High-Risk Neonate&neurodevlopmental outcome

High-Risk Neonate
&
neurodevlopmental outcome
By
Dr.Osama Arafa Abd EL Hameed
M. B.,B.CH - M.Sc Pediatrics - Ph. D.
Consultant
Pediatrician & Neonatologist
Head of Pediatrics Department - Port-
Fouad Hospital

GOALS
• Perinatal prevention
• Resuscitation and stabilization
• Evaluate and manage
• Monitoring and therapeutic
modalities
• Family centered care

Predisposing factors
• Pregnancy between the age of 15-19yrs
• Elderly women
• Wrong dates
• Multiple pregnancy
• Fetal anomalies
• Hereditary

Introduction:
Definition of High-risk Neonate:
Any baby exposed to any condition that
make the survival rate of the neonate at
danger.
Factors that contribute to have a High-risk
Neonate:
A) High-risk pregnancies: e.g.: Toxemias
B) Medical illness of the mother: e.g.:
Diabetes Mellitus

C) Complications of labor: e.g.:
Premature Rupture Of Membrane (PROM),
Obstructed labor, or Caesarian Section (C.S).
D) Neonatal factors: e.g.: Neonatal
asphyxia

Classification of High Risk
Newborns
• Gestational Age
– Preterm
– (Late Preterm)
– Term
– Postterm
• Gestational Age &
Birth Weight
– SGA
– AGA
– LGA

Some Definitions:
- Low Birth Weight Infant:
Is any live born baby weighing 2500 gram or
less at birth. (VLBW: <1500 gm, ELBW:<1000
gm).
- Preterm:
When the infant is born before term. i.e.:
before 38 weeks of gestation.
- Premature:
When the infant is born before 37weeks of
gestation.

- Full term:
When the infant is born
between 38 – 42 weeks of gestation.
- Post term:
When the infant is born
after 42 weeks of gestation.

Identification of some High-risk
Neonates:
The previous conditions often will result in:
Premature birth, Low birth weight infants, or
infants suffering from: Hypothermia,
Hyperthermia, Hypoglycemia, Infant of Diabetic
Mother (IDM), Neonatal Sepsis,
Hyperbilirubinemia, and Respiratory Distress
Syndrome (RDS).

Physiologic Challenges of the
premature infant

premature infant
• Respiratory and Cardiac
• Thermoregulation
• Digestive
• Renal

premature infant
• Respiratory and Cardiac
– Lack of surfactant
– Pulmonary blood vessels
– Ductus arteriosus

Definition:
It is a condition characterized by
lowering of body temperature than 36°C.
Types of Hypothermia:
It could be classified according to:
Causes and according to Severity.

I) According to Causes:
1- Primary Hypothermia: (immediately
associated with delivery)
In which the normal term infant delivered into a
warm environment may drop its rectal temperature
by 1 – 2°C shortly after birth and may not achieve a
normal stable body temperature until the age of 4 – 8
hours.
In low birth weight infants, the decrease of body
temperature may be much greater and more rapid
unless special precautions are taken immediately
after birth. (loss at least 0.25 °C/ min.) (careful
dryness).

Situations which contribute to develop
Primary Hypothermia:
e.g.: Low birth weight infants.
2- Secondary Hypothermia:
This occurs due to factors other than
those immediately associated with
delivery.
Important contributory factors are:
e.g.: Acute infection especially
Septicemia.

II) According to Severity:
(1) Mild Hypothermia:
When the
infant’s body temperature is less than 36°C.
(2) Moderate Hypothermia:
When
the infant’s body temperature is less than
35.5°C.
(3) Severe Hypothermia:
When the
infant’s body temperature is less than 35°C.

*) Clinical Picture:
1- Decrease in body temperature
measurement.
2- Cold skin on trunk and extremities.
3- Poor feeding in the form of poor
suckling.
4- Shallow respiration.
5- Cyanosis.
6- Decrease activity, e.g.: Weak crying.

The Four modalities by which the
infant lost his/ her body temperature:
1- Evaporation:
Heat loss that resulted from
expenditure of internal thermal energy to
convert liquid on an exposed surface to
gases, e.g.: amniotic fluid, sweat.
Prevention:
Carefully dry the infant
after delivery or after bathing.

