Physiology of pregnancy and pregnancy problems

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12 Physiology of pregnancy and pregnancy problems

Chapter Contents

Physiology of pregnancy

Gastrointestinal

Minor disorders of pregnancy

Nausea and vomiting

Urinary frequency

Symphysis pubis dysfunction

Carpal tunnel syndrome

Vaginal discharge

Hypertensive disorders of pregnancy

Pathophysiology

Clinical features

Treatment of hypertension

Timing of delivery

Severe hypertension or pre-eclampsia in labour

Postnatal management

Prevention of pre-eclampsia

Complications of pre-eclampsia

Antepartum haemorrhage

Infections of pregnancy

Urinary tract infection

Cytomegalovirus

Group B streptococcus

Bacterial vaginosis

Maternal systemic disorders

Haematological disorders

Endocrine disorders

Insulin-dependent diabetes mellitus

Gestational diabetes mellitus

Thyroid disease

Clinical features

Renal disorders

Asymptomatic bacteriuria

Urinary tract infection

Chronic renal disease

Neurological disorders

Multiple sclerosis

Liver disorders

Obstetric cholestasis

Acute fatty liver of pregnancy

Cardiac disease

Pathophysiology

Specific cardiac diseases

Psychiatric disorders

Hypomanic disorder

Domestic violence

Physiology of pregnancy

The major physiological changes occurring during pregnancy are outlined below. Many of the systemic problems associated with pregnancy, such as gestational diabetes, venous thromboembolism (VTE) and worsening cardiac disease, can be related to these physiological alterations.

Cardiovascular

Blood pressure falls in early pregnancy as a result of vasodilatation and reduced systemic vascular resistance. From the mid-trimester blood pressure rises again as cardiac output increases. Immediately after delivery blood pressure falls, but then increases to a maximum 3–4 days’ postpartum.

Cardiac output increases by 40% (20% within the first 8 weeks) to compensate for the fall in systemic vascular resistance caused by peripheral vasodilatation. This is achieved by an increase in both stroke volume and heart rate. The maximum cardiac output is achieved at 20–28 weeks.

The heart rate increases by 10–20 beats per minute in pregnancy.

The gravid uterus impairs venous return in the supine position and cardiac output can, therefore, fall by up to 25% when a pregnant woman lies on her back.

Respiratory

In response to the increased oxygen demand, maternal ventilation increases by 50% in pregnancy. This is mainly achieved through an increase in tidal volume rather than a high respiratory rate.

PaCO₂ is reduced due to the increased ventilation, with a compensatory fall in serum bicarbonate. This causes a mild compensated respiratory alkalosis.

Haematological

A physiological hypercoagulable state develops in pregnancy and hence thrombophilia screening can be unreliable during and shortly after pregnancy. This involves increases in factors VIII, IX, X and fibrinogen, with decreased fibrinolytic activity, antithrombin III, protein C and protein S (endogenous anticoagulants). Routine coagulation tests, however, remain normal. These coagulation changes last until 6 weeks after delivery. The hypercoagulability and venous stasis in the legs from the gravid uterus predispose to thrombosis.

There is a threefold increase in iron requirement and 10–20-fold increase in folate requirement in pregnancy. However, although red cell mass increases, the expansion in plasma volume is such that haemoglobin, haematocrit and red cell count fall. The platelet count also falls, though in 95% of women the level still remains within the normal non-pregnant range.

Renal

Renal plasma flow increases by 60–80% in pregnancy and glomerular filtration rate also increases. The creatinine clearance increases by 50% and there is a fall in serum urea and creatinine. Urinary protein excretion increases to up to 300 mg per 24 hours in normal pregnant women. Eighty per cent of women develop oedema due to physiological sodium and water retention, especially later in pregnancy.

The renal collecting system becomes dilated because of ureteric smooth muscle relaxation (a progesterone effect) and compression from the gravid uterus. This is more pronounced on the right than the left.

Hepatic

Serum protein decreases in pregnancy because of the 20–40% fall in serum albumin concentration. This is a dilutional effect from the increase in plasma volume. Alkaline phosphatase concentration increases due to production from the placenta. Alanine transaminase and aspartate transaminase fall in pregnancy.

