Stephen T. Webb

Intra-articular bupivacaine: potentially chondrotoxic?

The management of acute postoperative pain after orthopaedic surgery is a challenge for anaesthetists and surgeons. The administration of local anaesthetic drugs into the joint space, either by single injection or by continuous infusion, has become a well-recognized technique for postoperative analgesia, in particular after arthroscopic surgery. Bupivacaine is commonly used for intra-articular analgesia because of its long duration of action. Other local anaesthetics used for intra-articular analgesia include ropivacaine and lidocaine. Intra-articular use of these drugs has been widely regarded as safe, and adverse effects of local anaesthetic agents in the joint space have been reported only rarely. Peak plasma concentrations of bupivacaine are sufficiently low after intra-articular injection such that systemic toxicity is extremely unlikely. However, overdose or inadvertent intravascular injection may result in central nervous system and cardiovascular toxicity. 3 Despite their widespread use, the effects of intra-articular local anaesthetic agents on joint structures have not been fully elucidated. Early evidence from animal experiments suggested that bupivacaine acutely inhibits the synthesis of articular cartilage. A later study found that intra-articular bupivacaine 0.5% resulted in articular cartilage inflammation and synovial membrane changes in rabbit knee joints. However, clinical reports of postoperative chondrolysis of the shoulder joint – 9 and ankle joint after arthroscopic surgery, and the possible association with the use of intra-articular bupivacaine, have brought the safety of intra-articular local anaesthetics to the fore among orthopaedic surgeons. Chondrolysis is a condition in which extensive loss of articular cartilage occurs over a relatively short period of time. After arthroscopic shoulder surgery, the consequences of postoperative glenohumeral chondrolysis are clearly devastating. The condition typically occurs in young athletes and effective treatment options are limited. The pain and reduced mobility associated with chondrolysis tend to progress to severe osteoarthritis, which may eventually require joint arthroplasty. The largest series of cases of post-arthroscopic glenohumeral chondrolysis (PAGCL) described 12 cases. The authors state that the common factor in all cases was the postoperative administration of an intra-articular infusion of bupivacaine with epinephrine. In total, 27 cases of PAGCL have been reported, with 25 of these cases having received postoperative continuous intra-articular analgesia with bupivacaine. – 9 Recently, a number of experimental studies have suggested that local anaesthetics may damage articular cartilage. It has been shown that bupivacaine 0.5% is toxic to both bovine articular chondrocyte cultures and bovine articular osteochondral tissue. The effect of bupivacaine on human cartilage has also been analysed. The effects of bupivacaine 0.5%, bupivacaine 0.25%, bupivacaine 0.125%, and saline 0.9% on bovine and human articular chondrocyte cultures were compared. Both bupivacaine 0.5% and bupivacaine 0.25% displayed dose-dependent and time-dependent chondrotoxicity. The toxicity of bupivacaine 0.5% was more marked than bupivacaine 0.25% at all time points. The toxicity of both drugs increased as the duration of exposure increased (from 15 to 60 min) and as the time after exposure increased (from 1 h to 1 week). The effect of bupivacaine 0.125% on bovine and human articular chondrocytes was no different from 0.9% saline. The effects of different concentrations of bupivacaine on bovine articular osteochondral tissue were also compared. Again, both bupivacaine 0.5% and bupivacaine 0.25% demonstrated dose-dependent chondrotoxicity. However, the effect of bupivacaine 0.125% was not different from 0.9% saline. Although less profound than the effects of bupivacaine, lidocaine 1% and lidocaine 2% also exhibit dosedependent and time-dependent toxic effects on bovine articular chondrocytes. Ropivacaine is the third local anaesthetic to be associated with chrondrotoxicity. The effects of bupivacaine 0.5% and ropivacaine 0.5% on both human articular chondrocyte cultures and human articular

Transcatheter aortic valve insertion: anaesthetic implications of emerging new technology

Transcatheter aortic valve insertion is a new development that potentially offers a number of advantages to patients and healthcare providers. These include the avoidance of sternotomy and cardiopulmonary bypass, and much faster discharge from hospital and return to functional status. The procedure itself however is quite complex, and presents significant demands in planning and implementation to the multidisciplinary team. Anaesthetic input is essential, and patient care in the perioperative period can be challenging. Early results have shown a significant mortality and morbidity rate, but the majority of procedures to date have been carried out in elderly patients with multiple comorbidities, making comparison with surgical aortic valve replacement inappropriate. Long-term outcomes are not yet known, but randomized controlled trials should allow this procedure and its application to be properly assessed.

