Chapter 22 Hypertensive disorders of pregnancy
The hypertensive disorders of pregnancy represent the most significant complication of pregnancy affecting approximately 5% of all pregnancies and 11% of all first pregnancies (Villar et al 2003). They continue to be a major cause of maternal, fetal and neonatal morbidity and mortality. Between 40 000–70 000 maternal deaths annually worldwide are due to severe pre-eclampsia and eclampsia (Chhabra & Kakani 2007, Villar et al 2004). The majority of these deaths occur in the developing world due to lack of technological and therapeutic interventions. In the last triennial report of maternal deaths in the UK, pre-eclampsia and eclampsia caused 18 deaths and remains the second most common cause of direct maternal death. The majority of women died from intracranial haemorrhage, and inadequate antihypertensive therapy was the most common source of sub-standard care (Lewis 2007). The risk to the fetus includes growth restriction secondary to placental insufficiency and prematurity, accounting for approximately 25% of all infants with very low birth weight (<1500 g). Despite continued investigation throughout the world there is still limited understanding of the cause, pathophysiology and thus prevention of the hypertensive disorders which include a variety of vascular disturbances, such as gestational hypertension, pre-eclampsia, HELLP syndrome, eclampsia and chronic hypertension.
The definition and classification of the hypertensive disorders are complex as the pathophysiology remains poorly understood and there is considerable clinical variation in their presentation. It is important to recognize the distinction between a woman whose hypertension antedates pregnancy (pre-existing hypertension) and one who develops increased blood pressure during pregnancy (new hypertension). Work undertaken by the National High Blood Pressure Education Programme (NHBPEP), Working Group on High Blood Pressure in Pregnancy (2000) and the Pre-eclampsia Community Guideline Development Group (PRECOG 2004) describe the following main categories of hypertension during pregnancy:
An incremental rise in blood pressure is not included in this classification system. However, the working group considered that women who have a rise of 30 mmHg systolic or 15 mmHg diastolic blood pressure require close observation especially if proteinuria and hyperuricaemia (raised uric acid level) are also present.
The development of pre-eclampsia is generally considered to occur in two stages. The placenta is thought to be the primary cause of the hypertensive disorders of pregnancy as following birth of the baby the disease regresses. Early studies by Roberts & Redman (1993)indicated that abnormal placentation may be one of the initial events in the disease process. In normal pregnancy placentation involves invasion of the decidua by the syncytiotrophoblast. During early pregnancy, the muscular walls and endothelium of the spiral arteries are eroded and replaced by trophoblast to ensure an optimum environment for the developing blastocyst. A second phase of this invasive process occurs between 16 and 20 weeks’ gestation when the trophoblast erodes the myometrium of the spiral arteries. The loss of this musculoelastic tissue results in dilated vessels that are incapable of vasoconstriction; hence a system of low pressure and high blood flow into the placenta is produced with maximal placental perfusion (Sheppard & Bonnar 1989). In pre-eclampsia, trophoblastic invasion of the spiral arteries is thought to be inhibited resulting in decreased placental perfusion, which may ultimately lead to early placental hypoxia and oxidative stress (Borzychowski et al 2006). This first stage of the disease process occurs early in pregnancy and is difficult to detect clinically.
Stage two follows when the oxidatively stressed placenta triggers the release of one or more factors that damage the endothelial cells in the maternal circulation. Endothelial cells form the endothelium, which lines the cardiovascular system and serous cavities of the body. The subsequent maternal systemic inflammatory response and endothelial cell dysfunction results in the clinical signs of pre-eclampsia seen after 20 weeks’ gestation (Redman & Sargent 2003). Endothelial cells play an important role in regulating capillary transport, controlling plasma lipid contact and modulating vascular smooth muscle reactivity in response to various stimuli. They also synthesize several substances, two of which – prostacyclin and nitric oxide – are mediators in vasodilation and inhibit platelet aggregation, thus preventing blood clot formation. Damage to the endothelial cells with widespread inflammation will:
Several epidemiological studies suggest that the abnormal placentation is caused by a genetically pre-determined maternal immune response to fetal antigens, derived from the father, and expressed in normal placental tissue (Redman et al 1999, Robillard 2002). Additional evidence for the immune response theory includes the high incidence of hypertensive disease in primigravidae, increased inflammatory substances in the maternal circulation (Redman & Sargent 2003) and partner specificity (Li & Wi 2000).
Some women are thought to be more sensitive to endothelial cell dysfunction or have pre-existing endothelial cell dysfunction seen in conditions with associated microvascular disease such as diabetes, hypertension or thrombophilia. In addition it is more likely to occur where there is a large placental mass such as in multiple pregnancy or gestational trophoblastic disease (hydatidiform mole). Women with these conditions are at an increased risk of developing pre-eclampsia (Roberts & Redman 1993).
The combined effect of these events will cause:
These are the characteristic features of pre-eclampsia, which become manifest throughout the body resulting in pathological changes consistent with a multisystem disorder (Dekker & Sibai 2001).
Hypertension together with endothelial cell damage affects capillary permeability. Plasma proteins leak from the damaged blood vessels causing a decrease in the plasma colloid pressure and an increase in oedema within the extracellular space. The reduced intravascular plasma volume causes hypovolaemia and haemoconcentration, which is reflected in an elevated haematocrit. In severe cases the lungs become congested with fluid and pulmonary oedema develops, oxygenation is impaired and cyanosis occurs. With vasoconstriction and disruption of the vascular endothelium the coagulation cascade is activated.
