[Compartmental syndrome complicating endovascular treatment of ruptured abdominal aortic aneurysm]. / Cas clinique. Syndrome compartimental compliquant le traitement endovasculaire d'un anévrisme aortique abdominal rompu.

The Guide Line of the Society for Vascular Surgery now recommends endovascular repair (rEVAR) for ruptured abdominal aortic aneurysms (RAAA) when anatomical conditions are present. Abdominal compartment syndrome (ACS) can be one of the serious postoperative complications of rEVAR. ACS is usually associated with progressive development of organ dysfunctions and poor outcomes. We describe an ACS following a RAAA with hemorrhagic shock treated conservatively with a rEVAR.Decompression laparotomy were not performed because spontaneous improvement with conservative ICU treatment was effective.

La Société de Chirurgie Vasculaire recommande désormais la réparation endovasculaire (rEVAR) des anévrismes de l'aorte abdominale rompus (RAAA) lorsque les conditions anatomiques le permettent. Le syndrome compartimental abdominal (SCA) peut être l'une des complications postopératoires graves de la rEVAR. Le SCA est généralement associé au développement progressif d'une dysfonction de plusieurs organes. Nous décrivons ici un syndrome compartimental abdominal (SCA) consécutif à une RAAA avec choc hémorragique, traité de manière conservatrice avec une rEVAR aorto-mono-iliaque et un cross-over fémoro-fémoral. Le patient a été admis en post-opératoire en Unité de Soins intensifs et a développé, à 48 heures postopératoires, un SCA associé à une insuffisance rénale aiguë, une cytolyse hépatique, un œdème pulmonaire aigu et un iléus. Une laparotomie de décompression n'a pas été effectuée car l'amélioration spontanée avec un traitement conservateur aux soins intensifs s'est avérée efficace.

Establishing the ferret as a gyrencephalic animal model of traumatic brain injury: Optimization of controlled cortical impact procedures.

BACKGROUND: Although rodent TBI studies provide valuable information regarding the effects of injury and recovery, an animal model with neuroanatomical characteristics closer to humans may provide a more meaningful basis for clinical translation. The ferret has a high white/gray matter ratio, gyrencephalic neocortex, and ventral hippocampal location. Furthermore, ferrets are amenable to behavioral training, have a body size compatible with pre-clinical MRI, and are cost-effective. NEW METHODS: We optimized the surgical procedure for controlled cortical impact (CCI) using 9 adult male ferrets. We used subject-specific brain/skull morphometric data from anatomical MRIs to overcome across-subject variability for lesion placement. We also reflected the temporalis muscle, closed the craniotomy, and used antibiotics. We then gathered MRI, behavioral, and immunohistochemical data from 6 additional animals using the optimized surgical protocol: 1 control, 3 mild, and 1 severely injured animals (surviving one week) and 1 moderately injured animal surviving sixteen weeks. RESULTS: The optimized surgical protocol resulted in consistent injury placement. Astrocytic reactivity increased with injury severity showing progressively greater numbers of astrocytes within the white matter. The density and morphological changes of microglia amplified with injury severity or time after injury. Motor and cognitive impairments scaled with injury severity. COMPARISON WITH EXISTING METHOD(S): The optimized surgical methods differ from those used in the rodent, and are integral to success using a ferret model. CONCLUSIONS: We optimized ferret CCI surgery for consistent injury placement. The ferret is an excellent animal model to investigate pathophysiological and behavioral changes associated with TBI.

Transplanted Neural Progenitor Cells from Distinct Sources Migrate Differentially in an Organotypic Model of Brain Injury.

Brain injury is a major cause of long-term disability. The possibility exists for exogenously derived neural progenitor cells to repair damage resulting from brain injury, although more information is needed to successfully implement this promising therapy. To test the ability of neural progenitor cells (NPCs) obtained from rats to repair damaged neocortex, we transplanted neural progenitor cell suspensions into normal and injured slice cultures of the neocortex acquired from rats on postnatal day 0-3. Donor cells from E16 embryos were obtained from either the neocortex, including the ventricular zone (VZ) for excitatory cells, ganglionic eminence (GE) for inhibitory cells or a mixed population of the two. Cells were injected into the ventricular/subventricular zone (VZ/SVZ) or directly into the wounded region. Transplanted cells migrated throughout the cortical plate with GE and mixed population donor cells predominately targeting the upper cortical layers, while neocortically derived NPCs from the VZ/SVZ migrated less extensively. In the injured neocortex, transplanted cells moved predominantly into the wounded area. NPCs derived from the GE tended to be immunoreactive for GABAergic markers while those derived from the neocortex were more strongly immunoreactive for other neuronal markers such as MAP2, TUJ1, or Milli-Mark. Cells transplanted in vitro acquired the electrophysiological characteristics of neurons, including action potential generation and reception of spontaneous synaptic activity. This suggests that transplanted cells differentiate into neurons capable of functionally integrating with the host tissue. Together, our data suggest that transplantation of neural progenitor cells holds great potential as an emerging therapeutic intervention for restoring function lost to brain damage.