Consult 009 2013

consult The Australian Medical Magazine for Specialists and GPs Summer 2013

Magazine

Sudden Death in the Young Preventing Sudden Death from Inherited Heart Disease

Wisdom Teeth

What is Wise about Wisdom Teeth?

Breast Cancer

Mammography and Breast Cancer

Pulmonary Embolism Outcomes following Pulmonary Embolism

Opinion

Different CDP for all the Wrong Reasons?

Coronary Imaging

Which Imaging Test for Coronary Disease in 2013?

Dengue Fever

How to Diagnose and Prevent the Spread of Dengue Fever

Cancer in Pregnancy Gynaecological Cancers in Pregnancy

Informed Consent

Informed Consent - the Important Conversation

Lifestyle

What’s in a Name? It’s only Champagne.

medical director Season’s greetings!

There is something for everyone this issue – our talented Editorial Board have been busy writing articles from wide-ranging speciality areas that are essential reading for your everyday practice. And very importantly for this season, how to decide on your Christmas celebratory drinks, all about Champagnes and sparklings from around the world.

consult Magazine

wisdom teeth 4

What is wise about wisdom teeth?

Dr Ann Collins

breast canceR 8

Do we understand the effect of mammography screens on breast cancer incidence and mortality?

Dr Ashwini L Chand

Pulmonary Embolism

10 Long-term outcomes following acute PE Dr Austin Chin Chwan Ng

OPINION

13 Different CPD for all the wrong reasons?

Dr Joe Kosterich

We are very pleased to announce some important changes to the Virtual Medical Centre website. The patient website will be separating into a new website, www.myvmc. com. Top IT and graphic design developers have worked to ensure it is the most modern, user-friendly website possible, adapting seamlessly to use on desktops, laptops, tablets and mobiles. The clever search and navigation menus mean that you always find the particular page (out of our total 42,000 articles) which you are looking for.

Coronary imaging 2013

myVMC.com will go live in January 2014.

We look forward to hearing your and your patients’ feedback.

Cancer in pregnancy

Likewise, we are working hard on launching a modern and reinvigorated DrVMC website.

This will go live later in 2014. I would really appreciate your feedback on what you’d like to see in the new version (adean@ virtualmedicalcentre.com).

Thank you for your support, both for Consult magazine and our growing, evolving websites.

Andrew Dean MBChB MRCP(UK) FRACP Medical Director Virtual Medical Centre

contents

greetings from the

16 Which imaging test for coronary disease in 2013?

Dr Kenneth Lee

Dengue Fever 19 Dengue Fever

Prof John McBride

Sudden death in the Young

22 The family practitioner and preventing sudden death from inherited heart disease

Dr Jonathan R Skinner

24 Gynaecological cancers in pregnancy

Dr Padmaj Kulkarni

Informed consent

29 Informed consent - the important conversation Dr Jocelyne Benatar

lIFESTYLE

31 What’s in a Name? It’s only Champagne.

Prof Rod Underwood

We acknowledge the important contribution of the Medical Directors: • Dr Peter Bremner • Dr Andrew Dean • Dr Nick de Felice • Dr Clay Golledge • Dr Roger Goucke • Professor Jeffrey Hamdorf • Professor Graeme Hankey • Dr Andrew McQuillan

• Dr Brendan McQuillan • Dr Donald Ormonde • Dr Paul Snelling • Associate Professor Rob Will • Dr Garry Wilson • Dr Steve Wilson • Dr Joe Kosterich (Medical Spokesperson)

Published by Virtual Medical Centre.com Pty Ltd MANAGING EDITOR: Elizabeth Tysoe (elizabeth@virtualmedicalcentre.com) SUB EDITORS: Lizzie Lee Hoyle, Jennifer Browne, Michelle Brear CONTRIBUTION COORDINATOR: Sylvia Möllenbeck (sylvia@virtualmedicalcentre.com) LAYOUT DESIGNER: Sylvia Möllenbeck SUBSCRIPTIONS: www.virtualmedicalcentre.com/consultsubscribe.asp CIRCULATION: 10,000 copies Virtual Medical Centre PO Box 1173, Osborne Park, Western Australia, 6017 Ph: Perth (08) 9388 0344 Fax: (08) 9388 0611 Email: consult@virtualmedicalcentre.com Website: www.virtualmedicalcentre.com MEDICAL DIRECTOR: Dr Andrew Dean MANAGING DIRECTOR: Wayne Hughes GENERAL MANAGER: Thomas Maher COPYRIGHT WARNING: All editorial copy and some advertisements in this magazine are subject to copyright and cannot be reproduced in any form without the written permisson of the editor. Offenders will be prosecuted.

