A Rare Case of Epstein-Barr Virus: Infectious Mononucleosis Complicated by Guillain-Barré Syndrome.

Infectious mononucleosis (IM) is an acute disease caused by Epstein-Barr virus (EBV) infection affecting adolescents and young adults. Clinically, IM presents with fever, lymphadenopathy, and tonsillar pharyngitis. Guillain-Barré syndrome (GBS) has been reported as a possible rare complication of IM. IM-induced GBS is known but rarely reported in the literature. Here, we describe the case of a 19-year-old male with no significant medical history who was diagnosed with GBS following EBV-associated IM. A 19-year-old Caucasian male presented from a referring facility after complaining of generalized weakness involving the upper and lower extremity for about five days. Symptoms began with a sensation of tingling and numbness in the fingertips and toes that progressed over five days to where he was no longer able to ambulate. Physical examination was significant for oropharyngeal exudates, posterior oropharyngeal erythema, tonsillar hypertrophy, cervical lymphadenopathy, flaccid paralysis with areflexia, and paresthesia. Diagnostic workup was consistent with IM and GBS based on cerebrospinal findings. He was subsequently admitted to the intensive care unit, where he received plasmapheresis and intravenous immunoglobulin with significant improvement. This is a rare case of EBV-associated IM GBS. IM is a self-limiting disease but can lead to GBS as one of the known but rare complications. Neurological events have been reported in approximately 2% of patients. Only a few cases of IM leading to GBS have been reported in the literature. Detailed history and physical examination can help identify patients with IM-induced GBS. Moreover, increased awareness can help physicians easily identify and manage GBS, enabling timely recognition and initiation of prompt supportive care to improve recovery time.

Incidence of Venous Thromboembolism and Effect of Anticoagulant Dosing in Hospitalized COVID-19 Patients.

Background: Coronavirus disease 2019 (COVID-19) is characterized by coagulopathy and thrombotic events. We examined factors associated with development of venous thromboembolism (VTE) in COVID-19 and to discern if higher dose of anticoagulation was beneficial in these patients. Methods: This study involves an observational study of prospectively collected data in the setting of a large community hospital in a rural setting in Northeast Georgia with COVID-19 between March 1, 2020 and February 5, 2021. Anticoagulation dose (none, standard, intermediate, and therapeutic dosages) was studied in adult patients (≥ 18 years). We constructed multivariable logistic regression model to examine the association of clinical characteristics with VTE. To examine the effect of dose of anticoagulation in preventing VTE, we used inverse probability weighted regression adjustment. Results: Of the 4,645 patients with COVID-19, 251 (5.4%) patients were found to have VTE. Of these, 91 had pulmonary embolism, 148 had deep venous thrombosis (DVT) and 12 had both. A total of 129 of VTE cases were diagnosed at admission. Of all admissions, 12.9% did not receive any DVT prophylaxis, 70.4% received prophylactic dose, 1.3% received intermediate dose and 15.5% received therapeutic dose. Male gender (odds ratio (OR): 1.55, 95% confidence interval (CI): 1.0 - 2.4, P = 0.04) and Black race (OR: 2.0, 95% CI: 1.2 - 3.4, P = 0.01), along with higher levels of lactate dehydrogenase (LDH) and D-dimer were associated with higher odds of developing VTE. Patients receiving steroids had lower rates of VTE (3.9% vs. 8.3%, P < 0.001). Use of intermediate or therapeutic anticoagulation was not associated with lower odds of developing VTE. However, patients on therapeutic anticoagulation had lower odds of in hospital mortality when compared to standard dose (OR: 0.47, 95% CI: 0.27 - 0.80, P = 0.006). Conclusions: In COVID-19, D-dimer and LDH can be useful in predicting VTE. Steroids appear to have some protective role in development of VTE. Therapeutic anticoagulation did not result in lower rates of VTE but was associated with in-hospital mortality.

C1 esterase inhibitor for angiotensin-converting enzyme inhibitor-induced angioedema at a community teaching health system: A brief retrospective propensity-matched cohort study.

INTRODUCTION: Angiotensin-converting enzyme inhibitor (ACEi)-induced angioedema is a serious emergency that can cause life-threatening symptoms and death if not treated promptly. Potential treatment options for ACEi-induced angioedema include medications with limited evidence for use in this patient population. The purpose of this study was to evaluate the use, clinical efficacy, and angioedema-related medication costs of C1 esterase inhibitor (C1EI) for ACEi-induced angioedema. METHODS: This was a retrospective, propensity-matched cohort study comparing patients who received C1EI to those who did not receive C1EI for ACEi-induced angioedema. The primary outcome of interest was comparing the proportion of patients who required intubation secondary to ACEi-induced angioedema. Secondary endpoints of interest were also included. RESULTS: After propensity score matching, 22 patients were stratified into both the non-C1EI group and C1EI group, respectively. There was no difference between the groups with respect to the proportion of intubation (13.6% in the C1EI group vs. 9.1% in the non-C1EI group, p > 0.999). Mean cost of angioedema-related medication therapy was higher in the C1EI group compared to the non-C1EI group [$8758.95 (± $2959.30) vs. $15.91 (± $7.32), p < 0.001]. CONCLUSIONS: In this retrospective cohort study, the use of C1EI for ACEi-induced angioedema did not demonstrate improved outcomes with respect to intubation and resulted in increased costs. Larger, multicenter, prospective studies are needed to further validate the results of this study and to provide more clarity on the role of C1EI therapy in ACEi-induced angioedema.

Heparin-Induced Renal Tubular Acidosis Masquerading as Hyperkalemia in a SARS-CoV-2 (COVID-19) Patient: A Case Report.

Type 4 renal tubular acidosis (RTA) is a type of metabolic acidosis characterized by hyperchloremia and hyperkalemia resulting from the reduction in and/or resistance to aldosterone. RTA can be caused by multiple different medications including angiotensin-converting enzyme (ACE) inhibitor/angiotensin receptor blocker (ARB), potassium-sparing diuretics, and heparin. In this case, we discuss renal tubular acidosis caused by heparin use for the prevention of thromboembolic disease in COVID-19 infections.

Predictors and outcomes of healthcare-associated infections in COVID-19 patients.

INTRODUCTION: Healthcare-associated infections (HAI) after viral illnesses are important sources of morbidity and mortality. This has not been extensively studied in hospitalized COVID-19 patients. METHODS: This study included all COVID-19-positive adult patients (≥18 years) hospitalized between 01 March and 05 August 2020 at the current institution. The Centers for Disease Control and Prevention definition of HAI in the acute care setting was used. The outcomes that were studied were rates and types of infections and in-hospital mortality. Several multivariable logistic regression models were constructed to examine characteristics associated with development of HAI. RESULTS: Fifty-nine (3.7%) of 1565 patients developed 140 separate HAIs from 73 different organisms: 23 were Gram-positive, 39 were Gram-negative and 11 were fungal. Patients who developed HAI did not have higher odds of death (OR 0.85, 95% CI 0.40-1.81, p = 0.69). HAIs were associated with the use of tocilizumab (OR 5.04, 95% CI 2.4-10.6, p < 0.001), steroids (OR 3.8, 95% CI 1.4-10, p = 0.007), hydroxychloroquine (OR 3.0, 95% CI 1.0-8.8, p = 0.05), and acute kidney injury requiring hemodialysis (OR 3.7, 95% CI 1.1-12.8, p = 0.04). CONCLUSIONS: HAI were common in hospitalized Covid-19 patients. Tocilizumab and steroids were associated with increased risk of HAIs.