Pre eclampsia

PRE-ECLAMPSIA

Pre-Eclampsia

HYPERTENSION:Systolic BP > (or = to) 140 mmHgDiastolic BP > (or = to) 90 mmHg

confirmed by repeated readings over several hours

AND...

Pre-Eclampsia

RENAL INVOLVMENT:Protein > 0.3g / 24 hoursDipstick > 1 +PCR > 30mg / mmol

OR...

Pre-Eclampsia

MULTI-ORGAN COMPLICATIONS:Haemtological - Coagulopathy

- HaemolysisLiver - Dysfuntion

- Rupture of capsuleNeurological - Eclampsia

- StrokePulmonary OedemaFetal Growth RestrictionPlacental Abruption

Hypertension in 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)


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.


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.


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.


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.

Pre-Disposing Factors

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)

Pre-Disposing Factors

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

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

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

PathophysiologyRenal

SYMPTOMS: Oliguria, Concentrated Urine

Proteinuria PCR > 30mg/mmolSerum 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

PathophysiologyLiver

SYMPTOMS: Epigastric/Upper back pain, malaise, flu-like symptoms, nausea

Raised Serum Transaminases (AST & ALT most significant):

Aspartate transaminase (AST) > 60 U/LAlanine 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

PathophysiologyCardiovascular System

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

PathophysiologyNeurological

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

PathophysiologyHaematological

SYMPTOMS: Feeling hot/burning (unusual)

Thrombocytopenia Platelets <100 X 109/L HaemolysisDisseminated 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

PathophysiologyFetal Signs and Symptoms

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

PathophysiologyFetal Signs and Symptoms

PATHOPHYSIOLOGY: Reduced blood flow to the placenta Decreased placental circulation Placental ischaemia and infarction

EFFECTS: Intrauterine Growth Restriction, Placental Abruption, Preterm Labour

Tests and Investigations

GPH Bloods:

Full / Complete Blood Count+

Liver Group+

Renal +

Coagulation

Tests and Investigations: Complete Blood Count

HAEMOGLOBIN [Hb]: 100 – 140 g/LThe 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


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


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


PLATELETS: 150 – 400 109/LThe 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


MEAN PLATELET VOLUME [MPV]: 6.4 – 9.7 flA measurement of the average size of platelets

The average lifespan of platelets is 5 – 9 days, and immature platelets are larger than mature ones

Tests and Investigations: Renal Function Investigations

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


SERUM CREATININE: 0.04 – 0.08 mmol/LA 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


URATE (URIC ACID): 0.20 – 0.42 mmol/dEnd 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


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


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

Tests and Investigations: Liver Function Investigations

ASPARTATE TRANSAMINASE [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


ALKALINE PHOSPHATASE [ALP]: 90 - 250 U/LAn 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


ALANINE TRANSAMINASE [ALT]: 7 - 45 U/LAn 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


GAMMA GLUTAMYL TRANSPEPTIDASE [GGT]: < 50 U/LAn 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


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


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


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

Tests and Investigations: Coagulation

ACTIVATED PARTIAL THROMBOPLASTIN TIME [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.

Tests and Investigations: Coagulation

THROMBIN CLOTTING TIME: 10-18 secsA 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

Section 88 Maternity NoticeReferral Guidelines

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


Current Pregnancy - Eclampsia:

LEVEL 3 (Code 4006)


Previous Obstetric History - Pre-Eclampsia:

LEVEL 1 (Code 3007)


Previous Obstetric History - Pre-Eclampsia:

LEVEL 2 (Code 3008)WITH... - Significant IUGR- Requiring delivery <34 weeks

OR...- Multi-organ involvement

CLASP TrialCollaborative Low-dose Aspirin Studies in Pregnancy 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

CLASP TrialCollaborative Low-dose Aspirin Studies in Pregnancy 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

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

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

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

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

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

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

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

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

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

Management

Antihypertensive Therapy: 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

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

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

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

Management

Management After 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

Implications for Midwifery Care

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

Pre eclampsia

Health & Medicine

Transcript of Pre eclampsia