Pre-eclampsia: pathophysiology, diagnosis, and management

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Abstract

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Introduction
The criteria that define pre-eclampsia have not changed over the past decade. These are:
onset at >20 weeks’ gestational age of 24-hour proteinuria ≥30 mg/day or, if not available, a
protein concentration ≥30 mg (≥1+ on dipstick) in a minimum of two random urine samples
collected at least 4–6 hours but no more than 7 days apart, a systolic blood pressure >140
mmHg or diastolic blood pressure ≥90 mmHg as measured twice, using an appropriate cuff,
4–6 hours and less than 7 days apart, and disappearance of all these abnormalities before the
end of the 6th week postpartum. Nonetheless, some presentations of pregnancy-related
hypertension combined with clinical or laboratory abnormalities or intrauterine growth
restriction should also be considered as potential pre-eclampsia. (Kriteria yang menentukan pre -
eklampsia tidak berubah selama dekade terakhir. ini adalah serangan pada usia kehamilan > 20
minggu dari 24 jam proteinuria ≥30 mg / hari atau, jika tidak tersedia , konsentrasi protein ≥30 mg
(≥1+ pada dipstick ) dalam minimal dua sampel urin secara acak dikumpulkan di setidaknya 4-6 jam
tetapi tidak lebih dari 7 hari terpisah , tekanan darah sistolik > 140 mmHg atau tekanan darah diastolik
≥90 mmHg yang diukur dua kali, menggunakan manset yang tepat, 4-6 jam dan kurang dari 7 hari
terpisah, dan hilangnya semua kelainan ini sebelum akhir minggu postpartum 6 . Meskipun demikian,
beberapa presentasi hipertensi yang berhubungan dengan kehamilan dikombinasikan dengan
kelainan klinis atau laboratorium atau pembatasan pertumbuhan intrauterin juga harus
dipertimbangkan sebagai calon pre – eklampsia)

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Epidemiology
Pre-eclampsia is a multisystem disorder that complicates 3%–8% of pregnancies in Western
countries and constitutes a major source of morbidity and mortality worldwide. Overall,
10%–15% of maternal deaths are directly associated with pre-eclampsia and eclampsia. Some
epidemiological findings support the hypothesis of a genetic and immunological etiology.
The risk of pre-eclampsia is 2-fold to 5-fold higher in pregnant women with a maternal
history of this disorder. Depending on ethnicity, the incidence of pre-eclampsia ranges from
3% to 7% in healthy nulliparas and 1% to 3% in multiparas. Moreover, nulliparity and a new
partner have been shown to be important risk factors. (Pre - eklampsia adalah gangguan multisistem
yang mempersulit 3 % -8 % kehamilan di negara-negara Barat dan merupakan sumber utama morbiditas dan
mortalitas di seluruh dunia . Secara keseluruhan , 10 % -15 % dari kematian ibu secara langsung berhubungan
dengan pre - eklampsia dan eklampsia . Beberapa temuan epidemiologi mendukung hipotesis etiologi genetik
dan imunologi . Risiko pre - eklampsia adalah 2 kali lipat menjadi 5 kali lipat lebih tinggi pada wanita hamil
dengan riwayat ibu dari gangguan ini . Tergantung pada etnis , kejadian pre - eklampsia berkisar antara 3 %
sampai 7 % pada nulipara sehat dan 1 % hingga 3 % pada multipara . Selain itu , nulliparity dan pasangan
baru telah terbukti menjadi faktor risiko penting)

Major risk factors for pre-eclampsia (faktor risiko utama untuk pre – eklampsia)

Other risk factors have been identified, including a medical history of chronic hypertension,
kidney disease, diabetes, obesity, birthplace in Africa, age ≥35 years, and pregnancy
characteristics, such as twin or molar pregnancy, previous pre-eclampsia, or fetal congenital
abnormality. High altitude has also been shown to increase the incidence of pre-eclampsia,
and is attributed to greater placental hypoxia, smaller uterine artery diameter, and lower
uterine artery blood flow. (Faktor risiko lain telah diidentifikasi , termasuk riwayat medis hipertensi
kronis, penyakit ginjal , diabetes , obesitas , tempat kelahiran di Afrika , usia ≥35 tahun , dan karakteristik
kehamilan , seperti kembar atau kehamilan molar , sebelumnya pre - eklampsia , atau bawaan janin kelainan.
ketinggian tinggi juga telah ditunjukkan untuk meningkatkan kejadian pre - eklampsia , dan dikaitkan dengan
hipoksia lebih besar plasenta , diameter arteri uterina yang lebih kecil , dan aliran darah arteri rahim yang
lebih rendah)

Pre-eclampsia may be life-threatening for both mother and child, increasing both fetal and
maternal morbidity and mortality.5 In the mother, pre-eclampsia may cause premature
cardiovascular disease, such as chronic hypertension, ischemic heart disease, and stroke, later
in life, while children born after pre-eclamptic pregnancies and who are relatively small at
birth, have an increased risk of stroke, coronary heart disease, and metabolic syndrome in
adult life. (Pre - eklampsia mungkin bagi ibu dan anak , meningkatkan baik morbiditas dan mortality.5 janin
dan ibu Di ibu, pre - eklampsia dapat menyebabkan penyakit kardiovaskular prematur , seperti hipertensi
kronis, penyakit jantung iskemik, dan stroke yang mengancam jiwa, kemudian dalam hidup, sementara anak-
anak yang lahir setelah kehamilan pre - eklampsia dan yang relatif kecil saat lahir, memiliki peningkatan risiko
stroke, penyakit jantung koroner, dan sindrom metabolik dalam kehidupan dewasa)

The sole curative treatment being delivery, management must continuously balance the risk–
benefit ratio of induced preterm delivery and maternal–fetal complications. Screening women
at high risk and preventing recurrences are also key issues in the management of pre-
eclampsia. (Pengobatan kuratif satunya menjadi pengiriman , manajemen harus terus menyeimbangkan rasio
risiko -manfaat kelahiran prematur diinduksi dan komplikasi ibu-janin . Skrining wanita yang berisiko tinggi
dan mencegah kekambuhan juga isu-isu kunci dalam pengelolaan pre – eklampsia)
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Pathophysiology
During normal pregnancy, the villous cytotrophoblast invades into the inner third of the
myometrium, and spiral arteries lose their endothelium and most of their muscle fibers. These
structural modifications are associated with functional alterations, such that spiral arteries
become low-resistance vessels, and thus less sensitive, or even insensitive, to vasoconstrictive
substances. (Selama kehamilan normal, sitotrofoblas vili menyerang ke sepertiga bagian dalam miometrium ,
dan arteri spiral kehilangan endotelium dan sebagian besar serat otot mereka . modifikasi struktural ini terkait
dengan perubahan fungsional , sehingga arteri spiral menjadi kapal - resistance rendah , dan dengan demikian
kurang sensitif , atau bahkan tidak sensitif , untuk vasokonstriksi zat )

