Le Manach Research Articles

Validation of the Preoperative Score to Predict Postoperative Mortality (POSPOM) in Germany.

BackgroundThe Preoperative Score to Predict Postoperative Mortality (POSPOM) based on preoperatively available data was presented by Le Manach et al. in 2016. This prognostic model considers the kind of surgical procedure, patients' age and 15 defined comorbidities to predict the risk of postoperative in-hospital mortality. Objective of the present study was to validate POSPOM for the German healthcare coding system (G-POSPOM).Methods and findingsAll cases involving anaesthesia performed at the University Hospital Bonn between 2006 and 2017 were analysed retrospectively. Procedures codified according to the French Groupes Homogènes de Malades (GHM) were translated and adapted to the German Operationen- und Prozedurenschlüssel (OPS). Comorbidities were identified by the documented International Statistical Classification of Diseases (ICD-10) coding. POSPOM was calculated for the analysed patient collective using these data according to the method described by Le Manach et al. Performance of thereby adapted POSPOM was tested using c-statistic, Brier score and a calibration plot. Validation was performed using data from 199,780 surgical cases. With a mean age of 56.33 years (SD 18.59) and a proportion of 49.24% females, the overall cohort had a mean POSPOM value of 18.18 (SD 8.11). There were 4,066 in-hospital deaths, corresponding to an in-hospital mortality rate of 2.04% (95% CI 1.97 to 2.09%) in our sample. POSPOM showed a good performance with a c-statistic of 0.771 and a Brier score of 0.021.ConclusionsAfter adapting POSPOM to the German coding system, we were able to validate the score using patient data of a German university hospital. According to previous demonstration for French patient cohorts, we observed a good correlation of POSPOM with in-hospital mortality. Therefore, further adjustments of POSPOM considering also multicentre and transnational validation should be pursued based on this proof of concept.

Science, subsidies and the politics of the pulse trawl ban in the European Union

The decision to ban the pulse trawl by the European Parliament in early 2019 was influenced by public debate over its scientific and political legitimacy. In their 2019 paper in Marine Policy, Le Manach et al. continued this debate by making three claims. First, that the pulse trawl has substantial negative social and environmental impacts. Second, that it received ‘illegal’ subsidies from the European Union amounting to €20.8 million. And third, that the Dutch government and industry did not provide adequate transparency in the allocation of subsidies. These claims are misleading and, in some instances, demonstrably false: the ongoing science on the effects of the pulse trawl shows relatively positive impacts; following the conventional definitions of “harmful” and “fisheries subsidies” in the economic literature, harmful subsidies provided to pulse trawling only amount to €0.3 million, or less than 2% of Le Manach et al.‘s estimate; and there is no evidence of intentional non-disclosure of information related to the distribution of subsidies by the Dutch government. Finally, we reflect on the consequences of the inaccuracies presented by Le Manach et al. in the governance of fishing gear innovation and their wider effect on the legitimacy of advocacy-based science.

97 Can pre-operative troponin levels predict post-operative mortality following non-cardiac surgery?

IntroductionDespite advances in surgical and anaesthetic techniques, non-cardiac surgery still has a significant mortality. We hypothesised that pre-operative troponin levels might predict post-operative mortality.MethodsPatients undergoing elective and urgent/emergency non-cardiac surgery...

Reply to Collins and Le Manach.

We thank Collins and Le Manach for their insightful comments on our paper and also for drawing our attention to their article on sample sizes for external validation of prognostic models, which unfortunately was unavailable when our data were analysed. However, their article examined the effect of sample size for proportional hazards models and we used a logistic regression model (with previously published papers more applicable to the assessment of appropriate sample size).

Burden of traumatic injuries in Saudi Arabia: lessons from a major trauma registry in Riyadh, Saudi Arabia.

