ARDS-Diagnostik und -Therapie nach der Coronapandemie – alles beim Alten?

Die massiven wissenschaftlichen Aktivitäten zur Bewältigung der Coronapandemie haben für bestimmte intensivmedizinisch relevante Syndrome neue Blickwinkel und Perspektiven eröffnet. Neben der Sepsis betrifft dies das akute Lungenversagen als schwerste Manifestation der COVID-19-Infektion. In diesem Beitrag soll untersucht werden, ob sich daraus bereits neue Empfehlungen zur Diagnostik und Therapie des ARDS im Allgemeinen ableiten lassen.

Abstract

ARDS is a syndrome that can develop as a result of various underlying diseases. For a long time, the prevailing belief was that the course of the disease was comparable regardless of the underlying disease. However, even before the COVID-19 pandemic, it was suspected that there were different manifestations that could be treated more individually and thus reduce the high mortality rate of ARDS, which has remained unchanged for years. The various findings on the heterogeneity of the course of the disease in COVID-related ARDS appear to confirm these assumptions. It is therefore to be expected that the diagnosis and treatment of non-COVID-related ARDS will also have to be individualised according to such phenotypes in the future. However, as long as the effectiveness of such strategies has not been proven in clinical trials, the current recommendations for ARDS therapy will remain valid for the time being. However, the adjustments already formulated in this context to individual pathophysiological conditions with regard to respiratory mechanics, ventilation-perfusion distribution and possible cardiac dysfunction should be made more meticulously than has usually been the case to date.

Kernaussagen

• Die Letalität des ARDS bleibt trotz Beachtung der aktuellen Therapieempfehlungen unverändert.

• Bereits vor der COVID-19-Pandemie zeichnete sich ab, dass die Differenzierung des ARDS in verschiedene Phänotypen zusätzliche Therapieoptionen zulassen könnte. Insbesondere die Unterscheidung zwischen hyper- und hypoinflammatorischen Verläufen schien in dieser Hinsicht erfolgversprechend.

• Die im Rahmen der COVID-Pandemie gewonnenen Erkenntnisse zu heterogenen Krankheitsverläufen und entsprechend individualisierten Therapiestrategien lassen sich mit dieser Annahme in Einklang bringen.

• Es erscheint daher auch beim nicht COVID-bedingten ARDS sinnvoll, Subgruppen mit unterschiedlicher Krankheitsausprägung zu identifizieren.

• Die Steuerung einer entsprechend individualisierten Therapie mithilfe von Biomarkern ist dabei vielversprechend.

Schlüsselwörter

akutes Lungenversagen - ARDS - COVID-19 - maschinelle Beatmung - Bauchlagerung - Phänotyp - Biomarker

Keywords

acute respiratory distress syndrome - mechanical ventilation - prone position - phenotype - biomarkers

