Kul Blok Repro, Obs DNG Kompl HDK-JT-AB - dm14

1 Kul Blok Reprod, hdk-pj-ab,Daliman.
dm14 Senin, 16 Juli 2018

LATAR BELAKANG.
 Kematian ibu di Indonesia mengalami penurunan
yang belum signifikan dan masih jauh dari harapan.
 Menurut data dari Survey Demografi Kesehatan Indonesia

(SDKI), AKI 1996 sebanyak 450/100.000 kelahiran hidup,
1997 menjadi 373, 2003 yaitu 307 dan 2007 AKI menjadi
228, sedangkan 2008 sekitar 4.692 ibu, meninggal pada
masa kehamilan, persalinan dan nifas, tahun 2012 AKI
sebesar 359.
 Target MDGs 2015, AKI DI Indonesia menjadi 102.
2 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

CAUSE OF MATERNAL DEATH
HHS 2001
1. Bleeding 28%
2. Infection 11%
3. Eclampsia 24%  1+2+3 = 63% (2/3)
4. Abortion 5%
5. Prolong Labour 5%
6. Obstetric Emboli 3%
7. Obstetric Trauma 5%
8. Complication Puerperium 8%
9. Others 11%
Can not handled by Traditional Birth Attendant
We identified 23 eligible studies (published 2003—12). We included
417 datasets from 115 countries comprising 60 799 deaths in the
analysis.
About 73% (1 771 000 of 2 443 000) of all maternal deaths between
2003 and 2009 were due to direct obstetric causes and
deaths due to indirect causes accounted for 27·5% (672 000, 95% UI
19·7—37·5) of all deaths.
Haemorrhage accounted for 27·1% (661 000, 19·9—36·2),

hypertensive disorders 14·0% (343 000, 11·1—17·4), and
sepsis 10·7% (261 000, 5·9—18·6) of maternal deaths. The rest of
deaths were due to abortion (7·9% [193 000], 4·7—13·2), embolism
(3·2% [78 000], 1·8—5·5), and all other direct causes of death (9·6%
[235 000], 6·5—14·3). Regional estimates varied substantially.

MATERI:
1. HIPERTENSI DALAM
KEHAMILAN.
2. PENYAKIT JANTUNG.
3. ASMA BRONCHIALE.

Risk factors PE
1. Nulliparity (3.1)
2. Age >40 years (3:1)
3. Black race (1.5:1)
4. Family history (5:1)
5. Chronic renal disease (20:1)
6. Chronic hypertension (10:1)
7. Antiphospholipid syndrome (10:1)
8. Diabetes mellitus (2:1)
9. Twin gestation (but unaffected by zygosity) (4:1)
10. High body mass index (3:1)
11. Homozygosity for angiotensinogen gene T235 (20:1)
12. Heterozygosity for angiotensinogen gene T235 (4:1)
7 PE, pengelolaan dan sistem rujukan.DM13 Senin, 16 Juli 2018

Etiologi
Etiologi preeklamsia (Cunningham, 2014) belum jelas,
namun kondisi yang dianggap penting berhubungan
dengan etiologi preeklamsia, adalah:
1. Implantasi plasenta dengan ketidaknormalan invasi

trofoblast pada pembuluh darah uterus (a. Spiralis).
2. Maladaptasi toleransi imunologik maternal,
paternal (plasenta) dan jaringan janin.
3. Maladaptasi kardiovaskuler maternal atau
perubahan inflamasi dari kehamilan normal.
4. Faktor genetik termasuk gen predisposisi yang
diwariskan seperti pengaruh epigenetik.
Some Examples of Inherited Immunogenetic
Factors That May Modify Genotype and
Phenotype Expression in Preeclampsia
 "Immunization" from a prior gestation

 Inherited haplotypes for HLA-A, -B, -D, -Ia, -II
 Inherited haplotypes for NK-cell receptors—also
called killer-immunoglobulin-like receptors—KIR
 Possibly shared susceptibility genes with
diabetes and chronic hypertension
HLA = human leukocyte antigen; NK = natural killer.
From Ward and Lindheimer (2009).

Patogenesis
Patogenesis preeklamsia melibatkan kejadian
(Cunningham, 2014) :
1. Vasospasme.
2. Aktivasi sel endotel.
3. Peningkatan respon presor.
4. Nitrix oxide.
5. Endothelins.
6. Protein angiogenik dan antiangiogenik.

FIGURE 35–3 Etiology and
pathogenesis of preeclampsia.
HLA, human leukocyte
antigen-C; INF, interferon; IL,
interleukin; IUGR,
intrauterine growth
restriction; PLGF, placental
growth factor; TGF,
transforming growth factor;
VEGF, vascular endothelial
growth factor.
Copyright © 2011 Elsevier Inc. All

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Conditions of Use and our Privacy
Policy.
For problems or suggestions
concerning this service, please contact:
online.help@elsevier.com

Figure 1. Classic Renin-Angiotensin System Cascade ANG II, the key effector molecule of the RAS and potent
vasoconstrictor, acts through AT1receptors to increase blood pressure. AT1 receptors are found on many cell types.
Abbreviations - ADH: Antidiuretic hormone, ANG II: Angiotensin II, AT1 receptor: angiotensin-II type I receptor. Irani
and Xia Page 17 Placenta. Author
Plasma levels of renin, angiotensin II and aldosterone are increased during
normal pregnancy. However, these values in preeclampsia are decreased
to nearly that of a nonpregnant subject, and vascular sensitivity to
angiotensin II is increased. In preeclampsia, aldosterone is decreased less
than rennin. Therefore current studies were undertaken to determine the
relationship between aldosterone to renin ratio (ARR) and uterine artery
perfusion via RI value.
In the preeclampsia group, RI value of the uterine artery was

significantly higher than that of normal pregnant women. Both plasma
renin and aldosterone concentrations were lower in the preeclampsia
group. However, the ratio of these two parameters was significantly higher
(38.3 vs. 16.1, p < 0.001); the greater ARR, the higher the RI of the uterine
artery (r2=0.053, p = 0.048).
Conclusion
This study demonstrates that a high aldosterone to renin ratio may have a
negative effect on perfusion of the uterine artery and play an important
role in the pathophysiology of preeclampsia.
Yonsei Med J. 2008 February 29; 49(1): 138–143.

