Back To Search Results

Acute Respiratory Distress Syndrome

Editor: Sidharth Mahapatra Updated: 4/6/2023 2:30:55 PM

Acute respiratory distress syndrome (ARDS) is an acute, diffuse, inflammatory form of lung injury and life-threatening condition in seriously ill patients, characterized by poor oxygenation, pulmonary infiltrates, and acute onset. On a microscopic level, the disorder is associated with capillary endothelial injury and diffuse alveolar damage.

ARDS is an acute disorder that starts within seven days of the inciting event and is characterized by bilateral lung infiltrates and severe progressive hypoxemia in the absence of any evidence of cardiogenic pulmonary edema. ARDS is defined by the patient's oxygen in arterial blood (PaO2) to the fraction of the oxygen in the inspired air (FiO2). These patients have a PaO2/FiO2 ratio of less than 300. The definition of ARDS was updated in 2012 and is called the Berlin definition. It differs from the previous American European Consensus definition by excluding the term acute lung injury; it also removed the requirement for wedge pressure <18 and included the requirement of positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) of greater than or equal to 5.

Once ARDS develops, patients usually have varying degrees of pulmonary artery vasoconstriction and may subsequently develop pulmonary hypertension. ARDS carries a high mortality, and few effective therapeutic modalities exist to combat this condition.[1][2]


Earn CME credit as you help guide your clinical decisions.
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed.


$59 per month


$599 per year

ARDS has many risk factors. Besides pulmonary infection or aspiration, extra-pulmonary sources include sepsis, trauma, massive transfusion, drowning, drug overdose, fat embolism, inhalation of toxic fumes, and pancreatitis. These extra-thoracic illnesses and/or injuries trigger an inflammatory cascade culminating in pulmonary injury.[3]

A lung injury prevention score helps identify low-risk patients, but a high score is less helpful.[1]

Some risk factors for ARDS include:

  • Advanced age
  • Female gender
  • Smoking
  • Alcohol use
  • Aortic vascular surgery
  • Cardiovascular surgery
  • Traumatic brain injury[2]
  • Pancreatitis
  • Pulmonary contusion
  • Infectious pneumonia
  • Drugs (radiation, chemotherapeutic agents, amiodarone)

Estimates of the incidence of ARDS in the United States range from 64.2 to 78.9 cases/100,000 person-years. Twenty-five percent of ARDS cases are initially classified as mild, and 75% as moderate or severe. However, a third of the mild cases progress to moderate or severe disease.[3][4] Approximately 10 to 15% of patients admitted to the intensive care units and up to 23% of mechanically ventilated patients meet the criteria for ARDS.[5] A literature review revealed a mortality decrease of 1.1% per year for the period 1994 through 2006. However, the overall pooled mortality rate for all the studies evaluated was 43%.[6][7] The mortality of ARDS is commensurate with the severity of the disease; it is 27%, 32%, and 45% for mild, moderate, and severe disease, respectively.

ARDS represents a stereotypic response to various etiologies. It progresses through different phases, starting with alveolar-capillary damage, a proliferative phase characterized by improved lung function and healing, and a final fibrotic phase signaling the end of the acute disease process. The pulmonary epithelial and endothelial cellular damage is characterized by inflammation, apoptosis, necrosis, and increased alveolar-capillary permeability, which leads to the development of alveolar edema and proteinosis. Alveolar edema, in turn, reduces gas exchange, leading to hypoxemia. A hallmark of the pattern of injury seen in ARDS is that it is not uniform. Segments of the lung may be more severely affected, resulting in decreased regional lung compliance, which classically involves the bases more than the apices—this intrapulmonary differential in pathology results in a variant response to oxygenation strategies. While increased positive end-expiratory pressure (PEEP) may improve oxygen diffusion in affected alveoli, it may result in deleterious volutrauma and atelectrauma of adjacent unaffected alveoli.[8] The injury results in three main outcomes: 

  • Impaired gas exchange
  • Decreased lung compliance
  • Pulmonary hypertension[9]

