Acute respiratory distress syndrome: Difference between revisions

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==Background==
==Background==
*Non-cardiogenic pulmonary edema due to lung capillary endothelial injury
[[File:Lung and diaphragm.jpg|thumb|Lobes of the lung with related anatomy.]]
**Proteinaceous material accumulate in alveoli in a heterogeneous manner
*Non-cardiogenic [[pulmonary edema]] due to lung capillary endothelial injury (diffuse alveolar damage)
**Proteinaceous material accumulate in alveoli in a heterogeneous manner (hyalinosis)
*Symptom of an underlying disease
*Symptom of an underlying disease


==Clinical Features==
===Diagnostic Criteria<ref name="Ferguson">Ferguson ND et. al. The Berlin definition of ARDS: an expanded rationale, justification, and supplementary material. Intensive Care Med. 2012 Oct;38(10):1573-82.</ref>===
#New onset respiratory symptoms
#Bilateral pulmonary opacities
#Symptoms not explained by cardiac etiology or volume overload
===Severity by Berlin Definition<ref name="Ferguson" />===
{| class="wikitable"
| align="center" style="background:#f0f0f0;"|'''PaO2/FiO2'''
| align="center" style="background:#f0f0f0;"|'''Severity'''
| align="center" style="background:#f0f0f0;"|'''Mortality'''
|-
| 200-300||Mild||27%
|-
| 100-200||Mod||32%
|-
| <100||Severe||45%
|-
|}
===Presentation===
*Severe dyspnea
*Hypoxemia
*Diffuse crackles
===Imaging===
*Diffuse patchy pulmonary infiltrates
===Causes===
===Causes===
*[[Pneumonia]]
*[[Sepsis]]
*[[Sepsis]]
*[[Pancreatitis]]
*[[Pancreatitis]]
Line 39: Line 17:
*[[Toxicology (Main)|Overdose]]
*[[Toxicology (Main)|Overdose]]
*[[Massive transfusion]]
*[[Massive transfusion]]
*[[Transfusion-related acute lung injury]]
==Clinical Features==
*Severe [[dyspnea]]
*[[Hypoxemia]]
*Diffuse crackles


==Differential Diagnosis==
==Differential Diagnosis==
*[[Pneumonia]]
*[[Pneumonia]]
*[[PE]]
*[[PE]]
*Diffuse alveolar hemorrhage
*[[Diffuse alveolar hemorrhage]]
*[[DIC]]
*[[DIC]]
*[[CHF]]


{{Pulmonary edema types}}
{{Pulmonary edema types}}


==Evaluation==
==Evaluation==
[[File:ARDS.png|thumb]]
[[File:ARDSSevere.png|thumb|Classic ARDS on [[CXR]].]]
[[File:ARDS.png|thumb|ARDS on CXR]]
===Workup===
*[[CXR]]
*[[CXR]]
*CBC
*CBC
*Chem 10
*Chem 10
*[[Urinalysis]]
*[[Urinalysis]]
*LFT
*[[LFTs]]
*Lipase
*Lipase
*PT/PTT
*PT/PTT
*Influenza (seasonal)
*[[Influenza]] testing (seasonal)
*Blood cultures
*Blood cultures
*Lactate
*[[Lactate]]
*Consider bedside echo
*Consider bedside [[echocardiography|echo]]
*Consider ABG/VBG
*Consider [[ABG]]/[[VBG]]
*Consider BNP
*Consider [[BNP]]
 
===Diagnosis===
*'''Risk factors and origin of edema'''
**Precipitated by an acute predisposing risk factor, such as pneumonia, nonpulmonary infection, trauma, transfusion, aspiration, or shock. Pulmonary edema is not exclusively or primarily attributable to cardiogenic pulmonary edema/fluid overload, and hypoxemia/gas exchange abnormalities are not primarily attributable to atelectasis.
*'''Timing'''
**Acute onset or worsening of hypoxemic respiratory failure within 1 week of the estimated onset of the predisposing risk factor or new or worsening respiratory symptoms.
*'''Chest Imaging'''
**Bilateral opacities on chest radiography and computed tomography or bilateral B lines and/or consolidations on ultrasound
 