Pre-eclampsia has a complex pathophysiology, the primary cause being abnormal

placentation. Defective invasion of the spiral arteries by cytotrophoblast cells is observed
during pre-eclampsia. Recent studies have shown that cytotrophoblast invasion of the uterus
is actually a unique differentiation pathway in which the fetal cells adopt certain attributes of
the maternal endothelium they normally replace. In pre-eclampsia, this differentiation process
goes awry.13 The abnormalities may be related to the nitric oxide pathway, which contributes
substantially to the control of vascular tone. Moreover, inhibition of maternal synthesis of
nitric oxide prevents embryo implantation.14 Increased uterine arterial resistance induces
higher sensitivity to vasoconstriction and thus chronic placental ischemia and oxidative
stress. This chronic placental ischemia causes fetal complications, including intrauterine
growth retardation and intrauterine death. In parallel, oxidative stress induces release into the
maternal circulation of substances such as free radicals, oxidized lipids, cytokines, and serum
soluble vascular endothelial growth factor 1. These abnormalities are responsible for
endothelial dysfunction15 with vascular hyperpermeability, thrombophilia, and hypertension,
so as to compensate for the decreased flow in the uterine arteries due to peripheral
vasoconstriction. (Pre-eklampsia memiliki patofisiologi yang kompleks, penyebab utama adalah plasentasi
abnormal. invasi yang rusak dari arteri spiral oleh sel sitotrofoblas diamati selama pra-eklampsia. Studi
terbaru menunjukkan bahwa invasi sitotrofoblas rahim sebenarnya diferensiasi jalur yang unik di mana sel-sel
janin mengadopsi atribut tertentu dari endotelium ibu mereka biasanya mengganti. Dalam pre-eklampsia,
proses diferensiasi ini berjalan awry.13 Kelainan mungkin terkait dengan jalur oksida nitrat, yang memberikan
kontribusi besar terhadap kontrol tonus pembuluh darah. Selain itu, penghambatan sintesis ibu dari oksida
nitrat mencegah embrio implantation.14 Peningkatan resistensi arteri rahim menyebabkan sensitivitas yang
lebih tinggi untuk vasokonstriksi dan iskemia plasenta sehingga kronis dan stres oksidatif. iskemia plasenta
kronis ini menyebabkan komplikasi pada janin, termasuk hambatan pertumbuhan dalam kandungan dan
kematian intrauterin. Secara paralel, stres oksidatif menginduksi rilis ke dalam sirkulasi ibu dari zat-zat seperti
radikal bebas, lipid teroksidasi, sitokin, dan serum larut faktor pertumbuhan endotel vaskular 1. Kelainan ini
bertanggung jawab untuk endotel dysfunction15 dengan hyperpermeability vaskular, trombofilia, dan
hipertensi, sehingga untuk mengkompensasi aliran menurun pada arteri uterus akibat vasokonstriksi perifer)

Endothelial dysfunction is responsible for the clinical signs observed in the mother, ie,
impairment of the hepatic endothelium contributing to onset of the HELLP (Hemolysis,
Elevated Liver enzymes and Low Platelet count) syndrome, impairment of the cerebral
endothelium inducing refractory neurological disorders, or even eclampsia. Depletion of
vascular endothelial growth factor in the podocytes makes the endotheliosis more able to
block the slit diaphragms in the basement membrane, adding to decreased glomerular
filtration and causing proteinuria. Finally, endothelial dysfunction promotes microangiopathic
hemolytic anemia, and vascular hyperpermeability associated with low serum albumin causes
edema, particularly in the lower limbs or lungs. (disfungsi endotel bertanggung jawab untuk tanda-
tanda klinis yang diamati pada ibu , yaitu , penurunan endotel hati berkontribusi terhadap timbulnya HELLP
yang ( Hemolisis , enzim Peningkatan hati dan hitung Low Platelet ) sindrom , gangguan endotel otak
merangsang gangguan saraf tahan api , atau bahkan eklampsia . Penipisan faktor pertumbuhan endotel
vaskular di podocytes membuat endotheliosis lebih mampu memblokir diafragma celah di membran basal ,
menambah penurunan filtrasi glomerulus dan menyebabkan proteinuria . Akhirnya , disfungsi endotel
mempromosikan mikroangiopati anemia hemolitik , dan hyperpermeability vaskular yang terkait dengan
albumin serum yang rendah menyebabkan edema , khususnya di tungkai bawah atau paru-paru)

The crucial issue to understand is that the prime mover of pre-eclampsia is abnormal
placentation. Two common theories appear to be interlinked, ie, a genetic theory and an
immunological theory. Several susceptibility genes may exist for pre-eclampsia. These genes
probably interact in the hemostatic and cardiovascular systems, as well as in the
inflammatory response. Some have been identified, and in candidate gene studies they have
provided evidence of linkage to several genes, including angiotensinogen on 1-q42–43 and
eNOS on 7q36; other main important loci are 2p12, 2p25, 9p13, and 10q22.1. (Isu penting untuk
dipahami adalah bahwa penggerak utama dari pre - eklampsia adalah plasentasi abnormal. Dua teori umum
tampaknya saling terkait , yaitu, theory1, genetik dan gen kerentanan theory. Several imunologis mungkin ada
untuk pre - eclampsia. gen ini mungkin berinteraksi di hemostatik dan kardiovaskular sistem , serta di respon
inflamasi . Beberapa telah diidentifikasi , dan dalam studi gen kandidat mereka telah memberikan bukti
hubungan ke beberapa gen , termasuk angiotensinogen atas 1 - q42-43 dan eNOS pada 7q36 ; lokus penting
utama lainnya adalah 2p12 , 2p25 , 9p13 , dan 10q22.1)

