Pediatrics 1.1 DR.

SALAZAR
Neonatology I June 19, 2014

OUTLINE A. NONSTRESS TEST (NST)

I. Factors Affecting High Risk Neonates  Performed by auscultation of the fetal heart rate using an
II. Fetal Growth and Monitoring electronic monitor
III. Fetal Distress  monitors the presence of HR accelerations that follow fetal
IV. Maternal Conditions and Neonatal Outcome movement
V. Fetal Circulation  Reactive (normal) NST result demonstrates two fetal heart rate
VI. Fetal Lungs accelerates at least 15 beats/min lasting 15 secs
VII. Transition to Extrauterine Life  Nonreactive NST result suggest fetal compromise and requires
VIII. Newborn Circulation further assessment with a CST or the BPP
IX. Newborn Resuscitation  Goals of fetal monitoring: prevent intrauterine fetal demise and
X. Assessment hypoxic brain injury
XI. Initial Management: For all Deliveries
XII. Extended Algorithm INTERPRETATION OF THE FETAL HEART TRACING
XIII. Volume  Should follow a systematic approach with a full qualitative and
XIV. Immediate Essential New Born Care quantitative description of the following:
XV. High Risk Neonate o Baseline rate
XVI. Mortality o Baseline fetal heart rate (FHR) variability
XVII. Maternal Conditions that May Identify High Risk Neonates o Presence of accelerations
XVIII. Identification of SGA/IUGR o Periodic or episodic decelerations
XIX. Etiology of IUGR o Changes or trends of FHR patterns over time
XX. Post Natal Assessment o Frequency and intensity of uterine contractions
XXI. Multiple Gestation
XXII. Criteria for Intrapartum Fetal Distress BRADYCARDIA
XXIII. Perinatal Asphyxia  Mean FHR < 110 bpm
XXIV. Hypoxic Ischemic Encephalopathy (HIE)  A rate of 100-119 bpm in the absence of other non-reassuring
XXV. Hypothermia for HIE patterns is not usually a sign of compromise
XXVI. Seizure Management  Causes
o Heart block (little or no variability)
LEARNING OBJECTIVES o Occiput posterior or transverse position
Outline the clinical manifestations of pathologic conditions that would affect o Serious fetal compromise
the high risk neonate
 Patients with new onset bradycardia should be transferred to
Labor and Delivery for further observation and physician notified
FACTORS AFFECTING HIGH RISK NEONATES
 Risk factors that increase the likelihood of abortion, fetal death, TACHYCARDIA
premature delivery, intrauterine growth restriction, poor
 Mean FHR > 160 bpm
cardiopulmonary or metabolic transitioning at birth, fetal or
 In the presence of good variability tachycardia is not a sign of fetal
neonatal disease, congenital malformations, mental retardation or
distress
other handicaps.
 Causes:
o Maternal fever
FETAL GROWTH AND MONITORING
o Fetal hypoxia
 Assessed by ultrasound as early as 6-8 week
st o Fetal anemia
 Most accurate assessment of Gestational Age is by the 1
o Amnionitis- Inflammation resulting from infection of the
trimester (crown-rump length)
nd amniotic sac, which, in turn, often results from
 2 trimester (biparietal diameter): 30 weeks +/- 10 days premature rupture of the membranes (a condition often
 Full Term: abdominal circumference and femoral length associated with neonatal infection)
 18-20 weeks: GA and fetal anatomy (at this time, more o Normal variant
distinguished) – serial scans (congenital scans if needed) o Fetal tachyarrhythmia (usually > 100 bpm with abrupt
 onset little to no variability)
FETAL DISTRESS o SVT (Supraventricular Tachycardia)-200-240 bpm
 Antepartum fetal surveillance: stillbirth, IUGR, oligohydramnios or o Fetal heart failure
polyhydramnios, multiple gestation, Rh sensitization, hypertensive o Drugs
disorders, DM, other chronic maternal disease, decreased fetal  Beta sympathomimetics
movement and post term pregnancy  Vistaril
 Goals of antepartum surveillance: prevent intrauterine fetal  Phenothiazines
demise, prevent hypoxic brain injury, prolong or deliver fetus, or o Rebound transient tachycardia following a deceleration
termination even before it reaches term accompanied by decreased variability)
 Surveillance Tests Used:
A. Nonstress test (NST) DEVELOPMENT OF FHR (Fetal Heart Rate) VARIABILITY
B. Contraction stress test (CST)  Early in gestation the fetal heart rate is predominately under the
C. Biophysical profile (BPP) control of the sympathetic nervous system and arterial
chemoreceptors
 As the fetus develops its heart rate decreases in response to
parasympathetic (vagal stimulation) system maturation and
Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 1 of 15
 Pediatrics 1.1
variability becomes more pronounced. (which may lead to insults
to the fetus, one of which is hypoxia which may lead to acidosis
and FHR variability )
HOW HYPOXIA (LOW OXYGEN) LEADS TO ACIDOSIS AND DECREASED FHR
VARIABILITY
 Fetus uses oxygen to burn molecules and release energy
 Reaction: glucose + oxygen  carbon dioxide + water + energy
 Poor blood flow from the uterus and placenta causes the fetus to
constrict blood vessels in nonvital peripheral areas such as the
arms and legs in order to supply more blood flow to vital organs
such as the heart and brain
 With a limited supply of oxygen (hypoxia) the peripheral tissues
can only partially break down the sugar and converts it to lactic
acid (always refers to Kreb’s Cycle-aerobic and anaerobic
oxygenation)
 Significant levels of acid in the blood (acidemia) may suppress the
fetal nervous system and eventually lead to cardiovascular
collapse.
PRESENCE OF MODERATE FHR VARIABILITY IS REASSURING
 Persistently minimal/Absent FHR variability appears to be the
most significant intrapartum sign of fetal compromise.
 Presence of good FHR variability may not always be predictive of a
good outcome (such as may occur with an abruption).
Normally, the baseline FHR is variable. Variability is classified as follows:
absence variability (amplitude change is undetectable); minimal
variability (amplitude range is ≤5beats/min); moderate variability
(amplitude range 6-25 beats/min); marked variability (amplitude range
˃25 beats/min. The presence of moderate variability predicts the
[1]
absence of fetal metabolic acidemia.
CAUSES OF DECREASED VARIABILITY
 Fetal metabolic acidosis
 CNS depressants
 Fetal sleep cycles
 Congenital anomalies
 Prematurity
 Fetal tachycardia
 Preexisting neurologic abnormality
 Normal variant
 Betamethasone
LATE DECELERATIONS
 Late associated with no variability (where loss of variability has not
been caused by drug administration)
o With progressing hypoxia the decelerations become
deeper.
o As acidosis develops the brain stem reflexes become
blunted and direct myocardial depression causes shallow
decelerations (20.22)
o If myocardial depression is severe enough, lates may be
absent all together
 Causes
o Excessive uterine contraction (hyperstimulation),
maternal hypotension, or maternal hypoxemia
o Reduced placental exchange as in hypertensive
disorders, diabetes, IUGR, abruption
o Response to any maternal, placental, umbilical cord, or
fetal factor that limits effective oxygenation of the fetus-
Nelson
Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M
B. CONTRACTION STRESS TEST (CST)
 Observes fetal response to spontaneous, nipple-stimulated or
oxytocin-stimulated uterine contractions-Nelson
 Contraindicated in women with preterm PROM, previous uterine
scar from a classic cesarean section, multiple gestations,
incompetent cervix & placenta previa-Nelson
 Used by some antepartum testing centers to evaluate placental
function under stress. The test is performed by placing transducers
(ultrasound and toco), on patient’s abdomen as with the nonstress
test
 The tracing is then observed for late decelerations which suggest
fetal compromise
 The test requires three contractions in 10 minutes to be present
with the contractions lasting 40 – 60 seconds
 If uterine activity is absent then oxytocin is infused or nipple
stimulation is used
 Positive Test: if late decelerations are consistent and present with
more than 50% of the contractions
 Positive CST associated with an increased incidence of intrauterine
death, late decelerations in labor, low 5-minute Apgar scores, and
intrauterine growth restriction.
 CST is equivocal or suspicious if there are intermittent late
decelerations.
C. BIOPHYSCIAL PROFILE (BPP)
 Assess movement, fetal breathing, body movement, tone, heart
rate, and amniotic fluid volume; improve accurate and safe
identification of fetal compromise-Nelson
 24-28 weeks gestation: approximately 50% of NSTs are
nonreactive
 In contrast, sonographically evaluated variables are valid early in
gestation and account for 3-5 components of the biophysical
profile
 May be used to verify fetal well-being when the nonstress test is
not reactive
 Fetal movement and fetal tone develop between 7.5 and 9 weeks
menstrual age.
 Fetal breathing movements are detectable by, at least 17-18
weeks gestation.
 Amniotic fluid may be reduced as early as 17.5 weeks by fetal
acidosis.
 The components of the biophysical profile develop sequentially. In
order of appearance: (1) tone, (2) movement, (3) breathing,
(4)reactivity
COMPONENTS OF THE BIOPHYSCIAL PROFILE SCORE
Component Definition
Non-stress Two or more fetal heart rate accelerations peak (but do
test not necessarily remain) at least 15 beats per minute
above the baseline and last 15 seconds from baseline to
baseline within a 20 minute period with or without fetal
movement discernible by the woman.
Amniotic A single 2 cm x 2 cm pocket is considered adequate or
fluid volume AFI greater than 5.0 cm.
Fetal One or more episodes of rhythmic fetal breathing
breathing movements of 30 seconds or more within 30 minutes.
movements Hiccups are considered breathing activity.
Fetal At least three discrete bodies or limb movement.
movements Episodes of continuous movement are considered as a
single movement.
Fetal Tone One or more episodes of extension of a fetal extremity
or trunk with return to flexion, or opening or closing of
a hand.
Page 2 of 15
 Pediatrics 1.1