====Diagnostic Criteria<ref name="Matthay"> Matthay, M. et al. (2024). A New Global Definition of Acute Respiratory Distress Syndrome. American Journal of Respiratory and Critical Care Medicine, 30(1), 37-47. https://doi.org/10.1164/rccm.202303-0558WS </ref>====
*'''Nonintubated ARDS'''
**PaO2:FiO2 ≤ 300 mm Hg or SpO2:FiO2 ≤ 315 (if SpO2 ≤ 97%) on HFNO with flow of ≥ 30 L/min or NIV/CPAP with at least 5 cm H2O end-expiratory pressure
*'''Intubated ARDS'''
**Mild: 200 < PaO2:FiO2 ≤ 300 mm Hg or 235 < SpO2:FiO2 ≤ 315 (if SpO2 ≤ 97%)
**Moderate: 100 < PaO2:FiO2 ≤ 200 mm Hg or 148 < SpO2:FiO2 ≤ 235 (if SpO2 ≤ 97%)
**Severe: PaO2:FiO2 ≤ 100 mm Hg or SpO2:FiO2 ≤ 148 (if SpO2 ≤ 97%)
*'''Modified Definition for Resource Limited Settings'''
**SpO2:FiO2 ≤ 315 (if SpO2 ≤ 97%). Neither positive end-expiratory pressure nor a minimum flow rate of oxygen is required for diagnosis in resource-limited settings.


==Management==
==Management==
===General Care===
*Treat underlying cause
*Treat underlying cause
**Cover for sepsis
**Cover for [[sepsis]]
***Pneumonia in addition to other identified source
***[[Pneumonia]] in addition to other identified source
**Tamiflu 75mg BID oral or NGT if influenza season <ref>http://www.cdc.gov/flu/professionals/antivirals/summary-clinicians.htm</ref>
**[[Tamiflu]] 75mg BID oral or NGT if influenza season <ref>http://www.cdc.gov/flu/professionals/antivirals/summary-clinicians.htm</ref>
*Supplemental O2
 
*[[Noninvasive Ventilation|Noninvasive ventilation]]
===Pulse Dose [[Steroids]]===
**Limited data to support use
*Consider in early, established, severe ARDS in ICU setting<ref>Khilnani GC and Hadda V. Corticosteroids and ARDS: A review of treatment and prevention evidence. Lung India. 2011 Apr-Jun; 28(2): 114–119.</ref>
*Consider pulse dose steroids in early, established, severe ARDS in ICU setting<ref>Khilnani GC and Hadda V. Corticosteroids and ARDS: A review of treatment and prevention evidence. Lung India. 2011 Apr-Jun; 28(2): 114–119.</ref>
**'''NOT''' for prevention of ARDS (will increase risk for ARDS and worsening sepsis if not in ARDS already)
**'''NOT''' for prevention of ARDS (will increase risk for ARDS and worsening sepsis if not in ARDS already)
**In theory, may reduce fibro-proliferative inflammatory changes during exudative phase (< 1 wk)
**In theory, may reduce fibro-proliferative inflammatory changes during exudative phase (< 1 wk)
**No benefit to starting in late ARDS (> 2 wks)
**No benefit to starting in late ARDS (> 2 wks)
**Meduri protocol (21 vs. 43% mortality)<ref>Meduri GU, Golden E, Freire AX, Taylor E, Zaman M, Carson SJ, et al. Methylprednisolone infusion in early severe ARDS: Results of a randomized controlled trial. Chest. 2007;131:954–63.</ref>
*Meduri protocol (21 vs. 43% mortality)<ref>Meduri GU, Golden E, Freire AX, Taylor E, Zaman M, Carson SJ, et al. Methylprednisolone infusion in early severe ARDS: Results of a randomized controlled trial. Chest. 2007;131:954–63.</ref>
***1mg/kg loading dose methyprednisolone
**1mg/kg loading dose [[methylprednisolone]]
***Followed by infusion of 1mg/kg/day from day 1-14
**Followed by infusion of 1mg/kg/day from day 1-14
***Then 0.5mg/kg/day from day 15-21
**Then 0.5mg/kg/day from day 15-21
***Then 0.25mg/kg/day from day 22-25
**Then 0.25mg/kg/day from day 22-25
***Finally 0.125mg/kg/day from day 26-28
**Finally 0.125mg/kg/day from day 26-28
*[[Ventilation (Main)|Ventilator Settings]]
 
