Background:The increase in the incidence of iatrogenic injury to the extrahepatic biliary tree that has been documented since the introduction of laparoscopic cholecystectomy (LC) has been explained as a 'learning curve' problem. The early New Zealand experience has been published and the present study was undertaken to determine whether there had been any change in the incidence, nature and management of laparoscopic biliary injuries (LBI) after further experience with LC. Methods: A nationwide audit was undertaken in 1995 by two confidential postal questionnaires: to all active general surgeons (n = 184, response rate 60%), and to all endoscopists performing endoscopic retrograde cholangiopancreatography (ERCP) ( n = 18, response rate 100%). Results: The total number of LBI was 21, compared with 41 for 1991-92. The site and nature of the injuries were similar for the two survey periods. More of the injuries appeared to be diagnosed after the operation and prior to discharge (25% vs 47%). Calculating the national incidence of LBI was not possible without complete reporting, but in the subset of surgeons responsible for the LBI there was no apparent decrease in the incidence of all LBI (2.8% vs 2.9%), those requiring active re-intervention (2.4% vs 2.7%) and major duct injury (1.1 % vs 0.7%), despite a significant increase in the surgeons' prior experience with LC (20% vs 61 % of surgeons had performed more than 100 LC). There were some concerning trends in management: a less frequent use of ERCP in patients with LBI diagnosed after surgery (76% vs 65%) and a higher proportion of patients with minor injuries managed by re-operation (26% vs 50%). Conclusions:The present study indicates that iatrogenic biliary injury is a persistent problem in New Zealand, despite increasing experience with LC, and suggests the need for more intensive scrutiny of operative technique and training. There is scope to manage more patients with minor duct injuries conservatively.

A 66-year-old Chinese man developed corneal endothelial decompensation after intraocular lens (IOL) repositioning using intracameral epinephrine was performed. The presentation was compatible with toxic endothelial cell destruction syndrome, which is caused by prolonged, direct exposure of the corneal endothelium to relatively high concentrations of intracameral epinephrine. Despite its effective and immediate mydriatic effect, intracameral epinephrine is not recommended for intraoperative mydriasis in procedures such as IOL repositioning or secondary IOL implantation in which minimal irrigating solution is used.

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Vernal keratoconjunctivitis (VKC) is a chronic allergic inflammatory disease with unclear etiology and pathogenesis. We investigated the tear film proteome of patients with VKC to understand the pathologic characteristics of VKC. Methods: Tear samples were collected from healthy volunteers and patients with VKC. Electrophoresis was performed to display the tear proteomic profiles according to VKC severity. The identities of differentially expressed proteins were analyzed by mass spectrometry and quantified by enzyme-linked immunosorbent assay. Impression cytology was performed on VKC conjunctival samples to demonstrate the cellular protein expression. Allergic sensitization was performed in mice to study the pathologic role of these proteins in VKC. Results: Hemopexin, an inflammatory protein, was elevated in the tear film of patients with VKC. The increased hemopexin concentration in VKC tears was significantly associated with disease severity. Impression cytology showed specific high hemopexin expression in dekeratinized conjunctival epithelium and necrotic macrophages in patients with VKC. Immunohistochemical examination of normal lacrimal tissues from mice showed that hemopexin was not expressed in any lacrimal apparatus. Under systemic and topical sensitization and challenge using hemopexin in mice, the affected eye had mild to moderate bead discharge, chemosis, and edema with excessive macrophage infiltration and conjunctival necrosis. Conclusion: An association exists between tear hemopexin and the development and pathologic effects of VKC. Clinical Relevance: Increased hemopexin may have a role in the development of VKC.