Gastrointestinal

Pregnancy is associated with delayed gastric emptying and delayed lower gastrointestinal transit.

Metabolic

Human placental lactogen, cortisol and glucagon from the placenta cause a physiological insulin resistance and glucose intolerance during pregnancy. Insulin production doubles in response to this, with glucose tolerance decreasing with advancing gestation. Glucose metabolism also alters such that postprandial glucose is increased, though preprandial glucose is reduced when compared with non-pregnant values.

The renal threshold for glucose falls and glycosuria occurs in most normal women at some point in pregnancy.

Endocrine

Total thyroxine (T₄) and triiodothyronine (T₃) increase in pregnancy in response to increased thyroid-binding globulin production by the liver. In the first trimester thyroid-stimulating hormone (TSH) falls due to the excess human chorionic gonadotrophin beta-subunit (βhCG), which has a similar structure and effect.

In the third trimester, TSH increases and free T₄ and free T₃ are reduced.

Minor disorders of pregnancy

Nausea and vomiting

Incidence

Fifty per cent of pregnant women experience nausea or vomiting, which is excessive in 1% (hyperemesis gravidarum).

Pathophysiology

Nausea and vomiting occur probably due to βhCG secreted by the placenta, particularly in the first trimester. The problem is, therefore, exacerbated in multiple and molar pregnancies.

Clinical features of hyperemesis

Women may present with intractable vomiting, usually for weeks, and are often dehydrated and exhausted. Epigastric pain may occur secondary to prolonged vomiting and Mallory–Weiss tears occasionally cause haematemesis. Nutritional or electrolyte disturbances may occur, but there is rarely a detrimental effect on the fetus, unless maternal weight loss is significant. Most cases resolve between 12 and 14 weeks, and 90% have resolved by 20 weeks.

Psychological effects are commonly experienced relating to interference in relationships with other children, time off work and exhaustion. Some women feel anger or resentment towards the pregnancy and even consider termination.

Management

For mild to moderate symptoms, without ketonuria, women should be managed as an outpatient with support, oral fluids and small amounts of regular food. Oral or rectal antiemetics can be prescribed if needed.

Admission is indicated for severe hyperemesis. Full blood count (FBC) should be checked to exclude anaemia, or a leukocytosis, which would suggest an infective cause for the vomiting. Urea and electrolytes and liver function tests should be checked for abnormalities.

Thyroid function tests to exclude thyrotoxicosis as a cause of vomiting should be sent, but treatment should depend on clinical signs and symptoms of thyroid disease, as abnormal biochemical markers of thyroid function are common in hyperemesis.

Urinalysis is performed to check for ketonuria and a midstream urine (MSU) sample sent for culture to exclude a urinary tract infection (UTI) as a cause of the vomiting.

Ultrasound scan should be arranged to exclude multiple or molar pregnancy.

Intravenous fluids

Saline or Hartmann’s solution (0.9%) is used for rehydration. Sodium is important because of the hyponatraemia associated with hyperemesis. Dextrose should not be used (as it may precipitate Wernicke’s encephalopathy). Depending on the serum potassium result, potassium should usually be added to the intravenous fluids.

Antiemetics

Cyclizine, prochlorperazine and metoclopramide are commonly used antiemetics in pregnancy. They have not been shown to be harmful in pregnancy, but can occasionally cause oculogyric crises. Initial treatment should be intravenous, followed by oral or rectal administration.

Corticosteroids have been shown to improve symptoms of hyperemesis in intractable cases.

Ginger and acupressure are alternative evidence-based treatments.

Thiamine

Thiamine (oral 50 mg daily or intravenous 100 mg weekly) should be given to all women with hyperemesis as Wernicke’s encephalopathy has been reported from severe vitamin B₁ deficiency as a result of persistent vomiting.

Folic acid

Women with hyperemesis are usually folate-deficient and need to take 5 mg folic acid daily.

Any underlying cause of vomiting, such as UTI, should be treated.

Mallory–Weiss tears occur from prolonged vomiting and may be managed by ranitidine and antacids, though gastrointestinal referral is indicated if there is significant pain or the bleeding does not settle.

