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Respiratory Distress Syndrome Flashcards

1
Q

When was the subspecialty of Neonatology recognized?

A

1975

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2
Q

When did the NNP role emerge?

A

1970s

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3
Q

What was the first neonatal ventilator?

A

the baby bird I (followed by the bournes 200)

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4
Q

What therapies were introduced in the 1960’s?

A

1) phototherapy

2) PKU (beginning of NBS)

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5
Q

When was ECMO therapy for neonates introduced?

A

1975

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6
Q

What therapies were introduced in the 1980’s?

A

1) pulse oximeter
2) wide spread use of surfactant
3) growing used of perinatal steroids

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7
Q

How long does it take for the average practice change?

A

15-17 years

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8
Q

What is RDS?

A

respiratory distress syndrome; RDS is frequently complicated by CPIP; RDS = SURFACTANT DEFICIENCY and evolves into a compliance dz

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9
Q

What is CPIP?

A

chronic pulmonary insufficiency of the preterm; anatomic (under developed pulmonary/vascular anatomy) and functional immaturity (overly compliant chest wall, etc…) of the respiratory sytem

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10
Q

How does chronic lung disease differ from BPD?

A

CLD is used to designate the extremely PT infant who may be >28 dol of but is not yet CNA of 36 weeks with a refactory supplemental O2 requirement

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11
Q

How does the idea of old BPD differ from new BPD?

A

old BPD is essentially caused by O2 toxicity and barotrauma; new BPD is a function of dysmaturity as well as trauma

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12
Q

How does RDS differ from hyaline membrane dz?

A
  • RDS is a clinical dx

- HMD is a pathologic dx; cannot be assessed on CXR, its a histologic, pathologic ∆; dx via biopsy or autopsy

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13
Q

What population is RDS almost an exclusive dx for?

A

prematurity (some hereditary causes, ex: surfactant protein B &C deficiency)

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14
Q

What are the basic mechanisms that result in RDS?

A

1) surfactant deficiency (prematurity, hereditary, IDM, etc..)
2) surfactant production interruption/cessation (asphyxia)
3) surfactant deactivation (MAS, infx)

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15
Q

What are considered risk factors for the subsequent development of RDS?

A

1) PREMATURITY
2) sex (male)
3) maternal diabetes
4) family h/o infant with RDS
5) multiple gestation
6) CSX (r/t excessive lung fluid)
7) perinatal asphyxia
8) race (white)
9) lack of antenatal steroid therapy
10) lack of labor

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16
Q

What are the methods of preventing RDS?

A

1) prevention of PTB (incidence of 23-25 wk has been stable for decades; incidence of late PTB is decreasing)
2) antenatal steroids
3) appropriate & early recruitment (CPAP)
4) PIH (and chronic intrauterine stress reduces the incidence)
5) prevention of asphyxia
6) exogenous surf tx
7) surf + CPAP

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17
Q

What is the clinical duration of RDS?

A

if untreated, RDS will persist for 3-5 days (may improve after that time r/t physiologic diuresis); Avery’s- end of first week

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18
Q

What is the classic presentation of an infant with RDS?

A
  • grunting
  • tachypnea
  • increased WOB (nasal flaring & retractions)
  • cyanosis
  • pallor
  • lethargy
  • disinterest in feeding
  • apnea
  • diminished breath sounds
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19
Q

What is grunting?

A

physiologic CPAP; the infant is forcing air against a closed epiglottis; demonstrates that the babe is trying to help themselves; if they stop, the infant may have gotten better, or worse!

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20
Q

What is the typical RDS course from delivery room to day 3-5?

A

usually look alright coming out of the DR, FiO2 need is not excessive, may “honeymoon” for 24h. then the infant will get worse as they loose lung volume. By day 4, they diuresis with subsequent compliance improvment.

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21
Q

What is the typical RDS CXR look like?

A

1) low lung volumes
2) homogenous “ground glass”
3) air bronchograms

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22
Q

What accounts for the “ground glass” appearance on CXR?

A

micro-atelectasis; one alveoli open, one closed- creates a dotty pattern throughout all lung fields; “net like”

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23
Q

What accounts for peripheral air bronchograms?

