Научная статья на тему 'ОСТРЫЙ РЕСПИРАТОРНЫЙ ДИСТРЕСС-СИНДРОМ: НОВЫЕ ПОДХОДЫ ПРИ COVID-19'

ОСТРЫЙ РЕСПИРАТОРНЫЙ ДИСТРЕСС-СИНДРОМ: НОВЫЕ ПОДХОДЫ ПРИ COVID-19 Текст научной статьи по специальности «Клиническая медицина»

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Журнал
Re-health journal
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Ключевые слова
острый респираторный дистресс-синдром / COVID-19 / пневмония.

Аннотация научной статьи по клинической медицине, автор научной работы — Содиқова Дилрабохон Тожидиновна

Тяжелая коронавирусная болезнь 2019 года (COVID-19) представляет собой вирусную пневмонию от инфекции SARS-CoV-2 (тяжелый острый респираторный синдром коронавирус 2), приводящей к острому респираторному дистресс-синдрому (ОРДС). Его проявления можно рассматривать как сочетание двух процессов, а именно вирусной пневмонии и ОРДС. Наряду с другими серьезными коронавирусными инфекциями SARS и MERS, которые также вызывают ОРДС, COVID-19 представляет собой постоянную глобальную угрозу, поскольку это семейство вирусов может мутировать и инфицировать не-иммунизированные популяции.

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Текст научной работы на тему «ОСТРЫЙ РЕСПИРАТОРНЫЙ ДИСТРЕСС-СИНДРОМ: НОВЫЕ ПОДХОДЫ ПРИ COVID-19»

УДК 61-13058. 616-08

ОСТРЫЙ РЕСПИРАТОРНЫЙ ДИСТРЕСС-СИНДРОМ: НОВЫЕ ПОДХОДЫ ПРИ COVID-19

Содицова Дилрабохон Тожидиновна

Андижанский государственный медицинский институт

Тяжелая коронавирусная болезнь 2019 года (COVID-19) представляет собой вирусную пневмонию от инфекции SARS-CoV-2 (тяжелый острый респираторный синдром коронавирус 2), приводящей к острому респираторному дистресс-синдрому (ОРДС).

Его проявления можно рассматривать как сочетание двух процессов, а именно вирусной пневмонии и ОРДС. Наряду с другими серьезными коронавирусными инфекциями SARS и MERS, которые также вызывают ОРДС, COVID-19 представляет собой постоянную глобальную угрозу, поскольку это семейство вирусов может мутировать и инфицировать не-иммунизированные популяции.

Ключевые слова: острый респираторный дистресс-синдром, COVID-19, пневмония.

ACUTE РЕСПИРАТОРY DISTRESS SYNDROME: NEW APPROACHES FOR COVID-19

Severe Coronavirus disease 2019 (COVID-19) is a viral pneumonia from SARS-CoV-2 infection (severe acute респиратору syndrome coronavirus 2), leading to acute респиратору distress syndrome (ARDS).

Its manifestations can be considered as a combination of two processes, namely viral pneumonia and ARDS. Along with other serious coronavirus infections SARS and MERS, which also cause SARS, COVID-19 is a constant global threat, as this family of viruses can mutate and infect non-immunized populations.

Key words: acute респиратору distress syndrome, COVID-19, pneumonia.

УТКИР РЕСПИРАТОР ДИСТРЕСС СИНДРОМИ: COVID-19 УЧУН ЯНГИ

ЁНДАШУВЛАР

Огир коронавирус касаллиги 2019 (COVID-19)- SARS-CoV-2 инфекциясидан (огир уткир респиратор синдром коронавирус 2) вирусли пневмония булиб, уткир респиратор distress синдромига (УРДС) олиб келади.

Унинг намоён булиши икки жараённинг, яъни вирусли пневмония ва УРДСЛАРнинг комбинацияси сифатида царалиши мумкин. Бошца жиддий коронавирус инфекциялари SARS ва MERS билан бир цаторда, шунингдек, SARS сабаб, COVID-19 доимий глобал тахдид, вируслар бу оила айланмасдан ва ноозиц-immunized ах,оли суцилиб мумкин.

