HYPERTENSIVE DISORDERS

IN PREGNANCY

Betha Fe Manaois-Castillo M.D.

FPOGS,FPCS,FPSUOG
25 July 2013
HYPERTENSIVE DISORDERS
Most common medical complication in
pregnancy
5-10% incidence
Major cause of maternal and perinatal
morbidity worldwide

Report of the National High Blood Pressure Education Program. Working group
report on high blood pressure. Am J Obstet Gynecol. 2000;183:S1.; Sibai BM.
Diagnosis and management of gestational hypertension and preeclampsia.
Obstet Gynecol. 2003; 102:181.
 HYPERTENSION
BP > 140 mm Hg systolic OR 90 mm Hg
diastolic
Present on at least 2 occasions, at least 6
hours apart, but within a maximum of a 1-
week period
 Hypertensive Disorders
Related To Pregnancy
1. Gestational hypertension
2. Preeclampsia
3. Eclampsia
4. HELLP syndrome
5. Chronic/preexisting hypertension
6. Preeclampsia superimposed
upon chronic/preexisting hypertension
 Gestational Hypertension
systolic blood pressure 140 mHg and/or
diastolic blood pressure 90 mmHg in a
previously normotensive pregnant woman
who is 20 weeks of gestation and has no
proteinuria
BP returns to normal within 12 weeks after
delivery
Gestational HTN: DIAGNOSIS
Determine the severity of hypertension
Measure protein excretion
24-hour urine collection
Evaluate for signs/symptoms of severe
preeclampsia
Perform laboratory evaluation
+/- end - organ involvement
 Gestational HTN: DIAGNOSIS
CRITERIA FOR MILD GESTATIONAL HYPERTENSION
Blood Pressure > 140 to < 160 mm Hg, systolic
> 90 to < 110 mm Hg, diastolic
Proteinuria < 300 mg per 24-hr collection
Platelet count > 100,000/mm3
Liver enzymes Normal
Maternal symptoms Absent
IUGR / Oligohydramnios Absent
(UTZ)
Gestational HTN: MANAGEMENT
Mild Gestational HTN
Managed as outpatients (weekly antepartum visits)
Daily fetal movement/kick counting
NST + AFI OR BPS
Fetal growth monitoring every 3-4 weeks
No antihypertensive therapy
No antenatal corticosteroids
Deliver patients no later than their EDD
Gestational HTN: MANAGEMENT
Severe Gestational HTN
SBP 160 mmHg or DBP 105 mmHg is treated
with antihypertensive agents
> 34 wks AOG DELIVER!
< 34 wks AOG give steroids
Gestational HTN: Risk of Progression
to Preeclampsia
15-25% risk
Women with early onset of gestational
hypertension are more likely to progress to
preeclampsia than women with late onset
 Gestational HTN: RECURRENCE
Prevalence: 22 - 47 % (2nd pregnancy)
tends to recur with subsequent
pregnancies
Gestational HTN: LONG-TERM
PROGNOSIS

associated with development of HTN later

in life

associated with development of diseases

related to hypertension (CVD, CKD,DM)
 PREECLAMPSIA
Is a multi - system disorder characterized
by new onset of hypertension and
proteinuria after 20 weeks of gestation in a
previously normotensive woman

