Acute respiratory distress syndrome
Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs.[1] Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis).[1] For those who survive, a decreased quality of life is common.[4]
"ARDS" redirects here. For other uses, see Ards.Acute respiratory distress syndrome
Respiratory distress syndrome (RDS), adult respiratory distress syndrome, shock lung, wet lung
Shortness of breath, rapid breathing, bluish skin coloration, chest pain, loss of speech[1]
Blood clots, Collapsed lung (pneumothorax), Infections, Scarring (pulmonary fibrosis)[2]
Within a week[1]
Adults: PaO2/FiO2 ratio of less than 300 mm Hg[1]
Children: oxygenation index > 4[3]
35 to 90 % risk of death[1]
3 million per year[1]
Causes may include sepsis, pancreatitis, trauma, pneumonia, and aspiration.[1] The underlying mechanism involves diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the immune system, and dysfunction of the body's regulation of blood clotting.[5] In effect, ARDS impairs the lungs' ability to exchange oxygen and carbon dioxide.[1] Adult diagnosis is based on a PaO2/FiO2 ratio (ratio of partial pressure arterial oxygen and fraction of inspired oxygen) of less than 300 mm Hg despite a positive end-expiratory pressure (PEEP) of more than 5 cm H2O.[1] Cardiogenic pulmonary edema, as the cause, must be excluded.[4]
The primary treatment involves mechanical ventilation together with treatments directed at the underlying cause.[1] Ventilation strategies include using low volumes and low pressures.[1] If oxygenation remains insufficient, lung recruitment maneuvers and neuromuscular blockers may be used.[1] If these are insufficient, extracorporeal membrane oxygenation (ECMO) may be an option.[1] The syndrome is associated with a death rate between 35 and 50%.[1]
Globally, ARDS affects more than 3 million people a year.[1] The condition was first described in 1967.[1] Although the terminology of "adult respiratory distress syndrome" has at times been used to differentiate ARDS from "infant respiratory distress syndrome" in newborns, the international consensus is that "acute respiratory distress syndrome" is the best term because ARDS can affect people of all ages.[6] There are separate diagnostic criteria for children and those in areas of the world with fewer resources.[4]
Causes[edit]
There are direct and indirect causes of ARDS depending whether the lungs are initially affected. Direct causes include pneumonia (including bacterial and viral), aspiration, inhalational lung injury, lung contusion, chest trauma, and near-drowning. Indirect causes include sepsis, shock, pancreatitis, trauma (e.g. fat embolism), cardiopulmonary bypass, TRALI, burns, increased intracranial pressure.[11] Fewer cases of ARDS are linked to large volumes of fluid used during post-trauma resuscitation.[12]
Epidemiology[edit]
The annual rate of ARDS is generally 13–23 people per 100,000 in the general population.[40] It is more common in people who are mechanically ventilated with acute lung injury (ALI) occurring in 16% of ventilated people. Rates increased in 2020 due to COVID-19, with some cases also appearing similar to HAPE.[41][42]
Worldwide, severe sepsis is the most common trigger causing ARDS.[43] Other triggers include mechanical ventilation, sepsis, pneumonia, Gilchrist's disease, drowning, circulatory shock, aspiration, trauma—especially pulmonary contusion—major surgery, massive blood transfusions,[44] smoke inhalation, drug reaction or overdose, fat emboli and reperfusion pulmonary edema after lung transplantation or pulmonary embolectomy. However, the majority of patients with all these conditions mentioned do not develop ARDS. It is unclear why some people with the mentioned factors above do not develop ARDS and others do.
Pneumonia and sepsis are the most common triggers, and pneumonia is present in up to 60% of patients and may be either causes or complications of ARDS. Alcohol excess appears to increase the risk of ARDS.[45] Diabetes was originally thought to decrease the risk of ARDS, but this has shown to be due to an increase in the risk of pulmonary edema.[46][47] Elevated abdominal pressure of any cause is also probably a risk factor for the development of ARDS, particularly during mechanical ventilation.
Terminology[edit]
ARDS is the severe form of acute lung injury (ALI), and of transfusion-related acute lung injury (TRALI), though there are other causes. The Berlin definition included ALI as a mild form of ARDS.[51] However, the criteria for the diagnosis of ARDS in the Berlin definition excludes many children, and a new definition for children was termed pediatric acute respiratory distress syndrome (PARDS); this is known as the PALICC definition (2015).[52][53]
Research directions[edit]
There is ongoing research on the treatment of ARDS by interferon (IFN) beta-1a to aid in preventing leakage of vascular beds. Traumakine (FP-1201-lyo) is a recombinant human IFN beta-1a drug, developed by the Finnish company Faron Pharmaceuticals, which is undergoing international phase-III clinical trials after an open-label, early-phase trial showed an 81% reduction-in-odds of 28-day mortality in ICU patients with ARDS.[54] 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.[55]
Aspirin has been studied in those who are at high risk and was not found to be useful.[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.[56]