TUTORIAL OBSGIN

Refleksi Kasus Week 1

Juli 2019

Febri Indah Widhowati

Wicesa Nugraha
Winetta Celia Fairuza
 REFLEKSI KASUS OBS
1. Ny. MC, 26 tahun, G1P0A0, UK 26 minggu 6
hari
• Dx: PPROM 1 bulan, PAP e.c placenta previa
ANAMNESIS
30/6/2019 S: Pasien datang sendiri ke IGD RSS dengan keluhan keluar
21.45
IGD RSS darah dari jalan lahir. Awalnya sejak siang darah yang keluar
berupa bercak. Namun, habis maghrib darah menjadi lebih
G1P0A0, 26 thn banyak seperti menstruasi. Pasien mengeluh adanya kenceng-
HPHT 23/12/2018
HPL: 30/9/2019 kenceng tapi jarang. BAK dirasakan sering dan terasa anyang-
UK 26 weeks 6 days anyangan. Gerakan janin masih dirasakan. Pasien merasakan
sering keluar cairan sejak awal Mei. Pasien riwayat ANC di RS
TD : 109/77 mmHg Hidayatullah.
N : 99 kpm Sekitar 2 minggu lalu pasien mengaku mengalami keluar bercak
RR : 21 kpm dari jalan lahir beriksa ke SpOG, dikatakan letak plasenta di
S : 36.4
SpO2: 98 bawah, diberikan Premaston 3x1 (3 hari), 2x1 (3 hari), 1x1 (4
hari). Pasien tidak mengeluh mual muntah.
Riw peny hipertensi (-), DM (-), Asma (-), Alergi (-)
BW : 46 kg
BH : 150 cm Riw menikah:1x, +/- 7 bulan
BMI : 17,78 kg/m2 Riw KB belum pernah
Riw operasi disangkal
3
 PHYSICAL EXAM
KU : CM
Kepala : CA -/-, SI -/-,
Leher : KGB tidak membesar,
Pulmo : Vesikuler +/+, Rhonki -/-, Wh -/-
Jantung : S1 S2 tunggal
Abdomen : bising usus (+) N, janin tunggal, memanjang, preskep, punggung kanan, DJJ (+)
152 kpm, HIS (-), TFU = 17 cm
Ekstremitas : edema (-) semua ekstremitas
PD : V/U tenang, dinding vagina licin, cervix utuh, OUE menutup, pooling test (+),
nitrazin test (+), darah (+)
4
 ULTRASONOGRAPHY (30/6/19)
Janin tunggal memanjang, preskep, DJJ (+), Gerak (+), AK
sedikit (SDP 0.94 cm), placenta di corpus anterior, meluas ke
bawah. Tali menutup OUI.
BPD 6.74 cm~27W1D
HC 24,07cm~26W1D
AC 21.13cm~25W5D
TBJ 922gr

5
 DIAGNOSIS

Diagnosis: Presentasi kepala, G1P0A0 hamil

26 minggu 6 hari PPROM 1 bulan, PAP o/k
placenta letak rendah

6
 TATA LAKSANA
Manajemen Konservatif:
- Inj. Dexametason 1 amp/12 jam/IV
- Inj. Asam tranexamat 500 mg/8 jam/IV
- SF 1 tab/24 jam/PO
- Kalk 500 mg/8 jam/PO
- Rehidrasi RL 500cc
- USG ulang di bangsal
- Eritromisin 500mg/6 jam/oral
- Pengawasan KU, VS, his, DJJ, gerakan janin,
tanda-tanda chorioamnionitis

