16 - Acute lung injury/Atelectasis Flashcards

1
Q

Define atelectasis

A

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)

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2
Q

What are the 4 types of atelectasis?

A
  1. resorption
  2. compression
  3. loss of surfactant (neonatal)
  4. contraction
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3
Q

What causes resorption atelectasis?

A
  • Complete airway obstruction
    • mucus plug following surgery
    • aspiration of foreign material
    • bronchial asthma/bronchitis
    • bronchial neoplasms
  • In any part of the lung; collapse of all structures distally due to:
    • lack of new air flow
    • resorption of trapped air through pores of Kohn
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4
Q

What are the clinical findings of resorption atelectasis?

A
  • fever and dyspnea (within 24-36 hrs of collapse)
  • deviation of trachea TOWARDS lesion/collapse
  • ipsilateral diaphragm elevation
  • absent breath sounds/vocal vibration sensation
  • collapsed lung does not expand on inspiration
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5
Q

What causes compression atelectasis?

A

Air or fluid accumulation in pleural cavitiy (increases pressure and collapses underlying lung)

e.g. tension pneumothorax, pleural effusion

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6
Q

What is the tracheal shift in a compression atelectasis? In resorption?

A

Compression= shift AWAY from collapse

Resorption= shift TOWARDS collapse

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7
Q

What do you see on this chest xray?

A

Compression atelectasis due to pneumothorax

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8
Q

What is this image showing?

A

Atelectasis (no air in alveoli)

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9
Q

What causes neonatal atelectasis?

A

Loss of surfactant

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10
Q

Describe surfactant. What produces it and what stimulates that production?

A
  • Surfactant= lipoprotein
    • surface proteins A and D= innate immunity
    • surface proteins B and C= reduction of surface tension at air liquid barrier in alveoli
  • Synthesized by type 2 pneumocytes (beginning at 28 weeks gestation), stored in lamellar bodies
    • Synthesis increased by cortisol and thyroxine
    • Synthesis decreased by insulin
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11
Q

What risk factors decrease surfactant in neonatal lungs?

A
  • prematurity
  • maternal diabetes
    • fetal hyperglycemia stimulates insulin release which inhibits surfactant production
  • cesarean section
    • labor increases stress cortisol secretion to increase surfactant production
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12
Q

What does this image show?

A

Collapsed alveoli lined by hyaline membranes (arrow)

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13
Q

What are the clinical findings of neonatal atelectasis?

A
  • respiratory distress within a few hours of birth
  • hypoxemia and respiratory acidosis
  • “ground glass” appearance on chest xray
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14
Q

What are 5 complications of neonatal atelectasis?

A
  1. intraventricular hemorrhage
  2. PDA (persistent hypoxemia)
  3. necrotizing entercolitis (intestinal ischemia)
  4. hypoglycemia (excessive insulin release)
  5. O2 therapy can damage lungs and cause cataracts/blindness
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15
Q

What causes contraction atelectasis?

A

Fibrotic changes in lung or pleura that prevent full expansion (not reversible)

e.g. idiopathic pulmonary fibrosis or honeycomb lung in end stage lung disease

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16
Q

Define acute lung injury. How does it manifest?

A
  • acute lung injury= endothelial or epithelial injury initiated by numerous factors:
    • cytokines (TNF, IL1/6/10, TGF-B)
    • oxidants
    • growth factors
  • manifests as:
    • pulmonary edema
    • diffuse alveolar damage
17
Q

What are 2 main causes of pulmonary edema and examples of each?

A
  • alterations in starling pressure
    • increased hydrostatic pressure (left sided heart failure, volume overload)
    • decreased oncotic pressure (nephrotic syndrome, liver cirrhosis with decreased albumin)
  • microvascular/alveolar injury (increases capillary permeability)
    • infection
    • aspiration/trauma
    • drugs
    • high altitude
18
Q

What can cause noncardiogenic pulmonary edema?

A

Diffuse alveolar-capillary damage (direct or indirect)

Risk factors: gram negative sepsis, aspiration, severe trauma, pulmonary infection, heroin, smoke inhalation

19
Q

What are the clinical findings of ARDS? What is the prognosis?

A
  • respiratory insufficiency
  • dyspnea
  • cyanosis
  • severe hypoxemia NOT responsive to O2 therapy
  • respiratory acidosis
  • diffuse alveolar infiltration on chest x ray

**poor prognosis (~60% mortality)

20
Q

What is the pathogenesis of ARDS?

A
  • acute injury to alveolar epithelial or endothelial cells
    • repaired by type 2 pneumocytes (increased # in ARDS)
  • alveolar macrophages and other cells release cytokines
    • causes leakage of proteins/fibrin forming hyaline membranes
    • damage to pneumocytes causing surfactant deficienty
  • progressive fibrosis
21
Q

What does this image show?

A

Hyaline membrane (arrow) and diffuse alveolar damage of ARDS

22
Q

Describe the stages of acute lung injury

A
  1. edema
  2. hyaline membrane formation
  3. proliferation (interstitial inflammation and fibrosis)