Activation of the coagulation cascade results in formation of fibrin clots which trap platelets. This consumption of platelets produces thrombocytopenia. This process of disseminated intravascular coagulation (DIC) is characterized by low platelets, prolonged prothrombin time and low fibrinogen levels. As the process progresses fibrin and platelets are deposited, which will occlude blood flow to many organs, particularly the kidneys, liver, brain and placenta.
In the kidney, hypertension leads to vasospasm of the afferent arterioles resulting in a decreased renal blood flow, which produces hypoxia and oedema of the endothelial cells of the glomerular capillaries. Glomeruloendotheliosis (glomerular endothelial damage) allows plasma proteins, mainly in the form of albumin, to filter into the urine, producing proteinuria. Renal damage is reflected by reduced creatinine clearance and increased serum creatinine and uric acid levels. Oliguria develops as the condition worsens, signifying severe renal vasoconstriction.
Vasoconstriction of the hepatic vascular bed will result in hypoxia and oedema of the liver cells. In severe cases, oedematous swelling of the liver causes upper abdominal pain and can lead to intracapsular haemorrhages and, in very rare cases, rupture of the liver. Altered liver function is reflected by falling albumin and a rise in liver enzyme levels.
Hypertension, combined with cerebrovascular endothelial dysfunction, increases the permeability of the blood–brain barrier resulting in cerebral oedema and microhaemorrhaging. Clinically, this is characterized by the onset of headaches, visual disturbances and convulsions. Where the mean arterial pressure (MAP, i.e. the systolic blood pressure plus twice the diastolic pressure divided by 3) exceeds 125 mmHg, the autoregulation of cerebral flow is disrupted resulting in cerebral vasospasm, cerebral oedema and blood clot formation. This is known as hypertensive encephalopathy, which if left untreated can progress to cerebral haemorrhage and death (Vaughan & Delanty 2000).
In the uterus, vasoconstriction caused by hypertension reduces the uterine blood flow which can result in placental abruption and placental scarring. Reduction in blood flow to the choriodecidual spaces diminishes the amount of oxygen that diffuses through the cells of the syncytiotrophoblast and cytotrophoblast into the fetal circulation within the placenta. The result is that the placental tissue becomes ischaemic, the capillaries in the chorionic villi thrombose and infarctions occur, leading to fetal growth restriction (Odegard et al 2000). Hormonal output is also impaired with reduced placental function and this has serious implications for the survival of the fetus. This combination of factors often results in preterm labour and birth.
As the hypertensive disorders are unlikely to be prevented, early detection and referral by the midwife is crucial so that monitoring and treatment can be implemented to minimize the severity of the condition (PRECOG 2004, Sallah 2004). All women, particularly those from disadvantaged and vulnerable groups, must receive appropriate antenatal care (NICE 2008); women who do not receive antenatal care are more likely to die from complications related to the hypertensive disorders of pregnancy (Lewis 2007, Lewis & Drife 2001). The midwife is in a unique position to identify those women who are more likely to develop pre-eclampsia; a comprehensive history taking at their first meeting will identify the following risk factors (Duckitt & Harrington 2005):
On subsequent visits the midwife must take note of any further pregnancy-associated risk factors such as multiple pregnancy. The two essential features of pre-eclampsia, hypertension and proteinuria, are assessed for at regular intervals throughout pregnancy and diagnosis is usually based on the rise in blood pressure and the presence of proteinuria after 20 weeks’ gestation.
In order to detect increases in blood pressure, the midwife should take the woman’s blood pressure early in pregnancy and compare this with all subsequent recordings, taking into account the normal pattern in pregnancy (see Ch. 14). It is important to consider several factors in assessing blood pressure.
Blood pressure machines should be calibrated for use in pregnancy and regularly maintained. Mercury sphygmomanometry is still considered the gold standard for blood pressure measurement although the use of mercury for clinical purposes has been phased out in the UK. This raises problems with regard to the accurate assessment of blood pressure in pregnancy. If automated and ambulatory blood pressure monitoring devices are used they should be validated for use in pregnancy. In addition, automated blood pressure measuring devices such as the Dinamap need to be calibrated and checked regularly as they can systematically underestimate blood pressure by at least 10 mmHg in pre-eclampsia (Lewis & Drife 2004, Pomini et al 2001).
Blood pressure should not be taken immediately after a woman has experienced anxiety, pain, a period of exercise or has smoked. A 10 min rest period is recommended before measuring the blood pressure in these circumstances. The position of the person in whom the blood pressure is measured is important in pregnancy. The supine and right lateral positions are not recommended in view of the effect of the gravid uterus on venous return resulting in postural hypotension. Women should be seated or lying in the left lateral position at an angle of 45°, with the sphygmomanometer cuff approximately level with the heart (Duley et al 2006). Blood pressure can be overestimated as a result of using a sphygmomanometer cuff of inadequate size relative to the arm circumference. The length of the bladder should be at least 80% of the arm circumference. Appropriately sized cuffs should be available with inflation bladders of 35 cm (standard size), 41 cm (large size) and >42 cm (thigh size) (PRECOG 2004).
The rounding off of the blood pressure measurements should be avoided and an attempt made to record the blood pressure as accurately as possible to the nearest 2 mmHg. The use of Korotkoff V (disappearance of heart sounds) as a measure of the diastolic blood pressure has been found to be easier to obtain, more reproducible and closer to the intra-arterial pressure in pregnancy. This reading should be used unless the sound is near zero, in which case Korotkoff IV (muffling sound) should also be recorded (PRECOG 2004).
