OBSTETRICS & GYNECOLOGY

HYPERTENSIVE DISORDERS- OBSTETRICS o Delta Hypertension (not actually a classification of

hypertension in pregnancy, was just mentioned in
Dr. CCB the book because there are some women, though
Source: PPT + Williams 25th Ed.+ recordings the blood pressure is within the normal limit,
meaning the blood pressure does not go up to
140/90 mmhg, however, there is a transient
EPIDEMIOLOGY increase in the blood pressure. It can also
promote pre-eclampsia. It’s just that the mean
o
5 – 10% of all pregnancies are complicated with arterial pressure is increased and it is transient.
hypertensive disorders For example the normal BP of the mother is 90/60
o
Pre-eclampsia syndrome – alone or superimposed mmhg, then suddenly the BP became 120/90, then
on chronic hypertension is themost dangerous that is also hypertension).
o
WHO – 16% of maternal deaths worldwide (Khan, It is important to classify hypertension because they
2006)
have different management –GUIDE TO
o
USA – 2011-2013 – 7.4% of maternal deaths – pre- MANAGEMENT
eclampsia or eclampsia (Creanga, 2017)
CHRONIC HYPERTENSION
France – 2003-2007 – 10% (Saucedo, 2013)
o
Blood Pressure of ≥140/90 mmHg
HYPERTENSION o
Prior to pregnancy or
o
Half of these hypertensive-related deaths were o
Before 20 weeks age of gestation (or prior to
deemed preventable (Breg, 2005) pregnancy) and
o
In the Philippines, it is the most common
medical complication encountered in o
Persists after 12 weeks postpartum
pregnancy
If after 20 wks AOG: the BP is elevated, the
o mother does not know her previous BP, or prior to
Second most common cause of maternal mortality
and an important cause of perinatal mortality and her pregnancy, then you have to wait for the
morbidity(triad: hemorrhage, hypertension, delivery of the baby. If the BP persists as high as
infection). 140/90 mmhg 12 weeks postpartum, then she has
already hypertension.
o
Prevalent in young women of low socio-
economic status without prenatal care
PRE-ECLAMPSIA
o
WHAT IS HYPERTENSION IN PREGNANCY? Hypertension occurring after 20 weeks age
ofgestation with or without proteinuria(most
common and most dangerous complication of
o
Blood Pressure of = or > 140/90 mmHg hypertension in pregnancy).
o o
Blood Pressure must be manifested on at least If without proteinuria, it should have end
two occasions taken six hours apart organ involvement- cardiovascular
complication, cns problem, etc.)
CLASSIFICATION OF HYPERTENSION IN PREGNANCY o
NOTE: ONSET MAY SOMETIME BE EARLIER IN
EXTENSIVE HYDATIDIFORM CHANGES IN
o
Chronic Hypertension CHORIONIC VILLI(patients who has abnormal
placentation, like multifetal gestation)
o
Gestational Hypertension
o
GESTATIONAL HYPERTENSION
Pre-eclampsia
o o
Chronic Hypertension with Superimposed Pre- Hypertension with NO proteinuria and occursafter
eclampsia 20 weeks age of gestation or postpartum
o
o Eclampsia A temporary diagnosis during pregnancy which
has to be confirmed 12 weeks after delivery

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 OBSTETRICS & GYNECOLOGY

o Thrombocytopenia
If Blood Pressure is normalpost partum– Absent Present
Transient Hypertension (<100,000/µL)
o
If Hypertension persists 12 weeks post
partum – Chronic Hypertension Serum
Transaminase Minimal Marked
PRE-ECLAMPSIA WITH SEVERE FEATURES elevation

o
Blood Pressure of ≥160 mmHg (SystolicPressure) Fetal Growth
Absent Present
or ≥110 mmHg (Diastolic Pressure) Restriction
Either one of the following:
Pulmonary Edema Absent Present
o
Decreased Platelet count/Thrombocytopenia
o Gestational Age Late Early
Oliguria
o
Increased Serum Creatinine
o
Congestive Heart Failure CHRONIC HYPERTENSION WITH SUPERIMPOSED
o
Pulmonary Edema PRE-ECLAMPSIA
o
Epigastric/Right upper quadrant pain
o
o BP of >140/90 mmhg pre-exicting prior to
Elevated liver enzymes
pregnancy, or 20 weeks AOG (chronic
o
Persistent headache hypertension)
o
Pre-existing Chronic Hypertension with
o
Visual or Cerebral disturbance o
New-onset Proteinuria and/or

