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A 70-year-old man was referred to the pulmonary office for evaluation of a solitary lung nodule in September 2019. The patient was diagnosed with stage 1 adenocarcinoma of the rectum in November 2018 and underwent low anterior resection without any complications. No chemotherapy or radiation therapy

Idiopathic pulmonary hemosiderosis (IPH) is a rare cause of recurrent episodes of diffuse alveolar hemorrhage (DAH). IPH commonly manifests with hemoptysis, radiologic chest infiltrates and anemia. The etiology of IPH is unknown, but an immunologic mechanism is widely speculated. The definitive diagnosis of IPH requires a thorough exclusion of other causes of DAH, such as infections, inflammation, malignancy, cardiac diseases, drug and toxin exposure, and medications. Due to the rarity of the disease, a diagnosis is often delayed by years. We present the case of a 49-year-old man with ischemic cardiomyopathy who presented with hemoptysis for eighteen months. Serologic workup was negative for vasculitides and autoimmune diseases. Bronchoscopy revealed DAH. A surgical lung biopsy showed 'bland pulmonary hemorrhage.' A right heart catheterization ruled out cardiac causes of DAH. The patient was diagnosed with IPH and started on systemic corticosteroids with rapid improvement of hemoptysis.

Explosive pleuritis (EP) is an under-reported condition. Although there is no agreed-upon definition, generally, the term EP denotes a dramatic clinical and radiologic progression of pleural space inflammation in the setting of pneumonia. The pleural space inflammation leads to the formation of loculated complex pleural effusion or empyema, and pleural adhesion within a matter of hours, typically in less than 24 hours. Radiologically, these changes are manifested as opacification of the hemithorax with or without contralateral mediastinal shift. Streptococcal pneumonia is the most common cause of EP. Here we present a case and discuss the clinical, microbiologic, radiologic, and treatment aspects of EP. We also scrutinize the medical literature to compare the previously reported cases.

Background Secondary pulmonary infections (SPI) have not been well described in COVID-19 patients. Our study aims to examine the incidence and risk factors of SPI in hospitalized COVID-19 patients with pneumonia. Methods This was a retrospective, single-center study of adult COVID-19 patients with radiographic evidence of pneumonia admitted to a regional tertiary care hospital. SPI was defined as microorganisms identified on the respiratory tract with or without concurrent positive blood culture results for the same microorganism obtained at least 48 hours after admission. Results Thirteen out of 244 (5%) had developed SPI during hospitalization. The median of the nadir lymphocyte count during hospitalization was significantly lower in patients with SPI as compared to those without SPI [0.4 K/uL (IQR 0.3-0.5) versus 0.6 K/uL (IQR 0.3-0.9)]. Patients with lower nadir lymphocyte had an increased risk of developing SPI with odds ratio (OR) of 1.21 (95% CI: 1.00 to 1.47, p=0.04) per 0.1 K/uL decrement in nadir lymphocyte. The baseline median inflammatory markers of CRP [166.4 mg/L vs. 100.0 mg/L, p=0.01] and D-dimer (18.5 mg/L vs. 1.4 mg/L, p

A 78-year-old man presented with 1-month symptoms of dyspnoea and non-productive cough. He was initially diagnosed with biopsy-confirmed ulcerative colitis on a colonoscopy about 4-month ago. He was treated with intravenous methylprednisolone without any clinical improvement and required intravenous

Necrotizing sarcoid granulomatosis (NSG) is a rare inflammatory disease. Although considered by some to be a subtype of sarcoidosis, this opinion is not universal. NSG is histologically characterized by the presence of necrotizing sarcoid like granuloma and granulomatous vasculitis. The exclusion of potential etiologies for necrotizing granulomatous inflammation is necessary to establish a diagnosis of NSG. A 70-year old female presented to our office after she was incidentally found to have a right lung cavitary lesion on a shoulder X-ray. She had an extensive serologic workup for anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, mycobacterial and fungal etiologies, but they were all negative. She subsequently underwent bronchoscopic evaluation and biopsies. The histopathologic analysis revealed sarcoid-like granulomatous inflammation with large necrosis and mild granulomatous vasculitis. The pulmonary function test revealed a restrictive ventilatory defect. The patient was treated with steroid therapy with rapid radiologic and spirometric improvement.