Proteinuria in the absence of urinary tract infection is indicative of glomerular endotheliosis. The amount of protein in the urine is frequently taken as an index of the severity of pre-eclampsia. A significant increase in proteinuria coupled with diminished urinary output indicates renal impairment. Interobserver variation in the assessment of proteinuria and a high proportion of false positive and false negative results by dipstick analyses have been well documented (Gangaram et al 2005). It is important therefore to follow the instructions provided with the dipsticks in order to reduce the likelihood of error. Studies show that in routine clinical practice ‘nil’ or ‘trace’ proteinuria will miss significant proteinuria in one out of eight hypertensive women. Accuracy can be improved by using an automated device for dipstick analysis (Waugh et al 2005). Vaginal discharge, blood, amniotic fluid and bacteria can contaminate the specimen and give a false positive reading. A 24 hrs urine collection for total protein measurement will be required to be certain about the presence or absence of proteinuria and to provide an accurate quantitative assessment of protein loss (PRECOG 2004). A finding of >300 mg/24 hrs is considered to be indicative of mild-moderate pre-eclampsia, and >3 g/24 hrs is considered to be severe.
These used to be included in the diagnostic criteria for pre-eclampsia but both are variable findings and nowadays, are usually considered only when a diagnosis of pre-eclampsia has been made based on other criteria. Clinical oedema may be mild or severe in nature and the severity is related to the worsening of the pre-eclampsia. Oedema of the ankles in late pregnancy is a common occurrence. It is of a dependent nature, usually disappears overnight and is not significant in the absence of raised blood pressure and proteinuria. However, the sudden severe widespread appearance of oedema is suggestive of pre-eclampsia or some other underlying pathology and further investigations are necessary. This oedema pits on pressure and may be found in non-dependent anatomical areas such as the face, hands, lower abdomen, vulval and sacral areas.
These now make a significant contribution to the assessment and diagnosis of pre-eclampsia, particularly when the presentation is atypical and hypertension or proteinuria, or both, are absent. The expected normal blood values in pregnancy are outlined in Table 22.1. It is important to state that the data are limited and therefore the quoted normal range may vary (Nelson-Piercy 2006, Ramsay et al 2000). The following alterations in the haematological and biochemical parameters are suggestive of the onset of pre-eclampsia:
Table 22.1 Normal blood values in pregnancy
| Full blood counta | |
| Haemoglobin | 11.1–12 g/dL |
| Haematocrit | 33–39% |
| Platelets | 150–400 × 109/L |
| Fibrinogen | 3.63–4.23 g/L |
| Renal functionb | |
| Creatinine | 44–73 μmol/L |
| Urate | 2.4–4.2 mmol/L |
| Uric acid | 0.14–0.38 mmol/L |
| Liver functionc | |
| ALT | 10–30 IU/L |
| AST | 6–32 IU/L |
| GGT | 5–43 IU/L |
| Albumin | 28–35 g/L |
| Total protein | 48–65 g/L |
c Girling et al 1997, Ramsay et al 2000.
Symptoms may contribute to the diagnosis as described earlier, but these are rarely experienced by the woman until the disease has progressed to an advanced stage.
The aim of care is to monitor the condition of the woman and her fetus and if possible to prevent the hypertensive disorder worsening by using appropriate interventions and treatment. The ultimate aim is to prolong the pregnancy until the fetus is sufficiently mature to survive, while safeguarding the mother’s life. The maternal and fetal condition, together with the plan of care, need to be discussed with the woman and her partner and family. Helping the woman and her partner to interpret the situation, in particular the prognosis for the pregnancy and the potential for perinatal loss, is an important consideration (Kidner & Flanders-Stephans 2004). The midwife should be sensitive to the needs of the family if the woman requires admission to hospital, particularly if she is feeling well enough to be at home. She is likely to be anxious about the well-being of her children and visiting should be encouraged to allay her fears. The woman and her partner will be concerned for the current pregnancy; sensitive support and encouragement will be required of the midwife. The midwife has a key role in providing psychosocial support for these women (Hodnett 2000). Good communication with the multidisciplinary team involved in the care of the woman and her baby is essential (Mander 2001).
If the midwife diagnoses hypertension or pre-eclampsia during pregnancy, the woman should be referred to a doctor or directly to a maternity unit for assessment. Gestational hypertension will require close monitoring and if pre-eclampsia develops, then admission to hospital and more therapeutic interventions will be required. Care and management will vary depending on the degree of pre-eclampsia. Guidelines for the management of severe pre-eclampsia have been outlined by Lewis & Drife (2001) and Tufnell et al (2006) and these have been incorporated below.
Women are advised to rest as much as possible, but rest does not prevent the development of pre-eclampsia. Admitting women to hospital to facilitate this has not been found to be cost-effective, can be disruptive to family life and Meher et al (2005) found that inpatient care does not improve outcomes, nor prevent the development of proteinuria. It is recommended that women attend a day assessment unit as a means of reducing the need for antenatal admissions and the number of medical interventions. It is preferable for the woman to rest at home and to have regular visits by the midwife or GP and in some instances, this can be highly effective where there is the availability of distance monitoring. When proteinuria develops in addition to hypertension the risks to the mother and fetus are considerably increased. Admission to hospital is required to monitor and evaluate the maternal and fetal condition.