ANTEPARTUM RISK FACTORS MATERNAL CONDITIONS AND NEONATAL OUTCOME

 Maternal risk factors present during the antenatal period that can Eclampsia, Pre-eclampsia Circulatory and Nutritional
end up with a poor neonatal outcome Disorders due to vasoconstriction
o Maternal diabetes-does not only alter tissues because of of placental vessels diminishing
hyperinsulinemia but also the metabolic problem that nutrition to the neonate (ending
goes with it up with patients with SGA)
o Pregnancy-induced hypertension-affects the vascular Multiple births SGA due to crowding
supply due to the constriction of vessels of the placenta Prematurity
that diminishes the nutrition that would be given to the Feto-fetal transfusions
neonate leading to intrauterine growth restriction; BP High mortality risk
goes back to normal once there is already termination of Diabetes Macrosomia &Hypoglycemia due
pregnancy to hyperinsulinism
o Chronic hypertension Congenital anomalies
 Chronic maternal illness-taken from maternal history, includes the Insulin is a teratogen, hence there
medications of the mother since it can affect of neonatal outcome is congenital anomaly
o Cardiovascular Oligohydramnios (<500 ml) Postmaturity
o Thyroid Congenital malformations such as
o Pulmonary pulmonary hyperplasia &
o Renal Renal Agenesis (Potter’s
 Anemia or isoimmunization (ABO incompatibility & Rh Syndrome)
incompatibility) Polyhydramnios (>2L) Esophageal atresia
 Previous fetal or neonatal death Protracted Labor Asphyxia since breathing is

nd rd
Bleeding in 2 or 3 trimester compromised
 Fetal malformation Birth trauma
 Diminished fetal activity Brain damage
 Maternal infection
 Polyhydramnios CASE
 Oligohydramnios  A 16 year old girl arrives at the ER with abdominal pain.
 PROM (Premature Rupture of Membrane)  She states she is pregnant and is having abdominal pain about
every 1 to 2 minutes.
 Post-term gestation
 Her appearance is anxious but alert; she breathes rapidly with pain
 Size-dates discrepancy
but then slows her rate between episodes of pain.
 Drug therapy
 There are no retractions, and her skin color is normal.
o Lithium [4]
o Magnesium  According to the lecturer , this may be a case of high-risk
o Adrenergic-blocking drugs pregnancy due to the age of the mother. There may also be a risk
for premature birth and that doubles the problem that you are
 Maternal substance abuse
going to face with regards to the mother and neonatal outcome.
 No prenatal care
 Case Progression:
 Age < 16 or > 35 years
o Exam shows baby’s head crowning.
o What priorities of care should be initiated to resuscitate
INTRAPARTUM RISK FACTORS
the newly born? Antenatal care, surveillance, identify
 Emergency caesarian section-i.e. Uncontrolled hypertension,
maternal risk factors
malpresentation, reasons for termination of pregnancy
 Forceps or vacuum-assisted delivery (Assisted Operative Deliveries)
REVIEW: FETAL CIRCULATION
 Breech or other abnormal presentation
 One umbilical vein- oxygenated blood
 Premature labor
 Two umbilical arteries- deoxygenated blood
 Chorioamnionitis
 Three fetal shunts
 PROM (>18 hours) o Ductus venosus- hepatic system
 MSAF (Meconium Stain Amniotic Fluid) o Foramen ovale- between right and left atrium
 Prolapsed cord o Ductus arteriosus- vein connects pulmonary artery to
 Abruption placenta descending aorta; drives away the blood supply for the
 Prolonged labor (>24 hours) lungs since in utero, lungs are filled with water
nd
 Prolonged 2 stage (>2 hours)
 Fetal bradycardia ANATOMY
 Nonreassuring fetal heart rate patterns Characteristics:
 Use of general anesthesia 1. High pulmonary pressure
 Uterine tetany 2. Low systemic pressure
 Narcotics administered to mother within 4 hours of delivery 3. Presence of shunts or venous admixture
 Placenta previa - Foramen ovale (in between the future two atria)
- Ductus arteriosus (between the inferior surface of aortic arch to
the root of the pulmonary trunk)
- Ductus venosus (found in the liver used to bypass blood)

Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 3 of 15

 Pediatrics 1.1
Figure 1. Fetal Circulation-Blue: deoxygenated; Red-Oxygenated &Purple-
Mixed Blood
 Blood from placenta, which is about 80% oxygenated, returns to
embryo via the Left Umbilical Vein. Most of the blood goes to the
Ductus Venosus to enter the Inferior Vena Cava. Some of the blood
enters the liver sinusoids and would be mixed via the vein returning
from the Portal Circulation. In the Ductus Venosus, close to the
entrance of the left umbilical vein, a sphincter mechanism is present.
This sphincter mechanism prevents the sudden overloading of the heart,
especially when there are uterine contractions, wherein too much blood
would flow to the placenta. The sphincter mechanism would contract
and would close, so that the heart of the fetus would not be overloaded
with blood.
 Blood returning from the lower extremities mixes with blood in the
Inferior Vena Cava (but still well-oxygenated). From the Inferior Vena
Cava, blood would go to the Right Atrium. Most of the blood coming
from the Inferior Vena Cava is directed to the Left Atrium via the valve
of the Inferior Vena Cava, the Eustachian valve. This valve would direct
most of the blood to the Left Atrium. Some of the blood would be
prevented from entering the Left Atrium by the Septum Secundum, but
most of the oxygenated blood would flow to the Left Atrium. In the Left
Atrium, blood is mixed with deoxygenated blood from the Pulmonary
veins (blood coming from the lungs), and from the Left Atrium, would
go to the Left Ventricle, to the aorta. Since the initial portion of the
ascending aorta has the coronary arteries and the carotid arteries, this
ensures that the brain and the heart receive well-oxygenated blood.
Blood then flows to the aorta and then to the descending thoracic
aorta.
 The well-oxygenated blood that was prevented from entering the Left
Atrium now remains in the Right Atrium. This is mixed with
deoxygenated blood from the head via the Superior Vena Cava. Blood
from the Right Atrium would go to the Right Ventricle, to the
Pulmonary Trunk. Since the pressure is great in the lungs, only a small
amount of blood would go to right and left pulmonary trunks. Most of
the blood would be shunted through the Ductus Arteriosus, to be mixed
with the blood coming from the arch of the aorta. Blood would now go
to the Descending Thoracic Aorta, to the Descending Abdominal Aorta,
and finally, would return via the Umbilical Artery, to the placenta.
Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M
FETAL LUNGS
 Fluid filled
 Resistant
 Nourishment depends on placenta
TRANSITION TO EXTRAUTERINE LIFE
“Since fetal lungs are fluid-filled and resistant, fetus will derive their oxygen
and nutrients from the placenta. The transitional period (intrauterine to
extrauterine life) involves chemoreceptors and physical receptors that will
initiate the first breath. One factor would be the clamping of the umbilical
[4]
cord.”
Begins when the cord is CUT
 Placenta no longer works as the lungs
 Lungs begin to exchange gases
 First breath inflates lungs and causes circulatory changes- changes
in systemic and peripheral pressures
 Lungs inflate- resistance to blood flow through lungs and blood
flow from pulmonary arteries
 This results in Newborn Circulation
NEWBORN CIRCULATION
 At birth, with the onset of respiration, due to the presence of oxygen,
the muscle layer in the Ductus Arteriosus would contract, functionally
closing the Ductus Arteriosus. With the inflation of the lungs, blood
would now flow to the lungs and would be oxygenated. Oxygenated
blood now would go to the Left Atrium, thereby increasing the pressure
inside. With the increasing pressure, the septum primum would be
pressed onto the more rigid septum secundum, essentially closing the
Foramen Ovale. Blood would now flow from the Left Atrium, to the Left
Ventricle, to the aorta, to be distributed to the Systemic Circulation.
 When the umbilical cord is clamped, there is cessation of blood flow in
this area from the placenta. With this, the Left Umbilical Vein becomes
the Ligamentum Teres Hepatis or the Round Ligament of the Liver. The
Ductus Venosus becomes the Ligamentum Venosum. On the other
hand, the distal portion of the umbilical arteries becomes the Medial
Umbilical Ligaments, whereas the proximal portion becomes the
Superior Vesicle Arteries to supply the urinary bladder.
 Anatomically, the Ductus Arteriosus completely closes during the 2nd-
3rd week (some CVS books) or 1-3 months (Langman’s Medical
Embryology) while the closure of the Foramen Ovale, forming the fossa
st
ovalis, occurs within the first year of life. (1 year Anatomy Trans)
 Postnatal circulation
 Right atrium, SVC, IVC
 Poorly oxygenated blood
 Right ventricle, pulmonary artery, pulmonary circulation
 Oxygenated blood
 Left atrium, pulmonary veins
 Left ventricle, aorta, systemic circulation
Keeping those in mind, in premature babies the ductus arteriosus will not be
closed and there are factors that will keep the ductus close or patent.
Therefore, knowledge in neonatal resuscitation is needed. This would be
[4]
time- dependent.”
NEWBORN RESUSCITATION
*See IMAGE 1 on index page 
At birth, questions asked are the following:
 Is meconium clear?
o if there is hypoxic insult there would be relaxation of
sphincteric muscle leading to passage of meconium
o In utero, meconium would be sterile but once it is already
in the post natal circulation or when the patient starts to
breathe, meconium will be contaminated
o May lodge in the lungs and cause chemical pneumonitis
 Breathing or crying?
Page 4 of 15
 Pediatrics 1.1

 Good muscle tone?- differentiate if term or pre-term
 Is the baby pink? - No longer asked due to presence of
acrocyanosis which is due to constriction of vessels to conserve
heat
 Is the patient term or preterm?
 If the answer to any of the of the questions is no,
o Provide warmth by drying, stimulate, reposition and
provide oxygen if necessary to clear the airways
o Evaluate HR and color
 If HR is less than 100, provide positive pressure
ventilation (ambulatory bag)
 If HR is less than 60, initiate cardiac
compression
Figure 2. Primary and Secondary Apnea
 If there is apneic episode determine if it is more than 20 seconds
then classify whether it is:
o Primary apnea
 None of the HR and BP are affected; happens
during transitional period, the newborn adapts
to new environment
 spontaneous post-natal breathing, causing the
fluid out of the alveoli and stops fetal
respiration
o Secondary apnea
 a drop in HR and BP; tells you that you are not
successful in helping the patient in transition,
WHAT YOU WANT TO PREVENT
o Blood Pressure is affected to ensure stimulation of the
patient to avoid lagging in secondary apnea, affecting the
heart rate and making the patient bradicardic
Always Assess baby’s response to birth
Needed
Keep baby warm, Position, clear airway,
stimulate to breathe by drying, and give oxygen
(as necessary)
Needed Less Establish effective ventilation
Frequently Bag and mask
Endotracheal intubation
Provide chest
Compression
Rarely Needed
Administer
meds
Figure 3. Inverted pyramid of the priorities in initial resuscitation
 The inverted triangle gives you priorities in initial resuscitation
 Only 10% needs aggressive resuscitation-resuscitation in the
delivery room and emergency room mainly involves the drying,
stimulation and suctioning if needed
 Lowest is the medication
ASSESSMENT
ASSESSMENT BEFORE: APGAR SCORE
 This is a postnatal assessment for newborns which assesses and
grades the neonate’s 1st minute to 5th minute of life, based on
Appearance, Pulse, Grimace, Activity, and Respiration.
[4]
 “Still the best tool to evaluate physiologic parameters”
 10 is the highest score which equates to the best possible
condition but infants do not get 10 points because of acrocyanosis
in the 1st minute or even in the 5th minute of life.
 Normal score of 7-10
 Intermediate score of 4-7
 Poor score of 0-3 (requires immediate resuscitation)
 The 1st minute of life signifies the need for resuscitation while
the 5th minute of life tells the CNS outcome.
 APGAR score has limitations and is affected by gestational age,
maternal medications, resuscitation, congenital anomalies and
trauma.
 Low APGAR score on the 1st minute does not correlate with future
outcomes.
 Low APGAR score from 0-3 minutes may correlate with neonatal
mortality but not with neurologic dysfunction.
 APGAR scores of 0-3 in the 10th, 15th and 20th minute increases
[2]
the possibility of a neurologic problem.
Table 1. FACTORS AFFECTING THE APGAR SCORE
FALSE-POSITIVE (NO FETAL ACIDOSIS OR HYPOXIA; LOW APGAR SCORE
Prematurity
Analgesics, narcotics, sedatives
Magnesium sulfate
Acute cerebral trauma
Precipitous delivery
Congenital myopathy
Congenital neuropathy
Spinal cord trauma
Central nervous system anomaly
Lung anomaly (diaphragmatic hernia)
Airway obstruction (choanal atresia)
Congenital pneumonia and sepsis
Previous episodes of fetal asphyxia (recovered)
Hemorrhage-hypovolemia
FALSE-NEGATIVE (ACIDOSIS; NORMAL APGAR SCORE)
Maternal acidosis
High fetal cathecholamine levels
Some full term infants
ASSESSMENT NOW
 Physiologic parameters (Apgar is still the best tool)
 Breathing
 Heart rate
 Color
 Questions to ask yourself
 Clear of meconium
 Breathing or crying
 Good muscle tone
 Term gestation?

Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 5 of 15

 Pediatrics 1.1

INITIAL MANAGEMENT: FOR ALL DELIVERIES
 Provide warmth- to prevent evaporation as a loss for heat
 Position and clear airway
 Dry
 Give oxygen (as necessary)
o in premature babies: they at risk for retinopathy of  Indications for intubation
prematurity if you give 100% oxygen
o now it is accepted to do resuscitation in room care
 Indications for compressions
Figure 4. Providing Warmth: The Cycle of Hypothermia. Hypothermia will
increase oxygen utilization causing depletion of oxygen. This will increase
accumulation of lactic acid causing acidosis.
 Keep the mouth slightly open
 Delivering good and adequate pressure: chest rise is seen
 The manometer indicates pressure given
 don’t go beyond 40mmHg because it can cause
barotrauma leading to pneumothorax
 Meconium and baby is not vigorous
 PPV by bag-mask does not result in good chest rise
 PPV needed beyond a few minutes
 Chest compressions necessary
 Route to administer epinephrine
 Special indications
 prematurity
 lack of surfactant making lungs atelectatic
 Congenital Diaphragmatic Hernia - migration of GI
content into thoracic cavity. Thus, when you use ambu-
bag which distends the bowels, you compromise
respiratory status; clinically seen as scaphoid abdomen
 Heart rate<60 bpm after 30 secs of PPV
 Coordinated with ventilation
 4 events in 2 seconds
 90 compressions and 30 breaths per minute

MEDICATION: EPINEPHRINE
 Indication: HR <60 after 30 sec of coordinated ventilation and
compressions
 1:10,000 (0.1 mg/ml)
 Get 1 ml of 1:1,000 dilute in 9ml to make 1:10,000
 Route: Endotracheal tube or IV
 0.1-0.3 ml/kg
 1ml Term
 0.5 ml Preterm
 0.25 ml extreme preterm

EXTENDED ALGORITHM
 Endotracheal intubation if not already accomplished
 Establish IV access with UVC (Umbilical Venous Catheter)
 Stat Chest x-ray- to know if endotracheal tube is properly placed
and situated above the carina
 Discontinue efforts if no heart rate after 15 minutes

Figure 5. Continued algorithm of New Born Resuscitation

*If there is meconium staining and baby is vigorous- there is no need for
resuscitation/intubation
BREATHING OR CRYING
 Absence of crying- indicates APGAR score of 0-3
 Indications for Positive Pressure Ventilation
 Apnea or gasping
 Heart rate <100 even if breathing
 Persistent central cyanosis (saturation <90%) despite 100%
free flow oxygen (free flow oxygen in closed container is
100%; if it mixes in the environment it is not anymore 100%)
 PPV (positive pressure ventilation)
 Apply proper size of mask
 2 types
 Pear shaped
 Round mask
 Make sure the airway is clear
 Lift the baby’s jaw into the mask
Figure 6. Extended algorithm

Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 6 of 15

 Pediatrics 1.1

VOLUME 2. SPECIAL CARE REQUIREMENTS

 Indication: no response to resuscitation and evidence of blood  Those requiring special or assistive feeding techniques
loss  Those requiring respiratory assistance
 Normal saline (0.9% NSS)  Those with complex congenital anomalies requiring supportive
 Ringers or Blood as alternative and assistive devices
 10 ml/kg, may repeat
 Route: IV (umbilical vein) 3. GESTATIONAL AGE
 Need to evaluate cardiovascular output and closely monitor  37 completed weeks of gestation, regardless of birth weight-less
patient than 37 weeks puts them as high risk infants
 Full term infant – Born between 38 weeks and completion of the
CASE 42 weeks of gestation, regardless of birth weight
 Delivered a 34 weeks old (late pre-term)  Post term/ Post mature infant – Born after 42 weeks of gestation,
 Baby had poor tone and color initially but with suctioning, drying, regardless of birth weight
warming and stimulation, became vigorous with good cry, tone
and color 4. ACCORDING TO SIZE
 Baby did not need any intubation or chest compression, but just  LBW : < 2500 gm regardless of GA
STIMULATION which helped the patient sustain transition from  MLBW (moderately low): 1501- 2500 gm
intrauterine to extrauterine.  VLBW (very low) : <1500 gm
 ELBW (extremely low) : <1000 gm
th
IMMEDIATE ESSENTIAL NEWBORN CARE  AGA/SFD : <10 percentile on intrauterine growth curves (= IUGR)
 It is time bound- i.e. Drying in the first 30 sec, but wet linen should 
th
LGA/LFD : >90 percentile on intrauterine growth curves
be removed otherwise it would not help in preventing hypothermia
 Depends on risk factor and initial status of the newborn MORTALITY
 Focuses on the initial first 30 seconds which should involve  Live birth – Birth in which the neonate manifests any heart beat,
immediate drying of the newborn, while assessing if the newborn breathes or displays voluntary movement, regardless of birth
should be referred to a specialist or another institution. weight
 Prevention of hypothermia should be instilled.  Fetal death – Death of fetus after 20 weeks of gestation and
 Assessment of other interventions or care should be given to the before delivery, with absence of any signs of life after birth
patient after stabilization.  Neonatal Death – Death in the first 27 days of life (early – first 7
 Eye prophylaxis, Vit. K and other vaccines are not going to be the days)
initial measurements to be given to the neonate; instead, skin-to-  Post natal death – Deaths that occur at 28 days to 1 year
skin contact is the priority.  Perinatal Mortality – Total no of fetal and early neonatal deaths
There is no mention of the APGAR scoring. The only criterion is that if the per 1000 live births
patient is breathing or not, in which case resuscitation is done. *This is important because it gives you an index of the perinatal care
[4]
It is also important to assess BW of baby since if it less than 2.5 kg, it is an that was done to the mother.
[2]
index of potential problems with the mother and newborn.
MATERNAL CONDITIONS THAT MAY IDENTIFY A HIGH RISK NEONATE
PRINCIPLES OF ESSENTIAL NEWBORN CAARE  Age at delivery
 Early and immediate drying – should be done in first 30 secs.  Routine Prenatal Care
 Delayed cord clamping-when done within 30 seconds  Previous Pregnancies-low risk pregnancy has lesser visits to the
- 3 minutes will prevent preterm babies from developing obstetrician, high risk pregnancy has more visits to the obstetrician
intraventricular hypertrophy, but may increase the incidence  Maternal Laboratory Studies
hyperbilirubinemia because the increased RBC mass leads to  Maternal Illnesses and Infections
hemolysis  Pregnancy Induced Conditions
 Skin-skin contact  Maternal Medications and Drug Use
 Breastfeeding  Fetal Status Before Delivery
 Details of Delivery and Resuscitation
HIGH RISK NEONATE  Social Factors
 A newborn, regardless of gestational age or birth weight, who has
a greater than average chance of morbidity or mortality because
of conditions or circumstances superimposed on the normal
course of events associated with birth and the adjustment to extra
uterine existence