**Permissive hypercapnia
{{Lung Protective Ventilator Settings}}
**Tidal volume 6-8cc/kg of [http://www.mdcalc.com/ideal-body-weight/ predicted body weight]<ref>Brower RG, et al. "Ventilation With Lower Tidal Volumes As Compared With Traditional Tidal Volumes For Acute Lung Injury And The Acute Respiratory Distress Syndrome". The New England Journal of Medicine. 2000. 342(18):1301-1308.</ref>
{{Lung Protective FiO2 and PEEP Scale}}
***Limit barotrauma to healthy area of lung
 
***Increase PEEP to improve oxygenation
===Additional [[Ventilation (Main)|Ventilation]] Considerations===
****High FiO2 can cause absorptive atelectasis<ref>O'Brien J. Absorption Atelectasis: Incidence and Clinical Implications. AANA Journal. June 2013. Vol. 81, No. 3.</ref>
*Permissive hypercapnia
****Ardsnet PEEP/FiO2 [http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf protocol card]<ref>Kallet RH, et al. "Respiratory controversies in the critical care setting. Do the NIH ARDS Clinical Trials Network PEEP/FIO2 tables provide the best evidence-based guide to balancing PEEP and FIO2 settings in adults?" Respiratory Care. 2007. 52(4):461-75.</ref>
*Maintain plateau pressures < 30 <ref>Hansen-Flaschen et al. Acute respiratory distress syndrome: Clinical features and diagnosis.UpToDate accessed 3/26/14</ref>
**Maintain plateau pressures < 30 <ref>Hansen-Flaschen et al. Acute respiratory distress syndrome: Clinical features and diagnosis.UpToDate accessed 3/26/14</ref>
**Driving pressure (plateau pressure minus PEEP) <14 is most strongly associated with decreased mortality<ref>Amato MB, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372(8):747-755. doi:10.1056/NEJMsa1410639</ref>
**Ensure adequate sedation
*Ensure adequate [[sedation]]
***Better synchrony with vent
**Better synchrony with vent
***Decreased oxygen consumption
**Decreased oxygen consumption
***Less [[delirium]]
**Less [[delirium]]
***Increased patient comfort
**Increased patient comfort
**Prone ventilation <ref>Guerin, C. (2014) ‘Prone ventilation in acute respiratory distress syndrome’, European Respiratory Review, 23(132), pp. 249–257.</ref>  
*Prone ventilation <ref>Guerin, C. (2014) ‘Prone ventilation in acute respiratory distress syndrome’, European Respiratory Review, 23(132), pp. 249–257.</ref>  
***Increases survival for severe ARDS
**Increases survival for severe ARDS
***Consider for refractory hypoxemia
**Consider for refractory hypoxemia
***Many consider this a type of [[recruitment maneuver]]
**Many consider this a type of [[recruitment maneuver]]
**[[APRV]] ([[BiVent]]) to recruit alveoli, if minimal to no respiratory acidosis<ref>CritCareMed. 2005;33:S228 Other Approaches to Open-Lung Ventilation–Airway Pressure Release Ventilation.</ref><ref>CleveClinJMed 2011;78:101 Airway Pressure Release Ventilation–Alternative Mode of Mechanical Ventilation in Acute Respiratory Distress Syndrome.</ref>
*Consider [[Airway pressure release ventilation]] (APRV)
***Start PHigh at PPlat at 28, try not to go beyond 35 cmH2O
*[[Pressure control ventilation]] ([[PCV]]) if acidosis with APRV
***PPlateau = desired Pmean + 3 cmH2O
**Attempt to maintain same rate
***PLow at 0 cmH2O for maximal expiration
**Maintain same Pmean
***THigh at 4.5-6 seconds (inspiratory time)
*[[PRVC]] or [[Volume control ventilation]] with paralysis to prevent barotrauma in breath stacking and vent dyssynchrony<ref>Gainnier M, Roch A, Forel JM, et al. Effect of neuromuscular blocking agents on gas exchange in patients presenting with acute respiratory distress syndrome. Crit Care Med. 2004;32:113-119.</ref><ref>Papazian L, Forel JM, Gacouin A, et al. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010;363:1107-1116.</ref>
***Tlow at 0.5-0.8 seconds (expiratory time), with TV 4-6 cc/kg
**[[Cisatricurium]] loading dose 0.15 mg/kg, followed by 1-3 mcg/kg/min
***[[Automatic tube compensation]] ON if patient spontaneously breathing<ref>Guttmann J et al. Automatic tube compensation (ATC). Minerva Anestesiol. 2002 May;68(5):369-77.</ref>
**Titrated to less than 2 twitches in train of four
***Full benefit of APRV is in patients that are not paralyzed that can provide spontaneous breaths
**Cisatricurium preferred to pancuronium in renal impairment
***Wean by "dropping and stretching"
**Cannot use paralysis with APRV
****Every two hours or as tolerated, decrease PHigh by 1-2 cmH2O and increasing THight by 0.5 seconds per 1 cmH2O drop in PHigh
*[[Recruitment maneuver]]
****Monitor for drop in SpO2, increased work of breathing, tachypnea
**Varying methods and protocols
****Once PHigh reaches 10 cmH2O and THigh resaches 12-15 seconds with spontaneous respirations, change mode to CPAP with PEEP 10 cmH2O and PS 5-10 cmH2O, turn ATC off
**Controversial in risks and benefits
**[[Pressure control ventilation]] ([[PCV]]) if acidosis with APRV
***Attempt to maintain same rate
***Maintain same Pmean
**[[PRVC]] or [[Volume control ventilation]] with paralysis to prevent barotrauma in breath stacking and vent dyssynchrony<ref>Gainnier M, Roch A, Forel JM, et al. Effect of neuromuscular blocking agents on gas exchange in patients presenting with acute respiratory distress syndrome. Crit Care Med. 2004;32:113-119.</ref><ref>Papazian L, Forel JM, Gacouin A, et al. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010;363:1107-1116.</ref>
***[[Cisatricurium]] loading dose 0.15 mg/kg, followed by 1-3 mcg/kg/min
***Titrated to less than 2 twitches in train of four
***Cisatricurium preferred to pancuronium in renal impairment
***Cannot use paralysis with APRV
**[[Recruitment maneuver]]
***Varying methods and protocols
***Controversial in risks and benefits


