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Synopsis: Preeclampsia
Tim Ruangan Februari 2015

Ramie/Satriyo-Toni-Jeri/Wita-
Nia/Vira/Sandy/Darrell-Wicak/Mandy-Greg-Jaja-
Andy
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Introduction

 Preeclampsia is much more than hypertension and protein- uria

complicating pregnancy – it is a syndrome affecting virtually every
organ system.
 Some organ systems are predominantly affected more than others

 Early preeclampsia (onset <34 weeks) is associated with greater

morbidity than late-onset preeclampsia.
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Risk Factors
for PE
+ Risk Factors for PE
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Pathophysiology of PE
 Cytotrophoblast invasion of
the uterus is shallow, and
endovascular invasion does
not proceed beyond the
terminal portions of the spiral
arterioles.
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Normal Trophoblastic Invasion
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Abnormal Trophoblastic Invasion in PE
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Immunology of PE
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Immunology of Trophoblastic Cells
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Immunology of PE: Two Stage Model
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Role of
Seminal
Exposure
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Immunology of PE
Stage 1 of PE: Inadequate Trophoblastic Invasion

 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.
 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.
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Immunology of PE
Stage 2 of PE: Maternal Syndrome

 Associated with inflammatory response due to syncytiotrophoblastic

stress, hypoxia, or oxidative stress.
 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.
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Updated: 4 stages of PE
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Cerebrovascular Impact
 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.
 Vasogenic  more common
 Cytotoxic
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Cerebral Autoregulation

 Autoregulation: process by which cerebral blood flow (CBF)

remains relatively constant in the face of alterations in cerebral
perfusion pressure
 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 ~60–160mm Hg. Above and
below these limits, autoregulation is lost and CBF becomes
dependent on mean arterial pressure in a linear fashion
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Autoregulation
 Sudden elevations
in BP exceed the
normal CV
autoregulatory
capacity.
 Disruption of
endothelial tight
junctions (BBB) 
vasogenic edema
 Regions of
vasodilatation and
vasoconstriction
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Mechanism of Seizure

 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
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Cardiovascular Changes in PE

 Myocardial Function
 Ventricular remodeling  adaptive response to maintain normal
contractality due to increased afterload of PE
 Diastolic dysfunction

 Ventricular Function
 Increased cardiac afterload due to hypertension
 Preload may be diminished
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Cardiovascular Changes in PE
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Platelet Changes & Activation

 Increased platelet activation, due to:

 Extrinsic factors: endothelial damage
 Intrinsic factors: alterations in platelet-binding sites
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Platelet Changes & Activation
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The Liver in PE

 Macroscopic lesions:
 Periportal hemorrhage
 Ischemic parenchymal
lesions
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The Liver in PE
 Clinical aspects:
 Symptomatic involvement, typically manifest as moderate to
severe right upper, midepigastric or substernal pain and
tenderness
 Asymptomatic levation of serum hepatic transaminase levels –
AST and ALT.
 Hepatic hemorrhage or infarction may extend to form a hepatic
subcapsular hematoma under the Glisson capsule that may
rupture into the peritoneal cavity.
 Acute fatty liver of pregnancy
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Role of
Steroids
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Antihypertensive Agents
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Antihypertensive Agents
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Antihypertensive Agents
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Antihypertensive Agents
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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

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Preeklampsia ringan
vs berat
 ACOG 2013 tidak
merekomendasikan
pembagian ini, karena
morbiditas dan
mortalitas tetap
meningkat signifikan
pada keduanya.
 Disarankan:
preeclampsia without
severe features
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Perubahan pada Kriteria ACOG
2013
 Proteinuria tidak secara absolut dibutuhkan untuk
diagnosis preeklamsia.

 Proteinuria masif (> 5 g) dihapuskan dari kriteria beratnya

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

 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:
 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

 Aspirin dosis rendah (60-80 mg / hari)

 Direkomendasikan pada perempuan dengan risiko tinggi
 RR 0.90 (0.84-0.97), penurunan risiko hingga 17%.
 Efek samping minimal.

 Kalsium (1.5-2 g / hari)

 Direkomendasikan pada perempuan hamil dengan baseline
calcium intake rendah (< 600 mg/hari)
 RR 0.45 (0.31-0.65) pada semua perempuan hamil.
 RR 0.36 (0.20-0.65) pada perempuan hamil dengan baseline
calcium intake rendah.
+ Upaya Pencegahan yang
Tidak Direkomendasikan
 Suplementasi antioksidan dengan Vit C dan Vit E
 Bed rest
 Pembatasan asupan garam
 Penggunaan diuretik
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Prinsip Tatalaksana PE

1. Safety of the woman and her fetus

2. Delivery of a mature newborn that will not require

intensive or prolonged neonatal care.
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Maternal
CBC, liver enzyme, creatinine
at least once weekly

Fetal
Daily kick count
USG every 3 weeks
AFI once weekly
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TERIMA KASIH