Perfusion Index: Physical Principles, Physiological Meanings and Clinical Implications in Anaesthesia and Critical Care

Short title: Clinical Usefulness of Perfusion IndexInternational audiencePhotoplethysmography (PPG) has been extensively used for pulse oximetry monitoring in anaesthesia, perioperative and intensive care. However, some components of PPG signal have been employed for other purposes, such as non-invasive haemodynamic monitoring. Perfusion index (PI) is derived from PPG signal and represents the ratio of pulsatile on non-pulsatile light absorbance or reflectance of the PPG signal. PI determinants are complex and interlinked, involving and reflecting the interaction between peripheral and central haemodynamic characteristics, such as vascular tone and stroke volume. Recently, several studies have shed light on the interesting performances of this variable, especially assessing regional or neuraxial block success, and haemodynamic monitoring in anaesthesia, perioperative and intensive care. Nevertheless, no review has yet been published concerning the interest of PI in these fields. In this narrative review will be exposed first the physiological and pathophysiological determinants of PI, and then the mean to measure this value as well as its potential limitations. In the second part, the existing data concerning usefulness of PI in different clinical settings such as operating theatres, intensive care units and emergency departments will be presented and discussed. Finally, the perspectives concerning the use of PI and mentioned aspects that should be explored regarding this tool will be underlined

Peri-operative red blood cell transfusion in neonates and infants: NEonate and Children audiT of Anaesthesia pRactice IN Europe: A prospective European multicentre observational study

BACKGROUND: Little is known about current clinical practice concerning peri-operative red blood cell transfusion in neonates and small infants. Guidelines suggest transfusions based on haemoglobin thresholds ranging from 8.5 to 12 g dl-1, distinguishing between children from birth to day 7 (week 1), from day 8 to day 14 (week 2) or from day 15 (≥week 3) onwards. OBJECTIVE: To observe peri-operative red blood cell transfusion practice according to guidelines in relation to patient outcome. DESIGN: A multicentre observational study. SETTING: The NEonate-Children sTudy of Anaesthesia pRactice IN Europe (NECTARINE) trial recruited patients up to 60 weeks' postmenstrual age undergoing anaesthesia for surgical or diagnostic procedures from 165 centres in 31 European countries between March 2016 and January 2017. PATIENTS: The data included 5609 patients undergoing 6542 procedures. Inclusion criteria was a peri-operative red blood cell transfusion. MAIN OUTCOME MEASURES: The primary endpoint was the haemoglobin level triggering a transfusion for neonates in week 1, week 2 and week 3. Secondary endpoints were transfusion volumes, 'delta haemoglobin' (preprocedure - transfusion-triggering) and 30-day and 90-day morbidity and mortality. RESULTS: Peri-operative red blood cell transfusions were recorded during 447 procedures (6.9%). The median haemoglobin levels triggering a transfusion were 9.6 [IQR 8.7 to 10.9] g dl-1 for neonates in week 1, 9.6 [7.7 to 10.4] g dl-1 in week 2 and 8.0 [7.3 to 9.0] g dl-1 in week 3. The median transfusion volume was 17.1 [11.1 to 26.4] ml kg-1 with a median delta haemoglobin of 1.8 [0.0 to 3.6] g dl-1. Thirty-day morbidity was 47.8% with an overall mortality of 11.3%. CONCLUSIONS: Results indicate lower transfusion-triggering haemoglobin thresholds in clinical practice than suggested by current guidelines. The high morbidity and mortality of this NECTARINE sub-cohort calls for investigative action and evidence-based guidelines addressing peri-operative red blood cell transfusions strategies. TRIAL REGISTRATION: ClinicalTrials.gov, identifier: NCT02350348

Cardiovascular consequences of acute kidney injury : interaction renine angiotensin aldosterone system – galectin 3