Idiopathic pulmonary hemosiderosis (IPH) is a rare immunological disease with a genetic predisposition. It is characterized by recurrent episodes of diffuse alveolar hemorrhage (DAH). Timely use of immunosuppressive medications has significantly improved overall outcomes, including mortality. Still, uncontrolled and frequent episodes of DAH can eventually cause pulmonary fibrosis, leading to end-stage lung disease (ESLD). The objective of the present project was to scrutinize the literature and summarize the demographic, clinical, radiological, and histopathological features, as well as the overall outcomes, in this patient population following lung transplant. The Medline database was searched using the PubMed platform. Articles published in English between 1960 and 2020 were included in the search. Different search terms were used to identify all patients who underwent lung transplantation to manage ESLD due to IPH. Only four cases of lung transplantation have been reported in the literature in patients with IPH. All but one of these underwent deceased donor lung transplant; recurrence was reported in two of these patients and suspected in the third. One patient received living donor lung transplant and had no recurrence during a five-year follow-up. Patients with IPH should not be excluded from lung transplantation because the disease may not recur in all patients, and even when it does recur it can be promptly treated by increasing immunosuppression.

BACKGROUND: Bronchoscopy is an aerosol-generating procedure and routine use for patients with coronavirus disease 2019 (COVID-19) has been discouraged. The purpose of this review was to discuss the indications, clinical utility, and risks associated with bronchoscopy in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia. METHODS: A literature search was performed by using appropriate key terms to identify all relevant articles from medical literature databases up to August 1, 2021. RESULTS: Twelve cohorts (9 retrospective and 3 prospective) reported the performance of 2,245 bronchoscopies in 1,345 patients with COVID-19. The majority of the subjects were male. Nearly two thirds of the bronchoscopies (62%) were performed for therapeutic indications; the rest (38%) were for diagnostic purposes. Bronchoalveolar lavage had an overall yield of 33.1% for SARS-CoV-2 in subjects with negative results of real-time polymerase chain reaction on nasopharyngeal specimens. The incidence of a secondary infection ranged from 9.3% to as high as 65%. Antibiotics were changed in a significant number of the subjects (14%–83%) based on the bronchoscopic findings. Bronchoscopy was well tolerated in most subjects except those who required noninvasive ventilation, in whom the intubation rate after the procedure was 60%. The rate of transmission of SARS-CoV-2 among health-care workers was minimum. CONCLUSIONS: Bronchoscopy in patients with COVID-19 results in a significant change in patient management. Transmission of SARS-CoV-2 seems to be low with consistent use of appropriate personal protective equipment by health-care workers. Therefore, bronchoscopic evaluation should be considered for all diagnostic and therapeutic indications in this patient population.

Background Extracorporeal membrane oxygenation (ECMO) is a valuable rescue therapy to treat refractory hypoxemia caused by influenza. The present meta-analysis aimed to compare the clinical characteristics and outcomes of ECMO between COVID-19 and influenza. Methods We searched the PubMed, Cochrane Library, SCOPUS, and Web of Science databases from inception to May 1, 2021. The included studies compared the clinical characteristics and outcomes of ECMO between adults with COVID-19 and those with influenza. Results The study included four retrospective cohorts involving a total of 129 patients with COVID-19 and 140 with influenza who were treated using ECMO. Clinical characteristics were similar between the COVID-19 and influenza groups, including body mass index (BMI), diabetes mellitus, hypertension, and immunocompromised status. A higher proportion of patients with COVID-19 on ECMO were male (75.9% vs. 62.9%; P = 0.04). There was no difference between the groups in terms of illness severity based on sequential organ failure assessment (SOFA) score or serum pH. Patients with COVID-19 had a longer mean duration of mechanical ventilation before ECMO (6.63 vs. 3.38 days; P

Background: The use of extracorporeal membrane oxygenation (ECMO) in coronavirus disease 2019 (COVID-19) for refractory respiratory failure, severe cardiac dysfunction, and bridge to lung transplantation has been steadily increasing during the ongoing global pandemic. Objective: Our meta-analysis aims to compare the clinical characteristics between COVID-19 survivors and nonsurvivors requiring ECMO support. Methods: A systematic search of Pubmed, Cochrane, Embase, Scopus, and Web of Science databases was performed between December first, 2019, to June first, 2021. Studies with comparative data of COVID-19 ECMO patients were selected, in which clinical characteristics and complications were assessed. Results: Sixteen cohort studies involving 706 COVID-19 patients requiring ECMO support with pooled mortality rate of 40% were included. Younger age (mean 51 years vs 55 years; P

Case Presentation A 51-year-old White male never-smoker presented with intermittent cough and progressive dyspnea. His symptoms started after an exposure to bat guano while cleaning his attic approximately 9 months earlier. He has received several courses of antibiotic and corticosteroid for these symptoms, with short-term relief.

