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716 S P E C I A LT Y P R A C T I C E I N C R I T I C A L C A R E

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of the mother if necessary. The placenta is able to store need to accommodate for, and take into account, the
glucose by converting it to glycogen and reconverting it likely impact of the normal physiology of pregnancy
to glucose as required and is also able to store iron and on common ICU monitoring, interventions and care
some fat-soluble vitamins. (Table 26.4).
The placental membrane operates as a barrier between
the maternal and fetal circulations and provides a limited DISEASES AND CONDITIONS UNIQUE
protective function. Generally, few bacteria can cross the TO PREGNANCY
placenta, although viruses are able to cross fairly readily.
The placenta produces large volumes of hormones includ- There are a number of conditions unique to pregnancy
ing progesterone, oestrogens, placental lactogen, chori- that might cause a woman to become critically ill and
onic gonadotropin, growth factors, cytokine vasoactive result in admission to ICU including preeclampsia,
substances, placental growth hormone, thyrotropin and obstetric haemorrhage, amniotic fluid embolism and
corticotropin. The placenta does not have a nerve supply peripartum cardiomyopathy. These conditions are dis-
so all activities regulated by the placenta must be under- cussed in detail below.
taken by other mechanisms, e.g. chemical, hormonal
changes. PREECLAMPSIA
A full and comprehensive understanding of the placenta The umbrella term ‘hypertension in pregnancy’ is used to
remains elusive. We do know that the placenta is a highly describe a myriad of conditions in pregnancy where
complex organ with the ability to modulate a variety of hypertension is a major feature. These include gestational
metabolic effects in both the woman and the fetus. hypertension, pre-existing essential hypertension and
Disorders of the placenta are thought to be a major preeclampsia which incorporates eclampsia and Haemol-
contri butor to preeclampsia and small-for-gestational- ysis Elevated Liver enzymes and Low Platelets (HELLP)
age neonates. syndrome (Table 26.5). Comprehensive descriptions of
these conditions and their management have been pub-
Impact of Impaired Utero–placental lished by the Australian and New Zealand College of
Gas Exchange Obstetricians and Gynaecologists (RANZCOG) and the
Effective gas exchange across the placental membrane Society of Obstetric Medicine Australia and New Zealand
65,66
depends on sufficient maternal blood pressure and ade- (SOMANZ).
quate O 2 and CO 2 gradients for passive diffusion to occur. Preeclampsia is a condition unique to human pregnancy
In response to hypoxaemia, a fetal brain-sparing mecha- in that, whilst characterised by hypertension and protein-
nism goes into effect that increases fetal arterial pressure uria, it is a multisystem disorder consisting of variable
and redirects blood delivery to the main organs, namely clinical features caused by widespread vasospasm. The
the brain, heart and adrenal glands. This centralisation basis for preeclampsia remains unknown. The indication
64
of fetal blood flow is more apparent in response to mater- for ICU admission is usually related to organ failure,
nal hypoxaemia than to reduced utero–placental blood caused by the widespread vasospasm and reduced organ
flow. It appears that a less mature fetus (i.e. earlier gesta- perfusion that characterises the disease. Preeclampsia
67
tion) may be less susceptible to asphyxia than a fetus can be a very serious condition and remains a leading
at term. 64 cause of maternal death in both developed and develop-
ing countries. 68
Whether the fetus will die in utero or survive, and the
degree of any neurological compromise, depends on the
degree and duration of asphyxia, the recurrent nature of Aetiology
asphyxia, and the degree to which the fetus is able to The placenta is strongly implicated in the cause of pre-
compensate for the asphyxia. Antenatal asphyxia (asphyxia eclampsia; its removal is the only definitive treatment for
during pregnancy, not associated with labour) has been the condition. However, the exact mechanisms of the
linked to the development of cerebral palsy, behaviour aetiology of the disease remain elusive and are likely to
disorders and learning difficulties. The reasons and extent be complex and multifactorial. Theories explaining the
of individual variation in fetal outcome are unknown. pathophysiology of preeclampsia include immune mal-
adaptation, abnormal trophoblast embedding, endothe-
CLINICAL IMPLICATIONS OF lial activation and excessive inflammatory response, and
THE PHYSIOLOGICAL ADAPTATIONS a genetic susceptibility (Box 26.1). The contribution of
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OF PREGNANCY each component and whether all components are rele-
The beginning point of any nursing practice is an under- vant in all cases of preeclampsia is not known. It is fea-
sible that there are differing types of pathophysiology for
standing of normal anatomy and physiology. The normal mild preeclampsia that occurs at term, compared with
physiological adaptations of pregnancy can be used severe preeclampsia that often occurs prior to 34 weeks’
to explain the so-called ‘minor discomforts’ of pregnancy, gestation.
including constipation, varicose veins, indigestion,
breathlessness and fatigue. For a critically ill pregnant Preeclampsia is associated with impaired remodelling of
woman being nursed in ICU, these normal physiological the uterine spiral arteries and abnormal placental
changes are also highly relevant for her care. ICU nurses implantation. It is thought that maternal–fetal immune