KONFERENSI KLINIS

Kamis, 3 Agustus 2017

Erna Ashlihah R.
 JUMLAH KASUS
31 Juli – 3 Agustus 2017
• Persalinan fisiologis 0 kasus
• Persalinan patologis
– Spontan 3 kasus
– VE 0 kasus
– Gemeli 0 kasus
– Manual aid 0 kasus
• Kamar operasi mayor
– Seksio Sesarea
– Ginekologi 4 kasus
– Onkologi 0 kasus
6 kasus
– Histeroskopi Laparoskopi 3 kasus

• Kamar operasi minor 0 kasus

– Kuretase 14 kasus
– Sterilisasi Pomeroy
 Senin, 31 Juli 2017
1. Ny TKF, 37 th, G3P0A2, UK 38 minggu 1 hari
• RM. 01.45.58.xx 
• Dx: post SC emergency a/i GH, PROM, dengan
riwayat IVF 3x, P1A2.  
• Pada 10.10, bayi lahir perabdominal, jenis
kelamin laki-laki, BBL 3434g, PB 51cm, LK/LD
35/33cm, AS 7/8
 Senin, 31 Juli 2017
2. Ny YP, 21 th, G1P0A0, UK 41 minggu 2 hari
• RM. 01.81.88.xx
• Dx: post SC emergency a/i kala II tak maju, malposisi,
dengan riwayat induksi balon kateter+75ml aquadest
dilanjutkan stimulasi oxytocin dalam 500ml RL 20tpm
a/i post date, P1A0
• Pada 00.00, bayi lahir perabdominal, jenis kelamin laki-
laki,BBL 3732g, PB 52cm, LK/LD 34/35cm, AS 8/9
 Selasa, 1 Agustus 2017
1. Ny. BS, 37 th, G2P1A0, uk 37 migg 3 hr
RM. 01.81.86.xx
Dx: SC elektif a.i PEB superimposed, Riw SC 2 thn yll
obesitas gr III P2A0 
Pukul 15.20 bayi lahir spontan jenis kelamin ♀, BBL 3110
gr, PB 49 cm, LK/LD 34/33cm, A/S 9/10
Rabu, 2 Agustus 2017
 KASUS YANG DIDISKUSIKAN
1. Ny. SR, 37 th, G6P5A0 UK 30 minggu 2 hari
Dx: Grandemultigravida, hamil preterm, bdp, dengan multipel kongenital
anomali

2. An DNA, 10 th, P0A0

Dx: tumor padat ovarii pada anak

3. Ny. TP, 23 th, P0A2

Dx: GTN high risk, post MTX V, post EMACO IV, post EMA-EP IV, post BEP
III, post paclitaxel 200mg + carboplatin 450mg, post EMA-EP IIIA
KASUS I : FETOMATERNAL

Ny. SR, 37 th, G6P5A0 30 minggu 2 hari

Dx: Grandemultigravida, hamil preterm, bdp, dengan

multipel kongenital anomali
 IDENTITAS
Nama : Ny. SR
Umur : 37 th
Alamat: Semayan, Bantul
ANAMNESIS
G6P5A0 • Pasien datang ke poli kebidanan
HPM 1/1/17 dengan membawa surat pengantar
HPL 8/10/17 dari dr , SpOG(K), dengan keterangan
UK 30 minggu G6P5A0 hamil 30 minggu, kelainan
2 hari kongenital.
• Pasien merasa hamil 7,5 bulan, saat ini
tidak ada keluhan. Kenceng-kenceng
(-), lendir darah (-), air ketuban (-),
gerakan janin aktif.
• Riwayat obstetri:
1. 2003, laki-laki, BBL 3000 gram, spontan, dokter.
2. 2007, perempuan, BBL 2800 gram, spontan, bidan.
3. 2010, laki-laki, BBL 3400 gram, spontan, dokter.
4. 2012, perempuan, BBL 3400 gram, spontan, bidan.
5. 2014, laki-laki, BBL 3200 gram, SC a/I presentasi kaki
6. Hamil ini.
• Riwayat ANC di SpOG
• Riwayat menikah: 1x, 14 th
• Riwayat kontrasepsi: tidak ada
• Riwayat hipertensi (-), DM (-), asma (-), alergi (-), penyakit jantung
(-)
• Riwayat operasi (-)
• Riwayat minum alkohol, konsumsi obat-obatan tidak
ditemukan pada pasien maupun suaminya
• Riwayat demam saat kehamilan ini tidak ada.
• Riwayat adanya kelainan kongenital pada keluarga tidak
ditemukan
• Riwayat memelihara binatang peliharaan kucing.
 PEMERIKSAAN FISIK
• KU: baik, sadar
• VS: TD: 109/66mmHg, N: 84 kpm, RR: 20 kpm, t: 36,30C
• Kepala: konjungtiva anemia (-), sklera ikterik (-).
• Thorax:
– Paru: vesikular +/+, sonor +/+
– Jantung: S1/2 murni, reguler
• Abdomen: janin tunggal, letak memanjang, preskep, his (-), DJJ (+).
• PD/insp: tidak dilakukan
PEMERIKSAAN PENUNJANG (USG)
31/7/17
Tampak janin tunggal,
memanjang, preskep, DJJ
(+), gerak (+), tampak
multipel kelainan
kongenital yaitu tampak
labiopalatoschisis,
polidactyli pada
ekstremitas atas, tampak
dilatasi ureter sinistra,
tampak pelebaran calyx
ren dextra, tampak
hydrocele testis sinistra.
Kesan: multipel
kongenital anomali
 DIAGNOSIS
Grandemultigravida, hamil preterm, bdp, dengan
multipel kongenital anomali
 Analisis kasus
G6P5A0 UK 30
minggu 2 hari

