Increasing demand for surgery and anaesthesia has created an imperative to manage anaesthetic workforce and caseload. This may include changes to distribution of cases amongst anaesthetists of different grades, including non-physician anaesthetists. To achieve this safely, an assessment of case complexity is essential. We present a novel system for scoring complexity of cases in anaesthesia, the Oxford Anaesthetic Complexity score. This integrates patient, anaesthetic, surgical and systems factors, and is different from assessments of risk. We adopted an end-user development approach to the design of the score, and validated it using a dataset of anaesthetic cases. Across 688 cases, the median (IQR [range]) complexity score was 19 (17-22 [15-33]). Cases requiring a consultant anaesthetist had a significantly higher median (IQR [range]) score than those requiring a senior trainee at 22 (20-25 [15-33]) vs. 19 (17-21 [15-28]), p < 0.001. Cases undertaken in a tertiary acute hospital had a significantly higher score than those in a district general hospital, the median (IQR [range]) scores being 20 (17-22 [15-33]) vs. 17 (16-19 [17-28]), p < 0.001. Receiver-operating characteristic analysis showed good prediction of complexity sufficient to require a consultant anaesthetist, with area under the curve of 0.84. Any rise in complexity above baseline (score > 15) was strongly predictive of a case too complex for a junior trainee (positive predictive value 0.93). The Oxford Anaesthetic Complexity score can be used to match cases to different grades of anaesthetist, and can help in defining cases appropriate for the expanding nonphysician anaesthetist workforce.

We aimed to study the endothelial dysfunction among children and adolescents with transfusion-dependent β-thalassemia using von Willebrand factor antigen (VWF:Ag) and flow cytometric analysis of circulating CD144(+) endothelial microparticles (EMPs) and endothelial progenitor cells (CD34(+)VEGFR2(+)) and assess their relation to iron overload, erythropoietin and chelation therapy as well as echocardiographic parameters and carotid intima-media thickness. The VWF:Ag, EMPs, and CD34(+)VEGFR2(+) cells were significantly higher among patients with β-thalassemia than controls (P < .001). The type of chelation and patients' compliance did not influence the results. No significant correlations were found between the studied vascular markers. Patients with evident heart disease had higher VWF: Ag, EMPs, and CD34(+)VEGFR2(+) cells than those without. Carotid intima-media thickness was increased among patients but not correlated with vascular markers. We suggest that procoagulant EMPs and VWF: Ag are involved in cardiovascular complications in patients with young β-thalassemia. CD34(+)VEGFR2(+) cells were further increased in response to tissue injury contributing to reendothelialization and neovascularization.

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An 80-year-old lady suffered loss of cardiac output during an elective pacemaker lead exchange. Right ventricular perforation, cardiac tamponade, vascular lacerations and circulatory shock are known major complications of pacemaker lead exchange and may necessitate aggressive resuscitation. An emergency sternotomy revealed the administered fluid, blood products and resuscitative drugs, which were administered through an upper limb cannula, had likely extravasated at the site of an iatrogenic injury to the superior vena cava. Unfortunately, further resuscitation attempts were unsuccessful. There are no recommendations regarding sites for intravascular access during pacemaker lead exchange and we argue that lower limb veins should be considered for venous access, as the superior vena cava and innominate veins are possible sites of unintentional vascular injury.