ALL ABOUT

BABIES
Respiratory Diseases of the Newborn

 Transient Tachypnea of the Newborn

 Hyaline Membrane Disease
 Meconium Aspiration Syndrome
 Neonatal Pneumonia
Transient Tachypnea of the Newborn

 RDS Type II; Wet lung

 benign disease of near-term, term, or large premature infants
who have respiratory distress shortly after delivery
 Secondary to inadequate or delayed clearance of fetal
alveolar fluid
 tachypnea (>60 bpm), grunting, nasal flaring, rib retraction,
cyanosis
 classic "barrel chest" secondary to the increased AP diameter
Transient Tachypnea of the Newborn

 usually resolves within 48-72 hours days

 Pathophysiology
 At birth, the balance of fluid movement in the alveolus
switches from Chloride secretion to Sodium absorption
causing resorption of intra-alveolar fluid
 Absorption occurs in 2 steps:
 Na moves passively from the alveolar lumen into the cell through
Na-K-ATPase pump
 Na actively transported into the interstitium by Epithelial Sodium
Channel (ENaC)  cleared by the lymphatic and vascular systems
 Delayed resorption of fetal lung fluid
  lung compliance,  airway resistance
Risk Factors for TTN
 Elective cesarean  Delayed clamping of the
section delivery umbilical cord. (< 45 s)
 Male sex  Breech delivery
 Macrosomia  Fetal polycythemia
 Prolonged labor  Infant of a diabetic mother
 (-) amniotic fluid  Infant of drug-dependent
phosphatidylglycerol mother (narcotics)
 Birth asphyxia  Very low birth weight
neonates
 Fluid overload to the
mother  Exposure to B-mimetic agents

 Maternal asthma
TTN: Diagnostics
Laboratory studies
 Postnatal testing

 Arterial blood gas – mild hypoxia

 Sepsis evaluation

 Radiologic studies / Chest x-ray

TTN Radiographs

 Hyperexpansion of the lungs

 Prominent perihilar streaking (engorgement of periarterial lymphatics)
 Mild to moderately enlarged heart
 Depression (flattening) of the diaphragm
 Fluid in the minor fissure and pleural space
 Prominent pulmonary vascular markings
Management of TTN
 Oxygenation
 Antibiotics – broad spectrum
 Feeding
 < 60 – oral, 60-80 – OGT, >80 – NPO or IV nutrition
 Fluid and electrolytes
 Hyaline Membrane Disease
 RDS Type 1
 Preterm: ~50% of infants with BW 501-1500 g
 incidence is inversely proportional to the gestational age and
birth weight
 incidence and severity of HMD are expected to decrease
after the increase in use of antenatal steroids
 clinical course varies with the size of the infant, severity of
disease, use of surfactant replacement therapy, presence of
infection, degree of shunting of blood through PDA, and
whether or not assisted ventilation was initiated
 Surfactant
 surface-active material produced by type II pneumocytes
 synthesis begins at 24-28 weeks of gestation, appears in the
amniotic fluid at 28-32 weeks, and has reached mature levels
at 35 weeks of gestation
 Maturation delayed by fetal hyperinsulinemia
 Maturity enhanced by the administration of antenatal corticosteroids and
by chronic intrauterine stress
 Phospholipid (75%) and protein (10%)
 lipoprotein is released into the airways, where it functions to
decrease surface tension and maintain alveolar expansion at
physiologic pressures
Clinical Presentation
 Tachypnea
 Grunting: partial closure of the vocal cords to prolong
expiration and develop or maintain some FRC improves
alveolar ventilation
 Nasal flaring
 Retractions  to develop high transpulmonary pressure to
reinflate atelectatic air spaces
 may have cyanosis in room air
Diagnostics
 Chest X-ray - uniform reticulogranular pattern and
peripheral air bronchograms
 ABG
 Sepsis work-up
 Serum glucose and electrolyte levels (hypoglycemia and
hypocalcemia)
Bonsel Grading

SEVERITY GRADE RETICULOGRAM CARDIOTHYMIC AIR

PATTERN SHADOW BRONCHOGRAM
MILD 1 Mild, hazy Clearly defined Perihilar, within CT
generalized shadow
2 Moderate, Still discernible Just past CT
generalized borders
MODERATE 3 Heavier and more Hazy, barely Past 2/3 of lung
confluent discernible
SEVERE 4 White-out lung Up to lung Cardiac borders
fields periphery no longer visible
HMD Radiographs
Management of HMD
 Antenatal corticosteroids
 Administration to the mother of two 12-mg doses of
betamethasone given intramuscularly 24 h apart
 Dexamethasone is no longer recommended (cystic
periventricular leukomalacia ), 6 mg IV q6 x 4 doses
 Continuous fetal monitoring
 assessment of fetal lung maturity before delivery
(lecithin-sphingomyelin [L-S] ratio and
Phosphatidylglycerol), risk of RDS is low if L/S Ratio
>2
Surfactant Therapy
 Surface tension reduction and stabilization of the
alveolar air-water interface
 4 ml/kg
 PROPHYLACTIC THERAPY: (-) Sx, <28 weeks (InSurE)
 EARLY THERAPY: (+) Sx, < 2 hours from delivery and
initiate therapy
 RESCUE THERAPY: > 2 hours from delivery, repeat dose
every 6 hours
 Criteria for repeating surfactant: requiring FiO2 >30% to
maintain O2 sats >95%
 Direct tracheal instillation
 SE: pulmonary hemorrhage, secondary pulmonary
infections, air leak (pneumothorax) after bolus
administration
Meconium Aspiration Syndrome
 Term and post-term infants
 meconium-stained amniotic fluid may be aspirated by the fetus
 presence of meconium in the trachea may cause airway
obstruction as well as an inflammatory response, resulting in
severe respiratory distress
 meconium in an asphyxiated infant <34 weeks' gestation is
unusual and may represent bilious reflux secondary to
intestinal obstruction
Pathophysiology
 Passage of meconium in utero and aspiration of
meconium
 Effects of meconium:
 Chemical pneumonitis-due to release of cytokines and
vasoactive substances
 Ball-valve effect- meconium obstructing the small airways
causing atelectasis
 Persistent pulmonary hypertension-aspirated meconium
leads to vasospasm, hypertrophy of the pulmonary
musculature R-L shunting
Risk Factors
 Postterm pregnancy
 Preeclampsia-eclampsia
 Maternal hypertension
 Maternal diabetes mellitus
 Abnormal fetal heart rate
 Intrauterine growth retardation
 Abnormal biophysical profile
 Oligohydramnios
 Maternal heavy smoking, chronic respiratory, or cardiovascular
disease
Diagnostics
 Radiologic studies
 Hyperinflation of the lung fields and flattened diaphragms
 coarse, irregular patchy infiltrates
 pneumothorax or pneumomediastinum

 Arterial blood gas levels - hypoxemia

 respiratory alkalosis - hyperventilation
 respiratory acidosis (obstruction, atelectasis, and
pneumonitis)
 Cardiac echocardiogram: Pulmonary hypertension with
the resultant hypoxemia from right-to left atrial and
ductal shunt
MAS Radiographs
Management of MAS
 intubation and trachea suctioned using a meconium
aspirator
 Antibiotic coverage
 Meconium inhibits the normally bacteriostatic quality of
amniotic fluid.
 Neonatal Pneumonia
 Inflammatory pulmonary process that may originate in the lung or be a
focal complication of a contiguous or systemic inflammatory process
 Nonspecific defenses: glottis and vocal cords, ciliary escalator, airway
secretions, migratory and fixed phagocytes, nonspecific antimicrobial
proteins and opsonins, and the normal relatively nonpathogenic airway
flora
 Sterile respiratory mucosa at birth, with subsequent uncontested
colonization by microorganisms from the mother or environment
 Increased physical disruption of epithelial and mucous barriers also
occurs
 High oxygen concentrations, generous airway pressures, and large
intrapulmonary gas volumes may interfere with ciliary function and
mucosal integrity
Risk factors for Neonatal Pneumonia
 Unexplained preterm labor
 Rupture of membranes before the onset of labor
 Membrane rupture more than 18 hours before delivery
 Maternal fever (>38°C/100.4°F)
 Uterine tenderness
 Foul-smelling amniotic fluid
 Infection of the maternal genitourinary tract
 Previous infant with neonatal infection
 Nonreassuring fetal well-being test results
 Fetal tachycardia
 Meconium in the amniotic fluid
 Recurrent maternal urinary tract infection
 Gestational history of illness consistent with an organism known to have
transplacental pathogenic potential
Etiologic Agents
 Group B Streptococcus
 Escherichia coli
 Listeria monocytogenes
 Enterococci
 Staphylococcus aureus
 Gram Negative Bacilli
 Cytomegalovirus, Treponema pallidum, Toxoplasma
gondii Chlamydia
Diagnostics
 Chest X-ray
 Sepsis work up
Management
 O2 support
 Antibiotics
 Supportive
 Risk Factors
TTN HMD MAS NP
• CS or prolonged • Prematurity • Postterm • Preterm labor
labor • CS • IUGR • PROM, >18 hours
• Macrosomia • Male sex • Oligohydramnios before delivery
• Fetal polycythemia • Perinatal asphyxia • Maternal • Maternal fever
• Perinatal asphyxia • Chorioamnionitis hypertension, • Maternal UTI
• Maternal sedation • Hydrops preeclampsia- • Fetal tachycardia
and drug • Maternal diabetes eclampsia • Meconium staining
dependence • Maternal DM • Maternal illness
• Maternal asthma • Maternal smoking, with transplacental
and DM CVD, chronic pathogenic
respiratory disease potential
Radiographs

TTN HMD MAS NP

•Hyperaeration •Fine, diffuse •Bilateral, patchy, •Diffuse alveolar
with symmetric reticulogranular coarse infiltrates or interstitial
perihilar and pattern and hyperinflation disease, usually
interstitial streaky (microatelectasis of asymmetric
infiltrates the alveoli) •Pneumatoceles,
•Widening of the •Air bronchograms pleural effusion,
pleural space empyema
•Prominence of the
minor fissure
Clinical Course

TTN HMD MAS NP

• Respiratory • Peaks at 72 hours • Respiratory • May present
distress shortly • Resolves after 5- distress after within 24-72 hrs
after delivery 7 days aspiration of • Resolves after the
• Resolves within 3 meconium medications are
days taking effect
Persistent Pulmonary Hypertension
of the Newborn
 Cardiopulmonary disorder characterized by
systemic arterial hypoxemia secondary to elevated
pulmonary vascular resistance with resultant shunting
of pulmonary blood flow (Right Left shunt: PDA,
PFO) to the systemic circulation
 Term and near-term infants are affected
 Fetal circulation
 Placenta – organ for gas exchange, has a very
low resistance outlet for fetal systemic blood flow.
 Pulmonary Vascular Resistance > Systemic
Vascular Resistance
 RA & RV pressure > LA & LV pressure
 >1/3 of oxygenated blood from
placenta crosses through the
foramen ovale to LA LV and
perfuses head/neck/upper trunk
 Blood from Superior Vena Cava goes to Right
VentriclePulmonary Artery ductus arteriosus
 descending aorta, is mixed w/blood from RV =
lower PO2 to the lower body
 Only 8% of cardiac output perfuses the lungs
 With the loss of the placenta at the time of birth,
systemic vascular resistance increases
Circulatory adaptation
Fetal circulation is characterized by
– Low systemic vascular resistance
– High pulmonary vascular resistance

The post-natal circulation is characterized

– High systemic vascular resistance
– Low pulmonary vascular resistance
Transition at birth
Placental circulation removed  ↑ Systemic Vascular
Resistance  Rapid ↑ Peripheral Blood Flow  ↑
Blood Volume in Left Atrium  ↑ Left Atrial Pressure
> Right Atrial Pressure  closure of foramen ovale

Onset of ventilation ↑ 02 tension in alveolus and

blood  pulmonary vasodilatation  ↓ Pulmonary
Vascular Resistance ~ closure of ductus arteriousus,
redirection of blood into the lungs
Pathophysiology of PPHN
Abnormally Structurally Hypoplastic
Constricted Abnormal Pulmonary
Pulmonary Pulmonary Vasculature
vasculature vasculature
 Meconium  Idiopathic  CDH
Aspiration PPHN  Pulmonary
Syndrome (“black lung hypoplasia
 Pneumonia PPHN” )  Potter’s
normal lung on syndrome
 Respiratory
x-ray
distress
syndrome
MAS
 Most common cause of PPHN
 13% of all live births, meconium stained, 5% develop
MAS
 Recent studies: aspiration in utero
 Pathophysiology:
Meconium  lung injury
- mechanical obstruction of the airways
- chemical pneumonitis ( inflammation)
- activation of complement
- inactivation of surfactant
- vasoconstriction of pulmonary vessels
Idiopathic PPHN
 “black lung”
 Most common in term and near term (>34 wks AOG)
 Autopsy: vessel wall thickening & smooth mm
hyperplasia extending to intra-acinar arteries  no
appropriate pulmonary vasodilation profound
hypoxemia, clear hyperluscent lung fields on CXR
 Pathophysiology:
 under investigation
 Constriction of fetal ductus arteriosus in utero from exposure
to NSAIDs during the last trimester
 Disruptions of the NO-cGMP, PCA-cAMP, endothelin
pathways, ROS
Pulmonary hypoplasia
 Congenital Diaphragmatic Hernia: 1 / 2000-4000 live births
: 8% of all major congenital anomalies
 Herniation of abdominal contents due to a diaphragmatic
defect
 Posterolateral segment, 80% left side
 In utero compression of the lungs produce lung hypoplasia
 CDH develops early in the course of lung development
Clinical Manifestations
 become ill on the 1st 12 HOL
 Severe cyanosis with tachypnea
 Grunting, alar flaring, retractions, tachycardia, shock
 Cardiogenic shock: myocardial ischemia, papillary
mm dysfunction, MR, TR, biventricular dysfunction
 Very labile hypoxia
 CXR findings often out or proportion
Associated factors with PPHN
A. Lung disease : MAS, RDS, pneumonia, pulmo
hypoplasia, cystic lung disease, CCAM, congenital
lobar emphysema, CDH, congenital alveolar
capillary dysplasia
B. Systemic disorders : polycythemia, hypoglycemia,
hypoxia, acidosis, hypocalcemia, hypothermia,
sepsis
Associated factors with PPHN
C. Congenital heart disease: TAPVR, transient
trucuspid insufficiency, CoA, critical aortic stenosis,
endocardial cushion defects, Ebstein’s anomaly,
TGA
D. Perinatal : asphyxia, perinatal hypoxia, maternal
use of NSAIDs
E. Others: neuromuscular diseases, upper airway
obstruction, CNS do
Diagnosis
Hyperventilation test
 Hyperoxic hyperventilation thru ET or bag- mask

ventilation for 10 mins

 >30 mmHg PaO2, lowering PCO2 and inc pH

 Critical pH ~>7.55  dec PVR, less R L shunting

and PaO2 increases
 Used to differentiate with cyanotic CHD
 Diagnosis
Radiography
 Clear lung fields or only minor disease in the face of
severe hypoxemia ( CHD, cyanotic already ruled out)
Echocardiography
 Differentiate with cyanotic CHD

 Cardiac anatomy

 PAP ( systolic flow,TR jet, ductal shunt velocities)

 Shunting, ventricular output

Goals of Treatment
 Improve alveolar oxygenation
 Minimize pulmonary vasoconstriction
 Maintain systemic blood pressure and perfusion
 Consider induction of an alkalotic state
 Consider a trial of vasodilatation
 Consider extracorporeal membrane oxygenation
support
Management
A. Prevention
- adequate resuscitation from birth
- adequate & timely ventilation of asphyxiated
infant
- thermoregulation
B. General Management
- careful fluid mgt, normoglycemia, N calcium, temp
control, pulse oximetry
Management
C. Minimal Handling
 Patients are extremely labile
 ET suctioning
 Less noise
 Less physical manipulation
Management
D. Mechanical Ventilation
 Goal: maintain adequate and stable oxygenation
using the lowest possible mean airway pressures,
PEEP
: achieve optimal lung volume for lung
recruitment while minimizing lung injury
 Before: pH 7.5- 7.55/ pCO2 ~25 mmHg
 Now: Normal Acid base
 FiO2 100% (paO2 90-100 mmHg)
 Gradual weaning
 HFO, ECMO
Management
MAP = (PIP – PEEP) x IT x RR + PEEP
60

Hyperventilation, if possible, should be avoided.

PCO2 should be >30mmHg, 40-50mmHg are
acceptable.
100% oxygenation
Management
D. Surfactant
 With RDS, administration – fall in PVR

E. Pressor agents
 Increase BP will decrease RL shunt
 BP >40 mmHg
 Dopamine – most commonly used
Management
 Dobutamine, epinephrine, milrinone
 Hypotension refractory to inotropes 2 to
desensitization of the CV system to
catecholamines by overwhelming illness and
relative adrenal insufficiency.
 Hydrocortisone rapidly upregulates
cardiovascular adrenergic receptor expression
Management
G. Sedation & paralysis
 Labile patients
 Pancuronium, vecuronium

H. Alkalinization
 Inc pH - pulmonary vasodilatation & rapid
increase in pa02
Management
Pulmonary vasodilators
Inhaled Nitric oxide gas
 Colorless gas
 Relaxes vascular smooth mm
 2 RCT’s: reduce need for ECMO by 40%
 Optimal starting dose: 20ppm
Management

 Reduces PVR improves oxygenation

 Reducing extrapulmonary R to L shunting
 Redirecting blood from poorly aerated lung regions to
better aerated distal air spaces.
 Half-life is seconds
 If OI exceeds 25, iNO should be begun.
 Contraindicated in CHD that is depedent on
R to L shunting across the ductus arteriosus
Other pulmonary vasodilators
 Sildenafil
 Potent and highly specific PDE5 inhibitor
 PDE5 found in high concentrations in the lungs
 Selective pulmonary vasodilator
 Milrinone
 Selective inhibitor of PDE3 in cardiac myocytes &
vascular smooth muscles
 Decrease pulmonary artery pressure and resistance
and to act additively with iNO.
 Recombinant human superoxide dismutase
 Scavenger of ROS
 Augment responsiveness to iNO
 NO & PG signaling pathways in regulation of vascular tone