BACKGROUND AND OBJECTIVESIn Saudi Arabia (SA), injuries are the second leading cause of death; however, little is known about their frequencies and outcomes. Trauma registries play a major role in measuring the burden on population health. This study aims to describe the population of the only hospital-based trauma registry in the country and highlight challenges and potential opportunities to improve trauma data collection and research in SA.DESIGN AND SETTINGSUsing data between 2001 and 2010, this retrospective study included patients from a large trauma center in Riyadh, SA.PATIENTS AND METHODSA staff nurse utilized a structured checklist to gather information on patients’ demographic, physiologic, anatomic, and outcome variables. Basic descriptive statistics by age group (≤14 vs >14 years) were calculated, and differences were assessed using student t and chi-square tests. In addition, the mechanism of injury and the frequency of missing data were evaluated.RESULTS10 847 patients from the trauma registry were included. Over 9% of all patients died either before or after being treated at the hospital. Patients who were older than 14 years of age (more likely to be male) sustained traffic-related injuries and died in the hospital as compared to patients who were younger than or equal to years of age. Deceased patients were severely injured as measured by injury severity score and Glasgow Coma Scale (P<.001). Overall, the most frequent type of injury was related to traffic (52.0%), followed by falls (23.4%). Missing values were mostly prevalent in traffic-related variables, such as seatbelt use (70.2%).CONCLUSIONThis registry is a key step toward addressing the burden of injuries in SA. Improved injury classification using the International Classification of Disease-external cause codes may improve the quality of the registry and allow comparison with other populations. Most importantly, injury prevention in SA requires further investment in data collection and research to improve outcomes.

In-hospital Management of Diabetes

In-hospital Management of Diabetes

Do We Need to Monitor Cardiac Output during Major Surgery?

Do We Need to Monitor Cardiac Output during Major Surgery?

Erratum to “Unreported fishing, hungry people and political turmoil: The recipe for a food security crisis in Madagascar” [Mar. Policy 36 (1) (2012) 218–225

Erratum to ‘‘Unreported fishing, hungry people and political turmoil: The recipe for a food security crisis in Madagascar’’ [Mar. Policy 36 (1) (2012) 218–225] Frederic Le Manach , Charlotte Gough , Alasdair Harris , Frances Humber , Sarah Harper , Dirk Zeller c a University of Plymouth, Faculty of Science and Technology, Drake Circus, Plymouth PL4 8AA, United Kingdom b Blue Ventures Conservation, Aberdeen Centre, London, N5 2EA, United Kingdom c Sea Around Us Project, Fisheries Centre, University of British Columbia, 2202 Main Mall, Vancouver, Canada V6T 1Z4

Instructions for Obtaining Anesthesiology Continuing Medical Education (CME) Credit

Anesthesiology's Journal CME is open to all readers. Members of the American Society of Anesthesiologists (ASA) enjoy a preferred rate for their subscription. However, Journal CME is not limited to ASA members or Journal subscribers. To take part in Journal CME, complete the following steps:The American Society of Anesthesiologists is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.The American Society of Anesthesiologists designates this journal based CME activity for a maximum of 1 AMA PRA Category 1 Credit(s) ™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.Purpose: The focus of Anesthesiology Journal CME is to educate readers on current developments in the science and clinical practice of anesthesiology.Target Audience: Anesthesiology Journal CME is designed for physicians involved with anesthesiology education, clinical practice, and research.Editor-in-Chief: James C. Eisenach, M.D., returned a disclosure form indicating that he received consulting fees from Medtronic, Endo, and Solvay, and funded research from King Pharmaceuticals.CME Editors: Leslie C. Jameson, M.D., and Dan J. Kopacz, M.D., have no relevant financial relationships to disclose.ASA Staff: Employees involved in planning have no relevant financial relationships to disclose.All tests and requests for credit must be submitted through the Anesthesiology CME website at http://education.asahq.org/2011-journal-cme. Participants should claim credit in 15-minute increments, for a maximum of 1 AMA PRA Category 1 Credit(s) ™ per journal article.Two payment options are available:ASA Member Non-memberAnnual Fee $60 $120Per Issue $10 $20Payment may be made using Visa or MasterCard.Please direct any questions about Journal CME to:Joyce CanselorEducation Coordinator, CME(847) 268-9185j.canselor@asahq.orgRead the article by Cannesson et al . entitled “Assessing the diagnostic accuracy of pulse pressure variations for the prediction of fluid responsiveness: A ‘gray zone’ approach” on page 231 and the accompanying editorial by De Hert entitled “Assessment of fluid responsiveness: Insights in a ‘gray zone'” on page 229 of this issue.After completing this activity, the learner should be able to identify patients who would benefit from use of pulse pressure variation analysis, know when to administer a fluid bolus to optimize cardiac output, and be able to compare patient responses to fluids in specific clinical situations.Authors: Maxime Cannesson, M.D., Ph.D., received consulting fees from Edwards Lifesciences, Covidien, Masimo Corp., ConMed, Philips Medical Systems, CNSystems, BMEYE, and Fresenius Kabi. Yannick Le Manach, M.D., Ph.D., received consulting fees from Air Liquide Sante' and received lecture/travel fees from Masimo Corp. and Fresenius Kabi. Christoph K. Hofer, M.D., received consulting fees from Pulsion Medical Systems, Edwards Lifesciences, CSL Behring. Benoît Vallet, M.D., Ph.D., received lecture/travel fees from Masimo Corp. and Edwards Lifesciences, Fresenius Kabi, and Baxter Corp. Benoît Tavernier, M.D., Ph.D., received lectures/travel fees from Masimo Corp. and Fresenius Kabi. Jean Pierre Goarin, M.D., and Jean-Jacques Lehot, M.D., Ph.D., have no financial interest in or affiliation with any commercial supporter or providers of any commercial services discussed in this educational material.Author: Stefan G. De Hert, M.D., Ph.D., has no financial interest in or affiliation with any commercial supporter or providers of any commercial services discussed in this educational material.Registration and submission of answers must be completed by August 31, 2014.