Калит сузлар: уткир респиратор дистресс синдроми, COVID-19, пневмония.

Relevance. ARDS is defined as hypoxemia caused by the rapid occurrence of noncardiogenic pulmonary edema [2]. Etiological risk factors for ARDS include both direct and indirect lung damage, including, but not limited to, pneumonia, sepsis, non-cardiogenic shock, aspiration, trauma, bruising, blood transfusion, and lung injury from inhalation of toxic substances.

Despite the fact that the clinical diagnosis and treatment of ARDS has improved significantly over the past 25 years, it still remains the leading cause of death among patients in critical condition, with mortality rates constantly ranging from 30 to 40% [5]. ARDS treatment protocols have been developed to improve ARDS treatment outcomes

Infection caused by severe ARDS caused by coronavirus-2 (SARS-CoV-2) is mediated by binding of the virus spike to angiotensin converting enzyme-2 on type 2 alveolar epithelial cells [3] Viral infection causes cells to react by releasing chemokines and cytokines [1] Infection can also affect epithelial cells and cause their death through pyroptosis, which leads to the release of inflammatory lesions and molecular patterns associated with pathogens. Recognition of damage and pathogen-related molecular patterns and cytokines activates alveolar macrophages, and chemokines act by recruiting inflammatory immune cells into the lungs. Excessive release of antimicrobial effectors by immune cells, such as metallomatrix proteases, elastases and reactive oxygen species, causes damage to collateral tissues, which leads to loss of integrity of epithelial and endothelial barriers and penetration of protein fluid into the alveolar airspace [4].

In addition, there is more and more data confirming the important role of endothelial cells in the initiation of inflammation and the development of extensive intravascular coagulopathy of the lungs, which is often found in patients with COVID-19 [3]. In severe cases, patients with COVID-19 develop disseminated intravascular coagulation (DIC) [4].

Considering that the key pathological feature of COVID-19 is the prevalence of thrombotic coagulopathy in the pulmonary vascular network, much attention has been paid to whether anticoagulation or thrombolytic therapy can provide therapeutic efficacy in COVID-19 ARDS. In light of the current recognition of the pathophysiological role of coagulopathy in SARS-CoV-2 infection, several clinical trials have been initiated aimed at establishing the role of empirical therapeutic dosing with anticoagulants in COVID-19 ARDS.

In addition to anticoagulation, thrombolytic treatment of patients with COVID-19 ARDS has been proposed as a rescue therapy. The scientific justification of the use of fibrinolytic therapy in ARDS COVID-19, namely consistent data on pulmonary microvascular thrombosis, led to the beginning of much-needed clinical trials studying the role of antithrombotic agents in ARDS COVID-19 [2].

The purpose of the study. Based on clinical and laboratory indicators, it is based on the tactics of managing the state of ARDS in patients with COVID-19, taking into account the severity and nature of these diseases.

Research methods. ARDS develops in 42% of patients with COVID-19 pneumonia and 61-81% of them need treatment in the ICU. ARDS COVID-19 develops predictably within a few days with an average intubation time of 8.5 days after the onset of symptoms.

This is similar to previous reports where ARDS develops 8-9 days after the onset of symptoms. Therefore, it is important to monitor the development of ARDS in patients as their infection with COVID-19 progresses. Respiratory rate and SpO2 are two important parameters for assessing the clinical condition of patients and allow early recognition of ARDS. A patient who is suitable for any of the following conditions may have a serious medical condition and requires further evaluation:

1. Respiratory rate > 30 breaths /min;

2. SpO2< 92%;

3. PaO2 / FiO2= 300 mmHg.

The results of the study. Non-invasive ventilation (NIV) is not recommended. Clinical experience has found inconsistent benefits from NIV, and there is concern about aerosol formation and an increased risk of viral transmission. Light ventilation is useful for COVID-19 acute respiratory infections.

Placing a person in a position on his stomach contributes to a more uniform aeration of the lungs in ARDS and can improve oxygenation. While artificial lung ventilation is used only in about 16% of patients with typical ARDS in COVID-19, it is successfully used in the early course of ARDS, and it is recommended to use >12 hours a day. Venous extracorporeal membrane oxygenation (ECMO) can be used as a rescue for mechanically ventilated adults with COVID-19 and hypoxemia, which persists despite optimized ventilation, the use of rescue treatment methods and artificial lung ventilation.

