Anatomical Changes

The heart undergoes anatomical change during pregnancy including left ventricular hypertrophy and the cross-sectional areas of the aortic, pulmonary and mitral valves increase by 12–14%. ECG changes include non-specific ST segment changes, the development of a Q wave in Lead III and a left-axis deviation pattern.¹⁵ These are evident by the end of the first trimester and remain throughout the pregnancy.¹⁶ As with the interpretation of any ECG, consider other information like the patient presentation (signs and symptoms) and blood test results to form a complete assessment of the woman’s condition.

Blood Volume

Very early in the pregnancy there is generalised vasodilatation resulting in sodium and water retention. The causes of the vasodilatation are likely to include hormonal factors (e.g. progesterone), peripheral vasodilators like nitric oxide, and potentially, an as-yet unidentified pregnancy-specific vasodilatory substance.¹⁷ The end result is a 40–50% increase in blood volume as well as reduced normal serum sodium level, from 140 to 136 mmol/L and a reduced plasma osmolality from 290 to 280 mosmol/kg. These changes persist throughout pregnancy and the osmoreceptor system resets to accept these values as normal.¹⁸

The red cell mass increases 20–40% whilst the plasma volume increases 40–50%. The resultant physiological haemodilution produces a relative anaemia which is thought to be beneficial for utero-placental perfusion. Venous haematocrit typically falls from a non-pregnant value of 40% to 34% near term.¹⁹ The increase in blood volume is evident from seven weeks’ gestation and peaks at around 30–32 weeks’ gestation, normally remaining at a stable level until delivery.^17,20 Women who do not experience this normal increase in blood volume are more prone to adverse outcomes such as preeclampsia or small- for-gestational-age infant.²¹ The additional blood volume is also thought to accommodate the normal blood loss associated with birth (<500 mL). Pregnant women are renowned for being able to maintain stable vital signs, with blood losses as much as 1500 mL, before acutely deteriorating.

Blood Pressure

Blood pressure reduces in pregnancy, with the lowest normal blood pressure recorded during the second trimester (16–28 weeks), and returns to pre-pregnancy levels near term (see Table 26.2). Blood pressure begins dropping as early as 8 weeks’ gestation, in association with the generalised vasodilatation occurring at this time. If a woman does not experience the characteristic lowering of blood pressure, particularly during the second trimester, it is viewed with suspicion and as a potentially abnormal sign.

Heart Rate, Stroke Volume and Cardiac Output

Maternal heart rate increases by 10–15 beats per minute during pregnancy with an increase noted as early as 5 weeks’ gestation.^16,22 The increase in heart rate may be a compensatory response related to the generalised vasodilatation, although a hormone-related effect cannot be ruled out.²³ Tachycardia (>100 beats/min) is an abnormal sign and warrants further investigation.²⁴ The stroke volume is noted to increase between 18 and 32%, beginning as early as 8 weeks’ gestation.^25,26 An increase in cardiac output is detectable from 5 weeks gestation and continues to be 30–50% higher by 32 weeks gestation.^17,26 Hence, a normal cardiac output in pregnancy may be as high as 8 L/min. The increased cardiac output is achieved by a combination of the increases in heart rate and stroke volume.

Systemic Vascular Resistance

The generalised vasodilatation observed in early pregnancy reduces systemic vascular resistance by up to 35%, with some reduction already detectable by 8 weeks’ gestation.²⁷ The development of the low-resistance utero-placental junction was thought to act as an arteriovenous shunt and contribute to the lowered SVR seen in pregnancy. However, the very-early-observed decrease in SVR argues against this theory and perhaps circulating substances that exert a vasodilatory effect on the vasculature is a more likely proposition.

Effect of Posture on Maternal Haemodynamics

It is evident that from as early as 5–8 weeks’ gestation, pregnancy is characterised by general vasodilatation, increased blood volume, increased cardiac output and is generally a hyperdynamic state. As the pregnancy advances, the bulk of the uterus begins to have an impact on maternal haemodynamics. After 20 weeks’ gestation, a woman lying flat on her back may experience supine hypotension, secondary to compression of the inferior vena cava and aorta with subsequent reduction in venous return, cardiac output and placental flow. A reduction in placental flow may occur even without a recorded drop in blood pressure. Consequently, it is inadvisable to nurse a pregnant woman more than 20 weeks’ gestation, flat on her back. A left lateral lying position results in the best cardiac output, although manually displacing the uterus to the left whilst the woman remains supine is also effective in relieving the aorto-caval compression.²⁸ Otherwise, the use of a wedge or pillows to maintain a left lateral tilt of at least 15 degrees is recommended to minimise aorto-caval compression.²⁹

Postpartum Cardiovascular Changes

Heart rate returns to pre-pregnancy levels by 10 days postpartum; blood pressure has normally returned to pre-pregnancy levels by term and does not change during the puerperium.^23,27 The first few days of the puerperium are associated with a diuresis which reduces the circulating volume and results in haemoconcentration of blood. Consequently a postpartum haemoglobin level will increase over the first few days and the risk of thromboembolism is higher during the postpartum period than during pregnancy. Due care should be paid to postpartum women in ICU to prevent deep vein thrombosis, particularly as many of these women are in ICU with complications of preeclampsia or severe obstetric haemorrhage, both of which further increase the likelihood of thromboembolism.³⁰

Cardiac output increases briefly in the immediate postpartum period to compensate for blood losses and tends to increase by 50% of the pre-delivery value, at this point in the post partum phase stroke volume is increased while the maternal heart rate is often slowed.²³ For most women, the immediate postpartum elevation in cardiac output only lasts for an hour or so. By 2 weeks postpartum, many haemodynamic parameters have returned to pre-pregnancy levels for the majority of women, although some have been recorded as remaining above pre-pregnancy levels at 12 months postpartum, including cardiac output.^14,27 There is increasing acknowledgement that for many women following childbirth, there is a permanent modification to the cardiovascular system, although whether this persists into the menopausal era is not known and whether it impacts on cardiovascular disease risk is also unknown.²⁷