AA
L-arginine COX-1

NOS
PGH2
Endothelial cell
NO PGIS
iNO
PGI2

Guanylate cyclase Adenylate cyclase

ATP
GTP Smooth muscle cell cAMP
Sildenafil cGMP Milrinone AMP

GMP PDE5
VASODILATION PDE3
High frequency ventilation
 Rapid rates and very low tidal volume
 Decrease risk of barotrauma
 1 Hz ( 1 cycle ) = 60 breaths/min
 PPHN : HFV decreased the need for ECMO 25-
45% cases
ECMO
Extracorporeal membrane oxygenation
 Form of cardiopulmonary bypass that augments

systemic perfusion and provides gas exchange

 Used to patients with poor response to 100%

oxygenation, drugs & MV (5-10% )

 OI (oxygen index) or alveolar-arterial oxygen
gradient used to predict mortality rates >80%
ECMO
Oxygenation Index (OI)
OI= FiO2 x MAP x 100
post ductal PaO2

 > 620 for 8-12hrs and OI > 40 unresponsive of iNO –

predict high mortality
Criteria for ECMO
 Weight >1.8-2kg
 Gestational age >=34 weeks
 No more then 7 days continuous days of assisted
ventilation
 Reversible lung disease
 No major bleeding disorder or major intracranial
hemorhage
 No major cardiac lesion
 Alveolar to arterial oxygen gradient >605-
620mmHg for 4-12h
Criteria for ECMO
 PaO2 <35-50mmHg for 2-12h
 Oxygenation Index (OI) >35-45 for 0.5-6h
 Barotrauma
 Acute deterioration with intractable hypoxemia
 Gestation> 34 weeks
Contraindications

• Major intracranial hemorrhage (> Grade 2 PVH)

• Prolonged asphyxia predicted to cause brain damage

• Lethal congenital abnormality

Complications of ECMO
 IC bleed
 CNS infarction
 Seizures
 Brain death
 Pulmonary hemorrhage
 Hypertension
 Hypotension
 Cardiac tamponade
 Arrhythmias
 Hemolysis
 DIC
 Acute Renal Failure
 Mechanical failure
Prognosis
 Varies with the underlying diagnosis
 Long term outcome is related to HIE and ability to
reduce PVR
NEONATAL SEPSIS
 Neonatal sepsis
 A clinical syndrome of systemic illness accompanied by bacteremia
occuring in the 1st month of life
 3 clinical situations:
1. Early onset – 1st5-7days of life
 With respiratory symptoms
 Acquired the organisms during the intrapartum period from the maternal
genital tract
2. Late onset – after the 1st week of life
 Often with meningitis
 Acquired after birth from the maternal genital tract, human contact or
from contaminated equipment
3. Nosocomial sepsis – occurs in high-risk newborn infants
 Its pathogenesis is related to the underlying illness and debilitation of the
infant, the flora in the NICU and invasive techniques and monitoring
Neonatal sepsis
Causative organisms:
 Primary sepsis usually from the vaginal flora:

 Group B Strep (most common)

 Gram (-) enteric organisms (E. coli)

 Others: Listeria monocytogenes, Staphylococcus, other strep

(including enterococci), anaerobes and H. influenzae
 Nosocomial sepsis:
 Staphylcoccus (S. epidermidis), gram (-) rods (Pseudomonas,
Klebsiella, Serratia, Proteus)
 Fungal organisms
Neonatal sepsis
Risk factors:
 Prematurity and low birth weight

 Rupture of membranes (>18hrs)

 Maternal peripartum fever or infection

 Amniotic fluid problems

 Resuscitation at birth

 Multiple gestation

 Invasive procedures

 Infants with galactosemia (predisposition to E. coli sepsis), immune

defects or asplenia
 Iron therapy

 Low socioeconomic status

Neonatal sepsis
Clinical presentation: nonspecific
 Temperature instability

 Change in behavior

 Skin

 Feeding problems

 Cardiopulmonary

 Metabolic
Neonatal sepsis
 Diagnostics: blood culture and other work-ups
 Treatment:
 Primary sepsis: a penicillin (Ampicillin) +
aminoglycoside (Gentamicin or amikacin)
 Nosocomial sepsis: vancomycin + aminoglycoside or a
3rd gen Cephalosporines
 GBS – a penicillin is the drug of choice with
aminoglycoside for synergism
NECROTIZING ENTEROCOLITIS
Necrotizing Enterocolitis
 An acquired neonatal disorder representing an end expression
of serious intestinal injury after a combination of vascular,
mucosal and metabolic (and other unidentified) insults to a
relatively immature gut (Gomella, 2004)
 Most common acquired abdominal emergency in preterm
infants inquiring intensive care (Roger’s, 2008)
 Characterized by various degrees of mucosal or transmural
necrosis of the intestine (Nelson, 2007)
EPIDEMIOLOGY
 Predominant in preterm infants
 Incidence: 6-10 % in infants weighing <1.5 kg
 Incidence increases with decreasing gestational age
 70-90% occurs in high-risk, low birth weight infants
 10-25% occur in full-term newborns
 Infants with NEC represent 2-5 % of NICU admissions
ETIOLOGY
 Risk Factors
1. Prematurity – single most important risk factor
2. Asphyxia and acute cardiopulmonary distress
3. Enteral Feedings – formula milk
4. Polycythemia and hyperviscosity syndromes
5. Feeding volumes, timing of enteral feeding, and
rapid advancement in enteral feedings
6. Enteric pathogenic microorganisms
PATHOGENESIS

Intestinal
ischemia
(injury)

