An Epidemiological Update on COVID-19

By Manikandan Dhayalan, S.U.Mohammed Riyaz and S. Parveen

An Epidemiological Update on COVID-19 brings recent findings about the pandemic to the forefront. The reference is a compilation of eleven chapters contributed by expert scholars in epidemiology and medicine that cover topics of interest to anyone interested in COVID-19 monitoring and response measures. The topics also indicate some clinical areas of interest to COVID-19 researchers that have received attention due to the pandemic. It covers basic knowledge about respiratory conditions associated with SARS-CoV-2 infection and COVID-19 epidemiology. These topics are complemented with chapters detailing the symptoms and biochemical mechanisms of novel coronavirus infections intended for readers with an advanced level of understanding of life sciences and medicine. Special topics such as the immune response to Sars-CoV-2, and, recombinant drugs for COVID-19, are also covered in this book. Each chapter is organized in a reader-friendly format and includes a list of references.

• Language: English
• Publisher: Bentham Science Publishers
• Release date: Jul 13, 2022
• ISBN: 9789815050325

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Acute Respiratory Distress Syndrome (ARDS)

V. Shyamala¹, *, R. Harini², D. Manikandan³, S.U. Mohammed Riyaz⁴

¹ Department of Microbiology, Annai Violet Arts and Science College, Ambattur, Chennai– 600053, India

² Department of Biochemistry, Annai Violet Arts and Science College, Ambattur, Chennai-600053, India

³ Small Molecule Drug Discovery Group, Anticancer Bioscience, Tianfu International Biotown, Chengdu-610 000, China

⁴ Department of Biotechnology, Islamiah College (Autonomous), Vaniyambadi – 635752, India

Abstract

The lungs' air sacs are filled with fluid, leading to a life-threatening lung injury known as acute respiratory distress syndrome (ARDS). The tiny blood vessels of the lungs are damaged in this condition. The amount of oxygen in the bloodstream decreases, giving rise to carbon dioxide in blood circulation. This makes breathing extremely difficult, ultimately leading to organ failure. Usually, the organs damaged due to this condition are the kidneys or brain. The variations in the severity of ARDS are dependent on different signs and symptoms. Most of the time, ARDS is represented by shortness of breath, dry hacking cough, fever, headaches, and fast pulse rate. Labored and unusually rapid breathing, Low blood pressure, mental confusion, and extreme tiredness could also be other signs. ARDS can also be associated with old age, chronic lung disease, a history of alcohol misuse, or smoking.

Keywords: ARDS, Carbon dioxide, Lungs, Oxygen, Shortness of breath.

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* Corresponding author V. Shyamala: Assistant Professor, Department of Microbiology, Annai Violet Arts and Science College, Ambattur, Chennai– 600053, India; Tel: [phone]; E-mail: [e-mail]

INTRODUCTION

Ashbaugh and colleagues were the first to define acute respiratory distress syndrome (ARDS) in 1967. They believed that ARDS is associated with signs including acute non-cardiogenic, pulmonary oedema, and increased lung stiffness. In this condition, the process of breathing becomes difficult. It may give rise to pneumonia, trauma, sepsis, and aspiration, resulting in lung failure. It was defined as a condition associated with diffuse pulmonary oedema and respiratory failure by the American European Consensus Conference (AECC) in 1994. Its coexistence with left-sided heart failure was also pointed out at that time [8].

The European Society of Intensive Care Medicine (ESICM) ARDS Definition Task Force proposed some minor changes in the definition of ARDS after reevaluation. Keeping in mind the ‘mild’, ‘moderate’, and ‘severe’ oxygenation levels, these alterations were done. The first case of ARDS was also reported from Denver in 1967 [7].

Mild: 200 mm Hg < PaO2/FiO2 ratio ≤ 300 mm Hg with positive end-expiratory pressure (PEEP) or continuous positive airway pressure ≥ 5 cm H2O.