The key histologic changes in ARDS reveal the presence of alveolar edema in diseased lung areas. The type I pneumocytes and vascular endothelium are injured, which results in the leaking of proteinaceous fluid and blood into the alveolar airspace. Other findings may include alveolar hemorrhage, pulmonary capillary congestion, interstitial edema, and hyaline membrane formation. None of these changes are specific to the disease.[8]

History and Physical

The syndrome is characterized by dyspnea and hypoxemia, progressively worsening within 6 to 72 hours of the inciting event, frequently requiring mechanical ventilation and intensive care unit-level care. The history is directed at identifying the underlying cause that precipitated the disease. When interviewing patients that can communicate, they often start to complain of mild dyspnea initially, but within 12 to 24 hours, the respiratory distress escalates, becoming severe and requiring mechanical ventilation to prevent hypoxia. The etiology may be obvious in the case of pneumonia or sepsis. However, in other cases, questioning the patient or relatives on recent exposures may also be paramount in identifying the causative agent.

The physical examination will include findings associated with the respiratory system, such as tachypnea and increased breathing effort. Systemic signs may also be evident depending on the severity of the illness, such as central or peripheral cyanosis resulting from hypoxemia, tachycardia, and altered mental status. Despite 100% oxygen, patients have low oxygen saturation. Chest auscultation usually reveals rales, especially bibasilar, but can often be auscultated throughout the chest.


The diagnosis of ARDS is based on the following criteria: acute onset, bilateral lung infiltrates on chest radiography of a non-cardiac origin, and a PaO/FiO ratio of less than 300 mmHg. It is further sub-classified into mild (PaO2/FiO2 200 to 300 mmHg), moderate (PaO2/FiO2 100 to 200 mmHg), and severe (PaO2/FiO2 less than 100 mmHg) subtypes. Mortality and ventilator-free days increase with severity. A CT scan of the chest may be required in pneumothorax cases, pleural effusions, mediastinal lymphadenopathy, or barotrauma to properly identify infiltrates as pulmonic in location.

Assessment of left ventricular function may be required to differentiate from or quantify the contribution of congestive heart failure to the overall clinical picture. This assessment can be achieved via invasive methods, such as pulmonary artery catheter measurements, or non-invasively, such as cardiac echocardiography or thoracic bioimpedance, or pulse contour analysis. However, using pulmonary artery catheters (PAC) is controversial and should be avoided if clinically possible. Noninvasive assessment measures should be exhausted first; the use of PAC is discouraged by the new definition. Using bronchoscopy may be required to assess pulmonary infections and obtain material for culture.[2]

Other laboratory and/or radiographic tests will be guided by the underlying disease process, which has triggered the inflammatory process that has led to the development of ARDS. Also, laboratory tests will be needed as patients with ARDS are highly likely to develop or be affected by associated multi-organ failure, including but not limited to renal, hepatic, and hematopoietic failures. Regularly obtaining complete blood count with differential, comprehensive metabolic panel, serum magnesium, serum ionized calcium, phosphorus levels, blood lactate level, coagulation panel, troponin, cardiac enzymes, and CKMB are recommended if clinically indicated.[10][11][12]

Treatment / Management

The chief treatment strategy is supportive care and focuses on 1) reducing shunt fraction, 2) increasing oxygen delivery, 3) decreasing oxygen consumption, and 4) avoiding further injury. Patients are mechanically ventilated, guarded against fluid overload with diuretics, and given nutritional support until improvement is observed. Interestingly, the mode in which a patient is ventilated affects lung recovery. Evidence suggests that some ventilatory strategies can exacerbate alveolar damage and perpetuate lung injury in the context of ARDS. Care is placed on preventing volutrauma (exposure to large tidal volumes), barotrauma (exposure to high plateau pressures), and atelectrauma (exposure to atelectasis).[1][13]

