HYPOXIC ISCHEMIC ENCEPHALOPATHY:

Hypoxic encephalopathy is a condition in which the entire brain does not receive enough oxygen, but isn’t completely deprived. This
particular condition refers to an oxygen deficiency to the brain as a whole, rather than a part of the brain.

Neonatal encephalopathy, following severe birth asphyxia or perinatal hypoxia is referred to hypoxic- ischemic encephalopathy (HIE).
Following severe birth asphyxia, 25% infants are likely to develop syndrome of HIE. HIE may occur from a drop in blood
pressure, cardiac arrest, or a blocked or ruptured blood vessel.

Hypoxic ischemic encephalopathy can be fatal. The disease can also cause long-term damage, including mental retardation, delayed
development, seizures, and cerebral palsy.

BLOOD SUPPLY TO THE BRAIN:

CAUSES:

There are a variety of causes of hypoxic ischemic encephalopathy, as any injury and many health conditions may potentially cause
oxygen deprivation to the brain. Some common causes of the condition are:

 Drug overdose
 Drowning
 Lack of oxygen due to smoke inhalation
 Extremely low blood pressure
 Strangulation
 Injury or complication during birth
 Cardiac arrest
 Carbon monoxide poisoning
 High altitudes
 Choking
 Compression or injury to the trachea that reduces or stops breathing
 Complications from general anesthesia
 Diseases that cause paralysis of the respiratory organs or muscles (such asmyasthenia gravis or Guillane-Barre syndrome).

PATHOGENISIS:
Hypoxic damage to neurons may lead to both cytotoxic and vasogenic cerebral oedemas though brain swelling is not a prominent
feature of HIE in the human newborn. Severe hypoxia causes selective neuronal necrosis in hippocampus thalamus, basal ganglia,
brain stem and cerebellum. Asphyxia damage sets up a cascade of intracellular events which causes neuronal death after a few hours
of insult. During severe asphyxia energy failure occur leading to depletion of intracellular high- energy phosphate compounds like ATP.
Failure of ATP- dependent membrane bound Na + / K+ ATPase pump leads to depolarization of cells, allowing influx of Na + and Ca++ ions
with osmotic influx of water causing cytotoxic neuronal edema. Calcium ions inside the cells cause activation of intracellular protease
and lipase with generation of oxygen free radicals causing further damage to the cellular membranes. During reperfusion following
asphyxia insult, highly reactive oxygen- derived free radicals are generated in many organs including developing brain.
CLINICAL MANIFESTATIONS:
The clinical features of HIE are well preceded by at least one of the following three antecedents:

 Evidence of fetal hypoxia/ distress

 Apgar score of three or less at 5 minutes or later
 Cord arterial blood pH≤ 7.0

Other clinical manifestation: -

 Seizures
 CNS irritability
 Jitteriness
 Excessive crying
 Lethargy
 Inactivity
 Apnecic spells
 Stupor
 Generalised hypotonia followed by hypertonia
 Buldging anterior fontanelle
 Moro reflex may be hyper- reactive

DIAGNOSTIC EVALUATION:

1. Clinical monitoring: -
 Monitor vital signs with the help of multi- channel monitor
 Watch the color of the baby for cyanosis, pallor, jaundice
 Tissue perfusion should be evaluated by capillary refilling time on blanching which should be less than 2 seconds.
 Monitor abdominal girth
2. Biochemical monitoring: -
 Monitor acid base parameters
 Monitor blood gases
 Blood glucose
 Serum electrolytes
 Renal function test e.g. BUN
3. Laboratory investigation: -
 Skiagram of chest should be taken in all cases to exclude pneumothorax, diaphragmatic hernia and congenital pneumonia.
 Blood culture should be taken to make an early diagnosis of bacterial infection
 EEG preferably be taken during first 3 days of life to identify any abnormalities like burst suppression, low voltage or isoelectric
pattern.
 Ultrasound of the brain is best done during 4 to 7 days of life for the diagnosis of periventricular – intraventricular haemorrhage in
preterm babies.
 CT scan is more useful to diagnose parasagittal infarction and ischemia changes and it should preferably be done after the age
of 12 weeks.
4. Brain – oriented resuscitation: -
 Improve cerebral perfusion and prevent further ongoing neuronal damage due to hypoxia, ischemia and metabolic disturbances.
 The baby should be nursed in a thermoneutral environment with head raised by 30° to prevent further elevation of intracranial
pressure.
 The infant should be intubated and attach to a mechanical ventilator and provided with hyperventilation to maintain Pa O 2 above
80mm Hg and Pa CO2 between 25 – 30 mm Hg.
 Acidosis, hypoglycaemia, hyperkalemia and hypocalcaemia should be identified and appropriately managed.
 Blood glucose should be maintained between 60 – 100 mg/dl
 Hypotension or poor tissue perfusion should be identified and promptly managed by administration of normal saline or ringer
lactate.
 Neonates with moderate and severe HIE may manifest seizure activity within 12 hours after birth. It is recommended to
administer a loading dose of phenobarbitone 20 mg/kg followed by 5 mg/kg/dl as maintenance dose IV.
TREATMENT:

Treatment depends on the underlying cause of the condition, as well as the severity of the damage to the brain. Treatment options
include:

 Life-Sustaining Treatment
 If brain function has stopped but damage is not yet extensive, life-sustaining treatment is administered.
 Mechanical Ventilation
 Mechanical ventilation may be needed to sustain breathing.
 Treatments for the Circulatory System
 Treatments are administered to maintain heart function and control blood pressure.
 Seizure Control
 Medications and general anaesthesia may be administered to control seizures.
 Cooling Blankets
 Hypoxic brain damage is often caused by heat, so cooling blankets or other means of cooling may be applied to reduce the
body's temperature.

