OB-GYNE

Dr. Espinoza
HYPERTENSION IN PREGNANCY Midterms

Hypertension in Pregnancy Preeclampsia

 Proteinuria ≥ 300
 Most common medical disorder (8%) mg/day OR > +1 OR
 Major cause of maternal and neonatal Gestational
 Protein/ Crea ≥ 0.30 OR
morbidity and mortality Hypertension
– Gestational hypertension (6%)  Thrombocytopenia
+
– Preeclampsia (5-8%) (<100,000)
– Chronic Hypertension (3%) New onset of  Impaired liver fxn
– Superimposed preeclampsia (20- any of the
25%) following  Renal Insufficiency

PGH Causes of Maternal Mortality (%) (> 1.1 Creatinine)

 Pulmonary edema

Causes of  Cerebral disturbance

Maternal 2003 2004 2005 2006 2007 2008
Mortality  Visual impairment

Hemorrhage 35.71 33.44 17 19 27.78 26.32

Classification
Hypertension 28.67 26.91 8 38 0 31.58  Mild Preeclampsia
– increase morbidity
Infections 7.41 21 21 19 44.44 36.84 – increase mortality
– rapid progression is possible
Medical 28.31 54 54 24 27.78 0
 Early onset
 Co-morbidities
Definitions of terms  Preeclampsia
– increase morbidity
 Blood pressure
– increase mortality
– Mild: 140-159/90-109
– rapid progression is possible
– Severe: ≥ 160/110
 Early onset
 Proteinuria
 Co-morbidities
– 300 mg protein in 24 hour urine
 Preeclampsia without severe features
specimen
 Preeclampsia with severe features
Gestational Hypertension
Eclampsia
 Development of new, acute onset  Originally described by Hippocrates
hypertension after 19 weeks (2400 years ago) as:
– Previously normotensive – headache accompanied by
– SBP > 140 mmHg OR (not and/or) heaviness and convulsion during
– DBP > 90 mmHg pregnancy
– Persistent for 4 hours  1776: Thomas young Edinburg Scotland
 BP turns to normal < 6 weeks postpartum – Recognized that eclamptic
 Final diagnosis made only postpartum convulsion differed from non-
pregnant seizure

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 – Recommended prompt delivery Pathogenesis
and venesection for patients with
eclampsia to reduce uterine Preeclampsia Chronic Hypertension
pressure on the iliac vessels
 Palcental  Essential
 Pregnancy induced hypertension with:
hypoperfusion/ – Hypertension /
– Proteinuria ischemia presence of underlying
– Pathologic edema disorder (renal,
– Convulsions  New onset parenchymal, renal
hypertension vascular, endocrine
Chronic Hypertension with proteinuria etc.)
 BP 140/90 mmHg or greater before  Increase risk of IUGR
 Presents acute  Major acute morbidity-
pregnancy or diagnosed before 20
risk to mother secondary to the increased
weeks not attributable to gestational and fetus risk of superimposed
trophoblastic disease. preeclampsia
 Hypertension first diagnosed after 20  Greater risk for – well-established cause
weeks and persistent after 12 weeks cardiovascular of cadiovascular
postpartum disease later in morbidity and
life mortality
Classification
Preeclampsia
Superimposed preeclampsia (on Chronic
hypertension)  Widespread vascular endothelial
 New onset proteinuria in a woman with dysfunction and vasospasm with multi
hypertension but with no proteinuria organ system clinical features such as:
before 20 weeks – Hypertension
 Sudden increase in proteinuria or BP or a – Proteinuria
platelet count of < 100, 000/mm3 in a – Cerebral and hepatic dysfunction
woman with hypertension and  Secondary to placental perfusions thus
proteinuria before 20 weeks. lowering systemic BP and use of
antihypertensive medications
Criteria for Diagnosis of Preeclamsia with
Severe Features
 Sustained SBP > 160 mmHg or DBP >
110 mmHg
 Proteinuria > 3 g/24 hrs or 3+ on urine
dipstick
 Oliguria with urine output < 500 ml/24
hrs
 Serum creatinine > 1.2 mg/ dL
 Serum transaminase > 2x normal
 Lactate dehydrogenase >600 u/L
 Platelet count < 100,000/mm3
 CNS disturbance (headache, altered
vision)
 Pulmonary edema
 Evidence of fetal compromise (IUGR,
olygohydramnios, abnormal umbilical
artery)

