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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