PEDIATRICS- RESPIRATORY DISORDERS OF THE NEWBORN

DISEASES CLINICAL MANIFESTATIONS DIAGNOSIS & PROGNOSIS MANAGEMENT

Respiratory disorders: are the most frequent Signs & symptoms of respiratory distress Diagnostic tools:
cause of admission for neonatal intensive care includes: 1) Blood gas
in both term & preterm infants. 1) Cyanosis 2) Pulse oximetry determination
2) Nasal faring 3) Chest x-ray
Transition to pulmonary respiration: successful 3) Grunting
establishment of adequate lung function at 4) Retractions
birth depends on: 5) Tachypnea
1) Airway patency 6) Decreased breath sounds w/ or w/o
2) Functional lung development rales and/or rhonchi
3) Maturity of respiratory control 7) Pallor

Periodic breathing pattern: shifts from a regular

rhythmicity to cyclic brief episodes of
intermittent apnea.
- Common in preterm infants
- Apneic pauses of 5-10 sec followed by a
burst of rapid respirations at a rate of 50-60
sec bpm for 10-15 sec
APNEA - Onset: during the 1st 1-2 wks. after Prognosis: Treatment:
- Common problem in preterm infants birth, delayed if w/ RDS or other - Apnea of prematurity DOES NOT alter 1) Cardiorespiratory monitoring
- May be result of prematurity or an causes of respiratory distress infants’ prognosis unless severe, recurrent & 2) Gentle tactile stimulation for mild & intermittent
associated illness - Apneic episodes: frequent on day 1 refractory to therapy episodes
as throughout the 1st week in - Association of IVH & retinopathy of 3) Caffeine citrate/ theophylline: treatment for recurrent
Disorders that produce apnea: premature infants’ w/o respiratory prematurity are critical in determining apnea
1) Hypoglycemia distress prognosis for apneic infants  Caffeine citrate (less tachycardia & feeding
2) Meningitis - Serious apnea: cessation of breathing - Apnea of prematurity usually resolves by 37 intolerance)
3) Drugs for >20 sec. or for any duration if weeks of postconceptional age - LD: 20 mg/kg followed by 24 hr. later by MD
4) Hemorrhage accompanied w/ cyanosis &  May persist in extremely preterm infants of 5 mg/kg/24 hr. qd (PO or IV)
5) Seizure bradycardia <28 wks. AOG  Theophylline
6) Disturbances in O2 delivery (shock, sepsis, - Bradycardia: 1-2 sec. in >95% of cases - Infants w/ persisting apnea are discharged - LD: 5-7 mg/kg orally followed by
anemia)  Most often sinus (sometimes, w/ cardiorespiratory monitoring aminophylline (IV 1-2 mg/kg every 6-12 hr.)
7) Ventilation defects (obstructed airway, can be nodal)  Can be safely discontinued after 44 wk.  Monitoring:
pneumonia, muscle weakness postconceptional age - Vital signs
- Clinical response
Idiopathic apnea of prematurity: occurs in the Apnea & Sudden Infant Death Syndrome (SIDS) - Serum drug determination: therapeutic
absence of predisposing diseases. - Apnea of prematurity is not a risk for SIDS levels:
- Patterns:  Caffeine: 8-20 ug/ml
1) Obstructive apnea: char. by absence  Theophylline: 6-10 ug/ml
of airflow but persistent chest wall 4) Methylxanthines: increase central respiratory drive by
motion lowering the threshold response to hypercapnia &
 Pharyngeal instability enhancing contractility of the diaphragm & preventing
(collapse): results from diaphragmatic fatigue
incoordination of the tongue &  Higher does may be more effective
upper airway muscles involved  Do not necessarily result in more frequent side
in maintaining airway patency. effects
 Neck flexion  May reduce major neurodevelopmental
2) Central apnea: caused by disabilities
decreased CNS stimuli to respiratory 5) Doxapram: potent respiratory stimulant
muscles  Acts on peripheral chemoreceptors
 Both airflow & chest wall motion  Effective in neonates w/ apnea of prematurity
are absent that is unresponsive to methylxanthines
 Short apnea (10 sec) 6) Transfusion of packed RBC: for severely anemic infants
3) Mixed apnea: most common pattern  To reduce the incidence of idiopathic apnea
in preterm neonates
 50-75% of cases Therapy for mixed or obstructed apnea:
 Obstructive apnea followed by 1) Nasal CPAP 3-5 cm H2O: preferred for its efficacy
central apnea & safety
 Prolonged apnea (>20 sec) 2) High flow oxygenation using nasal cannula (1-2.5
L/min)

