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ICU Topicsrespiratory

ICU · respiratory

Acute Respiratory Distress Syndrome (ARDS) — Berlin Definition, Lung-Protective Ventilation, Proning, ECMO, and Phenotyping

Also known as ARDS · Acute respiratory distress syndrome · Berlin definition ARDS · Non-cardiogenic pulmonary oedema · Diffuse alveolar damage · Lung-protective ventilation · Prone ventilation · VV-ECMO · ARDS subphenotypes · PROSEVA · Baby lung

Acute respiratory distress syndrome (ARDS) — a syndrome of acute, diffuse, inflammatory lung injury causing increased pulmonary vascular permeability, loss of aerated lung, and severe hypoxaemia. The 2012 Berlin Definition replaces AECC: (1) Timing — within 1 week of a known clinical insult or new/worsening respiratory symptoms; (2) Chest imaging — bilateral opacities not fully explained by effusions, lobar/lung collapse, or nodules (CT or CXR); (3) Origin of oedema — respiratory failure NOT fully explained by cardiac failure or fluid overload (objective assessment — echo — required if no clear risk factor); (4) Oxygenation — PaO2/FiO2 ratio measured with PEEP/CPAP >=5 cmH2O: MILD 200-300 (inclusive), MODERATE 100-200, SEVERE <100. Causes are DIRECT/pulmonary (pneumonia — most common, aspiration of gastric contents, pulmonary contusion, inhalation injury, near-drowning) or INDIRECT/extrapulmonary (sepsis — most common indirect, severe trauma/shock, acute pancreatitis, massive transfusion/TRALI, severe burns, drug overdose). Pathophysiology — diffuse alveolar damage: exudative phase (type I pneumocyte + capillary endothelial injury → protein-rich alveolar oedema → hyaline membranes), proliferative phase (type II pneumocyte proliferation, fibroblast infiltration), fibrotic phase. The 'baby lung' concept (Gattinoni) — the aerated lung in ARDS is small, not stiff; high tidal volumes overdistend the small healthy portion → volutrauma. Management PILLARS: (1) Treat the cause (antibiotics, source control). (2) Lung-protective ventilation (ARDSNet — Vt 6 mL/kg PREDICTED body weight, plateau pressure <30 cmH2O, driving pressure <15 cmH2O, permissive hypercapnia pH >7.20). (3) PEEP optimisation (PEEP/FiO2 table, best compliance, oesophageal pressure). (4) Prone positioning (PROSEVA — >=16 h/day for moderate-severe ARDS P/F <150, ~50% relative mortality reduction). (5) Conservative fluid strategy (FACTT). (6) Corticosteroids (DEXA-ARDS — dexamethasone improves moderate-severe ARDS). (7) VV-ECMO for severe refractory ARDS (EOLIA). Neuromuscular blockade is NOT routine (ROSE). ARDS subphenotypes (Calfee 2014) — hyperinflammatory vs hypoinflammatory — differ in mortality and treatment response. Mortality ~35% overall (severe ~45%).

high16 referencesUpdated 26 July 202623 min readVerification in progress

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  • Severe ARDS (PaO2/FiO2 &lt;150 on FiO2 &gt;=0.6 and PEEP &gt;=5) within 7 days of onset and already on lung-protective ventilation = indication for EARLY prone positioning &gt;=16 h/day (PROSEVA) — a ~50% relative mortality reduction, the largest of any ARDS intervention after low Vt
  • Driving pressure (delta P = Pplat - PEEP) is the ventilation variable most strongly associated with survival in ARDS — an increment of ~7 cmH2O (1 SD) raises the relative risk of death to 1.41 — minimise it by reducing Vt or optimising PEEP; a 'safe' Vt of 6 mL/kg in a very small baby lung can still be injurious if delta P is high
  • Never escalate FiO2 and PEEP indefinitely without addressing the cause and considering adjuncts (prone, ECMO) — refractory hypoxaemia on PEEP &gt;=10 and FiO2 &gt;=0.8 in severe ARDS should trigger prone positioning and referral for VV-ECMO, not further incremental PEEP (which causes volutrauma, right heart failure, and hypotension)
  • Routine continuous neuromuscular blockade is NOT recommended for moderate-severe ARDS (ROSE 2019) — reserve for severe asynchrony, dangerous transpulmonary pressures, or to facilitate lung-protective ventilation/ proning; routine use increases sedation and does not improve mortality
  • Corticosteroids in ARDS are NOT for the late fibrotic 'fibroproliferative' rescue only — DEXA-ARDS (2020) showed dexamethasone started EARLY in established moderate-severe ARDS increases ventilator-free days and reduces mortality; steroids are contraindicated in active uncontrolled infection without cover
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Practise this topic8 MCQs with explanations

