(PEDIA II) 1.01 Neonatology I - Salazar

NEONATOLOGY I
Dr. Salazar, August 10, 2017 1.01

I. PREMATURITY Three important questions!
II. PRETERM BIRTH COMPLICATIONS
III. ASPHYXIA
A. Case
B. Hypoxia, Asphyxia, Ischemia, and HIE
IV. HYPOXIC-ISCHEMIC ENCEPHALOPATHY
V. THERAPEUTIC HYPOTHERMIA
VI. RDS: INTRODUCTION
VII. RESPIRATORY DISTRESS SYNDROME
VIII. APNEA OF PREMATURITY
IX. MECONIUM ASPIRATION SYNDROME
X. PERSISTENT PULMONARY HYPERTENSION OF THE
NEWBORN
XI. TRANSIENT TACHYPNEA OF THE NEWBORN
XII. PULMONARY AIR-LEAK SYNDROME
A. Pulmonary Interstitial emphysema
B. Pneumothorax
C. Pneumomediastinum
D. Pneumopericardium
E. Pneumoperitonium
XIII. NEONATAL SEPSIS
XIV. CONGENITAL VIRAL INFECTIONS
A. Rubella
B. Cytomegalovirus
C. Neonatal Herpes Simplex (1)
D. Parvovirus
E. Varicella-Zoster Virus
F. Neonatal Varicella
G. Zika Virus
XV. NEONATAL JAUNDICE
LEARNING OBJECTIVES
 Perinatal Asphyxia
o To be able to define hypoxia, anoxia, perinatal asphyxia,
ischemia, and HIE
o To discuss Sarnat stages for neurologic presentation
o To discuss Multisystemic effects of severe injury
o To discuss medical management
 Respiratory Distress Syndrome Figure 1. Overview of Newborn Resuscitation. The algorithm
o To review common neonatal respiratory disorders would just show you a step-wise approach with regards to when your
o To discuss the pathophysiology and clinical suppose to deliver your chest compressions, intubation, or giving
manifestations of neonatal respiratory disorders medications. Emergency medications are rarely given at the DR if
you’re good with the initial first steps.
OVERVIEW
th
Nelson, 20 Ed. page 845
 Read prescribed textbooks (Nelson and Navarro). According to Immediately after birth, an infant in need of resuscitation
Dr. Salazar, he only gave an insight of what we need to study. should be placed under a radiant heater and dried (to avoid
 I wanted to review with you first on the overview of newborn passive hypothermia), positioned with the head down and
resuscitation. He will give an URL (No URL provided). slightly extended; the airway should be cleared by suctioning,
 Stabilization at the delivery room is important but taking the and gentle tactile stimulation provided (slapping the foot,
maternal risk factors is more important. The only way to do that rubbing the back). Simultaneously, the infant’s color, heart
is to get a very good antenatal history. Once the patient is at the rate, and respiratory effort should be assessed
DR, it is ideal the place because it has the appropriate equipment The steps in neonatal resuscitation follow the ABCs: A,
and trained personnel to assist to the newborn and the mother. anticipate and establish a patent airway by suctioning and, if
Only 10% of the newborn needs stabilization at the DR. The first necessary, performing endotracheal intubation; B, initiate
few questions you need to ask is “Is this patient term? breathing by using tactile stimulation or positive-pressure
breathing?” There are three questions you need to fulfill. I would ventilation with a bag-and-mask or through an endotracheal
leave to you to review the steps on neonatal resuscitation. tube; C, maintain the circulation with chest compression and
 The reason I wanted to start with the overview for newborn medications, if needed.
resuscitation is its give you an idea with regards with what the Resuscitation with room air in term infants is equally effective
status of the newborn at birth. Are you familiar with APGAR? The and may reduce the risk of hyperoxia, which is associated with
st th
1 and 5 minute of APGAR score will give the state of well- decreased cerebral blood flow and generation of oxygen free
being of that particular neonate. radicals.
1 of 23 | Neonatology I (Gatbonton, Giron, Go, Hou, Ignacio) | Edited by: Sales
1.01 Neonatology I [Dr. Salazar]
 What is the difference between Dubowitz and Ballard?  Necrotizing Enterocolitis (NEC) – attributed secondary to
o Both utilize physical examination, and neurologic ischemic changes, the intestines would have interruption in
examination (passive and active reflexes). If you review your oxygenation and that particular portion becomes necrotic when
table (Ballard), you would see a negative sign. What does it not properly recognized
tell you? That’s utilizing it for your extremely premature  Retinopathy of prematurity (ROP) – secondary to increased
patient. That’s not going to be noted in Dubowitz. oxygenation
See Appendix 1. Ballard Score Chart.  Respiratory Distress Syndrome (RDS) – secondary to surfactant
deficiency
I. PREMATURITY
II. PRETERM BIRTH COMPLICATIONS
 Prematurity is defined as less than 37 weeks of gestation
 Prior to 32 weeks is considered a very premature birth  Respiratory distress syndrome
 Less than 28 weeks is extremely premature  Affects over 50% of premature infants
 The rate of premature single births is slightly increasing each  One of the leading cause of mortality and morbidity
year and that’s because of improvement and advancement in  Ventilator needed in some cases
taking care of the sick preterm. o There is a non-invasive ventilator support and that is with
 Of the babies born preterm: the use of CPAP. It depends on the development of lung.
o 84% are born between 32 and 26 weeks of gestation  Use different techniques to speed up pulmonary maturation or
o about 10% are born between 28 and 31 weeks of gestation assist lung function
o about 6% are born at less than 28 weeks of gestation o Administration of corticosteroids (Both 4 doses,
 The Philippines ranked number 8 for prematurity rate worldwide Betamethasone 12mg every 12 hours and Dexamethasone
next to China and India. 6mg every 6 hours) – Betamethasone is more superior but
 Preterm birth is the leading cause of neonatal mortality more expensive. In the Philippines, we have a good
o Lack of development of body systems is the underlying experience with Dexamethasone plus administration of
cause exogenous surfactant.
Preterm birth is common in high-risk pregnancies.  Reduce risk of RDS by 40-60%
Preterm Premature Rupture of Membranes (PROM) occurs in  Speeds up lung maturation
30-40% of preterm deliveries, and it is a leading identifiable  Max effect more than 24 hour prior to birth within 7
cause of prematurity. days of administration
A strong positive correlation exists between both preterm birth  What used to be a recommendation of giving
and IUGR and low socioeconomic status. Antenatal Dexamethasone on a weekly basis is no
longer recommended because it was found out that it
I-A. TERMINOLOGIES decrease the weight of the brain. Only given when
needed.
 Low birth weight: <2.5kg  Risks to corticosteroids
 Very low birth weight: <1.5kg  Increased susceptibility to infection
 Extremely low birth weight: <1.0kg
 Premature: <37 weeks II-A. CARDIOVASCULAR
 Immature: <28 weeks
 ELGAN: Extremely Low Gestational Age Newborn: <26 weeks  Patent Ductus Arteriosus (PDA) – A heart condition that causes
o Why is it important to even classify these neonates? For blood to divert away from the lungs
prognostication. The lower gestational age is the more  For full-term patients there would be anatomic and physiologic
problem these high-risk neonates will be encountering. closure but among premature patient it does not happen. But
 Small for gestational age: <2.5 percentile there would only be factors that would lead to a
 Lubchenco chart would give you whether the birth weight would hemodynamically unstable ductus of a preterm baby and that
be appropriate for gestational age or not. We all want our would be fluid overload, underlying infection, and hypoxemia.
newborns belong to the category of 1 which is AGA. SGA and Remember, the one that would trigger this ductus to remain
LGA are going to be high-risk. Sometimes they can have both the patent would be hypoxia. The danger in keeping the ductus
same problem like metabolic problem of hypoglycemia. For SGA, patent is the condition that lead to congestion. Keep close
it’s deficiency in your glucose store while in LGA it would be monitoring by PE, note PMI, character of pulses, and BP.
hyperinsulinemia leading to hypoglycemia.  Too low or too high blood pressure
See Appendix 2. Lubchenco Chart.  Low heart rate – often occurs with apnea
I-B. CONCERNS II-B. BLOOD AND METABOLIC
 Increasing morbidity and mortality  Anemia – may require blood transfusion

 Intraventricular hemorrhage (IVH) – due to prematurity o Most common cause: Iatrogenic – the amount of blood that
attributed to the presence of germinal matrix is extracted for diagnostic because only 10% of the total
 Periventricular Leukomalacia (PVL) – because of hypoxia the blood volume (TBV) is allowable. How to compute? Weight x
immature brain would liquify TBV (ex. Patient weighs 1kg multiply to 8 which is the TBV
 Cerebral Palsy – complication as a result of neurodevelopmental then get the 10% )
injury

o Why don’t you want anemia too be a problem? Because it  Necrotizing enterocolitis
would lead to a compensatory mechanism which you would o Cells in bowel are injured
now document in clinic as tachycardia to increase the o Infants who are exclusively breast fed are at a lower risk
cardiac output but in time that patient could go into high- because of the immunologic properties in breast milk.
output failure in contrast to your hypovolemia.  Spontaneous intestinal perforation
 Jaundice – due to immaturity of liver and gastrointestinal
function II-G. IMMUNITY
 Too low or too high levels of minerals and other substances in
the blood such as calcium and glucose (sugar)  Increased susceptibility to infection through childhood
 At birth, this patient would be started in parenteral solution and  Risk of bacterial infection
calcium is incorporated. The dextrosity of the solution for your o Prolonged intensive care
premature baby weighing less than 1kg should not be >10%. o NICU environment
Why? If you give 10% of glucose concentration, it would not be  Immunoglobulin G deficient at birth
tolerated.  Slower development of innate immune defense
 Immature kidney function  Prematurity affects all aspects of immunity
o Immune signaling
II-C. RENAL SYSTEM o Link between adaptive and innate immunity
 Limited neutrophil precursor pool
 Decreased ability to maintain blood pressure o Neutropenia
 Difficult time regulating electrolyte and water balance  Increase bacterial infection
 Water balance in physiology would consist extracellular and
rd
intracellular. By the 3 day of life, there would be contraction of II-H. LONG TERM
ECF compartment and can be clinically translated as patient with
rd
episodes of diuresis. But on the 3 day as well, the respiratory  Cerebral Palsy
distress secondary to surfactant deficiency improves but there is o 40%-50% of patients were born prematurely
no correlation with dieresis and improvement of your RDS. o Condition where infants are unable to control muscle
movement
II-D. NEUROLOGICAL o Affects movement and muscle tone
o Muscles become tight and uncontrolled
 Developmental issues o Results from CNS damage
 Intraventricular hemorrhage  poor circulation
o Blood vessels of the brain are not fully developed  insufficient oxygen and nutrient supply
o Premature infants are at a much higher risk  neural infection
o Increased risk if there are other problems o No treatment for this condition
o There are no prevention  Impaired cognitive skills
 Hydrocephalus – presence of fluid your ventricular system o Lag behind from full-term babies in mental development
 Periventricular leukomalacia - Contributing factors: o More likely to develop learning disabilities
o Premature infant brains are very fragile  Vision problems
o Hypoxia o Retinopathy of prematurity
o Early rupture of fetal membrane  Blood vessels swell and overgrow in the light
o Infection in-utero sensitive nerves of the retina
o Retinal scarring
II-E. THERMOREGULATION o Retinal detachment
 Possible blindness
 You don’t want your patient to be hypothermic because it leads
 Hearing problems
to metabolic acidosis. Review kreb’s cycle  Main Point:
o Increased risk of hearing loss
accumulation of lactic acid which clinically present as metabolic
 Dental problems
acidosis.
o Delayed tooth eruption
 Tend to lose body heat rapidly
o Tooth discoloration
 Less stored fat o Improper alignment of teeth
 At high risk to hypothermia  Behavioral and psychological problems
o Leads to breathing problems and low blood glucose o More likely to develop problems (Correlation of
o No brown fat prematurity with autism)
 Use available energy for heat o Attention deficit hyperactivity disorder (ADHD)
o Hypoglycemia o Depression or anxiety
o Decreased stores of glycogen o Interaction issues
 Chronic health issues
II-F. GASTROINTESTINAL
o Infections
 Immature systems o Asthma
 Majority of the immune system is from the GIT. o Feeding problems

