Perinatal asphyxia

PERINATAL ASPHYXIA/HIE
PRESENTER: Steven Akach
FACILITATOR: Professor Nyandiko
Steven Akach_Med VI
5/25/2021

Definition of Terms
• Asphyxia- Failure to initiate and maintain breathing soon after birth
(24 hours) hence the need for assisted breathing (Abdo et al., 2019).
• Perinatal asphyxia is a condition of impaired blood gas exchange that,
if persistent, leads to progressive hypoxemia and hypercapnia.
• Anoxia – Total depletion of oxygen level in circulation.
• Hypoxia – Decreased oxygenation to cells and organs.
• Hypoxemia – Decreased arterial concentration of oxygen.
• Ischemia – Blood flow to cells insufficient to maintain their normal
function leading to tissue or organ damage.
Steven Akach_Med VI
5/25/2021

Definition
• Hypoxic-ischemic encephalopathy (HIE),which is a subset of neonatal
encephalopathy (NE), can result from perinatal asphyxia whereby
inadequate oxygen delivery to the brain leads to compromised brain
metabolism (AAP & ACOG; Gomella’s Neonatology, p997).
• Local Definition of HIE: Manifestation of the asphyxial injury to the brain,
characterized in the early neonatal period by altered level of
consciousness, seizures within 12 hrs of birth or coma and altered tone.
• Neonatal encephalopathy (NE) is clinically defined as a disturbance in
neurologic function demonstrated by difficulty in maintaining respirations,
hypotonia, altered level of consciousness, depressed or absent primitive
reflexes, seizures, and poor feeding.
• NE does not imply HIE.
Steven Akach_Med VI
5/25/2021

Neonatal Signs of Acute HIE (UpToDate, 2020)
• Essential characteristics of HIE defined jointly by the AAP and the
ACOG include:
Apgar <5 at 5 & 10 mins.
Fetal umbilical artery acidemia pH <7 or base deficit >12mmol/L or
both.
Neuroimaging evidence of brain injury: Brain injury seen on MRI
consistent with acute hypoxic ischemia.
Evidence of multisystem organ dysfunction consistent with HIE.
Steven Akach_Med VI
5/25/2021

Epidemiology
• The top three causes of newborn death in Africa are severe infections
(28%), birth asphyxia (27%), and prematurity (29%)(KDHS, 2014).
• In Kenya, the main causes of neonatal death in 2015 were birth
asphyxia and birth trauma (31.6%), prematurity (24.6%), and sepsis
(15.8%).(UNICEF Data)
• Infant mortality: 39/1000 live births.
• Neonatal mortality rates: 22/1000 live births. (1/3 due to birth
asphyxia)
Steven Akach_Med VI
5/25/2021

Risk factors (incr chances)
• Pre conception risk factors; maternal age ≥ 35 years, social factors,
family history of seizures or neurologic disease, infertility treatment,
previous neonatal death.
• Ante partum risk factors include maternal pro-thrombotic disorders
and pro-inflammatory states, maternal thyroid disease, severe
preeclampsia, multiple gestation, chromosomal/ genetic
abnormalities, congenital malformations, intrauterine growth
restriction, trauma, breech presentation and ante partum
hemorrhage.
Steven Akach_Med VI
5/25/2021

Risk Factors
• Intra partum risk factors ; abnormal fetal heart rate during labor,
chorioamnionitis / maternal fever, thick meconium, operative vaginal
delivery, general anesthesia, emergency cesarean delivery, placental
abruption, umbilical cord prolapse, uterine rupture, maternal cardiac
arrest etc
• In the immediate postnatal period, asphyxia usually occurs
secondary to pulmonary, neurological or cardiovascular abnormalities
Steven Akach_Med VI
5/25/2021

Etiology
• HIE occurs as a result of an oxygen depriving event in the prenatal ,
intra partum or postnatal period.
• Etiology is divided into maternal , placental , umbilical ,fetal and
neonatal factors.
• Maternal factors - chronic hypertension ; pulmonary disorder causing
hypoxia eg hypoventilation during anesthesia , respiratory failure or
carbon monoxide poisoning ; low maternal blood pressure from acute
blood loss , spinal anesthesia or compression of the vena cava and
aorta by the gravid uterus ;uterine tetany causing inadequate
relaxation of the uterus to allow placental filling as in oxytocin
overdose.
5/25/2021 Steven Akach_Med VI

Etiology (Causes)
• Placental factors - abruption , infection , placental insufficiency from
toxiemia or postmaturity.
• Umbilical cord accidents – cord around the neck , compression ,
knotting.
• Fetal factors – infection, severe anemia , cardiac abnormalities.
• Neonatal factors(occur after birth) – congenital heart disease ,
septicemia with shock ,severe anemia from hemorrhage or hemolysis
,severe pulmonary disease.