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PEDIATRICS- RESPIRATORY DISORDERS OF THE NEWBORN

DISEASES CLINICAL MANIFESTATIONS DIAGNOSIS & PROGNOSIS MANAGEMENT

RESPIRATORY DISEASE SYNDROME (HYALINE - Deficient synthesis or release of - Clinical course Treatment:
MEMBRANE DISEASE) surfactant produces atelectasis & - Chest X-ray findings: 1) Confine in NICU
- Occurs primarily in premature infants results in perfused but not ventilated  Lungs may have a characteristic but not 2) Careful & frequent monitoring of HR, RR, O2 sat, PaCO2,
- Incidence is inversely related to gestational alveoli causing hypoxia pathognomonic appearance: PaO2, pH, serum bicarbonate, electrolytes, glucose,
age & birthweight - Hypercapnia is due to decreased 1) Fine reticular granularity of the hematocrit, BP, temperature
- Occurs 60-80% of infants <28 wks. AOG lung compliance, increased parenchyma 3) Arterial catheterization
- 15-30% of those b/w 32 & 36 wk. AOG physiologic dead space, & 2) Air bronchogram: prominent early 4) Place in the incubator or radiant warmer
- Rarely in those >37 wks. insufficient alveolar ventilation in the LLL  Maintain core temp. at 36.5 to 37 C
- Combination of hypercapnia, - Blood gas: hypoxemia, hypercapnia  Preferable in VLBW infants
Risk increases w/: hypoxia, & acidosis produces - Acid-base values: metabolic acidosis 5) IV therapy
1) Maternal DM pulmonary arterial vasoconstriction - Avoidance of unnecessary or poorly rimed  1st 24 hr.: 10% glucose solution w/ additional
2) Multiple births w/ increased R-to-L shunting through early CS (<39 wk.) or induction of labor amino acids in extremely premature infants
3) CS delivery the foramen ovale & ductus - Administration of antenatal corticosteroids - Through a peripheral vein at a rate of 65-75
4) Precipitous delivery arteriosus & w/in the lung itself - Prediction of pulmonary immaturity w/ Ml/KG/24HR
5) Asphyxia possible in utero acceleration of maturation  2nd day: additional electrolytes (most mature
6) Cold stress Signs & Symptoms: infants)
7) Maternal history of previously affected 1) Tachypnea  3rd to 7th day: additional electrolytes (more
infants 2) Prominent (audible) grunting immature infants
3) Intercostal & subcostal retractions  1st week: gradual increase of fluids
Risk reduced in pregnancies w/: 4) Nasal flaring - Excessive fluids (>140 ml/kg/day) may
1) Chronic or pregnancy-associated HPN 5) Cyanosis contribute to the development of PDA &
2) Maternal heroin use 6) Breath sounds may be normal or BPD
3) Prolonged rupture of membranes diminished w/ harsh tubular quality & 6) Warm humidified O2
4) Antenatal corticosteroids prophylaxis on deep inspiration fine crackles may  In concentration sufficient to keep arterial O2
be heard pressure b/w 50-70 mg (91-95% sat)
Etiology & Pathophysiology  If O2 sat cannot be kept >90% apply CPAP at a
- Primary cause: Surfactant deficiency Natural course if untreated: pressure of 5-10 cm H2O via nasal prongs
- Major constituents of surfactant: 1) Progressive worsening of cyanosis &  If CPAP cannot keep O2 sat at >90% give assisted
1) Lecithin (dipalmitoyl dyspnea ventilation & surfactant
phosphatidylcholine) 2) BP may fall  Reasonable measures of respiratory failure:
2) Phosphatidylglycerol 3) Cyanosis & pallor increase - Arterial blood pH <7.20
3) Apoproteins (SP-A, SP-B, SP-C, & SP-D) 4) Grunting decrease or disappears - Arterial blood PCO2 of 60mmHg or higher
4) Cholesterol 5) Mixed respiratory-metabolic acidosis - O2 Sat <90% at O2 concentration of 40-70%
- Surfactant is present in high concentrations 6) Edema and CPAP of 5-10cm H2O
in fetal lung by 20 wks. AOG 7) Ileus 7) Mechanical ventilation: intermittent positive pressure
- Mature levels are present after 35 wks. 8) Oliguria ventilation delivered by time-cycled, pressure-limited,
AOG 9) Respiratory failure (infants w/ rapid continuous flow ventilators
- Abnormalities in surfactant B & C genes & progression of the disease)  Goal: to improve oxygenation and elimination of
ABC transporter 3 (gene responsible for carbon dioxide without causing pulmonary injury
transporting surfactant across Improvement heralded by: or oxygen toxicity
membranes): is associated w/ severe & 1) Spontaneous diuresis  Other conventional ventilation:
often lethal familial respiratory disease. 2) Improved blood gas values at lower - Synchronized intermittent mandatory
- Other familial causes: inspired oxygen levels and/or lower ventilation: the set rate is synchronized with
1) Alveolar capillary dysplasia ventilator support patient’s own breaths
2) Acinar dysplasia - Pressure support: the patient triggers each
3) Pulmonary lymphangiectasia Death can result from: breath and a set pressure is delivered)
4) Mucopolysaccharidosis 1) Severe impairment of gas - Volume ventilation: a mode in which a
- Synthesis of surfactant depends on: exchange specific tidal volume is set and delivered
1) Normal pH 2) Alveolar air leaks (interstitial pressure varies
2) Temperature emphysema, pneumothorax) - Or combinations
3) Perfusion 3) Pulmonary hemorrhage  Sedation or pain reliefs:
- Factors that suppress surfactant synthesis: 4) IVH - Benzodiazepines
1) Asphyxia - Opiates (morphine, fentanyl)
2) Hypothermia BPD often develops in infants w/ severe - Midazolam
3) Pulmonary ischemia in associated w/ RDS  High frequency ventilation (HFV): achieves
hypovolemia desired alveolar ventilation by using smaller tidal
4) Hypotension volumes and higher rates (300-1,200 breaths/min
5) Cold stress or 5-20 Hz)