Published online 2008 February 20. doi: 10.3349/ymj.2008.49.1.138.
Patofisiologi
Patofisiologi preeklamsia, walaupun etiologinya belum
diketahui dengan pasti, mulai nampak sejak awal
kehamilan meliputi perubahan (Cunningham, 2014) :
 Sistem kardiovaskuler.
 Hemodinamik.
 Volume darah HEMOKONSENTRASI.
 Darah dan koagulasi, seperti trombositopenia
maternal dan neonatal, hemolisis, sindroma HELLP,
dan koagulasi.
 Homeostasis volume, seperti perubahan endokrin,
perubahan cairan dan elektrolit.
Lanjutan..
 Ginjal,seperti proteinuria, perubahan

anatomi, gagal ginjal akut (acute renal failure-
ARF atau acute kidney injury).
 Liver, seperti peningkatan serum

aminotransferase- aspartate transferase (AST)
dan alanine transferase (ALT).
 Otak, seperti lesi neuroanatomik – nekrosis

fibrinoid dinding arteri, infark mikrovaskuler
dan perdarahan, sakit kepala dan skotoma,
kejang eklamsia, kebutaan dan edema serebral
menyeluruh.
TERMINOLOGI
HIPERTENSI DALAM KEHAMILAN.
MENURUT The Working Group of the NHBPEP

(2000), HIPERTENSI DALAM KEHAMILAN, TA. :
1. GESTATIONAL HYPERTENSION.
2. PREECLAMPSIA AND ECLAMPSIA syndrome.
3. PREECLAMPSIA SUPERIMPOSED on chronic
hypertension.
4. CHRONIC HYPERTENSION of eny etiology.

 KLASIFIKASI HIPERTENSI DALAM KEHAMILAN
MENGGAMBARKAN BAHWA ETIOLOGI,
PATOGENESIS, DAN PENANGANAN KLINIK
KEHAMILAN BERBEDA DENGAN HIPERTENSI
DILUAR KEHAMILAN.
 PREEKLAMSIA TERIDENTIFIKASI SEBESAR

3.9% (MARTIN DKK, 2009) DARI SELURUH
KEHAMILAN.
 KEMATIAN IBU DI NEGARA MAJU 16%

OLEH KARENA KELAINAN HIPERTENSI DALAM
KEHAMILAN, 13 % PERDARAHAN, KOMPLIKASI
ABORSI 8% DAN 2% SEPSIS (WHO, 2006).

DIAGNOSIS.
 KENAIKAN TEKANAN DARAH ( MINIMAL ≥
140/90 mmHg ATAU 160/110)
 PROTEINURIA (KECUALI PADA GESTATIONAL

HYPERTENSION DAN HIPERTENSI KRONIK).
 GEJALA LAIN SEPERTI KENAIKAN SERUM

KREATININ, PENURUNAN TROMBOSIT,
PENINGKATAN ALT DAN AST, SAKIT KEPALA,
PANDANGAN KABUR, NYERI EPIGASTRIUM.

“Delta Hipertension” adalah
kenaikan MAP secara tiba-tiba pada
kehamilan trimester III, kenaikan tekan
Sistolik >30 mmHg atau Diastolik >15
mmHg, walaupun tekanan darah
<140/90.
Harus diwaspadai karena dapat timbul

kejang eklamsia dan sindroma
HELLP pada kondisi tersebut.
(Cunningham, et al., 2014)
24 Kul Blok Reprod, hdk-pj-ab,Daliman.14 Senin, 16 Juli 2018
GESTATIONAL HYPERTENSION.
 HIPERTENSI GESTASIONAL BERAT DIDEFINISIKAN SAMA,
KECUALI TEKANAN DARAH ≥ 160/110 mmHg.
 INSIDENSI 6-17% DARI WANITA NULLIPARA SEHAT.
 BATASAN : TEKANAN DARAH MENETAP, 2 KALI

PEMERIKSAAN INTERVAL 6JAM, ≥ 140/90 mmHg SETELAH
KEHAMILAN 20 MINGGU, TANPA PROTEINURIA.
 HIPERTENSI GESTASIONAL DIKAITKAN DENGAN KONDISI

KELUARAN YANG BAIK, WANITA HAMIL RISIKO RENDAH,
SEBALIKANYA PADA GESTASIONAL HIPERTENSI BERAT
DIKAITKAN DENGAN MORBIDITAS TINGGI DIBANDINGKAN
PREEKLAMSIA RINGAN, DALAM INSIDENSI SOLUSIO
PLASENTA, PERSALINAN PRETERM, DAN SGA SEPERTI PRE-
EKLAMSIA BERAT.
PRE-EKLAMSIA/ EKLAMSIA.
 PRE-EKLAMSIA DIDEFINISIKAN TEKANAN DARAH
(MENETAP, 2 KALI PEMERIKSAAN, INTERVAL 6JAM) ≥ 140/90
mmHg (TANPA HIPERTENSI KRONIS), DAN PROTEINURIA
(≥300 mg/ URINE 24 JAM, TANPA PROTEINURIA
SEBELUMNYA).
 PRE-EKLAMSIA BERAT DIDEFINISIKAN

DENGAN MINIMAL SALAH SATU DARI TEKANAN DARAH ≥
160/110 mmHg, PROTEINURIA ≥ 5 g/ 24 JAM URINE,
TROMBOSIT < 100 000, AST DAN/ ATAU ALT ≥ 70 U/L, SAKIT
KEPALA ATAU GANGGUAN SEREBRAL ATAU VISUAL YANG
MENETAP, NYERI EPIGASTRIK MENETAP, EDEMA
PULMONUM DAN OLIGURIA (<500 cc/ 24 JAM).

 SUPERIMPOSED PRE-EKLAMSIA DIDEFINISIKAN
SEBAGAI PROTEINURIA (>/= 300 mg/ 24 JAM, TANPA PROTEINURIA
SEBELUMNYA), SETELAH 20 mgg KEHAMILAN, DISERTAI HIPERTENSI
KRONIS.
 FAKTOR RISIKO DIKAITKAN DENGAN NULLIPARITAS, EKSPOSE

SPERMA TERBATAS, PRIMIPATERNITAS, DONOR SPERMA/ TELUR,
KEHAMILAN GANDA, RIWAYAT PRE-EKLAMSIA, HIPERTENSI KRONIS,
DIBETES, PENYAKIT VASKULER DAN JARINGAN IKAT, NEFROPATI,
ANTIPHOSPHOLIPID SYNDROME (APS), OBESITAS, RESISTEN
INSULIN, IBU USIA MUDA, IBU USIA LANJUT, RAS AFRIKA-AMERIKA,
RIWAYAT KELUARGA PRE-EKLAMSIA, WANITA LBW, STATUS SOSIAL
EKONOMI RENDAH, KENAIKAN sFlt 1, PENURUNAN PlGF, DAN LEBIH
TINGGINYA SEL FETUS DALAM SIRKULASI MATERNAL.

