Fulminant

About: Fulminant is a research topic. Over the lifetime, 3888 publications have been published within this topic receiving 74759 citations.

COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options.

Abstract: The novel coronavirus disease (COVID-19) outbreak, caused by SARS-CoV-2, represents the greatest medical challenge in decades. We provide a comprehensive review of the clinical course of COVID-19, its comorbidities, and mechanistic considerations for future therapies. While COVID-19 primarily affects the lungs, causing interstitial pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects multiple organs, particularly the cardiovascular system. Risk of severe infection and mortality increase with advancing age and male sex. Mortality is increased by comorbidities: cardiovascular disease, hypertension, diabetes, chronic pulmonary disease, and cancer. The most common complications include arrhythmia (atrial fibrillation, ventricular tachyarrhythmia, and ventricular fibrillation), cardiac injury [elevated highly sensitive troponin I (hs-cTnI) and creatine kinase (CK) levels], fulminant myocarditis, heart failure, pulmonary embolism, and disseminated intravascular coagulation (DIC). Mechanistically, SARS-CoV-2, following proteolytic cleavage of its S protein by a serine protease, binds to the transmembrane angiotensin-converting enzyme 2 (ACE2) -a homologue of ACE-to enter type 2 pneumocytes, macrophages, perivascular pericytes, and cardiomyocytes. This may lead to myocardial dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque instability, and myocardial infarction (MI). While ACE2 is essential for viral invasion, there is no evidence that ACE inhibitors or angiotensin receptor blockers (ARBs) worsen prognosis. Hence, patients should not discontinue their use. Moreover, renin-angiotensin-aldosterone system (RAAS) inhibitors might be beneficial in COVID-19. Initial immune and inflammatory responses induce a severe cytokine storm [interleukin (IL)-6, IL-7, IL-22, IL-17, etc.] during the rapid progression phase of COVID-19. Early evaluation and continued monitoring of cardiac damage (cTnI and NT-proBNP) and coagulation (D-dimer) after hospitalization may identify patients with cardiac injury and predict COVID-19 complications. Preventive measures (social distancing and social isolation) also increase cardiovascular risk. Cardiovascular considerations of therapies currently used, including remdesivir, chloroquine, hydroxychloroquine, tocilizumab, ribavirin, interferons, and lopinavir/ritonavir, as well as experimental therapies, such as human recombinant ACE2 (rhACE2), are discussed.

Long-term outcome of fulminant myocarditis as compared with acute (nonfulminant) myocarditis.

Abstract: Background Lymphocytic myocarditis causes left ventricular dysfunction that may be persistent or reversible. There are no clinical criteria that predict which patients will recover ventricular function and which cases will progress to dilated cardiomyopathy. We hypothesized that patients with fulminant myocarditis may have a better long-term prognosis than those with acute (nonfulminant) myocarditis. Methods We identified 147 patients considered to have myocarditis according to the findings on endomyocardial biopsy and the Dallas histopathological criteria. Fulminant myocarditis was diagnosed on the basis of clinical features at presentation, including the presence of severe hemodynamic compromise, rapid onset of symptoms, and fever. Patients with acute myocarditis did not have these features. The incidence of the end point of this study, death or heart transplantation, was ascertained by contact with the patient or the patient's family or by a search of the National Death Index. The average period of fol...

Fulminant Clostridium difficile: An underappreciated and increasing cause of death and complications

Abstract: Clostridium difficile is a spore-forming gram-positive bacteria first identified as the cause of antibiotic-associated diarrhea and colitis in the late 1970s. 1,2 The clinical symptoms range from mild diarrhea to hemodynamic collapse and death. Recent antimicrobial use (<2 months) is the most important risk factor for the development of C. difficile colitis; however, host and environmental factors also play a significant role. 3,4 Most cases can be treated by the administration of metronidazole or vancomycin to reverse the overgrowth of C. difficile and its toxin production in the colon, but a wide spectrum of disease exists; in some patients life-threatening systemic toxicity develops despite appropriate and timely medical therapy. 5,6 A classification scheme of disease severity is detailed in Table 1. Systemic symptoms are not derived from bacteremia, colonic perforation, or ischemia, but from toxin-induced inflammatory mediators (interleukin-8, macrophage-inflammatory protein-2, substance P, tumor necrosis factor-α) released locally in the colon. 7–9 Why some patients have more marked symptoms than others is unclear but may relate to the host’s ability to mount an effective antibody-mediated response to clostridial toxins. 10,11 Uncharacterized geographic factors also seem to play a major role in the incidence and severity of disease. Table 1. SEVERITY CLASSIFICATION SCHEME IN PATIENTS WITH CLOSTRIDIUM DIFFICILE Total abdominal colectomy and end ileostomy, the standard surgical treatment for patients with severe C. difficile colitis, has been described only in small series, the largest (n = 12) from our hospital published in 1992. 12–16 Recently we have noted an increase in the number of emergency colectomies for this disease. The purpose of the study was to define the epidemiology, clinical presentation, and risk factors peculiar to the fulminant syndrome. In addition, we tried to determine predictors of surgical death.