1. Hypoxic Ischemic Encephalopathy Dr Raghavendra . Fellow in
neonatology
2. 6/22/2015 Definitions Hypoxia/anoxia : denotes a partial or
complete lack of oxygen, respectively, in one or more tissues of
the body, including the blood stream. Asphyxia : is the state in
which pulmonary or placental gas exchange is affected leading to
progressive hypoxemia, which is severe enough to be associated with
acidosis. Ischemia : is a reduction in or cessation of blood flow
that arises from either systemic hypotension, cardiac arrest, or
occlusive vascular disease.
3. APGAR Score
4. Apgar Score Total Score = 10 score 7-10 normal score 5-6
mild birth asphyxia score 3-4 moderate birth asphyxia score 0-2
severe birth asphyxia
5. Hypoxic-Ischemic Encephalopathy Definition : It is the term
used to designate the clinical and neuropathological findings of an
encephalopathy that occurs in a full term infant who has
experienced a significant episode of intrapartum asphyxia.
6. Incidence of HIE Occurs in 1-6 per 1000 live term births in
developed countries 25% die or have multiple disabilities. 4% have
mild to moderate forms of cerebral palsy. 10% have developmental
delay .
7. Etiology of HIE Maternal: Cardiac arrest Asphyxiation Severe
anaphylaxis Status epilepticus Hypovolemic shock Uteroplacental:
Placental abruption Cord prolapse Uterine rupture Hyper stimulation
with oxytocic agents Fetal: Fetomaternal hemorrhage Twin to twin
transfusion Severe isoimmune hemolytic disease Cardiac
arrhythmia
8. Path physiology Immature brain is more resistant to
hypoxic-ischemic events compared to older children & adults
This may be due to: Lower cerebral metabolic rate Immaturity in the
development of the balance of neurotransmitters & Plasticity of
the immature CNS. Gestational age plays an important role in the
susceptibility of CNS structures < 20 weeks: Insult leads to
neuronal heterotopia or polymicrogyria 26-36 weeks: Insult affects
white matter, leading to periventricular leukomalacia Term: Insult
affects primarily gray matter
9. Other factors that influence the distribution of CNS injury:
Cellular susceptibility (neuron most susceptible) Vascular
territories (watershed areas) Regional susceptibility (areas of
higher metabolic rates, ie. Thalamus) Degree of asphyxia
10. PATHOPHYSIOLOGY OF BRAIN INJURY Mainly associated with two
phases 1. Primary energy failure . 2. secondary energy
failure.
11. Primary Energy Failure The impairment of cerebral blood
flow leads to decreases in oxygen and glucose, which leads to less
energy (ATP)) and increased lactate production. low ATP levels
cause failure of many of the mechanisms that maintain cell
integrity, particularly the sodium/potassium (Na/K) pumps and
mechanisms to maintain low intracellular calcium. This leads to the
release of glutamate, a prominent excitatory neurotransmitter. The
glutamate binds to glutamate receptors allowing additional influx
of intracellular calcium and sodium. Increased intracellular
calcium has detrimental effects leading to cerebral edema,
ischemia, micro vascular damage with resultant necrosis and/or
apoptosis Excitotoxic oxidative cascade get activated. necrosis
cell death.
12. Potential pathways for brain injury after hypoxia-ischemia.
Perlman J M Pediatrics 2006;117:S28-S33 2006 by American Academy of
Pediatrics
13. Secondary Energy Failure Continuation of excitotoxic
oxidative cascade . Activation of microglia inflammatory response .
Activation of caspase proteins. Reduction in levels of growth
factors , protein synthesis. Apoptosis cell death.
14. The interval between primary and secondary energy failure
represents an latent phase. That corresponds to a therapeutic
window. duration is approximately 6 hrs. Cell death in the brain
exposed to HI is delayed over several days to weeks after an injury
,apoptosis and necrosis continue depending on the region and
severity of the injury.
15. Status of infant at birth Depressed on initial assessment.
Generalized hypotonia. Apgars 3 or less @ 1min and 6 or less @
5min. Major resuscitation required. Large base deficit by blood
gas. Poor feeding to deep coma (encephalopathic)
16. Prognosis based on apgars Score at 1, 5 minutes does not
give prognosis indicator. The longer the score remains lower, the
greater its significance. 0-3 @ 1min has mortality of 5-10%. may be
increased to 53% if at 20min apgars score 0-3 0-3 @ 5min , CP risk
app. 1%. may be increased to 9% if for 15min. dramatic rise to 57%
CP risk if for 20min
17. Newborn neurological assessment Staging system of Sarnat
and Sarnat, levene score. Thompson score Means of recording
severity of insult to brain, to initiate med management and to
predict ultimate prognosis. Infants occasionally sustain insult to
brain arising from complication of systemic disease, Seizures in
50-70%
19. Assessment Tools in HIE Amplitude-integrated EEG (aEEG)
When performed early, it may reflect dysfunction rather than
permanent injury Most useful in infants who have moderate to severe
encephalopathy. Evoked Potentials Brainstem auditory evoked
potentials, visual evoked potentials and somatosensory evoked
potentials can be used in full-term infants with HIE More sensitive
and specific than aEEG alone However, not as available as aEEG and
there is a lack of experience among pediatric neurologists
Therefore aEEG is preferred because of easy access, application,
and interpretation
20. Standard 16-channel electroencephalogram showing a
typically abnormal burst suppression background pattern. (Courtesy
AC van Huffelen, PhD, Department of Neurophysiology, University
Medical Center, Utrecht, The Netherlands.)
21. Neuroimaging. Cranial ultrasound: Not the best in assessing
abnormalities in term infants. Echogenicity develops gradually over
days. CT: Less sensitive than MRI for detecting changes in the
central gray nuclei. MRI: Most appropriate technique and is able to
show different patterns of injury. Presence of signal abnormality
in the internal capsule later in the first week has a very high
predictive value for neurodevelopmental outcome.
22. Fetal hypoxia The umbilical placental impedance is so high
that the diastolic component shows flow in a reverse direction.
This finding is an indication of severe intrauterine hypoxia and
intrauterine growth restriction . Abnormal Doppler velocimetry. On
an umbilical artery Doppler flow velocity waveform
23. Patterns of periodic fetal heart rate (FHR) deceleration
Variable deceleration as a result of umbilical cord
compression
24. CT BRAIN OF HIE CHILD
25. 6/22/2015 Management Prevention, prevention, prevention
Insure physiological oxygen and acid-base balance Maintain
environmental temp and humidity Correct caloric, fluid and
electrolyte disturbances Maintain blood volume and hemostasis Treat
infection Neuro-resus measures to reduce cerebral oedema
ineffective Sz treated with PB, dilantin or lorazepam Newer
modalities- excitatory amino antagonists, oxygen free radical
inhibitors/scavengers, ca channel blockers, nitric oxide synthetase
inhibitors Hypothermia
26. References Allan WC. The clinical spectrum and prediction
of outcome in hypoxic-ischemic encephalopathy. Neoreviews 2002; 3;
e108-e115 Delivoria-Papadopoulos M, et al. Biochemical basis of
hypoxic- ischemic encephalopathy. Neoreviews 2010; 11; e184-e193
Fanaroff and Martins Neonatal-Perinatal Medicine: Diseases of the
Fetus and Infant, 9th edition. 2011, p 952-976 Marro, PJ, et al.
Pharmacology review: Neuroprotective treatments for
hypoxic-ischemic injury. Neoreviews 2010; 11; e311-e315. Newborn
Infant Nurs Rev. Author manuscript; available in PMC 2012 September
1.