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Asfiksia Neonatorum

Dr.Bambang Mulyawan SpA


Fakultas Kedokteran Universitas Muhammadiyah Malang

Pendahuluan (1)

Asfiksia Bayi Baru Lahir (BBL) : 15% kematian BBL (5 juta) /tahun Angka kejadian asfiksia di RS Propinsi : 25,2% (Jawa Barat) Angka kematian asfiksia di RS Pusat Rujukan Propinsi di Indonesia : 41% 10% BBL membutuhkan bantuan untuk mulai bernafas ( bantuan ringan res.lanjut yg ekstensif) 5% BBL membutuhkan tindakan resusitasi ringan 1% - 10% BBL di RS perlu bantuan ventilasi, hanya sedikit yg perlu intubasi dan kompresi dada

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Pendahuluan (2)

Sebagian besar bayi yaitu sekitar 90% tidak membutuhkan atau hanya sedikit memerlukan bantuan untuk memantapkan pernafasannya setelah lahir dan akan melalui masa transisi dari kehidupan intrauterin ke ekstrauturin tanpa masalah.

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Pendahuluan (3)
6-10 out of 130 mill newborns need intervention at birth 4 mill birth asphyxia 1 mill die and a similar number develop sequels due to birth asphyxia (CP, Epilepsia)

Most newborn infants are born outside hospitals without health personel attending

Pendahuluan (4)
Infant resuscitation required in 6% of all births. Asphyxia usually not anticipated. All labor and delivery units required to be skilled in neonatal resuscitation (Standard of Practice) NALS (Neonatal Advanced Life Support)

Definisi (1)
Asfiksia neonatorum : BBL yang tidak dapat bernafas secara spontan dan teratur pada saat lahir atau beberapa saat setelah lahir. BBL : Bayi Baru Lahir pada menit-menit pertama sp beberapa jam selanjutnya Periode neonatal : lahir 28 hari

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Definisi (2)
Asfiksia

BBL ditandai dg keadaan : *hipoksemia *hiperkarbia *asidosis

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Definisi (3)

Karakteristik asfiksia BBL /Perinatal (menurut AAP dan ACOG -2004 ) : 1. asidemia metabolik atau campuran (metabolik dan respiratorik) yang jelas, yaitu ph<7, pada sampel darah yang diambil dari a.umbilikal 2. nilai Apgar 0-3 pada menit ke 5 3. manifestasi neurologi pd periode BBL segera, termasuk kejang,hipotonia,koma atau ensefalopati hipoksisk isemik 4. terjadi disfungsi sistem multiorgan segera pada periode BBL

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Definisi (3-a)

Inconsistent Definitions Criteria for Neonatal Asphyxia (APA and ACOG, 1992) Profound metabolic (or mixed) acidosis (ph < 7.0) Persistence of Apgar score 0 - 3 for > 5 minutes Clinical neurological sequelae Evidence of multi-organ system dysfunction

Definisi (4)

This is pathologic condition referred to neonate who have no spontaneous breathing or represented irregular breathing movement after birth. Usually caused by perinatal hypoxia. It is emergency condition and need quickly treatment (resuscitation).

Definisi (4-a) birth asphyxia is defined simply as the failure to initiate and sustain breathing at birth The common worry of health professionals and parents is the permanent brain damage that birth asphyxia can cause.

Patofisiologi asfiksia (1)

BBL mempunyai karakteristik yg unik. Alveoli paru janin dalam rahim berisi cairan paru lahir nafas pertama udara masuk alveolicairan paru diabsorpsi oleh jaringan paru dstseluruh alveoli berisi udara oksigen. Paru membutuhkan tek.puncak inspirasi dan tek.akhir ekspirasi yg tinggialiran darah paru meningkat. Kegagalan penurunan resistensi vaskuler paru hipertensi pulmonal persisten pada BBL (Persisten pulmonary Hypertension of the neonate ) aliran drh paru inadekuat dan hipoksemia relatifekspansi par < gagal nafas ! ! !

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Patofisiologi (1-a)
Production of lung fluid diminishes 2-4 days before delivery 80-100 ml remain in the passageway of a full term infant during the birth, fetal chest is compressed and squeezes fluid

Patofisiologi (1-b)
First breath is inspiratory gasp Changes trigger aortic and caratoid chemo receptors that trigger brains respiratory center Natural result of a normal vaginal delivery

Patofisiologi (1-c)

Significant decrease in environmental temperature after birth Stimulates skin nerve endings Newborn responds with rhythmic respirations Excessive cooling may lead to profound depression of cold stress

Patofisiologi (1-d)

Onset of respiration stimulates cardiovascular changes As air enter the lungs, oxygen content rises in alveoli and stimulates relaxation of pulmonary arteries

Patofisiologi (1-e)

Patent ductus arteriosus closes With increased oxygenated pulmonary blood flow and loss of placenta, systemic blood flow increases, foreaman ovale closes, and PDA begins to close Leads to decrease in pulmonary vascular resistance-allows complete vascular flow to the lungs

Patofisiologi (2)
When fetal asphyxia happens, the body will show a self-defended mechanism which redistribute blood flow to different organs called interorgans shunt in order to prevent some important organs including brain, heart and adrenal from hypoxic damage.