increased risk for maternal and/or fetal

mortality or serious morbidity
Sibai BM, Caritis S, Hauth J, National Institute of Child Health and Human Development Maternal-Fetal
Medicine Units Network. What we have learned about preeclampsia. Semin Perinatol 2003; 27:239.;
Hutcheon JA, Lisonkova S, Joseph KS. Epidemiology of pre-eclampsia and the other hypertensive
disorders of pregnancy. Best Pract Res Clin Obstet Gynaecol 2011; 25:391.
www.uptodate.com 2013 UpToDate
 Preeclampsia
A 2 stage disease?
1. Asymptomatic Placental Stage
2. Symptomatic Maternal Stage
 Preeclampsia: PATHOGENESIS
Immunologic Factors
Systemic Endothelial Dysfunction
Diet
Genetic Factors
Increased sensitivity to Angiotensin II
Inflammation/Infection
 Preeclampsia: RISK FACTORS
Associated with the pregnant woman
Nulliparity
Preeclampsia in a previous pregnancy
Age >40 years or <18 years
Family history of preeclampsia (mother or sister)
Chronic hypertension
Chronic renal disease; APAS or inherited thrombophilia; Vascular or
connective tissue disease; DM (pregestational and gestational)
High body mass index
Black race / Filipino
Woman herself was small for gestational age
Prolonged interpregnancy interval
Preeclampsia: RISK FACTORS
Associated with the pregnant womans
husband or partner
First time father
Male partner whose mother or previous partner had
preeclampsia
Partner related factors (new partner, limited sperm exposure
[eg, previous use of barrier contraception])
Preeclampsia: RISK FACTORS
Associated with the fetus
Multifetal gestation
Hydrops fetalis / Triploidy
Unexplained fetal growth restriction
Fetal growth restriction, abruptio placentae, or fetal demise in
a previous pregnancy
Hydatidiform mole
 MEAN ARTERIAL PRESSURE

MAP = DBP + 1/3 (SBPDBP)

MAP 2 > 90 mmHg or a MAP3>
105 mmHg increased PIH and
perinatal deaths
Absence of a mid trimester drop in
BP may predict future PIH based
on the absence of arteriolar
vasodilatation
 Early Screening for PE (11-13 weeks)

Ultrasound Screening
Uterine arteries (PI)
Abnormal UA can identify 50%
of those who will develop pre-
eclampsia and 30% of those
who will develop IUGR. Nicolaides,
Placental and Fetal Doppler, Diploma in Fetal
Medicine Series, 2000.

Maternal Serum Markers

VEGF, PlGF, sFlt1
Endoglin

Courtesy of WWS
 Clinical Features and Pathophysiology

Cardiopulmonary
Hypertension
Intravascular volume and edema
Cardiac function - high afterload assoc w/ inc.
cardiac filling pressures
Pulmonary edema -
pulmo vascular hydrostatic P > plasma oncotic P
Capillary leak, left HF, iatrogenic volume overload
 Clinical Features and Pathophysiology

Renal
Proteinuria
0.3 grams protein in a 24-hour urine specimen or
persistent 1+ (30 mg/dL) on dipstick
random protein:creatinine ratio >30 mg/mmol
5 grams of protein in a 24-hour urine collection
(SEVERE)
Renal Function
GFR (30-40%), renal plasma flow
Rising creatinine and oliguria (UO<500mL/24h)
PES (sec to renal vasoconstriction and Na
retention)
 Clinical Features and Pathophysiology

Renal
Hyperuricemia /
Hypocalciuria
inc proximal Na resorption;
urate reabsorption sec to
renal ischemia
Urine sediment benign Light micrograph in preeclampsia showing

Histology Glomerular
glomerular endotheliosis. The primary
changes are swelling of damaged
endothelial cells, leading to partial closure
Endotheliosis of many of the capillary lumens (large
arrows). Mitosis within an endothelial cell
(small arrow) is a sign of cellular repair.
Courtesy of Helmut Rennke, MD.
Clinical Features and Pathophysiology

Hematologic
Thrombocytopenia
accelerated plt
consumption
<100,000/uL PES
PT, aPTT, Fibrinogen
not affected
Microangiopathic
hemolysis
+ schistocytes /
helmet cells (PBS)
Inc LDH;
hemoconcentration
Clinical Features and Pathophysiology

Hepatic
Periportal and sinusoidal fibrin deposition and
microvesicular fat deposition
RUQ pain, inc transaminase levels, coagulopathy,
subcapsular hemorrhage or hepatic rupture
Epigastric pain sec to stretching of Glissons
capsule due to hepatic swelling or bleeding
Clinical Features and Pathophysiology

