In humans, the acute inflammatory reaction caused by ultraviolet (UV) radiation is well studied and the sensory changes that are found have been used as a model of cutaneous hyperalgesia. Similar paradigms are now emerging as rodent models of inflammatory pain. Using a narrowband UVB source, we irradiated the plantar surface of rat hind paws. This produced the classical feature of inflammation, erythema, and a significant dose-dependent reduction in both thermal and mechanical paw withdrawal thresholds. These sensory changes peaked 48h after irradiation. At this time there is a graded facilitation of noxious heat evoked (but not basal) c-fos-like immunoreactivity in the L4/5 segments of the spinal cord. We also studied the effects of established analgesic compounds on the UVB-induced hyperalgesia. Systemic as well as topical application of ibuprofen significantly reduced both thermal and mechanical hyperalgesia. Systemic morphine produced a dose-dependent and naloxone sensitive reversal of sensory changes. Similarly, the peripherally restricted opioid loperamide also had a dose-dependent anti-hyperalgesic effect, again reversed by naloxone methiodide. Sequestration of NGF, starting at the time of UVB irradiation, significantly reduced sensory changes. We conclude that UVB inflammation produces a dose-dependent hyperalgesic state sensitive to established analgesics. This suggests that UVB inflammation in the rat may represent a useful translational tool in the study of pain and the testing of analgesic agents.

SummaryWe assessed how often bedside stethoscopes in our intensive care unit were cleaned and whether they became colonised with potentially pathogenic bacteria. On two separate days the 12 nurses attending the bedspaces were questioned about frequency of stethoscope cleaning on the unit and the bedside stethoscopes were swabbed before and after cleaning to identify colonising organisms. Twenty-two health care providers entering the unit were asked the same questions and had their personal stethoscopes swabbed. All 32 non-medical staff cleaned their stethoscopes at least every day; however only three out of the 12 medical staff cleaned this often. Out of 24 intensive care unit bedside stethoscopes tested, two diaphragms and five earpieces were colonised with pathogenic bacteria. MRSA cultured from one earpiece persisted after cleaning. Three out of the 22 personal stethoscope diaphragms and five earpieces were colonised with pathogens. After cleaning, two diaphragms and two earpieces were still colonised, demonstrating the importance of regular cleaning.

SummaryIn this article, we will discuss the pathophysiology of peripheral nerve injury in anaesthetic practice, including factors which increase the susceptibility of nerves to damage. We will describe a practical and evidence-based approach to the management of suspected peripheral nerve injury and will go on to discuss major nerve injury patterns relating to intra-operative positioning and to peripheral nerve blockade. We will review the evidence surrounding particular strategies to reduce the incidence of peripheral nerve injury during nerve blockade, including nerve localisation methods, timing of blocks, needle techniques and design, injection pressure-monitoring and local anaesthetic and adjunct choice. Pathophysiology of peripheral nerve injuryPeripheral nerve injury during the peri-operative period can occur when a nerve is subjected to stretch, compression, hypoperfusion, direct trauma, exposure to neurotoxic material or a combination of these factors [1,2].In many cases, no clear aetiology for nerve injury is apparent [3,4]. The shared pathophysiological precipitant of these injuries is often nerve hypoperfusion and consequent ischaemia due to physical disruption of the vasa nervorum, intraneural haemorrhage and/or endoneural oedema [5]. These result in a spectrum of histological neural abnormalities ranging from impaired axoplasmic transport, axonal degeneration, Schwann cell damage, myelin destruction, segmental demyelination and complete Wallerian degeneration [6][7][8]. Depending on the severity and duration of the ischaemic insult, either temporary or permanent disruption to nerve impulse transmission can result. There is a loose relationship between the severity of the original pathophysiological mechanism, degree of nerve ischaemia and subsequent clinical presentation, although in an animal model of compression injury, the degree of histological nerve damage has been correlated with the degree and duration of compression [8].Established peripheral neuropathy, pre-existing (but subclinical) peripheral neuropathy, profound hypothermia, hypovolaemia, hypotension, hypoxaemia, electrolyte disorders, malnutrition, small or large body mass index (BMI), tobacco use and anatomical variants (such as the presence of cervical ribs) may increase the susceptibility of peripheral nerves to peri-