NEWER THERAPEUTIC MODALITIES:

1. Oxygen free radical inhibitors and scavengers:
 Free radicals are known to initiate and perpetuate a cascade of chain reactions.
 Administration of specific enzymes including superoxidase dismutase (SOD), endoperoxidase and catalase to degrade highly
reactive radicals to non- reactive like vitamin E, vitamin C and mannitol.
 Indomthacin, a cycloxygenase and phospholipase A 2 inhibitor and allopurinol, a xanthine oxidase inhibitor have been shown to
be a benefit in ischemic neuronal damage.

2. Excitatory amino acid antagonists:

 The damage to neurons due to anoxia can be prevented by the presence of magnesium ions which block glutamate receptors or
by specific glutamate antagonists.
 Agents which block glutamate release or block its postsynaptic action may be useful in preventing neuronal injury.
 The role of magnesium sulphate as a neuroprotective agent for prevention of brain damage due to hypoxia- ischemia deserves
active consideration and evaluation in future.
PROGNOSIS:

Birth asphyxia is an important cause of neonatal mortality accounting for a case fatality rate of 15- 50 % depending upon the definition
of birth asphyxia and quality of newborn care facilities. Among term babies most deaths are attributed to HIE and systemic effects of
asphyxia while in preterm babies majority of deaths are accounted for by prematurity.

Following severe birth asphyxia 25% infants are likely to develop evidences of HIE. Infants with severe HIE have increased risk of long
term neurological sequelae and it is better predictor of subsequent handicap than poor Apgar scores or biochemical changes alone.
Apgar score have a poor predictive validity but when establishment of spontaneous breathing is delayed beyond 10 minutes or later
and Apgar scores remain low, it is associated with adverse long term outcome.

Development of seizures and other clinical and laboratory evidences of HIE are associated with increased risk of CP. If following
resuscitation of an asphyxiated newborn baby, there are no neurological abnormalities during early neonatal period, it guarantees
normal neuromotor development on follow up.

RESEARCH ABSTRACT:
■ Term infants with hypoxic-ischemic encephalopathy: outcome at 3.5 years
Charlene Robertson, Neil Finer

ABSTRACT:

A total of 167 term neonates with a diagnosis of hypoxic-ischemic encephalopathy (HIE) had detailed neurodevelopmental follow-up at
3–5 years of age. All 66 children with mild HIE were free from handicap; all seven with severe HIE were severely handicapped; and of
the 94 with moderate HIE at birth, 21-3 per cent were handicapped. Mean IQ was significantly related to the category of HIE. Within the
moderate HIE category, the neurological examination at discharge from the Neonatal Intensive Care Unit was more useful than the
presence of neonatal convulsions in identifying children with subsequent developmental delay. Abnormalities on this examination
related significantly to an increased number of handicapped children, decreased motor and language skills, and lower IQs. Although
neonatal convulsions were associated with an increased number of handicapped children, they did not significantly affect most other
developmental outcome measures. In term infants with documented HIE at birth, major neurodevelopmental dysfunction at 3–5 years
depended more on prospectively established category of HIE than on other perinatal or social factors.

I. High risk for infection related to deficient immunologic defences.

II. High risk of injury from increased intracranial pressure (ICP) related to immature central nervous system and physiologic stress
response
III. Altered family processes related to situational/ malnutritional crisis, knowledge deficit (birth of a preterm and / or ill infant) interruption
of parental attachment process
IV. Ineffective breathing pattern related to decreased energy and fatigue

BIBLIOGRAPHY:
 Marlow R. Dorothy, Redding A. Barbara, Textbook of Paediatric Nursing, 1st edition, , Noida, Saurabh Printers Pvt. Limited, India, Pp
293- 295
 Hockenberry. Marilyn. J, Wong’s Essential of Paediatric Nursing, 7 th Edition, Elsevier , New Delhi, 2007, Pp 280
 Wong. Donna. L, Wong and Whaley’s Clinical manual of Paediatric Nursing, 4 th Edition, Mosby, USA, 2006, Pp 350 - 354
 Potts. Nicki. L, Mandleco. Barbara. L, Paediatric Nursing – caring for children and their families, 2nd edition, 2007, Sanat Printers,
Haryana, Pp 569 - 570
 Singh Meharban, Textbook of Care of the Newborn,6 th Edition, 2004, New Delhi, Sagar Publications, Pp 106 -112.