UPDATES ON HPT DISORDERS OF PREGNANCY by dr yahya.pptx

HYPERTENSIVE DISORDERS
IN PREGNANCY
Presenter: DR Yahya Maryam
Postgraduate presentation.
Moderator : prof polite

OBJECTIVES
OUTLINE
 DEFINITIONS
 CATEGORIES OF HYPERTENSIVE DISORDERS OF PREGNANCY
 PATHOPHYSIOLOGY OF PREECLAMPSIA
 RISK FACTORS OF PREECLAMPSIA
 PREDICTION AND PREVENTION OF PREECLAMPSIA
 MANAGEMENT OF HYPERTENSIVE DISORDERS OF PREGNANCY
oANTENATAL
oPOST PARTUM
 COMPLICATIONS OF HYPERTENSIVE DISORDERS OF PREGNANCY.

INTRODUCTION
• Hypertension is the commonest medical disorder of pregnancy
• Affects about 8-10% of pregnancies
• PE/Eclampsia is the most important hypertensive disorders in
pregnancy in terms of incidence, morbidity and mortality.
• Worldwide incidence of PE is constant ( complicate 5% of all
pregnancies)
• The incidence of Eclampsia is higher in developing countries,
• It varies btw 10 to 50 /1000 deliveries(1-5%)

• Severe HDP are common in Nigeria,
• It is one of the leading causes of MM and perinatal mortality and morbidty
• There is a regional variation in its incidence. Commoner in the north than
in the south.
• Prevalence of HDP was 17% while pe was 6%
• Research done by swati singh et al. niger med 2014 in usman danfodiyo TH.
• Worldwide eclampsia is a disease of primigravida. In Nigeria over 80% of
eclamptic are primigravidas
• In kaduna the incidence was highest in lessthan 20yrs age group ( PI
onwuhafua 2001 ).

• Worldwide PE and Eclampsia are important causes of MM
• Causes >18% of MM in nigeria ( 2010-2016)
• Eclampsia account for morethan 42% ( y ahmed, EI nwobodo MM
associated with eclampsia in sokoto 2011)
• In Northern Nigeria, Eclampsia account >40% of MM.

Physiological changes of BP in pregnancy
• The blood pressure (BP) normally falls throughtout the first half of the
pregnancy under the influence of progesterone reaching a nadir in
mid pregnancy and returning to normal pre- pregnancy levels by the
end of third trimester
• This fall in BP in the first two trimesters occurs in both normotensive
and chronic hypertensive women
• the BP normally rises in third trimester and reaches pre-pregnancy
levels by term.
• This rise is associated with other cardiovascular change.

DEFINATIONS
Hypertension
• SBP ≥140 and/DBP ≥90 mm Hg.
• BP should be repeated in 4 -6 hours to confirm true hypertension.
• If BP is severe (SBP ≥160 and/DBP ≥110 mm Hg), then the BP should be
confirmed within 15 minutes
• The SBP value was reduced from 170 mmHg by most international societies
after recognition that a SBP ≥ 160 mmHg is associated with an increased
risk of stroke in pregnancy.
• A relative rise of SBP of 30mmHg and DBP of 15mmHg should no longer be
used to define hypertension in pregnancy due to its high false positive rate.
• Similarly MAP should also not be used for definition of hypertension in
pregnancy since there is no evidence relating MAP with clinical outcomes.

New definition of hypertension and effect on
HDP
• The American college of cardiology (ACC) and the American Heart
Association (AHA) have updated the definition of hypertension as follows;
(stage I hypertension 130–139/80–89 mmHg
stage 2 ⩾ 140/90 mmHg)
Though the ACOG and other bodies have acknowledged this definition, the
definition of hypertension in pregnancy has not changed.
This is likely to lead to an overall increase in patients classified with chronic
hypertension and will require co-decision by the obstetrician and
cardiologist, as well as by the patient regarding appropriate guideline
during pregnancy.
More women may have to be screened for preeclampsia.