rd
Ig would cross the placenta during the 3 trimester. So, if the o Sudden infant death syndrome
rd
patient would not reach the 3 trimester? There would be no  Possible risk of diabetes and cardiovascular disease such as
passage of the Ig G. More problem in the immunologic dev’t. hypertension

 Barker’s hypothesis is being monitored among these patients.  Infant flaccid with HR 40s. Intubated and chest compressions
What are these? Non-communicable disease. of 4 – 5 minutes. HR recovered without use of epinephrine.
Note: Barker’s hypothesis – IUGR, LBW, and premature birth Emergent UVC (ultraviolet c?) and NSS bolus x2.
have a causal relationship to the origins of hypertension,  Cord ABG 6.71/>130/5
coronary heart disease, and non-insulin dependent diabetes, in  Cord VBG 6.71/>130/26
middle age.  ABG at 30 minutes 6.8/86/65/-21
 Necrotizing enterocolitis  Posturing on exam
o Occurs 3-7 days after onset of feeding  Started passive cooling for HIE and transferred to NICU
o Hypertonicic feeding have a higher risk  Do you see a problem? Indication for cs is there was loss of FHT.
o Premature infants react abnormally to diet
o Bowels becomes inflamed and spontaneously necrose III-A-1. PE
o Treatment:
 Surgical intervention if the bowel is perforated  Flaccid, no response to painful stimuli, no spontaneous
 Feedings are withdrawn movement, no gag reflex, pupils reactive but sluggish and
 Contents of the stomach are suctioned out asymmetric (R>L), no dysmorphic features, no murmur
Diving reflex – when patient is toxic, there is preferential flow of
Table 1.Premature survival rate. The higher the gestational age the blood to vital organs like heart, brain, adrenals, and lungs.
higher the survival rate. Therefore expect that there will be damage due to ischemia in
Gestational age in weeks Survival rate (%) other organs like the kidney.
21 0-4 Anytime the uterus contracts, there is a rebound of fetal heart
22 1-12 tones. In this case, there was no rebound in the baby’s heart
23 8-36 tones which results to the flaccidity in the PE.
24 12-62 III-A-2. LAB RESULTS
25 31-79
26 53-85  Basic metabolic panels within normal limits
 Elevated LFTs (AST 347 ALT 68)
Table 2. Injury of ELGANs 1972-1990.  Elevated lactic acid (16.8)
<26 weeks <800 grams  Hyperglycemic >200
Minimal retardation 14% 14%  Slightly elevated coagulation parameters (PT 21 PTT50
Cerebral palsy 12% 8% Fibrinogen within normal limits)
Blindness 8% 8%  Urine dipstick 2+ protein 3+ blood
Deafness 3% 3%
“Major disability” 22% 24% III-A-3. HOSPITAL COURSE
Survival increased, however rate of injury was constant
 Respiratory: Required mechanical ventilation until withdrawal
of care
Best treatment for prematurity is PREVENTION of prematurity.
 FEN/GI/Renal: NPO, fluid retention with oliguria and elevated
Take care of the mother.
LFTs, developed bloody stools on DOL7 with presumed
II-I. SCHOOL PROBLEMS Necrotizing Enterocolitis (NEC)
 Cardiovascular: Hemodynamically stable
 A Dutch study showed that >50% with BW <1500 gram needed  ID: Treated with antibiotics for possible sepsis / meningitis,
extra support at school treatment continued for ?NEC
 Preterm infants have to be followed-up at least till school age  Heme: Few blood products required, coagulation parameters
because these problems have a late debut. Learning problems improved
picked up around 8 years.  Neurology
o ADHD o Therapeutic hypothermia x 72 hours
o Hyperactivity o HUS on DOL1 was within normal limits
o Intellectual problems (arithmetic, solving problems, o Low amplitude on aEEG initially then developed burst
cognitive functions) suppression pattern
o Short term memory o Phenobarbital was prescribed
o Coordinate problems o MRI spec on DOL4 showed severe and profound hypoxic
o Behavioral problems (shy, sport performance, socialize) brain injury with diffuse cytotoxic edema and extensive
o Boys > Girls lactate peaks.
o Low socioeconomic conditions The burst suppression pattern (will be talked about in more detail
later) is important because its presence indicates that this is a
III. ASPHYXIA case of HIE rather than an inborn error of metabolism
 Infant died within 24 hours after complete withdrawal of
III-A. CASE care
 3.5kg 39wk HF via emergent C/S for prolonged deceleration

and loss of fetal heart tones
 APGAR 1, 2, 2, 2, 5

III-A-4. AUTOPSY IV-D. MECHANISM OF INJURY

 Severe global diffuse hypoxic ischemic brain injury with neuron  Primary energy failure
loss in cerebral gray and white matter, basal ganglia, o There is a reduction in cerebral blood flow and oxygen /
cerebellum, and brain stem substrates
 No evidence of meningitis and encephalitis  Latent: “Therapeutic Window”
 Few changes of ATN in kidneys o Time when we can institute our intervention
 No gross or microscopic evidence of necrotizing enterocolitis  Secondary energy failure
(NEC), mild hepatocellular steatosis c/w hypoxic injury o The pathogenesis is not well understood but it is posited
 Placental slides with acute chorioamnionitis and funisitis with to be a combination of metabolic and neuronal loss after
acute umbilical phlebitis and arteritis indicating fetal infection primary injury
So in this case, there is an additional step in our Prolonged
III-B. HYPOXIA, ASPHYXIA, ISCHEMIA, AND HIE Hypoxia > Asphyxia > Ischemia paradigm. After ischemia, there is
a shift from aerobic to anaerobic glucogenesis to try and keep up
 Hypoxia and Anoxia – either partial or complete lack of with the body’s energy needs which leads to lactic acid
oxygen to the brain or blood production
 Asphyxia – when placental or fetal gas exchange is
compromised IV-E. PRODUCTION OF LACTATE
 Ischemia – when blood flow to an organ is compromised
leading to further decreased oxygen and substrate delivery  Brain consumes ~15% of the total energy generated in the
These terms are related in such a way that one condition body
eventually leads to the others. Prolonged hypoxia leads to  Most of the energy is used by the neurons to maintain ionic
asphyxia which eventually leads to ischemia gradients
o This is important for conductivity and synaptic function
IV. HYPOXIC ISCHEMIC ENCEPHALOPATHY (HIE)  Energy for these functions are derived from hydrolysis of ATP
o usually from oxidative phosphorylation of glucose
IV-A. CRITERIA FOR DIAGNOSIS  During hypoxia, anaerobic glycolysis is used as backup
HOWEVER
 Presence or absence of abnormal fetal heart rate  It is insufficient to meet the energy needs (3 ATP produced
 Cord pH <7 and / or BE > -12 from anaerobic vs. 36ATP formed from aerobic) which leads to
 5 minute Apgar score of 3 or less overproduction of lactic acid.
 Early onset of neurologic sequelae
o Like altered tone, coma, or seizures in infants ≥ 34 weeks
 Multiple Organ Dysfunction (heart, lungs, kidney, GI, and
hematologic changes)
IV-B. EPIDEMIOLOGY
 Occurs in 1 – 6% per 1000 live births in developed countries
 Up to ~50% asphyxiated infants with HIE die in the neonatal
period (first 28 days of life)
 25% of survivors with permanent neurodevelopmental injuries
like cerebral palsy and mental retardation
IV-C. RISK FACTORS

 Antepartum Risk Factors Figure 2. Illustration of Mechanism of Injury of HIE. It is very
o IUGR important to administer the intervention WITHIN 6 HOURS of the
o Severe pre – eclampsia insult. Further discussion of the diagram would be found in the
o Post dates following bullets.
o Abnormal appearance of the placenta
o Diabetes  Cellular injury / death (Initial primary phase) by release of
 Intrapartum Risk Factors excitatory amino acids
o Maternal Fever o Release of glutamate
o Emergency C/S  This release of excitatory amino acids is also the
o Operative VD reason why the patient would present with seizures
o Acute placenta or UC events (abruption / uterine rupture, o Influx of Calcium ions
tight nuchal cord, cord prolapse)  Apoptosis and Tissue injury (delayed secondary phase)
 Postpartum risk factors includes:
o Neonatal respiratory failure (severe RDS, MAS, o Release of glutamate
pneumonia) o Activation of catabolic enzymes (proteases,
o PPHN phospholipases, endonucleases, caspaces)
o A low perfusion state (septic shock) o Production of NO
o Cyanotic CHD o Release of oxygen – free – radicals (ROS)
IV-J. OUTCOMES
 3 clinical parameters predict death or severe disability:
o Chest compression for >1 minute
o Onset of regular respirations >30 minutes after birth
o Base deficit of >16 mmol/L on any blood gas analysis
within the first four hours from birth
 Range of Neurodevelopmental Injuries in HIE patients
o Mild
 Learning difficulties; attention deficit disorder
o Severe / disabling
 Cerebral Palsy; epilepsy, hearing / visual impairment
 severe cognitive and developmental disorders
Table 3. HIE-Outcomes.
Figure 3. Mechanisms of Damage in Fetal / Neonatal Model of Severity of Mild Moderate Severe
Hypoxia – Ischemia. Encephalopathy (Stage I) (Stage II) (Stage III)
EEG Normal Low Isoelectric Burst
IV-F. DURATION AND DAMAGE voltage Suppression
 Absolute duration of HI before brain injury occurs in the human Outcomes 100% 80% 100% Severe
fetus or infant is not known. Normal Normal Sequelae
 FT NB monkeys can sustain up to 10 minutes of complete and 15% CP > CP, MR
up to 30 minutes of incomplete ischemia before suffering (spastic) Epilepsy
permanent brain injury Deafness
Blindness
 Thus, the American Association of Pediatrics states you can
end resuscitation after 10 – 15 minutes of FULL resuscitation 7% Hearing
o Physicians used to resuscitate for 30 minutes to an hour but Loss
evidence shows that we can only do so much and the 8% Seizure
chances of saving a nonresponsive patient after 10 – 15 D/o
minutes are negligible. 3% Visual
IV-G. DIAGNOSIS V. THERAPEUTIC HYPOTHERMIA
 Diagnosis of HIE is made from:  Clinical reports of intact survival from prolonged cardiac arrest
o Perinatal history due to accidental cold water immersion convinced
o PE investigators that therapeutic hypothermia might work
o Metabolic Changes  Neuroprotection with hypothermia is temperature – specific,
o Respiratory failure with progressively increased protection associated with
o Presence of Seizure increasing depth of temperature.
o HUS, CT, +/- MRI
o +/- EEG V-A. MECHANISM
IV-H. STAGING  The mechanism of protection has been documented by many

