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USTMEDB2007

Pediatrics Neo-Nephro Module Respiratory Distress in the


NB
Dr. Josie Niu-Kho

o SP-A, B,C,D
10% neutral lipid primarily cholesterol
phosphatidylglycerol

Five Common Signs of RD


Tachypnea respiratory rate that exceeds 60 breaths
per minute
Retractions folding of the skin inwards in the chest
wall
nasal flaring
grunting expiratory sound made a baby w/ a
collapsed lungs; breathing w/ a closed glottis
cyanosis bluish discoloration

Surfactant Protein A
water soluble collectin
required for tubular myelin formation
contributes to the biophysical porp of surfactant
regulates surfactant secretion and catabolism
major function is as a non immune host defense
protein and regulator of inflammation in the lung
not present in sysnthetic surfactant used for RDS
treatment

Differential Dx in Neonatal Respiratory Distress


Pulmonary D/o
RDS
Transient tachypnea
Meconium aspiration syndrome
Pneumonia
Air leak syndrome
Pulmonary hypoplasia
Systemic D/o
hypothermia
metabolic acidosis
anemia/polycythemia
hypoglycemia
pulmonary hypertension
congenital heart dse closest differential
Anatomic Problems compromising the Respiratory Sys
upper airway obstruction
airway malformations
space occupying lesions
rib cage anomalies
phrenic nerve injury
neuromuscular disease

Surfactant Protein B
small hydrophobic protein
facilitates surface absorption of lipids and the devt of
low surface tension on surface area compression
lack of SP-B causes a loss of lamellar bodies in type
II cells
genetic absence of SP-B leads to a lethal form of
RDS after term birth

Respiratory Distress Syndrome (RDS I)


most common initial problem in the NICU
incidence is inversely related to gestational age and
birth weight
34-35 weeks AOG enough surfactant already
o less than 34-35 wk AOG -> high risk for RDS
Signs & Sx
difficulty initiating normal respiration
sternal and subcostal retractions
nasal flaring
rapid respiration
expiratory grunting
cyanosis
Etiology
primary absence or deficiency of a highly surface
active alveolar lining layer (pulmonary surfactant)

Surfactant Protein C
also a small hydrophobic protein
cooperates w/ SP-B for lipid absorption
main role is to spread phospholipids on alveolar
surface
Surfactant Protein D
hydrophilic protein w/ structural similiatities to SPA
binds pathogens and facilitates clearance

surfactant

Atelectasis

V/Q
inequality

hypoxemia

hypoventilation
hypercarbia

Respiratory + metabolic acidosis

Pulmonary vasoconstriction

Impaired endothelial and epithelial integrity

fig:
-

type 2 alveolar cell


lamellar body -> air space -> tubular myelin -> layer of
phospholipid (surfactant) -> dec surface tension of
alveoli & airways -> expansion -> recycling of
phospholipids
main component of surfactant -> reabsorbed by
vesicles -> endocytosis -> multivesicular body ->
lamellar body formation

Surfactant
70-80% phospholipids (sat phosphatidylcholine)
10% protein

Structural
lung
immaturity

Proteinaceous exudates

Respiratory Distress Syndrome

Phsyiologic Abnormalities
dec lung compliance
large areas of lung not ventilated (v/Q)
large areas of lung not perfused (V/q)
dec alveolar ventilation and inc work of breathing
reduced lung volume (dec FRC)
Pathologic Findings
Anatomic
gross: collapsed lung, firm, dark red and liver like
microscopic: alveolar collapse, pink staining
membrane on alveolar ducts (hyaline membrane),
thickened arteriolar wall
EM: disappearance of lamellar bodies, damage and
loss of type II pneumocytes
Biophysical and Biochemical
deficient or absent pulmonary surfactant
abnormal pressure volume curve
X-Ray
reticulgranular, ground glass appearance
(homogenous & bilateral)
bronchogram
diffuse haziness
white out lungs in severe RDS
General Preventive Measures
prolongation of pregnancy / inhibit premature labor
induction of pulmo surfactant w/ maternal steroids
(Bethamethasone)

X-Ray
-

o persistently high RR
other symptoms
o mild insignificant cyanosis, good air
exchange, minimal respiratory distress
confirm Dx
central perihilar streaking
hyperaeration
fluid in the minor fissure
increase in the vascular markings

Pathophysiology
delayed resorption of fetal lung fluid -> distress
inc risk
o cesarean delivery w/o labor fluid resorption
starts during labor
o infants of diabetic mothers
self limited course, resolves within 72 hours
Neonatal Pneumonia
route of transmission
o ascending infection from the genital tract
o transplacental passage
o predisposing factor
o prolonged rupture of membranes 18 hours
Group B Strep
major pathogen producing pneumonia

Clinical Management
Specific Treatment
exogenous surfactant administration
assisted ventilation

Other bacteria
E. coli most common in the Phil
Listeria
Klebsiella
Enterococcus

Principles of Basic Care


thermoregulation
provision of fluid and caloric requirements
maintainance of adequate oxygenation
non invasive monitoring of vital signs