Riwayat SC a/I
Multipel
presentasi kaki 3 Deteksi kelainan kongenital
th yg lalu kongenital.
Prognosis kehamilan
dan janin
 Infants with multiple congenital anomalies
(MCA) are typically infants with:
• two or more major malformations (e.g., a neural tube
defect, cardiac defect, missing limb), or
• three or more minor malformations (e.g., syndactly, a
club foot, abnormally formed pinnae). Common
abnormalities include cardiac defects, cleft lip/cleft
palette, neural tube defects, musculoskeletal
• defects, abnormalities of the eye, and gastrointestinal
or genitourinary defects.

Projects # U35MC02601 and # U35MC02602 from the Maternal and Child Health Bureau (Title V, Social
Security Act), #11223, Health Resources and Services Administration, Department of Health and Human
Services
 What causes MCA?
• Approximately 40-60% of congenital malformations have no
known origin.
• About 20% of birth defects are likely to result from genetic
and environmental factors combined.
– 7.5% are caused by single gene mutations
– 6% are caused by chromosome abnormalities
– 5% are caused by maternal illness and/or substance use
• Several factors must be considered in assessing MCA etiology:
maternal health history, prenatal history, family history, and
careful and detailed physical examination of the infant.
Projects # U35MC02601 and # U35MC02602 from the Maternal and Child Health Bureau (Title V, Social
Security Act), #11223, Health Resources and Services Administration, Department of Health and Human
Services
 How are MCA detected?
• Prenatal screening may identify a fetus at risk for MCA:
– Multiple marker maternal serum screening at 15 to 18
weeks gestation can identify fetuses at risk for MCA
associated with chromosomal aneuploid or open lesions.
– Ultrasound at 19 to 21 weeks gestation allows
sonographers to measure morphology.
– Fetal MRI, fetal echocardiographs, and amniocentesis with
cytogenetic or molecular testing may follow a positive
prenatal screen to identify potential diagnoses and to
predict prognosis. A woman or couple can then make
more informed decisions about the pregnancy.
Projects # U35MC02601 and # U35MC02602 from the Maternal and Child Health Bureau (Title V, Social
Security Act), #11223, Health Resources and Services Administration, Department of Health and Human
Services
• MCA are frequently not identified through prenatal screening
but are noted at the time of birth.
– Clinical geneticists document malformations, signs, and
symptoms in order to compare against known syndromes.
– Genetic testing may help to rule out or confirm a
suspected single gene disorder or chromosomal aneuploid
if maternal and pregnancy history are inconclusive.
– Biochemical studies, molecular testing, chromosomal
testing and/or fluorescent in-situ hybridization (FISH)
testing may help to provide a diagnosis
labiopalatoschisis, Differential diagnosis:
polidactyli pada 1. Patau syndrome
ekstremitas atas, tampak 2. Charge syndrome
dilatasi ureter sinistra,
tampak pelebaran calyx
ren dextra, tampak
hydrocele testis sinistra.
 Patau Syndrome
• Many fetuses never survive until term and are stillborn or
spontaneously abort. Features include:
• Intrauterine growth restriction and low birth weight.
• Congenital heart defects: these occur in 80%; they include atrial
septal defect, ventricular septal defect, patent ductus arteriosus,
dextrocardia.
• Holoprosencephaly: the brain doesn't divide into two halves; this can
present with midline facial defects including:
– Cleft lip and palate.
– Microphthalmia or anophthalmia.
– Nasal malformation.
– Hypotelorism (reduced distance between the eyes) or cyclops.
• Other brain and central nervous system abnormalities, including:
– Neural tube defects.
• Other anatomical defects of the brain
– Severe learning disability.
– Problems with control of breathing (central apnoea).
• Other craniofacial abnormalities include:
– Microcephaly.
– Scalp defects (cutis aplasia: skin missing from the scalp).
– Ear malformations and deafness.
– Capillary haemangiomata.
• Gastrointestinal abnormalities: omphalocele, exomphalos, hernias.
• Urogenital malformations: polycystic kidneys, micropenis or
hypertrophy of the clitoris.
• Abnormalities of hands and feet: polydactyly (extra fingers or toes),
small hyperconvex nails and rocker-bottom feet
• CHARGE is a mnemonic for coloboma, heart defects, choanal atresia,
retarded growth and development, genital abnormalities, and ear
anomalies. CHARGE syndrome is characterized by the following:
• Unilateral or bilateral coloboma of the iris, retina-choroid, and/or disc
with or without microphthalmos (80%-90% of individuals)
• Unilateral or bilateral choanal atresia or stenosis (50%-60%)
• Cranial nerve dysfunction resulting in hyposmia or anosmia,
unilateral or bilateral facial palsy (40%), impaired hearing, and/or
swallowing problems (70%-90%)
• Abnormal outer ears, ossicular malformations, Mondini defect of the
cochlea and absent or hypoplastic semicircular canals (>90%)
• Cryptorchidism in males and hypogonadotropic hypogonadism in
both males and females
• Developmental delay
• Cardiovascular malformations (75%-85%)
• Growth deficiency (70%-80%)
• Orofacial clefts (15%-20%)
• Tracheoesophageal fistula (15%-20%)
 Usulan
• Manajemen ekspektatif.
• Terminasi sesuai indikasi obstetri.
• Saat lahir, dilakukan pemeriksaan karyotyping.
KASUS II : ONKOLOGI