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PEDIATRICS- RESPIRATORY DISORDERS OF THE NEWBORN

- May improve elimination of carbon dioxide

and improve oxygenation in patients who
show no response to conventional
ventilators or those who have severe RDS,
interstitial emphysema, recurrent
pneumothoraces, or meconium aspiration
pneumonia.
- Methods:
 High-frequency Oscillatory Ventilation
(HFOV): Reduces BPD but may raise risk
for intracranial hemorrhage
 High-frequency Jet Ventilation (HFJV):
Facilitates resolution of air leaks
 Method of weaning from ventilator:
- Transition to nasal CPAP to avoid post-
extubation atelectasis and reduce re-
intubation
- High flow (1-2 L/min) or warmed, humidified
high flow (2-8 L/min) nasal cannula O2 is
commonly used to support term and near-
term infants following extubation and to
wean premature infants from nasal CPAP
- Preloading of Methylxanthines may
enhance success of extubation.
8) Surfactant replacement therapy
 Immediate effects:
- Improved alveolar-arterial oxygen gradients
- Reduced ventilator support
- Increased pulmonary compliance
- Improved chest radiograph appearance
 Should be initiated if CPAP failed
 Endotracheal surfactant should be initiated after
intubation
 Repeated dosing given every 6-12hrs for a total of
2-4 doses
 Complications:
- Transient hypoxia
- Hypercapnia
- Bradycardia
- Hypotension
- Blockage of endotracheal tube
- Pulmonary hemorrhage
9) Pharmacologic Therapies
 Systemic Corticosteroids
- Short term AE:
 Hyperglycemia
 Hypertension
 Gastrointestinal bleeding
 Gastrointestinal perforation
 Hypertrophic obstructive
cardiomyopathy
 Poor weight gain
 Poor growth of the head
 Periventricular Leukomalacia (PV
 Inhaled Nitric Oxide (INO): Decrease the need for
extracorporeal membrane oxygenation (ECMO)
in term and near-term infants with hypoxic
respiratory failure or persistent pulmonary
hypertension of the neonate
 Methylxanthines