DISCLAIMER: Virtual Medical Centre.com Pty Ltd (‘the publishers’), and its directors, employees and related entities do not make any warranty whatsoever as to the accuracy or reliability of any information, estimates, opinions, conclusions or recommendations contained in this publication and, to the maximum extent permitted by law, the publisher disclaims all liability and responsibility for any direct or indirect loss or damage which may be suffered by any person or entity through relying on anything contained in, or omitted from, this publication whether as a result of negligence on the part of the publisher or not.

Wise about wisdom teeth

DENTAL

What is wise about wisdom teeth?

Dr Ann Collins

Whether to leave or remove wisdom teeth is a common question that Oral and Maxillofacial surgeons face. This article will look into when they should be removed and its advantages.

Dr Ann Collins BDS (Lon), LDS RCS (Eng), MDS (Syd), FRACDS, FRACDS (OMS), Oral and Maxillofacial Surgeon; Editorial Advisory Board member: Virtual Medical Centre. Private practice: Suite 40, 163-171 Hawkesbury Road, WESTMEAD NSW 2145 (anncollins@westmeadomfs.com.au)

T

he removal of wisdom teeth is one of the most common procedures undertaken by Oral and Maxillofacial Surgeons.1 In an age of improved dental care, the use of fluoride, and the exception of orthodontic treatment and the possible removal of impacted teeth, the majority of young people grow up with little experience of dental treatment. Few people have large enough jaws and small enough teeth to accommodate the full complement of teeth that develop. The wisdom tooth (also known at the third molar tooth) is the last tooth to develop and often, there is insufficient room for it to erupt into

the oral cavity.1,2 There may be one, two, three or four wisdom teeth, a complete absence of wisdom teeth, or even the development of additional wisdom teeth.

The presence (or absence) and the position of wisdom teeth can be assessed using an orthopantomogram (OPG); this is an x-ray taken by a machine that rotates around the head and provides a full picture of the teeth and jaw.3 An impacted wisdom tooth is often in an ectopic position and not able to erupt into a functional position in the oral cavity;3 this may lead to disease with dental and medical consequences. To avoid known risks and complications, a decision should

Figure 1: Figure 1 shows an OPG of a patient with the lower left wisdom tooth (38) horizontally impacted, with the possibility of resorbing the adjacent second molar tooth and the lower right wisdom tooth (48), vertical but with only one cusp exposed in the oral cavity leading to localised infection due to insufficient room for the tooth to fully erupt into a functional position.

4

be made before the middle of the patient’s third decade to either remove or continue monitoring the status of impacted wisdom tooth. However, there is evidence to show that the retention of wisdom teeth that have erupted or have partially erupted may contribute to significant infections and periodontal disease.4,5

Surgical removal of impacted wisdom teeth

The surgical removal of an impacted wisdom tooth, before the middle of the patient’s third decade and when the tooth has incomplete root development, is usually associated with fewer risks of postoperative complications, as well as less pain and discomfort, than when the patient is older.3 The reasons for the removal of impacted wisdom teeth are outlined below.5

Pain, commonly associated with infection.5 Infection of a wisdom tooth is caused by exposure of a small portion of the tooth’s crown, allowing the ingress of bacteria and the subsequent development of pericoronal infection. This exposed tooth crown may be visualised by medical and dental practitioners, but if the communication to the tooth is via a periodontal (gum) pocket behind the last standing molar tooth, it may not be so easily seen. In this case, an infection can be clinically diagnosed by the dental practitioner by probing the periodontal pocket.

