Transcript Pre-eclampsia and PIH

Gestational Hypertension and
Pre-eclampsia
Karen Henderson
September 2009
Definition and Incidence
multisystem disorder pregnancy/ppart (16-44 %)
common worldwide:
leading cause of maternal and neonatal death
no change in 40 years
In UK:
~ 5 - 10 % gestational hypertension
~2–8%
pre-eclampsia (~ 73,000 p.a. UK)
< 0.01
eclampsia (~ 1:1200 to 1:100)
Presentation symptoms
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Commonly asymptomatic
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Vague
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headaches, irritability, confusion
visual problems, blurring flashing lights
abdominal pain, vomiting, feeling unwell
sudden swelling of ankles, feet, face with weight gain
shortness of breath
oliguria
Presentation findings
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Insidious or fulminant, rare before 20/40
asymptomatic or symptoms of severe disease
• intracerebral haemorrhage, liver, renal compromise
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Hypertension
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140/90
160/110
Proteinuria
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non severe
severe
0.3 gm/24 h, +1 proteinuria, 30 mg/dl single sample
Fluid retention
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Weak sign, swelling ankles, hands, face, weight gain >2 kg week
Risk Factors
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pre-existing hypertension: diastolic > 80 mmhg at booking
age: under 20, over 35 years
underlying medical problems: renal, DM (x 4), lupus, RA
first, multiples, >10 years between pregnancies (x 2-3)
family history (x 3), previous pre-eclampsia (x 7,~ 20 %)
high BMI, particularly over 35 or weight > 90Kg
vit D deficiency, UTI, peridontal disease, raised protein
hydatidiform mole, hydrops fetalis
known chromosomal abnormalities
first time fathers
race: black > white
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not long working hours or shift work!
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Pathophysiology
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initiating factors unknown
mechanism of disease clearer
two stage process
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abnormal embryo implantation and placental formation (20/40)
invasion of the spiral arteries by extravillous trophoblastic cells
reduced placental blood flow
leading to
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inactivation of placental growth factor
generalised endothelial dysfunction
Pathophysiology
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Number of immunological and inflammatory mediators
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relaxin
matrix metalloproteinases
growth factors
FMS-like tyrosine kinase 1
asymmetric dimethyl arginine
auto antibodies activate angiotensin receptors
Causes generalised vascular endothelial dysfunction including
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abnormal immune and inflammatory responses
failure to maintain integrity of vascular compartment
limits intravascular coagulation
modifies contractile response of smooth muscle
Consequences
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severe systemic vasospasm: decrease organ perfusion
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vascular haemoconcentration
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fluid relocation to interstitium
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exaggerated inflammatory response
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activate coagulation cascade:microthrombi
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end organ compromise and failure
Complications
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Fetal
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decrease blood flow to placenta: IUGR
placental abruption, APH
Maternal
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HELLP syndrome
• haemolysis, elevated liver enzymes, low platelets
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eclampsia
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cardiovascular, renal, DIC, death
The challenges of management
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progress of the disease difficult to determine
“eklampsis” = lightening
no single cost effective screening test
no established measure for primary prevention
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low dose aspirin, ? in high risk women (poor dopplers in 2nd trimester)
calcium supplementation NOT generally useful, ? dose
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appropriate antenatal care
early detection
careful monitoring
appropriate timely intervention and management
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72 % of care substandard (BMJ this week)
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management: GH and pre-eclampsia
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At or near term
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minimal maternal and neonatal morbidity
observation,
treatment unusual
Before 35/40 (depending on severity)
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significant maternal and perinatal complications
close evaluation of mother and fetus
expectant management
balance risk:benefit ratio of prolonging pregnancy
Management: pre-eclampsia
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adequate antenatal screening
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potential high risk evaluation
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Biochemical markers
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urinary C/P ratios > 30 and protein values < 1gm in 24 hr
serum uric acid: lacks sensitivity and specificity
24 hour urine collection
hepatic enzymes: transaminases, albumin, LAD,
FBC, platelet count, coagulation
Serum creatinine
ultrasound, doppler studies
frequency determined by disease process
Management: pre-eclampsia
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early warning scoring system
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regular observation as out/inpatient
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earlier onset, worsening symptoms, poor prognosis
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bedrest, avoid aorto-caval compression
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anti hypertensive drugs
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reduces complications to non-pre-eclamptic levels
decreases incidence of intracerebral haemorrhage
Antihypertensive drugs
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Potential adverse effects poorly quantified
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methyl dopa
central acting antiadrenergic agent, 1-3 g
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beta blockers
metoprolol, propranolol, NOT atenolol
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nifedipine
ca channel blocker, oral not S/L, 10 mg boluses
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hydralazine
direct acting dilator, oral, IV, 5 mg boluses
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labetolol
mixed BB, oral, IV, not in asthmatics
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Avoid:
ACE, ACE receptor antagonists, diuretics
observation and treatment
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Aim to lower BP gradually
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Systolic BP > 160-180 mmHg to be less than 140 mmHg