From Creatine Kinase-MB to Troponin

From Creatine Kinase-MB to Troponin

Perioperative Statin Therapy May Be Implicated in a Wide Array of Drug-Drug Interactions

We read with interest and appreciation the excellent article by Le Manach et al . in the June 2008 issue of Anesthesiology entitled “Statin Therapy within the Perioperative Period: Clinical Concepts and Commentary.”1However, there is an important area, namely drug-drug interactions involving statins, which merits more attention than the brief treatment in that review. We would like to make readers aware that a wide array of interactions can occur in the perioperative period and have been responsible for considerable morbidities.The authors are certainly correct that the risk of statin-induced rhabdomyolysis is associated with coadministration of such drugs as “cyclosporin, antifungal agents, calcium-channel blockers, and amiodarone.” However, there is a much broader array of medications that is likely to inhibit the metabolism or otherwise raise blood levels of statins to increase the risk of rhabdomyolysis. Atorvastatin, lovastatin, and simvastatin are primarily metabolized by the enzyme cytochrome P450 3A4 (CYP3A4). Coadministration of any of the many inhibitors on CYP3A4 (including cyclosporin, etc .) will raise blood levels of these specific statins. In addition, fluvastatin is metabolized by CYP2C9, and inhibitors of that enzyme's function will raise fluvastatin levels as well. Pravastatin's metabolism is primarily through phase II, or conjugative, metabolism, which is more difficult to inhibit to a clinically significant degree, so it is much less susceptible to these metabolic drug interactions. Rosuvastatin undergoes2*very little hepatic metabolism and it is generally excreted unchanged. However, through nonmetabolic mechanisms (probably inhibition of various transmembrane transporters), coadministration of either cyclosporin or gemfibrozil will significantly raise both pravastatin and rosuvastatin blood levels.There is an entire other dimension to drug-drug interactions involving statins that was not mentioned at all in the article: Coadministration of statins with enzymatic inducers. These drugs will, over the course of days to weeks, increase the quantity of enzymes available for metabolism of these statins. The addition of enzymatic inducers such as phenytoin, carbamazepine, and rifampin are likely to significantly decrease the concentrations of various statins. This is a particularly important interaction, especially in view of the ramifications for cardiac morbidity, as discussed in the authors' section on the risks of statin discontinuation in the perioperative period.In summary, this subject is clearly quite detailed and complex. A thorough treatment of this topic was published by Bellosta et al .2*University of Pennsylvania, Philadelphia Veterans Hospital, Philadelphia, Pennsylvania. sandson.marcucci@comcast.net