A lung-protective ventilatory strategy is advocated to reduce lung injury. The NIH-NHLBI ARDS Clinical Network Mechanical Ventilation Protocol (ARDSnet) sets the following goals: Tidal volume (V) from 4 to 8 mL/kg of ideal body weight (IBW), respiratory rate (RR) up to 35 bpm, SpO2 88% to 95%, plateau pressure (P) less than 30 cm H2O, pH goal 7.30 to 7.45, and inspiratory-to-expiratory time ratio less than 1. To maintain oxygenation, ARDSnet recognizes the benefit of PEEP. The protocol allows for a low or a high PEEP strategy relative to FiO2. Either strategy tolerates a PEEP of up to 24 cm HO in patients requiring 100% FiO2. The inspiratory-to-expiratory time ratio goal may need to be sacrificed and an inverse inspiratory-to-expiratory time ratio strategy instituted to improve oxygenation in a certain clinical situation.

Novel invasive ventilation strategies have been developed to improve oxygenation. These include airway pressure release ventilation (APRV) and high-frequency oscillation ventilation (children). Recruitment maneuvers and APRV have not been shown to improve mortality but may improve oxygenation. Patients with mild and some with moderate ARDS may benefit from non-invasive ventilation to avoid endotracheal intubation and invasive mechanical ventilation. These modalities include continuous positive airway pressure (CPAP), bi-level airway pressure (BiPAP), proportional-assist ventilation, and a high-flow nasal cannula. Adequate care should be taken to intubate and mechanically ventilate these patients if they get worse on the above non-invasive ventilation.

A plateau pressure of less than 30 cm HO can be achieved using several strategies. Again, this is to reduce the risk of barotrauma. One strategy is to maintain as low a V and PEEP as possible. Also, increasing the rise and/or inspiration times can also help maintain the P goal. Finally, the flow rate can be decreased as an adjunct to decreasing the P. High P is also a product of decreased lung compliance from non-cardiogenic pulmonary edema, a salient feature of ARDS pathophysiology.

Improving lung compliance will improve P and oxygenation goal attainment. The neuromuscular blockade has been used in this endeavor. Neuromuscular blockers instituted during the first 48 hours of ARDS improved 90-day survival and increased time off the ventilator.[13] However, the most recent trial published in 2019 showed no significant difference in mortality with continuous infusion of people with paralysis compared to lighter sedation goals.[14] 

Other causes of decreased lung compliance should be sought and addressed. These include, but are not limited to, pneumothorax, hemothorax, thoracic compartment syndrome, and intraabdominal hypertension. Prone position has shown benefits in about 50% to 70% of patients. The improvement in oxygenation is rapid and allows a reduction in FiO2 and PEEP. The prone position is safe, but there is a risk of dislodgement of lines and tubes. It is believed that in the prone position, there is the recruitment of dependent lung zones, improved diaphragmatic excursion, and increased functional residual capacity. To derive the benefits, the patient needs to be maintained in a prone position for at least 8 hours a day.

Non-ventilatory strategies have included prone positioning and conservative fluid management once resuscitation has been achieved.[15][16] Extracorporeal membrane oxygenation (ECMO) has recently been advocated as salvage therapy in refractory hypoxemic ARDS.[17] However, two major trials that compared venovenous (VV) ECMO to standard care showed no difference in mortality between the two groups.[18] Nutritional support via enteral feeding is recommended. A high-fat, low-carbohydrate diet containing gamma-linolenic acid and eicosapentaenoic acid has been shown in some studies to improve oxygenation. A moderately permissive strategy (i.e., target blood glucose 140 to 180 mg/dL [7.7 to 10 mmol/L]) is recommended for most hyperglycemic critically ill patients, rather than the intensive insulin therapy (IIT) targeting blood glucose 80 to 110 mg/dL. Critically ill patients are more prone to deep venous prophylaxis, so some form of thrombolysis is recommended. Likewise, prophylaxis against stress ulcers is advised for increased risk of gastrointestinal bleeding.