Changes to the Upper Airways and Thorax

Normal physiological changes of pregnancy include generalised vasodilatation of the upper airway vasculature, increased fat deposition around the neck and an increase in mucosal oedema. A combination of hormonal influences, likely progesterone and oestrogen, are at play. These physiological changes are thought to be responsible for the symptoms of rhinitis, nasal stuffiness and epistaxis that are common in pregnancy.¹⁷

Changes also occur to the chest wall with relaxation of ligaments resulting in an outwards flaring of the lower ribs and a 50% increase in the subcostal angle.³¹ Both the diameter and the circumference of the thorax increase by 2 cm and 5–7 cm respectively.^31,32 These physical changes are thought to cause the diaphragm to rise by 5 cm, with this occurring early in pregnancy and well before there is any pressure from the advancing uterus.³² Respiratory muscle function does not change significantly during pregnancy and rib cage compliance is unaltered.³¹ The functional reserve capacity (the amount of air left in the lungs after expiration) is reduced 17–20% making the pregnant woman more vulnerable to hypoxaemia during any apnoeic period. Chest X-ray interpretation is unchanged during pregnancy, despite the variety of changes to cardiovascular and respiratory flows.²³

Changes to the Physiology of Breathing

From as early as 5 weeks’ gestation, multiple factors result in an increased respiratory drive. The increase in progesterone levels is thought to lower the PaCO₂ threshold in the respiratory centre to stimulate respiration resulting in hyperventilation.¹⁵ Other related factors include an oestrogen-mediated progesterone response, lower serum osmolality, strong ion difference and increased level of wakefulness that are also present in pregnancy.^33–35 Increased minute ventilation begins soon after conception and peaks at 40–50% at term.¹⁵ The increase in minute ventilation is achieved by a 30–50% increase in tidal volume (e.g. an increase of 200 ± 50 mL at term), with no increase in respiratory rate.¹⁵

Due to the altered respiratory function, normal arterial blood gas values are different in pregnancy compared to the non-pregnant values (see Table 26.2). The reduced PaCO₂ level creates the necessary gradient for the fetal CO₂ to passively cross the placenta for maternal excretion. PaO₂ normally increases by 10 mmHg, although the PaO₂ level is affected by posture, particularly as the pregnancy progresses.³⁶ In advanced pregnancy, the supine position is associated with a reduction in PaO₂ of up to 10 mmHg when compared with the same woman in the sitting position.³⁷ The kidneys compensate for the lowered PaCO₂ by increasing bicarbonate excretion, which serves to maintain a normal pH.^36,38,39 Normal oxygen saturation in pregnancy has not been well investigated, however, it is likely to be 97–100% at sea level, with a healthy pregnant woman’s saturation not dropping below 95% during moderate exercise.^40,41

The notable hyperventilation of pregnancy is associated with a feeling of breathlessness in up to 75% of healthy pregnant women when attending to activities of daily living.³³ Distinguishing what is considered ‘physiological dyspnoea’ from pathological dyspnoea, for example developing cardiomyopathy, can present a challenge in pregnancy. Dyspnoea at rest is usually an abnormal sign in pregnancy.⁴²

Postpartum Respiratory Changes

There is complete resolution of the spirometry and arterial blood gas changes by 5 weeks postpartum.³⁶ Unfortunately there has been no study reporting the daily transition of these parameters over the first week postpartum – the timing when a postpartum woman is likely to be in ICU. One very old study reported that CO₂ levels took between two and five days to return to normal non-pregnant values postpartum.⁴³ Regardless, with the fetus delivered, it is probable that no harm will be done to a woman by the titration of her ventilation requirements according to non-pregnant conventions and arterial blood gas values.

Postpartum Renal Changes

The most significant renal change is the diuresis that occurs in the 1–3 days postpartum. This diuresis serves to offload the additional blood volume that the woman has had circulating for the duration of the pregnancy. There has been little examination of ‘normal urine output’ with the standard 0.5 mL/kg/hr reported as a minimum acceptable level, however a true ‘normal’ level is likely to be closer to 0.8 mL/kg/hr.⁴⁸ Creatinine levels are within the normal non-pregnancy range within 24 hours postpartum, whilst the lower urea levels remain for at least 48 hours.⁴⁶ The bladder returns to the pelvis in the early postpartum period as the uterus and other organs resume their pre-pregnancy position.

Hepatobiliary Changes in Pregnancy

There is no significant increase in hepatic arterial blood flow during pregnancy, despite the 40–50% increased cardiac output.⁵¹ There is, however, a doubling of bloodflow to the liver supplied by the portal vein,⁵¹ which may have an impact on oral medication metabolism in the liver. There are also changes in other hepatic enzymes responsible for drug metabolism, resulting in a change in pharmacokinetics of some medications, e.g. higher plasma levels of midazolam. Serum albumin levels reduce to 30–40 g/L for the majority of pregnancy, with levels as low as 25 g/L normal during the second postpartum week.⁴⁶ This low albumin level reduces colloid osmotic pressure that contributes to the dependent oedema, for example swollen ankles, that is common in pregnancy.

The general smooth muscle vasodilatation affects the hepatobiliary ducts, resulting in sluggish bile motility and delayed emptying of the gall bladder. These changes lead to an increased incidence of cholelithiasis and cholecystitis during pregnancy.

