Synopsis of symptoms of COVID-19 during second wave of the pandemic in India

COVID-19 was caused by the original coronavirus, severe acute respiratory syndrome associated coronavirus-2 (SARS CoV2), which originated in Wuhan, China. COVID-19 had a large breakout of cases in early 2020, resulting in an epidemic that turned into a pandemic. This quickly enveloped the global healthcare system. The principal testing method for COVID-19 detection, according to the WHO, is reverse transcription polymerase chain reaction (RT-PCR). Isolation of patients, quarantine, masking, social distancing, sanitizer use, and complete lockdown were all vital health-care procedures for everyone. With the ‘new normal’ and vaccination programmes, the number of cases and recovered patients began to rise months later. The easing of restrictions during the plateau phase resulted in a rebound of instances, which hit the people with more ferocity and vengeance towards the start of April 2021. Coronaviruses have evolved to cause respiratory, enteric, hepatic, and neurologic diseases, resulting in a wide range of diseases and symptoms such as fever, cough, myalgia or fatigue, shortness of breath, muscle ache, headache, sore throat, rhinorrhea, hemoptysis, chest pain, nausea, vomiting, diarrhoea, anosmia, and ageusia. Coronavirus infections can be mild, moderate, or severe in intensity. COVID-19 pulmonary dysfunction includes lung edoema, ground-glass opacities, surfactant depletion, and alveolar collapse. Patients who presented with gastrointestinal (GI) symptoms such as anorexia, nausea, vomiting, or diarrhoea had a higher risk of negative outcomes. COVID-19’s influence on cognitive function is one of COVID-19’s long-term effects. More clinical situations need to be reviewed by healthcare professionals so that an appropriate management protocol may be developed to reduce morbidity and death in future coming third/fourth wave cases.

Electrical Impedance Tomography Analysis Between Two Similar Respiratory System Compliance During Decremetal PEEP Titration in ARDS Patients

Purpose The positive end-expiratory pressure (PEEP) level with best respiratory system compliance (Crs) is frequently used for PEEP selection in acute respiratory distress syndrome (ARDS) patients. On occasion, two similar best Crs (where the difference between the Crs of two PEEP levels is < 1 ml/cm H2O) may be identified during decremental PEEP titration. Selecting PEEP under such conditions is challenging. The aim of this study was to provide supplementary rationale for PEEP selection by assessing the global and regional ventilation distributions between two PEEP levels in this situation. Methods Eight ARDS cases with similar best Crs at two different PEEP levels were analyzed using examination-specific electrical impedance tomography (EIT) measures and airway stress index (SIaw). Five Crs were measured at PEEP values of 25 cm H2O (PEEP25), 20 cm H2O (PEEP20), 15 cm H2O (PEEPH), 11 cm H2O (PEEPI), and 7 cm H2O (PEEPL). The higher PEEP value of the two PEEPs with similar best Crs was designated as PEEPupper, while the lower designated as PEEPlower. Results PEEPH and PEEPI shared the best Crs in two cases, while similar Crs was found at PEEPI and PEEPL in the remaining six cases. SIaw was higher with PEEPupper as compared to PEEPlower (1.06 ± 0.10 versus 0.99 ± 0.09, p = 0.05). Proportion of lung hyperdistension was significantly higher with PEEPupper than PEEPlower (7.0 ± 5.1% versus 0.3 ± 0.5%, p = 0.0002). In contrast, proportion of recruitable lung collapse was higher with PEEPlower than PEEPupper (18.6 ± 4.4% versus 5.9 ± 3.7%, p < 0.0001). Cyclic alveolar collapse and reopening during tidal breathing was higher at PEEPlower than PEEPupper (34.4 ± 19.3% versus 16.0 ± 9.1%, p = 0.046). The intratidal gas distribution (ITV) index was also significantly higher at PEEPlower than PEEPupper (2.6 ± 1.3 versus 1.8 ± 0.7, p = 0.042). Conclusions PEEPupper is a rational selection in ARDS cases with two similar best Crs. EIT provides additional information for the selection of PEEP in such circumstances.

Pulmonary surfactant: a unique biomaterial with life-saving therapeutic applications.

: Pulmonary surfactant is a complex lipoprotein mixture secreted into the alveolar lumen by type 2 pneumocytes, which is composed by tens of different lipids (approximately 90% of its entire mass) and surfactant proteins (approximately 10% of the mass). It is crucially involved in maintaining lung homeostasis by reducing the values of alveolar liquid surface tension close to zero at end-expiration, thereby avoiding the alveolar collapse, and assembling a chemical and physical barrier against inhaled pathogens. A deficient amount of surfactant or its functional inactivation is directly linked to a wide range of lung pathologies, including the neonatal respiratory distress syndrome. This paper reviews the main biophysical concepts of surfactant activity and its inactivation mechanisms, and describes the past, present and future roles of surfactant replacement therapy, focusing on the exogenous surfactant preparations marketed worldwide and new formulations under development. The closing section describes the pulmonary surfactant in the context of drug delivery. Thanks to its peculiar composition, biocompatibility, and alveolar spreading capability, the surfactant may work not only as a shuttle to the branched anatomy of the lung for other drugs but also as a modulator for their release, opening to innovative therapeutic avenues for the treatment of several respiratory diseases.

