Placental pathology as predictor of neonatal morbidity and neurological outcome in late preterm born infants

In industrialised countries, preterm birth is responsible for 75 percent of
neonatal morbidity and contributes to long-term neurodevelopmental problems.
Placental pathology may act as a causative factor in preterm birth. The
placenta plays a crucial role during pregnancy, with major implications for the
child if its function is impaired. Previous studies in term infants suggested
that several placental lesions are associated with long-term neurological
morbidity. It is also suggested that several placental lesions are associated
with early neonatal morbidity in preterm infants born <32 weeks gestational age
(GA). Recently, placental pathology was also reported as being the main cause
of foetal death. The most common cause of foetal death in the preterm period is
maternal hypoperfusion of the placenta in a pregnancy complicated by
hypertensive disorders. In the term period, foetal death is mainly caused by
developmental pathology of placenta parenchyma.
Little is known about placental pathology in preterm infants born between 32
and 36 weeks of gestational age, known as the late preterm infants. The
question arises whether the association between placental pathology and early
neonatal morbidity and neurological morbidity are the same as seen in early
preterm infants (born <32 weeks GA). A method to assess early morbidity is to
determine illness severity soon after birth by scoring several clinical
variables. A reliable instrument to measure illness severity in the first 24
hours after birth is the Score of Neonatal Acute Physiology Perinatal
Extension-II (SNAPPE-II). A non-invasive method to predict neurological outcome
in early infancy is the qualitative assessment of general movements according
to Prechtl*s method from videotape recordings.

The objective of this study is to determine whether placental pathology is
associated with early neonatal morbidity and the neurological development in
late preterm infants.
We hypothesise that more developmental pathology of the placenta will be found
compared to early preterm infants and that placental pathology will be
associated with higher illness severity shortly after birth and with a lower
quality of GMs.

Primary objectives:
- To determine the association between placental pathology and illness severity
during the first 24 hours after birth in infants born between 32 and 35+6 weeks
GA.
- To determine the association between placental pathology and neurological
outcome during the first 3 months after birth in infants born between 32 and
35+6 weeks GA.

Prospective observational cohort study in which 70 infants born in the UMCG
between 32 and 35+6 weeks gestation will be included. Only singleton infants
will be included, because placentas from a multiple pregnancy can show other
specific pathologies (e.g. twin-to-twin transfusion). Infants with chromosomal
abnormalities will be excluded. The inclusion will take place between 2011 and
2012.
Placentas will be examined by a perinatal pathologist as a part of normal
patient care. Illness severity during the first 24 hours after birth will be
determined by de SNAPPE-II score. This score consists of 9 clinical variables,
which will be retrospectively obtained from medical files. The neurological
condition will be evaluated by videotape recordings of the general movements on
day 5,8 and 15 after birht, term age and 3 months post term.

The qualitative assessment of GMs from videotape recordings is a sensitive
non-invasive, non-vulnerable method to assess brain function and to predict
neurological outcome. The non-invasive character of videotaping does not
interfere with routine clinical care since the camera will be placed in front
of or next to the incubator in a way that caregivers are not hindered by the
camera or lose sight on the monitor. Besides, the attending neonatologist and
the nurses will be informed that despite the infants being filmed, all
necessary care should be continued.
Data from this study can not be obtained in another population, as we are
interested in early neonatal morbidity in this specific late preterm infants
group. GMs are age-related and are only present from early fetal life onwards
until the end of the first half year of life.
The results of this study can help for a better understanding of the mechanisms
leading to neonatal morbidity and problems in neurological development in late
preterm infants. This insight might bring possible early interventions a step
closer.