Cardiac troponin and skeletal muscle oxygenation in severe post-partum haemorrhage

International audienceIntroductionCardiac troponin has been shown to be elevated in one-half of the parturients admitted for post-partum haemorrhage. The purpose of the study was to assess whether increased cardiac troponin was associated with a simultaneous alteration in haemoglobin tissue oxygen saturation in peripheral muscles in post-partum haemorrhage.MethodsTissue haemoglobin oxygen saturation of thenar eminence muscle (StO2) was measured via near-infrared spectroscopy technology. Two sets of StO2 parameters (both isolated baseline and during forearm ischaemia-reperfusion tests) were collected at two time points: upon intensive care unit admission and prior to intensive care unit discharge. Comparisons were performed using Wilcoxon paired tests, and univariate associations were assessed using logistic regression model and Wald tests.ResultsThe 42 studied parturients, admitted for post-partum haemorrhage, had clinical and biological signs of severe blood loss. Initial cardiac troponin I was increased in 24/42 parturients (0.43 ± 0.60 μrg/l). All measured parameters of muscular haemoglobin oxygen saturation, including Srecovery, were also altered at admission and improved together with improved haemodynamics, when bleeding was controlled. Multivariate analysis showed that muscular Srecovery ConclusionsOur study confirmed the high incidence of increased cardiac troponin, and demonstrated the simultaneous impairment in the reserve of oxygen delivery to peripheral muscles in parturients admitted for severe post-partum haemorrhage

Human Septic Myopathy: Induction of Cyclooxygenase, Heme Oxygenase and Activation of the Ubiquitin Proteolytic Pathway

Background: Skeletal muscle failure and wasting are manifestations of sepsis in humans that leads to serious and prolonged complications. The authors investigated the role of the major proinflammatory and antiinflammatory pathways, namely the inducible isoforms cyclooxygenase (COX-2) and heme oxygenase (HO-1), and the ubiquitin proteolytic pathway in skeletal muscle of septic patients. Methods: Protein expression was detected by Western blot techniques. Muscle biopsies were taken from two muscle groups, rectus abdominis and vastus lateralis, of septic and control patients. Results: The study showed an increase in COX-2 and HO-1 proteins expression and an activation of the proteolytic ubiquitin pathway with a parallel increase in free ubiquitin and ubiquitinated proteins in skeletal muscle of septic but not of control patients. In addition, those patients who would die from septic shock expressed more COX-2 and HO-1 proteins in muscle biopsies than did those patients who would survive. Conclusions: This study showed a marked involvement of local proinflammatory and antiinflammatory pathways and, more importantly, demonstrated the existence of an active ubiquitin proteolytic pathway in skeletal muscle of septic patients. Activation of ubiquitin pathway could be involved in sepsis-related muscle catabolism and wasting

Nitration et dégradation des protéines cardiaques et diaphragmatiques dans le Sepsis

Le choc septique entraîne fréquemment une atteinte musculaire qui se caractérise par un catabolisme protéique parfois majeur. Des données récentes suggèrent que la voie du NO via le peroxynitrite et celle de l'ubiquitine pourraient être impliquées dans cette dysfonction des muscles striés squelettiques au cours du sepsis. Aussi, nous nous proposons d'étudier ces voies dans deux autres muscles particuliers de l'organisme : le diaphragme et le cœur. Le but de notre étude est donc de révéler le rôle du NO et du peroxynitrite, en étudiant l'expression de la NOS-2 et des protéines nitrées, et d'évaluer le niveau d'expression et d'activation de la voie de l'ubiquitine dans la diaphragme et le cœur de patients présentant un choc septique. Pour cela, nous avons étudié, par une technique d'immuno-empreinte, l'expression de la NOS-2, des protéines nitrées, de l'ubiquitine et des protéines ubiquitinées dans le diaphragme, les parois des quatre cavités cardiaques et le muscle grand droit de l'abdomen de 7 patients décédés en choc septique en réanimation. Ces résultats ont été comparé à l'expression de ces protéines dans le muscle grand droit issu de 3 patients indemnes de tout sepsis (groupe contrôle). l'expression de la NOS-2, des protéines nitrées, de l'ubiquitine et des protéines ubiquitinées est plus importante chez les patients septiques que chez les patients contrôles. Le niveau d'expression de ces protéines est homogène dans tous les tissus étudiés des patients septiques. De plus, la voie de l'ubiquitine est active et son expression est adaptée à la quantité de protéines altérées...PARIS7-Villemin (751102101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls

Abstract Background Cognitive dysfunction and delirium after ICU are frequent and may partially result from brain ischemia episodes. We hypothesized that systemic inflammation (severe sepsis or septic shock) modifies the control of brain circulation and the relation between systemic and cerebral hemodynamic after a positive response to fluid challenge (FC). Methods Three groups of patients were studied if they increased stroke volume (SV) > 10% after 250 or 500 ml of crystalloids: control group: patients free of comorbidity anesthetized for orthopedic surgery; sepsis group: patients with severe sepsis or septic shock (classic definition); brain injury (BI) group: trauma brain jury or hemorrhagic stroke with no detectable systemic inflammation. The measurements before and after FC were mean arterial blood pressure (MAP) (radial catheter); SV and cardiac output (CO; transesophageal Doppler); bilateral middle cerebral artery (MCAv) velocity with peak systolic (PSV) and end diastolic (EDV) values (transcranial Doppler); end-tidal CO2. The role of MAP increase was investigated by an arbitrarily threshold increase of 5%, called responder in CO and MAP (RR). The remaining patients were call responders in CO and non-responders in MAP (RnR). Nonparametric tests were used for statistical analysis. Results Among the 86 screened patients, 66 have completed the protocol: 17 in control group; 38 in sepsis group; and 11 in BI group. All patients increased SV > 10% after FC. Only the sepsis group increased MAP [+ 12 (2–25%), p  baseline median MAP had similar MCAv. Conclusions After a FC-induced increase in SV, MCAv (PSV and EDV) increased only in septic group, mostly independently from MAP increase and from baseline MAP level. Cerebral perfusion becomes passively dependent on systemic blood flow, suggesting a modification of the control of cerebrovascular tone in sepsis-induced systemic inflammation. This information has been considered in the clinical management of septic patients

MOESM1 of Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls

Additional file 1: Table S1. Systemic and cerebral hemodynamics in patients responders-responders (RR) vs responders-non responders (RnR) in the control group. Table S2. Systemic and cerebral hemodynamics in patients responders-responders (RR) vs responders-non responders (RnR) in the brain injury group

Rapidly Progressive Diaphragmatic Weakness and Injury during Mechanical Ventilation in Humans

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A multicentre observational study on management of general anaesthesia in elderly patients at high-risk of postoperative adverse outcomes

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