2- Conduction:
Heat loss occurred from
direct contact between body surface
and cooler solid object.
Prevention:
Warm all objects before
the infant comes into contact with
them.

3- Convection:
Heat loss is resulted from
exposure of an infant to direct source of
air draft.
Prevention:
· Keep infant out of drafts.
· Close one end of heat shield in
incubator to reduce velocity of air.

4- Radiation:
It occurred from body
surface to relatively distant objects that
are cooler than skin temperature.

ISOLETTE/ RADIANT or
INCUBATOR OPEN
WARMER

*) General management:
1- Infant should be warmed quickly by wrapping
in a warm towel.
2- Uses extra clothes or blankets to keep the
baby warm.
3- If the infant is in incubator, increase the
incubator’s temperature.
4- Use hot water bottle (its temperature 50 °C).
5- Food given or even intravenous solution
should be warm.
6- Avoid exposure to direct source of air drafts.
7- Check body temperature frequently.
8- Give antibiotic if infection is present.

Definition:
It is a condition
characterized by an elevation in body
temperature more than 38°C.
Causes:
1- Disturbance in Heat Regulating Center
caused by intracranial hemorrhage, or
intracranial edema.
2- Incubator temperature is set too high.
3- Dehydrating fever

*) Management :
1) Undress the infant. If at home; keep light
cloths, cover that containing light sheet, Or only a
diaper if the infant is inside an incubator.
2) Reduction of incubator temperature.
3) Provide Tepid sponge bath.
4) If available; fill the water mattress with tape
water, and keep it in contact with the infant’s skin.
5) Increase fluid intake in the form of 5cc of
Glucose 5% between feeds to prevent dehydration.

HYPOGLYCEMIA
Untreated hypoglycemia can result in
permanent neurological damage or
death.

Ideally, neonatal hypoglycemia would be defined as the
blood glucose concentration at which intervention
should be initiated to avoid significant morbidity,
especially neurologic sequelae.
However, this definition remains elusive because the
blood glucose level and duration of hypoglycemia
associated with poor neurodevelopmental
outcome has not been established.
Neonatal hypoglycemia, defined as a plasma glucose
level of less than 30 mg/dL (1.65 mmol/L) in the first 24
hours of life and less than 45 mg/dL (2.5 mmol/L)
thereafter

Definition:
Neonatal hypoglycemia is usually defined as
a serum glucose value of < 40-45 mg/dl.
For the preterm infant a value of < 30 mg/dl is
considered abnormal (hypoglycemia).

N.B.: The normal plasma glucose
concentration in the neonate is
approximately 60 to 80 percent of the
maternal venous glucose level, or
nearly between 70 – 80 mg/dl in
neonates of normoglycemic mothers. A
steady-state level occurs by
approximately three hours after birth.

*) Neonates at risk for developing
hypoglycemia:
1- The main cause may become maternal
malnutrition during pregnancy which leads to fetal
malnutrition and of course a low birth weight.
2- Those infants whom are Small for
gestational age infants (SGA), that manifested
by decrease in their birth weight and
subcutaneous fat and hepatic glycogen.
3- Those infants’ of diabetic mothers (IDM) or
those named as large for gestational age
(LGA).

4- Those whom placentas were abnormal,
e. g.: placenta previa .
5- Those whom their mothers had toxemia
during pregnancy, e. g.: eclampsia or pre-eclampsia
induction of labor preterm
infant.
6- Those very ill or stressed neonates whom
their metabolic needs were increased due to
hypothermia, infection, respiratory distress
syndrome, or cardiac failure.

Pathophysiology:
The fetus receives glucose from the mother
continuously across the placenta. As soon as the cord is cut,
within 2 hours the normal neonate’s blood glucose level falls
from 70 – 80 mg/dl to 50 mg/dl. At this time, hepatic glucose is
released into the blood and the serum glucose level returns to
its normal level at birth (70 – 80 mg/dl). So, after birth the
neonate must kept well nourished because of the newly
acquired stressors as; abrupt transition from warm intrauterine
environment to a relatively cold extra-uterine one,
beginning the respiratory cycles by the neonate own
self, muscular activity, and suckling effort to prevent
carbohydrates storage consumption and the neonate become
at risk for developing hypoglycemia.

