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Pre-eclampsia

Definition
  • A hypertensive syndrome that occurs in pregnant women after 20 weeks' gestation
  • New-onset, persistent hypertension (defined as a BP of ≥140 mmHg systolic and/or ≥90 mmHg diastolic, based on at least 2 measurements taken at least 4 hours apart)
  • With proteinuria (defined as urinary excretion of ≥0.3 g protein/24 hours). [1] [2] [3] 
  • The severity of the condition is based on the BP measurement and the presence of systemic involvement. [1] [2] [3]
Risk Factors
  • Strong
    • Primiparity
    • Pre-eclampsia in previous pregnancy
    • Family history of pre-eclampsia
    • Body mass index >30
    • Maternal age >35 years
    • Multiple (twin) pregnancy
    • Gestational hypertension
    • Pre-gestational diabetes
    • Autoimmune disease
    • Renal disease
    • Chronic hypertension
  • Weak
    • BP ≥80 mmHg diastolic at booking
    • Interval of 10 years or more since previous pregnancy
Differential diagnosis
Epidemiology
  • Pre-eclampsia has been reported to occur in about 5% to 8% of all pregnancies in the US. [3] 
  • When figures include patients who develop pre-eclampsia postpartum, the incidence is between 4% to 6% of all pregnancies throughout the world. [4] [5]
  • The incidence of severe disease and complications varies.
    • Severe disease, which is associated with an increased risk of morbidity and mortality, has an incidence of only 0.5% in the developed world, [6]
    • Rises to 1% in low-income countries. [5] 
    • Similarly, the incidence of complications such as eclampsia is also variable.
    • In the UK, the incidence has decreased from 4.9 per 10,000 per year in 1992 [7] to 3.89 per 10,000 per year by 2000. [5] 
    • This decrease is observed mostly in the intrapartum and postpartum groups, suggesting a possible beneficial effect of prophylactic magnesium sulphate. [5] 
    • However, in low-income countries the incidence of eclampsia is 10-fold greater, at about 50 per 10,000 per year. [6]
Aetiology
  • Pre-eclampsia is associated with a failure of normal invasion of trophoblast cells leading to maladaptation of maternal spiral arterioles
  • Associated with hyperplacentation disorders such as diabetes, hydatidiform mole, and multiple pregnancy. [8]
  • There are numerous risk factors that increase the probability and severity
    • However, these risk factors do not account for all cases
  • Complications such as eclampsia, HELLP syndrome, and fetal growth restriction are not present in all patients.
    • HELLP is a subtype of severe pre-eclampsia characterised by haemolysis (H), elevated liver enzymes (EL), and low platelets (LP)
Clinical features
  • Common
    • >20 weeks' gestation
    • BP ≥140 mmHg systolic and/or ≥90 mmHg diastolic and previously normotensive
    • headache
    • upper abdominal pain
    • reduced fetal movement
    • fetal growth restriction
    • oedema
  • Uncommon
    • visual disturbances
    • seizures
    • breathlessness
    • oliguria
    • hyper-reflexia and/or clonus
Pathophysiology
  • Pre-eclampsia is associated with a failure of the normal invasion of trophoblast cells leading to maladaptation of maternal spiral arterioles. [8]
    • The maternal arterioles are the source of blood supply to the fetus.
    • Maladaptation of these vessels can interfere with normal villous development leading to placental insufficiency and fetal growth restriction.
  • Abnormalities of spiral artery adaptation are immunologically based, with genetic influences. [4] [8] 
  • Not all women with this potential placental trigger develop the syndrome
    • Therefore, the maternal response must be the decisive factor in development of systemic disease.
    • This systemic maternal response is what manifests itself as pre-eclampsia. [4]
  • Clinically, pre-eclampsia does not manifest until after 20 weeks' gestation.
  • However, more recent studies suggest that preclinical changes may occur, suggested by the presence of various biomarkers, although none are currently used in routine clinical practice. [4]
  • Hypertension and proteinuria are due to the vascular inflammatory response that produces vasoconstriction and capillary leak. [4] 
  • Other presentations are complications of the vascular inflammation and capillary leak
    • eclampsia (due to cerebral vascular dysregulation and oedema)
    • HELLP syndrome (due to liver vascular dysregulation and oedema causing abdominal pain)
    • pulmonary oedema (due to capillary leak).
Investigations
  • urinalysis
    • 1+ protein; urinary excretion of ≥0.3 g protein in 24 hours; or urine protein:creatinine ratio ≥30 mg/mmol
  • fetal ultrasound
    • variable depending on severity
  • fetal cardiotocography
    • no abnormalities in tracing indicate assured fetal wellbeing
  • fetal biometry
    • may reveal fetal growth restriction
  • umbilical artery Doppler velocimetry
    • absence of end diastolic flow is a sign that delivery will probably be necessary in the near future
  • amniotic fluid assessment
    • deepest vertical pocket ≥2 cm implies normality; <2 cm is associated with increased fetal morbidity and delivery should be considered
  • FBC
    • low platelet count is partly diagnostic for HELLP syndrome
  • LFTs
    • Increased transaminase levels are partly diagnostic for HELLP syndrome.
  • Serum creatinine
    • Elevated serum creatinine implies underlying renal disease.
    • Renal failure is a rare complication, and when it occurs, it is usually acute tubular necrosis associated with co-existing sepsis or placental abruption
  • coagulation screen
    • May be abnormal with advanced disease affecting the liver, or in association with abruption
Management
  • Before delivery
    • hospital admission and monitoring
    • decision regarding delivery
      • At <32 weeks' gestation: prolonging the pregnancy is beneficial for the fetus, as long as maternal and fetal assessments are satisfactory
      • At >36 weeks' gestation: delivery is the most sensible approach
    • corticosteroid
      • Antenatal corticosteroids are recommended before 34 weeks' gestation to mature fetal lungs
    • consider for outpatient follow-up when stable
    • with BP ≥150 mmHg systolic and/or ≥100 mmHg diastolic
      • antihypertensive therapy
        • Labetalol is considered the antihypertensive of choice, [2] [3] and is effective as monotherapy in 80% of cases
        • Acceptable alternatives include methyldopa, nifedipine (a calcium-channel blocker), and hydralazine
    • with seizures
      • magnesium sulphate
  • After delivery
    • close monitoring of fluid balance
    • continue antihypertensives and magnesium sulphate
Prognosis
  • Pre-eclampsia is a self-limiting condition of pregnancy that usually resolves once the placenta has been delivered, although it may persist for a few days post delivery.
  • There are few long-term sequelae; however, there are some long-term disease associations.
  • The course of pre-eclampsia is altered by treatment, and the condition can be controlled easily in the majority of cases, usually within a few hours of starting treatment.
  • Once controlled, the length of the disease depends on when delivery is decided.
  • After delivery, the condition normally settles within 2 to 4 days; however, some women have hypertensive problems and proteinuria for some weeks after.
  • The overall risk of recurrence in subsequent pregnancies ranges from about 10% to 50%
    • Depending on the severity of pre-eclampsia, the gestation it occurred at, and subsequent interventions in the next pregnancy. [2] [2] 
    • Generally, in previous severe or early onset (i.e., <30 weeks) pre-eclampsia, the risk of recurrence is 50%.
    • In mild to moderate or late-onset pre-eclampsia, the risk of recurrence is reduced to around 10%. [2]
  • There are good epidemiological data that suggest that women with pre-eclampsia have an increased long-term risk of cardiovascular disease, including hypertension and stroke. [2] [17]

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