What Constitutes Abnormal Proteinuria in
Pregnancy?
• 24- hour urine protein estimation of ≥ 300mg/ day is the gold standard
• In Practice the 24-hour urine protein has been replaced by spot urine protein/creatinine ratio
(PCr).
• A PCr ratio ≥30 mg/mmol (0.3 mg/mg) is abnormal.
• When neither 24 hour nor PCr measures of proteinuria are available, dipstick testing provides
reasonable assessment of true proteinuria, particularly when values are >1 g per liter, that is, 2+.
However it has a high false positive rate.
• A test result of 1+ proteinuria is false-positive in 71% of cases and even 3+ proteinuria test results
may be false-positive in 7% of cases. Overall accuracy is better if 2+ is used as the discriminant
value. A PCr should be done is suspicion is high.
• An Albumin/Creatinine ratio (Acr) of ≥ 8 mg/mmol indicates abnormal proteinuria
• However, at present, there is insufficient data to recommend using urinary ACr for assessment of
proteinuria.
• Proteinuria is not required for a diagnosis of preeclampsia. (P.Y.DEWANDRE, G.LAMBERT AND
OTHERS 2014 PRE ECLAMPSIA UPDATE)

Gestational proteinuria
• defined as the new onset proteinuria in pregnancy without other
obvious features of preeclampsia or primary renal disease
• PLGF levels are intermediate between those of normal pregnancies
and preeclampsia, indicating that these women have an early form of
preeclampsia.
• more frequently monitoring is required for the remainder of their
pregnancy.
• assess proteinuria at 3 months postpartum.

Hypertension categories in pregnancy
• The different categories of hypertensive Disorders of pregnancy do
not have the same level of risk for the pregnant woman and her
fetus/baby.
• PE and its complications are associated with the highest risk
• It is therefore important to classify or categorize hypertensive
disorders of pregnancy for optimum management to reduce the risk
of adverse outcome.
• Classification of HDP also facilitates communication among care
givers.

• The classification of HDP varies slightly among the various scientific
societies.
• ACOG, SOGC, RCOG and SOMANZ’s classifications are in line with
ISSHP’s classification which has been endorsed by FIGO.
• Accepted across international guidelines are the following four
categories.

Hypertensive categories in pregnancy
ACOG 2019
• Chronic hypertension
• Preeclampsia-Eclampsia
• Chronic hypertension with
superimposed preeclampsia
• Gestational hypertension
HYPERTENSION CANADA 2018
• Preeclampsia (includes non-
severe PE, severe PE, Hellp
syndrome,eclampsia

EUROPEAN SOCIETY OF
CARDIOLOGY 2018
• Pre-existing hypertension
• preeclampsia
• Pre-existing hypertension plus
superimposed gestational
hypertension with proteinuria
• Antenatally unclassifiable
hypertension
SOCIETY OF OBSTETRICIANS AND
GYNECOLOGISTS OF CANADA 2014
• Pre-existing(chronic) hypertension
 with comorbid condition(s)
 with evidence of preeclampsia
• Preeclampsia
• Other hypertensive effects
Transient hypertensive effect
White coat hypertensive effect
Masked hypertensive effect

SOCIETY OF OBSTETRIC MEDICINE
OF AUSTRALIA AND NEW
ZEALAND (SOMANZ) 2014
• Preeclampsia-eclampsia
• White coat hypertension
• Preeclampsia superimposed on
chronic hypertension
ROYAL COLLEGE OF
OBSTETRICIANS AND
GYNAECOLOGISTS (RCOG) 2011
• Preeclampsia
• Severe preeclampsia
• Eclampsia
• HELLP

• INTERNATIONAL SOCIETY FOR STUDY OF HYPERTENSION IN
PREGNANCY(ISSHP) 2018
Essential
Secondary
• Transient gestational hypertension
• Preeclampsia, de novo or superimposed on chronic hypertension
• White coat hypertension
• Masked hypertension

CHRONIC HYPERTENSION
• Chronic hypertension refers to high BP predating the pregnancy or recognized at <20
weeks’ gestation.
• In practice, this is often diagnosed for the first time at the first or early second trimesters
booking visit.
• The majority of cases are because of essential hypertension, family history or obesity.
• Secondary causes of hypertension are less common; in the age group of women who
conceive.
• The cause is usually an underlying primary renal parenchymal disorder (such as reflux
nephropathy or glomerulonephritis) and less commonly, fibromuscular hyperplasia of the
renal arteries or primary hyperaldosteronism.
• ISSHP does not recommend routine testing for any secondary cause of hypertension in
the absence of clinical clues to these conditions