Abnormality Non-severe Severe o

Signs and Symptoms of various End-Organ
Dysfunction or Pre-eclampsia
Diastolic BP < 110 mmHg ≥110 mmHg
ECLAMPSIA
Systolic BP <160 mmHg ≥160 mmHg
o
Diagnosed Pre-eclampsia with Convulsive
Proteinuria None to positive Seizures
o
Convulsion is not caused by coincidental
Headache Absent Present neurologic disease

Visual
Absent Present PATHOPHYSIOLOGY: PRE-ECLAMPSIA AND HELLP
Disturbances
SYNDROME
Upper Abdominal Maternal cause:
Absent Present
pain
• Secondary to underlying
maternaldisease (DM, CHVD, etc.)
Oliguria Absent Present • LATE in onset (>34 weeks)
• LESS severe
Convulsion • Hypertension should be aggressively
Absent Present addressed
(eclampsia)
Fetal cause:
Serum Creatinine Normal Elevated • Secondary to an abnormal placenta
• (+) Paternal contribution

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 OBSTETRICS & GYNECOLOGY

• EARLY onset (<34 weeks) PRE-ECLAMPSIA: RISK FACTORS

• MORE severe
Immunologic related
• Hypertension should be balanced
between maternal and fetal needs • Nulliparous- no exposure with sperm
• Previous Pre-eclampsia
• Multiple Gestation
PATHOPHYSIOLOGY: TWO-STAGE MODEL FOR • Abnormal Placentation
PRE-ECLAMPSIA Disease related – existing disease of the mother
• Chronic Hypertension
STAGE ONE • Chronic Renal Disease
• Abnormal placentation • Collagen Vascular Disease
• Reduced placental perfusion • Pregestational Diabetes Mellitus
• Asymptomatic Phasebecause it occurs
during the first or second trimester of Maternal Related
pregnancy • African American
• Obesity
STAGE TWO • 35<Age<20
• Maternal Syndrome • New paternity
• Symptomatic Phase – complications arise • Cohabilitation <1 year – living-in together,
not married
Second or third Trimester
Family History
WHAT CONSTITUTE NORMAL PLACENTATION? • Relatives
• Mother-in-law
Placental Vascular Development- normal
• Vasculogenesis – the process of new blood
vessel formation during embryonic development
of the

• Angiogenesis – the process by which new blood

vessels grow and develop fromexisting blood
vessels and thus, expanding the vascular
tree(increase in the number and sizes of
blood vessels)

- With all these risk factors, during the first and

second trimester, there would be abnormal placental
invasion of the spiral arteries of the uterus, there
would be placental dysfunction, and with this there
would be placental hypoperfusion. The placental
would become ischemic, so that it will release
debris, or vasoconstrictors which are angiogenic
factors, and after that, you will have now the
complications. This would be the second phase of
your pre-eclampsia.

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o
Placenta
o PIGF
o VEGF
o Normal Vascularity
o o Pro-Angiogenetic factors
o
o
Versus
o
o sFlt-1
o
o Endoglin
o o Abnormal Vascularity
o o Anti-Angiogenetic factors
o
o WHAT ARE THE EFFECTS OF PRO AND ANTI-
o ANGIOGENIC FACTORS IN THE VASCULAR
o EPITHELIUM?

o Pro-angiogenic factors (PLGF and VEGF) maintains the:

o • Smoothness of the endothelial walls
o
• Modulated response
tovasoconstrictors
• Regulated permeability
• Healthy vessels

Anti-angiogenic factors (sEndo/sFlt-1) promotes the:

STAGE I: ABNORMAL PLACENTATION • Adhesiveness and deposition of cellson
the endothelial walls
o
“ Placental vascular development stage ”
• Increased susceptibility of vessel wallsto
o Vasoconstrictors
Trophoblastic invasion – destruction of the Tunica • Increased permeability
Media of the spiral arterioles
o • Defective vessels
“Ballooning” (VD) of the vessels
o - Normally, the syncytiotrophoblast and
Advancing Age of Gestation – Vasodilatation in the U-
cytotrophoblast should invade the tunica media of
P Compartment
spiral artery of the decidua and the myometrium. So
that if you will invade the muscle of the arteries, you
should be able to transform the small and high
resistance vessels of spiral arterioles to a bigger
and flaccid spiral arteries. Kung na invade nya
yan,lalambot, kasi mai-invade nya yung muscle. So
that in increase in the AOG, you will be able to have
an increase in uterine blood flow, you will have a
normal pregnancy.
- The problem in pre-eclampsia is that your
syncytiotrophoblast will only invade up to the level
of decidua, but not to the level of myometrium. So
that during the increase blood flow, your blood
vessel will not vasodilate. So you will have increase
in pressure or peripheral resistance. Therefore, if
the blood flow is decreased, you will have placental
abnormality.

