Konsensus Pedoman Diagnosis Dan Terapi Diabetes Melitus Dalam Kehamilan DMK Hermanto
Konsensus Pedoman Diagnosis Dan Terapi Diabetes Melitus Dalam Kehamilan DMK Hermanto
DRAFT 1
Penyusun :
dr. Hermanto Tri Joewono, SpOG-K
Dr dr. H. Agung Pranoto, MSc. SpPD-KE
1
DAFTAR ISI
Pengantar
Klasifikasi
Batasan
Patofisiologi / Diabetologia
Metabolisme karbohidrat, protein dan
lemak selama hamil
Hipotesis Pedersen
Hipotesis Freinkel
DM Pragestasional
Angka kejadian
Skrining
Diagnosis
Penyulit obstetris
Penyulit neonatologis
Terapi medik
Terapi obstetri
Prognosis
DM Gestasional
Angka kejadian
Skrining
Diagnosis
Penyulit obstetris
Penyulit medis
Penyulit neonatologis
Terapi obstetris
Terapi medis
Penutup
2
I. PENDAHULUAN
Diabetes Mellitus (DM) dapat terjadi dalam dua bentuk jika
dihubungkan dengan kehamilan, yaitu DM yang mendahului
kehamilan atau wanita yang menderita DM yang hamil disebut
sebagai DM Pragestasi (DMPG) dan bentuk kedua adalah
wanita yang hamil kemudian menderita DM saat hamil dan
menghilang setelah persalinan yang disebut sebagai DM
Gestasi (DMG).
Adanya satu jenis diabetes khusus yang muncul hanya saat
kehamilan saja dan menghilang saat nifas masih belum
diterima oleh sebagian besar masyarakat kedokteran di
Indonesia, hal yang akan berdampak besar bagi
penatalaksanaan penyakit ini misalnya meningkatnya
morbiditas terutama pada janin atau neonatus dan
meningkatnya biaya perawatan yang tidak perlu (pemeriksaan
Hb A1C pada Diabetes Mellitus Gestasi atau ultrasonografi
untuk mencari kelainan bawaan janin pada DM Pragestasi ).
Kesepakatan akan adanya dua jenis DM dalam kehamilan
diharapkan dapat menurunkan morbiditas bahkan mortalitas
maternal maupun neonatal serta menurunkan biaya perawatan
ibu maupun bayi.
Pedoman Diagnosis dan Terapi ini membahas kedua jenis
DM tersebut mulai dari batasan, klasifikasi, skrining,
diagnosis, dan penatalaksaan baik medis maupun obstetris serta
neonatus, penyulit dan prognosisnya.
3
II. DEFINISI DAN KLASIFIKASI
4
Tabel 2. Perbedaan DM Gestasional
dan DM Pragestasional
DM G DMPG
Saat Sebelum
Onset
Kehamilan Kehamilan
Prevalensi 0,2 % 2%
Kelainan
= Populasi
bawaan Tinggi
N
janin
Makrosomia Tinggi Tinggi
Kematian = Populasi
Tinggi
Janin N
Pemeriksaan Tidak
Perlu
HBA1C perlu
Pemeriksaan Tidak
Perlu
USG u/ KBJ perlu
FWB usia Tidak
Perlu
34- 36 mgg perlu
5
TABLE 1–White Classification of Diabetes Complicating
Pregnancy (ACOG 1986)
Fasting 2-hour
Cl Onset Plasma Postprandial Therapy
ass Glucose Glucose
A1 Gestationa < 105 mg/dl < 120 mg/dl Diet
l
A2 Gestationa >105 mg/dl > 120 mg/dl Insulin
l
Cl Age of Duration (yr) Vascular Disease Therapy
ass Onset (yr)
B Over 20 < 10 None Insulin
C 10-19 10-19 None Insulin
D Before 10 > 20 Benign Insulin
Retinopathy
F Any Any Nephropathy*) Insulin
R Any Any Proliferative Insulin
Retinopathy or
Vitreous
Bleeding
H Any Any Atherosclerotic Insulin
Heart Disease
*)
When diagnosed during pregnancy: 500 mg or more
proteinuria per 24 hours measured before 20 weeks gestation.