Clinical manifestations:
1- Hypotonia.
2- Feeding poorly after feeding well.
3- Tremors.
4- Cyanotic spells.
5- Lethargy.
6- Seizures.

7- Hypothermia.
8- Irregular respiratory pattern (Apnea).
9- Irritability.
10- High pitched cry followed by weak cry.
11- poor reflexes, especially sucking reflex.

Management of the Neonate at Risk:
Prevention:
first of all, providing a warm environment.
Early enteral feeding is the single
most important preventive measure.
If enteral feeding is to be started,
breast or artificial milk should be used
if the infant is able to tolerate nipple or
naso-gastric tube feeding.

These infants should have glucose values
monitored until they are taking full feedings
and have three normal pre-feeding readings
above 40-45 mg/dl. Care must be taken to
ensure that breast-feeding mothers are
providing an adequate intake.
If the infant at risk for hypoglycemia is unable
to tolerate nipple or tube feeding,
maintenance IV therapy with 10% glucose
should be initiated and glucose levels
monitored.

Management of the Neonate with
Hypoglycemia:
Infants who develop hypoglycemia should
immediately be given 2cc/kg of 10% dextrose
over 5 minutes, repeated as needed.

A continuous infusion of 10% glucose at a
rate of 8-10 mg/kg/min should be started to
keep glucose values normal (NOTE: 10
mg/kg/min of 10%dextrose = 144cc/kg/day).
Frequent bedside glucose monitoring is
necessary.
When feedings are tolerated and
frequent bedside glucose monitoring
values are normal, the infusion can be
tapered gradually.

Introduction:
Good control of maternal
diabetes is the key factor in determining fetal
outcome. Recent data indicates that perinatal
morbidity and mortality rates in the offspring of
women with diabetes mellitus have improved
with dietary management and insulin therapy.
Infants of diabetic mothers are large plump
with plethora faces resembling patients
receiving cortisone.

Pathophysiology:
Maternal hyperglycemia fetal
hyperglycemia (because the placental barrier passes from
70 – 75% of maternal glucose level to the fetus) fetal
hyperinsulinemia which in turn increased glycogen
synthesis and storage in the liver and increased fat
synthesis weight and size of all infants organs
except the brain (Macrocosmic infant). Sudden placental
separation and cord clamping interrupts the transplacental
glucose supply to the newly born infant without a similar
effect on the hyperinsuilinemia (Pancreatic Hyperplasia),
this leads to hypoglycemia during the first 2 hours after
birth.

Specific Disorders frequently encountered
in Infants of Diabetic Mothers (IDM):
*) Hypoglycemia.
*) Hypocalcemia.
*) Hypomagnesemia.
*) Cardio-respiratory disorders.
*) Hyperbilirubinemia (Unconjugated)
*) Birth injuries
*) Congenital malformations

Management:
I) For the mother:
Through good antenatal
care for proper control of maternal
diabetes.

II) For an infant:
All IDMs should receive
continuous observation and intensive care.
Serum glucose levels should be checked at birth and
at half an hour, 1, 2, 4, 8, 12, 24, 36 and 48 hours of
age:
- If clinically well and normoglycemic; oral or
gavage feeding should be started and continued
within 2 hours intervals.
- If hypoglycemic; give 2 – 4 ml/kg of 10%
dextrose over 5 minutes, repeated as needed. A
continuous infusion of 10% glucose at a rate of 8-10
mg/kg/min. Start enteral feeding as soon as possible.
Give Corticosteroids in persistent hypoglycemia.

Treatment of other complications
should also start; oxygen therapy
for RDS, calcium gluconate 10%
for hypocalcemia, phototherapy
for hyperbilirubinemia……………..
etc.

Introduction:
The newborn infant is
uniquely susceptible to acquire infection,
whether bacterial, viral or fungal. Bacterial
sepsis and meningitis continue to be major
causes of morbidity and mortality in the
newborn. The mortality rate due to sepsis
ranges from 20% to as high as 80% among
neonates. Surviving infants can have
significant neurologic squeal because of CNS
involvement.