7
 PRETERM PREMATURE RUPTURE
OF MEMBRANES
DEFINISI
• Keadaan pecahnya selaput ketuban sebelum
persalinan atau dimulainya tanda inpartu dan
sebelum usia kehamilan lengkap 37 minggu.
• ꜛdurasi PPROM, ꜛ risiko infeksi asenden
• Rupture of membranes results from a variety of factors that
ultimately lead to accelerated membrane weakening. This is
caused by an increase in local cytokines, an imbalance in the
interaction between matrix metalloproteinases and tissue
inhibitors of matrix metalloproteinases, increased collagenase
and protease activity, and other factors that can cause
increased intrauterine pressure.
 SYMPTOMS
• Over 90% of women with PPROM report a
history of “gush of ™
fluid.”
 PATHOGENESIS
MOLECULAR CHANGES
• Related to increased apoptosis of membrane cellular components and to
increased levels of specific proteases in membranes and amnionic fluid.
• Strength of the membranes is provided by the amnionic extracellular matric
and interstitial amnionic collagens.
• The matric metaloproteinase (MMP) family involved particularly with
collagen degradation.
• The MMP-1, MMP-2, MMP-3, MMP-9 members of this family are found
higher concentrations in amnionic fluid from pregnancies with preterm
prematurely ruptured membranes.
 PATHOGENESIS
MOLECULAR CHANGES
• MMP activity is in part regulated by tissue inhibitors of matrix
metaloproteinases – TIMPs.
• Several of these inhibitors are found in lower concentrations in
amnionic fluid from women with ruptured membranes.
• Increased prostaglandin levels promote cervical ripening and uterine
con- tractions. Increased MMPs allow collagen breakdown in the
fetal membranes resulting in premature rupture.
• In conclusion, many PPROM cases result from collagen degrada-
tion, altered collagen assembly, and cell death, which all lead to a
weakened amnion.
•
 PATHOGENESIS
INFECTION
• Bacterial cultures of amniotic fluid support a role for infections in a
significant proportion.
• The inflammatory response that leads to membrane weakening is
currently being defined. Research is focused on mediators of this
process with a goal to identify early risk markers for PPROM.
 FAKTOR RISIKO
• Low socio-economic • Riwayat ketuban pecah
status dini pada kehamilan
• BMI < 19.8 sebelumnya
• Serviks pendek • Infeksi traktus genital
• Perdarahan antepartum
• Nutritional deficiencies
• Cigarette smoking
 KRITERIA DIAGNOSIS
• Pooling test (+)
– Visual pooling of clear fluid
in the posterior fornix of the
vagina or leakage of fluid
from the cervical ostium
– Ibu bisa diminta miring ke
lateral kiri untuk
membendung cairan amnion
demi kepentingan tes.
 KRITERIA DIAGNOSIS
• Nitrazine test (+)
– An alkaline pH of the cervicovaginal discharge, which is typically demonstrated by
seeing whether the discharge turns yellow nitrazine paper to blue.
– The normal pH of vaginal secretions is generally 4.5–6.0, whereas amniotic fluid
usually has a pH of 7.1–7.3. False-positive test results may occur in the presence of
blood or semen, alkaline antiseptics, or bacterial vaginosis. Alternatively, false-negative
test results may occur with prolonged membrane rupture and minimal residual fluid.
 KRITERIA DIAGNOSIS
• Ferning test (+)
– Microscopic ferning of the cervicovaginal
discharge on drying
– crystallization of amniotic ™
fluid due to its high
contents of salts and proteins.
– False positive results for contamination by
cervical– vaginal mucus, seminal ™ uid, •ngerprints,
and urine crystals. False negative results for
blood or meconium contamination or
inadequacy in slide preparation.
 KRITERIA DIAGNOSIS
• If the diagnosis remains unclear after a full evaluation,
membrane rupture can be diagnosed unequivocally with
ultrasonographically guided transabdominal instillation of
indigo carmine dye, followed by the passage of blue-dyed fluid
into the vagina, which is documented by a stained tampon or
pad. It is important to note that the maternal urine also will
turn blue and should not be confused with amniotic fluid.
 MANAJEMEN
1. Pembatasan aktivitas pasien
2. Apabila belum inpartu berikan Eritromisin
4x250mg selama 10 hari atau sampai tanda
inpartu (pilih yang lebih dulu)
3. Segera rujuk pasien ke fasilitas pelayanan
sekunder
4. Tokolitik tidak dianjurkan
 MANAJEMEN
4. Di RS rujukan
a. ≥ 34 minggu: lakukan induksi persalinan dengan oksitosin bila tidak ada kontraindikasi
b. 24 – 33 minggu:
• Bila terdapat amnionitis, abruptio plasenta, dan kematian janin, lakukan persalinan segera.
• Berikan Deksametason 6 mg IM tiap 12 jam selama 48 jam atau betametason 12 mg IM tiap 24
jam selama 48 jam.
• Lakukan pemeriksaan serial untuk menilai kondisi ibu dan janin.
• Bayi dilahirkan di usia 34 minggu, bila dapat dilakukan pemeriksaan kematangan paru dan hasil
menunjukan bahwa paru sudah matang.
c. <24 minggu:
• Pertimbangan dilakukan dengan melihat risiko ibu dan janin.
• Lakukan konseling pada pasien. Terminasi kehamilan mungkin menjadi pilihan.
• Jika terjadi infeksi (koroiamnionitis), lakukan tatalaksana koriamnionitis.
 COMPLICATION
Neonatal complication
• Respiratory distress syndrome
• Intraverticular Hemorrhage
(IVH)
• Perventricular leukomalacia
(PVL)
• infection and necrotizing
enterocolitis (NEC)
• Fetal pulmonary hypoplasia
• Skeletal deformities
• Cord compression and fetal
distress in labor
Maternal complication
• Chorioamnionitis
• Endometritis
• Cord prolapse
• Oligohydramnion
• Caesarean birth
• Abruptio placenta
 COMPLICATION ON <24wks GESTATION
• perinatal death
• pulmonary hypoplasia (PH)
• compression deformities
• long-term infant morbidities
• increased need for cesarean delivery (CD)
• retained placenta
 RELATED DIAGNOSIS
Perdarahan antepartum o/k plasenta letak rendah
(plasenta previa)
The major causes of APH are placenta previa and abruption placenta. Placenta previa is
one of the most serious complications during pregnancy and is associated with numerous
adverse maternal and fetal-neonatal complications. Many of these are direct
consequences of maternal antepartum and intrapartum hemorrhage. It was reported that
the prevalence of APH in pregnant women with placenta previa are at an approximately
ten times greater than that non-placenta previa women. Importantly, the prevalence of
placenta previa has been rising in parallel with the increasing rate of caesarean delivery
and varies throughout the world and it has become a serious public health problem
worldwide.
 USULAN
• dr. Irwan
– MgSO4 1gr/jam s/d 24 jam
– Vit C 1 tab/24 jam/PO
– Nifedipin 10 gr/8 jam/PO

– Monitor DJJ dan gerak janin

– Cek maturasi paru janin
– Terminasi kehamilan pada 34 weeks
 REFERENSI
• Cunningham. (2014). Williams Obstetrics, 24th ed. New York: Mc Graw-Hill Education
• Ikatan Dokter Indonesia. (2013). Panduan Praktik Klinis Bagi Dokter di Fasilitas Pelayanan
Kesehatan Primer. Jakarta: Ikatan Dokter Indonesia
• Kementerian Kesehatan RI. (2013). Pelayanan Kesehatan Ibu di Fasilitas Kesehatan Dasar dan
Rujukan. Jakarta: Kementeria Kesehatan RI
• ACOG
• RCOG
• https://www.ncbi.nlm.nih.gov/books/NBK532888/
• https://www.glowm.com/section_view/heading/Preterm%20Premature%20Rupture%20of%20the%20Me
mbranes/item/120
Thank You