Neonatal and Pediatric Respiratory Failure Flashcards

1
Q

What are the five stages of fetal lung development?

A
  1. Embryonic (weeks 4-7)
  2. Pseudoglandular (weeks 5-17)
  3. Canalicular (weeks 16-25)
  4. Saccular (weeks 24-birth)
  5. Alveolar (week 36 to age 8)
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2
Q

What occurs in the embryonic stage (weeks 4-7) of lung development?

A

Lung bud forms, develops into trachea, bronchial buds, and mainstem bronchi. Errors can lead to tracheoesophageal fistula.

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3
Q

What occurs in the Pseudoglandular (weeks 5-17) of lung development?

A
  • Endodermal tubules transition to terminal bronchioles.
  • Surrounded by modest capillary network.
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4
Q

At what stage do pneumocytes start developing?

A

Week 20 in the canalicular phase.

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5
Q

At what week is respiration viable?

A

Around week 25, when alveolar ducts and primitive air sacs start forming (saccular phase) where alveolar ducts and terminal sacs begin to develop. The terminal sacs are separated by 1° septae.

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6
Q

What major changes occur at birth to transition from fetal to neonatal respiration?

A

Air replaces lung fluid, leading to a decrease in pulmonary vascular resistance.

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7
Q

What are the cardinal symptoms for respiratory distress in newborns?

A
  • Tachypnea
  • Grunting
  • Nasal flaring
  • Subcostal and intercostal retractions
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8
Q

What is bronchopulmonary dysplasia (BPD)?

A

A chronic lung disease of premature infants characterized by prolonged oxygen dependence and lung injury. Infants born prematurely have arrested lung development, typically during the saccular stage (week 26-birth) when terminal sacs normally form and undergo septation. Disrupted alveolarization leads to decreased number and septation of alveoli, resulting in reduced surface area for gas exchange. In addition to prematurity, another risk factor for BPD is prolonged mechanical ventilation, which is associated with fibrotic lung injury and scarring. However, with increased use of noninvasive ventilation techniques and avoidance of oxygen toxicity, fibrocystic changes are less common and usually associated with more severe disease. BPD is diagnosed clinically in a premature infant with findings persistent oxygen requirement for ≥28 days, clinical signs of respiratory disease (eg, tachypnea, retractions, crackles, wheeze), and a chest x-ray with diffuse hazy infiltrates with variable lung volumes (low or normal in most cases). Treatment is supportive and includes optimizing nutrition, restricting fluids, and weaning supplemental oxygen as tolerated.

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9
Q

What are the highest risk factors for developing bronchopulmonary dysplasia?

A

Prematurity (most commonly), low birth weight, mechanical ventilation, and oxygen toxicity. The primary risk factor for this chronic lung condition is prematurity; the incidence of BPD is inversely correlated to gestational age, and most patients are born at gestational age <28 weeks.

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10
Q

How does bronchopulmonary dysplasia typically present in neonates?

A

Tachypnea, retractions, rales, and persistent oxygen requirement beyond 28 days after birth.

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11
Q

What imaging finding is characteristic of bronchopulmonary dysplasia?

A

Diffuse lung opacities with areas of atelectasis and hyperinflation on chest X-ray.

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12
Q

What is the primary management strategy for bronchopulmonary dysplasia?

A

Keep oxygen levels LOW, mechanical ventilation with minimal settings, fluid restriction, and diuretics if necessary.

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13
Q

How does lung function change in bronchopulmonary dysplasia patients as they age?

A

Lung function improves over months to years, with complete development by 8 years old.

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14
Q

What causes neonatal respiratory distress syndrome (NRDS)?

A

Insufficient surfactant production leading to alveolar collapse (atelectasis). What is deficient are lamellar bodies.

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15
Q

What are the risk factors for neonatal respiratory distress syndrome?

A

Prematurity, C-section delivery, and maternal diabetes.

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16
Q

What is the pathognomonic chest X-ray finding in neonatal respiratory distress syndrome?

A

Diffuse ground-glass opacities and low lung volumes.

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17
Q

What is the treatment for neonatal respiratory distress syndrome?

A

CPAP, supplemental oxygen, surfactant administration, and mechanical ventilation if severe.

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18
Q

What are the complications of neonatal respiratory distress syndrome?

A

PDA and bronchopulmonary dysplasia.

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19
Q

How can neonatal respiratory distress syndrome be prevented in premature infants?

A

Antenatal corticosteroids (e.g., betamethasone) given to mothers before preterm delivery.