Placenta

The placenta develops from the trophoblastic layer of the fertilised ovum and is completely formed and functioning ten weeks following fertilisation.⁶¹ The chorionic villi constitute the undersurface of the placenta and attach to the uterine wall via the decidua. The end result is an interface whereby maternal blood fills a space in which the nutritive villi float and are bathed in the maternal blood (Figure 26.1). A few villi are more deeply anchored in the decidua and these are referred to as anchoring villi.⁶¹ The blood drains back into the maternal circulation via maternal sinuses and the endometrial veins. Approximately 150 mL of maternal blood, replenished three to four times per minute, bathes the villi in the intervillous space.⁶¹ The chorionic villi maximise the available surface area to optimise the exchange of products across the maternal–placental interface. By term, this surface area is said to be as large as 13 m².⁶² Initially, four layers of cells separate the maternal blood from the fetal blood, reducing to three after 20 weeks’ gestation; these cell layers are collectively referred to as the ‘placental membrane’ or ‘placental barrier’.⁶³ Damage to villi, such as a threatened abortion or blunt trauma, may result in mixing of the blood circulations.

FIGURE 26.1 The maternal–placental interface.¹¹

Role of the Placenta

The placenta provides six major functions to sustain the pregnancy and fetus: respiration, nutrition, storage, excretion, protection and endocrine.⁶¹ Fetal lungs are filled with fluid and all oxygenation and removal of carbon dioxide must be provided via the placenta. Fetal haemoglobin has a slightly different structure to adult haemoglobin and has a higher affininity for oxygen. Both oxygen and carbon dioxide cross the placental membrane by simple diffusion. Nutrients are actively transported across the placental membrane, with the placenta able to select the substances needed by the fetus, even at the expense of the mother if necessary.⁶¹ The placenta is able to store glucose by converting it to glycogen and reconverting it to glucose as required and is also able to store iron and some fat-soluble vitamins.

The placental membrane operates as a barrier between the maternal and fetal circulations and provides a limited protective function. Generally, few bacteria can cross the placenta, although viruses are able to cross fairly readily. The placenta produces large volumes of hormones including progesterone, oestrogens, placental lactogen, chorionic gonadotropin, growth factors, cytokine vasoactive substances, placental growth hormone, thyrotropin and corticotropin. The placenta does not have a nerve supply so all activities regulated by the placenta must be undertaken by other mechanisms, e.g. chemical, hormonal changes.

A full and comprehensive understanding of the placenta remains elusive. We do know that the placenta is a highly complex organ with the ability to modulate a variety of metabolic effects in both the woman and the fetus. Disorders of the placenta are thought to be a major contributor to preeclampsia and small-for-gestational-age neonates.

Impact of Impaired Utero–placental Gas Exchange

Effective gas exchange across the placental membrane depends on sufficient maternal blood pressure and adequate O₂ and CO₂ gradients for passive diffusion to occur. In response to hypoxaemia, a fetal brain-sparing mechanism goes into effect that increases fetal arterial pressure and redirects blood delivery to the main organs, namely the brain, heart and adrenal glands.⁶⁴ This centralisation of fetal blood flow is more apparent in response to maternal hypoxaemia than to reduced utero–placental blood flow. It appears that a less mature fetus (i.e. earlier gestation) may be less susceptible to asphyxia than a fetus at term.⁶⁴

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 asphyxia, and the degree to which the fetus is able to compensate for the asphyxia. Antenatal asphyxia (asphyxia during pregnancy, not associated with labour) has been linked to the development of cerebral palsy, behaviour disorders and learning difficulties. The reasons and extent of individual variation in fetal outcome are unknown.

Prevention of eclampsia

Magnesium sulphate has received the most attention as an anticonvulsant in preeclampsia, with its mechanism of action thought to be connected to the release of prostacyclin from the endothelium, reversing the vasoconstriction that is the basis of the disease.^80,81 Magnesium is the anticonvulsant of choice to reduce the incidence of eclampsia.^82,83 A common magnesium regimen is:^68,82

The optimal therapeutic level of magnesium required to reduce the risk of fitting is not well understood and many advocate against the need to monitor serum magnesium levels on the basis that clinical assessment of deep tendon reflexes, urine output and respiratory rate is adequate to identify potentially toxic magnesium levels,^68,82 although evidence is inconsistent. Other opinions suggests a therapeutic serum magnesium level of 2 mmol/L but there is no rationale provided for this level.⁸⁴

Control hypertension

Obtaining control of high blood pressure remains a priority not only to improve organ perfusion but to minimise the risk of cerebral haemorrhage, a well-demonstrated hazard of hypertension in preeclampsia.²⁴ Both systolic and diastolic pressures are important and care should be taken to ensure a controlled lowering of blood pressure, as a rapid drop can compromise fetal wellbeing. There is no evidence for the superiority of any specific antihypertensive, although there is some evidence that diazoxide may result in a potentially-harmful rapid drop in the woman’s blood pressure, and that ketanserin may not be as effective as hydralazine.⁸³ Intravenous hydralazine is the most common drug used to treat very high blood pressure with IV labetalol increasingly being used. Severe hypertension may be treated with IV GTN or nitroprusside. The target blood pressure is not well described, other than to avoid precipitous drops in BP and to maintain adequate placental perfusion. Research has used a target diastolic BP of 85–95 mmHg.⁸⁵

Optimal fluid management

Despite being hypertensive, preeclamptic women are usually plasma-volume depleted.⁸⁶ In the past, intravenous fluid was administered in an attempt to restore the deficit, with no advantage noted between colloids and crystalloids. More recently, there has been a move towards more conservative plasma volume expansion due to the risk of pulmonary oedema. In reviews of maternal deaths associated with preeclampsia, it was noticed that some women were dying from complications of fluid overload. Careful titration of intravenous fluid is required with the use of pulmonary artery catheters advocated by some to guide the administration of fluid in women with severe preeclampsia, to optimise plasma volume and organ perfusion without the development of pulmonary oedema.⁸⁷ Central venous pressure is universally accepted as unhelpful to guide fluid management in preeclampsia. See also Box 26.3.

