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Multiple observational studies have described the similarities between COVID-19 pneumonia and organizing pneumonia (OP). These two entities clinically manifest with mild and subacute respiratory symptoms, often with a delayed diagnosis due to the atypical ARDS and silent hypoxemia presentation. Radiological features are often indistinguishable between the two. With the increase in antemortem lung biopsies and autopsies being performed, more histopathological findings of OP and its variant, acute fibrinous and organizing pneumonia (AFOP), are being diagnosed. These entities are known complications of viral infections as a delayed immunological process, explaining the favorable response to corticosteroids. Clinicians should be vigilant to diagnose this under-recognized entity of secondary OP in people with COVID-19 when clinical deterioration occurs, especially with compatible radiologic findings and recent cessation of corticosteroids. Despite the proven benefits of corticosteroids in treating COVID-19, treatment approaches can be more effective as OP often requires higher doses and a more prolonged therapy duration for remission and preventing relapses. The purpose of our narrative review is to compare the similarities between COVID-19 pneumonia and OP, emphasizing the clinical, radiological, and histopathological features based on the evidence available in the literature.

Introduction Calcium channel blockers (CCBs) are a potent class of medications that exert its action by blocking ‘L-type’ calcium channels. CCB overdose can be fatal even with appropriate and aggressive therapy. Death ensues from heart block, myocardial suppression, vasoplegia, and shock. Early use of methylene blue (MB) might provide additional means to improve outcomes. Case presentation A 25-year-old female presented after an attempted suicide. The patient ingested a substantial amount of diltiazem, promethazine, and trazodone. Seven hours following the ingestion, she became profoundly vasoplegic and hypotensive. Despite guideline-based therapy and high doses of vasopressors, she suffered from worsening lactic acidosis and multiorgan failure. Administration of an intravenous bolus dose of MB resulted in a rapid and sustained improvement of vasoplegia, and the patient subsequently went on to make a complete recovery. Discussion In addition to calcium channel blockade, CCBs cause vascular smooth muscle relaxation by the production of nitric oxide (NO). In cases of overdose, NO production can be significant. MB is a safe and inexpensive medication with the potential to reverse NO-mediated vasoplegia that is responsible for CCB induced shock state. In parts of the world where access to advanced medical care is not readily available, early use of MB might have a significant role in the management of CCB overdose.

Objective This narrative review aims to provide a detailed overview of pleural abnormalities in patients with coronavirus disease 19 or COVID-19. Background Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) is a novel beta coronavirus responsible for COVID-19. Although pulmonary parenchymal and vascular changes associated with COVID-19 are well established, pleural space abnormalities have not been the primary focus of investigations. Methods Narrative overview of the medical literature regarding pleural space abnormalities in COVID-19. The appropriate manuscripts were identified by searching electronic medical databases and by hand searching the bibliography of the identified papers. Pleural abnormalities on transverse and ultrasound imaging are discussed. The incidence, clinical features, pathophysiology, and fluid characteristics of pleural effusion are reviewed. Studies reporting pneumothorax and pneumomediastinum are examined to evaluate for pathogenesis and prognosis. A brief comparative analysis of pleural abnormalities among patients with COVID-19, severe acute respiratory syndrome (SARS), and Middle Eastern respiratory syndrome (MERS) has been provided. Conclusions Radiologic pleural abnormalities are common in COVID-19, but the incidence of pleural effusion appears to be low. Pneumothorax is rare and does not independently predispose the patient to worse outcomes. SARS-CoV-2 infects the pleural space; however, whether the pleural fluid can propagate the infection is unclear.

A 78-year-old woman presented to the hospital with generalised weakness and inability to walk 2 weeks after testing positive for COVID-19. Her COVID-19 symptoms were primarily limited to the upper respiratory tract. She received prednisone 40 mg for 5 days at home and also took non-steroidal

BACKGROUND: The clinical features and outcomes of mechanically ventilated patients with COVID-19 infection who develop a pneumothorax has not been rigorously described or compared to those who do not develop a pneumothorax. PURPOSE: To determine the incidence, clinical characteristics, and outcomes of critically ill patients with COVID-19 infection who developed pneumothorax. In addition, we compared the clinical characteristics and outcomes of mechanically ventilated patients who developed a pneumothorax with those who did not develop a pneumothorax. METHODS: This study was a multicenter retrospective analysis of all adult critically ill patients with COVID-19 infection who were admitted to intensive care units in 4 tertiary care centers in the United States. RESULTS: A total of 842 critically ill patients with COVID-19 infection were analyzed, out of which 594 (71%) were mechanically ventilated. The overall incidence of pneumothorax was 85/842 (10%), and 80/594 (13%) in those who were mechanically ventilated. As compared to mechanically ventilated patients in the non-pneumothorax group, mechanically ventilated patients in the pneumothorax group had worse respiratory parameters at the time of intubation (mean PaO2:FiO2 ratio 105 vs 150, P