This narrative review provides an overview of diffuse alveolar hemorrhage (DAH) associated with rheumatologic and autoimmune diseases and their differentiation from idiopathic pulmonary hemosiderosis (IPH). Relevant immunologic diseases associated with DAH are discussed, and a diagnostic flowchart is proposed to establish a “definitive” diagnosis of IPH within the spectrum of DAH. IPH is a rare cause of recurrent DAH both in children and adults. In adults, a definitive diagnosis of IPH requires a lung biopsy and histopathologic examination demonstrating intraalveolar hemorrhage, hemosiderin-laden macrophages, and a variable degree of fibrosis in the absence of both capillaritis and cellular inflammation. The presence of small vessel vasculitis points towards immunologic, well-differentiated, or sometimes undifferentiated rheumatologic diseases. However, it is essential to recognize that many rheumatologic diseases may in the initial phase present with DAH without any evidence of capillaritis, thus mimicking IPH. Although not definitely established, it is likely that immunologic processes are involved in IPH, and we, therefore, suggest the consideration of a more suitable term for the disease, e.g., “Immune-mediated Pulmonary Hemosiderosis” to acknowledge the aberrancy in the immune parameters and a positive response to immunosuppressive therapy.

Case Presentation A 75-year-old woman was referred to the pulmonary office in January 2020 for cough and progressive worsening of shortness of breath over the years. Her medical history was significant for asthma that was diagnosed approximately 10 years earlier, when she first developed dyspnea. A pre-bronchodilator spirometry at that time showed severe airflow obstruction ( Fig 1 ). The patient was incidentally found to have several noncalcified pulmonary nodules on a chest CT scan in 2015, which was obtained as a part of dyspnea workup. She underwent bronchoscopic evaluation with transbronchial biopsy of the largest nodule (1.6 × 1.2 cm) in the right middle lobe. She was diagnosed with low-grade neuroendocrine tumor (typical carcinoid) and had been under surveillance without any progression in the number of nodules or the size of the existing nodules. She was a lifelong nonsmoker and no family history of asthma. Over the years, she received multiple courses of systemic corticosteroids and different inhalers, without any improvement in her symptoms. The patient was frustrated by the lack of perceived benefit, and she discontinued all respiratory medications. She denied any fever, night sweats, exertional chest pain, or seasonal allergies but reported cough, wheezing, and severe exertional shortness of breath. She was unable to walk more than 20 feet at a time. She had no pets at home and did not travel outside the United States. Her only home medications were multivitamins and low-dose aspirin.

COVID-19-associated pulmonary aspergillosis (CAPA) is defined as invasive pulmonary aspergillosis occurring in COVID-19 patients. The purpose of this review was to discuss the incidence, characteristics, diagnostic criteria, biomarkers, and outcomes of hospitalized patients diagnosed with CAPA. A literature search was performed through Pubmed and Web of Science databases for articles published up to 20th March 2021. In 1421 COVID-19 patients, the overall CAPA incidence was 13.5% (range 2.5-35.0%). The majority required invasive mechanical ventilation (IMV). The time to CAPA diagnosis from illness onset varied between 8.0 and 16.0 days. However, the time to CAPA diagnosis from intensive care unit (ICU) admission and IMV initiation ranged between 4.0-15.0 days and 3.0-8.0 days. The most common diagnostic criteria were the modified AspICU-Dutch/Belgian Mycosis Study Group and IAPA-Verweij et al. A total of 77.6% of patients had positive lower respiratory tract cultures, other fungal biomarkers of bronchoalveolar lavage and serum galactomannan were positive in 45.3% and 18.2% of patients. The CAPA mortality rate was high at 48.4%, despite the widespread use of antifungals. Lengthy hospital and ICU stays ranging between 16.0-37.5 days and 10.5-37.0 days were observed. CAPA patients had prolonged IMV duration of 13.0-20.0 days. The true incidence of CAPA likely remains unknown as the diagnosis is limited by the lack of standardized diagnostic criteria that rely solely on microbiological data with direct or indirect detection of Aspergillus in respiratory specimens, particularly in clinical conditions with a low pretest probability. A well-designed, multi-centre study to determine the optimal diagnostic approach for CAPA is required.

