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1.
Ann Thorac Surg ; 112(4): e265-e266, 2021 10.
Article in English | MEDLINE | ID: covidwho-1056318

ABSTRACT

Tension pneumomediastinum is a rare but life-threatening cause of tamponade. Mechanical ventilation is a described source of tension pneumomediastinum. Here, we present a case of a 72-year-old man who developed cardiovascular collapse from tension pneumomediastinum in the setting of coronavirus disease 2019-related acute respiratory distress syndrome. We successfully performed bedside mediastinotomy and mediastinal tube placement under local anesthetic to alleviate his hemodynamic instability. Bedside mediastinotomy can be used to relieve tension pneumomediastinum in this setting.


Subject(s)
COVID-19/complications , Cardiac Tamponade/etiology , Mediastinal Emphysema/surgery , Mediastinum/surgery , SARS-CoV-2 , Aged , Humans , Male , Mediastinal Emphysema/complications , Mediastinal Emphysema/diagnostic imaging
2.
Mediators Inflamm ; 2021: 8874339, 2021.
Article in English | MEDLINE | ID: covidwho-1045644

ABSTRACT

Causes of mortality from COVID-19 include respiratory failure, heart failure, and sepsis/multiorgan failure. TLR4 is an innate immune receptor on the cell surface that recognizes pathogen-associated molecular patterns (PAMPs) including viral proteins and triggers the production of type I interferons and proinflammatory cytokines to combat infection. It is expressed on both immune cells and tissue-resident cells. ACE2, the reported entry receptor for SARS-CoV-2, is only present on ~1-2% of the cells in the lungs or has a low pulmonary expression, and recently, the spike protein has been proposed to have the strongest protein-protein interaction with TLR4. Here, we review and connect evidence for SARS-CoV-1 and SARS-CoV-2 having direct and indirect binding to TLR4, together with other viral precedents, which when combined shed light on the COVID-19 pathophysiological puzzle. We propose a model in which the SARS-CoV-2 spike glycoprotein binds TLR4 and activates TLR4 signalling to increase cell surface expression of ACE2 facilitating entry. SARS-CoV-2 also destroys the type II alveolar cells that secrete pulmonary surfactants, which normally decrease the air/tissue surface tension and block TLR4 in the lungs thus promoting ARDS and inflammation. Furthermore, SARS-CoV-2-induced myocarditis and multiple-organ injury may be due to TLR4 activation, aberrant TLR4 signalling, and hyperinflammation in COVID-19 patients. Therefore, TLR4 contributes significantly to the pathogenesis of SARS-CoV-2, and its overactivation causes a prolonged or excessive innate immune response. TLR4 appears to be a promising therapeutic target in COVID-19, and since TLR4 antagonists have been previously trialled in sepsis and in other antiviral contexts, we propose the clinical trial testing of TLR4 antagonists in the treatment of severe COVID-19. Also, ongoing clinical trials of pulmonary surfactants in COVID-19 hold promise since they also block TLR4.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/immunology , Gene Expression Regulation , SARS Virus , SARS-CoV-2 , Toll-Like Receptor 4/metabolism , Antiviral Agents/therapeutic use , Cell Proliferation , Humans , Immunity, Innate , Inflammation , Interferon Type I/metabolism , Lung/metabolism , Myocardium/metabolism , Protein Binding , Signal Transduction , Spike Glycoprotein, Coronavirus/metabolism , Surface-Active Agents
3.
Br J Pharmacol ; 177(21): 4975-4989, 2020 11.
Article in English | MEDLINE | ID: covidwho-998827

ABSTRACT

BACKGROUND AND PURPOSE: Resurgence in the use of chloroquine as a potential treatment for COVID-19 has seen recent cases of fatal toxicity due to unintentional overdoses. Protocols for the management of poisoning recommend diazepam, although there are uncertainties in its pharmacology and efficacy in this context. The aim was to assess the effects of diazepam in experimental models of chloroquine cardiotoxicity. EXPERIMENTAL APPROACH: In vitro experiments involved cardiac tissues isolated from rats and incubated with chloroquine alone or in combination with diazepam. In vivo models of toxicity involved chloroquine administered intravenously to pentobarbitone-anaesthetised rats and rabbits. Randomised, controlled treatment studies in rats assessed diazepam, clonazepam and Ro5-4864 administered: (i) prior, (ii) during and (iii) after chloroquine and the effects of diazepam: (iv) at high dose, (v) in urethane-anaesthetised rats and (vi) co-administered with adrenaline. KEY RESULTS: Chloroquine decreased the developed tension of left atria, prolonged the effective refractory period of atria, ventricular tissue and right papillary muscles, and caused dose-dependent impairment of haemodynamic and electrocardiographic parameters. Cardiac arrhythmias indicated impairment of atrioventricular conduction. Studies (i), (ii) and (v) showed no differences between treatments and control. Diazepam increased heart rate in study (iv) and as with clonazepam also prolonged the QTc interval in study (iii). Combined administration of diazepam and adrenaline in study (vi) improved cardiac contractility but caused hypokalaemia. CONCLUSION AND IMPLICATIONS: Neither diazepam nor other ligands for benzodiazepine binding sites protect against or attenuate chloroquine cardiotoxicity. However, diazepam may augment the effects of positive inotropes in reducing chloroquine cardiotoxicity. LINKED ARTICLES: This article is part of a themed issue on The Pharmacology of COVID-19. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.21/issuetoc.