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PEDIATRICS- RESPIRATORY DISORDERS OF THE NEWBORN
DISEASES
COMPLICATIONS OF RDS & INTENSIVE CARE
1) Tracheal intubation
 Most common:
- Pneumothorax and other air
leaks
- Asphyxia from obstruction or
dislodgement of the tube
- Bradycardia during intubation or
suctioning
- Subglottic stenosis
2) Umbilical arterial catheterization
3) PDA (Patent Ductus Arteriosus)
 Initially bidirectional or right-to-left
shunting but as RDS resolves PVR
decreases and left-to right shunting
may occur leading to left ventricular
volume overload and pulmonary
edema.
 Associated with:
- Hypoxia
- Acidosis
- Increased pulmonary pressure
secondary to vasoconstriction
- Systemic hypotension
- Immaturity
- Local release of prostaglandins
CLINICAL MANIFESTATIONS
Others:
 Bleeding from trauma during
intubation
 Posterior pharyngeal
pseudodiverticula
 Ulceration of the nares cause by
pressure from the tube
 Permanent narrowing of the nostril as
a result of tissue damage and
scarring from irritation or infection
around the tube
 Erosion of the palate
 Avulsion of a vocal cord
 Laryngeal ulcer
 Papilloma of a vocal cord
 Persistent hoarseness
 Stridor
 Edema of the larynx
Risks:
 Vascular embolization
 Thrombosis
 Spasm
 Vascular perforation
 Ischemic or chemical necrosis of
abdominal viscera
 Infection
 Accidental hemorrhage
 Hypertension
 Impairment of circulation to a leg
with subsequent gangrene
Manifestations:
 Hyperdynamic precordium
 Bounding peripheral pulses
 Wide pulse pressure
 Continuous or systolic murmur with or
without extension into diastole or an
apical diastolic murmur or multiple
clicks resembling the shaking of a
dice
DIAGNOSIS & PROGNOSIS MANAGEMENT
Measures to reduce complications:
 Skillful intubation
 Adequate securing of the tube
 Use of polyvinyl endotracheal tubes
 Use of the smallest tube that will provide effective
ventilation in order to reduce local pressure necrosis
and ischemia
 Avoidance of frequent changes and motion of the
tube in situ
 Avoidance of too frequent or too vigorous suctioning
 Prevention of infection through meticulous cleanliness
and frequent sterilization of all apparatus attached to
or passed through the tube
Diagnosis: Doppler flow imaging that Intervention:
demonstrates left-to-right or bidirectional a) Fluid restriction
shunting. b) Cyclooxygenase inhibitors (Indomethacin or
Ibuprofen)
 IV Indomethacin (0.1-0.2 mg/kg/day) given in 3
doses every 12-24 hr.
- Contraindications:
 Thrombocytopenia (<50,000 plt/mm3)
 Bleeding Disorders
 Oliguria (UO <1mL/kg/hr)
 Necrotizing enterocolitis
 Isolated intestinal perforation
 Elevated plasma creatinine
(>1.8mg/dL)
c) Surgical Closure
 Complications:
- Horner Syndrome
- Injury to the recurrent laryngeal nerve
- Chylothorax
- Transient hypertension
- Pneumothorax
- Bleeding from the surgical site
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PEDIATRICS- RESPIRATORY DISORDERS OF THE NEWBORN

DISEASES CLINICAL MANIFESTATIONS DIAGNOSIS & PROGNOSIS MANAGEMENT

4) Bronchopulmonary dysplasia (BPD)
 A result of lung injury in infants
requiring mechanical ventilation and
supplemental oxygen.
 Primarily seen on infants with
birthweight <1,000g born at <28wk of
