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Pathophysiology and Treatment of Acute Respiratory Distress Syndrome
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This entry is adapted from the peer-reviewed paper 10.3390/antiox12112016

Acute respiratory distress syndrome (ARDS) is a life-threatening pulmonary condition characterized by the sudden onset of respiratory failure, pulmonary edema, dysfunction of endothelial and epithelial barriers, and the activation of inflammatory cascades. Despite the increasing number of deaths attributed to ARDS, a comprehensive therapeutic approach for managing patients with ARDS remains elusive. To elucidate the pathological mechanisms underlying ARDS, numerous studies have employed various preclinical models, often utilizing lipopolysaccharide as the ARDS inducer. Accumulating evidence emphasizes the pivotal role of reactive oxygen species (ROS) in the pathophysiology of ARDS. Both preclinical and clinical investigations have asserted the potential of antioxidants in ameliorating ARDS. 

acute respiratory distress syndrome reactive oxygen species antioxidant acute lung injury superoxide dismutase glutathione vitamins

1. Introduction

Acute respiratory distress syndrome (ARDS) imposes a huge burden in the context of critical care medicine, demanding immediate attention and a comprehensive approach due to its life-threatening nature. Initially described in the 1960s by Petty and Ashbaugh [1], ARDS is characterized by the sudden onset of tachypnea, hypoxemia, and reduced lung compliance. The absence of a standardized or precise definition for ARDS has posed limitations in patient treatment and the statistical analysis of clinical outcomes [2]. In response to this challenge, the Berlin definition was introduced in 2012 as a novel diagnostic framework for ARDS [3]. This definition includes criteria such as (I) acute onset within 1 week; (II) bilateral lung infiltrates observable upon chest radiography; (III) the absence of a fully explanatory cause related to cardiac failure or fluid overload; and (IV) the categorization of ARDS severity based on a positive end-expiratory pressure (PEEP) level of at least 5 cm H2O, with lung injury classified into three grades of severity according to the PaO2/FiO2 ratio: mild (201–300 mm Hg), moderate (101–200 mm Hg), and severe (≤100 mm Hg). Historically, acute lung injury (ALI) referred to a milder form of lung injury, while ARDS signified a more severe lung condition [4]. However, the clinical use of the term ALI has been discontinued, and the classification is now based on the severity of ARDS, providing a clear and consistent categorization for clinical purposes.
ARDS can be attributed to various conditions, with trauma, aspiration, pneumonia, and sepsis serving as primary triggers for its development [5][6][7]. Additionally, the inhalation of harmful substances, aspiration of vomit, pancreatitis, blood transfusion, and near-drowning episodes can also induce ARDS. Recent retrospective observational studies have revealed that 67% of patients with severe COVID-19 develop ARDS, further emphasizing its significance as a primary cause of mortality [8]. Presently, ARDS stands as a leading cause of morbidity and mortality, with no effective treatments available [9]. Therefore, there is an urgent need to elucidate the pathogenesis of ARDS and develop innovative treatment strategies.

2. ARDS Incidence and Mortality

The incidence of ARDS varies globally, with data from population-based studies revealing significant diversity [9][10]. A study conducted in the United States from 1999 to 2000 reported an incidence rate of 78.9 per 100,000 person-years [11], while research in Iceland from 1988 to 2010 indicated incidence rates ranging from 3.65 to 9.63 [12]. These findings provide insights into mortality rates and severity distribution among patients with ARDS. In a large international, multicenter, prospective cohort study performed over a period of 4 weeks in 2014, patients with ARDS accounted for 10.4% of the total sample, with the proportions of mild, moderate, and severe cases being 30%, 46.5%, and 23.4%, respectively [13]. The mortality rates, according to severity, were 34.9% for mild, 40.3% for moderate, and 46.1% for severe. Another study conducted in China from March 2016 to February 2018 across 18 intensive care units (ICUs) reported that 3.6% of a total of 18,793 patients were diagnosed with ARDS [14]. Among these patients, 9.7% had mild ARDS, 47.4% exhibited moderate ARDS, and a substantial 42.9% were classified as having severe ARDS, with a reported mortality rate of 46.3%. Systematic research conducted since 2010 has indicated overall in-hospital, ICU, 28/30-day, and 60-day mortality rates of 45%, 38%, 30%, and 32%, respectively [15]. Multiple studies have highlighted the correlation between ARDS severity, high mortality, and prolonged ventilation duration.

3. ARDS Pathophysiology

Under normal physiological conditions, lung fluid balance is maintained through fluid clearance. However, dysfunction of the alveolar barrier can impair alveolar fluid clearance, a prominent hallmark of patients with ARDS, leading to hypoxemia and pulmonary bilateral edema [16][17]. Additionally, ARDS is characterized by an increased production of pro-inflammatory factors and an elevated expression of adhesion molecules, which play a crucial role in the recruitment of leukocytes. Specifically, activated neutrophils contribute to tissue damage by releasing cytotoxic agents, including granular enzymes, pro-inflammatory cytokines, bioactive lipids, and reactive oxygen species (ROS). Typical ARDS symptoms include dyspnea, an increased respiratory rate, tachycardia, and cyanosis. The pattern of injury observed in patients with ARDS is not uniform, and clinical symptoms can vary according to the severity or stage [18]. ARDS can be categorized into discrete stages, each with temporal evolution, pathophysiological alterations, histological features, and clinical implications. These stages encompass three simultaneous phases: exudative, proliferative, and fibrotic [19][20].
The acute phase, referred to as the exudative stage, typically spans from hours to the first week after the injury onset. During this stage, a cascading inflammatory response is activated, leading to an influx of neutrophils [21], a phenomenon that results in the disruption of the alveolar epithelial and endothelial barriers, and consequently, protein-rich edema in the interstitium and alveolar spaces. Hyaline membranes, composed of dead cells, surfactants, and plasma proteins, are also characteristic of diffuse alveolar damage [22]. The subsequent proliferative stage involves an organization and repair process that includes the proliferation of fibroblasts, primarily within the interstitium. In the late proliferative stage, most hyaline membranes are resorbed, although some remnants may persist along the alveolar septa [23]. Early fibrotic changes and thickening of the alveolar capillaries can also be observed. Finally, the fibrotic stage is marked by an increased deposition of collagen and enlarged air spaces, although not all patients progress to this stage. Established fibrosis reduces lung compliance, resulting in increased breathing effort, which is associated with poor lung function and a high risk of mortality [19].
To gain a deeper understanding of the intricate pathophysiology of ARDS and to develop novel therapeutic strategies, researchers have extensively utilized controlled experimental models to mimic clinical syndromes. These models serve as invaluable tools for exploring the mechanisms underlying ARDS and evaluating potential interventions. The workshop report published in 2011 by the American Thoracic Society (ATS) proposed the following four features of ARDS for preclinical models: histological evidence of tissue injury, alterations in the alveolar-capillary barrier, inflammatory response, and physiological dysfunction [24]. Histological evidence of tissue injury includes the infiltration of neutrophils in the alveolus or interstitium, the presence of hyaline membranes, and the accumulation of proteinaceous debris in the alveolus, along with thickening of the alveolar wall. Alveolar-capillary barrier disruption is reflected in increased extravascular lung water content, bronchoalveolar lavage fluid (BALF) protein levels, and microvascular filtration coefficient, and the accumulation of an exogenous tracer. The inflammatory response is characterized by an increase in the number of inflammatory cells in the BALF, lung myeloperoxidase (MPO) activity, BALF protein concentration, and pro-inflammatory cytokines in the lung or BALF. Lastly, physiological dysfunction comprises hypoxemia and an increased alveolar-arterial oxygen difference. To ensure ARDS in preclinical models, at least three of these four criteria should be fulfilled.
ARDS models have been generated through both direct and indirect methods to recapitulate human ARDS. The direct approach involves the stimulation of conditions such as pneumonia and acid aspiration, while the indirect approach involves the stimulation of pancreatitis and non-pulmonary sepsis. In direct models, ARDS is induced through the intranasal or intratracheal administration of agents such as lipopolysaccharides (LPS), HCl, bleomycin, bacteria, and viruses. Hyperoxia is also a direct cause of ARDS. In contrast, indirect lung injury can be induced via the intravenous injection of LPS, cecal ligation and puncture (CLP) to induce sepsis, hemorrhagic shock, mesenteric ischemia, and reperfusion.