Background Pneumocystis jirovecii (P. jirovecii) is increasingly identified on lower respiratory tract specimens of COVID-19 patients. Our narrative review aims to determine whether the diagnosis of pneumocystis jirovecii pneumonia (PJP) in COVID-19 patients represents coinfection or colonization based on the evidence available in the literature. We also discuss the decision to treat COVID-19 patients with coinfection by PJP. Methods A literature search was performed through the Pubmed and Web of Science databases from inception to March 10, 2021. Results We identified 12 COVID-19 patients suspected to have PJP coinfection. All patients were critically ill and required mechanical ventilation. Many were immunosuppressed from HIV or long-term corticosteroids and other immunosuppressive agents. In both the HIV and non-HIV groups, severe lymphocytopenia was encountered with absolute lymphocyte and CD4+T cell count less than 900 and 200 cells/mm, respectively. The time to PJP diagnosis from the initial presentation was 7.8 (range 2–21) days. Serum lactate dehydrogenase and beta-D-glucan were elevated in those coinfected with PJP. All patients were treated with anti-PJP therapy, predominantly sulfamethoxazole-trimethoprim with corticosteroids. The overall mortality rate was 41.6%, and comparable for both HIV and non-HIV groups. Conclusion As the current evidence is restricted to case reports, the true incidence, risk factors, and prognosis of COVID-19 patients with PJP coinfections cannot be accurately determined. Comorbidities of poorly controlled HIV with lymphocytopenia and multiple immunosuppressive therapies are likely predisposing factors for PJP coinfection.

Case Presentation A 74-year-old man was referred to a pulmonologist for evaluation of a 1-year history of nonproductive cough and progressive exertional dyspnea. He was initially evaluated by his primary care physician, where he had spirometry that was negative for any obstructive or restrictive lung disease. An echocardiogram showed a normal left ventricular ejection fraction, with no wall motion abnormality or valvular heart disease. He had an outpatient chest radiograph performed ( Fig 1 ), and he was subsequently treated empirically for a COPD exacerbation with 5 days of oral prednisone and azithromycin. He was eventually referred to a pulmonologist because of a lack of clinical improvement. On seeing his pulmonary physician, he described the same exertional dyspnea and a nonproductive cough. A review of systems was negative for fever, chills, wheezing, angina, arthralgia, myalgia, rash, or leg swelling. He denied any medical illness and was not taking any medications. He was currently retired and had worked as a cashier his entire adult life. He had no occupational exposure to asbestos, coal dust, beryllium, silica dust, or dust from hard metal objects, such as cobalt. However, he had smoked approximately 1 to 2 packs of cigarettes per day and had done so for the past 50 years. His vital signs were unremarkable, aside from an oxygen saturation of 94% on room air. His physical examination revealed bibasilar “velcro-like” inspiratory crackles on lung examination. There was no digital clubbing, nor was there peripheral edema in his lower extremities. He had no muscle tenderness and demonstrated normal muscle strength against resistance.

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.

The subpleural sparing pattern is a common finding on computed tomography (CT) of the lungs. It comprises of pulmonary opacities sparing the lung peripheries, typically 1cm and less from the pleural surface. This finding has a variety of causes, including idiopathic, inflammatory, infectious, inhalational, cardiac, traumatic, and bleeding disorders. Specific disorders that can cause subpleural sparing patterns include nonspecific interstitial pneumonia (NSIP), organizing pneumonia (OP), pulmonary alveolar proteinosis (PAP), diffuse alveolar hemorrhage (DAH), vaping-associated lung injury (VALI), cracked lung, pulmonary edema, pneumocystis jirovecii pneumonia (PJP), pulmonary contusion, and more recently, Coronavirus disease 2019 (COVID-19) pneumonia. Knowledge of the many etiologies of this pattern can be useful in preventing diagnostic errors. In addition, although the etiology of subpleural sparing pattern is frequently indistinguishable during an initial radiologic evaluation, the differences in location of opacities in the lungs, as well as the presence of additional radiologic findings, patient history, and clinical presentation, can often be useful to suggest the appropriate diagnosis. We did a comprehensive search on Pubmed and Google Scholar database using keywords of "subpleural sparing," "peripheral sparing," "sparing of peripheries," "CT chest," "chest imaging," and "pulmonary disease." This review aims to describe the primary differential diagnosis of subpleural sparing pattern seen on chest imaging with a strong emphasis on clinical and radiographic findings. We also discuss the pathogenesis and essential clues that are crucial to narrow the differential diagnosis.