 PRE-EKLAMSIA ADALAH SALAH SATU KOMPLIKASI
KEHAMILAN YANG SERING TERJADI. SATU HAL
PANTING YANG HARUS DIFAHAMI BAHWA TERAPI
UTAMA HANYA KELAHIRAN. PERBAIKAN TERJADI
ANTARA 24-48 JAM. INGAT ADA DUA PASIEN,
KELAHIRAN SELALU BAIK UNTUK IBU, TETAPI TIDAK
SELALU UNTUK BAYINYA, KHUSUSNYA BILA
SANGAT PREMATUR.
 PENCEGAHAN DENGAN PEMBERIAN ASPIRIN DOSIS

50-80 mg/ HARI (19%), KALSIUM (42%), SEMENTARA
PEMBERIAN ANTIOKSIDAN SEPERTI VIT C DAN VIT
E, Magnesium, SUPLEMENTASI FISH OIL, DAN
PEMBATASAN GARAM tidak direkomendasikan lagi.

MAGNESIUM SULFAT (MgSO4)
 MgSO4 ADALAH OBAT PILIHAN UNTUK

PENCEGAHAN EKLAMSIA, MENURUNKAN 59%
RISIKO EKLAMSIA, 36% SOLUSIO PLASENTA, 46%
(STATISTIK TIDAK SIGNIFIKAN) KEMATIAN
MATERNAL.
 SYARAT PEMBERIAN MgSO4 ADALAH REFLEKS

PATELLA +, URINE OUTPUT > 30 CC/JAM, DAN
RESPIRASI > 16 KALI/MENIT, SERTA TERSEDIA
ANTIDOTUMNYA YAITU Ca Gluconas.
 TOKSISITAS MgSO4 BERUPA HILANGNYA REFLEKS

PATELLA, DEPRESI RESPIRASI, PERUBAHAN
KONDISI JANTUNG, CARDIAC ARREST.
OBAT ANTIHIPERTENSI.
DIBERIKAN APABILA TEKANAN SISTOLIK ≥ 160 DAN
ATAU TEKANAN DIASTOLIK ≥ 100.
ALTERNATIF OBAT ANTIHIPERTENSI, ADALAH :
1. Labetalol 20 mg iv bolus, dilanjutkan 40 mg, 80 mg,

80 mg jika diperlukan, setiap 10 menit dengan dosis
maksimal total 220 mg.
2. Nifedipin 10-20 mg po, diulang tiap 30 menit.
3. Hydralazine 5-10 mg iv/ im, tiap 20 menit, dosis
maksimal 30 mg.
4. Sodium nitroprusside dimulai 0,25 ug/kg/min
sampai dosis maksimal 5 ug/kg/min.
KOMPLIKASI PRE-EKLAMSIA.
 IBU, BERUPA HELLP SYNDROME (20%), DIC

(10%), EDEMA PULMONUM (2-5%), SOLUSIO
PLASENTA (1-4%), GAGAL GINJAL (1-2%),
KEJANG EKLAMSIA (<1%), PERDARAHAN
SEREBRAL (<1%), PERDARAHAN HEPAR (<1%)
DAN KEMATIAN (JARANG).
 BAYI, BERUPA PERSALINAN PRETERM (15-

60%), IUGR (10-25%), KEMATIAN PERINATAL (1-
2%), TRAUMA HIPOKSEMIA-NEROLOGIK (<1%),
MORBIDITAS KARDIOVASKULER JANGKA
PANJANG (TIDAK DIKETAHUI)
HIPERTENSI KRONIK DALAM
KEHAMILAN.
 BATASAN – RIWAYAT HIPERTENSI SEBELUM
KEHAMILAN ATAU SEBELUM UMUR KEHAMILAN 20
MGG, DENGAN TEKANAN DARAH ≥ 140/90 mmHg.
 HIPERTENSI KRONIK BERAT APABILA

TEKANAN DARAH ≥ 160/110.
 PADA WANITA DEWASA TIDAK HAMIL TEKANAN

DARAH NORMAL < 120/80, TEKANAN DARAH 120-139/80-89
HIPERTENSI, TEKANAN DARAH 140-159/90-99 HIPERTENSI
DERAJAT I, ≥ 160/100 HIPERTENSI DERAJAT II.

TERAPI HIPERTENSI KRONIK
 PERUBAHAN GAYA HIDUP BERUPA DIET KAYA BUAH,
SAYUR, RENDAH LEMAK, MENGURANGI SATURASI DAN
TOTAL LEMAK, (MENGURANGI MASUKAN GARAM SAMPAI <
2,4 gram/ HARI  TIDAK DIANJURLKAN LAGI).
 BEDREST DI RS DIHUBUNGKAN PENGURANGAN 42%

HIPERTENSI BERAT, 47% PERSALINAN PRETERM.
 OBAT ANTIHIPERTENSI – METHYLDOPA, LABETALOL,

BETABLOKER, NIFEDIPIN, DIURETIK.
 ACE-INHIBITOR KONTRAINDIKASI DIBERIKAN PADA

TRIMESTER PERTAMA, DIHUBUNGKAN DENGAN
PENINGKATAN 2 KALI TERJADINYA MALFORMASI, DAN
JANGKA PANJANG IUGR, OLIGOHIDRAMNION, GAGAL
GINJAL DAN KEMATIAN NEONATUS.
HELLP (HEMOLYSIS, ELEVATED LIVER
ENZYMES AND LOW PLATELET COUNT)
SYNDROME.
 HEMOLYSIS (ANEMIA HEMOLITIK MIKROANGIOPATI,

DENGAN MINIMAL 2 DARI Burr CELL PADA
PEMERIKSAAN DARAH TEPI, SERUM BILIRUBIN
TOTAL ≥ 1,2 mg/dl, SERUM HAPTOGLOBIN RENDAH),
AST ATAU ALT DUA KALI NORMAL ATAU ≥ 70 u/L,
TROMBOSIT <100 000/mm3.
 EPIDEMIOLOGI SEKITAR 72% KASUS

TERDIAGNOSIS ANTEPARTUM DAN 28%
POSTPARTUM (80% < 48 JAM, DAN 20%> 48 JAM).

PENANGANAN HELLP SYNDROME.
 RUJUK KE FASILITAS PELAYANAN TERSIER (< 35 mgg).
 DIMASUKKAN KE AREA PERSALINAN DAN PELAHIRAN.
 MgSO4 IV,
 OBAT ANTIHIPERTENSI, JIKA TEKANAN DARAH >/= 160/110

mmHg.
 PADA KEHAMILAN < 24 DAN >/= 34mgg, NON-REASSURING

FETAL HEART TESTING (NRFHT), MATERNAL DISTRESS
(EKLAMSIA, DIC, RF, SOLUSIO PLASENTA, DISTRESS
RESPIRASI, SUSPEK HEMATOM LIVER  YA 
DILAHIRKAN, JIKA TIDAK (UMUR KEHAMILAN 24-33 mgg)
PEMBERIAN STEROID LENGKAP  DILAHIRKAN.