Some women are admitted repeatedly with hyperemesis and in these cases a social history may reveal other causes of difficulty coping with the pregnancy.

Heartburn

Delayed gastric emptying, the pressure effect of the gravid abdomen and smooth-muscle relaxation of the gastro-oesophageal sphincter cause a high incidence of gastro-oesophageal reflux in pregnancy. Heartburn is the symptom of retrosternal pain. Up to 70% of pregnant women report heartburn by the third trimester.

Treatment includes diet advice (reduced fat, small frequent meals and remaining upright after eating), posture advice (tilt head of bed up to reduce reflux), antireflux agents (e.g. Gaviscon or magnesium trisilicate) and antacids. Metoclopramide may help by increasing gastric emptying. H₂ antagonists such as ranitidine and proton pump inhibitors such as omeprazole are also effective and are not shown to be harmful in pregnancy, though they are not licensed for this indication.

Constipation

Constipation affects nearly half of pregnant women. The smooth-muscle effect of progesterone, the pressure of the gravid uterus, dietary changes or ferrous sulphate are contributing factors.

Severe constipation may lead to abdominal bloating and pain, nausea, vomiting, haemorrhoids and anal fissures.

Treatment is initially with dietary advice (high fibre, such as bran or wheat supplementation, balanced with appropriate fluid intake). Bulk-forming laxatives (e.g. ispaghula husk), stimulant laxatives (e.g. senna) or osmotic laxatives (e.g. lactulose) can also be used. Stimulant laxatives are more effective than bulk-forming agents but have a higher associated incidence of diarrhoea and abdominal pain.

Haemorrhoids

Haemorrhoids occur in 8% of pregnant women, due to increased intra-abdominal pressure causing decreased venous return, and are exacerbated by constipation. They may present with itching or bleeding. Pain occurs if haemorrhoids become thrombosed. Local preparations containing soothing agents are helpful and any constipation should be treated. Surgical treatment should only be considered very rarely, for unresolving thrombosed haemorrhoids. Haemorrhoids usually disappear spontaneously postpartum.

Urinary frequency

Frequency is normal in pregnancy, exacerbated by the pressure effect of the gravid uterus on the bladder. Infection should be excluded with an MSU sample if the symptoms are severe, suddenly worse or are associated with pain, offensive urine or pyrexia.

UTIs are discussed later in the chapter.

Breathlessness

Most women feel breathless during pregnancy because of increased ventilation, splinting of the diaphragm by the pregnant uterus, anaemia and general tiredness. Consideration should be given to the differential diagnoses if the symptoms are severe, sudden or associated with suspicious features such as pain, cough or wheezing. Other diagnoses include asthma, pulmonary embolism, pneumonia and cardiac causes. All women complaining of breathlessness should have a recent haemoglobin level checked, with iron supplementation as appropriate.

Skin problems

Itching

Many pregnant women experience itching, commonly over the abdomen. It is generally not associated with a rash, except for that due to excoriation, and liver function tests are normal. Suspicious features warranting further investigation are itching on the palms and soles, abnormal liver function or a rash (see obstetric cholestasis, below).

Pigmentation

Linea nigra (midline linear abdominal pigmentation), melasma (facial pigmentation), areolar darkening and striae gravidarum (stretch marks) all occur as features of normal pregnancy. There is no treatment and all fade after pregnancy, though striae never fully resolve.

Spider naevi and palmar erythema both occur in pregnancy, with spontaneous resolution in most cases.

Backache

Backache occurs in 40–60% of pregnant women as a result of progesterone causing relaxation of the ligamentous supports of the back and from the weight of the gravid uterus, with an exaggerated lumbar lordosis. Management, after assessing for neurological and orthopaedic abnormalities, is with reassurance, simple analgesia and physiotherapy for severe cases. Exercise in water, Ozzlo pillows (nest-shaped pillows to help sleep and posture in bed) and acupuncture are also shown to be effective at relieving symptoms.

