ABSTRACT
BACKGROUND: The COVID-19 infection which emerged in December 2019, is caused by the virus SARS-CoV-2. Infection with this virus can lead to severe respiratory illness, however, myocarditis has also been reported. The purpose of this study is to identify the clinical features of myocarditis in COVID-19 patients. METHODS: A systematic review was conducted to investigate characteristics of myocarditis in patients infected with COVID-19 using the search term "Coronavirus" or "COVID" and "myocarditis," "heart," or "retrospective." Case reports and retrospective studies were gathered by searching Medline/Pubmed, Google Scholar, CINAHL, Cochrane CENTRAL, and Web of Science databases. 11 articles were selected for review. RESULTS: COVID-19 myocarditis affected patients over the age of 50 and incidences among both genders were equally reported. Patients presented with dyspnea, cough, fever with hypotension and chest pain. Laboratory tests revealed leukocytosis with increased C-reactive protein, while arterial blood gas analysis demonstrated respiratory acidosis. All cardiac markers were elevated. Radiographic imaging of the chest showed bilateral ground glass opacities or bilateral infiltrates, while cardiac magnetic resonance imaging produced late gadolinium enhancements. Electrocardiography demonstrated ST-segment elevation or inverted T waves, while echocardiography revealed reduced left ventricular ejection fraction with cardiomegaly or increased wall thickness. Management with corticosteroids was favored in most cases, followed by antiviral medication. The majority of studies reported either recovery or no further clinical deterioration. CONCLUSION: Current available data on COVID-19 myocarditis is limited. Further research is needed to advance our understanding of COVID-19 myocarditis.
ABSTRACT
Coronavirus Disease-2019 (COVID-19) is currently a public health emergency and has been listed by the World Health Organization (WHO) as a pandemic. It has commonly been associated with pulmonary manifestations and there is a growing body of evidence of multisystem involvement of the virus. As evidenced by various case reports and cohort studies, COVID-19-associated coagulopathy has been a common manifestation amongst the critically ill and has been associated with increased mortality. The presence of venous thromboembolic events in patients who are critically ill due to COVID-19 has prompted the adoption of anticoagulation regimens aimed at preventing thromboembolic phenomena. Coagulation abnormalities have also been implicated in the progression and the severity of COVID-19 related acute respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC). There is strong evidence that D-dimer levels help predict which patients are at risk of thromboembolic events, progression to ARDS, DIC, immune dysregulation and mortality. We will review the utility of D-dimer as screening tool and in the risk stratification of COVID-19 patients prone to developing thromboembolic events, DIC, immune dysregulation and death. To date, the studies that have been published show the presence of elevated D-dimer levels in both the adult and pediatric populations and the measured level correlates with disease severity. Studies have also shown the relative increase of D-dimer levels in non-survivors compared to survivors. The elevation of D-dimer levels has shown to guide clinical decision making, namely the initiation of therapeutic anticoagulation and mortality benefit in patients with severe COVID-19 pneumonia compared to severe non COVID-19 pneumonia. Although the current body of literature suggested the use of D-dimer as a risk stratification tool and as a test to augment clinical judgement regarding the initiation of anticoagulation, randomized control trials are needed to fully understand the relationship between COVID-19 infection and the efficacy of D-dimer assays in clinical decision making.
