Australia E-mail Research Articles

A one-point technique for per-operative corneal meridian identification

Dear Editor, It is increasingly important for cataract and refractive surgery to achieve an emmetropic, astigmatic result. The efficacy of the many techniques that are available to achieve this is dependent upon the accurate identification of corneal meridia, to ensure the correct placement of corneal incisions or toric intraocular lenses. In cataract surgery, the incision can be astigmatically active, with a recent paper demonstrating a mean surgically induced astigmatism (SIA) of 0.66 dioptres in patients undergoing biaxial microincisional cataract surgery with enlargement of one wound to 2.8 mm [1]. Surgically induced astigmatism can be used to the surgeon’s advantage to reduce small cylinder errors with on-axis incisions [2]. This is facilitated by the pre-operative marking of a known meridian on the cornea. For our technique, we placed one drop of 1 % tetracaine hydrochloride (Minims, Bausch & Lomb, France) into the inferior fornix of the operative eye. The patient was then seated upright and instructed to look straight ahead (primary position) to avoid torsion brought on by postural change [3, 4]. The ophthalmic surgeon (MG), standing in front of the patient, then used the tip of a bevelled 25-gauge needle to mark the limbal epithelium with a radial vertical line at the most inferior point of the limbus. This line coincides with the 90° corneal meridian (Fig. 1a). Following routine peribulbar anaesthesia and sterile preparation of the eye, the 90° mark on a Mendez ring (Geuder, Germany) was aligned with the epithelial mark on the limbus whilst viewing through the operating microscope (Fig. 1b/c). The ring was then centred on the cornea. To ensure centration, the ring was placed to expose equal strips of conjunctiva on the vertical meridian above and below the limbus and similarly on the horizontal meridian, nasal and temporal to the limbus (Fig. 1d). The appropriate corneal meridian could then be chosen. The location of the main incision and paracentesis were measured at day 1 review using a slit lamp (Haag–Streit, Germany), with 10° graticules marked on the platform indicating the rotation of the slit beam about the z-axis. The positions of the main wound and paracentesis were recorded in the case notes, and compared with the targeted axes noted in the operation record. The technique was analysed for 41 patients who underwent phacoemulsification surgery by a single surgeon (MG) in the one centre. There were 24 right eyes (58.5 %) and 17 left eyes (41.5 %) operated upon. The majority (33, 80.5 %) of the main incisions were created at either 0 or 180°, and more than 78 % (32/41) of the paracenteses fell between 115 and 125°. Eighty-five percent (35/41) of the main wound incision sites were exactly aligned with their target site. Six main wounds (15 %) were misaligned by between 5° and 10°. No main wound incisions were misaligned by more than 10°. Misalignment was anti-clockwise from the intended site in all misaligned cases. Only four paracenteses (9.8 %) were 5 or more degrees away from the per-operatively recorded site. Each of these errors was made in favour of a more counter-clockwise position. There were two paracenteses that were on their per-operatively recorded merdia despite their associated main wounds being distant from their intended meridia. The authors have full control of all primary data, and agree to allow Graefe’s Archive for Clinical and Experimental Ophthalmology to review the data upon request. S. R. Durkin (*) :M. Goggin Department of Ophthalmology, The Queen Elizabeth Hospital, Woodville Rd, Woodville South, South Australia, Australia e-mail: shane.durkin@adelaide.edu.au

Helping trainees to become good pediatric anesthetists

Pediatric AnesthesiaVolume 23, Issue 8 p. 751-753 Vignette Helping trainees to become good pediatric anesthetists T.C.K. Brown, Corresponding Author T.C.K. Brown (Formerly) Royal Childrens Hospital Melbourne, Vic., Australia Correspondence T.C.K. Brown, 13 Alfred St., Kew, Vic. 3101, Australia Email: [email protected]Search for more papers by this author T.C.K. Brown, Corresponding Author T.C.K. Brown (Formerly) Royal Childrens Hospital Melbourne, Vic., Australia Correspondence T.C.K. Brown, 13 Alfred St., Kew, Vic. 3101, Australia Email: [email protected]Search for more papers by this author First published: 18 May 2013 https://doi.org/10.1111/pan.12188Citations: 1Read the full textAboutPDF 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 No abstract is available for this article.Citing Literature Volume23, Issue8August 2013Pages 751-753 RelatedInformation