===Adjuncts===
===Adjuncts===
Line 132: Line 126:
==Disposition==
==Disposition==
*Admit to ICU
*Admit to ICU
==Prognosis==
===Severity (Berlin Definition)<ref name="Ferguson"> Ferguson ND et. al. The Berlin definition of ARDS: an expanded rationale, justification, and supplementary material. Intensive Care Med. 2012 Oct;38(10):1573-82.</ref>===
{| class="wikitable"
| align="center" style="background:#f0f0f0;"|'''PaO2/FiO2'''
| align="center" style="background:#f0f0f0;"|'''Severity'''
| align="center" style="background:#f0f0f0;"|'''Mortality'''
|-
| 200-300||Mild||27%
|-
| 100-200||Mod||32%
|-
| <100||Severe||45%
|-
|}


==See Also==
==See Also==
*[[EBQ:ARDSnet Trial]]
*[[Pulmonary edema]]
*[[Pulmonary edema]]
*[[CHF]]
 
*[[EBQ:ARDSnet Trial]]
{{Mechanical ventilation pages}}
*[https://resusreview.com/2013/aprv-ventilation-mode-introduction-basic-use-management-and-advanced-tips/ APRV / BiVent]


==External Links==
==External Links==
[http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf ARDSnet Ventilator Settings]
*[http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf ARDSnet Ventilator Settings]
*[https://resusreview.com/2013/aprv-ventilation-mode-introduction-basic-use-management-and-advanced-tips/ APRV / BiVent]


==References==
==References==

Latest revision as of 15:57, 15 July 2025

Background

Lobes of the lung with related anatomy.
  • Non-cardiogenic pulmonary edema due to lung capillary endothelial injury (diffuse alveolar damage)
    • Proteinaceous material accumulate in alveoli in a heterogeneous manner (hyalinosis)
  • Symptom of an underlying disease