Definition:
Neonatal sepsis is a disease of
neonates (who are younger than one
month) in which they are clinically ill and
have a positive blood culture.

Risk Factors:
I) Maternal risk factors:
- e.g.: Premature rupture of
membrane.
II) Neonatal risk factors:
- e.g.: Prematurity (less immunologic
ability to resist infection + more liable
to penetrate their defensive barriers).

Bacteria can reach the fetus or newborn and cause
infection in one of the following ways:
• Bacteria can pass through the maternal blood through
placenta as rubella, toxoplasma, and syphilis.
• Bacteria from the vagina or cervix can enter the
uterus, as groups B streptococci.
• The newborn may be come contract with bacteria as it
passes through the birth canal as gram negative
organisms.
• The newborn may come in contact with bacteria in its
environment after birth (Coagulate positive or negative
staphylococci.)
• When a susceptible host acquires the pathogenic
organism, and the organism proliferates and
overcomes the host defense, infection results.

Classification of neonatal sepsis:
Neonatal sepsis may be categorized as
early or late onset .
Newborns with early-onset infection
present within 24 hours till 72 hours. Early-onset
sepsis is associated with acquisition
of microorganisms from the mother during
pregnancy (transplacental infection),
or during labor (an ascending infection
from the cervix).

Late-onset sepsis; occurs beyond the
first 72 hours of life (most common
after the 3rd day till the 7th day after
birth) and is acquired from the care
giving environment (Nosocomial
infection).

Clinical presentation of neonatal
sepsis:
Physical findings may be nonspecific and
are often subtle.
e.g.: apnea , Jaundice , Hypothermia ,
Bulging or full fontanel , Seizures ,
hypotonia

Laboratory indicators of sepsis
include:
- Total leukocytic count (WBC count)
- C – reactive Protein (CRP)
- Erythrocyte Sedimentation Rate
(ESR)
- Cultures:

Management of Sepsis:
- Prevention: through proper application
to infection control practices.
- Early onset sepsis; give intrapartum
antimicrobial prophylaxis (IAP) to the
mother.

- Neonates with clinically suspected
sepsis:
*) Culture should be obtained first.
*) The recommended antibiotics are ampicilin and
gentamicin.
*) Third generation cephalosporins (Cefotaxime) may
replace gentamicin if meningitis is clinically suspected or if
gram-negative rods are dominant in the unit.
- Late onset neonatal sepsis:
Vancomycin in combination with either gentamicin or
cephalosporins should be considered in penicillin
resistant cases.
Note: Administer all medications IV.

Nursing consideration
• Prevention
• Curative

Prevention
1- Demonstrate the effect of hand washing upon
the prevention of the noscomical infections.
2 -Standard precautions should be applied in the
nursery for infection prevention.
3- Instillation of antibiotics into newborn’s eye 1-2
hours after birth is done to prevent the infection.
4- Skin car should be done using worm water and
may use mild soup for removal of blood or
meconium and avoid the removal of vernix
caseosa.
5- Cord care should be cared out regularly using
alcohol or an antimicrobial agent.

Curative
• Encourage breast feeding from the mother.
• Adequate fluid and caloric intake should be
administered by gavage feeding or intravenous
fluid as ordered.
• Extra-measure for hypothermia or hyperthermia
that may take place to the newborn.
• Administering medications as doctor order.
• Follow the isolation precautions.
• Monitoring intravenous infusion rate and
antibiotics are the nurse responsibility.

• Administer the medication in the prescribed
dose, route, and time within hour after it is
prepared to avoid the loss of drug stability.
• Care must be taken in suctioning secretions
from the newborn as it may be infected.
• . Isolation procedures are implemented
according to the isolation protocols of the
hospital.
• Observe for the complication e.g. meningitis
and septic shock.
• Encourage in-service programs and
continuing education of nurses regarding the
infection control precautions.

Hypoxic Ischemic
Encephalopathy (HIE)

Grade I HIE:
- Alternating periods of lethargy and
irritability, hyper-alertness and jitteriness.
- Poor feeding.
- Exaggerated and/or a spontaneous Moro
reflex.
- Increased heart rate and dilated pupil.
- No seizure activity.
- Symptoms resolved in 24 hours.