L’insuffisance rénale aiguë est une pathologie fréquente qui est associée à une augmentation de la mortalité et morbidité à court et long terme. L’atteinte cardiaque secondaire à une agression rénale aiguë est désignée par le terme de syndrome cardio-rénale de type 3. Au-delà de l’altération de la fonction glomérulaire rénale qui définit l’IRA, et qui induit l’accumulation de toxines urémiques, les modèles animaux ont suggéré que le rôle de l’agression et du dommage tissulaire rénal est primordial dans l’activation des mécanismes induisant le dommage cardiovasculaire. Les mécanismes impliqués dans les conséquences cardiovasculaires de l’IRA sont cependant encore très imparfaitement identifiés. L’activation du système rénine-angiotensine-aldostérone qui est au centre de la physiopathologie de nombreuses maladies rénales et cardiovasculaires, pourrait jouer un rôle critique. Sur la base des travaux antérieurs de notre équipe, les objectifs de ce travail de thèse étaient de répondre à 2 questions : 1) Une ARA sans altération de fonction est-elle associée à un mauvais pronostic chez les patients de réanimation ? Afin de confirmer cette hypothèse chez l’homme nous avons exploré l’association entre la survenue d’une ARA sans altération de la fonction rénale (appelée sub-IRA) et le pronostic. Dans une cohorte de brûlés graves et dans deux cohortes de patients de réanimation polyvalente, nous avons mis en évidence qu’une sub-IRA était associée à un pronostic péjoratif à court terme. Ces résultats suggèrent fortement que l’ARA via le dommage tissulaire induit est critique dans l’activation des dommages cardiovasculaires plus que ne l’est la perte de la fonction rénale. 2) le SRAA est-il directement impliqué dans les dommages cardiovasculaires induit par l’IRA ? Dans une seconde partie expérimentale, nous avons étudié le lien entre IRA, dysfonction cardiaque et activation du SRAA. Nous avons particulièrement étudié l’interaction entre l’activation du SRAA et la Galectine-3 dans un modèle murin de SCR-3, sur la base de travaux de notre équipe qui ont mis en évidence le rôle de la Gal-3 dans la survenue de fibrose et de dysfonction cardiaque après IRA. Dans un modèle d’ischémie/reperfusion rénale associée à une néphrectomie du rein controlatéral, nous avons montré que l’IRR induisait une dysfonction rénale persistante à J28 associée à une élévation de la concentration d’angiotensine 2 et de Gal-3 plasmatiques et ceux jusqu’à J28. Concernant l’atteinte cardiaque, on observait une augmentation précoce des biomarqueurs d’agression cardiaque (Brain natriuretic peptide acide ribonucleique messager) persistante à J28 et d’inflammation (interleukine 1 [IL-1], cluster de différentiation 68 et Gal-3 ARNm). A J28, l’IRR induisait une inflammation et de la fibrose cardiaque (Rouge Sirius) et on observait une dysfonction contractile ventriculaire gauche (fraction de raccourcissement ventriculaire gauche diminuant de -5 à -10%). Pour déterminer le lien entre le SRAA et Gal-3 dans ce modèle, nous avons traité des souris sauvages avec un antagoniste du récepteur de type 1 de l’Ang-2 (Valsartan) ou l’association valsartan et inhibiteur de la neprilysine (salcubitril) en post IRR immédiat et ceux jusqu’à J28. L’inhibition pharmacologique d’AT-1 ou d’AT-1+NEP prévenait en partie l’augmentation plasmatique de l’Ang-2 et de Gal-3 ainsi que l’apparition de la fibrose et de la dysfonction cardiaque à J28 post-IRR. L’ensemble de ces résultats met en évidence que l’administration de Valsartan ou de Valsartan + Salcubitril après IRA prévient l’augmentation plasmatique et cardiaque de Gal-3 ainsi que la fibrose et la dysfonction cardiaque à J28.Acute kidney injury (AKI) is a common condition that is associated with short and long term increased mortality and morbidity. Cardiac damage secondary to acute kidney attack (AKA) is referred to as cardio-renal syndrome type 3 (CRS-3). Beyond the alteration of renal glomerular function, which defines AKI, and which induces the accumulation of uremic toxins, animal models have suggested that the role of renal tissue aggression and damage is paramount in the activation of the mechanisms inducing cardiovascular damage. However, the mechanisms involved in the cardiovascular consequences of AKA are still very imperfectly identified. Activation of the renin-angiotensin-aldosterone system (RAAS), which is central to the pathophysiology of many renal and cardiovascular diseases, could play a critical role. Based on the previous work of our team, the objectives of this thesis work were to answer 2 questions: 1) Is AKA without altered function associated with a poor prognosis in critically ill patients? In order to confirm this hypothesis in humans, we explored the association between the occurrence of AKA without alteration of renal function (called sub-AKI) and prognosis. In one cohort of severe burn patients and in two cohorts of critically ill patients, we demonstrated that sub-AKI was associated with a poor short-term prognosis. These results strongly suggest that AKA via induced tissue damage is more critical in the activation of cardiovascular damage than is the loss of renal function. 2) Is the RAAS directly involved in AKI-induced cardiovascular damage? In a second experimental part, we studied the link between AKI, cardiac dysfunction and activation of the RAAS. In particular, we studied the interaction between RAAS activation and Galectin-3 in a mouse model of CRS-3, based on our team's work that highlighted the role of Gal-3 in the development of fibrosis and cardiac dysfunction after AKI. In a model of renal ischemia/reperfusion (IRR) associated with contralateral kidney nephrectomy, we showed that AKI induced persistent renal dysfunction at D28 associated with elevated plasma angiotensin-2 and Gal-3 concentrations and those up to D28. With respect to cardiac involvement, there was an early increase in biomarkers of cardiac aggression (Brain natriuretic peptide ribonucleic acid messenger) persistent at D28 and inflammation (interleukin 1 [IL-1], differentiation cluster 68 and Gal-3 mRNA). At D28, AKI induced inflammation and cardiac fibrosis (Sirius Red) and left ventricular contractile dysfunction was observed (left ventricular shortening fraction decreasing from -5 to -10%). To determine the relationship between RAAS and Gal-3 in this model, we treated wild mice with an Ang-2 type 1-receptor antagonist (Valsartan) or the combination of valsartan and a neprilysin inhibitor (salcubitril) in the immediate post-IRR and those up to D28. Pharmacological inhibition of AT-1 or AT-1+NEP partially prevented plasma increases in Ang-2 and Gal-3 and the development of fibrosis and cardiac dysfunction at D28 post-IRR. All of these results demonstrate that the administration of Valsartan or Valsartan + Salcubitril after AKI prevents the plasma and cardiac increase of Gal-3 as well as fibrosis and cardiac dysfunction at D28