Causes

Clinical Features

Differential Diagnosis

Pulmonary Edema Types

Pulmonary capillary wedge pressure <18 mmHg differentiates noncardiogenic from cardiogenic pulmonary edema[1]

Evaluation

Classic ARDS on CXR.
ARDS on CXR

Workup

Diagnosis

  • Risk factors and origin of edema
    • Precipitated by an acute predisposing risk factor, such as pneumonia, nonpulmonary infection, trauma, transfusion, aspiration, or shock. Pulmonary edema is not exclusively or primarily attributable to cardiogenic pulmonary edema/fluid overload, and hypoxemia/gas exchange abnormalities are not primarily attributable to atelectasis.
  • Timing
    • Acute onset or worsening of hypoxemic respiratory failure within 1 week of the estimated onset of the predisposing risk factor or new or worsening respiratory symptoms.
  • Chest Imaging
    • Bilateral opacities on chest radiography and computed tomography or bilateral B lines and/or consolidations on ultrasound

Diagnostic Criteria[2]

  • Nonintubated ARDS
    • PaO2:FiO2 ≤ 300 mm Hg or SpO2:FiO2 ≤ 315 (if SpO2 ≤ 97%) on HFNO with flow of ≥ 30 L/min or NIV/CPAP with at least 5 cm H2O end-expiratory pressure
  • Intubated ARDS
    • Mild: 200 < PaO2:FiO2 ≤ 300 mm Hg or 235 < SpO2:FiO2 ≤ 315 (if SpO2 ≤ 97%)
    • Moderate: 100 < PaO2:FiO2 ≤ 200 mm Hg or 148 < SpO2:FiO2 ≤ 235 (if SpO2 ≤ 97%)
    • Severe: PaO2:FiO2 ≤ 100 mm Hg or SpO2:FiO2 ≤ 148 (if SpO2 ≤ 97%)
  • Modified Definition for Resource Limited Settings
    • SpO2:FiO2 ≤ 315 (if SpO2 ≤ 97%). Neither positive end-expiratory pressure nor a minimum flow rate of oxygen is required for diagnosis in resource-limited settings.

Management

General Care

  • Treat underlying cause

Pulse Dose Steroids

  • Consider in early, established, severe ARDS in ICU setting[4]
    • NOT for prevention of ARDS (will increase risk for ARDS and worsening sepsis if not in ARDS already)
    • In theory, may reduce fibro-proliferative inflammatory changes during exudative phase (< 1 wk)
    • No benefit to starting in late ARDS (> 2 wks)
  • Meduri protocol (21 vs. 43% mortality)[5]
    • 1mg/kg loading dose methylprednisolone
    • Followed by infusion of 1mg/kg/day from day 1-14
    • Then 0.5mg/kg/day from day 15-21
    • Then 0.25mg/kg/day from day 22-25
    • Finally 0.125mg/kg/day from day 26-28

Lung Protective Mechanical Ventilation

Lung Protective Ventilator Settings[6] should be the default for all intubated patients, unless contraindicated. It has demonstrated mortality benefit for ARDS-like pulmonary conditions; limits barotrauma and decreases complications of high FiO2[7][8]

  1. Mode
    • Volume-assist control
  2. Tidal Volume
    • Start 6-8cc/kg predicted body weight[9]
      • Predicted/"ideal" body weight is used because a person's lung parenchyma does not increase in size as the person gains more weight.
    • Titrate down if plateau pressure >30 mmHg
  3. Inspiratory Flow Rate (comfort)
    • More comfortable if higher rather than lower
    • Start at 60-80 LPM
  4. Respiratory Rate (titrate for ventilation)
    • Average patient on ventilator requires 120mL/kg/min for eucapnia
    • Start 16-18 breaths/min
    • Maintain pH = 7.30-7.45
  5. FiO2/PEEP (titrate for oxygenation)
    • Move in tandem to achieve:
    • SpO2 BETWEEN 88-95%
    • PaO2 BETWEEN 55-80mmHg

Lung Protective FiO2 and PEEP Scale[10][11][12]

