Neonatal Encephalopathy

Name: fatmah ahmed amer al abu hussain

ID: 434300426
SUPERVISION: DR. Majedah AL- razzaz
 Objective
• Defination
• Etiology and risk factor
• Incidence
• Pathophysiology
• Clinical manifestations
• Diagnosis
• Assessment tools
• Treatment
• Therapeutic hypothermia
• Outcomes
What is neonatal encephalopathy (NE)?

• Is a clinical and not an etiologic term that describes

an abnormal neurobehavioral state cosisting of an
altered level of consciousness usually other signs of
brainstem and or motor dysfunction.
Causes of neonatal encephalopathy

• Hypoxic ischemic encephalopathy

• Perinatal stroke
• Kernicterus
• Metabolic derangements (inborn errors of
metabolism or hypoglycemia )
• Intracranial hemorrhage
• Infection
• Maternal toxins
Etiology of HIE
Fetal factors Uteroplacental factors Maternal factors

•Fetomaternal •Placental abruption •Cardiac arrest

hemorrhage •Cord prolapse •Asphyxiation
•Twin to twin transfusion •Uterine rupture •Sever anaphylaxis
•Severe isoimmune •Hyper stimulation with •Status epilepticus
hemolytic DX oxytocic agents •Hypovolemic shock
•Cardiac arrhythmia •Pre eclamsia
•IUGR
INCIDENCE OF HIE
• Occurs in 1-6 per 1000 live term births
• Approximately 20-30% of infants with HIE die in the
neonatal period
• 33-50% of survivors are left with permanent
neurodevelopmental abnormalities (cerebral palsy
or mental retardation )
Pathophysiology
Cont…
• Gestational age plays an important role:
• < 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
Clinical picture
1. Neurological signs : Abnormal findings on
neurologic exam in the first few days after birth is
the single most useful predictor that brain insult
has occurred in the perinatal period .
2. Multiorgan dysfunction
Diagnosis
• There is no clear diagnostic test for HIE
Abnormal findings on the neurologic exam in the
first few days after birth is the single most useful
predictor that brain insult has occurred in the
perinatal period
Criteria for diagnosis of HIE
1. Metabolic acidosis (cord PH less than 7 or base
deficit of more than 12)
2. Early onset of encephalopathy
3. Multisystem organ dysfunction
4. 5 min apgar less than 4
Clinical staging of HIE
Assessment tools (investigations)
• Prenatal :
Doppler ultrasound (assess the cord blood flow)
• Perinatal :
Blood gas analysis
• Postnatal :
Monitoring of ABG –blood glucose serum
electrolytes – temperature – serum calcium –renal
function – LFT
CONT..
• Neuroimaging :
Amplitude-integrated EEG (aEEG) it reflect
dysfunction rather than permanent injury
Also it useful in infans who have moderate to severe
encephalopathy
So if the aEEG— normal the outcome is good
But if abnormal --- it raises the probability of death
or sever disability from 25%to 75%
Cont..
• MRI :
Most appropriate technique and is able to show
different patterns of injury
Treatment
1. Proper stabilization to minimize neuronal damage

2. Treatment of seizure by anticonvulsant

3. Treatment of hypotension by volume and
inotropic support
4. Treatment of hypoglycaemia and hypocalcemia
Emerging therapies
• Xenon – inhibits excitatory amino acid relese and
easily crosses blood – brain barrier
• Erythropoietin – possible neuroprotection against
apoptosis , anti inflammatory effect
• Melatonin – inhibit free radical , decreases
inflammatory cytokine level and stimulates
antioxidant enzymes
Treatment of complications
CNS complicatons management
• Monitor systemic blood pressure ,intracranial
pressure (by feel of fontanel) and structural
changes or damage (usually MRI)
• Pharmacologically management : anticonvulsants
(phenobarbiton , phenytoin) ,sedation especially if
ventilated and cooled (morphine, midazolam)
• Prevent fluid overloading
Cardiovascular and renal
complications
• hypovolaemia, hypotension , renal failure are most
serious sequelae of HIE and need to monitor ---
urine output, monitor electolyes, urea , creatinine
• hypovolaemia, hypotension ---management with
volume expanders ,blood transfusion and –or
inotrops (improve cardiac contractility and cardiac
output also improve renal function )
Pulmonary complication
management
• Monitor respiratory status by observation and
blood gases
• Provide respiratory support if required (CPAP or
ventilation)
• Treat underlying pathology
Metabolic complication
management
• Metabolic acidosis – (ventilate and use sodium
bicarbonate ).
• Hypoglycaemia (10% dextrose ), hypocalcaemia
correction
• Monitor BP
Outcomes
• The location and extent of damage , and the
immediate medical management will determine
the short and long term outcomes.
• Its possible to have no long term complication
• But complication that can occur are delayed as
failure to reach milestone , cerebral palsy , death .