Moderate: 100 mm Hg < PaO2/FiO2 ratio ≤ 200 mm Hg with PEEP ≥ 5 cm H2O.

Severe: PaO2/FiO2 ratio ≤ 100 mm Hg with PEEP ≥ 5cm H2O.

Since no method can measure lung injury, various clinical manifestations lead us to the diagnosis of ARDS. These clinical manifestations include pathological samples of lung tissue, distal airspace, or blood samples. In the beginning, ARDS may look like pneumonia (bacterial and viral most frequently: fungal sometimes) or major trauma (such as blunt or penetrating injuries or burns). The other possible clinical condition could be non-pulmonary sepsis or aspiration of gastric and/or oral and esophageal contents worsened due to some infection. Some other probable causes of ARDS may include acute pancreatitis, transfusion of fresh frozen plasma, RBCs and platelets, and smoke inhalation. Sometimes a drug overdose and inhalation of fresh or saltwater may lead to the development of ARDS. The hemorrhagic shock or cardiopulmonary bypass and lung resection etc. may also lead to ARDS. Acute respiratory distress syndrome (ARDS) may also be caused by primary graft dysfunction following lung transplantation, high-altitude pulmonary oedema, and neurogenic oedema. The clinical disorders associated with ARDS vary depending on geography so it may have different clinical manifestations in different parts of the world. Another factor is the healthcare system across the globe that makes ARDS show different manifestations clinically. The understating of epidemiology, pathogenesis, and pathophysiology of ARDS is not an easy job as it has different clinical manifestations in different parts of the world. Thus it is considered a heterogeneous syndrome. Its patients are segregated into sub-phenotypes based on clinical and biological features. Specific therapies of ARDS may have different effects on different patients.

Pathophysiology

Acute inflammation affects the process of gaseous exchange by affecting the lungs’ gas exchange surface as well as the alveolar-capillary membrane [1]. A direct pulmonary or indirect extra-pulmonary insult could be the other physiological processes associated with the disease, as these may cause the proliferation of inflammatory mediators. Some elements of the blood may pass into the tissues as a result of perspiration. As a result, some mediators are secreted by the Alveolar macrophages that accumulate inflammatory cells in the lung. This results in the inactivation of surfactants leading to the collapse of the alveolar epithelial barrier. Sometimes, there may be gaps in the alveolar epithelial barrier, leading to necrosis of types I and II alveolar cells. There is intravascular coagulation in the alveolar capillaries resulting in microthrombi. These physiological processes give rise to a condition known as pulmonary edema. There is a loss of surfactant, and dead cells or debris are deposited along the alveoli (hyaline membranes), resulting in compromising pulmonary compliance. There is a difficulty in the process of gaseous exchange. Chest radiography may reveal air space opacification or coarse reticular opacification, as shown in Fig. (1).

Fig. (1))

Chest X ray of ARDS patient.

In The Lancet Respiratory Medicine, Giacomo Grasselli and colleagues [2] reported stark similarities between the pulmonary injuries caused by COVID-19 and ARDS. They noticed decreased pulmonary compliance and increased lung weight in the patients of both conditions. There is an increase in the high D-dimer concentrations and mortality due to the lung damage caused by both diseases.

These results indicate that the death in COVID-19 may be caused by pulmonary vascular thrombosis. Further investigations of pulmonary arterial pressure and right-sided heart anatomy and function could also test this hypothesis. The pathophysiological role of the heart–lung interactions is reported to be changed due to the damage caused to the pulmonary circulation, leading to ventricular dysfunction.

Causes of ARDS

The causes of ARDS are not completely known and are being investigated. It has been reported that Direct or Indirect Injuries could possibly cause ARDS. Direct injuries are those which cause bruising of the lungs. The possible causes may be pneumonia or aspiration,injury to the chest or breathing of unwanted gases, including smoke. Indirect injures may include infections caused by viruses as well as bacteria. Other indirect injuries that may lead to ARDS are low blood pressure, injuries that require a blood transfusion, and acute pancreatitis.