modalities:
 Sarnat Staging – scoring system devised to help predict an o decrease in brain energy utilization measure by MRI spec
infant’s subsequent risk for neurodevelopmental injury (NDI) o reduced infarct size
See Appendix 3. HIE – Staging o decreased neuronal cell loss
Take note of the isopotential phases found on the severe (stage 3) o retention of sensory motor function
column on EEG findings. Another name for this is the isoelectric o preservation of hippocampal structures
burst suppression, which, as we have mentioned earlier, o recovery of EEG activity
differentiates hypoxic ischemia from errors of metabolism.
IV-I. SEIZURES IN INFANTS

 Most occur at 12 – 24 hours of age and resolves by 5 – 7 days
 Often are refractory to anticonvulsant treatment
 Majority are focal (eye or tongue twitching) but can be
multifocal and myoclonic
 Need to rule out metabolic deficiencies like low calcium,
glucose, or magnesium
 Treatment: Phenobarbital>Fosphenytoin>Ativan
Figure 4. Mechanism of Action of Hypothermia.

V-B. ADVERSE EFFECTS VI. RDS: INTRODUCTION

 Bradycardia VI-A. LUNG DEVELOPMENTAL ANATOMY
 Prolonged QT interval
 Thrombocytopenia  Assessment of the respiratory system includes the assessment
 Skin breakdown of other organ systems.
 Hypocalcemia  When we talk about respiratory distress syndrome, we talk
 Hypokalemia about its lung development.
 Metabolic acidosis  Studying the lung developmental anatomy gives us a better
 Coagulopathy understanding not only on congenital malformation, but like
 Clotting respiratory distress syndrome that is secondary to surfactant
 PPHN deficiency.
 Hypotension
V-C. INDICATIONS
 Physiologic criteria
st
o BG (cord or any blood gas 1 hr pH <7 or BE < 16)
o No BG or pH 7-7.15 or BE 10 – 15.9 with an acute event
and…
 10 minute Apgar <5
 Continued need for ventilation initiated at birth and
continued for at least 10 minutes. Figure 6. Stages of Pulmonary Development. Embryonic,
 Neurologic Criteria Pseudoglandular, Canalicular, Saccular, Alveolar
o Presence of seizures: automatic inclusion
o Physical exam consistent with moderate to severe VI-A-1. EMBRYONIC (26 days of gestation)
encephalopathy in 3 of the 6 categories.
 Appears as a protrusion of the foregut
V-D. RATIONALE  Initial branching of the lung occurs at 33 days gestation
forming the prospective main bronchi, which begin to extend
 Why start before 6 hours? into the mesenchyme
o Length of the “therapeutic window” for intervention in  Further branching forms the segmental bronchi as the lung
animal model enters the next stage of development
o
 Why cool to core temperature of 33.5 C?
o Animal studies: attenuation of brain injury at this VI-A-2. PSEUDOGLANDULAR (7th – 16th week of gestation)
temperature occurred without adverse effects seen at
 15 to 20 generations of airway branching occur starting from
lower temperatures
the main segmental bronchi and ending as terminal
 Why continue for 72 hours? bronchioles.
o No evidence to support benefit of shorter or longer
 At the end of this stage, the airways are surrounded by a
duration
loosely packed mesenchyme, which includes a few blood
V-E. TYPES OF COOLING vessels, and is lined by glycogen-rich and morphologically
undifferentiated epithelial cells with a columnar to cuboidal
 Whole body vs Selective Head Cooling shape.
 Therapeutic hypothermia significantly reduced the risk of  Epithelial differentiation is centrifugal so the most distal are
death or disability at 18 months lined with undifferentiated cells with progressive epithelial
 Less adverse effects with head cooling differentiation of the more proximal airways.
 Whole body cooling provides homogenous cooling to all brain
structures, including central brain
Figure 7. Stage of Lung Development.

Figure 5. Stage of HIE and response to Therapeutic hypothermia.

VI-A-3. CANALICULAR (16th – 25th week of gestation)  In your endoplasmic reticulum and golgi apparatus, your
surfactant is being produced by your active transport mechanism
 Transition from previable to a potential viable lung occurs as (exocytosis). The surfactant will line your alveoli that prevent its
the respiratory bronchioles and alveolar ducts of the gas collapse. If your lungs collapse there would be hypoxia which
exchange region of the lungs are formed. would lead to metabolic acidosis.
 Surrounding mesenchyme becomes more vascular and
condenses around the airways. The closer vascular proximity VI-B-1. SURFACTANT
ultimately results in fusion of the capillary and epithelial
 Lipids (phospholipids) (90%)
basement membranes.
o 70% Phosphaidylcholine
 After 20 weeks gestation, cuboidal epithelial cells being to
o 60% desaturated palmtoylphosphatidyl choline, the
differentiate into alveolar type II cells with formation of
major surfactant tension lowering component
cytoplasmic lamellar bodies. The glycogen in these cells is used
for surfactant production, which is stored in lamellar bodies.  Protein (10%: Four surfactant-specific proteins) – spreading
 This is when you consider surfactant production and the facto; keeps alveoli distended
administration of antenatal steroids. o Hydrophobic: SP-B and SP-C
o Hydrophilic: SP-A and SP-D
VI-A-4. SACCULAR (about 24th week of gestation)  If you want to test these in the delivery room, you get a sample of
the amniotic fluid and do a shake test. Shake the amniotic fluid
 There is potential for viability because gas exchange is possible and take note of the bubbles that would be formed in the upper
due to the presence of large and primitive forms of the future meniscus. The more bubbles there are, the more mature that lung
alveoli is going to be. But you still need to rely with your PE.
 Formation of alveoli (i.e. alveolarization) occurs by the
outgrowth of septae that subdivide terminal saccules into VI-B-2. TYPES OF SURFACTANT PROTEINS
anatomic alveoli, where air exchange occurs (APOPROTEINS) * lifted from 2018 trans
 Number of alveoli in each lung increases from zero at 32 week
gestation to between 50 and 150 million alveoli in term infants A. SP-A
and 300 million adults  Innate host defense protein and a regulator of inflammation
 Alveolar growth continues for at least two years after giving in the lung
birth at term  Facilitates phagocytosis of pathogens ad their clearance from
 Prematurity becomes an issue for your bronchopulmonary the airspace by macrophages
dysplasia (BPD) because it will halt the development of the  Patients with a deficiency of SP-A have not been identified
pulmonary system.  SP-A levels are low in surfactant from preterm lungs and
 BPD - chronic condition that usually is a result of an immature increase with corticosteroid exposure
lung being forced to open by the pressure being delivered, thus  Mice that lack SP-A have normal lung function and surfactant
destroying the histological architecture of the lung. metabolism indicating that SP-A is not critical to the
regulation of surfactant metabolism
VI-A-5. TERMINAL SAC PHASE  SP-A is not present in currently available surfactants used for
(27th to 36th week of gestation) treatment of RDS
 Refinement of the acini B. SP-B:

 Rudimentary primary saccules divide to subsaccules and alveoli
 facilitates aDsorption
 Capillary invasion
 Development of the surfactant system
C. SP-C
 Surfactant present in amniotic fluid between 28th and 32nd
 This has no bearing for us.
weeks of gestation.
 Deficiency (humans) do not have respiratory distress at birth,
VI-B. PULMONARY SURFACTANT but develop progressive interstitial pulmonary fibrosis as
infants and into early childhood.
 SP-C (animal model) deficient mice have normal lung and
surfactant function at birth the mice develop progressive
interstitial lung disease and emphysema as they age
(misprocessed SP-C results in SP-C deficiency in the airspaces
and injury to the type II cell)
NOTE: SP-B + SP-C work cooperatively to optimize rapid

adsorption and spreading of phospholipids on a surface and
to facilitate surface tension lowering and alveolar stability
on surface area compression at low lung volume.
D. SP-D
 Functions as an innate host defense molecule by binding
pathogens and facilitating their clearance.
Figure 8. Metabolism.Surfactant.