Pathophysiology
• Hypoxic Ischemia => physiologic and biochemical alterations.
• Consequences of cerebral ischemia => deprivation of energy substrates &
oxygen; and inability to clear accumulated toxic metabolites.
• Pathophysiologic mechanisms in HIE include:
 Cerebral Blood Flow and Energy Metabolism
 Excitotoxicity
 Oxidative Stress
 Inflammation
 Apoptosis

Cerebral Blood Flow & Energy Metabolism
• With brief asphyxia, there is
– a transient increase, followed by a decrease in heart rate (HR)
– mild elevation in blood pressure (BP)
– an increase in central venous pressure (CVP)
– and essentially no change in cardiac output (CO)
• Accompanied by a redistribution of CO with an increased
proportion going to the brain, heart, and adrenal glands
(diving reflex).

• Narrowing of autoregulatory window – due to increased expression of
iNOS, nNOS & eNOS.
• Downregulation of prostaglandin receptors due to increased circulating PG
levels; blunts the PG mediated vasoconstriction response to HTN =>
increased CBF.
• Loss of pressure autoregulation and CO2 vasoreactivity; due to prolonged
asphyxia. Worsened by hypotension & reduced CO.
• Inadequate supply of glucose/alternate substrates lead to hypoxic ischemic
neuronal cell death. Demand for substrate increase with increased brain
growth*.
• Decreased CBF => anaerobic metabolism & cellular energy failure; due to
increased glucose utilization in the brain and a fall in the concentration of
glycogen, phosphocreatine, and adenosine triphosphate (ATP).

• Cellular dysfunction results from diminished oxidative
phosphorylation and ATP production.
• Energy failure => impaired ion pump function => accumulation of
intracellular Na+, Cl-, H2O, and Ca2+; extracellular K+; and excitatory
neurotransmitters (e.g., glutamate).

Excitotoxicity
• Implies overactivation of excitatory amino acid receptors.
• Uptake of glutamate, the major excitatory amino acid is impaired.
• The result is high synaptic levels of glutamate and overactivation of
excitatory amino acid receptors ie NMDA, AMPA and kainate receptors.
• NMDA receptors; permeable to Ca & Na; Kainate and AMPA receptors
permeable to Na.
• Rapid Cytotoxic edema and necrotic cell death: caused by accumulation of
Na+ coupled with the failure of energy dependent enzymes such as Na+/ K+ -
ATPase.
• NMDA receptor activation=> intracellular Ca++ accumulation and further
pathologic cascades activation.

Excitotoxicity
• Susceptible regions: Putamen, thalamus, perirolandic cerebral cortex.
• Developing oligodendroglia also susceptible due to excitatory activity.
• Causes of intracellular Calcium rise:
NMDA receptor activation.
Release of Ca++ from intracellular stores (mitochondria and
endoplasmic reticulum [ER]), and
Failure of Ca++ efflux mechanisms due to Na/K ATPase impairment.

Excitotoxicity
• Consequences of increases intracellular Ca++ concentration include:
Activation of phospholipases, endonucleases, proteases, and, in
select neurons, nitric oxide synthase (NOS).
• Activation of proteases and endonucleases results in cytoskeletal and
DNA damage. (Apoptosis/necrosis)

Excitotoxicity

Oxidative Stress
• Def: Disruptions in cellular milieu result from an increase in free radical
production as a result of oxidative metabolism under pathologic
conditions.
• Superoxide production is consequence of mitochondrial dysfunction.
• Excitotoxicity energy depletion, mitochondrial dysfunction, and cytosolic
calcium accumulation, the generation of free radicals, such as
superoxide, nitric oxide derivatives, and the highly reactive hydroxyl radical.
• Reoxygenation mitochondrial oxidative phosphorylation is
overwhelmed and reactive oxygen species accumulate.
• Intrinsic antioxidant defenses depletedfree radicals directly damage
multiple cellular constituents (lipids, DNA, protein) activate pro-
apoptotic pathways.

Oxidative Stress (Nitric Oxide)
• Nitric oxide metabolism provides critical link between excitotoxicity
and oxidative injury in the hypoxic ischemic injured brain.
• Hypoxic-ischemic increases in nitric oxide production have multiple
potential beneficial and detrimental effects.
• Nitric oxide regulates vascular tone, influences inflammatory
responses to injury, and directly modulates NMDA receptor
function.
• Early endothelial NO is protective by maintaining blood flow, but
early neuronal NO and late inducible NO are neurotoxic by
promoting cell death

Inflammation
• Cytokines that have been strongly implicated as mediators
of brain inflammation in neonates include interleukin (IL)-
1b, tumor necrosis factor (TNF)a, IL-6,and membrane co-
factor protein-1
• After an asphyxial episode, there are many potential
sources of plasma cytokines,
– injured endothelium
– acutely injured organs, e.g brain by means of a disrupted
blood–brain barrier

Apoptosis
• Apoptosis is critical for normal brain development, but it is also an important
component of injury following neonatal hypoxia- ischemia and stroke.
• Immediate neuronal death (necrosis) can occur due to intracellular osmotic overload of
Na+ and Ca++ from ion pump failure or excitatory neurotransmitters acting on inotropic
receptors (such as the N-methyl-D-aspartate (NMDA) receptor.
• Apoptosis; secondary to uncontrolled activation of enzymes and second
messenger systems within the cell
– Ca2+-dependent lipases, proteases, and caspases);
– perturbation of mitochondrial respiratory electron chain transport;
– generation of free radicals and leukotrienes;
– generation of nitric oxide (NO) through NO synthase; and depletion of energy stores.

Apoptosis
• The pattern of injury after hypoxia-ischemia can be explained in
part on the basis of this metabolic demand;
• Brain regions most susceptible to hypoxic-ischemic injury in the term
infant (subcortical gray matter structures such as the basal ganglia
and thalamus) are the same regions that are most vulnerable to
mitochondrial toxins.

Summary of Pathophysiology
• HIE occurs in 3 stages:
1. Immediate primary neuronal Injury (interruption of O2 & glucose
in brain); Decreased ATP=>failure of ATP-Na/K pump. Na+
influx=>water influx=>Cellular swelling, depolarization & death. Cell
death & lysis causes release of glutamate(excitatory amino acid) =>
intracellular Ca2+ influx =>Further cell death.
2. Latent Period (6 hours); Reperfusion/recovery of cells.
3. Late Secondary Neuronal Injury (24-48 hours); reperfusion results
in blood flow to and from damaged areas, spreading toxic
neurotransmitters and widening the area of brain affected.

Neuropathology
1. Cortical edema, with flattening of cerebral convolutions, is followed
by cortical necrosis until finally a healing phase results in gradual
cortical atrophy, and may result in microcephaly.
2. Selective neuronal necrosis is the most common type of injury
observed in neonatal HIE. The pathogenesis most likely involves
hypoperfusion and reperfusion with injury promulgated by
glutamate.

3. Other findings
Status marmoratus-marbled histologic pathologic appearance caused
by hypermyelination of the basal ganglia and thalamus, and
parasagittal cerebral injury(bilateral and usually symmetric) with the
parieto-occipital regions affected more often than regions anteriorly.

4. Periventricular leukomalacia(PVL) is hypoxic-ischemic necrosis of
periventricular white matter resulting from cerebral hypoperfusion and
the vulnerability of the oligodendrocyte within the white matter to free
radicals, excitotoxin neurotransmitters, and cytokines.
-injury to the periventricular white matter is the most significant
problem contributing to long-term neurologic deficit in the premature
infant, although it does occur in sick full-term infants as well.

-the incidence of PVL increases with the length of survival and the
severity of postnatal cardiorespiratory disturbances.
-PVL involving the pyramidal tracts usually results in spastic diplegic or
quadriplegic CP.
-visual perception deficits may result from involvement of the optic
radiation.

PVL

5. Porencephaly, hydrocephalus, hydranencephaly, and multicystic
encephalomalacia may follow focal and multifocal ischemic cortical
necrosis, PVL, or intraparenchymal hemorrhage.
6. Brainstem damage is seen in most severe cases of hypoxic-ischemic
brain injury and results in permanent respiratory impairment.

Summary of Neurological Patterns
• Premature
– Selective subcortical neuronal necrosis
– Periventricular leukomalacia
– Focal/Multifocal ischemic necrosis
– Periventricular hemorrhage/infarction
• Term
– Selective Subcortical Neuronal necrosis
– Status Marmoratus of basal ganglia and thalamus
– Parasagittal cerebral injury
– Focal/Multifocal Ischemic cerebral necrosis

Part 2
Clinical Presentation & Management

Clinical presentation
• Perinatal asphyxia can result in :
- CNS injury alone(16% of cases),
- CNS and other end-organ damage(46%),
- isolated non-CNS organ injury(16%),
- or no end-organ damage(22%).
Steven Akach_Med VI
5/25/2021

Clinical Presentation
A. CNS injury in severe cases of HIE manifest with variable clinical
signs that evolve over time:
1. Birth to 12 hours.
- Deep stupor or coma,
- respiratory failure or periodic breathing,
- diffuse hypotonia,
- intact pupillary and oculomotor responses,
- and subtle or focal clonic seizures by 6-12 hours in term infants.
- Preterm infants can present with generalized tonic seizures.
Steven Akach_Med VI
5/25/2021

2. 12-24 hours.
- The level of alertness can appear to improve in less critical cases of
brain injury.
- However, severe seizures, marked jitteriness, and apnea also present
at this time.
- Term infants can present with weakness of the proximal upper limbs,
while preterm infants have lower extremity weakness.
Steven Akach_Med VI
5/25/2021

3. 24-72 hours.
- The consciousness level worsens leading to deep stupor and coma,
leading to respiratory failure.
- Pupillary and oculomotor disturbance are now present due to
brainstem involvement.
- Death due to HIE most often occurs at this time with a median time of
2 days.
- Preterm infants who die at this time often have severe intraventricular
hemorrhage(IVH) and periventricular hemorrhagic infarction.
Steven Akach_Med VI
5/25/2021

4. After 72 hours.
- Mild to moderate stupor may persist, but overall level of alertness
improves.
- Diffuse hypotonia may persist or hypertonia can become evident.
- Feeding difficulties becomes obvious due to abnormal sucking,
swallowing, and tongue movements.
Steven Akach_Med VI
5/25/2021

Clinical presentation
B. Non-CNS multi-organ dysfunction can present as follows:
1. Renal.
- Acute tubular necrosis can present with hematuria or renal
insufficiency or failure.
2. Pulmonary.
- Respiratory failure and meconium aspiration are due to fetal distress
and persistent pulmonary hypertension.
3. Cardiac.
- Myocardial dysfunction and congestive heart failure may result in
arrhythmias and hypotension.
Steven Akach_Med VI
5/25/2021

4.Hepatic.
- Abnormal liver enzymes, elevated serum bilirubin, and decreased
coagulation factors secondary to hepatic dysfunction.
5. Hematologic.
- Thrombocytopenia due to bone marrow suppression and decreased
platelet survival add to the coagulopathy.
6. Gastrointestinal .
- Paralytic ileus or necrotizing enterocolitis(NEC) are due to decreased
end-organ perfusion.
Steven Akach_Med VI
5/25/2021

7. Metabolic .
- acidosis( elevated lactate), hypoglycemia(hyperinsulinism),
hypocalcemia(increased phosphate load, correction of metabolic
acidosis), and hyponatremia/SIADH
Steven Akach_Med VI
5/25/2021

Clinical Presentation (National Guidelines)
Steven Akach_Med VI
5/25/2021

Diagnosis
A. Maternal data
1. History
- Prior pregnancy loss,
- thyroid disease,
- fever,
- drug use,
- infection
- and family history(thromboembolic disorders, seizure disorder) can
help identify causes of NE other than HIEs.
Steven Akach_Med VI
5/25/2021

2. Fetal heart rate (FHR) patterns.
3. Umbilical cord blood gases.
-provide objective evidence regarding the intrapartum metabolic status
of the fetus.
- An arterial cord pH<7 and base deficit ≥12 mmol/L are consistent with
fetal metabolic acidosis.
• For cord arterial pH >7.20, NE is unlikely to be a result of intrapartum
hypoxia (Gomella’s Neonatology, 2018 p 1000).
Steven Akach_Med VI
5/25/2021

4.Placental pathology.
- Pathological umbilical cord lesions, such as velamentous or marginal
cord insertion or cord hematoma or tears, may indicate a disruption
in the fetal vascular supply.
- Chorioamnionitis and funisitis may indicate an infectious etiology of
NE, while fetal thrombotic vasculopathy can point to a genetic
coagulopathic disorder.
Steven Akach_Med VI
5/25/2021

B. Neonatal data
1. Apgar scores.
• Not definite markers of an asphyxia event. Per ACOG, if the 5-minute Apgar score
is ≥7, peripartum HI is unlikely to be a major contributor to NE.
2. Physical examination.
- Findings determine grading of HIE severity based on Thompson’s scale.
- Normal: <7
- Abnormal: >/=7
- Mild HIE: 7-10
- Moderate :11-14
- Severe HIE: 15-22
Steven Akach_Med VI
5/25/2021

Thompson scoring for HIE
Elements 0 1 2 3
Level of
consciousness
Normal Hyperalert or
Stare
Lethargic Comatose
Fontanelle Normal Full, not tense tense
Posture Normal Fisting, cycling Strong, distal
flexion
Decerebrate
Tone Normal Hypertonia Hypotonia Flaccid
Moro Normal Partial Absent
Grasp Normal Poor Absent
Suck Normal Poor Absent +/- bites
Respiratory Normal Hyperventilate Brief apnoea IPPV (apnoea)
Seizures None Infrequent(<3/d
ay)
Frequent (>2 per
day)
Steven Akach_Med VI
5/25/2021

Investigations
Steven Akach_Med VI
5/25/2021

Imaging
• Echo for persistent pulmonary hypertension.
• Bedside cranial ultrasound; useful in 1st wk of life.
• Cranial ultrasound assessment directed at:
Basal ganglia injury
Presence of hemorrhage/echogenic parenchyma.
Size of lateral ventricles
Flow velocity in the anterior and middle cerebral artery.
Steven Akach_Med VI
5/25/2021

• Conventional electroencephalogram (cEEG).
• Amplitude-integrated EEG(aEEG).
• MRI of the brain.
• Magnetic resonance spectroscopy(MRS)
• Diffusion weighted imaging (DWI) and diffusion tensor imaging(DTI)
Steven Akach_Med VI
5/25/2021

Management
Post Resuscitation Management
• Begins with the identification of perinatal patients at high risk for asphyxia and
optimal resuscitation in the delivery room.
Resuscitation .
- The 2011 Neonatal Resuscitation Program guidelines(Kattwinkel et al, 2011)
recommend initiating resuscitation with room air or blended oxygen with a
targeted preductal Spo2 of 60-65% by 1 minute of life and 80-85% by 5 minutes
of life in all term and preterm infants.
- Hyperoxia should be avoided , as oxidative damage from oxygen-free radicals can
further exacerbate hypoxic-ischemic brain injury.
- Ensure effective airway and ventilation & offer circulatory support.
Thermoneutral Environment (TNE)
• Depends on birthweight & environment; Avoid hyperthermia.
• Maintain temperature at 37 ± 0.5ºC to prevent or minimize brain injury.
Steven Akach_Med VI
5/25/2021

Post Resuscitation Management
Ventilation/Respiratory Support
• Aim at maintaining arterial oxygen and carbon dioxide partial pressures within the
normal range. Continuously monitor oxygen saturation and arterial blood gas as the need
arises.
• Administer oxygen plus mechanical ventilation as needed for:
• Respiratory distress with or without meconium aspiration
• Severe encephalopathy need CPAP or mechanical ventilation
• Moderate encephalopathy
 Begin with room air; keep SPO2 at 90 -94% on supplemental oxygen.
 Keep PCO2 at 40-55mmHg.
 Risk for death; 16% for every 30s delay in initiating ventilation upto 6 min. Also 6% for
every minute in delay to initiate bag & mask ventilation (Shikuku et al., 2018).
Steven Akach_Med VI
5/25/2021

