[HYPERTENSION IN PREGNANCY]

[DRA. NAGTALON] [DATE: SEPTEMBER 16, 2010]

LEGEND o high BP but with diastole <100mm Hg; and

Normal text : lecture and recording with mild proteinuria. No other
Italics : book manifestations
Severe Pre-eclampsia
OUTLINE
-if with evidence of multi-organ involvement (e.g.
I. TYPES & CRITERIA
II. PREECLAMPSIA
liver pathology, renal pathology, abnormal platelet
A. AT RISK FOR PREECLAMPSIA count, headache, epigastric pain)
B. ETIOPATHOGENESIS
C. MANAGEMENT Indications of Severity of Hypertensive Disorders during Pregnancy
D. ADVERSE EFFECTS
E. EVALUATION Abnormality Mild Severe
F. INITIATION OF ANTI-HYPERTENSION
G. SEIZURE PREVENTION IN SEVERE PREECLAMPSIA Diastolic blood pressure < 100 mm Hg 110 mm Hg or higher
H. OPTIMAL MANAGEMENT Proteinuria Trace to 1+ Persistent 2+ or more
I. INDICATION FOR DELIVERY WITH EARLY-ONSET SEVERE
PREECLAMPSIA Headache Absent Present
J. CONDUCT OF DELIVERY
K. PREDICTION Visual disturbances Absent Present
III. ECLAMPSIA Upper abdominal pain Absent Present
A. PRIORITIES IN MANAGEMENT
B. MANAGEMENT Oliguria Absent Present
IV. HELLP SYNDROME
A. COMPONENTS Convulsion (eclampsia) Absent Present
V. POSTNATAL Serum creatinine Normal Elevated
VI. SUBSEQUENT PREGNANCY
VII. LONG-TERM SEQUELAE Thrombocytopenia Absent Present
VIII. CONTROLLING CHRONIC HYPERTENSION
IX. EARLY PRENATAL CARE FOR WOMEN
Liver enzyme elevation Minimal Marked
Fetal growth restriction Absent Obvious
I. TYPES & CRITERIA
Pulmonary edema Absent Present
*About 500,000 women die annually due to complications
due to pregnancy. 26% of that is due to HTN in pregnancy and
its complications.
C. Eclampsia
*What is HTN in pregnancy? - Seizures in a woman with preeclampsia
-Diastolic blood pressure of 110 mmHg or BP 140/90 mmHg. - seizures that cannot be attributed to other causes
(National Institute of Health)
- BP should be taken at two separate occasions about 4-6 hrs D. Superimposed Preeclampsia on Chronic Hypertension
apart. - In a woman with HTN, new onset proteinuria after 20 weeks
AOG
*A problem because morbidity and mortality with HTN in - Sudden increase in BP or proteinuria or platelet (<
pregnancy can also affect the baby. 100,000/ul) , after 20 weeks AOG, in a woman with HTN
- no proteinuria before 20 weeks' gestation
A. Gestational Hypertension - All chronic hypertensive disorders, regardless of their cause,
- BP=/> 140/90 during pregnancy, returns to normal before predispose to development of superimposed preeclampsia
12 weeks postpartum and eclampsia
- No proteinuria (difference from pre-eclampsia). SIDENOTE: just combine the features of chronic HTN with
preeclampsia
B. Preeclampsia
Minimum Criteria: E. Chronic Hypertension
- BP=/> 140/90 noted after 20 weeks AOG (if noted before 20 - BP=/> 140/90 antedating pregnancy or diagnosed even
weeks AOG, you might be dealing with CHRONIC HTN). before 20 weeks AOG (this is the only one with high BP before
- Proteinuria =/> 300mg/24hrs 20wks AOG)
- HTN after 20 weeks AOG and persists after 12 weeks
Increased certainty of Preeclampsia: postpartum
-BP=/>160/110 - will have greater complications if superimposed with pre-
- Proteinuria 2g/24hrs eclampsia (greater and earlier fetal morbidity and mortality
- Serum creatinine > 1.2mg/dl because the insult have been there early on in the pregnancy
- Platelets <100,000/ul (thrombocytopenia) or at the time of the embryonic stage.)
- Increased Lactate Dehydrogenase (LDH) -identify women at risk to predict this.
- Elevated ALT, AST -this is a concern because women are currently marrying at a
- Persistent headache, visual changes later age these days and may already have pre-existing
- Persistent epigastric pain conditions which can complicate pregnancy. The Assisted
Mild Pre-eclampsia Reproductive Technology is related to multiple births.

