PPHN and respiratory distress in the newborn Flashcards

1
Q

How does PPHN usually present

A
  1. Usually presents within first 12 hours of birth with severe hypoxemia, cyanosis with mild respiratory
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2
Q

Pathophysiology of PPHN

A
  1. Increased pulmonary resistance->persistence of fetal circulation
  2. Right to left shunt through PDA, foramen ovale
  3. Further reduction in lung blood flow= pulmonary vasoconstriction
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3
Q

Risk factors for secondary and primary PPHN

A
1. Secondary
Asphyxia
Meconium aspiration
Respiratory distress
Sepsis
Pneumonia
Structural defects (diaphragmatic hernia, pulmonary hypoplasia)
2. Primary->PPHN occurs without additional risk factors
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4
Q

Investigations in PPHN

A
  1. Measure pre and post ductal oxygen levels

2. Echo->increased pulmonary arterial pressure

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5
Q

Management in PPHN

A
  1. ABC, oxygen
  2. Minimise stress
  3. Normalise blood gases and circulation
  4. Mechanical ventilation
  5. Nitric oxide
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6
Q

Clinical presentation of respiratory distress in newborn

A
  • tachypnea: RR >60/min; tachycardia: HR >160/min
  • grunting, subcostal/intercostal indrawing, nasal flaring
  • duskiness, central cyanosis
  • decreased air entry, crackles on auscultation
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7
Q

Differential diagnosis of respiratory distress in newborn

A
1. Pulmonary
ƒƒRespiratory distress syndrome (RDS)
ƒƒTransient tachypnea of the newborn (TTN)
ƒMeconium aspiration syndrome (MAS)
ƒPleural effusions, pneumothorax
ƒƒCongenital lung malformations
2. Infectious
ƒƒ Sepsis, pneumonia
2. Cardiac
ƒƒCongenital heart disease (cyanotic, acyanotic)
ƒƒPersistent pulmonary hypertension of the newborn (PPHN)
3. Hematologic
ƒƒBlood loss, polycythemia
4. Anatomic
ƒTracheoesophageal fistula
ƒƒCongenital diaphragmatic hernia
ƒƒUpper airway obstruction (see Otolaryngology, OT44)
ŠŠChoanal atresia
ŠŠPierre-Robin sequence (retrognathia ± micrognathia, cleft palate, glossoptosis)
ŠŠLaryngeal (malacia)
ŠŠTracheal (malacia, vascular ring)
ŠŠMucous plug
ŠŠCleft palate
5. Metabolic
ƒƒHypoglycemia
ƒƒInborn errors of metabolism (amino acidemia, organic acidemia, urea cycle disturbance, galactosemia, 1° lactic acidosis)
6. Neurologic
ƒƒCNS damage (trauma, hemorrhage)
ƒƒdrug withdrawal syndromes
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8
Q

Investigations in respiratory distress of newborn

A
  1. CXR- in all infants once 02 requirements exceded 30%, repeat in prolonged or unusual
  2. ABG
  3. Echo, ECG if indicated
  4. FBE, BC before starting antibiotics if possible
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9
Q

Etiology of respiratory distress

A
  1. Surfactant deficiency ->poor lung compliance due to
    high alveolar surface tension ->atelectasis -> -vesurface area for gas exchange  hypoxia + acidosis -> respiratory distress
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10
Q

Risk factors of RDS

A
Maternal diabetes
Preterm delivery
Male sex
Low birth weight
Acidosis, sepsis
Hypothermia
Second born twin
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11
Q

Clinical features of RDS

A
  1. Onset in first few hours of life
  2. Worsens over 24-72 hours
  3. Respiratory distress
  4. Hypoxia
  5. Cyanosis
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12
Q

Homogenous CXR findings

A
  1. Homogenous ifiltrates
  2. Air bronchograms
  3. Decreased lung volumes
  4. May resemble pneumonia
  5. If severe->may have white out
  6. Reticulogranular pattern
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13
Q

What is TTN, risks, presentation, CXR

A
  1. Transient tachypN of newbord
  2. Delayed resorption of fetal lung fluid->accumulation of fluid in peribronchial lymphatics and vascular space= tachyP
  3. More common in term and late preterm
  4. Risks
    Maternal diabetes
    Maternal asthma
    Male
    Macrosomia
    Elective C section
    Late preterm
  5. TachyP w/i first few hours, resp distress, no hypoxia or cyanosis
  6. Perihilar infiltrates
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14
Q

Treatment for RDS

A
  1. ABC
  2. Oxygen
    Avoid hypoxemia->target 85-95% in 34 weeks
  3. Ventilation
  4. SUrfactant after ETT
  5. Thermoregulation
  6. Antibiotics->as differential, until BC proves negative. Penicillin + gentamicin
  7. Temperature control
  8. Prevent hypoglycemia
  9. IV fluids
  10. Minimal handling
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15
Q

Treatment of TTN

A
  1. Supportive
  2. Oxygen
  3. IV fluids and lavage feeds
  4. Observe for progression, consider other
  5. Ensure X respiratory fatigue
  6. Recovery usually within 3 days
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16
Q

What is retinopathy of prematurity

A
  1. Vasoproliferative
    • stage 1: faint demarcation line at the junction between the vascularized and avascular retina
    • stage 2: elevated ridge
    • stage 3: extra-retinal fibrovascular tissue extending into vitreous
    • stage 4: partial retinal detachment (4A: macula “on”, 4B: macula “off”)
    • stage 5: total retinal detachment
    • plus (+) disease: dilatation and tortuosity of retinal vessels
  2. Treated with cryptherapy or laser
  3. Important cause of blindness worldwide