Book Review: Acidic Pit Lakes: The Legacy of Coal and Metal Surface Mines

Acidic Pit Lakes: The Legacy of Coal and Metal Surface Mines, edited by Walter Geller, Martin Schultze, Bob Kleinmann, and Christian Wolkersdorfer, was recently published by Springer-Verlag (525 pp., 212 fig., 66 tab., ISBN 978-3-642-29383-2). This book can be viewed as an excellent update of the 1998 book, Acidic Mining Lakes: Acid Mine Drainage, Limnology and Reclamation, which was edited by Walter Geller, H. Klapper, and W. Salomons. This earlier book set the scene on what was then an emerging but fascinating field and synthesized a large amount of research conducted in the decommissioned lignite mines of former East Germany, as the legacy pits filled with water. Until that book was published, these acidic lake environments were rarely described in limnology textbooks or journal papers. Since the earlier book, an increasing numbers of acidic pit lakes have come into existence as legacy pits are filled with water; many of these pit have been subject to intensive studies, before, during and after filling. While much of this data continues to remain in the private sector, more and more data is being analyzed and released through journal publications. In the 2013 book, Chief Editor Walter Geller is assisted by 43 co-authors and international experts predominantly from Germany, but also from the USA, Spain, Canada, Australia, and Poland. An international network of acidic pit lake experts has been developing over the past decade, and many are indeed co-authors for this book, which succinctly outlines recent advances in our understanding of these complex systems. This new book provides a comprehensive overview of the origins, geochemistry, and limnology of pit lakes and possible remediation options. The book outlines all aspects of pit lake function— physical, chemical and biological limnology. The section on physical limnology includes descriptions of stratification and circulation, waves and currents, mixing and vertical transport in pit lakes. The section on chemical limnology includes detailed descriptions of sediment–water interactions, and iron and phosphorus cycling. Personally, I would have liked to have seen an overview of nitrogen cycling in these acidic systems also included in this section. The final section in the limnology chapter covers lake ecology, including phytoplankton, zooplankton, microbial and fungi dynamics, macrophytes, and benthic primary production. This chapter on limnology provides an excellent overview of current knowledge of pit lake processes and is very rich in data from existing pit lakes. This chapter in itself could have been the basis of a very useful book. The following two chapters outline remediation and management options and then a series of case studies from Germany, Australia, Canada, the USA, and Spain. The majority of research into pit lakes over the last decade has come from Germany, many of the authors are from Germany, and thus it is reasonable that the latter chapter is dominated by case studies from Germany, including the famous Mining Lake 111 with its plethora of superb data. The case study chapter is dominated by case studies from temperate climate regions—a shortfall that is of concern given a significant proportion of mining operations in the world are in tropical, semi-arid and arid regions. Mine water and lake management in these climate zones is particularly challenging and thus I hope that the next update from these authors includes many case studies from other climatic regions. One of the most interesting and valuable parts of this book is the chapter titled ‘‘Lessons learned, open questions and concluding remarks’’. This chapter is a very rare C. Oldham (&) School of Environmental Systems Engineering, The University of Western Australia, Crawley, WA, Australia e-mail: carolyn.oldham@uwa.edu.au

Autoimmune thyroid disease: a novel risk factor for atherosclerosis?

Atherosclerosis is the world’s leading cause of death [1]. Much, but not all, is known about atherosclerosis development. Classical modifiable risk factors include diabetes mellitus, hypertension, hyperlipidemia, and smoking, while other important risk factors include abdominal obesity, excessive alcohol intake, lack of fruit and vegetable intake, and psychosocial factors [2]. The suggestion that thyroid function may be related to atherosclerosis is not new [3]. There is general agreement that overt hypothyroidism promotes cardiovascular disease, including atherosclerosis. Mechanisms through which decreased thyroid hormone concentrations lead to atherosclerosis include elevated low-density lipoprotein cholesterol, diastolic hypertension, heightened coagulability, and actions on vascular smooth muscle [3]. However, much debate continues whether subclinical hypothyroidism similarly leads to increased cardiovascular events. A very large meta-analysis of previous studies suggested modestly increased risk with subclinical hypothyroidism [4], although there was significant heterogeneity of the results among the studies included. The meta-analysis also found that by age, the youngest patients had the most positive hazard ratio estimate, but statistical significance was not reached, likely because of small subgroup numbers [4]. Interestingly, a recent paper reported increased cardiovascular events in younger (B70 years) but not older ([70 years) patients with subclinical hypothyroidism [5]. This is interesting because subclinical hypothyroidism in some older individuals may not be pathologic, and is less likely to be due to autoimmune thyroid disease [6]. Some authors hypothesize that autoimmune thyroid disease per se may play a role in atherosclerosis development. Biochemically, it has been reported that Hashimoto’s thyroiditis causing subclinical hypothyroidism is associated with low-grade inflammation as measured by high-sensitivity C-reactive protein and interleukin-6 levels, and is linked to endothelial dysfunction [7]. That systemic lowgrade inflammation has been demonstrated in Hashimoto’s thyroiditis is not surprising given that peripheral (as opposed to simply intra-thyroidal) activation of the immune system in Hashimoto’s thyroiditis patients has also been reported [8]. At the organ level, another report showed that arterial stiffness, but not carotid intima-medial thickness (CIMT), was increased in euthyroid Hashimoto’s thyroiditis patients compared to controls [9]. Ciccone et al. [10] investigated overweight and obese euthyroid patients, finding that CIMT was indeed increased in patients with Hashimoto’s thyroiditis, compared to those without. At the population level, in a retrospective study, Nyirenda et al. [11] found that Scottish patients with Hashimoto’s thyroiditis over (but not under) the age of 50 years had more hospitalizations for cardiovascular disease than controls. Furthermore, using nationwide Swedish linked data registries, Zoller et al. [12] recently reported that patients hospitalized with Hashimoto’s thyroiditis (and numerous other autoimmune disorders) subsequently had higher rates of coronary heart disease and stroke [13]. In this issue of Endocrine, Topaloglu et al. [14] add further evidence to the debate. This study recruited 48 euthyroid premenopaual women with Hashimoto’s thyroiditis and compared them to 18 controls with respect to D. S. A. McLeod (&) Cancer Control Group, Queensland Institute of Medical Research, Herston, QLD 4029, Australia e-mail: donald.mcleod@qimr.edu.au