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Presence of multiple gestations is a risk for HTN in pregnancy.
(NAKU PO!!)
Hypertension in Pregnancy
- Strong genetic predisposition: Thrombophilia or family
history of HTN (4-8 fold increase)
o If your mother has HTN, you have a 4 fold chance of
having HTN in pregnancy.
o If your sister has HTN, you have a 8 fold chance of
having HTN in pregnancy.
- 3-10% of nulliparous women will develop HTN at some stage
during pregnancy
- 40% increase in the rate of preeclampsia since 1990, as a
result of a rise in advanced maternal age and ART-related
multiple births (Ventura et.al.)
- Major cause of maternal mortality & premature births
associated with worsening disease
II. PREECLAMPSIA
A. AT RISK FOR PREECLAMPSIA
1. Nulliparity/Pimipaternity
2. Advanced maternal age
3. Family history of HTN
4. Multiple gestation
5. Chronic renal disease
6. Insulin-dependent DM
7. Autoimmune disease: SLE, APAS
8. Thrombophilia
9. Previous pregnancy with pre-eclampsia
10. Chronic HTN
11. Gestational HTN in the current pregnancy
12. Connective tissue disease
13. Current fetal growth restriction
*There is a high risk if a woman is pregnant for the first time
or is pregnant for the first time with a DIFFERENT partner.
The exposure to the sperm and increase in chorionic villi
increases risk.
* Although a number of tests have been proposed to predict
those at greatest risk, NONE have risen to the level that they
can be recommended for general population screening
(Conde-Agudelo et.al.)
* A high index of suspicion for those at-risk will aid in the
management during the prenatal period.
B. ETIOPATHOGENESIS
1. Low resistance uteroplacental unit is prostacylin
dependent
In normal pregnancies, there is an increase need
for uteroplacental blood flow and so changes
occur in the uterine arteries: Endovascular
trophoblastic invasion of the arteries
dilatation with corkscrew like configuration at
the decidua and myometrial bed.
With HTN in pregnancy: faulty development at
the myometrium vessels are chronically
constricted decreased blood flow to
uteroplacental circulation ischemia
release inflammatory cytokines into the
maternal circulation.
TRANSCRIBED BY: Natz Quan, Abi Umayan
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2. Faulty Placentation
3. Immunologic Theory
Rejection of fetal allograft by maternal system.
Reduced extravillous immunosuppressive HLA-G
favors TH1 bias.
TH1 -bad cytokines. In pregnancies not
complicated wit pre-eclampsia, there is
dominance of TH2. In pre-eclamptic women,
TH1 is increased.
TH1 promote inflammatory cytokine secretion
(TNF, IL) which contribute to oxidative stress
and release of toxic free radicals, which injure
endothelial cells, modify NO production and
interfere with PG balance (decreased
prostacyclin: thromboxane favors increased
sensitivity to angiotensin II and
vasoconstriction).
Oxidative stress also results to production of
lipid-laden macrophage foam cells (invade and
ruin vascular bed lumen) seen in atherosis;
narrowing of lumen and activation of
microvascular coagulation, platelet aggregation,
and increased capillary permeability.
*Vasospasm explains seizures, renal affectation and oliguria,
abruption placenta, liver abnormalities, necrosis, and
hemolysis.
* Increased capillary permeability explains edema, pulmonary
edema, hemoconcentration and proteinuria.
*Microvascular complication explains thrombocytopenia
*All in all, the culprit is faulty placentation with reduced
uteroplacental perfusion.
* Compromised uteroplacental perfusion from vasospasm is
almost certainly a major culprit in the genesis of increased
perinatal morbidity and mortality associated with
preeclampsia
CASE: A 30 y/o G2P1, with preeclampsia in her previous
pregnancy, consults with a sonogram-established intrauterine
pregnancy, 8 weeks AOG, live twin gestation. What can be
offered to prevent recurrence of pre-eclampsia?
*At risk because of previous history and presence of multiple
gestation. Cannot offer anything for occurrence but
progression can be altered by Calcium or ASA.
ANSWER: Good prenatal care is a prerequisite. Allows early
identification which facilitates interventions, including
delivery, that will lessen risk of progression to severe
preeclampsia & eclampsia and reduce fetal & maternal
mortality and morbidity. Typical signs & symptoms indices of
suspicion are: (1) rapid weight gain; (2) increasing edema; (3)
persistent headache; (4) blurring of vision, & (5) tightness in
fingers.
* EARLY DETECTION IS CRITICAL.
C. MANAGEMENT
v In hospital evaluation for those diagnosed with
preeclampsia during prenatal care.
v Anti-HTN not recommended for women who was
previously normotensive unless BP>160/110.
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v Serial surveillance: detect disease progression;
assessment of maternal & fetal status
v Delivery is the optimal treatment
v MgSO4 for seizure prevention in severe preeclampsia
v Prevention for those AT RISK
a. LOW RISK
Calcium supplementations (ONLY if with low
dietary intake of 2g/day, reduce pre-eclampsia
by vasodilatation at uteroplacental bed and
increase placental blood flow) (RR 0.7, Cl 0.58-
0.83), most marked in those with low baseline
dietary calcium [I-A; Sibai & Cunningham 2009]
b.
HIGH RISK
Low dose Aspirin (reduce risk by prevents
thromboxane A2 synthesis increase
prostacyclin vasodilation). [I-A] & calcium
supplementation [I-A]
v Reduction:
a. 17% risk of pre-eclampsia
b. 8% preterm births
c. 14% fetal deaths
d. 10% SGA
CASE:
Supposed at 30 weeks AOG in this asymptomatic G2P1 with
twin pregnancy findings reveal:
BP=160/110 (checked 2x) severe pre-eclampsia!!
FH=29cm
FHT=150/min
U/A=+3 protein
PLAN OF ACTION: Hospitalization, in a tertiary care facility
that has critical care expertise, ICU, & NICU facility 7
personnel-on-site, is essential for severe disease for thorough
management. NO SHORTCUTS!
*in severe pre-eclampsia, hospitalization is important to
assess maternal and fetal status and progression of disease.
Management is delivery or termination but you cannot
deliver if youre not sure of the good chance of survival of the
baby. So it will be critical for the doctor to choose
conservative treatment (close monitoring) or delivery.
Maternal: CVA, cardiac failure, liver rupture,
eclampsia, HELLP(hemolysis, low platelet, and
elevated liver profile syndrome) pulmonary edema,
& preterm delivery
Fetal: Hypoxia IUGR, prematurity, IUFD, & anemia
secondary to abruption placenta
b. Others
Cerebrovascular (CV) overregulation leads to
vasospasm and diminished blood flow hence
ischemia, edema, & infarction.
Sudden elevations in systemic BP exceed normal CV
autoregulatory capacity forced arterial dilatation,
constriction with disruption of end-capillary pressure
causing increased hydrostatic pressure,
hyperperfusion, extravasation of plasma and RBCs
thru endothelial tight junction openings leading to
vasogenic edema.
Hemorrhagic strokes associated with preeclampsia
in women with CHR HTN with superimposed pre-
eclampsia due to affectation of the lenticulostriate
arteries dilate rupture or remarkable edema.
* Charcot-Bouchard Aneurysms in the deeply penetrating
arteries of the lenticulo-striate branch of the MCA which
supply the basal ganglia, putamen, thalamus, adjacent deep
white matter, pons, and deep cerebellum [Cunningham 2005]
Eclampsia
E. EVALUATION
1. Detailed exam with daily scrutiny: headache, visual
disturbances, epigastric pain, rapid weight gain
2. Weight determined daily (progressive edema if
increased)
Analysis for proteinuria (+2 and above with renal
impairment) on admission then q2 days
3. BP q4 hrs (Except between 12mn-6am)
4. CBC, creatinine, transaminase assessment (ALT and AST)
5. Fetal evaluation: AOG, fetal size, AFV non-stress test,
biophysical profile
F. INITIATION OF ANTI-HYPERTENSION