ACOG: The American College of Obstetricians and
Gynecologists
6
Many centres use simple classification, as seen in TABLE 2
(Inzucchi 1999), which primarily places the diabetes (either
type 1 or type 2 diabetes) in the context of the pregnancy (pre-
existing condition: Overt Diabetes = PDGM) or one that was
acquires during gestational (GDM)
1. Pregestational Diabetes Mellitus = PGDM (Overt DM),
which existed before the pregnancy, and subdivided into
Type 1 Diabetes Mellitus (T1DM) and Type 2 Diabetes
Mellitus (T2DM), in which each can be differentiated into
3 subtypes.
2. Gestational Diabetes Mellitus (GDM) which is defined as
any degree of glucose intolerance with onset or first
recognition during pregnancy (whether or not the condition
persist after pregnancy)
7
Gestational Diabetes Mellitus
Diet-controlled
Insulin-requiring
III. PATOFISIOLOGI
Metabolisme karbohidrat wanita hamil dan tidak hamil
sangat berbeda yang ditandai dengan adanya hipoglikemia
puasa, hiperglikemia postprandial yang memanjang dan
hiperinsulinisme terutama pada trimester tiga. Gambar dibawah
ini dapat memperjelas pernyataan diatas. Efek kehamilan yang
memperberat diabetes mellitus bila telah diderita ibu hamil
ataupun menimbulkan diabetes militus gestasi disebut sebagai
efek diabetogenik.
8
Penelitian terakhir membuktikan bahwa DMG terjadi
akibat kombinasi resistensi insulin dan sekresi insulin yang
berkurang dengan waktu paruh insulin yang tidak berubah.
Resistensi insulin ini terutama diakibatkan oleh hormon
Kortisol, Progesteron, hCS, Prolaktin dan Estradiol .Williams
Obstetrics 2001 masih menyatakan bahwa human Placental
Lactogen yang paling besar pengaruhnya terhadap resistensi
insulin.
Potensi
Elevasi diabetoje
Hormon puncak nik
minggu
Prolaktin Lemah
10
minggu Sangat
Estradiol
26 lemah
minggu
HCS Sedang
26
minggu Sangat
Kortisol
26 kuat
Progester minggu
Kuat
on 32
9
Rendahnya autoantibody ICA, IAA dan GAD menunjukkan
tidak adanya kerusakan sel B pankreas oleh autoantibody,
tetapi banyak ahli berpendapat bahwa ibu hamil dengan DMG
nampaknya merupakan fase awal proses IDDM.
Perubahan metabolisme karbohidrat ini seharusnya
menyebabkan penapisan ataupun diagnosis DMG tidak sama
dengan wanita yang tidak hamil.
Gambar 2.
Efek Kehamilan normal cukup bulan pada glukosa dan insulin
plasma
10
HIPOTESIS PEDERSEN 1
MATERNAL PLACENTAL FETAL
INSULIN INSULIN :
SENSITIVE INSENSITIVE
GROWTH
PLASMA
GLUCOSE
AMINO ACIDS INSULIN
LIPIDS
‘ MIXED
NUTRIENTS ‘
11
dari 4 kg) atau indikasi waktu (> 38 minggu). SC hanya
dilakukan atas indikasi obstetris dan menyusui tetap dianjurkan
pada ibu ibu dengan DMG..
Tindak lanjut pasca salin merupakan hal yang sangat
penting karena efek jangka panjang DMG yaitu timbulnya
diabetes nyata dengan melakukan TTGO 75 g 6 minggu pasca
salin. Dikatakan sebagai Gangguan Toleransi Glukosa bila
kadar glukosa plasma lebih atau sama dengan 110 mg/dl dan
kurang dari 126 mg/dl dan 2 jam pp lebih atau sama
dengan 140 mg/dl dan kurang dari 200 mg/dl. Dikatakan
Diabetes bila lebih atau sama dengan 126 mg/dl dan lebih atau
sama dengan 200 mg/dl. ADA tahun 1998 merekomendasikan
kriteria baru yang lebih menyederhanakan kriteria lama
dengan hanya 1 x pemeriksaan tanpa tahapan penapisan dan
diagnosis. Bila ditemukan kelainan harus segera diterapi
termasuk edukasi penderita. Pada bayi dan anak anak juga
harus dilakukan pemantauan akan tanda tanda obesitas dan atau
ganguan toleransi glukosa.