ABSTRACT
Pseudomonas mendocina is a Gram-negative bacillus from the family Pseudomonadaceae. The first P. mendocina-related infection was reported in 1992. Although a rare cause of infections, P. mendocina has been known to cause severe infections that require intensive treatment. We present the first documented case of urinary tract infection caused by P. mendocina. An 83-year-old male with a past medical history of diabetes, hypertension, coronary artery disease, and prostate cancer with bone metastases, currently being treated with abiraterone and prednisone, presented with subjective fever, fatigue, altered mental status, dysuria, and hematuria of one-week duration. He was found to have a complicated urinary tract infection with an incidental asymptomatic COVID-19 infection on admission. The patient was empirically treated with ceftriaxone and switched to cefepime for broader coverage on day two of hospitalization. Urine culture reported the presence of P. mendocina with resistance only to fluoroquinolones. Ceftriaxone was reinstated. The patient was successfully treated with a seven-day course of ceftriaxone (days 1-3, days 6-7) and cefepime (days 4-5) but continued to remain inpatient for a later symptomatic COVID-19 pneumonia with discharge on day 15. The majority of P. mendocina infections present as skin and soft tissue infections, infective endocarditis, meningitis, and bacteremia. Ours is the first documented case of urinary tract infection caused by P. mendocina, particularly in an immunocompromised COVID-19 patient, and the second to report P. mendocina with resistance to fluoroquinolones. This report contributes to the growing literature regarding P. mendocina-related infections.
ABSTRACT
BACKGROUND: The COVID-19 infection which emerged in December 2019, is caused by the virus SARS-CoV-2. Infection with this virus can lead to severe respiratory illness, however, myocarditis has also been reported. The purpose of this study is to identify the clinical features of myocarditis in COVID-19 patients. METHODS: A systematic review was conducted to investigate characteristics of myocarditis in patients infected with COVID-19 using the search term "Coronavirus" or "COVID" and "myocarditis," "heart," or "retrospective." Case reports and retrospective studies were gathered by searching Medline/Pubmed, Google Scholar, CINAHL, Cochrane CENTRAL, and Web of Science databases. 11 articles were selected for review. RESULTS: COVID-19 myocarditis affected patients over the age of 50 and incidences among both genders were equally reported. Patients presented with dyspnea, cough, fever with hypotension and chest pain. Laboratory tests revealed leukocytosis with increased C-reactive protein, while arterial blood gas analysis demonstrated respiratory acidosis. All cardiac markers were elevated. Radiographic imaging of the chest showed bilateral ground glass opacities or bilateral infiltrates, while cardiac magnetic resonance imaging produced late gadolinium enhancements. Electrocardiography demonstrated ST-segment elevation or inverted T waves, while echocardiography revealed reduced left ventricular ejection fraction with cardiomegaly or increased wall thickness. Management with corticosteroids was favored in most cases, followed by antiviral medication. The majority of studies reported either recovery or no further clinical deterioration. CONCLUSION: Current available data on COVID-19 myocarditis is limited. Further research is needed to advance our understanding of COVID-19 myocarditis.
ABSTRACT
BACKGROUND: The COVID-19 infection which emerged in December 2019, is caused by the virus SARS-CoV-2. Infection with this virus can lead to severe respiratory illness, however, myocarditis has also been reported. The purpose of this study is to identify the clinical features of myocarditis in COVID-19 patients. METHODS: A systematic review was conducted to investigate characteristics of myocarditis in patients infected with COVID-19 using the search term "Coronavirus" or "COVID" and "myocarditis," "heart," or "retrospective." Case reports and retrospective studies were gathered by searching Medline/Pubmed, Google Scholar, CINAHL, Cochrane CENTRAL, and Web of Science databases. 11 articles were selected for review. RESULTS: COVID-19 myocarditis affected patients over the age of 50 and incidences among both genders were equally reported. Patients presented with dyspnea, cough, fever with hypotension and chest pain. Laboratory tests revealed leukocytosis with increased C-reactive protein, while arterial blood gas analysis demonstrated respiratory acidosis. All cardiac markers were elevated. Radiographic imaging of the chest showed bilateral ground glass opacities or bilateral infiltrates, while cardiac magnetic resonance imaging produced late gadolinium enhancements. Electrocardiography demonstrated ST-segment elevation or inverted T waves, while echocardiography revealed reduced left ventricular ejection fraction with cardiomegaly or increased wall thickness. Management with corticosteroids was favored in most cases, followed by antiviral medication. The majority of studies reported either recovery or no further clinical deterioration. CONCLUSION: Current available data on COVID-19 myocarditis is limited. Further research is needed to advance our understanding of COVID-19 myocarditis.