Pre-eclampsia can be perceived as an impairment of the maternal immune system that

prevents it from recognizing the fetoplacental unit. Excessive production of immune cells
causes secretion of tumor necrosis factor alpha which induces apoptosis of the extravillous
cytotrophoblast. The human leukocyte antigen (HLA) system also appears to play a role in
the defective invasion of the spiral arteries, in that women with pre-eclampsia show reduced
levels of HLA-G and HLA-E. During normal pregnancies, the interaction between these cells
and the trophoblast is due to secretion of vascular endothelial growth factor and placental
growth factor by natural killer cells. High levels of soluble fms-like tyrosine kinase 1 (sFlt-1),
an antagonist of vascular endothelial growth factor and placental growth factor, have been
found in women with pre-eclampsia. Accordingly, assays of sFlt-1, placental growth factor,
endoglin, and vascular endothelial growth factor, all of which increase 4–8 weeks before
onset of the disease, may be useful predictors of pre-eclampsia. Recent data show the
protective role of heme oxygenase 1 and its metabolite, carbon monoxide, in pregnancy, and
identify this as a potential target in the treatment of pre-eclampsia. (Pre-eklampsia dapat dianggap
sebagai gangguan dari sistem kekebalan tubuh ibu yang mencegah dari mengenali unit fetoplasenta. produksi
berlebihan dari sel-sel kekebalan tubuh menyebabkan sekresi tumor necrosis factor alpha yang menginduksi
apoptosis dari cytotrophoblast. ekstravili The leukosit manusia antigen (HLA) sistem juga tampaknya
memainkan peran dalam invasi yang rusak dari arteri spiral, bahwa wanita dengan pra eklampsia
menunjukkan menurunnya tingkat HLA-G dan HLA-E. Selama kehamilan normal, interaksi antara sel-sel ini
dan trofoblas adalah karena sekresi faktor pertumbuhan endotel vaskular dan faktor pertumbuhan plasenta
oleh sel-sel pembunuh alami. Tingginya kadar larut fms-seperti tyrosine kinase 1 (sFlt-1), antagonis faktor
pertumbuhan endotel vaskular dan faktor pertumbuhan plasenta, telah ditemukan pada wanita dengan pre-
eclampsia. demikian, tes dari sFlt-1, plasenta faktor pertumbuhan, Endoglin, dan faktor pertumbuhan endotel
vaskular, yang semuanya meningkatkan 4-8 minggu sebelum timbulnya penyakit, mungkin indikator yang pre-
eklampsia. Data terbaru menunjukkan peran protektif dari heme oxygenase 1 dan metabolitnya, karbon
monoksida, kehamilan, dan mengidentifikasi ini sebagai target potensial dalam pengobatan pra-eclampsia.20)
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Clinical presentation and workup findings

Clinical and laboratory tests are intended to define and determine the severity of pre-
eclampsia. Headaches, tinnitus, phosphene signals, visual disorders, brisk tendon reflexes,
and vigilance disorders are related to cerebral edema; oliguria to acute renal failure; uterine
contraction, vaginal bleeding to placental abruption; vomiting to HELLP syndrome; band-
like epigastric pain to subcapsular hepatic hematoma; and dyspnea to cardiac failure.
Eclampsia, the major neurological complication of pre-eclampsia, is defined as a convulsive
episode or any other sign of altered consciousness arising in a setting of pre-eclampsia, and
which cannot be attributed to a pre-existing neurological condition. Clinical examination
should include resting blood pressure measurement using an appropriate cuff, and screening
for weight gain, edema (including signs of acute pulmonary edema and cerebral edema),
cardiomyopathy, and acute renal failure. The fetus should be assessed by
electrocardiotocography. Laboratory tests include: a complete blood count with platelets,
haptoglobin, and lactate dehydrogenase; a blood smear to test for schistocytes; bilirubin,
aspartate transaminase, and alanine transaminase in order to identify potential HELPP
syndrome; electrolyte, urea, and creatinine assessment to check for acute renal failure or
uremia; 24-hour proteinuria; prothrombin, activated thrombin time, and fibrinogen
(microangiopathic hemolytic anemia); blood group; and irregular antibody screening. Other
examinations include fetal ultrasound with Doppler velocimetry of the umbilical, cerebral,
and uterine arteries, estimation of fetal weight, assessment of fetal well-being by Manning
score, and examination of the placenta. (uji klinis dan laboratorium dimaksudkan untuk mendefinisikan
dan menentukan keparahan pre-eklampsia. Sakit kepala, tinnitus, sinyal phosphene, gangguan visual, refleks
tendon cepat, dan gangguan kewaspadaan terkait dengan edema serebral; oliguria gagal ginjal akut; kontraksi
uterus, perdarahan vagina untuk solusio plasenta; muntah untuk sindrom HELLP; Band-seperti nyeri
epigastrium ke subkapsular hematoma hati; dan dyspnea untuk gagal jantung. Eklampsia, komplikasi
neurologis utama pre-eklampsia, didefinisikan sebagai episode kejang atau tanda-tanda lain dari kesadaran
diubah timbul dalam pengaturan pra-eklampsia, dan yang tidak dapat dikaitkan dengan kondisi neurologis
yang sudah ada. pemeriksaan klinis harus mencakup beristirahat pengukuran tekanan darah menggunakan
manset yang tepat, dan penyaringan untuk mendapatkan berat badan, edema (termasuk tanda-tanda edema
akut paru dan edema serebral), kardiomiopati, dan gagal ginjal akut. Janin harus dinilai oleh
electrocardiotocography. Tes laboratorium meliputi: hitung darah lengkap dengan trombosit, haptoglobin, dan
laktat dehidrogenase; noda darah untuk menguji schistocytes; bilirubin, transaminase aspartat, dan
transaminase alanin untuk mengidentifikasi potensi sindrom HELPP; elektrolit, urea, dan penilaian kreatinin
untuk memeriksa gagal ginjal akut atau uremia; 24 jam proteinuria; protrombin, diaktifkan waktu trombin, dan
fibrinogen (anemia hemolitik mikroangiopati); golongan darah; dan skrining antibodi yang tidak teratur.
Pemeriksaan lainnya termasuk ultrasound janin dengan Doppler velocimetry dari pusar, dan arteri rahim
serebral, estimasi berat janin, penilaian kesejahteraan janin dengan skor Manning, dan pemeriksaan placenta.)

