Introduction

Hypertensive disorders of pregnancy are one of the most common antenatal complications, affecting 3–4% of all pregnancies:

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  They are a leading cause of direct maternal death in the UK and USA, with a rate of 0.83 and 0.99 per 100,000 maternities respectively

  
  
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  The necessity for urgent treatment of systolic hypertension (>160 mmHg) was one of the top ten recommendations in the last Maternal Mortality Report (CMACE 2006–2008):

  
  
  
  
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    There were seven deaths associated with inadequate control of systolic hypertension resulting in cerebral haemorrhage

    
    
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    Women with severe pre-eclampsia need to be managed by an effective multidisciplinary team

  
  
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  There is fetal morbidity and mortality associated with pre-eclampsia:

  
  
  
  
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    Iatrogenic preterm delivery

    
    
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    Fetal death in utero and stillbirth

    
    
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    Fetal growth restriction

  
  
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  There is also growing evidence of increased long term health risks in:

  
  
  
  
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    Women who have had pre-eclamptic pregnancies, including cardiovascular disease, type 2 diabetes mellitus and metabolic syndrome

    
    
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    Children of pre-eclamptic mothers also have an increased risk of hypertension and metabolic syndrome in later life.

Classification of hypertension in pregnancy

Hypertension in pregnancy is categorized according to gestation and cause (see Table 14.1). Before 20 weeks, it is likely to be due to chronic, pre-existing hypertension. Hypertension is often identified for the first time in early pregnancy and it is important to rule out any secondary causes. The commonest secondary cause is renal disease, but it is important to exclude vascular, endocrine and immunological causes. Approximately 20% of women with chronic hypertension will go on to develop superimposed pre-eclampsia.

Gestational hypertension complicates 10% of pregnancies and is defined as new-onset hypertension (>140/90 mmHg) after 20 weeks, without significant proteinuria or other features suggestive of multisystem disease.

Pre-eclampsia affects 3–4% of pregnancies, and is defined as new-onset hypertension with significant proteinuria: greater than 300 mg of urinary protein in 24 hours or a urinary protein:creatinine ratio (uPCR) > 30 mg/mmol.

Pre-eclampsia can occur at any time after 20 weeks’ gestation, even into the postpartum period. Early-onset pre-eclampsia (<34/40) represents around 30% of cases and is often associated with more severe fetal compromise. Severe maternal disease can develop at any gestation. The only cure for the condition is delivery of the placenta.

Pre-eclampsia may take several days to resolve post delivery. Blood pressure and proteinuria should resolve within 12 weeks of delivery. Women with early onset pre-eclampsia have a 25% chance of ongoing hypertension and proteinuria; this suggests an underlying cause, usually related to a renal condition, which requires further investigation.

Definitions

Pathogenesis

The cause of pre-eclampsia is not well understood; however, the placenta is the organ that drives pre-eclampsia.

The concept of a two-step model of trophoblast invasion has become widely accepted:

In pre-eclampsia the second stage of the process is impaired and results in impairment of remodelling the spiral arteries. The outcome is a poorly perfused and poorly developed placenta. Placental ischaemia is thought to be the reason for release of placental factors and the resultant imbalance of angiogenic factors. The altered placental function is associated with changes in the production and secretion of a number of placental-derived factors, which cause widespread maternal vascular endothelial dysfunction.

Widespread changes in the maternal vascular endothelium are characterized by vasoconstriction, capillary leak and an activation of the maternal inflammatory and clotting cascades.

A number of placental factors have been investigated in relation to pathogenesis of pre-eclampsia and it is likely that there is more than one aetiological mechanism that leads to placental dysfunction and pre-eclampsia. Research has been focused on a number of angiogenic markers. Angiogenesis is essential for normal placentation and two factors contribute to this:

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  Vascular endothelial growth factor (VGEF)

  
  
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  Placental growth factor (PlGF).

There are two antiangiogenic markers that have been studied:

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  Soluble FMS-like tyrokinase (sFlt-1): this peptide binds to and neutralizes the actions of VGEF and PlGF

  
  
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  Soluble endoglin (sEng): the levels of this peptide normally fall between the first and second trimesters; however, this is attenuated in women who go on to develop pre-eclampsia.

The result is an imbalance between proangiogenic and antiangiogenic peptides. These biomarkers may provide a way of detecting pre-eclampsia before the systemic signs of the disease appear. An elevation in sFlt and sEng with a reduction in VEGF and placental growth factor PlGF are currently being investigated as potential predictive, prognostic and diagnostic markers.

Risk factors

Many of the risk factors associated with pre-eclampsia identify a group of women with increased risk of vascular disease and these are the women at highest risk of developing the condition. It is likely that they are sensitized to the stressors of pregnancy and have an exaggerated response to placental dysfunction. The NICE guidelines recommend that women with risk factors for the development of pre-eclampsia should be prescribed 75 mg aspirin daily from 12 weeks until delivery. Aspirin is associated with a modest (around 15%) reduction in the rate of pre-eclampsia in high-risk groups. See Table 14.3 for risk factors related to development of pre-eclampsia.

Signs, symptoms and complications

Table 14.4 summarizes the diagnostic criteria for severe pre-eclampsia.

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