II. Is sedation by non-anaesthetists really safe?

Sedation is frequently given by non-anaesthetists but is it actually safe? The definition of ‘safe’ is inherently difficult, and depends upon one’s perspective, however, we believe most patients would expect mishaps to be rare (,1:10 000). Anaesthetists themselves may approach sedation with caution as in some circumstances its administration can be as difficult as general anaesthesia, often requiring equal skill. However some patients, and importantly, many of our professional colleagues, view sedation as a lesser and therefore safer procedure than a ‘full’ general anaesthetic, perhaps because an anaesthetist is ‘not needed’. Others believe themselves safer if a fully trained anaesthetist is present when their level of consciousness is to be altered in any way. These factors, together with the markedly varying techniques used and the inconsistent quality of published data, make quantification of risk very difficult, and comparison of risk between different techniques almost impossible. In 1995, Quine 1 published the findings of a prospective audit of upper gastrointestinal endoscopy in 14 149 patients in 36 UK hospitals. A mortality rate of 1:2000 and a morbidity rate of 1:200 were reported and poor sedation practice was identified as a frequent contributory factor. In 2001, the UK Academy of Medical Royal Colleges and Faculties (AoMRC) published crossspecialty recommendations for standards for sedation practice titled ‘Implementing and ensuring safe sedation practice for healthcare procedures in adults’. 2 The document reiterated a previous definition of ‘conscious sedation’ as ‘a technique in which the use of a drug or drugs produces a state of depression of the central nervous system enabling treatment to be carried out, but during which verbal contact with the patient is maintained throughout the period of sedation. The drugs and techniques used should carry a margin of safety wide enough to render loss of consciousness unlikely’. The document goes on to state ‘if verbal responsiveness is lost the patient requires a level of care identical to that needed for general anaesthesia’, clarifying that in the UK, what is termed ‘deep sedation’ by the American Society of Anesthesiologists (ASA), 3 is considered

5-Fluorouracil-induced cardiotoxicity mimicking myocardial infarction: a case report

BackgroundSevere cardiotoxicity is a documented, but very unusual side-effect of intravenous 5-fluorouracil therapy. The mechanism producing cardiotoxicity is poorly understood.Case presentationA case of 5-fluorouracil-induced cardiotoxicity, possibly due to coronary artery spasm, and mimicking acute anterolateral myocardial infarction is presented and discussed. Electrocardiographs highlighting the severity of the presentation are included in the report along with coronary angiograms demonstrating the absence of significant coronary atherosclerosis.ConclusionSevere 5-fluorouracil-induced cardiotoxicity is rare, but can be severe and may mimic acute myocardial infarction, leading to diagnostic and therapeutic dilemmas. Readministration of 5-fluorouracil is not advised following an episode of cardiotoxicity.

Anaesthesia for serial whole-lung lavage in a patient with severe pulmonary alveolar proteinosis: a case report

IntroductionPulmonary alveolar proteinosis is a rare condition that requires treatment by whole-lung lavage. We report a case of severe pulmonary alveolar proteinosis and discuss a safe and effective strategy for the anaesthetic management of patients undergoing this complex procedure.Case presentationA 34-year-old Caucasian man was diagnosed with severe pulmonary alveolar proteinosis. He developed severe respiratory failure and subsequently underwent serial whole-lung lavage. Our anaesthetic technique included the use of pre-oxygenation, complete lung separation with a left-sided double-lumen endotracheal tube, one-lung ventilation with positive end-expiratory pressure, appropriate ventilatory monitoring, cautious use of positional manoeuvres and single-lumen endotracheal tube exchange for short-term postoperative ventilation.ConclusionPatients with pulmonary alveolar proteinosis may present with severe respiratory failure and require urgent whole-lung lavage. We have described a safe and effective strategy for anaesthesia for whole-lung lavage. We recommend our anaesthetic technique for patients undergoing this complex and uncommon procedure.