*In general, if proteinuria >1gm/24hrs, in-hospital

* Use of anti-HTN in mild to moderate disease adversely
management is recommended, regardless of other
affect fetal growth.
parameters.
* Experts have stated that it is not advisable to initiate anti-
* Worsening of the condition as pregnancy progresses and rd
HTN therapy for a patient in the 3 trimester who was
crisis may occur anytime.
previously normotensive, because one runs the risk of
masking a key clinical parameter used to assess disease
* Hemorrhage is a common complication. Cardiac failure is
progression.
another problem.
DRUG for DOSAGE DIRECTIONS
* Concern is when best to terminate the pregnancy with a ACUTE HTN
favorable maternal and fetal outcome. Hydrazaline 5mg IV Repeat in 10mins, then give 5-
(Onset of 10mg IV q15-20mins until BP
CLOSE SURVEILLANCE RECOMMENDED. action: 10 stabilizes (140-150/90-
mins) 100mmHg); preferred for
COMPLETE ABATEMENT OF SIGNS & SYMPTOMS IS *vasodilator control of severe HTN in low-
UNCOMMON UNTIL AFTER DELIVERY! resourced settings; limit total
dose to 30mg per treatment
cycle
D. ADVERSE EFFECTS (Uncontrolled Hypertension) Labetalol 20mg IV After 10mins, give 40mg if BP
bolus has not decreased. The next
a. Maternal & Fetal 10min incremental dose is not