Thrombophylaxis

Preeclampsia is an independent risk factor for thromboembolic disease and when combined with prolonged bed rest, as may occur with caesarean section, ICU admission, obesity and age ≥35 years, due consideration must be made on the need for thrombophylaxis (in the absence of any contraindications). Thus women with severe preeclampsia admitted to ICU may meet the requirements for treatment with compression stockings and low molecular weight heparin for a minimum of 7 days.³⁰

Betamethasone

Women in late pregnancy with severe preeclampsia diagnosed prior to 34 weeks’ gestation are normally prescribed a single dose of betamethasone (11.4 mg IM), to promote fetal lung maturity and surfactant production. A Cochrane Review has shown that treatment with antenatal corticosteroids reduces the risk of neonatal death, respiratory distress syndrome, cerebroventricular haemorrhage, necrotising enterocolitis, infectious morbidity, need for respiratory support and neonatal intensive care unit admission, with no adverse effects on the mother.⁸⁹

Optimal timing of delivery

Women with severe preeclampsia can only be definitively cured by delivery, no matter what the gestation. A number of studies have trialled ‘temporising treatments’, aimed at prolonging the pregnancy especially when a woman develops early onset severe preeclampsia (<34 weeks’ gestation). Whilst some have found that treatment with vasodilators and fluid administration prolongs pregnancy with no adverse effect, the general belief is that prolonging the pregnancy is associated with an increased chance of the maternal complications of preeclampsia, such as eclampsia, pulmonary oedema and cerebral haemorrhage.^68,90 Consequently, a woman with severe preeclampsia is usually stabilised (magnesium sulphate commenced and hypertension controlled) and arrangements for delivery are made. Ideally, women <34 weeks’ gestation should be transferred to a tertiary obstetric centre prior to delivery.

Placental abruption (or abruptio placentae)

Placental abruption is premature separation (i.e. before the birth of the baby) of a normally-sited placenta from the uterine wall and is responsible for about 25% of APH.⁹² Only a portion of the placenta separates with two-thirds separation considered severe. There are two relevant matters to consider with placental abruption: how much blood the woman has lost and how much placenta remains attached and functionally able to support the fetus. If the placenta partially separates along an edge of the placenta, blood loss is usually visible via the vagina. In some cases the centre part of the placenta detaches, leaving the rim attached all the way around (like the rim of a dinner plate) and in these cases, the blood loss is usually not visible via the vagina (i.e. is concealed). However, the woman may have lost substantial blood volume and be in hypovolaemic shock. This type of placental abruption is usually accompanied by severe abdominal pain and DIC commonly develops in response to blood being forced into uterine muscle tissue; referred to as a couvelaire uterus. Once half to two-thirds of the placenta is detached, the likelihood of fetal survival is low, especially if the woman is also hypotensive. In the majority of cases, only women with severe placental abruption are admitted to ICU and usually admission occurs following an emergency caesarean section. Understanding of the aetiology of placental abruption is not complete with approximately 20% of cases unexplained. For most women, placental abruption is associated with a known related factor like preeclampsia, blunt trauma (e.g. car crash) and sudden reduction in uterine volume (e.g. after delivery of the first baby in a twin pregnancy).

Placenta praevia

Placenta praevia is when some or the entire placenta is abnormally sited in the lower segment of the uterus, often referred to as a low-lying placenta. Placenta praevia is graded into four categories of severity according to the location of the placenta in relation to the cervix (Box 26.5). A vaginal birth is not possible with Grades III and IV as the placenta blocks the passage for the baby, necessitating a caesarean section. The lower uterine segment does not fully form until 28–32 weeks’ gestation and the shearing stress as the lower uterine segment forms may precipitate detachment of the placenta from the uterine wall causing maternal bleeding. However, bleeding can occur at any time, is usually painless and may be massive. Placenta praevia is the main cause of APH accounting for 30% of cases.⁹² As with placental abruption, management is dictated by the size of the blood loss and maternal condition, how much functioning placenta remains and fetal wellbeing, and whether bleeding is ongoing. In severe cases, the woman is usually taken to theatre for an emergency caesarean section.

Placenta accreta is a serious complicating condition that may occur in conjunction with placenta praevia. The attachment of the placenta to the uterine wall is abnormal and is considered morbidly adherent. There are three levels of severity, although often all three are referred to as placenta accreta (Box 26.6). Placenta accreta is strongly associated with prior caesarean section and a woman with an anterior placenta praevia and a prior caesarean section should be actively screened for placenta accreta (by ultrasound or MRI) prior to any elective caesarean section. Placental tissue can be very invasive and may infiltrate local structures like the bladder. Many women with placenta accreta undergo emergency hysterectomy at the time of caesarean section, as a means to remove the placenta and control bleeding. An alternative management is to deliver the baby by caesarean section and leave the placenta in situ.⁹³ As long as a portion of the placenta does not detach, there will be no bleeding and in most cases, the placenta will autolyse and be re-absorbed by the woman.

Maintaining circulating volume, oxygenation and perfusion

Haemodynamic instability following substantial blood loss is a frequent reason for admission to ICU.⁹⁹ Accurate estimation of blood loss is difficult as bleeding can be concealed, and the presence of amniotic fluid makes accurate blood volume loss estimation a challenge, potentially leading to an underestimation of fluid resuscitation needs. Furthermore, peripartum women are at an increased risk of acute pulmonary oedema, which further complicates fluid resuscitation.^100,101 Standard resuscitation fluids, such as normal saline, should be infused according to routine practice of the non-obstetric haemorrhage, remembering that large volumes of blood products may also be required.