Perioperative Myocardial Infarction

More than 230 million major surgeries are performed annually worldwide,1 and this number grows continuously. The 30-day mortality associated with moderate- to high-risk noncardiac surgery in recent large cohorts and population-based studies exceeds 2%2–4 and surpasses 5% in patients at high cardiac risk.5 Cardiac complications constitute the most common cause of postoperative morbidity and mortality,4,6 having considerable impact on the length and cost of hospitalization.7 As our population ages, more high-risk cardiac patients will undergo surgery, and perioperative myocardial infarction (PMI) can be an increasing problem. Traditionally, MI was defined by the World Health Organization criteria, ECG criteria, and cardiac enzymes. Defining PMI, however, is often difficult because most PMIs occur without symptoms in anesthetized or sedated patients, ECG changes are subtle and/or transient, and the creatine kinase-MB isoenzyme has limited sensitivity and specificity because of coexisting skeletal muscle injury.8 Consequently, PMI was often recognized late (postoperative day 3 to 5), resulting in high (30% to 70%9) mortality. Cardiac troponin assays have changed this definition.10 The recent universal definition of MI11 is based on a rise and/or fall of cardiac biomarkers (preferably troponin) in the setting of myocardial ischemia: cardiac symptoms, ECG changes, or imaging findings. Studies using serial troponin measurements demonstrate that most PMIs start within 24 to 48 hours of surgery during the greatest postoperative stress.12–15 Le Manach et al15 observed early ( 24 hours) peaks in troponin in 1136 patients after abdominal aortic aneurysmectomy. Yet, 90% of troponin elevations began within <24 hours. Two distinct mechanisms may lead to PMI: acute coronary syndrome and prolonged myocardial oxygen supply-demand imbalance in the presence of stable coronary artery disease (CAD), designated type 1 and type 2 by the universal definition of MI.11 This distinction …

Procalcitonin and its utility as a diagnostic and prognostic assay in patients with renal dysfunction and immunosuppressive conditions

1. Endo S, Aikawa N, Fujishima S, Sekine I, Kogawa K, Yamamoto Y, et al. Usefulness of procalcitonin serum level for the discrimination of severe sepsis from sepsis: a multicenter prospective study. J Infect Chemother 2008;14:244–9. 2. Hirakata Y, Yanagihara K, Kurihara S, Izumikawa K, Seki M, Miyazaki Y, Kohno S. Comparison of usefulness of plasma procalcitonin and C-reactive protein measurements for estimation of severity in adults with community-acquired pneumonia. Diagn Microbiol Infect Dis 2008;61:170–4. 3. Amour J, Birenbaum A, Langeron O, Le Manach Y, Bertrand M, Coriat P, et al. Infl uence of renal dysfunction on the accuracy of procalcitonin for the diagnosis of postoperative infection after vascular surgery. Crit Care Med 2008;36:1147–54. 4. Dornbusch HJ, Strenger V, Sovinz P, Lackner H, Schwinger W, Kerbl R, et al. Non-infectious causes of elevated procalcitonin and C-reactive protein serum levels in pediatric patients with hematologic and oncologic disorders. Support Care Cancer 2008 Sep;16(9): 1035–40. 5. Ciaccio M, Fugardi G, Titone L, Romano A, Giordano S, Bivona G, et al. Procalcitonin levels in plasma in oncohaematologic patients with and without bacterial infections. Clin Chim Acta 2004;340: 149–52. 6. Stolzel F, Babatz J, Thiede C, Siegert G, Illmer T, Ehniger G, et al. Cyclic severe elevated procalcitonin serum levels in a patient with post polycythemic myelofi brosis carrying a V617F-JAK2 mutation. Ann Hematol 2008;87:1021–2. 7. Viallon A, Guyomarc’h S, Marjollet O, Berger C, Carricajo A, Robert F, et al. Can emergency physicians identify a high mortality subgroup of patients with sepsis: role of procalcitonin. Eur J Emerg Med 2008;15:26–33. Received: December 9, 2008 / Accepted: December 16, 2008

