Sub-Tenon's anaesthesia: complications and their prevention

The advent of a new technique that is considered much safer than previously established one leads to its rapid adoption. This usually leads to the identification of previously unreported complications of the new technique, and a re-assessment of its position in clinical care, which is precisely the state of play with the sub-Tenon's block. The sub-Tenon's block was introduced into the clinical practice in early 1990. A systematic recent search of subject headings such as complications of sub-Tenon's block, subtenon, orbital block, orbital block complications, and orbital anaesthesia was performed in Medline, EMBASE, and Cochrane database. Indeed there are complications of sub-Tenon's block published as case reports and the exact incidence of these complications is not known. Management and preventive measures of these complications are described. Although the sub-Tenon's block appears to be relatively safer than needle-based blocks but a proper prospective, randomized, double-blind controlled trial is essential for scientific proof that sub-Tenon's block is better than needle-based blocks

Platelet hyperaggregability: Impaired responsiveness to nitric oxide (“platelet NO resistance”) as a therapeutic target

The original publication can be found at www.springerlink.comPlatelet hyperaggregability and associated thrombosis have been documented in a number of cardiovascular disease states. While one of the current mainstays of anti-thrombotic treatment (i.e. aspirin, clopidogrel, glycoprotein IIb/IIIa antagonists) has been directed at reducing platelet activation and aggregation, it is apparent that there are limitations to the effectiveness of these therapies. Nitric oxide (NO) plays an important role in platelet physiology. The ability of NO to regulate cyclic guanosine-3,′5′-monophosphate (cGMP), via activation of soluble guanylate cyclase, is the principal mechanism of negative control over platelet activity. NO is not only of the endothelial source, it is also released from activated platelets, providing a negative feedback. Studies in patients with symptomatic ischemia, chronic heart failure, diabetes and various risk factors for cardiovascular disease have demonstrated that platelets from these subjects exhibit reduced responsiveness to the anti-aggregating efficacy of NO: a phenomenon termed “platelet NO resistance”. It constitutes an impaired physiological response to endogenous NO (endothelium-derived relaxing factor or EDRF), and as such may contribute to the increased risk of ischemic events. NO resistance also accounts for reduced pharmaco-activity of exogenous NO donors, e.g. organic nitrates. Platelet NO resistance results largely from a combination of “scavenging” of NO by superoxide anion radical and inactivation of soluble guanylate cyclase. NO resistance has both diagnostic and prognostic implications. The current review examines the association of platelet NO resistance with pathological hyperaggregability and discusses potential therapeutic strategies targeting this abnormality.Sharmalar Rajendran and Yuliy Y. Chirko