Structural Alterations of Lung Parenchyma in the Adult Respiratory Distress Syndrome

Bachofen, M; Weibel, Ewald R.

doi:10.1016/s0272-5231(21)00143-x

Cited by 509 publications

(77 citation statements)

References 14 publications

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“…[74][75][76] Some of these insults cause epithelial apoptosis or necrosis, whereas others disrupt intercellular junctions, which increase epithelial permeability. 75,77,78 Circulating factors (eg, DAMPs or cell-free haemoglobin) and microbial products, toxins, and circulating immune cells and inflammatory mediators can damage the epithelium. 56,57,79…”

Section: Alveolar Epithelial Injury Permeability and Dysfunctionmentioning

confidence: 99%

Acute respiratory distress syndrome

2021

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Acute respiratory distress syndrome (ARDS) is an acute respiratory illness characterised by bilateral chest radiographical opacities with severe hypoxaemia due to non-cardiogenic pulmonary oedema. The COVID-19 pandemic has caused an increase in ARDS and highlighted challenges associated with this syndrome, including its unacceptably high mortality and the lack of effective pharmacotherapy. In this Seminar, we summarise current knowledge regarding ARDS epidemiology and risk factors, differential diagnosis, and evidence-based clinical management of both mechanical ventilation and supportive care, and discuss areas of controversy and ongoing research. Although the Seminar focuses on ARDS due to any cause, we also consider commonalities and distinctions of COVID-19-associated ARDS compared with ARDS from other causes.

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Section: Alveolar Epithelial Injury Permeability and Dysfunctionmentioning

confidence: 99%

Acute respiratory distress syndrome

2021

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“…It has been known for several decades that extravascular fibrin deposition promotes lung dysfunction and the acute inflammatory response in diverse forms of ALI [204]. Within 3 days of disease onset, disordered coagulation (increased procoagulant activity) and fibrinolysis (decreased) promote extravascular fibrin deposition manifesting as alveolar fibrin deposition and intravascular thrombosis or disseminated intravascular coagulation.…”

Section: Microthrombosis and A Role For Anticoagulants And Thrombolysis With Or Without Surfactant As Treatment Agents In Covid-19 And VImentioning

confidence: 99%

An overview of acute lung injury in general and in particular viral infections with specific reference to nebulized surfactant and anticoagulation

Smith¹,

Coetzee²,

Zyl³

2020

J Respir Dis Med

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The coronavirus 2 (SARS-CoV-2) has resulted in an international pandemic. The SARS-CoV-2 affects cardiovascular, digestive and urogenital systems. In an attempt to develop a multimodal and targeted approach to the pathophysiology associated with viral lung injury, we reviewed lung histopathology, inflammation, surfactant biology and pathophysiology related to viral associated acute lung injury (ALI / ARDS). Histopathology of viral pneumonia/ARDS cases of the past 100 years has revealed that lung parenchymal and vascular pathologic changes described in the 1918 influenza pandemic, are no different from the histopathology observed in other viral pandemics. Given the inflammatory storm which can occur in COVID-19 infection, the patient is a candidate to develop the classic multi-organ dysfunction and / or failure (MOD/F) which may well include ALI and ARDS. Because there is a well described temporal change in the pathophysiology associated with ALI /ARDS, a "one size fit al" remedy will not suffice, hence our attempt at a targeted functional approach. For instance, variable results in adults treated with surfactant have relegated the use of surfactant in adult ARDS to an uncertainty. We speculate that early and repeated surfactant installation in adults is required in adults. Surfactant may also have beneficial effects on the inflammatory process in the ARDS lung. The increased clotting tendency associated with the inflammation (and ARDS), particularly the effect on the lung vasculature (acute pulmonary hypertension and increased dead space), causes mechanical pressure overload (and failure) of the right ventricle and mechanical respiratory failure. Active management of these should include inhibition of the accelerated coagulation and thrombolysis (via nebulization) and early inotropic support.

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“…In humans, the histological appearance can be divided into three interrelated and overlapping phases 15,16 . The first exudative phase is marked by alveolar and interstitial inflammation, oedema and hyaline membrane formation 17,18 . Later, a proliferative phase predominated by organisation and repair 16 with proliferation of type II epithelial cells increases the volume of the interstitium 18 .…”

Section: Introductionmentioning

confidence: 99%

Acute interstitial pneumonia in foals: A severe, multifactorial syndrome with lung tissue recovery in surviving foals

Punsmann¹,

Hoppe

Klopfleisch

et al. 2020

Equine Veterinary Journal

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Background Acute interstitial pneumonia in foals has been sparsely described in literature, and the individual authors disagree on the underlying aetiology. Histopathological follow‐up from surviving foals is not available. Objectives Description of clinical and histopathological findings in the course of acute interstitial pneumonia and in recovery. Investigating the aetiology and possible triggering factors of acute interstitial pneumonia. Study design Case series. Methods Post‐mortem examination of nine affected foals; seven died during the acute phase, and two had recovered from acute interstitial pneumonia. Data from clinical examinations on the day of death were recorded for all foals. Complete necropsy, special histological staining, virological and microbiological examinations were performed. Results Seven foals died during the acute phase with severe respiratory distress, fever and increased numbers of comet tail artefacts in lung ultrasound. In post‐mortem examination, a wide variety of possible triggering factors was identified. Microbiology revealed Escherichia coli, Rhodococcus equi and Klebsiella pneumoniae as the most common bacterial pathogens. Equine herpesvirus 2 was detected in all foals by PCR. Those with high viral loads also displayed histopathological changes suggestive of viral infections. Pneumocystis carinii was detected in all acutely affected foals. Histopathological changes in lung parenchyma clearly differed between the foals that had recovered from acute interstitial pneumonia and those dying in the acute phase. While lungs in acute phase featured marked parenchymal collapse and necrosis, the recovered foals revealed nearly normal ventilated lung parenchyma and alveolar structure. Main limitations Small number of cases. Because all foals are from the same breeding farm with endemic occurrence of pathogens, it is not certain whether the results of this study can be transferred to other foals without restrictions. Conclusions Acute interstitial pneumonia seems to be based on a multifactorial aetiology. Lungs from foals that have survived acute interstitial pneumonia appear to be able to regenerate completely, leaving no permanent changes.

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Structural Alterations of Lung Parenchyma in the Adult Respiratory Distress Syndrome

Cited by 509 publications

References 14 publications

Acute respiratory distress syndrome

Acute respiratory distress syndrome

An overview of acute lung injury in general and in particular viral infections with specific reference to nebulized surfactant and anticoagulation

Acute interstitial pneumonia in foals: A severe, multifactorial syndrome with lung tissue recovery in surviving foals

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