Pathogenic Enteral nutrition

organisms (metabolic
substrate)
CLINICAL MANIFESTATION

Gastrointestinal Systemic

• Abdominal distention • Lethargy

• Abdominal tenderness • Apnea/respiratory
• Feeding intolerance distress
• Delayed gastric • Temperature instability
emptying • “not right”
• Vomiting • Acidosis (metabolic
• Occult/gross blood in and/or respiratory)
stool • Glucose instability
• Change in stool • Poor perfusion/shock
pattern/diarrhea • Disseminated
• Abdominal mass intravascular coagulation
 MODIFIED BELL’S STAGING CRITERIA
Stage Systemic signs Intestinal signs Radiographic signs Management
I: Suspected NEC Temperature instability, Elevated gastric Normal or mild ileus NPO for 3 days
apnea, bradycardia residuals, mild Antibiotics
abdominal distention, IV fluids, total
occult blood in the parenteral nutrition
stool

IIA: Mild NEC Similar to stage I Prominent abdominal Ileus, dilated bowel NPO and Antibiotics
distention+/- loops with focal for 14 days
tenderness, absent pneumatosis IV fluids, total
bowel sounds, grossly parenteral nutrition,
bloody stools Cardiorespiratory
support, surgical
consultation

IIB: Moderate NEC Mild acidosis and Abdominal wall Extensive pneumatosis, Same as IIA
thrombocytopenia edema and tenderness early ascites, +/-
+/- palpable mass portal venous gas

IIIA: Advanced NEC Respiratory and metabolic Worsening wall edema Prominent ascites, Same as IIA
acidosis, mechanical and erythema with persistent bowel loop, Inotropic and
ventilation, hypotension, induration no free air ventilatory support
oliguria, DIC Monitor UO
IIIB: Advanced NEC Vital signs and laboratory Evidence of Absent bowel gas Surgery (Laparotomy
evidence of deterioration, perforation Pneumoperitoneum or penrose drain)
shock
Pneumatosis intestinalis Pneumoperitoneum
PERINATAL ASPHYXIA
Perinatal Asphyxia
 ACOG Criteria
1. Profound metabolic or mixed acidemia (pH <7) on
umbilical cord arterial blood sample
2. Persistence of an Apgar score of 0-3 for > 5 mins
3. Neurologic manifestations in the immediate neonatal
period - seizures, hypotonia, coma, or HIE
4. Evidence of multi-organ system dysfunction in the
immediate neonatal period
Mechanisms of Asphyxia
 Interruption of umbilical circulation (cord compression)
 Inadequate perfusion of the maternal side of the
placenta (maternal hypotension, hypertension, abN
uterine contractions)
 Impaired maternal oxygenation (cardiopulmonary dse,
anemia)
 Altered placental gas exchange (placenta abruptio,
previa, insufficiency)
 Failure of the neonate to accomplish lung inflation and
transition from fetal to neonatal cardiopulmonary
circulation
 Effects of Asphyxia

Stages of HIE
Clinical Manifestations of HIE

 IUGR w/ increase vascular resistance

 may be 1st indication of fetal hypoxia
 bradycardia; beat-to-beat variability declines

 At delivery

- meconium-staining of amniotic fluid

- depressed infants; fail to breath
- hypotonic, hypertonic or normal
- pallor, cyanosis, apnea, unresponsiveness
 Clinical Manifestations
 Next 24 hrs
- cerebral edema
- profound brainstem depression
- seizure
a. Phenobarbital ( DOC)
- LD 20mg/Kg + 5-10mg/kg
(up to 40-50mg/kg)
-MD 5mg/kg/24h
b. Phenytoin –LD 20mg/Kg
c. Lorazepam- 0.1mg/kg
 Clinical Manifestations

 Heart failure & cardiogenic shock, PPHN, RDS, GI

perforation, hematuria, ATN
 Symptoms may develop over a series of days  serial
neurologic exam
 INITIAL: depressed level of consciousness
 Clinical Manifestations
 Periodic breathing with apnea or bradycardia
 Cranial nerve function – SPARED

(intact PLR & spontaneous eye movt)

 Seizures are common

 Hypotonia (early manifestation)

 Diagnosis
 Ultrasound –limited utility
 CT scans – identification of focal hemorrhagic lesions,
diffuse cortical injury, & damage to the basla ganglia
 MRI- preferred imaging modality

- ability to outline topography

of the lesion
 Amplitude integrated EEG (aEEG)

- good reliability; (+) predictive value – 85%;

detects seizure activity
 Treatment
 Systemic or selective cerebral hypothermia
- decrease rate of apoptosis &
suppresses production of mediators
e.g glutamate, free radicals, NO
 Selective head cooling
- effective in less severe aEEG changes
 supportive care ( adequate oxygenation, BP, acid-base

balance)
Criteria for therapeutic or
neuroprotective hypothermia (Stable)
 Intentional body cooling (between 33.5-34C) for 72hrs
 Reduces mortality rate and in survivors, decreases the
chance that the infant will have major disability
 Should be started w/in 6 hours of birth
1. Infants ≥36 weeks gestation
2. ≥1800 grams
3. Abnormal neurologic exam
4. Blood gas (cord or neonatal w/in 1st hr of life) pH ≤7.0 or
base deficit ≥16
 Rewarming speeds not exceed 0.5C per hour to avoid
sudden vasodilatation and hypotension
 Prognosis of HIE
 Poor -Severe encephalopathy
- flaccid coma, apnea, absent
oculocephalic reflexes, &
refractory seizure
- low apgar score at 20 min.
- persistent abnormal
neurologic signs at 2 wks
 Prognosis of HIE

BRAIN DEATH:
1) coma unresponsive to stimulus
2) apnea w/ PCO2 rising to 40 to over 60mmHg w/o
ventilatory support
3) absent brain stem reflexes
- must occur in the absence of hypothermia,
hypotension and elevated levels of anticonvulsants
INTRAVENTRICULAR
HEMORRHAGE
 Intraventricular hemorrhage

 trauma or asphyxia & rarely, from a primary hemorrhagic

disturbance or congenital vascular anomaly
 assoc with DIC, iso-immune thrombocytopenia,& neonatal
vitamin K deficiency
 Epidemiology

- 30% of PT <1,500 g
- severe (grade 3 or 4) in 5% of 1,250 g-1,500g
- 60-70% in 500 g – 750 g infants
 Intraventricular hemorrhage