There is little evidence to support dietary intervention for preventing or restricting the advance of pre-eclampsia. As for any pregnant woman, a diet rich in protein, fibre and vitamins may be recommended. There is some evidence to suggest that prophylactic fish oil in pregnancy may act as an anti-platelet agent, thereby preventing hypertension and proteinuric pre-eclampsia (Roberts & Redman 1993). Calcium supplementation has also been investigated and appears to be beneficial for women at high risk of developing hypertension in pregnancy and in communities with low dietary calcium intake (Hofmeyr et al 2007). Studies have been undertaken to find out whether the use of antioxidant Vitamin C and E supplements could reduce the incidence of pre-eclampsia. However the Vitamins in Pre-eclampsia (VIP) Trial Consortium found that supplementation with vitamins C (1000 mg) and E (400 IU) does not prevent pre-eclampsia in women at risk, but does increase the rate of babies born with low birth weight. Therefore, these high dose antioxidants should not be given in pregnancy (Poston et al 2006).
The value of routine weighing during antenatal visits has been questioned and in many areas has now been abandoned as a form of antenatal screening for pre-eclampsia. However, weight gain may be useful for monitoring the progression of pre-eclampsia in conjunction with other parameters. The initial BMI (see Ch. 13) is considered a more useful predictor of hypertension in pregnancy, since this is higher in women who subsequently develop pre-eclampsia (Duckitt & Harrington 2005).
If hypertension is detected during pregnancy, the blood pressure is monitored daily at home or every 4 hrs when in hospital. Urine should be tested for protein daily. If the woman or midwife identifies protein in a midstream specimen of urine, a 24 hrs urine collection is required in order to determine the amount of proteinuria. The level of protein indicates the degree of vascular damage. Reduced kidney perfusion is indicated by proteinuria, reduced creatinine clearance and increased serum creatinine and uric acid.
Abdominal examination is carried out daily. Any discomfort or tenderness should be recorded and reported immediately to a doctor, as this may be a sign of placental abruption. Upper abdominal pain is highly significant and indicative of HELLP syndrome associated with fulminating (rapid onset) pre-eclampsia.
Doppler assessment of uterine arteries can demonstrate increased placental vascular resistance as a result of failure of the trophoblastic invasion of the spiral arteries early in pregnancy (<20 weeks).
Biophysical profile assessment is recommended in order to determine fetal health and well-being. This can be done by the use of the following: fetal movement charts, CTG monitoring, serial ultrasound scans to check for fetal growth, assessment of liquor volume and fetal breathing movements and umbilical artery Doppler blood flow (see Ch. 18).
These are often referred to as ‘PET’ bloods and include full blood count (haemoglobin, haematocrit and platelet count), urea and electrolytes, serum creatinine level, serum uric acid level, liver function tests including albumin levels, clotting studies if platelet count <100 × 109/L. In severe pre-eclampsia, there should be blood studies undertaken every 12–24 hrs (Lewis & Drife 2001).
The use of antihypertensive therapy as prophylaxis is controversial, as this shows no benefit in significantly prolonging pregnancy or improving maternal or fetal outcome in women with mild to moderate hypertension (Abalos et al 2007). Its use is, however, advocated as short-term therapy in order to prevent an increase in blood pressure and the development of severe hypertension (diastolic of 110 mmHg and systolic of 170 mmHg), thereby reducing the risk to the mother of cerebral haemorrhage (Duley et al 2007). The aim of treatment is to gradually reduce the blood pressure to a level that is safe for both mother and fetus and to maintain the systolic blood pressure between 140–155 mmHg and the diastolic 90–100 mmHg. A review undertaken by Duley et al (2006) concludes that there is no one antihypertensive which is preferable to others and clinicians should use the one/s with which they are familiar.
Methyldopa is the most widely used drug in women with mild to moderate gestational hypertension. Drowsiness is a common side effect and it can cause depression, however it is considered to be safe and effective for both mother and fetus. An α- and β-blocker such as labetalol is an alternative and is considered safe in pregnancy except for women with asthma or congestive heart failure. Atenolol used over the long term is not recommended as this is linked with fetal growth restriction and the use of angiotensin-converting enzyme (ACE) inhibitors are contraindicated in pregnancy. Calcium channel blockers such as nifedipine, are increasingly used to treat severe hypertension in pregnancy (Duley et al 2006). These act on arteriolar smooth muscle to induce vasodilation by blocking calcium entry into cells thus decreasing cerebral vasospasm and increasing urinary output and uteroplacental blood flow. Maternal side-effects include tachycardia, palpitations and headache (Frishman et al 2005).
Early activation of the clotting system may contribute to the later pathology of pre-eclampsia and as a result the use of anticoagulants or antiplatelet agents has been considered for the prevention of pre-eclampsia and fetal growth restriction. Aspirin is thought to inhibit the production of the platelet-aggregating agent thromboxane A2. The PARIS (Perinatal Antiplatelet Review of International Studies) Collaboration systematic review and meta-analysis found that women receiving antiplatelet agents had a 10% reduced risk of: developing pre-eclampsia, pre-term birth before 34 weeks’ gestation and having a pregnancy with serious adverse outcome (Askie et al 2007).
Timing and mode of delivery is dependent on the maternal and fetal condition as well as the gestation of the pregnancy. Where possible, spontaneous onset of labour and vaginal birth is preferable (NHBPEP Working Group 2000). The midwife should remain with the woman throughout the course of labour as pre-eclampsia can suddenly worsen at any time. It is essential to monitor the maternal and fetal condition carefully. Marked deviations should be noted and medical assistance sought. The woman with gestational or mild pre-eclampsia will require less intensive care than a woman with severe pre-eclampsia or eclampsia.
