COVID-19-associated acute respiratory distress syndrome: Difference between revisions
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{{CMG}} {{AE}} {{AyeshaFJ}} {{S.M.}} | {{SI}} | ||
{{CMG}}; {{AE}} {{AyeshaFJ}}, {{S.M.}} | |||
==Overview== | ==Overview== | ||
Revision as of 15:12, 1 July 2020
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ayesha Javid, MBBS[2], Sara Mohsin, M.D.[3]
Overview
Historical perspective
- The novel coronavirus was named as the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) due to its high similarity to SARS-CoV, which caused acute respiratory distress syndrome (ARDS) in 2002–2003.
- SARS-CoV-2 virus primarily affects the respiratory system causing a wide variety of respiratory symptoms which can range from symptoms of lower respiratory tract infection to severe hypoxia to acute respiratory distress syndrome within a very short span of time.
- The acute respiratory distress syndrome (ARDS) is a common cause of morbidity and mortality in critically ill COVID-19 infected patients. It is defined by the acute onset of noncardiogenic pulmonary edema, hypoxaemia and the need for mechanical ventilation
Epidemiology and demographics
- Incidence is higher in the elderly and much lower in children
- Higher mortality rate is seen in the elderly.
Pathophysiology
- ARDS arises as a complication of COVID-19 infection due to acute inflammation of the alveolar space which prevents normal gas exchange. The increase in proinflammatory cytokines within the lung leads to recruitment of leukocytes, further propagating the local inflammatory response.[1]
- The cytokine storm and the deadly uncontrolled systemic inflammatory response resulting from the release of large amounts of proinflammatory cytokines including interferons and interleukins and, chemokines by immune effector cells resulting in acute inflammation within the alveolar space. The exudate containing plasma proteins, including albumin, fibrinogen, proinflammatory cytokines and coagulation factors will increase alveolar-capillary permeability and decrease the normal gas exchange and plasma proteins, including albumin, fibrinogen, proinflammatory cytokines and coagulation factors.[2]
- The COVID-19 patients with ARDS show elevated levels of IL-6, IFN-a, and CCL5, CXCL8, CXCL-10 in serum as compared to those with the mild to moderate disease.[3]
- This inflammatory process leads to the fibrin deposition in the air spaces and lung parenchyma and contributes to hyaline-membrane formation and subsequent alveolar fibrosis.[4]
- Patients infected with COVID‐19 also exhibit coagulation abnormalities.[5] This procoagulant pattern can lead to acute respiratory distress syndrome.[5]
Diagnosis
Laboratory findings
- Blood plasma has elevated levels of IL-6, IL-1, tumour necrosis factor-α (TNF α) and C-reactive protein.[6]
- Thrombocytopenia.[7]
- Increased D-dimer levels. The elevated level of D-dimer is strongly associated with a higher mortality rate.[8]
- Increased fibrin degradation products.[8]
- Increased fibrinogen.[8][9]
- Prothrombin time and activated partial thromboplastin time may be slightly elevated.[8]
Imaging studies
- Chest CT scan shows characteristic ground-glass opacities (GCO). This indicates the presence of exudate in the bronchoalveolar airspace.[1]
- Lung biopsy shows fibrin deposition.[1] [10]
Signs and Symptoms
Treatment
Fluid and electrolytes management
- Studies have shown that in ARDS, conservative fluid management may help patients by reducing oedema formation. [15] [16]
- Conservative fluid management with buffered or non-buffered crystalloid is recommended for ARDS patients.
- The conservative fluid strategy results in an increased number of ventilator-free days and a decreased length of ICU stay. However, its effect on mortality remains uncertain. [17]
Corticosteroids
- Recent studies have shown that the corticosteroid dexamethasone may reduce mortality of severe COVID-19 patients.[18] In England, a non-peer-reviewed randomized trial was issued as a press release suggesting a potential survival benefit from dexamethasone in hospitalized patients with COVID-19 who require oxygen.[19]
- The Society of Critical Care Medicine (SCCM) provided a conditional, weak recommendation in favor of glucocorticoids in patients with COVID-19 who have severe ARDS; with a partial arterial pressure of oxygen/fraction of inspired oxygen PaO2:FiO2] <100 mmHg). This recommendation suggest benefit in patients with moderate to severe ARDS which is refractory to low tidal volume ventilation.[20]
Mechanical Ventilation
- Mechanical ventilation along with supportive therapies are the mainstay of treatment of ARDS.[21]
- Invasive mechanical ventilation (ie, ventilation via an endotracheal tube or tracheostomy with breaths delivered by a mechanical ventilator) is preferred for patients with ARDS, particularly those with moderate or severe ARDS (ie, arterial oxygen tension/fraction of inspired oxygen PaO2/FiO2 ≤200 mmHg on positive end-expiratory pressure (PEEP) ≥5 cm H2O).[22]
- It is recommended to use low tidal volume ventilation (LTVV) with 4 to 8 mL/kg predicted body weight [PBW]. Several meta-analyses and randomized trials that report a mortality benefit from LTVV in patients with ARDS.[23]
- The aim is to maintain oxygen saturation between 90% to 96%. The severe hypoxemia of the COVID-19 ARDS best responds when Positive end-expiratory pressure (PEEP) is high with Pplat ≤30 cm H2O. It is beneficial if the physician starts with higher than usual levels of PEEP (10 to 15 cm H2O).[24]
Anticoagulant or thrombolytic therapy
- Fibrinolytic drugs such as tissue-type plasminogen activator (tPA) degrade pre-existing fibrin in the lungs.[8]
- Nebulizer plasminogen activators may provide more targeted therapy to degrade fibrin and improving oxygenation in critically ill patients. It is in Phase II of the clinical trial.