Patofisiologi (3)

Hypoxic cellular damage : _reversible ( early stage ) _unreversible damage Primary apnea Secondary apnea Other damage : persisten pulmonary hypertension, hypo/hyperglicemia, hyperbilirubinemia

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Etiologi / Faktor resiko (1)


Maternal factor: hypoxia, anemia, diabetes, hypertension, smoking, nephritis, heart disease, too old or too young,etc Delivery condition: Abruption of placenta, placenta previa, prolapsed cord, premature rupture of membranes,etc Fetal factor: Multiple birth, congenital or malformed fetus,etc

Etiologi / faktor resiko (2)

Anticipate Asphyxia Preterm delivery Thick meconium Acute fetal or placental hemorrhage Use of narcotics in labor Maternal infection Polyhydramnios: GI obstruction Oligohydramnios: Hypoplastic lungs

Manifestasi klinis (1)


Fetal asphyxia fetal heart rate: tachycardia bradycardia fetal movement: increase decrease amniotic fluid: meconium-stained

Manifestasi klinis (2)


Apgar score: A: appearance(skin color) P: pulse(heart rate) G: grimace(reactive ability) A: activity(muscular tension) R: respiration

manifestasi klinis (2-a)


Assign Apgar Score at 1, 5, and 10 Minutes. Apgar Score more useful in Term than Preterm Infant, but not specific for diagnosis of neonatal asphyxia. Cord Arterial Blood Gases: Ph (< 7) and Base Deficit ( > - 4 ).

Manifestasi klinis (2-b)

Degree of asphyxia: Apgar score 8~10: no asphyxia Apgar score 4~8: mild/cyanosis asphyxia Apgar score 0~3: severe/pale asphyxia

Apgar Score
Score Heart Rate Respiratory Effort 0 Absent Absent, irregular 1 <100 Slow, crying 2 >100 Good

Muscle Tone
Reflex irritability (nose suctioning) Color

Limp
No response Blue, pale

Some flexion of extremities


Grimace Acrocyanosis

Active motion
Cough or sneeze Completely pink

Apgar V. Anesth Analg 1953; 32:260 Scoring at 1 and 5 minutes of age Additional scoring could be continued at 5 minute intervals if needed

Resusitasi BBL (1)


Tujuan resusitasi BBL adalah untuk memperbaiki fungsi pernafasan dan jantung bayi yang tidak bernafas. Penilaian pada bayi yang terkait dengan penatalaksanaan resusitasi dibuat berdasarkan keadaan klinis.

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Resusitasi BBL (1-a)


Tujuan :
1 Expansion of lungs(by clearing upper airways & ensuring patent route to the trachea) 2 Increasing the arterial PO2 (by providing adequate alveolar ventilation,with O2 if needed) 3 Supporting adequate cardiac output 4 Ensuring that O2 consumption by newborn is minimized (by reducing heat losses in the immediate postpartum period)

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Resusitasi BBL (2)

Tindakan yang paling penting dan efektif pada resusitasi neonatus adalah pemberian ventilasi pada paru-paru bayi baru lahir dengan oksigen

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Resusitasi BBL (2)

1) Basic Resuscitation

2)Advanced Resuscitation

ABCs of Resuscitation
A B C (A: Airway, B: Breathing, C: Circulation)

A - establish open airway Position, suction B - initiate breathing Tactile stimulation Oxygen C - maintain circulation Chest compressions Medications D. Drug E. Evaluation

Resusitasi BBL (2-a)

Neonatal Resuscitation Program

Johns Hopkins: The Harriet Lane Handbook: A Manual for Pediatric House Officers, 16th ed., Copyright 2002 Mosby, Inc.

BASIC RESUSCITATION

Basic Resuscitation

Initial steps: Thermal management Positioning Suctioning Tactile stimulation

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The important steps in resuscitation are: 1.Prevention of heat loss, 2.Opening the airway and 3.Positive pressure ventilation that starts within the first minute of life

The surface on which the baby is placed should always be warm as well as flat, firm and clean

This consists of : drying, positioning the neonate under radiant warmer to minimize heat loss and suctioning of mouth and nose (Tracheal suctioning if meconium present).
This should only take approximately 20 seconds

Drying provides sufficient stimulation of breathing in mildly depressed newborns and no further stimulation is appropriate

The second step (within 20-30 seconds of birth) is assessment of neonatal respiration

If the newborn is crying and breathing is normal, no resuscitation is needed

The upper airway (the mouth then the nose) should be suctioned to remove fluid if stained with blood or meconium

If there is no cry, assess breathing: if the chest is rising symmetrically with frequency >30/minute, no immediate action is needed

If the newborn is not breathing or gasping: immediately start resuscitation.

Occasional gasps are not considered breathing.

Open the airway Put the baby on its back Position the head so that it is slightly extended .

Position of Newborn for Resuscitation

Illustrations courtesy to Resuscitation of Babies at Birth (Royal College of Paediatrics and Child Health and Royal College of Obstetricians and Gynaecologists. London: BMJ Publishing, 1997)

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Place Under warmer Dry thoroughly Remove wet linen Position Suction mouth then nose Tactile stimulation

Evaluate Respirations

Overview of Resuscitation

None
Inj. Narcan

Spontaneous

Yes
Drug Depressed

Evaluate HR No
HR <60 Ct Ventilation + Chest compression

PPV
15-30 sec

HR
<100
>100

HR 60-100
-HR increasing Ct ventilation -HR not increasing (<80) Ct chest compression

HR >100 look for spont. Resp DC ventilation

Evaluate color
Blue Oxygen Dr.Said Alavi

Drugs if: HR <80,after 30 secs PPV +100% O2 +chest compression 15/06/1999

Observe Monitor

Pink

46 Association American Heart

Hubungan antara prosedur resusitasi dan jumlah bayi yang perlu prosedur tsb.
Most common treatment
Keep dry & warm Suction & stimulation