STAGE 2: MATERNAL SYNDROME

Abnormal placentation----Microvascular endothelial
damage----Intravascular platelet activation and
deposition----Stimulates secretion of Thromboxane A2---
(potent vasoconstrictor)

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• Damage to the vascular endothelium
• Vasocontriction
• Platelet deposition/aggregation
• Increased vascular permeability
----HYP AND ORGAN HYPOPERFUSION
PATHOPHYSIOLOGY OF PRE-ECLAMPSIA IN THE
KIDNEYS
In one sequence: Renal hypoperfusion----Ischemic
damage to the renal tissues----Proteinuria----
• Decreased IV oncotic pressure and Increased
Hydrostatic pressure----Edema
• Decreased Serum Albumin and Increased
Protein in the urine
In another sequence: Renal hypoperfusion----
Decreased Glomerular Filtration Rate----
• Oliguria
• Increased BUN, Creatinine and Uric acid
Dx: Serum Creatinine and Urine Protein
PROTEINURIA
- >300 mg protein/L in a 24 hour
urinecollection
- >1000 mg/L in Random urine collectiontwice, 6
hours apart
- Qualitative/dipstick:
PATHOPHYSIOLOGY OF PRE-ECLAMPSIA IN THE CNS
• Trace – 1+ ---- Mild Proteinuria
• 2+ – 4+ ---- Heavy Proteinuria
In one sequence: CNS----
• Retinal ischemia----Blurring of vision
• Neuronal Ischemia/Irritation----Convulsion
In another sequence: CNS----CVA
In another sequence: Meningeal irritation----Headache
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OBSTETRICS & GYNECOLOGY
Dx: Fundoscopy – retinal detachment: observe until
delivery
PATHOPHYSIOLOGY OF PRE-ECLAMPSIA IN THE CVS
AND PULMONARY SYSTEM
Increased peripheral resistance----Increased afterload---
-Left sided heart failure----CHF (tachycardia)----
Pulmonary edema
Dx: ECG and CXR
PATHOPHYSIOLOGY OF PRE-ECLAMPSIA IN THE GIT
In one sequence: Gastrointestinal tract----liver: common
affected organ; complain: RUQ pain
Liver edema and Hydropic degeneration of the liver cells-
---Stretching of the Glisson’s capsule----
• Liver rupture
• Right upper quadrant/epigastric pain
In another sequence: Gastrointestinal tract----
Liver ischemia----Liver cell necrosis----Release of liver
enzymes (SGPT/ALT) into the blood
Dx: SGPT/ALT and LDH (not SGOT: it is for the heart)
PATHOPHYSIOLOGY OF PRE-ECLAMPSIA IN THE
UTEROPLACENTAL UNIT
In one sequence: Uteroplacental unit----VC and hypoxia to
the inplantation site----Abruptio placenta----
• Disseminated Inravascular
Coagulopathy
• Acute Renal Failure
In another sequence: Uteroplacental unit----
• In Utero Growth Restriction
• Oligohydramnios
• Fetal Death In Utero
Dx: UTZ and Electro-fetal monitoring as well as
Coagulation profile(DIC)
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 OBSTETRICS & GYNECOLOGY

Hemoglobulin – Anemia due to Microangiopathic Hemolysis

VASOCONSTRICTION, PLATELET
DEPOSITION/AGGREGATION AND DAMAGE TO Platelet count – Thrombocytopenia
THE BLOOD VESSEL WALL LDH - ≥600 IU/L (increased)

In one sequence: Vasoconstriction, platelet Blood smear – (+) schistocytes or spherocytes

deposition/aggregation and damage to the blood vessel wall-
---Hypertension Coagulation profile – DIC:
• Protime
In another sequence: Vasoconstriction, platelet • Activated Platelet Count
deposition/aggregation and damage to the blood vessel wall---- • D-dimer test
Decreased circulating platelets----Decreasedactual platelet • Fibrinogen test
count
MINIMUM MATERNAL LABORATORY TESTS THAT
In another sequence: Vasoconstriction, platelet SHOULD BE REQUESTED
deposition/aggregation and damage to the blood vessel wall----
Furthur vessel narrowing---- • Hematocrit and Hemoglobin
• Actual Platelet Count
• Hepatocellular hypoxia and Periportal necrosis-
• Serum Creatinine levels
---Increased liver enzymes
• SGPT/ALT
• Red Blood Cell damage---- • LDH
Microangiopathic hemolysis----Increased LDH • Serum albumin
and Decreased Hemoglobin • Urine protein