Grade II HIE:
- Lethargy.
- Poor feeding, depressed gag reflex.
- Hypotonia.
- Low heart rate and papillary constriction.
- 50-70% of infants display seizures,
usually in the first 24 hours after birth.
- Oliguria.

Grade III HIE:
- Coma.
- Flaccidity.
- Absent reflexes.
- Pupils fixed, slightly reactive.
- Apnea, bradycardia, hypotension.
- Oliguria.
- Seizures are uncommon.

Management of Hypoxic Ischemic
Encephalopathy:
- Prevention is the best management.
- Primary supportive measures.
- Treat seizures: e.g: Phenobarbital

Definition:
Hyperbilirubinemia is an
elevation in the neonatal serum bilirubin
characterized by JAUNDICE, which is
defined as “yellowish discoloration of skin
and mucous membranes”. In the neonate
clinical jaundice is diagnosed if the total
serum bilirubin is ≥ 7 mg/dl.

N.B.:
The normal adult range of Total
Serum Bilirubin is 0.2 – 1 mg/dl (Direct:
0 – 0.2 mg/dl and Indirect: 0.2 – 0.8
mg/dl).

Pathophysiology: = Neonatal Bile Pigment
Metabolism.
Destruction of RBCs
Hemoglobin Salts
Water
Heme globin
(protein portion reused by
the body).
+ O2
Biliverdin

+
more O2
Unconjugated Bilirubin
+
Plasma protein
Liver
Which released from plasma protein inside the liver and
connected with Glucuronic acid and Glucuronyl Transferese
Enzyme (in the presence of normal Ph, O2, and normal body
temperature) to become Conjugated Bilirubin , that has 3
pathways:
Bile duct Kidney Gastrointestinal
tract
To digest fat. (Urobilin Urobilinogen) (Stercobilin
Stercobilinogen)
to obtain normal color of urine. to obtain normal
color of stool.

The following are possible causes of
hyperbilirubinemia in the newly born
infants:
1. Over production of bilirubin.
2. Under excretion of bilirubin.
3. Combined over production and
under excretion.
4. Physiological jaundice.
5. Breast milk associated jaundice.

Complication:
The most common
complication of hyperbilirubinemia is Kernicterus
(Bilirubin Encephalopathy), which usually
occurs when the unconjugated serum bilirubin level
exceeds than 20 mg/dl. In small, sick preterm
infants, even a bilirubin level in a low range may
cause Kernicterus.

Clinical Presentation:
Kernicterus progresses through 4 stages:
Stage I: Poor Moro reflex, poor feeding, vomiting,
high-pitched cry, decreased tone and lethargy.
Stage II: Spasticity, seizures, fever. Neonatal
mortality is high at this stage (80%).
Stage III: A symptomatic (Spasticity decreases
and all remaining clinical signs and symptoms may
disappear).
Stage IV: Appears after the neonatal period.
Long-term sequelae can include: spasticity
quadriplegia, deafness and mental retardation (for
the 20%).

•Management of unconjugated
hyperbilirubinemia:
·

•Phototherapy:
Nursing care for those infants receiving
Phototherapy:
1. Cover the infant’s eyes and genital
organs.
2. The infant must be turned frequently
to expose all body surface areas to the
light.
3. Serum bilirubin level /4 – 12 hours.
4. Each shift, eyes are checked for
evidence of discharge or excessive
pressure on the lids and eye care should
be done using warm water, then apply eye
drops or ointment.

5. Eye cover should be removed during
feeding, and this opportunity is taken to
provide visual and sensory stimuli.
6. Avoid oily lubricants or lotion on the
infant’s exposed skin, because this can act
as a barrier that prevent penetration of light
through the skin.
7. Increase feeds in volume and calories.
Add 20% additional fluid volume to
compensate for insensible and intestinal
water loss.
8. Intake and output chart.

• Blood exchange transfusion
Carry out this technique Beside the
Crash Cart.

