This document discusses perinatal asphyxia, which is a lack of oxygen and blood flow to the fetus or newborn during delivery resulting in tissue injury. It can be caused by issues with the placenta, umbilical cord, prolonged compression of the fetal head during delivery, or other maternal or fetal conditions. Left untreated, perinatal asphyxia can damage multiple organs but particularly impacts the brain, kidneys, and heart. Management involves maintaining adequate oxygen and blood flow as well as controlling seizures. Hypothermia therapy, keeping the infant's core temperature at 33°C for 72 hours, may help reduce brain injury from severe asphyxia. While multisystem effects are common, failure to breathe

1. PERINATAL
ASPHYXIA
Abate Y.

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

3. PERINATAL ASPHYXIA
There may be associated lactic
acidosis
If there is hypoventilaiton there
may be hypercarbia

4. Definition
Profound umbilical arterial metabolic or
mixed acidemia with PH <7.2
 APGAR score of <3 for > 5 minutes
Neonatal neurologic sequelae: seizures,
hypotonia, coma
Multiorgan dysfunction

5. PERINATAL ASPHYXIA
Western
Scenario
India
Incidence
Cause of Perinatal death
Still Birth + P. Mort.
1 – 1.5 / 1000
20%
50%
10%
26%
59%

6. 12/11/2022 6
4 million newborn deaths – Why?
almost all are due to preventable conditions

7. 35% 35%
20% 10%
During delivery
During labor
After delivery
Before labor

8. ETIOLOGY
 Intrapartum or Antepartum (90%)
Placental Insufficiency
Cord accident
MAS
Maternal CP arrest

9. ETHIOLOGY
Post partum (10%)
Pulmonary
Cardiovascular
neurological

10. ETHIOLOGY
I - MATERNAL CAUSES: (conditions
leading to imperfect oxygenation
of maternal blood)
 Severe anemia, Hemorrhage &
shock, Respiratory failure, and heart
failure.
 Eclamptic seizure, pneumonia, and
pulmonary edema.

11. ETHIOLOGY
II- PLACENTAL CAUSES:
 Placental compression: interfering with its
circulation as in tonically contracted uterus,
prolonged labour after rupture of the
membranes or as a method of control of
bleeding in placenta previa.
 Placental separation as in accidental
hemorrhage.
 Placental insufficiency e.g. extensive
degeneration, multiple infarcts & abnormally
small placenta.

12. ETHIOLOGY
III- CAUSES IN THE UMBILICAL CORD:
Obstruction of the circulation, which may be
due to:
 Tight nucal cord
 True knots
 Prolapsed cord
 Compression of the vessels by hematoma of
the cord
 Rupture of vasa praevia.

13. ETIOLOGY ( cont…)
IV-PROLONGED COMPRESSION OF THE FETAL
HEAD:
This will cause edema and ischemia, which
interfere with the blood supply of the medulla
leading to depression of the respiratory center.
Prolonged compression may be due to:
 Contracted pelvis (C/P disproportion).
 Rigid perineum.
 Intracranial hemorrhage.
 Forceps application for a long time.
 Depressed fracture

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

15. Circulatory depression
Respiratory depression
Hypoxemia
Hypercarbia
Respiratory acidosis
Low cardiac output
Decreased tissue perfusion
Ischemia
Metabolic acidosis
Capillary leak, edema
Multi-organ dysfunction

16. NONE BRAIN ORGAN DAMAGE
PATHOPHYSIOLOGY
Acute asphyxia
Diving reflex
Shunting of blood
to brain adrenals
& heart
Away from
lungs, kidney
gut & skin

17. CEREBRAL CORTICAL LESIONS
PATHOPHYSIOLOGY
Asphyxia continues
Shunting within the brain
Anterior
Circulation
Suffers
Posterior
Circulation
Maintained

20. THALAMUS & BRAIN STEM INJURY, CORTEX SPARED
PATHOPHYSIOLOGY
 Hypoxia – ABRUPT & SEVERE
 Complete abruption
 Cord accident
 Maternal CP arrest

21. Clinical grading OF HIE

22. PATHOLOGY
 Target organs of perinatal asphyxia
 Kidneys 50%
 Brain 28%
 Heart 25%
 Lung 23%
 Liver, Bowel, Bone marrow < 5%

23. NEUROPATHOLOCIAL CHANGES
Pattern seen in term infants
 Selective neuronal necrosis (Spastic CP)
 Status Marmoratus (Chorea, Athetoid, Dystonia)
 Parasagittal cerebral injury (Prox Spastic
Quadriparesis)
 Focal and multifocal ischemic brain injury (sp.
Hemiparesis, cognitive defects, seizure)
Pattern predominant in preterm
 Periventricular leukomalacia

24. PATHOLOGY
Cerebral O2 
Substrate supply 
Synaptic inactivation (Reversible)
Energy failure
Memb. pump failure
Further  in perfusion
At cellular level

26. CHANGES IN SUBSTRATE METABOLISM
AND NEURTRANSMITTERS
Hypoxic effect
Changes that are increased
An initial increase Cerebral blood
flow
Increase of glucose influx to brain
Increase in glycogenolysis (increase
cAMP)
Increase in glycolysis (increase
cAMP)

27. CHANGES IN SUBSTRATE METABOLISM
AND NEURTRANSMITTERS
Changed that are decreased
Decreased oxidative
phosphorylation
Eventual decrease brain glucose
Decreased phosphocreatinine
(PCr) and ATP
These changes are more pronouned
in the white matter compared to the
gray matter

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GASTROINTESTINAL EFFECTS
 The asphyxiate infants is at risk for bowel
ischemia and
 NECROTIZING ENTEROCOLITIS

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HEMATOLOGICS EFFECTS
 DIC
 THE LIVER MAY FAIL TO MAKE CLOTTING FACTORS
 THE BONE MARROW MAY NOT PRODUCE
PLATELETS

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PULMONARY EFFECTS
 Increased pulmonary resistance
 pulmonary hemorrhage
 Pulmonary edema secondary to cardiac failure
 Failure of surfactant production with secondary HMD
 Meconium aspiration may be present.

31. Management of HIE
1. Maintain O2 and CO2 in normal ranges.
2. Hyperventilation not recommended and may be
detrimental.
3. Monitor arterial blood pressure because cerebra perfusion
pressure is dependent on MAP
4. Administer volume slowly: overall fluid restriction
5. Monitor electrolytes and glucose
6. Control seizures
7. HYPOTHERMIA THERAPY

32. HYPOTHERMIA THERAPY
 Entry criteria
 PH < 7.0
 Base deficit 16mmole/l in 1st hour
 APGAR score < 5 at 10 minutes.
 Less than 6 hrs old.
 Technique
 Keep core temp at 33 *C for 72 hrs
 Continuous EEG monitoring
 Continue medical management

33. MULTISYSTEMIC EFFECTS
 Seizures
 Often resitant to anticonvulsant therapy in severe HIE
(possibly because of a lack of cortical inhibition Vs.
excesive cortical activity
 50% are subtle, focal ,multifocal or myoclonic
 Typically first noted at age 12 to 24 hrs and often
resolve by 5 to 7 days
 Must also assess for other metabolic derangements
(eg; hypoglycemia, hypocalcemia,
hypomagnesemia)
 Phenobarbital is the first line agent followed by
dilantin (may also consider lorazepam)

34. MULTISYSTEMIC EFFECTS
 ACUTE ASPHYXIA
 elicits diving reflex with preferred blood flow to the brain,
heart, and adrenal gland
 CARDIAC MANIFESTATIONS
 Transient myocardial ischemia, congestive heart failure,
left or right ventricular dysfunction, tricuspid
regurgitation murmur within the first 24 hrs
 RENAL
 Oliguria and possible acute tubular necrosis
 PULMONARY
 Pulmonary hypertension especially after MAS

35. PREDICTORS OF POOR
NEURO DEVELOPMENTAL OUTCOME
 Failure to establish respiration by 5 minutes
 Apgar 3 or less in 5 mts
 Onset of Seizure in 12 hrs
 Refractory convulsion
 Inability to establish oral feed by 1 wk
 Abnormal EEG & failure to normalise by 7 days
of life
 Abnormal CT, MRI in neonatal period

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PREVETION IS THE BEST MEDICINE!