Acute Respiratory Distress Syndrome (ARDS)


Article Author:
William Gossman
Hector Peniston Feliciano


Article Editor:
Sidharth Mahapatra


Editors In Chief:
Marie Amma
Jennifer Barrow
Darcy Duncan


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
7/11/2019 11:13:52 PM

Introduction

Acute respiratory distress syndrome (ARDS) is a life-threatening condition of critically ill patients, characterized by poor oxygenation and non-compliant or "stiff" lungs. The disorder is associated with capillary endothelial injury and diffuse alveolar damage.

ARDS is defined as an acute disorder 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 arterial blood (Pa02) to the fraction of the oxygen in the inspired air (Fi02). These patients usually have a Pa02/Fi02 ratio of less than 200.

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

Etiology

ARDS has many risk factors. Besides pulmonary infection or aspiration, extra-pulmonary sources include sepsis, trauma, massive transfusion, drowning, drug overdose, fat embolism, and pancreatitis. These extra-thoracic illnesses and/or injuries trigger an inflammatory reaction resulting in remote pulmonary damage.[3]

Risk factors for ARDS include:

  • Advanced age
  • Female gender
  • Smoking
  • Alcohol use

Epidemiology

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 go on to progress to moderate or severe disease.[4] 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 still a very significant 43%.[5] 

Pathophysiology

ARDS represents a stereotypic response to various etiologies. It progresses through different phases, starting with alveolar capillary damage, to lung resolution, culminating in a fibroproliferative phase. 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. Alveolar edema, in turn, worsens oxygenation, leading to hypoxemia. A hallmark of the damage seen in ARDS is that it is not uniform. Segments of the lung may be more severely affected resulting in more decreased regional lung compliance. This intra-pulmonary differential in pathology results in differential response to oxygenation strategies. While increased positive end-expiratory pressure (PEEP) may improve oxygen diffusion of affected alveoli, it may result in deleterious volutrauma, barotrauma, or atelectrauma of adjacent unaffected alveoli. [6]

Histopathology

The key histologic changes in ARDS reveal the presence of diffuse alveolar damage. Other findings may include alveolar hemorrhage, pulmonary capillary congestion, interstitial edema, and hyaline membrane formation. None of these changes are specific for the disease. [7]

History and Physical

The syndrome is characterized by the development of dyspnea and hypoxemia which progressively gets worse within hours to days, requiring mechanical ventilation and intensive care unit (ICU)-level care. The history is directed at identifying the underlying disease which has precipitated the ARDS. Bear in mind that this disease may be extra-thoracic. Patients start to initially complain of mild dyspnea but within 12-24 hours, the respiratory distress can become severe requiring mechanical ventilation.

The physical examination will include findings associated with the respiratory system such as tachypnea and increased work of breathing. Despite 100% oxygen, patients have low oxygen saturation. There is associated peripheral vasoconstriction, hypotension, and cold extremities. Cyanosis in the extremities is not uncommon.

Chest auscultation usually reveals bilateral rales.

The physical exam should also be directed to identify associated organ failures such as shock or coma.

Evaluation

The diagnosis of ARDS is made based on the following criteria: acute onset, bilateral CXR infiltrates non-cardiogenic and a PaO2/FiO2 ratio of less than 300. It is further sub-classified into mild (PaO2/FiO2 200 to 300), moderate (PaO2/FiO2 100 to 200), and severe (PaO2/FiO2  less than 100) forms. Mortality and ventilatory free days increase with severity as expected.

CT scan may be required in cases of pneumothorax, pleural effusions, medicational adenopathy, and barotrauma.

Assessment of 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-invasive methods such as thoracic bioimpedance or pulse contour analysis.

Invasive monitoring using a central line may be required in most patients. The use of pulmonary artery catheters is controversial and should be avoided.

Bronchoscopy may be required to assess pulmonary infections and obtain material for culture.

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 ARDS. Also, laboratory tests will be needed as patients with ARDS are highly likely to develop or be to suffer from associated multiorgan failure including but not limited to renal, hepatic, and hematopoietic failures. [8][9][10]

Treatment / Management

No drug has proven to be effective in preventing or managing ARDS. The major treatment is supportive along with adequate nutrition. Evidence suggests that ventilatory strategies if left unchecked, can exacerbate alveolar damage and perpetuate lung injury in the context of ARDS. Care is placed in preventing volutrauma (exposure to large tidal volumes), barotrauma (exposure to high plateau pressures), and atelectrauma (exposure to atelectasis). [1][11]

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: TV 4 to 8 ml per kg IBW, RR up to 35 bpm, SpO2 88% to 95%, plateau pressure less than 30 cm H2O, pH goal 7.30 to 7.45, 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 H2O 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.