GESTATIONAL HYPERTENSION
• Gestational hypertension is persistent de novo hypertension that
develops at or after 20 weeks’ gestation in the absence of features of
preeclampsia.
• Associated with 25-50 % risk of progression to preeclampsia
especially in women who develop the hypertension prior to 32W.
• no tests have reliably predicted which women with gestational
hypertension will later develop preeclampsia.
• Gestational hypertension, like preeclampsia, is also associated with
cardiovascular disease in the long term.

PREECLAMPSIA SUPERIMPOSED ON CHRONIC HYPERTENSION
• There is about 25% risk of women with chronic hypertension developing
preeclampsia.
• Risk is higher in women with underlying renal disease.
• Diagnosis is made when a woman with chronic hypertension develops
new-onset proteinuria and or evidence of maternal organ dysfunction. The
following per se are not considered diagnostic criteria for PE in women
with chronic hypertension.
Rises in BP. This may be difficult to distinguish from the usual increase in BP
after 20 weeks’ gestation.
an increase in proteinuria In women with proteinuric renal disease.
 FGR since it may be due to chronic hypertension itself

PREECLAMPSIA
Pregnancy specific multi-system disorder with affects 2-8% of pregnant women.
Preeclampsia is defined as gestational hypertension accompanied by ≥1 of the following new-onset conditions
at or after 20 weeks’ gestation:
 Proteinuria
 Other maternal organ dysfunction, including:
• AKI (creatinine ≥90umol/L( 1.1 mg/dl)
• Liver involvement (elevated transaminases ALT and AST >40 IU/L) with or without right upper quadrant or
epigastric pain.
• Neurological complications (e.g. altered mental status, blindness, stroke, clonus, severe headaches, and
persistent visual scotomata)
• Hematological complications (thrombocytopenia–platelet count <150 000/μL, disseminated intravascular
coagulation, hemolysis)
• Uteroplacental dysfunction (such as fetal growth restriction, abnormal umbilical artery [UA] Doppler wave
form analysis, or stillbirth).

WHITE-COAT HYPERTENSION
• refers to elevated office/clinic (≥140/90 mm Hg) BP, but normal BP
measured at home or work (<135/85 mm Hg); it is not an entirely
benign condition and conveys an increased risk for preeclampsia.
MASKED HYPERTENSION
• is a form of hypertension, more difficult to diagnose, characterized by
BP that is normal at a clinic or office visit but elevated at other times,
most typically diagnosed by 24-hour ambulatory BP monitoring
(ABPM) or automated home BP monitoring.

TRANSIENT GESTATIONAL HYPERTENSION
Transient gestational hypertension is de novo hypertension that
develops at any gestation that resolves without treatment during the
pregnancy

Pre eclampsia
• Pre‐eclampsia is a multi‐organ syndrome of pregnancy that manifests
after 20 weeks' gestation with new‐onset hypertension alongside
maternal end‐organ dysfunction and/or fetal growth restriction (Lowe
2009).
• It is responsible for 50,000 - 60,000 maternal deaths annually
worldwide and complicates 5% of all pregnancies.
• It is responsible for hospital admissions, inductions of labour and high
morbidity and mortality to both mother and foetus

• it is the commonest cause of iatrogenic prematurity
• Currently no effective treatment for pre‐eclampsia
• Delivery is the only cure

• Definition of severe Preeclampsia –
• severe hypertension (systolic BP≥160 mmHg or diastolic BP≥110 mmHg) with or
without proteinuria and with any one of the following features of maternal organ
dysfunction ie
Rise in creatinine concentration (≥90 μmol/L, ≥1.1 mg/dL) or or2×baseline
Rise in ALT and AST (>70 IU/L or twice upper limit of normal range or severe RUQ
or epigastricpain
Fall in platelet count (<100 000/μL)
Signs of impending eclampsia
pulmonary oedema
Suspected fetal compromise
New-onset cerebral or visual disturbances

