ABSTRACT
Objectives: Reporting a case of a COVID-19 vaccinated patient admitted to our intensive care unit with severe acute respiratory failure due to SARSCoV2 - Omicron variant, rapidly deteriorating requiring intubation, prone ventilation, and ECMO support. Method(s): A 62 years old Caucasian male was admitted in ICU for rapidly deranging respiratory failure and fever which occurred over the previous 24h. The patient received two doses of SARS-CoV2 vaccine (Oxford, AstraZeneca), the last one over five months before onset of symptoms. The patient was admitted to the intensive care unit (ICU) with tachypnea, low peripheral saturation (80%), elevated serum creatinine (2.4 mg/dl), and mild obesity (BMI 34,6). Pressure support ventilation trial (2 hours) failed carryng out to orotracheal intubation and protective ventilation. Worsening of respiratory exchanges (5 th day from the admission) required a rescue prone ventilation cycle, in the meantime an indication was given to the placement of veno-venous ECMO. The cannulation site was femoro-femoral and the configuration used was Vivc25- Va21, according to the current ELSO nomenclature;ECMO flow was progressively increased until a peripheral saturation of 95% was obtained. Result(s): The patient passed out after 2 month of extracorporeal support with no sign of recovery of pulmonary and renal function. Conclusion(s): Unlike evidences showing a lower symptomatic engagement of the Omicron variant SARSCoV2 positive patients, we have witnessed a rapid and massive pulmonary involvement. The short time that passed from the onset of symptoms and the rapid decay of respiratory function required rapid escalation of the intensity of care up to extracorporeal support. The patient showed previous pathologies that can lead to suspicion of a loss of immune coverage given by the vaccine, in addition to the long time elapsed since the last dose. (Figure Presented).
ABSTRACT
Background/Introduction: The bactericidal/permeability-increasing fold-containing family-B-member-4 (BPIFB4) serves as a biomarker of healthy aging [1,2] and displays prognostic relevance in vascular pathology [3–5]. We recently described a drop in plasma BPIFB4 level in patients with severe COVID-19 compared to low-grade disease patients [6]. Purpose: As COVID-19 is associated with autoimmune features, we developed the methods for determination of Anti-BPIFB4 IgG (autoAbs) and then characterized their neutralizing activity in COVID-19 patients. Methods: A sandwich ELISA-based colorimetric assay followed by immunoblot analysis detected the presence of autoAbs against BPIFB4 in 60 hospitalized COVID-19 patients and in 30 healthy volunteers. Compared to the healthy controls, the optical density (OD) level of autoAbs in COVID-19 showed considerable variability distributing over a range between 0.13 and 0.85. We thus divided the patients into two groups, one with OD >0,29 and the other one with a OD >0,29, where 0,29 represents the OD mean value of autoAbs against BPIFB4 in physiological conditions. Results: Since patients with higher OD are mainly those who spend in average a higher number of days in hospital, we stratified the patients according to the Length of Stay (LoS) in hospital (Figure 1), and found a trend towards a positive correlation between AutoAbs OD level and length of hospitalization within COVID-19 patients.When present, autoAbs exclusively target the WT-BPIFB4 autoantigens and neglect the recognition of the Longevity-associated-variant-(LAV) of the BPIFB4 gene known for its therapeutic efficacy in cardiomyopathy, atherosclerosis (4), diabetes (6) and platelets' reactivity.As expected, the pre-treatment of human PrP with the recombinant rhLAV-BPIFB4 reduces platelets' aggregation in response to ADP and collagen in COVID-19 patients in vitro.On the other hand, at functional level, the well established LAV-BPIFB4-regulated M2 macrophage polarization (4,7), is neutralized in presence of anti-BPIFB4 autoAbs-enriched plasma. Conclusion: We conclude that a significant proportion of hospitalized COVID-19 patients displays BPIFB4-AutoAbs which are positively correlated with the Length of Stay (LoS) in hospital. In future, it will be of utmost importance to clarify if the 4 missense SNPs which distinguish LAV-BPIFB4 gene from its WT-counterpart, are instrumental to prevent the self-tolerance brake-down and the potential development of specific antibodies against endogenous cardiovascular protectors. Funding Acknowledgement: Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Cariplo Foundation (n.2016-0874) to AAP and CV;Ministry of Health (RF-2016-02364864) to AAP and CVFigure 1
ABSTRACT
The inodilator levosimendan, in clinical use for over two decades, has been the subject of extensive clinical and experimental evaluation in various clinical settings beyond its principal indication in the management of acutely decompensated chronic heart failure. Critical care and emergency medicine applications for levosimendan have included postoperative settings, septic shock, and cardiogenic shock. As the experience in these areas continues to expand, an international task force of experts from 15 countries (Austria, Belgium, China, Croatia, Finland, France, Germany, Greece, Hungary, Italy, the Netherlands, Spain, Sweden, Switzerland, and the USA) reviewed and appraised the latest additions to the database of levosimendan use in critical care, considering all the clinical studies, meta-analyses, and guidelines published from September 2019 to November 2021. Overall, the authors of this opinion paper give levosimendan a “should be considered” recommendation in critical care and emergency medicine settings, with different levels of evidence in postoperative settings, septic shock, weaning from mechanical ventilation, weaning from veno-arterial extracorporeal membrane oxygenation, cardiogenic shock, and Takotsubo syndrome, in all cases when an inodilator is needed to restore acute severely reduced left or right ventricular ejection fraction and overall haemodynamic balance, and also in the presence of renal dysfunction/failure.
ABSTRACT
Between March 21 and May 18 2020 we admitted 98 patients with COVID-19 to our ICU of whom 72 required invasive mechanical ventilation. Of these, 3 patients required extracorporeal support: One V-V ECMO for respiratory failure, one V-V ECMO for tracheoesophageal fistula, and one V-AV ECMO for cardiogenic shock due to pulmonary thromboembolism, to which we had to add an extra return cannula to improve oxygenation. Coagulation abnormalities have been described in COVID-19 with an increase in D-dimer, a modest decrease in platelet count, and delay in the prothrombin time (1). Pro-coagulant states however, may not be highlighted by a standard coagulation essay that's why we decided to assess them by ROTEM. Even with an ACT level kept between 180-200s, we found a normal value of aPTT and a ROTEM profile consistent with hypercoagulability: An acceleration of blood clot formation (CFT below the lower limit in INTEM and EXTEM) and a significantly higher clot strength (MCF above the upper limit in INTEM and EXTEM in two patients and in FIBTEM in all patients). For this reason, we titrate heparin infusion to maintain INTEM CT in a range between normal and 100 sec longer for all the ECMO run, without thrombotic complications. Despite the superiority of ROTEM to monitor anticoagulation in ECMO is not yet proven in literature, this test could help us to understand the coagulation profile of each patient and to titrate heparin where the coagulation function is greatly altered by the virus and by the circuit.