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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Dr.Bambang M

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
kehidup-an intrauterin ke ekstrauturin
tanpa ma-salah.

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Dr.Bambang M

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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Dr.Bambang M

Definisi (2)
Asfiksia

BBL ditandai dg
keadaan :
*hipoksemia
*hiperkarbia
*asidosis

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Dr.Bambang M

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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Dr.Bambang M

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

Absent

<100

>100

Respiratory Effort

Absent, irregular

Slow, crying

Good

Muscle Tone

Limp

Some flexion of
extremities

Active motion

Reflex irritability
(nose suctioning)

No response

Grimace

Cough or sneeze

Color

Blue, pale

Acrocyanosis

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

Spontaneous

None
Inj.
Narcan

Evaluate
HR

Yes
Drug
Depressed

No
HR <60
Ct Ventilation +
Chest compression

HR

PPV

<100

15-30 sec

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

Drugs if:
HR <80,after 30 secs PPV
+100% O2
+chest compression
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Overview of
Resuscitation

>100

HR >100
look for spont. Resp
DC ventilation

Observe
Monitor

46 Association
American Heart

Evaluate
color

Pink

Blue
Oxygen
Dr.Said Alavi

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

Drugs

Least common treatment

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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 surfactant PS
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

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

40
17
7
6
6
5
4
3
2
10

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
More severe and rapid development of complications
3050% mother-newborn transmission rate
C. trachomatis

89

Normal Newborn Care

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
Giving prophylaxis after first hour
Flushing of eyes after silver nitrate application
Using old prophylactic solutions

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 hospital-acquired
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

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10

Asphyxia
Contrls

75

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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, self-defended
mechanism could 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
(several of this may be present in a single baby)

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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

Heart rate
Respiratory

Score

Nil

<100

Absent

effort

Gasping or
irregular

2
>100
Regular or
crying

Muscle tone

Flaccid

Some tone

Response to
stimulation

None

Grimace

Cry or cough

Color

White

Blue

Pink centrally

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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

Dr.Said Alavi

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..)

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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
Dr.Said Alavi

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

TERMINAL (SECONDARY) APNEA

HR<60, pale,apneic,poor tone & reflexes,

Apgar score usually 1-3
Spontaneous respiration is never established
unless actively resuscitated by intubation & PPV

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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)
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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)
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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/o drug 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)
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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

HR- Zero or
HR <80/Mt after 30 sec PPV
+chest compression
Can be repeated every
5 Minutes

Adrenaline

Sodium Bicarbonate
HR>100

Metabolic
Acidosis
Soda Bicarbonate

Yes

No

DC drugs

A/c bleeding +
Hypovolemia
Volume expanders

? Shock

Resp. depression &

H/o Narcotics given to
Mother <4hr
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Dopamine
Narcan

American Heart
155Association

Dr.Said Alavi

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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