• SEVERITY OF PREECLAMPSIA
• “Mild” is no longer used to distinguish the severity of preeclampsia; those who
meet criteria simply have preeclampsia either with or without severe features.
• Massive proteinuria of > 5g is no longer used to define severe preeclampsia due
to lack of correlation between degree of proteinuria and outcomes.
• It is necessary for every healthcare provider to recognize that there are no “mild”
cases, which can be managed non-aggressively, among HDP cases.
• The term severe preeclampsia should not be used in clinical practice (ACOG,
2013).
• Even though ACOG and other societies prefer to call the severe form of
preeclampsia ‘’ Preeclampsia with severe features’’ others still refer to it as ‘’
severe preeclampsia’’

Pathophysiology of preeclampsia
• Actual cause of PE unknown
• A placental disorder since delivery of the placenta leads to resolution
of symptoms
• Interplay of several factors; Genetic, immunological and placental
• Abnormal trophoblastic invasion of the maternal spiral arteries results
in defective remodelling thereby resulting in failure to convert them
to low resistance high capacitance vessels.
• This causes reduced blood flow to the placenta.
• Placenta ischaemia is critical for the development of preeclampsia.

• The exact pathogenesis of pre‐eclampsia is unknown but it is likely that its
evolution is multi‐factorial involving a complex interplay between the mother,
fetus and the placenta
• There are many theories pastulated about pre eclampsia but the commonest
theories include
• Utero placental theory : in early pregnancy the cytotrophoblast of the embryo
invade the decidual arteries making their musculature more flaccid and dilated (
making them low resistance vessels that are capable of accommodating adequate
fetal placental blood flow during pregnancy ( low resistance, low pressure and
high capacitance system).
• During the second trimester of normal pregnancy second invasion occurs but if its
does not occur, it will ultimately generate a state of utero placental hypoxia as
seen in pt with PE and fetal growth restrictions

OXIDATIVE STRESS THEORY
• The observation that women with pre‐eclampsia have decreased plasma and
placental concentrations of antioxidants (Hubel 1999) led to the proposal that
placental hypoperfusion may induce a state of oxidative stress.
• This includes overproduction of highly reactive oxygen molecules or free radicals,
depleting the body’s stores of antioxidants.
• Oxidative stress, coupled with an exaggerated inflammatory response, may cause
the release of maternal factors that result in inappropriate endothelial cell
activation and endothelial cell damage

• Vascular endothelial damage plays a vital role in the disorder
VED result in decrease secretion of prostaglandin I2 ( prostacyclin
and NO) e- are potent vasodilator and inhibitor of platelet aggregator.
VED also triggers platelat aggregation and activation then release
of its derivatives like TXA2 which is a potent vasoconstrictor and
platelet aggregator so decrease in prostaglandin and increase in TXA2 is
responsible for imbalance between the 2 which will cause hypertension
and vasoconstriction which are the main features of the disorder.

Pathological changes
• The vasospasm leads to vascular changes and local hypoxia of
surrounding tissues which lead to haemorrhage, necrosis and other
pathological changes on different site of the body;
• A. Brain Cerebral injury includes fibrinoid necrosis, thrombosis, micro
infarcts, cerebral edema, and petechial hemorrhages, primarily in the
cerebral cortex. CT scan findings include focal white matter
hypodensities in the posterior hemispheres, temporal lobes, and
brainstem, reflecting petechial hemorrhage with resultant edema.
MRI may reveal occipital and parietal abnormalities in the watershed
area of major cerebral arteries and lesions in the brainstem and basal
ganglia. Rarely, subarachnoid or intraventricular hemorrhage occurs.

• B and C Heart and lungs
• endocardial and myocardial hemorrhage and necrosis, lungs shows
hemorrhage fluid accumulation predisposing to pulmonary edema
secondary bronchopneumonia.
• D. Liver Centrilobular necrosis may result from reduced perfusion.
Subcapsular hematomas may develop and, in severe cases, may
progress to liver rupture. Right upper quadrant or epigastric pain are
classic symptoms attributed to stretching of Glisson's capsule.
Elevation of serum transaminases is a hallmark of HELLP (hemolysis,
elevated liver enzymes, and low platelets) syndrome.