Antisynthetase syndrome (AS) is a rare disease that affects patients with inflammatory myopathies such as polymyositis (PM) and dermatomyositis (DM). In patients with AS, up to 95% of patients develop antisynthetase syndrome-associated interstitial lung disease (AS-ILD). Although AS-ILD commonly occurs in patients with a well-established diagnosis of AS, it can be the first or only manifestation of an occult AS. The frequency of interstitial lung disease (ILD), myopathy, and skin involvement are often dependent on the type of myositis-specific antibodies present. AS-ILD patients who are positive for both anti-Jo-1 and anti-SSA/RO-52 autoantibodies often present with a severe degree of lung restriction on pulmonary function tests and radiologic imaging with an inadequate response toward immunosuppressive therapies. We describe a 65-year-old woman who presents with chronic dyspnea. She was initially diagnosed with corticosteroid-resistant cryptogenic organizing pneumonia based on the radiological findings on her CT chest. Her symptoms did not improve, and she suffered from intolerable corticosteroid-related side effects. Reviews of systems were positive for arthritis and Raynaud's phenomenon. She was found to have elevated inflammatory markers and autoantibodies such as anti-Jo-1, anti-RO-52, and anti-SSA. A diagnosis of AS-ILD resistant to corticosteroid therapy was made. Her lung function improved with combination therapy of mycophenolate and rituximab. Our case highlights that a detailed history and physical exam, compatible radiologic imaging, and autoantibodies are essential for the diagnosis of AS-ILD.

Background The incidence of secondary pulmonary infections is not well described in hospitalized COVID-19 patients. Understanding the incidence of secondary pulmonary infections and the associated bacterial and fungal microorganisms identified can improve patient outcomes. Objective This narrative review aims to determine the incidence of secondary bacterial and fungal pulmonary infections in hospitalized COVID-19 patients, and describe the bacterial and fungal microorganisms identified. Method We perform a literature search and select articles with confirmed diagnoses of secondary bacterial and fungal pulmonary infections that occur 48 h after admission, using respiratory tract cultures in hospitalized adult COVID-19 patients. We exclude articles involving co-infections defined as infections diagnosed at the time of admission by non-SARS-CoV-2 viruses, bacteria, and fungal microorganisms. Results The incidence of secondary pulmonary infections is low at 16% (4.8–42.8%) for bacterial infections and lower for fungal infections at 6.3% (0.9–33.3%) in hospitalized COVID-19 patients. Secondary pulmonary infections are predominantly seen in critically ill hospitalized COVID-19 patients. The most common bacterial microorganisms identified in the respiratory tract cultures are Pseudomonas aeruginosa, Klebsiella species, Staphylococcus aureus, Escherichia coli, and Stenotrophomonas maltophilia. Aspergillus fumigatus is the most common microorganism identified to cause secondary fungal pulmonary infections. Other rare opportunistic infection reported such as PJP is mostly confined to small case series and case reports. The overall time to diagnose secondary bacterial and fungal pulmonary infections is 10 days (2–21 days) from initial hospitalization and 9 days (4–18 days) after ICU admission. The use of antibiotics is high at 60–100% involving the studies included in our review. Conclusion The widespread use of empirical antibiotics during the current pandemic may contribute to the development of multidrug-resistant microorganisms, and antimicrobial stewardship programs are required for minimizing and de-escalating antibiotics. Due to the variation in definition across most studies, a large, well-designed study is required to determine the incidence, risk factors, and outcomes of secondary pulmonary infections in hospitalized COVID-19 patients.