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Maternal Factors for Preeclampsia (NICE Management of Preeclampsia
Guidelines 2010)  CBC
High risk factors:  Urinalysis
 Hypertensive disease in previous pregnancy  Serum ALT and AST
 Chronic renal disease  Creatinine
 Chronic hypertension  Uric acid
 Diabetes mellitus  LDH
 Autoimmune disease  24 hour urine protein
 PT, APTT and fibrinogen
Moderate risk factors
 Maternal lifestyle: Fetal Surveillance
– Obesity  Assess status of the fetus (Biophysical
– Smoking profile)
 Other maternal:  Evaluate for growth restrictions
– African-american race  Doppler flow studies
– Age > 40 years  Cardiotocography (NST)
 Paternal obstetrics:
– Paternity by male who fathered a Initiating Antihypertensive Medications
previous preeclamptic pregnancy in  Minimize fetal exposure to medication that
another woman may have adverse effects
– Paternity by male born from a  Cochrane meta-analysis:
preclamptic.  Insufficient data to determine the
benefits and risk of antihypertensive
Mean Arterial Pressure (MAP) Test therapy for mild to moderate
MAP = DBP + 1/3 (SBP- DBP) hypertension.
 Combined MAP @ 11-14 weeks + MF  – ↓ risk of severe hypertension
62.5% of PE cases – no difference in outcomes of:
 MAP - 2 > 90 mmHg - ↑ Preeclampsia  Preeclampsia
 MAP - 3 > 105 mmHg- ↑ Perinatal deaths  Neonatal deaths
 Preterm births
Prevention of Eclampsia  SGA babies
 Low dose aspirin (80mg/day)
 Calcium supplementation (1 g daily)  Safe BP target: 140-155/ 90-105
 Low dose heparin  Chronic hypertension and mild to
 Antioxidant supplementation moderately elevated BP before pregnancy
 Fish oil supplementation with no known target organ damage
– Discontinue antihypertensive,
Screening provided they are closely
 No clinically used screening test to predict monitored
preeclampsia – Reinitiated if BP 140-150/90-100
 Abnormal uterine artery doppler at first
trimester (11-14 weeks)
– Early onset of Eclampsia
 No single biochemical marker
– PAPP-A
– PP-13
– PIGF
– VEGF