A

air bronchograms are commonly seen because the lareg airways beyond the second or third generation are more visible than usual as a result of radiodensity from engorged peribronchial lymphatics and fluid-filled or collapsed alveoli

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24
Q

How quickly might hyaline membranes develop?

A

as early as 30 minutes

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25
How are hyaline membranes formed?
1) begin with insufficient alveoli (surf deficient/dysfx) are unstable and tend to collapse and force (spontaneous or assisted) aeration and ventilation 2) net effect on a non-compliant lung is stretched epithelium, tissue damage, acidosis & vasoconstriction (cumulative shearing stresses from opening and reclosing and overdistension damage to pulmonary epithelium) 3) damaged tissue starts to swell, leak and form proteinaceous sludge 4) proteinaceous sludge in the pulmonary parenchyma forms hyaline membranes in the alveolar space 5) creates a physical barrier to efficient and adequate gas exchange
26
What is meant by proteinaceous sludge?
the proteins and inflammatory mediators that come into the lung parenchyma
27
What percentage of LBW newborns will have some type of respiratory distress?
approximately half
28
If supportive therapy is successful, when can the repair phase of RDS be expected to being?
during dol 2
29
What occurs in the repair phase of RDS?
- appearance of macrophages and polymorphonuclear cells - sludge/ debris is then phagocytosed and the damaged epithelium is regenerated - edema fluid in the interstitium is mobilized into the lymphatics, leading to the "diuretic" phase of RDS characterized by high UOP
30
What population of infants is at greatest risk of impaired healing from RDS?
- infants born at < 1250g | - larger newborns needing higher FiO2 and PPV for severe RDS
31
What are the consequences of impaired healing from RDS?
newborns may develop inflammation and inappropriate repair of the growing lung, leading to emphysema and fibrosis
32
What is Laplace's Law?
the pressure required to inflate a bubble is proportional to the surface tension divided by the radius of the bubble
33
How does Laplace's law r/t two connected alveoli?
if you try to simultaneously inflate two interconnected bubbles, the smaller one with deflate into the larger one; a smaller radius requires greater amounts of pressure to stay inflated - if one alveoli has greater compliance of has surfactant, it's easier to move air into an already opened alveoli - net effect is that air will preferentially move into the dilated alveoli and the other is more likely to collapse
34
What are the classic diagnostic results c/w RDS?
1) V/Q mismatch 2) hypoventilation with resultant hypoxemia and hypercarbia 3) blood gases show respiratory and metabolic acidosis
35
What is the function of surf?
a surface active material that lowers surface tension | - causes fluid to spread out instead of beading up
36
How does surfactant cause alveoli to remain at relatively the same size?
- lung surfactant has the miraculous property of reducing surface tension as the size of the alveoli decreases - when the radius is very small, the surface tension falls to almost 0 - the pressure required then to keep the smaller bubble open is negligible (preventing collapse) - so as the radius of the alveoli increases, the surface tension increases; following the path of least resistance, air flows along the pressure gradient causing alveoli to be about the same size
37
How does wide spread alveolar collapse result in R > L shunting?
collapsed atelectatic lung > decreased compliance > decreased FRC > increased dead space > V/Q mismatch > R-L shunt
38
How does intrapulmonary shunting occur?
with increased intrapulmonary pressures, generated from collapsed alveoli, blood is shunted away without the opportunity for blood in pulmonary capillaries to pick up O2 from, or deliver Co2 to, the alveoli
39
How does alveolar collapse contribute to PPHN?
lungs that are poorly inflated have widespread collapse of pulmonary vessels, leading to pulmonary hypertension
40
How does alveolar collapse exacerbate a PDA?
the elevated pulmonary artery pressures lead to R > L shunting of unoxygenated blood across the ductus to the descending aorta
41
What are common complications of RDS?
1) alveolar rupture 2) infection 3) IVH (r/t hypoxic injury) 4) PDA exacerbation 5) pulmonary hemorrhage 6) CLD 7) death
42
What are common complications resulting from RDS treatment and intervention?