POTENTIAL TERATOLOGY :
GESTATIONAL DIABETES
WEEKS OF PREGNANCY
12
PREGESTATIONAL DIABETES MELLITUS
Patients with either type 1 diabetes mellitus (T1DM) or
type 2 diabetes mellitus (T2DM), which existed before the
pregnancy have pregestational diabetes mellitus (PGDM).
Whereas, those with diabetes mellitus during pregnancy itself
have gestational diabetes mellitus (GDM).
Criteria for the diagnosis of diabetes mellitus are based
on PERKENI-CONSENSUS (2002) and the Report of the
Expert Committee on the Diagnosis and Classification of
Diabetes Mellitus (ADA-2003) and can be seen in TABLE 3.
13
DM, diabetes mellitus; FPG, fasting plasma glucose; 2-h PG,
2-h postload glucose. *) A diagnosis of diabetes must be
confirmed on a subsequent day by any one of the three
methods included in the chart. In clinical settings, the FPG test
is greatly preferred because of ease of administration,
convenience, acceptability to patients, and lower cost. Fasting
is defined as no calorie intake for at least 8 h. † This test
requires the use of a glucose load containing the equivalent of
75g anhydrous glucose dissolved in water.
Expert Committee
IGF (mg/dl) was Redefined from
110-125 to 100-125
(ADA-Fall 2003)
14
regression (sacral agenesis). Meticulous glycemic control may
reduce the malformation rate, which in poorly controlled
diabetic pregnancies may be 30% (about 12 times the
background rate).
Accelerated fetal growth is due to increased delivery of
glucose and other nutrients from the mother to the fetus, which
induce fetal hyperinsulinemia that promotes nutrient storage.
Global obesity, rapid skeletal maturation and hypertrophy of
the heart and liver may occur. Large for-gestational-age infants
are twice as common in diabetic as in non-diabetic
pregnancies.
Systematically, the multiple deleterious effects of the
pregnancy of diabetic patients on the offspring, during the
various periods of fetal and postnatal was be summarized by
Inzucchi 1999 (complications on: Fetus, Delivery, Neonate,
and Child - Adult).
* The complications on the fetus in the 1st trimester
Congenital Anomalies: if AIC in the 1st trimester higher
6SD above normal mean (Ryan 2003)
Spontaneous Abortions
Embryonic Growth Delay (EGD): Considerable data
indicate that embryonic growth may be inhibited in
hyperglycemic pregnancies; it has been postulated an
important role for hyperglycemia as an “improper
culture medium” for the developing blastocyst
(Pedersen et al 1986).
Intra Uterine Growth Restriction (IUGR)
Extrinsic IUGR results from nutrient limitation
associated with maternal hypertension and advanced
diabetic vasculopathy (Moore 1999). On ultrasound
examination, extrinsic growth retardation is
characterized by slowing abdominal growth and
plateauing or cessation of weight gain. If allowed to
progress uncheck, extrinsic IUGR leads to
olygohydramnios, hypoxia, asphyxia, or fetal death. In
15
diabetic pregnancy, asymmetric IUGR is most common
in patients with vasculopathy (retinopathy,
nephropathy, chronic hypertension). Diabetic women in
long-standing disease (> 10 years) and coexisting
nephropathy are particularly at risk for IUGR.
16
d. Pyelonephritis ± 4%
e. Cesarean Section (two-fold higher than for non-
diabetic).
2. Diabetic Complications
a. Retinopathy10-55% progression from preconception
to one month postpartum (Ryan 2003)
b. Nephropathy (as in Retinopathy): increased risk of
hypertension and pre-eclampsia, proportional to pre-
pregnancy proteinuria (Ryan (2003)
c. Neuropathy
d. Macrovascular Diseases.