Diffuse alveolar hemorrhage (DAH) is a rare condition with reported mortality ranging between 20 and 100%. There are many etiologies of DAH. Cardiac diseases are likely underreported causes of DAH. Heart failure and mitral valve diseases are the most common cardiac causes of DAH. The DAH results from pulmonary venous hypertension leading to stress failure of the pulmonary capillaries. There is also a contribution of the bronchial circulation. The Alveolar-capillary membrane or blood-gas barrier is an extremely thin structure that allows rapid and passive diffusion of oxygen from the inhaled air to the pulmonary capillaries while preventing pulmonary edema and DAH with chronic elevation of the transmural hydrostatic pressure. The purpose of this manuscript is to inform the clinician about this rare cause of DAH, which may be overlooked unless specifically sought after. We also discuss the pathophysiologic aspects of DAH and the safety mechanisms in place to prevent such occurrences.

Case Presentation A 69-year-old woman with a medical history significant for COPD, ulcerative colitis (UC), and tobacco dependence was referred to a pulmonologist for lung nodules found on routine annual low-dose CT scan for lung cancer screening. Her review of systems was negative for dyspnea, angina, hemoptysis, fever, night sweats, anorexia, and weight loss. She had a successful total proctocolectomy with ileal pouch-anal anastomosis performed 5 years ago because of acute fulminant UC refractory to corticosteroids and biologic agents. Her home medications were albuterol inhaler, umeclidinium, and vilanterol inhalation powder. She denied any history of lung cancers in her family. She was an active smoker and had a 35-pack-year smoking history. She worked as a cashier in a local supermarket and had been doing so for the past 25 years.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus responsible for the coronavirus disease -19 (COVID-19). Since December 2019, SARS-CoV-2 has infected millions of people worldwide, leaving hundreds of thousands dead. Chloroquine (CQ) and Hydroxychloroquine (HCQ) are antimalarial medications that have been found to have in vitro efficacy against SARS-CoV-2. Several small prospective studies have shown positive outcomes. However, this result has not been universal, and concerns have been raised regarding the indiscriminate use and potential side effects. The clinicians are conflicted regarding the usage of these medications. Appropriate dose and duration of therapy are unknown. Here, we will discuss the pharmacokinetic and pharmacodynamic properties of CQ and HCQ, as well as review the antiviral properties. The manuscript will also examine the available data from recent clinical and preclinical trials in order to shed light on the apparent inconsistencies.

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.

Type A aortic dissection is an uncommon cause of chest pain that carries a high morbidity and mortality rate. A previous history of hypertension and coronary artery bypass grating (CABG) are recognized risk factors for Type A aortic dissection. We present a case of an elderly man who presents with acute onset chest pain and was found to have an acute ruptured Type A aortic dissection that has a “saddle pulmonary embolism”‐like appearance on computed tomography (CT) imaging. We also describe the clinical, laboratory, and radiological workup done leading up to the diagnosis of Type A aortic dissection in the emergency setting.

Idiopathic pulmonary hemosiderosis (IPH) is a rare disease that causes diffuse alveolar hemorrhage (DAH). The latest data suggests an immunologic origin of IPH, and a new name, immune mediated pulmonary hemosiderosis (ImPH), has been proposed. However, the exact immunologic mechanism has remained elusive for nearly eight decades despite extensive research, including detailed histopathologic analysis. Although several hypotheses have been proposed to describe the pathobiology of IPH, none of them explain the clinical and histopathologic findings conclusively. In this manuscript, we have presented a new hypothesis for the pathogenesis of DAH in IPH. We hypothesize that DAH in IPH is not immunocomplex mediated but due to histamine, eosinophilic cationic protein (ECP), and possibly vascular endothelial growth factor (VEGF). These bioactive proteins induce endothelial and alveolar epithelial damage, leading to the peri-capillary and intraalveolar escape of RBCs. The deformability of the RBC likely also plays a role. The supranormal secretion of histamine, ECP and VEGF occurs in genetically predisposed individuals with an aberrant immunologic response. The histamine is released from the basophils and possibly the mast cells in response to cytokines secreted by activated lymphocytes. The lymphocyte activation occurs after exposure to a known (gluten) or unknown antigen. The same lymphocyte-derived cytokines also induce eosinophilic degranulation of ECP and VEGF in the pulmonary circulation. We believe that our hypothesis unifies the observed clinical variabilities and histopathologic findings in IPH, and we hope that would promote future research in the field of IPH.

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.

