Lung Injury in COVID-19—An Emerging Hypothesis

Alharthy, Abdulrahman; Faqihi, Fahad; Memish, Ziad A.; Karakitsos, Dimitrios

doi:10.1021/acschemneuro.0c00422

Cited by 31 publications

(26 citation statements)

References 33 publications

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“…Also, the fact that SARS-CoV-2 can bind to the ACE-2 receptors that are expressed on type II pneumocytes and vascular endothelial cells within the lung could reflect direct injury to the pulmonary vasculature [ 13 ]. This vascular pathology along with the parenchymal lung injury (“dual-hit” underlying mechanism) could be at least partially responsible for the refractory ARDS observed in critically ill patients with COVID-19 [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

A Retrospective Analysis of Thromboembolic Phenomena in Mechanically Ventilated Patients with COVID-19

Faqihi

Alharthy

Balhamar

et al. 2021

Critical Care Research and Practice

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Background. Recent studies have shown an increased prevalence of thromboembolic disease in critically ill patients with the novel SARS-CoV-2 disease (COVID-19). However, the use of enhanced anticoagulation therapy in these patients remains controversial. Objectives. To determine the incidence of thromboembolic phenomena (TEP) and hemorrhagic events (HEs) in intensive care unit (ICU) COVID-19 patients. Methods. One hundred and sixty ICU patients with COVID-19 were enrolled. Clinical examination results, laboratory data, and imaging studies (computed tomography/Doppler ultrasound scans) for these patients were retrospectively collected and analyzed. Outcome measures including days on mechanical ventilation, ICU length of stay, and day-28 mortality were recorded. Results. Sixty patients (37.5%) developed TEP including thirty patients with deep vein thrombosis, 55 patients with pulmonary embolism, and 7 patients with arterial thromboembolism. Cardiac arrhythmias, lymphocytopenia, and increased D-dimers were more frequently observed in the TEP group compared to the non-TEP group of patients (all p < 0.05 ). The sensitivity, specificity, and positive and negative predictive values of a cutoff D-dimer level of 3.0 μg/mL for predicting PE were 74.5%, 95.1%, 86.8%, and 91.9%, respectively. Thirteen patients experienced HEs, which were more frequently observed in the TEP group ( p < 0.05 ). Twenty-eight-day mortality was higher in the TEP group (60%) compared to the non-TEP group (30%) of patients ( p = 0.02 ). Conclusions. The rates of TEP and HEs in mechanically ventilated critically ill COVID-19 patients were 37. 5% and 8.1%. Twenty-eight-day mortality was higher in the TEP group (60%) compared to the non-TEP group (30%) of patients.

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Section: Discussionmentioning

confidence: 99%

A Retrospective Analysis of Thromboembolic Phenomena in Mechanically Ventilated Patients with COVID-19

Faqihi

Alharthy

Balhamar

et al. 2021

Critical Care Research and Practice

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“…The pathophysiology of COVID-19-induced lung disease with the development of air leak has not been discussed. It is plausible that direct viral infiltration of the lung parenchyma and visceral and parietal pleura caused disruption of parenchymal and pleural integrity or ruptured alveoli leading to subsequent air leak, called the Macklin effect [ 1 , 2 ]. A cytokine release syndrome (CRS) or overexaggerated immune response could trigger parenchyma and microvascular inflammation with microthrombosis and hypercoagulable states.…”

Section: Discussionmentioning

confidence: 99%

“…A cytokine release syndrome (CRS) or overexaggerated immune response could trigger parenchyma and microvascular inflammation with microthrombosis and hypercoagulable states. We suspect that a substantial increase in inflammatory response along with direct viral invasion of the pleura and provoking thromboembolic phenomena are the three major mechanisms or triple hit for the development of air leak [ 1 ]. Hence, pneumomediastinum and/or pneumothorax are associated with poor prognoses given the significant inflammatory cascade and viral destruction of lung architecture.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, our study was performed at a single institution and may not be generalizable to the entire population. Further studies are needed to identify the incidence of air leak in patients with COVID-19 disease as this may suggest a worse overall prognosis [ 1 , 6 ].…”

Section: Discussionmentioning

confidence: 99%

“…An interesting complication that has been reported in COVID-19 hospitalized patients is that of spontaneous pneumomediastinum and/or pneumothorax. Majority of the literature has cited high rates of patients on mechanical ventilation with such complications, and it has been theorized that the likely cause is from barotrauma during mechanical ventilation [ 1 – 3 ].…”