3.1. LPS-Induced Sepsis Model

The most frequently utilized ARDS model involves the instillation of LPS via either the intratracheal or intranasal routes. Research has also explored variations based on species, age, sex, and LPS concentrations. In the LPS-induced ARDS model, several key observations include a reduced PaO2/FiO2 ratio, increased total protein concentration in the BALF, infiltration of inflammatory cells, disruption of alveolar barrier function, and excessive generation of ROS and oxidative stress [25][26][27]. These changes are often accompanied by local hemorrhage and edema [28]. However, the limitations of this model include the fact that alveolar and interstitial edema is mild, hyaline membrane formation is absent, and the decrease in PaO2 is not sustained for an extended period [29]. These limitations can be mitigated by employing a two-hit approach involving LPS stimulation, where both intratracheal LPS and intravenous LPS are administered [29]. This two-hit model involves the intraperitoneal injection of a small dose of LPS (1 mg/kg), followed by tracheal instillation with a moderate dose of LPS (5 mg/kg). In this model, the decrease in PaO2 is sustained for more than 72 h and induces more pronounced hyaline membrane formation and edema. Additionally, several studies have reported that the intraperitoneal injection of LPS can lead to lung injury [30][31].

3.2. Acid Aspiration Model

In the clinical setting, the aspiration of gastric contents is a major contributor to ARDS. Given the role of pH in lung injury, hydrochloric acid (HCl) has been employed to mimic human ARDS. The orotracheal and intratracheal instillation of HCl leads to reduced oxygenation, increased respiratory elastance, and pulmonary inflammation [32]. Furthermore, HCl aspiration induces histological changes, lung edema, and inflammatory responses in rabbits [33].

3.3. Oleic Acid Injection Model

The intravenous injection of oleic acid induces ARDS characterized by intra-alveolar edema and an increased infiltration of inflammatory cells [34][35]. An advantage of the oleic acid method is the rapid and reversible development of sparse inflammatory lung injury [36]. In research involving pigs, the administration of oleic acid resulted in a high mortality rate and extensive histological changes, as well as elevated levels of IL6 and IL8 [37]. Additionally, the intratracheal injection of oleic acid, employed in a mouse ARDS model, resulted in elevated neutrophil and protein levels in the BALF, the activation of leukocytes, and the production of inflammatory mediators [38].

3.4. CLP-Induced Sepsis Model

CLP is a method commonly utilized to induce sepsis in models [39]. In brief, in this method, the cecum is ligated, punctured with a needle, and compressed to expel a small amount of feces [39]. The severity of the injury can vary depending on factors such as the percentage of ceca ligated, the number of punctures, and the size of the needle used. Puncturing the cecum, which contains bacteria, leads to bacterial peritonitis and the translocation of bacteria into the bloodstream, ultimately resulting in septic shock. CLP mice exhibit high mortality and histopathological changes associated with ARDS, including the destruction of the alveolar structure, thickening of the pulmonary septa, hemorrhaged lung tissue, and the infiltration of inflammatory cells [40][41].