An DNA, 10 th, P0A0

Dx: tumor padat ovarii pada anak
 IDENTITAS
Nama : An DNA
RM : 01.81.58.xx
Umur : 10 th
Alamat: Sewon, Bantul
Anamnesis S: pasien datang ke IGD, kiriman dari poli ER dengan
(25/7/17) keterangan kista ovarii bilateral dengan keluhan nyeri
perut sebelah kanan bawah sejak tadi pagi, nyeri
berkurang bila minum obat (Na diklofenak).
P0A0, 10 th
Keluhan utama berupa nyeri perut, dirasakan sejak 2
Belum menikah bulan yang lalu, hilang timbul, meningkat saat
HPM 24/7/17 menstruasi. Perut BAB dan BAK tidak ada keluhan.
Awalnya pasien periksa di puskesmas (juli 2017) karena
terasa benjolan di perut  rujuk RSUD Bantul.
Dilakukan USG, hasil tampak kista ovarium bilateral 
rujuk RSS.
Riwayat menarche: 7 bulan yang lalu (januari 2017)
Riwayat menstruasi: siklus 26-30 hari, durasi 6-7 hari,
ganti pembalut 3x, nyeri saat menstruasi (+).
Riwayat asma, alergi, DM, penyakit jantung disangkal.
 PEMERIKSAAN FISIK
• KU: tampak kesakitan
• VS:TD: 130/70mmHg, N 98 kpm, RR 22 kpm, BB 60 kg, TB 154 cm,
BMI 25,3
• VAS: 6/10
• Abd: teraba massa suprapubik, nyeri tekan (+).
• PD: tidak dilakukan (Pasien tidak kooperatif)
• RT: tidak dilakukan (Pasien tidak kooperatif)
PEMERIKSAAN PENUNJANG
USG:
VU terisi cukup,
tampak uterus ukuran
3,63 x 1,16cm, tampak
massa kistik 3 lobus.
Lobus 1 uk 7,4 x
5,15cm. Lobus 2 uk
3,94 x 2,4cm. Lobus 3
uk 2,93 x 2,28cm.
Septa (+)
USG staf:
Tampak gambaran massa echoic kesan dari
adnexa kiri uk 8x7 cm. uterus kesan membesar.
 MSCT abdomen dengan kontras
(19/7/17)
• Lesi inhomogen di cavum pelvis dominasi kistik (cairan kental)
dengan lesi solid minimal di tepinya yang meluas hingga ke
cavum abdomen, mengarah gambaran complex cyst ovarium.
• Agenesis ren dextra.
• Tak tampak kelainan pada VF, pankreas, ren sinistra, VU,
uterus, maupun rectum.
• Tak tampak limfadenectomy paraaorta, mesenterica, maupun
para iliaca.
• Tak tampak gambaran bone metastasis pada sistem tulang
yang tervisualisasi.
 Laboratorium
Nilai rujukan 7/7/17 25/7/17