Neonatal Respiratory
Disorders

Common Neonatal Respiratory
disorders:
· Respiratory distress syndrome (RDS)
= Hyaline membrane disease (HMD).
· Transient tachypnea of the newborn
(TTN).
· Meconium aspiration syndrome
(MAS).
· Apnea.

A) Respiratory distress syndrome
(RDS) = Hyaline membrane disease
(HMD).
Definition:
Respiratory distress
syndrome is A low level or absence of
surfactant system.

Risk factors (High risk group):
e.g: Prematurity and low birth weight.

Clinical Presentation:
Grade I: (Mild distress): Rapid respiratory rate
(tachypnea >60 breaths per minute) + nasal flaring
(alae nasai).
Grade II: (Moderate distress): GI +
intercostals and substernal retractions.
Grade III: (Severe distress): GI + GII +
expiratory grunting.
Grade IV: (Advanced distress): GI + GII + GIII
+ central cyanosis and disturbed consciousness.

Management of RDS:
A) General:
* Basic support including thermal
regulation and parentral nutrition and
medications (antibiotics).
* Oxygen administration, preferably
heated and humidified
B) Specific:
Surfactant replacement therapy
through ET tube.

B) Transient Tachypnea of the
Newborn (TTN).
Definition:
TTN is a benign disease of near-term
or term infants who display respiratory
distress shortly after delivery. It occurs when
the infant fails to clear the airway of lung fluid
or mucus or has excess fluid in the lungs, this
limit the amount of alveolar surface available
for gas exchange, leading to respiratory rate
and depth to better use of the surface
available.

Risk factors:
· Secondary to hypothermia.
· Infant born by Cesarean section, in
which the thoracic cavity is not squeezed by
the force of vaginal pressure, so that less
lung fluid is expelled than normally happen.

Clinical presentation:
* The infant is usually near-term or term.
* Exhibits tachypnea (> 80 breaths/min)
shortly after delivery.
* The infant may also display mild grunting,
nasal flaring, intercostals retraction, and
cyanosis.
* Spontaneous improvement of the neonate,
which considered as the most important
marker of TTN.

Management of TTN:
- Oxygenation.
- Fluid restriction.
- Start feeding as tachypnea improves.
Outcome and prognosis:
·Peaks intensity reached at 36 hours of infant’s life.
·The disease is self-limited (respiratory symptoms
improve as intrapulmonary fluid is naturally
absorbed or artificially mobilized using diuresis).
·No risk of recurrence or further pulmonary
dysfunction.

C) Meconium Aspiration Syndrome
(MAS).
Definition:
This respiratory disorder is
caused by meconium aspiration by the fetus
in utero or by the newborn during labor and
delivery. MAS is often a sign that the neonate
has suffered asphyxia before or during birth.
The mortality rate can be as high as 50% and
survivors may suffer long-term sequelae
related to neurological damage.

Causes and Pathophysiology:
1. Fetalis hypoxia; e.g. cord prolapse that
comes around the neck of the fetus many
days before delivery.
2. Babies born breech presentation.
In both cases; intrauterine hypoxia Or breech
presentation vagal nerve stimulation
relaxation of the sphincter
muscle
releasing of the first stool (meconium) in the
intrauterine life and becomes mixed with the
amniotic fluid, with the first breath the baby
can inhale meconium.

Dangerous of MAS:
The aspirated meconium can cause
airway obstruction clinical
manifestations of RDS, and an
intense inflammatory reaction.

Management of MAS:
*) Suctioning of the oropharynx by
obstetricians before delivery of the shoulders.
*) Immediate insertion of an ET tube and
tracheal suctioning before ambu bagging
(Maintain a neutral thermal environment).
*) Gastric lavage, and emptying of the stomach
contents to avoid further aspiration.

*) Postural drainage and chest vibration
followed by frequent suctioning.
*) Pulmonary toilet to remove residual
meconuim if intubated.
*) Antibiotic coverage (Ampicillin &
Gentamicin).
*) Oxygenation ( maintain a high saturation
> 95%)
*) Mechanical ventilation to avoid
hypercapnia & respiratory acidosis.

D) Apnea.
Definition:
Apnea is the cessation of respiration
accompanied by bradycardia and/or cyanosis for
more than 20 second.
Types:
1- Pathological apnea:
Apnea within 24 hours of
delivery is usually pathological in origin.
2- Physiological apnea:
Apnea developing
after the first three days of life and not associated
with other pathologies, may be classified as apnea
of prematurity.

