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 1week period
Hypertensive Disorders
Related To Pregnancy
1.
2.
3.
4.
5.
6.
Gestational hypertension
Preeclampsia
Eclampsia
HELLP syndrome
Chronic/preexisting hypertension
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
(UTZ)
Absent
Gestational HTN: MANAGEMENT
• Mild Gestational HTN
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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
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Immunologic Factors
Systemic Endothelial Dysfunction
Diet
Genetic Factors
Increased sensitivity to Angiotensin II
Inflammation/Infection
Preeclampsia: RISK FACTORS
• Associated with the pregnant woman
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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 woman’s
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
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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 preeclampsia 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
• Histology – Glomerular
Endotheliosis
Light micrograph in preeclampsia showing
glomerular endotheliosis. The primary
changes are swelling of damaged
endothelial cells, leading to partial closure
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
–
–
•
PT, aPTT, Fibrinogen
–
•
accelerated plt
consumption
<100,000/uL  PES
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 Glisson’s
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 diseasemanaged 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
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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 antiseizure prophylaxis
Pathogenesis of Seizures
1. Cerebral overregulation in response to
high systemic blood pressure
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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
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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
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Identify Risk Factors
Prediction
Diagnosis (Classify)
Ambulatory or In Patient Management
Tertiary Care
Postpartum care
Prevention
Thank you…