Hypertension in pregnancy, pre-eclampsia and eclampsia

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Chapter 14 Hypertension in pregnancy, pre-eclampsia and eclampsia


Suna Monaghan, Jenny Myers and Lorna A. Howie



Introduction


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




  • 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



  • 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):




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



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



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




    • Iatrogenic preterm delivery



    • Fetal death in utero and stillbirth



    • Fetal growth restriction



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




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



    • 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.



Table 14.1 Hypertension in pregnancy
























Condition Diagnosis
Chronic hypertension

Hypertension (BP >140/90):




  • Present at booking



  • Present before 20/40



  • Being treated at the time of referral to maternity services

Gestational hypertension

New hypertension (BP >140/90):




  • Presenting after 20/40



  • Without significant proteinuria



  • Also known as pregnancy-induced hypertension (PIH)



  • Affects 1 in 10 pregnancies

Pre-eclampsia

New hypertension (BP >140/90):




  • After 20/40



  • With significant proteinuria



  • Affects 2–3% of pregnancies



  • 2% can go on to develop eclampsia (worldwide)

Severe pre-eclampsia

New severe hypertension (BP >160/110):




  • After 20/40



  • With significant proteinuria



  • +/– symptoms (see below)



  • +/– biochemical impairment



  • +/– haematological impairment



  • HELLP – severe expression of PET, associated with haemolysis, elevated LFTs and low platelets

Eclampsia Convulsive condition associated with 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



Hypertension


This can be deemed mild, moderate or severe (NICE) (see Table 14.2). Blood pressure readings should be made with manual sphygmomanometers instead of an automated machine, as these tend to underestimate systolic blood pressure.



Table 14.2 Definition of hypertension


















Hypertension BP reading
Mild 140–149/90–99
Moderate 150–159/100–109
Severe >160/110


Proteinuria


Significant proteinuria:




  • Protein >300 mg/24 hours or



  • Urinary protein:creatinine ratio (uPCR) >30 mg/mmol on a spot sample.


NB. A degree of proteinuria is a normal physiological change in pregnancy.



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:




1. Invasion of the decidual segments of the spiral arteries (10–12 weeks)



2. Invasion of the myometrial segments (15–16 weeks).


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:




  • Vascular endothelial growth factor (VGEF)



  • Placental growth factor (PlGF).


There are two antiangiogenic markers that have been studied:




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



  • 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.



Table 14.3 Risk factors associated with pre-eclampsia












Moderate risk High risk



  • 1st pregnancy



  • Age > 40



  • Pregnancy interval of > 10 years



  • Family history of pre-eclampsia



  • Multiple pregnancy



  • BMI 35




  • Hypertensive disease during a previous pregnancy



  • Chronic renal disease



  • Autoimmune diseases (SLE, antiphospholipid syndrome etc.)



  • Diabetes



  • Chronic hypertension



Signs, symptoms and complications


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



Table 14.4 Diagnostic criteria for severe pre-eclampsia









Severe pre-eclampsia: hypertension and proteinuria in addition to any one of the following features:

CVS




  • Severe hypertension (SBP >160 or DBP >110)



  • Chest pain



  • Sudden swelling of face/hands/feet



Renal




  • Oliguria (decrease in GFR)



  • Creatinine >100 mmol/L



  • Cortical/tubular necrosis



CNS




  • Severe frontal headache



  • Visual disturbance including blurring and flashing in front of the eyes



  • Cortical blindness



  • Retinal oedema



  • Clonus



  • Eclampsia



  • Cerebral haemorrhage/oedema



Respiratory




  • Dyspnoea



  • Pharyngeal/laryngeal oedema



GIT




  • Nausea and vomiting



  • Right upper quadrant pain (as a result of liver capsule tension)



  • Epigastric pain



  • ALT > 50 IU/L



  • HELLP



Haematological




  • Thrombocytopenia (platelets <100 × 109)



  • Falling fibrinogen



  • Disseminated intravascular coagulation (DIC)



  • Prolonged clotting times



  • Microangiopathic haemolysis



Feto-placental




  • IUGR



  • Oligohydramnios



  • Abruption



  • Abnormal umbilical Doppler



  • Preterm delivery (50% in severe pre-eclampsia)



  • Still birth

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Jan 28, 2017 | Posted by in ANESTHESIA | Comments Off on Hypertension in pregnancy, pre-eclampsia and eclampsia
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