Epidemiology

Acute respiratory distress syndrome (ARDS) has been recognized as a major clinical problem worldwide. It was first described by Ashbaugh et al. [1] in 1967 and is reported to be associated with high morbidity and mortality [2-4]. A notable variation has been found in epidemiology and clinical outcomes in different healthcare settings [4]. The occurrence of ARDS may vary from 1 to 79 cases per 100 000 [3]. A less number of cases of ARDS has been reported in Europe as compared to the USA [6], while the number of cases in Brazil ranges from 1.8 to 31 per 100 000 [7, 8].

The survival rate in patients with ARDS is improving gradually [9, 10], but the differences in in-hospital mortality and several observational studies [2-4, 8-11] have remained significant. It can be explained by the variations in risk factors associated with ARDS, differences in diagnostic techniques, ability to diagnose ARDS, and biases involved in the clinics while undergoing trials [12]. A recent study on ARDS involved 459 ICUs in 50 different countries across the globe [13], and all the patients were included in the trial, keeping in mind the Berlin criteria [5]. The diagnosis of these patients under trial was compared with those patients who were diagnosed in the clinics by various physicians. It was found that the incidence of ARDS is far higher in North America, Oceania, and Europe than in South America, Asia, and Africa. In all, 30.0% of the patients with mild, 46.6% with moderate, and 23.4% with severe ARDS were diagnosed as per Berlin criteria. Out of it, 34% of the patients were diagnosed with ARDS at day 1, while 60.2% of the patients were diagnosed only at the end of their stay in ICUs [13]. Many of the patients with ARDS were not treated well [14-16], and optimal mechanical ventilation was less utilized. 82% of the patients received less than 12 cm H2O positive end-expiratory pressure (PEEP), while ventilation in more than 35% of the patients was more than 8 mL·kg−1 ideal body weight without measurement of their plateau pressure [17, 18]. In addition, adjunctive treatments were also less utilized (pronation 16%, corticosteroids 23%, recruitment manoeuvres 33% and neuromuscular blockade 38%) [13]. It was witnessed that the severity has been increased in 19% of patients, mortality in hospitals remained 40%, while mortality was worsened with the increase in diving pressure (Pplateau−PEEPextrinsic) and with ARDS severity (46% severe ARDS) [19]. Drug-based preventive strategies remain a major challenge, since two recent trials on aspirin and statins failed to reduce the incidence in atrisk patients. A new disease-modifying therapy is awaited: some recent studies promised to improve the prognosis of ARDS, but mortality and disabling complications are still high in survivors in intensive care [20]. Chest ultrasonography was conducted to check bilateral chest opacities with chest radiographs. The previous pieces of evidence also supported the use of ultrasonography [21].

Risk Factors

ARDS is not considered a disease but a clinical condition. It is usually caused by acute respiratory failure due to pulmonary and non-pulmonary insults. Usually, there is a lack of education about environmental and individual risk factors that may lead to ARDS [3, 22, 23]. This condition is associated with alcoholism as well as smoking [24]. Numerous studies have also pointed out the relation between environmental pollution and disease occurrence. A study was conducted by Ware et al. [25] to investigate the effect of long-term ozone exposure in individuals with risk for ARDS. These individuals resided within 50 km of one of the 163 air quality monitoring stations nearby Nashville (TN, USA). The record about levels of ozone, nitrogen dioxide (NO2), sulfur dioxide, and particles with a 50% cut-off aerodynamic diameter of 10 µm and 2.5 µm was kept daily, and its exposure was estimated on those individuals. The result showed that there is an increased risk of ARDS if the individuals are exposed to ozone exposure (p<0.001). If such individuals have a history of trauma as well assmoking, the risk for ARDS becomes higher in such cases. Although the role of NO2 and other pollutants in causing ARDS was not well-established. This study has some limitations as well since it was associated with a single region and the measurement of the pollutants levels was also difficult, yet the relation between the Incidence of ARDS and air pollution was