Ventilation and Respiratory Support Ctd
• Avoid hyperventilation because the ↑PCO2 is the only respiratory
stimulant.
• Ranges:
• (PaO2), 80-100 mm Hg
• (PaCO2), 35-40 mm Hg
• pH, 7.35-7.45.
Effects:
• Hypoxemia – cell damage
• Hyperoxia – vasoconstriction ----decreased CBF, Increased free oxygen radical damage
• Hypercapnia – Cerebral vasodilation + acidosis – uneven/increased CBF
• Hypocapnia PCO2 < 25 ---- decreased CBF

Perfusion
- Arterial blood pressure should be maintained in the normotensive range
for gestational age and weight.
- Limit fluid intake to 60-80% of recommended levels in 1st 48 to 72 hours.
- Treat hypovolaemia with infusion of 10ml/kg human albumin solution or
blood
- Acidosis corrects spontaneously; give K+ free Neonatylate or 10% dextrose
water with no added alkali.
- Fluid boluses are not indicated. Use vasopressors 1st before IV fluids unless
the cause is sure.
- Hypotensive: vasopressors; dobutamine* and dopamine (5-20ug/kg/min)
Steven Akach_Med VI
5/25/2021

Fluid and Electrolyte management
Steven Akach_Med VI
5/25/2021

Hematology
• Administer Vitamin K (1mg IM) on admission
• Maintain normal hemoglobin
• Treat DIC with vitamin K 1mg daily for 7 days, platelet
• transfusion if bleeding
Sepsis
• Assume presence of sepsis until proven otherwise – treat
Steven Akach_Med VI
5/25/2021

Seizure Management
• R/O metabolic causes – hypoglycaemia, hypocalcaemia, pyridoxine deficiency( common
in Moderate HIE, rare in Severe HIE)
• Phenobarbital – loading dose 20mg/kg slow iv infusion; maintenance dose 5-8mg/kg/day
• If no response: repeat with loading dose of 10mg/kg/day up to max 3 times followed by
maintenance of 5-8mg/kg/day
• If seizures persist: give phenytoin – loading dose of 20mg/kg/d slow iv followed by 3-
8mg/kg/d maintenance dose.
• If seizures persist: give a benzodiazepine(as 3rd drug) Lorazepam 0.05 – 0.1mg/kg/dose.
• If no iv access – diazepam, valproate, paraldehyde given rectally.
• Most seizures are refractory in 1st 72 hrs. If the infant has been stable for 3-5 days – all
anticonvulsants should be weaned except phenobarbital(taper over several weeks)
• If EEG abnormal – continue Phenobarbital for 3-6 months

Hyperglycemia and Hypoglycemia
• Maintain blood glucose at 75-100mg/dL (4.2 -5.6 mmol/l)
• Higher rate of infusion (9-10mg/kg)
• Use higher concentrations to avoid volume overload.
• Monitor blood glucose.
• Discontinue slowly to avoid rebound hypoglycaemia.
• Effects:
• Hypoglycemia – detrimental to neurons
• Hyperglycemia – increases brain lactate
• Cell damage
• Increased edema

Special considerations
• Admit to TICU if resuscitation lasts >5 min or signs of encephalopathy.
• Monitor temp hourly to avoid hyperthermia which may insult
hypothalamus. Use antipyrexic agent for pyrexia.
• Antibiotics if the cause is infections; monitor renal fxns with
aminoglycosides.
• Postpone feeding for 24-48 hours in cases of convulsions or severe or
moderate encephalopathy. When improved, feed at 40ml/kg/day.
• No benefits of withholding feeds >24hours without signs of
encephalopathy.
• EEG within to hours of resuscitation, confirms the need for hypothermia.
• Monitor development of seizures and treat promptly. 1st line drug
Phenobarbitone.
Steven Akach_Med VI
5/25/2021

