Perinatal asphyxia refers to lack of oxygen and poor perfusion experienced by the fetus or newborn during delivery or birth. This can lead to hypoxic ischemic encephalopathy and multi-organ system dysfunction in the newborn. Key criteria for diagnosing perinatal asphyxia include an umbilical cord pH less than 7.0, low Apgar scores for more than 5 minutes, and neurological or multi-organ abnormalities in the newborn period. The pathophysiology involves hypoxia, ischemia and reperfusion injury damaging cells and organs. Management focuses on supporting oxygenation, circulation, temperature and metabolism to prevent further brain injury.

2. PERINATAL ASPHYXIA
Insult to the fetus / Newborn
Lack of oxygen (Hypoxia)
Lack of perfusion (Ischemia)
 Effect of hypoxia & Ischemia
inseperable
Both contribute to tissue injury

3. DEFINITION
 WHO
 NNPD
 AAP

4. ESSENTIAL CRITERIA FOR
PERINATAL ASPHYXIA
 Prolonged metabolic or mixed acidemia (pH < 7.00) on an
umbilical cord arterial blood sample
 Persistence of an Apgar score of 0-3 for > 5 minutes
 Clinical neurological manifestations e.g. seizure,
hypotonia, coma or hypoxic-ischaemic encephalopathy in
the immediate neonatal period
 Evidence of multiorgan system dysfunction in the
immediate neonatal period

5. DEFINITION
 ANOXIA - complete lack of oxygen as a result of a
number of primary causes
 HYPOXIA -decreased arterial concentration of oxygen
leading to tissue anoxia
 ISCHEMIA refers to blood flow to cells or organs that
is insufficient to maintain their normal function

6. INCIDENCE
 THE FREQUENCY OF PERINATAL HYPOXIA IS
APPROXIMATELY 1% TO 1.5% in the west
 INVERSELY RELATED TO BIRTH WEIGHT
&GESTATIONAL AGE
 O.5%OF LIVE BORN INFANTS >35 WEEKS
 ACCOUNTS FOR 20% OF PERINATAL DEATHS

7. FACTORS  Mat. Oxygenation
 Blo
Blood flow
mother to
placenta
 Blood flow
placenta to fetus
 Gas Exchange
across placenta or
fetal tissue
 Fetal O2 Req.

8. PATHOPHYSIOLOGY
 Hypoxia
 Diving seal reflex
 Shunting of blood to brain adrenals & heart
 Away from lungs, kidney gut & skin
 NON BRAIN ORGAN INJURY
Shunting of blood
to brain adrenals
& heart

9. Shunting of blood to brain adrenals & heart

10. PATHOPHYSIOLOGYBRIEF ASPHYXIA
 TRANSIENT INCREASE AND THEN DECREASE OF
<HR>
 MILD ELEVATION IN <BP>
 INCREASE IN <CVP>
 NO CHANGE IN <CO>
 DIVING REFLEX

 REDISTRIBUTION OF<CO>
 BRAIN HEART ADRENALS

11. PROLONGED ASPHYXIA
 CEREBRAL BLOOD FLOW BECOMES DEPENDENT
ON SYSTEMIC BLOOD FLOW
 LOSS OF CEREBROVASCULAR AUTOREGULATION
 HYPOTENSION
 DECREASED CEREBRAL BLOOD FLOW
 ANAEROBIC METABOLISM
 INTRACELLULAR ENERGY FAILURE{due to increased
utilisation of glucose in the brain }
 FALL IN THE CONCENTRATION OF
 GLYCOGEN
 PHOSPHOCREATINE
 ATP

12. PATHOGENESIS OF HYPOXIC
ISCHEMIC BRAIN INJURY
ADENOSINE
•HYPOXANTHINE XO
•XANTHINE O2 FREE
RADICALS
DECREASED
ATP
•GLUTAMATE RELEASE
NMDA RECEDPTOR
•INTRACELLULAR Ca
activates lipase
•FREE FATTY ACIDS,arachadonic
acis o2
•Free radicals
INCREASED
LACTATE
•ANAEROBIC METABOLISM
•HYPOGLYCEMIA DUE TO LOSS
OF STORES

13. CELLULAR CHANGES
 DIMINISHED OXIDATIVE PHOSPHORYLATION
AND ATP PRODUCTION
 ENERGY FAILURE
 IMPAIRS ION PUMP FUNCTION
 ACCUMULATION OF INTRACELLULAR Na,Cl,H2O&
Ca
 EXTRACELLULAR K
 EAA eg.GLUTAMATE