4. Treatment

The primary goal of managing ARDS is to improve blood oxygen levels. Despite administering high levels of inspired oxygen, oxygen saturation often remains inadequately low, underscoring the severity of impaired gas exchange or the failure to respond to conventional respiratory therapy in patients with ARDS. Furthermore, due to the diversity of ARDS causes and the complexity of the syndrome, there is currently no single therapy tailored specifically to ARDS. Additionally, a decline in the quality of life is frequently observed even after recovering from ARDS.
Various professional societies, including the Faculty of Intensive Care Medicine and Intensive Care Society [42], The French Society of Intensive Card Medicine (Société de Réanimation de Langue Française) [43], The ATS, the European Society of Intensive Care Medicine [44], the Korean Society of Critical Care Medicine and Korean Academy of Tuberculosis and Lung Diseases of South Korea [45], the Society of Critical Care Medicine, and the World Health Organization, offer recommendations for managing ARDS, taking into account the patient’s condition. These guidelines have been thoroughly documented in review papers [46][47] and propose various management strategies for patients with ARDS; these strategies can be categorized into two main groups: (1) ventilation strategies, including non-invasive ventilation, low tidal volume ventilation (LTVV), high positive end-expiratory pressure (PEEP) strategies, recruitment maneuvers, and high-frequency oscillatory ventilation, and (2) non-ventilation strategies, including interventions such as neuromuscular blockade, inhaled vasodilators, corticosteroids, and other pharmacological agents [47][48].
Mechanical lung ventilation is a standard therapeutic approach used to enhance oxygenation in patients with ARDS. However, it can also lead to ventilation-induced lung injury (VILI) [49][50]. VILI manifests as clinical symptoms such as shallow breathing, respiratory distress, and cyanosis, as well as chest X-ray findings indicating bilateral lung infiltrates, reduced blood oxygen levels (hypoxemia), and impaired lung elasticity, among other pulmonary functional impairments. Minimizing VILI through mechanical ventilation and effectively managing refractory hypoxemia are critical aspects of supportive ARDS management.
VILI is characterized by four primary mechanisms: volutrauma, barotrauma, atelectrauma, and biotrauma [49]. Volutrauma is closely linked to the use of high tidal volumes during mechanical ventilation. When mechanical ventilation is applied with a typical tidal volume without considering collapsed lung regions, it can result in the overdistension of lung cells, ultimately leading to increased alveolar-capillary permeability and alveolar destruction, culminating in pulmonary edema. Barotrauma arises from high airway pressure during positive pressure ventilation, causing lung damage through overinflation and the rupture of lung cells. The repeated opening and closing of lung cells contributes to increased lung size and shear stress forces, resulting in lung injury and surfactant dysfunction, known as atelectrauma. Biotrauma refers to the biochemical processes that occur when mechanical forces cause the collapse of lung cell membranes, triggering an inflammatory response. This can lead to systemic inflammatory response syndrome and multiple organ failure, ultimately resulting in death. Importantly, these four mechanisms are interconnected and can mutually influence each other. Various lung-protective ventilation methods are employed to minimize VILI.

4.1. Low Tidal Volume Ventilation

Patients with ARDS often exhibit reduced lung volume due to edema and inflammation, colloquially referred to as the “baby lung”. Consequently, traditional tidal volume ventilation (10 mL/kg or more) can lead to lung overdistension in patients with ARDS. LTVV is a technique that involves reducing the tidal volume, a strategy commonly used in individuals with healthy lungs to prevent lung tissue overdistension [17]. In 1998, Amato et al. first reported the potential clinical benefits of LTVV in patients with ARDS [51]. An extensive ARDS Network study involving 861 patients demonstrated that LTVV (6 mL/kg of predicted body weight) reduced mortality from 39.8% to 31% compared to traditional tidal volume ventilation (12 mL/kg of predicted body weight) and also increased the number of ventilator-free days [52]. Recent research suggests that the effects of mechanical ventilation can be enhanced with different tidal volumes (depending on lung compliance), with patients exhibiting low respiratory system compliance being more vulnerable to damage at higher driving pressures [53]. Furthermore, patients with COVID-19 receiving LTVV have shown reduced 28-day mortality [54].