Alb 3,97-4,94 d/dL 4,08

SGOT <=32 U/L 13

SGPT <=33 U/L 9

BUN 6,00-20,00 mg/dL 9,4

Cr 0,50-0,9 mg/dL 0,56

GDS 80-140 mg/dL 109 95

Na 136-145 mmol/L 140 135

K 3,50-5,10 mmol/L 4,22 4,85

Cl 98-107 mmol/L 102 98

 Nilai rujukan 7/7/17 25/7/17

PPT 12,3-15,3 detik 15,4/14,2 15,2/14,9

APTT 27,9-37,0 detik 32,1/28,6 29,5/29,8

INR 0,9-1,1 1,14 1,12

HBsAg Non reaktif Non reaktif

AE 4,0-5,4 10^6/ 5,61 5,75

AL 4,5-13,5 10^3/ 6,92 10,59

AT 150—450 x 10^3/ 368 327

Hb 12-15 g/dL 14,3 14,4

Hmt 35-49 % 42,2 43,6

gol. darah B

Ca-125 179,4
 Nilai rujukan hasil

Protein negatif +- (15-29 mg/dL)

leukosit 0-20 / 22

Sel epitel 0-40 / 63,3

silinder 0,0-1,2 / 4,6

bacteria 0-100 / 424,5

Small round cell 0-6 / 18,9

Nitrit negatf negatif

keton negatif negatif

Lekosit esterase negatif Negatif (25 sel/

 DIAGNOSIS
• Tumor padat ovarii pada anak
 TS bedah urologi
S: demam (-), ngompol (-), BAK lancar
O: CT scan:
A: agenesis ginjal dextra, TPO
P: observasi
 Diskusi
• Massa organ ginekologis pada anak
• Apakah manajemen yang tepat?
• Ovarian neoplasms are uncommon in the pediatric
population, with an estimated incidence of 2.6 cases
per 100,000 girls per year. Ovarian malignancy in
children and adolescents is reported in 10%– 20% of all
ovarian masses or neoplasms and comprises
aproximately 1%–2% of all childhood malignancies.

Heo, S.H. et al. review of ovarian tumor in children and

adolescent. Radiographic. 34 (7), 2014.
M. Zhang et al.J Pediatr Adolesc Gynecol 27 (2014) e73 - e77
Heo, S.H. et al. review of ovarian tumor in children and
adolescent. Radiographic. 34 (7), 2014.
Heo, S.H. et al. review of ovarian tumor in children and
adolescent. Radiographic. 34 (7), 2014.
M. Zhang et al.J Pediatr Adolesc Gynecol 27 (2014) e73 - e77
• The patient’s ranged in age from 2 to 18 years (mean = 15.6 years),
with 30 being premenarchal (14.8%). The incidence of ovarian tumor
increases with age, especially in patients older than 14 years. The
main complaint was abdominal pain or abdominal distension in 117
patients (57.7%). A high AFP level in a pre-pubic girl with an adnexal
mass is indicative of a malignant ovarian tumor. The 214 adnexal
masses (11 patients had bilateral cysts) consisted of benign tumorous
oophoropathy (107 masses, 50.0%), borderline and malignant tumors
(29 masses, 13.6%), and nontumorous oophoropathy (78 masses,
36.5%). Of the 136 neoplasia, germ cell tumors accounted for 71.5%.
Surgical intervention was performed in 98.5% of cases. There were
statistically decreased blood loss, surgery duration and days of
hospitalization with the laparoscopic procedure when compared with
open surgery.