Glucocorticoids can be administered in patients in whom ARDS has been precipitated by a steroid-responsive process (e.g., acute eosinophilic pneumonia) and to those with refractory sepsis or community-acquired pneumonia. Most patients who have persistent or refractory moderate to severe ARDS are relatively early in the disease course (within 14 days of onset with a partial arterial pressure of oxygen/fraction of inspired oxygen [PaO/FiO] ratio <200) despite initial management with standard therapies, including low tidal volume ventilation, can also be managed with glucocorticoids.[19] However, glucocorticoids are generally avoided in patients with less severe ARDS or those with persistent ARDS beyond 14 days. Moreover, their use is associated with worse outcomes in patients with certain viral infections, including influenza.[20]

Central venous catheters can draw blood, administer pressors, and measure central venous pressure.

Care must also be taken to prevent pressure sores; thus, frequent patient repositioning or turning is recommended when feasible. Skin checks per nursing routine are also advised. Physical therapy should involve exercising the patient when they are liberated from mechanical ventilation and stable to participate in treatment. No role for the routine administration of mucolytics is proven in these patients.[21]

Differential Diagnosis

  • Cardiogenic edema
  • Exacerbation of interstitial lung disease
  • Acute interstitial pneumonia
  • Diffuse alveolar hemorrhage
  • Acute eosinophilic lung disease
  • Organizing pneumonia
  • Bilateral pneumonia
  • Pulmonary vasculitis
  • Cryptogenic organizing pneumonia
  • Disseminated malignancy


The prognosis for ARDS was abysmal until very recently. There are reports of 30 to 40% mortality up until the 1990s, but over the past 20 years, there has been a significant decrease in the mortality rate, even for severe ARDS. These accomplishments are secondary to a better understanding of and advancements in mechanical ventilation and earlier antibiotic administration and selection. The primary cause of death in patients with ARDS was sepsis or multiorgan failure. While mortality rates are now around 9 to 20%, it is much higher in older patients. ARDS has significant morbidity as these patients remain in the hospital for extended periods and have significant weight loss, poor muscle function, and functional impairment. Hypoxia from the inciting illness also leads to various cognitive changes that may persist for months after discharge. As measured by functional testing, there is an almost near-complete return of pulmonary capacity for many survivors. Nonetheless, many patients report feelings of dyspnea on exertion and decreased exercise tolerance. This ARDS sequela makes returning to a normal life challenging for these patients as they adjust to a new baseline.[22][23]


  • Barotrauma from high PEEP
  • Prolonged mechanical ventilation -thus the need for tracheostomy
  • Post-extubation laryngeal edema and subglottic stenosis
  • Nosocomial infections
  • Pneumonia
  • Line sepsis
  • Urinary tract infection
  • Deep venous thrombosis
  • Antibiotic resistance
  • Muscle weakness
  • Renal failure
  • Post-traumatic stress disorder

Postoperative and Rehabilitation Care

Tracheostomy and Percutaneous Endoscopic Gastrostomy (PEG)

Many patients with ARDS require a tracheostomy and a percutaneous feeding tube in the recovery phase. The tracheostomy facilitates weaning from the ventilator, making it easy to clear the secretions and more comfortable. The tracheostomy is usually done at 2 to 3 weeks, followed by a percutaneous feeding tube.

Nutritional Support

Most patients with ARDS have difficulty eating, and muscle wasting is very common. These patients are either given enteral or parenteral feeding, depending on the condition of the gastrointestinal tract. Some experts recommend a low-carbohydrate, high-fat diet as it has anti-inflammatory and vasodilating effects. Almost every type of nutritional supplement has been studied in patients with ARDS, but so far, none has proven to be the magic bullet.


Since patients with ARDS are bed-bound, frequent position changes are highly recommended to prevent bedsores and deep venous thrombosis. In alert patients, one can minimize the sedation and sit them in a chair.