CLASSIFIED ACCORDING TO:

1. ETIOLOGIC FACTORS
 Low birth weight (LBW) infant-less than 2.5kg, premature, SGA
 Infant who requires technological support-i.e. May be needing
ventilators or other devices to keep proper monitoring
 Infant primarily at risk because of family issues
 The infant whose irreversible condition will result in an early
death
Figure 5. Birth weight for gestational age.

Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 7 of 15

 Pediatrics 1.1

Discussion for Figure 5: Patient A is a 35-weeker with a BW of 2kg-AGA;  Chronic fetal infections (cytomegalic inclusion disease,
Patient B is full term with a BW of 2kg-SGA. congenital rubella, syphilis)
Better to have patient A, since the problem with patient B may already be  Congenital anomalies – syndrome complexes
chronic and there may also be a lot of problems even in the intrauterine  Irradiation
[4]
period. Classification based on weight is for PROGNOSTICATION.  Multiple gestation
 Pancreatic hypoplasia
LARGE FOR GESTATIONAL AGE (LGA)  Insulin Deficiency
th th
 Appropriate for Gestational Age = 10 – 90 centile  Insulin-like growth factor type 1 deficiency
th
 Small for Gestational Age – below the 5 centile

th
Large Gestational age – above the 95 centile  Placental
 *the evaluation of the newborns will predict complications which  Decreased placental weight or cellularity, or both
may occur during the fetal and neonatal transition period and  Decrease in surface area
closely monitor them  Villous placentitis (bacterial, viral and parasitic)
 Appears large and plump  Infarction
 LGA babies are at risk for difficult delivery that can result in birth  Tumor (chorioangioma, hydatidiform mole)
injuries/ distress  Placental Separation
 Prone to hypoglycemia; polycythemia  Twin transfusion Syndrome
 Ex. Infants of diabetic mother; fetal hydrops; Beckwith-Weidmann
(chronic hypoglycemia with omphalocele); postterm infants;  Maternal
constitutionally large infants  Toxemia
 Hypertension or renal disease
SMALL FOR GESTATIONAL AGE (SGA)  Hypoxemia (high altitude, cyanotic cardiac or pulmonary
 Accounts for 1/3 of low birth weight (<2500) in western countries disease)
 Appear scrawny with large head; alert; more mature than what  Malnutrition (micro/macro deficiencies)
their BW would suggest  Chronic Illness
 Babies who either have not received enough nutrition in utero to  Sickle cell Anemia
grow appropriately or have poor use of nutrients, such as those  Drugs (narcotics, alcohol, cigarettes, cocaine, anti-
with chromosomal defects metabolites)
 Higher risk of mortality than AGA or LGA babies
PROBLEMS OF IUGR/SGA INFANTS
 They have experienced chronic stress in utero and diminish
Problem Pathogenesis
reserves to withstand stresses of labor and delivery
Intrauterine Fetal Demise Hypoxia, acidosis, infection and
 Premature SGA infants are at lower risk for RDS
lethal anomaly
 They are at risk for hypoglycemia; need higher caloric
Perinatal Asphyxia Decreased utero- placental
requirements
perfusion during labor with or
* If you have a mother with chronic hypertension or pregnancy-induced
without chronic fetal hypoxia
hypertension, the effect of hypertension on pulmonary maturity is
resulting to acidosis, meconium
hastened. Therefore, these patients do not have an increased incidence
[4] aspiration syndrome
of hyaline membrane or respiratory distress.
Hypoglycemia Decrease tissue glycogen stores
and gluconeogenesis,
IDENTIFICATION OF SGA/IUGR
hyperinsulinism, increased
 An infant may be small at birth due to genetic factors. Non genetic glucose needs due to hypoxia,
factors may not be apparent before 32-34 weeks of gestation and hypothermia and large brain
this could be due to: Polycythemia – Hyperviscosity Fetal hypoxia with increased EPO
1. Placental insufficiency from maternal disease involving small production
blood vessel as seen in maternal conditions such as pre- Reduced oxygen Hypoxia, hypoglycemia starvation
eclampsia or primary hypertension, renal disease or long consumption/hypothermia effect, poor subcutaneous fat
standing diabetes stores
2. Placental involution which is noted in post-mature babies Dysmorphology Syndrome anomalads,
3. Infectious agents such as cytomegalovirus, rubella virus or chromosomal-genetic disorders,
toxoplasma gondii oligohydramnios- induced
4. Small head circumference: head bigger than chest by >3 cm deformation, TORCH infection
5. Physical characteristics such as skin appearance (loose folds
of skin), ear cartilage (small amount of ear cartilage), sole IUGR VS SGA
creases (less creases) lack of subcutaneous tissues SGA IUGR
6. Patient’s behavior? Does he have a vigorous suck? Alert? BW less than population norms BW less than expected inhibition of
7. Feeding behavior normal growth potential
8. Maternal History: opioid or cocaine user? Alcohol and th
<10 % OR Implies pathology
smoking during pregnancy? < 2 SD below the mean A term used by OB to describe a
9. Growth restriction pattern of growth over a period of
time
FACTORS ASSOCIATED WITH IUGR Pathologic or non-pathologic causes
 Fetal A term used by PEDIA
 Chromosomal disorders UENT MANAGEMENT OF ASP

Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 8 of 15

 Pediatrics 1.1

ETIOLOGY: IUGR COMPLICATIONS

I. An infant may be small at birth  due to genetic factors  Hypoxia – Perinatal asphyxia
II. Nongenetic factors = Restricted intrauterine growth  not apparent - Persistent pulmonary hypertension
before 32 to 35 weeks gestation - Meconium aspiration
o Placental insufficiency from maternal disease involving the  Thermoregulation – Hypothermia (diminished subcutaneous fat)
small blood vessels (pre-eclampsia, primary hypertension,  Metabolic – hypoglycemia, hypocalcemia
renal disease, or long-lasting diabetes)  Hematologic – Hyperviscosity , polycythemia (Decreased
o Placental involution accompanying post maturity; and oxygenation that stimulates RBC production)
infectious agents such as cytomegalovirus, rubella virus, or  Immunologic-increased protein catabolism and decreased in
Toxoplasma gondii protein, prealbumin decreased Ig = decreased humoral and
o Clinical Manifestations: cellular immunity
 Toxoplasmosis – Rash, seizures,
microcephaly/micropthalmia MANAGEMENT
 Rubella – Heart defects, neurologic abnormalities  Antenatal – diagnosis and management is the key to proper
 Cytomegalovirus – IUGR, purpura, chorioretinitis, management
microcephaly  Delivery and Resuscitation – appropriate timing of delivery,
 Herpes simplex virus – Disseminated or localized HSV Skilled resuscitation should be available, and Prevention of heat
(CNS, skin, eye) loss
 Syphilis – Snuffles, rash of trunk, palm and soles  Hypoglycemia – close monitoring of blood glucose early treatment
because glucose is the main substrate in the CNS, once patient
WHEN DO YOU THINK OF TORCH INFECTIONS? becomes hypoglycemic, they can present with seizures
th
 IUGR-BW classified as less than 10 percentile  Hematologic Disorder – central Hct to detect polycythemia (Hct of
 HSM (Hepatosplenomegaly) 65)
 Thrombocytopenia  Congenital Infection – examined for signs of congenital infection
 Unusual Rash (e.g. rash, microcephaly, hepatosplenomegaly, lymphadenopathy,
 Concerning maternal history cardiac anomalies, etc.), Torch titer screening
 Classic findings of any specific infection  Genetic anomalies – screening as indicated by PE
- chromosomal analysis/karyotyping
CLASSIFICATION
1) Symmetric: weight, length and head circumference are all below MULTIPLE GESTATION
th
the 10 %, associated to stunted and wasted patients (33% of IUGR INCIDENCE
infants; 2ndary to genetics & congenital infections)  spontaneous twins 1 in 80 pregnancies: triplets 1 in 8000
th
2) Asymmetric: weight is below the 10 and head circumference and pregnancies
length are preserved (55% of IUGR; placental insufficiency   Monozygotic twins 1 in 3.5 per 1000
under nutrition)  Dizygotic – incidence varies by locale, race, maternal age
3) Combination: Infant may have skeletal shortening some reduction
of tissue mass (12% of IUGR) TYPE OF TWINS
1. Monozygotic – 1 fertilized egg splits during 2 weeks of
development
2. Dizygotic – fertilization of 2 eggs leading to fraternal twins
*Identifying twins as monozygotic or dizygotic require detailed blood typing,
gene analysis or tissue HLA typing.
*Still have physical and cognitive differences because their utero
environment may be different as these differences can still exist in the
mitochondrial genome, post-translational gene product modification and in
the epigenetic modifications of genes depending on environmental factors

TWIN TO TWIN TRANSFUSIONS

Figure 6. IUGR  Incidence--5-15% of monochorionic, diamniotic twins
 Etiology – Placental vascular anastomoses
POST NATAL ASSESSMENT  Diagnosis – US findings: size disparity between fetuses
1. Growth parameters: weight, height, HC (directly related to
developmental outcome) ASPHYXIA: DEFINITION OF RELATED TERMS
2. Assess Gestational Age with Ballard score-Neurologic and Physical  Hypoxic Ischemic Injury to the CNS: failure to initiate and sustain
Maturity=Pediatric Dating for Patient’s Age breathing immediately after birth
3. Plotted growth parameters in growth chart  Hypoxic Ischemic Encephalopathy: clinical manifestations (e.g. Seizure)
 Neonatal Encephalopathy: not always possible to document the
PHYSICAL APPEARANCE hypoxic insult and there may be potential several other etiologies
 Heads are disproportionately large for their trunks and extremities operating; does not point to a single etiologic cause (Dr. Salazar)
 Facial appearance has been likened to that of a “wizened old man”  A gold standard definition of birth asphyxia does not exist
 Long nails  Perinatal Asphyxia: in-utero, at birth or in the postnatal period
 Scaphoid abdomen  Moderate Asphyxia/AS 4-6: slow gasping breathing
 Severe Asphyxia/AS 0-3: no breathing

Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 9 of 15

 Pediatrics 1.1

4 CRITERIA FOR INTRAPARTUM FETAL DISTRESS o More seizures

(According to the American Association of Pediatrics [AAP] and American o Jitteriness
College of OB-GYN) o Weakness in hip/shoulder
1. Persistence of an Apgar score of 0-3 for > 5 minutes  24-72 hours
2. An umbilical arterial blood pH < 7 o More stuporous
3. A sustained neonatal neurologic syndrome that includes hypotonia, o Respiratory arrest
coma, seizures o Brainstem oculomotor abnormalities
4. Evidence of multiorgan dysfunction are manifestations of perinatal  Greater than 72 hours
asphyxia o Persistent, though diminishing, stupor
[4]
*ALL HAVE TO BE MET TO SAY THAT PATIENT HAS ASPHYXIA o Disturbed sucking, swallowing, gag and tongue movements
o Hypotonia greater than hypertonia
ETIOLOGY
 Intrapartum or ante partum (90%) PERINATAL ASPHYXIA
o Placental insufficiency  Insult to the fetus/newborn
[3]
o Intrapartum disorders that causes fetal hypoxia o Lack of oxygen (hypoxia)
1. Inadequate oxygenation of maternal blood from o Lack of perfusion (ischemia)
hypoventilation during anesthesia, cyanotic heart disease, o Effect of hypoxia and ischemia are inseparable and both
respiratory failure, or carbon monoxide poisoning contribute to tissue injury
2. Low maternal BP from acute blood loss, spinal anesthesia or
compression of the vena cava and aorta by the gravid uterus
3. Inadequate relaxation of the uterus to permit placental
filling as a result of uterine tetany cause by the
administration of excessive oxytocin Shunting of
Away from
blood to
4. Premature separation of the placenta Diving seal lungs,
Hypoxia brain,
5. Impedance to the circulation of blood through the umbilical reflex kidney, gut,
adrenals,
cord as a result of compression or knotting of the cord and skin
and heart
6. Placental insufficiency from toxemia and postmaturity
 Post partum (10%)
o Pulmonary
o Cardiac
o Post partum disorders that causes hypoxia (Nelson page 569) Figure 8. Priority organs: brain, adrenals, and heart; that’s why in an
1. Failure of oxygenation as a result of severe forms of cyanotic asphyxiated patient the skin is pale because it is not a priority organ; one of
congenital heart disease or severe pulmonary disease the complications would be acute kidney injury since blood is shunted away
2. Severe anemia (severe hemorrhage, hemolytic disease) from the kidney
3. Shock severe enough to interfere with the transport of
oxygen to vital organs from overwhelming sepsis, massive  Results in adverse effects on all major body systems
blood loss, intracranial or adrenal hemorrhage  Fatal complications
 Term: renal 50%, CNS 28%, Cardiac 25%, Lungs 25% Dysfunction
 Extent of organ system dysfunction determines the early outcome of an
asphyxiated neonate

Table 2. Organ System Dysfunction determining early outcome of

asphyxiated neonate
CNS HIE, ICH Seizures Neurologic
sequelae
CVS Myocardial Valvular Rhythm ab
dysfunction dysfunction CHF
Figure 7. APGAR. RENAL Hematuria ATN RVT
*APGAR Score- is a useful tool that is used that will guide us with regards to METABOLIC Acidosis Hypoglycemia Hypocalcemia
the post-asphyxia treatment of the neonate and in predicting the long-term hyponatremia
outcome in patients with perinatal asphyxia (Dr. Salazar)
*See Image 4 on Index  Table 3. Multiorgan systemic effects of asphyxia (Clinical Manifestation
based on magnitude of involvement) (Nelson page 569)
HYPOXIC BABIES (5-minute APGAR score of 0-3) SYSTEM EFFECT
Clinical features Central nervous Hypoxic-ischemic encephalopathy (HIE),
 Birth-12 hours system infarction, intracranial hemorrhage (ICH),
o Deep stupor or coma seizures, cerebral edema, hypotonia,
o “Periodic” breathing hypertonia
o Intact papillary responses Cardiovascular Myocardial ischemia, poor contractility, cardiac
o Intact oculomotor reflexes stun, tricuspid insufficiency, hypotension
o Hypotonia, minimal movement Pulmonary Pulmonary hypertension, pulmonary
o Seizures hemorrhage, respiratory distress syndrome
 12-24 hours Renal Acute tubular or cortical necrosis
o Less stuporous Adrenal Adrenal hemorrhage
Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 10 of 15
 Pediatrics 1.1

