1. PRE-ECLAMPSIA

2. Pre-Eclampsia
 HYPERTENSION:
Systolic BP > (or = to) 140 mmHg
Diastolic BP > (or = to) 90 mmHg
confirmed by repeated
readings over several hours
AND...

3. Pre-Eclampsia
 RENAL INVOLVMENT:
Protein > 0.3g / 24 hours
Dipstick > 1 +
PCR > 30mg / mmol
OR...

4. Pre-Eclampsia
 MULTI-ORGAN COMPLICATIONS:
Haemtological - Coagulopathy
- Haemolysis
Liver - Dysfuntion
- Rupture of capsule
Neurological - Eclampsia
- Stroke
Pulmonary Oedema
Fetal Growth Restriction
Placental Abruption

5. Hypertensionin Pregnancy
There are four major types of high blood
pressure that may occur during pregnancy:
 Pre-eclampsia
 Chronic hypertension
 Preeclampsia superimposed upon chronic
hypertension
 Gestational hypertension (also called
transient hypertension)

6. Hypertensionin Pregnancy
Chronic Hypertension:
 Chronic hypertension is defined as a blood
pressure ≥140/90 mmHg diagnosed either:
- Before pregnancy
- Before the 20th week of pregnancy
- Or that persists more than 12 weeks after
delivery.

7. Hypertensionin Pregnancy
Pre-Eclampsia Superimposed Upon Chronic
Hypertension:
 This refers to a woman with chronic
hypertension who develops signs of pre-
eclampsia after the 20th week of pregnancy.

8. Hypertensionin Pregnancy
Gestational Hypertension:
 Women with gestational hypertension have all of
the following:
- Blood pressure ≥140/90 mmHg
- No protein in the urine (proteinuria)
- Are ≥20 weeks pregnant
- No previous history of high blood pressure.

9. Hypertensionin Pregnancy
Gestational Hypertension:
Over time, some pregnant women with gestational
hypertension will develop proteinuria and be
considered preeclamptic, while others will be
diagnosed with chronic hypertension because of
persistently high blood pressure after delivery.

10. Pre-DisposingFactors
 Age: <20 years / >35 years
 Ethnicity: Indian, Pacific
 Obesity
 Diet: <2 servings of fruit per week, high fat
 Lifestyle: Working in pregnancy, high stress
 Booking BP >130/80: Predisposing hypertension
 Miscarriage: 1 x lowers risk (immune response)
3 x increases risk (underlying)

11. Pre-DisposingFactors
 Partner: Relationship < 3 months, Father
previously involved in pre-eclamptic
pregnancy
 Woman born SGA
 Family History: Pre-eclampsia, hypertension,
diabetes, PCOS, underlying
thrombophilias
 Obstetric History: Previous pre-eclampsia,
donated gamate
 Multiple Pregnancy

12. Pathogenesis
NORMAL PREGNANCY:
 Fetal trophoblast invade walls of spiral arteries
 This disrupts their smooth muscle layer and
converts them into venous-like channels
 Remodelling begins about 5-6 weeks and
continues until around 20-22 weeks
 This allows blood supply to uterus to increase
from 10-15 mls (pre-pregnancy) to 600-800 mls
per minute to meet placental blood flow
requirements at term

13. Pathogenesis
In pre-eclampsia, this process is
DEFECTIVE
1. fewer of the arteries
undergoing these changes
2. changes may not extend throughout the
myometrium of the spiral arteries

14. Pathophysiology
Renal
 SYMPTOMS: Oliguria, Concentrated Urine
Proteinuria PCR > 30mg/mmol
Serum plasma creatinine > 90 umol/L
 PATHOPHYSIOLOGY: Endothelial damage in glomeruli 
GFR impaired Tubular necrosis and renal failure (rare)
 EFFECTS: Reduced glomerular filtration rate, Reduced urea
clearance and increased uric acid concentration, Proteinuria
and hypoproteinaemia, Oliguria, Acute renal failure

15. Pathophysiology
Liver
 SYMPTOMS: Epigastric/Upper back pain, malaise, flu-like
symptoms, nausea
Raised SerumTransaminases (AST & ALT most significant):
Aspartate transaminase (AST) > 60 U/L
Alanine transaminase (ALT) > 40 U/L
 PATHOPHYSIOLOGY: Endothelial damage  Impaired
function  Capillary haemorrhage  Haemotoma 
Ruptured capsule
 EFFECTS: Abnormal liver function tests, Subcapsular
haemorrhage and epigastric pain, Liver rupture