Achieving haemostasis and correct coagulopathy

Specific interventions to control haemostasis include radiological arterial embolisation or balloon occlusion of the internal iliac arteries and emergency hysterectomy. It is not uncommon for women to need to return to theatre for abdominal packing for ongoing ‘ooze’ that may continue after a hysterectomy. Most women with severe obstetric haemorrhage in ICU have developed DIC that requires treatment with the appropriate blood products.¹⁰² DIC is particularly common in these women in part because of the normal changes in the clotting factors during pregnancy and in part due to the potential for an amniotic fluid embolism to have been the triggering event for the haemorrhage.^86,103,104

Large volumes of blood products, such as packed red cells, fresh frozen plasma, platelets and cryoprecipitate are often required. Guidelines recommending the ratio of red blood cells:fresh frozen plasma:platelets in acute major haemorrhage are under development in many countries. Increasingly it is thought that more aggressive use of fresh frozen plasma and platelets in line with red blood cell usage is needed to prevent and/or correct haemorrhage coagulopathy. A recent large trauma study found that a 1 : 1 ratio for both red blood cells/fresh frozen plasma and red blood cells/platelets, if given early following a major blood loss, resulted in significantly improved mortality.¹⁰⁵ There has been no similar study conducted in obstetric patients, although it is likely that obstetric patients may also benefit from more liberal early use of fresh frozen plasma and platelet transfusions. Importantly, the large trauma study found the increased ratios of FFPs and platelets were not associated with an increase in transfusion-related acute lung injury and acute respiratory distress syndrome from inflammatory mediators.¹⁰⁵ Finally, recombinant Factor VIIa has been used successfully in the management of severe obstetric haemorrhage and should be considered for use early in the management of the bleeding woman, with treatment more likely to be effective if administered before the woman becomes hypothermic and acidotic.¹⁰⁶

Preventing complications

Strategies to prevent the following complications should be implemented:

Epidemiology and Course of Asthma During Pregnancy

Asthma is the most common chronic health disease in pregnant women, affecting 4–8% of all pregnancies in the US.¹³² However, the incidence in Australia may be higher given the higher prevalence, 12–14%, of ‘current asthma’ in women of childbearing age.¹³³ The course of asthma during pregnancy is highly variable and not predictable for any individual woman. Approximately one-third of women experience an improvement in asthma symptoms, one-third report no change and one-third experience exacerbation of asthma.¹³⁴ Curiously, the fetal gender may be a relevant factor with the female fetus associated with a worsening of asthma symptoms.¹³⁵ Generally speaking, the more severe asthma symptoms a woman exhibits pre-pregnancy, the more likely she will experience an exacerbation during pregnancy resulting in hospitalisation.^136,137 Very severe exacerbations of asthma during pregnancy requiring ICU admission are rare. A persisting problem in pregnant women with asthma is the potential for reluctance to treat (by physicians) and decreased medication compliance (by women), based on concerns about the safety of medication during pregnancy, with a substantial number of asthma exacerbations in pregnancy associated with non-adherence to prescribed drugs.^138,139 Studies comparing medication use have shown that pregnant women are also less likely to be prescribed systemic corticosteroids than non-pregnant asthmatics.^138,140 The second and third trimesters are commonly the time when a worsening of asthma symptoms will develop, although women tend to have an improvement in symptoms for the last four weeks of a term pregnancy.¹³⁸

Effect of Asthma on Pregnancy

The relationship between asthma in pregnancy and adverse maternal and neonatal outcomes including preeclampsia, gestational diabetes, small-for-gestational-age neonates and preterm birth is inconsistent. The general belief is that poor maternal and neonatal outcomes are associated with poor asthma management and not a result of the treatment itself.¹³⁷

Management and Treatment Priorities

A pregnant woman admitted to ICU with asthma may be experiencing new-onset asthma or an exacerbation of preexisting asthma. Regardless, the management and treatment priorities are the same. Accurate diagnosis and evaluation of the disease is necessary and should involve the advice of a thoracic medicine specialist and an obstetrician, who will continue the care of the woman once discharged from ICU. Methacholine testing, used as a diagnostic tool for asthma, is contraindicated in pregnancy, and a woman with a clinical picture consistent with new-onset asthma, should be treated as such, until diagnostic testing can be conducted postpartum.¹⁴¹ Treatment of severe asthma in pregnancy is no different to the treatment in non-pregnant patients (see Chapter 14), apart from the additional needs to monitor fetal wellbeing and consider the normal respiratory parameters in pregnancy (Figure 26.2). Severe hypoxaemia associated with an exacerbation of asthma places the fetus at risk and should be avoided; maternal SaO₂ should remain ≥95%. Peak flow measures are recommended to be used during pregnancy to assess and monitor the woman’s condition, with the normal values unchanged in pregnancy.¹³⁷ The risks associated with current asthma medication use in pregnancy are far less than the risks associated with uncontrolled asthma, and the regular schedule of asthma medications should be prescribed in pregnancy according to asthma symptom level.¹⁴¹ Likewise, none of the common drug categories such as inhaled corticosteroids, long-acting β-agonists and leukotriene-receptor antagonists, is contraindicated during lactation.¹⁴¹

FIGURE 26.2 Acute management of exacerbation of asthma in pregnancy.¹³⁷

Treatment Priorities

All women with cardiac disease are considered to have a ‘high risk’ pregnancy and should receive maternity care by a multidisciplinary team including as a minimum, obstetrician, midwife, cardiologist and anaesthetist.¹⁵¹ The timing and location of delivery, choice of anaesthesia and delivery mode should each be discussed by the team with the woman, and planned well in advance. If a pregnant woman with cardiac disease is admitted to ICU, this multidisciplinary team should be consulted about her care. Priorities of care include:

Initial Evaluation of the Pregnant Patient: The Primary Survey

Consideration should be given to all women of childbearing age as to whether she may be pregnant. Determination of the presence of a pregnancy and the estimated gestation may be obtained from the woman (or friend/relative) or may require blood tests/physical examination/ultrasound.¹⁶⁰ If the woman is obviously pregnant, a rough estimate of gestation can be made by measuring the height of the fundus from the symphysis pubis. The height in cm equates to the number of weeks’ gestation, e.g. 22 cm = 22 weeks’ gestation. The presence of fetal movement is a quick assessment of fetal wellbeing and if the woman is conscious and over 18–20 weeks’ gestation, she should be able to communicate if she feels fetal movements. The physiological adaptations of pregnancy may initially mask serious injury, with vital signs and patient symptoms not reflective of the underlying injuries.¹⁶³ A pregnant woman’s condition can rapidly deteriorate.

