Pulmonary Disorders I
First described in 1967; several definitions have evolved over the years
Variable
Criteria
Timing
Onset within 1 wk of a known clinical insult or new or worsening respiratory symptoms
Chest imaging
Bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules
Origin of edema
Respiratory failure not fully explained by cardiac failure or fluid overload
Need objective assessment (ie, ECHO) to exclude hydrostatic edema if no risk factors present
Oxygenation
Mild
200 mm Hg < Pao2/Fio2 โค 300 mm Hg with PEEP or CPAP โฅ 5 cm H2O
Moderate
100 mm Hg < Pao2/Fio2 โค 200 mm Hg with PEEP โฅ 5 cm H2O
Severe
Pao2/Fio2 โค 100 mm Hg with PEEP โฅ 5 cm H2O
ARDS = acute respiratory distress syndrome; CPAP = continuous positive airway pressure; ECHO = echocardiogram; Fio2 = fraction of inspired oxygen; Pao2 = partial
pressure of oxygen; PEEP = positive end-expiratory pressure..
In 2014, ARDS represented 10.4% of all ICU admissions and 23.4% of patients requiring mechanical
Of these, mild ARDS accounted for 30%, moderate for 46.6%, and severe for 23.4%.
Hospital mortality was 34.9% for mild ARDS, 40.3% for moderate ARDS, and 46.1% for severe
ARDS.
During the COVID-19 pandemic, ARDS occurred at a rate of 50% to 80% compared with the
general ICU population (BMJ. 2024;369:e076612).
| d. | Multisystem organ failure is the leading cause of death in patients with ARDS, with the number of |
|---|
Med 2011;37:1932-41).
Direct and indirect causes of lung injury
Direct: Pneumonia, aspiration, trauma
Indirect: Sepsis, transfusion injury, pancreatitis, burn injury, trauma
The hallmark clinical manifestation of ARDS is hypoxemia from alveolar collapse and edema.
The exudative phase is characterized by increased permeability from the alveolar epithelium and
capillary endothelial complex damage, leading to diffuse alveolar edema with fluid and cellular
debris (e.g., neutrophils, cytokines, platelets). In addition, type II cells responsible for surfactant
production are damaged. The peak incidence of this phase typically occurs within the first week
after the initial insult.
The fibroproliferative phase marks either recovery or progression of ARDS. Patients may partly
or fully recover pulmonary function from drainage of the alveolar fluid, type II cellular repair,
and improvement in the integrity of the endothelium-epithelium complex. However, patients whose
conditions are progressively worsening may develop significant alveolar, interstitial, and capillary
fibrosis. This phase typically manifests later in the course of ARDS (i.e., more than 7 days after the
initial insult).