gestation.
 Associated with:
- Interstitial emphysema
- Male
- Low PaCO2 during the
treatment of RDS
- PDA
- High peak inspiratory
pressureIncreased a
- irway resistance in the 1st wk. of
life Increased pulmonary artery
pressure Family history of atopy
or asthma
TRANSIENT TACHYPNEA OF THE NEWBORN (TTN)
- Most common after term caesarean
delivery
- Secondary to slow absorption of fetal lung
fluid resulting in decreased pulmonary
compliance and tidal volume and
increased dead space.
- A.k.a. “Malignant Transient Tachypnea of
the newborn”
Classifications:
 Mild: those who need O2
supplementation for >28days but are
breathing room air at 36 wk. or at
discharge
 Severe: neonates pressure support or
≥30% supplemental O2 at 36 wk. or a
discharge
- Requires prolonged mechanical
ventilation
Risks:
 Increased risk:
- Genetic polymorphisms
- Over hydration during the 1st
days of life
 Decreased risk:
- Vitamin A supplementation
(5,000 IU IM 3x/wk for 4wks) in
VLBW infants
- Early use of nasal CPAP
- Rapid extubation with transition
to nasal CPAP
Characterized by:
1) Early onset of tachypnea
2) Retractions
3) Expiratory grunting
4) Cyanosis (relieved by minimal oxygen
sup <40%)
5) Chest sound generally clear without
crackles or wheeze
Most infants recover within 3 days
Diagnosis: Treatment:
 Chest Radiograph  Nutritional Support
- Pulmonary interstitial emphysema - To provide 24-30 cal/30mL formula
- Wandering atelectasis with - Protein (3-3.5 g/kg/24hr)
concomitant hyperinflation - Fat (3g/kg/24hr
- Cyst formation  Fluid restriction
 Pathologic Stages:  Drug therapy
- Acute Lung Injury a) Diuretics:
- Exudative Bronchiolitis - Furosemide (1mg/kg/dose IV BID or
- Proliferative Bronchiolitis 2mg/kg/dose PO BID) – treatment of choice
- Obliterative Fibroproliferative for acute fluid overload
Bronchiolitis  AE:
 Histologic Findings:  Hyponatremia
- Residual hyaline membrane formation  Hypokalemia
- Progressive alveolar coalescence with  Alkalosis
atelectasis of the surrounding alveoli  Azotemia
- Interstitial edema  Hypocalcemia
- Coarse focal thickening of the  Hypercalciuria
basement membrane  Cholelithiasis
- Widespread bronchial and bronchiolar  Renal stones
mucosal metaplasia and hyperplasia  Nephrocalcinosis
 Ototoxicity
Prognosis: - Thiazide
 Early provision of intensive observation and  AE: Electrolyte imbalance
care of high-risk newborn infants can b) Inhaled Bronchodilators
significantly reduce the morbidity and - Albuterol
mortality associate with RDS and other  AE: HPN, tachycardia
neonatal illnesses. - Ipratropium
- Combination therapy of albuterol &
ipratropium
c) Methylxanthines
d) Caffeine citrate
e) Theophylline: half-life of 30-40 hrs.
- AE: tachycardia, gastroesophageal reflux,
agitation, seizures
f) Postnatal dexamethasone
 Maintenance of adequate oxygenation
 Prompt treatment of infection
Chest radiograph: Treatment is supportive.
1) Prominent pulmonary vascular markings
2) Fluid in the intralobar fissures
3) Overaeration
4) Flat diaphragms
5) Small pleural effusion (rare)
Distinctive feature: Rapid recovery of the infant
and absence of radiographic findings for RDS
(hypoaeration, diffuse reticulogranular pattern, air
bronchogram) and other lung disorders