Although the definition of severe pre-eclampsia varies, several components of this definition
are usually accepted: maternal systolic blood pressure ≥160 mmHg or diastolic blood
pressure ≥110 mmHg; maternal neurological disorders such as persistent headaches,
phosphene signals, tinnitus, and brisk, diffuse, polykinetic tendon reflexes, eclampsia, acute
pulmonary edema, proteinuria ≥5 g/day, oliguria <500 cc/day, creatinine >120 μmol/L,
HELLP syndrome, thrombocytopenia <100,000/mm3, and fetal criteria, especially
intrauterine growth retardation, oligohydramnios, or fetal death in utero. Mild pre-eclampsia
is defined as diastolic blood pressure ≥90 mmHg measured on two occasions at least 6 hours
apart, combined with proteinuria (two or more occurrences of protein on dipstick, >300 mg
total protein in a 24-hour urine collection, or a protein creatinine ratio >30 mg/mmol).1
(Meskipun definisi pre - eklampsia berat bervariasi , beberapa komponen dari definisi ini biasanya diterima :
tekanan darah sistolik ibu ≥160 mmHg atau tekanan darah diastolik ≥110 mmHg ; gangguan neurologis ibu
seperti sakit kepala terus-menerus , sinyal phosphene , tinnitus , dan cepat , menyebar , refleks tendon
polykinetic , eklampsia , edema paru akut , proteinuria ≥5 g / hari , oliguria < 500 cc / hari , kreatinin > 120
umol / L , HELLP sindrom , trombositopenia < 100.000 / mm3 , dan kriteria janin , terutama intrauterine
keterbelakangan pertumbuhan , oligohidramnion , atau kematian janin dalam rahim . Mild pre - eklampsia
didefinisikan sebagai tekanan darah diastolik ≥90 mmHg diukur pada dua kesempatan setidaknya 6 jam
terpisah , dikombinasikan dengan proteinuria ( dua atau lebih kejadian dari protein pada dipstick , > 300 mg
protein total dalam koleksi urin 24 - jam , atau rasio kreatinin protein > 30 mg / mmol ) )

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Immediate emergency management

Delivery is the only curative treatment for pre-eclampsia. Management is multidisciplinary,
involving an obstetrician, an anesthetist, and a pediatrician. In some cases consultation of
maternal fetal medicine and hypertension or nephrology subspecialists may be required.
Management decisions must balance the maternal risks of continued pregnancy against the
fetal risks associated with induced preterm delivery. The criteria for delivery are based on
two often interrelated factors, ie, gestational age at diagnosis (estimated fetal weight) and
severity of pre-eclampsia.(Persalinan adalah satu-satunya pengobatan kuratif untuk Manajemen pra -
eclampsia. adalah multidisiplin , yang melibatkan seorang dokter kandungan , ahli anestesi , dan dokter anak .
Dalam beberapa kasus konsultasi kedokteran janin ibu dan hipertensi atau nefrologi subspecialists mungkin
diperlukan . keputusan manajemen harus menyeimbangkan risiko ibu hamil terus terhadap risiko janin terkait
dengan prematur disebabkan delivery. Kriteria untuk pengiriman didasarkan pada dua faktor sering saling
terkait, yaitu , usia kehamilan saat diagnosis ( perkiraan berat janin ) dan beratnya pre - eklampsia)

Severe pre-eclampsia requires treatment with a dual aim, ie, preventing the harmful effects of
elevated maternal blood pressure and preventing eclampsia. Management of severe pre-
eclampsia begins with transfer of the mother in a fully equipped ambulance or helicopter to a
maternity ward providing an appropriate level of care for both mother and child. At
admission and daily thereafter, clinical, cardiotocographic, laboratory, and ultrasound testing
are required to detect the severity of pre-eclampsia and tailor management accordingly.(Parah
pre - eklampsia memerlukan pengobatan dengan tujuan ganda , yaitu , mencegah efek berbahaya dari tekanan
darah ibu tinggi dan mencegah eclampsia . Manajemen pre - eklampsia berat dimulai dengan pemindahan ibu
dalam ambulans yang lengkap atau helikopter ke bangsal bersalin menyediakan tingkat perawatan yang tepat
bagi ibu dan child. Pada penerimaan dan setiap hari setelahnya , klinis , cardiotocographic , laboratorium ,
dan USG pengujian yang diperlukan untuk mendeteksi tingkat keparahan pre - eklampsia dan manajemen
penjahit sesuai)

Regardless of the severity of pre-eclampsia, there is no advantage in continuing the

pregnancy when pre-eclampsia is discovered after 36–37 weeks. Nor is expectant
management justified for severe pre-eclampsia before 24 weeks, in view of the high risk of
maternal complications and the poor neonatal prognosis. The obstetric team must then
discuss with the parents the possibility of a medical interruption of pregnancy. Prolongation
of pregnancy in the event of mild pre-eclampsia can be discussed and re-evaluated on a
regular basis. At 34 –37 weeks, management depends on the severity of the pre-eclampsia.
Expectant management is possible for mild pre-eclampsia to limit the risk of induced preterm
delivery, but for severe pre-eclampsia, delivery remains the rule due to the increased risk of
maternal and fetal complications.(Terlepas dari keparahan pre - eklampsia , tidak ada keuntungan dalam
melanjutkan kehamilan ketika pre - eklampsia ditemukan setelah 36-37 weeks. Juga tidak manajemen hamil
dibenarkan untuk pre - eklampsia berat sebelum 24 minggu , mengingat risiko tinggi komplikasi ibu dan
prognosis. neonatal miskin tim obstetri kemudian harus mendiskusikan dengan orang tua kemungkinan
gangguan medis kehamilan . Perpanjangan kehamilan dalam hal ringan pre - eklampsia dapat dibahas dan
dievaluasi secara teratur . Pada 34 -37 minggu , manajemen tergantung pada tingkat keparahan pra eklampsi .
manajemen hamil mungkin untuk ringan pre - eklampsia untuk membatasi risiko kelahiran prematur diinduksi ,
tapi untuk pre - eklampsia berat , pengiriman tetap aturan karena peningkatan risiko komplikasi ibu dan janin )

Similarly, at 24–34 weeks, management depends on the severity of pre-eclampsia. The

presence of one or more of the following signs indicates the need for immediate delivery:
uncontrolled severe hypertension (not responsive to dual therapy), eclampsia, acute
pulmonary edema, abruptio placentae, subcapsular hepatic hematoma, or thrombocytopenia
<50,000/mm3. Delivery after corticosteroid therapy for pulmonary maturation is necessary if
any of the following criteria is present: persistent epigastric pain, signs of imminent
eclampsia (headaches or persistent visual disorders), de novo creatinine >120 μmol/L,
oliguria below 20 mL/hour, progressive HELLP syndrome, prolonged or severe variable
decelerations with short-term variability less than 3 milliseconds. When emergency delivery
is not required, labor can be induced by cervical ripening.(Demikian pula , di 24-34 minggu ,
manajemen tergantung pada tingkat keparahan pre - eklampsia . Kehadiran satu atau lebih dari tanda-tanda
berikut ini menunjukkan kebutuhan untuk pengiriman segera : hipertensi berat yang tidak terkontrol ( tidak
responsif terhadap terapi ganda ) , eklampsia , edema paru akut , solusio plasenta , hematoma hati subkapsular
, atau trombositopenia < 50.000 / mm3 . Pengiriman setelah terapi kortikosteroid untuk pematangan paru
diperlukan jika salah satu kriteria berikut hadir : nyeri epigastrium terus-menerus , tanda-tanda eklampsia
dekat ( sakit kepala atau gangguan visual yang terus-menerus ) , de novo kreatinin > 120 umol / L , oliguria
bawah 20 mL / jam, sindrom HELLP progresif , lama atau berat variabel deselerasi dengan variabilitas jangka
pendek kurang dari 3 milidetik . Ketika pengiriman darurat tidak diperlukan , tenaga kerja dapat disebabkan
oleh pematangan serviks)