Use of Imaging in Pregnancy

All radiological investigations and imaging that are clinically indicated by the maternal condition should be attended to without delay over concerns for the fetus.¹⁶³ When possible and appropriate, use of a pelvic/abdominal lead shield may be used to protect the developing embryo/fetus. If a chest tube is necessary for a haemothorax, care should be taken to position the catheter 1–2 spaces higher than normal due to the raised diaphragm.

Obstetric Assessment in Trauma

If the woman’s gestation is estimated to be 22–24 weeks or more, then a CTG should be conducted to assess fetal wellbeing (see section on fetal assessment). If there has been any likelihood of blunt trauma to the abdomen (i.e. by the steering wheel or seatbelt position), then a continuous four-hour duration CTG should be done to identify any fetal distress resulting from a potential placental abruption. An abdominal ultrasound is commonly done to assess fetal wellbeing and to identify any trauma to the fetus. Ultrasound is also useful in detecting free peritoneal fluid, maternal haemorrhage and may assist in the diagnosis of placental abruption.¹⁶³ The possibility of uterine rupture should also be considered even though it is rare (<1% of pregnant trauma patients).¹⁶³ Also remember that the bladder becomes an abdominal organ after 12 weeks’ gestation and is more prone to traumatic injury.

Potential for Perimortem Caesarean Section

If the woman is ≥20 weeks’ gestation, perimortem caesarean section should be considered early if the woman requires resuscitation. Effective CPR is virtually impossible after midpregnancy and the likelihood for fetal survival is low.

Pregnancy and Influenza

The WHO has recommended that all pregnant women receive the seasonal influenza vaccination since 2006, in recognition of the known increased risk that influenza poses during pregnancy and because vaccination during pregnancy is safe and confers immunity to the newborn for the first few vulnerable months. In developing countries, this policy has the potential to save the lives of many women and in particular, their babies. In developed countries, maternal death caused by seasonal influenza is rare. However, the pandemic influenza, H1N1 09 (referred to as ‘swine flu’), which swept across the world in 2009, demonstrated how vulnerable pregnant women are to influenza and emphasised the importance of influenza vaccination to prevent severe disease.

The H1N1 2009 flu epidemic killed seven pregnant/postpartum women in Australia and New Zealand in three months.¹⁶⁵ Over 60 women were admitted to ICU and a number of their babies died (see the Research vignette at the end of the chapter for more details on this study). Women in the second half of pregnancy were over 13 times more likely to be admitted to ICU with H1N1 influenza than non-pregnant women of child-bearing age. Pregnant and postpartum women admitted to ICU with H1N1 influenza were particularly unwell, with 14% of women requiring ECMO.¹⁶⁶

Interestingly, the severe impact of the pandemic influenza on pregnant women seen during the H1N1 2009 epidemic is not dissimilar to that seen during the Spanish influenza epidemic of 1918 (also caused by H1N1 influenza A) and the influenza epidemic of 1957. Each of these influenza epidemics has demonstrated an increased likelihood of maternal death from influenza and poor maternal and neonatal outcomes.

Preexisting Mental Health Disorders

The underlying principles of management of pregnant women with a preexisting mental health disorder are the same as for non-pregnant women: safety of the woman, stabilisation of the mental illness and empowerment of, and support for, the woman to make her own choices. A considerable additional challenge is maintaining stability of the mental health disorder if changes to medication are required due to potential teratogenesis or contraindication for use during pregnancy. Generally speaking, if the indication for treatment is unchanged, then treatment should be continued during pregnancy.¹⁶⁷

Pregnant women with preexisting mental health disorders may require admission to ICU due to acute deterioration in their mental health. This is most likely to be as a result of cessation or alteration of their regular medications.^168,169 Most relapses occur in the first trimester and many women who initially stop their medication, recommence it during the pregnancy.¹⁶⁸ Routine care should be provided as clinically indicated, keeping in mind the additional requirements to monitor fetal wellbeing, conduct standard antenatal assessment and consider the impact of the physiological adaptations on treatments.

Mental Health Disorders Related to Pregnancy

Suicide related to unwanted pregnancy remains a cause of maternal death in countries like Australia and New Zealand, especially in adolescents and in women from cultures where childbirth outside of marriage is unacceptable.⁵² Depression may arise during pregnancy (antenatal depression) although is more likely to present during the postpartum (postpartum depression). The most severe mental health disorder related to pregnancy is puerperal psychosis.

Cardiotocograph

Cardiotocographs (CTGs) consist of two pieces of information: a Doppler recording fetal heart rate pattern and a pressure transducer detecting uterine muscle contraction. Both elements are recorded on a timed graph so that one may consider the fetal response to uterine contraction (Figure 26.4). Thus, CTGs provide information about the fetal heart rate and whether there is any uterine contraction. A normal fetal heart rate is 120–160 beats/min with variability in the rate. Details of the patient’s condition and treatment, and the date and time the recording was taken should be documented on the trace. Many tertiary obstetric hospitals offer a fax CTG interpretation service for general hospitals without maternity staff to assist with interpretation of CTGs. A CTG provides superior information to an intermittent fetal heart rate (by stethoscope or Doppler) and should be used when possible. The required frequency and duration of a CTG recording will vary according to clinical condition. For example, suspected placental abruption following blunt trauma may require four hours of continuous monitoring. A CTG is recommended during and following elective cardioversion and any other major procedure. CTGs are usually only indicated if the fetus is >22–24 weeks’ gestation and there is the potential to act on adverse findings, such as emergency delivery. The CTG is an indication of fetal wellbeing at the time the trace is recorded and the fetal condition can change rapidly according to changes in maternal condition.

FIGURE 26.4 Normal CTG trace. FHR = fetal heart rate; UA = uterine activity.