Prevention
- The ARDS patients have an increased risk of hospital-associated venous thromboembolism (VTE).[25]
- Due to this reason, it is advised to take low molecular weight heparin (LMWH) prophylactically in patients who do not have the contraindications. Studies have shown that the heparin, either unfractionated or LMWH, can also reduce inflammatory biomarkers hence could help in reducing the inflammation.[26]
References
- ↑ 1.0 1.1 1.2 Whyte CS, Morrow GB, Mitchell JL, Chowdary P, Mutch NJ (2020). "Fibrinolytic abnormalities in acute respiratory distress syndrome (ARDS) and versatility of thrombolytic drugs to treat COVID-19". J Thromb Haemost. doi:10.1111/jth.14872. PMC 7264738 Check
|pmc=value (help). PMID 32329246 PMID: 32329246 Check|pmid=value (help). - ↑ Meduri GU, Annane D, Chrousos GP, Marik PE, Sinclair SE (2009). "Activation and regulation of systemic inflammation in ARDS: rationale for prolonged glucocorticoid therapy". Chest. 136 (6): 1631–1643. doi:10.1378/chest.08-2408. PMID 19801579 PMID: 19801579 Check
|pmid=value (help). - ↑ Tezer H, Bedir Demirdağ T (2020). "Novel coronavirus disease (COVID-19) in children". Turk J Med Sci. 50 (SI-1): 592–603. doi:10.3906/sag-2004-174. PMC 7195991 Check
|pmc=value (help). PMID 32304191 PMID: 32304191 Check|pmid=value (help). - ↑ Bertozzi P, Astedt B, Zenzius L, Lynch K, LeMaire F, Zapol W; et al. (1990). "Depressed bronchoalveolar urokinase activity in patients with adult respiratory distress syndrome". N Engl J Med. 322 (13): 890–7. doi:10.1056/NEJM199003293221304. PMID 2314423 PMID: 2314423 Check
|pmid=value (help). - ↑ 5.0 5.1 Ranucci M, Ballotta A, Di Dedda U, Bayshnikova E, Dei Poli M, Resta M; et al. (2020). "The procoagulant pattern of patients with COVID-19 acute respiratory distress syndrome". J Thromb Haemost. doi:10.1111/jth.14854. PMID 32302448 PMID: 32302448 Check
|pmid=value (help). - ↑ Matthay MA, Zemans RL, Zimmerman GA, Arabi YM, Beitler JR, Mercat A; et al. (2019). "Acute respiratory distress syndrome". Nat Rev Dis Primers. 5 (1): 18. doi:10.1038/s41572-019-0069-0. PMC 6709677 Check
|pmc=value (help). PMID 30872586 PMID: 30872586 Check|pmid=value (help). - ↑ Lippi G, Plebani M, Henry BM (2020). "Thrombocytopenia is associated with severe coronavirus disease 2019 (COVID-19) infections: A meta-analysis". Clin Chim Acta. 506: 145–148. doi:10.1016/j.cca.2020.03.022. PMC 7102663 Check
|pmc=value (help). PMID 32178975 PMID: 32178975 Check|pmid=value (help). - ↑ 8.0 8.1 8.2 8.3 8.4 Tang N, Li D, Wang X, Sun Z (2020). "Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia". J Thromb Haemost. 18 (4): 844–847. doi:10.1111/jth.14768. PMC 7166509 Check
|pmc=value (help). PMID 32073213 PMID: 32073213 Check|pmid=value (help). - ↑ Dowton SB, Colten HR (1988). "Acute phase reactants in inflammation and infection". Semin Hematol. 25 (2): 84–90. PMID 2455348 PMID: 2455348 Check
|pmid=value (help). - ↑ Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J; et al. (2020). "Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China". JAMA. doi:10.1001/jama.2020.1585. PMC 7042881 Check
|pmc=value (help). PMID 32031570 PMID: 32031570 Check|pmid=value (help). - ↑ Yang X, Yu Y, Xu J, Shu H, Xia J, Liu H; et al. (2020). "Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study". Lancet Respir Med. 8 (5): 475–481. doi:10.1016/S2213-2600(20)30079-5. PMC 7102538 Check
