obs

2. INTRODUCTIO
■ Birth asphyxia can & deùned as a dinical condiüon
chaæ4erised by inability/failure to iniûate or sustain
sponBnæus regular rœpiætion leading to varying
degræ of hypoxic and iuhaemic injuûœ to body üuuœ
and organs.
• Histoûcally categorized into two gedes
• asphyxia livida (due asphyxia) - blue appearance of the
newborn. MuscleRne is good and the infant is responsive D
stimuli
• asphyxia pallâa (white/pale asphyxia) moe sevee, ba@is
pale, Aaccid and unresponsive to stimuli
3

3. INTRODUCTIO
• Currently, biÆ asphyxia is gæded into 3 categoriœ
(mild, moderate and severe) using Öe AŒAR ŒORE 1
■ According to the American College of Ob2ePicians and
Gyrieologists andDe American Academy of PediaPics, a
neonate is labelled to beasphyxiated if the following
condiâons are satisfied:
• Umbilical œrd arteñal pH <7
• Apgar score of 0-3 fôr tanger than Smin
• Neonatal neurological manifèstaóons (e.g. seizures, coma or hypotonia);
and
• Hulôsystem organ dysfunction, e.g. œrdiovascular, gastrointesônal,
haematological, pulmonary or æna system

4. INTRODUCTION
• Currendy, birth asphyxia is gaded into 3 categories
(mild, modeate and sevee) as proposed by Sanart and
Sanart 2
• This goding depends mainly onDe severity of the
clinical symptoms and signs
• Birth asphyxia can be caused by evens in De
antepartum, De intraparGm or De postpaCm periods
or combinations of all Dree.
• Arecent review suggests Dat asphyxia is probably
primarily antepartum in 50°/o of cases, intraparGm in
40% and postpartum in De remaining 10°/o of cases

5. INTRODUCTION
• In developing counPies intrapartum causes aceunt Ör
a larger proporüon of cases
• Poverty, ignorance, abence of standard hœlÖ facilitiæ
and tæined biÆ aRendanS are impedimenÖ to Öe
management of biR asphyxia in Nigeria, and mo2
developing counPiæ

6. PREDISPOSI FACTORS
• Any factors which interfere wiÖ De circulation
between maternal and fetal blood exchange (Iœding
to hypoxia) could rœult in Öe happens of peûnaBl
asphyxia.
■ Thèse factors can be matemal factor, feæl factor,
delivery fa4or or combinaôon.

7. PREDISPOSI FACTORS
ry›oe«sio»
Hypertension
Diabetes
Anaemia
Smoldng
Nephritls
l1eandisease
Extreme of age
Congenital
malfonziabon
Nalpresentatlori
Preterm/premaNrity
u«maurity
IUGR
Chorioamnionitis
Abruptio placentae
Racenta piaeda
cedacddenb
PAOM
Obstructed labour
Neconium aspiradori
Oxytocin excess

8. AETIOPATHOGENESIS
Interference to cerebral blood flow
(hypotension, failure of autoregulation)
Hypoxia
Ischemia to the brain
Generation of free radicals
Reduced energy production (ATP)+ anaerobic glycolysis, lactic acidosis
Glutamate release + receptors (excitotoxic)
Change in membrane function (accumulation of Na+, NO in cells and release of Ca2+)
Cellular damage + oedema
(by affectation of mitochondrial function)

9. CLINICAL PRESENTATIO
• Acidaemia, leading to an abnormal heart rate or rhythm
• &IIor
• Cyanosis
• Decreased tonœ and reäexœ
• Poor or absent cry
• Gasping or poor respiraory ePort
• Hypotonia
• Hyporeäexia
■ Neconium stained liquor
■ Œular manifestation (ùxed dilated pupils, nystagmus)
• SNpor
■ Comma 12

10. INVESTIGATIONS
• No œnùrmatory test to dÂgnose asphyxÂ
• Iwestigahons ae done to assess the severity of brain injury
and % moniQr De Lnctional status of systemic organs.
• FBC
• Œpôc culhiR
• Urlnalysis (ketonœ, ammonia)
• E/U/Cr
• UlæDund scan
• CT diffue hypoaRenuaüon
• MRî
» ElectroenœphalogHm (EEG)

11. S Y S T E M
C N S
EARLY COMPLICATIONS
E F F E C T f S )
FTE. intracranial hemorrhage. seizures,
cerebral edema, hypotoMa hypeoonia
Car‹:JiovascuIar Myc›carcJiaI ischemia. cc›ntractiIity, carcliac
stunnin‹g, trici spicl insufficiency, hypc›tensic›r›
P u l m a n a r y h y p ertension. p u l m o n a r y hemorrha‹ge.
R D S
A c u t e t u b u la r o r cortical n e c r o s i s
Aclren al h e m o r r h a g e
Perforatic›n. u lceration 'with hemorrha‹ge. n e c r o s i s
inappropriate s e c r e t c n o f a o t o u r e t c hormone.
P u l m o n a r y
R e n a l
Aclrenal
G a s t r o int e st in a l
Meta b oh c
h onatremia. bypc›pIyc emia, hypc›caIcem›a.
myo‹gIobin iria
S u b c u t a n e o u s fat necrosis
Disseminatecl intravascular coa‹guIation
lntegurnent
Mematology

12. LATE COMPLICATIO
• Developmen@I delay
" Ceebral palsy
" Nen@I re@rdaéon
" Nicrocephaly
" Behavioral abnormaliâes
" Seizure disorder (epilepsy)

13. CLINICÅL PRESENTATION
n›u›

14. MANAGFM NT
■ Supportive therapy
• Inidally N
P
O
• Oxygen via fae mask of nasal caDeter
• Assisted wn5lation whenrequired
• Correction of hypoglycaemia
• Correcaon of electrolye derangement andacidosis
• Fluid restrlcuon to prevent ceebal oedema
■ ?Pophylactic anabiotio

15. MANAGEM€NT
• Control seizure with anticonvulsanQ
• 1° - phenbarbitone (loading 20m@kg sDwly, maintain with
5-10mg/kg/6y in 2 divided doses
» If seizue persists add phenytén (20mg/kg loading dose)
• Diazepam (0.1-0.2mg/kg) 6 hrly
• lorazepam (0.1mg/kg)

16. MANAGEMENT
• Reduction of cerebral injury by induced hypothermia
• Whole body (systemic) or elective cembral Deapeutic
hypothermia reduces mortality or ma@r neurodevelopmenBl
impairment in term and near-term infbnts.
• Deoeases %erate of apopNsis and suppresses production
of neurotoxic mediaRrs e.g. extTacellular glutama&, free
radicals, nibic oxâe, and ladate
• Reduces mortality and neurodevelopmenBlimpairment 1
instituted within 6 hrs

17. MANAGEM NT
■ Commence feeding as soon as clinical condiñon
improves
■ Complicañons of induced hypoDermia include
» thrombocytopenia (usually without bleeding)
• reduced heart rae, and
• subcutaneous fat necrosis
• overcooling

18. PREVENTION
• This en@ils prevenüon of birth asphyxia and
prevenüon of iu complicaüons when itoccurs
• Follows Øe five levels of prevenüon
HœIÒ educaüon (pńmary)- eduœR the masses about it
z Specl€c protection(pńmary)- idenôŞ dsks in pregnancy and
institute prevendve mœsures
› Early diagrosis and Pœtment (secondary) - idenüȘ and
Pœt asphyxia pæmpdy
‹ Ümitaüon of dčability (tertiary) - physiotheæpy
RehablliNbon (teoary) integaüon of Øe baby and Øe
moDer into Øe community