.
  1. Nair MKC, Geroge B. Early Detection and Early Intervention Therapy for Developmental Delay. In: IAP Textbook of Pediactrics, Jaypee Brothers Medical Publishers,  New Delhi,  Third edition 2006; 834–835.
  1. Sharma P, Gupta T, Ganguly NK, Mahajan RC, Malla N. Increasing Toxoplasma seropositivity in women with bad obstetric history and in new borns. Natl Med J 1997;10:65–66.
  1. Seth P, Manjunath N, Balaya S. Rubella infection: the Indian scene. Rev Infect Dis 1985;7 (Suppl. 1):S64.
  1. Peekham C. Congenital infections in the United Kingdom before 1970; the prevaccine era. Rev Infect Dis 1985; (7 Suppl. 1):S1.
  1. Stagno S, Pass RF, Cloud G, et al. Primary cytomegalovirus in pregnancy. Incidence transmission to fetus and clinical outcome. JAMA 1986;256:1904–86.
  1. Sergio S, Whitley RJ. Herpes infections of pregnancy. N Eng J Med 1985;313:1327–30.
  1. Juliet M. Coscia, Bruce K. etal. Effects of Home Environment, Socioeconomic Status, and Health Status on Cognitive Functioning in Children with HIV-1 Infection. Journal of Pediatric Psychology 2001;26(6):321–9.
  1. Janet A. DiPietro - Department of Population and Family Baby and the Brain: Advances in Child Development Annual Review of Public Health Vol. 21:455–71.
  1. National Scientific Council on the Developing Child, Young Children Develop in an Environment of Relationships, 2006.
  1. Nair MKC. Neonatal Survival - Role of Family Counsellor. Indian Pediatr 2004; 41:1201–2.
  1. Nair MKC, Armida Fernandez. Indian Academy of Pediatrics and National Neonatology Forum–Areas of Partnership. Indian Pediatr 2004;41:987–8.