Statin Therapy within the Perioperative Period

STATINS are highly effective in lowering serum cholesterol concentrations through 3-hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase inhibition and thus are central to the primary and secondary prevention of cardiovascular disease. More than 50% of patients undergoing major vascular surgery and 80% undergoing cardiac surgery are on chronic statin therapy. 1,2 Statins also exert numerous lipid-independent or “pleiotropic” effects (effects that were not expected during drug development) as a result of their ability to inhibit the inflammatory response, reduce thrombosis, enhance fibrinolysis, decrease platelet reactivity, inhibit cell growth, reduce ischemia–reperfusion injury, and restore endothelial function. These beneficial effects result predominantly from the modulation of the complex interplay between the pathologic triad of inflammation, dynamic obstruction, and thrombosis. 3 This triad is integral to the surgical stress response and central to postoperative outcomes. However, recent reports noted that patients who undergo postoperative statin withdrawal experience increased cardiac morbidity when compared with patients who undergo early postoperative readministration of statins or with patients not treated with statins. 1,4 These facts raise several important questions for the anesthesiologist regarding statin therapy during the perioperative period: (1) Do statins modify perioperative risk? (2) Is continuation or discontinuation of statin therapy during the perioperative period associated with additional risk? (3) Do the potential benefits of statin therapy outweigh the potential risks? This review of the literature explores the risks and benefits associated with perioperative statin therapy.

Perioperative Statin Therapy: Are Formal Guidelines and Physician Education Needed?

Charles D. Collard, MD In this issue of Anesthesia & Analgesia, Le Manach et al. add to the growing evidence that perioperative statin therapy reduces surgical morbidity and mortality (1–6). Moreover, data from these same authors and others suggest that postoperative discontinuation of statin therapy is associated with worsened cardiac outcomes after major cardiovascular surgery (1,2). Thus, administration of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or “statins,” may be one of the most important perioperative therapeutic regimens to reduce the risk of postoperative cardiovascular complications in high-risk surgical patients since the introduction of -blockers into the operative setting (6). However, unlike the situation with perioperative -blocker therapy, the American College of Cardiology/American Heart Association Task Force on Practice Guidelines have yet to publish a consensus statement regarding perioperative statin therapy. Current National Cholesterol Education Program Adult Treatment Panel guidelines recommend decreasing LDL levels to 100 mg/dL in patients with known coronary disease, and more aggressive statin therapy to decrease LDL levels to 70 mg/dL in patients with coronary disease and high risk factors such as diabetes, hypertension, obesity, smoking, the metabolic syndrome, and acute coronary syndromes (ACS) (7). Thus, on the basis of these guidelines, most patients undergoing major cardiovascular surgery would qualify for statin therapy. Yet, despite these guidelines, it is estimated that up to two-thirds of eligible candidates may not be receiving statin therapy at hospital discharge (8). Explanations for not starting or reinitiating statin therapy after cardiovascular surgery may include patients’ decreased tolerance of oral medications secondary to nausea and vomiting, transient renal dysfunction, concerns pertaining to hepatic toxicity or myositis, or failure of the responsible physician to reimplement preoperative medications. The most serious potential statin side effect is rhabdomyolysis. Cerivastatin, which is no longer on the market, carried the greatest risk of this complication (3.16 per million prescriptions). In contrast, the risk of statin-induced rhabdomyolysis ranges only from 0 to 0.19 per million prescriptions for the other commonly used statins (9). Furthermore, the risk for rhabdomyolysis is associated with factors that increase serum statin concentrations, such as small body size, advanced age, renal or hepatic dysfunction, diabetes, hypothyroidism, and drugs that interfere with statin metabolism, such as cyclosporin, antifungal drugs, calciumchannel blockers, and amiodarone (9). When this small risk is compared with the incidence and socioeconomic cost of cardiac perioperative morbidity and mortality after major cardiovascular surgery, the benefits of statin therapy seem to largely outweigh any potential risks in the vast majority of patients. Moreover, in a recent study by Schouten et al., perioperative statin use in a large group of patients was not associated with an increased risk of perioperative myopathy or increased creatine phosphokinase levels after major vascular surgery (10). Indeed, after correcting for cardiac risk factors and clinical risk factors for myopathy, length of surgery remained the only independent predictor for myopathy From the Division of Cardiovascular Anesthesiology, Baylor College of Medicine, Texas Heart Institute, St. Luke’s Episcopal Hospital, Houston, Texas. Accepted for publication March 6, 2007. Address correspondence to Charles D. Collard, MD, Baylor College of Medicine, Texas Heart Institute, St. Luke’s Episcopal Hospital, 6720 Bertner Ave., Houston, TX 77030. Address e-mail to ccollard@heart.thi. tmc.edu. Copyright © 2007 International Anesthesia Research Society

