B4.058 - Acute Lung Injury and Respiratory Distress Syndrome Flashcards
cardiogenic pulmonary edema
microhemorrhages –> hemosiderin-containing macrophages in thealveoli
“heart cells”
if prolonged, numerous hemosiderin laden macrphages nad fibrosis make brwon induration
B. Hemodynamic pulmonary edema
RDS gross appearance
congested, atelectatic lung (like liver)
usually sink in water
DAD fibrosis
what is ARDS
clinical syndrome characterized by the rapid onset of severe life threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia that is refractory to oxygen therapy. Chest radiographs show diffues aveolar infilatrates. May progress to extrapulmonary multisystem organ failure.
pulmonary hypoplasia
managemenf of RDS
assess lung maturity using amniotic fluid phospholipids
prevent labor
induce maturity with corticosteroids
surfactant replacement therapy
oxygenation/ventilation
immature lung
histo manifestation of ALI and ARDS
DAD
diffuse alveolar damage
lamellar bodies (precursor of surfactant) within a type 2 pneumocyte
pulmonary hypoplasia
another cause of acute respiratory distress in infants, due to poorly developed lungs
causes of ARDS
diffuse pulmonary infections (viral, mycoplasma, miliary TB, pneumocystis
gastric aspiration
sepsis
trauma (incl. head injury)
causes of pulmonary edema
hemodynaminc - cadiogenic
microvascular injury - direct increase in vasc permeability
undetermined origin - head injury, HAPE
cardiogenic pulmonary edema
resolution of ARDS/DAD
resorption of the exudate and dead cell removal by macrophages
macrophages also discharge fibrogenic cytokines (TGFbeta and PDGF) –> fibroblastic proliferation and collagen deposition –> alveolar wall fibrosis
Epithelial cell repopulation from proliferation fo bronchilar stem cells
endothelial repopulation from proliferation of undamaged capillaries
other causes of respiratory distress syndrome in neonate
pathogenesis of ARDS
endothelial activation
pneumocyte injury –> sensed by resident alveolar macrophages –> secrete mediators TNF –> endothelium
Circulating mediators activate pulmonary endothelium (severe tissue injury or sepsise)
endothlelial cells expresss increased adhesion molecules, procoagulant proteins and chemokines.
management of DAD
treat underlying cause and supportive care. average mortaility is 40%
potential complications of acute lung injury in adults
air leaks
unresolved fibrosis
superinfection
can be fatal
renal abnormalities seen with pulmonary hypoplasia due to oligohydramnios
pulmonar edema - cardiogenic
retinopathy of prematurity phases
1 - hyperoxic phase, marked reduction of VEGF, endothelial cell apoptosis
2 - comparatively hypoxic room air, retinal vessel proliferatiol (neovascularization)
pathophys of RDS
prematurity means reduced surfactant –> incfased ST –> atelectasis –> uneven perfusion and hypoventilation –> hypoxemia and CO2 retention –> acidosis, pulm vasoconstriction –> pulm hypoperfusion –> ednothelial and epithelial damage –> leaky plasma –> hyaline mebrane
commonest cause fo respiratory distress in infants
RDS lack of surfactant in immature lungs
organization phase of ARDS/DAD
describe the adhesion and migration of neutrophils in ARDS
neutrophils degraulate –> inflammatory mediators, including proteases, reactive oxygen species, and cytokines. Macrophage migration inhibitory factor (MIF) helsp to sustain proinflammatory reponse –>increase recruitement of leukocytes –> more endothelial injury and local thrombosis
what is acute lung injury
concardiogenic pulmonary edema
abrupt onset of significant hypoxemia nad diffuse pulmonary infiltrates in the absesce of cardiac failure
ARDS is severe ALI
inflammation associated increase in pulmonary vascular permeability and epithelial and endothelial cell death
histo of RDS
presence of hyaline membranes in peripheral airspaces
CXR for RDS
ground glass opacification
what reparative changes happen after 48 hrs in RDS
alveolar epithelium growsn under hyaline membrane
may detach into airspace
partial digestion or phagocytosis by macrophages
signs of cardiogenic pulmonary edema
perivascular and isterstitial fluid accumulation, particularly in theinterlobular septa, responsible for Kerleys B lines on x ray
progressive edematous widening of alveolar septa
accumulation of edema fluid in alveolar spaces –> wet, heavy lungs with frothy blood tinged fluid
pathogenensis of intraalveolar fluid and hyaline membranes in ARDS