 Absence of SP-D results in increased surfactant lipid pools in  Use of accessory muscles
the airspaces and emphysema, but no major deficits in  Nasal flaring
surfactant function in mice.  Atelectasis and respiratory failure progress, symptoms
 Treatment of preterm lambs with recombinant surfactant worsen with cyanosis, lethargy, irregular breathing, and apnea
protein D has been shown to inhibit lung inflammation, which  On examination, breath sounds are decreased. Peripheral
reduces surfactant inactivation, and may hold promise for pulses may be decreased with peripheral extremity edema and
future human investigation. decreased urine output.
 All these are available in surfactant preparations. Because part of
the management of surfactant deficiency would be the VII-B. ETIOLOGY
exogenous administration of your surfactant which is either done
to all premature babies (prophylactic) or whenever the patient  Surfactant is not produced in adequate amounts until relatively
becomes symptomatic (rescue). late in gestation: thus, risk of RDS increases with greater
 The limiting factor of its usage is its cost (Php 25,000-30,000). prematurity.
 It does not assure you that this would lessen the complications. It  That is the reason why there is going to be respiratory distress,
only shortens the time you put the patient on ventilation. atelectasis and clinical sign and symptoms
 When doing PE, there is decreased air entry.
VI-B-3. SYNTHESIS, SECRETION, AND ADSORPTION  When you do X-ray, you’ll see a ground-glass or white lung
appearance.
Synthesis of surfactant depends in part on normal pH,  Other risk factors include maternal factors (multifetal
temperature and perfusion (Nelson, p851). pregnancies, maternal diabetes), labor (cesarean delivery,
Asphyxia, hypoxemia, and pulmonary ischemia (particularly in precipitous delivery), and neonatal factors (asphyxia, cold
association with hypovolemia, hypotension, and cold stress) stress, being male and white).
may suppress surfactant synthesis (Nelson, p851). Race and gender is a factor. Incidence is highest in preterm
 Surfactant is synthesized within the alveolar type II cells male or white infants (Nelson, p850).
starting with phospholipid synthesis in the endoplasmic  Females have a lower mortality risk at birth but may become
reticulum, and then is processed through the Golgi apparatus sickly later on
to the lamellar bodies.  Males have a higher mortality risk, but if they survive, they are
 Phospholipids combine with the surfactant proteins SP-B less likely to get sick later on.
and SP-C to form the surfactant lipoprotein complex within  Risk decreases with fetal growth restriction, pre-eclampsia or
the lamellar bodies. eclampsia, maternal hypertension, prolonged rupture of
 Lamellar bodies localize to the apical surface of the type II cell membranes, and maternal corticosteroid use.
and are released by exocytosis and line your alveoli.  Stress enhances the development of your surfactant.
 Type II cells with lamellar bodies appear in the human lung  Rare cases are hereditary, caused by mutations in surfactant
after 22 weeks with very little surfactant protein mRNA protein (SP-B and SP-C) and ATP-binding cassette transporter
expression until later in gestation. A3 (ABCA3) genes.
 Expression of the four surfactant proteins varies with
gestational age: VII-C. PATHOPHYSIOLOGY
o SP-A increases after 32 weeks gestation
o SP-B increases after 34 weeks gestation  Pulmonary surfactant is a mixture of phospholipids and
o SP-C is highly expressed at the tip of branching lipoproteins secreted by type II pneumocytes
o airways during early lung development  It diminishes the surface tension of the water film that lines
o Expression of SP-D in mRNA is low until late gestation alveoli, thereby decreasing the tendency of alveoli to collapse
and the work required to inflate them
VII. RESPIRATORY DISTRESS SYNDROME
VII-D. PATHOGENESIS
Also known as Hyaline Membrane Disease
 Caused by pulmonary surfactant deficiency in the lungs of
neonates
 Most commonly in those born at <37 weeks gestation
 Risk increases with degree of prematurity
 Neonates weighing <1000g may have lungs so stiff that they
are unable to initiate or sustain respirations in the delivery
room
VII-A. SIGNS AND SYMPTOMS

 Rapid, labored, grunting respirations appearing immediately
or within a few hours after delivery
 Tachypnea increases RR and all these are efforts to increase
oxygenation.
 Grunting respirations – forced expiration against a closed
Figure 9. Pathogenesis of RDS. The pathogenesis of RDS, the
glottis, which distends your alveoli in order to increase
multi-factors, and the sequence of events that occurs.
oxygenation. But because of the size of these patients, they
eventually tire out.
 Surfactant deficiency, the lungs become diffusely atelactic, VII-F. CLINICAL PICTURE
triggering inflammation and pulmonary edema.
 Because blood passing through the atelactic portions of lung
is not oxygenated (forming a right-to-left intrapulmonary
shunt) infant becomes hypoxemic.
 Lung compliance is decreased, thereby increasing the work
of breathing. That’s why you see retractions, the use of
accessory muscles, in these patients.
 In severe cases, the diaphragm and intercostal muscles
fatigue, and CO2 retention and respiratory acidosis develop
VII-E. COMPLIANCE
Figure 11. Chest x-ray.

 This is the clinical picture where you can visualize the
retractions. This is what you would see in the X-ray. When you
auscultate, there would be decreased air entry.
Figure 10. Lung Compliance.
 The normal lung would need a very small pressure to inflate. But
in sick or premature babies, you need a higher pressure to distend
that volume. This is what you see in your volume-pressure curve.
Alveolar atelectasis hyaline membrane formation, and
interstitial edema make the lungs less complaint in RDS, so
great pressure is required to expand the alveoli and small
airways (Nelson, p851).
 Low compliance: stiff lungs, extra work is required to bring
in a normal volume of air
The chest wall of the preterm infant however is highly
compliant, which offers less resistance than that of the mature
infant to the natural tendency of the lungs to collapse (Nelson,
p851).
Deficient synthesis or release of surfactant, together with small
respiratory units and a compliant chest wall, produces Figure 12. Histology.
atelectasis and results in perfused but not ventilated alveoli,  This is your air bronchogram where it depicts the histologic
causing hypoxia (Nelson, p.851). picture of the hyaline membrane, named after the dye it was
Decreased lung compliance, small tidal volumes, increased used to name its appearance.
physiologic dead space, ad insufficient alveolar ventilation
eventually results in hypercapnia (Nelson, p851).
The combination of hypercapnia, hypoxia, and acidosis
produces pulmonary arterial vasoconstriction with increased
right-to-left shunting through the foramen ovale and ductus
arteriosus and within the lung itself (Nelson, 851).
Progressive injury to epithelial and endothelial cells from
atelectasis, volutrauma, ischemic injury, and oxygen toxicity
results in effusion of proteinaceous material into the alveolar
spaces (Nelson, p851).
Figure 13. Illustration of Silverman-Anderson Score. The higher

the score, the more severe the respiratory condition of you rpatient.
The graphic representation (below) can tell you to observe the chest
rise (the upper and lower parts), retractions, dilatation of nares, and
the grunting (audible or noted only on auscultation). These would be
indications of severity of respiratory distress.

VII-G. DIAGNOSIS  Severe hypoxemia can result in multiple organ failure and
death
 Clinical presentation Warm humidified oxygen should be provided at a
 Recognition of risk factors concentration initially sufficient to keep arterial oxygen
 ABG’s showing hypoxemia and hypercapnia; and chest x-ray pressure at 50-70mmHg (91-95% saturation) (Nelson,
 Blood gas is going to reveal the patient is hypoxemic because p853)
of the atelectasis. CO2 would accumulate causing the acidosis. If oxygen saturation cannot be kept >90% at inspired
 Chest x-ray shows diffuse atelectasis classically described as oxygen concentrations of 40-70% or greater, applying
having a ground-glass appearance with visible air CPAP at a pressure of 5-10cm H2O via nasal prongs is
bronchograms; appearance correlates loosely with clinical indicated (Nelson, p853).
severity. Alternative approach: Intubate the preterm infant,
 Expectation on PE: decreased breath sounds on both lung fields. administer intratracheal surfactant, and then extubate the
 RDS can be anticipated prenatally using tests of fetal lung infant and begin CPAP (Nelson, p853).
maturity, which measure surfactant obtained by amniocentesis  Specific treatment is Intratracheal Surfactant Therapy
or collected from the vagina. o Requires endotracheal intubation, which also may be
 Risk of RDS is low when: necessary to achieve adequate ventilation.
o Lecithin/sphingomyelin ratio is > 2 Repeated dosing is given every 6-12hours for a total of 2-4
o Phosphatidyl glycerol is present doses, depending on the preparation (Nelson, p854).
o Foam stability index = 47. Surfactant albumin o Surfactant therapy is associated with significant decrease
ratio(measured by fluorescence polarization) is >55mg/g in duration of mechanical ventilation, lesser incidence of
o Combination air leak syndromes, and lower incidence of
bronchopulmonary dysplasia.
Infants with respiratory failure or persistent apnea require
assisted mechanical ventilation (Nelson, p853).
o Reasonable measures of respiratory failure are:
 Arterial blood pH <7.20
 Arterial blood PCO2 of 60mmHg or higher
 Oxygen saturation <90% at oxygen concentrations of
40-70% and CPAP of 5-10cm H2O
o Intermittent positive pressure ventilation delivered by
time-cycled, pressure-limited, continuous flow ventilators
is a common method of conventional ventilation for
newborns
o Goal of mechanical ventilation: to improve oxygen and
eliminate CO2 without causing pulmonary injury or
Figure 14. Left: Patient with severe RDS; Right: Patient with
toxicity.
intubation which cleared up the patient’s condition
VII-H. TREATMENT VII-I. PREVENTION

 When a fetus must be delivered between 24 weeks and
 Prognosis with treatment is excellent; mortality <10%
34weeks, giving the mother
 With adequate ventilator support alone, surfactant production
o 2 doses of betamethasone 12mg IM 24 hours apart
eventually begins, and once production begins RDS resolves
o 4 doses of dexamethasone 6mg IV or IM q12h at least 48
within 4 or 5 days
hours before delivery
o Resolution may start on the 3rd day, but often times are
Betamethasone is preferred because it reduces neonatal
associated with diuresis of your patient.
mortality to a greater extent as compared to dexamethasone
Because most cases of RDS are self-limited the goal of
(Nelson p852).
treatment is to minimize abnormal physiologic variations
 But recent drawback of betamethasone is its cost.
and superimposed iatrogenic problems (Nelson, p853).
Dexamethasone is cheaper and has the same benefits as
 General principles for supportive care of any premature infant
betamethasone, but coupled with the exogenous surfactant,
should be adhered to.
the outcome is better.
o Avoid hypothermia and minimize oxygen consumption,
 Antenatal steroids – induces fetal surfactant production and
infant should be placed in an incubator or radiant warmer.
o reduces the risk of RDS or decreases its severity
Core temperature (36.5-37 C) should be maintained.
o Calories and fluids should be initially provided by IV.  The administration of antenatal glucocorticoids reduces the
 First 24 hours: 10% glucose solution with additional risk of RDS in premature infants because:
amino acids in extremely premature infants via o Improves neonatal lung function by enhancing
peripheral vein at rate of 65-75mL/24hours maturational changes in lung architecture by inducing
 Electrolytes should be added on day 2 in the most enzymes that stimulate phospholipid synthesis and
mature infants, and on days 3-7 in the more release of surfactant.
immature ones CPAP started at birth is as effective as prophylactic or early
o Fluid volume is increased gradually over the first week. surfactant and is the approach of choice for the delivery room
Excessive fluids (>140mL/kg) contribute to the management of a preterm neonate as risk for RDS (Nelson,
development of PDA and BPD. p852).