Oxygen
Establish effective ventilation Bag &mask Tracheal Intubation Chest compressions

Least common treatment

Drugs

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Gangguan napas pada bayi baru lahir


Apnea attack Respiratory Distress Syndrome Hyaline Membrane Disease

Apnea attack ( serangan apnu, episode apnu )


Keadaan bayi tidak bernafas untuk beberapa saat Abnormal : > 20 detik, disertai sianosis, bradikardi Pada hari-hari I kelahiran, biasanya berulang-ulang Sering pada bayi prematur ( berat lahir < 1.500 gr, kehamilan < 32 minggu )

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Etiologi

Imaturitas pusat pernafasan Obstruksi jalan nafas oleh lendir / susu Pada bbrp kelainan paru berat ( peny. hialin membran, pneumonia, perdarahan paru ) Gangguan SSP ( perdarahan intrakaranial, Kern icterus) Gangguan metabolik ( hipoglikemi, perubahan keseimbangan asam-basa cairan dan elektrolit )

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Sikap dan tindakan


Lakukan rangsangan mekanis ( mengubah letak bayi, memukul telapak kaki ) Bersihkan saluran nafas Berikan O2 dg sedikit tekanan Mencari dasar etiologinya Sikap selanjutnya sesuai dengan etiologi

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Respiratory Distress Syndrome

Sindroma Gangguan Nafas / SGN

Pendahuluan

Merupakan masalah yg sering dijumpai pd hari I kehidupan Bayi Baru Lahir Ditandai : takipnea, napas cuping hidung (NCH), retraksi interkostal, sianosis dan apnu Penyebab : - di dalam paru ( pneumotoraks/mediastinum, penyakit membran hialin, pneumonia aspirasi sindroma Wilson Mikity ) - di luar paru
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Definisi / pengertian

Definisi Gangguan Napas adl. suatu keadaan meningkatnya kerja pernafasan yg ditandai dengan : Takipnea : > 60 - 80 kali/menit Retraksi interkostal dan atau substernal slm inspirasi Napas Cuping Hidung ( NCH ) Merintih/ grunting saat inspirasi Sianosis ( sentral/bibir : jantung, hematologik, nafas ) Apnu atau henti napas ( dalam jam2 I : takipnea, retraksi, NCH, grunting, kadang dijumpai pd BBL normal. Jika menetap bbrp jam, waspada adanya ggn nafas/RDS )
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Hyaline membrane disease


Penyakit membran hialin Sindroma gangguan pernafasan idiopatik

Brief Introduction
Neonatal Hyaline Membrane Disease,
almost exclusively occurred in premature infants, with progressive dyspnea-respiratory distress: expiratory grunting, cyanosis and the vicious cycle of hypoxia if not be hindered. Respiratory distress defined as respiratory rate > 60, some grunting, retraction, flaring, and cyanosis in room air. Expiratory grunting is due to partial closure of the glottis, why?

Why?
Deficiency-pulmonary surfactant Symmetric alveolar atelectasis

HMD-CHEST X-RAY

Definition
Hyaline membrane disease HMD Deficiency of pulmonary surfactantPS Pulmonary alveoli collapse at the end of expiration Progressively aggravated respiratory distress shortly after birth Mainly in preterm infant Higher incidence rate with smaller gestational age Infant of DM mother, cesarean section, the second baby of twins

Etiologi

Belum sepenuhnya jelas Pematangan paru yg belum sempurna Berkaitan dg faktor pertumbuhan sal. nafas/paru Sering pd bayi prematur Pd ibu pend.gangguan perfusi darah uterus slm kehamilan : DM, toksemia grav.,hipotensi, SC, perdarahan Penyebab utama kematian prematur ( 50 70 %)

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patofisiologi

Pembentukan substansi surfaktan paru tidak sempurna alveoli kolaps pd akhir ekspirasi utk nafas berikut perlu tek.negatif> dan usaha inspirasi yg kuat hipoksia, retensi CO2 dan asidosis. Asidosis : oksigenasi jaringan <, kerusakan endotel terbentuk fibrin, jar.epitel rusak lapisan/membran hialin.

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Patofisiologi

( lanj.)

Atelektasis hipoksia asidosis transudasi penurunan aliran darah paru hambatan pembentukan substansi surfaktan atelektasis. Hal ini berlangsung terus : penyembuhan / kematian

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Gambaran klinis

Pada bayi BB 1.000 2.000 gram / masa gestasi 30 36 minggu, riwayat asfiksia atau gawat janin. Tanda gg pernafasan dlm 6 8 jam I, karakteristik pd 24 jam 72 jam Gejala gg nafas ok. atelektasis dan perfusi yg menurun : dispneu/hiperpnu, sianosis, retraksi suprasternal, epigrastium, interkostal, ekspiratory grunting. Bradikardi, hipotensi, kardiomegali, edema, hipotermi, tonus menurun.

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Gambaran radiologis
Gambaran klasik foto rontgen paru : bercak difus infiltrat retikulogranuler Untuk diagnosis dini, walaupun klinis belum jelas Untuk menyingkirkan DD : pneumotoraks, hernia diafragma.

