Fracture panfaciale: un challenge thérapeutique: à propos d’une observation et revue de la littérature

La gestion des traumatismes de la face a subi plusieurs progrès dans la dernière décennie. Avec l'avènement de la tomodensitométrie bi- ettridimensionnelle, qui permet de dresser une cartographie précise des lésions osseuses, le développement du matériel d'ostéosynthèse, et lesprocédés de réduction des fractures. L'objectif est la restauration totale de la forme et la fonction de la face, seul garant pour empêcher lasurvenue de préjudices esthétiques et fonctionnels. Nous rapportons l'observation de Mme assal khadija, âgée de 38 ans, admise le 25 Aout 2010, au service des urgences d'ORL et maxillo-faciales, à l'hôpital 20 aout de Casablanca, victime d'un AVP, occasionnant un traumatisme facial grave, avec un important délabrement de la face, et asphyxie. Une trachéotomie a été réalisée en urgence. Le bilan lésionnel a objectivé un important fracas du massif facial intéressant l'étage supérieure, moyen et inférieur. Dans l'immédiat, un parage a été réalisé sous anesthésie  générale, la réparation des parties molles délabrées a été effectuée en endobuccale (vestibules, langue et plancher buccal) et pour les téguments de la face. Une semaine après, la patiente a été reprise pour la  reconstruction du massif facial, nous avons opté pour le «inside-out, de bas en haut" pour la réduction des fractures. Nous avons procédé à la fixation de la mandibule qui a précédé la reconstruction du maxillaire, de la pyramide nasale, et de l'orbite. L'évolution a été marquée par  l'apparition d'un orostome, qui fera l'objet après tarissement de l'infection, d'une réparation grâce à un lambeau myocutané, et une nécrose cutanée de la région zygomatique laissée à la cicatrisation dirigée. Toutes les  lésions traumatiques de la face ont des répercussions esthétiques et fonctionnelles à moyen et long termes, dont le degré dépend de la qualité de la prise en charge, qui étant la plus précoce et la plus complète possible avant la consolidation des fractures est le meilleur garant d'un résultat satisfaisant à long terme

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

EPIdemiology of Surgery-Associated Acute Kidney Injury (EPIS-AKI) : Study protocol for a multicentre, observational trial

More than 300 million surgical procedures are performed each year. Acute kidney injury (AKI) is a common complication after major surgery and is associated with adverse short-term and long-term outcomes. However, there is a large variation in the incidence of reported AKI rates. The establishment of an accurate epidemiology of surgery-associated AKI is important for healthcare policy, quality initiatives, clinical trials, as well as for improving guidelines. The objective of the Epidemiology of Surgery-associated Acute Kidney Injury (EPIS-AKI) trial is to prospectively evaluate the epidemiology of AKI after major surgery using the latest Kidney Disease: Improving Global Outcomes (KDIGO) consensus definition of AKI. EPIS-AKI is an international prospective, observational, multicentre cohort study including 10 000 patients undergoing major surgery who are subsequently admitted to the ICU or a similar high dependency unit. The primary endpoint is the incidence of AKI within 72 hours after surgery according to the KDIGO criteria. Secondary endpoints include use of renal replacement therapy (RRT), mortality during ICU and hospital stay, length of ICU and hospital stay and major adverse kidney events (combined endpoint consisting of persistent renal dysfunction, RRT and mortality) at day 90. Further, we will evaluate preoperative and intraoperative risk factors affecting the incidence of postoperative AKI. In an add-on analysis, we will assess urinary biomarkers for early detection of AKI. EPIS-AKI has been approved by the leading Ethics Committee of the Medical Council North Rhine-Westphalia, of the Westphalian Wilhelms-University Münster and the corresponding Ethics Committee at each participating site. Results will be disseminated widely and published in peer-reviewed journals, presented at conferences and used to design further AKI-related trials. Trial registration number NCT04165369

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease