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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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Gestational hypertension
Preeclampsia-eclampsia
Chronic hypertension
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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Gestational hypertension
Preeclampsia-eclampsia
Chronic hypertension
Preeclampsia superimposed upon
chronic hypertension
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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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Gestational hypertension
Preeclampsia-eclampsia Chronic hypertension
Superimposed preeclampsia upon
chronic hypertension
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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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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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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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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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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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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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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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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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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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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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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)
chronic hypertension
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