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DEFINITION


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Gestational hypertension

Preeclampsia

Eclampsia

Chronic hypertension

Preeclampsia superimposed uponchronic hypertension


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Elevated BP first detected after 20

weeks of gestation without proteinuria

= transient hypertension

Gestational Hypertension

20th week

of pregnancy

Proteinuria

(

)

Proteinuria

( )

BP N BP

12weeks

postpartum

BP N


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Preeclampsia-eclampsia


Preeclampsia superimposed upon

chronic hypertension


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The syndrome of new onset of hypertension

& proteinuria after 20 weeks of gestation in a

previously normotensive woman

Preeclampsia - Eclampsia

20th week

of pregnancy

Proteinuria

(

)

Proteinuria

( + )

BP N BP

12weeks

postpartum

BP N/


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Preeclampsia-eclampsia


Preeclampsia superimposed upon



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SBP > 140 mmHg and / or DBP > 90 mmHg

that antedates pregnancy, is present before

the 20th week of pregnancy, and persists

longer than 12 weeks postpartum

Chronic Hypertension

Proteinuria

(

)

20th week

of pregnancy

Proteinuria

(

)

BP BP BP BP

12weeks

postpartum

delivery


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Preeclampsia-eclampsia Chronic hypertension

Superimposed preeclampsia upon



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Worsening HT w/ new onset proteinuria

in a woman w/ chronic HT

20th week

of pregnancy

Proteinuria

( )

Proteinuria

( + )

BP BP

Superimposed preeclampsia upon

Underlying HT

12weeks

postpartum

Proteinuria

( - )/(+)

BP


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Endothelial cell dysfunctionappears to be the central

pathomechanism in the pathogenesis

of preeclampsia

Functions of the endothelium Regulate vascular permeability

Regulate vascular cell growth

Mediate inflammatory and

immune mechanism Modulate lipid oxidation

( metabolic activity )

Endothelial dysfunction

An imbalance between relaxing and

contracting factors between

anti -and pro-coagulant mediators

or growth-inhibiting and growth

promoting factors.


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FIGURE 1. Abnormal placentation in preeclampsiaIn normal placental development, invasive cytotrophoblasts of fetal origin invade the maternal spiral arteries,

transforming them from small-caliber resistance vessels to high-calibercapacitance vessels capable of providing

placental perfusion adequate to sustain the growing fetus. During the process of vascular invasion, the

cytotrophoblasts differentiate from an epithelial phenotype to an endothelial phenotype, a process referred to as

pseudovasculogenesis orvascularmimicry ( left) . In preeclampsia, cytotroph oblasts fai l to adopt an inv asiveendothelial pheno type. Instead, invasion of the spiral arteries is shallow, and they remain small caliber, resistance

vessels (r ight). Maynard S,,Annu. Rev. Med. 2008. 59:6178


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1. Placental ischemia

2. Very low-density lipoprotein versus

toxicity-preventing activity3. Immune maladaptation

4. Genetic imprinting

5. Deficiency of catechol-O-

methyltransferase / 2-methoxyestradiol

6. The role of RAS


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Placentaischemia

Endothelial dysfunctionPlacental release of factors

ET-1 TBX NO PG2 ANG II Sensitivity

Renalpressure

natriuresis

Totalperipheral

resistance

HYPERTENSION

Decreased

uterine placental

blood flow

Am J Physiol Heart Circ Physiol 294: H541H550,2008


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Endothelial cell damage Platelet aggregation

Systemic

vasoplasm

Organ flow

Intravascular

coagulation

Placental

ischemia

Lipid peroxides

Cytokines

PGI2 NO Endothelin Mitogenic factors

(eg, PDGF)

Thrombin

Thromboxane A2 Serotonin, PDGF


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Endothelial cell

ICAM 1

oxLDL ANG II TNF-

TNFRAT1RLOX-1

NAD(P)H oxidase

O2

ONOO

eNOS iNOS

NO NF - BMMP-2

Big ET-1

PGI2synthase

ET-1 (132 )

Role of oxidative stress in the mediation of endothelial cell dysfunction

in preeclampsia

Expert Reviews in Molecular Medicine 2006


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The place of oxidative stress in the

three-stage model of the disease

HUM ONTOGENET2(1), 2008, 2938


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6. The role of RAS


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FFA 15 - 20 weeks beforethe onset of clinical

disease

Sera from preeclampsia

women have both a higher

ratio of FFA to albumin

lipolitic activity resultingin enhanced endothelial

cell uptake of FFA

FFA levelsendothelial cell

triglyceride

accumulation

cytokine-mediated

oxidative stress

ischemia-reperfusion mechanisms

activated leukocytesor / and


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6. The role of RAS


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Normal : Interact ion between decidual leukocy tes and

invading cy totrophob last cel ls is essent ial for n ormal

trophob last invasion and development.

NK cells Th1 predominant inflammatory response profile increased

interferon- and TNF- endothelial damage and inflammation systemically

Further investigation !!!!

Shallow invasion of spiral arteries by endovascular cytotrophoblast cells and

endothelial cell dysfunction mediated by an increased decidual release ofcytokines, proteolytic enzymes, and free radical species

Immun maladaptation


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6. The role of RAS


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Genetic factors

Environment factor(deficiency in nutritions?)

Endothelial

damage Placental

deficiency

Increased

demand from

embryo?

Clinical signs of

preeclampsia

??

?

Kanasaki K,Kalluri R, Kidney International,2009


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6. The role of RAS


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Figure 2.The putative role of COMT/2-methoxyestradiol (2-ME) in pregnancy. In

normal pregnancy, 2-ME may have a role in regulating hypoxia-inducible factor (HIF)-

1a in diverse ways. In preeclampsia, low COMT/2-ME levels may induce accumulation

of HIF-1a, vascular defect, placental hypoxia, and inflammatory responses in the

placenta. Such a response may induce placental defects and result in suppression of

placental-derived estradiol and further reduction in 2-ME levels. COMT, catechol-O-

methyltransferase; CYP450, cytochrome 450.


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6. The role of RAS


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Deficient uteroplacental perfusion

pressure and blood flow

Progesterone and

other mediators

Vascular dysfunction:

systemic and multi-organ

effectsReciprocalrenal RAS

Chronic subpressor

angiotensin II

UteroplacentalRAS

Figure 3. Pathogenesis of preeclampsia

Proximate biochemical-molecular event is the activation of uterine RAS. Uterus is

the clipped kidney with reduced perfusion pressure, and the two kidneys are the

nonclipped kidney with reciprocal suppression of renal RAS, which is manifested

in the systemic circulation. RASrenin-angiotensin system.


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Deficient

vascular

remodeling

Vascular

dysfunction

Uteroplacental

insufficiency

Elevated

subpressor

Ang II

Activation

of decidualRAS

Proteinuria

HYPERTENSION

sFLT1 s EnG

Vascular

maladaptation

Placental hypoxia

Kidney

Current Opinion in Nephrology and Hypertension 2007, 16:213220

Figure 4 : Decidual RAS activation and the placental release of antiangiogenic factors may

explain the manifestations of human preeclampsia


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Maternal Outcome

Severe Disease Mild Disease

Hypovolemia Vasoconstriction Platelet Aggregation

presence of underlying disorders:

(maternal susceptibility genes)


hyperhomocysteinemia

thrombophilic disorders

obesity, syndrome X

diabetes mellitus

Placental

Ischemia

Fetal Compromise

Increased STB Deportation

In End-Stage Disease

Cytokine-MediatedOxidative Stress

EC Dysfunction

EC Adhesion

Molecules

(neutrophilrecruitment)

Immune Maladaptation

Genetic Conflict

Shallow Trophoblast

Invasion in

Spiral Arteries

Acute

Atherosis

Balance

abnormal CTB integrin switching

abnormal decidual CK activity ?


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Risk FactorsUnadjusted relative risk

(95% confidence interval)

Age > 40 years, primiparae 1.68 (1.23 2.29)

Age > 40 years, multiparae 1.96 (1.34

2.87)Family history 2.90 (1.70 4.93)

Nulliparity 2.91 (1.28 6.61)

Multiple pregnancy 2.93 (2.04 4.21)

Preexisting diabetes 3.56 (2.54 4.99)

Prepregnancy body mass index

> 354.29 (3.52 5.49)

Previous preeclampsia 7.19 (5.85 8.83)

Antiphospholipis syndrome 9.72 (4.34 21.75)


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SUMMARY THE PATHOMECHANISM OF PREECLAMPSIA


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PENCEGAHAN

PEMBATASAN KALORI, CAIRAN, DIITRENDAH GARAM TIDAK MENCEGAH

HIPERTENSI DALAM KEHAMILANBAHKAN MEMBAHAYAKAN JANIN

MANFAAT ASPIRIN, KALSIUM DLL.BELUM TERBUKTI

DETEKSI DINI DAN PENANGANANCEPAT-TEPAT


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ALUR TERAPI

HIPERTENSI

KARENA

KEHAMILAN

TANPA

PROTEINURIA

HAMIL

< 37 MG

PREEKLAMPSIA

PEMANTAUAN

TEKANAN

DARAH

TERMINASI

KEHAMILAN

HAMIL

> 37 MG

MENINGKAT


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PENGELOLAAN

HIPERTENSI DALAM KEHAMILAN

TANPA PROTEINURIA

JIKA KEHAMILAN < 37 MINGGU

RAWAT JALAN PEMANTAUAN TEKANAN DARAH, PROTEINURIA &

KONDISI JANIN TIAP MINGGU

BILA KONDISI JANIN MEMBURUK / GANGGUAN PER-

TUMBUHAN JANIN RAWAT DAN PERTIMBANGKANTERMINASI KEHAMILAN

JIKA KEHAMILAN > 37 MINGGU

TERMINASI KEHAMILAN


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ALUR TERAPI

PREEKLAMPSIARINGAN

HAMIL

< 37 MG

RAWAT INAP

PEMANTAUAN

TEKANAN DARAH,

PROTEINURIA,

REFLEKS, KONDISI

JANIN

TERMINASI

KEHAMILAN

HAMIL

> 37 MG

KENAIKAN

TEKANAN

DARAH

KENAIKAN

PROTEINURIAGANGGUAN

PERTUMBUHAN

JANIN

PREEKLAMPSIA TERMINASI

KEHAMILAN


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PENGELOLAAN

PREEKLAMPSIA RINGAN

JIKA KEHAMILAN < 37 MINGGU DAN TIDAK

TERJADI PERBAIKAN, LAKUKANPENILAIAN 2 KALI/MG RAWAT JALAN

PEMANTAUAN TEKANAN DARAH, urin, refleks,

kondisi janin.

Banyak istirahat. Dieet biasa

TIDAK PERLU PENGOBATAN

Konseling pasien dan keluarga tntang tanda dan bahaya

preeklamsia dan eklamsia


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PENGELOLAAN

PREEKLAMPSIA RINGAN

JIKA KEHAMILAN < 37 MINGGU DAN TIDAK MEMUNG-KINKAN RAWAT JALAN, RAWAT DI RS

PEMANTAUAN TEKANAN DARAH 2X/HR, PROTEINURIA 1X/HR &KONDISI JANIN

BANYAK ISTIRAHAT

DIIT BIASA

TIDAK PERLU PENGOBATAN

TIDAK PERLU DIURETIK, KECUALI TERDAPAT EDEMA PARU,DEKOMPENSASI KORDIS & GAGAL GINJAL AKUT

PERTUMBUHAN JANIN TERHAMBAT PERTIMBANGKANTERMINASI

PROTEINURIA KELOLA SEBAGAI PREEKLAMPSIA BERAT TEKANAN DIASTOLIK TURUN SAMPAI NORMAL

PASIEN DIPULANGKAN

ISTIRAHAT & PERHATIKAN TANDA PREEKLAMPSIA BERAT

TEKANAN DIASTOLIK NAIK RAWAT


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PENGELOLAAN

PREEKLAMPSIA RINGAN

JIKA KEHAMILAN > 37 MINGGU

PERTIMBANGKAN TERMINASIKEHAMILAN

SERVIKS MATANG LAKUKAN INDUKSIOKSITOSIN 5 IU / 500 ml DEKSTROSE 5% 10

TETES/MENIT ATAU PROSTAGLANDIN SERVIKS BELUM MATANG PROSTA-

GLANDIN / MISOPROSTOL / KATETERFOLEY / BEDAH CAESAR


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ALUR TERAPI

PREEKLAMPSIA

BERAT DAN

EKLAMPSIA ANTI KONVULSAN ANTI HIPERTENSIPASANG INFUS KESEIMBANGAN CAIRAN PENGAWASAN OBSERVASI TANDA

VITAL, REFLEKS, DJJ, EDEMA PARU, UJI

PEMBEKUAN DARAH

ANTI KONVULSAN

GAWAT JANINOLIGURIA

SINDROM

HELLP

KOMA

PERSALINAN 12

JAM (EKLAMPSIA)

/ 24 JAM

(PREEKLAMPSIA)

RUJUK

PARTUS

PERVAGINAM

KEJANG

BEDAH

CAESAR


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PENGELOLAAN

PREEKLAMPSIA BERAT & EKLAMPSIA

PENGELOLAAN KEJANG

ANTI KONVULSAN

PERLENGKAPAN PENGELOLAAN KEJANG

LINDUNGI DARI TRAUMA

BARINGKAN PASIEN UNTUK MENGURANGIRRESIKO ASPIRASI

O2 4-6 LITER/MEN


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PENGELOLAAN

PREEKLAMPSIA BERAT & EKLAMPSIA

PENGELOLAAN UMUM

JIKA DIASTOLIK > 110 mmHg BERIKAN ANTI HIPERTENSI

SAMPAI DIASTOLIK ANTARA 90-100 mmHg PASANG INFUS RINGER LAKTAT

UKUR KESEIMBANGAN CAIRAN

KATETERISASI URIN

JIKA JUMLAH URIN < 300 ML/JAM PANTAU EDEMAPARU

PENGAWASAN

OBSERVASI TANDA VITAL, REFLEKS & DJJ TIAP 1 JAM

LAKUKAN UJI PEMBEKUAN DARAH


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PENGELOLAAN

MAGNESIUM SULFAT

DOSIS AWAL MgSO4 40% 4 g , diencerkan , IV SELAMA 5-10MENIT

DOSISPEMELIHARAAN

MgSO4 40% 6 g drip DENGAN 500cc rl 15 tetesper menit

SEBELUM MgSO4PERIKSA RR

16 KALI/MENITREFLEKS PATELLA +

URIN 30 ML/JAM DALAM 4 JAM TERAKHIRHENTIKANPEMBERIAN

REFLEKS PATELLA

URIN < 30 ML/JAM . FREKUENSIPERNAPASAN


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PENGELOLAAN

DIASEPAM

DOSIS AWAL DIASEPAM 10 MG IV SELAMA 2 MENIT

DOSISPEMELIHARAAN

DIASEPAM 40 MG / 500 ML RINGER LAKTAT

TIDAK MELEBIHI 100 MG/JAM

PEMBERIANMELALUIREKTUM

DIASEPAM 20 MG DALAM SEMPRIT 10 ml

JIKA MASIH ADA KEJANG DOSISTAMBAHAN 10 MG/JAM

DAPAT DIBERIKAN MELALUI KATETER URIN

KE DALAM REKTUM


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PENGELOLAAN

ANTI HIPERTENSI

DOSIS AWAL HIDRALAZIN 5 MG IV SELAMA 5 MENIT

DOSIS

PEMELIHARAAN

HIDRALAZIN TIAP JAM ATAU 12.5 MG IM

TIAP 2 JAM

JIKA TIDAKTERSEDIAHIDRALAZIN

NIFEDIPIN 5 MG SUBLINGUAL, RESPONSTIDAK MEMBAIK 10 MENIT TAMBAHAN 5 MGSUBLINGUAL

LABETOLOL 10 MG IV RESPONS TIDAKMEMBAIK 20 MG IV

METILDOPA 3X 250-500 mg/hari


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PENGELOLAAN PERSALINAN

Harus diusahakan segera setelah keadaan pasien stabil.PREEKLAMPSIA BERAT PERSALINAN DALAM 24 JAM Periksa serviks

Serviks matang, lakukan pemecahan ketuban, induksi persalinan

dengan oksitosin

Jika pervaginam tdk dpt diharapkan PREEKLAMPSIA PERSALINAN DALAM 24 JAM, EKLAMPSIA PERSALINANDALAM 12 JAM, lakukan seksio sesarea

Gawat janin lakukan seksio sesarea

Serviks belum matang, janin hidup , lakukan seksio sesarea


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BILA DILAKUKAN BEDAH CAESAR TIDAK ADA KOAGULOPATI

ANESTESIA TERPILIH ANESTESIA UMUM

JIKA TIDAK TERSEDIA ANESTESI UMUM

JANIN MATI

BBLR

LAKUKAN PERSALINAN PERVAGINAM

JIKA PEMATANGAN SERVIKS BAIK INDUKSI OKSITOSIN 5IU / 500 ML DEKSTROSE 5% ATAU PROSTAGLANDIN


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LAKUKAN RUJUKAN

BILA:

OLIGURIA ( 24 JAMSETELAH KEJANG


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PERAWATAN POSTPARTUM

ANTI KONVULSAN DITERUSKANSAMPAI 24 JAM POSTPARTUM /

KEJANG TERAKHIR

ANTI HIPERTENSI JIKA TEKANAN

DIASTOLIK > 110 mmHg

PEMANTAUAN JUMLAH URIN


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Hipertensi kronik

Jika pasien sblm hamil sudah mndapat obatanti hipertensi dan terkontrol dgn baik,

lanjutkan

Jika tekanan diastol 110 mmHg atau tekanasistol 160 mmHg atau lbh, berikan

antihipertensi

Jika terdapat proteinuri, pikirkan

superimposed preeklamsia, tangani sepertipre eklamsia


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Pantau pertumbuhan dan kondisi janin

Tdk ada komplikasi tunggu sampai aterm

Gawat janin : terminasi

Pertumbuhan janin terhambat : nilai serviks,serviks matang induksi persalinan , belum

matang ya matangkan dulu dgn

prostaglandin atau kateter foley


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Gangguan Plasentasi

(remodelling arteri spiralis)

Hipoperfusi Plasenta

Pelepasan Faktor-faktor dari Plasenta(TNF-, stress oksidatif)

Disfungsi Endotel

Gangguan

Pressure Natriuresis GinjalVasokonstriksi Sistemik

Hipertensi

Patofisiologi Preeklampsia

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