Gastrointestinal Perforation, ulceration with hemorrhage, Posture Normal Flexion Decerebrate

necrosis Tendon Hyperactive Hyperactive Absent
Metabolic Inappropriate secretion of antidiuretic reflexes/clonus
hormone, hyponatremia, hypoglycemia, Myoclonus Present Present Absent
hypocalcemia, myoglobinuria Moro reflex Strong Weak Absent
Integument Subcutaneous fat necrosis Pupils Mydriasis Miosis Unequal, poor
Hematology Disseminated intravascular coagulation light reflex
Seizures None Common Decerebration
CLINICAL CONSEQUENCES Electro- Normal Low voltage Burst
A. Brain (Hypoxic Ischemic Encephalopathy)- hypoxic insult presented as encephalo- changing to suppression to
seizures graphic findings seizure isoelectric
o Autonomic disturbances (hypotension, increase salivation, activity
abnormal papillary reflex) Duration <24hr if 24hr-14days Days to weeks
o Altered neonatal reflexes (Moro, sucking, swallowing) progresses;
o Seizures otherwise,
o Asphyxiated patients do not develop seizures due to hypoxia but may remain
due toIncreased glutamate (excitatory) release  NMDA normal
receptor  Calcium accumulation  neurotoxic Outcome Good Variable Death, severe
B. Heart deficits
o Myocardial dysfunction resulting in hypotension or CHF
C. Kidney
o Tubular damage may cause ARF EVOLUTION OF HIE
[2]
 Gradually evolving process: Begins during the insult  extends beyond
Patterns in term infants affected by perinatal asphyxia the resuscitation period
 Selective neuronal necrosis: ends up with a patient having a spastic  Initial brain injury  Hypoxia and ischemia
cerebral palsy  Subsequent reperfusion and generation of free radicals contribute to
 Status marmoratus: this presents as involuntary movements such as ongoing injury
chorea, athetoid, and dystonia
 Parasagittal cerebral injury: this results to a quadric-paretic patient
 Focal and multifocal ischemic brain injury INFARCTION (initial hypoxic-ishemic inury)

[2] PENUMBRA (immediate area surrounding

Patterns in pre-term babies affected by perinatal asphyxia
 Periventricular leukomalacia where the brain seems to liquefy the infarcted area)

HYPOXIC ISHCEMIC ENCEPHALOPATHY (HIE) NEURONAL NECROSIS

 This is an important cause of permanent damage to CNS tissues that
may result in neonatal death or manifest later as cerebral palsy or APOPTOSIS (programmed cell death)
developmental delay/mental deficiency-Nelson
 CNS dysfunction Figure 8. Evolution of HIE
 Foremost concern in an asphyxiated neonate  long-term neuromotor It is possible that these post-hypoxic changes in the penumbra may be
sequelae amenable to therapeutic intervention
 Sarnat and Sarnat Classification Good supportive therapy is essential for the first 48 hours of post-asphyxial
 Levine Classification: simple and practical classification by severity of period to reduce neuronal injury in the penumbra
manifestations
PRINCIPLES OF MANAGEMENT
Table 4. Levine classification  Admit in newborn unit-NICU(Neonatal Intensive Care Unit)
o
Feature Mild Moderate Severe  Thermo-neutral temperature to maintain skin temp at 36.5 C
(<24 hours) (2-14 days) (Hours to  IV line, fluids two-third of maintenance (because in the first 3 days
weeks) there’s going to be cerebral edema due to hypoxic insult- Dr. Salazar)
Consciousness Irritable Lethargy Comatose  Fluid bolus (0.9 NSS at 10cc/kg-Dr. Salazar) if Capillary Refill Time > 3
Tone Hypotonia Marked Severe seconds or low BP
o o
hypotonia hypotonia  Normal range: 36.5 C – 37.5 C
o o
Seizures No Yes Prolonged  Cold stress: 36.1 C – 36.4 C
o o
Sucking/ Poor suck Unable to suck Unable to  Moderate hypothermia: 32.0 C – 36.0 C
o
Respiration sustain  Severe hypothermia: <32.0 C
spontaneous  Hypothermic therapy (discussed further in subsequent pages)
respiration o Isolated cerebral cooling or systemic hypothermia to a core temp
o [5]
of 33.5 C w/in the first 6hrs after birth
[5]
Table 5. Sarnat and Sarnat Classification o All infants with gestational age of 35 weeks + 6 days or more are
Signs Stage 1 Stage 2 Stage 3 going to be exposed to hypothermia because it decreases the
[2]
Level of Hyperalert Lethargic Stuporous, coma metabolic need of the body
consciousness o However, it can only be done for the first 48-72 hrs just so the
[2]
Muscle tone Normal Hypotonic Flaccid body, specifically the brain will be able to recover

Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 11 of 15

 Pediatrics 1.1

 Good supportive care is essential in the first 48 hours after asphyxia to SUBSEQUENT MANAGEMENT OF ASPHYXIATED NEONATES
prevent ongoing brain injury in the penumbra region
 Strict monitoring and prompt correction is needed for common
problems including temperature maintenance, blood sugars, blood
pressure and oxygenation to see if patients are showing signs of
improvement/deterioration
[2]
Guidelines to be followed in managing patients with HIE
 Meconium stained, amniotic fluid
o If the patient is vigorous and crying, there’s no need for intubation
and suctioning
o If the patient is depressed, you need to suction the amniotic fluid
even before the first breath to avoid aspiration. If aspiration lodges
in the lungs, chemical pneumonitis may be a complication. Figure 9. Subsequent Management
o Meconium aspiration syndrome is the end result if patient is not
able to recover from this condition A. Ventilate if there is respiratory depression especially in the setting
 Avoid hyperthermia of:
o Full-term patients: 100% FiO2 is recommended but if supplemental  Severe encephalopathy
oxygen is not available room air can be utilized.  Frequent seizures
o Pre-term patients: 100% FiO2 is detrimental because it can lead to  Post anticonvulsant medication-ie. Phenobarbital can
blindness or retrolental fibroplasia. cause respiratory depression, although a high dose of this
 Chest compression is given when seizure is intractable
o Initiated if the heart rate is absent or remains to be <60 bpm. B. Aim for O2 Saturation= 90-93% in the term baby to minimize the
o If it is <100 bpm, just do positive pressure ventilation. risk of pulmonary hypertension
 Give epinephrine: 1:10,000 at 0.01 to 0.03mg per kg C. Avoid hypocapnia (pCO2<50mmHg) will worsen cerebral
vasoconstriction
Prevent Further Organ Damage D. Consider crystalloid boluses (10-20ml/kg of 0.9% saline)
 Maintain oxygenation, ventilation and perfusion  Perfusion is poor
 Correct and maintain normal metabolic and acid base milieu  Lactate not improving
 Prompt management of complications  Mean BP <40mmHg in a term baby
In the NICU set-up, if your patient shows metabolic acidosis,
Clinical Monitoring sodium bicarbonate is not the answer.You must evaluate the
 HR, RR, color, CRT (Capillary Refill Time), O2 saturation, BP and fluid status of your patient first before you administer
temperature bicarbonate infusion.-Dr. Salazar
 Assessment of neurologic status-tone, seizures, consciousness, E. Consider blood transfusion if there has been fetal blood loss and
pupillary size & reaction, sucking and swallowing poor perfusion and metabolic/ lactic acidosis persists-
 Abdominal circumference-since GI is not a priority organ F. If hypotension persists start inotropes
 Urine output-good output is 1cc/kg  Dobutamine (5-20 micrograms/kg/minute)
Biochemical Monitoring  Dopamine (5-20 micrograms/kg/minute)
 Blood gases & pH G. Acidosis usually improves with improved ventilation and
 Bedside blood sugar by Destrostix perfusion. Consider a half bicarbonate correction, if severe
 Hematocrit metabolic acidosis persists. However, persisting acidosus suggests
 S electrolytes (Na, K) impaired cardiac output and attention should be directed towards
 S calcium treating this
H. Restrict fluids to 40-50 ml/kg/day until urine output (of
 BUN, creatinine
1ml/kg/hour) is established.
Other Investigations
I. Give 10% glucose in the first 24 hours and monitor blood glucose
 Neuroimaging
levels. Once renal function is stable sodium and potassium
1. CT scan
additives can be commenced
o Brain edema as suggested by small compressed vessels
J. If oliguria/anuria, consider:
o Hemorrhage
 Urinary catheterization
2. Ultrasound
 Fluid challenge (20ml/kg 0.9% saline over 30 mins.) with
o Small compressed vessels
diuretic (Furosemide 1-2 mg/kg IV)
o Intraventricular hemorrhage
 Dopamine (renal dose 2.5-5 micrograms/kg/minute)
3. EEG
 Withholding aminoglycoside antibiotic if prescribed.
*Sepsis Screen should be part of your work-up to exclude in utero or acquired
infections during resuscitation esp. if you have utilized your umbilical cord as
[4] AIMS OF SPECIFIC MANGAMENT
your vascular access.
 Maintain temperature, perfusion, oxygenation and normal metabolic
*Sometimes if you suspect barotrauma (intubated patient doing all right
state
then suddenly experiences desaturation, becomes cyanotic and there is o
1. Temperature: 36.5- 37.5 C
absence of breath sounds on auscultation-PNEUMOTHORAX), you can do
2. Perfusion:
transillumination. Transillumination is when you put a bright source light on
 BP: Mean 40-60 mmHg
the chest and the area of pneumothorax lightens up. Documentation of this
[4]  CRT: Maintain <3 sec.
should be done through chest x-ray. Thoracocentesis can also be done.

Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 12 of 15

 Pediatrics 1.1

3. Oxygen ADVERSE EFFECT

 PaO2 : 60-80 mmHg  Sinus bradycardia
 Saturation: 90-93% o Borderline increase in the need for inotrope support
4. CO2: 35-45 mmHg  Significant increase in the evidence of thrombocytopenia (Platelet
9
5. Glucose: 70-110 mg/dl count <150x10 /L)-may be related to acid-base problem thus should
6. Calcium: 9-11mg/dl only be given within 72 hours

SEIZURE MANAGEMENT
 Peaks on the first 48 hours
 Anticonvulsant therapy-AE: respiratory depression
A. Phenobarbital
st
 1 line anticonvulsant, drug of choice for maintenance
monotheraphy in the first 6 months of life due to its
relale absorption and long safety record
 Initial Dose: 20mg/kg/dose, if seizures continue, up to
40mg/kg can be given safely. Stop IV once seizure is
controlled
 Maintenance: 5mg/kg/day once daily
B. Phenytoin
nd
 2 line anticonvulsant
 Loading Dose: 15-20mg/kg/dose IV
 Phenytoin absorption orally is unreliable, thus this
agent is discontinued after the immediate stabilization
period
C. Midazolam
rd
 3 line anticonvulsant can be titrated for continuous
The patient would actually meet the criteria for asphyxia. These are the infusion.
guidelines used for infants who are asphyxiated and usually apply for term D. Clonazepam
patients where they usually institute the HYPOTHERMIA THERAPY.  Safe and effective alternative

HYPOTHERMIA THERAPY FOR HIE PREVENTING ASPHYXIA

BRAIN HYPOTHERMIA  Perinatal assessment
o
 Induced by colling a baby to around 33 C for 3 days after birth  Regular antenatal check ups
 Been proven to be the only medical intervention which reduces brain  High risk approach-high risk pregnancies
damge and improves an infants chance of survival  Anticipation of complication during labor
 Reduces infarcted size by about 50% following focal ischemia  Timely intervention-very good neonatal assessment
 Reduces histological injury in cortex, thalamus, and hippocampus  Management of maternal complication
following global hypoxia-ischemia
 Improves long term functional outcome following traumatic and NEURODEVELOPMENTAL OUTCOME
hypoxia ischemic insults.  Failure to establish respiration by 5 minute
 APGAR score of 3 or less at 5 minutes
COOLING
 Onset of seizures within 12 hours
 2 types of Cooling:
o  Refractory seizures
1. Head Cooling with mild cooling to 34.5 C-brain expected to
 Inability to establish oral feedigs by 1 week
be a degree cooler which decreases metabolic activity
o  Abnormal EEG, neuro imaging
2. Whole body Cooling to 33-34 C
 Cooling for 72 hours will start within 6 hours after birth
PROGNOSIS
 APGAR Score<5 at 10 mins: nearly 50 % death or disability
CURRENT EVIDENCE
 No spontaneous respiration after 20 mins.:60% disability in
 Hypothermic neural rescue therapy is an evidence based clinical
survivors
treatment which increases a severely injured FT infant’s chance of
 No spontaneous respiratiuon afet 30 mins: nearly 100% disability
survivng without brain damage at 18 month by 50%
in survivors
 Only restricted to FT (>36 weeks)
 Potentially transformiung therapy for low-resource environments
References
where birth asphyxia remains a major cause of death and disability th
1. Nelson 19 ed.
 Reduces the elevation of dopamine, free FA and glutamate
2. 2015B trans
 Preserves cerebral energy metabolism th
3. Nelson’s 19 ed., page 569
 Reduces delayed increase in extracellular glutamate 4. Recording
 Reduces secondary rise in cortical impedance (cytotoxic edema) th
5. Nelson’s 19 ed., page 571
 Inhibits apoptosis cell death
“But seek first His Kingdom and His righteousness, and all these things will
be given to you as well. Therefore do not worry about tomorrow, for
tomorrow will worry about itself. Each day has enough trouble of its own.”
(Matthew 6:33-34)
Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 13 of 15
 Pediatrics 1.1 DR. SALAZAR
Neonatology I June 19, 2014

INDEX

Image 2: Algorithm of New Born Resuscitation Image 3: Algorithm of New born Resuscitation

Image 4: APGAR Score

Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 14 of 15

 Pediatrics 1.1

Image 5: Ballard’s Score: Post Natal Assessment

Group # 28 | Sorsona, Sunga M, Sunga P, Sy C, Sy M Page 15 of 15