1) equipment injuries (nasal/ septum erosions, palatal grooving, palatal cleft) 2) hyperoxic injuries (ROP) 3) lung injuries (BPD)
43
How do air leaks occur in patients with RDS?
r/t the asymmetry of alveolar inflation and the sheer stresses in terminal bronchioles, leading to disection of air into the interstitium (PIE) and through the visceral pleura (pneumothorax)
44
What conditions are included in the term alveolar rupture?
1) pneumomedistium 2) pneumothorax 3) pneumopericardium 4) pneumoperitneum 5) collection of air underneath the skin
45
What is the incidence of PIE and pneumothorax in newborns treated with exogenous surfactant?
PIE: up to 50% pneumothorax: 5-10%
46
What is the pathophysiology of pulmonary hemorrhage secondary to RDS?
probably d/t left ventricular failure and excessive L > R flow through a PDA with resultant disruption of the pulmonary capillaries - may also be r/t insufficient vent weaning s/p surf tx with improved lung compliance
47
In what population does pulmonary hemorrhage secondary to RDS most frequently occur?
the most PT
48
What is the clinical progression and presentation of pulmonary hemorrhage secondary to RDS?
- onset is typically 1-3 days - sudden respiratory deterioration - pink or red frothy fluid in the ETT - wide spread white out on CXR
49
What are the indicated treatments for pulmonary hemorrhage?
1) increase PEEP | 2) some evidence that surf may be beneficial
50
What is the pathophysiology of BPD secondary to RDS?
probably d/t abnormal lung repair following injury from RDS
51
What are the goals of CPAP?
1) to prevent end- expiratory alveolar collapse 2) reduce the WOB 3) better match ventilation to perfusion
52
What are the disadvantages of CPAP?
1) challenge of keeping proper seal 2) difficulty handling patient 3) less risk of pressure necrosis to nares/ septum
53
What are the indicated interventions for RDS?
- increase FiO2 with spontaneous ventilation - mechanical ventilation - CPAP - surfactant replacement
54
What is the intended effect of PPV?
- alveolar recruitment | - maintenance of FRC
55
What are the functions of surf?
1) spreads out as a thin layer at air liquid interface 2) lowers surface tension 3) prevents alveolar collapse at end of expiration 4) stabilizes alveoli 5) reduces pressure needed for subsequent alveolar inflation 6) maintains FRC the composition of surfactant has evolved to balance the need for low viscosity for optimal spreading and redistribution along the smallest airways with the need for a stable and low surface tension.
56
What is DPPC?
dipalmitoylphosphatidylcholine; the main phospholipid in surfactant; also called lecithin
57
What else does DPPC need to cause surf to act efficiently?
DPPC by itself does not adsorb efficiently at the air-liquid interface and is in the form of a gel at body temperature. the presence of some unsaturated phospholipids and cholesterol help to make it more fluid.
58
What is PG?
phosphatidylglycerol; sometimes used as a marker of lung maturation (not necessary for lung function) - interacts with the hydrophobic surf proteins to improve biophysical activity
59
What is the function of free fatty acids with pulmonary surfactant?
improve the stability of the interfacial film, especially after repeated compression
60
Where is surfactant synthesized?
in the golgi apparatus of the type II pneumocytes of the lung epithelium into lamellar bodies in the form of bilayered membranes; also scavenger mechanism, recycle building blocks and "remake surfactant".
61
How is surfactant secreted?
secreted by exocytosis into the lumen of the alveolus
62
What is the function of SP-A?
hydrophilic; is an innate host defense- has some inflammatory fx
63
What are the functions of SP-B and SP-C?
1) small, hydrophobic proteins 2) facilitate rapid absorption and spreading of DPPC as a monolayer 3) this works to lower the surface tension at alveolar air-liquid interface and prevents atelectasis * available in commercially available preparations
64
What is the effect of an absent SP-B?
fatal neonatal respiratory failure
65
What is the function of SP-D?
hydrophillic; appears to bind to pathogens and assists in clearance
66
What is surfactant composed of?
90% phospholipids (6 kinds) and 10% proteins (4 kids of apoproteins)
67
Why does an infant with RDS p/w cyanosis?
cyanosis results from inadequate oxygenation
68
Why does an infant with RDS p/w pallor?
from acidosis due to poor elimination of CO2
69
What is the cumulative effect of increased WOB, cyanosis and acidosis?
causes lethargy, disinterest in feeding and eventually apnea
70
What can be appreciated on auscultation with an infant with RDS?