Blood pressure is measured half-hourly, 15–20 min in severe pre-eclampsia. Because of the potentially rapid haemodynamic changes in pre-eclampsia, a number of authors recommend the measurement of the MAP. As mentioned earlier this can be calculated manually or by the use of an automated blood pressure recorder such as the Dinamap. MAP reflects the systemic perfusion pressure, and therefore the degree of hypovolaemia, whereas manual measurement of diastolic pressure alone is a better indicator of the degree of hypertension (Churchill & Beevers 1999). Observation of the respiratory rate (>14/min) will be complemented with pulse oximetry in severe pre-eclampsia; this is a non-invasive measure of the saturation of haemoglobin with oxygen and gives an indication of the degree of maternal hypoxia. Temperature should be recorded as necessary. In severe pre-eclampsia, examination of the optic fundi can give an indication of optic vasospasm and papilloedema. Cerebral irritability can be assessed by the degree of hyper-reflexia or the presence of clonus (significant if more than three beats).
The reduced intravascular compartment in pre-eclampsia together with poorly controlled fluid balance can result in circulatory overload, pulmonary oedema, adult respiratory distress syndrome and ultimately death (Lewis & Drife 2001). In severe pre-eclampsia, a central venous pressure (CVP) line may be considered in order to monitor the fluid status more effectively (see Ch. 33). If the value is >10 mmHg, then 20 mg furosemide (frusemide), a diuretic drug, should be considered. Intravenous fluids are administered using infusion pumps and the total recommended fluid intake in severe pre-eclampsia is 85 mL/hr. Oxytocin should be administered with caution as it has an antidiuretic effect. Urinary output should be monitored closely and urinalysis undertaken every 4 hrs to detect the presence of protein, ketones and glucose. In severe pre-eclampsia a urinary catheter should be in situ and urine output is measured hourly; a level >30 mL/hr reflects adequate renal function.
Although women with pre-eclampsia have oedema, they are hypovolaemic. The blood volume is low, as shown by a high haemoglobin concentration and a high haematocrit level. This results in movement of fluid into the extravascular compartment causing oedema. The oedema initially occurs in dependent tissues, but as the disease progresses oedema occurs in the liver and brain giving rise to the symptoms described previously. Nevertheless, this cannot be corrected simply by plasma volume expansion. Treatment is controversial as colloids can seep into the tissues and ‘hold’ fluid there and they can thus cause even worse pulmonary oedema than crystalloids. Any fluids are therefore given with caution.
Epidural analgesia may procure the best pain relief, reduce the blood pressure and facilitate rapid caesarean section should the need arise. It is important to ensure a normal clotting screen and a platelet count >100 × 109/L prior to insertion of the epidural.
The fetal heart rate should be monitored closely and deviations from the normal reported and acted upon.
When the second stage commences, the obstetrician and paediatrician should be notified. The midwife will continue her care of the woman and will usually assist the woman during the birth. A short second stage may be preferred depending on the maternal and fetal conditions; in this instance a ventouse extraction or forceps delivery will be performed by the obstetrician. If the maternal or fetal condition shows significant deterioration during the first stage of labour, a caesarean section will be undertaken. Oxytocin is recommended for the management of the third stage of labour. Ergometrine and Syntometrine will cause peripheral vasoconstriction and increase hypertension and therefore should not normally be used in the presence of any degree of pre-eclampsia unless there is severe haemorrhage.
The maternal condition should continue to be monitored at least every 4 hrs for at least the next 24 hrs following childbirth, as there is still the potential danger of the mother developing worsening pre-eclampsia or eclampsia. The blood pressure may initially rise after delivery but should gradually return to normal by the end of the first postnatal week. Persistent hypertension will need to be treated. Methyldopa should be avoided postpartum because of the risk of postpartum depression; the drug of choice is atenolol and/or nifedipine. Most antihypertensive drugs are compatible with breastfeeding (James & Nelson-Piercy 2004).
The signs and symptoms described in Box 22.1 will signal the onset of eclampsia. The midwife should be alert to any of these signs and summon medical assistance immediately. The aim of care at this time is to preclude death of the mother and fetus by controlling hypertension, inhibiting seizures and preventing coma.
The syndrome of haemolysis (H), elevated liver enzymes (EL) and low platelet count (LP) was first described by Weinstein in 1982 and is generally thought to represent a variant of the pre-eclampsia/eclampsia syndrome but can occur on its own or in association with pre-eclampsia. The incidence of the disease is reported as being 0.17–0.85% of all livebirths (Rath et al 2000).
HELLP syndrome typically manifests itself between 32 and 34 weeks’ gestation and 30% of cases will occur postpartum. With postpartum presentation, the onset is typically within the first 48 hrs following birth. Women with HELLP syndrome often complain of malaise, nausea and vomiting, upper abdominal pain with tenderness; some will have non-specific viral-syndrome-like symptoms. Hypertension and proteinuria may be minimal or absent (Rath et al 2000) (see Sharon’s story, Box 22.2).
At 31 weeks pregnant, I felt really good. Ten days later I was attending an aquanatal class in which I really struggled to bend my ankles to swim. The following day I saw my midwife who after taking my blood pressure phoned the hospital as my readings were of concern and I had protein in my urine.
I was admitted to the maternity ward, my blood pressure was taken regularly and I was told to rest. I found this quite difficult, as I felt a fraud being on the ward as I felt well. How naive was I.
Late one evening the midwife took my blood pressure and was alarmed by the reading, ‘I can’t fit it on the chart’, she said, so after a few minutes she re-took it with a manual pump. The second readings were the same, so at around midnight I was wheeled down to the labour ward. Still at this stage I didn’t realize how serious this was. I was monitored all night and my baby was monitored as well. The doctors wanted to take blood but my hands and forearms had now swollen up, so trying to extract blood from me was very difficult, so the decision was taken that I should have a central venous pressure line with three parts. This was quite uncomfortable in my neck, and heavy with all the parts coming out to the machines.
