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SURVIVAL CAREER
As part of the process-context approach, Hutter (1998a, 1998b) and Padmadas (2000)
developed a model of reproductive health that incorporates the childs survival career next to
the mothers reproductive career and her health career. A central element in this model is the
link between health and survival of the child and the reproductive health of the mother. As in
the life course approach to health (see Section 3.2.1), this model thus looks back across
generations and considers the intergenerational transmission of health.
The model is based on two well-known models used by demographers: the fertility
model of Bongaarts and Potter (1983) and the model on child survival by Mosley and Chen
(1984), which has been elaborated by Van Norren and Van Vianen (1986). An important
notion in the fertility model is the idea of proximate determinants that have a direct effect on
the outcome of interest. Bongaarts and Potter (1983) distinguish between variables that affect
fertility directly (the proximate determinants) and factors that affect fertility indirectly. The
proximate determinants of fertility, or intermediate fertility variables, are the biological and
behavioural factors through which social, economic, and environmental variables affect
fertility (1983, p.1), or:
Social, economic,
environmental
factors
Proximate
determinants
Fertility
Similarly, Mosley and Chen (1984) identify proximate determinants or intermediate variables
that directly affect child survival. All social and economic factors operate through these
determinants.
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Figure 3.1: Integrated model of mothers reproductive career and childs survival career
Heart rate
Respiratory effort
Muscle tone
Reflex irritability
Colour
Absent
Absent
Flaccid
No response
Blue, pale
< 100/min.
Slow, irregular
Some flexion of extremities
Grimace
Body pink, extremities blue
> 100/min.
Good, crying
Active motion
Vigorous cry
Completely pink
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Source: Van der Veen 2001, adapted from Dancis and Schneider 1986
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Days from
ovulation
Days from
LMP
Characteristic
Zygote
Morula
Blastocyst
Implantation
Embryo
Foetus
Viable infant
Term and newborn infant
0
1-2
3-6
6-7
7-48
49-181
154+
245+
14
15-16
17-20
20-21
21-62
63-195
168+
259+
Celldivision
Differentiation
Differentiation
Interaction
Organogenesis
Growth and maturation
Growth and maturation
Adaptation
Source: Van der Veen (2001) who adapted it from Kline et al. (1989) and Moore and
Persaud (1998)
The term gestation is used to denote the developmental process evolving within the
embryo and foetus (Van der Veen 2001, p.52). A model of gestation thus represents the
schedule of foetal development including the processes of organogenesis and physical growth.
The developmental process from zygote to full-term foetus may be divided into stages of
variable length, as shown in Table 3.2. These stages were also discussed in Section 3.2.3.
Figure 3.3: Gestation as a process of interaction
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Risk factors
(VI)
(V)
Neonatal process
(I)
Final outcome
(IV)
Intermediate outcome
(III)
Gestation/pregnancy
and birth outcome
Risk factors
Birth process
(II)
Gestation/pregnancy
process
Final outcome
(VIII)
Neonatal survival
status
Intermediate outcome
(VII)
Neonatal outcome
Context
Risk
factors
(I)
Adverse
pregnancy and
birth outcome
(III)
Foetal loss /
death (IV)
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Neonatal
death
(VIII)
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including:
- maternal factors
- complications of
placenta, cord, and
membranes
- birth complications
Chapter 9
Risk factors
RISK FACTORS
congenital anomalies
low birth weight
preterm birth / low gestational
age
intrauterine growth retardation
/ small-for-gestational-age
birth asphyxia
Chapters 6, 7, and 8
INTERMEDIATE OUTCOMES /
RISK FACTORS
spontaneous
abortion
stillbirth
Chapters 5 and 8
Foetal loss
early neonatal
death
neonatal death
Chapters 5 and 8
Neonatal death
FINAL OUTCOME
(survival status)
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%
7.5
6
5
2
1.4
3.5
1.3
20
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Medication
Androgenic hormones (androgens
and certain progestins)
Anticonvulsant drugs
Coumarin
Diethylstilbestrol (DES)
Folic acid antagonists
(e.g. aminopterin)
Isotretinoin
Lithium
Retinol (vitamin A)
Tetracycline
Thalidomide
Other environmental agents
Ionizing irradiation
Methylmercury
Polychlorinated biphenyls
Sources: Kalter and Warkany 1983; Moore 1986; Beckman and Brent 1987; Kline et al. 1989;
Cunningham et al. 1993; Keeling and Boyd 1993; Leck 1994 cited by Shibuya and Murray 1998c
Environmental or exogenous factors and agents that damage the unborn child or cause
abnormal development are labelled teratogens. Kline et al. (1989) define a teratogen as a
factor extrinsic to the developing organism that acts in the interval between conception and
birth to injure the progeny or provoke abnormal development (p.3). Teratogens include
micro-organisms, medication and other drugs, chemical substances, and radiation (see Table
3.4). In addition, Beckman and Brent (1987) note mechanical problems (e.g.