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20
Q

What causes transient tachypnea of the newborn (TTN)?

A

Delayed clearance of alveolar fluid leading to mild pulmonary edema.

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21
Q

What are the risk factors for transient tachypnea of the newborn?

A

TTN is a condition caused by retained fetal lung fluid after delivery. Prematurity, C-section delivery, maternal diabetes are the main risk factors. Newborns have respiratory distress and the imaging findings consistent with transient tachypnea of the newborn (TTN). Patients born prematurely or by cesarean section are at increased risk, as typical resorptive mechanisms are activated at term and during labor. TTN also occurs more frequently in infants born to mothers with diabetes due to impaired fluid clearance in the diabetic fetal lung. TTN presents shortly after birth with tachypnea, increased work of breathing (eg, retractions, nasal flaring), and often cyanosis. However, breath sounds are usually clear on examination.

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22
Q

What chest X-ray finding is seen in transient tachypnea of the newborn?

A

Bilateral perihilar linear streaks. Hyperinflation (ie, flattened diaphragm), mild cardiomegaly, prominent vascular markings, fluid in the interlobar fissures, and pleural effusions may be seen on chest x-ray.

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23
Q

How is transient tachypnea of the newborn managed?

A

Supportive care with supplemental oxygen; self-resolves in 24-72 hours. The symptoms usually resolve spontaneously within 72 hours with no long-term complications.

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24
Q

What is the pathophysiology of persistent pulmonary hypertension of the newborn (PPHN)?

A

Failure of normal pulmonary vascular resistance decline, leading to persistent right-to-left shunting.

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25
Q

What are the risk factors for persistent pulmonary hypertension of the newborn?

A

Meconium aspiration, perinatal asphyxia, congenital diaphragmatic hernia.

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26
Q

What is the unique clinical sign of persistent pulmonary hypertension of the newborn?

A

Differential cyanosis: oxygen saturation is higher in the right hand than in the lower extremities.

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27
Q

What is the treatment for persistent pulmonary hypertension of the newborn?

A

100% oxygen, inhaled nitric oxide, sildenafil, or ECMO in severe cases.

28
Q

What causes meconium aspiration syndrome?

A

Aspiration of meconium-stained amniotic fluid causing airway obstruction and chemical pneumonitis.

29
Q

What is the hallmark chest X-ray finding in meconium aspiration?

A

Patchy infiltrates with hyperinflation.

30
Q

How is meconium aspiration syndrome managed?

A

Intubation with suction avoidance, oxygen support, antibiotics for possible secondary infection.

31
Q

What is a significant long term complication of meconium aspiration syndrome?

A

Permanent neurocognitive impairment is a severe complication of birth asphyxia due to meconium aspiration syndrome, which presents at delivery with respiratory distress from meconium-stained amniotic fluid.

32
Q

What is apnea of prematurity?

A

Cessation of breathing for >20 sec in a premature infant due to an immature respiratory drive.

33
Q

How is apnea of prematurity managed?

A

Supportive care, CPAP, caffeine therapy (methylxanthines).

34
Q

What is the most common cause for neonatal pneumonia?

A
  • Before 72 hours, Group B Streptococcus (GBS) and Escherichia coli.
  • After 72 hours, MRSA, Pseudomonas aeruginosa, Klebsiella pneumoniae, and Acinetobacter species.
35
Q

How do you differentiate a pulmonary cause from a cardiac cause of neonatal respiratory failure?

A

If supplemental oxygen improves saturation, the cause is pulmonary; if not, it is likely cardiac (e.g., congenital heart disease with right-to-left shunting).

36
Q

What is the first-line treatment if a congenital heart defect is suspected?

A

Prostaglandin E1 to keep the ductus arteriosus open.

37
Q

What is Laryngomalacia?

A

The most common congenital cause of inspiratory stridor in infants due to collapse of supraglottic structures during inspiration.

38
Q

What causes Laryngomalacia?

A

Immature, soft, and floppy laryngeal cartilage leading to dynamic airway obstruction.

39
Q

What is the most common presentation of Laryngomalacia?

A

Chronic, intermittent inspiratory stridor that worsens when supine, crying, or feeding and improves when prone.

40
Q

At what age does Laryngomalacia typically present?

A

Within the first 4-8 weeks of life.

41
Q

What position improves Laryngomalacia symptoms?

A

Prone position, due to gravity stabilizing the airway.

42
Q

How is Laryngomalacia diagnosed?