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Gambaran laboratorium
Darah : asam laktat >, bilirubin >, kadar PaO2 <, kadar PaO2 > o.k.atelektasis dan pH < : asidosis metabolik dan respiratorik Funsi paru : frek.nafas >, tidal vol <, lung compliance <, fungsi ventilasi dan perfusi terganggu, dll

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Gambaran patologi dan histopatologi

Otopsi : atelektasis, membran hialin dlm alveolus atau duktus alveolaris, emfisema. Membran hialin : febrin, sel eosinofilik, dari darah atau sel epitel alveolus yg rusak

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Pencegahan
Mencegah kelahiran bayi prematur Pemberian kortikosteroid ibu hamil trimester III ( ? )

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Penatalaksanaan
Memberikan lingkungan yg optimal : suhu, humiditas Oksigen Pemberian cairan, glukosa, elektrolit Antibiotika

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Prognosis
Tergantung tingkat prematuritas Terjadinya displasia bronkopulmoner umumnya akibat tekanan positif terus menerus ( respirator )

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SEPSIS PADA BAYI BARU LAHIR

DEFINISI
Sepsis adalah infeksi aliran darah yang bersifat invasif dan ditandai dengan ditemukannya bakteri dalam cairan tubuh seperti darah, cairan sumsum tulang atau air kemih Sering terjadi pd bayi resiko : BKB, BBLR, Sindroma Ggn Nafas, lahir dari ibu berisiko

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Neonatal Infections
Sepsis Meningitis Pneumonia
Otitis Media Diarrheal Disease UTI Osteomyelitis Suppurative Arthritis Conjunctivitis Orbital Cellulitis Cellulitis - - Omphalitis

Bacterial / Viral / Fungal

Definisi

(lanj.)

Pembagian : - sepsis awitan dini - sepsis awitan lambat Sepsis awitan dini : di bawah 3 hari. Terjadi secara vertikal dari ibu hamil, selama persalinan/ kelahiran Sepsis awitan lambat : > 3 hari, kuman dari lingkungan, horizontal, nosokomial
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Neonatal Immune System


All neonates relatively immunocompromised Immature and Ineffective: Antibodies Complement Neutrophils Skin / mucosal barriers

Neonatal Bacterial Sepsis:


Disease Patterns

Early Onset Neonatal Sepsis (EONS)


Fulminant, multisystem illness < 5 days old Obstetrical complications Prematurity Perinatal acquisition High mortality, 5-50%

Late Onset Neonatal Sepsis (LONS) Sepsis or meningitis 5 days to 3 months old Perinatal or postnatal acquisition Lower mortality, 2-6%

Risk Factors for Early Onset Neonatal Sepsis

Primary (significant) Prematurity or low birth weight Preterm labor Premature or prolonged rupture of membranes Maternal fever / chorioamnionitis Fetal hypoxia Traumatic delivery Secondary Male Lower socioeconomic status African-American race

Remington and Klein, Sixth Edition, 2006

Early Onset Neonatal Sepsis:


Signs/Symptoms Strongly suggestive
hypoglycemia / hyperglycemia hypotension metabolic acidosis apnea shock DIC hepatosplenomegaly bulging fontanelle seizures petechiae hematochezia respiratory distress

Early Onset Neonatal Sepsis:


Signs/Symptoms

Nonspecific
lethargy, irritability temperature instability -- hypothermia or fever poor feeding cyanosis tachycardia abdominal distention jaundice tachypnea

Early Onset Neonatal Sepsis:


Summary

GBS is still the predominant organism isolated in EONS


Our efforts at IAP have reduced, but not eliminated, early onset GBS sepsis Obstetrical risk factors, including premature/near-term delivery and maternal intrapartum fever, help to identify the infants at highest risk for EONS Ancillary laboratory evaluations, including the CRP value, may assist in determination of the most appropriate length of therapy

Late Onset Neonatal Sepsis

Perinatal acquisition with later onset


Term or preterm Bacterial: GBS, Chlamydia Viral: HSV, CMV, HepB, HIV Fungal: Candida

Nosocomial acquisition
Health care associated infections Preterm or sick term infant

Late Onset GBS

Transmission - Perinatally or postnatally -- intrapartum prophylaxis


or neonatal treatment of early onset disease does not decrease risk of late onset disease

Symptoms -

7days - 3 months. Typically 3-4 weeks old.

Occult bacteremia or meningitis most common. However, focal infections (pneumonia, UTI, cellulitis, osteomylelitis, septic arthritis) may occur.

Diagnosis - Culture of blood, sputum, urine, abscess or other body


fluid.

Treatment - Penicillin, as with early onset disease.

Beberapa istilah

Sepsis sindroma respon inflamasi sistemik (Systemic Inflamatory Respons Syndrome SIRS) yg terjadi akibat infeksi bakteri, virus, jamur, parasit. Sepsis berat : disertai disfungsi organ kardiovaskuler dan ggn nafas akut atau terdapat ggn dua organ lain ( neurologi, hematologi, urogenital, dan hepatologi ) Syok sepsis terjadi bila masih dlm keadaan hipotensi walau telah mendapatkan cairan adekuat/cukup ) Sindroma disfungsi multi organ : bayi tidak mampu lagi mempertahankan homeostasis tubuh terjadi perubahan fungsi dua atau lebih organ tubuh.
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Neonatal Sepsis: Incidence

2/1000 live births with culture proven sepsis


Bacterial / Viral / Fungal 80% infants develop bacterial sepsis 20% infants perinatally acquired viral infections

~ 25% of infected infants have meningitis

Higher rate with preterm birth


26/1000 preterm infants with BW < 1000g 8-9/1000 preterm infants with BW 1000-2000g

Remington and Klein, Sixth Edition, 2006

Diagnosis

Masalah : gambaran klinis tidak spesifik tanda/gejala = peny.non infeksi ( sin. gn nafas, perdarahan intrakranial, gjl sepsis klasik ( pd anak besar) jarang pd bayi Baku emas : biakan darah Pemeriksaan penunjang : C reactive protein, biomolekuler, respon imun/sitokin ?

