Atelectasis and Acute Respiratory Distress Syndrome (Acute Lung Injury and Disease)

Question 1

What is Atelectasis?

Answer 1

The lung, partially or whole, collapsed or without air. This results in loss of lung volume due to inadeq expansion of air spaces.

Question 2

What types of Atelectasis are there?

Answer 2

1. Resorption
2. Compression
3. Loss of surfactant (neonatal)
4. Contraction

Question 3

What is Resorption?

Causes?

Answer 3

Complete airway obstruction in bronchi, subsegmental bronchi, or bronchiooles. Preventing air reaching the alveoli.

Resorption of air trapped in distal airspaces thru pores of Kohn. (lack of air in distal airspaces)

Causes: Mucus/mucopurulent plug after surgery

Aspiration of foreign material

Bronchial asthma, bronchitis, bronchiectasis

Bronchial neoplasms (caveat of total obstruction)

Question 4

Clinical findings of Resorption Atelectasis?

Answer 4

Fever and dyspnea within 24-36 hrs of collapse. most common cause of fever following surgery.

Ipsilateral deviation of trachea and Ipsilateral diaphragmatic elevation

Absent breath sounds and absent vocal vibratory sensations (tactile fremitus)

Collapsed lung does not expand on inspiration

Question 5

What is Compression Atelectasis?

(What can cause it)

How does it present?

Answer 5

Air or fluid accumulation in pleural cavity, increases pressure and collapses underlying lung

(Tension pneumothorax or Pleural effusion)

Trachea and medastinum shift away from atelectatic lung

Question 6

What produces surfactant, where is it stored, when is it synthesized, what is it comprised of?

Answer 6

Surfactant is produced by Type II pneumocytes, stored in lamellar bodies, synthesized by 28th week of gestation.

Comprised of Phosphatidylcholine (lecithin)/ Phosphatidylglycerol/Proteins (A and D for innate immunity, B and C for reducing surface tension at air liquid barrier in alveoli)

Question 7

What increases surfactant production

What decreases surfactant production

What causes loss of surfactant in neonates?

Answer 7

Cortisol and Thyroxine increase

Insulin decrease

Prematurity/Maternal diabetes/Cesarian section

Question 8

What is seen on microscope for loss of surfactant atelectasis?

Answer 8

Collapsed alveoli lined by hyaline membranes (THIS IS ALSO CALLED HYALINE MEMBRANE DISEASE/Infant Respiratory Distress Syndrome)

Question 9

Complications of Infant RDS/Hyaline membrane disease?

Answer 9

Intraventricular hemmorhage

PDA

Necrotizing enterocolitis

Hypoglycemia

O2 therapy damaging lungs and cataracts

Question 10

Steps to infant RDS/Hyaline membrane disease

Answer 10

Prematurity–>Reduced surfactant–>Atelectasis–>Uneven perfusion and Hypoventilation–>Hypoxemia and CO2 retention–>acidosis–>pulmonary vasoconstriction–>pulmonary hypoperfusion–>epithelial and endothelial damage–>Plasma leak into alveoli–>Fibrin and necrotic cells (hyaline membrane formation)

Question 11

What is Contraction Atelectasis

Answer 11

Fibrotic change in lung of pleura preventing full expansion (irreversible

Question 12

What is Acute lung injury?

Mediators?

Manifestations?

Answer 12

Endothelial or epithelial injury, initiated by numerous factors

Mediators: Cytokines/oxidants/Growth factors/TNF/IL-1, 6, 10/TGF beta

Manifestations: Pulmonary edema and Diffuse alveolar damage (acute respiratory distress synrome)

Question 13

How does pulmonary edema occur?

Answer 13

Alterations in Starling pressure (either increased hydrostatic pressure or decreased oncotic pressure)

Left sided HF, volume overload, mitral stenosis, Hemodynamic distrubances like cardiogenic pulmonary edema.

Nephrotic syndrome, Liver cirrhosis

Microvascular or alveolar injury (increase in capillary permeability)

Infections, aspirations, drugs shock trauma, high altitude

Undetermined origin

Question 14

How does pulmonary edema present?

Answer 14

Transudate fluid, edema fluid accumulates in alveoli with Heart Failure cells and “Brown induration” (HEmosiderin laden macrophages)

Question 15

What is Acute Respiratory Distress Syndrome?

What causes it (what percent in patients)

Clinical findings?

Answer 15

Noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage (SEVERE END OF SPECTRUM OF ACUTE LUNG INJURY)

Caused by Direct or indirect (systemic disease) lung injury

Gram- sepsis (40%)

Aspiration (30%)

Severe trauma (10%)

Pulmonary infection, heroin, smoke inhalation

Clinical findings: Dyspnea, severe hypoxemia NOT RESPONSIVE TO O2 therapy

Respiratory acidosis

Question 16

Pathogenesis of Acute Respiratory Distress Syndrome?

What stages are there and what are seen?

Specifically what happens when alveolar macrophage and other cells release cytokines? (Part of the pathogenesis)

Answer 16

Acute injury to alveolar epithelial or endothelial cells–>Alveolar macrophage and other cells release cytokines–>Repair by Type 2 pneumocytes–>Progressive interstitial fibrosis

Exudative (early) and Proliferative (late) phases, separated by 7 days. Edema immediately seen then goes away followed by Hyaline membranes which decreases slowly. Then slow increase in Interstitial inflammation and fibrosis

Alveolar Macrophage and other cells relasing cytokines–>(neutrophic chemotaxis, transmigration of neutrophils from capillaries into alveoli, leakage of protein (fibrin) rich exucate leading to hyaline membrane, damage to pneumocytes causing surfactant deficiency leading to atelectasis