14. • INTRACELLULAR OSMOTIC
OVERLOAD OF Na and Ca
• EXCESSIVE EAA ACTING ON
NMDA RECEPTORS
IMMEDIATE
NEURONAL
DEATH
• UNCONTROLLED ACTIVATION OF
ENZYMESAND SECONDARY
MESSENGERS eg. Calcuim dependend
lipases,proteases,caspases
• PERTUBATION OF MITICHONDRIAL
RESPIRATORY ETC
• GENERATION OF FREE RADICALS
AND LT
• GENERATION OF NO THROUGH NO
SYNTHETASE
• DEPLETION OF ENERGY STORES
DELAYED
NEURONAL
DEATH

15. REPERFUSION INJURY
 REPERFUSION OF PREVIOUSLY ISCHEMIC TISSUE MAY
CAUSE INJURY AS IT CAN PROMOTE FORMATION OF
EXCESS REACTIVE O2 SPECIES
 Eg. SUPEROXIDE,HYDROGEN
PEROXIDE,HYDROXYL,SINGLET O2
 ACTIVATE ENDGENOUS SCVENGER MECHANISM
 DAMAGE TO CELLULAR PROTEINS LIPIDS AND
NUCLEIC ACIDS
 DAMAGE TO BBB
 INFLUX OF NEUTROPHILS
 RELEASE OF INJURIOUS CYTOKINS- IL I B,TNF ALPHA,
MICROGLIA

16. NEUROPATHOLOGY OF PERINATAL
ASPHYXIA
• HIE
• NECROSIS OF BRAINSTEM
NUCLEI
• SAH
TERM
NEWBORN
• PERIVENTRICULAR
HAEMORRAGIC INFARTION
• PERIVENTRICULAR IV BLEED
• PERIVENTRICULSR
LEUCOMALACIA
PRETERM
NEWBORN

17. SYSTEMIC EFFECTS OF ASPHYXIA
 CNS …….
HIE,SEIZURES,ICH,INFARTS,CEREBRAL
EDEMA,HYPOTONIA,HYPERTONIA
 CVS …… MI ,TR,POOR
CONTRACTILITY,HYPOTENSION
 RENAL …… ATN OR CORTICAL NECROSIS
 ADRENAL …… HEMORRAGE

18.  GI …… PERFORATION,ULCERATION WITH
HAEMORRAGE AND NECROSIS
 METABOLIC…… ADH,
HYPONATREMIA,HYPOGLYCEMIA,HYPOCALCEMI
A,
MYOGLOBINUREA
 HEMATOLOGICAL …… DIC
 INTEGUMENT …… SUBCUTANEOUS FAT
NECROSIS

19. INTRODUCTION
 PERINATAL ASPHYXIA
impaired gas exchange
PERSISTENT
FETAL HYPOXIA AND HYPERCARBIA
{estimated by fetal acidosis UMBELICAL ARTERY p H <
7.0}

20. AT RISK INFANTS
 NEONATAL DEPRESSION: prolonged transition from
INTRA to EXTRA uterine life WITH f/s/o
 FETOMATERNAL COMPROMISE-CORD ROUND NECK
 NRNST
 BABY BORN THROUGH MECONIUM STAINED LIQOUR
SUGGESTIVE OF INTRAUTERINE STRESS
 DIABETIC OR TOXEMIC mother
 IUGR
 BREECH
 POST DATED

21. ETIOLOGY
 Intrapartum or Antepartum (90%)
 Placental Insufficiency
 Post partum (10%)
 Pulmonary
 Cardiovascular
 Neurologic Insufficiency

22. SPECIFIC MANAGEMENT
PREVENT FURTHER BRAIN
DAMAGE
 Maintain temperature, perfusion, oxygenation &
ventilation
 Correct & maintain normal metabolic & acid base
milieu
 Prompt management of complications

23. SUMMARY OF INITIAL
MANAGEMENT
 Admit in newborn unit
 Maintenance of temp
 Check vital signs
 Check hematocrit, sugar, ABG, electrolyte
 I.V line
 Consider vol. expander
 Vit K, stomach wash, urine vol

24. SUPPORTIVE CARE
 T - Temperature
 A - Airway
 B - Breathing
 C - Circulation
 F - Fluid
 M - Medications
 F - Feed
 M - Monitoring
 C - Communication
 F - Followup

25. SUBSEQUENT MANAGEMENT
 Oxygenation & ventilation
 Adequate perfusion
 Normal glucose & calcium
 Normal hematocrit
 Treat seizure

26. TREATMENT OF SEIZURES
 Correction of hypoglycemia, hypocalcemia & electrolyte
 Prophylactic Phenobarbitone ?
 Therapeutic Phenobarbitone
20 mg / kg (loading), 5 mg / kg / d (maintenance)
 Lorazepam – 0.05 – 0.1 mg / kg
 Diazepam to be avoided

27. CEREBRAL OEDEMA
 Avoid fluid overload (SIADH, ATN)
 30 Head raise
 Maintain PaCo2 25-30mm Hg in ventilated infants
 Mannitol 20% (0.5 - 1g / kg) 6 hrly. x 24 hrs.
 Frusemide 1.0 mg / kg every 12 hrs.