EKLAMSIA.
 INSIDENSI 1 DIANTARA 2000-3400 KELAHIRAN
DI EROPA DAN NEGARA MAJU, DAN 1 DIANTARA
100 SAMPAI 1 DIANTARA 11.700 KELAHIRAN DI
NEGARA BERKEMBANG.
 DITANDAI DENGAN TERJADI KEJANG ≥ 1 YANG

DIHUBUNGKAN DENGAN PRE-EKLAMSIA.
 KEJANG MUNCUL PADA ANTEPARTUM (40-50%),

INTRAPARTUM (20-35%) ATAU POSTPARTUM (10-
40%). EKLAMSIA POSTPARTUM LANJUT (>48 JAM
TETAPI < 4 mgg), JARANG TETAPI DAPAT
TERJADI.
PENANGANAN EKLAMSIA.
 SEKITAR 15% KASUS, TANPA HIPERTENSI DAN
PROTEINURIA SEBELUM EKLAMSIA, LEBIH DARI
50% KASUS TERJADI PADA KASUS YANG TIDAK
DIDIAGNOSIS PRE-EKLAMSIA, TETAPI HANYA
PENYAKIT RINGAN, PRETERM, DAN TANPA DAPAT
DICEGAH.
 PRIORITAS PERTAMA, ADALAH PENANGANAN

AIRWAY, BRETHING, AND CIRCULATION (ABCs),
PERAWATAN MULTIDISIPLIN, DAN BEBERAPA
PERLU STABILISASI. INTERVENSI TERMASUK
PENILAIAN AIRWAY, POSISI LATERAL DECUBITUS,
MAINTENANCE OKSIGEN 8-10 L/m DENGAN MASK.
TERAPI :
 MgSO4, DOSIS AWAL 6 gram IV BOLUS,
DILANJUTKAN DENGAN DRIPS 2 gram/ JAM,
PEMBERIAN ULANG IV 2 gram MINIMAL 3-5
MENIT KEMUDIAN (JARANG), JIKA PERLU DAPAT
DIBERIKAN Na-AMOBARBITAL 250 mg IV
MINIMAL 3-5 MENIT.
 TEKANAN DARAH DIPERTAHANKAN SEKITAR

140-159/ 90-109 DENGAN OBAT ANTIHIPERTENSI,
SELANJUTNYA DITANGANI SEBAGAIMANA PRE-
EKLAMSIA.

KOMPLIKASI EKLAMSIA
 KEMATIAN MATERNAL 1-2% DI NEGARA MAJU,
LEBIH DARI 10% DI NEGARA BERKEMBANG.
 KEMATIAN PERINATAL 6-12% DI NEGARA

MAJU, LEBIH DARI 25% DI NEGARA BERKEMBANG.
 SOLUSIO PLASENTA 7-10%, DIC 7-11%, HELLP 10-

15%, EDEMA PULMONUM 3-5%, GAGAL GINJAL 5-
9%, PNEUMONIA ASPIRASI 2-3%,
CARDIOPULMONARY ARREST 2-5%, PERSALINAN
PRETERM 50%.

Measurement of Blood Pressure (BP)
1. BP should be measured with the woman in the sitting position with the
arm at the level of the heart. (II-2A)
2. An appropriately sized cuff (i.e., length of 1.5 times the circumference
of the arm) should be used. (II-2A)
3. Korotkoff phase V should be used to designate diastolic BP. (I-A)
4. If BP is consistently higher in one arm, the arm with the higher values
should be used for all BP measurements. (III-B)
5. BP can be measured using a mercury sphygmomanometer, calibrated
aneroid device, or an automated BP device that has been validated for
use in preeclampsia. (II-2A)
6. Automated BP machines may underestimate BP in women with
preeclampsia, and comparison of readings using mercury
sphygmomanometry or an aneroid device is recommended. (II-2A)
7. Ambulatory BP monitoring (by 24-hour or home measurement) may be
useful to detect isolated office (white coat) hypertension. (II-2B)
8. Patients should be instructed on proper BP measurement technique if
they are to perform home BP monitoring. (III-B)
J Obstet Gynaecol Can 2008 Mar;30(3 Suppl 1):S9-15.

40 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 JuliNGC.
2018
Diagnosis of Hypertension
 The diagnosis of hypertension should be based on
office or in-hospital BP measurements. (II-2B)
 Hypertension in pregnancy should be defined as a
diastolic BP of > 90 mm Hg, based on the average of
at least two measurements, taken using the same
arm. (II-2B)
 Women with a systolic BP of > 140 mm Hg should be
followed closely for development of diastolic
hypertension. (II-2B)
 Severe hypertension should be defined as a systolic
BP of ≥160 mm Hg or a diastolic BP of > 110 mm Hg.
(II-2B)
NGC.
Lanjutan…
 For non-severe hypertension, serial BP

measurements should be recorded before a
diagnosis of hypertension is made. (II-2B)
 For severe hypertension, a repeat measurement

should be taken for confirmation in 15 minutes. (III-
B)
 Isolated office (white coat) hypertension should be

defined as office diastolic BP (dBP) of > 90 mm Hg,
but home BP of < 135/85 mm Hg. (III-B)

NGC.
Measurement of Proteinuria
1. All pregnant women should be assessed for proteinuria. (II-2B)
2. Urinary dipstick testing may be used for screening for

proteinuria when the suspicion of preeclampsia is low. (II-2B)
3. More definitive testing for proteinuria (by urinary

protein: creatinine ratio or 24-hour urine collection) is encouraged
when there is a suspicion of preeclampsia, including in
hypertensive pregnant women with rising BP or in normotensive
pregnant women with symptoms or signs suggestive of
preeclampsia. (II-2A)

NGC.

Diagnosis of Clinically Significant
Proteinuria
1. Proteinuria should be strongly suspected when
urinary dipstick proteinuria is > 2+. (II-2A)
2. Proteinuria should be defined as > 0.3 gram/day

(g/d) in a 24-hour urine collection or > 30 mg/mmol
in a spot (random) urine sample. (II-2B)
3. There is insufficient information to make a
recommendation about the accuracy of the urinary
albumin: creatinine ratio. (II-2 I)
NGC.
The basic management
objectives for any pregnancy
complicated by preeclampsia are
(Cunningham, 2014):
1. Termination of pregnancy with the least
possible trauma to mother and fetus
2. Birth of an infant who subsequently thrives
3. Complete restoration of health to the mother.

