Lung Diseases Flashcards
1
Q
Most common cause of respiratory failure in preterm infant?
A
- RDS
2
Q
Incidence and severity seen in males or females?
A
- male infants
- increased circulating androgens, decreased lung maturity, and surfactant production by type II pneumocytes
- more common and more severe in white infants vs black
3
Q
Increased incidence - RFs for RDS?
A
- low gestation
- male sex
- white race
- maternal diabetes: increased insulin decreases lung maturation and surfactant production
- C section pre-onset of labor
- perinatal asphyxia: CV shock and pulm HTN
- maternal HTN
4
Q
Decreased incidence RFs?
A
- prolonged rupture of membranes
- chronic congenital infections
- maternal substance abuse
- antenatal corticosteroid exposure
- female
5
Q
2 major issues in RDS?
A
- immature lungs
- lack of surfactant
6
Q
Diff. lung stages?
A
- canalicular stage: 16-26 wks
- saccular stage: 24-38 wks
- may have primitive airspaces with undiff pneumocytes
- no juxtaposition of airway epithelium and capillaries
7
Q
Surfactant:
when does it appear, when is adequate amt produced?
Fxn?
A
- appears at 23-24 wks
made by type II pneumocyte - adequate amts not produced until about 35 wks
- reduces surface tension in alveolar spaces:
facilitates lung expansion
prevents alveolar collapse
8
Q
Premature infants usually have what other respiratory problems along with RDS?
A
- excessively compliant chest walls
- weakness of the respiratory muscles
- these may further contribute to alveolar collapse
9
Q
PP behind RDS?
A
- alveolar collapse alters normal ventilation/perfusion relationship
- produces pulm shunting - progressive arterial hypoxemia - metabolic acidosis
- hypoxemia and acidosis - lead to vasoconstriction - decreased pulmonary blood flow (pulm HTN)
- may produce R - L shunting through PFO and PDA - worsening hypoxemia
- pulm blood flow may subsequently increase - this leads to decreased vascular resistance and persistence of PDA
- increased pulm blood flow leads to acccum of fluid and protein in interstitial and alveolar spaces
- protein in alveolar spaces deactivates surfactant
10
Q
What is hyaline membrane disease?
A
- lungs appear solid and congested with diffuse atelectasis
- hyaline membranes line most of remaining airspaces
- hyaline membranes are made up of plasma proteins leaked from damaged epithelium
- HMD and epithelial necrosis is less severe in infants tx with surfactant
11
Q
What will you see on PE of child with RDS?
CXR?
ABGs?
A
- progressive tachypnea, subcostal and sternal retractions, grunting, cyanosis, and decreased breath sounds present in minutes to hours of life
- CXR: increased density of both lung fields with reticulogranular infiltrates, air bronchograms, and elevation of diaphragm
- O2 requirement varies with disease severity
- ABGs: hypoxemia, hypercarbia, and metabolic acidosis
12
Q
Clinical course and prognosis of RDS?
A
- severity of resp failure increases during first 2-3 days of life
- in infants greater than 32-33 wks respiratory status usually improves by 1 wk of life
- in infant less than 26-28 wks course usually prolonged and complicated by volutrauma and/or barotrauma, PDA, infection, and intraventricular hemorrhage
13
Q
Tx of RDS?
A
- exogenous surfactant has drastically changed course of disease, rapidly decreases need for O2 and mechanical ventilation,
reduces incidence of gas leaks - careful stabilization in delivery room and NICU, proper monitoring of cardiopulmonary fxn, adequate resp support: O2, CPAP, mechanical ventilation
- proper thermal, metabolic and nutritional support
14
Q
Prevention of RDS?
A
- prevention of premature delivery
- antenatal corticosteroids: rapid change, within 15 hrs in lung structure: improved compliance, increased lung volume, decreased capillary protein leak
- slower (longer than 24 hrs): increased synthesis and secretion of surfactant by type II cells
15
Q
Complications of RDS?
A
- hemorrhagic pulmonary edema
- capillary rupture and interstitial fluid
- may be seen with exogenous surfactant
- usually occurs in first 5-7 days of life
- may be rapidly fatal