|pmc=value (help). PMID 32105632 PMID: 32105632 Check|pmid=value (help). - ↑ Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J; et al. (2020). "Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China". JAMA. doi:10.1001/jama.2020.1585. PMC 7042881 Check
|pmc=value (help). PMID 32031570 PMID 32031570 Check|pmid=value (help). - ↑ Gattinoni L, Coppola S, Cressoni M, Busana M, Rossi S, Chiumello D (2020). "COVID-19 Does Not Lead to a "Typical" Acute Respiratory Distress Syndrome". Am J Respir Crit Care Med. 201 (10): 1299–1300. doi:10.1164/rccm.202003-0817LE. PMC 7233352 Check
|pmc=value (help). PMID 32228035 PMID: 32228035 Check|pmid=value (help). - ↑ Repessé X, Vieillard-Baron A (2017). "Hypercapnia during acute respiratory distress syndrome: the tree that hides the forest!". J Thorac Dis. 9 (6): 1420–1425. doi:10.21037/jtd.2017.05.69. PMC 5506150. PMID 28740647 PMID: 28740647 Check
|pmid=value (help). - ↑ National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Wiedemann HP, Wheeler AP, Bernard GR, Thompson BT, Hayden D; et al. (2006). "Comparison of two fluid-management strategies in acute lung injury". N Engl J Med. 354 (24): 2564–75. doi:10.1056/NEJMoa062200. PMID 16714767 PMID 16714767 Check
|pmid=value (help). Review in: ACP J Club. 2006 Nov-Dec;145(3):69 - ↑ Grissom CK, Hirshberg EL, Dickerson JB, Brown SM, Lanspa MJ, Liu KD; et al. (2015). "Fluid management with a simplified conservative protocol for the acute respiratory distress syndrome*". Crit Care Med. 43 (2): 288–95. doi:10.1097/CCM.0000000000000715. PMC 4675623. PMID 25599463 PMID 25599463 Check
|pmid=value (help). - ↑ Silversides JA, Major E, Ferguson AJ, Mann EE, McAuley DF, Marshall JC; et al. (2017). "Conservative fluid management or deresuscitation for patients with sepsis or acute respiratory distress syndrome following the resuscitation phase of critical illness: a systematic review and meta-analysis". Intensive Care Med. 43 (2): 155–170. doi:10.1007/s00134-016-4573-3. PMID 27734109 PMID 27734109 Check
|pmid=value (help). - ↑ Theoharides TC, Conti P (2020). "Dexamethasone for COVID-19? Not so fast". J Biol Regul Homeost Agents. 34 (3). doi:10.23812/20-EDITORIAL_1-5. PMID 32551464 PMID: 32551464 Check
|pmid=value (help). - ↑ "World first coronavirus treatment approved for NHS use by government - GOV.UK".
- ↑ Annane D, Pastores SM, Rochwerg B, Arlt W, Balk RA, Beishuizen A; et al. (2017). "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 Med. 43 (12): 1751–1763. doi:10.1007/s00134-017-4919-5. PMID 28940011 PMID 28940011 Check
|pmid=value (help). - ↑ Fanelli V, Vlachou A, Ghannadian S, Simonetti U, Slutsky AS, Zhang H (2013). "Acute respiratory distress syndrome: new definition, current and future therapeutic options". J Thorac Dis. 5 (3): 326–34. doi:10.3978/j.issn.2072-1439.2013.04.05. PMC 3698298. PMID 23825769 PMID: 23825769 Check
|pmid=value (help). - ↑ "www.who.int" (PDF).
- ↑ Weiss CH, Baker DW, Weiner S, Bechel M, Ragland M, Rademaker A; et al. (2016). "Low Tidal Volume Ventilation Use in Acute Respiratory Distress Syndrome". Crit Care Med. 44 (8): 1515–22. doi:10.1097/CCM.0000000000001710. PMC 4949102. PMID 27035237 PMID: 27035237 Check
|pmid=value (help). - ↑ "www.who.int" (PDF).
- ↑ "b-s-h.org.uk" (PDF).
- ↑ Thachil J, Tang N, Gando S, Falanga A, Cattaneo M, Levi M; et al. (2020). "ISTH interim guidance on recognition and management of coagulopathy in COVID-19". J Thromb Haemost. 18 (5): 1023–1026. doi:10.1111/jth.14810. PMID 32338827 PMID: 32338827 Check
|pmid=value (help).