 In many women with preeclampsia,
especially those at or near term, all three
objectives are served equally well by
induction of labor.
 One of the most important clinical questions

for successful management is precise
knowledge of fetal age.
 Termination of pregnancy is the

only cure for preeclampsia
 Once severe preeclampsia is diagnosed, labor
induction and vaginal delivery have

traditionally been considered ideal.
 Temporization with an immature fetus is

considered subsequently. Several concerns,
including an unfavorable cervix, a perceived
sense of urgency because of the severity of
preeclampsia, and the need to coordinate
neonatal intensive care, have led some to advocate
cesarean delivery.
At that time, most eclampsia regimens used in the
United States adhered to a similar philosophy still in use
today, and the tenets of which include the following:
1. Control of convulsions using an intravenously
administered loading dose of magnesium sulfate.
This is followed by a continuous infusion of
magnesium sulfate
2. Intermittent administration of an antihypertensive
medication to lower blood pressure whenever it is
considered dangerously high
3. Avoidance of diuretics unless there is obvious
pulmonary edema, limitation of intravenous fluid
administration unless fluid loss is excessive, and
avoidance of hyperosmotic agents
4. Delivery of the fetus to achieve a "cure."
Magnesium Sulfate Dosage Schedule Dosage
Schedule for Severe Preeclampsia and
Eclampsia (Cunningham, 2014).
Continuous Intravenous Infusion
1. Give 4- to 6-g loading dose of magnesium sulfate diluted in

100 mL of IV fluid administered over 15–20 min
2. Begin 2 g/hr in 100 mL of IV maintenance infusion. Some
recommend 1 g/hr
3. Monitor for magnesium toxicity: Assess deep tendon reflexes
periodically. Some measure serum magnesium level at 4–6 hr
and adjust infusion to maintain levels between 4 and 7 meq/L
(4.8 to 8.4 mg/dL) Measure serum magnesium levels if serum
creatinine 1.0 mg/dL
4. Magnesium sulfate is discontinued 24 hr after delivery.

 Only offer women with pre-eclampsia
antihypertensive treatment other than
labetalol after considering side-effect
profiles for the woman, fetus and newborn
baby.
 Alternatives include methyldopa† and

nifedipine.†
© 2011 Royal College of Obstetricians and
Gynaecologists
Timing of birth
 Manage pregnancy in women with pre-eclampsia
conservatively (that is, do not plan same-day
delivery of the baby) until 34 weeks.
 Consultant obstetric staff should document in the
woman’s notes the maternal (biochemical,
haematological and clinical) and fetal thresholds for
elective birth before 34 weeks in women with pre-
eclampsia.
 Consultant obstetric staff should write a plan for

antenatal fetal monitoring during birth.
© 2011 Royal College of Obstetricians and Gynaecologists
 Offer birth to women with pre-eclampsia before 34
weeks, after discussion with neonatal and
anaesthetic teams and a course of corticosteroids
has been given if:
 severe hypertension develops refractory to

treatment
 maternal or fetal indications develop as specified
in the consultant plan.

Lanjutan…
 Recommend birth for women who have pre-eclampsia with

severe hypertension after 34 weeks when their blood
pressure has been controlled and a course of corticosteroids
has been completed (if appropriate).
 Offer birth to women who have pre-eclampsia with mild or

moderate hypertension at 34+0 to 36+6 weeks depending
on maternal and fetal condition, risk factors and availability of
neonatal intensive care.
 Recommend birth within 24–48 hours for women who have pre-
eclampsia with mild or moderate hypertension after 37+0
weeks.

Postnatal investigation, monitoring and
treatment (including after discharge from critical care)
Blood pressure
In women with pre-eclampsia who did not take antihypertensive treatment
and have given birth, measure blood pressure:
 at least four times a day while the woman is an inpatient
 at least once between day 3 and day 5 after birth
 on alternate days until normal if blood pressure was abnormal on days
3–5.
In women with pre-eclampsia who did not take antihypertensive

treatment and have given birth, start antihypertensive
treatment if blood pressure is 150/100 mmHg or higher

Offer women with pre-eclampsia who have
given birth transfer to community
care if all of the following criteria have been
met:
 there are no symptoms of pre-eclampsia

 blood pressure, with or without treatment, is
149/99 mmHg or lower

 blood test results are stable or improving.

Severe gestational hypertension or pre-
eclampsia
1. Carry out cardiotocography at diagnosis of
severe gestational hypertension or pre-eclampsia.
2. If conservative management of severe gestational

hypertension or pre-eclampsia is planned carry out
all the following tests at diagnosis:
 ultrasound fetal growth and amniotic fluid volume
assessment.
 umbilical artery Doppler velocimetry.
Some Indications for Delivery with Early-
Onset Severe Preeclampsia (Cunningham 2010):
Maternal
1. Persistent severe headache or visual changes; eclampsia
2. Shortness of breath; chest tightness with rales and/or SaO2 < 94
percent breathing room air; pulmonary edema
3. Uncontrolled severe hypertension despite treatment
4. Oliguria < 500 mL/24 hr or serum creatinine 1.5 mg/dL
5. Persistent platelet counts < 100,000/L
6. Suspected abruption, progressive labor, and/or ruptured
membranes
AFI = amnionic fluid index; EGA = estimated gestational age; SaO2 = oxygen
saturation.
From Sibai and Barton (2007).

Lanjutan…
Fetal
1. Severe growth restriction—< 5th percentile
for EGA
2. Persistent severe oligohydramnios—AFI < 5
cm
3. Biophysical profile 4 done 6 hr apart
4. Reversed end-diastolic umbilical artery flow
5. Fetal death

 Menurut the Centers for Disease Control and
Prevention, penyakit jantung menjadi penyebab
utama kematian wanita umur 25-44 tahun (Kung and
coll., 2008).
 Kelainan jantung dengan berbagai variasi berat dan

komplikasi diperkirakan 1% dari seluruh kehamilan,
bermakna berkontribusi terhadap angka kesakitan
dan kematian maternal.
 Cardiomyopathy dikaitan dengan kematian maternal di USA

sebesar 8% (Chang and coll., 2003).
 Angka Kematian Maternal sebagai akibat komplikasi
penyakit jantung di Brazil sebesar 2,7% (Avila and ass.,
2003), sementara di USA tahun 1991 pada pasien selama
dirawat di RS untuk melahirkan sebesar 7,6% (Callaghan
and ass., 2008).
Kondisi fisiologis pada kehamilan.
 Peningkatan perubahan hemodinamik sebesar
lebih dari 50% puncaknya pada trimester kedua
(midpregnancy) selama 8 minggu dapat
memberikan efek pada wanita berlatarbelakang
penyakit jantung.
 Pada awal kehamilan peningkatan stroke volume

sebagai akibat hasil penurunan resistensi
perifer, sedangkan pada akhir kehamilan
peningkatan stroke volume dan penurunan nadi
akibat dari penambahan pengisian atrium oleh
karena hipervolemia kehamilan.
PERUBAHAN HEMODINAMIK PADA HAMIL ATERM
DAN 12 MINGGU POSTPARTUM (Clark and coll., 1989)
PARAMETER PERUBAHAN (%) KETERANGAN

Cardia output + 43
Heart rate + 17
Left ventricular stroke + 17
work index
Vascular resistance:
 systemic - 21
 pulmonary -34
Mean arterial pressure +4
Colloid osmotic pressure - 14

 Penjelasan adaptasi maternal terhadap kondisi
overload volume natural pada ibu hamil
melibatkan kontrol ekspresi/ fungsi gen dari sinyal
molekul memediasi hipertrofi reversibel (Eghbali
and co-workers, 2006). Kondisi ini diaktivasi oleh
estrogen atau G-protein-couple receptor agonist
seperti endothelin-1 atau angiotensin II.
 Wanita dengan latar belakang penyakit

jantung kemungkinan tidak dapat
beradaptasi dengan perubahan di atas dan
disfungsi ventrikel menyebabkan gagal jantung
kardiogenik.