VII-J. PROGNOSIS VIII-C. DIAGNOSIS

 Antenatal steroids, postnatal surfactant use, and improved  Attributable to immature respiratory control mechanisms
modes of ventilation have resulted in low mortality from RDS  Can be a sign of major infectious, metabolic,
(~10%) thermoregulatory, respiratory, cardiac, GI, or CNS dysfunction
 Mortality increases with decreased gestational age.  Careful history, physical assessment
 Optimal results depend on the availability of experienced and  Diagnosis of apnea is usually made by
skilled personnel, care in specially designed and organized o Visual observation
regional hospital units, proper equipment, and lack of o Use of impedence – type cardiorespiratory monitors used
complications such as severe asphyxia, intracranial continuously during assessment and ongoing care of
hemorrhage, or irremediable congenital malformation. preterm infants
 Surfactant therapy has reduced mortality from RDS by o Multichannel recordings of multiple physiologic
approximately 40% parameters (e.g. chest wall movement, airflow, O2
 BPD mortality ranges from 10-25% saturation, heart rate, brain electric activity) take for up to
 Highest in infants who remain ventilator dependent for longer 24h can be used as adjuncts for diagnosis and planning
than 6 months and monitoring treatment
 Outlook is much better for those weighing >1500g.
 Long-term prognosis of pulmonary function in most infants VIII-D. CAFFEINE AS TREATMENT
surviving RDS is excellent.
 Caffeine is not available in the Philippines. You can get it in
 Poor prognosis signs: Prolonged ventilation, IVH, pulmonary, Singapore.
hypertension, cor pulmonale, and oxygen dependence beyond
 Caffeine is the safest and most commonly used respiratory
1 year of life.
stimulant drug
o Caffeine base (LD: 10mg/kg; MD: 2.5mg/kg po q24h)
VIII. APNEA OF PREMATURITY
o Caffeine citrate, a caffeine salt that is 50% caffeine (LD
 Defined as respiratory pauses 20mg/kg; MD5 to 10 mg/kg q 24h)
o > 20 sec or airflow interruption and respiratory pauses  Caffeine is preferred because of ease of administration, fewer
>20 sec associated with bradycardia (<80 beats / min), adverse effects, larger therapeutic and less need to monitor
central cyanosis, or O2 saturation < 85% in neonates drug levels
born at <37 weeks gestation and with no underlying  Treatment:
disorders causing apnea o 34 – 35 wk gestation
 Cause may be CNS immaturity (central) or airway o free from apnea requiring physical intervention for at least
obstruction 5 – 7 days
 Diagnosis is by multichannel respiratory monitoring o Monitoring continues until the infant is free of apnea
 Most common: Mixed type requiring intervention for 5 – 10 days
VIII-A. PROGNOSIS IX. MECONIUM ASPIRATION
 Excellent; Death is rare  Meconium in-utero is in a sterile environment therefore it does

Apnea resolves in most neonates by 37 weeks not cause any problem. Your preterm patients are not a
 ~25% of preterm infants have apnea of prematurity  begins 2 candidate but your full term patients are. Why? There would be
to 3 days after birth and only rarely on the first day hypoxia. With hypoxia you have your external and internal
 Apnea that develops >14 days after birth in an otherwise sphincter muscles and that would lead to the relaxation and
healthy infant signifies a serious illness other than apnea of passage of meconium BUT in-utero this patient can already
prematurity (eg sepsis) aspirate and if it lodges in the lungs, nothing is going to happen
 Risk increases with earlier gestational age because in-utero the lungs is non-functional and submerge in
amniotic fluid. So, once this patient is delivered and there would
VIII-B. PATHOPHYSIOLOGY be cast which is a foreign body leading to chemical pneumonitis
that would give all the clinical presentation. What are you afraid
 Central apnea is caused by: of? It is your patient going to persistent fetal circulation or your
o Immaturity of medullary respiratory control centers persistent pulmonary hypertension. There is no issue with the air
o Insufficient neural impulses from the respiratory centers in going to the lungs but going out the alveoli or when you expire it
the medulla reach the respiratory muscles becomes trap which leads to build up to a point of air leak.
 Obstructive apnea is caused by:  Intrapartum meconium aspiration can cause
o Obstructed airflow o Inflammatory pneumonitis
o Neck flexion causing opposition of hypoharyngeal soft o Mechanical bronchial obstruction
tissues  Findings include
o Nasal occlusion o Tachypnea
o Reflex o Rales
 Hypoxemia and hypercarbia stimulate respiratory efforts o Rhonchi
 Both types of apnea can cause hypoxemia, cyanosis, and o Cyanosis
bradycardia if the apnea is prolonged o Desaturation

 Diagnosis is suspected when there is respiratory distress:  Symptoms and signs

o After delivery through meconium – tinged amniotic fluid o Tachypnea
o Confirmed by chest x – ray (patchy lung) o Retractions
 Treatment o Severe cyanosis
o Vigorous suction immediately on delivery before neonates o Desaturation
take their first breath (From the PPT) o Unresponsive to o2
o Followed by respiratory support as needed  Treatment
o If you have a patient who is born with meconium stained o O2
amniotic fluid, however that patient is vigorous you do NOT o Alkanization
have to suction or intubate the patient. You just have to o High-frequency ventilation
observe. We encourage the OB to hand him to the o Nitric oxice
resuscitating team rather than the OB suctioning the oral o Pressors, intropes, or both
cavity. Suction first the oral cavity before nasal cavity
because you do not want this child to be aspirating the
meconium which would give the complication.
 Prognosis depends on the underlying physiologic stressors.
IX-A. ETIOLOGY
 The mechanisms by which aspiration induces the clinical
syndrome probably include
o Nonspecific cytokine release
o Airway obstruction
o Surfactant inactivation
o Chemical pneumonitis
IX-B. SIGNS
 Tachypnea Figure 15. Pathophysiology of Persistent Pulmonary
 Nasal flaring Hypertension of the Newborn.
 Retractions  Pulmonary and systemic resistances are high  increased load
 Cyanosis or desaturation on the heart
 Rales, rhonchi  This load increase may result in (1) right heart dilation (2)
 Greenish yellow staining of the umbilical cord, nail beds, or skin tricuspid insufficiency, and (3) right heart failure
Meconium staining may be visible in the oropharynx and (on
intubation) in the larynx and trachea XI. TRANSIENT TACHYPNEA OF THE NEWBORN
Neonates with air trapping may have barrel – shaped chest
and also symptoms and signs of pneumothorax, and  Also called neonatal wet lung syndrome
pulmonary interstitial emphysema  Affects premature infants, term infants delivered by cesarean
section because they lack “vaginal squeeze” – passage to the
IX-C. DIAGNOSIS birth canal during NSD may squeeze the thoracic cage and
facilitate reabsorption of fetal lung fluid at a faster rate
 Meconium passage  Infants born with respiratory depression
 Respiratory distress  All of whom have delayed clearance of fetal lung fluid
 Characteristic x-ray findings showing hyperinflation (floppy)  For unknown reasons: maternal diabetes and asthma are also
with variable areas of atelectasis and flattening of the risk factors
diaphragm  Pneumonia and sepsis may have similar manifestations, so
CXR, CBC, and blood cultures are usually done
X. PERSISTENT PULMONARY HYPERTENSION OF THE
 Expect that the patient is tachypneic, blood gas is blowing off
NEWBORN your CO2 so expect alkalosis.
 Persistence of or reversion to pulmonary arteriolar  CXR shows hyperinflated lungs with streaky perihilar
constriction, causing a severe reduction in pulmonary blood markings (because of tachypnea), giving the appearance of a
flow and right to left shunting. shaggy heart border while the periphery of the lungs is clear
 Diagnosis is by history, examination, CXR, and response to O2  Fluid is often seen in the lung fissures
 Persistent pulmonary hypertension of the newborn is a  If initial findings are indeterminate or suggest infection, give
disorder of pulmonary vasculature that affects term or post antibiotics
term infants.
XII. PULMONARY AIR LEAK SYNDROME
 You see the symptoms in RDS but what becomes obvious as the
condition becomes more serious would be the observation of  Involve dissection of air out of the normal pulmonary airspaces
cyanosis and desaturation which is not responsive with your 0 2.  Types
This also has a triad: acidosis, hypercarbia, and hypoxemia. You o Pulmonary Interstitial emphysema
might need to intubate or ventilate this patient. o Pneumothorax
o Pneumomediastinum
o Pneumopericardium XII-B. PNEUMOTHORAX

o Pneumoperitonium
o Subcutaneous emphysema  Dissection of air into the pleural space; sufficient accumulation
 Risk Factors of air causes tension pneumothorax
o Diseases
 RDS XII-B-1. ETIOLOGY
 Meconium Aspiration Syndrome
Most common cause: over inflation resulting in alveolar
 Amniotic Fluid Aspiration
rupture
 Infection
May be spontaneous or may be due to underlying pulmonary
 Prematurity <32 weeks
disease, trauma, or bronchial or bronchiolar obstruction
o Procedures
Associated with disorders of decreased amniotic fluid volume,
 Intubation
decreased fetal breathing movement, pulmonary space-
 Suctioning
occupying lesions, and thoracic abnormalities.
 Tracheostomy
 Resuscitation XII-B-2. CLINICAL MANIFESTATION
o Ventilation
 Use of increased peak inspiratory pressure (PIP)  Sometimes asymptomatic
PE reveals hyperresonance and decreased breath sounds
on affected side
Irritability and restlessness or apnea may be the earliest
signs.
 Pneumothorax typically causes worsening of tachypnea,
grunting, and cyanosis
 Chest enlarges on the affected side
Inc. AP diameter
Bulging of ICS
Heart is displaced towards unaffected side
Displaced apex beat and PMI
Diaphragm is displaced downward, as is the liver with
Figure 16. Pulmonary Air-Leak Syndrome. right-sided pneumothorax → abdominal distention
10% of cases are bilateral → symmetry does not rule it out
XII-A. PULMONARY INTERSTITIAL EMPHYSEMA  Tension pneumothorax causes cardiovascular collapse
Why do patients die? Because of the tamponade effect
 If leakage of air from alveoli into the pulmonary interstitium, Air is going to compress the heart
lymphatics, or subpleural space. ↓
 Commonly seen among premature babies who are ventilated for Restrict the contractility of the heart
a long time ↓
 Occurs in infants with poor lung compliance  respiratory Dec the cardiac output
distress syndrome treated with mechanical ventilation ↓
 One or both lungs may be involved, and pathology may be Dec the heart rate
focal or generalized within each lung ↓
 If dissection of air is widespread, respiratory status may acutely Dec the stroke volume
worsen because lung compliance suddenly is reduced ↓
 Pathophysiology Patient will die
o Collect air in the interstitium
o Compress the small airway and vessels XII-B-3. DIAGNOSIS
o V/Q mismatches  Transillumination of the thorax
o Deterioration of blood gas o Helpful in the emergency diagnosis of pneumothorax
o Affected side transmits excessive light.
XII-A-1. IMAGING
 By radiography, with the edge of the collapsed lung standing
 X-ray out in relief against the pneumothorax
o Increase lung volume
o Small heart size
o Cysts containing air and bleb
o Mainly associated with pneumothorax
XII-A-2. TREATMENT
 Supportive
 Decrease vent volumes (decrease MAP)
 Minimize ET suction and hand bagging
 HFOV (low strategies volume)

Figure 19. X-ray of patient with pneumothorax affecting both lungs.