 Pathogenesis
 occurs in the gelatinous subependymal germinal matrix
 immature vessels in this highly vascular region + poor
tissue vascular support – predispose PT to hemorrhage
 Predisposing factors:
 prematurity, RDS, hypoxic-ischemic or hypotensive injury,
reperfusion injury of damaged vessels, increased or decreased
cerebral blood flow, reduced vascular integrity, increased
venous pressure, pneumothorax, hypervolemia, & hypertension
 Clinical Manifestations (IVH)
 apnea, pallor, or cyanosis; poor suck; abnormal eye signs; a
high-pitched, shrill cry; muscular twitching, convulsions, or
decreased muscle tone; metabolic acidosis; shock & a
decreased hematocrit or failure of the hematocrit to increase
after transfusion
 rarely present at birth ;

50% - 1st day

75% within 1st 3 days
LATE : days 14-30
Periventricular Leukomalacia (PVL)

 focal, necrotic lesions in the periventricular white matter &/or

more diffuse white matter damage
 due to hypoxia-ischemia, venous obstruction from an IVH,
or undetected fetal stress  decreased perfusion to the brain
 increases in infants w/ severe IVH
 Clinical Manifestations (PVL)

 usually asymptomatic until the neurologic sequelae of white

matter damage become apparent in later infancy (spastic
motor deficits)
 may be present at birth

 usually occurs later as an early echodense phase (3-10

days of life), followed by the typical echolucent (cystic)
phase (14-20 days of life)
 Grading of IVH
Grade I
- bleeding at subependymal area
Grade II
- bleeding within the ventricle but without ventricular
dilatation
Grade III
- IVH with ventricular dilatation
Grade IV
- intraventricular & parenchymal hemorrhage
NORMAL NEONATAL BRAIN , LEFT SAGITTAL SCAN
GRADE I IVH
GRADE II IVH
GRADE III IVH
IVH WITH PERIVENTRICULAR
HEMORRHAGIC INFARCTION
 Diagnosis of IVH
High index of Suspicion
 Cranial Ultrasound

- preterm <34 wks

- <1,000g ( 1st 3-5 days)
-1,001-1,500g (7-14 days)
* ff-up at 35-40wks postmenstrual age
 evaluate PVL (cystic changes may
not be visible for at least 2-4 wks)
 Prognosis of IVH
Grade I and II- normal

Grade III or IV- progressive hydrocephalus, VP shunting,

intraparenchymal hemorrhage and PVL  CP
• Up to 30% of infants with birth weight <1,000 g with
normal cranial ultrasounds have CP or low cognitive
performance at 18 mos adjusted age.
• Most infants with IVH and acute ventricular distention do
not develop post-hemorrhagic hydrocephalus (PHH).
 Prevention of IVH

 judicious mgt of CPD & operative (forceps, vacuum) delivery

 antenatal steroids, IVIG, fetal platelet transfusion;

Caesarian section
- reduce fetal or neonatal hemorrhage caused by maternal
ITP or alloimmune thrombocytopenia
- Antenatal corticosteroids at 24-34wks
 Prevention of IVH

IV Vit K – mothers taking phenobarbital or phenytoin

during pregnancy

 adequate neonatal respiratory status & fld &

electrolytes mgt
 Treatment of IVH
 Symptomatic
Seizures – anti-convulsant
Anemia and coagulopathy
- FFP & PRBC
Shock and acidosis
- Fluids & NaHCO3
Hydrocephalus- VP shunt
 Newborn screening diseases
 Universal Newborn Screening has been recommended by the Philippine
Newborn Screening Program of the Department of Health. The Newborn
Screening Act of 2004
 (RA No. 9288) is an act promulgating a comprehensive policy and a national
system for ensuring newborn screening.
 Newborn Screening (NBS) is a simple procedure usually done on the 24th to
48th hour of life to find out if a neonate has a congenital metabolic disorder
that may lead to mental retardation and even death if left unrecognized and
untreated.
 The goal of newborn screening is to give all newborns a chance to live a
normal life.
 It provides the opportunity for early treatment of diseases that are
diagnosed before symptoms appear.
 Included in the panel of disorders under the Philippine Newborn Screening
Program are: Congenital Hypothyroidism (CH), Congenital Adrenal Hyperplasia
(CAH), Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency, Galactosemia
(Gal), Maple Syrup Urine Disease (MSUD) and Phenylketonuria (PKU).
JAUNDICE
Jaundice

 Benign
Physiologic
Breast Milk
Breastfeeding

 Pathologic
Jaundice
Breastfeeding Jaundice
 Aka “breastfeeding associated jaundice”
 Aka “human milk jaundice syndrome”
 Occurs in 20-30% of all breastfeeding infants
 Fewer calories  increased enteroheptic circulation

Breastmilk Jaundice
 Pregnane-3-alpha-20-beta-diol , a UDP glucuronosyl
transferase inhibitor  decreased conjugation
 Increased Beta glucoronidase  increased enteroheptic
circulation
 Physiologic Jaundice

Increased rbc
Shortened rbc lifespan

Immature hepatic
uptake & conjugation

Increased
enterohepatic
circulation
Pathologic Jaundice

Categories
 Increased bilirubin load
 Decreased conjugation
 Impaired bilirubin excretion
Jaundice
 A search to determine the cause of jaundice should
be made if
 Appears in the 1st 24 h of life
 Serum bilirubin is rising at a rate faster than 5
mg/dL/24h
 Serum bilirubin is > 12mg/dL in fullterm infants (in the
absence of risk factors), or 10-14 mg/dL in preterm
 Jaundice persists after 10-14 days of life

 Direct reacting bilirubin is > 2 mg/dL at any time

 Increased Bilirubin Load

Hemolytic Disease

 Features: elevated reticulocytes, decreased Hgb

 Coomb’s (+) Rh incompatibility, ABO
incompatibility
 Coomb’s (-) G6PD, spherocytosis, pyruvate kinase
deficiency, etc
Hemolysis consider present

 Hct < 45%

 Abnormal blood smear with 3-4+ spherocytes
 Reticulocyte count is 4.5% in the first 72 hrs, or
 Reticulocyte count is >1-2% in the first 1-2 wks
Increased Bilirubin Load
Non-hemolytic Disease