16. Pathophysiology
CardiovascularSystem
 SYMPTOMS: Oedema
 PATHOPHYSIOLOGY: Endothelial damage Altered
prostaglandin metabolism  Increased thromboxane and
decreased prostacyclin concentration  vasoconstriction
 EFFECTS: Widespread vasoconstriction, Normal or
increased systemic vascular resistance, Left ventricular
failure, Increased vascular permeability and oedema,
Decreased circulating blood volume

17. Pathophysiology
Neurological
 SYMPTOMS: Severe headache, convulsions, persistant
visual disturbances
 PATHOPHYSIOLOGY: Endothelial damage  Retinopathy
 Cerebral oedema  CVA (rare)
 EFFECTS: Headaches,Visual disturbances, Hyper-reflexia,
Sustained clonus, Cerebral haemorrhage, Convulsions

18. Pathophysiology
Haematological
 SYMPTOMS: Feeling hot/burning (unusual)
Thrombocytopenia Platelets <100 X 109/L
Haemolysis
Disseminated Intravascular Coagulation
 PATHOPHYSIOLOGY: Endothelial damage  Leaky
capillaries  Activated coagulation  Inflammatory
Response  Haemolysis  DIC
 EFFECTS: Increased turnover fibrinogen, fibrin and
platelets, Thrombocytopaenia, Impaired platelet function,
Disseminate Intravascular Coagulation, HELLP syndrome

19. Pathophysiology
FetalSignsandSymptoms
 SYMPTOMS: Slowed or slowing fetal growth, signs and
symptoms related to abruption and/or preterm labour
Abnormal biophysical profile score
Slowed growth of the baby, based upon customised
growth chart and/or an ultrasound
Decreased amount of amniotic fluid around the baby, noted
on ultrasound
Decreased blood flow through the umbilical cord,
noted on Doppler tests

20. Pathophysiology
FetalSignsandSymptoms
 PATHOPHYSIOLOGY: Reduced blood flow to the placenta
 Decreased placental circulation  Placental ischaemia
and infarction
 EFFECTS: Intrauterine Growth Restriction, Placental
Abruption, Preterm Labour

21. TestsandInvestigations
 GPH Bloods:
Full / Complete Blood Count
+
Liver Group
+
Renal
+
Coagulation

22. TestsandInvestigations:
CompleteBloodCount
HAEMOGLOBIN [Hb]: 100 – 140 g/L
The iron-containing protein, which transports
oxygen within the red blood cells
 In normal pregnancy, there is a natural decrease
in Hb, due to haemodilation
 In pre-eclampsia, expected plasma volume
increase is impaired, affecting Hb estimation
 If at 28/40 bloods, Hb is not lower than booking
bloods, this could be significant, and therefore
need to be vigilant

23. TestsandInvestigations:
CompleteBloodCount
HAEMOGLOBIN [Hb]:
 As the pregnancy progresses, and capillaries
become more damaged, they begin to leak,
causing fluid to shift from the blood vessels to
extravascular spaces
 Blood therefore becomes more concentrated,
and a raised Hb may indicate reduced plasma
(haemoconcentration)
 Plasma volume normal with mild disease, but
reduced with severe pre-eclampsia

24. TestsandInvestigations:
CompleteBloodCount
HAEMATOCRIT [PCV]: 0.28 – 0.41 (ratio)
The proportion of total blood volume that is
occupied by erythrocytes
 High PCV is suggestive of hypovolaemia (low
volume), which therefore may affect placental
perfusion
 No exact levels for Hb and PCV define significant
haemoconcentration, serial measurements are
more useful for monitoring the disease course

25. TestsandInvestigations:
CompleteBloodCount
PLATELETS: 150 – 400 109/L
The total number of thrombocytes, which play
an integral role in haemostasis
 Platelet levels decrease as they aggregate
following damage to the endothelial cells of the
capillaries
 Day-to day variations common so serial
measurements are necessary and more
informative

26. TestsandInvestigations:
CompleteBloodCount
MEAN PLATELETVOLUME [MPV]: 6.4 – 9.7 fl
A measurement of the average size of platelets
 The average lifespan of platelets is 5 – 9 days,
and immature platelets are larger than mature
ones