ASPIRATION OF FOREIGN MATERIAL (FETAL Pneumonia may ensue due to pathogenic Gradual improvement generally occurs over 3- Treatment is symptomatic
ASPIRATION SYNDROME, ASPIRATION bacteria that may accompany the 4days 1) Respiratory support
PNEUMONIA) aspirated material 2) Systemic antibiotics
- Aspiration of amniotic fluid containing
vernix caseosa, epithelial cells, meconium,
blood, or material from the birth canal
which may block the smallest airways and
interfere with alveolar exchange of O2 and
CO2

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PEDIATRICS- RESPIRATORY DISORDERS OF THE NEWBORN
DISEASES
PERSISTENT PULMONARY HYPERTENSION OF THE
NEWBORN (PERSISTENT FETAL CIRCULATION)
- PPHN occurs mostly in term and post-term
infants
- Often idiopathic
- Incidence: 1/500 – 1,500 live births
Pathophysiology:
- Excessively high PVR  Persistence of the
fetal circulatory pattern of right-to-left
shunting through the PDA and foramen
ovale
- Increase PVR may be:
1) Maladaptive from an acute injury
2) Result of increased pulmonary artery
medial muscle thickness and
extension of smooth muscle layers
into the usually non-muscular, more
peripheral pulmonary arterioles in
response to chronic fetal hypoxia
3) Consequence of pulmonary
hypoplasia
4) Obstructive as a result of
polycythemia or total anomalous
pulmonary venous return
5) Alveolar capillary dysplasia, which is
a lethal autosomal recessive disorder
characterized by thickened alveolar
septa, increased masculinization of
the pulmonary arterioles, reduce
number of capillaries, and
misalignment of the intrapulmonary
veins
CLINICAL MANIFESTATIONS DIAGNOSIS & PROGNOSIS MANAGEMENT
Manifestations: Diagnosis: - Correcting any predisposing condition:
- Become ill in the delivery room or - Should be suspected in all term infants with  Hypoglycemia
within 1st 1st hr. after birth cyanosis independent of a history of fetal  Polycythemia
distress, intrauterine growth restriction - Improving poor tissue oxygenation
PPHN related to: meconium-stained amniotic fluid, or birth - Initial management:
1) Polycythemia asphyxia.  O2 administration
2) Idiopathic causes - Real-time echocardiography combined with  Correction of acidosis, hypotension, and
3) Hypoglycemia Doppler flow imaging hypercapnia
4) Hypothermia - Chest X-ray findings are associated with - Persistent hypoxemia should be managed with
5) Asphyxia pneumonia and diaphragmatic hernia, intubation and mechanical ventilation
- Result in: parenchymal opacification and bowel - Inotropic therapy is frequently needed to support
 Severe cyanosis with tachypnea and/or liver in the chest are seen. blood pressure perfusion
 Initial signs of respiratory distress  Dopamine
may be minimal Prognosis:  Dobutamine
- >80-90% survive  Epinephrine
PPHN assoc. with: - 60-75% appear normal at 1-3.5 yr of age  Milrinone
1) Meconium aspiration - iNO reduces the need for ECMO support by
2) Group B streptococcal pneumonia Predisposing factors: approximately 40%
3) Diaphragmatic hernia 1) Birth asphyxia  starting dose is 20 ppm
4) Pulmonary hypoplasia 2) MAS  maximal safe duration of iNO therapy is unknown
- Exhibit: 3) Early onset sepsis  can be weaned to 5 ppm after 6-24 hr. of therapy
 Cyanosis 4) RDS  dose can be weaned slowly and discontinued
 Grunting 5) Hypoglycemia when the FIO2 is <0.6 and the iNO dose is 1 ppm
 Flaring 6) Polycythemia - Therapy with continuous inhaled or IV Prostacyclin
 Retractions 7) Maternal use of nonsteroidal anti- (Prostaglandin I2)
 Tachycardia inflammatory drugs with in utero constriction - Extracorporeal Membrane Oxygenation (ECMO)
 Shock of the ductus arteriosus  Used to treat carefully selected, severely ill infants
8) Maternal late trimester use of selective with hypoxemic respiratory failure caused by RDS,
serotonin reuptake inhibitors meconium aspiration pneumonia, congenital
9) Pulmonary hypoplasia caused by diaphragmatic hernia, PPHN, or sepsis
diaphragmatic hernia  A form of cardiopulmonary bypass that augments
10) Amniotic fluid leak systemic perfusion and provides gas exchange
11) Oligohydramnios  Indication: Alveolar-arterial gradient >620 for 8m-
12) Pleural effusion 12 hr and an oxygenation index >40 that is
unresponsive to iNO
 Site:
1) Venoarterial Bypass: requires carotid artery
ligation and the placement of large
catheters in the right internal jugular vein
and carotid artery
2) Venovenous Bypass: avoids carotid artery
ligation and provides gas exchange but it
does not support cardiac output
 Blood is initially pumped through a membrane
oxygenator and returns to the aortic arch in
Venoarterial ECMO and the right atrium in
Venovenous ECMO
 Cannot be used in patients with or at high risk of
IVH (weight <2kg, gestational age <34wk)
 Complications:
- Thromboembolism - Thrombocytopenia
- Air embolism - Neutropenia
- Bleeding - Hemolysis
- Stroke - Infectious
- Seizures complications of
- Atelectasis blood transfusions
- Cholestatic jaundice - Edema formation
- Systemic
hypertension
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PEDIATRICS- RESPIRATORY DISORDERS OF THE NEWBORN

DISEASES CLINICAL MANIFESTATIONS DIAGNOSIS & PROGNOSIS MANAGEMENT

MECONIUM ASPIRATION Manifestations: Chest radiograph: Prevention:
- Meconium stained amniotic fluid found in 1) Tachypnea 1) Patchy infiltrate 1) Rapid identification of fetal distress
10-15% of births, usually occurs in term or 2) Retractions 2) Coarse thickening of both lung fields 2) Initiation of prompt delivery in the presence of late
post-term infants 3) Grunting 3) Increased anteroposterior diameter fetal heart rate deceleration or poor beat-to-beat fetal
- Meconium Aspiration Syndrome (MAS) 4) Cyanosis 4) Flattening of the diaphragm heart rate variability
develops 5% of such infants
- 30% require mechanical ventilation Normal chest roentgenogram in infant with severe Treatment:
- 3-5% die hypoxemia and no cardiac malformation 1) Supportive care
suggests Pulmonary Hypertension 2) Standard management for respiratory distress
3) HFV or ECMO for infant refractory to conventional
Prognosis: mechanical ventilation
- Mortality rate of meconium-stained infants is
higher than non-stained infants
- Ultimate prognosis depends on the extent of
CNS injury from asphyxia and the presence
of associated problems (like pulmonary
hypertension)