Ultrasound

An ultrasound is able to measure core components of fetal anatomy, such as head circumference and femur length, to determine fetal size as well as quantify adequacy of amniotic fluid volume. Thus ultrasound is used to consider adequacy of fetal growth in relation to the gestation and is a component of the biophysical profile regarding fetal movement and swallowing patterns. Serial ultrasounds, e.g. weekly, are used to monitor adequate fetal growth and would be a helpful adjunct to the care of a pregnant woman in ICU with a long term problem, such as Guillain–Barré syndrome.

Potential for Teratogenesis

A teratogen is any agent that increases the incidence of a congenital anomaly.¹⁹¹ The major organs are developed by 10 weeks’ gestation, however, the recommendation is to avoid any teratogenic drug throughout the first trimester (14 weeks).¹⁹² Some medications exert an adverse effect in the second or third trimesters of pregnancy, such as ACE inhibitors (fetal anuria and stillbirth), indomethacin (potential premature closure of the ductus arteriosus) and selective serotonin uptake inhibitors (neonatal withdrawal syndrome).¹⁹² Medical staff prescribing drugs and nursing staff administering them should each check the potential impact of the medication in pregnancy, and consult a pharmacist when possible.

Immediately Prior to Delivery

Besides effects on the structural development of the fetus in the first trimester, the other key time for consideration of drug administration is immediately prior to delivery. Common sedative agents like midazolam, morphine, fentanyl and propofol cross the placenta readily and exert an action on the fetus.^193–195 Consequently, even mature term babies may be born sedated and require assistance with breathing. Planning for delivery of a pregnant woman in ICU should include the involvement of a paediatrician/neonatologist or the local newborn emergency transport service (NETS) if no paediatricians are on site.

Therapeutic Routine Drug Therapy in Pregnancy

For women admitted to ICU for prolonged periods of time, for example those with Guillain–Barré syndrome, consideration may be given to routine therapeutic medication in pregnancy. For example, folic acid (400 µg daily) is recommended pre-conception and throughout the first trimester to prevent neural tube defects.¹⁹² Similarly, iron and Vitamin D supplementation may be indicated dependent on blood levels. Vitamin D deficiency is common, yet often unrecognised in critically ill patients.¹⁹⁶ Maternal vitamin D deficiency is associated with childhood asthma and increased risk of osteoporotic fracture in their offspring.^197,198 Due attention should be paid to a pregnant woman’s nutritional status in ICU as poor nutrition during pregnancy is associated with many poor birth outcomes and pregnancy is associated with increased nutritional requirements.¹⁹⁹

Uterine Involution

The term ‘involution’ means the return of the uterus to its normal size, tone and position. The vagina, ligaments of the uterus and muscles of the pelvic floor also return to their pre-pregnant state during the involution process. During this process, the lining of the uterus is cast off in the lochia, more commonly referred to as PV loss, and is later replaced by the new endometrium. Postdelivery of the baby and postexpulsion of the placenta, the muscles of the uterus constrict the blood vessels, so the blood circulating within the uterus is dramatically decreased. Redundant muscle, fibrous and elastic tissue is disposed of – the phagocytes of the blood stream deal with this –  but the process is usually incomplete and some elastic tissue remains. So a uterus that has once been pregnant will never return fully to its pre-pregnant state. The decidual lining of the uterus is shed in the form of lochia. The new endometrium grows from this basal layer, beginning to be formed at the tenth day and completed by 6 weeks postpartum.

The rate of involution is measured by the rate of descent of the uterine fundus (the top of the uterus) in relation to either the belly button or the symphysis pubis. Important markers include:

A normally contracted uterus is very hard; as you palpate the fundus to locate the top and feel the texture of the uterus, you can not push your fingertip into the tissue of the uterus. A so-called boggy uterus is one that is not contracted properly and the fundus does not feel very hard on palpation. Reasons for a ‘boggy uterus’ include uterine atony, retained tissue/membrane/clot or a full bladder that is impeding the uterine nerve stimulus to contract. The uterus responds well to tactile stimulation, and the first treatment for a ‘boggy uterus’ is to ‘rub-up’ the fundus. This involves palpating the top of the uterus and literally giving it a rub. The uterus will usually respond and you will feel it tighten and become harder. Such an action may result in a small gush of PV loss. On some occasions, an uterotonic, a drug that causes the uterus to contract, may be needed to ensure the uterus is contracting properly. If the uterus does not contract properly, then the vessels that fed the placental bed will not be closed off by the uterine muscle contraction (called the living ligature) and the woman will continue to bleed.

Lochia and Perineal Care

The changes in the appearance of the lochia are described in three stages: lochia rubra, lochia serosa and lochia alba.²⁰⁰ Lochia rubra consists of blood coming chiefly from the placental site, mixed with shreds of the decidua. Three or four days post delivery, the lochia changes to brownish in colour, and consists of altered blood and serum containing leucocytes and organisms; this is called lochia serosa. Seven days post delivery the lochia again changes, the PV loss is now yellowish in appearance, and consists mainly of cervical mucus, leucocytes and organisms; this is called lochia alba. Normal lochia is not offensive in odour. Offensive lochia coupled with or without maternal pyrexia may indicate a uterine infection. High and low vaginal swabs for culture and sensitivity, and the commencement of antibiotic cover, should be initiated. Offensive lochia coupled with a high non-involuting (and boggy) uterus may require ultrasound to exclude retained placental tissue. An infected placental site may result in a secondary postpartum haemorrhage.

Regular assessment of the PV loss is required in the early postpartum phase. Generally this includes 1–2 hourly checks if the PV loss is relatively heavy (pad soaked within 1–2 hours) for the first day, progressing to 4 hourly checks on day 2, with further reductions in observation frequency based on clinical condition. Essentially, you need to check the fundus and PV loss regularly enough to detect any excessive blood loss or loss of uterine tone. The colour and volume of PV loss is usually documented along with any pad changes.

When checking the PV loss, the perineum should also be examined twice a day, even for women that have had a caesarean birth. A vulval haematoma or varicosities may have formed and require attention. For women that have had a vaginal birth, check the perineum to see if there was any tear or episiotomy at delivery. If there is a tear or any sutures, make sure to keep the region clean and observe for signs of infection or wound dehiscence. Ice packs applied to the perineum may help with any swelling and discomfort.

Increased Potential for Deep Vein Thrombosis

All postpartum women have an increased likelihood for DVT. Preeclampsia and obstetric haemorrhage are additional risk factors, as is an emergency operative procedure and postpartum immobility. Most postpartum women admitted to ICU would fulfil the criteria that recommend medical thrombophylaxis. Routine postpartum care involves examining the legs for signs of DVT and appropriate use of thromboembolic stockings, sequential compression devices and thrombophylaxis as required (see www.rcog.org.uk for more details).³⁰

Initiation and Establishment of Lactation

The establishment and maintenance of lactation is a hormone-mediated process. The physiological trigger for the establishment of lactation is a fall in progesterone combined with maintained levels of prolactin and cortisol.²⁰¹ In the initial postnatal period colostrum is produced. The normal timing for milk to ‘come in’ is between 3 and 4 days post-delivery,²⁰² although establishment and ‘coming in’ of breast milk may be delayed in critically ill women. Additionally, the drug dopamine may hinder lactation, as it inhibits prolactin secretion.²⁰³ It is not likely that the severity of maternal illness plays much of a role in the initial capacity to produce milk; anecdotally, 100 mL of breast milk has been expressed 4 hourly from a postpartum woman on ECMO. The initial regularity of hand expression and milk removal provide the stimulus to produce milk.

For women who prefer to breastfeed the infant, reasonable attempts to support this decision should be made. Most women make a decision regarding infant feeding either before becoming pregnant or during the first trimester and in all pregnant women, the breasts have developed and are capable of producing milk from 22 weeks onwards.^204,205

There is some debate regarding how crucial the first 24–48 hours are for the successful establishment of lactation.^206,207 In many cultures, colostrum is considered poisonous and breastfeeding is withheld until after 48 hours and so clearly the absence of breast stimulation in the first 48 hours does not prohibit the establishment of lactation.²⁰⁸ Hand expressing is recommended for the first few days until the milk ‘comes in’, and then to start and finish each expressing episode along with the use of a breast pump²⁰⁹ (see Box 26.12 for principles and Figure 26.5 for process). It is not uncommon for only a few drops of colostrum to be expressed each time in the first couple of days.²¹⁰ It is believed that even a small total expressed volume of 5–10 mL per day of colostrum may be of value to stimulate the ‘coming in’ of full milk production.²⁰¹ The two key factors that support the establishment of lactation are breast stimulation (infant suckling, hand expression) and milk removal. The more often you express and remove milk, the positive feedback mechanisms ensure that more milk is produced. Frequent, short expression of the breasts is more effective than prolonged infrequent expressing. Overnight expression is also important.

FIGURE 26.5 How to hand express.

Oxytocin is most commonly known for its role in the ‘let-down reflex’ of milk during breastfeeding, but also has known effects on brain areas involved in emotion and stress response, increased levels of oxytocin lower blood pressure among mothers who breast feed their babies. this is known to improve a mother’s mood, increases pain tolerance, and also has a possible positive association in wound healing. Prolactin may also be responsible for intense ‘mothering’ feelings.²⁰³

If the mother’s intention was to formula feed, or if the baby has died, then the lactation process may be suppressed. In practice, this means providing no stimulation to the breasts (i.e. no hand expression). Although used in the past, medications are no longer used to influence this process. With no breast expression, some women may still experience milk ‘coming in’ at or after Day 4 postpartum and comfort measures may assist if the breasts become very uncomfortable. Cold compresses may be of use²⁰⁹ and it is important for the critical care nurse to observe for signs like reddened hot areas on the breast that may be an indication of mastitis.

Medication Administration and Lactation

Many drugs are safe to use in breastfeeding, although most common critical care drugs have not been well evaluated.²¹¹ Even if the woman is receiving a medication that is contraindicated during breastfeeding, you can still express (and discard) the milk to establish the process of lactation, unless the woman is likely to stay on the medication long term.

The safety of the expressed milk for the baby depends on three factors: the amount of the medication in the milk, the oral bioavailability of the medication, and the ability of the infant to metabolise the medication.²¹² The gestation and condition of the infant are relevant as the function of the gut, liver and kidney varies with maturity and illness. Consequently, advice from the baby’s neonatologist or paediatrician can help determine whether the neonate can receive the expressed breast milk, or whether it should be discarded.

Promoting Maternal–infant Attachment

Promoting maternal–infant attachment depends on the condition of both the mother and her baby, and their physical locations. The best case scenario is that the baby is able to ‘room in’ with the mother for periods of time in ICU. Skin to skin contact is usually recommended to promote bonding.²¹⁴ Alternatively, the baby may be able to visit the mother in ICU or the mother may be able to visit the baby in NICU. Physically seeing and touching the baby may be an important step for the mother. Newer technologies, like Skype, have been used by some ICUs to enable the mother to see her baby in a different hospital and to watch significant events, such as the first bath.

The use of diaries, one about the mother’s condition and one about the baby’s progress, complete with photos, visitor and clinician entries is another strategy that may be useful to promote maternal-infant attachment. The first few days following birth are often a blur for the mother with little recollection of events. It is also common to have photographs of the baby for the mother to look at and clinicians keep in touch with the nursery where the baby is being cared for and gives the mother regular updates on the baby’s condition.

Caring for the Partner and Other Family Members

The partner is similarly ‘bowled over’ by the sudden and severe illness of the mother. The partner is often torn between two ICUs, with the newborn admitted to NICU in one hospital and the mother in ICU in another hospital. This situation is further compounded if there are other children who also need the care and attention of their father and need an explanation about what has happened to their mother. Most women recover and do so fairly quickly, so there is usually hope that the woman will survive and fully recover. Usual strategies such as explanation, open visiting and social work support are important.