Symphysis pubis dysfunction

Symphysis pubis dysfunction presents as discomfort or pain in the pelvic area, which may radiate to the upper thighs or perineum. The pain usually occurs initially with walking. It occurs in 3% of pregnant women and it may be severe enough to reduce mobility. On examination, the woman often reports severe pain on pressure over the symphysis pubis or on compression of the pelvis.

Treatment is supportive with crutches, pelvic support braces and analgesia.

Carpal tunnel syndrome

Oedema of the wrist causes compression of the median nerve and pain, numbness or paraesthesia, with possible impaired motor function or muscle wasting. Wrist splints are generally helpful and corticosteroid injections can be considered for intractable symptoms in pregnancy, with limited evidence of benefit. The symptoms usually resolve spontaneously postnatally.

Concentration

Some women report impaired concentration in pregnancy. The cause of this is not clear and it may relate to poor sleep and general tiredness.

Oedema

Dependent oedema occurs in 80% of pregnant women and may be mild or severe and uncomfortable. Simple measures such as elevation of the legs are helpful. Blood pressure and urinalysis are necessary to exclude pre-eclampsia as the cause of the oedema. Oedema often worsens immediately after delivery, with a natural diuresis then occurring within the next 72 hours.

Varicose veins

Varicose veins are common, due to impaired venous return and progesterone effect on valve function and the vein wall. They may be asymptomatic or cause aching or itching. Vulval varicosities are rare, but cause a throbbing discomfort and may bleed excessively at delivery. Varicose veins are generally treated by ligation and stripping, injection or avulsion after the completion of the family. During and after pregnancy, compression stockings may be helpful to relieve symptoms.

Vaginal discharge

Physiological discharge increases in pregnancy. It is white and smooth. Any itching, offensive odour, blood or change in the nature of the discharge should be investigated with swabs for Candida, bacterial vaginosis and sexually transmitted infection. It should be noted that endocervical swabs are not recommended in pregnancy.

Candida occurs more commonly in pregnancy due to the state of relative glucose intolerance. Antifungal pessaries and creams are safe in pregnancy, but oral treatments are not recommended. Creams or pessaries are most effective when given for a 1-week course. There is no evidence that the fetus or neonate is affected by maternal vaginal candidiasis.

Hypertensive disorders of pregnancy

Definitions

Hypertension in pregnancy

There are various definitions in use for the diagnosis of hypertension in pregnancy. Generally accepted criteria for diagnosis are:

• Diastolic blood pressure > 90 mmHg on two occasions or > 110 mmHg on a single occasion

• An increase in diastolic blood pressure of 20 mmHg or more above booking

• An increase in systolic blood pressure of 30 mmHg or more above booking.

Chronic hypertension

This is hypertension diagnosed before pregnancy or in the first trimester.

Essential hypertension

Essential hypertension is diagnosed before pregnancy or in the first trimester, not secondary to another cause.

Pregnancy-induced hypertension

Pregnancy-induced hypertension is diagnosed after 20 weeks’ gestation (most hypertension developing between 12 and 20 weeks will be chronic hypertension, but it may occasionally be due to severe early-onset pre-eclampsia).

Pre-eclampsia

Pre-eclampsia is a pregnancy-specific multisystem disorder with various clinical manifestations. The classic definition involved hypertension, proteinuria and oedema, but now the diagnosis may be made on a combination of possible maternal and fetal features. These include intrauterine growth restriction (IUGR), haematological abnormalities, biochemical abnormalities and clinical symptoms or signs.

Incidence

Ten per cent of women develop high blood pressure or mild pre-eclampsia in pregnancy. Of these, 10% develop severe pre-eclampsia. Women with pre-existing hypertension have double the risk of developing superimposed pre-eclampsia. The incidence of pregnancy-induced hypertension and pre-eclampsia is higher in first pregnancies than in multiparous women.

Aetiology

Chronic hypertension may be due to endocrine disease (e.g. Cushing’s and Conn’s syndromes) or secondary to renal disease or cardiac disease.

The aetiology of pre-eclampsia is still poorly understood. There is, however, a known genetic component (20% risk of daughters of affected women developing pre-eclampsia).

Prediction

Risk factors for the development of pre-eclampsia are shown in Table 12.1.

