COVID-19-associated acute respiratory distress syndrome: Difference between revisions
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* [[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. | * [[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]] | * 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]] | ||
==Classification== | ==Classification== | ||
Several authors in a case report highlighted the nonuniformity of patients with COVID-19-associated ARDS and proposed the existence of two primary phenotypes: | |||
* | * Type L (low values of elastance, pulmonary ventilation/ perfusion ratio, lung weight, and recruitability) | ||
* Type H (high values of elastance, right-to-left shunt, lung weight, and recruitability), more consistent with typical severe ARDS. | |||
==Pathophysiology== | ==Pathophysiology== | ||
| Line 38: | Line 33: | ||
==Clinical Features== | ==Clinical Features== | ||
Clinical presentations of COVID-19 range from asymptomatic (81.4%), through mildly symptomatic with or without seasonal flu-like symptoms, to severe pneumonia (13.9%) [15]. | |||
* Usually, respiratory problems manifest about one week after virus entry and dyspnea ranges from effort dyspnea to dyspnea occurring at rest [16,17]. | |||
* Patients with dyspnea can revert to an asymptomatic phase or progress to ARDS, requiring positive pressure oxygen therapy and intensive care therapy [18] in 17–19.6% of symptomatic patients [19,20]. ARDS, in turn, can progress to multi-organ failure [21] and, in this phase, disseminated intravascular coagulation (DIC) can also be observed [22]. The main cause of death worldwide in infected patients is a combination of both ARDS and DIC in 13.9% of cases | |||
==Differentiating [disease name] from other Diseases== | ==Differentiating [disease name] from other Diseases== | ||
Revision as of 09:25, 13 July 2020
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For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ayesha Javid, MBBS[2]
Overview
ARDS has been distributed over different phenotypes over the last decade. The management of COVID-19 related ARDS has been therefore led to different proposal for the management strategies that are stratified according to the type of phenotype. ARDS developed in 20 percent a median of eight days after the onset of symptoms; mechanical ventilation was implemented in 12.3 percent. [1] The mortality rate of COVID-19 related ARDS is higher in elderly patients. Given the importance of heterogeneity of ARDS profile , appropriate intervention at appropriate time is needed to help preventing the deterioration of lung function. Recent advances in RECOVERY trial has further strengthened this notion that the use of dexamethasone in patients on ventilator can reduce the mortality rate of patients by 1/3rd. The treatment of COVID-19 related ARDS is evolving with time and different treatment options are now available for the better management of ARDS.
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
Classification
Several authors in a case report highlighted the nonuniformity of patients with COVID-19-associated ARDS and proposed the existence of two primary phenotypes:
- Type L (low values of elastance, pulmonary ventilation/ perfusion ratio, lung weight, and recruitability)
- Type H (high values of elastance, right-to-left shunt, lung weight, and recruitability), more consistent with typical severe ARDS.
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.[2]
- 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.[3]
- 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.[4]
- 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.[5]
- Patients infected with COVID‐19 also exhibit coagulation abnormalities.This procoagulant pattern can lead to acute respiratory distress syndrome.[6]
Clinical Features
Clinical presentations of COVID-19 range from asymptomatic (81.4%), through mildly symptomatic with or without seasonal flu-like symptoms, to severe pneumonia (13.9%) [15].
- Usually, respiratory problems manifest about one week after virus entry and dyspnea ranges from effort dyspnea to dyspnea occurring at rest [16,17].
- Patients with dyspnea can revert to an asymptomatic phase or progress to ARDS, requiring positive pressure oxygen therapy and intensive care therapy [18] in 17–19.6% of symptomatic patients [19,20]. ARDS, in turn, can progress to multi-organ failure [21] and, in this phase, disseminated intravascular coagulation (DIC) can also be observed [22]. The main cause of death worldwide in infected patients is a combination of both ARDS and DIC in 13.9% of cases
Differentiating [disease name] from other Diseases
- [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:
- [Differential dx1]
- [Differential dx2]
- [Differential dx3]
Epidemiology and Demographics
- Incidence is higher in the elderly and much lower in children
- Higher mortality rate is seen in the elderly.
- A systematic review showed that ARDS occurred in 14% of patients (95% PI, 2 to 59%; 999/6322 patients; 23 studies).
Age
- Patients of all age groups may develop [disease name].
- [Disease name] is more commonly observed among patients aged [age range] years old.
- [Disease name] is more commonly observed among [elderly patients/young patients/children].