(+) Suspicion of HELLP syndrome

HELLP SYNDROME  Coagulation profile
 Blood smear
Hemolysis
SCREENING AND DIAGNOSIS: PREEMPTIVE
• Decreased Haptoglobin (Earliest) - ≤25 mg/dL MANAGEMENT
• Increased LDH - ≥600 IU/L
Risk Identification
• PBS – Damaged Red Blood Cell
(Schistocytes and Burr Cell) • Clinical History

• Decreased Hemoglobin • Physical Examination – Mean Arterial

Pressure and Roll Over Test
Elevated Liver enzymes
• Laboratory Examinations
Low Platelets
• Doppler Velocimetry

PE: Mean Arterial Pressure

RECOMMENDED LABORATORY EVALUATION AND
RATIONALE • MAP = DBP+1/3(SBP-DBP)

• MAP-2 >90 mmHg ---- Increased PIH and

Serum Creatinine – Increased levels = 1.1 mg/dL Perinatal deaths

Serum albumin – Decreased levels • MAP-3 >105 mmHg ---- Increased PIH and
Perinatal deaths
Proteinuria – 300mg/24 hr urine collection
• Absence of a mid-trimester drop in Blood
Urine Protein/Creatinine – 0.3 Pressure may predict future PIH on the
absence of arteriolar
Hematocrit – Increased/Hemoconcentration

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The Roll-Over Test Preclinical In Utero Growth Restriction

and/or Pre-eclampsia
• At 28-32 weeks age of gestation, Baseline BP
reading is taken at Left Lateral Decubitus • Clinical Significance: Early Prediction----
position (to ease the aortocaval Prophylactic Management
compression, increase blood
Combined with sFlt-1 and PLGF predicted onset PE
flow=decrease blood pressure kasi with 83% sensitivity and 95% specificity
maganda ang flow)----Patient is rolled over
to the supine position----BP readings taken Doppler velocimetry plus sFlt-1 increase the sensitivity for
after five minutes----An increase of at least 20 PreTermDelivery because of complication of Pre-
mmHg Diastolic constitutes a positive ROT Eclampsia from 64% to 79% and specificity from 63% to
and you can also predict pre-eclampsia 80%

• Because of Sudden decrease in blood CLINICAL SIGNIFICANCE

volume will lead to Vasoconstriction
(increase blodd pressure) due to Detection rate for pre-eclampsia
Hypereactivity of the vessels to Screening tool:
vasoconstrictors
• Maternal history----46.5%
Serum Markers in the Blood
• Uterine artery Doppler----64.6%
• Elevated sFlt-1/PLGF ratio----High
Predictability for the development of Pre- • History+Doppler----69.4%
Eclampsia
AMONG PATIENTS WITH UTERINE ARTERY
• Clinical Significance: Aids well in the
NOTCHING BY DOPPLER VELOCIMETRY WHERE
prediction and as monitoring guide to
“NOTCHING” MANAGEMENT WE CAN OFFER TO
management
PREVENT/ALLEVIATE THE COMPLICATIONS OF PE?
Doppler velocimetry principle:
Low Dose Aspirin – 80-150 mgs/d (USA - 81 and
• A visual translation of the velocity of blood 100mgs/d)
flow in a vessel
High dose Calcium – 1-2 g/d
• Fast flow----Low Resistance----
Vasodilated LOW DOSE ASPIRIN

• Slow flow----High resistance----  TX-A2/Vasoconstrictor in Platelets < PGI2/Vasodilator

Vasoconstricted or Obstructed
• Uterine Artery Notching is due to“delayed
dilatation” or “resistance to flow” in the
placental vessels following systole when blood
gushes into the vessels during the “relaxed”
state of diastole
(-) Uterine artery notching (18-24 weeks):
• 50% probability the patient will develop pre-
eclampsia
• 30% will develop In Utero Growth
Restriction
• Doppler velocimetry of the uterine
arteries helps in the prediction of
(Prostacyclin) in the Endothelium = Normal
Pregnancy
 TX-A2/Vasoconstrictor in Platelets > PGI2/Vasodilator
in the Endothelium = Pre-eclampsia
Why Low Dose Aspirin?
Aspirin----(-)PG synthetase----Prostaglandin----
• TX-A2----Vasoconstrictor and Platelet
aggregator in Platelets (target of aspirin)
• PC----Vasodilator and (-) Platelet
aggregator in the Endothelium
Why High Dose Calcium?
 Calcium (periphery-cells)----Smooth muscle
contraction (vasoconstriction) in theca media