The challenge of integrating science for landscape management

‘Ecosystem restoration is now a global priority’ announced a recent editorial (Aronsen and Alexander 2013), reporting on the outcomes of the 11th Conference of the Parties (in Oct 2012) of the Convention on Biological Diversity. Large-scale programs to restore, or more sustainably manage, ecosystems exist in many countries and landscape ecologists often are at the forefront of those actively contributing their expertise. In Australia, for example, the Federal Government has invested some $6.5 billion since 1990 in a series of natural resource management and restoration programs (Hajkowicz 2009), primarily in agricultural environments to respond to the consequences of excessive clearing of native vegetation. But how do we know whether such management interventions are effective? How do we measure their impact? Is the environment in a better condition as a result of these investments? Could these restoration actions be carried out in a more effective and efficient way? These kinds of challenging questions were the stimulus for a research project in southern Australia, documented in this volume. ‘Landscape Logic’ was a four-year, nationally funded project, which set out to ‘measure the effects of past human intervention on the environment using a combination of biophysical and social evidence, and the experience of land and water managers’. It was large in scale, scope and ambition: personnel were drawn from four Universities, three state agencies, and six catchment management organisations. From the outset, the project was planned to be interdisciplinary and participatory, with scientists working alongside managers. The structure of the book reflects the priority issues identified in consultation with land managers in two study areas. Thus, Part 1. ‘Managing water quality in agricultural catchments’ relates to project components undertaken in the state of Tasmania (Chaps. 2–9), where the issue of water quality was of greatest concern. Part 2, ‘Vegetation change in rural landscapes’, relates to components in Victoria (Chaps. 10–17), where the effects of management intervention on the condition and quality of native vegetation was a priority. Part 3, ‘Integrating science and practice’, includes four chaps. (18–21) that synthesize aspects of the overall project. Two questions kept recurring as I read this book: ‘who is this written for?’ and ‘what is its purpose?’. My initial expectation was that the book would provide an array of new scientific evidence evaluating ecological outcomes of the extensive restoration and management activities undertaken in Australia over the last two decades. However, while the bulk of the chapters are centred on various research components of the project, communication of research findings is not the sole intention of the book. Rather, it documents the ‘anatomy’ of a major project, including what it set A. F. Bennett (&) School of Life & Environmental Sciences, Deakin University, 221 Burwood Highway, Burwood, VIC 3125, Australia e-mail: Andrew.Bennett@deakin.edu.au

Imaging in patients with obstructed defecation

Piloni et al. make an important contribution with ‘‘MRdefecography in obstructed defecation syndrome (ODS): technique, diagnostic criteria, and grading’’ [1]. It is pleasing to see an increasing trend toward comprehensive assessment of patients suffering from ODS in the gray zone between gynecology, urogynecology, gastroenterology, and colorectal surgery inhabited by women experiencing the effects of rectocele, enterocele, rectal intussusception, and anismus. Consensus can only be built on scientific fact, but such fact has first to be uncovered. At the moment, we are still enveloped in ignorance when it comes to the etiology, pathogenesis, and interactions of the conditions that underlie ODS and it is not surprising that there is so little agreement regarding treatment. Piloni et al. make a bold step toward an all-encompassing classification based on images of disorders of functional anatomy associated with ODS. However, the true value of the paper lies in the detailed descriptions of the patterns of altered anatomy and the ability of magnetic resonance imaging (MRI) to demonstrate them. Classification and categorization may have to wait, eventually to be informed by a more solid understanding of etiology and pathophysiology, but the authors are to be congratulated for their efforts and for making such a compelling case for the inclusion of the imaging specialist (rather than the image alone) in the multidisciplinary approach to this disorder. The use of MRI is restricted by availability and cost and it must be acknowledged that MRI is not as dynamic as translabial or transperineal ultrasound imaging which has been developing in this field over the last 20 years. Indeed, 4D translabial imaging allows multiplanar or tomographic real-time imaging in any freely definable plane, has excellent tissue discrimination, and also visualizes the modern mesh implants that are virtually invisible to radiological techniques including MRI [2]. The dynamic nature of ultrasound (allowing acquisition speeds of 30 Hz and more in a single plane and 4–8 Hz in volumes encompassing the entire pelvic floor) continues to inform the understanding of functional anatomy and tissue biomechanical properties and is an alternative to defecography [3, 4]. Ultrasound has provided a wealth of insight into the role of the levator ani for pelvic organ support and anorectal function. We now know that the levator ani is commonly damaged in childbirth [5, 6], that the use of forceps is the main risk factor [7], and that such tears and overdistension lead to excessive distensibility of the levator hiatus, the largest potential site for herniation in the human body [8]. This damage is associated with symptoms and signs of female pelvic organ prolapse [8, 9], with rectal intussusception [10] and with prolapse recurrence after pelvic reconstructive surgery [11–13]. It is no surprise that a radiologist is likely to prefer MRI and a clinician the convenience and instant availability of an ultrasound machine: each has its strengths and weaknesses. It is likely that each imaging modality may complement the other, with the MRI’s ‘‘reach’’ and the ultrasound’s sense of compliance and movement complementing one another. MRI is not as good as ultrasound for demonstrating ‘‘ballooning,’’ for example, and ultrasound cannot show the pudendal nerves. One paradoxical ‘‘disadvantage’’ of ultrasound is that it may be too inexpensive and too simple. The formality, expense, and inconvenience of an MRI lend the technique a gravitas that may be out of proportion to its value in this syndrome at the moment. H. P. Dietz (&) J. Cartmill University of Sydney, Penrith, NSW, Australia e-mail: hpdietz@bigpond.com

