ABSTRACT
Guillain-Barré syndrome (GBS) in an immune mediated disease that affects peripheral nerves with possible life-threatening complications. GBS has multiple subtypes including acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN) and acute motor sensory axonal neuropathy (AMSAN), which can make GBS difficult to diagnose. GBS commonly presents after viral infections such as influenza virus, campylobacter jejuni, and zika virus. GBS commonly presents with a prolonged clinical course leading to increased morbidity among affected patients. It is not surprising that COVID-19 has been connected with multiple cases of GBS, which may alter the recovery course for several patients post-COVID. In this report, we present a case of 69-year-old-female who presented with progressive motor weakness and loss of sensation in her extremities after testing positive for antibodies to COVID-19 one-month prior to presentation. Her presentation and treatment of GBS in the setting of COVID-19 is an example of one of the many COVID-19 complications and sheds light on the prolonged recovery course that we may experience as clinicians in the wake of this pandemic.
ABSTRACT
Coronavirus disease 2019 (COVID-19) is a pandemic that started in the Wuhan province of China in December 2019. It is associated with increased morbidity and mortality mainly due to severe acute respiratory syndrome 2 (SARS-Cov-2). Cardiac manifestations related to COVID-19 include demand ischemia, fulminant myocarditis, myocardial infarction and arrhythmias. In this report, we present a case of ST-segment elevation myocardial infarction (STEMI) in a 68-year-old man with COVID-19 who initially presented with chest pain and shortness of breath. Patient's STEMI was managed with pharmaco-invasive strategy with tissue plasminogen activator (t-PA). He then developed acute hypoxic respiratory failure that was managed in the intensive care unit (ICU), together with multi-organ failure from which the patient died 2 days after presentation. Although the pathophysiologic mechanisms of STEMI in COVID-19 patients has not been clearly established, we hypothesize that interrelated pathogenetic factors, that we highlight in this report, can play a role in the development of STEMI, including plaque rupture secondary to systemic inflammation, increased pro-coagulants, endothelial dysfunction, impaired fibrinolysis and impaired oxygen utilization leading to demand/supply mismatch and myocardial ischemia.
ABSTRACT
Coronavirus disease 2019 (COVID-19) is a pandemic that started in China in December 2019 and carries a high risk of morbidity and mortality. To-date (4-22-2020) it affected over 2.6 million people and resulted in nearly 200,000 death worldwide mainly due to severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2). Among the major underlying pathophysiologic mechanisms in COVID 19 is hypercoagulability, leading to increased risk for deep vein thrombosis and pulmonary embolism that contribute to increased morbidity and mortality. In this report, we present the case of a 55-year-old man who presented with COVID-19 pneumonia, and was found to have a thrombus in transit by routine point of care ultrasound (POCUS). While computer tomography (CT) angiography is the test of choice, the utilization of point of care ultrasound (POCUS) has gained traction as an adjunctive means of surveillance for the development of VTE in patients with COVID-19. In this report, we discuss the clinical utility of POCUS in diagnosing thrombus in transit in COVID 19 populations.
ABSTRACT
COVID-19 is a pandemic that started in Wuhan city, Hubei province in China in December 2019 and is associated with high morbidity and mortality. It is characterized by a heightened inflammatory and prothrombotic state that are known to cause various cardiovascular manifestations such as thromboembolism, acute coronary syndrome and stroke. We here present a 72-year-old woman with multiple cardiovascular risk factors and COVI 19 pneumonia who presented with acute ischemic stroke. She was also noted to have ST segment elevation myocardial infarction (STEMI) on the electrocardiogram however the imaging and clinical presentation was consistent with apical takotsubo cardiomyopathy. We here discuss the various pathophysiologic mechanisms by which COVID-19 can result in acute stroke. The patient likely developed takotsubo cardiomyopathy because of stroke and acute COVID-19 induced sympathetic stimulation and catecholamine surge. To the best of our knowledge this is the first case of apical variant of takotsubo cardiomyopathy in a COVID-19 report.
ABSTRACT
Immune checkpoint inhibitors have opened a new era in treating advanced malignancies, resulting in a rapid increase in utilization, given the remarkable clinical outcomes. The incidence of immune-related adverse events increased due to the immunologic effects of these therapeutic agents. However, immune-related renal adverse events remain low, representing only a small incidence of reported cases. Common renal toxicity described includes acute interstitial nephritis, minimal change disease, and immune complex glomerulonephritis. Renal tubular acidosis has occasionally been reported but is highly uncommon. This report presents a case of a 68-year-old woman with a known history of metastatic melanoma undergoing treatment with ipilimumab+nivolumab, who developed distal renal tubular acidosis requiring stress dose steroids and sodium bicarbonate for treatment. We describe the clinical characteristics, potential mechanisms, and management of this case, highlighting the need among clinicians utilizing immune check inhibitors to be aware of this immune-related disease entity.