Management of apnea:
· Monitor at-risk neonates of less than 32
weeks of gestation.
Begin with tactile stimulation ; gentle
shaking or prick the sole of the foot often
stimulate the infant to breath again.

· If no response to tactile stimulation, bag
and mask ventilation should be used
during the spell.
· Provide CPAP or ventilatory support
in recurrent and prolonged apnea.
· Pharmacological therapy:
- Theophylline.
Treat the cause, if identified, e.g., Sepsis,
Hypoglycemia, Anemia ………….. etc.

Monitoring the neonatal brain
Can we do more?
More direct monitoring parameters are needed:
• Stable and recognizable parameters
• Bedside monitoring possible for extended periods of time

Monitoring the brain
• Near Infrared Spectroscopy (NIRS)
• 1 or 2 channel EEG: aEEG

Near Infrared Spectroscopy (NIRS)
• Monitoring technique for cerebral oxygenation and
haemodynamics
• Based on absorption of near-infrared light by
oxygenated [O2Hb] and deoxygenated Hb [HHb]
• Absorption-changes in NIR-light (D ODs) can be
converted in changes of [DO2Hb] and [DHHb]
• Regional (mixed) cerebral O2-saturation: rScO2

Reproducibility is good when used for
trend monitoring
Menke et al, Biol Neon 2003
Fronto-parietal
position
(r= 0.88,
p <0.01)
rScO2-Right (%)
rScO2-Left (%)
Lemmers et al, Pediatr Res, 2009

100
90
80
70
60
50
40
30
20
10
0
Interpretation of rScO2 values
High values (>
+2SD)
Avoid if possible!1,2,3
2:02
2:05
2:08
2:11
2:14
2:17
2:20
2:23
2:26
2:29
2:32
2:35
2:38
2:41
2:44
2:47
2:50
2:53
2:56
2:59
3:02
3:05
3:08
3:11
3:14
3:17
3:20
3:23
3:26
3:29
3:32
rScO2 %
Expected “normal” values
(±2SD)
Low values (<
-2SD)
1) Hou, Physiol Meas 2007; 2) Kurth, J Cereb Blood Flow Metab 2005;
3) Dent, J Thorac Cardiovasc Surg 2002

aEEG
• Filtered (2-15 Hz)
• Amplification
• Compressed (6 cm/hr)
• Semilogarithmic scale
• 1 channel (2 parietal leads)
• 1 channel for impedance

Continuous
Background patterns
Burst Suppression
Discontinuous
Cont. Low Voltage Flat Trace
= 10 min
Thanks to
LdeVries/MToet

Has cerebral monitoring add any
additional value in clinical care for the
neonate in N.I.C.U

Brain monitoring in clinical practice
non invasive monitoring
Preterm infants <32 wks
Term infants after hypoxic
ischemic events
Preterm infants <32 wks for 72 h
Neonates after perinatal asphyxia

Brain monitoring in clinical practice
• Arterial saturation
(pulse oxymetry)
• Arterial blood
pressure
• Heart rate
• Cerebral oxygenation
by NIRS (rScO2)
• aEEG

Monitoring the neonatal brain
• aEEG and NIRS in clinical practice
• Relation with other clinical conditions
• Blood pressure
• Patent ductus arteriosus
• Autoregulatory ability
• (Mechanical) ventilation
• Surgery

Relation brain monitoring
• Blood pressure
• Patent ductus arteriosus
• Autoregulatory ability
• (Mechanical) ventilation
• Surgery

Limits of normal blood pressure in neonates
• Not well defined
• Mostly used definition MABP (mmHg)<GA (wks)
• Hypotension is related with brain damage
• Hypotension is not directly related to outcome
(Dammann 2002; Limperopoulos 2007)
• Recent papers show good outcome when accepting
lower limits for MABP (Dempsey 2013)

Dopamine
5μg/kg/min
$
*
$ p<0.05 vs controls;
* p<0.05 vs before
dopa
N=38
Bonestroo et al, Pediatrics 2011
$
N=39

