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Flashcards in Respiratory Distress Syndrome Deck (94)
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When was the subspecialty of Neonatology recognized?



When did the NNP role emerge?



What was the first neonatal ventilator?

the baby bird I (followed by the bournes 200)


What therapies were introduced in the 1960's?

1) phototherapy
2) PKU (beginning of NBS)


When was ECMO therapy for neonates introduced?



What therapies were introduced in the 1980's?

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


How long does it take for the average practice change?

15-17 years


What is RDS?

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


What is CPIP?

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


How does chronic lung disease differ from BPD?

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


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

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


How does RDS differ from hyaline membrane dz?

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


What population is RDS almost an exclusive dx for?

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


What are the basic mechanisms that result in RDS?

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


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

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


What are the methods of preventing RDS?

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


What is the clinical duration of RDS?

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


What is the classic presentation of an infant with RDS?

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


What is grunting?

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!


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

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.


What is the typical RDS CXR look like?

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


What accounts for the "ground glass" appearance on CXR?

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


What accounts for peripheral air bronchograms?

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


How quickly might hyaline membranes develop?

as early as 30 minutes


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


What is meant by proteinaceous sludge?

the proteins and inflammatory mediators that come into the lung parenchyma


What percentage of LBW newborns will have some type of respiratory distress?

approximately half


If supportive therapy is successful, when can the repair phase of RDS be expected to being?

during dol 2


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


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