- breath sounds may be distant or shallow from the fast inspiratory rate and low tidal volume - fine inspiratory rales may be heard due to reopening of moist, collapsed air sacs
71
How can the duration of clinical presentation be useful in the differential diagnosis?
clinical improvement during the first 12h after birth suggests TTNB and onset after 24 h suggests PNA or sepsis
72
What can present with tachypnea without increased WOB?
cyanotic heart disease
73
What else should be included in the differential diagnosis with a "white out" CXR?
obstructed pulmonary veins from TAPVR
74
What should be suspected with hypoventilation without increased WOB?
CNS problem (ICH) or perinatal asphyxia
75
Why will the infant with RDS present with both a respiratory and metabolic acidosis?
- as the infant tires and can no longer compensate for respiratory distress, the PaCo2 will rise (r/t hypoventilation) causing respiratory acidosis - with imminent respiratory failure, there may be metabolic acidosis due to inadequate oxygen delivery to tissues and from poor peripheral perfusion (d/t respiratory acidosis) causing metabolic acidosis
76
What has research demonstrated concerning the efficacy of exogenous surfactant therapy?
compared to no tx: 1) reduces risk of pneumothorax by 58% 2) reduces risk of PIE by 55% 3) reduces mortality by 32% 4) reduces the combined outcome of BPD or death by 17%
77
What was the first commercially available exogenous surfactant?
Exosurf; entirely synthetic with no surfactant proteins in it; entirely DPPC
78
What are the protein-containing animal surfactants?
Curosurf- porcine lung tissue (lower vol req'd, little more thick and viscous) Infasurf- bovine (calf) lung lavage; the only brand that has been studied in late administration Survanta- bovine lung tissue (+ natural proteins)
79
What is the current clinical recommendation for surfactant choice (natural v synthetic)?
strongly support natural because of reduced risk of air leak and more rapid response to treatment
80
What are the supported advantages of Curosurf given prophylactically?
fewer doses req'd, quicker O2 weaning and potentially less cost (later down the road)
81
What is considered prophylactic surf tx?
administration of doses within 15 min of life
82
What should be done to avoid giving an unnecessary, expensive medication and avoid the risks of intubation when giving prophylactic surf?
should only be given to the patients who would have eventually developed RDS and met treatment criteria anyway
83
What percentage of very preterm babes have a true surfactant deficiency?
50-75%
84
What is considered early rescue surfactant therapy?
given 1-2 hours of life
85
What is considered late rescue surfactant therapy?
needing mechanical ventilation and > 40% FiO2; typically 4-6 h post birth
86
What populations should be considered for prophylactic surfactant therapy?
1) < 26 wk GA | 2) 26-30 wk if a) no antenatal steroids, or b) needs intubation anyway
87
What populations should be considered for early rescue surfactant therapy?
< 30 wk GA at first signs of RDS
88
What populations should be considered for treatment of established RDS surfactant therapy?
all newborns with established RDS, regardless of GA, if they need a ventilator and at least 30-40% FiO2
89
What are the risks of immediate intubation in the DR?
significant procedure morbidity (including apnea and bradycardia)
90
What are complications of surfactant therapy?
- plugging - desaturation and need for supplemental O2 - bradycardia - tachycardia - right main stem lavage
91
What are current recommendations as it pertains to dosing interval?
1) give as a bolus rather than infusing slowly 2) no data to suggest subsequent doses if vent settings and O2 requirements are at minimal levels 3) no data to suggest > 4 doses 4) interval between doses should be at least 6 h 5) most protocols dc surf > 48h of life
92
What are the potential effects of not weaning ventilator settings s/p surf?
1) air leak 2) lung injury 3) pulmonary hemorrhage
93
Under what conditions might an infant have a poor response to surf tx?
1) lung hypoplasia 2) PNA 3) congenital heart dz 4) poor distribution of surf (main stem intubation, poor ETT placement, plugging of the tube, esophageal intubation) 5) inadequate dosing
94
How is PDA exacerbation related to surfactant therapy?
the rapid improvement in lung compliance in response to surfactant therapy may lead to excessive pulmonary blood flow from L > R shunting from the PDA

Neonatal Pathophysiology (17 decks)

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