A

Clinical diagnosis confirmed by flexible laryngoscopy showing an omega-shaped epiglottis and inspiratory collapse of supraglottic structures.

43
Q

What is the treatment for mild Laryngomalacia?

A

Reassurance and close follow-up, as it resolves spontaneously by 12-18 months.

44
Q

When is surgical intervention needed for Laryngomalacia?

A

Severe symptoms such as feeding difficulties, apnea, significant hypoxia, or failure to thrive warrant supraglottoplasty.

45
Q

What associated condition should be considered in Laryngomalacia?

A

Gastroesophageal reflux disease (GERD), as it can exacerbate symptoms.

46
Q

What is the surgical procedure for severe Laryngomalacia?

A

Supraglottoplasty.

47
Q

What is the differential diagnosis for Laryngomalacia?

A

Vascular rings (biphasic stridor, feeding difficulties), Tracheomalacia (expiratory stridor), and Foreign body aspiration (sudden onset, localized wheezing).

48
Q

What is the prognosis for infants with Laryngomalacia?

A

Excellent prognosis; symptoms typically resolve by 12-18 months as the laryngeal cartilage matures.

49
Q

How does Laryngomalacia differ from Tracheomalacia?

A

Laryngomalacia causes inspiratory stridor, while Tracheomalacia causes expiratory stridor.

50
Q

What classic finding is seen on laryngoscopy in Laryngomalacia?

A

Omega-shaped epiglottis and inspiratory collapse of supraglottic structures.

51
Q

Why does Laryngomalacia worsen when supine?

A

Increased airway collapse due to gravity affecting the weak supraglottic structures.

52
Q

Why is GERD often associated with Laryngomalacia?

A

GERD can contribute to inflammation and worsening airway collapse, exacerbating symptoms.

53
Q

How is GERD managed in infants with Laryngomalacia?

A

Acid suppression therapy such as H2 blockers or PPIs if significant reflux symptoms are present.

54
Q

What is the typical age group for foreign body aspiration?

A

1-3 years old.

55
Q

What are the symptoms of foreign body aspiration?

A

Sudden onset of coughing, wheezing, stridor, and unilateral decreased breath sounds. Children can also assume the tripod position.

56
Q

How can signs and symptoms guide the acute management for airway obstruction?

A
  • For a partial obstruction, the worst signs are simply coughing and/or gagging.
  • For a complete obstruction, the worst signs are respiratory distress and cyanosis, along with hands clutched at throat with the inability to breath, cough or speak.
57
Q

What are the immediate steps for a child who has a complete airway obstruction?

A
  • Children age <1 should be placed face and head down on the rescuer’s arm and receive 5 back blows and then turned on the back and receive 5 chest thrusts; abdominal thrusts are generally avoided due to potential damage to the liver in infants. Chest thrusts are not recommended in children age ≥1.
  • In children age ≥1, abdominal thrusts (Heimlich maneuver) should be performed to dislodge the aspirated object. The rescuer should stand behind the child, lean the child forward, and perform upward thrusts into the abdomen just above the navel; this produces a rapid increase in intrathoracic pressure and may dislodge the object. As an alternative, 5 back blows alternating with 5 abdominal thrusts can be performed with the child leaning forward in front of the rescuer.
58
Q

How is foreign body aspiration diagnosed?

A

Chest x-ray with inspiratory/expiratory views or CT scan if equivocal.

59
Q

What is the management for partial obstruction?

A

Flexible bronchoscopy.

60
Q

What is the management for complete obstruction?

A

Back blows (infants), Heimlich maneuver (older children), emergent rigid bronchoscopy.

61
Q

What are the risk factors for foreign body aspiration in children?

A

Playing with small objects, eating while running, lack of molars.

62
Q

Foreign bodies in the pharynx or laryngeal inlet can often be extracted by

A

Magill forceps

These are used after laryngeal exposure with a standard laryngoscope. The patient will usually vomit, so suction is mandatory.

63
Q

Bronchial foreign bodies will require ______ for removal.

A

Operative bronchoscopy

Occasionally, a tracheotomy will be required, such as for a patient who has aspirated a partial denture with imbedded hooks.

These patients can present as airway emergencies, although they more typically present with unexplained cough or pneumonia.

64
Q

If a ball-valve obstruction results, hyperinflation of the obstructed lobe or segment can occur and this is easier to visualize on __________ .

A

inspiration-expiration films

65
Q

hyperinflation of the obstructed lobe or segment following an aspiration is due to to a … ?

A

ball-valve obstruction