 Features : normal reticulocytes

 Extravascular sources – cephalhematoma

 Polycythemia

 Exaggerated enterohepatic circulation - GI

obstruction
Decreased Bilirubin Conjugation
 Elevated unconjugated bilirubin

 Genetic Disorders
 Crigler-Najjar
 2 types
 Severe hyperbilirubinemia
 Gilbert Syndrome
 Mild hyperbilirubinemia

 Hypothyroidism
Impaired Bilirubin Excretion

 Elevated conjugated bilirubin (> 2 mg/dL or > 20% of

TSB)

 Biliary Obstruction
 Structural
defects – I.e. biliary atresia
 Genetic defects – Rotor’s & Dubin-Johnson syndromes
 10 Commandments of Preventing and
Managing Hyperbilirubinemia
Clinicians should:
 Promote and support successful breastfeeding.
 Establish nursery protocols for the identification and evaluation of hyperbilirubinemia.
 Measure the total serum bilirubin (TSB) or transcutaneous bilirubin (TcB) level on infants
jaundiced in the first 24 hours.
 Recognize that visual estimation of the degree of jaundice can lead to errors, particularly in
darkly pigmented infants.
 Interpret all bilirubin levels according to the infant’s age in hours.
 Recognize that infants at less than 38 weeks’ gestation, particularly those who are breastfed,
are at higher risk of developing hyperbilirubinemia and require closer surveillance and
monitoring.
 Perform a systematic assessment on all infants before discharge for the risk of severe
hyperbilirubinemia.
 Provide parents with written and verbal information about newborn jaundice.
 Provide appropriate follow-up based on the time of discharge and the risk assessment.
 Treat newborns, when indicated, with phototherapy or exchange transfusion.
1 Promote and support
successful breastfeeding
 Clinicians should advise mothers to nurse their infants
at least 8 to 12 times per day for the first several
days

 Poor caloric intake and/or dehydration associated

with inadequate breastfeeding may contribute to
the development of hyperbilirubinemia
2 Establish nursery protocols for the identification and evaluation
of hyperbilirubinemia
Algorithm for the management of jaundice in the newborn nursery
 3 Measure the total serum bilirubin (TSB) or
transcutaneous bilirubin (TcB) level on infants
jaundiced in the first 24 hours.

 Ongoing assessments for risk of developing severe

hyperbilirubinemia
 Monitor at least every 8-12 hours
 Blood testing

 All pregnant women should be tested for ABO and Rh

(D) blood types and have a serum screen for unusual
isoimmune antibodies
Laboratory investigation
Indicated (if bilirubin concentrations reach phototherapy levels)
 Serum TB DB IB

 Blood typing and Coombs’ test

 Hemoglobin and hematocrit determinations

Optional (in specific clinical circumstances)

 CBC with diff count

 Blood smear for red cell morphology

 Reticulocyte count

 Glucose-6-phosphate dehydrogenase screen

 Serum electrolytes and albumin

4 Recognize that visual estimation of the degree
of jaundice can lead to errors, particularly in
darkly pigmented infants

5  Zone 1 head - clavicle 5 mg/dl

1 5  Zone 2 clavicle - umbilicus 6-8 mg/dl

8 Zone 3 umbilicus- knee 9-12 mg/dl

10 12


 Zone 4 knees-ankles 13-15 mg/dl

 Zone 5 palms + soles >15 mg/dl

5 Interpret all bilirubin levels according to
the infant’s age in hours.
 Nomogram for designation of risk in 2840 well newborns at 36 or more weeks'
gestational age with birth weight of 2000 g or more or 35 or more weeks' gestational
age and birth weight of 2500 g or more based on the hour-specific serum bilirubin
values
6 Recognize that infants at less than 38
weeks’ gestation, particularly those who are
breastfed, are at higher risk of developing
hyperbilirubinemia and require closer
surveillance and monitoring
Risk Factors for Severe Hyperbilirubinemia

Major risk factors

 Bilirubin levels in high-risk zone
 Jaundice in 1st 24 hrs
 Blood group incomp with + direct antiglobulin test, other
known hemolytic disease (eg, G6PD deficiency)
 Gestational age 35–36 wk
 Previous sibling received phototherapy
 Cephalohematoma or significant bruising
 Exclusive breastfeeding
 East Asian race
Risk Factors for Severe Hyperbilirubinemia

Minor risk factors

 Bilirubin levels in high intermed-risk zone
 Gestational age 37–38 wk
 Jaundice before discharge
 Previous sibling with jaundice
 Macrosomia infant with diabetic mother
 Maternal age ≥ 25
 Male
Risk Factors for Severe Hyperbilirubinemia

Decreased Risk
 Bilirubin levels in low-risk zone
 ≥ 41 wks gestation
 Exclusive bottle feed
 Black race
 D/c from hospital > 72hrs
 Nomogram for designation of risk in 2840 well newborns at 36 or more weeks'
gestational age with birth weight of 2000 g or more or 35 or more weeks' gestational
age and birth weight of 2500 g or more based on the hour-specific serum bilirubin
values
7 Perform a systematic assessment on all
infants before discharge for the risk of
severe hyperbilirubinemia

8 Provide parents with written and verbal

information about newborn jaundice.

9 Provide appropriate follow-up based on

the time of discharge and the risk
assessment
Discharge
 Close follow-up necessary
 Individualize
based on risk
 Weight, % change from BW, intake, voiding habits,
jaundice

Infant Should be Seen

Discharge by
< 24 hours 72 hours
24-48 hours 96 hours

48-72 hours 120 hours

10 Treat newborns, when
indicated, with phototherapy or
exchange transfusion.
Phototherapy
 Mechanism: converts bilirubin to water soluble form
that is easily excreted
 Forms
 Fluorescent lighting
 Fiberoptic blankets

 Goal is to decrease TSB by 4-5 mg/dL or < 15

mg/dL total
 Breastfed infants are slower to recover
Phototherapy
 Severe rebound hyperbilirubinemia is rare
 Average increase is 1mg/dL
 Intensive
 Special blue tube with light in blue-green spectrum
 Close to infant  10-15cms