Novel invasive ventilation strategies have been developed to improve oxygenation. These include airway pressure release ventilation and high-frequency oscillation ventilation. These open-lung ventilation strategies can be supplemented with recruitment maneuvers.

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), bilevel airway pressure (BiPAP), proportional-assist ventilation, and high flow nasal cannula.

Plateau pressure less than 30 cm H2O can be achieved using several strategies. The first one is to maintain as low VT and PEEP as possible. Also, increasing the rise and/or inspiration times can also help maintain the Pplat goal. Finally, the flow rate can be decreased as an adjunct to decreasing the Pplat. High Pplat is also a product of decreased lung compliance, a salient feature of ARDS pathophysiology.

Improving lung compliance will improve Pplat and oxygenation goals attainment. Neuromuscular blockers have been used in this endeavor. Neuromuscular blockers instituted during the first 48 hrs of ARDS was found to improve 90-day survival and increase time off the ventilator.[12] 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 benefit in about 50-70% of patients. The improvement in oxygenation is rapid and allows reduction in Fi02 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 recruitment of dependent lung zones, improved diaphragmatic excursion and increased functional residual capacity. To derive the benefits, the patient needs to be maintained in the prone position for at least 8 hours a day.

Non-ventilatory strategies have included prone positioning [13] and conservative fluid management once resuscitation has been achieved.[14] Recently, extracorporeal membrane oxygenation has also been advocated as salvage therapy in refractory hypoxemic ARDS.[15]

Nutritional support via enteral feeding is recommended. A high fat low carbohydrate diet containing gamma linolenic acid and eicosapentaeenoic acid have been shown in some studies to improve oxygenation.

To prevent pressure sores and improve muscle function, frequent patient positioning is recommended. Physical therapy should be involved in exercising the patient.

Differential Diagnosis

  • CHF
  • Aspiration pneumonia
  • Bacterial pneumonia
  • Hypersensitivity pneumonitis
  • Septic shock

Prognosis

The prognosis for ARDS was abysmal until very recently. There were reports of 30% to 40% mortality up until the 90s, but over the past 2 decades, improvements in technology, a better understanding of mechanical ventilation and better antibiotics, the mortality rates have dropped significantly. The major cause of death in ARDS patients was from sepsis or multiorgan failure. While mortality rates are now around 9% to 20%, the disorder has significant morbidity. Patients remain in the hospital for months and have significant weight loss, poor muscle function, and functional impairment. The hypoxia also leads to a variety of cognitive changes which persist for many months after discharge. For many survivors, returning to a normal life is not possible as they continue to have poor weight gain and no exercise endurance. The quality of life of survivors is poor.[16][17]

Complications

  • Barotrauma from high PEEP
  • Prolonged mechanical ventilation -thus the need for tracheostomy
  • Post extubation laryngeal edema and subglottic stenosis
  • Nosocomial infections
  • Pneumonia
  • Line sepsis
  • UTI
  • DVT
  • Antibiotic resistance
  • Muscle weakness
  • Renal failure
  • PTSD

Postoperative and Rehabilitation Care

Tracheostomy and PEG 

Many patients with ARDS end up requiring a tracheostomy and a percutaneous feeding tube in the recovery phase. The tracheostomy facilitates weaning from the ventilator, make it easy to clear up the secretions and is more comfortable for the patient, compared to the oral endotracheal tube. The tracheostomy is usually done at 2 to 3 weeks, followed by a percutaneous feeding tube.

Nutritional Support

The majority of 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 benefits. Almost every type of nutritional supplement has been studied in ARDS patients, but so far, none has proven to be the magic bullet.

Activity

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

Consultations

Management of ARDS patients requires a multidisciplinary team of healthcare workers that include:

  • Pulmonologist
  • Respiratory therapist
  • Intensivist
  • Infection disease
  • Dietitian

Deterrence and Patient Education

Even though many risk factors for ARDS are known, there is no way of preventing ARDS. However, careful management of fluid in high-risk patients can be helpful. Steps should be taken to prevent aspiration by keeping the head of bed elevated before feeding.