A clinical prediction model was sensitive but not specific for predicting mortality in pulmonary embolism

Source Citation Aujesky D, Roy PM, Le Manach CP, et al. Validation of a model to predict adverse outcomes in patients with pulmonary embolism. Eur Heart J. 2006;27:476-81. 16207738

Accessory myocardial pathway mimicking an inferior myocardial infarction after major vascular surgery

Accessory myocardial pathway mimicking an inferior myocardial infarction after major vascular surgery

Is a New Classification of Postoperative Myocardial Infarction Justified?

Royal Brompton Hospital, London, United Kingdom. dylanbould@yahoo.co.ukI read with interest the prospective audit of routinely measuring cardiac troponin I (cTnI) levels postoperatively in infrarenal aortic surgery by Le Manach et al. 1The authors have proposed a classification of two separate groups of postoperative myocardial infarction (PMI) based on their findings. However, I think that aspects of both the methodology of the study and the presentation of results are open to criticism and that the validity of their distinction between early and delayed PMI is questionable.It is not clear why the value for cTnI that the authors consider to be abnormal changed in the study and in their participating institution from 0.5 ng/ml from September 1995 to November 1999 to 0.2 ng/ml from November 1999 onward. It seems that the same machine was used for testing cTnI throughout the study period. This parameter is the basis of the definitions of both myocardial damage and delayed PMI and also the proposed difference between the early and delayed PMI groups and is clearly a key issue. Regardless of whether the institution changed its normal values for cTnI, it would seem that the most appropriate methodology would be to analyze the whole population by the same rules. It would be of interest whether the endpoints would differ from that reported if all patients were reanalyzed together at 0.2 ng/ml and at 0.5 ng/ml.The abstract states that the cTnI profiles between the delayed PMI group before the cTnI threshold for PMI was reached and the myocardial damage group were identical. In the main part of the Results, it is only written that the profiles are comparable. Even so, the only evidence presented for this is a graph of two “representative” patients. To describe the two profiles mentioned as identical would require descriptive statistics of cTnI values to be presented against time for each of the different groups, with a mathematical analysis of their difference. I also note that there was not even a “representative” example described of the other two groups.The timing of the 24-h cutoff for the difference between early and delayed PMI was predetermined and arbitrary. The authors state that in the early PMI group, PMI was not preceded by subinfarction myocardial damage, but did any of the early PMI group patients have abnormal cTnI for 18 rather than 24 h? If so, how do we know that this was not significant myocardial damage? It would seem to be a more robust choice of timing if at first the pattern within the population was examined and then the most appropriate cutoff was chosen.The authors note that only the early PMI group had an increased incidence of previous myocardial infarction and hint that this supports their hypothesis of different etiology in the two PMI groups. I note that 57 comparisons are made in table 2. Because the P values are only described as less than 0.05 and not specified, it is hard to know how significant their four P values of less than 0.05 in table 2 really are when you would expect almost three to occur just by statistical probability. Defining two groups on their differing temporal characteristics, proving statistical difference in a clearly related temporal parameter in the absence of any other differences in nonrelated parameters, and then inferring that the two groups are fundamentally different is a weak argument.The opinion that the time when the cTnI is abnormal but not diagnostic of PMI should be considered a “golden period,” and the hypothesis that intensive interventions may influence outcome is attractive. The description of the natural history of cTnI changes would be more useful if we knew whether the ischemia was silent or associated with evidence that would have resulted in appropriate therapy anyway. I would like to know whether the myocardial damage group or the patients with abnormal cTnI before PMI had chest pain, dyspnea, heart failure, arrhythmias, or other electrocardiographic changes suggestive of ischemia.In conclusion, the authors have not shown a bimodal distribution that would justify the classification of PMI as early and delayed, nor have they conclusively shown a fundamental difference between rapid-onset and delayed-onset PMI groups on the evidence as presented. Moreover, I think the suggestion that early PMI is “hitherto unrecognized in the postoperative setting” is unfounded.Royal Brompton Hospital, London, United Kingdom. dylanbould@yahoo.co.uk