CNS and eye

headache
visual symptoms constriction of retinal arteries
Photopsia (flashing lights); scotomata (dark
areas/gaps); diplopia or amaurosis fugax (unilat
blindness)
generalized hyperreflexia
sustained ankle clonus
Stroke
Clinical Features and Pathophysiology

Fetus and placenta

FGR
Oligohydramnios
Fetal hydrops (mirror or Ballantyne syndrome)
 PE: MANAGEMENT
Definitive treatment: DELIVERY!
Based on the ff:
AOG
Severity of PE
Maternal / Fetal condition
 PES: MANAGEMENT
Deliver regardless of gestational age
if proteinuria ( 5 grams) is the only criteria for
severe diseasemanaged as mild PE
mild fetal growth restriction with reassuring
Doppler velocimetry treat conservatively *
severe hypertension treat conservatively *

NOTE: * remote from term

 MILD PE: MANAGEMENT
Deliver at 37 weeks of gestation
Labor induction encouraged
EXPECTANT ANTEPARTUM MANAGEMENT OF
MILD PREECLAMPSIA

Inpatient vs outpatient care

Close maternal monitoring upon diagnosis of
preeclampsia is important to establish disease
severity and the rate of progression

Hospitalization is useful for making these

assessments and facilitates rapid intervention in
the event of rapid progression

Outpatient care is a cost-effective option for

women with stable mild preeclampsia after initial
dx evaluation
EXPECTANT ANTEPARTUM MANAGEMENT OF
MILD PREECLAMPSIA

Laboratory follow up
platelet count, serum creatinine, serum AST
1-2x/wk, assess disease progression

Assessment of fetal well-being

daily fetal movement count
twice weekly fetal NST with AFI or
twice weekly BPS
UMA Doppler indices evaluation
EXPECTANT ANTEPARTUM MANAGEMENT OF
MILD PREECLAMPSIA

Assessment of fetal growth

sonographic estimation of fetal weight done to look
for growth restriction and oligohydramnios at the
time of diagnosis of PE , repeated every 3 weeks if
the initial examination is normal
Antenatal corticosteroids
< 34 weeks AOG
 INTRAPARTUM MANAGEMENT

Intrapartum monitoring
Fluids
monitored closely to avoid excessive
administration, since women with severe disease
are at risk of pulmonary edema and significant
third-spacing
 Acute Management of PES
Labetalol
first-line therapy (rapid onset of action, good safety
profile)
20 mg IV over 2 minutes followed at 10-minute
intervals by doses of 20 to 80 mg
up to a maximum total cumulative dose of 300 mg
E.g. Give 20 mg, then 40 mg, then 80 mg, then 80 mg,
then 80 mg
 Acute Management of PES
Hydralazine
5 mg IV over 1 to 2 minutes
if BP goal is not achieved within 20 minutes, give a
5 to 10 mg bolus depending upon the initial
response
The maximum bolus dose is 20 mg
If a total dose of 30 mg does not achieve optimal
blood pressure control, another agent should be
used.
The fall in blood pressure begins within 10 to 30
minutes and lasts from 2 to 4 hours.
 Target BP
130 to 150 mm Hg systolic and 80 to 100
mm Hg diastolic OR reduce MAP by no
more than 25% over 2hrs

Cerebral or myocardial ischemia or infarction can be

induced by aggressive antihypertensive therapy if the
blood pressure falls below the range at which tissue
perfusion can be maintained by autoregulation
 Seizure Prophylaxis
MgS04 given to mild / severe PE
Loading dose: 4-6 g, slow IV push, over 15-20 mins
Continuous infusion: 1-2 g/hr OR 5g IM into each
buttock (total 10 g) followed by 5 g IM, alternate
buttocks ever 4h
continued for 24 hours postpartum
 MgS04 Toxicity
loss of DTRs: 9.6 to 12.0mg/dL(4.0 -5.0 mmol/L)
respiratory paralysis: 12.0 to 18.0 mg/dL (5-7.5 mmol/L)
cardiac arrest: 24 to 30 mg/dL (10 to 12.5 mmol/L)

