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Since the first description of orbital blowout fractures, there has been much confusion as to their etiology. Two principal mechanisms have been proposed to explain their production, the buckling and the hydraulic mechanisms caused, respectively, by trauma to the orbital rim and the globe of the eye. The aim of this study was to evaluate both mechanisms qualitatively and quantitatively. Our protocol used intact cadavers, quantifiable intraocular pressure, variable and quantifiable force, and quantifiable bone strain distribution with strain gauge analysis. One orbit of each cadaver was used to simulate each of the two mechanisms, allowing direct comparison. Fractures produced by the buckling mechanism were limited to the anterior part of the orbital floor, with strain readings reaching up to 3756 microepsilon. Posteriorly, strain did not exceed 221 microepsilon. In contrast, hydraulic-type fractures were much larger, involving anterior and posterior parts of the floor as well as the medial wall of the orbit. Here, strain exceeded 3756 microepsilon in both parts of the floor. Furthermore, we have demonstrated that the average energy required to fracture the orbital floor by the buckling mechanism is 1.54 J, whereas an average energy of 1.22 J is needed to produce this fracture by the hydraulic mechanism. Our results suggest that efforts to establish one or another mechanism as the primary etiology are misplaced. Both mechanisms produce orbital blowout fractures, with different and specific characteristics. We believe this provides the basis for our reclassification of such fractures.

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INTRODUCTION The management of bile leaks following laparoscopic cholecystectomy has evolved with increased experience of ERCP and laparoscopy. The purpose of this study was to determine the impact of a minimally invasive management protocol.PATIENTS AND METHODS Twenty-four patients with a bile leak following laparoscopic cholecystectomy were recorded consecutively between 1993 and 2003 . Between 1993-1998, 10 patients were managed on a case-by-case basis. Between 1998-2003, 14 patients were managed according to a minimally invasive protocol utilising ERC/biliary stenting and relaparoscopy if indicated.RESULTS Bile leaks presented as bile in a drain left in situ post laparoscopic cholecystectomy (8/10 versus 10/14) or biliary peritonitis (2/10 versus 4/14). Prior to 1998, neither ERC nor laparoscopy were utilised routinely. During this period, 4/10 patients recovered with conservative management and 6/10 (60%) underwent laparotomy. There was one postoperative death and median hospital stay post laparoscopic cholecystectomy was 10 days (range, 5-30 days). In the protocol era, ERC ±s tenting was performed in 11/14 ( P = 0.01 versus pre-protocol) with the main indication being a persistent bile leak. Relaparoscopy was necessary in 5/14 ( P = 0.05 versus preprotocol). No laparotomies were performed ( P < 0.01 versus pre-protocol) and there were no postoperative deaths. Median hospital stay was 11 days (range, 5-55 days).CONCLUSIONS The introduction of a minimally invasive protocol utilising ERC and re-laparoscopy offers an effective modern algorithm for the management of bile leaks after laparoscopic cholecystectomy.

Therapeutic, IV.

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Background Pain is the most debilitating symptom of migraine. The cause of migraine pain likely requires activation of meningeal nociceptors. Mast cell degranulation, with subsequent meningeal nociceptor activation, has been implicated in migraine pathophysiology. Degranulating mast cells release serine proteases that can cleave and activate protease activated receptors. The purpose of these studies was to investigate whether protease activated receptor 2 is a potential generator of nociceptive input from the meninges by using selective pharmacological agents and knockout mice. Methods Ratiometric Ca imaging was performed on primary trigeminal and dural cell cultures after application of 2at-LIGRL-NH, a specific protease activated receptor 2 agonist. Cutaneous hypersensitivity and facial grimace was measured in wild-type and protease activated receptor 2 mice after dural application of 2at-LIGRL-NH or compound 48-80, a mast cell degranulator. Behavioral experiments were also conducted in mice after dural application of 2at-LIGRL-NH (2AT) in the presence of either C391, a selective protease activated receptor 2 antagonist, or sumatriptan. Results 2at-LIGRL-NH evoked Ca signaling in mouse trigeminal neurons, dural fibroblasts and in meningeal afferents. Dural application of 2at-LIGRL-NH or 48-80 caused dose-dependent grimace behavior and mechanical allodynia that were attenuated by either local or systemic application of C391 as well as in protease activated receptor 2 mice. Nociceptive behavior after dural injection of 2at-LIGRL-NH was also attenuated by sumatriptan. Conclusions Functional protease activated receptor 2 receptors are expressed on both dural afferents and fibroblasts and activation of dural protease activated receptor 2 produces migraine-like behavioral responses. Protease activated receptor 2 may link resident immune cells to meningeal nociceptor activation, driving migraine-like pain and implicating protease activated receptor 2 as a therapeutic target for migraine in humans.

Background: Microwave ablation is an in situ method of tumour destruction