Atelectasis and Acute Respiratory Distress Syndrome (ARDS)

Question 1

what is atelectasis?

Answer 1

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

Question 2

Types of atelectasis

Answer 2

– Resorption
– Compression
– Loss of surfactant (neonatal) – Contraction

Question 3

what causes resorption Atelectasis?

Answer 3

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

Question 4

what are possible causes of obstruction that can lead to respiration atelectasis?

Answer 4

Cause of obstruction:
–Mucus/mucopurulent plug following surgery
– Aspiration of foreign material
– Bronchial asthma, bronchitis,
bronchiectasis
– Bronchial neoplasms (caveat-total obstruction)

Question 5

Clinical findings in resorption atelectasis

Answer 5

• 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

Question 6

what happens to the trachea and diaphragm with resorption atelectasis?

Answer 6

• Ipsilateral deviation of trachea

* Ipsilateral diaphragmatic elevation

Question 7

causes of compression atelectasis?

Answer 7

• Air or fluid accumulation in pleural cavity – increased pressure – collapses underlying lung

Question 8

possible causes of compression atelectasis?

Answer 8

• tension pneumotorax

- pleural effusion

Question 9

what happens to the trachea with compression atelectasis?

Answer 9

• Trachea and mediastinum shift away from the atelectatic lung

Question 10

what causes neonatal atelectasis?

Answer 10

loss of surfactant

Question 11

what is surfactant made up of?

Answer 11

– 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

Question 12

what cells synthesize surfactant? when does synthesis start?

Answer 12

– Synthesized by type 2 pneumocytes

• Synthesis begins by 28th week of gestation

Question 13

where is surfactant stored?

Answer 13

• Stored in lamellar bodies

Question 14

what is the role of surfactant?

Answer 14

Reduces surface tension in small airways and prevents collapse on expiration

Question 15

what has an effect on surfactant synthesis?

Answer 15

hormones

Question 16

which hormones have effects on surfactant synthesis and what are the effects?

Answer 16

– ↑ by cortisol and thyroxine

– ↓ by insulin

Question 17

what are causes of respiratory distress syndrome (RDS) in newborns?

Answer 17

• 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

Question 18

what lines collapsed alveoli in neonatal atelectasis?

Answer 18

hyaline membranes

Question 19

clinical findings of neonatal atelectasis?

Answer 19

– Respiratory distress within a few hours of birth
– Hypoxemia and respiratory acidosis
– “Ground glass appearance” on chest x-ray

Question 20

complications of neonatal atelectasis?

Answer 20

– 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)

Question 21

what causes contraction atelectasis?

Answer 21

fibrotic changes in lung

or pleura prevent full expansion (not reversible)

Question 22

damage where causes acute lung injury?

Answer 22

fibrotic changes in lung

or pleura prevent full expansion (not reversible)

Question 23

what can cause acute lung injury?

Answer 23

• Nonheritable AND heritable causes (response and survival depends on multiple loci on different chromosomes)

Question 24

what are mediators of acute lung injury?

Answer 24

• Mediators Cytokines, oxidants, growth factors– TNF; IL-1, 6 and 10; TGF-β.

Question 25

manifestations of acute lung injury

Answer 25

• Manifestations–Pulmonary edema, Diffuse Alveolar Damage (Acute respiratory distress syndrome)

Question 26

causes of pulmonary edema?

Answer 26

– Edema due to alterations in Starling pressure
– Microvascular or alveolar injury – increase in capillary permeability
– Undetermined origin
– Therapy and outcome depend on underlying etiology

Question 27

what changes in starling pressure can cause pulmonary edema?

Answer 27

• 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”

Question 28

what microvascular or alveolar injuries (causing increase in capillary permeability) can cause pulmonary edema?

Answer 28

• Infections
• Aspiration
• Drugs, shock, trauma
• High altitude

Question 29

what is ARDS?

Answer 29

• Noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage
– Direct lung injury
– Indirect lung injury (systemic diseases)

Question 30

what are risks for ARDS?

Answer 30

• Gram negative sepsis (40%)
• Aspiration (30%)
• Severe trauma (10%)
• Pulmonary infections, heroin, smoke inhalation

Question 31

what four causes account for >50% of ARDS cases?

Answer 31

• sepsis
• diffuse lung infections
• gastric aspiration
• physical injury/trauma

Question 32

clinical findings in acute respiratory distress syndrome

Answer 32

– Dyspnea, severe hypoxemia NOT responsive to O2 therapy.

– Respiratory acidosis

Question 33

pathogenesis and pathology of ARDS

Answer 33

– 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

Question 34

prognosis of ARDS

Answer 34

Poor (~60%mortalityrate)

Question 35

what happens to alveoli in ARDS?

Answer 35

• diffuse alveolar damage!
• hyaline membranes
• hyperplastic type 2 pneumocytes

Question 36

main findings of the exudative state of ARDS?

Answer 36

• edema

- hyaline membranes (main one!!)

Question 37

main findings of the proliferative state of ARDS

Answer 37

• interstitial infammation

- interstitial fibrosis