• E kidneys ; decrease in reanal blood flow- glomerular damage
(glomerular endotheliosis) – decrease GFR by 50%
_ loss of protein in urine
_ elavated serum level of uric acid , urea and creatinine ,( serum uric
acid is diagnostic as well as prognostic for SPE)
F . Placenta –reduced uteroplacental blood flow leading to IUGR and
even death.
placental thrombosis infarction and abruptio.

Eclampsia
• Eclampsia is defined by new-onset tonic-clonic, focal, or multifocal
seizures in the absence of other causative conditions such as epilepsy,
cerebral arterial ischemia and infarction, intracranial hemorrhage, or
drug use
• alternative diagnoses may be more likely in cases in which new-onset
seizures occur after 48–72 hours postpartum
• 20–38% of patients do not demonstrate the classic signs of
preeclampsia (hypertension and proteinuria).

Risk factors for PE
Moderate risk
• Age 40 years or more First pregnancy
• Multiple pregnancy Interval since last pregnancy of more than 10 years
• Body mass index of 35 or more at presentation
• Family history of pre-eclampsia
High risk
Chronic hypertension
Chronic kidney disease
Hypertensive disease during a previous pregnancy
Diabetes
Autoimmune disease

Screening of pre eclampsia
• Routine screening for pre‐eclampsia is based on measurement of blood
pressure and urinalysis for proteinuria. Overall, 15% to 25% of women with
gestational hypertension progress to pre‐eclampsia (Saudan 1998).
• Numerous physiological and biochemical screening tests and algorithms
have been developed, however, none so far has proved to be of good
predictive value and few are used in clinical practice (Akolekar
2011; Oliveira 2014; Poon 2013).
• Increased resistance of the uterine arteries measured through Doppler
ultrasound is a commonly used safe and non‐invasive test to assess for
abnormal blood flow to the placenta, and at present holds some promises
(Papageorghiou 2004).

Predictors of PE
• Glycosylated Fibronectin
• A new test used for the prediction of pre-eclampsia is the
measurement of glycosylated fibronectin (GlyFn) serum levels in the
first trimester
• A longitudinal cohort study by Rasanen et al. (2015) showed levels to
be significantly higher in women with pre-eclampsia and to remain
higher throughout pregnancy
• Increased GlyFn levels were significantly associated with increased
blood pressure and small-for-gestational-age neonates

PREDICTORS 2
• Studies have shown that levels of cell-free fetal DNA (cffDNA) are
raised in women with pre-eclampsia.
• The hypothesis for increased levels of cffDNA is of abnormal
placentation, hypoxia reperfusion injury, and release of apoptotic
fragments containing cffDNA into maternal circulation .
• A systematic review showed that whilst cffDNA may have a role in
disease prediction in pre-eclampsia, its use is probably limited to the
early second trimester because its detection rate is too low at later
gestations (Contro et al, 2017)

Prevention of PE
Prevention of PE
• The use of low-dose aspirin 75-162mg mg has a small to moderate
effect on the prevention of preeclampsia
• Aspirin is given from 12 weeks to 36 weeks
• the effect is greatest in women at highest risk of developing
preeclampsia
• Does not prevent term PE
• Calcium supplementation of 1.2-2.5g daily is recommended in
women with low intake (<600mg daily) or unknown intake.

PREVENTION CNT
Antithrombotic therapies (such as low molecular weight heparin) may decrease
the risk of pre‐eclampsia in women at high risk of placental dysfunction (Dodd
2013).
 Supplementing women with melatonin, a potent antioxidant, may increase
their resistance to oxidative stress and subsequently limit the systemic and
uteroplacental endothelial damage that is observed in pre‐eclampsia (Hobson
2013).

