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IDENTITAS
Nama : By. Ny. DF
Tgl Lahir : 8 Januari 2014
Alamat : Krapyak
No.RM : 74.03.43
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MASALAH UTAMA
Takipneu, Ibu DM
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Riwayat Penyakit Sekarang:
1 minggu yll,lahir bayi perempuan dari ibu P3A0, secara spontan,
saat lahir bayi tidak menangis, tidak bergerak, sianosis seluruh tubuh,
Apgar score 3/7, dilakukan resusitasi s/d oksigen aliran bebas. Air ketuban
hijau keruh, meconium (-).
Ibu bayi adalah penderita hipertensi, tidak kontrol rutin, tensi
dikatakan 130-140an, selama hamil tensi 160an. Diketahui DM saat
mondok di RSS.
ayah bayi meninggal 6 bulan yll, dikatakan sakit jantung(?)
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RIWAYAT KELUARGA
Tidak ada riwayat atopik pada keluarga
Tidak ada riwayat penyakit kongenital lainpada keluarga
Curiga ada penyakit jantung di keluarga
Terdapat riwayat hipertensi pada ibu
pasien
Terdapat riwayat DM pada ibu
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Silsilah keluarga
27th,
obese(+),
Hipertensi
(+),DM(+)
45th,peny.jantung
(+),DM(-)
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RIWAYAT KEHAMILAN DAN KELAHIRANANC:rutin kontrol di bidan puskesmas, rutin minumvitamin, hamil ke-3, riwayat trauma -, minum jamu -,minum obat-obatan -, sakit hingga mondok -,perdarahan -, hipertensi (+)
NC:lahir di RSS, spontan, BBL: 5280 gram, umurkehamilan 38minggu, PB 54cm , lingkar kepala38cm,lingkar dada 38.5cm, LLA 14cm, tidak menangis,biru +, kekuningan -
PNC:NICU
Kesan: simpulan riwayat kehamilan,dan persalinankurang baik
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Anamnesis sistem
Demam (-)
Sistem CNS: kejang (-), penurunan kesadaran (-)
Sistem respirasi: sesak (-), batuk (-), pilek (-)
Sistem kardiovaskular: sesak (+), kebiruan (-),bengkak (-)
Sistem gastrointestinal: meconium(+), intake SF
12x10-15cc
Sistem genitourinaria : miksi (+)
Sistem integumentum:sianosis (-), ikterik (-)
Sistem muskuloskeletal: deformitas (-),
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Kesan Umum: gerak aktif, kesan gizi cukup
Tanda Utama:
HR 125x/menit, R 65x/menit, retraksi (-)
T 36,8C, suhu aksila
SpO2: 97% (NCPAP, FiO2 4lpm)
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Pemeriksaan Antropometri BB 5280 g,
TB 54 cm,
LLA 14 cm, LK 38 cm,
LP 36 cm,
LD 38.5cm
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JVP meningkat (-), limfonodi tidak teraba
LEHER
DP//DD,BU (+) dbn,Hepar& Lien tak teraba
PERUT
perempuan
ANOGENITAL
Gerakan bebas, akral hangat, perfusi baik CRT
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petechiae (-), kering
Atrofi (-), tonus menurun
Deformitas (-), Fraktur (-)
Deformitas (-), dislokasi (-)
KULI T
OTOT
TULANG
SENDI
Pemeriksaan Jasmani
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Kepala
Ukuran : normal
Mata : konjungtiva anemis, sklera tak ikterik
Pulmo : Insp. : simetris, KG (-), retraksi (-)
Palp. : stem fremitus kanan = kiri
Perk. : sonor
Ausk. : vesikuler (+) N, menurun pada SIC VI kebawah
RBK -/+,RBB -/-, wheezing -/-
Cor : Insp. : IC tak tampak
Palp. : IC teraba di SIC VI LMCS, thrill (-), RV heaving (-)Perk. : kesan kardiomegali (+)
Ausk. : S1N S2 split tak konstan, reguler, bising sdn
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LABORATORIUM
Hb : 14.1
AL : 25.9
AE : 4.29
AT : 277
Hmt : 44
S : 54
L : 37
M : 6.1
E : 0.4B : 0
Alb : 3.28
BUN : 31.7
Cre : 12.3
GDS : 47
Tbil :7.33Dbil : 0.55
Na :142
K : 3.92
Cl : 103Ca : 1.73
CRP :
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BBLB, CB, BMK, spontan, ibu PEB, DM
Sepsis neonatorum
Hipoglikemia neonatus
Problem:
Kardiomiopati?