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CICMFFICMEDIC

Red flags

  • Severe ARDS (PaO2/FiO2 &lt;150 on FiO2 &gt;=0.6 and PEEP &gt;=5) within 7 days of onset and already on lung-protective ventilation = indication for EARLY prone positioning &gt;=16 h/day (PROSEVA) — a ~50% relative mortality reduction, the largest of any ARDS intervention after low Vt
  • Driving pressure (delta P = Pplat - PEEP) is the ventilation variable most strongly associated with survival in ARDS — an increment of ~7 cmH2O (1 SD) raises the relative risk of death to 1.41 — minimise it by reducing Vt or optimising PEEP; a 'safe' Vt of 6 mL/kg in a very small baby lung can still be injurious if delta P is high
  • Never escalate FiO2 and PEEP indefinitely without addressing the cause and considering adjuncts (prone, ECMO) — refractory hypoxaemia on PEEP &gt;=10 and FiO2 &gt;=0.8 in severe ARDS should trigger prone positioning and referral for VV-ECMO, not further incremental PEEP (which causes volutrauma, right heart failure, and hypotension)
  • Routine continuous neuromuscular blockade is NOT recommended for moderate-severe ARDS (ROSE 2019) — reserve for severe asynchrony, dangerous transpulmonary pressures, or to facilitate lung-protective ventilation/ proning; routine use increases sedation and does not improve mortality
  • Corticosteroids in ARDS are NOT for the late fibrotic 'fibroproliferative' rescue only — DEXA-ARDS (2020) showed dexamethasone started EARLY in established moderate-severe ARDS increases ventilator-free days and reduces mortality; steroids are contraindicated in active uncontrolled infection without cover

Overview

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Acute respiratory distress syndrome (ARDS) is acute, diffuse, inflammatory lung injury causing non-cardiogenic pulmonary oedema and severe hypoxaemia, defined by the Berlin criteria (2012): onset within 1 week of a known insult, bilateral opacities on imaging not explained by cardiac failure/overload, and hypoxaemia graded by PaO2/FiO2 with PEEP >=5: mild 200-300, moderate 100-200, severe <100. Causes are direct (pneumonia — commonest; aspiration, contusion, inhalation, near-drowning) or indirect (sepsis, pancreatitis, massive transfusion/TRALI, major trauma, burns). The lung in ARDS is a small, heterogeneous 'baby lung' — so management is built on lung-protective ventilation (ARDSNet: Vt 6 mL/kg predicted body weight, plateau pressure <30, driving pressure <15, permissive hypercapnia) — the single most evidence-supported intervention (31% vs 40% mortality). In moderate-severe ARDS escalate to: prone positioning >=16 h/day (PROSEVA — the largest mortality benefit after low Vt, ~50% relative reduction), conservative fluids (FACTT), and dexamethasone (DEXA-ARDS — improved survival in moderate-severe ARDS). For severe refractory disease, VV-ECMO (EOLIA). Routine neuromuscular blockade is NOT recommended (ROSE). ARDS has two reproducible subphenotypes — hyperinflammatory (high mortality, responds to fluids/PEEP/steroids) and hypoinflammatory (lower mortality) — the foundation of ARDS precision medicine.[1][2][6]

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References16ShowHide
  1. [1]Brower RG, Matthay MA, Morris A, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome N Engl J Med, 2000.PMID 10793162
  2. [2]Guérin C, Reignier J, Richard JC, et al. Prone positioning in severe acute respiratory distress syndrome N Engl J Med, 2013.PMID 23688302
  3. [3]Moss M, Huang DT, Brower RG, et al. Early Neuromuscular Blockade in the Acute Respiratory Distress Syndrome N Engl J Med, 2019.PMID 31112383
  4. [4]Combes A, Hajage D, Capellier G, et al. Extracorporeal Membrane Oxygenation for Severe Acute Respiratory Distress Syndrome N Engl J Med, 2018.PMID 29791822
  5. [5]Villar J, Ferrando C, Martínez D, et al. Dexamethasone treatment for the acute respiratory distress syndrome: a multicentre, randomised controlled trial Lancet Respir Med, 2020.PMID 32043986
  6. [6]Calfee CS, Delucchi K, Parsons PE, et al. Subphenotypes in acute respiratory distress syndrome: latent class analysis of data from two randomised controlled trials Lancet Respir Med, 2014.PMID 24853585
  7. [7]Ranieri VM, Rubenfeld GD, Thompson BT, et al. Acute respiratory distress syndrome: the Berlin Definition JAMA, 2012.PMID 22797452
  8. [8]Bellani G, Laffey JG, Pham T, et al. Epidemiology, Patterns of Care, and Mortality for Patients With Acute Respiratory Distress Syndrome in Intensive Care Units in 50 Countries JAMA, 2016.PMID 26903337
  9. [9]Amato MB, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome N Engl J Med, 2015.PMID 25693014
  10. [10]Wiedemann HP, Wheeler AP, Bernard GR, et al. Comparison of two fluid-management strategies in acute lung injury N Engl J Med, 2006.PMID 16714767
  11. [11]Brower RG, Lanken PN, MacIntyre N, et al. Higher versus lower positive end-expiratory pressures in patients with the acute respiratory distress syndrome N Engl J Med, 2004.PMID 15269312
  12. [12]Briel M, Meade M, Mercat A, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis JAMA, 2010.PMID 20197533
  13. [13]Ferguson ND, Cook DJ, Guyatt GH, et al. High-frequency oscillation in early acute respiratory distress syndrome N Engl J Med, 2013.PMID 23339639
  14. [14]Young D, Lamb SE, Shah S, et al. High-frequency oscillation for acute respiratory distress syndrome N Engl J Med, 2013.PMID 23339638
  15. [15]Gattinoni L, Pesenti A. The concept of 'baby lung' Intensive Care Med, 2005.PMID 15812622
  16. [16]Horby P, Lim WS, Emberson JR, et al. Dexamethasone in Hospitalized Patients with Covid-19 N Engl J Med, 2021.PMID 32678530

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