Figure 17. Pneumothorax. See the pulmonary markings outside of
which is air; “basta itim that is air”. XII-C. PNEUMOMEDIASTINUM
 Dissection of air into connective tissue of the mediastinum
 The air may further dissect into the subcutaneous tissues of the
neck and scalp
XII-C-1. CLINICAL MANIFESTATIONS

 Usually causes no symptoms or signs, though subcutaneous air
causes crepitus
If amount of trapped gas is great → midthoracic area bulge,
distended neck veins, and hypotension → tamponade of
systemic and pulmonary veins
Pathognomonic sign: subcutaneous emphysema
XII-C-2. DIAGNOSIS
 Diagnosis is by x-ray; in an anteroposterior view, air may form
a lucency around the heart, whereas on a lateral view, air lifts
Figure 18. Pneumothorax. A, Right-sided tension pneumothorax the lobes of the thymus away from the cardiac silhouette
and widespread right lung pulmonary interstitial emphysema in a (spinnaker snail sign)
preterm infant receiving intensive care. B, Resolution of
pneumothorax with a chest tube in place.
Patient hooked on ventilator, doing all right, then, suddenly

became cyanotic. First check the system. Is it functioning? Is the
level of oxygen adequate? If system is all right, then do a full PE,
auscultate. If there are no breath sounds, you might be dealing
with pneumothorax. Do transillumination, it lightens up. You do
an x-ray you see the evidence of pneumothorax.
XII-B-4. TREATMENT
You will have to decompress
Goal is resumption of cardiac contractility
 Without a continued air leak, asymptomatic and
mildlysymptomatic small pneumothoraces require only Figure 20. Pneumomediastinum in a newborn infant. The
closeobservation. anteroposterior view (left) demonstrates compression of the lungs,
 Needle aspiration – both diagnostic and therapeutic – and the lateral view (right) shows bulging of the sternum, each
immediately relieves tension resulting from distention of the mediastinum by trapped air.
 Definitive treatment: chest tube thoracostomy on affectedside
and draining the tube to remove pleural air XII-C-3. TREATMENT
 General measure: thermoregulation, proper
 No treatment is usually needed, and the condition resolves
nutrition,correction of electrolyte and metabolic imbalances
spontaneously.
 Frequent small feedings may prevent gastric dilatation
andminimize crying
 If the air leak is ongoing, continuous suction (−5 to −20 cmH2O)
may be needed to evacuate the pneumothorax completely

XII-E. PNEUMOPERITONIUM
 Dissection of air into the peritoneum
XII-E-1. CLINICAL MANIFESTATIONS

 Clinical symptoms that include abdominal rigidity, absent
bowel sounds, and signs of sepsis suggest abdominal viscus
injury
 It is generally not clinically significant but must be
distinguished from pneumoperitoneum due to ruptured
abdominal viscus, which is surgical emergency 
Figure 21. Pneumomediastinum. The arrows point to the XII-E-2. DIAGNOSIS

pulmonary markings and outside of that would be air outside the
alveolus.  Diagnosis is made by abdominal x-ray and physical
examination
XII-D. PNEUMOPERICARDIUM Paracentesis can be helpful in differentiating
pneumoperitoneum from intestinal perforation.
 Dissection of air into the pericardial sac
 Affects mechanically ventilated infants almost exclusively
XII-D-1. CLINICAL MANIFESTATIONS

 Most cases are asymptomatic, but if sufficient air accumulates,
it can cause cardiac tamponade
 Usually manifests as sudden shock with tachycardia, muffled
heart sounds, and poor pulses suggesting tamponade.
XII-D-2. DIAGNOSIS
 Diagnosis is suspected if infants experience acute circulatory
Figure 24.Pneumoperitoneum. Air in the abdominal cavity
collapse and is confirmed by lucency around the heart on x-
ray or by return of air on pericardiocentesis using an XII-E-3. TREATMENT
angiocatheter and syringe
 Occasionally, pneumoperitoneum can result in an abdominal
compartment syndrome requiring decompression.
XII-F. RESPIRATORY SUPPORT IN NEONATES

 SupplementalO2
 Continuous positive airway pressure(CPAP)
 Bag and mask ventilation or mechanical ventilation
XIII. NEONATAL SEPSIS

 Clinical syndrome of bacteremia with systemic signs and
symptoms of infection in the first 4 weeks of life
Figure 22. Pneumopericardium. See air outside the heart. Observer
 Septicemia is the presence of the organism PLUS clinical signs
air outlining the heart (black space around the heart).
and symptoms whereas bacteremia is the presence of the
XII-D-3. TREATMENT organism WITHOUT clinical signs and symptoms.
 Treatment is pericardiocentesis followed by surgical insertion

of a pericardial tube
Figure 25. Most common cause of neonatal deaths.

Figure 23. Pericardiocentesis.
May be asymptomatic, requiring only general supportive
treatment

 Common organisms: Mostly found on the vaginal flora XIII-D-1. SEPSIS SCREEN
o Klebsiella pneumoniae
o Escherichia coli – no 1 cause in developing country  Leukopenia (TLC < 5000mm )
3
o Staphylococcus aureus  3
Neutropenia (ANC < 1800/mm )
o Pseudomonas
 Immature Neutrophil to total neutrophil ( I/T) ratio (>0.2)
Table 4. Early vs Late Onset Sepsis  st
Micro-ESR (>15mm 1 hour) – affected by patient’s age; only
Early Late time to request this is if your done to clear the risk factors and
(usually involves respiratory) (usually involves CNS) your definite if you’re going to treat an infection or not
Onset Up to 72 hours After 72 hours  CRP + ve – good as blood culture but the only thing it does not
Source Maternal Postnatal Environment probably give you is the isolation of the organism
Presentation Fulminant multisystem Slowly progressive, focal  If two or more tests are positive treat infant as neonatal sepsis.
Pneumonia frequent Meningitis frequent
Mortality 15-50% 10-20% XIII-E. MENINGITIS
XIII-A. SYMPTOMS OF NEONATAL SEPSIS  10-15% cases of sepsis have meningitis
 CNS  Can be often missed clinically
o Lethargy, refusal to suckle, limp, not arousable, poor or  Lumbar puncture must be done in all cases of late onset and
high pitched cry, irritable, seizures symptomatic early onset sepsis
 CVS
o Pallor, cyanosis, cold clammy skin XIII-F. MANAGEMENT
 Respiratory
o Tachypnea, apnea, grunt, retractions XIII-F-1. SUPPORTIVE CARE
 GIT  Keep the neonate warm
o Vomiting, diarrhea, abdominal distention  If sick, avoid enteral feed
 Hematological  Start IV fluids, infuse 10% dextrose- 2ml/kg over 2-3 minutes to
o Bleeding, jaundice maintain normoglycemia; for premature <1kg you cannot go
 Skin higher than 5% because they cannot tolerate it
o Rashes, purpura, pustules  Maintain fluid and electrolyte balance and tissue perfusion. If
CRT>3 sec, infuse 10 ml/kg normal saline
XIII-B. SIGNS OF NEONATAL SEPSIS
 Start oxygen by hood, if cyanosed or having RR> 60/min or
 Cold to touch ( hypothermia) severe chest retractions
 Poor perfusion (CRT)  Consider exchange blood transfusions, if there is sclerema
 Hypotension XIII-F-2. CHOICE OF ANTIBIOTICS
 Renal Failure
 Sclerema  It is empirical and it would depend on the organism you’re most
 Bulging fontanels, neck retraction likely considering
 Poor weight gain (indicates low grade sepsis)  Pneumonia or sepsis
o Penicillin (Ampicillin or Cloxacillin) + Aminoglycoside
XIII-C. CLINICAL FEATURES OF SEVERE INFECTIONS (Gentamicin or Amikacin)
 Meningitis
 Feeding ability reduced o Ampicillin + Gentamicin or Gentamicin or Amikacin +
 No spontaneous movement Cefotaxime

o
Temperature >38 C
 Prolonged capillary refill time
XIII-F-3. SUSPECTED NEONATAL SEPSIS
 Lower chest wall indrawing  Start parenteral antibiotics
 RR >60/minute  Send cultures (report in 72 hours)
 Grunting
 Cyanosis
 H/o of convulsions
XIII-D. DIAGNOSIS OF NEONATAL SEPSIS

 Direct
o Isolation of organisms from blood, CSF, urine is diagnostic
 Indirect
o Screening tests (like CRP, ESR)
Figure 26. Suspected Neonatal Sepsis.

XIII-G. SUPERFICIAL INFECTIONS XIII-I. FUMIGATION

 Pustules  Use Potassium permanganate 70gm with 170ml of 40%
o After puncturing, clean with betadine and apply local formalin for 1000 cubic feet area for 8-24 hours alternatively
antimicrobial Bacillocid spray for 1-2 hours may be equally effective
 Conjunctivitis
o Chlorampenicol eyedrops XIII-J.CONCLUSION
 Oral thrush
o Local application of nystatin or Clotrimazole  High index of clinical suspicion
 Look for lab evidence of sepsis
XIII-H. PREVENTION OF INFECTIONS
 Start parenteral antibiotics (IV)
 Exclusive breastfeeding  Provide supportive care
 Keep cord dry  Review culture reports
 Hand washing by care givers  Practice barrier nursing to prevent cross-infection
 Hygiene of baby
 No unnecessary interventions XIV. CONGENITAL VIRAL INFECTIONS
XIII-H-1. HAND WASHING NOTE: This part onwards was not discussed in our class and was left
as a reading assignment. It was based on the ppt slides and 2019A & C
 Simplest, most effective measure for preventing hospital recordings.
acquired infections
 2 minutes hand washing prior to entering nursery
 15 seconds hand washing before touching baby
 Alcohol based hand rub, effective but costly
Figure 27. Six Steps of Handwashing.
XIII-H-2. CONTROL OF HOSPITAL INFECTIONS Figure 28. Clinical Manifestations of Different Congenital Viral
Infections.
 Hand washing by all staff
 Isolation of infectious patient Table 5. Clinical Mannifestations of Rubella, Cytomegalovirus
 Use of plenty of disposable items and Toxoplasmosis.
 Avoid overcrowding Rubella CMV Toxoplasmosis
 Aseptic work culture Eye involvement ++ ++ +++
 Infection surveillance Microphthalmia + + +
Chorioretinitis + ++ ++
XIII-H-3. WORK CULTURE Cataracts ++ - -
IUGR +++ + +
 Sterile gowns and linen for babies
Brain ++ ++ +++
 Hand washing by all
Hydrocephaly - - ++
 Regular cleaning of unit
Microcephaly + ++ +
 No sharing of baby belongings
Calcification ++ ++ ++
 Dispose waste-product in separate bins
Deafness +++ +++ ++
XIII-H-4. CONTROL OF HOSPITAL OUTBREAKS OF Hepatosplenomegaly ++ ++ ++
INFECTIONS Cardiac ++ - +-
Purpura ++ ++ -
 Epidemiologic investigation Pneumonitis + ++ +
 Increased emphasis on handwashing Bony involvement ++ + -
 Reinforce all preventive measures  First to rule out is TORCH (Toxoplasmosis, Other – syphilis,
 Review of protocols of nursery varicella-zoster, parvovirus B-19, Rubella, Cytomegalovirus,
 Screen all personnel Herpes)
 Review of antibiotic policy
 Cohorting of infants