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Diagnosis ( lanj.)

Beberapa informasi yg diperlukan : - faktor resiko ( pd awitan dini/ lambat) - gambaran klinik - pemeriksaan penunjang Faktor resiko awitan dini : - faktor ibu : persalinan dan kelahiran kurang bulan, ketuban pecah lebih dari 18-24 jam, chorioamnionitis, persalinan dg tindakan, demam pd ibu (> 38.4 C ), infeksi sal.kencing ibu, faktor sosial dan gizi ibu. - faktor bayi : asfiksia perinatal, lahir rendah, kurang bulan, prosedur infasif, cacac bawaan
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Diagnosis ( lanj.)

Faktor resiko sepsis awitan lambat : - dirawat di ruang intensif, perawatan lama, nutrisi parenteral lama, dari alat perawatan bayi, infeksi nosokomial dari bayi lain/ perawat

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Etiologic Agents of Neonatal Sepsis


Frequency(%)

Group B Streptococci Escherichia coli Streptococcus viridans Staphylococcus aureus Enterococcus spp Coagulase-negative staphylococci Klebsiella pneumoniae Pseudomonas spp Serratia marcescans Others

40 17 7 6 6
5 4 3 2 10

*Schuchat et al, Pediatrics 105: 21-26, 2000

Congenital nasolacrimal duct obstruction


5% of all newborns
*absence of conjunctival injection! Warm compresses, gentle massage, watchful waiting 95% resolve by 6 months; if not, refer for probing (earlier if multiple episodes of dacryocystitis)

Conjunctivitis

Close contacts affected Unilateral bilateral Sticky discharge Diffuse redness Cornea and pupil normal Chloramphenicol
Cellulitis- Refer urgently Neonatal conjunctivitis: refer urgently

Risk of corneal perforation from n. gonorrhoea

Eye Care To Prevent or Manage Ophthalmia Neonatorum


Ophthalmia neonatorum Conjunctivitis with discharge during first 2 weeks of life Appears usually 25 days after birth Corneal damage if untreated Systemic progression if not managed Etiology N. gonorrhea 89 Normal Newborn Care More severe and rapid

Eye Care To Prevent or Manage Ophthalmia Neonatorum (continued)


Prophylaxis Clean eyes immediately 1% Silver nitrate solution Not effective for chlamydia 2.5% Povidone-iodine solution 1% Tetracycline ointment Not effective vs. some N. gonorrhea strains Common causes of prophylaxis failure

90 Normal Newborn Care

Summary
The essential components of normal newborn care include: Clean delivery and cord care Thermal protection Early and exclusive breastfeeding Monitoring Eye care Immunization
91 Normal Newborn Care

Dacryocystitis
Bacterial infection of nasolacrimal gland with duct obstruction Mgt:
Swab C+S

Topical + systemic antibiotics

Gonorrheal conjunctivitis
Hyperpurulent discharge at day 2-4

Potentially a disaster!! Mgt?


Need FSW Admit for antibiotics, eye irrigation, mgt of complications: corneal ulceration, scarring, synechiae formation Rx concomitantly for Chlamydia Rx mom and her partner

Chlamydial conjunctivitis
C. trachomatis : presents on day 3-10 (but may be up to 6 weeks) Mom with active untreated chlamydia: babe has 40% chance of infection Whats the real worry here?

10-20% have associated pneumonia untreated can lead to chronic cough and pulmonary impairment well with pneumonia and staccato cough Creps/wheezes; patchy infiltrates w/ hyperinflation CBC: eosinophilia Rx: systemic erythro x 14 days Treat mom and her partner,

Herpetic conjunctivitis

Day 2-16 Flourescein stain: dendritic ulcer Do FSW

Rx: IV acyclovir, topical vidarabine 30-50% of cases recur w/i 2 years

Omphalitis

When should the umbilical cord separate?

Usually w/i 2 weeks

Delayed separation: think of possible leukocyte adhesion defect

Omphalitis
erythema

and edema of umbilical area excellent medium for bacterial colonization poor hygiene or hospitalacquired infection Staphylococcus, Streptococcus, Gram (-) rods

Omphalitis

Purulent, foul-smelling discharge with erythema of surrounding skin Secondary to poor cord hygiene S. aureus/Group A Strep/Gm s Tx; topical care and systemic antibiotics (

Omphalitis: complications

Necrotizing fasciitis Sepsis Portal vein thrombosis Hepatic abscesses

Treatment
IV

Antibiotics Local cleaning Can rapidly progress to Necrotizing fasciitis (16%) Usually polymicrobial Rapidly fatal (50%) Surgical debridement necessary

10
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Physical Eamination

Vital signs RR 40-60 HR 120-160 Temperature axilary 35.5-37.5 Over bundling Heater

Etiology

Pathologically, any factors which interfere with the circulation between maternal and fetal blood exchange could result in the happens of perinatal asphyxia. These factors can be maternal factor, delivery factor and fetal factor.

Pathophysiology(I)

a.

