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RESP 5017 > 4. Pulmonary Disorders (RDS, TTN, BPD) > Flashcards

4. Pulmonary Disorders (RDS, TTN, BPD) Flashcards

1
Q

What are the 6 classic signs of neonatal distress?

A
  1. Nasal Flaring
  2. Cyanosis
  3. Expiratory Grunting
  4. Tachypnea
  5. Retractions
  6. Hyperdynamic Precordium
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2
Q
  1. What is nasal flaring?

2. Why does this occur, and why is it seen more in neonates?

A
  1. Dilatation of nostrils on inspiration
  2. Occurs due to increased demand & attempt to decrease resistance, neonates are obligate nose breathers until 3-4 months
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3
Q
  1. How many g/dL of deoxygenated Hb is needed to cause cyanosis?
  2. Does central or peripheral cyanosis pose more of a threat to the infant? Why?
A
  1. 5 g/dL Hb will generate the dark blue colour

2. Central cyanosis is more of a threat because the baby needs O2 right away, peripheral is OK in first 24 hrs of life

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4
Q
  1. What is expiratory grunting?

2. Why would an infant grunt?

A
  1. Exhalation against a partially closed glottis

2. To ↑ FRC, lungs are a bit collapsed, so baby grunts to ↑ lung volumes (creates back pressure)

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5
Q
  1. What is tachypnea in a newborn classified as?
  2. What about in paediatrics?
  3. Usual causes of tachypnea in a newborn?
A
  1. RR > 60 bpm in newborns
  2. Age dependent in peds
  3. Hypoxemia, acidosis, anxiety, pain
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6
Q

What breathing pattern is seen with poor lung compliance?

A

Rapid, shallow breathing

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7
Q
  1. What are chest retractions caused by?
  2. What is observed when retractions are present, and why?
  3. What are the 6 types of retractions?
A
  1. Lung compliance is stiffer than chest wall compliance
  2. Chest wall sucked in due to high negative pressure
  3. -Sternal
    - Substernal
    - Supraclavicular
    - Suprasternal
    - Intercostal
    - Subcostal
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8
Q
  1. What is a hyperdynamic precordium?

2. What is it usually associated with?

A
  1. ↑ motion visualized through the chest in the area of the heart
  2. ↑ volume load on the heart secondary to L → R shunt through the PDA
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9
Q
  1. What is RDS?
  2. What is incidence inversely related to?
  3. Leading cause of ____?
A
  1. Deficiency of pulmonary surfactant and immature lungs
  2. Incidence inversely related to gestational age
  3. Death among premature infants
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10
Q
  1. Causes of RDS?

2. Who does RDS affect more often & how much?

A
  1. Surfactant deficiency or abnormality, prematurity, immature lungs, pulmonary hypoperfusion d/t hypoxia, idiopathic
  2. Occurs more often in males and is usually more severe
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11
Q

Pathophysiology of RDS

A
  1. Surfactant deficiency (↑ surface tension)
  2. ↓ lung compliance ( ↓ FRC, atelectasis)
  3. V/Q mismatch w/ poor gas exchange (hypoxia, hypercarbia, acidosis)
  4. Interstitial and intra-alveolar edema
  5. Leakage of proteinaceous exudate and formation of hyaline membranes
  6. Hypoxia induced pulmonary vasoconstriction (↑ PVR)
  7. R → L shunt across patent FO and DA
  8. Lung hypoperfusion → ischemia → decreased lung metabolism
  9. Pulmonary surfactant reduced even further
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12
Q
  1. Secondary Surfactant deficiency may occur in infants with the following:
  2. What can SSD lead to ?
A
  1. Intrapartum asphyxia, pulmonary infections, pulmonary hemorrhage, meconium aspiration pneumonia, oxygen toxicity along w/ barotrauma or volutrauma
  2. RDS
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13
Q

Causes of ↓ surfactant production

A

Prematurity, familial predisposition, C section w/o labour, perinatal asphyxia, maternal diabetes, chorioamnionitis, cold stress

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14
Q

Causes of ↑ surfactant production

A

Chronic intra-uterine stress, prolonged pPROM, maternal HTN, IUGR/SGA, Antenatal glucocorticoids, maternal use of narcotics, tocolytics

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15
Q

What can be used to prevent/minimize RDS? (7 things)

A
  1. Delay/prevent premature birth
  2. Antenatal steroids
  3. Early intervention (prevent cold stress, hypoglycaemia, hypoxemia) “warm, sweet, pink”
  4. O2 therapy
  5. Surfactant replacement
  6. Nasal CPAP
  7. Nasal NIV
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16
Q

S&S of RDS?

A

Tachypnea, tachycardia, ↑ WOB (nasal flaring, grunting, retractions), cyanosis requiring O2, crackles, ↓ activity, apnea

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17
Q

How is a diagnosis of RDS made? (ex. what is seen in the newborn/what can be done for confirmation of diagnoses?)

A

Clinical history (is baby premature?), clinical assessment, onset of progressive resp failure shortly after birth, CXR

18
Q

What is seen in an RDS CXR?

A

Low lung volumes, diffuse reticular granular pattern (frosted appearance), air bronchograms to the periphery

19
Q

What is the RDS clinical course? (4 features)

A

Resp. failure beginning at birth
Max severity by 24-48 hrs
Rapid improvement over 3-5 days
May progress to chronic changes = BPD

20
Q

What is the RDS management protocol?

A

Early CPAP, surfactant if indicated, extubate after surfactant if able and place on CPAP/NIPPV, avoid lung derecruitment, avoid hyperoxia

21
Q

What are the RDS mcvent strategies?

A

Avoid volutrauma, effective lung recruitment, extubate ASAP to NIV

22
Q

What are the RDS supportive care strategies?