L' hémorragie sous arachnoïdienne induit une dysfonction cardiaque précoce et réversible associée à la libération de catécholamines

LE KREMLIN-B.- PARIS 11-BU Méd (940432101) / SudocSudocFranceF

Les électorats sous la 5ème République: Données d'enquête

info:eu-repo/semantics/publishe

Perfusion Index: Physical Principles, Physiological Meanings and Clinical Implications in Anaesthesia and Critical Care

Short title: Clinical Usefulness of Perfusion IndexInternational audiencePhotoplethysmography (PPG) has been extensively used for pulse oximetry monitoring in anaesthesia, perioperative and intensive care. However, some components of PPG signal have been employed for other purposes, such as non-invasive haemodynamic monitoring. Perfusion index (PI) is derived from PPG signal and represents the ratio of pulsatile on non-pulsatile light absorbance or reflectance of the PPG signal. PI determinants are complex and interlinked, involving and reflecting the interaction between peripheral and central haemodynamic characteristics, such as vascular tone and stroke volume. Recently, several studies have shed light on the interesting performances of this variable, especially assessing regional or neuraxial block success, and haemodynamic monitoring in anaesthesia, perioperative and intensive care. Nevertheless, no review has yet been published concerning the interest of PI in these fields. In this narrative review will be exposed first the physiological and pathophysiological determinants of PI, and then the mean to measure this value as well as its potential limitations. In the second part, the existing data concerning usefulness of PI in different clinical settings such as operating theatres, intensive care units and emergency departments will be presented and discussed. Finally, the perspectives concerning the use of PI and mentioned aspects that should be explored regarding this tool will be underlined

The role of CD146 in renal disease: from experimental nephropathy to clinics

International audienceVascular endothelial dysfunction is a major risk factor in the development of renal diseases. Recent studies pointed out a major interest for the inter-endothelial junction protein CD146, as its expression is modulated during renal injury. Indeed, some complex mechanisms involving this adhesion molecule and its multiple ligands are observed in a large number of renal diseases in fundamental or clinical research. The purpose of this review is to summarize the most recent literature on the role of CD146 in renal pathophysiology, from experimental nephropathy to clinical trials

Comparison of a short versus long-course antibiotic therapy for ventilator-associated pneumonia: a systematic review and meta-analysis of randomized controlled trials

International audienceBackground For ventilator-associated pneumonia (VAP), the safety of short-course versus long-course antibiotic therapy is still debated, especially regarding documented VAP due to non-fermenting Gram-negative bacilli (NF-GNB). The aim of this meta-analysis was to assess the rates of recurrence and relapse of VAP in patients receiving short-course (= 10-15 days) of antibiotic therapy. Methods The protocol for this study was registered in the PROSPERO database (ID: CRD42022365138). We per-formed an electronic search of the relevant literature and limited our search to data published from 2000 until September 1, 2022. We searched for randomized controlled trials (RCTs) in the United States National Library of Medicine, Cochrane Database of Systematic Reviews (CDSR) and the Cochrane Central Register of Controlled Trials (CENTRAL), Embase, National Institutes of Health PubMed/MEDLINE, web of science and Google Scholar data-bases. The primary endpoint was the recurrence and relapses of VAP, secondary endpoints were 28-day mortality, mechanical ventilation duration, number of extra-pulmonary infections and length of ICU stay.Findings We identified five relevant studies involving 1069 patients (530 patients in the short-course group and 539 patients in the long-course group). The meta-analysis did not reveal any significant difference between short and long-course antibiotic therapy for recurrence and relapses of VAP (odd ratio "OR" = 1.48, 95% confidence intervals (CI) [0.96, 2.28], p = 0.08 and OR = 1.45, 95% CI [0.94, 2.22], p = 0.09, respectively), including those due to NF-GNB (OR = 1.90, 95% CI [0.93, 3.33], p = 0.05 and OR = 1.76, 95% CI [0.93, 3.33], p = 0.08, respectively). No difference was found for 28 days-mortality (OR = 1.24, 95% CI [0.92, 1.67], p = 0.16), mechanical ventilation duration, number of extra-pulmonary infections and length of ICU stay. However, short-course therapy significantly increased the number of antibiotic-free days.Interpretation Our meta-analysis showed that short-course antibiotic therapy did not result in increased number of recurence and relapses of VAP, suggesting that short-course should be preferred to reduce the exposure to antibiotics