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 to exceed 220mg total dose per *Any manifestation related to severe pre-eclampsia to
treatment episode. prevent occurrence of seizures.
Nifedipine (first 10mg oral Repeat in 30mins for 4 doses *Woman with new onset proteinuric HTN. At onset, one
line oral (max: 40mg); then give 10-20mg of the following is required:
therapy) orally q4-6hrs to achieve BP
BP=/> 160/110
*Calcium 140-150/90-100mmHg; caution
antagonist with concomitant MgSO4
Proteinuria +2 or >
because it can cause cardiac Serum creatinine >1.2mg/dl
depression. Platelet count <100,000/ul
Aspartate transaminase (AST) elevated 2x above
* Only give anti-hypertensive drugs if with progression of upper limit of normal
disease with increase in BP at 160/100mmHg. Persistent headache, scotoma
Persistent mid-epigastric, RUQ pain
*Dont go lower than 90 mmHg diastolic because that could
further compromise blood flow. H. OPTIMAL MANAGEMENT
*Delivery is best.
PERSISTENT UNCONTROLLED HYPERTENSION v Once concerns about prematurity have been eliminated
-there is affectation of the cerebrovascular autoregulation (achieving 37 weeks AOG), further expectant
system (extreme headache, vomiting, and change in management is NOT indicated.
sensorium) which explains ischemia, edema, and infarction. v Its a problem if its before 34 weeks AOG because you
have to weigh things and try to see if its better to deliver
*If a patient develops a true hypertensive crisis with now, or later but with the risk of having a still born baby.
hypertensive encephalopathy (generally occurs at BP=/> v In severe preeclampsia, it is generally not recommended
240/140mmHg), then emergent intervention with a rapidly to continue the pregnancy beyond 34 weeks AOG
acting agent such as sodium nitroprusside is necessary and because of the associated perinatal mortality rate
should be managed by someone skilled in critical care and the (PMR)=87%.
use of such drugs. v Preeclampsia

G. SEIZURE PREVENTION IN SEVERE PREECLAMPSIA Expectant management for mid trimester severe
a. MgSO4 (anti-convulsant and vasodilator) for seizure preeclampsia
prophylaxis (Level Ia, A) STUDY NUMBER MATERNAL PERINATAL
Relative risk (RR) of eclampsia 0.33 (95% Cl 0.11- OUTCOME % MORTALITY %
1.02) Hall et al 8 36% 88%
2001
MgSO4 superior than phenytoin
Jenkins et al 39 54% 90%
MOA: reduce presynaptic release of glutamate;
2002
block glutamatergic N-CH3-D-aspartate (NMDA) Budden et 31 71% 71%
receptors; potentiation of adenosine action; al 2006
improved mitochondrial Ca buffering; blockade of Ca Gaugler- 26 65% 82%
entry via voltage-gated channels (Duley et al & Senden et al
Altman D. et al) 2006
magnesium sulfate administered parenterally is an Bombrys et 46 38-64% (sorry hindi ko
effective anticonvulsant agent without producing al 2008 po mabasa)
central nervous system depression in either the AVERAGE 140 60% 65%
mother or the infant
v Glucocorticoid Therapy
b. MgSO4 Maternal & Fetal Effects Treatment decreased incidence of RDS and
Maternal improved fetal survival; did not worsen maternal
Depressed cardiovascular function with HTN [Leveno & Cunningham 2009]
exceedingly high serum levels (best to maintain Enhances pulmonary maturity.
at 4-7meq/L Corticosteroid use to ameliorate HELLP syndrome -
Inhibit myometrial contractility (8-10meq/L) Recovery times for platelet counts and serum AST
Relaxes the uterus so it takes some time for were identical in the treatment and placebo group
induction of labor if given this drug. [Katz et al 2008]
DTR loss at 10 meq/L
Respiratory changes and changes in sensorium I. INDICATION FOR DELIVERY WITH EARLY-ONSET SEVERE
12 meq/L PREECLAMPSIA [Sibai et al]
a. Maternal
Fetal Persistent severe headache or visual changes;
No significant changes in beat-to-beat FHR ECLAMPSIA
variability [Hallack et al] Shortness of breath with rales or O2 sat <94%;
Protective effect against development of PULMONARY EDEMA
cerebral palsy in VLBW infants (0.6 Cl 0.44- UNCONTROLLED severe HTN
0.85)[Nelson et al] OLIGURIA <500ml/24h, or serum creatinine 1.5mg/dl
or > PLATELET count <100,000/ul
c. Who should be given MgSO4? Suspected ABRUPTIO, progressive labor, PROM

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b. Fetal
Severe IUGR<5 percentile for estimated gestational
age (EGA)
Persistent oligohydramnios; Amniotic Fluid Index
(AFI) of <5cm
Biophysical Profile (BPP)<4 done 6hr apart
Reversed end-diastolic umbilical artery flow
IUFD
J. CONDUCT OF DELIVERY
a. Mode
Trial of vaginal birth for mild preeclampsia
Induction of labor for severe preeclampsia, CS for
dystocia/fetal indication [Nasaar et al & Alexander
JM et al]
CS for very tight and long cervix.
b. Anesthesia
Lumbar epidural anesthesia(LEA) provides good
control of HTN & improves uteroplacental blood
flow; CAUTION with aggressive fluid therapy
Sub-arachnoid block (SAB) with appropriate preblock
hydration, posture & judicious administration of
vasopressors for hypotension also suitable
GA/General anesthesia for severe fetal distress,
hemodynamic compromise from placental abruption
[Hogg B et al]
Lumbar epidural anesthesia is better because there
is no sudden drop in the BP versus spinal anesthesia.
K. PREDICTION
v At triage for prenatal care, women with markers of
increased risk should be offered OB consultation [II-2B]
Markers are:
o Roll-over test hypertensive response induced by
having women at 28 to 32 weeks assume the supine
position after lying laterally recumbent predicted
gestational hypertensive
o Uric acid - Elevated serum uric acid levels due to
decreased renal urate excretion are frequently found
in women with preeclampsia
o Fibronectin- Endothelial cell activation likely is the
cause of elevated serum cellular fibronectin levels in
some women with preeclampsia
o Coagulation activation- Thrombocytopenia and
platelet dysfunction are integral features of
preeclampsia
o Oxidative stress- Increased levels of lipid peroxides,
coupled with decreased activity of antioxidants in
women w/ preeclampsia
o Cytokines- There are over 50 cytokines, and a
number of these are elevated in preeclampsia
o Placental peptides - a number of peptides are
produced by the placenta, and some may prove to be
markers for prediction of preeclampsia
o Fetal DNA- Identification of fetal DNA in maternal
serum may be predictive of preeclampsia
o Uterine artery doppler velocimetry
v Women at increased risk should be considered for risk
stratification involving a multivariable clinical &
laboratory approach [II-2B]
III. ECLAMPSIA
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*Severe pre-eclampsia + seizures (over secretion of the
epileptogenic/hyper-excitatory transmitters in the brain.)
A. When eclampsia develops, the priorities in management:
Prevent maternal injury & aspiration
Support respiration & CV functions: oxygenation 8-
10L/min
MgSO4 7 H2O to prevent recurrence
Maintain BP 140-160/90-100mmHg
Correct maternal hypoxemia, hypercarbia
Deliver an infant with good chance of survival
B. MANAGEMENT
Like managing a woman with seizures: prevent
aspiration, injury, cardiovascular and respiratory
support, maintain BP (to prevent another seizure),
Magnesium sulfate to prevent recurrence of seizure,
correct hypoxemia, deliver baby.
Do not proceed to emergent C-Section! *Because V/S
not yet stable and manipulation can trigger another
seizure attack. So control the BP, administer
magnesium sulfate and after 4-6 hours, may start
induction of C/S.
Delivery after conditions are stabilized (method of
delivery depends on GA, fetal presentation and status
of the cervix) [Cochrane Lib, 2001; Sibai, 2009]
IV. HELLP SYNDROME
- 1) hemolysis, 2) elevated liver enzymes, 3) low platelets
- complication of severe pre-eclampsia
A. COMPONENTS:
1. Hemolysis (presence of at least 2)
peripheral smear (schistocytes, burr cells)
serum bilirubin (1.2mg/dl))
low haptoglobulin
severe anemia unrelated to blood loss
2. Elevated liver enzymes
AST or ALT 2x upper limit of normal
LDH 2x upper limit of normal
3. Low platelets (<100,000/cu mm)lower means
hemorrhage!!
* When HELLP syndrome arises..
Continue MgSO4 (decrease BP and prevent
eclampsia)until there is laboratory evidence of
improvement in platelet count & transaminase
Delivery when condition has stabilized; presence of
fetal compromise
Use of dexamethasone / glucocorticoid therapy
remains controversial.[Fonseca et al, 2005]
Recovery times for platelet counts and serum AST
were identical in the treatment and placebo group
[Katz et al, 2008]
V. POSTNATAL
PREECLAMPSIA & ECLAMPSIA
*complete magnesium sulfate 24 hours postpartum
v Maintain high-dependency care for 24-48 hr
v STOP anticonvulsants 24 hr after last fit/when brisk
dieresis is observed
v Use anti-HTN as necessary (12 weeks postpartum) and
closely monitor BP
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v Counsel about risks of recurrence: Highest for gestational
hypertension.
v Long-term follow-up SHOUTOUT
Boss CARLO, after mo maproofread pwede po bang maglagay ng
Neuro assessment for atypical fits
greeting?..hehe..this is my first trans ever..so first time din ako makakabati sa
Monitor BP and proteinuria, investigate if they mga madam..thanx.--abi
remain abnormal beyond 12 weeks postpartum
Yehey! Thanks glenny, sa pagw8 ng pabati ko.

