The coronavirus disease 2019 (COVID-19) pandemic due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has challenged health-care systems and physicians worldwide to attempt to provide the best care to their patients with an evolving understanding of this unique pathogen. This disease and its worldwide impact have sparked tremendous interest in the epidemiology, pathogenesis, and clinical consequences of COVID-19. This accumulating body of evidence has centered around case series and often empiric therapies as controlled trials are just getting underway. What is clear is that patients appear to be at higher risk for thrombotic disease states including acute coronary syndrome (ACS), venous thromboembolism (VTE) such as deep vein thrombosis (DVT) or pulmonary embolism (PE), or stroke. Patients with underlying cardiovascular disease are also at higher risk for morbidity and mortality if infected. These patients are commonly treated with anticoagulation and/or antiplatelet medications and less commonly thrombolysis during hospitalization, potentially with great benefit but the management of these medications can be difficult in potentially critically ill patients. In an effort to align practice patterns across a large health system (Jefferson Health 2,622 staffed inpatient beds and 319 intensive care unit (ICU) beds across 14 facilities), a task force was assembled to address the utilization of anti-thrombotic and anti-platelet therapy in COVID-19 positive or suspected patients. The task force incorporated experts in Cardiology, Vascular Medicine, Hematology, Vascular Surgery, Pharmacy, and Vascular Neurology. Current guidelines, consensus documents, and policy documents from specialty organizations were used to formulate health system recommendations. Objective: Our goal is to provide guidance to the utilization of antithrombotic and antiplatelet therapies in patients with known or suspected COVID-19.
In a tertiary, academic, advanced CICU, patients are elderly with a high burden of non-cardiovascular comorbid conditions. Care has shifted from ACS toward predominantly shock and cardiac arrest, as well as non-ischemic conditions, and the mortality of these conditions is high. These data may be useful to guide cardiac critical care redesign.
Pump‐induced thrombosis continues to be a major complication of continuous‐flow left ventricular assist devices (CF‐LVADs), which increases the risks of thromboembolic stroke, peripheral thromboembolism, reduced pump flow, pump failure, cardiogenic shock, and death. This is confounded by the fact that there is currently no direct measure for a proper diagnosis during pump support. Given the severity of this complication and its required treatment, the ability to accurately differentiate CF‐LVAD pump thrombosis from other complications is vital. Hemolysis measured by elevated lactate dehydrogenase (LDH) enzyme levels, when there is clinical suspicion of pump‐induced thrombosis, is currently accepted as an important metric used by clinicians for diagnosis; however, LDH is a relatively nonspecific finding. LDH exists as five isoenzymes in the body, each with a unique tissue distribution. CF‐LVAD pump thrombosis has been associated with elevated serum LDH‐1 and LDH‐2, as well as decreased LDH‐4 and LDH‐5. Herein, we review the various isoenzymes of LDH and their utility in differentiating hemolysis seen in CF‐LVAD pump thrombosis from other physiologic and pathologic conditions as reported in the literature.
The purpose of this study was to determine the incidence of patient-reported numbness following anterior cruciate ligament reconstruction (ACLR), if postoperative numbness dissipates with time, and how the graft type affects numbness severity. A total of 218 patients undergoing ACLR were prospectively enrolled. At 6 weeks, 6 months, and 1 year postoperatively, patients completed a questionnaire assessing numbness severity and location. Each time, patients rated their sensory deficit from 0 to 10 (0 = no deficit; 10 = complete lack of sensation) and indicated the location of their sensory deficit by marking a picture of a knee divided into nine rectangular segments. A mixed effect linear regression model was used to identify predictors for the patient-reported numbness severity. Overall, 69.8% (150/218) of patients reported numbness at 6 weeks, 50.0% (97/194) at 6 months, and 42.2% (78/185) at 1 year. Allograft patients reported a mean numbness severity of 2.9 ± 0.3 (mean ± standard error), 1.7 ± 0.2, and 1.4 ± 0.3 at 6 weeks, 6 months, and 1 year, respectively. The 6-week, 6-month, and 1-year averages were 4.7 ± 0.4, 2.7 ± 0.4, and 1.7 ± 0.4 for bone-patellar tendon-bone (BTB) autograft patients and 4.3 ± 0.4, 2.9 ± 0.4, and 2.5 ± 0.4 for hamstring autograft patients. The model indicated that the use of hamstring autografts increased patient-reported numbness by an average of 1.4 ± 0.5 across all time points, and the use of a BTB autograft increased patient-reported numbness by 1.2 ± 0.4 across all time points. Time from surgery decreased the severity of patient-reported numbness for all graft types (-1.3 ± 0.2 at 6 months and -1.7 ± 0.2 at 1 year). Hypoesthesia in the distribution of the infrapatellar branch of the saphenous nerve is common after ACLR but is likely to dissipate with time. Patients undergoing ACLR with allograft may be less likely to develop sensory deficits, and these deficits may be less severe.
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