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Echo (8januari 2014)
Situs solitus, AV-VA concordance
Muara vv pulmonales dan sistemik normal
IVS dan LVPWD menebal ringan (IVS 6mm,
LVPWD 5.7mm, LVIDd 16 mm) IAS dan IVS intak
Katup-katup baik
Kontraaktilitas LV baik
Arc.Ao ada di kiri, tak tampak CoA maupun PDA Kesimpulan : LVH konsentrik ringan
Saran: propanolol 0-5-1mg/kgBBhari
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Infants of Diabetic Mothers
Prevalensi: 1.3% dari seluruhan
kehamilan
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Patofisiologi
DM mempengaruhi multi-organ
Prevalensi malformasi kongenital padaa
bayi dengan ibu DM 6-9% (3-4x > bayi
biasa)
Neural tube
defect(anencephali/myelomeningocele),
congenital heart defect, sacraldysgenesis/agenesis adalah yang
tersering
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Congenital heart defect, cardiomyopathy,
persistent pulmonary hipertensi of the
newborn
Tersering: VSD, TGA, truncus
arteriosus, tricuspid coarc aorta
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CLINICAL
MANIFESTATIONS 1. The history usually reveals gestational or insulin-dependent diabetes mellitus in the mother. The
patient often has a history of progressive respiratory distress with tachypnea (80 to 100
breaths/minute) from birth.
2. These large-for-gestational-age babies are often plethoric and mildly cyanotic and may have
tachypnea and tachycardia (>160 beats/minute). Signs of congestive heart failure (CHF) with gallop
rhythm may be found in 5% to 10% of these babies. The patient may have a systolic murmur along
the left sternal border, which may be caused by an outflow tract obstruction or an associated defect.
3. Chest x-ray films may reveal a varying degree of cardiomegaly. Pulmonary vascular markings are
normal or mildly increased because of pulmonary venous congestion.
4. The ECG is usually nonspecific, but a long QT interval caused by a long ST segment secondary to
hypocalcemia may be found. Occasionally, RVH, LVH, or biventricular hypertrophy (BVH) may be
seen.
5. Echo may show the following:
a. The ventricular septum is often disproportionately thicker than the LV free wall, but even
free walls are thicker than normal (see Fig. 18-7 ). The degree of asymmetrical septal hypertrophy has
no relationship to the severity of the maternal diabetes.
b. Supernormal contractility of the LV and evidence of LVOT obstruction appear in about 50% of
infants with cardiomyopathy.
c. Rarely, the LV is dilated, and its contractility is decreased.
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General supportive measures are provided, such as intravenous
fluids, correction of hypoglycemia and hypocalcemia, and
ventilatory assistance, if indicated.
2.In most cases, the hypertrophy spontaneously resolves within the
first 6 to 12 months of life. - Adrenergic blockers, such as
propranolol, may help the LVOT obstruction, but treatment isusually not necessary. Digitalis and other inotropic agents are
contraindicated because they may worsen the
obstruction.
3. If the LV is dilated with decreased LV contractility, the usual
anticongestive measures (e.g., digoxin,diuretics) are indicated.
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Transient Hypertrophic Cardiomyopathy in Neonates
Recently, transient HCM in neonates who had perinatal
injury with acute fetal distress has been described.
Initially, echo studies showed abnormal LV systolic anddiastolic function but the LV wall thickness was normal. The
hypertrophy of the LV occurred between days 2 and 7 and
affected initially the interventricular septum and later the LV
posterior wall, but it disappeared in all cases between 1 and
5 months of life. Acute fetal distress with myocardial
ischemia is believed to have caused the hypertrophy. The
prognosis of this type of HCM is good, in contrast to that of
other primitive HCM occurring in neonates ( Vaillant et al,
1997).
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THANK YOU