Table 12.1. Risk factors for pre-eclampsia

Primiparity

Multiple pregnancy

Obesity

Extremes of age

New partner

In vitro fertilization – egg donation

Diabetes

Chronic hypertension

Antiphospholipid syndrome

Renal disease

Molar pregnancy

Uterine artery Doppler studies at 20–24 weeks can be used to identify women at high risk of pre-eclampsia, in whom a high resistance and ‘notched’ waveform is seen. This is still a research tool and has not been widely accepted in the general antenatal population

Pathophysiology

The features of pre-eclampsia originate from abnormal placental trophoblast invasion in early pregnancy. The usual low resistance and high flow do not develop in the spiral arteries of the uterus and diffuse maternal vascular endothelial dysfunction results, with vasoconstriction and platelet aggregation.

Clinical features

Hypertension may be the first sign of pre-eclampsia and women with chronic hypertension are likely to develop pre-eclampsia. Differentiation between the two conditions may be difficult clinically.

History

Women with hypertension may report headache or visual disturbance. Pre-eclampsia may also present with epigastric pain, nausea, vomiting and oedema. Oedema is commonly in the face and fingers and women may notice that they cannot take off their rings. Alternatively, their partner may have noticed facial swelling.

Examination

Blood pressure should be measured at 45°, with an appropriate cuff. If the circumference of the arm is more than 80% of the cuff size, a larger cuff should be used to avoid underestimation of the blood pressure.

The first Korotkoff sound (phase I), that is, the beginning of the audible beats, signifies the systolic blood pressure. The diastolic reading is taken at the level of the fifth Korotkoff sound (phase V), that is, when silence occurs. In a minority of women silence does not occur, in which case the phase IV sound (muffling) is used.

The legs, hands and face should be examined for oedema and the reflexes checked for hyperreflexia and clonus (signs of cerebral irritability). Palpation of the abdomen may reveal epigastric tenderness. The symphyseal–fundal height should be measured and a subjective assessment made of liquor volume.

Investigations

The following investigations should be performed for all women with pregnancy-induced hypertension or other features suggestive of possible pre-eclampsia. In established pre-eclampsia the tests should be repeated twice weekly, or more often if the clinical condition deteriorates.

Urinalysis

If + 1 proteinuria or more is present, then an MSU sample should be sent to exclude UTI as the cause and a 24-hour urine collection commenced. More than 0.3 gram of protein per 24 hours is diagnostic of pre-eclampsia in the absence of other causes such as infection or chronic renal disease.

Full blood count

Platelets usually fall in pre-eclampsia. Low haemoglobin and very low platelets are suspicious signs as they may signify the syndrome of haemolysis, elevated liver enzymes and low platelet count (HELLP).

Urea and electrolytes

Urea and creatinine may rise in pre-eclampsia. The normal range for creatinine is lower in pregnancy, so creatinine concentration greater than about 80 μmol/l is significant.

Uric acid (urate)

Uric acid is a non-specific marker of pre-eclampsia. As a general rule in singleton pregnancies, the value of the uric acid should be less than the number of weeks’ gestation, divided by 100. For example, at 36 weeks, uric acid is normally < 0.36. Serial values are more beneficial as a marker of disease progression rather than one level in isolation.

Liver function tests

Alanine and aspartate transaminases rise in pre-eclampsia. If gamma glutamyl transaminase and bilirubin are raised, then HELLP syndrome is the likely diagnosis.

Albumin

Albumin falls in pre-eclampsia as the kidneys lose protein.

Coagulation tests

International normalized ratio (INR) and activated partial thromboplastin time (APTT) only become prolonged in severe pre-eclampsia and do not need to be checked in all cases of suspected pre-eclampsia.

Ultrasound scan

Fetal well-being should be confirmed with growth, liquor volume and umbilical artery Doppler studies.

Management

Delivery of the baby is the only cure for pre-eclampsia. Otherwise, management of hypertensive disorders involves monitoring the disease process, monitoring fetal well-being, treatment of hypertension, diagnosis and treatment of complications, and appropriate timing of the delivery of the baby.