Summer 2013 | Consult Magazine

Wise about wisdom teeth

Infections may initially be of a minor nature and can be treated with good local oral hygiene along with appropriate antibiotic therapy. However, without appropriate intervention the infection can progress to be of a major nature, leading to significant facial swelling associated with airway embarrassment, difficulty in opening the mouth as well as difficulty with swallowing and speech. Such major presentations can be of rapid onset and require urgent hospital admission for airway management together with appropriate surgical and medical management. Delay in management of such severe odontogenic infections can be life threatening.5,6 Once a patient has had an infection with an impacted wisdom tooth, careful assessment should be undertaken for the appropriate surgical management, as recurrent infections are more severe and often associated with significant complications (see figure 1).

Figure 2a: Figure 2a shows on OPG of an 8-year-old boy. A large radiolucent lesion in the right mandible can be seen, displacing the wisdom tooth up to the coronoid region. Incisional biopsy confirmed this was an odontogenic keratocyst.

Management was initially by marsupialisation and packing with a BIPP pack which allowed the cystic lesion to shrink in size. This also allowed more bone to form and reduced the risk of damage to the ID nerve when the lesion was finally excised together with the impacted wisdom tooth. Yearly review was then undertaken.

Prophylactic tooth removal when medically or surgically indicated.5 Medical or surgical indications for prophylactic extraction may include: • Cardiac and renal patients especially those who are undergoing organ transplants, • Patients who are having alloplastic implants placed, • Patients undergoing donor transplant or stem cell harvest, and • Patients undergoing such therapies as chemotherapy, radiation therapy and bisphosphonate therapy.

A careful clinical and radiographic assessment of the dental status of these patients with an overview of their medical conditions is essential. Prior to medical and surgical management, these patients should have their dental treatment completed and their oral hygiene should be excellent in order to avoid odontogenic infections.

The need to remove impacted wisdom teeth and/or other teeth will be part of this overview.

Pathology associated with the tooth follicle.5 When a tooth is developing within the jawbone, there is a soft tissue sac around the crown of the tooth known as the tooth follicle; this disappears when the tooth erupts into the oral cavity. When a tooth remains within the jawbone, the

Consult Magazine | Summer 2013

Figure 2b: The OPG in Figure 2b is the same patient from figure 2a, five years later. It shows complete resolution of the lesion with the formation of normal bone in the right mandible. The other three wisdom teeth, which are mesioangularly impacted, can be seen and were subsequently removed. Odontogenic keratocyst has now been re-classified as odontogenic keratocystic tumour and such lesions should be monitored for recurrence with a yearly OPG x-ray for ten years from the definitive management of the lesion.

dental follicle has the potential to become pathological and form odontogenic cysts and tumours. As these lesions enlarge, there is destruction of the jawbone together with disruption of the wisdom tooth and adjacent teeth. These lesions may become quite significant in size before the patient experiences any symptoms. The first indication that such a lesion exists may be when it causes enough erosion of the bone that it becomes infected, or when a routine/ post-trauma x-ray is undertaken. This will then reveal the associated pathology. (See figure 2a and 2b).

Abnormalities of tooth size or shape precluding normal function.5 Teeth which are an abnormal size or shape may not erupt into functional positions and may be associated with dental caries and periodontal disease, or cause disruption to the smooth function of

the occlusal relationship of the jaws.5 Management of periodontal disease.5 Even though a wisdom tooth may become fully or partially erupted into the oral cavity, it may still be associated with dental caries and/or significant periodontal disease as the position of the tooth precludes good oral hygiene.4 This can result in loss of bone support, chronic periodontal disease and possible damage to adjacent teeth.

Resorption of adjacent tooth due to the position of the impacted tooth.5 There may be resorption of the adjacent tooth root, crown or both, and this may occur without the patient experiencing any symptoms.7 Once significant resorption has occurred, the tooth cannot be restored and will be lost in association with the wisdom tooth.

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Wise about wisdom teeth

Quick reference guide: Indications for surgical removal of the third molars5-10

Indication

Possible outcomes

Pain, commonly associated with infection.

Infections may progress in severity leading to: • facial swelling • airway embarrassment • difficult mouth opening • difficulty with swallowing & speech.

Delay in management of severe odontogenic infections can be life threatening.

Prophylactic tooth removal when medically or surgically indicated.