Antihypertensive treatment is useful only in severe pre-eclampsia because the sole proven
benefit of such management is to diminish the risk of maternal complications (cerebral
hemorrhage, eclampsia, or acute pulmonary edema). There is no international consensus
concerning antihypertensive treatment in pre-eclampsia. The four drugs authorized for the
treatment of hypertension in severe pre- eclampsia in France are nicardipine, labetalol,
clonidine, and dihydralazine. There is no ideal target blood pressure value, and too aggressive
a reduction in blood pressure is harmful to the fetus. Therapy with a single agent is advised as
first-line treatment, followed by combination treatment when appropriate. The algorithm for
antihypertensive treatment proposed by French experts is shown in Figure 1. (pengobatan
antihipertensi hanya berguna di pre - eklampsia berat karena manfaat terbukti satunya manajemen tersebut
adalah untuk mengurangi risiko komplikasi maternal ( pendarahan otak , eklampsia , atau edema paru akut )
Tidak ada konsensus internasional mengenai pengobatan antihipertensi di pra eklampsia . Empat obat
berwenang untuk pengobatan hipertensi pada preeklamsia berat di Perancis adalah nicardipine , labetalol ,
clonidine , dan dihydralazine . Tidak ada yang ideal nilai tekanan darah sasaran , dan terlalu agresif
penurunan tekanan darah yang berbahaya bagi Therapy fetus. dengan agen tunggal disarankan sebagai
pengobatan lini pertama , diikuti dengan pengobatan kombinasi saat yang tepat . Algoritma untuk pengobatan
antihipertensi yang diusulkan oleh experts Perancis ditunjukkan pada Gambar 1)

Figure 1
Algorithm for antihypertensive treatment of pre-eclampsia.

Pulmonary maturation using corticosteroids must be considered, taking gestational age into
account. Betamethasone remains the gold standard at a dosage of two injections of 12 mg 24
hours apart; this treatment reduces the risk of hyaline membrane disease, intraventricular
hemorrhage, and neonatal mortality. (pematangan paru menggunakan kortikosteroid harus
dipertimbangkan , mengambil usia kehamilan ke rekening. Betametason tetap standar emas dengan dosis dua
suntikan 12 mg 24 jam terpisah ; perawatan ini mengurangi risiko penyakit hialin membran , perdarahan
intraventrikular , dan mortalitas neonatal)

Magnesium sulfate (MgSO4) may be part of the therapeutic armamentarium for severe pre-
eclampsia. It is indicated in the treatment of eclamptic convulsions as well as for secondary
prevention of eclampsia, thus replacing treatment by diazepam, phenytoin, or the
combination of chlorpromazine, promethazine, and pethidine. The efficacy of MgSO4 in the
reduction of maternal and neonatal complications of eclampsia is well established. It is
administered intravenously, first at a loading dose of 4 g over 15–20 minutes, which can be
repeated at a half dose (2 g) if convulsion recurs, and then at a maintenance dose of 1 g/hour
for 24 hours. MgSO4 treatment must be monitored in the intensive care unit because organ
failure may occur. This monitoring is based on repeated checking for a Glasgow score of 15,
tendon reflexes, respiratory frequency >12 per minute, and diuresis >30 mL/hour. Any
manifestation of overdose requires stopping the infusion, considering injection of calcium
gluconate, and measuring blood magnesium levels. (Magnesium sulfat (MgSO4) mungkin menjadi
bagian dari armamentarium terapi untuk pre-eklampsia berat. Hal ini diindikasikan dalam pengobatan kejang
eklampsia serta untuk pencegahan sekunder dari eklampsia, sehingga menggantikan pengobatan dengan
diazepam, fenitoin, atau kombinasi dari klorpromazin, prometazin, dan pethidine. Kemanjuran MgSO4 dalam
pengurangan komplikasi ibu dan bayi eklampsia mapan. Hal ini diberikan intravena, pertama dengan dosis 4 g
lebih 15-20 menit, yang dapat diulang di setengah dosis (2 g) jika kejang berulang, dan kemudian pada dosis
pemeliharaan 1 g / jam selama 24 jam. pengobatan MgSO4 harus dipantau di unit perawatan intensif karena
kegagalan organ dapat terjadi. Pemantauan ini didasarkan pada diulang memeriksa skor Glasgow dari 15,
refleks tendon, frekuensi pernapasan> 12 per menit, dan diuresis> 30 mL / jam. Setiap manifestasi overdosis
memerlukan menghentikan infus, mengingat injeksi kalsium glukonat, dan mengukur tingkat magnesium darah)
Eclampsia is generally considered an indication for emergency cesarean section. Nonetheless,
a decision to delay a cesarean, albeit rare, may be based on fetal status and justified if the
mother’s condition is stable and reassuring after treatment.(Eklampsia umumnya dianggap sebagai
indikasi untuk operasi caesar darurat . Meskipun demikian , keputusan untuk menunda bedah caesar , meskipun
jarang , mungkin didasarkan pada status janin dan dibenarkan jika kondisi ibu stabil dan meyakinkan setelah
pengobatan)
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Management following delivery

Although delivery is the only effective treatment for pre- eclampsia, and despite the fact that
clinical symptoms and laboratory abnormalities usually regress in the hours afterwards, the
risk of complications persists for some time following delivery. Pre-eclampsia is associated
with long-term morbidity and mortality. Approximately 20% of women with pre-eclampsia
develop hypertension or microalbuminuria during long-term follow-up, and the risk of
subsequent cardiovascular and cerebrovascular disease is doubled in women with pre-
eclampsia and gestational hypertension compared with age-matched controls. A recent
prospective epidemiological study with a median follow-up duration of 30 years provides
evidence that pre-eclampsia is a marker of increased mortality from cardiovascular disease.
(Meskipun persalinan adalah satu-satunya pengobatan yang efektif untuk preeklamsia , dan meskipun fakta
bahwa gejala klinis dan kelainan laboratorium biasanya regresi dalam jam setelah itu, risiko komplikasi
berlanjut untuk beberapa waktu berikut delivery. Pre - eklampsia berhubungan dengan jangka panjang
morbiditas dan mortalitas . Sekitar 20 % dari wanita dengan pre - eklampsia mengembangkan hipertensi atau
mikroalbuminuria selama jangka panjang tindak lanjut , dan risiko penyakit kardiovaskular dan
serebrovaskular berikutnya adalah dua kali lipat pada wanita dengan pre - eklampsia dan hipertensi
gestasional dibandingkan dengan usia yang sama controls. A baru-baru ini studi prospektif epidemiologi
dengan median durasi tindak lanjut dari 30 tahun memberikan bukti bahwa pre - eklampsia adalah penanda
peningkatan mortalitas akibat penyakit kardiovaskuler)

Hemodynamic, neurological, and laboratory monitoring is necessary following delivery for

patients with severe preeclampsia. Hemodynamic monitoring includes frequent blood
pressure measurements to enable adjustment of antihypertensive treatment and frequent
monitoring of diuresis and weight according to intake (oliguria should prompt progressive
fluid resuscitation and sometimes diuretic use). Neurological monitoring consists of checking
for signs of imminent eclampsia, including headaches, phosphene signals, tinnitus, and brisk
tendon reflexes. Clinical monitoring must be done several times daily during the week after
delivery, a period considered at high risk for complications. If necessary, monitoring can be
performed in an intensive care unit. (Hemodinamik , neurologis , dan laboratorium pemantauan
diperlukan setelah persalinan untuk pasien dengan preeklamsia berat . pemantauan hemodinamik termasuk
pengukuran tekanan darah sering mengaktifkan penyesuaian pengobatan antihipertensi dan pemantauan sering
diuresis dan berat sesuai dengan asupan ( oliguria harus meminta progresif resusitasi cairan dan penggunaan
kadang-kadang diuretik ) . pemantauan neurologis terdiri dari memeriksa tanda-tanda eklampsia dekat,
termasuk sakit kepala , sinyal phosphene , tinnitus , dan refleks tendon cepat . pemantauan klinis harus
dilakukan beberapa kali sehari selama seminggu setelah melahirkan , periode dianggap berisiko tinggi untuk
komplikasi . Jika perlu , monitoring dapat dilakukan di unit perawatan intensif )

Laboratory monitoring should be done several times daily in the first 72 hours after delivery
and thereafter adapted according to progress of the indices. It must include a complete blood
count, liver function tests, and measurement of lactate dehydrogenase. Discharge from
hospital cannot be considered until all clinical and laboratory indices have returned to normal,
and regular monitoring by the patient’s general practitioner as necessary if treatment for
hypertension is to be continued after discharge. (pemantauan laboratorium harus dilakukan beberapa
kali sehari dalam 72 jam pertama setelah melahirkan dan selanjutnya disesuaikan sesuai dengan kemajuan
indeks . Ini harus mencakup jumlah darah lengkap , tes fungsi hati , dan pengukuran dehidrogenase laktat .
Keluar dari rumah sakit tidak bisa dianggap sampai semua indeks klinis dan laboratorium telah kembali
normal , dan pemantauan rutin oleh dokter umum pasien yang diperlukan jika pengobatan untuk hipertensi
adalah untuk dilanjutkan setelah debit )

The risk of recurrence of pre-eclampsia during a subsequent pregnancy has to be considered.

This risk is estimated to be less than 10% for all cases of pre-eclampsia, but is greater when
pre-eclampsia is discovered before 28 weeks. The relative risk is 15 if pre-eclampsia occurs
at 20–33 weeks, 10 at 33–36 weeks, and 8 after 37 weeks. (Risiko kekambuhan dari pre - eklampsia
selama kehamilan berikutnya harus dipertimbangkan . Risiko ini diperkirakan kurang dari 10 % untuk semua
kasus pre - eklampsia , 37 tetapi lebih besar ketika pre - eklampsia ditemukan sebelum 28 minggu . Risiko
relatif adalah 15 jika pra - eklampsia terjadi pada 20-33 minggu , 10 di 33-36 minggu , dan 8 setelah 37
minggu)

Three months after delivery, screening for underlying renal or hypertensive disease may be
requested by the patient’s primary physician. Such screening is intended to check for
normalization of blood pressure values and disappearance of proteinuria, and if abnormalities
persist, a referral should be made to a nephrologist or a hypertension expert to determine the
cause. This examination is important because pre-eclampsia may unmask previously
undiagnosed systemic or kidney disease or thrombophilia. It should include a specific set of
questions, blood pressure measurement, a clinical examination looking for signs of
autoimmune conditions, and a urinary dipstick test. Testing for antiphospholipid antibodies is
recommended after severe pre-eclampsia. The search for hereditary thrombophilia by assays
for protein C and S, antithrombin III, and a test for resistance to activated protein C is
recommended in the case of a personal or family history of venous thromboembolic disease,
early pre-eclampsia, or pre-eclampsia with any intrauterine growth retardation, abruptio
placentae, or in utero death. Percutaneous needle biopsy of the kidney should be performed
only if kidney failure persists at three months postpartum or if signs of a systemic underlying
condition or proteinuria persist at 6 months. (Tiga bulan setelah melahirkan, skrining untuk penyakit
ginjal atau hipertensi yang mendasari dapat diminta oleh dokter utama pasien. skrining tersebut dimaksudkan
untuk memeriksa normalisasi tekanan nilai darah dan hilangnya proteinuria, dan jika kelainan bertahan,
rujukan harus dibuat untuk sebuah nephrologist atau ahli hipertensi untuk menentukan penyebabnya.
Pemeriksaan ini penting karena pre-eklampsia dapat membuka topeng penyakit sistemik atau ginjal yang
sebelumnya tidak terdiagnosis atau trombofilia. Ini harus mencakup satu set khusus dari pertanyaan,
pengukuran tekanan darah, pemeriksaan klinis mencari tanda-tanda dari kondisi autoimun, dan tes dipstick
urin. Pengujian untuk antibodi antifosfolipid dianjurkan setelah pre-eklampsia berat. Pencarian trombofilia
herediter dengan tes untuk protein C dan S, antitrombin III, dan tes untuk ketahanan terhadap diaktifkan
protein C dianjurkan dalam kasus riwayat pribadi atau keluarga dari penyakit tromboemboli vena, awal pra-
eklampsia, atau pre-eklampsia dengan hambatan pertumbuhan dalam kandungan, solusio plasenta, atau di
dalam rahim death. biopsi jarum perkutan ginjal harus dilakukan hanya jika gagal ginjal terus berlanjut di tiga
bulan setelah melahirkan atau jika tanda-tanda dari kondisi yang mendasarinya sistemik atau proteinuria
menetap di 6 bulan.)

Patients who have had severe pre-eclampsia may share predispositions with nonpregnant
patients who have cardiovascular risk factors. Accordingly, long-term monitoring of
cardiovascular, renal, and metabolic risk factors is recommended after severe pre-eclampsia.
(Pasien yang memiliki pre - eklampsia berat dapat berbagi kecenderungan dengan pasien hamil yang memiliki
risiko kardiovaskular factors. demikian , pemantauan jangka panjang kardiovaskular , ginjal , dan faktor-faktor
risiko metabolik dianjurkan setelah pre - eklampsia berat )
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Prevention
Primary prevention of pre-eclampsia is based on the detection of modifiable risk factors. The
literature is plentiful regarding the risk factors for pre-eclampsia, but should be interpreted
with caution. Women at high risk are those with a personal history of severe pre-eclampsia,
while those at low risk are defined as those who have never had pre-eclampsia but have at
least one risk factor. There are numerous risk factors, including genetic risk factors, family
history of pre- eclampsia, immunologic factors, nulliparity, a new partner, and demographic
factors such as a maternal age >35 years, the woman’s own gestational age and birth weight
(with elevated risks for women born before 34 weeks or weighing less than 2500 g at birth),
factors related to the pregnancy, such as multiple pregnancy, congenital or chromosomal
anomalies, a hydatidiform mole, or urinary infection, risk factors associated with maternal
disease, including chronic hypertension, kidney disease, obesity, insulin resistance, and
diabetes, as well as thrombophilia, and environmental factors such as living at a high altitude
and stress. Although the search for these risk factors is important, they may not effectively
predict this pre-eclampsia by themselves. (pencegahan primer dari pre-eklampsia didasarkan pada
deteksi faktor risiko yang dapat dimodifikasi. literatur berlimpah mengenai faktor risiko pre-eklampsia, tetapi
harus ditafsirkan dengan hati-hati. Perempuan yang berisiko tinggi adalah mereka yang memiliki riwayat
pribadi pre-eklampsia berat, sementara mereka yang berisiko rendah didefinisikan sebagai orang-orang yang
tidak pernah memiliki pre-eklampsia tapi memiliki setidaknya satu faktor risiko. Ada banyak faktor risiko,
termasuk faktor genetik risiko, riwayat keluarga preeklamsia, faktor imunologi, nulliparity, pasangan baru, dan
faktor-faktor demografi seperti usia ibu> 35 tahun, wanita itu sendiri usia kehamilan dan kelahiran berat
(dengan ditinggikan risiko bagi wanita yang lahir sebelum 34 minggu atau berat badan kurang dari 2500 g saat
lahir), faktor yang berhubungan dengan kehamilan, seperti kehamilan ganda, bawaan atau kromosom anomali,
mola hidatidosa, atau infeksi saluran kemih, faktor risiko yang terkait dengan penyakit ibu, termasuk kronis
hipertensi, penyakit ginjal, obesitas, resistensi insulin, dan diabetes, serta trombofilia, dan faktor lingkungan
seperti hidup di dataran tinggi dan stres. Meskipun pencarian faktor-faktor risiko penting, mereka tidak dapat
secara efektif memprediksi ini pre-eklampsia sendiri.)

However, accurate prediction of pre-eclampsia would enable early and optimal management
of women at high risk. Several predictive tests are being assessed currently. These include
clinical tests, such as blood pressure measurement during the second trimester or 24-hour
ambulatory blood pressure monitoring, but these lack sensitivity and specificity. Laboratory
tests for oxidative response have been assessed, including assays for uric acid, urinary
kallikrein, and fibronectin, but no evidence of their relevance has so far been found. Among
the markers used to screen for trisomy 21 during the second trimester (beta human chorionic
gonadotropin, alpha fetoprotein, and unconjugated estriol), elevated alpha fetoprotein is
associated with a higher risk of pre-eclampsia (unless there are neural tube abnormalities, as
when beta human chorionic gonadotropin is elevated). Frequent monitoring of women with
elevated levels could be useful, but these tests may not be carried out for screening purposes
due to their low negative predictive value. Serum markers for trisomy 21 in the first trimester
(pregnancy- associated plasma protein A, inhibin A, corticotropinreleasing hormone, and
activin) have been tested, but their likelihood ratios seem to be insufficient. (Namun, prediksi
yang akurat dari pre-eklampsia akan memungkinkan manajemen awal dan optimal wanita yang berisiko tinggi.
Beberapa tes prediktif sedang dinilai saat ini. Ini termasuk uji klinis, seperti pengukuran tekanan darah selama
trimester kedua atau 24 jam pemantauan tekanan darah rawat jalan, tapi ini kurang sensitivitas dan
spesifisitas. Tes laboratorium untuk respon oksidatif telah dinilai, termasuk tes untuk asam urat, kallikrein
kemih, dan fibronektin, tetapi tidak ada bukti relevansi mereka sejauh ini telah ditemukan. Di antara penanda
digunakan untuk layar untuk trisomi 21 selama trimester kedua (beta manusia chorionic gonadotropin, alpha
fetoprotein, dan estriol tak terkonjugasi), peningkatan alpha fetoprotein dikaitkan dengan risiko yang lebih
tinggi dari pre-eklampsia (kecuali ada kelainan tabung saraf, seperti ketika beta human chorionic gonadotropin
ditinggikan). pemantauan sering wanita dengan kadar bisa berguna, tetapi tes ini tidak dapat dilakukan untuk
skrining tujuan karena nilai prediktif negatif rendah. penanda serum untuk trisomi 21 pada trimester pertama
(pregnancy- terkait protein plasma A, inhibin A, corticotropinreleasing hormon, dan aktivin) telah diuji, namun
rasio kemungkinan mereka tampaknya tidak cukup.)