Monitoring of the disease

Confirmed pre-eclampsia should be managed as an inpatient because of the risk of fulminating disease or placental abruption. Bed rest itself does not alter the outcome of pre-eclampsia. Blood pressure should be checked every 4 hours, urinalysis daily and 24-hour protein clearance weekly. Outpatient management may be suitable for well-controlled hypertension without other features, or in mild pre-eclampsia, with frequent assessment as a day case.

All pre-eclamptic women should have twice-weekly FBC, urea and electrolytes and liver function checked, with more frequent tests if clinically indicated.

Monitoring fetal well-being

In established pre-eclampsia, fetal ultrasound scan should be repeated regularly (between twice weekly and every 2 weeks depending on the findings). Fetal movements should be monitored by the mother but the value of regular cardiotocography (CTG) is debated if scans and fetal movements are normal.

Treatment of hypertension

Hypertension should be treated in both pregnancy-induced hypertensive and pre-eclamptic women, to prevent stroke. However, although antihypertensives correct blood pressure, they do not alter the underlying disease process and the risk of worsening pre-eclampsia or eclampsia remains.

The systolic and diastolic values at which antihypertensive treatment should be commenced are debated, but treatment should always be started if the diastolic reading is repeatedly greater than 100 mmHg or systolic greater than 160 mmHg.

Antenatal management

First-line management

Methyldopa (centrally acting) should be given at a dosage of 250 mg three times a day, increased up to 1 gram three times daily. Methyldopa has the best safety record in pregnancy, but side effects include drowsiness, depression and reduced fetal movements, though these often settle after a few days. Women on other hypertensives prior to pregnancy are usually converted to methyldopa once pregnancy has been confirmed.

Second-line management

Labetalol (beta-blocker and arterial vasodilator) can be given at a dosage of 100 mg twice daily, increased up to 600 mg four times a day. Rare side effects include fetal growth restriction and neonatal bradycardia. Asthma is a contraindication for use.

Slow-release nifedipine (calcium antagonist) can also be given at a dosage of 10 mg twice daily, increased to 40 mg twice daily. Care is needed, as nifedipine particularly may cause a sudden drop in blood pressure, compromising the uteroplacental circulation.

Other beta-blockers are rarely used in pregnancy due to concerns over growth restriction and fetal bradycardia.

Angiotensin-converting enzyme (ACE) inhibitors are contraindicated in pregnancy and diuretics are only used with extreme caution.

Intrapartum management

Severe hypertension developing in labour or in women presenting with severe sudden pre-eclampsia for whom delivery is indicated may need intravenous treatment with hydralazine or labetalol. A bolus of colloid (250–500 ml) should be given prior to this, to avoid a sudden drop in blood pressure as a result of the depleted intravascular volume in pre-eclampsia. The fetus is monitored with continuous CTG, in case of sudden hypotension causing acute uteroplacental insufficiency.

The mean arterial blood pressure (MAP) should be maintained below 125. MAP is calculated as follows:

MAP = diastolic blood pressure + (systolic – diastolic)/3

Hydralazine

Intravenous hydralazine is given at a dosage of 2.5–5 mg over 5 minutes and the dose repeated after 15 minutes if the MAP has not fallen below 125 mmHg. If more than three doses are required, then an infusion is commenced.

Labetalol

Intravenous labetalol is given at a dosage of 20 mg/hour, doubled every 30 minutes, according to the blood pressure, up to a maximum of 160 mg/hour.

Nifedipine

Slow-release nifedipine may be given intrapartum at a dosage of 10 mg, but careful monitoring of the fetus is important, in case of a sudden severe drop in blood pressure.

Postnatal management of hypertension

Methyldopa should be discontinued after delivery, because of the possible side effect of depression. If hypertension has been moderate or severe, then labetalol or atenolol should be commenced. Calcium antagonists and ACE inhibitors are also safe, even with breastfeeding. If hypertension antenatally or during labour was mild, then consideration should be given to stopping all hypertensives and monitoring the blood pressure for 72 hours.

Discharge should only be arranged when the blood pressure is consistently less than 140/90 mmHg. The woman should have regular blood pressure measurement by the community midwife and see her general practitioner in 6 weeks to consider discontinuing treatment.