27. TestsandInvestigations:
RenalFunctionInvestigations
SERUM UREA: 2.0 – 4.0 mmol/L
An organic chemical compound which
essentially is the waste produced when the body
metabolizes protein
 A late sign of renal injury as a result of
pre-eclampsia is impairment of glomerular
filtration which causes an increase in serum urea

28. TestsandInvestigations:
RenalFunctionInvestigations
SERUM CREATININE: 0.04 – 0.08 mmol/L
A breakdown product of creatine (muscle waste
material), which is constantly produced and
filtered by the kidneys
 Creatinine is removed from the body entirely by
the kidneys
 If kidney function is abnormal, creatinine levels
will increase in the blood

29. TestsandInvestigations:
RenalFunctionInvestigations
URATE (URIC ACID): 0.20 – 0.42 mmol/d
End product of protein metabolism
 Excreted by renal tubule, in preeclampsia this
function is impaired by damage to kidney and
blood levels rise
 High levels associated with poor fetal outcome
 Useful diagnostic feature of early preeclampsia
 Diet may affect level

30. TestsandInvestigations:
RenalFunctionInvestigations
PROTEIN-CREATININE RATIO: 0 – 30 mg/mmol
 Random (spot) urine protein-creatinine ratio
collected during normal daytime activity
 Provides an accurate and rapid quantitation of
proteinuria in pregnant women with systemic
arterial hypertension and increased risk of pre-
eclampsia

31. TestsandInvestigations:
RenalFunctionInvestigations
CREATININE CLEARANCE: 120 – 160 ml/min
The volume of plasma completely cleared of
creatinine per unit of time
 Assesses the glomerular filtration rate
 Gives an indication of renal function
 Creatinine clearance may be reduced in pre-
eclampsia as a result of decreased GFR
 Assessed via 24 hour specimen

32. TestsandInvestigations:
LiverFunctionInvestigations
ASPARTATETRANSAMINASE [AST]: < 45 U/L
An enzyme, involved in cellular metabolism
that has raised levels in acute liver damage
 Also found in high concentrations in heart,
muscle, kidney, pancreas and red blood cells
 If any of these areas are damaged the blood
levels of the enzyme will increase
 Not specific for liver function

33. TestsandInvestigations:
LiverFunctionInvestigations
ALKALINE PHOSPHATASE [ALP]: 90 - 250 U/L
An enzyme made in the liver, bone, and the
placenta, released into the blood during injury and
during such normal activities as bone growth and
pregnancy
 Involved in cell metabolism and present in nearly all
tissues
 Levels reach up to 3 times normal in pregnancy due
to placental phosphatase
 Exaggerated increases may point to placental and
hepatic damage in preeclampsia

34. TestsandInvestigations:
LiverFunctionInvestigations
ALANINETRANSAMINASE [ALT]: 7 - 45 U/L
An enzyme involved in cellular respiration, found in
highest amounts in the liver. It is released into the
blood through liver injury.
 Found in low levels in other tissues
 High levels are specific for hepatic damage
In normal pregnancy AST and ALT
usually remain unchanged.
In severe preeclampsia they may be elevated

35. TestsandInvestigations:
LiverFunctionInvestigations
GAMMA GLUTAMYLTRANSPEPTIDASE [GGT]: < 50 U/L
An enzyme that participates in the transfer of amino
acids across the cell membrane, and in glutathione (an
anti-oxidant) metabolism
 Found almost entirely in the liver
 Elevated in severe preeclampsia

36. TestsandInvestigations:
LiverFunctionInvestigations
LACTATE DEHYDROGENASE [LDH]: 120 – 250 U/L
An enzyme that catalyzes the conversion of
lactate to pyruvate
 Found in liver, heart, skeletal muscle and red
blood cells
 As cells die, their LDH is released and finds its
way into the blood

37. TestsandInvestigations:
LiverFunctionInvestigations
BILIRUBIN: 2 – 20 mmol/L
Bilirubin is a product that results from the
breakdown of hemoglobin
 Serum bilirubin levels do not usually rise in
pre-eclampsia, unless complicated by HELLP
syndrome