 Sebagian kecil wanita disfungsi kardiak berat
muncul sebelum midpregnancy, sebagian yang lain
gagal jantung muncul setelah kehamilan 28 minggu,
setelah kehamilan memicu hipervolemia dan
cardaic output meningkat encapai maksimum.
 Kebanyakan kegagalan jantung berkembang

peripartum, ketika kondisi obstetrik pada
umumnya lebih membebani fungsi jantung.
 Pada 542 wanita dengan penyakit jantung,

dilaporkan oleh Etheridge dan Pepperell (1977), 8
dari 10 kematian ibu terjadi peripartum.

INDIKATOR KLINIS PENYAKIT JANTUNG PADA
KEHAMILAN.
TANDA-TANDA:
 SESAK NAFAS PROGRESIF ATAU SESAK NAFAS SAAT
BERBARING.
 BATUK PADA MALAM HARI.
 HEMOPTISIS.
 PINGSAN.
 NYERI DADA.
TEMUAN KLINIK.
 SIANOSIS, CLUBBING OF FINGER.
 DISTENSI V JUGULARIS MENETAP.
 SISTOLIK MUMUR DERAJAT 3/6 ATAU LEBIH.
 DIASTOLIK MUMUR.
 KARDIOMEGALI.
 ARITMIA MENENTAP.
 SPLIT SUARA JANTUNG KEDUA MENETAP.
 KRITERIA HIPERTENSI PULMONAL.
PREDIKTOR KOMPLIKASI KARDIAL,
DIANTARANYA:
1. KEGAGALAN JANTUNG SEBELUMNYA, TRANSIENT

ISCHEMIC ATTACK, ARITMIA ATAU STROKE.
2. BERBASIS NYHA KLAS III ATAU IV, ATAU SIANOSIS.
3. Left-sided obstruction didefinisikan sebagai area

katup mitral kurang dari 2 cm2, area katup aorta
kurang dari 1,5 cm2, atau puncak aliran ventrikel kiri
tract gradient diatas 30 mmHg dengan
echocardiography.
4. Fraksi ejeksi kurang dari 40%.

PENANGANAN PENYAKIT JANTUNG PADA
KEHAMILAN.
1. NYHA I-II, BIASANYA TANPA MORBIDITAS, PERSALINAN
PERVAGINAM, SC JIKA ADA INDIKASI OBSTETRI.
2. NYHA III-IV, 3%, KASUS BERAT, JARANG TERJADI (DI

NEGARA MAJU), DITAWARKAN TERMINASI, JIKA
DILANJUTKAN BERI PENJELASAN RISIKO, PERAWATAN
KETAT DI RS, DAPAT LAHIR PERVAGINAM DENGAN
EPIDURAL ANESTESI, SC JIKA ADA INDIKASI OBSTETRI.
3. KOREKSI PEMBEDAHAN PADA KELAINAN JANTUNG

BAWAAN ATAU DIDAPAT, DILAKUKAN SEBELUM HAMIL
(MORTALITAS MATERNAL 3-4%, LEBIH BANYAK KEMATIAN
JANIN), PERLU PEMILIHAN ANTIKOAGULAN YANG TEPAT.

BEBERAPA PENYAKIT JANTUNG PADA KEHAMILAN.
1. PENAYKIT KATUP JANTUNG (stenosis mitral, insufisiensi

mitral, stenosis aorta, insufisiensi aorta, stenosis pulmonal).
2. PENYAKIT JANTUNG BAWAAN, SEPERTI defek septum (ASD,
VSD, ATRIOVENTRICULAR SEPTAL DEFECT), PERSISTEN
DUCTUS ARTERIOSUS, PENYAKIT JANTUNG SIANOSIS
(tetralogi Fallot, Ebstein anomaly), EISENMENGER
SYNDROME.
3. HIPERTENSI PULMONAL (Idiopatik, left-side atrial or ventricel
disease, left-side valvular disease, chronic obstructive
pulmonary disease, interstitial lung disease, dsb).
4. Kondisi kardiovaskuler lain (Mitral valve prolaps, peripartum
cardiomyopathy, hypertrophic cardiomyopathy, inefective
endocarditis, aritmia).
5. PENYAKIT PADA AORTA (aortic dissection, Marfan syndrome,
coaortasio aortae).
6. ISCHEMIC HEART DISEASE (IHD).
Professional Guide to Diseases (Eighth Edition),
2005
Cardiovascular disease in pregnancy: Causes and
incidence
(Professional Guide to Diseases (Eighth Edition))
Approximately 1% to 2% of pregnant females have cardiac disease,

but the incidence is rising because medical treatment today allows
more females with rheumatic heart disease (present in more than
80% of patients who develop cardiovascular complications) and
congenital defects (present in 10% to 15% of patients) to reach
childbearing age. Coronary artery disease accounts for about 2%
of cardiovascular complications.
Read more at
http://www.wrongdiagnosis.com/h/heart_disease/causes.htm?ktrack=kcplink

The diseased heart is sometimes unable to meet the
normal demands of pregnancy: 25% increase in
cardiac output, 40% to 50% increase in plasma
volume, increased oxygen requirements,
retention of salt and water, weight gain, and
alterations in hemodynamics during delivery. This
physiologic stress often leads to the heart’s failure to
maintain adequate circulation (decompensation).
The degree of decompensation depends on the patient’s

age, the duration of cardiac disease, and the heart’s
functional capacity at the pregnancy’s outset.
Read more at
http://www.wrongdiagnosis.com/h/heart_disease/causes.htm?ktrack=kcplink

Professional Guide to Diseases (Eighth Edition), 2005
Cardiomegaly/Congestive Heart Failure: Differential
Overview
(Field Guide to Bedside Diagnosis)
❑ Congestive heart failure
❑ Hypertensive left ventricular hypertrophy
❑ Anterior myocardial ischemia ❑ Athlete’s heart
❑ Mitral regurgitation, ❑ Aortic stenosis
❑ High output ❑ Hypertrophic obstructive
cardiomyopathy
❑ Pulmonary hypertension ❑ Cor pulmonale
❑ Dilated cardiomyopathy ❑ Endocarditis
❑ Pericardial effusion ❑ Left ventricular aneurysm
❑ Mitral stenosis ❑ Amyloidosis
Read more at
http://www.wrongdiagnosis.com/h/heart_disease/causes.htm?ktrack=kcplin
k
Source: Field Guide to Bedside Diagnosis, 2007
Heart failure: Causes (Handbook of Diseases)

