ACUTE RESPIRATORY DISTRESS SYNDROME

Exudative Proliferative Fibrotic

Time frame  First seven days after exposure  Day 7 to day 21

CXR  Alveolar and interstitial opacities – ¾ of the

lung fields
 Rarely shows:
- Cardiomegaly
- Pleural effusion
- Pulmonary vasculature redistribution

Chest CT  Extensive heterogeneity of lung involvement

Lung Biopsy  Evidence of PULMONARY FIBROSIS – increased risk of mortality

Pathology  Injury of ACEC and Type I pneumocytes  Progressive lung injury  Extensive alveolar duct and interstitial
 Loss of normal tight alveolar barrier  Early changes of pulmonary fibrosis fibrosis
 Accumulation of edema fluid in interstitial and  FIRST SIGNS OF RESOLUTION:  EMPHYSEMA-like changes
alveolar spaces  Initiation of lung repair o W/ large bullae
 Pulmonary vascular injury  Organization of alveolar exudates o Results from marked disruption of
 Vascular obliteration – microthrombi  Shift from neutrophil to acinar architecture
 Fibrocellular proliferation LYMPHOCYTE predominant  INTIMAL PROLIFERATION
 Dependent portions of the lung pulmonary infilltrate o Site: pulmonary microcirculation
- Alveolar edema  Proliferation of type II pneumocytes along o Causes:
- Diminished aeration alveolar basement membrane 1. Vascular occlusion
- Atelectasis  Synthesize new pulmonary surfactant 2. Pulmonary hypertension
 Collapse of lung sections (dependent lung)  Differentiate into type I pneumocytes 
- Decrease lung compliance
 Intrapulmonary shunting and hypoxemia
- Work of breathing increases  dyspnea
 Pathophysiologic alterations in alveolar spaces
- Exacerbated by microvascular
occlusion
- Reductions in pulmonary arterial
blood flow to ventilated portions of
the lung
 Increase in DEAD SPACE
- Pulmonary hypertension

Involved  Alveolar capillary endothelial cells  Predominant: LYMPHOCYTE  Acinar architecture

cells/structures  Type I pneumocytes (A. epithelial cells)  Type II pneumocytes
 Cytokines
- IL-1
- IL-8
- TNF - alpha
 Lipid mediators – LTB4
 Leukocytes & NEUTROPHILS 
pulmonary interstitium and alveoli

Pathognomonic  HYALINE MEMBRANE WHORLS  Emphysema-like changes with large bullae

Clinical  Usually presenting 12 – 36 hours after initial  Most patients: ***Many patients – recover lung function after
Manifestation insult  Rapid recovery initial pulmonary injury and some enter fibrotic
 Can be delayed (5 – 7 days)  Liberated from mechanical ventilation phase
 HYPERCAPNEA – secondary to an increase Despite improvement:  FIBROTIC PHASE:
in pulmonary dead space  Dyspnea  Long term support on mechanical ventilators
 DYSPNEA  Tachypnea and/or supplemental oxygen
- Inability to get enough air  Hypoxemia  Patients experience substantial burden of
- Rapid shallow breathing excess morbidity
 Increased work of breathing  Physiologic consequences:
 TACHYPNEA 1. Increased risk of pneumothorax
Result in: 2. Reductions in lung compliance
- Respiratory fatigue 3. Increased pulmonary dead space
- Respiratory failure