* Calcium gluconate (1 gram intravenously over 5 to 10

minutes)
should be administered only to counteract life-threatening symptoms of
magnesium toxicity (such as cardiorespiratory compromise)
 Postpartum Management
NSAIDs
for pain control should be avoided in women with
poorly controlled hypertension, oliguria, renal
insufficiency, or thrombocytopenia
Monitor VS q 2h while on MgS04
Treat PES
 Prevention of Recurrence
Prepregnancy
Weight loss to ideal BMI
Control of glucose in diabetes
Control of BP in CHTN (diet, exercise)
Low dose aspirin in select patients (from 12 wks)
Not recommended
Vitamins C & E
Dietary salt restriction
Anti-HTN therapy to prevent preeclampsia
 ECLAMPSIA
development of grand mal seizures in a
woman with preeclampsia, in the absence
of other neurologic conditions that could
account for the seizure
occurs in 2 to 3 percent of severely
preeclamptic women not receiving anti-
seizure prophylaxis
 Pathogenesis of Seizures
1. Cerebral overregulation in response to
high systemic blood pressure
vasospasm of cerebral arteries
underperfusion of the brain
localizedischemia/infarction
cytotoxic (intracellular) edema
 Pathogenesis of Seizures
2. Loss of autoregulation of cerebral blood
flow in response to high systemic
pressure
E.g., hypertensive encephalopathy
Hyperperfusion
endothelial damage
vasogenic (extracellular) edema
 Management
Iinitial Mx: Maintenance of airway patency
and prevention of aspiration
Gravida rolled onto her left side
Protect from trauma
Supplemental O2 (8-10L/min via face
mask)
 Management of severe hypertension, if
present
Prevention of recurrent seizures
Evaluation for prompt delivery
definitive treatment of eclampsia is delivery,
irrespective of gestational age
 Management of Persistent
Convulsions
additional bolus of 2 grams MgS04 over
15 to 20 minutes
with careful monitoring for signs of magnesium
toxicity
 HELLP Syndrome
Hemolysis
Elevated Liver enzymes
Low Platelets

severe form of preeclampsia or an independent

D/O
 HELLP Syndrome
Initiate IV Dexamethasone EARLY:
Always when PLTS <100,000/uL
Selectively when Class 3 plus
(a) Eclampsia; (b) Severe Epigastric Pain;
(c) Fulminant Disease; (d) Severe HTN
Antepartum: Dex 10mg q12 hrs
Postpartum: Dex 10+10+5+5
@ 0,12,24,36 hrs
 CHRONIC / PREEXISTING
HYPERTENSION
SBP 140 mmHg and/or DBP 90 mmHg
that antedates pregnancy or is present
before the 20th week of pregnancy (on at
least two occasions) or persists longer
than 12 weeks postpartum
 PREECLAMPSIA SUPERIMPOSED
UPON CHRONIC /
PREEXISTING HYPERTENSION
the new onset of proteinuria after 20
weeks of gestation in a woman
with chronic/preexisting hypertension
 Hypertensive Disorders particularly
PREECLAMPSIA
Major life-threatening morbidity
Leading reason for preterm labor and birth
RISK factor for FUTURE maternal cardiovascular
and metabolic DISEASE
Affects long term maternal survival
 GOALS
Development of effective strategies
for the prevention and/or treatment
of preeclampsia

Prolong the pregnancy and improve

maternal and neonatal health
 Key Points
Identify Risk Factors
Prediction
Diagnosis (Classify)
Ambulatory or In Patient Management
Tertiary Care
Postpartum care
Prevention
Thank you