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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

15/06/1999 2 Dr.Bambang M
Pendahuluan (2)

 “Sebagian besar bayi yaitu sekitar 90%


tidak membutuhkan atau hanya sedikit
memerlukan bantuan untuk memantap-
kan pernafasannya setelah lahir dan
akan melalui masa transisi dari kehidup-
an intrauterin ke ekstrauturin tanpa ma-
salah.”

15/06/1999 3 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

15/06/1999 6 Dr.Bambang M
Definisi (2)

 Asfiksia BBL ditandai dg


keadaan :
*hipoksemia
*hiperkarbia
*asidosis

15/06/1999 7 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

15/06/1999 8 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
alveolicairan paru diabsorpsi oleh jaringan paru
dstseluruh alveoli berisi udara oksigen. Paru
membutuhkan tek.puncak inspirasi dan tek.akhir
ekspirasi yg tinggialiran 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 relatifekspansi
par <  gagal nafas ! ! !

15/06/1999 12 Dr.Bambang M
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 brain’s
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 “inter-
organs 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

15/06/1999 19 Dr.Bambang M.
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 0 1 2
Heart Rate Absent <100 >100
Respiratory Effort Absent, irregular Slow, crying Good
Muscle Tone Limp Some flexion of Active motion
extremities
Reflex irritability No response Grimace Cough or sneeze
(nose suctioning)
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.

15/06/1999 27 Dr.Bambang M
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)

15/06/1999 28 Dr.Bambang M
Resusitasi BBL (2)

 Tindakan yang paling penting dan


efektif pada resusitasi neonatus adalah
pemberian ventilasi pada paru-paru bayi
baru lahir dengan oksigen”

15/06/1999 29 Dr.Bambang M
Resusitasi BBL (2)

1) Basic Resuscitation
2)Advanced Resuscitation
ABC’s 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
15/06/1999 35 Dr.Bambang M
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)

15/06/1999 45 Dr.Bambang M
•Place Under warmer
•Dry thoroughly Overview of
•Remove wet linen Evaluate
•Position Respirations Resuscitation
•Suction mouth then nose
•Tactile stimulation

None Spontaneous
Inj.
Narcan
Yes

Evaluate Drug
HR Depressed PPV HR
<100
No 15-30 sec
>100
HR <60 HR 60-100 HR >100
Ct Ventilation + -HR increasing look for spont. Resp Evaluate
Chest compression Ct ventilation DC ventilation
-HR not increasing (<80)
color
Ct chest compression
Blue
Drugs if: Pink
HR <80,after 30 secs PPV Observe
+100% O2 Monitor Oxygen
+chest compression
15/06/1999 American Heart
46 Association Dr.Said Alavi
Hubungan antara prosedur resusitasi dan
jumlah bayi yang perlu prosedur tsb.
Keep dry & warm
Most common Suction & stimulation
treatment
Oxygen

Establish effective ventilation


Bag &mask
Tracheal Intubation

Chest compressions

Least common treatment Drugs

15/06/1999 47 Dr.Bambang M
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 )

15/06/1999 49 Dr.Bambang M
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 )

15/06/1999 50 Dr.Bambang M
Sikap dan tindakan

 Lakukan rangsangan mekanis ( mengu-


bah letak bayi, memukul telapak kaki )
 Bersihkan saluran nafas
 Berikan O2 dg sedikit tekanan
 Mencari dasar etiologinya
 Sikap selanjutnya sesuai dengan
etiologi

15/06/1999 51 Dr.Bambang M
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

15/06/1999 53 Dr.Bambang M
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 )
15/06/1999 54 Dr.Bambang M
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 %)

15/06/1999 59 Dr.Bambang M
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.

15/06/1999 60 Dr.Bambang M
Patofisiologi ( lanj.)

 Atelektasis  hipoksia  asidosis 


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

15/06/1999 61 Dr.Bambang M
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.