462 THE ASSOCIATION BETWEEN HAEMOGLOBIN DECLINE AND SVR IS INDEPENDENT OF ITPA GENOTYPE DURING PEG-INTERFERON PLUS RIBAVIRIN THERAPY FOR HCV-1: ANALYSIS FROM THE CHARIOT STUDY

461 SPONTANEOUS CLEARANCE OF ACUTE HCV INFECTION IS ASSOCIATED WITH FEMALE SEX, IL28B GENOTYPE AND HCV GENOTYPE 1 INFECTION J. Grebely, K. Page, R. Sacks-Davis, M. Schim van der Loeff, T.M. Rice, J. Bruneau, M.D. Morris, B. Hajarizadeh, J. Amin, A.L. Cox, A.Y. Kim, B.H. McGovern, J. George, N. Shoukry, G. Lauer, L. Maher, A.R. Lloyd, M. Hellard, G.J. Dore, M. Prins, on behalf of the InC3 Study Group. Kirby Institute, University of New South Wales, Sydney, NSW, Australia; University of California San Francisco, San Francisco, CA, USA; Burnet Institute, Melbourne, VIC, Australia; GGD Public Health Service of Amsterdam, Amsterdam, The Netherlands; Universite de Montreal, Montreal, QC, Canada; Johns Hopkins Medical Institutions, Baltimore, MD, Harvard Medical School, Tufts Medical School, Boston, MA, USA; Westmead Millennium Institute, University of Sydney, School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia E-mail: jgrebely@kirby.unsw.edu.au

The child in hospital – changes in the last 50 years

Pediatric AnesthesiaVolume 23, Issue 6 p. 565-566 Vignette The child in hospital – changes in the last 50 years T.C.K. Brown, Corresponding Author T.C.K. Brown Royal Children's Hospital, Melbourne, Vic., Australia Correspondence T.C.K. Brown, 13 Alfred Street, Kew, Vic. 3101, Australia Email: [email protected]Search for more papers by this author T.C.K. Brown, Corresponding Author T.C.K. Brown Royal Children's Hospital, Melbourne, Vic., Australia Correspondence T.C.K. Brown, 13 Alfred Street, Kew, Vic. 3101, Australia Email: [email protected]Search for more papers by this author First published: 23 March 2013 https://doi.org/10.1111/pan.12150Read the full textAboutPDF 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 No abstract is available for this article. Volume23, Issue6June 2013Pages 565-566 RelatedInformation

Oesophageal atresia and diaphragmatic hernia as it was 40 + years ago

Pediatric AnesthesiaVolume 24, Issue 4 p. 449-452 Vignette Oesophageal atresia and diaphragmatic hernia as it was 40 + years ago T.C.K. Brown, Corresponding Author T.C.K. Brown Royal Childrens Hospital, Melbourne, Vic., Australia Correspondence T.C.K. Brown, 13 Alfred St., Kew, Vic. 3101, Australia Email: [email protected]Search for more papers by this author T.C.K. Brown, Corresponding Author T.C.K. Brown Royal Childrens Hospital, Melbourne, Vic., Australia Correspondence T.C.K. Brown, 13 Alfred St., Kew, Vic. 3101, Australia Email: [email protected]Search for more papers by this author First published: 23 March 2013 https://doi.org/10.1111/pan.12161Read the full textAboutPDF 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 Volume24, Issue4April 2014Pages 449-452 RelatedInformation

Unexpected complications during anesthesia

Pediatric AnesthesiaVolume 24, Issue 3 p. 335-338 Vignette Unexpected complications during anesthesia T.C.K. Brown, Corresponding Author T.C.K. Brown (Formerly) Royal Children's Hospital, Melbourne, Vic., Australia Correspondence T.C.K. Brown, 13 Alfred St., Kew, Vic. 3101, Australia Email: [email protected]Search for more papers by this author T.C.K. Brown, Corresponding Author T.C.K. Brown (Formerly) Royal Children's Hospital, Melbourne, Vic., Australia Correspondence T.C.K. Brown, 13 Alfred St., Kew, Vic. 3101, Australia Email: [email protected]Search for more papers by this author First published: 23 March 2013 https://doi.org/10.1111/pan.12160Citations: 2Read the full textAboutPDF 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 onFacebookTwitterLinkedInRedditWechat Citing Literature Volume24, Issue3March 2014Pages 335-338 RelatedInformation

Heat-related deaths

While vigorous debate continues concerning the nature and/or extent of global warming, it has been suggested that the number, length, and intensity of heat waves experienced globally is increasing [1, 2]. Certainly, forensic pathologists are continually encountering cases where deaths may have either been caused by, or associated with, high environmental temperatures, and in many parts of the world there does appear to have been an increase in numbers of heat-related deaths [3, 4]. In January–February 2009, summer temperatures in Adelaide, the capital of South Australia, reached record levels, with 8 days having maximum temperatures above 40 C, including the hottest day in 70 years with a temperature of 45.7 C [5]. The results of this heat wave included a marked increase in deaths, particularly of elderly individuals with underlying cardiovascular disease. Other studies have shown that children are also at risk [6]. Given the unprecedented numbers of victims in the South Australian heat wave, a refrigerated container had to be hired and installed next to the state mortuary to deal with the increased storage requirements, something that had never previously been required. These events create a number of problems for forensic pathologists ranging from simple logistical issues of having to deal with markedly increased numbers of cases, to diagnostic issues around determining causes of death. Making a diagnosis of a heat-related death may be quite difficult at autopsy as commonly found features such as skin slippage, pleural petechiae, and pulmonary and cerebral edema are entirely nonspecific [7]. Only very rarely will a core temperature of a body proximate to the time of death be available, and heat often accelerates decomposition which further complicates post mortem assessment [8]. Occasionally there may be convincing evidence of prolonged exposure to high temperatures, for example in a sweat lodge [9], or a history of coma or muscle spasm resulting from a significant elevation of core temperature. Dehydration may be an associated feature at autopsy [9, 10]. While survival for some time with a high temperature may be associated with the development of acute pancreatitis, centrilobular necrosis of the liver, cerebral neuronal degeneration, acute tubular necrosis of the kidneys, and rhabdomyolysis [7], the latter may also suggest drug exposure [11]. The association of hyperthermia with drugs such as cocaine and the ring derivate amphetamines such methylenedioxymethamphetamine, MDMA or ‘‘ecstasy,’’ and paramethoxyamphetamine or PMA is well recognized and necessitates full toxicological evaluation of each case [12, 13]. In addition, certain prescription medications such as tricyclic antidepressants and antihistamines with anticholinergic effects, certain antiparkinsonian drugs, and neuroleptic drugs such as some of the major tranquilizers, may all predispose to hyperthermia [14]. As periods of high environmental temperatures may be associated in various parts of the world, such as Australia, with serious brush/bushfire outbreaks, the autopsy load may also be added to by fire deaths [15]. For example, in the Australian state of Victoria in February 2009 the hottest day to date of 46.4 C was recorded, with heat-related deaths occurring in of over 400 people around this time, and a further 173 deaths occurring associated directly with the bushfires [16]. To standardize the approach to, and the diagnosis of, hyperthermic deaths certain criteria have been proposed R. W. Byard (&) Discipline of Anatomy and Pathology, Level 3 Medical School North Building, The University of Adelaide, Frome Road, Adelaide, SA 5005, Australia e-mail: roger.byard@sa.gov.au

Reporting uncertainties in measurement: what approach should be followed?

Much of the work of a scientist or engineer involves taking measurements. For example, a radiation oncology medical physicist measures the absorbed dose in a water phantom. However any measurement has some limit in the accuracy of the final value you obtain. This is due to limits in the accuracy of the measuring equipment, any bias in the measurements, calibration issues or simple mistakes you make. All of these contribute to an uncertainty in the value of the parameter you are measuring. For example, the absorbed dose of radiation from a linear accelerator can be measured in a water phantom using a well characterised ionisation chamber. In this particular case of radiation dose measurement, there will be uncertainties due to the equipment consisting of an ionisation chamber, electrometer and the water phantom. There will also be uncertainties in the setup of the equipment, the linear accelerator. Traditionally these uncertainties are characterised as random errors or systematic errors. Random errors can be minimised by taking multiple measurements while the reduction of systematic uncertainties requires a good understanding of the equipment. Systematic errors are often ‘‘fixed’’ by application of some calibration factor or may be even missed. The method used to determine the uncertainty of a measurement is widely varied. For example, you can repeat the measurements a number of times usually between 3 and 5, and from this calculate the standard deviation. A more systematic approach is to determine random and systematic errors and summate these together to give the final uncertainty in your parameter. This takes a bit more time and requires that you have a good understanding of your equipment. Finally, you can ignore your errors, assume your equipment is working correctly and just quote your results. A review of published papers in any medical physics or biomedical engineering journal will show a similar variation in reporting of uncertainties. This can give the impression of a much lower uncertainty in your measurements. For example, the IAEA TRS 398 dosimetry protocol reports that the estimated relative uncertainty in the dose calibration of megavoltage X-ray beams is ±1.5 % [1]. Therefore any absolute dose measurements using these X-ray beams must have an uncertainty larger than this. There is a more uniform approach for uncertainty analysis as prescribed by the International Organization for Standardization (ISO). The ISO has published a document called the ‘‘Guide to the expression of uncertainties in R. Hill (&) Department of Radiation Oncology, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050, Australia e-mail: robin.hill@email.cs.nsw.gov.au

The law and the laboratory

Forensic pathologists are continually being asked in court to provide opinions on the possible causes, mechanisms, manifestations and effects of specific injuries. Although the pathological findings in some cases may not be of legal importance, the interpretation in others may have profound effects on the outcome of a particular trial by significantly influencing the decisions of judges and/or juries. For this reason pathologists must formulate opinions carefully. Unfortunately this may be difficult, as many traumatic conditions are not completely understood, the understanding of mechanisms may be in evolution, and individual pathologists may lack personal experience of particular types of cases [1, 2]. Blunt craniocerebral trauma is a good example of an injury type that may be associated with a wide range of outcomes. Unfortunately, the clinical manifestations may be nonspecific and there is often little experimental data to help with the evaluation of cases [3]. Histories may also be unreliable as they are often formulated in cases of inflicted head trauma to protect the perpetrator, rather than to provide a clear explanation of the events leading to the injury or death. This means that cases such as this are among the most challenging, particularly in terms of determining mechanisms, predisposing factors, time frames and the degree of force [4]. Involvement of forensic pathologists in experimental work in the laboratory may, however, be one way to answer some of these questions. For a variety of reasons, forensic pathologists are not generally involved in laboratory work. This has the unfortunate effect of isolating pathologists from academic activities such as hypothesis testing using experimental methodology. Although standard and new techniques may be used to clarify or focus on certain diagnostic issues, for example with post-mortem toxicology [5–7], the following studies demonstrate how useful direct collaboration between forensic pathology and the laboratory may be in providing answers to other questions that potentially arise in court. Examples that will be discussed include i) the development of an anesthetized sheep model of traumatic brain injury that has enabled the monitoring of intracranial pressure (ICP) and brain oxygenation following closed head injury, and ii) the measurement of cerebral free magnesium concentrations after blunt cranial trauma in alcohol-intoxicated rats. Studies involving biomechanical testing also demonstrate other fruitful areas of laboratory activity [8]. The first study measuring ICP and brain oxygen levels in anesthetized sheep following blunt head trauma revealed that a dramatic increase in ICP occurred within minutes of trauma [9]. Although this was followed by a gradual decrease, and then a steady increase in ICP, at no stage after injury was the ICP ever normal. We propose that this biphasic response resulted from reactive vasodilation in the first instance, followed by developing cerebral edema. The latter was confirmed by positive staining of sections for albumin, which showed that leakage of serum proteins into tissues had occurred, a hallmark of vasogenic edema. The questions asked in court in this area are often centered around how rapidly manifestations of severe blunt head trauma arise and/or appear. In infants and young children this includes debate over the possibility of the child appearing completely normal following injury, i.e., having a ‘‘lucid interval.’’ The R. W. Byard (&) R. Vink Discipline of Anatomy and Pathology, Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Level 3 Medical School North Building, Frome Road, Adelaide 5005, Australia e-mail: roger.byard@sa.gov.au; roger.byard@adelaide.edu.au

Deeply infiltrating endometriosis of the rectum: shave, disc or segmental excision?

Dear Editor, The article by Ruffo et al. [1] describes a single-center series of 750 segmental resections of the mid or low rectum for deeply infiltrating endometriosis. Although the authors’ relatively low complication rate is impressive, we are concerned about the large number of low or very low anastomoses being performed in otherwise well and young (median age, 33 years) women without accompanying report of bowel function. Anterior resection syndrome is well documented, particularly after low rectal anastomoses, the management of which can be difficult [2–4]. Considering that endometriosis surgery is in many ways a quality-of-life operation to alleviate symptoms, we are interested in the authors’ comments. In our experience as well as that of others, most rectal endometriosis can be managed with shave or disc excisions without recourse to segmental resection [5, 6]. Although Ruffo et al. describe pathological confirmation of endometriosis, it will be important to determine the extent of disease on pathology. In our opinion, segmental resection should be reserved for patients with multicentric involvement or where a less invasive procedure is deemed inadequate. The authors did not make any comments on discs or shave excisions; if all patients were managed with segmental resection, then we consider this approach overly aggressive. We recently published our experience with rectal endometriosis and reported that the majority of patients (71 %) can be spared the morbidity of segmental resection by undergoing a disc excision of the anterior rectal wall because most will have focal rectal wall involvement [5]. This avoids the morbidity of full rectal mobilization, which risks rectal denervation and preserves the native rectal reservoir, which in turn reduces the likelihood of bowel dysfunction. Routine mobilization of the splenic flexure, as highlighted by Ruffo et al., necessarily implies a generous segmental resection. We are concerned about the appropriateness of this aggressive approach. We do not contest the safety and feasibility of laparoscopic management of rectal endometriosis, and recent publications testify that rectal resection can indeed be performed with low complication rates. Other than cyclical bleeding in 20 % and a preoperative median dyschezia score of 6.7, it was difficult to grasp the severity of patients’ symptoms in the series of Ruffo et al. to justify such aggressive surgical management. One could argue that even a 3 % anastomotic leak rate, 2 % rectovaginal fistula rate, 0.7 % risk of ureteric injury, and 14.5 % temporary ileostomy rate is excessive if the rectal resection was unwarranted in the first place. As we discuss in our recent article, the literature seems divergent in that there seems to be a lack of consensus as to whether bowel resection is warranted [6]. In the absence of definitive evidence to support one approach or the other, and in an era of patient-centered care, we urge all authors to move away from only reporting on short-term surgical outcomes and instead focus on functional outcomes with regard to symptom control, fertility, and bowel function outcomes. C. E. Koh (&) M. J. Solomon Surgical Outcomes Research Center, Royal Prince Alfred Hospital, Camperdown, NSW, Australia e-mail: cherry_koh@hotmail.com

Tom Allen and the Adelaide Childrens Hospital

Pediatric AnesthesiaVolume 23, Issue 7 p. 665-666 Vignette Tom Allen and the Adelaide Childrens Hospital T.C.K. Brown, Corresponding Author T.C.K. Brown Royal Childrens Hospital, Melbourne, Vic., Australia Correspondence T.C.K. Brown, 13 Alfred St., Kew, Vic. 3101, Australia Email: [email protected]Search for more papers by this author T.C.K. Brown, Corresponding Author T.C.K. Brown Royal Childrens Hospital, Melbourne, Vic., Australia Correspondence T.C.K. Brown, 13 Alfred St., Kew, Vic. 3101, Australia Email: [email protected]Search for more papers by this author First published: 02 January 2013 https://doi.org/10.1111/pan.12110Citations: 1Read the full textAboutPDF 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 onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume23, Issue7Special Issue: Special Themed Issue on Quality ImprovementJuly 2013Pages 665-666 RelatedInformation

Toward a guided approach to platelet activation in diabetes

Diabetes is associated with substantially poorer cardiovascular outcomes. Furthermore, people with diabetes are at greatly increased risk of not responding to standard antiplatelet therapy for acute coronary syndromes, leading to higher mortality and stent thrombosis [1]. Poor glucose control likely contributes to these cardiovascular events through changes in platelet membrane fluidity and signalling, increased production of platelets leading to a greater fraction of younger and more reactive platelets not yet exposed to antiplatelet therapy, and increased triggering of platelet activation arising from an underlying thromboinflammatory milieu [2]. While patients with higher thrombotic risk may be prospectively identified through laboratory identification of elevated blood glucose or HbA1c [3], the approach to treatment for diabetic platelet hyper-responsiveness remains unclear. Options such as increasing frequency of antiplatelet therapy, additional and more aggressive antiplatelet therapy or more intensive glucose control have been suggested (Fig. 1). However, the data to support these are limited and, particularly where more aggressive antiplatelet therapy is proposed, must be measured against the potential for increased bleeding risk in patients with hyperglycemia. In patients with type-2 diabetes, Capodanno et al. [4] demonstrated enhanced inhibition of platelet function when patients took 81 mg of aspirin twice per day compared with 81 mg daily. Spectre et al. [5] showed greater inhibition of platelet function with 75 mg twice per day when compared to 75 mg daily in patients with type-2 diabetes and vascular complications. In a recent study Rocca et al. [6] showed that increasing frequency of dose better attenuated platelet activation over 24 h in both diabetic and non-diabetic patients. Therefore increasing the frequency of antiplatelet therapy dosing represents an appealing strategy in patients with diabetes and poor glycemic control. However, the clinical effectiveness of this approach on cardiovascular outcome, as well as the net benefit against increased bleeding risk remains to be investigated. Similarly, the addition of more aggressive antiplatelet therapy, such as newer ADP receptor antagonists with greater potency and bioavailability, or emerging thrombin receptor antagonists have been suggested [2]. The use of these must be weighed against the potentially increased risk of bleeding. While altering antiplatelet therapy strategies in patients with diabetes and poor glycemic control is an appealing avenue for further clinical investigation, a potential alternative or complimentary approach might be to achieve improved glycemic control in order to attenuate platelet activation. Several studies have assessed the ability of infused insulin in patients with diabetes to attenuate platelet function and improve cardiovascular outcome in acute coronary syndromes [7]. While evidence of improvement in cardiovascular outcome is variable, intensive treatment with insulin in patients with diabetes may attenuate platelet activation relative to conventional approaches to glycemic control [8]. In this issue of the Journal of Thrombosis and Thrombolysis, Vivas et al. [9] explore whether tight glycemic control with insulin infusion attenuates platelet reactivity in patients with an acute coronary syndrome and hyperglycemia at admission. In a post hoc analysis of the prospective, randomized, open-label CHIPs study, 67 patients with poor glycemic control (as measured by HbA1c [ 6.5 %) were M. D. Linden (&) Centre for Microscopy, Characterisation and Analysis, M510, University of Western Australia, 35 Stirling Highway, Nedlands, WA 6009, Australia e-mail: matthew.linden@uwa.edu.au

Looking Back and Moving Forward

Looking Back and Moving Forward

Letter to the editor: decompressive craniectomy for acute subdural hematoma

Dear Editor, We read with interest the recent paper published in Acta Neurochirurgica by Li et al. [14]. In this paper, the authors have compared the outcome of craniotomy versus decompressive craniectomy in patients who have had an acute subdural hematoma evacuated. This is a well-written paper that addresses the important and topical issue of the role of decompressive craniectomy in the management of patients with severe traumatic brain injury and the authors should be congratulated. We would however, like to raise a few issues for further discussion. In the first instance, the authors concluded that “This is the first time that the CRASH head injury prediction model has been applied in a cohort of patients with traumatic ASDH”. This statement was incorrect. A review of the recent literature published in Acta Neurochirurgica would not support this statement [8]. Indeed, a wider review of the literature would reveal that this methodology has been used in a number of studies not only when considering evacuation of a mass lesion but also in the context of diffuse cerebral swelling [5, 6]. In our previous work, we stratified patients according to injury severity using a method that is similar to the standard method by which a prediction model is calibrated [2]. By comparing the predicted risk of an unfavorable outcome with the observed outcomewe can actually see differences between the predicted and observed risks of unfavorable outcomes across the full spectrum of severity of illness, rather than just the overall difference by the standardized morbidity ratio. Secondly, we can see from their results that the patients who had decompressive craniectomy were significantly sicker than the patients who had had a craniotomy.We would recommend the authors conduct a multivariable analysis to assess whether decompressive craniectomy was better than craniotomy, after adjusting for the CRASH-predicted risks of unfavorable outcome. Although the confidence interval of the two standardized morbidity ratios overlapped with one another, this did not confirm that these two estimates were statistically different. Because the standardized morbidity ratios between the groups appeared different, the authors should analyze the differences in their standardized morbidity ratio by a formal statistical testing before concluding that they were not different. Finally, this study was underpowered to detect a difference in outcomes between the two groups. At the very least, the risk of a type II error should be emphasized and any extrapolation of the negative results should be taken with extreme caution. Unfortunately, the authors did not highlight this important limitation in their discussion of the limitations of the study. Notwithstanding these issues, we would agree with the authors that one of the major confounding issues when interpreting the results of the many studies that have investigated the role of decompressive craniectomy is the failure to adjust for initial injury severity. Using the CRASH model to stratify patients according to injury severity provides an objective assessment of outcome (Fig. 1) and while we would agree with the CRASH collaborators that the use of this model should only be used to support and not replace clinical judgment, we feel that it can provide supportive S. Honeybul (*) : C. R. P. Lind Department of Neurosurgery, Sir Charles Gairdner Hospital and Royal Perth Hospital, Perth, Western Australia, Australia e-mail: stephen.honeybul@health.wa.gov.au

The painful path

Pediatric AnesthesiaVolume 23, Issue 5 p. 453-456 Vignette The painful path T.C.K. Brown, Corresponding Author T.C.K. Brown (Formerly) Royal Children's Hospital, Melbourne, Australia Correspondence T.C.K. Brown, 13 Alfred St., Kew, Melbourne, Vic. 3101, Australia Email: [email protected]Search for more papers by this author T.C.K. Brown, Corresponding Author T.C.K. Brown (Formerly) Royal Children's Hospital, Melbourne, Australia Correspondence T.C.K. Brown, 13 Alfred St., Kew, Melbourne, Vic. 3101, Australia Email: [email protected]Search for more papers by this author First published: 19 October 2012 https://doi.org/10.1111/pan.12062Read the full textAboutPDF 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 Volume23, Issue5May 2013Pages 453-456 RelatedInformation

Auditory pathway changes mirror overall disease progress in individuals with Friedreich ataxia

Friedreich ataxia (FRDA) is a neurodegenerative disease affecting both motor and sensory systems through mutations of the FXN gene. Electrophysiologic changes consistent with axonopathy in the cochlear nerve and auditory brainstem have been reported in a high proportion ([90 %) of affected individuals, as have functional effects including disruption of temporal-resolution and speech perception [1, 2]. We present longitudinal findings for two males with FRDA in whom auditory deterioration mirrored overall disease progress. Patient 1 reported walking difficulties evident from his late teens. Molecular diagnosis confirmed homozygosity for GAA expansions in intron 1 of the FXN gene (repeat lengths: 527/1058). When last examined (at 32 years old), he could walk independently but required a motorisedscooter for community mobility. He also had mild dysarthria, upper limb dysmetria, lower limb areflexia and scoliosis. Patient 2 also reported walking problems in adolescence (15 years). Molecular diagnosis confirmed homozygosity for GAA expansions in intron 1 of the FXN gene (repeat lengths: 569/884). At diagnosis he was independently ambulant, but his physical difficulties progressed rapidly, and at 22 years old he required a walker for short distances and wheelchair for community access. He also had upper limb dysmetria, dysarthria, lower limb areflexia, scoliosis and hypertrophic cardiomyopathy. Both individuals underwent annual auditory brainstem response (ABR) and binaural speech-processing (Listening in Spacialized Noise [LiSN-S]) evaluations over a 3 year period. Patient 1 was 29–32 years and Patient 2, 18–21 years old at assessment. Overall disease severity was equivalent in the two subjects at initial assessment with both achieving scores of about 65 on the Friedreich Ataxia Rating Scale (FARS) [3]. Disability levels for Patient 1 remained stable, but Patient 2 had significant functional deterioration across the study period (Fig. 1). Both subjects showed evidence of cochlear nerve axonopathy despite maintaining normal sound detection. Patient 1 presented with ABRs of normal latency and low amplitude at each test point (Fig. 2a), suggesting normal transmission efficiency but reduced neural populations in the central auditory pathways [1]. Patient 2 showed normal ABRs at first assessment, which decreased in amplitude over the study period and became unidentifiable in the final year (Fig. 2b). ‘‘Spatial listening’’ is the ability to localize sound sources (and hence improve perception) through the integration of subtle timing and level differences in the acoustic-signal reaching the two ears [4]. These interaural cues are initially processed in the lower brainstem, where neural impulses from left and right nerves meet at the G. Rance (&) Department of Audiology and Speech Pathology, The University of Melbourne, 550 Swanston Street, Parkville, Melbourne, VIC 3010, Australia e-mail: grance@unimelb.edu.au