Hongqian Liu, Xiangao Wang, Donghao Lu, Zhihong Liu and Gang Shi.Journal of Ovarian Research20136:47

https://doi.org/10.1186/1757-2215-6-47©  Liu et al.; licensee BioMed Central Ltd. 2013.Received:
9 April 2013Accepted: 2 July 2013
Usulan
- Usul pengangkatan massa tumor + frozen
section dengan konsep fertility preservation
surgery
KASUS III: ONKOLOGI

Ny. TP, 23 th, P0A2

RM: 01.63.37.xx

Dx: GTN high risk resisten, post MTX IV, post EMACO IV, post
EMA-EP IV, post BEP III, post paclitaxel 200mg + carboplatin
450mg, post EMA-EP IIIA
 IDENTITAS
Nama : Ny. T
RM : 01.63.37.xx01.81.72.93
Umur : 23 thn
Alamat: Cerme, Panjatan, Kulonprogo
Anamnesis Pasien adalah penderita GTN high risk resisten, post
kemoterapi MTX V, post EMACO IV, post EMA-EP IV,
(31/1/17) post BEP III, post paclitaxel 200mg + carboplatin
P0A2, 22 th 450mg, post EMA-EP IIIA.
PA: Molahidatidosa Saat ini pasien tidak ada keluhan. BAB dan BAK
HPHT: Januari 2017 lancar. Perdarahan (-).
Riwayat kuret 2x:
TD 153/89 mmHg 1. 2013, kuret, PA: mola hidatidosa, Tx: MTX
N 120 kpm 2. 2015, kuret, PA (-), Tx: MTX V, EMACO IV, EMA-EP
RR 20 kpm IV, BEP III, paclitaxel 200mg + carboplatin 450mg,
EMA-EP IIIA.
T 36,3 C
Riwayat menikah 1x.
Riwayat kontrasepsi: kondom, injeksi KB 3 bulan
BW 76 kg
Riwayat hipertensi, DM, asma, alergi, penyakit
BH 158 cm
jantung disangkal
BMI 30,44 kg/m2
BSA 1,777 m2
 Pemeriksaan Fisik
• KU: baik, sadar
• Abdomen: supel, nyeri tekan (-), massa tak
teraba (-)
• PD: vulva uretra normal, dinding vagina licin,
serviks licin, kaku di belakang, parametrium
kanan kiri lemas, cavum douglas tak
menonjol.
 Foto Thorax (01/12/2016)
• Kesimpulan:
– Bronkhitis
– Jantung dalam ukuran normal
 MSCT abdomen (27/7/17)
• Uterus ukuran 6,35 x 5,62 x 8,47 (ukuran sebelumnya tanggal 3/2/17
adalah 6,35 x 5,6 x 4,5 cm) dengan area hipodense di corpofundal
dextra, bentuk irreguler, batas sebagian tak tegas densitas
prekontras.
• Kesan:
– Massa di corpofundal uteri suspek malignansi
– Tak tampak kelainan pada hepar, lien, VF, pancreas, ren dextra et sinistra, VU
maupun rectum, tak tampak metastase pada organ tersebut.
– Tak tampak limfadenopathy paraaorta, mesenterica, maupun parailiaca.
– Tak tampak gambaran bone metastasis pada sistema tulang yang tervisualisasi.
• Dibandingkan MSCT sebelumnya tanggal 3/2/2017 secara radiologis
membesar (progressive
 Chronology
Sept 2015, RSU Feb 2016,
Juni 2016,
Kharisma RSS
Des 2012 RSS
Paramedika Tak Juni 2016, RSS
RSUD wates Kulonprogo Tak respon Des 2016,
respon Tak respon EMA CO RSS
Kehamilan Kehamilan ke- MTX EMA CO
ke-1, kuret 2, kuret
PA: mola PA (-) Beta hcg : Evaluasi 1
Beta hcg : Beta hcg :
hidatidosa 19117 bulan
Beta hcg : 5378 502,1 19117
Βeta hcg = Dx: GTN Beta hcg :
Dx: GTN low Dx: GTN Dx: GTN high
9873,26 high risk 1686
risk high risk risk
Dx GTN low Tx: EMA- BEP I
Tx: MTX 20 Tx: EMA- Tx: EMA- EP
risk EP
mg/i.m/5 hari/ CO
Tx: MTX 2 minggu Beta hcg :
/oral (5x) Beta hcg : 3,9
Beta hcg : 1648
Beta hcg :
3,9
Beta hcg: 502,1 19117
 Januari 2017 Februari 2017 Maret 2017 Mei 2017 Juni 2017 Juli 2017