SummarySpinal cord injury arising during anaesthetic practice is a rare event, but one that carries a significant burden in terms of morbidity and mortality. In this article, we will review the pathophysiology of spinal cord injury. We will then discuss injuries relating to patient position, spinal cord hypoperfusion and neuraxial techniques. The most serious causes of spinal cord injury -vertebral canal haematoma, spinal epidural abscess, meningitis and adhesive arachnoiditis -will be discussed in turn. For each condition, we draw attention to practical, evidence-based measures clinicians can undertake to reduce their incidence, or mitigate their severity. Finally, we will discuss transient neurological symptoms. Some cases of spinal cord injury during anaesthesia can be ascribed to anaesthesia itself, arising as a direct consequence of its conduct. The injury to a spinal nerve root by inaccurate and/or incautious needling during spinal anaesthesia is an obvious example. But in many cases, spinal cord injury during anaesthesia is not caused by, related to, or even associated with, the conduct of the anaesthetic. Surgical factors, whether direct (e.g. spinal nerve root damage due to incorrect pedicle screw placement) or indirect (e.g. cord ischaemia following aortic surgery) are responsible for a significant proportion of spinal cord injuries that occur concurrently with the delivery of regional or general anaesthesia. Pathophysiology of spinal cord injuryInjury to the spinal cord and its nerve roots occurs following a range of insults, including: compression; stretch; hypoperfusion; direct trauma; exposure to neurotoxic material; or a combination of these factors. Like peripheral nerves, the spinal cord responds poorly to ischaemia, which is the common histopathological endpoint of these insults.In contrast to peripheral nerve injury during anaesthesia, many cases of spinal cord injury have a clear aetiology. Certain predispositions may render patients more at risk of spinal cord injury during anaesthesia, including: spinal canal deformity; abnormal coagulation; abnormal vascular supply; or immunosuppression.Spinal canal stenosis is a common spinal canal deformity and can result from arthritic change, ankylosing spondylitis, Paget's disease or acromegaly. It is rarely caused by congenital malformations. Pre-existing stenosis may contribute to spinal cord injury because the narrower canal cross-sectional area in such patients renders them more at risk of nerve compression or

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By reading this article you should be able to:Plan the intraoperative conduct of shoulder surgery with the patient either awake, sedated, or using general anaesthesia. Describe the steps required to safely perform interscalene brachial plexus blockade for shoulder surgery. Describe the complications and adverse effects of interscalene nerve block. Discuss the differences between regional anaesthetic techniques performed for anaesthesia to facilitate awake surgery and techniques used to provide postoperative analgesia.

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BackgroundThe optimal anesthetic modality for endovascular treatment (EVT) in acute ischemic stroke (AIS) is undetermined. Comparisons of general anesthesia (GA) with composite non-GA cohorts of conscious sedation (CS) and local anesthesia (LA) without sedation have provided conflicting results. There has been emerging interest in assessing whether LA alone may be associated with improved outcomes. We conducted a systematic review and meta-analysis to evaluate clinical and procedural outcomes comparing LA with CS and GA.MethodsWe reviewed the literature for studies reporting outcome variables in LA versus CS and LA versus GA comparisons. The primary outcome was 90 day good functional outcome (modified Rankin Scale (mRS) score of ≤2). Secondary outcomes included mortality, symptomatic intracerebral hemorrhage, excellent functional outcome (mRS score ≤1), successful reperfusion (Thrombolysis in Cerebral Infarction (TICI) >2b), procedural time metrics, and procedural complications. Random effects meta-analysis was performed on unadjusted and adjusted data.ResultsEight non-randomized studies of 7797 patients (2797 LA, 2218 CS, and 2782 GA) were identified. In the LA versus GA comparison, no statistically significant differences were found in unadjusted analyses for 90 day good functional outcome or mortality (OR=1.22, 95% CI 0.84 to 1.76, p=0.3 and OR=0.83, 95% CI 0.64 to 1.07, p=0.15, respectively) or in the LA versus CS comparison (OR=1.14, 95% CI 0.76 to 1.71, p=0.53 and OR=0.88, 95% CI 0.62 to 1.24, p=0.47, respectively). There was a tendency towards achieving excellent functional outcome (mRS ≤1) in the LA group versus the GA group (OR=1.44, 95% CI 1.00 to 2.08, p=0.05, I2=70%). Analysis of adjusted data demonstrated a tendency towards higher odds of death at 90 days in the GA versus the LA group (OR=1.24, 95% CI 1.00 to 1.54, p=0.05, I2=0%).ConclusionLA without sedation was not significantly superior to CS or GA in improving outcomes when performing EVT for AIS. However, the quality of the included studies impaired interpretation, and inclusion of an LA arm in future well designed multicenter, randomized controlled trials is warranted.