Fever and Hyponatremia Unmasking Brugada Pattern Electrocardiogram in a Patient With SARS-CoV-2 Infection.

Brugada syndrome is an autosomal dominant genetic disorder that primarily affects myocardial sodium channels and has been associated with an increased risk of ventricular tachyarrhythmias and sudden cardiac death. Here, we report a case of a 58-year-old Hispanic male with a history significant for prior pulmonary tuberculosis infection who presented with pleuritic left-sided chest pain associated with body aches, productive cough, fevers, and chills and was found to be positive for SARS-CoV-2 by real-time reverse-transcription-polymerase chain reaction (rRT-PCR). Electrocardiogram (ECG, EKG) on presentation demonstrated a coved ST-segment elevation in V1-V2, suggesting Brugada pattern type 1 without evidence of ischemic changes. EKG changes normalized once fever and hyponatremia improved.

Does Baseline Diuretics Use Affect Prognosis in Patients With COVID-19?

The rapid emergence of coronavirus disease 2019 (COVID-19) has become the biggest healthcare crisis of the last century, resulting in thousands of deaths worldwide. There have been studies that evaluated the role of angiotensin-converting enzyme (ACE) inhibitors (ACEi) and angiotensin receptor blockers (ARBs) in treating patients with COVID-19. However, the prior use of diuretics and their effect on mortality in this setting remains unknown. The aim of the study was to evaluate the effect of diuretics in patients admitted with COVID-19. The current study was conducted between March 15, 2020, and April 30, 2020, during the COVID-19 pandemic in three different hospitals in Northern New Jersey, USA. The primary outcome was survival or in-hospital mortality from COVID-19 from the day of admission. The secondary outcome was severe or non-severe illness from COVID-19. This retrospective study included a total of 313 patients with a median age of 61.3 ± 14.6 years. There was a total of 68 patients taking diuretics at home and 245 patients who were not taking diuretics. There was a total of 39 (57.35%) deaths in patients taking diuretics as compared to 93 (37.96%) deaths in patients not taking diuretics (p-value 0.0042). Also, 54 (79.41%) patients who took diuretics had severe COVID-19 illness as compared to 116 (47.35%) who did not take diuretics (p-value <.0001). However, after adjusting for the confounding factors, there was no difference in mortality or severity of illness in COVID-19 patients taking diuretics at the time of admission. In conclusion, there was no effect of the baseline use of diuretics in the prognosis of COVID-19.

A 22-year-old COVID-19 positive male with no prior medical history presented to the emergency department with pulmonary infarction.

Rapidly growing evidence has now shown a high incidence of venous thrombosis in patients with severe acute respiratory syndrome secondary to novel coronavirus 2, a disease now named COVID-19. Accumulating case reports and series have also shown a higher prevalence of arterial thrombosis in these patients as well. Although the pathophysiology remains unknown but likely multifactorial - including endotheliitis from direct viral damage and an underlying hyper-inflammatory state, arterial and venous thrombosis occurrence does not appear to be linked with underlying classic risk factors for venous thromboembolism and may present in healthy patients without significant comorbidities. We present a case of a 22-year-old healthy patient with COVID-19 who developed a pulmonary embolism with a pulmonary infarction, a complication that results from arterial and venous thrombosis of the pulmonary vascular supply resulting in tissue necrosis.

COVID-Induced Spontaneous Pneumothoraxes: Case Series.

Severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) is a communicable disease leading to COVID-19 infection that resulted in worldwide flooding of medical centers with the shortage of ventilators in some areas. The respiratory system is the most affected by the novel virus. Clinical manifestations are diverse in severity, with the most common symptoms including fever, chills, cough, and shortness of breath. The contributing factor to the morbidity and mortality associated with this virus is the rapid clinical deterioration as a result of a heightened inflammatory response, requiring supplemental oxygen. Pneumothorax is an unusual complication that may further worsen the hypoxia and require immediate intervention. We present a case series of two patients with no risk factors for pneumothorax besides recent COVID-19 infection, who were found to have spontaneous pneumothoraxes.

Invasive Pneumococcal Disease in a Patient With COVID-19: A Case Report.

