Acute (Adult) Respiratory Distress Syndrome

Authored by , Reviewed by Dr Adrian Bonsall | Last edited | Meets Patient’s editorial guidelines

Added to Saved items
This page has been archived. It has not been updated since 21/01/2019. External links and references may no longer work.
This article is for Medical Professionals

Professional Reference articles are designed for health professionals to use. They are written by UK doctors and based on research evidence, UK and European Guidelines. You may find the Sepsis (Septicaemia) article more useful, or one of our other health articles.

Read COVID-19 guidance from NICE

Treatment of almost all medical conditions has been affected by the COVID-19 pandemic. NICE has issued rapid update guidelines in relation to many of these. This guidance is changing frequently. Please visit to see if there is temporary guidance issued by NICE in relation to the management of this condition, which may vary from the information given below.

Acute respiratory distress syndrome (ARDS) is a common and devastating condition which can affect all adult patients - eg, medical, surgical and obstetric patients. It occurs when non-cardiogenic pulmonary oedema (secondary to acute damage to the alveoli) leads to acute respiratory failure. The terms ARDS and acute lung injury (ALI) are used interchangeably, although the American-European Consensus Conference Committee devising a consensus definition in 1994, describes them as different entities - ALI having less severe hypoxaemia than ARDS[1].

More recently, a conference of experts in Berlin developed a new definition (see Diagnostic criteria, below)[2].

There is some evidence that the Berlin definition provides a better prediction of mortality than the American-European Consensus Conference Committee definition.

Various population-based studies have revealed a huge global variation in incidence - eg, South America (10.1 per 100,000 person-years), Europe, (17.9 per 100,000 person-years), Australia (34 per 100,000 person-years), USA (78.9 per 100,000 person-years). Even within Europe, considerable variation exists: 10.6 per 100,000 person-years in Finland, 17.9 per 100,000 person-years in Scandinavia, 25.5 per 100,000 person-years in Spain.

In the UK, in one prospective six-month study to determine the incidence and outcome of ARDS in a UK adult University Hospital ICU, 344 patients were admitted during the study period, of which 43 (12.5%) were determined to have ARDS[4].

The more risk factors present, the greater the chance of ARDS.

Most common risk factors[5]

  • Sepsis.
  • Massive trauma with shock and multiple transfusions.
  • Hypovolaemic shock.
  • Pneumonia.
  • Gastric aspiration.

Other risk factors

  • Smoke inhalation
  • Burns
  • Near drowning
  • Diabetic ketoacidosis
  • Pregnancy
  • Eclampsia
  • Amniotic fluid embolus
  • Drugs - paraquat, heroin, aspirin
  • Acute pancreatitis
  • Disseminated intravascular coagulation (DIC)
  • Head injury/raised intracranial pressure (ICP)
  • Fat emboli
  • Transfusions of blood products
  • Heart/lung bypass
  • Tumour lysis syndrome
  • Pulmonary contusion

Increased permeability of pulmonary microvasculature causes leakage of proteinaceous fluid across the alveolar-capillary membrane. This may be one manifestation of a more generalised disruption of endothelium, resulting in hypoxia and multiple organ failure. There is also a reduction in surfactant production. Some patients progress to fibrosis, whilst others recover. The reason for this is not known. However, it is known that there is genetic variability between patients who respond to treatment (particularly corticosteroids) and those who do not. There is also evidence of inflammation in the lung tissue which can be seen on metabolic imaging methods.

  • Symptoms: history of relevant injury and increasing dyspnoea which may occur some time after the precipitating event.
  • Signs: cyanosis (reflecting hypoxia refractory to oxygen therapy), tachypnoea, tachycardia, peripheral vasodilatation, bilateral fine inspiratory crackles.
  • FBC, U&E, LFTs, amylase, clotting, CRP, blood cultures, ABG.
  • CXR shows bilateral alveolar shadowing, often with air bronchograms.
  • Other investigations as deemed by the clinical scenario - eg, echocardiography.

According to the Berlin definition, ARDS is an acute form of diffuse lung injury occurring in patients with a predisposing risk factor, meeting the following criteria:

  • Onset within one week of a known clinical insult or new/worsening respiratory symptoms.
  • Presence of bilateral opacities on CXR, not fully explained by effusion, lobar/lung collapse, or nodules.
  • Diagnosis of respiratory failure not fully explained by cardiac failure or fluid overload.
  • Presence of hypoxaemia, as defined by a specific threshold of the PaO2/FiO2 ratio measured with a minimum requirement of positive end-expiratory pressure (PEEP) ≥5 cm H2O.