38. TestsandInvestigations:
LiverFunctionInvestigations
SERUM ALBUMIN: 35 – 45 g/L
Albumin transports many small molecules in the
blood (for example, bilirubin, calcium,
progesterone, and drugs). It is also of prime
importance keeping the fluid from the blood from
leaking out into the tissues.
 Because albumin is made by the liver, decreased
serum albumin may result from liver disease
 In pre-eclampsia low levels of albumin may also be
the result of protein lost through proteinuria

39. TestsandInvestigations:
Coagulation
ACTIVATED PARTIALTHROMBOPLASTINTIME [APTT]:
35 - 45 secs
When you bleed, the body launches the coagulation
cascade. There are three pathways to this event.
The APTT test looks at special proteins, called
factors, found in two of these pathways (intrinsic).
 A blood test that looks at how long it takes for
blood to clot
 It can help tell if there are bleeding or clotting
problems
 A prolonged APTT time can be indicative of
disorders such as DIC, haemophilia, lupus, etc.

40. TestsandInvestigations:
Coagulation
THROMBIN CLOTTINGTIME: 10-18 secs
A test which measures time required for plasma
fibrinogen to form thrombin. Exogenous
thrombin is added to citrated plasma and the
time to clot formation is measured.
 TCT is prolonged with abnormalities of
fibrinogen and in the presence of heparin or of
fibrin/fibrinogen degradation products
 Prolonged in DIC as clotting mechanism fails

41. Section88 MaternityNotice
ReferralGuidelines
Current Pregnancy - Pre-Eclampsia:
 LEVEL 3 (Code 4022)
- Blood Pressure >140/90 (or rise of >30/15)
AND...
- Proteinuria > 0.3g / 24 hours
- Platelets < 150 x 109 / L
- Abnormal renal or liver function
- Imminent eclampsia / eclampsia

42. Section88 MaternityNotice
ReferralGuidelines
Current Pregnancy - Eclampsia:
 LEVEL 3 (Code 4006)

43. Section88 MaternityNotice
ReferralGuidelines
Previous Obstetric History - Pre-Eclampsia:
 LEVEL 1 (Code 3007)

44. Section88 MaternityNotice
ReferralGuidelines
Previous Obstetric History - Pre-Eclampsia:
 LEVEL 2 (Code 3008)
WITH...
- Significant IUGR
- Requiring delivery <34 weeks
OR...
- Multi-organ involvement

45. CLASPTrial
CollaborativeLow-doseAspirinStudiesinPregnancy
 Aspirin and Calcium thought to produce
modest reductions in blood pressure in
pregnant women who are at above-average
risk for PE
 Debate continues over gestation at which
prophylactic treatment should begin, but
earlier the better (approx. 6/40 gestation)
 Aspirin may also be beneficial in the
treatment of IUGR

46. CLASPTrial
CollaborativeLow-doseAspirinStudiesinPregnancy
 For women who are at high risk of pre-
eclampsia (>20%)
 Aspirin 100 mg daily
 Calcium 1.5 g daily
 For women who are at very high risk of pre-
eclampsia or previous pregnancy had very
early onset
 Heparin 7500 u BD or enoxaparin 40mg daily
 Aspirin 100 mg daily

47. Management
Depends on many factors:
 Gestational age of the pregnancy
 Severity of the disease
 Presence of complicating factors
 Evidence of maternal compromise
 Evidence of fetal compromise
The definitive treatment for pre-eclampsia is
delivery of the fetus and placenta

48. Management
 Expectant Management:
 No evidence that hospital admission for mild PE
improves maternal or fetal outcomes
 Admission to hospital is stressful, emotionally and
financially costly
 Women with mild PE without significant
proteinuria may be treated as outpatient or
admitted as a ‘day case’ for assessment and
evaluation

49. Management
 Expectant Management:
 Expectant management at home or hospital requires:
 Reduced activity
 Woman may be advised to stop working
 May be advised to go on bed rest – although this is logical
it has not been proved to improve outcomes
 Careful recording and daily checking of:
 Fetal activity
 Blood pressure
 Urine protein
 Any other signs and symptoms of PE

50. Management
 Collaborative Management:
The goal is to:
 Recognise pre-eclampsia early
 Monitor the woman for evidence of disease
progression that would mandate either delivery
of more intensive fetal surveillance