DIAPHRAGMATIC HERNIA
- A communication between the
abdominal and thoracic cavities with or
without abdominal contents in the thorax
- Etiology: congenital but may be traumatic
- Location:
1) Esophageal Hiatus (Hiatal)
2) Paraesophageal (adjacent to the
hiatus)
3) Retrosternal (Morgagni)
4) Posterolateral portion of the
diaphragm (Bochdalek)
CDH/Bochdalek - Respiratory distress (cardinal sign) Diagnosis: - Aggressive respiratory support
- congenital diaphragmatic hernia  Seen after birth or a 1) Prenatal UTZ (between 16 and 24wk of 1) Rapid endotracheal intubation
- 90% of the hernias seen in newborn “honeymoon” period of up to gestation) 2) Sedation
- 80-90% occur on the left side 48hr  Polyhydramnios 3) Paralysis
- Incidence 1/2,000 and 1/5,000 live births  Characterized by:  Chest mass - Ventilation Strategies
- Female affected twice as often as males 1) Tachypnea  Mediastinal shift 1) Conventional Mechanical Ventilation
- Defects are common on the left (85%) and 2) Grunting  Gastric bubble 2) HFOV
are occasionally (<5%) bilateral 3) Use of accessory muscles  Fetal hydrops 3) ECMO
- Sporadic, but familial cases are reported 4) Cyanosis 2) High-speed MRI can further define the lesion - Goal: Maintain oxygenation and carbon dioxide
- Scaphoid abdomen with increased 3) Chest radiograph (after delivery) elimination without inducing volume trauma
Associated anomalies: chest wall diameter  Echogenic chest mass - Novel Strategies: Fetal ultrasonography
1) CNS lesions - Bowel sound may also be heard in - Surgical Repair
2) Esophageal atresia the chest with decreased breath Characterized by a structural diaphragmatic
3) Omphalocele sound bilaterally defect, major limiting factor for survival is the
4) Cardiovascular lesions - Point of maximal impulse may be associated pulmonary hypoplasia
5) Chromosomal syndromes: displaced away from the side of the - Pulmonary Hypoplasia: reduction in
 Trisomy 21, 13, 18 hernia if mediastinal shift has pulmonary mass and the number of
 Fryns occurred bronchial divisions, respiratory bronchioles,
 Branchmann-de Lange - Vomiting is seen on patients with and alveoli
 Pallister-Kilian delayed presentation  Pathology: abnormal septa in the
 Turner - Incarceration of intestine proceeds to terminal saccules, thickened alveoli,
ischemia with sepsis and shock. and thickened pulmonary arterioles.
 Biochemical abnormalities: relative
surfactant deficiencies, increased
glycogen in the alveoli, and decreased
levels of phosphatidylcholine, total
DNA, and total lung protein.

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PEDIATRICS- RESPIRATORY DISORDERS OF THE NEWBORN

DISEASES CLINICAL MANIFESTATIONS DIAGNOSIS & PROGNOSIS MANAGEMENT

Foramen of Morgagni Hernia Manifestations: - Chest X-ray radiograph Surgical repair:
- Anteromedial diaphragmatic defect 1) Recurrent respiratory infection  Structure behind the heart, and a 1) Laparoscopic
through the foramen of Morgagni 2-6% of 2) Cough lateral film localizes the mass to the 2) Open
diaphragmatic defects 3) Vomiting retrosternal area
- Failure of the sternal and crural portions of 4) Reflux - Chest CT or MRI: will confirm the diagnosis
the diaphragm to meet and fuse produces 5) Incarceration (rare)
this defect.
- Defects are small with a greater transverse
than anteroposterior diameter
- Commonly right-sided (90%) but may be
bilateral
Paraesophageal Hernia Risk factors: Prompt surgical repair
- GEJ is in normal location 1) Previous Nissen fundoplication
- Herniation of the stomach is alongside or 2) Other diaphragmatic procedures
adjacent to the GEJ and is prone to
incarceration with strangulation and
perforation
EVENTRATION - Elevation produces a paradoxical - Association with: - Do not require repair
- An abnormal elevation motion of the affected hemi 1) Pulmonary sequestration
- Consisting of a thinned diaphragmatic diaphragm 2) CHD
muscle that causes elevation of the entire - Asymptomatic 3) Chromosomal trisomy
hemi diaphragm or its anterior aspect
EXTRAPULMONARY AIR LEAKS (PNEUMOTHORAX, PNEUMOMEDIASTINUM, PULMONARY INTERSTITIAL EMPHYSEMA, PNEUMOPERICARDIUM)
Pneumothorax Manifestations: Definition:
- Asymptomatic Pneumothorax: - Asymptomatic Pneumothorax - Pneumomediastinum: the volume of
 Unilateral  Hyperresonance escaped air is great enough to collect in the
 Occur in 1-2% of all newborn infants  Diminished breath sounds over mediastinal space.
- Symptomatic Pneumothorax & the involved side - Pneumothorax: the volume of escaped air is
Pneumomediastinum: less common  With or without tachypnea great enough to rupture into the pleural
- Incidence is increased in infants with lung - Symptomatic Pneumothorax space
diseases, those who receive assisted  Respiratory distress - Subcutaneous Emphysema: escaped air in
ventilation, and in infants with urinary track  Tachypnea the subcutaneous tissue
anomalies or oligohydramnios  Cyanosis - Pneumoperitoneum: escaped air in the
 Early signs: peritoneal cavity
Etiology & Pathophysiology: 1) Irritability - Pneumopericardium: escaped air in the
- Most common cause is Overinflation 2) Restlessness peritoneal cavity and/or pericardial sac
resulting to alveolar rupture 3) Apnea - Pulmonary air embolism: air may embolize
- May be spontaneous or caused by  Onset: sudden, may be gradual into the circulation
underlying pulmonary disease  Chest appear asymmetric with - Tension pneumothorax: occurs if an
- Pneumothorax with pulmonary hypoplasia an increased AP diameter and accumulation of air within the pleura space
is common & occurs during the 1st few hr bulging of the intercostal space is sufficient to elevate intrapleural pressure
after birth – caused by reduced alveolar on the affected side above atmospheric pressure.
surface area and poorly compliant lungs  Hyper-resonance
- Associated with:  Diminished or absent breath
1) Disorders of decreased amniotic fluid sounds
 Potter syndrome  Heart is displaced towards the
 Renal agenesis unaffected side
 Renal dysplasia  Diaphragm is displaced
 Chronic amniotic fluid leak downward
2) Decreased fetal breathing movement - Tension Pneumothorax
 Oligohydramnios  Signs of shock may be noted
 Neuromuscular disease
3) Pulmonary space-occupying lesions
 Diaphragmatic hernia
 Pleural effusion
 Chylothorax
4) Thoracic abnormalities
 Thoracic dystrophies

