ABSTRACT
I. Definition 390
II. Radiologic Findings 392
A. Initial, Early Exudative Stage/Stage I (1st-24th Hour) 394 B. Exudative Stage/Stage II (2nd-7th Day) 395 C. Proliferative and Fibrotic Stages/Stages III and IV
(.7th Day) 397
III. CT Scan Protocols 397
A. Advantages and Indications of CT 398
IV. Pulmonary or Extrapulmonary ARDS 399
V. Basic Concepts of Therapy and
Potential Complications 400
A. Prone Positioning 401
VI. Ventilator-Associated Lung Injury 402
VII. Long-Term CT Findings 402
VIII. Deeper Insights in ARDS and Mechanical
Ventilation by Functional CT 403
IX. Alternative to Radiological Imaging:
Electrical Impedance Tomography 407
X. Conclusion 408
References 409
I. Definition
The term “acute respiratory distress syndrome” (ARDS) was coined in 1967 by
Asbaugh et al. (1), who described a syndrome of severe dyspnea, tachypnea,
hypoxemia refractory to oxygen therapy, decreased pulmonary compliance,
and diffuse alveolar opacities on chest radiography. Autopsy findings consisted
of atelectasis, vascular congestion, hemorrhage, and pulmonary edema. His-
tology revealed diffuse alveolar damage with hyaline membrane formation.
Although this description reflected clinical and pathological findings, the clinical
entity of the ARDS at the time was still poorly defined. As similar findings were
also observed in children and adolescents, the term “acute respiratory distress
syndrome” was adopted and is preferred to the initial name, “adult respiratory
distress syndrome”. ARDS is characterized by a general inflammatory reaction
of the lung, which results in severe pulmonary capillary permeability with the
subsequent development of interstitial and alveolar edema. The production of
mediators, such as leukotrienes, prostaglandins, and proteolytic enzymes, leads
to severe alterations in normal pulmonary physiology and respiratory failure.
The primary clinical finding is hypoxemia with an oxygenation index [arterial
oxygen partial pressure (PaO2)/inspiratory oxygen concentration (FiO2)] of less than 200. The hypoxemia is also associated with reduced pulmonary compli-
ance due to interstitial edema, depletion of surfactant, atelectasis, formation of
hyaline membranes, and eventually, the development of fibrosis.