Management of patients with ARDS requires an interprofessional team of healthcare workers that includes:

  • Pulmonologist
  • Respiratory therapist
  • Intensivist
  • Infectious disease
  • Dietitian

Deterrence and Patient Education

Even though many risk factors for ARDS are known, there is no way to prevent ARDS proactively. However, careful management of fluids in high-risk patients can be helpful. Steps should be taken to prevent aspiration by keeping the head of the bed elevated before feeding. Lung protective mechanical ventilation strategy in patients without ARDS who are high risk would help prevent ARDS.

Enhancing Healthcare Team Outcomes

ARDS is a severe disorder of the lung which has the potential to cause death. Patients with ARDS may require mechanical ventilation because of hypoxia.[24] The management is usually in the ICU with an interprofessional healthcare team. ARDS has effects beyond the lung. Prolonged mechanical ventilation often leads to bedsores, deep venous thrombosis, multi-organ failure, weight loss, and poor overall functioning. It is essential to have an integrated approach to ARDS management because it usually affects many organs in the body. These patients need nutritional support, chest physiotherapy, treatment for sepsis if present, and potentially hemodialysis. Many of these patients remain in the hospital for months, and even those who survive face severe challenges due to a loss of muscle mass and cognitive changes (due to hypoxia). There is ample evidence showing that an interprofessional team approach leads to better outcomes by facilitating communication and ensuring timely intervention.[25] The team and responsibilities should consist of the following:

  • Intensivist for managing the patient on the ventilator and other ICU-related issues like pneumonia prevention, deep venous thrombosis prophylaxis, and gastric stress prevention
  • Dietitian and nutritionist for nutritional support
  • Respiratory therapist to manage the ventilator settings
  • Pharmacist to manage the medications, which include antibiotics, anticoagulants, and diuretics, among others
  • Pulmonologist to manage the lung diseases
  • Nephrologist to manage the kidneys and oversee renal replacement therapy if needed
  • Nurses to monitor the patient, move the patient in bed, educate the family
  • Physical therapist to exercise the patient, regain muscle function
  • Tracheostomy nurse to assist with maintaining tracheostomy and weaning
  • Mental health nurse to assess for depression, anxiety, and other psychosocial issues
  • Social worker to assess the patient's financial situation, transfer for rehab, and ensure there is an adequate follow-up
  • Chaplain for spiritual care


Despite advances in critical care, ARDS still has high morbidity and mortality. Even those who survive can have a poorer quality of life. While many risk factors are known for ARDS, there is no way to prevent the condition. Besides restricting fluids in high-risk patients, close monitoring for hypoxia by the team is vital. The earlier the hypoxia is identified, the better the outcome. Those who survive have a lengthy recovery period to regain functional status. Many continue to have dyspnea even with mild exertion and thus depend on care from others.


(Click Image to Enlarge)
Acute Respiratory Distress Syndrome
Acute Respiratory Distress Syndrome
Image courtesy S Bhimji MD



Gajic O,Dabbagh O,Park PK,Adesanya A,Chang SY,Hou P,Anderson H 3rd,Hoth JJ,Mikkelsen ME,Gentile NT,Gong MN,Talmor D,Bajwa E,Watkins TR,Festic E,Yilmaz M,Iscimen R,Kaufman DA,Esper AM,Sadikot R,Douglas I,Sevransky J,Malinchoc M, Early identification of patients at risk of acute lung injury: evaluation of lung injury prediction score in a multicenter cohort study. American journal of respiratory and critical care medicine. 2011 Feb 15     [PubMed PMID: 20802164]


Wang Y,Zhang L,Xi X,Zhou JX,China Critical Care Sepsis Trial (CCCST) Workgroup., The Association Between Etiologies and Mortality in Acute Respiratory Distress Syndrome: A Multicenter Observational Cohort Study. Frontiers in medicine. 2021;     [PubMed PMID: 34733862]


Zambon M,Vincent JL, Mortality rates for patients with acute lung injury/ARDS have decreased over time. Chest. 2008 May;     [PubMed PMID: 18263687]


