[7][8] Other common symptoms include muscle fatigue and general weakness, low blood pressure, a dry, hacking cough, and fever.

Indirect causes include sepsis, shock, pancreatitis, trauma (e.g. fat embolism), cardiopulmonary bypass, TRALI, burns, increased intracranial pressure.

[12] ARDS is a form of fluid accumulation in the lungs not explained by heart failure (noncardiogenic pulmonary edema).

[13] Additional common findings in ARDS include partial collapse of the alveoli (atelectasis) and low levels of oxygen in the blood (hypoxemia).

The triggering insult to the tissue usually results in an initial release of chemical signals and other inflammatory mediators secreted by local epithelial and endothelial cells.

[citation needed] Neutrophils and some T-lymphocytes quickly migrate into the inflamed lung tissue and contribute in the amplification of the phenomenon.

[citation needed] One research group has reported that broncho-alveolar lavage fluid in later-stage ARDS often contains trichomonads,[14] in an amoeboid form (i.e. lacking their characteristic flagellum) which makes them difficult to identify under the microscope.

[16][17] In addition to generally broadening the diagnostic thresholds, other notable changes from the prior 1994 consensus criteria[6] include discouraging the term "acute lung injury", and defining grades of ARDS severity according to degree of decrease in the oxygen content of the blood.

Generally, radiographic findings of fluid accumulation (pulmonary edema) affecting both lungs and unrelated to increased cardiopulmonary vascular pressure (such as in heart failure) may be suggestive of ARDS.

[20] Ultrasound findings suggestive of ARDS include the following: Acute respiratory distress syndrome is usually treated with mechanical ventilation in the intensive care unit (ICU).

The role of non-invasive ventilation is limited to the very early period of the disease or to prevent worsening respiratory distress in individuals with atypical pneumonias, lung bruising, or major surgery patients, who are at risk of developing ARDS.

[citation needed] The overall goal of mechanical ventilation is to maintain acceptable gas exchange to meet the body's metabolic demands and to minimize adverse effects in its application.

Recent studies have shown that high tidal volumes can overstretch alveoli resulting in volutrauma (secondary lung injury).

Low tidal volumes (Vt) may cause a permitted rise in blood carbon dioxide levels and collapse of alveoli[10] because of their inherent tendency to increase shunting within the lung.

[citation needed] A patient with ARDS, on average, spends between 8 and 11 days on a mechanical ventilator; APRV may reduce this time significantly and thus may conserve valuable resources.

[27] Positive end-expiratory pressure (PEEP) is used in mechanically ventilated people with ARDS to improve oxygenation.

[citation needed] The 'best PEEP' used to be defined as 'some' cmH2O above the lower inflection point (LIP) in the sigmoidal pressure-volume relationship curve of the lung.

A large randomized controlled trial of patients with ARDS found that lung recruitment maneuvers and PEEP titration was associated with high rates of barotrauma and pneumothorax and increased mortality.

[29][30] However, attention should be paid to avoid the SIDS in the management of the respiratory distressed infants by continuous careful monitoring of their cardiovascular system.

[33] Inhaled nitric oxide (NO) selectively widens the lung's arteries which allows for more blood flow to open alveoli for gas exchange.

[citation needed] Acute respiratory distress syndrome was first described in 1967 by Ashbaugh et al.[10][50] Initially there was no clearly established definition, which resulted in controversy regarding the incidence and death of ARDS.

In 1994, a new definition was recommended by the American-European Consensus Conference Committee [6][10] which recognized the variability in severity of pulmonary injury.

These recommendations were an effort to both update classification criteria in order to improve clinical usefulness and to clarify terminology.

[16] The Berlin definitions represent the current international consensus guidelines for both clinical and research classification of ARDS.

[54][55] There is ongoing research on the treatment of ARDS by interferon (IFN) beta-1a to aid in preventing leakage of vascular beds.

[56] The drug is known to function by enhancing lung CD73 expression and increasing production of anti-inflammatory adenosine, such that vascular leaking and escalation of inflammation are reduced.

[1] An intravenous ascorbic acid treatment was tested in the 2019 RCT, in people with ARDS due to sepsis and there was no change in primary endpoints.