Acute Respiratory Distress Syndrome (ARDS)

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Overview

Acute respiratory distress syndrome (ARDS) is sudden, life-threatening lung failure. ARDS inflames the alveoli, causing them to fill with liquid and collapse. Once the alveoli collapse, gas exchange ceases, and the body becomes starved of oxygen. ARDS requires treatment with mechanical ventilation or some other form of assisted breathing.

ARDS is a syndrome, not a specific disease. A variety of underlying conditions, from blood-borne infections to major trauma, can cause the characteristic inflammation and accumulation of fluid (edema) in the alveoli (see causes).

ARDS usually develops within 24 to 48 hours of the injury or illness. The duration and intensity of the condition can vary considerably from patient to patient. The mortality rate from ARDS ranges from 35—50%. In most cases, death results from underlying disease or from complications of mechanical ventilation. In patients who survive, normal lung function usually resumes within 6 to 12 months.

Incidence and Prevalence
According to the American Lung Association, the incidence of ARDS ranges from 1.5 to 71 per 100,000 persons in the United States.

Pathophysiology
The respiratory system resembles an upside-down, hollow tree. Indeed, the passageways leading from the mouth to the interior of the lungs are referred to as the tracheobronchial tree. The parts of the body through which air enters and exits the body (i.e., the mouth, nose, larynx, and trachea) make up the "trunk" of the tree. The tubes that lead to the lungs (bronchi) and the tiny tubes inside the lungs (bronchioles) are the tree's "branches" and "twigs."

Air moves through the respiratory system from the base of the trunk to the tips of the twigs. Clustered at the tips of the trachiobronchial twigs are tiny air sacs called alveoli, where inhaled oxygen passes into the blood stream. This is where ARDS occurs.

Injury to the alveoli
About 90% of the cells that make up the alveoli are very thin "type I epithelial cells" across which actual gas exchange takes place. Oxygen normally diffuses very easily through this layer of cells into the capillaries where it binds with the hemoglobin in the red blood cells.

The alveolar epithelial cells normally form a very tight barrier around the alveolar space, preventing any fluid from entering and disrupting gas exchange. In ARDS, the alveolar epithelial barrier breaks, allowing flooding of the alveolar space and making it difficult or impossible for oxygen to diffuse into the capillaries.

ARDS also can affect the "type II alveolar cells". Type II cells are thicker, square-shaped cells and the main function of these cells is to produce surfactant. Surfactant plays an essential role in preventing the alveoli from collapsing. The flooding through the broken type I cell barrier and the diminished production of surfactant by the type II cells collapse the alveoli.

Alveolar damage is increased by the activity of immune system cells (neutrophils) that rush to the site of injury, ironically, to help out. The activity of these cells and the inflammation they cause create a cascade of further injury that may extend into the capillaries as well.

Injury to the alveolar capillaries
If the original injury is in the alveolar capillaries that lie just beneath the alveoli, chemical mediators (usually cytokines) that the immune system releases in response, rush to the site of the injury, damaging and causing inflammation to the cells that line the capillaries (i.e., the capillary endothelium).

As a result, cells and fluid leak through the capillaries and into the alveolar spaces; the capillaries become blocked with cellular debris and fibrin (i.e., protein that makes up blood clots); surfactant production ceases; and the alveoli collapse.

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