Hypoxic cellular damages: Reversible damage(early stage): Hypoxia may decrease the production of ATP, and result in the cellular functions . But these change can be reversible if hypoxia is reversed in short time.

b. Unreversible damage: If hypoxia exist in long time enough, the cellular damage will become unreversible that means even if hypoxia disappear but the cellular damages are not recovers. In other words, the complications will happen.

Pathophysiology(II)
Asphyxia development: a. Primary apnea breathing stop but normal muscular tone or hypertonia, tachycardia(quick heart rate), and hypertension Happens early and shortly, selfdefended mechanismcould not be damage to organ functions if corrected quickly

b. Secondary apnea features of severe asphyxia or unsuccessful resuscitation, usually result in damage of organs function.

Pathophysiology(III)

a.

b.
c.

Other damages: Persistent pulmonary hypertension (PPHN) Hyper/hypoglycemia Hyperbilirubinemia

Clinic manifestations
Complications: CNS: HIE, ICH RS: MAS, RDS, pulmonary hemorrhage CVS: heart failure, cardiac shock GIS: NEC, stress gastric ulcer Others: hypoglycemia, hypocalcemia, hyponatremia

Management
ABCDE resuscitation A (air way) B (breathing) C (circulation) D (drug) E (evaluation)

1.Anticipation. 2.Adequate preparation. 3.Timely recognition. 4.Quick and correct action are critical for the success of resuscitation

Resuscitation must be anticipated at every birth. Every birth attendant should be prepared and able to resuscitate

Good management of pregnancy and labour/delivery complications is the best means of preventing birth asphyxia

For resuscitation: 1. A self-inflating Ambou bag (newborn size) 2. Two infant masks (for normal and small newborn), 3. A suction device (mucus extractor), 4. A radiant heater (if available), warm towels, a blanket and 5. A clock are needed

Neonatal Resuscitation Program

Johns Hopkins: The Harriet Lane Handbook: A Manual for Pediatric House Officers, 16th ed., Copyright 2002 Mosby, Inc.

Perinatal Asphyxia

Normal Birth Transition: Lung Expansion (after negative intrathoracic pressure) Cry (expiration against a partially closed glotis) Umbilical Cord Clamping BP Increases Massive Stimulation of Sympathetic Nervous System Pulmonary Vascular Resistance Falls
Gradual

Transition to Neonatal Circulation ( with

closure of Foramen Ovale and Ductus Arteriosis)

Perinatal Asphyxia

Transition in the Asphyxiated Neonate Primary Apnea: Spontaneous respiration can be induced with stimulation. May require Narcan Secondary Apnea: Following 1 minute of apnea 4 - 5 minutes of deep gasping Last gasp Requires vigorous ventilatory support within a few minutes or death will occur.

Apgar Score

Originally proposed as a predictor for newborns at risk for complications for bad outcomes (cerebral palsy) Outcomes If the Apgar score at twenty minutes after delivery is less than five, there is still only a 20% chance of a handicapping condition. Level of evidence (LOE) 5

Causes of Delayed Onset of Regular Respiration After Delivery

Acute asphyxia Chronic partial asphyxia Pre existing brain diseases Depression of respiratory center-drugs Trauma to CNS Prematurity Sepsis (GBS) Primary maternal diseases Anemia
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Failure to breath after birth


PO2 falls immediately to near zero
Acidosis Biophysical stigmata of Asphyxia

Brain damage or Aggravation of an existing CNS injury

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Effects of Asphyxia on Body Systems


CNS-most serious impact,neurologic sequelae CVS-heart failure, myocardial ischaemia, necrosis, cardiac dilatation,TR Lungs-RDS,massive pulmonary hemorrhage, pul.edema,suppression of surfactant production Kidneys-ATN,renal failure,myoglobinuria Temp. homeostasis-hypothermia,hyperthermia Others-NEC,SIADH,GH deficiency,liver necrosis, jaundice,coagulation defects, DIC

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One out of 50 requires active resuscitation in labor ward 5.7% of all deliveries found to be apneic & 25% of them need intubation 70% of infants that require resuscitation come from predictably high-risk situations 30% infants who need active resuscitation are born after an apparently normal labor, in which no e/o fetal compromise At every delivery someone capable of resuscitating the newborn baby needed -midwife -anesthetist -pediatrician -obstetrician (Gupta & Tizard 1967,Primhak 1984, Milner & Vyas-1985)
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Perinatal Complications Requiring a Pediatrician at Delivery


CS (6.2% will need intubation & ppv) Forceps Ventouse Breech (8% will need intubation & PPV) Malpresentations Multiple pregnancy Thick meconium staining of amniotic fluid Gestational age <36 weeks Fetal distress(sustained bradycardia,scalp pH <7.1) Fetal complications:
Rh disease & Hydrops Serious congenital malformations (by antenatal USG)

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At every delivery, wherever it takes place, there should be at least one person who is responsible for giving basic care to the baby, initiating resuscitation if necessary, and summoning more help if needed

(British Pediatric Association,1993)


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Assessment of Newborn After Delivery


As quickly after delivery as possible Record the response to resuscitation as a narrative in babies notes

Methods of assessment
Traditional way-Apgar score Cord blood analysis Other biochemical methods Clinical examination
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Apgar scores for different signs in Newborns


Sign Score

0
Heart rate Nil

1
<100

2
>100

Respiratory
effort Muscle tone

Absent
Flaccid

Gasping or
irregular Some tone Grimace Blue

Regular or
crying Active Cry or cough Pink centrally

Response to None stimulation Color White

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Factors Affecting Apgar Score


False positive score

False negative score


Prematurity Drugssedatives,narcotics,mgso4 A/c cerebral trauma Precipitate labor Cong. Myopathy Cong. Neuropathy Spinal cord trauma CNS anomaly Lungs-diaphragmatic hernia Airway-choanal atresia Cong. Pneumonia (GBS)
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Maternal acidosis High fetal catecholamine levels Some full term infants

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Limitations of Apgar Score

Affected by many factors, so low apgar score do not necessarily signify fetal asphyxia Do not predict neonatal mortality or subsequent development of CP (score normal in most cases with CP & incidence of CP is very low in those with apgar score 0-3 at 5 Mts..)