Management of HDP
preconception care
• Substitute ACE inhibitors, ARBs, chlorothiazide diuretics with safer options
(due to the increased risk of congenital anomalies).
ACE inhibitors, ARBs, chlorothiazide diuretics
• Acceptable initial antihypertensive include labetalol, oxprenolol,
methyldopa, nifedipine, diltiazem;
• prazosin and hydralazine are usually used as second or third line agents
• Assess for maternal organ dysfunction

Management of HDP
antenatal care
• discontinue ‘unsafe’ anti-hypertensives
• Substitute with safer options
• Aim to keep BP < 150/100 if they have no comorbidities and < 140/90 if they have
comorbidities but diastolic BP should not be <80mmHg
• At booking, assess for maternal organ dysfunction by doing FBC, BUE, Urea, uric acid
LFTS, ECG, Echocardiogram.
• Monitor for superimposed PE by checking urine protein at each visit, regular tests ie FBC,
LFTs, RFTs, electrolytes… at least once each trimester
• Assess fetal growth with ultrasound scan from 26 weeks of gestation and subsequently
every 2-4 weeks( EFW and centile, AFI with or without umbilical artery Doppler PI).
• If maternal and fetal condition remain stable aim to deliver by 39 weeks.

Management of HDP
 Serum uric acid is not a diagnostic criterion for preeclampsia, but are
associated with worse maternal and fetal outcomes.
 should prompt a detailed assessment of fetal growth, even in women
with gestational hypertension.
 should not be used to determine the timing of delivery.

Management of HDP
Summary of the management of chronic hypertension in pregnancy
• tight BP control ( target: SBP110–140 and DBP 85-100 mm Hg)
• monitoring fetal growth
• repeatedly assessing for the development of preeclampsia and
maternal complications.
• Often can be done in an outpatient setting.

Management of HDP
GESTATIONAL HYPERTENSION
The Key Principles of Management of Gestational Hypertension
• Control BP to levels to < 150/100 mm Hg
• . Monitor for development of preeclampsia.
• Monitor fetal growth, especially if maternal uric acid is elevated.
 Delivery can be delayed until 39+6 weeks provided BP is controlled
fetal condition is reassuring, and preeclampsia has not developed.

Management of HDP
PREECLAMPSIA
• IF BP ≥160/110 mm Hg; treat urgently.
• acceptable agents for this include oral nifedipine or intravenous
labetalol or hydralazine
• Maintain BP at < 150/100
• Antihypertensive drugs should be reduced or discontinued if diastolic
BP falls <80 mm Hg
• Acceptable agents include oral methyldopa, labetalol, oxprenolol,
nifedipine, with second or third line agents hydralazine and prazosin

Management of HDP
PREECLAMPSIA
• Assess the patient and determine whether PE is with or without
severe features
• Women with PE without severe features who are stable and can be
relied on to monitor their BP regularly at home and report promptly
when complications develop, may be managed on out patient basis.
• Women with PE with severe features should be admitted
• Women with PE with severe features should be given MgS04 for
seizure prophylaxis

Management of HDP
PREECLAMPSIA
For Fetal monitoring,
• ultrasound scan Surveillance comprising for fetal biometry, EFW and centile,
amniotic fluid, and UA Doppler AND CTG should be done at first diagnosis
• If normal, repeat USG surveiilance 2 weekly
• If FGR is diagnosed continue USG surveillance 2 weekly
• If Umbilical artery Doppler PI is > 95th centile, AFI and U A Doppler should be
done weekly
• If U A Doppler shows absence of flow < 34 Weeks, Do AFI and U A Doppler twice
weekly, CTG daily. Delivery should be considered not later than 34 Weeks
• .

Management of HDP
• If U A Doppler shows reversed end diastolic flow, Do U A Doppler PI and AFI
3X weekly, CTG at least once daily. Delivery should be considered not later
than 30 weeks
• Prenatal corticosteroids for fetal lung maturation should be given between
24+0 and 34+0 weeks gestation.
• MgSO4 for fetal neuroprotection should be administered in gestations
before 32 weeks.
• Mode of delivery needs to be discussed on an individual basis
• however CS is likely when absent or reversed end-diastolic flow UA Doppler
waveforms are present, or in very preterm gestations.
• If induction of labor is considered in women with abnormal UA Doppler, a
continuous cardiotocograph should be performed once contractions have
started, with a low threshold for caesarean delivery.

Management of HDP
PREECLAMPSIA
Maternal monitoring comprises of
• BP monitoring
• repeated assessments for proteinuria if not already present
• clinical assessment including clonus, and twice weekly blood tests for
Hb, platelet count, liver transaminases, creatinine, and uric acid.
• In addition, Blood test evaluation should be repeated in response to a
change in clinical status in most women with preeclampsia.