A

Thermoregulation, fluid management, nutrition (breast milk, vitamin A, E

23
Q

What are the complications of RDS?

A

Air leaks, chronic changes leading to BPD, tracheal stenosis, reactive airway disease, ↑ risk of infection, intraventricular hemorrhage (IVH), retinopathy of prematurity (ROP), necrotizing enterocolitis (NEC)

24
Q
  1. What is Transient Tachypnea of a Newborn (TTN)? What does this do to the lungs?
  2. What is TTN also known as?
  3. Who does it affect most?
  4. When does it present? Resolve?
A
  1. Fast and shallow breathing pattern, causes delayed reabsorption of fetal lung fluid (fluid in air spaces, wet lung)
  2. RDS Type II
  3. Term or near term infants
  4. Presents at or shortly after birth, resolves within 24-48 hrs
25
Q

Physiology of Fetal Lung Fluid at Birth (3 stages!)

A
  1. Labour → high circulating conc. of epi activates the switch w/i lungs from net secretion to net reabsorption
  2. Vaginal squeeze of thorax contributes to very small portion of lung fluid re-absorption
  3. Interstitial lung fluid moves into the pulmonary circulation (giving baby self transfusion of fluid) or drains via lung lymphatics
26
Q
  1. Why is lung fluid retained in TTN?

2. What does this cause? (3 things)

A
  1. Incomplete absorption of pulmonary fetal fluid, ↓ removal of fluid by pulmonary lymphatics
  2. Alveolar fluid, interstitial edema, compressed bronchial airways (from excessive A-C interstitial fluid, causes air trapping and alv. hyperinflation)
27
Q

Causes of TTN?

A

Full term pregnancy, delivery by C/S (esp. cold section, ↓ squeeze, ↓ catecholamines) precipitous vaginal deliveries (↓ squeeze, ↓ catecholamines), maternal analgesia/anesthesia during labour and delivery, intrauterine hypoxia, prematurity or SGA/IUGR babies

28
Q

S&S of TTN?

A

Tachypnea (as high as 120 bpm), rapid shallow breathing, nasal flaring, grunting, retractions, barrel shape chest from hyperinflation, wheezes and crackles may be present

29
Q

What do you see on a CXR of a baby with TTN?

A

Perihilar vascular markings, fluid in fissures (AP & lateral view), blunted costophrenic angles (small pleural effusions), hyperinflation (flattened diaphragms, bulging intercostals), patchy infiltrates

30
Q

How is TTN diagnosed?

A

History, CXR, clinical presentation, rule out other causes

31
Q
  1. How is TTN treated?
  2. What does NOT affect the clinical course of TTN?
  3. When pneumonia is suspected, what meds are indicated?
A
  1. Stabilization, monitoring, tests, oxygen therapy, CPAP, NIPPV, rarely intubation, fluid restriction is usually ordered until S&S resolve
  2. Diuretics
  3. Antibiotics
32
Q

What is BPD and who is it most common in?
What are these patients treated with?
What is BPD associated with?

A
  1. Chronic Lung Disease , most common in preterm infants w/ RDS (lower gestational age = ↑ incidence, worse severity)
  2. Mechanical ventilation, NIV, O2 therapy
  3. Significant mortality, short/long term morbidity, including growth and neurodevelopment delay
33
Q

What are the 3 risk factors for BPD?

A
  1. Prematurity, low BW
  2. White boys
  3. Genetic heritability
34
Q

What is the official BPD definition?

A

Need for oxygen based on GA and severity of disease, a trial on room air should be performed if infant on minimal O2 requirements to ensure need for O2 at time of assessment

35
Q
  1. If baby is born < 32 wks, when should assessment for BPD be done?
  2. What about >/= 32 wks?
A
  1. < 32 wks: 36 wks PMA or discharge, whichever first

2. >/= 32 wks: > 28 days but < 56 days postnatal age or discharge, whichever first

36
Q

How is a baby born < 32 wks old treated for mild, moderate, and severe BPD?

A

Treatment w/ O2 >21% for at LEAST 28 days plus…
Mild: RA at 36 wks PMA/discharge
Moderate: Need < 30% O2 at 36 wks PMA/discharge
Severe: Need >/= 30% O2 and/or PPV/NCPAP at 36 wks PMA/discharge

37
Q

How is a baby born >/= 32 wks old treated for mild, moderate, and severe BPD?

A

Treatment w/ O2 >21% for at LEAST 28 days plus…
Mild: RA by 56 days postnatal age/discharge
Moderate: Need < 30% O2 at 56 days postnatal age/discharge
Severe: Need >/= 30% O2 and/or PPV/NCPAP at 56 days postnatal age/discharge

38
Q
  1. What does “Old BPD” (before surfactant and steroids) show as on a CXR?
  2. Is this a more or less severe form of BPD? Is this commonly seen?
A
  1. Cystic changes, heterogeneous aeration

2. More severe form of BPD, not commonly seen now (only in severe cases)

39
Q

What does “New BPD” (after surfactant and steroids) show as on a CXR?

A
  1. More uniform inflation and less fibrosis
  2. Some parenchymal opacities, but more homogenous aeration and less cystic areas
  3. Larger simplified alveoli and dysmorphic pulmonary vasculature
40
Q
  1. The pathogenesis of BPD is ________.

2. What could it include? (examples!)

A
  1. Multifactorial (RDS → BPD)
  2. Prematurity, resp. distress, mechanical ventilation, NIV, O2 supplementation/toxicity, infection & inflammation, pulmonary edema as result of/and PDA, fluid overloading, nutritional deficiencies, genetics

RESP 5017 (19 decks)

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