Abstract
Acute respiratory distress syndrome (ARDS) is a serious affection of the lung caused by a variety of pathologies. Great interest is currently focused on ARDS induced by viruses (pandemic influenza and corona viruses). The review describes pulmonary changes in ARDS and specific effects of the pandemic viruses in ARDS, and summarizes treatment options. Because the known pathogenic mechanisms cannot explain all aspects of the syndrome, the contribution of pulmonary lymphatics to the pathology is discussed. Organization and function of lymphatics in a healthy lung and in resorption of pulmonary edema are described. A future clinical trial may provide more insight into the role of hyaluronan in ARDS but the development of promising pharmacological treatments is unlikely because drugs play no important role in lymphedema therapy.
Highlights
Respiratory Distress Syndrome: Adult acute respiratory distress syndrome (ARDS) was first described as a noncardiogenic pulmonary edema and is currently defined according to the “Berlin Definition of ARDS” as the acute onset of hypoxia and bilateral pulmonary opacities not fully explained by a cardiac cause [1]
Lung tissue of infants is less prone to inflammation and fibrosis and the relative amount of endogenous surfactant is higher in children than in adults, inflammation, cellular damage, and surfactant dysfunction occur in a similar way as in adults [2]
Characteristics of SARS-CoV-2-induced ARDS in contrast to ARDS caused by other pathologies were listed as follows: patients display little breathlessness despite marked hypoxemia; lung compliance is well preserved; hypoxemia is associated with large intrapulmonary shunt; and the benefit of prone ventilation is larger than for typical ARDS [31]
Summary
Respiratory Distress Syndrome: Adult acute respiratory distress syndrome (ARDS) was first described as a noncardiogenic pulmonary edema and is currently defined according to the “Berlin Definition of ARDS” as the acute onset of hypoxia and bilateral pulmonary opacities not fully explained by a cardiac cause [1]. Despite the similarities to adult ARDS, the Pediatric Acute Lung Injury Consensus Conference (PALICC) published, in 2015, a pediatric-specific definition for ARDS [3]. Affections of the lung (pneumonia, aspiration, and pulmonary contusion) cause direct ARDS, extrapulmonary (systemic) diseases (non-pulmonary sepsis, non-thoracic trauma, and transfusion) indirect ARDS. The majority of ARDS cases are caused by severe pneumonia (30–50%), sepsis (25–30%), and severe trauma 10–25%. Neonatal ARDS is due to immaturity of the lung, and standard treatment consists of the administration of an exogenous surfactant. In contrast to neonate ARDS, there is no standardized pharmacological treatment for adult ARDS. The large LUNGSAFE study, published in 2016, reported mortality of 40%, highlighting the need for better treatments [5]. The role of pulmonary lymphatic vessels will be discussed as an additional parameter in ARDS by describing the architecture and function of the pulmonary lymphatic system
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