17
regulatory hormonal responses (Diamond et al 1992). Severe
hypoglycemia does indeed occur frequently during tightly
controlled diabetic pregnancies. One study reported: 80% cases
occurred before the 20th gestational week (median at the 12th
week) and 77% occurred during sleep. Fortunately, despite
this, however, no permennet maternal sequelae were seen and
fetal outcome was favorable, with no perinatal mortality or
congenital anormalies (Kimmerle et al 1992).
Importantly, the tendency toward ketosis in women
with diabetes is accentuated. Hence, omission of insulin
injections or the development a superimposed infection may
result in diabetic ketoacidosis more rapidly than would
normally occur in the nonpregnant situation.
18
for patients with PGDM, whereas the Diet-B1 is prescribed for
those with GDM pregnant women.
602 12
19
Tabel 4. Luaran perinatal
Jm
Ket
l
Makrosomia 2
Kematian janin -
intra uterine
Kematian 2
neoanatus
Kelainan bawaan 1 meningg
janin al
SC 2
Ekstraksi vakum 1
BMI >31 3
DM paska salin 1
19
Ekstraksi
Vakum, 23%
SC, 47%
Spt. B, 30%
20
BERAT BADAN LAHIR PENDERITA DIABETES MELLITUS
PERIODE JANUARI – AGUSTUS 2003
DI RSU DR. SOETOMO (64/2392)
5001-5500 gr,
3000-3500 gr, 2%
3501-4000 gr, 4501-5000 gr,
2%
27% 14%
4001-4500 gr,
55%
IV.SKRINING ( PENAPISAN )
DIABETES MELLITUS
GESTASIONAL
21
Semua wanita hamil (universal screening bukan selective
screening )berarti tanpa melihat adanya faktor risiko termasuk
usia diatas 30 tahun , riwayat keluarga diabetes, pernah
melahirkan bayi besar / mati / cacat, obesitas, hipertensi dan
glukosuria. Bila yang diperiksa hanya yang mempunyai faktor
risiko, hampir 50 % DMG tidak terdiagnosis. Dan dalam
kriteria ADA, yang termasuk indikasi universal screening ,
salah satunya adalah keturunan Asia. Kecenderungan yang
sekarang dilakukan adalah penapisan hanya atas indikasi.
Dilakukan penapisan pada minggu ke 24 - 28 karena DMG
jarang yang terjadi minggu awal karena kadar hormon
kehamilan mencapai puncak pada trimester tiga awal dan tidak
lebih dari 28 minggu supaya sel B janin belum terangsang
sehingga hiperinsulin janin belum terjadi.
Penapisan ini cukup sederhana dengan sensitivitas dan
spesifisitas cukup baik dan harga yang masih terjangkau. Dari
Workshop yang ke empat 1998,dianjurkan penapisan pada
kunjungan antenatal pertama dengan membagi ibu hamil
menjadi risiko rendah, sedang dan tinggi untuk terjadinya
DMG. (Berubah dari universal screening menjadi selective
screening). Nilai ambang 140 mg/dl dapat mengidentifikasi 90
% kasus DMG dimana 15 %nya harus di TTGO. Bila
diturunkan menjadi 130 mg/dl sensitivitas meningkat tetapi
yang harus di TTGO menjadi 25 %.
22
Nilai yang dianggap standar adalah kadar gula puasa 105
mg/dl, 1 jam 190 mg/dl, 2 jam 165 mg/dl dan 3 jam 145
mg/dl. Dua angka ini diambil lebih berdasarkan timbulnya DM
berikutnya dibanding luaran perinatalnya sehingga beberapa
ahli menyarankan kriteria yang spesifik untuk kehamilan dan
luarannya. Misalnya Tallarigo dkk menemukan bahwa
kejadian makrosomia berhubungan dengan nilai 2 jam pp.
Bila hasil penapisan > 185 mg/dl atau puasa > 126 mg/dl
diagnosis dapat langsung dibuat tanpa TTGO.
DIAGNOSIS DM GESTASIONAL
23
VII. PENYULIT DIABETES MELITUS
GESTASIONAL
24
Banyak bukti yang menyatakan bahwa insulin dan insulin-like
growth factors (IGF -I dan II) merupakan faktor pertumbuhan
janin dengan merangsang diferensiasi dan divisi sel.
25
SUMMARY
Normal pregnancy induces insulin resistance through
the diabetogenic effects of the placental steroid and peptide
hormones, e.g., prolactine, estrogens, progesterone, hCS and
cortisol (bound and free) with their maximal effects in the late
2nd and 3rd trimester. In non-diabetic women, pregnancy may
induce gestational diabetes mellitus (GDM) or impaired
glucose tolerance (IGT), while subjects with pre-exiting
glucose intolerance may become overtly diabetic.
The classification recommended by the American
College of Obstetrician and Gynecologists (ACOG) in 1986
subdivided women with GDM according to their degree of
glycemia. Class-A in White Classification was placed into
GDM. Specifically, those with fasting plasma glucose (FPG) <
105 mg/dl and 2-hour Postprandial Glucose (2-h PG) < 120
mg/dl are classified into Class-A1 (Diet-treated), whereas those
with FPG > 105 mg/dl and 2-h PG > 120 mg/dl are placed into
Class-A2 (Insulin-treated).
For practical and clinical reasons, alternative
classification of diabetes in pregnancy into Progestational
Diabetes Mellitus (PGDM) and GDM can be rationally
accepted.
Multiple deleterious effects of the pregnancy of a
diabetic patient should be recognized, and tight glycemic
control is really essential to minimize perinatal morbidity and
mortality.
Particularly before 8 weeks’ gestation, during the
period of organogenesis, hyperglycemia is teratogenic. The
malformation rate is related to the severity of hyperglycemia
(via myoinositol depletion and generation of free radicals).
Pregnancy may worsen renal function (occasionally
irreversible) and retinopathy (especially preproliferative and
proliferative stages).
Healthy lifestyle (medical nutrition therapy = MNT,
regular exercise, etc) should be well socialized to women with
26
diabetes. If FPG > 105 mg/dl and 2-h PG > 120 mg/dl, human
insulin therapy should be started, otherwise the goals targeted
for blood pressure (< 130/80 mmHg) and lipid profiles (LDL-
Chol. < 100-130 mg/dl, Triglycerides < 150-200 mg/dl) should
be reached as well.
Based on clinical experiences, Diet-KV (for PGDM) or
Diet-B1 (for GDM), Diets T1, T2, T3, and Diet-L (for Trimester
1, 2, 3, and Lactation, respectively) can be prescribed.
Otherwise, Formula 2.5-1, Formula 1-2-3, and Formula-12
may be used to get good glycemic control during Bagor and
delivery.
Breast-feeding should be encouraged in women with
GDM; education on diabetes mellitus and long-term
therapeutic considerations for patients with GDM must be well
programmed and closely monitored.
Offspring of women with GDM should be followed up
closely for the possibility of insulin resistance and the
development of obesity and / or glucose intolerance.
Conclusions: Pregnancy induces insulin resistance with
its metabolic and clinical consequences. Maternal diabetes can
adversely affects the fetus, neonates, and may cause other
multiple deleterious effects. For clinical point of view, PGDM
and GDM should be differentiated. Diet-KV (for PGDM),
Diet-B1 (for GDM), and Diets-T1, T2, T3, and L (for Trimester
1, 2, 3, and Lactation, respectively) can be prescribed on
appropriate indications.
Otherwise, Formula 2.5-1, Formula 1-2-3, and Formula-12 can
be used for rapid glycemic control and its maintenance during
Bagor and delivery. Importantly, pregnancy may worsen pre-
existing nephropathy, retinopathy, neuropathy, and other
macrovascular disease. Good preconception care of diabetic
women and high risk groups of GDM, and meticulous
glycemic control of maternal diabetes may improve perinatal
morbidity and mortality. Women with GDM and the offsprings
should be closely followed-up.