Preoperative percutaneous patent foramen ovale closure before neurosurgery in the sitting position

ent hospitals’. This is an important point. Despite using a range of concentration of ADP activator for LTA in their study (2–5 mM), when analysing agreement between LTA and modified thrombelastography (mTEG), a concentration of 5 mM was used. Chen and colleagues used a concentration of 2 mM again, extrapolating predictive values for bleeding between the two papers, in our opinion, requires caution. Agarwal and colleagues demonstrated good agreement between LTA and mTEG in patients on clopidogrel therapy, k 0.81, with agreement in 14 of 20 patients. In 10 patients identified as having a definitive response to clopidogrel by LTA, seven patients were also identified by mTEG. However, conversely, three patients (30%) were false negatives. In patients taking both clopidogrel and aspirin, mTEG correctly identified only five out of 10 patients, a 50% false negative rate. Therefore, if mTEG was used alone, a proportion of patients would have been cleared for surgery and anaesthesia, despite having definitive ADP receptor platelet inhibition. Perhaps most importantly in our paper, the finding of a wide range of both platelet ADP and TxA2 receptor inhibition in the control group remains unexplained. The issue concerning the concentration of platelet receptor agonists has been discussed. The potential for a high false-positive rate is therefore of concern and, as we highlighted, requires further investigation. Finally, we are equally excited about the potential of point of care tests of platelet function. There is huge potential for tailoring the timing of surgery, informing the use of neuroaxial anaesthesia, guiding blood product transfusions, and identifying at-risk non-responders to antiplatelet agents. However, as we concluded, more work is required with TEG platelet mapping before truly evidence-based guidance can be offered.

The Assessment of Risk in Cardiothoracic Intensive Care (ARCtIC): prediction of hospital mortality after admission to cardiothoracic critical care.

The models used to predict outcome after adult general critical care may not be applicable to cardiothoracic critical care. Therefore, we analysed data from the Case Mix Programme to identify variables associated with hospital mortality after admission to cardiothoracic critical care units and to develop a risk‐prediction model. We derived predictive models for hospital mortality from variables measured in 17,002 patients within 24 h of admission to five cardiothoracic critical care units. The final model included 10 variables: creatinine; white blood count; mean arterial blood pressure; functional dependency; platelet count; arterial pH; age; Glasgow Coma Score; arterial lactate; and route of admission. We included additional interaction terms between creatinine, lactate, platelet count and cardiac surgery as the admitting diagnosis. We validated this model against 10,238 other admissions, for which the c index (95% CI) was 0.904 (0.89–0.92) and the Brier score was 0.055, while the slope and intercept of the calibration plot were 0.961 and −0.183, respectively. The discrimination and calibration of our model suggest that it might be used to predict hospital mortality after admission to cardiothoracic critical care units.

Acute leukaemoid reaction following cardiac surgery.

Chronic myelomonocytic leukaemia is an atypical myeloproliferative disorder with a natural history of progression to acute myeloid leukaemia, a complex and poorly understood response by the bone marrow to stress. Cardiac surgery activates many inflammatory cascades and may precipitate a systemic inflammatory response syndrome. We present a case of undiagnosed chronic myelomonocytic leukaemia who developed rapidly fatal multi-organ dysfunction following cardiac surgery due to an acute leukaemoid reaction.

Tied up in knots

demonstrates that in doubtful situations attaching an air-tight plastic bag or ETCO2 monitoring line to the external end of the feeding tube can be used to diagnose tracheal placement, provided the tube is not kinked or obstructed. We also suggest that in addition to the usual precautions recommended while inserting feeding tubes, cleaning and draping of the chest and abdomen should not occur until correct placement has been confirmed.

Do inotropes really have a future

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