BackgroundWith recent emphasis placed on workplace based assessment (WBA) as a method of formative performance assessment, there is limited evidence in the current literature regarding the role of feedback in improving the effectiveness of WBA. The aim of this systematic review was to elucidate the impact of feedback on the effectiveness of WBA in postgraduate medical training.MethodsSearches were conducted using the following bibliographic databases to identify original published studies related to WBA and the role of feedback: Medline (1950-December 2010), Embase (1980-December 2010) and Journals@Ovid (English language only, 1996-December 2010). Studies which attempted to evaluate the role of feedback in WBA involving postgraduate doctors were included.Results15 identified studies met the inclusion criteria and minimum quality threshold. They were heterogeneous in methodological design. 7 studies focused on multi source feedback, 3 studies were based on mini-clinical evaluation exercise, 2 looked at procedural based assessment, one study looked at workplace based assessments in general and 2 studies looked at a combination of 3 to 6 workplace based assessments. 7 studies originated from the United Kingdom. Others were from Canada, the United States and New Zealand. Study populations were doctors in various grades of training from a wide range of specialties including general practice, general medicine, general surgery, dermatology, paediatrics and anaesthetics. All studies were prospective in design, and non-comparative descriptive or observational studies using a variety of methods including questionnaires, one to one interviews and focus groups.ConclusionsThe evidence base contains few high quality conclusive studies and more studies are required to provide further evidence for the effect of feedback from workplace based assessment on subsequent performance. There is, however, good evidence that if well implemented, feedback from workplace based assessments, particularly multisource feedback, leads to a perceived positive effect on practice.

The Wilderness Medical Society convened an expert panel to develop a set of evidence-based guidelines for the prevention and treatment of frostbite. We present a review of pertinent pathophysiology. We then discuss primary and secondary prevention measures and therapeutic management. Recommendations are made regarding each treatment and its role in management. These recommendations are graded based on the quality of supporting evidence and balance between the benefits and risks/burdens for each modality according to methodology stipulated by the American College of Chest Physicians.

Frostbite presentation to hospital is relatively infrequent, and the optimal management of the more severely injured patient requires a multidisciplinary integration of specialist care. Clinicians with an interest in wilderness medicine/freezing cold injury have the awareness of specific potential interventions but may lack the skill or experience to implement the knowledge. The on-call specialist clinician (vascular, general surgery, orthopaedic, plastic surgeon or interventional radiologist), who is likely to receive these patients, may have the skill and knowledge to administer potentially limb-saving intervention but may be unaware of the available treatment options for frostbite. Over the last 10 years, frostbite management has improved with clear guidelines and management protocols available for both the medically trained and winter sports enthusiasts. Many specialist surgeons are unaware that patients with severe frostbite injuries presenting within 24 h of the injury may be good candidates for treatment with either TPA or iloprost. In this review, we aim to give a brief overview of field frostbite care and a practical guide to the hospital management of frostbite with a stepwise approach to thrombolysis and prostacyclin administration for clinicians.

Syndromes thought to have cerebral venous hypertension as their core, such as idiopathic intracranial hypertension and jugular foramen outlet obstruction, classically result in headaches. Do they provide an insight into the cause of the headache that commonly occurs at altitude? The classic theory of the pathogenesis of high altitude headache has been that it results from increased intracranial pressure (ICP) secondary to hypoxemia in people who have less compliant intracranial volumes (Roach and Hackett, 2001). However, there does not appear to be a correlation between the headache of acute mountain sickness (AMS) and the presence of cerebral edema (Bailey et al, 2006; Wilson et al, 2009). Research has concentrated on arterial perfusion to the brain in hypoxia, but there has been little study of venous drainage. Hypoxia results in markedly increased cerebral blood flow; however, if it has been considered at all, venous outflow has to date been assumed to be of little consequence. Retinal venous distension and the increased venous blood demonstrated by near infra-red spectroscopy and more recently by MRI imply that, in hypoxia, a relative venous insufficiency may exist. Similarly, there is increasing evidence that manifestations of the fluid shift during microgravity is of similar nature to idiopathic intracranial hypertension, which is thought to be primarily a venous insufficiency condition. The unique anthropomorphic adaptations of large brained biped humans with cerebral venous systems that have to cope with large changes in hydrostatic pressure may predispose us to conditions of inflow/outflow mismatch. In addition, slight increases in central venous pressures (e.g., from hypoxia-induced pulmonary vasoconstriction) may further compromise venous outflow at altitude. A better understanding of cerebral venous physiology may enlighten us with regards the pathogenesis of headaches currently considered idiopathic. It may also enable us to trigger headaches for study and hence enable us to develop new treatment strategies.

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These results show that resting blood flow in the gastrointestinal tract is increased during exposure to high-altitude hypoxia, and that the vascular response of increased blood flow following food ingestion is maintained. Therefore, reduced flow is unlikely to cause gastrointestinal symptoms and reduced appetite at HA.

Current methods of measuring ABO antibody levels based on the hemagglutination (HA) titers have the disadvantages of relatively poor reproducibility and do not offer fine discrimination of antibody concentration. We therefore developed a simple and rapid method of measuring ABO antibody levels using flow cytometry (FC). For validation, we analyzed plasma samples from 79 blood donors. Both IgM and IgG were detected and measured with IgG essentially restricted blood group O donors. Forty-two successive samples were collected from a patient with blood group O undergoing antibody removal and subsequent transplantation from a group A2 donor and tested by both HA and FC. Changes in IgG measured by FC (relative median fluorescence) correlated well with HA titers and importantly rejection episodes were preempted by a rising relative median fluorescence. The method allowed quantitative discrimination in the range of antibody levels relevant to ABO incompatible transplantation and has the advantages over HA of objective measurement and reproducibility.

The SRT was easy to perform and provided a quantitative assessment of truncal ataxia in the field without the need for specialized equipment.