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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

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]

Lungs: (volutrauma), pulmonary embolism (PE), pulmonary fibrosis, ventilator-associated pneumonia (VAP)

barotrauma

Gastrointestinal: bleeding (ulcer), dysmotility, , bacterial translocation

pneumoperitoneum

Neurological: brain damage

hypoxic

Cardiac: , myocardial dysfunction

abnormal heart rhythms

Kidney: , positive fluid balance

acute kidney failure

Mechanical: vascular injury, (by placing pulmonary artery catheter), tracheal injury/stenosis (result of intubation and/or irritation by endotracheal tube)

pneumothorax

Nutritional: (catabolic state), electrolyte abnormalities

malnutrition

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]

lung injury of acute onset, within 1 week of an apparent clinical insult and with the progression of respiratory symptoms

bilateral opacities on chest imaging ( or CT) not explained by other lung pathology (e.g. effusion, lobar/lung collapse, or nodules)

chest radiograph

respiratory failure not explained by heart failure or volume overload

positive end expiratory pressure (PEEP)

Prognosis[edit]

The overall prognosis of ARDS is poor, with mortality rates of approximately 40%.[29] Exercise limitation, physical and psychological sequelae, decreased physical quality of life, and increased costs and use of health care services are important sequelae of ARDS.

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.

acute onset, persistent dyspnea

bilateral infiltrates on chest radiograph consistent with pulmonary edema

hypoxemia, defined as PaO
2
:FiO
2
 < 200 mmHg (26.7 kPa)

pulmonary artery wedge pressure

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]

Marino, Paul (2006). The ICU Book. Baltimore: Williams & Wilkins.  978-0781748025.

ISBN

Martin GS, Moss M, Wheeler AP, Mealer M, Morris JA, Bernard GR (1 August 2005). "A randomized, controlled trial of furosemide with or without albumin in hypoproteinemic patients with acute lung injury". Crit. Care Med. 33 (8): 1681–7. :10.1097/01.CCM.0000171539.47006.02. PMID 16096441. S2CID 38941988.

doi

Jackson WL, Shorr AF (1 June 2005). "Blood transfusion and the development of acute respiratory distress syndrome: more evidence that blood transfusion in the intensive care unit may not be benign". Crit. Care Med. 33 (6): 1420–1. :10.1097/01.CCM.0000167073.99222.50. PMID 15942365.

doi

Mortelliti MP, Manning HL (May 2002). . Am Fam Physician. 65 (9): 1823–30. PMID 12018805. Archived from the original on 2008-09-06. Retrieved 2005-08-28.

"Acute respiratory distress syndrome"

Metnitz, P. G. H.; Bartens, C.; Fischer, M.; Fridrich, P.; Steltzer, H.; Druml, W. (17 February 1999). "Antioxidant status in patients with acute respiratory distress syndrome". Intensive Care Medicine. 25 (2): 180–185. :10.1007/s001340050813. PMID 10193545. S2CID 11377820.

doi

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]

Respiratory monitoring

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—the NIH / NHLBI ARDS Network

ARDSNet

—information for patients with ARDS

ARDS Support Center