51. Management
 Collaborative Management:
Education for the family begins as soon as the diagnosis is
confirmed:
 Should include information about the disease process
 Signs and symptoms
 Proposed course of treatment
 Physical and laboratory investigations
 Medications
 Potential complications to mother and baby
 Plan for birthing
 Baseline laboratory evaluations:
 Should be performed early in pregnancy for all women known to be
at high risk of PE

52. Management
 Collaborative Management:
 Blood pressure:
 Should be recorded more frequently in women at high risk of
PE
 Rapid increases warrant closer observation
 Fundal height:
 Should be measured at each visit
 A measurement less than expected may indicate IUGR or
oligohydramnios
 Presence of either IUGR or oligohydramnios may occur
before any other diagnostic criteria for PE become apparent
 Oedema:
 Rapidly increasing generalised, facial and/or periorbital
oedema requires further assessment

53. Management
 Collaborative Management:
 Once hypertension is documented in second half of
pregnancy, or onset of PE is suspected laboratory
investigations to track progression:
 Full blood count
 Liver function tests
 Renal tests
 Coagulation screening
 Urinanalysis

54. Management
 Collaborative Management:
 Fetal monitoring:
 Antepartum surveillance (CTG’s)
 Symphyseal-fundal height measurements
 Record of fetal movements
 Ultrasonography:
 Amniotic fluid index
 Fetal growth
 Biophysical profiles
 Umbilical artery Doppler studies
Used to monitor fetal growth and to ascertain the most
appropriate and safest time for delivery

55. Management
 Hospital Management:
May be necessary for woman who:
 Feel safer in hospital
 Hypertension worsens
 Presence of significant proteinuria
 Signs of end organ involvement
 There are concerns about fetal wellbeing
 Baseline laboratory evaluations as with Collaborative
management to monitor progression of disease
 Crucial that an accurate fluid-balance chart maintained to
ensure that renal impairment detected early

56. Management
 AntihypertensiveTherapy:
 Indicated once the BP is persistently above
>160/100 mmHg, with the aim of achieving a
diastolic reading of 90 – 100 mmHg
 This is to avoid ‘overcorrection’ and the risk of
exacerbating placental hypoperfusion
 Drugs used include methyldopa, atenolol and
labetalol
 ACE inhibitors contraindicated in pregnancy

57. Management
 Timing of Delivery:
 Delivery is the only cure for clinically diagnosed PE
 Should be accomplished once the fetus is mature
 Earlier if maternal condition deteriorates or if there is
evidence of significant fetal compromise
 Delivery should always take place in a level 2 hospital,
where there are obstetric and paediatric facilities
readily available
 Timing and management of delivery requires close
collaboration between the woman, midwifery,
obstetric, paediatric and anaesthetic teams

58. Management
 Timing of Delivery:
 If fetus is between 24 -34 weeks gestation and urgent
delivery is required, corticosteroids are administered
to the mother
 Vaginal birth preferable
 Epidural anaesthesia preferred choice of pain relief as
the maternal stress response releases catecholamines
and increases BP, although contraindicated if there is
evidence of coagulopathy
 Continuous monitoring of fetus
 Syntometrine to be avoided for third stage due to
ergometrine component

59. Management
 Timing of Delivery:
 Fetal indications for immediate delivery:
 Intrauterine Growth Restriction
 Non-reassuring CTG
 Oligohydramnios
 Maternal indications for immediate delivery:
 Progressive deterioration of liver function
 Progressive deterioration of renal function
 Suspected placental abruption
 Persistent severe headache or visual changes
 Persistent severe epigastric pain, nausea or vomiting

60. Management
 ManagementAfter Delivery:
 30% of cases of PE only diagnosed in postpartum
period
 Following initial improvement, 60% of women will
worsen within 48 hours of delivery
 Antihypertensive drugs usually continued for a
further 48 hours
 Close monitoring of BP should continue, as well as a
meticulous fluid balance chart
 Good analgesia cover to reduce maternal stress
 Follow-up consultation and/or debrief

61. ImplicationsforMidwiferyCare
 Must begin with an accurate record of a woman’s
history to identify risk factors and establish
baseline recordings of BP and laboratory values
 Early recognition and diagnosis of physical signs
rather than symptoms, as woman may feel well,
yet have severe pre-eclampsia
 Scope of care depends on severity of disease
 Referral guidelines encompass a three-way
discussion between the woman, her midwife,
and specialist – therefore availability of the
midwife paramount