Three categories of severity are identified:

  • Mild (200 millimeters of mercury (mm Hg) < PaO2/FiO2 ≤ 300 mm Hg).
  • Moderate (100 mm Hg < PaO2/FiO2 ≤ 200 mm Hg).
  • Severe (PaO2/FiO2 ≤ 100 mm Hg).

Admit to ITU, give supportive therapy and treat the underlying cause.

Respiratory support

In early ARDS, continuous positive airway pressure (CPAP) with 40-60% oxygen may be adequate to maintain oxygenation. But most patients need mechanical ventilation.

Indications for ventilation[7]

  • Severe hypoxaemia: PaO2: <60mm Hg (8.3 kPa) despite 0.6 FiO2
  • PaCO2: >45mm Hg (6 kPa)

The large tidal volumes (10-15 mL/kg) produced by conventional ventilation plus reduced lung compliance in ARDS may lead to high peak airway pressures ± pneumothorax. PEEP increases oxygenation but at the expense of venous return, cardiac output, and perfusion of the kidneys and liver. Low tidal volume ventilation, ie ≤6 mL/kg predicted body weight is the only form of ventilation associated with improved survival[8, 9, 10]. Newer approaches include inverse ratio ventilation (inspiration > expiration), and high-frequency jet ventilation, and other low tidal volume techniques[11]. [12, 13]. Permissive hypercapnia (allowing the patient's carbon dioxide level to rise) has had its advocates, but recent evidence suggests that the risks may well outweigh the benefits[14].

Prone ventilation has been shown to improve alveolar gaseous exchange[13]. This has also been used with good effect in a pregnant patient who experienced blunt chest trauma[15].

Circulatory support

Invasive haemodynamic monitoring with an arterial line and Swan-Ganz catheter may be helpful in monitoring pulmonary capillary wedge pressure and cardiac output.

Maintaining cardiac output and thus oxygen delivery usually needs inotropes (eg, dobutamine), vasodilators and blood transfusion. Fluid rehydration needs to be carefully balanced and in some cases negative fluid balance is the objective. This may require haemofiltration in extreme cases.

Pulmonary hypertension has been treated with inhaled nitric oxide, a selective pulmonary vasodilator. However, studies found that it was associated with renal dysfunction and is no longer routinely recommended. There may be a place for it for short periods in severe right ventricular dysfunction or extreme hypoxaemia, but further research is required[8].

Other therapies

There is a range of opinion on whether the benefits of corticosteroids in ARDS outweigh the risks. Further research is needed[16].

The role of ketoconazole has also proved to be disappointing[17]. Essentially, the treatment of ARDS has been supportive, and no emerging therapies have been identified which make any difference to the clinical outcome[18].


Identify organism(s) and treat accordingly. If clinically septic, but no organisms cultured, use empirical broad-spectrum antibiotics, but avoid nephrotoxic antibiotics.

Other supportive care[19]

  • Nutritional support - enteral feeding is better than parenteral feeding.
  • Venous thromboembolism prevention with low molecular weight heparin.
  • Gastric ulcer prevention with prophylactic medications.
  • Mortality rate in ARDS remains significant. One study reported a rate of 38%, but this was reduced to 31% after the introduction of low-volume ventilatory support[20].
  • A number of methods to determine prognosis have been developed including the use of[21]:
    • Clinical characteristics.
    • Physiological parameters and oxygenation.
    • Genetic polymorphisms and biomarkers.
    • Scoring systems.
  • In most cases, survivors' lung function returns almost to normal. However, some may have reduced exercise capacity and neuropsychological disorders up to five years after their illness[22].
  • Patients with ALI recover lung function in 12 months but can have persistent muscle weakness and reduced health-related quality of life for up to 24 months[23].

Are you protected against flu?

See if you are eligible for a free NHS flu jab today.

Check now

Further reading and references

  • Wohlrab P, Kraft F, Tretter V, et al; Recent advances in understanding acute respiratory distress syndrome. F1000Res. 2018 Mar 57. doi: 10.12688/f1000research.11148.1. eCollection 2018.

  1. Tsushima K, King LS, Aggarwal NR, et al; Acute lung injury review. Intern Med. 200948(9):621-30. Epub 2009 May 1.

  2. Umbrello M, Formenti P, Bolgiaghi L, et al; Current Concepts of ARDS: A Narrative Review. Int J Mol Sci. 2016 Dec 2918(1). pii: ijms18010064. doi: 10.3390/ijms18010064.

  3. Rezoagli E, Fumagalli R, Bellani G; Definition and epidemiology of acute respiratory distress syndrome. Ann Transl Med. 2017 Jul5(14):282. doi: 10.21037/atm.2017.06.62.

