HIE

Instructor : Abed- Alhameed

awawda
student Name : Aya Qattoush
Outline :
• Definition
• Risk factors
• Etiology
• Pathophysiology
• Stages of HIE
• Diagnosis
• Management
Definition
• Hypoxic-ischemic
encephalopathy Is an
abnormal neurobehavioral
state in which the
predominant pathogenic
mechanism is impaired
cerebral blood flow that may
result in neonatal death or be
manifested later as cerebral
palsy or mental deficiency.
 Ante partum
Risk factors •Sever preeclampsia
•Placental abruption
•IUGR
•APH
Pre conceptual
•IDDM
•Thyroid disease
•Fertility treatment
•Nulliparity
•Advanced maternal age
Intra partum
•Breech
•Cord prolapse
•Emergency C-section
•induction
•Maternal Pyrexia
Etiology of HIE
• Maternal:
1. Cardiac arrest
2. Severe anaphylaxis
3. Status epilepticus
4. Hypovolemic shock

• Fetal:
1. Fetomaternal hemorrhage
2. Severe isoimmune hemolytic disease
3. Cardiac arrhythmia
• Uteroplacental:
1. Placental abruption
2. Cord prolapse
3. Uterine rupture
4. Hyper stimulation with oxytocic agents
Path physiology
• Mainly associated with two phases
1. Primary energy failure .
2. secondary energy failure.
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
• necrosis cell death
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
Stages of HIE
• Mild(stage1) : Hyper alertness, uninhibited
reflexes, sympathetic over activity

• Moderate(stage2) : Lethargy-stupor, hypotonia,

suppressed primitive reflexes, seizures

• Severe(stage3) : Coma, flaccid tone, suppressed

brainstem function, seizures, increased ICP
Diagnosis
• Severe acid levels — pH less than 7.00 — in the
arterial blood of the umbilical cord.
• APGAR score of zero to three for longer than five
minutes. The Apgar test is used just after birth to
evaluate a newborn's color, heartbeat, reflexes,
muscle tone and respiration.
• Neurological problems, such as seizures, coma
and poor muscle tone.
• Respiratory distress, low blood pressure
Tests and studies are conducted once medical professionals have
observed signs and symptoms of HIE. These include:

• CT scan
• MRI scan
• EKG
• Blood tests (arterial blood gases)
• Evoked potential test
• Ultrasound
• Echocardiogram: This test uses high-frequency sound waves to
examine the size, shape, and motion of the baby’s heart.
• Blood glucose levels
Management
• Secure an appropriate airway & maintain
adequate circulation.
• Corticosteroids are not beneficial in
management of cerebral edema.
• Controlled hyperventilation and use of
furosemide or mannitol may actually be
harmful.
• Monitoring of seizure activity and control by
anticonvulsants.
1. Phenobarbital (Luminal)
2. Phenytoin (Dilantin)
3. Lorazepam (Ativan)

• aEEG or EEG should be used to monitor subclinical

seizure.
• Monitor multiorgan function carefully
• Maintenance of adequate cerebral perfusion, use
inotropic agents in pts with evidence of myocardial
dysfunction
• Avoid both systemic hypotension and
hypertension.
• Prevent SIADH.
• Avoid fluid overload
• Monitor serum glucose and electrolytes closely
• Closely monitor body temperature and avoid
hyperthermia.
• Careful attention to possible infection is
important.
Therapeutic hypothermia
• Selective head or whole body hypothermia of a core temperature of
33.5 C applied within 6 hours of birth for 48-72 hours is
neuroprotective

• How does therapeutic hypothermia work?

Lowering the body’s temperature slows the metabolic rate and allows
cells more time to recover from neurological damage.
When should doctors perform
therapeutic hypothermia?
• The baby is less than six hours of age* and was born after
at least 36 weeks of pregnancy.

• At least one of the following:

▫ A complication before delivery, such as cord prolapse,
uterine rupture, or profound fetal bradycardia
▫ An Apgar score of five or lower at 10 minutes of life
▫ Prolonged resuscitation at birth
▫ Severe acidosis
▫ Abnormal base excess within 60 minutes of birth, as shown
in umbilical cord gas or neonate blood gas

• At least one of the following:

▫ Signs of neonatal seizures
▫ Evidence of neonatal encephalopathy in a clinical exam