The Role of Pulmonary Surfactant in COVID-19 Understanding

Background: In Covid-19 the virus infects the respiratory tract in human. When lung tissue becomes diseased, the walls and lining of the alveoli and capillaries are damaged. At this point lung compliance and ventilation decrease. Pulmonary surfactant that is produced and dispersed into alveolar space, has a significant role in understanding how heavily covid-19 interferes and infects lung cells. The importance of pulmonary surfactant in alveoli is to lower surface tension at air/liquid interface in the lung. This is achieved by reducing the work of breathing and preventing alveolar collapse. The main constituent of pulmonary surfactant is dipalmitoylphosphatidylcholine (DPPC) (C40H80NO8P). It is a phospholipid containing two non polar palmitic acid C16 chains as hydrophobic tails linked to a polar head group of a phosphatidylcholine (also known as lecithin). Rationale of the Review and Objective Method: When DPPC molecules are in contact with a polar solvent, micelles which grow further into bilayers are formed considering their cylindrical structures. This trait makes the whole structure of pulmonary surfactant as amphipathic and surface active molecules. The head group of phosphatidylcholine in the pulmonary surfactant is attracted by polar liquid molecules causing a reduction of the liquid surface tension. Conclusion: This review complements the quoted information analysing them theoretically and integrates recent advances in pulmonary surfactant research with the global pandemic.

The Experience of Surfactant Therapy in Severe COVID-19 Pneumonia: A Case Report

The COVID-19 pandemic has presented challenges to finding effective treatment for lung damage. Medical researchers from different countries recognize the deficiency of pulmonary surfactant (PS) as a significant cause of the alveolar collapse, followed by microatelectasis and severe disturbances in the ventilation-perfusion relationship. Due to the pathophysiological rationale, experimental confirmations, and accumulated clinical experience, the PS preparations can be used to treat patients with severe COVID-19. The article provides a description of a case when ST was successfully used in a patient with severe COVID-19 pneumonia.

Proposal of selective wedge instillation of pulmonary surfactant for COVID-19 pneumonia based on computational fluid dynamics simulation

Background The most important target cell of SARS-CoV-2 is Type II pneumocyte which produces and secretes pulmonary surfactant (PS) that prevents alveolar collapse. PS instillation therapy is dramatically effective for infant respiratory distress syndrome but has been clinically ineffective for ARDS. Nowadays, ARDS is regarded as non-cardiogenic pulmonary edema with vascular hyper-permeability regardless of direct relation to PS dysfunction. However, there is a possibility that this ineffectiveness of PS instillation for ARDS is caused by insufficient delivery. Then, we performed PS instillation simulation with realistic human airway models by the use of computational fluid dynamics, and investigated how instilled PS would move in the liquid layer covering the airway wall and reach to alveolar regions. Methods Two types of 3D human airway models were prepared: one was from the trachea to the lobular bronchi and the other was from a subsegmental bronchus to respiratory bronchioles. The thickness of the liquid layer covering the airway was assigned as 14 % of the inner radius of the airway segment. The liquid layer was assumed to be replaced by an instilled PS. The flow rate of the instilled PS was assigned a constant value, which was determined by the total amount and instillation time in clinical use. The PS concentration of the liquid layer during instillation was computed by solving the advective-diffusion equation. Results The driving pressure from the trachea to respiratory bronchioles was calculated at 317 cmH2O, which is about 20 times of a standard value in conventional PS instillation method where the driving pressure was given by difference between inspiratory and end-expiratory pressures of a ventilator. It means that almost all PS does not reach the alveolar regions but moves to and fro within the airway according to the change in ventilator pressure. The driving pressure from subsegmental bronchus was calculated at 273 cm H2O, that is clinically possible by wedge instillation under bronchoscopic observation. Conclusions The simulation study has revealed that selective wedge instillation under bronchoscopic observation should be tried for COVID-19 pneumonia before the onset of ARDS. It will be also useful for preventing secondary lung fibrosis.

6-Gingerol Ameliorates Sepsis Induced Acute Lung Injury by Regulating Nuclear Factor-κB and Nuclear-Factor Erythroid 2-Related Factor 2/Heme Oxygenase-1 Signaling Pathways

Acute lung injury initiated systemic inflammation leads to sepsis. Septic mice show a series of degenerative changes in lungs as demonstrated by pulmonary congestion, alveolar collapse, inflammatory cell infiltration, and increased wet-todry weight in lungs. 6-Gingerol ameliorates histopathological changes and clinical outcome of the sepsis. The increase in the levels of tumor necrosis factor-α, interleukin-1 beta, interleukin-6, and interleukin-18 in septic mice were reduced by administration with 6-Gingerol. Also, 6-Gingerol attenuates sepsis-induced increase of malonaldehyde and decrease of catalase, superoxide, and glutathione. Enhanced phospho-p65, reduced nuclear factor erythropoietin-2-related factor 2, and heme oxygenase 1 in septic mice were reversed by administration with 6-Gingerol. In conclusion, 6-Gingerol demonstrates anti-inflammatory and antioxidant effects against sepsis associated acute lung injury through inactivation of nuclear factor-kappa B and activation of nuclear-factor erythroid 2-related factor 2 pathways.

Recent progress on surfactant protein A: cellular function in lung and kidney disease development

Pulmonary surfactant is a heterogeneous active surface complex made up of lipids and proteins. The major glycoprotein in surfactant is surfactant protein A (SP-A), which is released into the alveolar lumen from cytoplasmic lamellar bodies in type II alveolar epithelial cells. SP-A is involved in phospholipid absorption. SP-A together with other surfactant proteins and phospholipids prevent alveolar collapse during respiration by decreasing the surface tension of the air-liquid interface. Additionally, SP-A interacts with pathogens to prevent their propagation and regulate host immune responses. Studies in human and animal models have shown that deficiencies or mutations in surfactant components result in various lung or kidney pathologies, suggesting a role for SP-A in the development of lung and kidney diseases. In this mini-review, we discuss the current understanding of SP-A functions, recent findings of its dysfunction in specific lung and kidney pathologies, and how SP-A has been used as a biomarker to detect the outcome of lung diseases.