1 min. Apgar scorestrongly correlated with cord pH & an index of intrapartum asphyxia Apgar score beyond 1 min. (5,10,15 & 20min)reflective of childs changing condition & indicative of adequacy of resuscitative efforts Score 0-3 at 20 Mts.indicate high mortality & morbidity
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Cord Blood Analysis


Objective way to assess asphyxia Collection from a double clamped segment of umbilical artery Ideally should be done in all deliveries- at least in all high-risk cases Help to diagnose the neonates failure to breathe other than asphyxia

Limitations: -Poor relationship with Apgar score


-2% babies with normal Apgar score has pH<7.1 -Most babies with pH<7.1 have normal Apgar

If both Apgar & pH abnormal & no other cause detected, strongly s/o recent Asphyxia

Other biochemical indicesLactate,hypoxanthine,CPK


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Examination of the Newborn


Area Examination
Head-Fontanelle, sutures, ears, eyes,face, lip, and palate Arms-Numbers of fingers, palmar creases

Chest-Listen to heart and lungs


Abdomen-Umbilicus, groins, anus, genitalia

Back-Skin, spine
Legs -Toes, ankles, hips

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Conditions to Exclude in Initial External Examination of Newborns


Birth injuries

Abnormalities of limbs or digits


Cyanosis, tachypnoea, or grunting Imperforate anus

Cleft lip or palate


Significant naevi Ambiguous genitalia

Esophageal atresia (if polyhydramnios)


Other obvious congenital abnormality
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Labor Ward Management of Resuscitation


Preparation history equipment & drugs equipment check on arrival Initial care of baby after delivery (60-90 sec) start clock & note gestational age assess HR,RR,tone,reflexes dry,cover with warm blanket traditional apgar score at 1 minute if baby did not breathe quick assessment whether apnea primary or terminal
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Apnea
PRIMARY APNEA

HR>80,good peripheral perfusion,tone & reflexes Apgar score usually 4-7 The onset of gasping & regular respiration can be established by peripheral(tactile) stimulation HR<60, pale,apneic,poor tone & reflexes, Apgar score usually 1-3 Spontaneous respiration is never established unless actively resuscitated by intubation & PPV

TERMINAL (SECONDARY) APNEA


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Care After Initial Assessment


Most infants fall into four groups
Group 1. Fit & healthy,crying well (90-95%) Group 2. (primary apnea) (5-6%) Not breathing well,blue, Group 3. (terminal apnea) (0.2-0.5%) Pale,limp, apneic, HR<60 Group 4. Dead but resuscitatable (<0.1%)

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Management(contd.)
Group 1-Fit & healthy
Leave

this baby alone ! No vigorous suction Dry & wrap in warm blanket Inj.Vitamin K Give to mother for breast feeding
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Group 2-Primary Apnea

Prems <32 weeks


all with no respiration & fail to turn pinkintubate & IPPV

Full term
peripheral stimulation small percentage need bag & mask if no resp.By 1-3 min. Intubation & IPPV majority extubated & given to mother by 2-3 min. If still no respiration, consider terminal apnea, drug depression, neurologic illness or congenital defects

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Resuscitation With Bag & Mask

Illustrations courtesy to Resuscitation of Babies at Birth (Royal College of Pediatrics and Child Health and Royal College of Obstetricians and Gynecologists. London: BMJ Publishing, 1997) 15/06/1999 140 Dr.Said Alavi

Positive Pressure Ventilation - Correct Position & Size of Face Mask

Illustrations courtesy to Resuscitation of Babies at Birth (Royal College of Pediatrics and Child Health and Royal College of Obstetricians and Gynecologists. London: BMJ Publishing, 1997) Dr.Said Alavi

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Group 3-Terminal Apnea


5-10% of all apneic infants at 2 min Severely asphyxiated,never spontaneous respiration Intuabtion & IPPV,O2-most respond If HR<60-ECM & soda bicarb- majority improve,breathe & turn pink by 4-5 min If still no respiration, s/odrug depression-naloxone severe asphyxia & acidemia- soda bicarbonate

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Correct Positioning of Laryngoscope

Illustrations courtesy to Resuscitation of Babies at Birth (Royal College of Pediatrics and Child Health and Royal College of Obstetricians and Gynecologists. London: BMJ Publishing, 1997) 15/06/1999 143 Dr.Said Alavi

Group 4-Dead but resuscitatable


ECM Laryngoscopy,clear airways Intubation & IPPV(some respond & vigorous cry by 5-10 min) Endotracheal adrenaline UVC insertion & sodabicarb ECG monitoring Still no cardiac activity-sodabicarb,10% dextrose,ca.Gluconate,adrenaline Repeat adrenaline-still no response by 10 min-abandon resuscitation except in acute episode of asphyxia like shoulder dystocia or difficult breech (in these try resuscitation for 10 min more)
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External Chest Compression