Gender
- [Disease name] affects men and women equally.
- [Gender 1] are more commonly affected with [disease name] than [gender 2].
- The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.
Race
- There is no racial predilection for [disease name].
- [Disease name] usually affects individuals of the [race 1] race.
- [Race 2] individuals are less likely to develop [disease name].
Risk Factors
- Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
Natural History, Complications and Prognosis
- The majority of patients with [disease name] remain asymptomatic for [duration/years].
- Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
- If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
- Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
- Prognosis is generally [excellent/good/poor], and the [1/5/10year mortality/survival rate] of patients with [disease name] is approximately [#%].
Diagnosis
Diagnostic Criteria
- The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
- [criterion 1]
- [criterion 2]
- [criterion 3]
- [criterion 4]
Symptoms
Physical Examination
- Patients with [disease name] usually appear [general appearance].
- Physical examination may be remarkable for:
- [finding 1]
- [finding 2]
- [finding 3]
- [finding 4]
- [finding 5]
- [finding 6]
Laboratory Findings
- Blood plasma has elevated levels of IL-6, IL-1, tumour necrosis factor-α (TNF α) and C-reactive protein.[11]
- Thrombocytopenia.[12]
- Increased D-dimer levels. The elevated level of D-dimer is strongly associated with a higher mortality rate.[13]
- Increased fibrin degradation products.[13]
- Increased fibrinogen.[13][14]
- Prothrombin time and activated partial thromboplastin time may be slightly elevated.[13]
Imaging Findings
- Chest CT scan shows characteristic ground-glass opacities (GCO). This indicates the presence of exudate in the bronchoalveolar airspace.[2]
- Lung biopsy shows fibrin deposition.[2] [15]
Other Diagnostic Studies
- [Disease name] may also be diagnosed using [diagnostic study name].
- Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
Fluid and electrolytes management
- Studies have shown that in ARDS, conservative fluid management may help patients by reducing oedema formation. [16] [17]
- 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. [18]
Corticosteroids
- Recent studies have shown that the corticosteroid dexamethasone may reduce mortality of severe COVID-19 patients.[19]
- In England, a non-peer-reviewed randomized trial was issued as a press release which suggested that dexamethasone has a potential survival benefit in hospitalized COVID-19 patients requiring oxygen.[20]
- The Society of Critical Care Medicine (SCCM) provided a weak conditional recommendation in the 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 suggests benefit in patients with moderate to severe ARDS which is refractory to low tidal volume ventilation.[21]
Mechanical Ventilation
- Mechanical ventilation along with supportive therapies are the mainstay of treatment of ARDS.[22]
- 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).[23]
- 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.[24]
- 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).[25]
Anticoagulant or thrombolytic therapy
- Fibrinolytic drugs such as tissue-type plasminogen activator (tPA) degrade pre-existing fibrin in the lungs.[13]
- 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).[26]
- 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.[27]
Surgery
- Surgery is the mainstay of therapy for [disease name].
- [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
- [Surgical procedure] can only be performed for patients with [disease stage] [disease name].
Prevention
- There are no primary preventive measures available for [disease name].
- Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
- Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].
References
- ↑ Wang, Dawei; Hu, Bo; Hu, Chang; Zhu, Fangfang; Liu, Xing; Zhang, Jing; Wang, Binbin; Xiang, Hui; Cheng, Zhenshun; Xiong, Yong; Zhao, Yan; Li, Yirong; Wang, Xinghuan; Peng, Zhiyong (2020-03-17). "Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China". JAMA. American Medical Association (AMA). 323 (11): 1061. doi:10.1001/jama.2020.1585. ISSN 0098-7484. PMC 7042881 Check
|pmc=value (help). PMID 32031570 Check|pmid=value (help). - ↑ 2.0 2.1 2.2 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). - ↑ 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). - ↑ 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). - ↑ 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). - ↑ 13.0 13.1 13.2 13.3 13.4 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). - ↑ 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).
|
COVID-19 Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
COVID-19-associated acute respiratory distress syndrome On the Web |
|
American Roentgen Ray Society Images of COVID-19-associated acute respiratory distress syndrome |
|
FDA on COVID-19-associated acute respiratory distress syndrome |
|
CDC on COVID-19-associated acute respiratory distress syndrome |
|
COVID-19-associated acute respiratory distress syndrome in the news |
|
Blogs on COVID-19-associated acute respiratory distress syndrome |
|
Risk calculators and risk factors for COVID-19-associated acute respiratory distress syndrome |