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- Why do you need calcium, if may constriction na?
 PTH – normally, Increases Ca levels in the blood by
releasing Ca from the bones ang alam ng katawan
mo mababa, at kailangan niya ng maraming Ca
because you are pregnant, so it will release Ca
load to the bones so, therefore Ca will lead to
vasoconstriction
In one sequence: High Dose Calcium----
Central (-) PTH----(-) Ca from the bones to the intravascular
space akala ng katawan marami ng Ca, so will not release
Ca anymore----Decreased Ca concentration intracellularly----
NO Vasoconstriction = Vasodilation
In another sequence: High Dose Calcium/ excess----Increased
Ca excretion in the urine----UROLITHIASIS ask the patient to
increase water intake
REGIMEN TO PREVENT HPN IN PREGNANCY
Yes - (do not interchange!)
• Low Dose Aspirin
• High Dose Calcium
No
• Progestogens
• Low salt intake
• Aerobic Exercise
• Vit C and E
• Bed rest
• Vit B9/Folic acid
• DHA/Fish oils
NICE TO KNOW
 General Principles of Management Pre-eclampsia
with severe features
 Root of all the problems in the definitive management-
---Placenta
 If the baby is TERM or NEAR term with GOOD
survival rate in the nursery----Delivery
 SEVERELY PRETERM FETUS----May TEMPORIZE
Delivery to push the baby to more maturity
What about the risk to the mother while temporizing the
delivery?
Safety of the mother and the fetus should be balanced
Initial Management:
• Stabilization of the mother’s condition
kailangan una lagi ang mommy, kung wala
ang mommy, wala yung baby
• Assessment of fetal well-being
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OBSTETRICS & GYNECOLOGY
• Confirmation of Age of Gestation you can ask
for her first ultrasound, the earliest that
would be the confirmation
• If no ultrasound at all, you have to rely and
trust her with LMP
Universal consensus:
• Delivery at >/= 34 weeks age of gestation
after maternal stabilization
At 34 weeks age of gestation, most Philippine nurseries
have a 80% neonatal survival rate
<24 weeks – pregnancy termination after maternal
stabilization baby not viable
24 - <34 weeks – Expectant management push to a more
maturity, kung pwede until 37weeks as long as mother
is stable and no end-organ damage – Improve perinatal
outcome without increasing maternal morbidity
• Corticosteroids – maturation of lungs of the
baby
• MgSO4 – neuroprotection of both the
mother and baby
- If with end-organ damage, you have to deliver the
baby
PRE-ECLAMPSIA WITH SEVERE FEATURES
Maternal and Fetal Monitoring while TEMPORIZING delivery
for fetal maturity
Maternal:
• VS, Urine Output and S/SX monitoring
• Laboratory monitoring
- CBC with APC
- Creatinine
SGPT, LDH, etc.
Fetal:
• FMC- count movements of baby after eating,
after 2 hrs it should be >10 fetal movements
• BPS
• Fetal Growth Monitoring with (-)/(+) Doppler
velocimetry request for US today, if you
would like to monitor, request again
another 2 weeks, after 2 weeks, every week
you are expecting a growth of 200g/wk.
After 2 weeks the baby should be able to
gain 400mg or more, if not, then the baby is
IUGR. Pero kung lumalaki siya and the baby
is still small, that is constitutionally small
baby.
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 OBSTETRICS & GYNECOLOGY

Indications for delivery:

• At 34 weeks or older
• (+) Maternal deterioration (S/SX and/or
laboratory results)
• (+) Fetal deterioration
What should we do while temporizing the delivery?
Maternal
• Anti-convulsant – MgSO4
• Anti-hypertensives
- Hydralazine
- Labetalol
- Calcium blocker (Nifedipine)
- Low dose Diazoxide
- Nitroprusside
• Delivery
• Maternal Support
Fetal
• Steroids – Enhance fetal lung maturity
• MgSO4 – Enhance CNS maturity

MONITORING WHILE ON MgSO4

 Urine output of at least 30 cc/hr

 (+) Patellar reflex (+1-+2) sx/ssx of Mg toxicity

Monitor every hr
 Respiratory Rate of not <12/min

 Calcium gluconate (10mL in 10% solution) – at the

bedside

 Ideally, MgSO4 level monitoring

 Anticonvulsants must be given at least 24 hours after

the delivery

ECLAMPSIA RECOMMENDATIONS

 Even in the absence of strong evidences, DELIVERY

(CS or Vaginal?) is indicated as soon as the patient
regains consciousness and is oriented

 Since temporization to gain fetal maturity in eclampsia

is very risky

 May opt to do INDUCTION especially if bishop

score is >6/7 of labor because among this group of
patients, uterus is very sensitive to Oxytonin

BLACK – PPT, BOOK

BLUE- recordings

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