 Intrauterine Viral Infections  Permanent

o Rubella o Sensorineural deafness, Heart defects (peripheral
o Cytomegalovirus(CMV) pulmonary stenosis, pulmonary valvular stenosis, patent
o Parvovirus B19 ductus arteriosus, ventricular septal defect) Eye defects
o Varicella-Zoster (VZV) (retinopathy, cataract, microphthalmia, glaucoma, severe
myopia) Other defects (microcephaly, DM, thyroid
o Enterovirus
disorders, dermatoglyptic abnormalities)
o HIV
 Developmental
o HTLV-1 o Sensorineural deafness, Mental Retardation, DM, Thyroid
o Hepatitis C disorder
o Hepatitis B
o Lassa Fever XIV-A-3. OUTCOME*
o Japanese Encephalitis
 Perinatal and Neonatal Infections  1/3 will lead to normal independent lives
o Human Herpes Simplex  1/3 will live with parents
o VZV  1/3 will be institutionalized
 The only effective way to prevent CRS is to terminate the
o Enterovirus
pregnancy
o HIV
o Hepatitis B XIV-A-4. PREVENTION*
o Hepatitis C
o HTLV-1  Antenatal screening
o All pregnant women attending antenatal screenings are
XIV-A. RUBELLA tested for immune status against rubella
o Non- immune women are offered rubella vaccination in
 Characteristics: the immediate postpartum period.
o RNA enveloped virus, member of the togavirus family
 Since 1968, a highly effective live attenuated vaccine has been
o Spread by respiratory droplets
available with 95% efficacy
o In the pre-vaccination era, 80% of women were already
 Universal vaccination is now offered to all infants as part of the
infected by childbearing age
MMR regimen in the USA, UK, and a number of other countries
 Clinical Features
 Some countries such as Czech Republic continue to selectively
o Maculopapular rash
vaccinate school girls before they reach reproductive age.
o Lymphadenopathy
 Both universal and selective vaccination policies will work
o Fever
provided that the coverage is high enough
o Arthropathy (up to 60% of cases)
XIV-A-5. LABORATORY DIAGNOSIS*
XIV-A-1. RISK OF RUBELLA INFECTION DURING
PREGNANCY  Diagnosis in acute infections
o Rising titers of antibody (mainly IgG)-HAI, EIA)
 Preconception o Presence of rubella-specific IgM-EIA
o Minimal risk
 Immune status screen
 0-12 weeks o HAI is too insensitive for immune status screening
o 100% risk of fetus being congenitally infected resulting in o SRH, EIA, and latex agglutination are routinely used
major congenital abnormalities. Spontaneous abortion o 15 IU/ml is regarded as the cutoff for immunity
occurs in 20% of cases
 13-16 weeks
o Deafness and retinopathy 15%
 After 16 weeks
o Normal development, slight risk of deafness and
retinopathy
 If you get it in early trimester of pregnancy, there are more
complications and that it is precisely why it’s important to give
MMR to all women of child-bearing age.
XIV-A-2. CONGENITAL RUBELLA SYNDROME

 Classical triad consists of cataracts, heart defects, and
sensorineural deafness. Many other abnormalities ad been
described and these are divided into transient, permanent, and
developmental.
 Transient
o LBW, hepatosplenomegaly, thrombocytopenic purpura, Figure 29. Typical serologic events following acute rubella
bone lesions, meningoencephalitis, hepatitis, hemolytic infection. Note that in reinfection, IgM is usually absent or present
anemia, pneumonitis, lymphadenopathy only transiently at low levels.

XIV-B. CYTOMEGALOVIRUS  Premature rupturing of the membranes is a well recognized

risk factor
 Member of the herpesvirus  The risk of perinatal transmission is greatest when there is
 Primary infection usually asymptomatic. Virus then becomes florid primary infection of the mother
latent and is reactivated from time to time  There is appreciably smaller risk from recurrent lesions in the
 Transmitted by infected saliva, breast milk, sexually and mother, probably because of the lower viral load and the
through infected blood presence of specific antibody
 60% of the population eventually becomes infected. In some  The baby may also be infected from other sources such as oral
developing countries, the figure is up to 95% lesions from the mother or a herpetic whitlow in a nurse.
 The spectrum of neonatal HSV infection varies from a mild
XIV-B-1. CONGENITAL INFECTION disease localized to the skin to a fatal disseminated infection
 Defined as the isolation of CMV from the saliva or urine within  Infection is particularly dangerous in premature infants
3 weeks of birth.  Where dissemination occurs, the organs most commonly
 Commonest congenital viral infection, affects 0.3-1%of all live involved are the liver, adrenals, and the brain
births. The second most common cause of mental handicap  Where the brain is involved, prognosis is particularly severe.
after Down’s syndrome and is responsible for more cases of The encephalitis is global and of such severity that the brain
congenital damage than rubella may be liquefied
 Transmission to fetus may occur following primary or recurrent  A large proportion of survivors of neonatal HSV infection have
CMV infection. 40% chance of transmission to the fetus residual disabilities.
following a primary infection  Acyclovir should be promptly given in all suspected cases of
 May be transmitted to the fetus during all stages of pregnancy neonatal HSV infection.
 No evidence of teratogenicity, damage to the fetus results  The only means of prevention is to offer C section to mothers
from destruction of target cells once they are formed. with florid genital HSV lesions.
XIV-B-2. CYTOMEGALIC INCLUSION DISEASE* XIV-D. PARVOVIRUS

 CNS abnormalities- microcephaly, mental retardation,  Causative agent of Fifth disease (erythema infecticeum),
spasticity, epilepsy, periventricular calcification clinically difficult to distinguish from rubella
 Eye- choroidoretinitis and optic atrophy  Also causes aplastic crisis in individuals with hemolytic anemia
 Ear- sensorineural deafness as erythrocyte progenitors are targeted
 Liver- hepatosplenomegaly and jaundice which is due to  Spread by respiratory route, 60-70% of the population is
hepatitis eventually infected
 Lung- pneumonitis  50% of women of childbearing age are susceptible to infection
 Heart- myocarditis
 Thrombocytopenic purpura, hemolytic anemia XIV-D-1. CONGENITAL PARVOVIRUS
 Late sequelae in individuals asymptomatic at birth- hearing
defects, and reduced intelligence  Known to cause fetal loss through hydrops fetalis, severe
anemia, congestive heart failure, generalized edema, and fetal
XIV-B-3. DIAGNOSIS death
 No evidenced teratogenicity
 Isolation of CMV from the urine or saliva of the neonate
 Risk of fetal death highest when infection occurs during the
 Presence of CMV IgM from the blood of the neonate
second trimester of pregnancy (12%)
 Detection of Cytomegalic Inclusion bodies from affected
 Minimal risk to the fetus if infection occurred during the first or
tissues ( rarely used)
third trimesters of pregnancy
XIV-B-4. MANAGEMENT  Maternal infection during pregnancy does not warrant
termination of pregnancy
 Primary infection- consider termination of pregnancy
 Cases of diagnosed hydrops fetalis had been successfully
 40% chance of fetus being infected treated in utero in intrauterine transfusion and administration
 10% chance that congenitally infected baby will be of digoxin to the fetus.
symptomatic at birth or develop sequelae later in life
 Therefore in case of primary infection, there is a 4% chance of XIV-E. VARICELLA-ZOSTER VIRUS
giving birth with an infant with CMV problems
 Recurrent Infection- termination not recommended as risk of  90% of pregnant women already immune, therefore primary
transmission to fetus is much lower infection is rare during pregnancy
 Antenatal screening- Impractical  Primary infection during pregnancy carries a greater risk of
 Vaccination- may become available in the near future severe disease, in particular pneumonia
XIV-C. NEONATAL HERPES SIMPLEX (1)  First 20 weeks of pregnancy- up to 3% chance of transmission
to the fetus, recognized congenital varicella syndrome
 Incidence of neonatal HSV infection varies inexplicably from o Scarring of skin
country to country e.g. from 1 in 4,000 live births in US to 1 in o Hypoplasia of limbs
10,000 live births in the UK o CNS and eye defects
 The baby is usually infected perinatally during passage through o Death in infancy normal
birth canal
XIV-F. NEONATAL VARICELLA  Why does physiologic jaundice develop?