Background Pneumothorax has been frequently described as a complication of COVID-19 infections. Objective In this systematic review, we describe the incidence, clinical characteristics, and outcomes of COVID-19-related pneumothorax. Methods Studies were identified through MEDLINE, Pubmed, and Google Scholar databases using keywords of “COVID-19,” “SARS-CoV-2,” “pneumothorax,” “pneumomediastinum,” and “barotrauma” from January 1st, 2020 to January 30th, 2021. Results Among the nine observational studies, the incidence of pneumothorax is low at 0.3% in hospitalized COVID-19 patients. However, the incidence of pneumothorax increases to 12.8–23.8% in those requiring invasive mechanical ventilation (IMV) with a high mortality rate up to 100%. COVID-19-related pneumothorax tends to be unilateral and right-sided. Age, pre-existing lung diseases, and active smoking status are not shown to be risk factors. The time to pneumothorax diagnosis is around 9.0–19.6 days from admission and 5.4 days after IMV initiation. COVID-19-related pneumothoraces are associated with prolonged hospitalization, increased likelihood of ICU admission and death, especially among the elderly. Conclusion COVID-19-related pneumothorax likely signify greater disease severity. With the high variability of COVID-19-related pneumothorax incidence described, a well-designed study is required to better assess the significance of COVID-19-related pneumothorax.

Diffuse alveolar hemorrhage (DAH) in cardiac diseases results from pulmonary capillary stress failure due to pulmonary venous hypertension. The most common cardiac causes of DAH are heart failure and mitral valvular disease. Patients typically manifest with hemoptysis, radiologic chest abnormalities, and anemia. The chest infiltrates are generally bilateral, similar to pulmonary edema. Rarely, the chest infiltrates can be unilateral, mimicking an infectious etiology. We present the case of an 88-year-old female with critical aortic stenosis, who presented with shortness of breath, unilateral right lung infiltrates, and mild leukocytosis. The patient was misdiagnosed with pneumonia as pulmonary edema or DAH was expected to be a bilateral finding on chest imaging. The patient deteriorated and DAH was eventually diagnosed by bronchoscopy.

Background: There is conflicting data in the literature about the association of ABO blood type and susceptibility to COVID-19 infection. Moreover, very few studies have examined the effect of blood type on severity of COVID-19 infection. Methods: This was a retrospective, single-center analysis of adult patients with COVID-19 infection who were hospitalized between March 8(th) to July 31(st), 2020 at a regional tertiary care hospital. All patients who were hospitalized with a diagnosis of severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection and had a documented ABO blood type were enrolled in this analysis. Aims of this study were to examine the prevalence of ABO blood types in patients with COVID-19 infection and to determine the frequency of severe COVID-19 infection among ABO blood types. Results: A total of 227 cases were identified. Our cohort had a mean age of 63.3 years and 60% were males. The most common blood type was O (49%) followed by A (36%), which was similar to the prevalence of ABO blood types in our regional population. Moreover, there was no significant difference in the frequency of severe COVID-19 infection between ABO blood types (O: 50%, A: 53%, B: 56%, AB: 57%; P=0.93), or any additional outcomes including in-hospital mortality rate (P=0.72), need for ICU admission (P=0.66), ICU free days at day 28 (P=0.51), hospital free days at day 28 (P=0.43), or need for acute renal replacement therapy (P=0.09). Conclusion: We did not find an increased susceptibility of any blood type to COVID-19 infection, nor was there an increased risk of severe COVID-19 infection in any ABO blood types.

A 72-year-old man with chronic obstructive pulmonary disease and depression presented to the emergency department (ED) with progressive worsening of shortness of breath. He required intubation and mechanical ventilation. The patient improved with therapy, but his endotracheal aspirate culture was positive forNocardia cyriacigeorgica. The patient was started on high dose Bactrim and discharged. He presented to the office 5 days later with confusion, and his serum sodium was 113 mmol/L. Based on a euvolemic physical examination, consistent serum and urine studies, he was diagnosed with syndrome of inappropriate antidiuretic hormone secretion (SIADH) likely from citalopram. However, treatment for SIADH failed to improve his serum sodium level. A bedside ultrasound revealed an inferior vena cava diameter of 0.7 cm with a complete inspiratory collapse that was inconsistent with SIADH. The patient was correctly diagnosed with salt-losing nephropathy from trimethoprim, and the medication was discontinued. He received therapy initially with intravenous normal saline and then salt tablets. His sodium improved within 2 weeks.