FiO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0 1.0 1.0
PEEP 5 5 8 8 10 10 10 12 14 14 14 16 18 20 22 24

Additional Ventilation Considerations

  • Permissive hypercapnia
  • Maintain plateau pressures < 30 [13]
    • Driving pressure (plateau pressure minus PEEP) <14 is most strongly associated with decreased mortality[14]
  • Ensure adequate sedation
    • Better synchrony with vent
    • Decreased oxygen consumption
    • Less delirium
    • Increased patient comfort
  • Prone ventilation [15]
    • Increases survival for severe ARDS
    • Consider for refractory hypoxemia
    • Many consider this a type of recruitment maneuver
  • Consider Airway pressure release ventilation (APRV)
  • Pressure control ventilation (PCV) if acidosis with APRV
    • Attempt to maintain same rate
    • Maintain same Pmean
  • PRVC or Volume control ventilation with paralysis to prevent barotrauma in breath stacking and vent dyssynchrony[16][17]
    • Cisatricurium loading dose 0.15 mg/kg, followed by 1-3 mcg/kg/min
    • Titrated to less than 2 twitches in train of four
    • Cisatricurium preferred to pancuronium in renal impairment
    • Cannot use paralysis with APRV
  • Recruitment maneuver
    • Varying methods and protocols
    • Controversial in risks and benefits

Adjuncts

Disposition

  • Admit to ICU

Prognosis

Severity (Berlin Definition)[18]

PaO2/FiO2 Severity Mortality
200-300 Mild 27%
100-200 Mod 32%
<100 Severe 45%

See Also

Mechanical Ventilation Pages

External Links

References

  1. Clark SB, Soos MP. Noncardiogenic Pulmonary Edema. In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 1, 2020.
  2. Matthay, M. et al. (2024). A New Global Definition of Acute Respiratory Distress Syndrome. American Journal of Respiratory and Critical Care Medicine, 30(1), 37-47. https://doi.org/10.1164/rccm.202303-0558WS
  3. http://www.cdc.gov/flu/professionals/antivirals/summary-clinicians.htm
  4. Khilnani GC and Hadda V. Corticosteroids and ARDS: A review of treatment and prevention evidence. Lung India. 2011 Apr-Jun; 28(2): 114–119.
  5. Meduri GU, Golden E, Freire AX, Taylor E, Zaman M, Carson SJ, et al. Methylprednisolone infusion in early severe ARDS: Results of a randomized controlled trial. Chest. 2007;131:954–63.
  6. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000;342(18):1301-1308.
  7. ARDSnet
  8. O'Brien J. Absorption Atelectasis: Incidence and Clinical Implications. AANA Journal. June 2013. Vol. 81, No. 3.
  9. Brower RG, et al. "Ventilation With Lower Tidal Volumes As Compared With Traditional Tidal Volumes For Acute Lung Injury And The Acute Respiratory Distress Syndrome". The New England Journal of Medicine. 2000. 342(18):1301-1308.
  10. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med. 2000;342(18):1301-1308.
  11. Kallet RH, et al. "Respiratory controversies in the critical care setting. Do the NIH ARDS Clinical Trials Network PEEP/FIO2 tables provide the best evidence-based guide to balancing PEEP and FIO2 settings in adults?" Respiratory Care. 2007. 52(4):461-75.
  12. ARDSnet protocol card
  13. Hansen-Flaschen et al. Acute respiratory distress syndrome: Clinical features and diagnosis.UpToDate accessed 3/26/14
  14. Amato MB, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372(8):747-755. doi:10.1056/NEJMsa1410639
  15. Guerin, C. (2014) ‘Prone ventilation in acute respiratory distress syndrome’, European Respiratory Review, 23(132), pp. 249–257.
  16. Gainnier M, Roch A, Forel JM, et al. Effect of neuromuscular blocking agents on gas exchange in patients presenting with acute respiratory distress syndrome. Crit Care Med. 2004;32:113-119.
  17. Papazian L, Forel JM, Gacouin A, et al. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010;363:1107-1116.
  18. Ferguson ND et. al. The Berlin definition of ARDS: an expanded rationale, justification, and supplementary material. Intensive Care Med. 2012 Oct;38(10):1573-82.