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Saint-Léger-du-Bourg-Denis, France

Dubory A.,Laboratoire Detude Of La Microcirculation | Dubory A.,Bicetre Universitary Hospital | Laemmel E.,Laboratoire Detude Of La Microcirculation | Badner A.,University of Toronto | And 6 more authors.
Journal of Visualized Experiments | Year: 2015

Reduced spinal cord blood flow (SCBF) (i.e., ischemia) plays a key role in traumatic spinal cord injury (SCI) pathophysiology and is accordingly an important target for neuroprotective therapies. Although several techniques have been described to assess SCBF, they all have significant limitations. To overcome the latter, we propose the use of real-time contrast enhanced ultrasound imaging (CEU). Here we describe the application of this technique in a rat contusion model of SCI. A jugular catheter is first implanted for the repeated injection of contrast agent, a sodium chloride solution of sulphur hexafluoride encapsulated microbubbles. The spine is then stabilized with a custom-made 3D-frame and the spinal cord dura mater is exposed by a laminectomy at ThIX-ThXII. The ultrasound probe is then positioned at the posterior aspect of the dura mater (coated with ultrasound gel). To assess baseline SCBF, a single intravenous injection (400 μl) of contrast agent is applied to record its passage through the intact spinal cord microvasculature. A weight-drop device is subsequently used to generate a reproducible experimental contusion model of SCI. Contrast agent is re-injected 15 min following the injury to assess post-SCI SCBF changes. CEU allows for real time and in-vivo assessment of SCBF changes following SCI. In the uninjured animal, ultrasound imaging showed uneven blood flow along the intact spinal cord. Furthermore, 15 min post-SCI, there was critical ischemia at the level of the epicenter while SCBF remained preserved in the more remote intact areas. In the regions adjacent to the epicenter (both rostral and caudal), SCBF was significantly reduced. This corresponds to the previously described “ischemic penumbra zone”. This tool is of major interest for assessing the effects of therapies aimed at limiting ischemia and the resulting tissue necrosis subsequent to SCI. © 2015 Journal of Visualized Experiments. Source

Fullana J.-M.,University Pierre and Marie Curie | Gelade P.,Laboratoires Innothera | Vicaut E.,Laboratoire Detude Of La Microcirculation | Flaud P.,University Paris Diderot
Journal des Maladies Vasculaires | Year: 2011

Objective: Compression therapy for venous and lymphatic edema of the lower limbs raises a major challenge concerning the optimal pressure ensuring both efficacy and patient compliance. We present a mathematical model of tissue fluid transfers which is aimed at determining the lowest pressure required to prevent edema. Methods: The model is based on a set of equations, derived from published experimental data, which describe the fluid and solute transfers between blood, interstitium and lymphatics, and the mechanical properties of interstitial compartment. It enables us to compute the changes in tissue volume, at the ankle level, resulting from increases of capillary pressure in case of venous insufficiency, and from an impairment of lymph drainage; as well as the effect of various external pressures upon this volume. Results: An increase of capillary pressure to 40 and 50. mmHg results in an ankle edema which is completely prevented by an external pressure of 10. mmHg. This result is in keeping with the observation by Partsch that vesperal leg swelling is reduced by low compression stockings. The dose effect reported in this study is also found by simulation. The complete blockade of lymphatic return leads to an edema, the prevention of which requires a counterpressure of at least 30. mmHg. When an increase of venous pressure to 60. mmHg, and a reduction by 2/3 of lymphatic drainage are combined, simulating chronic venous insufficiency, the resulting edema is prevented by a 25. mmHg counterpressure. Conclusion: These first results of simulation are in reasonable agreement with clinical experience. As nearly every combination of disturbances may be simulated, the computer model could help to understand and treat edemas, as long as their cause can be identified. © 2010 Elsevier Masson SAS. Source

Duret J.,Hopital Michallon | Pottecher J.,Hopitaux Universitaires Of Strasbourg | Pottecher J.,University of Strasbourg | Bouzat P.,Hopital Michallon | And 10 more authors.
Critical Care | Year: 2015

