16 - Acute lung injury/Atelectasis Flashcards
Define atelectasis
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)
What are the 4 types of atelectasis?
- resorption
- compression
- loss of surfactant (neonatal)
- contraction
What causes resorption atelectasis?
-
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
What are the clinical findings of resorption atelectasis?
- 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
What causes compression atelectasis?
Air or fluid accumulation in pleural cavitiy (increases pressure and collapses underlying lung)
e.g. tension pneumothorax, pleural effusion
What is the tracheal shift in a compression atelectasis? In resorption?
Compression= shift AWAY from collapse
Resorption= shift TOWARDS collapse
What do you see on this chest xray?
Compression atelectasis due to pneumothorax
What is this image showing?
Atelectasis (no air in alveoli)
What causes neonatal atelectasis?
Loss of surfactant
Describe surfactant. What produces it and what stimulates that production?
- 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
What risk factors decrease surfactant in neonatal lungs?
- prematurity
- maternal diabetes
- fetal hyperglycemia stimulates insulin release which inhibits surfactant production
- cesarean section
- labor increases stress cortisol secretion to increase surfactant production
What does this image show?
Collapsed alveoli lined by hyaline membranes (arrow)
What are the clinical findings of neonatal atelectasis?
- respiratory distress within a few hours of birth
- hypoxemia and respiratory acidosis
- “ground glass” appearance on chest xray
What are 5 complications of neonatal atelectasis?
- intraventricular hemorrhage
- PDA (persistent hypoxemia)
- necrotizing entercolitis (intestinal ischemia)
- hypoglycemia (excessive insulin release)
- O2 therapy can damage lungs and cause cataracts/blindness
What causes contraction atelectasis?
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
Define acute lung injury. How does it manifest?
- 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
What are 2 main causes of pulmonary edema and examples of each?
-
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
What can cause noncardiogenic pulmonary edema?
Diffuse alveolar-capillary damage (direct or indirect)
Risk factors: gram negative sepsis, aspiration, severe trauma, pulmonary infection, heroin, smoke inhalation
What are the clinical findings of ARDS? What is the prognosis?
- respiratory insufficiency
- dyspnea
- cyanosis
- severe hypoxemia NOT responsive to O2 therapy
- respiratory acidosis
- diffuse alveolar infiltration on chest x ray
**poor prognosis (~60% mortality)
What is the pathogenesis of ARDS?
-
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
What does this image show?
Hyaline membrane (arrow) and diffuse alveolar damage of ARDS
Describe the stages of acute lung injury
- edema
- hyaline membrane formation
- proliferation (interstitial inflammation and fibrosis)