Clinical Course
signs of RDS
o tachypnea
o retractions
o cyanosis
-

* ensure survival with minimal risk of chronic morbidity


Bronchopulmonary Dysplasia
chronic lung disease of the newborn
a complication of HMD, results from lung injury in
infants requiring mechanical ventilation and inc
oxygen concentration
defined as a need for supplemental O2 36 wks after
conception
CXR radiolucent areas alternating w/ areas of
irregular density resembling a sponge
Treatment nutritional support, fluid restriction, O2
support, infection control (infxn worsen pulmonary
fxn), drug therapy (diuretics, bronchodilators,
dexamethasone postnatal steroid given directly to
the baby to help lessen degree of bronchopulmonary
dysplasia)
Fig: Bronchopulmonary Dysplasia CXR
sponge like
honey combing
areas of lucencies, white densities
very patchy in lower areas of the lungs
Transient Tachypnea of the NB
follows an uneventful delivery at or near term
major presenting symptom

X-Ray
-

non specific signs


o
apneic spells
o thermal instability
o jaundice (E. coli)
streaky densities
confluent opacified areas
diffusely granular appearance w/ air bronchograms

Dx
-

high index of suspicion starting from maternal hx


labs
o CBC high or low WBC
o Blood culture bacterial growth
Isolated pneumonia usually
negative
o Tracheal aspirate culture

Treatment
Penicillin (Group B Strep) and aminoglycoside (E.
coli)
late onset
o Staphylococcus Oxacillin / Vancomycin
o Chlamydia erythromycin
o Fungi ampothericin B
Duration of treatment 10 days

Air Leak Syndromes: Pneumothorax


spontaneous pneumothorax in 1% of all live births
should be suspected in any NB w/ respiratory distress
or in an infant on a respirator whose condition
suddenly worsens
increased risk in the following
o vigorous resuscitation at birth overinflate
the lungs
o RDS pathologic lungs
o MAS (meconium aspiration syndrome)
read!
o Pulmonary hypoplasia collapsed lungs
usually secondary to barotraumas
Pathophysiology
air from ruptured alveolus dissects up the vascular
sheath into the mediastinum and into the pleural
space
Clinical Findings
unilateral pneumothorax should be able to dx on PE
alone!
o cardiac impulse shifted contralaterally
o decreased ipsilateral breath sounds
o distended abdomen
Diagnosis
transillumination of the chest
CXR
o Hyperluscent area
o Shifting of midline structures to contralateral
side
o Diaphragm may be pushed down ->
distended abdomen
Fig: Massive tension pneumothorax
tension -> medical emergency
o decreased venous return to the heart
o decreased in cardiac output
o babies are hypotensive and bradycardic ->
may die
Management
nonspecific therapy for asymptomatic pneumothorax
thoracentesis
thoracostomy tube placement
o left until there is healing of the alveoli
Pneumomediastinum
may be asymptomatic
degree of respiratory distress depends on the amount
of trapped air
subcutaneous emphysema is pathognomonic
diagnosis is confirmed by CXR: air in the anterior
mediastinum
Mx close observation, may progress to
pneumothorax

seen predominantly in the preterm who requires


prolonged assisted ventilation w/ high pressures
presence of PIE signals barotraumas
associated w/ subsequent bronchopulmonary
dysplasia

fig: pulmonary interstitial emphysema


multiple lucencies
Extrapulmonary Causes of Respiratory Distress
Approach
Hx: pregnancy, delivery, neonatal transition
PE
o May not always help but one will have to do
a good PE bec there are conditions that will
give dx based on PE alone
Analysis of simple laboratory data: blood gases
(hypoxemia), blood sugar (hypoglycemia can give
RD), CBC (rule out infection), radiographic studies
High index of suspicion!
CNS
-

most commonly secondary to cerebral edema or


hemorrhage
medications administered to mother (narcotics)
o Demerol
o Tx: give Naloxone

Neuromuscular
Werdnig-Hoffmann disease (Infantile Spinal Muscular
Atrophy)
Myasthenia gravis
Hypotonia and respiratory insufficiency
Airway Obstruction
location of obstruction
o larynx and upper trachea -> stridor
laryngomalacia, tracheomalacia
o mediastinal trachea -> wheezing
will require auscultation
Choanal Atresia
obstruction of nasal passage by a membrane
cyanosis relieved w/ crying of the infant
dx established by inability to pass a catheter through
the nose
o quiet -> blue; crying -> pink
Laryngomalacia
most common cause of stridor in an infant
stridor lessens in the prone position; tends to
exacerbate during agitation
fiberoptic nasolaryngoscopy
Cystic Hygroma
anomalous devt of lymphatic channels in the neck
surgical excision

Fig: Pneumomediastinum
lungs being compressed
lobulated -> accumulation of air in the mediastinum
Pulmonary Interstitial Emphysema
rupture of air from alveoli or small airways into the
perivascular tissues of the lung
primary a radiographic diagnosis

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