endothelial damage –> pulmonary capillaries leaky –> interstitial and itraaveolar edema
necrosis of type 2 alveolar pneumocytes leads to surfactant abnormailities –> comprominsing alveolar gas exchange
protein rich edema fluid and debris from dead alveolar epthelial cells organize int hyaline membranes
what is wide spread pulmonary edema from microvascular injury
significant contributor to ARDS
causes of hemodynaic pulonary edema
increased hydrostatic pressure - left sided heart failure, volume overload, pulm vein obsturction
decreased oncotic pressure - low protein states, hypoalbuminemia, renal disease
lymphatic obstruction
bronchopulmonary dysplasia
potentially reversible abnormality in avleolar septation –> fewer, larger alveoli –> reduction in surface area available for gas exchange
dysregulation of pulmonary vasculature
superimposed effects of hyperoxia, hyperventilation, prematurity, inflammation, vascular maldevelopment
causes of pulmonary edema from microvascular injury
infections
inhaled gases
liquid aspiration
drugs and chemicals
shock
trauma
radiation
transfusion related
normal mature alveoli
what are hyaline membranes
debris consisting of damaged cells, exudative necrosis, leaked protein lining the alveolar sacs
hyaline membrane disease
hyaline membrane is composed of fibrin and necrotic cells within peripheral airspaces
DAD - fibrosis
role of surfactant in initial respiration
first brewth of life needs high inspiratory pressures to expand lungs, in subsequent breaths it requries much less
in surfactant deficiency each breath takes as much effort as the first because the lungs collapse with additional breath
pulmonary edema
anatomic compartment
pathogenesis
pathphys
histo
anatomic compartment - alveolar-capillary interface
pathogenesis - hemodynamic disturbances or injury to the the alveolar septa leading to extravasation of fluid
pathophys - decreased diffusing capacity and compliance
histo - congestion of alveolar capillaries and fluid filled aveoli
what is persistent fetal circulation
PDA
foramen ovale
pulmonary edema
increase in insterstitial fluid which then accumulates within the alveolar sacs
what kinds of inhalants can cause ARDS
oxygen in high concentrations
pathogenesis of pulmonary edema form microvascular injury
alveolar septa affected
damage to vascular endo/epithelium with secondary vascular injury
inflammatory exudate –> interstitial space –> alveoli (severe)
increased risk of transient tachypnea of the newborn
C section
diabetic mother
what produces surfactant
T2 pneumocytes
lecithin, phosphatidyl, glycerol are components of surfactant
summarize ARDS effects of epithelial and endothelial injury
neonatal respiratory distress syndrome
observed worldwide in premature infants of all racial and ethnic groups
lack of surfactant and lung immaturity
complications of bronchopulmonary dysplasia
severe disease requires prolonged mechanical ventilation, may develop pulmonary hypertension and cor pulmonale
pathogenic factors of RDS
insulin (moms diabetic) and congenital surfacatnt deficiency lead to decreaseds surfactant - baby senses high blood sugar and increases insulin production which negatively affects surfactant production
glucocorticoids lead to increased surfactant - this is why labor instead of C section is protective, it puts stress on the body which increases endogenous steroid release which helps produce surfactant. C sections do not cause endogenous steroid release
full term lung
diaphragmantic hernia seen with pulmonary hypoplasia due to chest wall abnormalities
typical clinical scenario of RDS
preterm, male infant, maternal diabetes, delivered by C section
labored breathing and cyanosis
fine rales, flaring nostrils, increased RR
potential complications of neonatal RDS
air leaks
complications of oxygen therapy - bronchopulmonary dysplasia, retrolental fibroplasia
PDA
intraventricular hemorrhage
necrotizing enterocolitis
what is acute interstitial pneumonia
ALI/DAD of unknown etiology
rare, usually older
usually follows upper respiratory tract like illness
a male infant born at 28 weeks to a diabetic mother develops severe respiratory difficulty 30 minutes after birth. Most likely Dx>
RDS of the neonate
what is transient tachypnea of the newborn
pulmonary edema resulting from delayed resoption and clearance of fetal aveolar fluid
shortly after deliveryin full term or late preterm babies
DAD hyaline membranes