Introduction: Early alterations in tissue oxygenation may worsen patient outcome following traumatic haemorrhagic shock. We hypothesized that muscle oxygenation measured using near-infrared spectroscopy (NIRS) on admission could be associated with subsequent change in the SOFA score after resuscitation. Methods: The study was conducted in two Level I trauma centres and included 54 consecutive trauma patients with haemorrhagic shock, presenting within 6 hours of injury. Baseline tissue haemoglobin oxygen saturation (StO2) in the thenar eminence muscle and StO2 changes during a vascular occlusion test (VOT) were determined at 6 hours (H6) and 72 hours (H72) after the admission to the emergency room. Patients showing an improved SOFA score at H72 (SOFA improvers) were compared to those for whom it was unchanged or worse (SOFA non-improvers). Results: Of the 54 patients, 34 patients were SOFA improvers and 20 SOFA non-improvers. They had comparable injury severity scores on admission. SOFA improvers had higher baseline StO2 values and a steeper StO2 desaturation slope at H6 compared to the SOFA non-improvers. These StO2 variables similarly correlated with the intra-hospital mortality. The StO2 reperfusion slope at H6 was similar between the two groups of patients. Conclusions: Differences in StO2 parameters on admission of traumatic haemorrhagic shock were found between patients who had an improvement in organ failure in the first 72 hours and those who had unchanged or worse conditions. The use of NIRS to guide the initial management of trauma patients with haemorrhagic shock warrants further investigations. © Duret et al.; licensee BioMed Central. Source

Harrois A.,University Paris - Sud | Harrois A.,Laboratoire Detude Of La Microcirculation | Hamada S.R.,University Paris - Sud | Duranteau J.,University Paris - Sud | Duranteau J.,Laboratoire Detude Of La Microcirculation
Current Opinion in Critical Care | Year: 2014

Purpose of review To discuss the fluid resuscitation and the vasopressor support in severe trauma patients. Recent findings A critical point is to prevent a potential increase in bleeding by an overly aggressive resuscitative strategy. Indeed, large-volume fluid replacement may promote coagulopathy by diluting coagulation factors. Moreover, an excessive level of mean arterial pressure may induce bleeding by preventing clot formation. Summary Fluid resuscitation is the first-line therapy to restore intravascular volume and to prevent cardiac arrest. Thus, fluid resuscitation before bleeding control must be limited to the bare minimum to maintain arterial pressure to minimize dilution of coagulation factors and complications of over fluid resuscitation. However, a strategy of low fluid resuscitation needs to be handled in a flexible way and to be balanced considering the severity of the hemorrhage and the transport time. A target systolic arterial pressure of 80-90 mmHg is recommended until the control of hemorrhage in trauma patients without brain injury. In addition to fluid resuscitation, early vasopressor support may be required to restore arterial pressure and prevent excessive fluid resuscitation. It is crucial to find the best alchemy between fluid resuscitation and vasopressors, to consider hemodynamic monitoring and to establish trauma resuscitative protocols. Copyright © Lippincott Williams & Wilkins. Source

Tanaka S.,University Paris - Sud | Harrois A.,University Paris - Sud | Harrois A.,Laboratoire Detude Of La Microcirculation | Nicolai C.,University Paris - Sud | And 5 more authors.
Critical Care | Year: 2015

Introduction: We aimed to determine i) the feasibility of nurses taking bedside measurements of microcirculatory parameters in real time in intensive care patients; and ii) whether such measurements would be comparable to those obtained by the classical delayed semi quantitative analysis made by a physician. Methods: This prospective observational study was conducted in a university hospital and was approved by our local Institutional Review Board (IRB 00006477). After ICU admission and study inclusion, a set of measurements of macrocirculatory and microcirculatory parameters was taken by the nurse in charge of the patient every 4h within the first 12h after admission and before and after every hemodynamic therapeutic intervention. Seventy-four sublingual microvascular measurements were performed with incident dark field illumination (IDF) microscopy in 20 mechanically ventilated patients hospitalized in the ICU. Results: There were no significant differences between the microvascular flow index (MFI) taken in real time by the nurses and the delayed evaluation by the physician. In fact, the nurses' real-time measurement of MFI demonstrated good agreement with the physician's delayed measurement. The mean difference between the two MFIs was -0.15, SD=0.28. The nurses' real-time MFI assessment showed 97% sensitivity (95% CI: 84-99%) and 95% specificity (95% CI: 84-99%) at detecting a MFI<2.5 obtained by a physician upon delayed semiquantitative measurement. Concerning the density, 81% of the paramedical qualitative density measurements corresponded with the automatized total vessel density (TVD) measurements. The nurses' real-time TVD assessment showed 77% sensitivity (95% CI: 46-95%) and 100% specificity (95% CI: 89-100%) at detecting a TVD<8 mm/mm2. Conclusion: A real-time qualitative bedside evaluation of MFI by nurses showed good agreement with the conventional delayed analysis by physicians. The bedside evaluations of MFI and TVD were highly sensitive and specific for detecting impaired microvascular flow and low capillary density. These results suggest that this real-time technique could become part of ICU nurse routine surveillance and be implemented in algorithms for hemodynamic resuscitation in future clinical trials and regular practice. These results are an essential step to demonstrate whether these real-time measurements have a clinical impact in the management of ICU patients. © 2015 Tanaka et al. Source

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