The spread of the new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), has resulted in a global health pandemic and caused profound morbidity and mortality worldwide. The virus is known to cause severe hypoxemic respiratory failure and has been associated with extrapulmonary manifestations and end-organ dysfunction in the setting of extensive inflammatory response. Recently, the association between COVID-19 and pneumococcal pneumonia co-infection or superinfections has gained increasing interest. In this report, we present the case of a 58-year-old man with a past medical history significant for pulmonary tuberculosis, diagnosed over two decades ago, who presented with pleuritic chest pain, myalgia, intermittent fevers, chills, and productive cough and was found to have invasive pneumococcal disease and COVID-19. To our knowledge, this is the first reported case of invasive pneumococcal infection in a patient with COVID-19.

Unfortunate Outcomes in Patients With SARS-CoV-2 Superimposed on Pneumococcal Pneumonia.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the disease it causes, coronavirus disease 2019 (COVID-19), continue to have socioeconomic as well as health implications worldwide. The virus has already led to over 200,000 deaths in the United States alone. This is most likely secondary to quick respiratory deterioration seen in patients inflicted with the virus. In other words, the heightened inflammatory response leads to major organ system damage, which leads to rapid decompensation of the patient's clinical condition. Interestingly enough, some patients present with both the novel virus as well as a superimposed bacterial infection that further complicates the management of the disease. We present a case of a patient with a positive polymerase chain reaction (PCR) test for SARS-CoV-2 as well as a pneumococcal urine antigen; he was treated with both appropriate antibiotics as well as dexamethasone and remdesivir for pneumonia and novel virus, respectively. The patient's hypoxemia continued to worsen with appropriate means of oxygenation and eventually led to cardiac arrest.

Subacute COVID-19 Infection Presenting as Indolent Large Pericardial Effusion.

Reports of complications as a result of COVID-19 infection are emerging since the virus became a pandemic. Although not fully understood, reports show that the COVID-19 virus has shown acute pericardial involvement resulting from this infection. It can cause a wide range of manifestations from minimal effusion to large effusion with tamponade; however, there is little or no data on an indolent course of COVID-19 infection and its resulting manifestations. Here we describe a patient who had minimal disease symptoms for weeks, resulting in sizeable pericardial effusion formation.

A Novel Case of Hypoparathyroidism Secondary to SARS-CoV-2 Infection.

Hypoparathyroidism is usually caused by postsurgical or autoimmune damage to the parathyroid gland. We present the case of a 46-year-old Hispanic male with no significant past medical history who was admitted to the hospital with hypoxic respiratory failure due to coronavirus disease 2019 (COVID-19) infection and had a prolonged hospital course. He was incidentally found to have hyperphosphatemia and low parathyroid hormone (PTH) levels. During the second month of hospitalization, his phosphorus levels rose to 6.9 mg/dL (normal range: 2.4-4.7 mg/dl). His PTH levels were found to be at 8 pg/mL. Vitamin D levels obtained were also low (7 ng/dL), phosphorus was at 5.8 mg/dL with albumin of 2.9 g/dL, and calcium level was normal at 9.2 mg/dl. Parathyroid hormone-related peptide (PTHrP) level was low at 10. Malignancy and genetic causes were ruled out. The patient was started on 50,000 units of ergocalciferol once a week. He was also started on calcium acetate 1,334 mg three times a day for hyperphosphatemia. Phosphorus levels remained elevated, and sevelamer was added on discharge after he was weaned off oxygen and cleared by physical therapy. No explanation for persistent hyperphosphatemia and hypoparathyroidism was found. To date, there have been some reports linking severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to widespread tissue injury; however, there have been no reports so far on the effect of the parathyroid gland. Further studies are necessary to elaborate and to confirm the causative relationship between SARS-CoV-2 and hyperphosphatemia.

A Rare Complication of Myocardial Infarction: Ventricular Septal Defect.

Ventricular septal defect (VSD) is a rare but lethal complication of myocardial infarction. We present a case of a 65-year-old male who presented with a history of progressive shortness of breath associated with productive cough. Physical examination was significant for crepitation in both lower lung fields and bilateral lower extremity edema. Chest X-ray revealed bilateral reticular opacities with small bilateral pleural effusions. Polymerase chain reaction (PCR) for COVID was positive. Echo showed a left ventricular ejection fraction (LVEF) of 30-35%, ischemic cardiomyopathy, and muscular ventricular septal defects with left to right shunting and severely elevated pulmonary artery systolic pressure. Overtime during the hospital course, he developed respiratory and fulminant hepatic failure. Our patient had VSD due to an undiagnosed old myocardial infarction (MI). Initially heart failure was compensated and treated with medical management. Later on, he developed respiratory complications related to COVID-19 infection as well as hepatic failure in addition to a cardiomyopathy which made him a poor surgical candidate leading to death.