Shrestha GS,Khanal S,Sharma S,Nepal G, COVID-19: Current Understanding of Pathophysiology. Journal of Nepal Health Research Council. 2020 Nov 13;     [PubMed PMID: 33210623]

Level 3 (low-level) evidence


Bellani G, Laffey JG, Pham T, Fan E, Brochard L, Esteban A, Gattinoni L, van Haren F, Larsson A, McAuley DF, Ranieri M, Rubenfeld G, Thompson BT, Wrigge H, Slutsky AS, Pesenti A, LUNG SAFE Investigators, ESICM Trials Group. Epidemiology, Patterns of Care, and Mortality for Patients With Acute Respiratory Distress Syndrome in Intensive Care Units in 50 Countries. JAMA. 2016 Feb 23:315(8):788-800. doi: 10.1001/jama.2016.0291. Epub     [PubMed PMID: 26903337]


Sedhai YR,Yuan M,Ketcham SW,Co I,Claar DD,McSparron JI,Prescott HC,Sjoding MW, Validating Measures of Disease Severity in Acute Respiratory Distress Syndrome. Annals of the American Thoracic Society. 2020 Dec 21;     [PubMed PMID: 33347379]


Sharma NS,Lal CV,Li JD,Lou XY,Viera L,Abdallah T,King RW,Sethi J,Kanagarajah P,Restrepo-Jaramillo R,Sales-Conniff A,Wei S,Jackson PL,Blalock JE,Gaggar A,Xu X, The neutrophil chemoattractant peptide proline-glycine-proline is associated with acute respiratory distress syndrome. American journal of physiology. Lung cellular and molecular physiology. 2018 Nov 1     [PubMed PMID: 30091378]


Huang D,Ma H,Xiao Z,Blaivas M,Chen Y,Wen J,Guo W,Liang J,Liao X,Wang Z,Li H,Li J,Chao Y,Wang XT,Wu Y,Qin T,Su K,Wang S,Tan N, Diagnostic value of cardiopulmonary ultrasound in elderly patients with acute respiratory distress syndrome. BMC pulmonary medicine. 2018 Aug 13;     [PubMed PMID: 30103730]

Level 2 (mid-level) evidence


Vieillard-Baron A,Schmitt JM,Augarde R,Fellahi JL,Prin S,Page B,Beauchet A,Jardin F, Acute cor pulmonale in acute respiratory distress syndrome submitted to protective ventilation: incidence, clinical implications, and prognosis. Critical care medicine. 2001 Aug     [PubMed PMID: 11505125]


Chen WL,Lin WT,Kung SC,Lai CC,Chao CM, The Value of Oxygenation Saturation Index in Predicting the Outcomes of Patients with Acute Respiratory Distress Syndrome. Journal of clinical medicine. 2018 Aug 8     [PubMed PMID: 30096809]


Rawal G,Yadav S,Kumar R, Acute Respiratory Distress Syndrome: An Update and Review. Journal of translational internal medicine. 2018 Jun;     [PubMed PMID: 29984201]


Cherian SV,Kumar A,Akasapu K,Ashton RW,Aparnath M,Malhotra A, Salvage therapies for refractory hypoxemia in ARDS. Respiratory medicine. 2018 Aug;     [PubMed PMID: 30053961]


Guérin C,Reignier J,Richard JC,Beuret P,Gacouin A,Boulain T,Mercier E,Badet M,Mercat A,Baudin O,Clavel M,Chatellier D,Jaber S,Rosselli S,Mancebo J,Sirodot M,Hilbert G,Bengler C,Richecoeur J,Gainnier M,Bayle F,Bourdin G,Leray V,Girard R,Baboi L,Ayzac L, Prone positioning in severe acute respiratory distress syndrome. The New England journal of medicine. 2013 Jun 6;     [PubMed PMID: 23688302]