15/06/1999 62 Dr.Bambang M
Gambaran radiologis

 Gambaran klasik foto rontgen paru :


bercak difus infiltrat retikulogranuler
 Untuk diagnosis dini, walaupun klinis
belum jelas
 Untuk menyingkirkan DD :
pneumotoraks, hernia diafragma.

15/06/1999 63 Dr.Bambang M
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

15/06/1999 64 Dr.Bambang M
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

15/06/1999 65 Dr.Bambang M
Pencegahan

 Mencegah kelahiran bayi prematur


 Pemberian kortikosteroid ibu hamil
trimester III ( ? )

15/06/1999 66 Dr.Bambang M
Penatalaksanaan

 Memberikan lingkungan yg optimal :


suhu, humiditas
 Oksigen
 Pemberian cairan, glukosa, elektrolit
 Antibiotika

15/06/1999 67 Dr.Bambang M
Prognosis

 Tergantung tingkat prematuritas


 Terjadinya displasia bronkopulmoner
umumnya akibat tekanan positif terus
menerus ( respirator )

15/06/1999 68 Dr.Bambang M
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

15/06/1999 70 Dr.Bambang M
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

15/06/1999 71 Dr.Bambang M
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.

15/06/1999 72 Dr.Bambang M
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  ?

15/06/1999 73 Dr.Bambang M
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

15/06/1999 74 Dr.Bambang M
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

15/06/1999 75 Dr.Bambang M
10
Asphyxia
Contrls
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15/06/1999 78 Dr.Bambang M
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)

 Hypoxic cellular damages:


a. 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)

 Other damages:
a. Persistent pulmonary hypertension
(PPHN)
b. Hyper/hypoglycemia
c. 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 1 2

Heart rate Nil <100 >100


Respiratory Absent Gasping or Regular or
effort irregular crying
Muscle tone Flaccid Some tone Active
Response to None Grimace Cry or cough
stimulation
Color White Blue Pink centrally

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Factors Affecting Apgar Score
False positive score False negative score
 Prematurity  Maternal acidosis
 Drugs-  High fetal
sedatives,narcotics,mgso4 catecholamine levels
 A/c cerebral trauma  Some full term infants
 Precipitate labor
 Cong. Myopathy
 Cong. Neuropathy
 Spinal cord trauma
 CNS anomaly
 Lungs-diaphragmatic hernia
 Airway-choanal atresia
 Cong. Pneumonia (GBS)

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Limitations of Apgar Score
 Affected by many  1 min. Apgar score-
factors, so low apgar strongly correlated with
score do not necessarily cord pH & an index of
signify fetal asphyxia intrapartum asphyxia
 Do not predict neonatal  Apgar score beyond 1
mortality or subsequent min. (5,10,15 & 20min)-
development of CP reflective of child’s
(score normal in changing condition &
most cases with CP & indicative of adequacy of
incidence of CP is very resuscitative efforts
low in those with apgar  Score 0-3 at 20 Mts.-
score 0-3 at 5 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 indices-


Lactate,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 pink-
intubate & 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 µg/ml)
Dose 1st and 2nd dose 10 µg/kg (0.1 ml/kg); 3rd dose 100 µg/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 µg/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 drugs-
delay further treatment until blood
gas,glucose & CXR results
 Then treat according to results
 If all investigations WNL & apnea persists-
s/o profound neurologic problem with bad
prognosis or underlying neurologic disorder
or intractable cerebral edema
 Those fulfill criteria of brain death-
discontinue 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

•Ondine’s curse
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ABCD of Neonatal Resuscitation

+
Drugs
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Begin
•HR- Zero or
Medications •HR <80/Mt after 30 sec PPV
+chest compression
•Adrenaline
•Volume expander Can be repeated every
Adrenaline
5 Minutes
•Sodium Bicarbonate

Yes
HR>100 DC drugs

Metabolic No A/c bleeding +


Acidosis Hypovolemia
Soda Bicarbonate Volume expanders

? Shock

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

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129Association 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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