Neonatal case presentation on hypoxic ischemic encephalopathy
15 days old female baby Mariyam, weighing 2.9kg
and K/C of birth asphyxia delievered via LSCS due to
breech presentation at 38 weeks of gestation was
admitted on 15-9-2013 with C/O
for 1 day
reluctant to feed
for 1 day
HISTORY OF PRESENTING COMPLAIN:
According to attendent, baby was in usual state of
health 1 day back when she started having fits in the
morning. Fits were focal and involved either one limb at
one time with flickering of eyes and lasting 5-10 secs
occuring every 2 to 3 hrs. There was no loss of
consciousness, fecal or urinary incontinence and
uprolling of eyeballs.There is no history of fever and
vomiting .Baby is also reluctant to feed since then.
It was a fullterm pregnancy and a booked case at some private hospital
U/S scan was done twice at 8th and 9th mth
Mother had no c/o gestational DM, hypertension,fever,rash or anemia during
She took multivitamins and got tetanus toxoid.
Mother underwent LSCS due to breech presentation of baby at 38 wks of gestation.
There is no H/O PROM, preeclampsia or any other maternal complication at birth
Baby had delayed and weak cry.
There was peripheral cyanosis.There was no jaundice.
Baby had episode of fits half hr after birth.They took the baby to Jinnah hospital
and upon their refusal to admit due to lack of incubators, they took the babyto
Naseem centre.The baby was admitted there as a case of perinatal asphyxia for 9
days.No fits were observed during this period.Platelets and FFPs were
tranfused.Baby was on tanzo and vancomycin and was discharged on 9-9-2013.
No BCG vaccination done.
Baby was kept NPO after birth.Breast feeding was
started at 8th day of life and she was taking feed normally.
She is reluctant to feed for 1 day.
Baby is 5th product of cosanginuous marriage.She has
3 normal siblings.There is no significant family history of any
Their socioeconomic status is average.
They use unboiled water for drinking.
GRAM STAIN: no organism seen
No bacterial growth
no bacterial growth seen
Widening of sutures and anterior fontanelle suggestive of raised
no solid or cystic lesion seen
mild hydrocephalus with dilated all 4 ventricles
grade 2 parenchymal and IVH including germinal matrix
Grade 2 intracranial hemorrhage
CT SCAN brain:
Extensive white matter edema invlving the subcortical regions of
frontal,parietal and temporal lobes causing effacement of
right lateral ventricle.
No hemorrhagic density identified
Ischemic encephalopathy involving frontal,parietal and temporal
ENCEPHALOPATHY SECONDARY TO
Pt was kept NPO initially ,then mother feed was given 2cc 2hrly via
Inj 1/5th in 10% D/S 150cc/kg/day
i.e 450cc in 24 hrs
Inj cefotaxime 150mg/kg/day
i.e 225 mg iv B.D
Inj amikacin 15mg/kg/day
i.e 22 mg iv B.D
Tab phenobarbitone 30 mg
Inj diazepam 0.3mg/kg iv sos
Inj Phenytoin 20 mg/kg loading dose
i.e 60mg iv stat,then 10mg iv BD in infusion
Neb with N/S 6hrly
Hypoxic-ischemic encephalopathy, is
characterized by clinical and laboratory
evidence of acute or subacute brain injury
due to asphyxia. The primary causes of this
condition are systemic hypoxemia and/or
reduced cerebral blood flow (CBF).
The cerebral blood flow (CBF) of adults is typically
maintained at constant levels despite fluctuations in the
systemic blood pressure.
In the infant, CBF autoregulation is not as responsive;
therefore, when hypoxia occurs, the infant's initial systemic
response is to maintain perfusion to the brain and end
organs with increased heart rate and the endogenous
release of epinephrine.
These measures can only maintain CBF for a short time
(minutes), and when the hypoxic state persists, the
systemic blood pressure falls and neuronal cells are
damaged through progressive intracellular energy failure
and eventual cell death via apoptosis.
THIS IS THE FIRST PHASE OF HYPOXIA.
The second or latent stage of this process,
which occurs 6 to 24 hours after the initial
insult, is the recovery of cerebral circulation
and oxygenation leading to a progression of
inflammatory response and significant
cerebral edema, onset of seizures, secondary
cytotoxic edema, and additional cell death.
In the United States and in most developed countries,
the incidence of hypoxic-ischemic encephalopathy is 18 cases per 1000 births.
The incidence of hypoxic-ischemic encephalopathy is
reportedly high in developing countries.
SIGNS AND SYMPTOMS
Clinical manifestations and course vary depending on
hypoxic-ischemic encephalopathy severity.
Mild hypoxic-ischemic encephalopathy
Muscle tone may be slightly increased and deep tendon
reflexes may be brisk during the first few days.
Transient behavioral abnormalities, such as poor
feeding, irritability, or excessive crying or sleepiness.
The neurologic examination findings normalize by 3-4 days
Moderately severe hypoxic-ischemic
The infant is lethargic, with significant hypotonia and
diminished deep tendon reflexes.
The grasping, Moro, and sucking reflexes may be sluggish
The infant may experience occasional periods of apnea.
Seizures may occur within the first 24 hours of life.
Full recovery within 1-2 weeks is possible and is associated
with a better long-term outcome.
Severe hypoxic-ischemic encephalopathy
Stupor or coma is typical. The infant may not respond to any physical stimulus.
Breathing may be irregular, and the infant often requires ventilatory support.
Generalized hypotonia and depressed deep tendon reflexes are common.
Neonatal reflexes (eg, sucking, swallowing, grasping, Moro) are absent.
