WALANT technique versus locoregional anesthesia in the surgical management of metacarpal and phalangeal fractures: Lessons from the Covid-19 crisis.

Wide Awake Local Anesthesia No Tourniquet (WALANT) is an anesthetic method which uses a local injection of anesthetic and epinephrine, avoiding use of a tourniquet. During the COVID-19 pandemic, human and logistic resources had to be reorganized, and WALANT ensured resilience in our department to maintain access to surgical care. The objective of the present study was to compare hand function recovery 3 months after surgery for unstable metacarpal or phalangeal fracture under regional anesthesia versus WALANT. From November 2020 to May 2021, 36 patients presenting a metacarpal or phalangeal fracture requiring surgical treatment were included in a single-center study in a university hospital center. Nineteen patients underwent surgery under locoregional anesthesia with tourniquet, and 17 under WALANT. The main endpoint was functional recovery at 3 months on QuickDASH score. Need for complementary anesthesia, surgery duration, analgesic consumption, reintervention rate, and patient satisfaction were also assessed. There was no significant difference between groups in functional recovery at 3 months or on the secondary endpoints. In the COVID-19 context, WALANT proved to be a safe and effective method in hand fracture surgery, ensuring access to surgical care. It should be included in surgical training to optimize day-to-day surgical care and face future crises.

An angiotensin receptor blocker in the presence of sars cov2 pseudovirus does not change protein expression of ace2 in human heart cell models

Introduction: ACE inhibitor (ACEI) or angiotensin receptor blocker (ARB) use in COVID-19 raised concern due to reported increases in ACE2, the cell receptor for SARS-CoV2. We tested the hypothesis that ARB (Losartan) and ACEI (Captopril) do not impact SARS-CoV2 associated ACE2 expression in cardiomyocytes (CMs). Methods: Beating monolayer ventricular CMs were generated from human iPSCs and grown as engineered heart tissue constructs (EHTs), which mimic a more mature phenotype than monolayer CMs. Drug treatments (24hrs) without pseudovirus were applied to EHTs: (A) Vehicle, 1μM Losartan (ARB), 1μM Angiotensin II (AngII), 1μM Losartan+1μM Ang II;(B) Vehicle, 1μM Captopril, 1μM Ang I, or 1μM AngI+1μM Captopril with 2-3 replicates for each combination and RNAseq as outcome. Drug treatment A only was repeated in monolayer CMs with a 5-6 day to rVSV-SARS-Cov2SpikeLuciferase-FLAG tagged pseudovirus (2-4 replicates) with immunoblotting for ACE2, Cathepsin B (CTSB) and Furin proteins. Results: Immunoblot densitometry showed abundant ACE2 protein in untreated CMs and EHTs. A focused mRNA analysis of 12 genes associated with SARS-Cov2 entry and processing (EHTs) revealed no significant changes in expression of ACE2, NRP1, CTSB, CTSL and FURIN due to Losartan or Captopril treatment. There was a nonsignificant trend towards Losartan-induced increase in AGTR1 with attenuation when AngII was administered, while ITGA5 trended upwards with Losartan+AngII. AGTRI also trended upwards with Captopril and AngI+Captopril. Upon pseudoviral challenge, CMs demonstrated increased ACE2 (55%) and slightly decreased Furin (24%) protein, with unchanged CTSB, although results were not statistically significant. Losartan addition, regardless of AngII, did not alter SARS-CoV2Spike pseudovirus mediated changes of ACE2, Furin or CTSB proteins. Conclusions: Losartan or Captopril did not substantially alter gene expression of ACE2, CTSB, CTSL, FURIN and NRP1 in EHTs without pseudovirus. Losartan did not show convincing evidence for pseudoviral mediated changes of proteins important for viral entry and processing in CM cell models.