  4. Summers C, Singh NR, Worpole L, et al; Incidence and recognition of acute respiratory distress syndrome in a UK intensive care unit. Thorax. 2016 Nov71(11):1050-1051. doi: 10.1136/thoraxjnl-2016-208402. Epub 2016 Aug 22.

  5. Matthay MA, Ware LB, Zimmerman GA; The acute respiratory distress syndrome. J Clin Invest. 2012 Aug 1122(8):2731-40. doi: 10.1172/JCI60331. Epub 2012 Aug 1.

  6. Confalonieri, M et al; Acute respiratory distress syndrome, European Respiratory Review 2017 26: 160116 DOI: 10.1183/16000617.0116-2016

  7. Bein T, Grasso S, Moerer O, et al; The standard of care of patients with ARDS: ventilatory settings and rescue therapies for refractory hypoxemia. Intensive Care Med. 2016 May42(5):699-711. doi: 10.1007/s00134-016-4325-4. Epub 2016 Apr 4.

  8. The Faculty of Intensive Care Medicine; Guidelines on the management of acute respiratory distress syndrome, 2018.

  9. Wheeler AP, Bernard GR; Acute lung injury and the acute respiratory distress syndrome: a clinical review. Lancet. 2007 May 5369(9572):1553-64.

  10. Girard TD, Bernard GR; Mechanical ventilation in ARDS: a state-of-the-art review. Chest. 2007 Mar131(3):921-9.

  11. Kotani T, Katayama S, Fukuda S, et al; Pressure-controlled inverse ratio ventilation as a rescue therapy for severe acute respiratory distress syndrome. Springerplus. 2016 Jun 145(1):716. doi: 10.1186/s40064-016-2440-x. eCollection 2016.

  12. Guerin C, Reignier J, Richard JC, et al; Prone positioning in severe acute respiratory distress syndrome. N Engl J Med. 2013 Jun 6368(23):2159-68. doi: 10.1056/NEJMoa1214103. Epub 2013 May 20.

  13. Bein T, Grasso S, Moerer O, et al; The standard of care of patients with ARDS: ventilatory settings and rescue therapies for refractory hypoxemia. Intensive Care Med. 2016 May42(5):699-711. doi: 10.1007/s00134-016-4325-4. Epub 2016 Apr 4.

  14. Repesse X, Vieillard-Baron A; Hypercapnia during acute respiratory distress syndrome: the tree that hides the forest! J Thorac Dis. 2017 Jun9(6):1420-1425. doi: 10.21037/jtd.2017.05.69.

  15. Kenn S, Weber-Carstens S, Weizsaecker K, et al; Prone positioning for ARDS following blunt chest trauma in late pregnancy. Int J Obstet Anesth. 2009 May 21.

  16. Meduri GU, Rochwerg B, Annane D, et al; Prolonged corticosteroid treatment in acute respiratory distress syndrome: impact on mortality and ventilator-free days. Crit Care. 2018 May 2422(1):135. doi: 10.1186/s13054-018-2007-z.

  17. Jung HS, Kaplan LJ, Park PK; Reviewing the studies of the National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome Network: outcomes and clinical findings. Curr Probl Surg. 2013 Oct50(10):451-62. doi: 10.1067/j.cpsurg.2013.08.009.

  18. Derwall M, Martin L, Rossaint R; The acute respiratory distress syndrome: pathophysiology, current clinical practice, and emerging therapies. Expert Rev Respir Med. 2018 Dec12(12):1021-1029. doi: 10.1080/17476348.2018.1548280. Epub 2018 Nov 21.

  19. Saguil A, Fargo M; Acute respiratory distress syndrome: diagnosis and management. Am Fam Physician. 2012 Feb 1585(4):352-8.

  20. Baron RM, Levy BD; Recent advances in understanding and treating ARDS. F1000Res. 2016 Apr 225. doi: 10.12688/f1000research.7646.1. eCollection 2016.

  21. Chen W, Ware LB; Prognostic factors in the acute respiratory distress syndrome. Clin Transl Med. 2015 Dec4(1):65. doi: 10.1186/s40169-015-0065-2. Epub 2015 Jul 2.

  22. Chiumello D, Coppola S, Froio S, et al; What's Next After ARDS: Long-Term Outcomes. Respir Care. 2016 May61(5):689-99. doi: 10.4187/respcare.04644.

  23. Fan E, Dowdy DW, Colantuoni E, et al; Physical complications in acute lung injury survivors: a two-year longitudinal prospective study. Crit Care Med. 2014 Apr42(4):849-59. doi: 10.1097/CCM.0000000000000040.