7. Clinical Timeline:
What Happens Next in ARDS?
High power photomicrograph shows alveoli containing capillaries within
a narrow interstitium. The alveoli are lined with thin, elongated type I
pneumocytes (arrow) and smaller numbers of cuboidal type II
pneumocytes (dashed arrow).
Courtesy of Steven E Weinberger, MD.
Graphic 80140 Version 2.0
Photomicrograph shows early diffuse alveolar damage with
minimal alveolar septal thickening, hyperplasia of pneumocytes,
and eosinophilic hyaline membranes (arrow).
Courtesy of Jeffrey L Myers, MD.
Graphic 57964 Version 3.0
Images: UpToDate
Editor's Notes
This is the first of two modules that discuss ARDS. This first module aims to discuss the epidemiology, pathophysiology, and clinical timeline of this disease.
ARDS is acute respiratory distress syndrome. Although the formal definition will be discussed in module 2, it is important to note that ARDS is “acute” – occurring suddenly and can progress rapidly. ARDS is a respiratory distress syndrome in which patients often suffer from dyspnea, and associated tachypnea.
ARDS can develop in 10-15% of ICU admissions and in 20% of MV patients. 80% of ARDS patients will require MV.
ARDS is a syndrome describing a disease process. ARDS can have many different etiologies that result in the same physiology, pathology and treatment strategy. Causes of ARDS include both direct lung injury such as PNA, Aspiration, Inhalation injury, and pulmonary contusions, or indirect lung injuries such as in sepsis, pancreatitis, TRALI, or from medications and toxins. The common pathologic feature is diffuse alveolar damage.
ARDS lung injury and diffuse alveolar damage leads to Vascular permeability and Protein-rich edema fluid that fills the alveoli and interstitial space. This then leads to impaired gas-exchange and hypoxemia. Over time this parenchymal damage can also lead to Hyaline membrane formation, disordered healing, and fibrosis
In early ARDS, between days Day 1-4, alveolar filling leads to pulmonary edema. This is soon associated with interstitial inflammation. Edema and inflammation lead to diffusion limitations and hypoxemia.
Between Days 10-14 there may be formation of eosinophilic hyaline membranes and scar formation which is called the fibroproliferative phase of the disease.
In addition to hypoxemia, when lung tissue such as the alveoli and interstium become fluid filled and inflamed, the lung compliance will decrease. Decreased compliance leads to an increased risk of barotrauma. Additionally, there can be pulmonary vascular congestion and disruption leading to pulmonary hypertension.
In summary, the hallmark characteristics of ARDS include hypoxemia and bilateral infiltrates seen on radiographic imaging of the chest.