Complications associated with retaining wisdom teeth particularly disastrous for: • cardiac and renal patients (especially transplant recipients) • patients having alloplastic implants • stem cell donors • chemotherapy, radiation therapy and bisphosphonate therapy patients.

Pathology associated with the tooth follicle.

When a tooth remains within the jawbone the dental follicle may become pathological, forming odontogenic cysts and tumours. As these lesions enlarge, can lead to: • destruction of the jawbone • disruption of the wisdom tooth • disruption of adjacent teeth Symptoms and thus presentation may be delayed.

Abnormalities of tooth size or shape precluding normal function.

Teeth which are an abnormal size or shape may: • not erupt into functional positions • be associated with dental caries and periodontal disease • cause disruption to the occlusal relationship of the jaws.

Management of periodontal disease.

Both fully and partially erupted wisdom teeth may be difficult to clean, leading to: • dental caries and/or significant periodontal disease • loss of bone support • chronic periodontal disease • possible damage to adjacent teeth.

Resorption of adjacent tooth due to the position of the impacted tooth.

Resorption of the adjacent tooth root, crown or both, may occur without symptoms.

With significant resorption, the tooth cannot be restored and will be lost.

Management of orthodontic tooth movement & stability of the dental occlusion.

•

Facilitation of prosthodontic rehabilitation.

Abnormal position of wisdom teeth can impede prosthodontic rehabilitation (e.g. dentures, bridges, dental implants).

Tooth impeding the normal eruption of the adjacent tooth.

The impacted wisdom tooth may prevent the eruption of the adjacent second molar teeth (erupting age 12–13).

Tooth in the line of facial fracture.

Many mandibular fractures are situated at the angle of the jaw associated with an impacted wisdom tooth, as this provides a line of weakness.

It is prudent to remove the impacted tooth disrupted from its socket due to risk of delayed healing or infection.

Tooth involved in tumour resection.

Impacted wisdom tooth may be associated with both benign and malignant tumours and removed with the tumour

Tooth interfering with orthognathic and/or reconstructive jaw surgery.

Impacted wisdom teeth may be removed 3–6 months ahead of major jaw surgery to ensure no interference to the surgery.

Allows for sufficient bone healing to have occurred, thus facilitating plating techniques.

Management of orthodontic tooth movement and stability of the dental occlusion.5 Orthodontic treatment aims to provide co-ordination of the teeth and jaws to provide a stable dental relationship. It is an area of significant debate whether wisdom teeth in their growth spurts cause movement of the dentition once orthodontic treatment is completed.8 There is no doubt, however, that the careful clinical and radiographic assessment of

6

•

Wisdom teeth in their growth spurts may cause movement of the dentition once orthodontic treatment is completed.

Careful clinical and radiographic assessment is warranted.

the teeth should be undertaken when orthodontic treatment has been completed to facilitate stability in the long term.

dental bridges or the placement of dental implants. For these treatments, wisdom teeth may have to be removed.9

Facilitation of prosthodontic rehabilitation.5 Wisdom teeth may cause a problem due to their abnormal position and relationship with other teeth; this can impede prosthodontic rehabilitation, such as the provision of dentures, the construction of

Tooth impeding the normal eruption of the adjacent tooth.5 The impacted wisdom tooth may prevent the eruption of the adjacent second molar tooth which erupt between the ages of twelve and thirteen years. The removal of impacted wisdom teeth in a patient at this

Summer 2013 | Consult Magazine

Tooth in the line of facial fracture.5 Many mandibular fractures are situated at the angle of the jaw and are associated with an impacted wisdom tooth as this provides a line of weakness.10 In the management of jaw fractures, it is often prudent to remove the impacted tooth as it usually has been disrupted from its socket and may cause delayed healing or infection if left in position. When the patient is having surgery to reduce and fix the fractured jaw, this is an ideal opportunity to remove the offending tooth because of the easy access it provides to that area.10 In limited circumstances where there is minimal or no displacement of the fractured bones then the impacted wisdom tooth may be left in the line of the fracture until healing References 1. Mettes TD, Ghaeminia H, Nienhuijs ME et al. Surgical removal versus retention for the management of asymptomatic impacted wisdom teeth. Cochrane Database Syst Rev. 2012; 6:CD003879.

2. Biswari1 G, Gupta P, Das D. