Abstract
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 [3].
The normal human heart is able to tolerate recurrent episodes of pregnancy-related volume overload without compromising normal function [4]. 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.
Physiological Changes to Fluid Status in Pregnancy
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 [3].
The normal human heart is able to tolerate recurrent episodes of pregnancy-related volume overload without compromising normal function [4]. 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. While in the first and second trimester maternal fluid regulation appears normal, water load is not easily excreted in the last trimester and fluid regulation is more vulnerable with the risk of overload and underload. During labour and postpartum, demands on the regulatory systems further increase. In the postpartum period, mobilisation of fluids can lead to a drop in colloid osmotic pressure of up to 30%. The outlined physiological changes to maternal fluid balance through the stages of pregnancy emphasise the need for careful fluid management, especially in patients with underlying medical disease or acute illness.
Fluid Overload
Fluid overload can lead to pulmonary oedema, which is a significant cause of morbidity and mortality in pregnancy and early postpartum. The incidence in pregnancy is estimated between 0.08% and 0.5 % [5, 6]. In patients with preeclampsia, fluid overload can also cause cerebral oedema with high maternal mortality. Attention to volume status is important in any woman in labour, but strict attention must be paid to fluid balance in patients with any pre-existing medical disease. This includes careful monitoring of fluid input and output on an early-warning or high-dependency chart in a dedicated high-dependency unit. A senior clinician should have overall responsibility for the management of the patient. There should be early involvement of consultant obstetric anaesthetists and/or intensivists as part of a multidisciplinary approach. Always check for signs of fetal distress due to maternal compromise and consider early delivery to improve maternal outcome.
Risk Factors for Fluid Overload
Maternal Cardiac Disease
Diminished myocardial function or cardiac outflow tract obstruction frequently deteriorates in pregnancy with a high risk of peripheral and/or pulmonary oedema and congestive cardiac failure. Women with pre-existing hypertension, pregnancy-induced hypertension or preeclampsia may develop diastolic cardiac dysfunction and left ventricular hypertrophy with reduced cardiac compliance to fluid challenges. Most cardiac deaths in pregnancy occur in women with no previous cardiac history; therefore it is important to pay attention to potential cardiac risk factors (maternal age, lifestyle, ethnicity, clinical history) when administering intravenous fluids.
Severe Infection
In patients with sepsis and generalised increase in capillary permeability, fluid resuscitation should be guided by invasive haemodynamic monitoring due to the risk of fluid overload.
Preeclampsia
Preeclampsia leads to endothelial damage with increased capillary permeability and decreased colloid osmotic pressure [5]. In addition, there is a frequent increase in peripheral vascular resistance with myocardial diastolic dysfunction. These women are at a high risk of fluid overload and should be treated with fluid restriction and close monitoring of their fluid balance. Acute pulmonary oedema is a sign of disease severity and a leading cause of death in women with this condition.
Use of Tocolytic Agents
Simultaneous use of (multiple) tocolytic agents, particularly ritodrine and terbutaline, is a common cause of maternal pulmonary oedema. This may be explained by the prolonged catecholamine exposure, which can lead to maternal myocardial dysfunction, changes in pulmonary capillary permeability and also iatrogenic volume overload to treat maternal tachycardia and attempted fetal resuscitation and the concurrent use of steroid medication.
Other Risk Factors
Corticosteroids lead to water retention and illicit drug misuse can lead to disturbed fluid balance. Obesity, multiple pregnancy, underlying endocrine disorder such as hyperthyroidism or phaeochromocytoma and pre-existing renal disease can increase the risk for disturbances in fluid balance and volume overload [6].
Iatrogenic Fluid Overload
This occurs commonly in patients with long, complicated labour and frequent episodes of fetal distress, when fluid boluses are given in an attempt to restore normal maternal haemodynamic state. This is a major preventable factor and it is important to monitor the fluid intake of all women at risk during labour and postpartum [7].
Clinical Signs
Peripheral oedema, dyspnoea, tachypnoea, inappropriate weight gain
Paroxysmal nocturnal dyspnoea, inability to lie flat
End-expiratory crackles on auscultation, pink frothy sputum
Hypoxia and radiological signs of pulmonary oedema on chest radiograph (Figure 33.1)
Figure 33.1 Chest radiograph showing pulmonary oedema.
Management of Fluid Overload
If the patient is in respiratory distress with clinical signs of pulmonary oedema, start treatment before investigations.
Principles of Management
Look for causes of volume overload, for example, underlying cardiac disease, sepsis, tocolytic therapy or preeclampsia
Administer oxygen. Position the patient upright. Check airway, breathing and circulation. Remember laryngeal swelling can make mask ventilation and/or intubation significantly more difficult; therefore careful airway assessment is essential.
Establish venous access. Peripheral oedema may make this difficult. Consider central venous access and invasive heamodynamic monitoring [8, 9]. Non-invasive cardiac output monitoring and echocardiography may be useful to distinguish cardiac and non-cardiac causes of fluid overload in women with severe preeclampsia and/or underlying cardiac disease.
Urinary catheter with hourly fluid balance. Aim for urine output > 0.5 mL/kg per hour [8]. Women with preeclampsia frequently have a brief period of oliguria up to 6 hours after delivery. This should be anticipated and not overcorrected [10].
Fluid restriction. Pay attention to intravenous drug therapy and fluid maintenance. Overall fluid input should not exceed 85 mL/hour or 1 mL/kg per hour. It may often be necessary to use double/triple concentrations of drugs to avoid infusion of excessive amounts of fluid. The choice between colloid or crystalloid solutions remains controversial. Crystalloid may reduce plasma colloid pressure even further. Colloid solutions may contribute to volume overload during postpartum fluid mobilisation [11]. Consider colloid solutions if the colloid osmotic pressure is markedly decreased (<12 mm Hg).
Take blood for renal and liver function (including albumin) tests and full blood count. Consider blood gas analysis, especially in cases where the cause of fluid overload is unclear.
Arrange for a chest radiograph to identify pulmonary oedema but also look for other underlying causes (pneumonia, cardiac disease).
Use diuretics in cases of acute pulmonary oedema and respiratory compromise with underlying cardiac disease or iatrogenic fluid overload. The use of diuretics in women with preeclampsia remains controversial because of the intravascular hypovolaemic state of preeclamptic women, despite the presence of peripheral oedema [9].