o Increased bilirubin load
 VZV can cross the placenta in the late stages of pregnancy to o Defective uptake from plasma
infect the fetus congenitally o Defective conjugation
 Neonatal varicella may vary from a mild disease to a fetal o Decreased excretion
dissemination o Increased entero-hepatic circulation
 If rash in mother occurs more than 1 week before delivery, then
sufficient immunity would have been transferred to the fetus XV-A-1. CAUSES OF HYPERBILIRUBINEMIA
 Zoster immunoglobulin should be given susceptible pregnant
 Increased production
women who had contact with suspected case of varicella o Short RBC lifespan
 Zoster immunoglobulin should also infants whose mothers o Increased shunt bilirubin
develop varicella during the last 7 days of pregnancy or the 14
 Decreased clearance
days of after delivery
o Portal vein shunting via ductus venosus
XIV-G. ZIKA VIRUS  Decreased conjugation
o Decreased UDPGA synthesis
 Zika virus is a flavivirus that is primarily transmitted by Aedes o Decreased UDPG transferase
mosquitoes. It can also be sexually transmitted and possibly via  Increased enterohepatic circulation
transfusions. o High concentration of bilirubin in meconium
 Most infections are asymptomatic. When symptoms are o Decreased bowel motility
present, they are usually mild and resemble dengue.
 The distribution of Zika virus is similar to Dengue, being found XV-A-2. HYPERBILIRUBINEMIA: ELEVATION IN DISEASE
usually in tropical areas of Asia, Africa, and America. STATES
 Zika virus was first reported to be associated with
 Overproduction
microcephaly and Guillain-Barre syndrome by Brazil in 2015.
o Short RBC lifespan
 The risk of infected pregnant women giving birth to a live or
 Underproduction
dead baby with congenital abnormalities including
o Portal vein shunting via ductus venosus
microcephaly is in the region of around 4-5% (based on US
 Mixed
data)
o Decreased UDPGA synthesis
 Infected pregnant women should be followed up routinely by
ultrasound. XV-B. PATHOLOGIC JAUNDICE
XV. NEONATAL JAUNDICE  Characteristics:
o Appears within 24 hours of age
 Visible form of bilirubinemia o Increase of bilirubin > 5mg/dL/day
o Adult sclera >2 mg/dl o Serum bilirubin >15mg/dL
o Newborn skin >5 mg/dl o Jaundice persisting after 14 days
 Occurs in 60% of term and 80% of preterm neonates o Stool: clay white colored and urine staining clothes yellow
 However, significant jaundice occurs in 6% of term babies o Direct bilirubin >2mg/dL
 How do you observe this condition? These would be in a cephalo-
caudal progress which would be referred as Kramer's XV-C. CAUSES OF JAUNDICE
classification. The area of the body that would be affected with
the equivalent bilirubin levels.  Appearing within 24 hours of age
o Hemolytic disease of NB : Rh, ABO
Table 6. Clinical Assessment of Jaundice. o Infections: TORCH, malaria, bacterial
Area of body Bilirubin levels (mg / dl) o G6PD deficiency
Face 4-8  Appearing between 24-72 hours of life
Upper trunk 5-12 o Physiological
Lower trunk & thighs 8-16 o Sepsis
Arms and lower legs 11-18 o Polycythemia
o Concealed hemorrhage
Palms & soles >15
o Intraventricular hemorrhage
XV-A. PHYSIOLOGIC JAUNDICE o Increased enterohepatic circulation
 After 72 hours of age
 Characteristics: o Sepsis
o Appears after 24 hours o Cephalhaematoma
o Maximum intensity by 4th-5th day in term and 7th day in o Neonatal hepatitis
premature babies o Extra-hepatic biliary atresia
o Serum level less than 15 mg / dl o Breast mile jaundice
o Clinically not detectable after 14 days o Metabolic disorders
o Disappears without any treatment
o Note: Baby should, however, be watched for worsening
jaundice

XV-D. RISK FACTORS FOR JAUNDICE XV-F-1. PHOTOTHERAPY

 JAUNDICE  Principle
o J – jaundice within first 24 hours of life o Native bilirubin: Insoluble
o A – a sibling who was jaundiced as neonate o Photo isomers of bilirubin: Soluble
o U – unrecognized hemolysis  Side Effects
o N – non-optimal sucking/nursing o Increased insensible water loss
o D- deficiency of G6PD o Loose stools
o I – infection o Skin rash
o C – cephalhematoma / bruising o Bronze baby syndrome
o E – East Asian / North Indian  Seen among babies who has direct hyperbilirubinemia
meaning to say there is conjugation, therefore you do
XV-E. WORKUP not need to put the patient into phototherapy and if
you do your patient will present with bronze
 Maternal and perinatal history discoloration.
 Physical examination o Hyperthermia
 Laboratory tests (must in all)* o Upsets maternal baby interaction
o Total and direct bilirubin* o May result in hypocalcemia
o Blood group and Rh for mother and baby*
o Hematocrit, retic count and peripheral smear* XV-F-2. EXCHANGE TRANSFUSION
o Sepsis screen  Reserve for hemolytic disease with bilirubin >20mg/dL
o Liver and thyroid function  Patients who appears jaundice but when you look at CBC, there
o TORCH titers, liver scan when conjugated is anemia. It indicates that there is a hemolytic process.
hyperbilirubinemia
 Those unresponsive to intensive phototherapy with bilirubin
>25mg/dL
 Choice of blood for exchange blood transfusion
o ABO incompatibility
 Use O blood of same Rh type, ideal O cells suspended
in AB plasma
o Rh isoimmunization
 Emergency O -ve suspended in AB plasma or baby’s
blood group but Rh -ve
o Other situations
 Baby’s blood group
XV-G. PROLONGED INDIRECT JAUNDICE

 Causes
Figure 30. Normogram of Total Serum Bilirubin. This is the o Crigler Najjar syndrome
normogram that we used in the clinics depending on the level of o Breast milk jaundice
bilirubin and the postnatal age of your patient. Qualify the patient and o Hypothyroidism
it would tell you what kind of intervention you need to do. o Pyloric stenosis
o Ongoing hemolysis, malaria
XV-F. MANAGEMENT
XV-H. PREVENTION OF KERNICTERUS
 Rationale: reduce level of serum bilirubin (FIRST) and prevent
bilirubin toxicity  Identifying infants at risk of Hyperbilirubinemia
 Prevention of hyperbilirubinemia: early feeding and adequate  Prenatal maternal blood type and antibody screen
hydration  Blood type and direct coombs on the baby
 Reduction of bilirubin levels: phototherapy, exchange o Or type only babies of:
transfusion, drugs  Rh negative mothers (necessary for Rhogam eval)
 Other antibody screen positive
Table 7. Age of Patient and Treatment Modality.  O mother (for ABO incompatibility), or hold cord
Age (h) Bilirubin Level Treatment blood 5-7 days for testing
<12 <10 Observe  Good follow up and check bilirubin levels
≥10 Phototherapy
<18 <12 Observe XV-I. CLASSIFICATION OF KERNICTERUS
≥12 Phototherapy
 Acute
<24 <14 Observe
o Phase 1 (first 1-2 days): poor sucking, stupor, hypotonia,
≥14 Phototherapy
seizures
>24 >15 Phototherapy
o Phase 2 (mid first week): hypertonia of extensors,
opisthotonus, retrocollis, fever
o Phase 3 (after first week): hypertonia

 Chronic REFERENCES
o First year: hypotonia, active DTRs, obligate tonic neck
reflexes, delayed motor skills  JBSalazar, MD’s PowerPoint Presentation & Lecture Recording
o After first year: movement disorders (choreoathetosis,  Fundamentals of Pediatrics Navarro
ballismus, tremor). Upward gaze, sensorineural hearing  Nelson Essentials of Pediatrics
loss.  2018 Transcriptions
 2019A & C recordings
XV-J. CONJUGATED HYPERBILIRUBINEMIA
REVIEW QUESTIONS
 Suspect
Choose the letter of the correct answer.
o High colored urine 1. In neonates with RDS affected, alveolar atelectasis will result to:
o White or clay colored stool a. Less compliant lungs, more compliant chest wall
 Caution b. More complaint lungs, less compliant chest wall
o Always refer to hospital for investigations so that biliary c. Equally complaint lungs and chest wall
atresia or metabolic disorders can be diagnosed and 2. Prematurity is defined as:
managed early a. Very early onset neonatal sepsis
b. Late onset neonatal sepsis
 Causes
c. Very late onset neonatal sepsis
o Idiopathic neonatal hepatitis 3. Which week of gestation does the administration of antenatal
o Infections – Hepatitis B, TORCH, sepsis corticosteroids to pregnant women can significantly reduce the
o Biliary atresia, choledochal cyst incidence and mortality of RDS?
o Metabolic – Galactosemia, tyrosinemia, hypothyroidism a. Between 20-30 weeks
o Total parenteral nutrition b. Between 24-34weeks
c. Between 28-38weeks
Answers: A, A, B
APPENDIX
Appendix 1. Ballard Score Chart. Appendix 2. Lubchenco Chart.
Appendix 3. HIE Staging.

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NEONATOLOGY I

Dr. Salazar, August 10, 2017 1.01

I-B. CONCERNS II-B. BLOOD AND METABOLIC

 Increasing morbidity and mortality  Anemia – may require blood transfusion

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 3.5kg 39wk HF via emergent C/S for prolonged deceleration

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III-A-4. AUTOPSY IV-D. MECHANISM OF INJURY

IV-C. RISK FACTORS

IV-G. DIAGNOSIS V. THERAPEUTIC HYPOTHERMIA

IV-H. STAGING  The mechanism of protection has been documented by many

IV-I. SEIZURES IN INFANTS

Figure 4. Mechanism of Action of Hypothermia.

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V-B. ADVERSE EFFECTS VI. RDS: INTRODUCTION

Figure 7. Stage of Lung Development.

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 Refinement of the acini B. SP-B:

NOTE: SP-B + SP-C work cooperatively to optimize rapid

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VII-A. SIGNS AND SYMPTOMS

Figure 11. Chest x-ray.

Figure 10. Lung Compliance.

Figure 13. Illustration of Silverman-Anderson Score. The higher

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VII-H. TREATMENT VII-I. PREVENTION

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VII-J. PROGNOSIS VIII-C. DIAGNOSIS

VIII-A. PROGNOSIS IX. MECONIUM ASPIRATION

 Excellent; Death is rare  Meconium in-utero is in a sterile environment therefore it does

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 Diagnosis is suspected when there is respiratory distress:  Symptoms and signs

o Pneumopericardium XII-B. PNEUMOTHORAX

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Figure 19. X-ray of patient with pneumothorax affecting both lungs.

XII-C-1. CLINICAL MANIFESTATIONS

Patient hooked on ventilator, doing all right, then, suddenly

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XII-E-1. CLINICAL MANIFESTATIONS

Figure 21. Pneumomediastinum. The arrows point to the XII-E-2. DIAGNOSIS

XII-D-1. CLINICAL MANIFESTATIONS

XII-F. RESPIRATORY SUPPORT IN NEONATES

XIII. NEONATAL SEPSIS

 Treatment is pericardiocentesis followed by surgical insertion

Figure 25. Most common cause of neonatal deaths.

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XIII-D. DIAGNOSIS OF NEONATAL SEPSIS

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XIII-G. SUPERFICIAL INFECTIONS XIII-I. FUMIGATION

Figure 27. Six Steps of Handwashing.

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 Intrauterine Viral Infections  Permanent

XIV-A-2. CONGENITAL RUBELLA SYNDROME

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XIV-B. CYTOMEGALOVIRUS  Premature rupturing of the membranes is a well recognized

XIV-B-2. CYTOMEGALIC INCLUSION DISEASE* XIV-D. PARVOVIRUS

XIV-F. NEONATAL VARICELLA  Why does physiologic jaundice develop?

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