Pupils may be dilated, fixed, or poorly reactive to light.
Seizures occur early and often and may be initially resistant to conventional
treatments. They are usually generalized.
Irregularities of heart rate and blood pressure (BP) are common during the
period of reperfusion injury, as is death from cardiorespiratory failure.
Infants who survive severe hypoxic-ischemic encephalopathy;
The level of alertness improves by days 4-5 of life.
Hypotonia and feeding difficulties persist, requiring tube feeding for weeks to
Serum electrolyte levels
Renal function studies
Cardiac and liver enzymes - These values are an
adjunct to assess the degree of hypoxic-ischemic injury
to the heart and liver
Coagulation system - Includes prothrombin time,
partial thromboplastin time, and fibrinogen levels
Arterial blood gas - Blood gas monitoring is used to
assess acid-base status and to avoid hyperoxia and
hypoxia, as well as hypercapnia and hypocapnia
Findings include global increase in cerebral
echogenicity and obliteration of cerebrospinal fluid
(CSF) containing spaces suggestive of cerebral edema.
Head CT scanning
A CT scan of the head shows cerebral edema,
manifested as narrowness of the lateral ventricles and
flattening of gyri. Areas of reduced density that
indicate evolving zones of infarction may be present.
Evidence of hemorrhage in the ventricles or in the
cerebral parenchyma may also be seen.
MRI is the imaging modality of choice for the
diagnosis and follow-up of infants with moderate-tosevere hypoxic-ischemic encephalopathy (HIE).
Demonstrates the injury pattern as area of
aEEG performed within a few hours of birth can
help evaluate the severity of brain injury in the infant
with hypoxic-ischemic encephalopathy.
1. Transfer the baby to special care newborn unit.
A baby who fails to initiate and sustain respiration at birth is at risk
of hypoxic brain injury and needs regular monitoring. All these babies
should have a cord gas analysis performed.
Infants with moderate asphyxia (Apgar score 4-6 at 1 minute of age)
may be transferred to the mother. However, these infants should also
be monitored frequently in the first 48-72 hours for features suggestive
Infants with severe asphyxia (Apgar score 0-3 at 1minute or need for
prolonged bag and mask ventilation >5 minutes) should be transferred
to a special care newborn unit for observation and treatment.
2. Maintain temperature
Place the baby under the radiant warmer after drying the baby.
3. Check vital signs
Immediate clinical assessment should be made by recording
respiration, heart rate, blood pressure, capillary refill time,
temperature and oxygen saturation. Urine output monitoring
should be done.
4. Start intravenous fluids
5. Check blood sugar, hematocrit and blood gases.
Check blood sugar (to detect hypoglycemia or
hyperglycemia), hematocrit (to detect anemia and polycythemia)
and blood gases (to detect metabolic acidosis, hypoxia,hyperoxia
and respiratory failure).
6. Consider infusion of volume expander
If the capillary refill time is more than 3 seconds or if there is
metabolic acidosis, volume expansion with normal saline (or
Ringer’s lactate) 10 ml/kg over 5-10 min should be instituted.
This may be repeated.Maintain the mean BP above 35 mm Hg
(for term infants). Dopamine or dobutamine can be used to
maintain adequate cardiac output.
a) Maintain oxygenation and ventilation.
b) Maintain adequate perfusion: Use saline, Ringer’s lactate and blood to maintain
c) Vasopressors: Dopamine and dobutamine are the drugs of choice.
d) Maintain normal blood glucose
e) Treat seizures:
The anticonvulsant of choice for controlling seizures is phenobarbitone.The initial
dose is 20 mg/kg, intravenously slowly over 20 minutes.Two additional doses of 10 mg/kg
can be given every 15 minutes. The maximum loading dose is thus 40 mg/kg.
If convulsions are still uncontrolled, phenytoin sodium should be added in a dose of
20 mg/kg intravenously slowly over 20 minutes. Maintenance therapy of both
phenobarbitone and phenytoin is started 12 hours later in a dose of 5 mg/kg/day in a
For intractable seizures Clonazepam, Midazolam, Paraldehyde, and Valproate may be
f)One promising modality on the horizon is cerebral hypothermia.Mil dreductions in
temperature of the body as a whole or of the head (brain) has been shown to minimize
the effects of hypoxic ischemic encephalopathy.
In most cases (particularly in moderately severe
and severe hypoxic-ischemic encephalopathy), the
infant is restricted to nothing by mouth (NPO) during
the first 3 days of life or until the general level of
alertness and consciousness improves. In addition,
infants undergoing hypothermia therapy should
remain NPO until rewarmed. Enteral feeds should be
carefully initiated about 5 mL every 3-4 h.
In severe hypoxic-ischemic encephalopathy, the mortality rate is 25-50%. Most
deaths occur in the first week of life due to multiple organ failure or . Some
infants with severe neurologic disabilities die in their infancy from aspiration
pneumonia or systemic infections.
The incidence of long-term complications depends on the severity of hypoxicischemic encephalopathy.
80% of infants who survive severe hypoxic-ischemic encephalopathy develop
serious complications, 10-20% develop moderately serious disabilities, and
10% are healthy.
Among the infants who survive moderately severe hypoxic-ischemic
encephalopathy, 30-50% may have serious long-term complications, and 1020% have minor neurological morbidities.
Infants with mild hypoxic-ischemic encephalopathy tend to be free from
serious CNS complications
• Cerebral palsy - 30%
• Epilepsy - 16%
• Blindness - 14-17%
• Severe hearing impairment - 6