Special Considerations ctd
Investigations (Depends on pt presentation)
• FBC & Blood culture to exclude infection
• UECs in the 1st 24hrs to assess renal fxn and hyponatremia
• Serum glucose, calcium, phosphate and magnesium;
hypomagnesaemia occurs within 1st day. Hypocalcemia btn day 2 & 3.
• Lumbar puncture in patients with moderate to severe
encephalopathy.
• LFTs and Cardiac enzymes.
Steven Akach_Med VI
5/25/2021

CNS Function/Neuroprotection
CNS Function
• Treat convulsions
• Therapeutic hypothermia as indicated
• Occupation therapy/physiotherapy: Refer & Start therapy as soon as the
baby has stabilised.
Enhancing Endogenous Protection (brain)
• This can be done by providing Therapeutic Hypothermia(TH) to babies with
moderate or severe asphyxia within six hours of birth.
• Therapeutic hypothermia attenuates secondary energy failure by
decreasing cerebral metabolism, inflammation, excitotoxicity, oxidative
damage, and cellular apoptosis.
Steven Akach_Med VI
5/25/2021

Requirements for Therapeutic Hypothermia
Steven Akach_Med VI
5/25/2021

Principles used in providing TH
• Achieve rectal temperature of 33ºC – 34.5ºC within 3 to 4 hours
• Maintain rectal temperature steadily between 33ºC and 34.5ºC for 72
hours.
• Rewarm the baby at a steady rate of 0.5ºC per hour until a rectal
temperature of 37 +/- 0.5 ºC is attained
• Monitor the baby closely until 80 hours
• Maintain adequate supportive care and close monitoring throughout
the TH and continue intensive care after the TH
Steven Akach_Med VI
5/25/2021

Other Neuroprotective Approaches
(Pharmacotherapy)
• Antagonists of excitatory neurotransmitters: eg.ketamine
• Free Radical Scavengers: Superoxide, dismutase, Vit E
• Calcium Channel Blockers: magnesium sulphate; nicardipine
• Antioxidant enzymes such as superoxide dismutase and catalase.
• Free radical inhibitors such as allopurinol and deferoxamine.
• NMDA glutamate receptor antagonist such as Magnesium.
• Prophylactic use of calcium channel blockers, such as flunarizine. Use in
infants currently c/I due to adverse cardiovascular effects.
• Erythropoietin has been shown to improve outcomes for term infants with
mild to moderate HIE by modulating neuronal injury and promoting neural
regeneration.

Neuroprotective Approaches Summary

Monitoring
Steven Akach_Med VI
5/25/2021

Supportive care
• Involve an occupational therapist as soon as the baby stabilise for feeding
and motor function
Counsel parents:
• Start early and involve them in care as much as possible. Teach them how
to recognize a convulsion. As the baby recovers plan for discharge and long
term follow up according to complications
Planning for discharge
• Reviewability to feed and advise accordingly
• Do a full neurological evaluation to plan for long term care
• Some may need to continue phenobarbitone.
Steven Akach_Med VI
5/25/2021

Prognosis
Depends on severity of hypoxia and timing of intervention
• Mild (7-10)
• 98-100% normal neurological outcome
• Moderate(11-14)
• 20-40% die/abnormal neuro outcome
• Signs >7 days have poorer outcome
• Severe(15-22)
40-50% die – All survivors have major neurodevelopment impairment.
• Cardiac, GIT, pulmonary, hepatic & hematological problems usually
resolve if the infant survives except the KIDNEY

References
• Abdo, R. A., Halil, H. M., Kebede, B. A., Anshebo, A. A., & Gejo, N. G.
(2019). Prevalence and contributing factors of birth asphyxia among
the neonates delivered at Nigist Eleni Mohammed memorial teaching
hospital, Southern Ethiopia: a cross-sectional study. BMC Pregnancy
and Childbirth, 19(1), 536.
• National Newborn Guidelines For Hospitals (2018)
• Shikuku, D. N., Milimo, B., Ayebare, E., Gisore, P., & Nalwadda, G.
(2018). Practice and outcomes of neonatal resuscitation for newborns
with birth asphyxia at Kakamega County General Hospital, Kenya: A
direct observation study. BMC pediatrics, 18(1), 167.
• UpToDate 2020
Steven Akach_Med VI
5/25/2021

Perinatal asphyxia

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