Enhancing Healthcare Team Outcomes

ARDS is a serious disorder of the lung which has the potential to cause death. Patients with ARDS require mechanical ventilation because of hypoxia.[18] The management is usually in the ICU with a team of healthcare workers. ARDS has repercussions beyond the lung. The prolonged mechanical ventilation often leads to bed sores, deep vein thrombosis, multiorgan failure, weight loss, and poor overall functioning. It is important to have an integrated, streamlined approach to management of ARDS because it usually affects many other organs in the body. These patients need nutritional support, chest therapy, treatment for sepsis, and even dialysis. Many of these patients remain in the hospital for months and even those who survive face severe challenges as a result of 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 as it facilitates communication and ensures timely intervention.[19] The team should consist of the following:

  • Intensivist for managing the patient on the ventilator and other ICU related issues like pneumonia prevention, DVT prophylaxis and gastric stress prevention
  • Dietitian for nutritional support
  • Respiratory therapist to manage the ventilator
  • Pharmacist to manage the medications which include antibiotics, blood thinners, diuretics, among others
  • Pulmonologist to manage the lung problems, oxygenation
  • Nephrologist to manage the kidneys
  • 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 weaning
  • Mental health nurse to assess for depression, anxiety
  • Social worker to assess the patient financial situation, transfer for rehab and ensure there is an adequate follow-up

Outcomes

Despite advances in critical care, ARDS still has high morbidity and mortality. Even those who survive have a very poor quality of life. While many risk factors are known for ARDS, there is no way to prevent the condition. Besides the restriction of fluids in high-risk patients, close monitoring by the nurses for hypoxia is vital. The earlier the hypoxia is identified, the better the outcome.[20]

Unfortunately, even those who survive have a long recovery period and most never regain full functional status and remain disabled for life. Many continue to have dyspnea even with mild exertion and thus are dependent on care from others. (Level V)[21]


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Acute Respiratory Distress Syndrome (ARDS) - Questions

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What is the approximate mortality for patients with acute respiratory distress syndrome?

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Why is pulmonary vasoconstriction present in acute respiratory distress syndrome?



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What is a key feature when ventilating ARDS patients?



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What is not a criterion for a diagnosis of acute respiratory distress syndrome?



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After an injury, when do the symptoms of acute respiratory distress syndrome usually begin?



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Which of the following diagnoses is associated with adhesive atelectasis?



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Which of the following is most characteristic of acute respiratory distress syndrome?



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Which of the following is most likely to improve oxygenation in a patient with acute respiratory distress syndrome?



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Which of the following is not characteristic of acute respiratory distress syndrome?



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What is the major alteration in acute respiratory distress syndrome?



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Which of the following is not true of acute respiratory distress syndrome?



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A 71-year-old male is admitted to the intensive care unit with a diagnosis of acute respiratory distress syndrome. Which of the following findings is unlikely in this patient?



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A 71-year-old has been diagnosed with acute respiratory distress syndrome following a bout with sepsis. What is the most common feature on a chest x-ray in the first day or two of the disease?



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Which statement about adult respiratory distress syndrome (ARDS) is false?



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Which of the following is not a requirement for the diagnosis of acute respiratory distress syndrome?



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Prone position for ventilation is used in patients with which of the following disorders?



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Use of low tidal volume ventilation has only been shown to be beneficial in patients with which diagnosis?



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Which choice best describes radiographic features of acute respiratory distress syndrome?



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Which statement about acute respiratory distress syndrome (ARDS) is false?



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Which medical disorder is least associated with acute respiratory distress syndrome?



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Which is not considered a standard risk factor for acute respiratory distress syndrome (ARDS) in hospitalized patients?



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Which of the following is used to treat acute respiratory distress syndrome?



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Which lung parameter is associated with acute respiratory distress syndrome?



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Why do the pulmonary capillaries leak in acute respiratory distress syndrome?



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In acute respiratory distress syndrome, there is a picture of hypoxemia without hypercapnia. Select the most likely explanation of this.



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Formation of hyaline membranes in the alveoli is characteristic of which process?



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Which of the following is least likely to cause acute respiratory distress syndrome (ARDS)?



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Which of the following is least likely seen in acute respiratory distress syndrome?



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When positive end expiratory pressure (PEEP) is used to treat acute respiratory distress syndrome, which of the following is least likely to occur?



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Which of the following findings would help differentiate acute respiratory distress syndrome from cardiogenic pulmonary edema?



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Pathogenesis of acute respiratory distress syndrome involves:



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Which of the following is not a risk factor for acute respiratory distress syndrome?



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A patient has severe hypoxemia that is unresponsive to O2 therapy, a pulmonary artery wedge pressure less than 18 mm Hg, and CXR findings of widespread alveolar consolidation with air bronchograms. What is the most likely diagnosis?



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Which statement regarding the treatment and prognosis of acute respiratory distress syndrome is correct?



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What is the mortality rate for adults with acute respiratory distress syndrome (ARDS)?



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Which of the following is required when acute respiratory distress syndrome patients are mechanically ventilated?