VI. SUBSEQUENT PREGNANCY Just want to say hi to my gang (yaya,bebe,xena d warrior princess, & to
princess of d republic of mexico); to all my groupmates sa med (tiu to
villaflor), neuro (tiu to versoza esp. YELLOW), pedia (tan to valdez) & surge
RISK OF RECURRENCE (tengco to villaflor); MADAM MARO (ayan na ha capslock pa yan) at sa mga
v 70% with gestational HTN TITAs; BABSKI (u know who u r) & his friends; & to medicine class 2012!!!
v 40% if with very early-onset preeclampsia Thanks to our pres. (kasi kung ndi cya nagtaray, ndi ako sasali sa transcom at
v 25-65% with severe preeclampsia ndi din ako makakagrit, HEHE ). Many thanks din sa aming boss (Mr.
v 5-26% for HELLP syndrome Carlo Benjamin Tanada) & to my trans sub-groupmate Ms. Nats Quan & ang
v 1-1.9% for eclampsia pinakamabait daw na AGAPEman Mr. Glentanilla (kunin mo na zagu mo sa
akin,tunaw na kaya). Thats all.

VII. LONG-TERM SEQUELAE The early worm dies first. HEHE! Kaya magpalate tayong lahat.
- DOLLETE

CVD
A. 50 years follow-up National database from ICELAND
[Arnadottir et al, 2005]
1. Mortality: 60% of HTN women vs 53% of controls
2. Ischemic cerebrovascular disease (ICVD): 25% vs 15%
3. Stroke: 9.5% vs 6.5%

B. SWEDISH data (1973-1982) showed

1. Increased ICVD in those with HTN in pregnancy

C. DANISH registry (1978-2007) mean follow-up of 15 years:

1. Chronic HTN increased 5.2-fold in those with
gestational HTN
2. 3.5-fold after mild preeclampsia
3. 6.4-fold after severe preeclampsia
4. 3.5-fold increase in DM-Type II

VIII. CONTROLLING CHRONIC HYPERTENSION

v BP=140/90mmHg before 20 weeks AOG and likely to

cause adverse effects on baby (seek prenatal care before
20 weeks of gestation due to physiologic maternal
nd
hypotension in 2 trimester and may have a masked
hypertension during this time).
v Fetal:
30% SGA
60% pre-term delivery (esp. with chronic HTN with
superimposed HTN without prenatal care before 20
weeks AOG.)
high Perinatal Mortality Rate with preeclampsia
v Maternal: Abruptio placenta
* 1.5% in mild HTN, 5-10% with severe HTN, 30% with
superimposed preeclampsia

IX. EARLY PRENATAL CARE FOR WOMEN

* Diagnostic complication may arise for those who seek

consult after 20 weeks GA considering the physiologic
decrease in BP that normally occurs in the second trimester
[Garovic, 2000]

Recap:
*HTN in pregnancy if noted AFTER 20 weeks.
*earlier than 20 weeks is CHRONIC HTN.
*Mild pre-eclampsia BP at 140/90 mmHg with proteinuria.
*Severe eclampsia 160/100-110mmHg and proteinuria.

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