Publikationsverlauf

Artikel online veröffentlicht:
08. Januar 2024

• Literatur

• 1 Ranieri VM, Rubenfeld GD, Thompson BT. et al. Acute respiratory distress syndrome: the Berlin Definition. JAMA 2012; 307: 2526-2533
• 2 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; 315: 788-800
• 3 Slutsky AS, Villar J, Pesenti A. Happy 50th birthday ARDS!. Intensive Care Med 2016; 42: 637-639
• 4 Brower RG, Matthay MA, Morris A. Acute Respiratory Distress Syndrome Network. 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; 342: 1301-1308
• 5 Gattinoni L, Pesenti A. The concept of “baby lung”. Intensive Care Med 2005; 31: 776-784
• 6 Deutsche Gesellschaft für Anästhesiologie und Intensivmedizin e.V. (DGAI) (federführend). S3-Leitlinie „Invasive Beatmung und Einsatz extrakorporaler Verfahren bei akuter respiratorischer Insuffizienz“. 04.12.2017 Zugriff am 28. November 2023 unter: https://www.awmf.org/leitlinien/detail/ll/001-021.html
• 7 Amato MB, Meade MO, Slutsky AS. et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med 2015; 372: 747-755
• 8 Huppert LA, Matthay MA, Ware LB. Pathogenesis of Acute Respiratory Distress Syndrome. Sem Respir Crit Care Med 2019; 40: 31-39
• 9 Ashbaugh DG, Bigelow DB, Petty TL. et al. Acute respiratory distress in adults. Lancet 1967; 2: 319-323
• 10 Lewis SR, Pritchard MW, Thomas CM. et al. Pharmacological agents for adults with acute respiratory distress syndrome. Cochrane Database Syst Rev 2019; (07) CD004477
• 11 Pham T, Rubenfeld GD. Fifty Years of Research in ARDS. The Epidemiology of Acute Respiratory Distress Syndrome. A 50th Birthday Review. Am J Respir Crit Care Med 2017; 195: 860-870
• 12 McAuley DF, Laffey JG, O’Kane CM. et al. Simvastatin in the acute respiratory distress syndrome. N Engl J Med 2014; 371: 1695-1703
• 13 Calfee CS, Delucchi KL, Sinha P. et al. Acute respiratory distress syndrome subphenotypes and differential response to simvastatin: secondary analysis of a randomised controlled trial. Lancet Respir Med 2018; 6: 691-698
• 14 Fan E, Beitler JR, Brochard L. et al. COVID-19-associated acute respiratory distress syndrome: is a different approach to management warranted?. Lancet Respir Med 2020; 8: 816-821
• 15 Gattinoni L, Coppola S, Cressoni M. et al. COVID-19 Does Not Lead to a “Typical” Acute Respiratory Distress Syndrome. Am J Respir Crit Care Med 2020; 201: 1299-1300
• 16 Gattinoni L, Chiumello D, Rossi S. COVID-19 pneumonia: ARDS or not?. Crit Care 2020; 24: 154
• 17 Busana M, Giosa L, Cressoni M. et al. The impact of ventilation-perfusion inequality in COVID-19: a computational model. J Appl Physiol (1985) 2021; 130: 865-876
• 18 Camporota L, Cronin JN, Busana M. et al. Pathophysiology of coronavirus-19 disease acute lung injury. Curr Op Crit Care 2022; 28: 9-16
• 19 Gattinoni L, Gattarello S, Steinberg I. et al. COVID-19 pneumonia: pathophysiology and management. Eur Respir Rev 2021; 30: 210138
• 20 Zhang Y, Geng X, Tan Y. et al. New understanding of the damage of SARS-CoV-2 infection outside the respiratory system. Biomed Pharmacother 2020; 127: 110195
• 21 Iba T, Levy JH, Levi M. et al. Coagulopathy of Coronavirus Disease 2019. Crit Care Med 2020; 48: 1358-1364
• 22 Lin SH, Zhao YS, Zhou DX. et al. Coronavirus disease 2019 (COVID-19): cytokine storms, hyper-inflammatory phenotypes, and acute respiratory distress syndrome. Genes Dis 2020; 7: 520-527
• 23 Deutsche Gesellschaft für Internistische Intensivmedizin und Notfallmedizin e.V. (DGIIN), Deutsche Interdisziplinäre Vereinigung für Intensiv- und Notfallmedizin e.V. (DIVI), Deutsche Gesellschaft für Pneumologie und Beatmungsmedizin e.V. (DGP), Deutsche Gesellschaft für Infektiologie e.V. (DGI). S3-Leitlinie „Empfehlungen zur Therapie von Patienten mit COVID-19“. 02.03.2023 Zugriff am 30. Oktober 2023 unter: https://register.awmf.org/de/leitlinien/detail/113–001LG
• 24 Kalfon P, Payen JF, Rousseau A. et al. Effect of intravenous almitrine on intubation or mortality in patients with COVID-19 acute hypoxemic respiratory failure: A multicentre, randomised, double-blind, placebo-controlled trial. E Clin Med 2022; 52: 101663
• 25 Goligher EC, Bradbury CA, McVerry BJ. et al. Therapeutic Anticoagulation with Heparin in Critically Ill Patients with Covid-19. N Engl J Med 2021; 385: 777-789
• 26 Karagiannidis C, Strassmann S, Merten M. et al. High In-Hospital Mortality Rate in Patients with COVID-19 Receiving Extracorporeal Membrane Oxygenation in Germany: A Critical Analysis. Am J Respir Crit Care Med 2021; 204: 991-994
• 27 Meduri GU, Headley AS, Golden E. et al. Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: a randomized controlled trial. JAMA 1998; 280: 159-165
• 28 Steinberg KP, Hudson LD, Goodman RB. et al. Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome. N Engl J Med 2006; 354: 1671-1684
• 29 Tang BM, Craig JC, Eslick GD. et al. Use of corticosteroids in acute lung injury and acute respiratory distress syndrome: a systematic review and meta-analysis. Crit Care Med 2009; 37: 1594-1603
• 30 Sinha P, Delucchi KL, Chen Y. et al. Latent class analysis-derived subphenotypes are generalisable to observational cohorts of acute respiratory distress syndrome: a prospective study. Thorax 2022; 77: 13-21
• 31 Sinha P, Furfaro D, Cummings MJ. et al. Latent Class Analysis Reveals COVID-19-related Acute Respiratory Distress Syndrome Subgroups with Differential Responses to Corticosteroids. Am J Respir Crit Care Med 2021; 204: 1274-1285
• 32 Famous KR, Delucchi K, Ware LB. et al. Acute Respiratory Distress Syndrome Subphenotypes Respond Differently to Randomized Fluid Management Strategy. Am J Respir Crit Care Med 2017; 195: 331-338