Diastolic BP > 105-110 mmHg to be less than 90-105 mmHg
Worsening symptoms
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severe headache, visual disturbance
epigastric pain or vomiting
clonus
papilloedema
liver tenderness, elevated liver enzymes (ALT etc > 70 IU)
platelet count < 100, elevated liver enzymes, HELLP
Management of pre-eclampsia
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delivery: timing important, grey zone 34-37 weeks
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fetal: IUGR, non-reassuring fetal surveillance, oligohydramnios
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maternal:>38/40, hepatic, renal dysfunction, APH, + symptoms
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do not compromise life of the mother
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vaginal delivery preferable
avoids physiological stress response of LSCS
regional technique less risk to mother
GA if coagulopathy
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Eclampsia
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unpredictable, unpreventable
progression of pre-eclampsia, 38 % spontaneous
rare before 20/40 and 3 weeks after delivery
80 % third trimester or within 48 hr of delivery
25 % before labour, 50 % during labour, 25 % post partum
Pathogenesis uncertain, possibilities include:
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cerebral vasoconstriction
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hypertensive encephalopathy
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cerebral oedema
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haemorrhage or infarction
Signs and Symptoms of Eclampsia
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headache
hyperactive reflexes
marked proteinuria
peripheral oedema
visual disturbances
epigastric pain
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seizures:
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83 %
80 %
52 %
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44 %
20 %
2 phases
first:
15-20 secs, facial twitching, rigidity,
second: 60 secs, generalised tonic clonic seizures
coma, variable length, hyperventilation
Management of Eclampsia
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Prevention: 1 % die, > 50,000 deaths pa, 11.9->7.0 /million in UK
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A,B,C
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MgSO4:
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cerebral vasodilator, catecholamine antagonist
1st line treatment for eclampsia (dec mortality cf diazepam, phenytoin)
MAGPIE study: 58 % reduction in seizures
IV or IM, 4 gm bolus in 5 mins, 1-2 gm/hr, therapeutic level 2-4 mmol/l
continue for 24 hr post delivery or last seizure
care if oliguria
Ca gluconate 1 gm over 10 mins if neuromuscular block, loss of reflexes
MgSO4: important points
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recommended as a prophylaxis in severe pre-eclampsia
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controversy over use in mild disease
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50 % reduction in progression to eclampsia, red 1st seizure
morbidity from pneumonia, ITU admission reduced
side effects more common
increase in LSCS
does not reverse or prevent disease progression
not recommended as an antihypertensive agent
measure levels, toxicity > 3.5 mmol/l
HELLP syndrome
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Severe form of pre-eclampsia
Haemolytic anaemia, ELevated liver enzymes, Low Platelets
spontaneous, 10–25 % pre-eclampsia
symptoms:
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headaches, vision, parasthesia, nausea, abdo pain
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activation clotting cascade,DIC, multi organ failure,
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diagnosis
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clinical, coagulation abnormalities, platelets, D-Dimer
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treatment:
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symptomatic, prompt delivery irrespective of gestation, steroids?
HELLP syndrome: points to note
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exact levels of biochemical and haematological values and criteria
used to make diagnosis debatable
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insufficient evidence to refute/support corticosteroid therapy
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antepartum dexamethasone inc platelets, no improvement in outcome
postpartum dexamethasone no improvement in M & M
platelet transfusion
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local guidelines but < 50 x 109 significant
plasma exchange, plasmapheresis documented but not recommended
Role of anaesthetist
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Integral part of multi-disciplinary team
understand underlying processes: multiorgan
operative and non-operative care
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particularly:
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treatment of BP
control of seizures
fluid therapy and treatment of oliguria
decision when to deliver
management of coagulation abnormalities
ICU, CVS, CNS, pain management
Fluid therapy
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accurate monitoring
central venous pressure, UO, arterial BP or more?
no evidence maintaining specific UO of benefit
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fluid restriction: less is more, better outcome
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colloids
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85 mls hr, 1 ml/kg/hr or UO plus 30 mls/hr standard regimes
no evidence of benefit of fluid expansion
diuretics +/- dopamine
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poss for pulmonary oedema
Regional
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Decision on an individual basis
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Regional preferred but normal rules apply: fasting etc
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no one technique preferred, spinal, epidural, CSE
platelet > 75, absence of coagulation abnormalities
pain control, stress response obtunded
doses same as for non pre-eclamptic
hypotension less common
ephedrine or phenylephrine, ? metaraminol
GA
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may be necessary: small number of cases
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care with:
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coagulopathy,
pulmonary oedema, may herald peripartum cardiomyopathy
decreased conscious level, cerebral oedema present
eclampsia
hypertensive response to intubation: direct cause of maternal death
no clear advantage with opioids, esmolol, lignocaine, MgSO4
airway assessment, intubation and extubation
monitoring e.g. arterial,
BUT regional preferred if stable, normal conscious level, no
neurological deficits
Finally, other things to think about
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oxytoxic agents
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avoid syntometrine (syntocinon and ergometrine)
avoid ergometrine unless life threatening emergency
NSAID’s
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Care if renal problems, volume depletion, coagulopathy
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thromboprophylaxis
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HDU care
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delivery of the baby is only the first step to recovery