28. SUPPORTIVE CARE (RECENT
ADVANCES)
 Role of Mannitol, Steriod & Hyperglycemia ??
 Regulatory gene (Regulon)
 Hypothermia
 Pentoxifylline
 Enhancement of natural defence
- Neurotrophic factor & fibroblast growth factor

29. IMPACT
 BRAIN INJURY THAT OCCURS IN THE PERINATAL
PERIOD IS ONE OF THE MOST COMMON
RECOGNISABLE CAUSES OF SEVERE LONG TERM
SEQUELAE…
{NEUROLOGICAL DEFICITS IN CHILDREN OFTEN
REFFERED TO AS CEREBRAL PALSY}

30. HYPOXIC ISCHEMIC
ENCEPHALOPATHY
 FULFILLING CRITERIA
 1)APGAR<3@ >5min
 2)fetal heart rate <60beats/min
 3)prolonged >1hr acidosis
 4)seizures within 24 to 48 hrs
 5)burst suppression pattern on eeg

31. PATHOLOGY
 DEPENDENT ON AFFECTED ORGAN AND
SEVERITY
 COAGULATION NECROSIS AND CELL DEATH
 CONGESTION AND PETICHIAE SEEN IN
PERICARDUIN PLEURA THYMUS HEART
ADRENALS AND MENINGES
 PULMONARY ARTERY SMOOTH MS
HYPERTROPHIES LEADING TO PULMONARY HTN
 PROLONGED IU HYPOXIA INADEQUATE
PERFUSION OF WHITE MATTER PVL

32. CEREBRAL BLOOD FLOW
ASSESMENT
 XENON CLEARENCE TECHNIQUE
 JUGULAR VENOUS OCCLUSION
PLETHISMOGRAPHY mean cerebral blood
flow=50-60ml/min/100g brain wt…..in asphysiated
term babies it is one half of normal at 2 days and
remains decreased for 4 days ,cbf of 20ml/min/100mg
in term or preterm results in permanent brain damage
 NONINVASIVE DOPPLER
pulsatility index =( systolic amplitude – diastolic
amplitude)/systolic amplitude ….normal in mildly
asphysiated and and low in severe asphyxia

33. PRINCIPLES OF PATHOPHYSIOILOGY
USED IN MANAGEMENT
• CO ORDINATE WITH OBSTRETRIC TEAM
• NEWBORN RESUCITATION
IDENTIFICATION OF HIGH RISK
INFANT
• VENTILLATION MAINTAIN p CO2WITHIN NORMAL RANGE(STEAL PHENOMENON HYPERCAPNIA,HYPOCAPNIA
DECREASES CBF)
• Perfusion promptly treat hypotension avoid hypertension
• Fluid status initial fluid restriction follow serum sodium and daily weight
• Blood glucose maintain within normal levels
• Seizures treat wit eeg corelates
• Electrolyte imbalance monitor calcium magnesuim and electrolytes
• Infection lp in suspected cases of cns infection
SUPPORTIV E CARE
• Hypothermia…selective cooling to 2-4 degree celcius reduce incidence if tissue damage
• O2 free radical scavenger,inhibitors
• Eaa antagonists
• Prevention of no formation
• Ca channel blockers
POTTENTIAL
NEUROPROTECTIVE
STRATEGIES…AMEILORATING
SECONDARY BRAIN DAMAGE

34. BIBILIOGRAPHY
 MANUAL OF NEONATAL CARE CLOHARTY 6TH
EDITION
 NELSON TEXTBOOK OF PAEDIATRICS 18TH EDIYION
 NEUROLOGY OF THE NEWBORN VOLPE4TH EDITION
 NEONATAL NEUROLOGY GERALD M FENICHEL 3RD
EDITION
 RECENT ADVANCES IN PAEDIATRICS EDITED BY
T.J.DAVID 18

35. THANK YOU

36. Pathophysiology
 Within minutes of onset of fetal hypoxia :
 Bradycardia
 Hypotension
 Decreased cardic output
 Severe metabolic as well as respiratory acidosis

37. Initial circulatory response of the
fetus
 Increased shunting through the ductus venosus,ductus
arteriosus and foramen ovale