Fernando Schiraldi

Objective. In physiological conditions, arterial blood lactate concentration is equal to or lower than central venous blood lactate concentration. A reversal in this rate (i.e., higher lactate concentration in central venous blood), which could reflect a derangement in the mitochondrial metabolism of lung cells induced by inflammation, has been previously reported in patients with ARDS but has been never explored in COVID-19 patients. The aim of this study was to explore if the COVID-19-induced lung cell damage was mirrored by an arterial lactatemia higher than the central venous one; then if the administration of anti-inflammatory therapy (i.e., canakinumab 300 mg subcutaneous) could normalize such abnormal lactate a-cv difference.Methods. A prospective cohort study was conducted, started on March 25, 2020, for a duration of 10 days, enrolling 21 patients affected by severe COVID-19 pneumonia undergoing mechanical ventilation consecutively admitted to the ICU of the Rimini Hospital, Italy. Arterial and central venous blood samples were contemporarily collected to calculate the difference between arterial and central venous lactate (Delta a-cv lactate) concentrations within 24 h from tracheal intubation (T-0) and 24 hours after canakinumab administration (T-1).Results. AtT0, 19 of 21 (90.5%) patients showed a pathologic Delta a-cv lactate (median 0.15 mmol/L; IQR 0.07-0.25). In the 13 patients undergoing canakinumab administration, atT(1), Delta a-cv lactate decreased in 92.3% of cases, the decrease being statistically significant (T-0: median 0.24, IQR 0.09-0.31 mmol/L;T-1: median -0.01, IQR -0.08-0.04 mmol/L;p=0.002).Conclusion. A reversed Delta a-cv lactate might be interpreted as one of the effects of COVID-19-related cytokine storm, which could reflect a derangement in the mitochondrial metabolism of lung cells induced by severe inflammation or other uncoupling mediators. In addition, Delta a-cv lactate decrease might also reflect the anti-inflammatory activity of canakinumab. Our preliminary findings need to be confirmed by larger outcome studies.

Objective: In physiological conditions arterial blood lactate concentration is equal or lower than central venous. The aim of this study was to explore if the COVID-19 induced lung cells damage was mirrored by an arterial lactatemia higher than the central venous one; then if the administration of immunosuppressant drugs (i.e. canakinumab) could normalize such abnormal lactate a-cv difference. Methods: Prospective cohort study started on March 25 ^th 2020 for a duration of 10 days, enrolling 21 patients affected by severe COVID-19 pneumonia undergoing mechanical ventilation consecutively admitted to the ICU of the Rimini Hospital, Italy. Arterial and central venous blood samples were contemporary collected to calculate the difference between arterial and central venous lactate (Delta a-cv lactate) concentration within 24 h from tracheal intubation (T ₀ ), and 24 hours after canakinumab administration (T ₁ ). Results: At the T ₀ 19/21 (90.5%) patients showed a pathologic Delta a-cv lactate (median 0.22 mmol/L; IQR 0.07–0.36), suggesting severe inflammation. In the 13 patients undergoing canakinumab administration, at the T ₁ Delta a-cv lactate decreased in 92.3% of cases, being the decrease statistically significant (T ₀ : median 0.15, IQR 0.07–0.25 mmol/L; T ₁ : median −0.01, IQR 0.09–0.04 mmol/L; p=0.002). Conclusion: A reversed Delta a-cv lactate is likely to be one of the effects of COVID-19 related cytokine storm, that could reflect a derangement in the lung cells mitochondrial metabolism induced by inflammation or other uncoupling mediators. Delta a-cv lactate decrease may reflect the anti-inflammatory activity of canakinumab. Our preliminary findings need to be confirmed by larger outcome studies.

Background: Dyspnea is one of the most frequent complaints in the Emergency Department. Thoracic ultrasound should help to differentiate cardiogenic from non-cardiogenic causes of dyspnea. We evaluated whether the diagnostic accuracy can be improved by adding a point-of-care-ultrasonography (POC-US) to routine exams and if an early use of this technique produces any advantage. Methods: One hundred sixty-eight patients were enrolled and randomized in two groups: Group 1 received an immediate POC-US in addition to routine laboratory and instrumental tests; group 2 received an ultrasound scan within 1 h from the admission to the Emergency Department. The concordance between initial and final diagnosis and the percentage of wrong diagnosis in the two groups were evaluated. Mortality, days of hospitalization in Emergency Medicine department and transfers to other wards were compared. Sensitivity and specificity of the routine protocol and the one including ultrasonography for the diagnosis of the causes of dyspnea were also analyzed. Results: Eighty-eight patients were randomized in group 1 and 80 in group 2. The concordance rate between initial and final diagnoses was significantly different (0.94 in group 1 vs. 0.22 in group 2, p < 0.005). The percentage of wrong initial diagnosis was 5% in group 1 and 50% in group 2 (p < 0.0001). Conclusions: Adding POC-US to routine exams improves the diagnostic accuracy of dyspnea and reduces errors in the Emergency Department.