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In the treatment of acute respiratory distress syndrome, why are high levels of positive-end respiratory pressure are needed?



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Which of the following PaO2/FiO2 ratios defines moderate acute respiratory distress syndrome?



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Which of the following is the most common risk factor for acute respiratory distress syndrome?



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Which of the following is not a risk factor for acute respiratory distress syndrome?



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Which of the following is not a characteristic of acute respiratory distress syndrome?



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Which of the following will most likely present as hypoxia, pulmonary edema, and respiratory failure?



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A 4-year-old child is diagnosed with aspiration pneumonia and requires intubation and mechanical ventilation. The initial chest X-ray showed left lower lobe pneumonia but when repeated the next day, show bilateral upper and lower infiltrates. Her FIO2 is 100 percent with a PEEP of 5, but her oxygen saturation is only 87 percent. What is the next step in management?



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A 4-year-old child is diagnosed with aspiration pneumonia and requires intubation and mechanical ventilation. The initial chest x-ray showed left lower lobe pneumonia but the next day, the x-ray shows bilateral upper and lower infiltrates. Her FIO2 is 1.0 with a PEEP of 15 cmH2O but arterial blood gas shows pH=7.27, PaO2=60 mmHg, and PaCO2=60 mmHg. What is the next step?



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What is the expected pathologic finding in a patient that dies of acute respiratory distress syndrome?



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Which is not a characteristic of acute respiratory distress syndrome (ARDS)?



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Which of the following is associated with a conservative fluid management strategy among patients with acute respiratory distress syndrome?



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A male is involved in a motor vehicle collision and is brought to the emergency department intubated. He is resuscitated and admitted to the intensive care unit because of severe brain injury. The following day his chest x-ray reveals bilateral fluffy infiltrates. Which of the following is the earliest finding of acute respiratory distress syndrome within 12 to 24 hours after the onset of the disorder?



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Acute Respiratory Distress Syndrome (ARDS) - References

References

Hypoxemia in the ICU: prevalence, treatment, and outcome. Annals of intensive care. 2018 Aug 13     [PubMed]
Calfee CS,Delucchi KL,Sinha P,Matthay MA,Hackett J,Shankar-Hari M,McDowell C,Laffey JG,O'Kane CM,McAuley DF, Acute respiratory distress syndrome subphenotypes and differential response to simvastatin: secondary analysis of a randomised controlled trial. The Lancet. Respiratory medicine. 2018 Aug 2     [PubMed]
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. 2018 Aug 7     [PubMed]
Zambon M,Vincent JL, Mortality rates for patients with acute lung injury/ARDS have decreased over time. Chest. 2008 May     [PubMed]
Sharma NS,Lal CV,Li JD,Lou XY,Viera L,Abdallah T,King R,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 (ARDS). American journal of physiology. Lung cellular and molecular physiology. 2018 Aug 9     [PubMed]
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]
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]
Rawal G,Yadav S,Kumar R, Acute Respiratory Distress Syndrome: An Update and Review. Journal of translational internal medicine. 2018 Jun     [PubMed]
Chamarthy MR,Kandathil A,Kalva SP, Pulmonary vascular pathophysiology. Cardiovascular diagnosis and therapy. 2018 Jun     [PubMed]
Cherian SV,Kumar A,Akasapu K,Ashton RW,Aparnath M,Malhotra A, Salvage therapies for refractory hypoxemia in ARDS. Respiratory medicine. 2018 Aug     [PubMed]
Papazian L,Forel JM,Gacouin A,Penot-Ragon C,Perrin G,Loundou A,Jaber S,Arnal JM,Perez D,Seghboyan JM,Constantin JM,Courant P,Lefrant JY,Guérin C,Prat G,Morange S,Roch A, Neuromuscular blockers in early acute respiratory distress syndrome. The New England journal of medicine. 2010 Sep 16     [PubMed]
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]
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]
Brodie D,Bacchetta M, Extracorporeal membrane oxygenation for ARDS in adults. The New England journal of medicine. 2011 Nov 17     [PubMed]
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]
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]
Chiumello D,Coppola S,Froio S,Gotti M, What's Next After ARDS: Long-Term Outcomes. Respiratory care. 2016 May     [PubMed]
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]
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]
Walkey AJ,Summer R,Ho V,Alkana P, Acute respiratory distress syndrome: epidemiology and management approaches. Clinical epidemiology. 2012;     [PubMed]
Bein T,Weber-Carstens S,Apfelbacher C, Long-term outcome after the acute respiratory distress syndrome: different from general critical illness? Current opinion in critical care. 2018 Feb;     [PubMed]

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