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Synopsis: Preeclampsia
Tim Ruangan Februari 2015
Ramie/Satriyo-Toni-Jeri/Wita-Nia/Vira/Sandy/
Darrell-Wicak/Mandy-Greg-Jaja-Andy

Introduction
n

Preeclampsia is much more than hypertension and proteinuria complicating pregnancy it is a syndrome affecting
virtually every organ system.
n

Some organ systems are predominantly affected more than others

Early preeclampsia (onset <34 weeks) is associated with

greater morbidity than late-onset preeclampsia.

Risk Factors
for PE

+ Risk Factors for PE

Pathophysiology of PE
n

Cytotrophoblast invasion
of the uterus is shallow,
and endovascular
invasion does not
proceed beyond the
terminal portions of the
spiral arterioles.

Normal Trophoblastic Invasion

Abnormal Trophoblastic Invasion in PE

Immunology of PE

Immunology of Trophoblastic Cells

Immunology of PE: Two Stage Model

Role of
Seminal
Exposure

Immunology of PE
Stage 1 of PE: Inadequate Trophoblastic Invasion
n

Endometrium in an immune tissue.

Uterine NK cells interact with HLA expressed by

trophoblastic tissue have capacity to secrete cytokines and
angiogenic factors promote infiltration of spiral arteries by
invasive trophoblast.
n

Inadequate activation of uterine NK cells may lead to inadequate

invasion.

Maternal T-cells may be activated as well to fetal HLA-C, but

its role is undefined.

Immunology of PE
Stage 2 of PE: Maternal Syndrome
n

Associated with inflammatory response due to

syncytiotrophoblastic stress, hypoxia, or oxidative stress.
n

PIGF, sVEGFR-1, soluble endoglin

Endothelial cells mediate systemic and local inflammatory

responses by upregulation of adhesion molecules that anchor
marginated leukocytes (granulocytes, macrophages, NK
lymphocytes).

Coagulation system, liver, and adipose tissue also contribute

factors to the inflammatory response.

Updated: 4 stages of PE

Cerebrovascular Impact
n

Gross intracerebral
hemorrhage was seen in
up to 60% of eclamptic
women, but it was fatal in
only half .

Most common in the

occipital lobes and least
common in the temporal
lobes

Cerebral edema may

occur, but is frequently
reversible.
n
n

Vasogenic more
common
Cytotoxic

Cerebral Autoregulation

Autoregulation: process by which cerebral blood flow (CBF)

remains relatively constant in the face of alterations in
cerebral perfusion pressure
n

Physiological protective mechanism that prevents brain

ischemia during drops in pressure and prevents capillary damage
and edema from hyperperfusion during pressure increases

In normotensive adults, CBF is maintained at approximately

50mL per 100g of brain tissue per minute (mL/100g/min),
provided perfusion pressure is in the range ~60160mm Hg.
Above and below these limits, autoregulation is lost and
CBF becomes dependent on mean arterial pressure in a
linear fashion

Autoregulation
n Sudden

elevations in BP
exceed the
normal CV
autoregulatory
capacity.
Disruption of
endothelial tight
junctions (BBB)
vasogenic edema
n Regions of
vasodilatation and
vasoconstriction
n

Mechanism of Seizure
n

Seizures consist of excessive release of excitatory

neurotransmitters (especially glutamate), massive
depolarization of network neurons, and bursts of action
potentials.