 Expose maximum surface area

 Circular phototherapy
Guidelines for phototherapy in hospitalized infants of 35 or more weeks' gestation
Double Volume Exchange Transfusion
(DVET)
 Mechanism: removes bilirubin and antibodies from
circulation and correct anemia
 Most beneficial to infants with hemolysis and sepsis
 Double Volume Exchange Transfusion
(DVET)
Total Volume needed
 Preterm - wt X 100cc X 2

 Term – wt X 80cc X 2

Volume per exchange - Total Volume needed / 40

Number of exchanges - 40
Guidelines for exchange transfusion in hospitalized infants of 35 or more weeks'
gestation
 Complications of Hyperbilirubunemia

 Toxicity to Basal Ganglia and brainstem nuclei

 2 terms
 Acute bilirubin encephalopathy - acute manifestations of
bilirubin toxicity seen in the first weeks after birth
 Kernicterus – chronic and permanent clinical sequelae of
bilirubin toxicity
Human Milk
 Colostrum
 Higher concentration of protein and antibodies
 Transitions around days 3-5

 Mature by day 10
 Distribution of Kcals

Breastmilk Formula

% Protein 6 9

% Fat 52 48

% Carbohydrate 42 42
Protein

Predominant protein of human milk is whey & predominant

protein in cow’s milk is casein
 Casein: proteins of the curd (low solubility at pH 4.6)

 Whey: soluble proteins (remain soluble at pH 4.6)

 Ratio of casein to whey is between 40:60 and 30:70 in

human milk and 82:18 in cow’s milk
 some formulas provide more whey proteins than others
Characteristics and Advantages of
Human Milk
 Low renal solute load
 Immunologic, growth and trophic factors
 Decrease illness, infection, allergy
 Improved digestion and absorbtion
 Nutrient Composition: CHO, Protein, Fatty Acid, etc
 Cost
AAP: Breastfeeding and the Use of
Human Milk, 1997
 “Exclusive breastfeeding is ideal nutrition and
sufficient to support optimal growth and
development for approximately the first 6 months
after birth….It is recommended that breastfeeding
continue for at least 12 months, and thereafter for
as long as mutually desired.”
AAP: Breastfeeding and the Use of
Human Milk, 1997
 Human milk is the preferred feeding for all infants
 Breastfeeding should begin as soon as possible
after birth
 Newborns should be nursed 8 to 12 times every 24
hours until satiety, usually 10 to 15 minutes per
breast. (Crying is a late indicator of hunger.)
AAP: Breastfeeding and the Use of
Human Milk, 1997
 “Should hospitalization of the breastfeeding mother
or infant be necessary, every effort should be made
to maintain breastfeeding preferably directly or by
pumping the breasts.”
AAP: Breastfeeding and the Use of
Human Milk, 1997
 Formal evaluation of breastfeeding by trained
observers at 24-48 hours and again at 48 to 72
hours.
 No supplements should be given unless a medical
indication exists.
 When discharged at <48 hours, should have FU
visit at 2 to 4 days of age, assessment at 5 to 7
days, and be seen at one month.
AAP statement on breastfeeding
(continued)
 Supplements (water, glucose, formula) should be
avoided (unless medically necessary). Pacifiers
should also be avoided.
 Exclusive breastfeeding is ideal for the first 6
months. Breastfeeding should continue for at least
12 months.
AAP statement on breastfeeding
(continued)
 In the first 6 months, water, juice and other foods
are generally unnecessary. Vitamin D and iron may
be needed. Fluoride should not be given during the
first 6 months.
 AAP: Breast milk and allergy

 1.Breast milk is an optimal source of nutrition for infants

through the first year of life or longer. Those breastfeeding
infants who develop symptoms of food allergy may benefit
from:
 a.maternal restriction of cow's milk, egg, fish, peanuts
and tree nuts and if this is unsuccessful,
 b.use of a hypoallergenic (extensively hydrolyzed or if
allergic symptoms persist, a free amino acid-based
formula) as an alternative to breastfeeding.
Breast feeding and allergy
a.Breastfeeding mothers should continue breastfeeding for the
first year of life or longer. During this time, for infants at
risk, hypoallergenic formulas can be used to supplement
breastfeeding. Mothers should eliminate peanuts and tree
nuts (eg, almonds, walnuts, etc) and consider eliminating
eggs, cow's milk, fish, and perhaps other foods from their
diets while nursing. Solid foods should not be introduced into
the diet of high-risk infants until 6 months of age, with dairy
products delayed until 1 year, eggs until 2 years, and
peanuts, nuts, and fish until 3 years of age.
Infant Formula: Categories
 Term vs. Preterm
 Standard Infant Formula
 Cows Milk Based

 Soy Formula

 Specialty Formulas
 Hypoallergenic: Peptide hydrolysates, amino acid
based
 Metabolic Products

 other
Milk Based Formulas
Characteristics
 Blend of Whey and Casein Proteins (8.2-
9.6 % total calories)

 Carbohydrate: lactose
 Fats: long chain
 Meet needs of healthy infant
 Premature Formulas
General Characteristics compared to Standard
 Increased Protein,Vitamins & Minerals

 For infants born at <1.5kg

 up to 2000-2500gm
 Feeding of infants > 2500 gm
 risk of vitamin toxicities

 Premature formulas vary in nutrient content

 WHO/UNICEF TEN STEPS TO SUCCESSFUL
BREASTFEEDING
1. Have a written breastfeeding policy that is routinely communicated to all health
care staff.
2. Train all health care staff in skills necessary to implement this policy.
3. Inform all pregnant women about the benefits and management of
breastfeeding.
4. Help mothers initiate breastfeeding within 1 hour of birth.
5. Show mothers how to breastfeed and how to maintain lactation, even if they are
separated from their infants.
6. Give newborn infants no food or drink other than breast milk, unless medically
indicated.
7. Practice rooming-in—allow mothers and infants to remain together—24 hours a
day.
8. Encourage breastfeeding on demand.
9. Give no artificial teats or pacifiers to breastfeeding infants.
10. Foster the establishment of breastfeeding support groups and refer mothers to
them, on discharge from the hospital or clinic.
THANKS SUPER FOR YOUR
ATTENTION! 