Atelectasis and Acute Respiratory Distress Syndrome (ARDS) Flashcards
what is atelectasis?
Atelectasis is defined as a state in which the lung, in whole or in part, is collapsed or without air.
– Loss of lung volume due to inadequate expansion of airspaces
Types of atelectasis
– Resorption
– Compression
– Loss of surfactant (neonatal) – Contraction
what causes resorption Atelectasis?
Consequence of complete airway obstruction
– Obstruction in bronchi, subsegmental bronchi or bronchioles
– Prevents air from reaching the alveoli
– Resorption of air trapped in distal airspaces through the pores of Kohn
– Lack of air in distal airspaces
– Collapse
what are possible causes of obstruction that can lead to respiration atelectasis?
Cause of obstruction:
–Mucus/mucopurulent plug following surgery
– Aspiration of foreign material
– Bronchial asthma, bronchitis,
bronchiectasis
– Bronchial neoplasms (caveat-total obstruction)
Clinical findings in resorption atelectasis
- Fever and dyspnea – within 24-36 hours of collapse (commonest cause of fever 24-36 hrs following surgery)
- Absent breath sounds and absent vocal vibratory sensation (tactile fremitus)
- Collapsed lung does not expand on inspiration
what happens to the trachea and diaphragm with resorption atelectasis?
- Ipsilateral deviation of trachea
* Ipsilateral diaphragmatic elevation
causes of compression atelectasis?
• Air or fluid accumulation in pleural cavity – increased pressure – collapses underlying lung
possible causes of compression atelectasis?
- tension pneumotorax
- pleural effusion
what happens to the trachea with compression atelectasis?
• Trachea and mediastinum shift away from the atelectatic lung
what causes neonatal atelectasis?
loss of surfactant
what is surfactant made up of?
– Lipoprotein
• Phosphatidylcholine (lecithin)
• Phosphatidylglycerol
• Proteins
– Surfactant proteins (SP) A and D: innate immunity
– Surfactant proteins (SP) B and C: reduction of surface tension at air liquid barrier in alveoli
what cells synthesize surfactant? when does synthesis start?
– Synthesized by type 2 pneumocytes
• Synthesis begins by 28th week of gestation
where is surfactant stored?
• Stored in lamellar bodies
what is the role of surfactant?
Reduces surface tension in small airways and prevents collapse on expiration
what has an effect on surfactant synthesis?
hormones
which hormones have effects on surfactant synthesis and what are the effects?
– ↑ by cortisol and thyroxine
– ↓ by insulin
what are causes of respiratory distress syndrome (RDS) in newborns?
• Decreased surfactant in fetal lungs
– Prematurity
– Maternal diabetes
» Fetal hyperglycemia stimulates insulin release
– Cesarean section
» Labor and vaginal delivery ↑es stress related cortisol secretion - ↑es surfactant production
what lines collapsed alveoli in neonatal atelectasis?
hyaline membranes
clinical findings of neonatal atelectasis?
– Respiratory distress within a few hours of birth
– Hypoxemia and respiratory acidosis
– “Ground glass appearance” on chest x-ray
complications of neonatal atelectasis?
– Intraventricular hemorrhage
– Patent ductus arteriosus (persistent hypoxemia)
– Necrotizing enterocolitis (intestinal ischemia)
– Hypoglycemia (excessive insulin release)
– O2 therapy – damage to lungs (bronchopulmonary dysplasia) and cataracts (blindness)
what causes contraction atelectasis?
fibrotic changes in lung
or pleura prevent full expansion (not reversible)
damage where causes acute lung injury?
fibrotic changes in lung
or pleura prevent full expansion (not reversible)
what can cause acute lung injury?
• Nonheritable AND heritable causes (response and survival depends on multiple loci on different chromosomes)
what are mediators of acute lung injury?
• Mediators Cytokines, oxidants, growth factors– TNF; IL-1, 6 and 10; TGF-β.
manifestations of acute lung injury
• Manifestations–Pulmonary edema, Diffuse Alveolar Damage (Acute respiratory distress syndrome)
causes of pulmonary edema?
– Edema due to alterations in Starling pressure
– Microvascular or alveolar injury – increase in capillary permeability
– Undetermined origin
– Therapy and outcome depend on underlying etiology
what changes in starling pressure can cause pulmonary edema?
• Increased hydrostatic pressure in pulmonary capillaries
– Left sided heart failure, volume overload, mitral stenosis
– Hemodynamic disturbances- cardiogenic pulmonary edema
• Decreased oncotic pressure
– Nephrotic syndrome, liver cirrhosis
• Transudate
• Edema fluid accumulation in alveoli with “heart failure” cells and “brown induration”
what microvascular or alveolar injuries (causing increase in capillary permeability) can cause pulmonary edema?
- Infections
- Aspiration
- Drugs, shock, trauma
- High altitude
what is ARDS?
• Noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage
– Direct lung injury
– Indirect lung injury (systemic diseases)
what are risks for ARDS?
- Gram negative sepsis (40%)
- Aspiration (30%)
- Severe trauma (10%)
- Pulmonary infections, heroin, smoke inhalation
what four causes account for >50% of ARDS cases?
- sepsis
- diffuse lung infections
- gastric aspiration
- physical injury/trauma
clinical findings in acute respiratory distress syndrome
– Dyspnea, severe hypoxemia NOT responsive to O2 therapy.
– Respiratory acidosis
pathogenesis and pathology of ARDS
– Acute injury to alveolar epithelial or endothelial cells
– Alveolar macrophages and other cells release cytokines
• Neutrophilic chemotaxis
• Transmigration of neutrophils from capillaries into alveoli
• Leakage of protein (fibrin) rich exudate forming hyaline membranes
• Damage to pneumocytes causing surfactant deficiency leading to atelectasis
– Repair by type 2 pneumocytes
– Progressive interstitial fibrosis
prognosis of ARDS
Poor (~60%mortalityrate)
what happens to alveoli in ARDS?
- diffuse alveolar damage!
- hyaline membranes
- hyperplastic type 2 pneumocytes
main findings of the exudative state of ARDS?
- edema
- hyaline membranes (main one!!)
main findings of the proliferative state of ARDS
- interstitial infammation
- interstitial fibrosis
