Perinatal asphyxia is caused by lack of oxygen and perfusion to organs before, during, or after birth. It can lead to hypoxic-ischemic encephalopathy (HIE) and brain damage in newborns. Key criteria for diagnosis include low Apgar scores, metabolic acidosis in umbilical cord blood, and neurological symptoms. Management focuses on preventing further brain injury through ventilation, temperature control, seizure management, and maintaining circulation. Outcomes range from normal to death or disabilities like cerebral palsy. Prognosis depends on severity of encephalopathy.

1. Perinatal Asphyxia
Natangwe Shimhanda
201208214

2. PERINATALASPHYXIA
Definition
An insult to the fetus or newborn due to lack of
oxygen (hypoxia) and /or lack of perfusion
(ischemia) to various organs.
Associated with
– Tissue lactic acidosis
– Hypoventilation
– Hypercapnea
2

3. Definitions
• Birth Asphyxia - failure to initiate
spontaneous and sustained respiration after
delivery (may result in severe hypoxia)
• Fetal Hypoxia - refers to inadequate
oxygenation before delivery (may predispose
the fetus to birth asphyxia)

4. • Hypoxia during labour in term babies is the
most common cause of neonatal brain
damage and is the leading cause of cerebral
palsy in the developing word.
• The effects of hypoxia & Ischemia inseparable
and they both contribute to tissue injury

5. 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 periods

6. Phases of Asphyxia
• Primary Apnea (30-60s)
– short series of respiratory
efforts
– convulsion or a series of
clonic movements
– abrupt fall in heart rate
– then no muscle tone
– skin cyanotic and then
blotchy
• Gasping (8m)
– 3-6/minute
– heart rate and blood pressure
continue to fall
• Secondary/Terminal Apnea

7. Apgar score
APGAR Score:
8-10 No asphyxia
5-7 Mild asphyxia
3-4 Moderate asphyxia
0-2 Severe asphyxia

8. ETIOLOGY
• 90% Antepartum/ Intrapartum
• 10% Postpartum
Maternal
– Hypertension - chronic / pre-eclampsia
– Diabetes, Anemia, Malnutrition, Maternal health
– Hypoxia - Pulmonary/Cardiac Diseases, Bronchial asthma,
Hypotension
– anesthetics and analgesics
– Intrauterine infections
– Prolonged and difficult 2nd stage of labour
– Placental: Infarction/fibrosis/abruption/insufficiency
– Cord Accidents: Prolapse / True knots / compression/Abn. vessels

9. Fetal Factors
• Infections - Intrauterine
• Anemia - Feto-fetal or Feto-maternal transfusion
• Growth restriction (IUGR)/ Postmaturity -
Meconium aspiration, tracheal plug by bloody
mucus
• Congenital malformations - choanal atresia,
laryngeal web, diaphragmatic hernias,
• Hydrops fetalis
• Prematurity, multiple births and rhesus
isoimmunization

10. Pathophysiology
Diving reflex:
Shunting of blood to brain ,heart, adrenals and away
from gut, kidney, liver, spleen ,skeletal muscle and
skin

11. Progressive asphyxia:
Hypoxia, Hypercapnea, acidosis
Pulmonary vasoconstriction,
Decrease in HR, CO, BP
Cerebral edema- Petechial hemorrhage,
SIADH,
Na- intracellular accumulation

12. Acute Sequelae Of Asphyxia

13. Late effects
• Microcephaly
• MR
• Developmental delay
• Cerebral palsy
• Epilepsy
• Visual, hearing impairement
• Behavioral disturbances

14. Management
• Presence of a health professional skilled in
Neonatal resuscitation
• Necessary equipment for resuscitation: infant size
laryngoscpoe and margill’s forceps, ETT 2.5-
3.5mm, neonatal Ambu-bag mask, suction
catheters 8FG and 6FG, umbilical catheters if
peripheral IV line is not possible, necessary fluids,
etc.
• Emergency medicines e.g. naloxone, adrenaline

15. Management
Aimed to prevent further Brain Damage
• Determine your APGAR score
• Ensure warmth and not allowing hypothermia to occur
• Administer 100% O2, reduce as soon as the colour
improves
• Apply gentle nasopharyngeal suction if indicated
• Administer bag mask ventilation
• Administer Naloxone when indicated
• Undertake external Cardiac massage for bradycardia

18. HIE
• In perinatal asphyxia, gas exchange, either
placental or pulmonary, is compromised or
ceases altogether, resulting in cardiorespiratory
depression.
• Hypoxia, hypercarbia and metabolic acidosis
follow.
• Compromised cardiac output diminishes tissue
perfusion, causing hypoxic-ischaemic injury to the
brain and other organs.
• The neonatal condition is called hypoxic-
ischaemic encephalopathy (HIE).

19. • It remains an important cause of brain damage,
resulting in disability or death, and its prevention
is one of the key aims of modern obstetric care.
• In developed countries, approximately 0.5–
1/1000 liveborn term infants develop HIE and
0.3/1000 have significant neurologic disability.
• The incidence is higher in developing countries.
• Most cases of hypoxic-ischaemic encephalopathy
(HIE) follow a significant hypoxic even
immediately before or during labour or delivery.

20. TARGET ORGAN-BRAIN
HIE:PATHOPHYSIOLOGY
Hypoxia Alteration in glucose and energy
metabolism loss of autoregulation & decreased
cardiac function ischemia
Severe hypoxia and ischemia failure of oxidative
phosphorylation & ATP production
Accumulation of Na, Cl,Ca intracellular and K and
excitatory neurotransmitters extracellular
neuronal death
20

21. Pathology and Pattern seen in term
babies
• Selective neuronal necrosis - cerebral and
cerebellar cortex, Thalamus, brain stem nuclei
(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

22. Grading
The clinical manifestations start immediately or up to
48 h after asphyxia, and can be graded:
• Mild – the infant is irritable, responds excessively to
stimulation, may have staring of the eyes and
hyperventilation and has impaired feeding
• Moderate – the infant shows marked abnormalities of
tone and movement, cannot feed and may have seizures
• Severe – there are no normal spontaneous movements
or response to pain; tone in the limbs may fluctuate
between hypotonia and hypertonia; seizures are
prolonged and often refractory to treatment; multi-organ
failure is present.

23. Management (Prevent Further Brain
damage)
• Ventilation-For hypoxia and hypercapnea
• Maintain cerebral perfusion
• Correction of hypoglycemia and
hypocalcemia
• Temperature maintenance
• Control of seizure- Anticonvulsants
• Cardiac effects-Ionotropes
• Renal effects- Dopamine

24. 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

25. Cerebral Edema
• Avoid fluid overload (SIADH, ATN)
• 30 degrees 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.

26. Prognosis
• Overall mortality - 10-20%
• Neurological sequele - 20-45%
Sarnat Stages
• 1- 100% Normal neurological outcome
• 2- 80% Normal neurological outcome
• 3- 50% deaths, 50% major neurological sequelae
Risk for CP - 5-10%
• Subtle school problems in neurologically and
mentally normal survivors of HIE stage 1-nil, stage 2-
18-35%

27. References
• Lissauer T, Clayden G, 2012. Illustrated
Textbook Of Paediatrics. Fourth edition. ©
2012 Elsevier Ltd
• Wittenberg D.F. (2009), Coovadia’s Paediatrics
and Child Health. Oxford University Press
Southern Africa (pty) Ltd