Section: Introductionmentioning

confidence: 99%

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Pneumothorax and Pneumomediastinum Secondary to COVID-19 Disease Unrelated to Mechanical Ventilation

Tucker

Patel

Vatsis

et al. 2020

Case Reports in Critical Care

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In the recent worldwide coronavirus 2019 pandemic, a notable rise in pneumomediastinum and pneumothorax complications has been witnessed in numerous mechanically ventilated patients infected with severe acute respiratory syndrome coronavirus 2. Most cases have reported these complications as barotrauma from mechanical ventilation with COVID-19 disease. We aim to report three polymerase chain reaction-confirmed COVID-19 patients who developed pneumomediastinum and pneumothorax unrelated to mechanical ventilation. We originally analyzed 800 patients with COVID-19 disease at Orlando Regional Medical Center from March 1, 2020, to July 31, 2020, of which 12 patients developed pneumomediastinum and pneumothorax in their hospital course. Interestingly, three patients developed pneumomediastinum on chest imaging prior to intubation. We present these three patients, one female and two males, ages of 42, 64, and 65, respectively, who were diagnosed with COVID-19 disease through nasopharyngeal sampling tests with acute respiratory distress syndrome. Spontaneous pneumomediastinum and pneumothorax are potential complications of COVID-19 disease in the lungs unrelated to mechanical ventilation. This is similar to previous outbreaks of severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) diseases. Further investigation is needed to define the causality of pneumomediastinum in nonintubated COVID-19 patients to define the incidence of disease.

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Residual Lung Injury in Patients Recovering From COVID‐19 Critical Illness

Alharthy

Abuhamdah

Balhamar

et al. 2020

J of Ultrasound Medicine

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Scarce data exist regarding the natural history of lung lesions detected on ultrasound in those who survive severe COVID-19 pneumonia.Objective-We performed a prospective analysis of point-of-care ultrasound (POCUS) findings in critically ill COVID-19 patients during and after hospitalization.Methods-We enrolled 171 COVID-19 intensive care unit patients. POCUS of the lungs was performed with phased array (2-4 MHz), convex (2-6 MHz) and linear (10-15 MHz) transducers, scanning 12 lung areas. Chest computed tomography angiography was performed to exclude suspected pulmonary embolism. Survivors were clinically and sonographically evaluated during a 4 month period for evidence of residual lung injury. Chest computed tomography angiography and echocardiography were used to exclude pulmonary hypertension (PH) and chest high-resolution-computedtomography to exclude interstitial lung disease (ILD) in symptomatic survivors.Results-Cox regression analysis showed that lymphocytopenia (hazard ratio [HR]: 0.88, 95% confidence intervals [CI]: 0.68-0.96, p = .048), increased lactate (HR: 1.17, 95% CI: 0.94-1.46, p = 0.049), and D-dimers (HR: 1.21, 95% CI: 1.03-1.44, p = .03) were mortality predictors. Non-survivors had increased incidence of pulmonary abnormalities (B-lines, pleural line irregularities, and consolidations) compared to survivors (p < .05). During follow-up, POCUS with clinical and laboratory parameters integrated in the semi-quantitative Riyadh-Residual-Lung-Injury scale had sensitivity of 0.82 (95% CI: 0.76-0.89) and specificity of 0.91 (95% CI: 0.94-0.95) in predicting ILD. The prevalence of PH and ILD (non-specific-interstitial-pneumonia) was 7% and 11.8%, respectively. Conclusion-POCUSshowed ability to monitor the evolution of severe COVID-19 pneumonia after hospital discharge, supporting its integration in clinical predictive models of residual lung injury.

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Lung Injury in COVID-19—An Emerging Hypothesis

Cited by 31 publications

References 33 publications

A Retrospective Analysis of Thromboembolic Phenomena in Mechanically Ventilated Patients with COVID-19

A Retrospective Analysis of Thromboembolic Phenomena in Mechanically Ventilated Patients with COVID-19

Pneumothorax and Pneumomediastinum Secondary to COVID-19 Disease Unrelated to Mechanical Ventilation

Residual Lung Injury in Patients Recovering From COVID‐19 Critical Illness

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