ABSTRACT
Coronavirus disease 2019 (COVID-19) is associated with various cardiovascular manifestations, including myocarditis, myocardial infarction, and arrhythmias. A prothrombotic state is the primary underlying pathogenic mechanism. While cardiac arrhythmias manifest more commonly amongst critically ill COVID-19 populations, ventricular arrhythmias have been reported only in few cases. This report describes a case of a 95-year-old African American man with COVID-19, who developed sustained monomorphic ventricular tachycardia, which progressed to an electrical storm. The case highlights the importance of high clinical suspicion, early recognition of electrical abnormalities in patients with active COVID-19 infection, and its ability to precipitate fatal ventricular arrhythmia. Also, we provide a literature review on the electrical storm in COVID-19 patients, highlighting the pathophysiologic mechanisms and the management of this deadly arrhythmia.
ABSTRACT
COVID-19 caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is associated with significant cardiovascular dysfunction in patients with, and without, pre-existing cardiovascular disease [1]. There are now well-documented cardiac complications of COVID-19 infection which include myocarditis, heart failure, and acute coronary syndrome [2]. There is growing evidence showing that arrhythmias are also one of the major complications of COVID-19. We report a patient with no known cardiac conduction disease who presented with syncope, positive SARS-CoV-2 PCR, who was persistently bradycardic and subsequently developed sinus node dysfunction (SND). To date, there are a limited number of reports of sinus node dysfunction (SND) associated with COVID-19. We describe the clinical characteristics, potential pathophysiologic mechanisms and management of COVID-19 patients who experienced de novo SND.
ABSTRACT
Various electrocardiographic (EKG) manifestations have been reported in patients with coronavirus disease 2019 (COVID-19). There is growing evidence showing that new onset QT-prolongation is a common EKG finding in COVID-19 patients. In this report, we present a case of a 71-year-old man who was found to have a new onset, irreversible, prolonged QT-interval requiring permanent biventricular pacemaker despite testing negative twice for RT-PCR COVID-19 and correction of all known reversible causes. To date, there are a limited number of reports of irreversible QT-prolongation associated with COVID-19. This case report emphasizes the importance of a physician's clinical judgment in the setting of negative RT-PCR COVID-19 testing. A robust systemic inflammatory state seen in active COVID-19 infection is possibly the key mechanism precipitating the new EKG findings.
ABSTRACT
Thrombosis is one of the major underlying pathogenetic mechanisms leading to increased morbidity and mortality among COVID-19 patients. Thromboembolic events as well as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) are the major causes of death in this continued pandemic. While elevated D-dimer level suggests worse thrombotic outcomes, levels at which benefits of anticoagulation outweigh the bleeding risk is yet to be determined. In this report, we present a case of a 72-year-old man with COVID-19 presented with confusion and subsequently developed acute hypoxic respiratory failure. On hospital day 7, patient developed extensive peripheral arterial thrombosis with acute rise of D-dimer from 800 to 14,899 ng/ml. He was treated with heparin drip and underwent urgent brachial, radial and ulnar embolectomy under general anesthesia. In this report, we also discuss the pathogenetic mechanisms and management of thromboembolism in COVID-19 patients, highlighting the role of early detection and aggressive therapeutic interventions that could be life and / or limb saving strategy.
ABSTRACT
Coronavirus disease 2019 (COVID-19) has rapidly evolved into a global pandemic, with affecting to-date over 23 million people and causing over 800,000 deaths around the globe. The major pathogenetic mechanisms include inflammation, vasoconstriction and thrombogenesis. Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) typically manifests as fever, cough, shortness of breath, and exhibits radiographic evidence of bilateral pneumonic infiltrates. Recent meta-analyses have shown that myocardial injury, including viral myocarditis, is prevalent among infected patients, especially in patients requiring ICU level care. Diagnosis of viral myocarditis is multifactorial and involves detection of elevated cardiac biomarkers and echocardiographic evidence of cardiomyopathy, in the absence of diseased coronary arteries. Endomyocardial biopsy with histopathologic examination provides definitive confirmation. We present a case of a previously healthy 52-year-old male who presented clinically with suspected myocarditis with new-onset dilated cardiomyopathy (DCM) and systolic dysfunction as a sequela of infection with SARS-CoV-2. In this report we highlight the clinical presentation of echocardiographic findings and proposed pathogenetic mechanisms of myocarditis associated with COVID-19 which has a varied presentation, ranging from clinically silent to life-threatening arrhythmias with hemodynamic compromise.