oligohydramnios2, uterine malformations, extrinsic pressure, and uterine contractions) as
causes of malformations. Furthermore, advanced maternal age and family history are wellknown and important risk factors for chromosomal aberrations.
Further refinement: three important types of anomalies
The large range of congenital anomalies makes it difficult, and sometimes even irrelevant, to
study all types of anomalies. Indeed, many studies and articles focus on only one specific type
of anomaly. The most frequent congenital anomalies among newborns in the Netherlands are
neural tube defects plus heart defects, skeletal defects, and mental retardation (Bonsel and
Van der Maas 1994). These are also important causes of death. In developed countries, the
major causes of death in the neonatal period and in infancy among all congenital anomalies
are those of the cardiovascular system and those of the central nervous system, or more
specifically congenital heart disease and neural tube defects. Moreover, anomalies of the
2
Oligohydramnios: a volume of amniotic fluid below the normal limits (Cunningham et al. 1993).
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A large part of the information below is derived from Kramer (1987a), Kline et al. (1989), and
Pittard (1993). Additional sources include Batcup (1993), Cunningham et al. (1993), Keeling
(1993), Ott (1995), Bakketeig (1998), Shibuya and Murray (1998a), Van der Veen (2001).
Low birth weight
The WHO (1993) describes birth weight as the first weight of the foetus or newborn obtained
after birth. For live births, birth weight is preferably measured within the first hour of life
before significant postnatal weight loss. Low birth weight (LBW) is defined as a birth weight
of less than 2,500 grams. Furthermore, very low birth weight (VLBW) is less than 1,500
grams and extremely low birth weight (ELBW) below 1,000 grams (WHO 1993). However, it
is worth noting that these absolute cut-off points are somewhat arbitrary. In developing
countries average birth weight is often lower than the weights observed in developed regions,
yet birth weight-specific neonatal mortality rates may be lower. Some authors propose
adjusting the defining limit of LBW for newborns in developing regions to a more pragmatic
weight threshold such as 2,000 grams.
It is generally recognised that birth-weight distributions are essentially normal
(Gaussian) but slightly negatively skewed with additional births in the lower or left tail, i.e. an
excess of newborns with low birth weights (Wilcox and Russell 1983a; Wilcox and Russell
1986; Chen et al. 1991). It is assumed that the birth weight distribution in any population is a
mixture of two distributions: a predominant distribution that is Gaussian and a residual
distribution with a smaller mean. The predominant distribution is regarded as the distribution
of the normal population while the residual component may imply less organised, perhaps
pathological, influences (Wilcox and Russell 1983a, p.318). Breaking down the distribution
into these two components has been used in the analysis of mortality in relation to birth
weight (Wilcox and Russell 1986) and for the calculation of population-specific low birth
weight thresholds (Chen et al. 1991).
The cause of low birth weight is multifactorial. Numerous factors have been associated
with LBW or are thought to affect birth weight, among them genetic and constitutional factors
such as sex of the foetus/infant, maternal height and weight, race, and birth order or parity
(Kramer 1987a, 1987b; Klln 1988; Cunningham et al. 1993). However, there are two
pathological mechanisms or processes that may directly lead to low weight at birth: (1) short
duration of gestation and (2) retarded foetal growth. In other words, a pathological low birth
weight may be the result of preterm birth, intrauterine growth retardation (IUGR), or a
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Meconium: the first faeces of the newborn. In the situation of foetal distress and suffocation, it is
sometimes excreted before birth, into the amniotic fluid.
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5
6
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Pre-eclampsia: hypertension in pregnancy accompanied by protein in the urine and/or oedema (see
Section 9.2.1).
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