• Chemotherapy • Chenotherapy • MSCT • EP EMA I • EP EMA II • EP EMA III

BEP II BEP III Abdomen: • BHCG 8021 • BHCG 4536 • BHCG 5076
• BHCG 465 • BHCG360 uterus uk 6,35 x • MSCT
5,6 x 4,5 cm. abdomen:
Terdapat massa uterus uk 6,35 x
kistik di corpus 5,62 x 8,47 cm
fundal uterus dg area
• Ganti regimen hipodense di
dengan paxus corpofundal
carbo dextra, ireguler,
• BHCG 3800 batas sebagian
tak tegas
 BHCG RESULTS 2013-2017
100000
90000 88495
80000
70000 EMA CO
60000 EMA - EMA -
EP EP
50000 MTX
40000 BEP
38295
30000 26748
20000 19117

10000 9873.26 8021

53785378 4502.1 3411 3800 4536 5076
185536.3 13.4 6.36 5.9 5.36 6.81 6.35 1366256 265 1365 392.18.7 3.9 16861648465 360
0 171.21
1 3 1 3 1 3 1 3 13 1 3 1 3 1 3 1 3 1 3 1 3 1 5 1 5 1 5 15 1 6 1 6 1 6 1 6 1 6 1 6 1 6 1 6 1 6 1 6 17 1 7 1 7 1 7 1 7 1 7 1 7 1 7
/5 /20 /1/ /20 10/ /20 /8/ /20 12/ /20 /9/ /6/ /2/ /9/ /8/ /7/ /3/ 11/ /20 10/ 11/ 10/ /8/ 10/ /3/ /5/ /20 i 20 i 20 t 20 pr- i 20 i 20
/
1 25 5 20 6/ 24 7 22 8/ 26 9 10 10 11 12 1 2 3/ 23 6/ 7/ 8/ 9 0/ 11 12 17 ar ar re A e n
1/ 5/ 6/ 7/ 8/ 5/ 1 1/ anu bru Ma m Ju
J Fe
 DIAGNOSIS
GTN high risk resisten, post MTX V, post EMACO IV, post
EMA-EP IV, post BEP III, post paclitaxel 200mg +
carboplatin 450mg, post EMA-EP IIIA
 Diskusi
• Apakah manajemen yang tepat?
• Patients whose WHO scores are less than 7 are considered to be at
low risk
• Patients with scores greater than 6 are considered to be at high risk
of developing drug resistance.
• Patients with nonmetastatic disease (Stage I) and low-risk metastatic
GTN (Stages II and III, score <7) can be treated initially with single-
agent chemo-therapy with cure rates approaching 80% to 90%.
• Patients classified as having high-risk metastatic disease (Stage IV and
Stages II–III with scores >6) require multiagent chemotherapy,
possibly with adjuvant radiation and/or surgery, as indicated, to
achieve similar cure rates.

Donald Peter Goldstein, MDa,*, Ross S. Berkowitz, MDb

• In patients who resisted second line chemotherapy,
third line chemotherapy may be considered. Several
regimens were proposed as third line treatment such
as TP/TE, BEP, ICE, Carboplatin/ Gemcitabine (Bianconi
et al., 2007; Wong et al., 2008; Patel et al., 2010; Feng
et al., 2011; Alazzam et al., 2012; Lurain et al., 2012).
The efficacy of those regimens was acceptable
(Bianconi et al., 2007; Feng et al., 2011; Lurain et al.,
2012).
• Approximately one half of patients with high-risk GTN will require
some form of surgical procedure during the course of therapy to
either remove disease or treat complications.
• Adjuvant surgical procedures, especially hysterectomy and
pulmonary resection, are used most frequently to remove foci of
chemotherapy-resistant disease in patients with persistent or
recurrent GTN.
• Conservative resection of chemotherapy-resistant disease within the
myometrium may be considered in highly selected patients with no
other evidence of disease who wish to preserve fertility.
• Surgery may also be required in the therapy of patients with high-risk
GTN as a means of controlling hemorrhage or dealing with other life-
threatening complications.

John R. Lurain. John & Ruth Brewer Professor of Gynecology and Cancer Research, John I. Brewer
Trophoblastic Disease Center, Northwestern University Feinberg School of Medicine, 250 E. Superior St.
Suite 05-2168, Chicago, IL 60611, USA
 Usulan
• Usul pelacakan metastase ke organ lain, yaitu
dengan CT scan whole body.
• Usul reseksi massa di fundus sampai dengan
kemungkinan histerektomi.
• Motivasi pasien dan keluarga.

68
TERIMA KASIH