27
KEPUSTAKAAN
1. Adam JMF. 1999. Beberapa Ketidaksepakatan pada Diabetes
Mellitus Gestasional. Dalam Asdie HAH, Wiyono P. (eds).
Naskah Lengkap Pertemuan Ilmiah Tahunan Nasional Endokrin,
Jogyakarta.
2. American Diabetes Association. 1999. Clinical Practice
Recommendations. Gestational Diabetes Mellitus. Diabetes Care
vol 22 (Suppl. 1).
http://www.diabetes.org/diabetescare/supplement199/S74
3. Carr DB, Gabbe S. 1998. Gestational Diabetes : Detection,
Management, and Implications. Clinical Diabetes.16:1.
http://www.diabetes.org/clinicaldiabetes//v16n1j-f98/pg4.htm.
4. Cunningham FG, Gant NF, Leveno K.J. et al. 2001. Williams
Obstetrics (21st ed); New York: Mc GrawHill
5. Hermanto Tri Joewono., Agus Abadi. 1991. Luaran Perinatal
Kehamilan dengan Diabetes Mellitus Gestasional di RSUD Dr
Soetomo Surabaya. Penelitian untuk Tugas Akhir PPDS I.
6. Hermanto Tri Joewono. 2001. Diabetes Mellitus Gestasional.
Dari Sullivan-Mahan sampai PERKENI. Dari Gold Standard
sampai Konsensus. Grahabik: Surabaya Diabetes Update VI.
7. Hermanto Tri Joewono. 2002. Diabetes Mellitus Gestasional.
Makalah untuk Buku Ajar K Feto-Maternal
8. Hermanto Tri Joewono. 21 2002. Sekali Lagi tentang Diabetes
Mellitus Gestasional. Pertemuan Ilmiah Tahunan POGI. Batu.
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1997
10. Kuhl C. 1998. Etiology and Pathogenesis of Gestational
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R.K., Resnik, R. (eds). Maternal-Fetal Medicine(4th ed).
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Buku Acuan Nasional Pelayanan Kesehatan Maternal dan
Neonatal. 290-299. Jakarta: YBPSP
28
REFERENCES
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29
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30
SUSUNAN ORGANISASI
Pelindung : Direktur RS
Ka Bag/SMF Obs Gin
Ka Bag/SMF IPD minat PDN
Ka Bag/SMF Anak & Neonatologi
Ka Bag/SMF Anesthesi
Ka Instalasi Gizi
Anggota
1. Seluruh anggota Divisi Kedokteran Fetomaternal
2. Seluruh anggota Sub Bagian Neonatologi
3. Pusat Diabetes & Nutrisi,
Minat : dr……………………
4. Seluruh anggota Bag/SMF Anestesi
Minat : dr……………………
5. Instalasi Gizi,
Minat : dr……………………
31
Organisasi Tim Diabetes dalam Kehamilan :
RS
PANMED
RSSIB
TIM
DMK
32
USULAN PENELITIAN MULTISENTER
JUDUL:
PREVALENSI DM GESTASIONAL DI RS INDONESIA
PATOFISIOLOGI
DIABETES
MELLITUS
GESTASIONAL
SKRINING/ PENGOBATAN
DIAGNOSIS DIABETES
DIABETES MELLITUS
MELLITUS GESTASIONAL
GESTASIONAL
DIABETES
MELLITUS
DALAM
KEHAMILAN
PROFIL
PROFIL METABOLIK
METABOLIK DIABETES
MELLITUS
MAKROSOMIA
PRAGESTASIONAL
OBESITAS
DAN DM
DALAM
KEHAMILAN
33
LATAR BELAKANG MASALAH
TUJUAN PENELITIAN
METODE PENELITIAN
34
TABEL HASIL PENELITIAN:
4. LUARAN PERINATAL
a. BB BAYI
b. SKOR APGAR BAYI
c. CARA PERSALINAN
d. MORBIDITAS DAN MORTALITAS
NEONATAL
35