Timing of delivery

Delivery is the only ‘cure’ for pre-eclampsia and is indicated by uncontrolled hypertension, severe clinical, biochemical or haematological abnormalities or fetal concerns. Ideally, delivery should be delayed until after 37 weeks to allow for fetal lung maturity, but each case must be assessed individually and delivery may be much earlier. Usual indications for delivery are:

• Severe hypertension not responsive to double or triple therapy

• Symptomatic pre-eclampsia (e.g. epigastric pain, visual symptoms)

• Severe fetal growth restriction with abnormal umbilical artery Doppler flow

• Decreasing platelets

• Increasing creatinine, alanine transaminase (ALT) and aspartate transaminase (AST)

• HELLP syndrome

• Placental abruption.

Women with likely premature delivery under 36 weeks should be given a course of steroids to aid fetal lung maturity.

Severe hypertension or pre-eclampsia in labour

A protocol should be adhered to for all women with significant disease. Important considerations in the management are summarized in Figure 12.1 and include:

a. Blood pressure should be monitored every 15–60 minutes, depending on the severity of disease.

b. Fluid balance should be calculated with urinary catheter and measurement of all intravenous and oral intake. Low urine output is common and should be managed expectantly unless urine output is less than 80 ml over 4 hours, in which case a central venous pressure line should be inserted to guide fluid management.

c. Full blood count, coagulation, renal and liver function, and urate should be checked every 6 hours in severe disease.

d. Clinical signs of hyperreflexia and clonus should be checked.

e. Fetal well-being should be monitored with continuous CTG.

2. Fluid restriction: fluid input should be restricted to 85 ml/hour, due to the intravascular depletion associated with pre-eclampsia.

3. Treatment of blood pressure: the treatment of blood pressure is outlined above.

4. Delivery: induction of labour or caesarean section (depending on obstetric factors) should be initiated when the maternal haemodynamic condition is stable. Epidural is encouraged as it reduces blood pressure, though platelets should be checked first as there is a risk of epidural haematoma if the platelet count is less than 80 × 10⁹/l. Syntocinon alone is used for the third stage as ergometrine may precipitate a further rise in blood pressure.

5. Magnesium sulphate: magnesium sulphate decreases the likelihood of an eclamptic fit and should be considered in severe pre-eclampsia. A loading dose of 2 grams (diluted in 20 ml normal saline) over 5 minutes is followed by an infusion of 1–2 g/hour. Side effects are hot flushing sensation, loss of tendon reflexes, respiratory depression and cardiac arrest. The urine output, reflexes, blood pressure, respiratory rate and oxygen saturation should be monitored closely, with cardiac monitoring. Magnesium sulphate also lowers blood pressure and care is needed with other hypertensives to prevent a sudden drop in blood pressure, which may cause fetal distress. Magnesium sulphate should be continued for 24 hours postpartum.

Figure 12.1 Management of severe pre-eclampsia. BP, blood pressure; MAP, mean arterial pressure; HR, heart rate; FBC, full blood count; LFT, liver function tests; CTG, cardiotocograph; CVP, central venous pressure; IV, intravenous; RR, respiration rate; ECG, electrocardiogram.

Postnatal management

Haematology and biochemistry results need to be monitored postnatally until normal. The fluid balance chart should be continued until diuresis occurs, which may be up to 72 hours following delivery. Management of postnatal hypertension is outlined above.

Prognosis

In most women, blood pressure returns to normal within 6 weeks. However, a few women remain hypertensive in the long term.

Pregnancy-induced hypertension commonly recurs in subsequent pregnancies. The risk of recurrence of pre-eclampsia in otherwise healthy women is 10%. However, it is more likely in women with hypertension or other medical risk factors. The severity of the disease tends to reduce with each subsequent pregnancy.

Prevention of pre-eclampsia

Aspirin reduces the incidence of pre-eclampsia in women with a history of previous severe pre-eclampsia necessitating delivery prior to 34 weeks’ gestation. Calcium helps to prevent pre-eclampsia in women with inadequate dietary supply or who are vitamin D-deficient, and vitamin C and E supplements may provide benefit in women at high risk of pre-eclampsia.

