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Hypoxic ischemic encephalopathy: Lecture on HIE
1. DR SUJIT SHRESTHA
NEONATOLOGY ( SGRH)
MD PEDIATRICS ( IOM, TUTH)
LECTURER, DEPARTMENT OF PEDIATRICS
NMCTH
Hypoxic Ischemic Encephalopathy
(Neonatal Asphyxia): MBBS
2. Definition: Birth asphyxia
Birth asphyxia is defined as a reduction of
oxygen delivery and an accumulation of carbon
dioxide owing to cessation of blood supply to the
fetus around the time of birth.
4. APGAR score
Score 0 1 2
Heart rate none <100 > 100
Respiration none irregular regular
Muscle tone limp reduced normal
Response to none grimaced cough
stimulation
Color of trunk white blue pink
7. Diagnosis
1/ Evidence of fetal distress
2/ Fetal metabolic acidosis
3/ Abnormal neurological state
4/ Multiorgan involvement
8. HIE Definition
Refers to CNS dysfunction or encephalopathy
associated with Perinatal asphyxia.
Potential to cause mortality and long term sequele
like disabilities and cerebral palsy.
9. Etiology
Pathologically, any factors which interfere with
the circulation between maternal and fetal blood
exchange
maternal factor, delivery factor and fetal factor.
10. Etiology—High Risk Factors
Maternal factor:
hypoxia, anemia, diabetes, hypertension, smoking,
nephritis, heart disease, too old or too young,etc
Delivery condition:
Abruption of placenta, placenta previa, prolapsed
cord, premature rupture of membranes,etc
Fetal factor:
Multiple birth, congenital or malformed fetus,etc
11. Pathophysiology
Asphyxia self-defensive mechanism
redistribution of blood flow to vital organs
( brain, heart and adrenal) to prevent from
hypoxic damage. ‘ Diving Reflex’
12. Pathophysiology
Hypoxic cellular damages:
a. Reversible damage(early stage):
Hypoxia may decrease the production of ATP,
and result in the cellular dysfunctions . But these
change can be reversible if hypoxia is reversed in
short time.
14. Pathophysiology
Cerebral blood flow
Early stage: normal (intraorgans shunt)
then slow down (selective vulnerability)
finally ischemia – Watershed regions
Cerebral metabolism – altered
Cellular electrolyte alteration- Na, Ca
17. Status Marmoratus: basal ganglia lesion resulting from
asphyxia. The lesions have a marbled appearance caused by
neuronal loss and an overgrowth of myelin in the putamen,
caudate, and thalamus.
Selective vulnerability - The hippocampal pyramidal
cells of CA1, pyramidal neocortical neurons (layers 3, 5, and
6), Purkinje cells, and striatal neurons have the highest
vulnerability.
18. Clinically, more term babies suffered
from this disease than premature
babies.
Pathologically, more premature
babies suffered from this disease
than term babies.
27. Electrolytes- Na and Calcium should be monitored.
Avoid Polycythemia: If Hct>65-70 , partial exchange
transfusion is done to bring Hct level to 55.
28. Control of seizures: HIE seizures are difficult to
control
Phenobarbital
loading dose 15-20mg/kg, iv
maintenance dose 3-5mg/kg, iv
Phenytoin
loading dose 15-20mg/kg, iv
maintenance dose 5mg/kg, iv
Midazolam: 0.1-0.3mg/kg, iv
Leveracetam, Topiramate
29. Special Investigations
EEG
Routine EEG does not help
Continous aEEG- Amplified EEG used for cerebral function
monitoring
Detects voltage pattern- burst, low voltage, isoelectric
Detects electrical seizure activity
Cranial Ultrasound:
Not good modality
Preterm – IVH, Periventricular leukomalacia
Severe cases- hypoechoic areas.
31. CT scan: only indicated in emergency
Generalized low attenuation of brain parenchyma in acute
stage.
local or patchy hypodensity, extensive & generalized hypodensity,
usually combined with brain hemorrhage
MRI
Time consuming
DWI ( Diffusion weighted imaging) is helpful in early stage.
Within hours shows restricted diffusion to hypoxic areas.
32. Recent advances in Management
Cerebral Hypothermia
Selective head cooling ( CoolCap trial ) vs Whole body cooling
Decreases brain metabolism and injury.
>=36 weeks and >=2000gm
Cooling upto 33-34 C.
Provided for 72 hours
Seen to have better outcomes specially for moderate HIE cases.
34. Prognosis
Depend on the severity of brain damage & medical
treatment, usually:
Mild or moderate cases could be cured completely, but
severe cases represent poor prognosis with high mortality
or cerebral complications such as mental retardation &
cerebral palsy.
35. Overall mortality – 20%
Overall incidence of sequele - 30%
Mild : 100% good prognosis
Mod : 80% normal
Severe : 50% death, 50% sequele
Presence of seizure increases chance of Cerebral
palsy by 50-70 times.