The doctors wanted to induce me, so they broke my waters. Some hours passed and I was only 3 cm, I had an epidural but nothing seemed to ease the blood pressure. Then my baby’s heart rate dropped, so I was taken for an emergency caesarean section.
In the early hours of the following morning and 6 weeks premature, I had a baby boy weighing 3 lb 5 oz. I saw him briefly but he was rushed into the neonatal intensive care unit. I was then taken back to high dependency, where I had further complications. My blood was taken every 6 hrs to monitor the platelets in my red blood cells, as they were getting very low, down to 30 at it lowest stage. Platelets had been ordered in preparation for a transfusion, but luckily after 2 days they started to increase. After 7 days, I was transferred to the postnatal ward where I stayed for a further 5 days.
The hardest thing of all was that it was 36 hrs after birth before I got to see my son and this was only for 1 hr. The following 4 weeks were also very difficult, as my husband was at home and work, I was in the postnatal ward and our son was on the neonatal unit. We both felt as if we were renting our own son from the hospital and the house felt so empty when we got home.
Now that we are both well, I can reflect on what happened. I didn’t realize how serious pre-eclampsia and HELLP syndrome were or what the implications could have been for me and my baby.
Early diagnosis of HELLP syndrome is critical; any woman presenting with the above symptoms should have a full blood count, platelet count and liver function tests, irrespective of maternal blood pressure. Haemolysis with elevated lactate dehydrogenase (LDH) and raised bilirubin levels, low (<100 × 109/L) or falling platelets and elevated liver transaminases (AST, ALT and GGT) assist in confirming the diagnosis of HELLP syndrome (Knappen et al 1999). A positive D-dimer test (indicator of coagulopathy) in conjunction with pre-eclampsia has also been found to be predictive of women who will develop HELLP syndrome (Padden 1999).
HELLP syndrome may be classified as partial (one or two features of the syndrome) or full (all three features). It may also be classified on the basis of the platelet count: Class I <50 × 109/L, Class II 50–100 × 109/L, Class III 100–150 × 109/L. Women with Class I HELLP syndrome are at increased risk for maternal and perinatal morbidity and mortality (Padden 1999).
Serious maternal complications include abruptio placentae, disseminated intravascular coagulation (DIC), eclampsia, acute renal failure and subcapsular haematoma of the liver (Deruelle et al 2006, Haddad et al 2000, Vigil-De 2001). Rupture of the liver is a very rare but potentially fatal complication of the HELLP syndrome and usually presents with severe upper abdominal, neck and shoulder pain, which may persist for several hours. Radiographic imaging of the liver is required to assess the extent of the damage; surgical intervention and/or liver transplantation, may be required to prevent haemorrhagic shock and liver failure (Reck et al 2001). Infants whose mothers have HELLP syndrome are often small for gestational age and are at risk of perinatal asphyxia (Rath et al 2000).
Prompt recognition of HELLP syndrome and initiation of therapeutic interventions are essential to ensure the best outcome for mother and fetus. Women with the HELLP syndrome should be admitted to a consultant unit with intensive or high dependency care facilities available. Treatment and interventions are based on the gestational age and the health of the mother and fetus. Corticosteroids may stabilize some of the abnormal biochemical and clinical parameters, as well as aid fetal lung maturity (Clenney & Viera 2004). However, further research is required to determine if maternal and perinatal morbidity and mortality is significantly reduced (Matchaba & Moodley 2004). In term pregnancies, or where there is a deteriorating maternal or fetal condition, immediate delivery is recommended (Curtain & Weinstein 1999). A significant number of women with HELLP syndrome also require blood product transfusions to correct the coagulation abnormalities (Deruelle et 2006, Haddad et al 2000, Padden 1999).
Eclampsia is rarely seen in developed countries today, especially if there are good facilities for antenatal care. Leith et al (1997) demonstrated that over a 60-year period, the incidence of eclampsia had fallen from 74 to 7.4 per 10 000 deliveries. More recently, the reported rate of eclampsia in Europe and other developed countries is 1 in 2000–3000 deliveries (Mattar & Sibai 2000). In the UK, there was an incidence of 4.8/10 000 maternities (Lewis & Drife 2004) but a more recent UKOSS (UK Obstetric Surveillance System) study found an incidence of 2.1/10 000 births (UKOSS 2006). Usually pre-eclampsia is diagnosed and treatment instituted to prevent eclampsia but occasionally pre-eclampsia is so rapid in onset and progress that eclampsia ensues before any action can be taken. In this situation, pre-eclampsia is termed ‘fulminating’ (Katz et al 2000).
Eclampsia is associated with increased risks of maternal and perinatal morbidity and mortality. Significant maternal life-threatening complications as a result of eclampsia include placental abruption and haemorrhage, DIC, pulmonary oedema, multi-organ failure including cardiac, renal and liver, HELLP syndrome and brain haemorrhage (Lewis & Drife 2001, 2004).
There is a proposed link between the hypertension in eclampsia, which may not be extreme, and cerebral disease; Vaughan & Delanty (2000) identify the clinical similarities between eclampsia and hypertensive encephalopathy. A significant finding, however, is that hypertension is not necessarily a precursor to the onset of eclampsia but will almost always be evident following a seizure (Sibai 2005). MRI studies suggest that there is cerebral vasospasm causing ischaemia and cellular oedema, especially in the territory of the posterior cerebral arteries.