Heart failure may result from a primary abnormality of the heart muscle (such
as an infarction), inadequate myocardial perfusion due to coronary artery
disease, or cardiomyopathy. Other causes include:
 mechanical disturbances in ventricular filling during diastole when there’s too little
blood for the ventricle to pump, as in mitral stenosis secondary to rheumatic heart
disease or constrictive pericarditis and atrial fibrillation
 systolic hemodynamic disturbances such as excessive cardiac workload due to
volume overloading or pressure overload that limit the heart’s pumping ability.
These disturbances can result from mitral or aortic insufficiency, which causes volume
overloading, and aortic stenosis or systemic hypertension, which results in
increased resistance to ventricular emptying.
Reduced cardiac output triggers three compensatory mechanisms: ventricular dilation,

hypertrophy, and increased sympathetic activity. These mechanisms improve cardiac
output at the expense of increased ventricular work.
Read more at http://www.wrongdiagnosis.com/h/heart_disease/causes.htm?ktrack=kcplink

Handbook of Diseases, 2003
Cardiovascular disease in pregnancy: Causes
(Handbook of Diseases)
 Rheumatic heart disease is present in more than 80% of patients
who develop cardiovascular complications. In the rest, these
complications stem from congenital defects (10% to 15%) and coronary
artery disease (2%).
 The diseased heart is sometimes unable to meet the normal demands of

pregnancy: a 25% increase in cardiac output, a 40% to 50% increase in
plasma volume, increased oxygen requirements, retention of salt and
water, weight gain, and alterations in hemodynamics during delivery. This
physiologic stress commonly leads to the heart’s failure to maintain
adequate circulation (decompensation).
 The degree of decompensation depends on the patient’s age,

the duration of cardiac disease, and the functional capacity of the heart
at the outset of pregnancy.
Read more at http://www.wrongdiagnosis.com/h/heart_disease/causes.htm?ktrack=kcplink
Asthma in Pregnancy
 Asthma is one of the most common coexisting medical
conditions affecting reproductive-aged woman. The course of
asthma during pregnancy is variable; one third of patients
improve, one third remain stable, and one third worsen.
 In patients with symptomatic asthma, gestational

weeks 24-36 tend to be the most difficult.
 Only 10% of women experience asthma exacerbation

during labor and delivery, and the severity tends to
revert to that of pregnancy by 3 months' postpartum.
 Asthma is generally expected to follow a similar

course during successive pregnancies.

 A summary of observations during the 20th century
suggests that infant outcome might be worse as
asthma severity increases and that outcome with
aggressive asthma management is usually good.
 A systematic review of the literature revealed that

asthma exacerbations during pregnancy that require
medical intervention occur in about 20% of
women, with approximately 6% of women being
admitted to the hospital. These exacerbations occur
primarily in the late second trimester and are either
triggered by viral infection or nonadherence to
inhaled corticosteroid medication. Severe
exacerbations during pregnancy are a significant risk
factor for a low birth weight baby and inhaled
corticosteroid use may
Kul Blok Reprod, hdk-pj-ab,Daliman.dm14
reduce the risk. [5 ]
78 Senin, 16 Juli 2018
 Clinical features of asthma during pregnancy are the same as
those in the nonpregnant patient. Objective assessment with
pulmonary function tests is essential to assess the presence of
airflow obstruction.
 Inadequate asthma control or factors that are associated with

increased asthma severity during pregnancy leads to lower
pulmonary function, which is associated with increased gestational
hypertension and premature delivery.[6 ]
 One cohort study (performed to estimate the racial differences in

maternal asthma outcomes in a low-income population of pregnant
women in which blacks and whites have similar medical care
access and benefits) found that black women had clinically
significantly more morbidity than whites, thus indicating a racial
difference between the 2.[35 ]
 For excellent patient education resources, visit eMedicine's

Asthma Center. Also, see eMedicine's patient education articles,
Asthma and Asthma in Pregnancy.

Therapy[7,8 ]
Avoidance and control of asthma triggers

Asthma can be triggered by several factors, including allergy, upper
respiratory tract infection, sinusitis, exercise, aspirin, nonsteroidal
anti-inflammatory agents, and irritants (eg, tobacco smoke, chemical
fumes, humidity, emotional upset). Paying close attention to asthma
triggers might improve symptom control, and pregnant patients with
asthma might require less medication.
Strongly encourage smoking cessation in patients with asthma or in

any pregnant patient.
Gastroesophageal reflux is commonly recognized as an asthma
trigger, and approximately one third of pregnant woman have
symptomatic reflux. Initial therapy might consist of small meals and
raising the head of the bed by 6 inches. Some patients might require
antacids or H2-receptor–blocking medications.

Medications during pregnancy
While a natural reluctance exists to prescribe drug therapy in
pregnancy, poorly controlled asthma is potentially more
dangerous for the fetus than medication. The classic teratogenic
period in humans occurs from 4-10 weeks after the last
menstrual period.
Medications are added in a sequential fashion, with few

differences from the nonpregnant patient. A stepped approach
to asthma therapy generally is used.
Also see the clinical guideline summary from the National

Asthma Education and Prevention Program, Managing asthma
during pregnancy: recommendations for pharmacologic
treatment.[9 ]

Office management of asthma
In outpatient asthma management, beta-2 agonists are used for
symptomatic benefit. Inhaled corticosteroids remain the mainstay of
therapy for asthma control. Initiate treatment with the lowest
possible dose of inhaled steroids; the dose can be increased further
as required by symptomatic and objective asthma assessment.
Long-acting adrenergic agonists, such as salmeterol or formoterol,

might be used in symptomatic patients on adequate corticosteroid
therapy. The leukotriene antagonists are the newest agents available
for asthma management. Their exact role in the treatment of asthma
during pregnancy is unclear. No widespread experience has been
gained with the use of these agents in pregnant patients.
Theophylline might be used as a third-line agent after beta-agonist
therapy and inhaled steroids. Extensive experience has been gained
with the use of theophylline during pregnancy, and it does not
appear to cause developmental risk.
Fetal outcome
Asthma can have a number of deleterious effects on pregnancy outcome. An increased
incidence of preterm births, low birth weight, and increased prenatal
mortality largely related to poor asthma control has been reported. Physicians and
patients should not inappropriately avoid the use of effective pharmacologic therapy
because of concerns for fetal effects of drugs.
One recent study examined the effect of inhaled corticosteroids, systemic

corticosteroids, and beta 2-agonists on fetal growth in 654 infants born to
women with asthma compared with 303 infants born to controls without
asthma. Treatment with systemic corticosteroids resulted in a deficit of about 200 g in
birth weight compared with controls and exclusive beta 2-agonist users and no
increased incidence of infants who were small for gestational age. Asthma management
with beta 2-agonists and/or inhaled corticosteroids during pregnancy did not impair
fetal growth.[10 ]

Acute asthma exacerbation[11 ]
Acute exacerbations that necessitate emergency department
visits typically require a course of systemic
corticosteroids. Oxygen should be used liberally, and the
oxygen saturation should be maintained at or above 95% to
ensure fetal well-being. A beta-agonist with or without
ipratropium should be given via a metered-dose inhaler with a
spacer or in nebulized form. Theophylline has limited use in
acute exacerbations. Aggressive management of asthma
exacerbation is recommended because of greater risk to the
fetus from untreated asthma.