4.2. Positive End-Expiratory Pressure

PEEP involves maintaining a pressure higher than atmospheric pressure at the end of expiration, which helps prevent atelectrauma and corrects hypoxemia resulting from alveolar hypoventilation [55]. Physiologically, PEEP increases functional residual capacity, recruits collapsed alveoli, and redistributes fluid to the interstitial space to improve oxygenation [56]. These physiological effects are expected to reduce VILI. However, it has been reported to have side effects, including a decrease in cardiac output and the potential for barotrauma. Studies on the effectiveness of high levels of PEEP in patients with ARDS have yielded inconsistent results. Some meta-analyses suggest that higher PEEP can enhance oxygenation during the first and third days of ventilation [57]. However, other meta-analyses have indicated that there is no significant difference in the 28-day mortality between high- and low-PEEP groups [58][59]. Additional studies are needed to accurately determine the impact and outcomes of PEEP application in patients with ARDS.

4.3. Lung Recruitment Maneuvers (LRMs)

LRMs are strategies designed to transiently increase the driving pressure to facilitate the recruitment of collapsed alveoli. This recruitment process improves oxygenation, promotes uniform volume distribution in the lungs, and mitigates the risk of overdistension [60]. Sustained inflation is employed at pressures ranging from 35 to 50 cm H2O for 20 to 40 s, with continuous monitoring for any adverse effects [61][62]. The use of LRMs in the treatment of ARDS remains a subject of debate. A meta-analysis that included data from 10 trials involving 1658 patients indicated that the implementation of LRMs in patients with ARDS led to reduced ICU mortality [63]. However, this study had limitations, primarily due to co-interventions with other mechanical ventilation strategies. Conversely, a more recent study with 10 trials involving 3025 patients suggested that LRMs did not affect the mortality of patients with ARDS, only reducing the duration of hospital stay [64]. Further research is necessary to clarify the precise impact and potential benefits of the isolated application of LRMs on the overall management and outcomes of patients with ARDS.

4.4. Prone Position

The prone position is commonly employed to facilitate breathing in ventilated patients. It involves turning the patient from the supine (back) position to the prone (face down) position to improve oxygenation. ARDS patients in the supine position are affected by the weight of the heart and abdominal organs, leading to increased pleural pressure in the dorsal lung regions, resulting in lung collapse. In such cases, the leveraging of the prone position can help redistribute blood and airflow more evenly [65][66]. The Prone Positioning in Severe ARDS (PROSEVA) study in 2013 demonstrated that employing the prone position during ventilation reduced both the 28- and 90-day mortality rates [67]. A meta-analysis of eight randomized controlled trials (RCTs) involving 2129 patients conducted by Munshi et al. suggested that employing the prone position for more than 12 h daily is likely to reduce mortality among patients with severe ARDS [68]. Furthermore, the PaO2/FiO2 ratio was significantly higher in the prone position group on day 4. A recent meta-analysis also indicated that prone positioning during venovenous extracorporeal membrane oxygenation improved survival [69][70]. Nevertheless, PEEP in the prone position is approached with caution due to potential adverse effects, including endotracheal tube obstruction, pressure sores, and facial edema [71].

4.5. Corticosteroids

Corticosteroids are potent anti-inflammatory and immunomodulatory drugs commonly employed to treat various inflammatory diseases, including asthma, allergic rhinitis, chronic obstructive pulmonary disease (COPD), and pneumonia [72]. The use of corticosteroids in patients with ARDS has yielded varying results. A meta-analysis of corticosteroid use in ARDS encompassing seven RCTs involving 851 patients indicated that corticosteroids reduced mortality and the duration of mechanical ventilation while increasing the number of ventilator-free days [73]. Furthermore, another meta-analysis demonstrated that patients with ARDS, both with COVID-19 and non-COVID-19 cases, exhibited reduced mortality and decreased mechanical ventilation duration when treated with corticosteroids [74]. However, a separate meta-analysis found that corticosteroids reduced mortality in non-COVID-19 patients with ARDS but had no effect in the COVID-19 subgroup [75]. It is important to exercise caution when using corticosteroids, as they may be associated with a higher mortality rate or the development of hyperglycemia [73][76].

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Subjects: Biology
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Eun Yeong Lim
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So-Young Lee
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Hee Soon Shin
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Gun-Dong Kim
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Update Date: 13 Dec 2023
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