Atelectasis and ARDS Flashcards
causes of obstruction in resorption atelectasis
Mucus/mucopurulent plug following surgery
foreign material
bronchial asthma, bronchitis, bronchiectasis
neoplasm
contraction atelectasis
fibrotic changes in lung or pleura prevent full expansion (not reversible)
hemosiderin laden macrophages found in
pulmonary edema (heart failure cells)
histo compression atelectasis
collapsed, slit-like alveoli
manifestations acute lung injury
Pul edema
Diffuse Alveolar Damage
ARDS
ARDS presenetation
dypsnea
severe hypoxemia not responsive to O2
Respiratory acidosis
clinical presentation resorption atelectasis
Fever+dypsnea within 24-36 hours of collapse
ispilateral trachea deviation
ipsilateral diaphragmatic elevation
absent breath sounds+vocal vibratory sensation (fremitius)
no expansion on inspiration
histo neonatal atelactaiss
collapsed parenchyma
reduced open alveoli
open alveolie lined with pink hyaline membrane
risk factors ARDS
gram negative sepsis
aspiration
severe trauma
pulmonary infections, heroin, smoke
associations decreased neonatal surfactant
premature
maternal diabetes (fetal hyperglycemia)
Cesarean
pathogenesis ARDS
acute injury to alveoli/capillary
macrophage cytokine release >
PMN chemotaxis > migrate to alveoli >
fibrin leakage > hyaline membrane
damage to type 2 pneumocytes
Repair by type 2 leads to interstitial fibrosis
histology ARDS
hyaline membrane
hyperplastic type 2 pneumocytes
neonatal atelactasis due to
loss of surfactant
hormonal drivers of surfactant
increased by cortisol and thyroxine
decreased by insulin
surfactant proteins implicated in atelactasis
B and C
reduce surface tension