PENANGANAN ASTHMA PADA KEHAMILAN.
1. AKUT.
 PENANGANAN ASTHMA AKUT PADA IBU HAMIL SAMA SEPERTI
WANITA TIDAK HAMIL.
 IV HIDRASI, PEMBERIAN OKSIGEN MEMEPERTAHANKAN
saturasi pO2 > 60 mmHg, lebih disukai normal, dengan Oksigen
95%, BETA-ADRENERGIC AGONONIST (terbutalin, albuterol,
isoetharine, epinephrine, isoproterol, atau metaproterenol 
subcutan, oral atau inhalasi), corticosteroid bersama beta-
adrenergic agonist (metyl prednisolon 40-60 mg /6 jam, atau
hydrocortison infus, atau prednison oral dng dosis yang sesuai).
2. KRONIS.
 Edukasi pasien, menjauhi atau mengontrol faktor presipitasi
lingkungan, penilaian objektif fungsi paru dan kesejahteraan
janin, terapi farmakologi.
3. Status asthmaticus (30-60 menit tidak respon terapi intensif)

 RAWAT ICU.
Daftar Pustaka
Cunningham FG, et.al., 2014. Williams Obstetrics, 24rd ed, The McGraw-
Hill Companies,Inc, USA.
James D., 2011. High Risk Pregnancy Management Options, 4th ed, by
Saunders, an imprint of Elsevier Inc. St Louis.
Magee LA, Helewa M, Moutquin JM, von Dadelszen P, Hypertension

Guideline Committee, Society of Obstetricians and Gynaecologists of
Canada. Diagnosis and classification. In: Diagnosis, evaluation, and
management of the hypertensive disorders of pregnancy. J Obstet
Gynaecol Can 2008 Mar;30(3 Suppl 1):S9-15.
National Collaborating Centre for Women’s and Children’s Health,

Commissioned by the National Institute for Health and Clinical
Excellence, 2011. Hypertension in pregnancy : the management of
hypertensive disorders during pregnancy, Published by the Royal
College of Obstetricians and Gynaecologists, 27 Sussex Place,
Regent’s Park, London NW1 4RG, First published August 2010,
revised reprint January 2011

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1 Kul Blok Reprod, hdk-pj-ab,Daliman.

dm14 Senin, 16 Juli 2018

 Menurut data dari Survey Demografi Kesehatan Indonesia

2 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

Haemorrhage accounted for 27·1% (661 000, 19·9—36·2),

4 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

5 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

7 PE, pengelolaan dan sistem rujukan.DM13 Senin, 16 Juli 2018

1. Implantasi plasenta dengan ketidaknormalan invasi

 "Immunization" from a prior gestation

11 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

14 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

Copyright © 2011 Elsevier Inc. All

15 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

In the preeclampsia group, RI value of the uterine artery was

Yonsei Med J. 2008 February 29; 49(1): 138–143.

 Ginjal,seperti proteinuria, perubahan

 Liver, seperti peningkatan serum

 Otak, seperti lesi neuroanatomik – nekrosis

MENURUT The Working Group of the NHBPEP

21 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

 PREEKLAMSIA TERIDENTIFIKASI SEBESAR

 KEMATIAN IBU DI NEGARA MAJU 16%

22 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

 PROTEINURIA (KECUALI PADA GESTATIONAL

 GEJALA LAIN SEPERTI KENAIKAN SERUM

23 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

Harus diwaspadai karena dapat timbul

 INSIDENSI 6-17% DARI WANITA NULLIPARA SEHAT.

 BATASAN : TEKANAN DARAH MENETAP, 2 KALI

 HIPERTENSI GESTASIONAL DIKAITKAN DENGAN KONDISI

 PRE-EKLAMSIA BERAT DIDEFINISIKAN

26 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

 FAKTOR RISIKO DIKAITKAN DENGAN NULLIPARITAS, EKSPOSE

27 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

 PENCEGAHAN DENGAN PEMBERIAN ASPIRIN DOSIS

28 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

 MgSO4 ADALAH OBAT PILIHAN UNTUK

 SYARAT PEMBERIAN MgSO4 ADALAH REFLEKS

 TOKSISITAS MgSO4 BERUPA HILANGNYA REFLEKS

ALTERNATIF OBAT ANTIHIPERTENSI, ADALAH :

1. Labetalol 20 mg iv bolus, dilanjutkan 40 mg, 80 mg,

 IBU, BERUPA HELLP SYNDROME (20%), DIC

 BAYI, BERUPA PERSALINAN PRETERM (15-

 HIPERTENSI KRONIK BERAT APABILA

 PADA WANITA DEWASA TIDAK HAMIL TEKANAN

32 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

 BEDREST DI RS DIHUBUNGKAN PENGURANGAN 42%

 OBAT ANTIHIPERTENSI – METHYLDOPA, LABETALOL,

 ACE-INHIBITOR KONTRAINDIKASI DIBERIKAN PADA

 HEMOLYSIS (ANEMIA HEMOLITIK MIKROANGIOPATI,

 EPIDEMIOLOGI SEKITAR 72% KASUS

34 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

 DIMASUKKAN KE AREA PERSALINAN DAN PELAHIRAN.

 OBAT ANTIHIPERTENSI, JIKA TEKANAN DARAH >/= 160/110

 PADA KEHAMILAN < 24 DAN >/= 34mgg, NON-REASSURING

35 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

 DITANDAI DENGAN TERJADI KEJANG ≥ 1 YANG

 KEJANG MUNCUL PADA ANTEPARTUM (40-50%),

 PRIORITAS PERTAMA, ADALAH PENANGANAN

 TEKANAN DARAH DIPERTAHANKAN SEKITAR

38 Kul Blok Reprod, hdk-pj-ab,Daliman.dm14 Senin, 16 Juli 2018

 KEMATIAN PERINATAL 6-12% DI NEGARA