58 Abstracts / Pregnancy Hypertension: An International Journal of Womens Cardiovascular Health 7 (2017) 5664
problems. The association of proteinuria with bad outcomes, partic-
ularly eclampsia and intrauterine death helped to strengthen these
believes. But the risk to mother is largely associated with high blood
pressure pulmonary oedema and renal failure is a rare cause of
maternal mortality. These complications are relatively easily man-
aged. However, the falls in the the incidence of maternal death
and eclampsia preceded the use of antihypertensive drugs or magne-
sium sulphate, implying environmental and basic care factors to be
preeminent in reducing the complications. As far as the baby is con-
cerned it is placental insufficiency and prematurity that are the main
complications. The current preeminence of the placenta as the driv-
ing force in pre-eclampsia is undermined by the fact that most pre-
eclampsi pregnancies are not associated with IUGR and most IUGR
are not associated wth pre-eclamspia. This is a multifaceted disease
that presents at different gestations and in different and the out-
comes can vary greatly due to the modifiers that exist such as obe-
sity and genetics. The fact that there is a strong association with
long term cardiovascular complications imply a maternal suscepti-
bility which could be environmental or genetic in nature. Pre-
eclampsia is still a disease of theories but they have changed and
there may be more than one answer.
doi:10.1016/j.preghy.2016.10.009
Computerised analysis of the antepartum cardiotocogram (CTG)
for care of the compromised fetus
Chris Redman a, , David Stanger b, Beth Albert a (a Nuffield
Department of Obstetrics and Gynaecology, John Radcliffe
Hospital, Oxford, United Kingdom, b Obstetric Systems at
Huntleigh Healthcare, Cardiff, UK)
Fifty years ago the fetus was inaccessible to objective measure-
ment. But the development of electronic fetal heart rate (FHR) mon-
itoring and ultrasound imaging revolutionised fetal care. Continuous
FHR monitoring was introduced and quickly implemented for intra-
partum monitoring. Its ability to detect fetal distress before labour
(antepartum CTG was also rapidly appreciated. But there were prob-
lems. The diagnosis of a terminal state is easy, but its prediction is
more difficult. The unresolved issue is calibrating the grey zone
between normality and the terminal trace. Conventional visual
assessment is well known to be very unreliable, both inter- and
intra-observer variations are unacceptably large. Computerised anal-
ysis has helped by standardising the interpretation and measure-
ment of grey-zone features which allows a more evidence- based
approach.
The DawesRedman system of computerised analysis was first
marketed in 1991, after nearly 15 years of development in the high
risk pregnancy unit in Oxford. It is currently commercially available
(Huntleigh Healthcare) and widely used in the UK, Europe, and the
Middle and Far East. It is based on the DawesRedman criteria of
normality which cover many aspects of the CTG including short term
variation, fetal heart rate, accelerations, deceleration, fetal move-
ments, fast sinusoidal patterns and the electronic quality of the
trace. Some of the criteria are specific for gestational age. As would
be expected the preterm fetus has different limits of normality from
the term fetus. These criteria are comparable to the FIGO and NICE
criteria, but more extensive, more sophisticated and based on better
evidence. Application of the DawesRedman system abolishes the
requirement for a trace of fixed duration. When all criteria of nor-
mality have been met, advice is given that the CTG can be stopped.
This might be after 10 min or after 55 min. The average is about
1618 min. If criteria are not met at 60 min the CTG is classified as
Christopher.Redman@obs-gyn.ox.ac.uk
abnormal (criteria are not met), the underlying features are high-
lighted and further investigation and management decisions are nec-
essary. Overall the flexibility of the duration of monitoring saves
time. The criteria are evidence based on more than 100,000 antepar-
tum CTGs in the Oxford archive.
In this meeting three aspects of the system will be presented: its
pathophysiological basis (Redman), its clinical implementation
(Stanger) and its use by midwives in a high risk unit (Albert).
doi:10.1016/j.preghy.2016.10.010
Early and late onset preeclampsia: Two sides of the same coin
C.W. Redman (Nuffield Department of Obstetrics and
Gynaecology, John Radcliffe Hospital, Oxford OX3 9DU, UK)
Pre-eclampsia is caused by the placenta. Although its pathogene-
sis is not clear, a critical risk factor is inadequate antenatal care,
because it can prevent most of the secondary complications of the
disorder.
Pre-eclampsia is clinically defined by the secondary features of a
primary placental disorder. There are probably several subtypes of
preeclampsia of which early (EO-PE) and late onset disease (LO-PE)
are the best known. These are classified by the time of delivery-
EO-PE, delivered before 34 weeks and LO-PE, after 37 weeks; while
intermediate onset disease (3437w_eeks) is a mixture of both types.
One of the major differences is that EO-PE is usually complicated by
intrauterine growth restriction (IUGR) while LO-PE is not. Another
difference is that there is clear placental pathology with EO-PE while
LO-PE placentas are usually normal to routine clinicopathological
examination. The pathology of EO-PE comprises lesions of uteropla-
cental malperfusion. These are associated with maladaptation of the
uteroplacental spiral arteries in early pregnancy (818 weeks, poor
placentation) such that they are too small and too contractile to sus-
tain the non-pulsatile, high volume, low pressure flow needed by the
third trimester placenta. The result is oxidative stress and even
infarction that damage placental tissue. The spiral arteries may also
be obstructed by acute atherosis and atherosclerosis-like lesion that
causes arterial thrombosis which underlies the infarctions.
The surface syncytiotrophoblast layer, in direct contact with
maternal blood, appears to be particularly vulnerable to damage. It
is also the source of pre-eclampsia biomarkers such as sFlt-1 or pla-
cental growth factor (PlGF). It will be explained why these are, in
fact, markers of syncytiotrophoblast damage. Changes in the circu-
lating sFlt-1 and PlGF levels at term indicate that syncytiotro-
phoblast damage is an increasing feature of normal pregnancy.
Moreover the pathology, visible only to electron microscopy reveals
widespread syncytiotrophoblast damage. Evidence is presented that
this results from diffuse placental hypoxia, which develops as the
placenta outgrows the capacity of the uterus and its vasculature to
support the increasing demands of the term placenta, Hence EO-PE
and LO-PE both result from the same problem, malperfusion, which
has very different causes.
doi:10.1016/j.preghy.2016.10.011
Circulating levels of natural killer T cells and EPC cells in pre-
eclamptic pregnant women
F. Basile, A. Santamaria, L. Rizzo, G. Zoccali, D. Giordano, S. Loddo,
R. DAnna (Department of Human and Developmental Pathology,
University of Messina, Italy)
Natural killer T cells are bone marrow origin, they represent
about 70% of decidua leukocytes and play an important role in the
remodeling of spiral arteries [1]. Endothelial progenitor cells (EPC)