SUMMARY In a retrospective three year study 13 cases of xanthogranulomatous cholecystitis (XGC) (seven female, six male) were found in 724 gallbladders (1 8%), an estimated incidence of 1 7 cases per 1O00000 population per annum. Symptoms often began with an episode of acute cholecystitis and persisted for up to five years. There was extension of xanthogranulomatous tissue into adjacent organs in nine cases. Three patients had fistulae from the gall bladder, one to skin, and two to the duodenum; this is the first report of this complication in XGC. In two patients XGC sufficiently resembled carcinoma for the surgeon to request intraoperative frozen section diagnosis. There was a high rate of postoperative infective complication, with one subphrenic abscess and three wound infections (one fatal), two in patients with fistulae.

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Aims-To determine the sites, mechanisms, and clinical significance of injuries to the eyes and brains of children with non-accidental injuries in relation to differing levels of trauma. Methods-A forensic pathological study of injuries in the eyes and brains of 23 consecutive children dying of non-accidental injuries over a 4 year period

Clinical, radiological and pathological findings in 31 patients with xanthogranulomatous cholecystitis have been reviewed. The spectrum of presentation was similar to that of cholelithiasis but fewer patients had biliary colic (17 per cent) and there were more complications (32 per cent). Four patients had a biliary fistula and four a perforated gallbladder with abscess formation. Patients characteristically had gallstones. Appearances often mimicked carcinoma of the gallbladder at ultrasonography and/or laparotomy, with xanthogranulomatous tissue extending to adjacent structures. Xanthogranulomatous cholecystitis and carcinoma of the gallbladder coexisted in three patients. The possibility should be considered that an 'inoperable tumour' of the gallbladder may in fact be xanthogranulomatous cholecystitis, a benign condition that frozen-section biopsy may confirm.

Aim: The potential causes of the optic nerve injury as a result of blunt object trauma, were investigated using a computer model. Methods: A finite element model of the eye, the optic nerve, and the orbit with its content was constructed to simulate blunt object trauma. We used a model of the first phalanx of the index finger to represent the blunt body. The trauma was simulated by impacting the blunt body at the surface between the globe and the orbital wall at velocities between 2-5 m/s, and allowing it to penetrate 4-10 mm below the orbital rim. Results: The impact caused rotations of the globe of up to 5000˚/s, lateral velocities of up to 1 m/s, and intraocular pressures (IOP) of over 300 mm Hg. The main stress concentration was observed at the insertion of the nerve into the sclera, at the side opposite to the impact. Conclusions:The results suggest that the most likely mechanisms of injury are rapid rotation and lateral translation of the globe, as well as a dramatic rise in the IOP. The strains calculated in the study should be sufficiently high to cause axonal damage and even the avulsion of the nerve. Finite element computer modelling has therefore provided important insights into a clinical scenario that cannot be replicated in human or animal experiments.A nterior traumatic optic neuropathy and optic nerve avulsion may result from a blunt injury where a foreign object intrudes between the globe and the orbital wall.