Anaphylaxis to rocuronium

AnaesthesiaVolume 58, Issue 2 p. 196-196 Free Access Anaphylaxis to rocuronium First published: 23 September 2008 https://doi.org/10.1046/j.1365-2044.2003.03005_20.xCitations: 6AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat We present this case in response to recent recommendations [1] that cases of anaphylaxis to rocuronium should be fully reported. A 47-year-old, ASA II woman presented for elective gynaecological surgery. Her past medical history included a prior admission to the intensive care unit following an allergic reaction to iodine contrast media. Previous general anaesthesia had been uneventful. Anaesthesia was induced with fentanyl, propofol (containing 1% lidocaine) and rocuronium. Intubation was uneventful, but within 5 min, an allergic reaction was diagnosed on the basis of bronchospasm, tachycardia (150 bpm), severe hypotension (60/30 mmHg) and the development of a widespread, florid and erythematous rash. She was given epinephrine 100 µg and 1 L of crystalloid intravenously. The situation improved rapidly with a return to baseline of cardiovascular parameters and improved lung compliance. Whilst recovery from neuromuscular block was awaited, a discussion was held with the surgeon and senior anaesthetic colleagues. Surgery was postponed, as the intended procedure could have involved significant blood loss. She was extubated 1 h post induction, once neuromuscular function had returned to normal. As a precaution she was admitted to a high dependency area overnight. She recovered fully and ultimately elected not to have surgery. Anaphylaxis was confirmed by elevated serum tryptase of 65 nmol.ml−1 1 h after the reaction. Skin prick testing 2 months after the event identified rocuronium as the causative agent (1/10 diluted solution). Interestingly, she also demonstrated sensitivity to succinylcholine, vecuronium and morphine (1/10 diluted solutions). Yellow card reporting was undertaken, the patient was counselled by the anaesthetic assessment clinic and MedicAlert warnings obtained. We agree with Baillard [1] and others that close monitoring of drug-related adverse events is desirable, but stress that all drugs are included in such a process. Unless this precaution is taken, reporting bias may over-exaggerate the dangers of one particular drug (as may well be occurring presently with rocuronium). The determination of the anaphylaxis risk of a drug is difficult as neither the numerator nor denominator are accurately known: Adverse events are known to be under-reported [2], and little information exists as to how many patients have been exposed to any one drug. R. ThomasM. Wood Queen Alexandra Hospital, Portsmouth PO6 3LY, UK References 1 Baillard C, Korinek AM, Galanton V, Le Manach Y, Larmignat P, Cupa M, Samama CM. Anaphylaxis to rocuronium. British Journal of Anaesthesia 2002; 88: 600 – 2.CrossrefCASPubMedWeb of Science®Google Scholar 2 Jayasuriya JP, Anandaciva S. Compliance with an incident report scheme in anaesthesia. Anaesthesia 1995; 50: 846 – 9.Wiley Online LibraryCASPubMedWeb of Science®Google Scholar Citing Literature Volume58, Issue2February 2003Pages 196-196 ReferencesRelatedInformation

Sir Robert Mond, F.R.S

ROBERT LUDWIG MOND, the elder son of the late Dr. Ludwig Mond, F.R.S., was born at Farnworth, near Widnes, Lancashire, on September 9, 1867, and was brother of Alfred Moritz Mond, the late Lord Melchett. He was educated at Cheltenham and at Peterhouse, Cambridge. Later he worked at the Polytechnicum, Zurich, and at the Universities of Edinburgh and Glasgow, and had the privilege of being private assistant to Sir William Thomson (Lord Kelvin). His first wife, the mother of his two daughters, died tragically in Egypt in 1905 ; and he married in 1922 Marie Louise Le Manach, of Belle Isle en Terre, Brittany.