The compelling arguments for the need of microvascular investigation in COVID-19 critical patients

Abstract

The burden of pandemic COVID-19 is growing worldwide, as the continuous increases of contagion. Only 10-15% of the entire infected population has the necessity of intensive care unit (ICU) treatments. But, this relatively low rate of patients has absorbed almost the whole availability of ICU during few days, becoming at least in Italy, an emergency for the national health system. In COVID-19 ICU patients massive aggression of lung with severe pulmonary failure, as well as kidney and liver injuries, heart, brain, bowel and spleen damages with lymph nodes necrosis and even cutaneous manifestations have been observed. Moreover, increased levels of cytokines so-called "cytokines storm (CS), and overt intravascular disseminated coagulation have been also reported. The hypercoagulation and CS would speculate about a microvascular dysfunction. Unfortunately, no specific observations have been performed on microcirculatory dysfunction in COVID-19 patients. Hence the presumed pathophysiological pathways and models about a microvascular involvement can be gathered by sepsis models studies. But despite this lack of evidence, the COVID-19 has emphasized the compelling need for microcirculation monitoring at the bedside in ICU patients.

Cerebrovascular comorbidity, high blood levels of C-reactive protein and D-dimer are associated with disease outcomes in COVID-19 patients

“…Stroke incidence and cerebrovascular disease have been reported in 5% and 5.7% of COVID-19 pateints, repectively [7]. However, the thrombotic changes are generalized and occur in all regions of the body -not only in the brain), as it was demonstrated by previous studies like thromboses in the lung [8], kidney infractions [9], as well as overt intravascular disseminated coagulation [10]. The pro-inflammatory biomarkers were elevated signicantly due to the COVID-19…”

Immunity, endothelial injury and complement-induced coagulopathy in COVID-19

“…TNF can activate glucuronidases that might degrade the endothelial glycocalyx but might also upregulate hyaluronic acid synthase 2, leading to increased deposition of hyaluronic acid in the extracellular matrix and promoting fluid retention 113 . Additional mechanisms, such as a reduction of endothelial nitric oxide synthase activity and nitric oxide levels, as well as the release of vascular endothelial growth factor (VEGF) as a consequence of the systemic hypoxia induced by ARDS, have also been proposed as key pathogenic processes underlying endothelial dysfunction following SARS-CoV-2 infection 136 . Below, we focus on the possible role of the complement system in inducing systemic endothelial dysfunction in COVID-19.…”

Interstitial lung opacities in patients with severe COVID-19 pneumonia by bedside high-resolution ultrasound in association to CO2 retention

“…Severe ARDS is reported in up to 15 to 31 % of patients with pneumonia [14,15]. However, also beyond the massive aggression of the lung with severe pulmonary failure, as well as kidney and liver injuries, heart, brain, bowel and spleen damages with lymph nodes necrosis and even cutaneous manifestations have been observed [16]. Ultrasound diagnostic is a cost effective and world-wide accessible device to assess pneumonia [17,18].…”