Background: The dissecting posterior cerebral artery (PCA) aneurysms are very rare. These aneurysms pose significant treatment challenge and need careful evaluation to formulate an optimal treatment plan in case of ruptured or un-ruptured presentations. Methods: Retrospective review of a prospectively collected data. Results: Seven patients with dissecting aneurysms of the PCA were identified. Six out of seven presented with subarachnoid hemorrhage (SAH) and one with ischemic stroke. Three out of seven were treated with endovascular coil embolization without sacrifice of the parent artery and the rest had parent artery occlusion (PAO) with coil embolization. None of the patients developed new neurological deficits post-procedure. Aneurysm re-occurred in two patients that were treated without PAO. Conclusion: Endovascular treatment of the dissecting PCA aneurysm is safe and feasible. It can be performed with or without PAO. Recurrence is more common without PAO and close follow-up is warranted.

Endovascular tumor embolization as adjunctive therapy for head and neck cancers is evolving and has become an important part of the tools available for their treatment. Careful study of tumor vascular anatomy and adhering to general principles of intra-arterial therapy can prove this approach to be effective and safe. Various embolic materials are available and can be suited for a given tumor and its vascular supply. This article aims to summarize current methods and agents used in endovascular head and neck tumor embolization and discuss important angiographic and treatment characteristics of selected common head and neck tumors.

Premedication with clopidogrel, in contrast to aspirin, does not achieve adequate platelet inhibition in about two-third of the patients. Same day antiplatelet loading may be insufficient to achieve adequate platelet inhibition and should be avoided if clinically feasible.

Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...

Background: Mechanical thrombectomy is a promising adjuvant or stand-alone therapy for acute