Detecting and managing imminent eclampsia is also made more difficult in that, unlike other types of seizure, warning symptoms are not always present before onset of the convulsion. Variations also exist according to the gestational period with 38–53% occurring antenatally, 18% intrapartum and 28–44% postpartum (Douglas & Redman 1994, Mattar & Sibai 2000). Late postpartum eclampsia has also been described, where eclampsia can occur between 48 hrs and 4 weeks after birth (Chames et al 2002, Munjuiuri et al 2005).
In fulminating pre-eclampsia or eclampsia, delivery of the mother should take place as soon as possible once the condition has been stabilized by the following measures.
The aims of immediate care are to:
The midwife must remain with the mother constantly and provide assistance with medical treatment. In the first instance, all effort is devoted to the preservation of the mother’s life and the well-being of the baby is secondary. This may seem arbitrary, but if the mother dies then fetal death is inevitable. The woman will require intensive/high dependency care as she may remain comatose for a time following the seizure or may be sleepy. Clinical observations should be measured and recorded. The midwife must observe for periodic restlessness associated with uterine contraction, which indicates that labour has commenced. The woman’s partner should be kept informed and the midwife will need to give emotional support through this unexpected and anxious time. It is usual to deliver the baby as soon as possible when eclampsia occurs, initial seizures are usually of short duration but may become prolonged while the woman remains pregnant; in this instance caesarean section is the usual mode of delivery. The following therapeutic interventions are essential (Tufnell et al 2006).
Magnesium sulphate (MgSO4) is now the recommended drug of choice to treat and prevent eclampsia rather than diazepam or phenytoin. It is thought to aid vasodilation thereby reducing cerebral oedema and preventing seizures. There is a reduction in the incidence of pneumonia, artificial ventilation and admission to intensive care in women treated with MgSO4 compared with those treated with diazepam (ETCG 1995, Lewis & Drife 2001, 2004, Magpie Trial Collaborative Group 2002). Diazepam is used to control other types of seizures and has a sedative effect and should only be used in the treatment of pre-eclampsia if MgSO4 is not available.
MgSO4 is administered intravenously according to a protocol. The Confidential Enquiries into Maternal Deaths (Lewis & Drife 2001) recommend that a loading dose of 4 g is given over 5–10 min i.v. followed by a maintenance dose of 5 g/500 mL normal saline given as an i.v. infusion at a rate of 1–2 g/hr until 24 hrs following delivery or the last seizure. Recurrent seizures should be treated with a further bolus of 2 g. Continuous infusion of MgSO4 can be toxic particularly in women with renal insufficiency. Early signs and symptoms of toxicity include nausea, weakness, slurred speech, double vision and loss of patellar reflexes. In more severe cases muscular paralysis, respiratory arrest and cardiac arrest ensue. The respiratory rate (>14/min) and oxygen saturation levels (>95%) and deep tendon reflexes should be monitored hourly. In women with oliguria, serum magnesium levels should be monitored and maintained within the therapeutic range (2–3 mmol/L). In the event of toxicity, the MgSO4 infusion should be stopped and ventilatory and circulatory support given as required. Calcium gluconate (10–20 mL of 10% solution) is the antidote for magnesium toxicity and should be readily available.
Severe hypertension is defined as >160/110 mmHg or a mean arterial pressure >125 mmHg. The aim of treating severe hypertension is to avoid the loss of cerebral autoregulation and prevent cerebral haemorrhage without significantly reducing cerebral perfusion or uteroplacental blood flow. Intravenous hydralazine is the most useful agent to gain control of the blood pressure quickly; 5–10 mg should be administered slowly intravenously and the blood pressure measured at 5 min intervals until the diastolic pressure reaches 90–100 mmHg. The diastolic blood pressure may be maintained at this level by titrating the infusion of hydralazine against the blood pressure. Labetalol may be used in preference to hydralazine, in which case 20 mg is given i.v. followed at 10-min intervals by 40 mg, 80 mg and 80 mg up to a cumulative dose of 300 mg (Lewis & Drife 2001, p 92). Care should be taken when using nifedipine in conjunction with MgSO4 as this may result in excessive calcium channel blockade and potentiate hypotension.
Care must be taken not to overload the maternal system with intravenous fluids as discussed in the management of pre-eclampsia. Frequent assessment of the fluid intake (intravenous, oral and blood products) and urine output, as well as monitoring by pulmonary function (pulse oximetry and respirations) is essential (Lewis 2007, Lewis & Drife 2001, 2004).
Use of anaesthesia in eclampsia is difficult, as the condition of women with eclampsia varies considerably. Both general and regional (epidural/spinal) anaesthesia carry a degree of risk (Levy 2003); epidural is preferred in eclamptic women who are conscious, haemodynamically stable and cooperative (Moodley et al 2001).
As soon as the baby is born, the woman’s partner should be encouraged to hold him and accompany him to the neonatal intensive care unit if that is where he will be cared for. It is important that the partner has early interaction with the baby so that an account can be given of the baby’s progress from the time of birth. Likewise, the midwife should liaise with the neonatal unit staff and explain the treatment given to the baby and the likely prognosis. A photograph should be taken of the baby so that the mother can see him as soon as she recovers. Postpartum care should be given, as recommended by NICE (2006) and as soon as the mother’s condition permits, she should be taken in her bed or a chair to see her baby. Alternatively, if the baby’s condition is good, he may be returned to his mother.
As almost half of eclamptic seizures occur following childbirth, intensive surveillance of the woman is required in a high dependency or intensive care unit. Parameters to monitor are: a return to normal blood pressure, an increase in urine output, reduction in proteinuria, a reduction in oedema and a return to normal laboratory indices. Antithrombotic agents and the use of thromboelastic stockings will prevent deep vein thrombosis. Antihypertensive therapy should be maintained and gradually reduced as the blood pressure returns to normal; this may take up to 12 weeks. Most antihypertensive drugs are compatible with breastfeeding.
There is no indication that the hypertensive disorders of pregnancy cause later hypertensive disease but it can bring to the fore an inherent disposition towards hypertension. Women with a history of severe pre-eclampsia before 32 weeks’ gestation have a 5% risk of recurrence by this gestational age and a 15% risk of recurrence overall (Mattar & Sibai 2000). Recent studies have also identified that women who have a history of pre-eclampsia are more likely to develop cardiovascular disease in later life (Manton et al 2007, Wilson et al 2003).
Usually the blood pressure returns to normal within several weeks but the proteinuria may persist for a longer period. Six weeks after the birth of her baby, the mother is examined by the obstetrician and if all is well, she will be discharged and advised to seek advice as soon as a subsequent pregnancy occurs. Referral to voluntary organizations, such as Action on Pre-eclampsia (www.apec.org.uk) may provide additional information, advice and support following a pregnancy complicated by hypertensive disorders.
The mother may have very little recollection of the birth and the events surrounding it if she was unconscious or heavily sedated at the time. It is essential that the midwife enquire further if a mother gives no clear history of a previous birth or if she says that she was ill. It is advisable to obtain the previous case notes where possible. In this way good care can be provided and prophylactic management established where indicated.
Pre-existing (chronic) hypertension has the following possible causes:
Consistent blood pressure recordings of ≥140/90 mmHg, on two occasions more than 24 hrs apart during the first 20 weeks of pregnancy, suggest that the hypertension is pre-existing and unrelated to the pregnancy. The diagnosis may be difficult to make because of the changes seen with blood pressure in pregnancy. This is a particular problem in women who present late in their pregnancy with no baseline blood pressure measurement. These women may appear normotensive in early pregnancy and hypertension identified later in pregnancy is considered gestational. The diagnosis may only be made when the blood pressure remains elevated at 12 weeks postpartum.
When taking a history, the midwife may identify potential or existing medical problems. Women with pre-existing (chronic) hypertension tend to be older, parous and have a family history of hypertension.
Accurate measurement of blood pressure is important and the midwife needs to consider the guidelines mentioned earlier. Serial blood pressure recordings should be made in order to determine the true pattern as even normotensive women show occasional peaks.
The doctor’s physical examination of the woman may reveal the long term effects of hypertension such as retinopathy, ischaemic heart disease and renal damage. Renal function tests may be performed although alterations in the physiological norms may affect clinical interpretation in pregnancy. Elevated serum uric acid levels may assist in identifying women with chronic hypertension. Admission to a hospital or day assessment unit for initial assessment may be necessary.
The perinatal outcome in mild pre-existing (chronic) hypertension is good. However, the perinatal morbidity and mortality are increased in those women who develop severe chronic hypertension or superimposed pre-eclampsia. Other complications are independent of pregnancy and include renal failure and cerebral haemorrhage. In 1–2% of cases, hypertensive encephalopathy may develop if the blood pressure suddenly rises above 240/140 mmHg; this is a hypertensive emergency requiring admission to an intensive care unit (Vidaeff et al 2005). Maternal mortality is high if phaeochromocytoma is not diagnosed and left untreated.
This is defined as a systolic blood pressure of <160 mmHg and a diastolic blood pressure of <110 mmHg. All women with pre-existing (chronic) hypertension should be referred to a specialist either preconception or early in pregnancy in order to arrange shared care, review the diagnosis and review their medication. Women who are already taking antihypertensive therapy will need to discontinue those drugs which may be harmful to the fetus, e.g. ACE inhibitors and atenolol and replace them with medications considered to be safe in pregnancy. Most of these women are at low risk of pregnancy complications and are unlikely to need antenatal admission to hospital. The woman’s condition should be carefully monitored in the community by the midwife and GP in order to identify if superimposed pre-eclampsia develops.
The systolic blood pressure is >160 mmHg and the diastolic blood pressure is >110 mmHg. The woman should be cared for by the obstetric team in conjunction with a physician. Frequent antenatal visits are recommended in order to monitor the maternal condition. This includes blood pressure monitoring, urinalysis to detect proteinuria and blood tests to measure the haematocrit and renal function. Antihypertensive therapy is used in order to prevent maternal complications but has no proven benefit for the fetus and does not stop the development of pre-eclampsia. The midwife may do much to settle anxiety by the use of counselling skills and by mobilizing resources to meet social needs if required. In the rare event of a phaeochromocytoma being present, the blood pressure will be treated with appropriate antihypertensive drugs during the pregnancy and the tumour resected postnatally.
Monitoring of fetal well-being and of placental function should be carried as there is an increased risk of placental abruption and growth restriction (see Ch. 18). If the maternal or fetal condition causes concern, the woman will be admitted to hospital.
The timing and mode of the birth is planned according to the needs of mother and fetus, if early delivery is required, induction of labour is preferred to caesarean section. Postnatally, the woman should be seen by a physician to review the management and treatment of persistent hypertension and renal function should also be reassessed. The midwife who is advising the woman on family planning should be aware of the hypertensive effect of the combined oral contraceptive pill.
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