Management of HDP
PREECLAMPSIA
• Women with severe features at GA 26 0/7 to 33 6/7 weeks may be
offered expectant management for as long as maternal and fetal
condition remain stable. Antenatal corticosteroid therapy is indicated.
• Women with severe features at 24 0/7 weeks or lower should be
counselled and offered TOP
• women with PE without severe features should be delivered by 37
weeks
• Women with PE with severe features should be delivered by 34 weeks

Management of HDP
PREECLAMPSIA
• Other indications for delivery include;
o repeated episodes of severe hypertension despite maintenance treatment with 3 classes
of antihypertensive agents.
o thrombocytopenia; abnormal renal or liver enzyme tests
o Severe epigastric pain, oliguria
o pulmonary edema
o abnormal neurological features, such as severe intractable headache, repeated visual
scotomata
o Convulsions
o Non-reassuring fetal status.
o Neither the serum uric acid nor the level of proteinuria should be used as an indication
for delivery

Principles of Management of Eclamptic Seizures
Maintain situational awareness.
• maintain a purposeful calm and to avoid unnecessary interventions
that can result in iatrogenic complications.
Avoid polypharmacy.
• Do not attempt to shorten or abolish the initial convulsion by using
drugs such as diazepam (Valium) or phenytoin (Dilantin).
• Magnesium sulfate is the drug of choice for initial and recurrent
convulsions.
• Polypharmacy can lead to maternal or neonatal respiratory
depression, aspiration, or other adverse effects.

Principles of Management of Eclamptic
Seizures
Protect the airway, and minimize the risk of aspiration.
• Place the patient on her left side and suction her mouth.
• Call for someone skilled in intubation to be immediately available.
Prevent maternal injury.
• Falls from the bed can result in contusions or fractures, and head
injury may result from violent seizure activity.
• Close observation and use of soft padding and side rails on the bed
may help prevent injuries.

Principles of Management of Eclamptic
Seizures
• Administer magnesium sulfate to control convulsions.
• If the patient has already received a prophylactic loading dose when
the seizure occurs, an additional 2 g should be given intravenously..
• Avoid the temptation to perform immediate caesarean delivery for a
self-limited seizure episode.

Post partum management
• continue management of hypertension.
• Medication selected in relation to breast feeding and long-term
cardiovascular health of the mother
• Methyl Dopa might aggravate postnatal depression
• labetalol, nifedipine, enalapril, captopril, atenolol, and metoprolol
have no known adverse effects on babies receiving breast milk.
• There is insufficient evidence on the safety of angiotensin II receptor
blockers, amlodipine, and angiotensin converting enzyme inhibitors
other than enalapril and captopril in babies receiving breast milk.

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4. Shennan AH, Redman C, Cooper C, et al. : Are most maternal deaths from pre-eclampsia avoidable? Lancet. 2012;379(9827):1686–7.
10.1016/S0140-6736(11)60785-X
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Rev. 2007; (2):CD004659.
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7. Mol BW, Roberts CT, Thangaratinam S, et al. : Pre-eclampsia. Lancet. 2016;387(10022):999–1011. 10.1016/S0140-6736(15)00070-7
8. Achkar M, Dodds L, Giguère Y, et al. : Vitamin D status in early pregnancy and risk of preeclampsia. Am J Obstet Gynecol. 2015;212(4):511.e1–7.
10.1016/j.ajog.2014.11.009
9. Kiely ME, Zhang JY, Kinsella M, et al. : Vitamin D status is associated with uteroplacental dysfunction indicated by pre-eclampsia and small-for-
gestational-age birth in a large prospective pregnancy cohort in Ireland with low vitamin D status. Am J Clin Nutr. 2016;104(2):354–61.
10. Boyle VT, Thorstensen EB, Mourath D, et al. : The relationship between 25-hydroxyvitamin D concentration in early pregnancy and pregnancy
outcomes in a large, prospective cohort. Br J Nutr. 2016;116(8):1409–15.
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UPDATES ON HPT DISORDERS OF PREGNANCY by dr yahya.pptx