Complications of pre-eclampsia

Fetal growth restriction

Pre-eclampsia is associated with uteroplacental insufficiency, which causes impaired fetal growth and reduced liquor volume. Eventually fetal blood flow is impaired and reduced, absent and eventually reversed end-diastolic flow occurs in the umbilical artery. Ultrasound monitoring, fetal movement recording and CTG are used to determine timing of delivery. In rare severe cases, fetal growth restriction occurs early, before the fetus has reached a viable weight and intrauterine death occurs.

Haemolysis, elevated liver enzymes and low platelets

HELLP syndrome presents with epigastric pain, nausea, vomiting and right upper quadrant tenderness. Onset is often acute, with patients not necessarily having presented with pre-eclampsia symptoms or signs prior to the development of HELLP.

Management is as for severe pre-eclampsia, with monitoring of haematological and biochemical abnormalities, treatment of hypertension and urgent delivery. Renal failure, liver haematoma or rupture and abruption are all complications.

Pulmonary oedema

Pulmonary oedema occurs as a result of the hypoalbuminaemia and vascular endothelial dysfunction.

Disseminated intravascular coagulation

Disseminated intravascular coagulation (DIC) results from a generalized stimulation of coagulation activity and subsequent depletion in clotting factors and platelets. The clinical presentation is, therefore, of uncontrolled bleeding and the diagnosis is confirmed by increased fibrin degradation products, decreased fibrinogen and platelets, and prolonged TT, APTT and INR. It is most likely after HELLP syndrome or abruption.

Cerebral haemorrhage

Stroke is the result of uncontrolled hypertension and is one of the main causes of death in pre-eclamptic women.

Abruption

Placental abruption is a common complication of pre-eclampsia and cannot be predicted by the clinical severity of the disease. It usually presents with sudden severe abdominal pain, with or without vaginal bleeding. Initial management involves stabilization of the haemodynamic status of the mother by blood transfusion and correction of any coagulopathy. Urgent delivery by caesarean section should be arranged if the fetus is alive, otherwise by induction of labour if intrauterine death has already occurred.

Eclampsia

Eclampsia affects 0.05% of pregnancies (about 1 in 2000). Forty per cent of episodes occur postpartum and eclampsia commonly occurs in women not previously diagnosed with pre-eclampsia. Seizures are generalized and generally self-limiting within 2–3 minutes.

Specific management is covered in Chapter 17.

Antepartum haemorrhage

Antepartum haemorrhage (APH) is a significant cause of maternal mortality. Any bleeding should be taken seriously, with a high index of suspicion for placenta praevia or placental abruption. It should always be remembered that hypovolaemic shock can occur rapidly, despite minimal vaginal loss, where a concealed placental abruption has occurred.

Definition

APH is vaginal bleeding occurring once the fetus has reached viability. This is usually defined as more than 24 weeks’ gestation.

Incidence

Two to 10% of women report an APH at some stage in pregnancy.

Aetiology

Bleeding may occur from a maternal, fetal or placental site (Table 12.2). Both placental and maternal sites involve loss of maternal blood, whereas in the case of vasa praevia fetal blood is lost.

Table 12.2 Causes of antepartum haemorrhage

Maternal	Placental	Fetal
Vaginal infectionstart=”row” colname=”col1″ align=”left”(e.g. Candida, Trichomonas)	Placenta praevia	Vasa praevia
Cervical ectropion	Placental abruption
Cervical infection
Cervical malignancy
Bloody show
Uterine rupture

In many cases the cause of bleeding cannot be identified. It is likely that these small bleeds represent minor abruptions and such women should be carefully monitored as they are at risk of further abruption. If repeated bleeds occur, then fetal growth restriction also may develop. The term ‘marginal bleed’ is sometimes used to refer to such bleeding.

Non-vaginal causes of bleeding also may occur. Bleeding from haemorrhoids is common in pregnancy, for example, and haematuria may also be mistaken for vaginal blood loss.

History

Important features in the history of a woman presenting with suspected APH are:

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