ABSTRACT
Background: Central venous catheter (CVC) is the preferred vascular access in critically-ill patients needing kidney replacement therapy (KRT). Non-tunneled CVC (NT-CVC) is frequently selected for bedside placement and provider familiarity. With hemodynamic instability, tunneled CVC (T-CVC), despite its known advantages of lower infection risk, lower mechanical complications, better blood flow rates and patient comfort, is infrequently considered due to competing demands for central vein access, and provider inexperience. We report our early experience of building a collaborative training program to improve vascular access approach in the critically-ill patients. Methods: A single center retrospective study of T-CVC placed in an adult medical ICU between March 1, 2020 and December 31, 2020 by a nephrologist or an intensivist. The T-CVCs were placed in hemodynamically unstable patients for KRT and other medical therapies. Statistical analysis was limited to assess feasibility and safety of implementing a collaborative procedural service in an academic medical ICU. Results: A total of 120 CVC related procedures were completed during the study period. 106 were T-CVC placements (68 for KRT, 38 small bore non-KRT), seven T-CVC removals, one difficult NT-CVC for KRT, one T-CVC exchange, one fluoroscopy guided repositioning of NT-CVC, four aborted for suspected central vein occlusion. Twentyseven T-CVC (23 in COVID-19 positive and 4 for other compelling reasons) were placed at bedside with ultrasound guidance and anatomical landmarks without fluoroscopy. A safety pre-procedure checklist was developed for eligibility based on this experience. A minimum of 48-hr sterile blood culture report was essential to proceed. Complex comorbidities included coagulopathic patients. A minimum training competency was established and 2 critical care staff physicians were credentialed during this period. No major complications were encountered. Conclusions: A collaborative care model between nephrology and medical ICU for T-CVC focused strategy is feasible. T-CVC can be placed safely in a carefully selected critically-ill patient population. Training intensivists with basic procedural skills for T-CVC procedure is achievable over a short period.
ABSTRACT
Background: Acute kidney injury (AKI) can be a severe complication of COVID-19, particularly in those who require intensive care. Its relationship to the incidence of proteinuria, hematuria, and elevated inflammatory markers has not been well characterized. Our objective is to describe the incidence of AKI in COVID-19, and its association with inflammatory markers. Methods: Retrospective cohort study of adult patients hospitalized at the Cleveland Clinic with COVID-19. SARS-CoV-2 infection was confirmed by virus detection in respiratory specimens using RT-PCR. AKI was diagnosed per KDIGO serum creatininebased classification. We selected stage 2 and higher as our primary endpoint for the study. Baseline creatinine was defined as the most recent pre-admission level available within 3 months of presentation. Acute lung injury was defined by the need for mechanical ventilation. Results: The incidence of AKI was 14% in 621 hospitalized COVID-19 patients, with half requiring kidney replacement therapy (KRT). The incidence of proteinuria and microscopic hematuria were high in these patients (83% and 77% respectively). Seventy five percent of patients with AKI needed mechanical ventilation, and timing of KRT overlapped with time of mechanical ventilation. Inflammatory markers and acute phase reactants, including LDH, ferritin, and C reactive protein were significantly higher in patients with AKI compared to those with no AKI. On adjusted analysis, hematuria and elevated LDH levels were significantly associated with AKI (Figure). Conclusions: Elevated lactate dehydrogenase levels and microscopic hematuria on presentation are independently associated with 50% probability of moderate to severe AKI. Our findings suggest a possible pathogenetic mechanism of endothelial cell injury and thrombotic microangiopathy as a cause of AKI in COVID-19 patients. Additional studies are needed to explore this potential mechanism of AKI in COVID-19.