Fluctuations in neurosteroid levels (progesterone and its

metabolites) during pregnancy result in selective changes in
the expression and function of GABA (inhibitory receptor)
receptors that cause neuronal hyperexcitability

Preeclampsia is a state of altered neuronal GABA receptor

function as well, further making the brain hyperexcitable

Cardiovascular Changes in PE
n

Myocardial Function
n

Ventricular remodeling adaptive response to maintain normal

contractality due to increased afterload of PE

Diastolic dysfunction

Ventricular Function
n

Increased cardiac afterload due to hypertension

Preload may be diminished

Cardiovascular Changes in PE

Platelet Changes & Activation

n Increased
n Extrinsic

platelet activation, due to:

factors: endothelial damage

n Intrinsic factors: alterations in platelet-binding sites

Platelet Changes & Activation

The Liver in PE

n Macroscopic
n Periportal

lesions:

hemorrhage
n Ischemic parenchymal
lesions

The Liver in PE
n Clinical

aspects:

n Symptomatic

involvement, typically manifest as

moderate to severe right upper, midepigastric or
substernal pain and tenderness
n Asymptomatic levation of serum hepatic transaminase
levels AST and ALT.
n Hepatic hemorrhage or infarction may extend to form a
hepatic subcapsular hematoma under the Glisson
capsule that may rupture into the peritoneal cavity.
n Acute fatty liver of pregnancy

Role of
Steroids

Antihypertensive Agents

Antihypertensive Agents

Antihypertensive Agents

Antihypertensive Agents

Pengukuran tekanan darah dilakukan pada posisi duduk nyaman,

cuff pada lengan atas sejajar dengan atrium kiri, pasien tenang dan tidak
berbicara selama pemeriksaan. Pengukuran dilakukan setelah 5 menit
Proteinuria is not absolutely required for the diagnosis of preeclampsia

+
Preeklampsia ringan
vs berat
n

ACOG 2013 tidak

merekomendasikan
pembagian ini, karena
morbiditas dan
mortalitas tetap
meningkat signifikan
pada keduanya.
Disarankan:
preeclampsia without
severe features

Perubahan pada Kriteria ACOG 2013

n Proteinuria

tidak secara absolut dibutuhkan untuk

diagnosis preeklamsia.

n Proteinuria

masif (> 5 g) dihapuskan dari kriteria beratnya

preeklampsia, karena hubungan antara jumlah protein urin dan
luaran kehamilan sangat minimal.

n Pertumbuhan

janin terhambat dihapuskan dari kriteria

beratnya preeklampsia, karena tatalaksananya sama saja
pada pasien dengan atau tanpa preeklamsia.

Temuan yang Membutuhkan

Pengawasan Lebih
Bila diagnosis preeklamsia belum ditegakkan tetapi
ditemukan gejala/tanda berikut, diperlukan pengawasan
lebih ketat:
n

New-onset headache or visual disturbances

Nyeri abdomen, terutama kuadran kanan atas atau epigastrium

PJT

New-onset proteinuria pada paruh kedua masa kehamilan

Peningkatan TD sistolik > 30 mmHg atau diastolik > 15 mmHg

Edema atau peningkatan berat badan yang cepat bukan

kriteria diagnostik dan tidak sensitif maupun spesifik
untuk preeklamsia.

+ Upaya Pencegahan yang

Direkomendasikan
n Aspirin

dosis rendah (60-80 mg / hari)

Direkomendasikan pada perempuan dengan risiko tinggi

n RR 0.90 (0.84-0.97), penurunan risiko hingga 17%.
n Efek samping minimal.
n

n Kalsium

(1.5-2 g / hari)

Direkomendasikan pada perempuan hamil dengan baseline

calcium intake rendah (< 600 mg/hari)
n RR 0.45 (0.31-0.65) pada semua perempuan hamil.
n RR 0.36 (0.20-0.65) pada perempuan hamil dengan baseline
calcium intake rendah.
n

+ Upaya Pencegahan yang

Tidak Direkomendasikan
n Suplementasi
n Bed

antioksidan dengan Vit C dan Vit E

rest

n Pembatasan

asupan garam

n Penggunaan

diuretik

Prinsip Tatalaksana PE
1.
2.

Safety of the woman and her fetus

Delivery of a mature newborn that will not require

intensive or prolonged neonatal care.

Maternal
CBC, liver enzyme, creatinine
at least once weekly
Fetal
Daily kick count
USG every 3 weeks
AFI once weekly

TERIMA KASIH