Hipertensi Dalam Kehamilan

dr. Adib Ahmad S, SpOG

Tingginya Angka Kematian Ibu Disebabkan :
     Perdarahan
     PE / E  15 - 18%
     Infeksi

UNICEF 2000 : Perdarahan dan PE / E ---- 58,1 %

• Sasaran Th 2010 :
AKI / AKN : 125 / 100.000
AKP : 16 / 1000
 Preeklampsi Salah Satu Penyebab
Kematian Maternal dan Perinatal
   Di RSCM (1994) 687 PE / E dari 4217 persalinan dengan 13 kematian ibu
dan
68 kematian bayi (Noroyono Wibowo)
 Di Negara industri, preeklampsi dijumpai (5-7%) pada wanita
hamil dan menimbulkan kematian pada ibu dan bayi terbanyak
(Prof.Gulardi HW)
 Di Amerika, terjadi pada 6-8% kehamilan dan menyebabkan 15%
kematian ibu (Maternal Mortality Collaborate)
 Di Negara berkembang diprediksi akan menjadi penyebab 1 pada
kematian ibu (WHO)
Major changes of  
PIH
PIH
new classification
 HDP is defined as hypertension in pregnancy.
 Eclampsia was removed from the major
classification.
 Chronic hypertension was added to the major
classification.
 If pregnant women with new onset of hypertension
have either maternal organ dysfunction or
uteroplacental dysfunction, they should be
diagnosed with preeclampsia, even in the
absence of proteinuria.
Major changes of  
PIH
PIH
new classification
 The severity classification should be ‘severe’ when
hypertension is severe, or when hypertension is
mild but there is maternal organ dysfunction or
uterine placental dysfunction. The term ‘mild’
was excluded from the criteria of HDP
because it can be misinterpreted to mean
‘not at high risk’.
 The definition of ‘early onset type’ is that which
appears earlier than 34 weeks gestation, in
accordance with international standards.
 The New Vs. the Old  
PIHPIH
classifications
 Pre-eclampsia does not require the presence
of proteinuria for Dx.
 Pre-eclampsia may be diagnosed if HTN+
– Thrombocytopenia (PLTs<100k)
– Liver injury (ALT/AST > x2 UNL)
– Renal dysfunction (SCr>1.1 or x2 from
baseline)
– Pulmonary edema
– New onset cerebral or visual disturbances
201
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Updated Classification of  
Hypertensive disorders of   PIH
PIH
pregnancy ( ACOG,2013)
201
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 MACAM HIPERTENSI DALAM
KEHAMILAN 

1. Gestational Hipertensi / Transient HT

2. Preeklampsia

3. HT Kronis Superimposed PE

4. HT Kronis
Gestasional Hipertensi
• T  140 / 90 mm Hg selama hamil
• Tidak ada proteinuria
• Tekanan normal < 12 minggu post partum
• Diagnosa biasanya dibuat setelah post partum
• Kadang-kadang ada tanda-tanda preeklampsi
seperti trombositopeni dan epigastric discomfort 
 Predisposisi Preeklampsia
1. Primigravida
2. Hiperplacentosis
             -   Mola Hidatidosa
             -  Gemelli
             -   DM
             -   Hydropsfetalis
3. Umur ekstrem
4. Riwayat Keluarga
5. Penyakit ginjal & HT sebelumnya
• Zweifsi (1916)  " PE the disease of theories "
 banyak teori ttg kemungkinan etiologi PE
1. Teori imunologi
2. Teori genetik
3. Teori iskemik plasenta
4. Teori Hormonal
5. Teori Gizi
Hypertension
 systolic BP ≥140 and/or diastolic BP ≥90 mm Hg.
 Repeated to confirm true hypertension.
 Severe BP (systolic BP ≥160/110 mm Hg), then the BP
should be confirmed within 15 minutes
 Less severe BP, repeated within a few hours.
 Use a liquid crystal sphygmomanometer .If unavailable,
validated calibrated automated device.
 confirmed by 24-hour ABPM or home BP monitoring
Proteinuria
 not required for a diagnosis of preeclampsia.
 assessed initially by automated dipstick urinalysis,
if not available, careful visual dipstick urinalysis
 If positive (≥1+, 30 mg/dL), then spot urine
protein/creatinine (PCr) ratio
 PCr ratio ≥30 mg/mmol (0.3 mg/mg) is abnormal.
 Negative dipstick accepted, not require PCr.
 24hr urine collection still gold standard
 Urine albumin/creatinine ratio (UACR) Quantifies
urine albumin Steps toward standardization
 Massive proteinuria (>5 g/24 h) is associated with
more severe neonatal outcomes
1.Chronic Hypertension
 high BP predating the pregnancy or recognized at
<20 weeks’ gestation.
 often diagnosed at the first or early booking
visits.
 should be confirmed by 24-hour ABPM or home
BP monitoring, or at minimum, after repeated
measurements over hours at the same visit
 The majority because of essential hypertension
 White-coat hypertension not an entirely benign
condition..
 Masked hypertension more difficult to diagnose
2.Gestational Hypertension
 Persistent de novo hypertension that develop at
or after 20 weeks’ gestation in the absence of
features of preeclampsia
 Of women with apparent gestational hypertension,
about ⅓ develop preeclampsia
 maternal and fetal outcomes are usually normal
 High risk of chronic hypertension later in life
3.Preeclampsia
 4. Chronic Hypertension with Superimposed  
Preeclampsia ( CHSP)
 Develop in 25 % of women with chronic
hypertension
 higher in women with underlying renal disease.
Diagnosis
 Experience a sudden exacerbation of hypertension
(not sufficientalone)
 Develop maternal organ dysfunction
 New-onset proteinuria
 Increase in proteinuria in proteinuric renal disease
Severe Preeclampsia
Crises in Preeclampsia
 Eclampsia
 HELLP syndrome
 Pulmonary Edema
 Placental Abruption
 Cerebral
Hemorrhage
 Cortical Blindness
 DIC
 Acute Renal Failure
Early Vs. Late Preeclampsia
EDEMA
Cronic hipertensi superimposed preeklampsia
Hipertensi sebelum 20 minggu
Gejala PE

Cronic Hipertensi
T  140 / 90 sebelum hamil atau didiagnosis sebelum
20 mg
Tetap tinggi setelah 12 mg post partum
 PATOLOGI PREEKLAMSIA
• Vasospasme _______ arteri kecil
Nail beds
Occular fundi
Bulbar conjunctiva

• Resistensi blood flow (angiotensi II ) vasoconstriksi

--------- kerusakan sel endothel

kerusakan intersel endothel
kebocoran pembuluh darah
trombosit dan fibrinogen dalam sub endothel
 Lokal hipoksia jaringan sekitar

Perdarahan, nekrosis, 
gangguan fungsi organ
Iskemik plasenta radical bebas
destruksi endotel keseimbangan komponen
vasodilator dan vasokonstriktor terganggu
Bloodflow menurun perfusi fetomaternal menurun
Isufisiensi plasenta fetal compromise
IUGR
IUFD 
 PREEKLAMPSI

DISFUNGSI ENDOTEL

Struktur Fungsi
NO, Prostacycline ↓
HT
-sintesa
Tromboxan, Endothelin ↑
rusak
-barier Permeabilitas Vasc. ↑ Oedem
proteinuri
Sirk. Endothel -metabolisme

Fibronektin ↑
dll
PATOFISIOLOGI Kegagalan
Plasenta
Penyakit Vaskuler Excessive
Trophoblast
Genetik
Imunologi
Inflamasi

Bahan Vasoaktif Cytokine

Pe  Perfusi Uteroplasenta
Lipid Peroksidase
PG
NO
Endothelin Aktivasi endotel

Vasospasme Kebocoran kapiler Aktivasi koagulasi

Edema Proteinuria

HT
Kejang Hemokonsentrasi
Oligouri Trombositopenia
Solusio
Iskemia hepar
 MARKER UNTUK PREDIKSI PREEKLAMPSI

GLUCOSA OXIDATIVE ABNORMAL TROPHOBALST

INTOLERENCE STRESS INVASION
GCT, Insulin LDL, TRIGLISERIDA, FFA, Dopler Waveform Velocity
Anti Oxidants

ENDOTHELIAL DYSFUNCTION PLACENTAL

Fibrinectin, PGI2, NO, Endothelin
PLATELET FUNCTION
Thromoglobulin, CD63, TxA2, P
Selectin, Fibronectin, Mean
Platelet Volume
PEPTIDES
Activin, Inhibin, bHCG
PREEKLAMPSI
RENAL FUNCTION
Creatinine, Uric Acid
FIBRINOLYTIC ACTIVITY
CYTOKINES PAI-1, PAI-2, TAT III

TNF α, IL-1, IL-6

MULTIORGAN YANG TERLIBAT PADA PE

PLASENTA

GINJAL
PEMBULUH
OTAK
DARAH

HEPAR
KOAGULASI
HEMOPOESIS
Prediction
 No single test or set of tests can reliably
predict the development of preeclampsia
 the routine clinical use of rule-in or rule-out
tests
not recommended
 PlGF or sFlt-1 [soluble fms-like tyrosine kinase-
1]/PlGF ratio for preeclampsia continue to be
evaluated
 Risk Factors ( ACOG, 2019)
High
 History of preeclampsia,
especially when
accompanied by an adverse
outcome
 Multifetal gestation
 Chronic hypertension
 Type 1 or 2 diabetes
 Renal disease
 Autoimmune disease
( SLE, antiphospholipid
syndrome)
moderate
 Nulliparity
 Obesity (BMI > 30)
 Family history of preeclampsia
(mother or sister)
 Sociodemographic
characteristics (African
American race, low socioeconomic
status)
 Age 35 years or older
 Personal history factors
(LBW, SGA, Previous adverse
pregnancy outcome, > 10-year
Prevention
 supplemental calcium (1.2–2.5g/d)
 Low molecular weight heparin is not
indicated
 exercise during pregnancy
 low salt diet
Aspirin prophylaxis
 low-dose aspirin ( preferred dose 81 - 150 mg)
 High risk patient
 Ideally before 16 weeks but definitely
before20 weeks to prevent preterm but not
Prevention ( ACOG , 2019)
Chronic Hypertension
 To maintain BP in the range 110-140/80-85
mmHg.
Home BP monitoring adjunct to clinic visits
 Home device accuracy against a
sphygmomanometer
 Monitor for developing preeclampsia using
urinalysis at each visit with clinical assessment
Blood tests at 28 and 34 weeks as a
minimum.
Indications for delivery similar to preeclampsia
 Gestational hypertension  
Preeclampsia without severe features

ACOG,2019 Level A Recommendation

Gestational Hypertension
Preeclampsia
NO Expectant Management (ACOG,2019)
Maternal Fetal
 Uncontrolled severe BP  Abnormal fetal
( not responsive to antihypertensive ) testing
 Persistent refractory headaches  Fetal death
 Epigastric pain or right upper pain
Persistent  Fetus without
 Visual disturbances, motor deficit or altered expectation for
sensorium
survival at the time
 Stroke
of maternal
 Myocardial infarction
diagnosis
 HELLP syndrome
( lethal anomaly,
 New or worsening renal dysfunction
 Pulmonary edema extreme prematurity)
 Persistent reversed
 Eclampsia
 end-diastolic flow in
Severe Preeclampsia
PENATALAKSANAAN
•Preeklampsia ringan
- Konservatif
- Pantau kesejahteraan janin

Evaluasi Kesejahteraan Janin:

 Non Stress Test
 Profil Biofisik
 Penentuan Biometri (USG)
 Pematangan Paru
 PREEKLAMPSIA BERAT
• Konservatif
– Kehamilan preterm  tidak ada tanda impending 
Eklampsia
• Aktif :
– Kesejahteraan janin jelek
– Ada tanda impending Eklampsia
– Adanya HELLP syndrome
– Kehamilan aterm
– PEB prematur dengan tensi tidak terkendalikan
PEMBERIAN MgSO4 PADA PE / E
Dosis Awal :
 4 gram MgSO4 IV sebagai larutan 20% selama 5 menit
 Dilanjutkan 6 gram MgSO4 dalam 500 cc RL 28 tetes / menit
 Kejang ulang setelah 15 mnt diberikan MgSO4 2 gr (lar. 20%) IV 5 mnt
Pemberian MgSO4 sampai 24 jam post partum atau kejang terakhir

Setelah Pemberian MgSO4 Periksa :

 Frekuensi pernafasan minimal 16 kali / mnt
 Reflek patela +
 Urin minimal 30 cc/jam dalam 4 jam terakhir

Hentikan Pemberian MgSO4 jika Syarat Tak Terpenuhi

Siapkan Antidotum : Ca glukonas 1 gr IV (20 cc dlm larutan 10%)
 KOMPLIKASI
A.Ibu
- CVA
- Decompensasi cordis
- Edema paru
- Gagal ginjal & Hepar
- DIC
-Solusio plasenta
- HELLP syndrome

B. Janin
- Prematuritas
- IUGR
- Gawat Janin
 PENCEGAHAN

Faktor Resiko:
-Primigravida
-Hiperplacentosis
-Umur Ekstrem Janin
-Riw. Keluarga
SEMBUH
-Peny. Ginjal & HT
CACAT
GRAVIDA GX KLINIK
MATI

primer sekunder tersier

ECLAMPSIA
• KONVULSI TONIK – KLONIK
• ANTE – INTRA – POST PARTUM
• TRIMESTER III ATERM
• MATERNAL MORTALITAS
• PROGNOSIS
D D/
• EPILEPSY
• ENCEPHALITIS
• MENINGITIS
• CEREBRAL TUMOR
• RUPTUR CELEBRAL ANORYSMA
EXCLUDED WANITA HAMIL + KONVULSI
ECLAMPSIA
 GEJALA  KLINIS
• Konvulsi Dimulai dari mulut (Facial Twitching)
• Seluruh Badan Rigid (Muscular Contraction) 15 – 20 detik.
• Rahang membuka dan menutup, juga mata
• Bertahap kontraksi otot menurun dan jarang lemas
• Diafragma Fixed Pernafasan Berhenti
• Koma
 KOMPLIKASI ECLAMPSIA
 PULMONARY EDEMA
1. ASPIRASI PNEUMONITIS
2. CARDIAC FAILURE
 BLINDNESS (10 %)
1. RETINAL DETASHMENT
2. OCCIPITAL LOBE ISCHEMIA
INFARCTION EDEMA
PROGNOSA BAIK
 DEATH
– INVASIVE CEREBRAL HAEMORHAGE
 SINDROMA HELLP

Definisi :
Preeklampsia / Eklampsia yang disertai
dengan hemolisis, disfungsi hepar dan
trombositopenia

H : HEMOLISIS
EL : ELEVATED LIVER ENZYMES
LP : LOW PLATELET COUNT
DIAGNOSIS
A. Tidak Khas, seperti infeksi viral : mual,
muntah, nyeri kepala, malaise, lemah
B. Tanda & Gejala PE
Hipertensi
Protein uria
Nyeri epigastrium
Edema
Peningkatan asam urat
C. Tanda kerusakan / disfungsi Sel Hepatosit
kenaikan ALT, AST, LDH

E. Trombositopenia
Trombosit ≤ 150.000 / ml

C. Tanda Hemolisis Intravaskular

peningkatan LDH, ASt dan bilirubin
indirek
Penurunan haptoglobin
Apusan tepi : fragmentasi eritrosit
Kenaikan urobilinogen urin
KLASIFIKASI
A. Klasifikasi Missisipi
Klas I : Trombosit ≤ 50.000 / ml
Serum LDH ≥ 600.000 IU / l
AST dan atau ALT ≥ 40 IU / l

Klas II : Trombosit > 50.000 - ≤ 100.000 / ml

Serum LDH ≥ 600.000 IU / l
AST dan atau ALT ≥ 40 IU / l

Trombosit > 100.000 - ≤ 150.000 / ml

Klas III :
Serum LDH ≥ 600.000 IU / l
AST dan atau ALT ≥ 40 IU / l
B. Klasifikasi Tennesse

Klas Lengkap :

Trombosit < 100.000 / ml

LDH ≥ 600.000 IU / l
AST ≥ 70 IU / l

Klas Tidak Lengkap :

Bila ditemukan hanya satu atau dua

tanda-tanda tersebut di atas
Diagnosis Banding PE – Sindroma HELLP
1. Trombotik angiopati
2. Kelainan konsumtiv fibrinogen ( acute
fatty liver of pregnancy, hipovolemia
berat/perdarahan berat, sepsis )
3. Kelainan jaringan ikat : SLE
4. Penyakit ginjal primer
TERAPI MEDIKAMENTOSA
1. Mengikuti terapi medikamentota PE / E
2. Pemeriksaan laboratorium trombosit dan
LDH tiap 12 jam
3. Bila trombosit < 50.000/ ml atau ada tanda
koagulopati konsumtif maka harus
diperiksa waktu protrombin, waktu
tromboplastin partial dan fibrinogen
4. Dapat dipertimbangkan pemberian :
• Transfusi trombosit bila trombosit
< 50.000 / ml
• antioksidan
5. Pemberian ‘DEXAMETHASONE RESCUE’
a. Antepartum diberikan ‘double strength dexamethasone’
( double dose ) jika didapatkan :
• Trombosit < 100.000 / ml atau
• tro,mbosit 100.000 – 150.000 / ml dan dengan eklampsia,
nyeri epigastrium, hipertensi berat dan atau ‘gejala
fulminan’
Diberikan deksametason 10 mg iv tiap 12 jam
b. Post partum
deksametason 10 mg iv tiap 12 jam sebanyak 2 kali,
kemudian diikuti 5 mg iv tiap 12 jam sebanyak 2 kali
c. Terapi deksametason dihentikan bila telah terjadi :
• Perbaikan laboratorium berupa trombosit > 100.000 / ml
• Penurunan LDH
PENGELOLAAN OBSTETRIK
• Sikap : AKTIF
→ terminasi kehamilan tanpa
memandang usia kehamilan
• pervaginam mapun perabdominam
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Terima Kasih