Conclusion
aEEG should be continued for at least 48 hrs to be able
to detect late onset seizure after HI

Suggestion
• Brain monitoring by NIRS and aEEG
could be a useful approach to judge the
need of blood pressure support in
infants with low blood pressures

Hemodynamically important
PDA
• Ductal steal phenomenon in cerebral arteries
is a risk factor for cerebral damage in the
preterm infant (Perlman 1981)

PDA surgery after failure medication
*
GA 26.7 ±1.8 wks
PNA 7 days [4-39]
surger
y
p<0.05 vs pre-clip

Suggestions
• Monitoring of rScO2 during surgical ductal closure
can prevent surgery-related brain damage
• Cerebral oxygenation should play a role in the
ultimate decision to close of a hemodynamically
important ductus arteriosus

Autoregulatory ability
rScO2
CCeerreebbrraall bblloooodd ffllooww
(corr)
(no corr)
(corr)
MABPBrady, Stroke 2007/2010
CCeerreebbrraall ppeerrffuussiioonn
pprreessssuurree
Wong, Pediatrics 2008
De Smet Adv Exp Med Biol. 2010
Aciado Ped Res 2011

200
180
160
140
120
100
80
60
40
20
0
Absence of cerebral autoregulation
0:00:07
0:18:07
HR
(b/min)
21:00
21:18
21:36
21:54
22:12
22:30
22:48
23:06
23:24
23:42
0:54:07
1:12:07
1:30:07
1:48:07
2:06:07
2:24:07
2:42:07
3:00:07
3:18:07
3:36:07
3:54:07
4:12:07
0:36:07
4:48:07
4:30:07
5:06:07
5:24:07
5:42:07
Erythrocyt
es
Thrombo+FF
P
Dopamine
15
Dobutamine and
steroids
Dopamine
10
♂, sepsis, †
SaO2
(%)
rScO2
(%)
MABP
(mmHg)

Presence cerebral autoregulation
40
50
60
70
80
90
100
18:01
18:03
18:05
18:07
18:09
18:11
18:13
18:15
18:17
18:19
18:21
18:23
18:25
18:27
18:29
18:31
18:34
18:36
18:38
18:40
18:42
18:44
18:46
18:48
18:50
18:52
18:54
18:56
18:58
19:00
19:02
19:04
19:06
19:08
19:10
19:12
19:14
19:16
19:18
19:20
10
MABP
(mmHg)
20
30
40
SaO 50 2
(%)
rScO2
(%)
♂, 30 wk 945 g, day 1

Suggestions
• Monitoring MABP and rScO2 can, within certain limits,
identify infants with absence of autoregulatory ability
• Identification of absence of autoregulatory ability may
help to prevent brain damage

Suggestion
• Brain monitoring during (artificial)
ventilation can help to prevent
hypo/hyper perfusion and
hyper/hypoxemia and so brain damage

Relat ion br ain monit or ing
Hypotension
Patent ductus arteriosus
Autoregulatory ability
(Mechanical) ventilation
Surgery

Neonatal cardiac surgery
Low cerebral saturations (<35%-45% )
related with adverse outcome
Toet et al Exp Brain Res 2009
Phelps et al 2009
Sood et al J Thorac Cardiovasc surg 2013

Conclusions
• The current results of these studies in
neonates strongly suggest that SaO2 does not
always reflect oxygenation of the neonatal
brain.
• Thus monitoring of cerebral oxygenation by
NIRS and brain function by aEEg in addition to
SaO2 and blood pressure, can help to prevent
brain damage but also prevent unnecessary
treatment.

• The number of infants with (minor)
neurodevelopmental problems is high in infants
undergoing surgical procedures in neonatal period
So
• Neurodevelopmental delay needs to be investigated
in relation to brain injury :
• brain monitoring
• (pre-existing) riskfactors
• brain injury by neuro-imaging
• longterm follow-up
• larger cohorts
• collaboration between disciplines in hospitals and
multi-center

Neonatal brain damage
• Leading to neuro
developmental
problems
• Cerebral palsy
• Behaviour/sch
ool problems

High-Risk Neonate&neurodevlopmental outcome

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