Subject(s)
Arrhythmias, Cardiac/chemically induced , Cardiotoxicity/etiology , Chloroquine/poisoning , Diazepam/pharmacology , Animals , Arrhythmias, Cardiac/prevention & control , Benzodiazepinones/pharmacology , COVID-19 , Cardiotoxicity/prevention & control , Clonazepam/pharmacology , Coronavirus Infections/drug therapy , Diazepam/administration & dosage , Dose-Response Relationship, Drug , Drug Overdose , Electrocardiography , Female , Hypokalemia/chemically induced , Male , Pandemics , Pneumonia, Viral/drug therapy , Rabbits , Random Allocation , Rats , Rats, Wistar
4.
3D Print Med ; 6(1): 27, 2020 Sep 29.
Article in English | MEDLINE | ID: covidwho-802427

ABSTRACT

PURPOSE: Many commonly used mask designs are secured by elastic straps looping around the posterior auricular region. This constant pressure and friction against the skin may contribute to increased wearer pain, irritation, and discomfort. The purpose of this work is to report a modified 3D printed mask extender to alleviate discomfort and increase mask wearability by relieving posterior auricular pressure from isolation masks. METHODS: Our institutional review board designated this project as non-human research and exempt. As part of resourcing 3D printing laboratories along with individual 3D printers to provide resources to healthcare workers, mask extenders were printed to relieve posterior auricular pressure from individuals wearing isolation masks. The authors modifed an existing mask extender, increasing its length with accompanying peripheral rungs for isolation mask securement. 3D printing was performed with Ultimaker S5 (Ultimaker B.V.; Geldermalsen, Netherlands) and CR-10 (Creality3D; Shenzhen, China) 3D printers using polylactic acid filaments. The author's modified extended mask extenders were printed and freely delivered to healthcare workers (physicians, nurses, technologists, and other personnel) at the authors' institution. RESULTS: The final mask extender design was printed with the two 3D printers with a maximum 7 straps printed simultaneously on each 3D printer. Mean print times ranges from 105 min for the Ultimaker S5 printer and 150 min for the CR-10. Four hundred seventy-five mask extenders were delivered to healthcare workers at the authors' institution, with the demand far exceeding the available supply. CONCLUSION: We offer a modification of a 3D printed mask extender design that decreases discomfort and increases the wearability of isolation mask designs with ear loops thought to relieve posterior auricular skin pressure and ability to control strap tension. The design is simple, produced with inexpensive material (polylactic acid), and have been well-received by healthcare providers at our institution.

5.
JMIR Med Inform ; 8(9): e20477, 2020 Sep 22.
Article in English | MEDLINE | ID: covidwho-789079

ABSTRACT

BACKGROUND: The widespread death and disruption caused by the COVID-19 pandemic has revealed deficiencies of existing institutions regarding the protection of human health and well-being. Both a lack of accurate and timely data and pervasive misinformation are causing increasing harm and growing tension between data privacy and public health concerns. OBJECTIVE: This aim of this paper is to describe how blockchain, with its distributed trust networks and cryptography-based security, can provide solutions to data-related trust problems. METHODS: Blockchain is being applied in innovative ways that are relevant to the current COVID-19 crisis. We describe examples of the challenges faced by existing technologies to track medical supplies and infected patients and how blockchain technology applications may help in these situations. RESULTS: This exploration of existing and potential applications of blockchain technology for medical care shows how the distributed governance structure and privacy-preserving features of blockchain can be used to create "trustless" systems that can help resolve the tension between maintaining privacy and addressing public health needs in the fight against COVID-19. CONCLUSIONS: Blockchain relies on a distributed, robust, secure, privacy-preserving, and immutable record framework that can positively transform the nature of trust, value sharing, and transactions. A nationally coordinated effort to explore blockchain to address the deficiencies of existing systems and a partnership of academia, researchers, business, and industry are suggested to expedite the adoption of blockchain in health care.

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