This document discusses perinatal asphyxia, including its causes, effects, management, and prevention. Some key points: - Perinatal asphyxia can be caused by issues with maternal oxygenation, placental blood flow, umbilical cord complications, or prolonged fetal head compression during delivery. - Effects of asphyxia include hypoxemia, metabolic acidosis, multi-organ dysfunction affecting particularly the brain, kidneys, heart and lungs. Cerebral effects range from reversible synaptic changes to selective neuronal necrosis. - Management involves maintaining normal oxygen and carbon dioxide levels, fluids, seizures control, and therapeutic hypothermia for severe cases meeting certain criteria. - Prevention of perin

1. Professor Bogale Worku
Oct 2009

2. 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. 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. Western
Scenario
India
(NNF data Base)
Incidence
Cause of Perinatal death
Still Birth + P. Mort.
1 – 1.5 / 1000
20%
50%
10%
26%
59%

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4 million newborndeaths – Why?
almostallareduetopreventableconditions

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Estimated causes of neonatal deaths
(2000)
34%
22%
15%
15%
4%
4% 6%
Infection
Asphyxia
Preterm
Tetanus
Diarrhea
Congenital
Others

8. 35% 35%
20% 10%
During delivery
During labor
After delivery
Before labor

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

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

11. 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.

12. 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.

13. 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 hamatoma of the
cord
 Rupture of vasa praevia.

14. 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

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

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

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

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

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

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

22. 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

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

25. 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)
Increase lactate and hydrogen ions

26. 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.

30. 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

31.  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

32.  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)

33.  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

34.  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

35. PREVETION IS THE BEST MEDICINE!!!!

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PREVETION IS THE BEST MEDICINE!!!!
Thank you