Lipoid pneumonia occurs due to the accumulation of lipids within the lung tissue. Autopsy series have reported an incidence of 1.0-2.5% in adult and 8.8% in children. Lipoid pneumonia can be from an exogeneous or an endogenous source. Exogenous lipoid pneumonia is often associated with aspiration of fatty materials, whereas endogenous lipoid pneumonia is associated with an accumulation of lipid-rich debris from destroyed alveolar cells. We describe a 75-year-old man who presented with spiculated lung nodules found incidentally on abdominal CT. Reviews of systems were positive for weight loss, and a history of constipation. A PET/CT revealed spiculated nodules with positive fluorodeoxyglucose (FDG) uptakes. A wedge resection was performed with histopathologic findings consistent with exogenous lipoid pneumonia with granulomatous reaction. We report clinical, radiological, and pathological features of exogenous lipoid pneumonia secondary to chronic aspiration mimicking invasive adenocarcinoma. A high index of suspicion for exogenous lipoid pneumonia should be maintained, especially when evaluating patients with abnormal chest radiographic findings and risk factors for aspirations.

Background Multiple studies describing the benefits of intrapleural fibrinolytic over placebo and DNase therapy have been published, but few have been published on intrapleural fibrinolytic and DNase therapy. Objective Our meta-analysis aims to compare the outcomes of surgical intervention, mortality, and hospital length of stay between intrapleural fibrinolytic and DNase therapy with either intrapleural fibrinolytic or DNase therapy alone in patients with pleural space infections. Methods We searched Pubmed, EMBASE, Web of Science, and Cochrane library databases for observational studies and randomized controlled trials (RCTs) containing comparative data for hospitalized adults and children with pleural infections receiving intrapleural therapy of fibrinolytic and DNase versus those receiving intrapleural fibrinolytic or DNase alone. Meta-analysis was performed using the Review Manager software, and heterogeneity was tested using I 2 statistics. Results A total of 2 cohorts and 2 RCTs involving 362 adult and children was included. There was significant reduction in surgical intervention requirement among patients who received intrapleural fibrinolytic and DNase (OR 0.30; 95% CI 0.11–0.83; I2 = 31%; P = 0.02) than those receiving either intrapleural fibrinolytic or DNase alone. No difference was observed for mortality (OR 0.72; 95% CI 0.31–1.71; I2 = 0%; P = 0.46) and complication rates (OR 3.09; 95% CI 0.75–12,74; I2 = 54%; P = 0.12). The hospital length of stay (mean 13.70 vs. 16.67 days; P = 0.19) and duration of chest tube drainage (mean 6.47 vs. 6.30 days; P = 0.58) was similar between the two groups. Conclusion Combination of intrapleural fibrinolytic and DNase, compared to single-agent intrapleural therapy alone, is associated with a lesser need for surgical interventions. However, no difference was found in mortality, hospital length of stay, and chest tube drainage duration.

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.

Purpose Invasive pulmonary aspergillosis has been increasingly recognized in COVID-19 patients, termed COVID-19-associate pulmonary aspergillosis (CAPA). Our meta-analysis aims to assess the clinical characteristics and outcomes of patients diagnosed with CAPA compared to those without CAPA. Methods We searched the Pubmed, Cochrane Library, SCOPUS, and Web of Science databases for studies published between January 1, 2020 and August 1, 2021, containing comparative data of patients diagnosed with CAPA and those without CAPA. Results Eight cohort studies involving 729 critically ill COVID-19 patients with comparative data were included. CAPA patients were older (mean age 66.58 vs. 59.25 years; P = 0.007) and had underlying chronic obstructive pulmonary disease (COPD) (13.7 vs. 6.1%; OR 2.75; P = 0.05). No differences in gender, body mass index (BMI), and comorbidities of diabetes and cancer were observed. CAPA patients were more likely to receive long-term corticosteroid treatment (15.0 vs. 5.3%; OR 3.53; P = 0.03). CAPA patients had greater severity of illness based on sequential organ failure assessment (SOFA) score with a higher all-cause in-hospital mortality rate (42.6 vs. 26.5%; OR 3.39; P

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.