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Drugs for Gestational or Chronic HPN
Drug Dose
Preferred Agent 0.5-3 g/day in 2 divided
 Methyldopa (B) doses
Second-line Agents 200-1200 mg/day in 2-3
 Labetalol (C) divided doses
 Nifedipine (C) 30-120 mg/dl of a slow
release preparation
 Hydralazine (C) 50-300 mg/day in 2-4
divided doses
 B-receptor blockers Depends on specific
(C) agent
 Hydrochlorothiazide 12.5-25 mg/day
For Urgent Control of severe HPN
Drug Dose
Hydralazine (C) 5 mg IV or IM then 5-10 mg
every 20-40 mins, infusion
0.5-10 mg/hr; if no success
with 20 mg IV or 30 mg IM
consider another drug
Nifedipine (C ) Tablets recommended only
10-30 mg PO, repeat in 45
minutes if needed
Nicardipine Start at 1 mg/hr, maximum
of 10 mg/hr (D5W 90 cc +
Nicardipine 10 mg in a
soluset- concentration 0.1
mg/ml-10 ugtt/min
increments of 1 mg/hr)
Labetalol ( C) 10-20 mg IV, then 20-80 mg
every 20-30 minutes.
MOA: Nonselective B- Maximum of 300 mg for
blocker/ alpha 1 infusion 1-2 mg/minute
blocking activity
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Concerns/Comments
Drug of choice
Adverse side effect
– Postural hypotension
– Sedation
Associated with IUGR
May inhibit labor and have symptomatic
May cause neonatal thrombocytopenia
– Decrease uteroplacental flow
– Impair fetal response to hypoxic stress
– Risk of growth restrictions when started
in 1st and 2nd trimester
– Risk of neonatal hyperglycemia at higher
doses
May cause volume contraction and
electrolyte disorders
Concerns/Comments
Drug of choice
Adverse effects:
– Tachycardia
– Hypotension
– Headache
– Decrease placental perfusion
Contraindication:
– Mitral valve
– RHD
– Coronary artery disease
– Stroke
 Long acting preparation is preferred
although obstetrrics experience with short
acting has been favourable
 It is not approved by the FDA
Used with caution if concomitantly used with
MgSo4
Adverse effects:
– Flushing
– Headache
– Reflex tachycardia
– Uterine atony
Side effects:
– IUGR
– Fetal/neonatal bradycardia
– Hypoglycemia in higher doses
Containdications:
– Bronchial asthma
– Congestive Heart Failure
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Management of Preeclampsia
 Objective:
– Safety of the mother and delivery
of healthy new born
 Delivery is the only cure
 Optimal management depends on the
gestational age and disease severity
 The further the pregnancy from term
the greater the impetus to manage the
patient medically
 The severity of disease must be weighed
against the risks of infant prematurity
 Hospitalized and monitored carefully for
development of worsening or
complications
 Bed rest
 Should be delivered at:
 ≥ 40 weeks AOG
 ≥ 37 weeks AOG with favourable
cervix ( BS >5)
 ≥ 37 weeks AOG
Patients having all of the following maybe
manage at home:
 Ability to comply with
recommendations
 Diastolic pressure < 100 mmHg
 Systolic Pressure < 140 mmHg
 Proteinuria < 1 gm/24 hr or < 2+ on
dipstick
 Platelet count > 120,000
 Normal fetal growth and testing
Management of Mild Preeclampsia
 Antepartum testing:
– NST, BPP 2x/week
– Fetal growth monitoring every 2
weeks
– Doppler velocimetry
 Delivery ≥ 34 weeks, ruptured
membranes, abnormal fetal testing,
progressive labor or FGR
 Vaginal delivery
Management of Severe Preeclampsia
 After 34 weeks, delivery is appropriate.
– Vaginal delivery: attempted
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–CS: reserved for routine obstetric
indications
 Should be delivered regardless of
gestational age:
– Non reassuring fetal status
– Ruptured membranes
– In labor
– Maternal distress
 > 32 weeks and received course of
steroid, should be delivered
Criteria for Delivery
Guidelines for Expedited delivery (within 72
hours) of patients with Preeclampsia
 Nonreassuring fetal heart status
 Uncontrolled BP
 Oligohydramnios with AFI < 5cm
 Severe IUGR in EFW < 5%
 Oliguria (< 500/24 hr)
 Serum creatinine 1.5 mg/dL
 Pulmonary edema
 Shortness of breath or chest pain with
pulse oximetry < 94% on room air.
 Headache persistent and severe
 Right upper quadrant tenderness
 Fundoscopic changes: hemorrhage or
papilledema
 Development of HELLP syndrome
 Absent end diastolic or reversed
umbilical artery flow on doppler
velocimetry.
Seizure Treatment and prophylaxis with
Magnesium sulfate
 ABC (airway, breathing and circulation)
 Magnesium Sulfate
– IM route: LD 4 g slow IV over 5-
10 minutes and 10 grams deep
IM (5 g on each buttocks), then 5
gram IM every 4 hours until 24
hours after delivery
– IV route: LD 4 g slow IV followed
byy IV infusion 2 g/hr
 Lorazepam and Phenytoin
 Active seizure:
– IV Magnesium sulphate: first line
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  Prophylactic treatment:
– Magnesium sulphate: severe
preeclampsia
Superimposed Preeclampsia
 Antihypertensive treatment are
extrapolated from the evidence based
on CH and preeclampsia
 Same drugs and dosage regimen for
urgent control and oral maintenance
 Corticosteroids at ≤ 34 weeks
 MgSo4 as first line treatment of
eclampsia and prophylaxis
 Wihout severe features and with stable
maternal and fetal conditions expectant
management until 37 weeks
 Delivery soon after maternal
stabilizations is recommended
irrespective of gestation age for women
with SPE and complicated by any of the
ff:
– Uncontrollable severe
hypertension
– Eclampsia
– Pulmonary edema
– Abruption placenta
– DIC
– Nonreassuring FHR pattern
Chronic Hypertension
 With complicated and secondary
hypertension appear to be at greater
risk for maternal and fetal
complications benefit from
antihypertensive therapy with goal of
lower BP levels.
 Close fetal surveillance is warranted
when there is uteroplacental
vasculopathy
 With mild uncomplicated preexisting
hypertension can be allowed to into
spontaneous labor and deliver at term
 Possible adverse pregnancy outcomes
are:
– Superimposed preeclampsia
– Abruption placenta
– Preterm birth <37 weeks
– IUGR
Joan CONSTANTIAM 2020
 Baseline laboratory:
– Urinalysis
– Urine culture
– Serum creatinine
– Glucose
– Electrolyte
 Uncomplicated preexisting
hypertension who are normotensive or
mildly hypertensive on medication may
continue their therapy or have their
antihypertensive stopped or tapered
during pregnancy.
Postpartum Hypertenson
 Antihypertensive agents may be
required temporarily postpartum if
hypertension is severe.
 If pre pregnancy BP was normal, it is
reasonable to stop antihypertensive
after 3 weeks to assess whether
treatment is indicated.
 Beta-blockers and calcium channel
blockers enter breast milk but most
appear safe during lactation
Long Term Maternal Outcome
 Recurrent Preeclampsia
 Chronic hypertension (4 fold)
 Ischemic heart diesase (2 fold)
 Stroke (2 fold)
 Venous Thromboembolism (2 fold)
 All cause mortality (1.5 fold)
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