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The incidence of maternal collapse and severe maternal morbidity is unknown. Recent studies estimate that maternal collapse occurs in between 0.14 and 6 per 1000 births [1, 2]. In hospital, maternal collapse and sudden cardiac arrest are usually related to peripartum events and the outcome depends on effective resuscitation and identification and effective treatment of the underlying cause . Therefore, staff on the delivery suite must be expertly trained in advanced life-support techniques and resuscitation equipment should be readily available.
The maternal body accumulates water in pregnancy. Total body water can increase by up to 8 L. Oestrogens increase plasma renin activity with enhanced renal sodium absorption and water retention (renin–angiotensin–aldosterone system). Plasma osmolality decreases by about 10 milliosmol/kg below non-pregnant levels [1, 2]. These changes promote sufficient placental perfusion as the plasma volume rises steadily throughout the first two trimesters and plateaus at around 32 weeks. Reduced maternal plasma volume is associated with abnormal pregnancy outcome .
The normal human heart is able to tolerate recurrent episodes of pregnancy-related volume overload without compromising normal function . Disturbances in the cardiovascular system and the regulation of fluid balance can lead to changes in blood pressure and to hypotension or hypertension. Imbalance in salt and fluid regulation is common and can cause oedema in later stages of pregnancy.
Maternal collapse is an acute life-threatening event where the mother becomes unconscious due to cardiorespiratory or neurological compromise at any stage in pregnancy or up to 6 weeks postpartum. During resuscitation, aortocaval compression reduces cardiac output during chest compression. The risk of aspiration during resuscitation is increased due to a more relaxed lower oesophageal sphincter muscle and elevated gastric acid volume production. Amniotic fluid embolism (AFE) can also lead to fetal collapse of unknown origin that precedes maternal collapse. Uncontrolled hypertension can lead to intracranial haemorrhage. Typical clinical signs are severe, never-experienced headache preceding maternal collapse. Hypervolaemia, hypoxia, hyperkalaemia/metabolic disorders, hypothermia, thromboembolism, toxicity, cardiac tamponade, tension pneumothorax are some of reversible causes for maternal cardiac arrest. A cardiac arrest trolley and defibrillator, including wedge for left lateral tilt should be available on all maternity units and checked daily.
This chapter discusses the key implications, diagnostic signs and management techniques for fluid overload and underload during pregnancy. Pulmonary oedema, although uncommon in pregnancy, is associated with an increase in maternal and fetal morbidity and mortality. Inadequate plasma volume expansion in pregnancy is linked to poor fetal outcome. Volume loss due to hyperemesis gravidarum or haemorrhage can lead to maternal hypotension, collapse and fetal distress due to poor placental perfusion. Hypoxia and radiological signs of pulmonary oedema in chest X-ray are some diagnostic signs. Management for fluid over load is to look for causes of volume overload, e.g. underlying cardiac disease, sepsis, tocolytic therapy or preeclampsia. Hypovolaemic shock with cardiac, renal or other organ failure is causes of volume under load. If facilities for high-dependency care and invasive haemodynamic monitoring are unavailable, it is important to concentrate eforts on strict control of fluid balance.
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