Among critically ill patients treated in Wuhan, artificial ventilation and ECMO treatment were not found to be as effective as in ARDS caused by other pathogens. Possible causes include:

1. COVID-19 pneumonia was still progressing and was not under control;

2. Lung injuries were not completely dependent on gravity under the influence of ultrasound, so the effect of the position on the stomach was limited;

3. The patient's immune status was not restored, and a secondary nosocomial infection worsened the condition;

4. When the number of cases is high as a result of the epidemic, treatment regimens, isolation and human resources still needed to be discussed and strengthened.

The protective ventilation strategy used in typical ARDS provides for a low respiratory volume (6 ml/kg) and higher PEEP targets. For COVID-19 ARDS, it is proposed to change more generous respiratory volume targets, allowing up to 8 ml/kg, and lower PEEP levels to prevent lung damage in the patient (P-SILI).

Conclusion. The last 25 years of large-scale randomized clinical trials have made a huge contribution to the development of clinical practice of mechanical ventilation with lung protection. Indeed, the introduction of clinically proven therapeutic interventions, such as the use of low respiratory volumes and lying on the stomach, has significantly improved the results of ARDS treatment.

However, mortality remains high, and there are no targeted treatment options. Nevertheless, new fundamental scientific research has led to the emergence of new therapeutic targets, such as hypoxia, adenosine, and microRNA signaling, which may pave the way for new pharmacological treatments for ARDS [29]. In addition, the recent COVID-19 pandemic has stimulated the rapid start of clinical trials aimed at treating ARDS.

References:

1. Asfar p, Schortgen F, Boisrame-Helms J, Charpentier J, Gero E, Megarbain B, Grimaldi D, Grelon F, Anguel N, Lasocki S, Henri-Lagarrig M, Gonzalez F, Legay F, Guitton C, Schenck M, Doise JM, Devaquet J, Van der Linden T, Chatelier D, Rigaud JP, Dellamonica J, Tamion F, Mesiani F, Mercat A, Dreyfus D, Seegers V, Radermacher p; HYPER2S Investigators; REVA Research Network. Hyperoxia and hypertonic solution in patients with septic shock (HYPERS2S): a factorial multicenter randomized clinical trial two by two // Lancet Respir Med. - 2017. - No. 5. - pp. 180-190.

2. Barro L, Asfar P, Mauni F, Vinishevsky HOUR, Montini F, Badi J, Quenot JP, Pili-Fluri S, Bouhemad B, Louis gram, Souweine B, Collange O, Gonchar J, Levi B, Puyraveau M, Vettoretti L, Constantin JM, Capelier gram; LOCO2 researchers and the REVA research Network. Liberal or conservative oxygen therapy in acute respiratory distress syndrome // N Engl J Med. -2020. - No.382. - p. 999-1008.

3. Pan C, Chen L, Lu C, Zhang W, Xia JA, Sklar MC, Du B, Brochard L, Qiu H. Lung recruitability in COVID-19-associated acute respiratory distress syndrome: a single-center observational study // Am J Respir Crit Care Med. - 2020. - No.201. - p. 1294-1297.

4. Neudecker V, Haneklaus M, Jensen O, Hailova L, Masterson JC, Tai H, Biette K, Edlichka p, Brodsky KS, Gerich ME, Mack M, Robertson AAB, Cooper MA, Furuta GT, Dinarello CA,

O'Neill LA, Eltschig HK, Masters SL, McNamee EN. MiR-223, derived from myeloid, regulates intestinal inflammation by repression of inflammasome NLRP3 // J Exp Med. - 2017. - No.214. - P. 1737-1752.

5. Lang M, Som A, Mendoza DP, Flores EJ, Reed N, Carey D, Lee MD, Witkin A, Rodriguez-Lopez JM, Shepard JOE, Little BP. Hypoxemia associated with COVID-19: vascular and perfusion disorders on dual-energy CT // Lancet Infection Dis. - 2020. - No. 20. - p. 3036730374.

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