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
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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
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
16.
17.
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
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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%
*choanal atresia – congenital disorder where by the back of the nasal passage (choana) is blocked
* Hydrops fetalis- abnormal accumulation of fluid in 2/more fetal compartments e.g ascities, pleural effusion, pericardial efusion
Syndrome of inappropriate antidiuretic Hormone secretion - SIADH