Imaging tests have been evaluated, including uterine artery Doppler ultra-sound. Uterine
artery Doppler ultrasound is not advised during the first or second trimester in low-risk
populations due to the excessive variability of likelihood ratios in this population, which
allows for the prediction of only one-third of pre-eclampsia cases. In a high-risk population,
the definition of which is often imprecise, uterine artery Doppler can be performed during the
second trimester morphologic ultrasound examination and checked 1 month later in case of
abnormal results (resistance index >0.58 or 90–95th percentile, unilateral or bilateral notch).
The combination of a uterine artery Doppler examination during the first trimester and a
three-dimensional ultrasound assessing placental volume may predict the risk of pre-
eclampsia as early as the first trimester. (tes pencitraan telah dievaluasi , termasuk rahim Doppler arteri
ultra- sound . Rahim Doppler arteri USG tidak disarankan selama trimester pertama atau kedua dalam
populasi berisiko rendah karena variabilitas berlebihan rasio kemungkinan pada populasi ini , yang
memungkinkan untuk prediksi hanya sepertiga dari kasus pre - eklampsia . Pada populasi berisiko tinggi ,
definisi yang sering tidak tepat , Doppler arteri uterina dapat dilakukan selama pemeriksaan trimester kedua
morfologi USG dan diperiksa 1 bulan kemudian dalam kasus hasil abnormal ( resistance indeks> 0.58 atau
persentil 90-95th , unilateral atau kedudukan bilateral ) . Kombinasi pemeriksaan Doppler arteri uterine
selama trimester pertama dan USG tiga dimensi menilai volume yang plasenta dapat memprediksi risiko pre -
eklampsia sedini trimester pertama)

In clinical practice, because no single marker effectively predicts the risk of pre-eclampsia,
the current trend is to test a combination of markers. The most commonly used combination
of markers assesses sFlt-1, placental growth factor, endoglin, and vascular endothelial growth
factor during the first or second trimester. Increased vascular endothelial growth factor and
endoglin levels, combined with increased sFlt-1 and decreased placental growth factor during
the first trimester, is associated with a significantly increased risk of pre-eclampsia. (Dalam
praktek klinis , karena tidak ada penanda tunggal secara efektif memprediksi risiko pre - eklampsia , tren saat
ini adalah untuk menguji kombinasi penanda . Kombinasi yang paling umum digunakan penanda menilai sFlt -
1 , faktor pertumbuhan plasenta , Endoglin , dan faktor pertumbuhan endotel vaskular selama trimester
pertama atau kedua . Peningkatan faktor pertumbuhan endotel vaskular dan Endoglin tingkat , dikombinasikan
dengan peningkatan sFlt - 1 dan penurunan faktor pertumbuhan plasenta selama trimester pertama , terkait
dengan peningkatan risiko yang signifikan dari pre – eklampsia)

Improved prediction of pre-eclampsia has been noticed when serum markers are combined
with Doppler indices. In a recent nested case-control study, second trimester maternal serum
cystatin C, C-reactive protein, and uterine artery mean resistance index were observed to be
independent predictors of pre-eclampsia. (Peningkatan prediksi pre - eklampsia telah melihat ketika
penanda serum digabungkan dengan indeks Doppler . Dalam studi kasus-kontrol baru-baru ini , trimester
kedua serum ibu cystatin C , protein C - reaktif , dan arteri uterina berarti indeks resistensi yang diamati
menjadi prediktor independen dari pre – eklampsia)

Secondary prevention is based on antiplatelet aspirin therapy, which reduces the risk of pre-
eclampsia by 10% in women who have at least one risk factor. No study currently allows
determination of the exact dosage or the best time for initiation of aspirin. However, aspirin
should be initiated as early as possible, ie, before 12–14 weeks, which corresponds to the
beginning of the first phase of trophoblast invasion. The efficacy of aspirin has been shown
only in women with previous pre-eclampsia associated with intrauterine growth retardation
and without thrombophilia. Low molecular weight heparin is indicated only in cases of
complicated thrombophilia (history of thromboembolic complications or of pre-
eclampsia). Calcium supplementation at a dosage of 1.5 g/day, beginning at 15 weeks and
continued throughout the pregnancy, is recommended for prevention of pre- eclampsia in
women with a daily calcium intake <600 mg/day. The statins, which stimulate HO-1
expression and inhibit sFlt-1 release, could have the potential to ameliorate early-onset pre-
eclampsia. Other treatments, such as antioxidant treatment by vitamins C and E,
oligoelements, and nitric oxide have no proven efficacy. (Pencegahan sekunder adalah terapi
aspirin antiplatelet, yang mengurangi risiko pre-eklampsia sebesar 10% pada wanita yang memiliki setidaknya
satu faktor risiko. Tidak ada studi saat ini memungkinkan penentuan dosis yang tepat atau waktu terbaik untuk
inisiasi aspirin. Namun, aspirin harus dimulai sedini mungkin, yaitu, sebelum 12-14 minggu, yang sesuai
dengan awal tahap pertama invasi trofoblas. Khasiat aspirin telah terbukti hanya pada wanita dengan
sebelumnya pre-eclampsia yang terkait dengan hambatan pertumbuhan dalam kandungan dan tanpa
trombofilia. heparin berat molekul rendah diindikasikan hanya dalam kasus trombofilia rumit (sejarah
komplikasi tromboemboli atau pre-eklampsia). suplemen kalsium dengan dosis 1,5 g / hari, dimulai pada 15
minggu dan berlanjut sepanjang kehamilan, dianjurkan untuk pencegahan preeklamsia pada wanita dengan
asupan kalsium harian <600 mg / hari. Statin, yang merangsang HO-1 dan menghambat sFlt-1 rilis, bisa
memiliki potensi untuk memperbaiki awal-awal pre-eklampsia. Pengobatan lain, seperti perawatan antioksidan
oleh vitamin C dan E, oligoelements, dan oksida nitrat memiliki khasiat terbukti.)

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Conclusion
Pre-eclampsia is a rare pregnancy-related disease with an unpredictable course that can have
serious consequences for both the mother and the fetus. The treatment is simple, ie, delivery.
Nonetheless, induced preterm delivery requires careful weighing of both maternal and fetal
risk– benefit. Accordingly, identifying delivery criteria in case of pre- eclampsia is crucial to
optimal management. Current research focuses on the prediction of onset of pre-eclampsia or
even severe pre-eclampsia so as to allow early management and improve the morbidity and
mortality associated with this disease. Specific tools for secondary prevention must also be
developed for recurrent pre-eclampsia. (Pre - eklampsia adalah penyakit yang berhubungan
dengan kehamilan langka dengan kursus tak terduga yang dapat memiliki konsekuensi serius bagi
ibu dan janin . Pengobatan ini sederhana , yaitu , pengiriman . Meskipun demikian , kelahiran
prematur diinduksi membutuhkan hati berat dari kedua manfaat -risiko ibu dan janin . Dengan
demikian , mengidentifikasi kriteria pengiriman dalam kasus preeklamsia sangat penting untuk
pengelolaan yang optimal . Penelitian saat ini berfokus pada prediksi awal pre - eklampsia atau pre-
eklampsia bahkan parah sehingga memungkinkan manajemen awal dan meningkatkan morbiditas
dan mortalitas yang terkait dengan penyakit ini . alat khusus untuk pencegahan sekunder juga harus
dikembangkan untuk berulang pre – eklampsia)

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Footnotes
Disclosure
The authors report no conflicts of interest in this work.
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