Technique of chest compression-Note the position of


the thumbs on the midsternum,just below the nipples

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Group 4 (contd.)
Heart beat returns but cardiac output low or bradycardic-atropine 0.1 mg iv Lignocaine 1-2 mg/kg for V-tach or fibrillation Ca.gluconate 1-2 mmol 0f 10% soln. Albumin/plasma 10 cc/kg Admit in NICU Further management as terminal apnea

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Drugs for use in neonatal resuscitation


Adrenaline
Preparation 1 in 10 000 dilution (100 g/ml) Dose 1st and 2nd dose 10 g/kg (0.1 ml/kg); 3rd dose 100 g/kg ,(1 ml/kg) Route 1st dose, tracheal tube (provided that lungs are inflated); 2nd and 3rd doses, umbilical venous catheter

Sodium bicarbonate
Preparation 4.2% (0.5 mmol/ml) or 8.4% (1 mmol/ml) solution with equal volume of dextrose Dose 1-2 mmol/kg (2-4 ml/kg of 4.2% solution) via umbilical venous catheter; 2 doses may be given

Volume expanders
Preparations Plasma, or group O Rh negative blood that is not cross matched; 4-5% human albumin Dose 10-20 ml/kg via umbilical venous catheter over 5-10 minutes (may be repeated)

Naloxone hydrochloride*
Dose 100 g/kg (0.25 ml/kg) intramuscularly
*Never give to the baby of an opiate dependent mother
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Continuing Therapy After Terminal Apnea A.Infants with regular respiration If not pink by 5-10 min admit in NICU Monitor BP,PCV,hypocount,blood gases, CXR (in most all WNL, no further treatment, transfer to mother by 24-36hrs) Symptomatic >24-48 hrs-problems HIE Renal failure Myocardial damage
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B.Infants who do not start to breathe


Pink,good cardiac output,but by 20 min. No spont.respiration despite empirical drugsdelay further treatment until blood gas,glucose & CXR results Then treat according to results If all investigations WNL & apnea persistss/o profound neurologic problem with bad prognosis or underlying neurologic disorder or intractable cerebral edema Those fulfill criteria of brain deathdiscontinue from IPPV with parental consent
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Infants Who Do Not Respond to IPPV & Resuscitation


A Babies clinically assessed as asphyxiated, but despite all procedures still cyanosed & bradycardic at 5-10 min. B Vigorous & active babies with good respiratory efforts,yet cyanosed & fail to go pink- s/o unasphyxiated baby with serious malformations of CVS or RS C Babies born apneic with feeble efforts,needed intubation,goes pink but remain hypotonic with no or poor respiratory efforts - s/o primary neurologic or muscle diseases
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A.Asphyxiated Baby Not Responding to Resuscitation

Technical error in procedure(commonest) disconnection of equipment,tube in esophagus or in right main bronchus, insufficient inflation pressure,tubal block Very ill infant with serious underlying lung disease-RDS,MAS,congenital pneumonia, anemia Pneumothorax Profound & severe asphyxial insult Congenital structural anomalies preventing oxygenation
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B.Vigorous but Persistently Cyanosed


URT-choanal atresia,Pierre-Robin syndrome, laryngeal webs & cleft

Lung-hypoplasia(PPROM,Potters syndrome), pleural effusion,cong.cystic adenomatiod malformation,cong.lobar emphysema Extra pulmonary-diaphragmatic hernia (commonest), eventration,intrathoracic tumors, gross abdominal distention (ascitis, tumor, hepatosplenomegaly), small chest(asphyxiating thoracic dystrophy, thanatophoric dwarfism)
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C.Persistent Apnea,Hypotonia,good Cardiovascular Response


Severe terminal apnea Structural CNS or muscle disorder
Severe antenatal brain damage Fracture cervical spine or cord Dystropia myotonica Congenital myopathies Werdnig-Hoffman disease Brain tumor Degenerative brain disorder Ondines curse
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ABCD of Neonatal Resuscitation

Drugs
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Begin

Medications
Adrenaline Volume expander Sodium Bicarbonate

HR- Zero or HR <80/Mt after 30 sec PPV +chest compression


Can be repeated every 5 Minutes

Adrenaline

HR>100

Yes DC drugs

Metabolic Acidosis Soda Bicarbonate

No

A/c bleeding + Hypovolemia Volume expanders

? Shock

Resp. depression & H/o Narcotics given to Mother <4hr


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Dopamine Narcan

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References
American Academy of Pediatrics Committee on Drugs.Emergency Drug Doses for Infants & Children.Pediatrics.1988;81:462 American Academy of Pediatrics.Use & Abuse of the Apgar Score.Pediatrics.1996;98:141-142 Apgar,V.A Proposal for New Method for Evaluation of the Newborn Infant.Anesth.Analg.1953:32:260-267 Ballard R.A.Schaffer & Avery's Diseases of the Newborn-6th Ed.1991; 193-206

British Pediatric Association. Neonatal Resuscitation. London: BPA, 1993


Bloom R.S, Cropley C.S. Textbook of Neonatal Resuscitation. American Heart Association, American Academy of Pediatrics,1987;1-37 Hamilton P.Care of the Newborn in the Delivery Room.BMJ 1999;318:1403-1406

Royal College of Obstetricians and Gynecologists. Working Party Report on Maternity Care in Obstetrics and Gynecology. London: Royal College of Obstetricians and Gynecologists, 1990
Roberton N.R.C.Resuscitation of the Newborn.Textbook of Neonatology 2nd Edn.Churchill Livingstone.1992;173-198
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