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PEDIATRICS- RESPIRATORY DISORDERS OF THE NEWBORN

DISEASES CLINICAL MANIFESTATIONS DIAGNOSIS & PROGNOSIS MANAGEMENT

Pneumomediastinum - Usually Asymptomatic
- Can occur in patients with pneumothorax  Degree of RD depends on the
amount of trapped gas
 If it is great, bulging of the
midthoracic area is observed,
neck veins distended, BP is low
 Subcutaneous Emphysema
(pathognomonic sign)
Pulmonary interstitial emphysema Radiography Treatment:
- May precede the development of a - Edge of the collapsed lung standing out in - Bronchoscopy in patients with evidence of mucous
pneumothorax or may occur relief against the pneumothorax plugging
independently - Pneumomediastinum – hyperlucency - Selective intubation and ventilation of uninvolved
- Lead to increasing RD as a result of around the heart border and between the bronchus
decreased compliance, hypercapnia, & sternum and the heart border - Oxygen
hypoxemia - General respiratory care
- Progressive enlargement of blebs of gas - HFV
may result in cystic dilation and respiratory
deterioration resembling pneumothorax.
- In severe cases – precedes BPD
Pneumopericardium General Treatment:
- May be asymptomatic - without continued air leak, asymptomatic, and mildly
- Usually manifested as sudden shock with symptomatic small pneumothoraces:
tachycardia, muffled heart sounds, and  Close Observation
poor pulses suggesting tamponade  Conservation management
Pneumoperitoneum  Frequent small feedings
- Can result in an abdominal compartment  Breathing 100% O2
syndrome requiring decompression. Severe respiratory or circulatory embarrassment
- Emergency aspiration
- Chest tube insertion
- Prompt evacuation (for Pneumopericardium)
- Sedation (for infant fighting intubation)
- Surfactant therapy for RDS
PULMONARY HEMORRHAGE Manifestations: Radiography: Treatment:
- Relatively uncommon - Respiratory distress - Varied and nonspecific 1) Blood replacement
- But with high risk of morbidity and mortality - Severe cases: - Ranging from minor steaking or patchy 2) Suctioning
- Occurs in about 10% of ELBW  Sudden cardiovascular collapse infiltrates to massive consolidation 3) Intratracheal administration of epinephrine
 Poor lung compliance - Usually Bilateral pleural infiltrate 4) HFV (in some cases)
Associated with:  Profound cyanosis 5) Intensive supportive treatment
1) Significant ductal shunting  Hypercapnia Incidence increased in association with:
2) High pulmonary blood flow - Hemoptysis 1) Acute pulmonary infection
3) Severe left-sided heart failure - Blood in nasopharynx or airway with 2) Severe asphyxia
no evidence of upper respiratory or 3) RDS
GIT bleeding 4) Assisted ventilation
5) PDA
6) CHD
7) Erythroblastosis fetalis
8) Hemorrhagic disease of the newborn
9) Thrombocytopenia
10) Inborn errors of ammonia metabolism
11) Cold injury
12) Surfactant treatment – only seen in
Pulmonary hemorrhage