Moss M,Huang DT,Brower RG,Ferguson ND,Ginde AA,Gong MN,Grissom CK,Gundel S,Hayden D,Hite RD,Hou PC,Hough CL,Iwashyna TJ,Khan A,Liu KD,Talmor D,Thompson BT,Ulysse CA,Yealy DM,Angus DC, Early Neuromuscular Blockade in the Acute Respiratory Distress Syndrome. The New England journal of medicine. 2019 May 23     [PubMed PMID: 31112383]


Wiedemann HP,Wheeler AP,Bernard GR,Thompson BT,Hayden D,deBoisblanc B,Connors AF Jr,Hite RD,Harabin AL, Comparison of two fluid-management strategies in acute lung injury. The New England journal of medicine. 2006 Jun 15;     [PubMed PMID: 16714767]


Brodie D,Bacchetta M, Extracorporeal membrane oxygenation for ARDS in adults. The New England journal of medicine. 2011 Nov 17     [PubMed PMID: 22087681]


Combes A,Hajage D,Capellier G,Demoule A,Lavoué S,Guervilly C,Da Silva D,Zafrani L,Tirot P,Veber B,Maury E,Levy B,Cohen Y,Richard C,Kalfon P,Bouadma L,Mehdaoui H,Beduneau G,Lebreton G,Brochard L,Ferguson ND,Fan E,Slutsky AS,Brodie D,Mercat A, Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome. The New England journal of medicine. 2018 May 24     [PubMed PMID: 29791822]


Yang P,Formanek P,Scaglione S,Afshar M, Risk factors and outcomes of acute respiratory distress syndrome in critically ill patients with cirrhosis. Hepatology research : the official journal of the Japan Society of Hepatology. 2019 Mar;     [PubMed PMID: 30084205]


Annane D,Pastores SM,Rochwerg B,Arlt W,Balk RA,Beishuizen A,Briegel J,Carcillo J,Christ-Crain M,Cooper MS,Marik PE,Umberto Meduri G,Olsen KM,Rodgers S,Russell JA,Van den Berghe G, Correction to: Guidelines for the diagnosis and management of critical illness-related corticosteroid insufficiency (CIRCI) in critically ill patients (Part I): Society of Critical Care Medicine (SCCM) and European Society of Intensive Care Medicine (ESICM) 2017. Intensive care medicine. 2018 Mar     [PubMed PMID: 29476199]


Rodrigo C,Leonardi-Bee J,Nguyen-Van-Tam J,Lim WS, Corticosteroids as adjunctive therapy in the treatment of influenza. The Cochrane database of systematic reviews. 2016 Mar 7;     [PubMed PMID: 26950335]

Level 1 (high-level) evidence


Anand R,McAuley DF,Blackwood B,Yap C,ONeill B,Connolly B,Borthwick M,Shyamsundar M,Warburton J,Meenen DV,Paulus F,Schultz MJ,Dark P,Bradley JM, Mucoactive agents for acute respiratory failure in the critically ill: a systematic review and meta-analysis. Thorax. 2020 Aug     [PubMed PMID: 32513777]

Level 1 (high-level) evidence


Gadre SK,Duggal A,Mireles-Cabodevila E,Krishnan S,Wang XF,Zell K,Guzman J, Acute respiratory failure requiring mechanical ventilation in severe chronic obstructive pulmonary disease (COPD). Medicine. 2018 Apr;     [PubMed PMID: 29703009]


Chiumello D,Coppola S,Froio S,Gotti M, What's Next After ARDS: Long-Term Outcomes. Respiratory care. 2016 May;     [PubMed PMID: 27121623]


Villar J,Schultz MJ,Kacmarek RM, The LUNG SAFE: a biased presentation of the prevalence of ARDS! Critical care (London, England). 2016 Apr 25;     [PubMed PMID: 27109238]


Bos LD,Cremer OL,Ong DS,Caser EB,Barbas CS,Villar J,Kacmarek RM,Schultz MJ, External validation confirms the legitimacy of a new clinical classification of ARDS for predicting outcome. Intensive care medicine. 2015 Nov;     [PubMed PMID: 26202043]

Level 3 (low-level) evidence