ABSTRACT
Mounting evidence shows a disproportionate COVID-19 burden among Blacks. Early findings indicate pre-existing metabolic burden (eg, obesity, hypertension and diabetes) as key drivers of COVID-19 severity. Since Blacks exhibit higher prevalence of metabolic burden, we examined the influence of metabolic syndrome on disparate COVID-19 burden. We analyzed data from a NIH-funded study to characterize metabolic burden among Blacks in New York (Metabolic Syndrome Outcome Study). Patients (n=1035) were recruited from outpatient clinics, where clinical and self-report data were obtained. The vast majority of the sample was overweight/obese (90%); diagnosed with hypertension (93%); dyslipidemia (72%); diabetes (61%); and nearly half of them were at risk for sleep apnea (48%). Older Blacks (age≥65 years) were characterized by higher levels of metabolic burden and co-morbidities (eg, heart disease, cancer). In multivariate-adjusted regression analyses, age was a significant (p≤.001) independent predictor of hypertension (OR=1.06; 95% CI: 1.04-1.09), diabetes (OR=1.03; 95% CI: 1.02-1.04), and dyslipidemia (OR=0.98; 95% CI: 0.97-0.99), but not obesity. Our study demonstrates an overwhelmingly high prevalence of the metabolic risk factors related to COVID-19 among Blacks in New York, highlighting disparate metabolic burden among Blacks as a possible mechanism conferring the greater burden of COVID-19 infection and mortality represented in published data.
ABSTRACT
Novel coronavirus disease (COVID-19) is a pandemic affecting over 10 million people in 160 countries. Its spread, and the medical communities' response, cast light on an important deficiency in the speed and effectiveness for evidence-based recommendations to reach the bedside in academic medical practice. We built a clinical decision support tool on the avoMD platform that systematizes and personalizes the treatment of COVID-19 by bringing point-of-care access to the guidelines specific to individual cases to the clinician's hands. This app has the potential to improve the mortality for COVID-19.
ABSTRACT
Coronavirus disease 2019 (COVID-19) is a pandemic that started in Wuhan city, Hubei province in China in December 2019 and is associated with high morbidity and mortality. This pandemic has overwhelmed health care systems in the USA, Europe and many other countries around the globe. Several health care institutions, including ours, SUNY-Downstate Health Science University in Brooklyn, New York, were designated as COVID-only hospitals. At the same time, patients with other serious illnesses refrained from seeking medical care because of the fear of contracting the virus at the health care facilities. In this report, we present a case of an octogenarian woman with breast cancer who was treated initially with radical mastectomy and chemotherapy, who then developed back pain in mid-March 2020, that later progressed to bilateral lower extremity weakness secondary to cord compression, which was diagnosed nearly 4 weeks after her initial symptoms started. The patient had refrained from seeking medical care citing fear of contracting COVID-19 in the hospital. This case illustrates the dire need to establish mechanisms within our health care system to manage oncologic (and other life or limb threatening) emergencies during times such as the COVID-19 pandemic.
ABSTRACT
The severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, is the most serious pandemic in modern times. The disease was first reported in January of 2020 in China's city of Wuhan, Hubei province, and since then it has spread worldwide. Given the rapid spread of the virus and the burden it has taken on the healthcare systems it has swept through, there is the need for a concise description of current understanding of the pathogenesis of organ failure in SARS-CoV-2 infection while acknowledging that more is yet to be uncovered. This review will not only inform decision making at the bedside but will also help illustrate potential therapeutic targets for research. We searched the available literature to-date, and present the pathophysiology underlying increased morbidity and mortality of SARS-CoV-2 infection in the lungs, heart and kidneys in a highly illustrated presentation that is easy-to-understand for the clinician, researcher, and student alike.
ABSTRACT
Cardiac manifestations of COVID-19 include myocarditis, demand ischemia, myocardial infarction and arrhythmias with prothrombotic state being a major underlying pathogenetic mechanism. In this report we present a case of a 57-year-old, otherwise healthy, woman who presented with chest pain and nausea and was found to have an inferior wall ST-elevation myocardial infarction (STEMI) in the setting of an active COVID-19 infection. Angiography revealed tortuous coronary arteries with a 100% right coronary artery occlusion with high thrombus burden and normal left coronary system. In light of the available literature regarding the pro-thrombotic effects of this novel corona virus, we continued full dose anticoagulation with Enoxaparin after the cardiac catheterization and transitioned to rivaroxaban and we also continued the patient on dual antiplatelet therapy prior to discharge.