Arterial blood gas (ABG) analysis is used in critical care units to determine the degree of oxygenation, adequacy of ventilation, and the presence and severity of acid-base disturbances in the body. However, arterial puncture may result in complications, and the difficulty in acquiring arterial blood may delay care. Central venous blood gas (VBG) is a potentially more accessible alternative to ABG sampling. Current evidence suggests that pH and Pco2 obtained via peripheral VBG correlate well with ABG measurement. Nevertheless, the value of using central VBG to guide clinical decisions or as a surrogate for ABG is unclear. The purpose of this review is to explore the relationship between ABGs and central VBGs in critically ill patients. We performed a MEDLINE search using the following search terms: venous blood gas, arterial blood gas, and central venous blood gas. We excluded studies that did not involve human subjects, and only pH and Pco2 values were reviewed and examined from the studies included. All cited references from included studies were also reviewed to identify relevant literature. We identified 7 studies that met our criteria. In studies of hemodynamically stable patients, the mean difference between arterial and central venous pH and Pco2 was 0.03 units and 4-6.5 mm Hg, respectively. However, in patients with circulatory failure, the difference between central venous and arterial pH/Pco2 was 4-fold greater. We concluded that central VBG parameters of pH and Pco2 are potentially good surrogates for determining arterial pH and Pco2 in a stable patient without severe acid-base disturbances. Furthermore, central VBG can be used as a useful screening tool for arterial hypercapnia. In addition, we derived an adjustment formula for ABG conversion from central VBG: (1) arterial pH = venous pH + 0.05 units and (2) arterial Pco2 = venous Pco2 - 5 mm Hg.

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.

Human pulmonary dirofilariasis (HPD) is a rare zoonotic disease caused by Dirofilaria immitis, the nematode responsible for canine cardiopulmonary dirofilariasis (dog heartworm). The incidence of HPD is on the rise throughout the world due to increased awareness and factors affecting the vector (mosquito). Humans are accidental hosts for D. immitis. Most patients are asymptomatic and present with an incidental pulmonary nodule that mimics primary or metastatic pulmonary malignancy. Some patients suffer from pulmonary and systemic symptoms in the acute phase of pneumonitis caused by pulmonary arterial occlusion by the preadult worms resulting in pulmonary infarction and intense inflammation. These patients may have ill-defined pulmonary infiltrate on chest radiology. Pulmonary nodules represent the end result of initial pneumonitis. There are no specific clinical, laboratory, or radiologic findings that differentiate HPD from other causes of a pulmonary nodule. Although serologic tests exist, they are usually not commercially available. The majority of patients are diagnosed by histopathologic identification of the decomposing worm following surgical resection of the lesion.

Diffuse alveolar hemorrhage (DAH) is a rare condition with reported mortality ranging between 20 and 100%. There are many etiologies of DAH. Cardiac diseases are likely underreported causes of DAH. Heart failure and mitral valve diseases are the most common cardiac causes of DAH. The DAH results from pulmonary venous hypertension leading to stress failure of the pulmonary capillaries. There is also a contribution of the bronchial circulation. The Alveolar-capillary membrane or blood-gas barrier is an extremely thin structure that allows rapid and passive diffusion of oxygen from the inhaled air to the pulmonary capillaries while preventing pulmonary edema and DAH with chronic elevation of the transmural hydrostatic pressure. The purpose of this manuscript is to inform the clinician about this rare cause of DAH, which may be overlooked unless specifically sought after. We also discuss the pathophysiologic aspects of DAH and the safety mechanisms in place to prevent such occurrences.

Background COVID-19-related pleural effusions are frequently described during the ongoing pandemic. Objectives We described the incidence, characteristics, and outcomes of COVID-19-related pleural effusions based on the current evidence available in the literature. Methods We searched MEDLINE, Pubmed, and Google Scholar databases using keywords of “coronavirus disease 2019 (COVID-19),” “severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2),” “pleural effusion,” “pleural fluid,” and “pleura” from January 1st, 2020 to January 31st, 2021. Results The incidence of pleural effusions was low at 7.3% among the 47 observational studies. Pleural effusions were commonly observed in critically ill patients and had Multisystem Inflammatory Syndrome (MIS). COVID-19-related pleural effusions were identified 5–7 days and 11 days, after hospital admission and onset of COVD-19 symptoms. The characteristic findings of pleural fluid were exudative, lymphocytic or neutrophilic-predominant pleural fluid with markedly elevated lactate dehydrogenase (LDH) levels and pleural fluid to serum LDH ratio. Conclusion A well-designed study is required to assess the significance of COVID-19-related pleural effusions during this current pandemic.

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.

A 61-year-old man presented to the ED with fever, chills, cough, purulent sputum, and progressive shortness of breath for 7 days. The patient was an active smoker with at least 80 pack-year smoking history. He had no other medical or surgical history and was not on any medication at home.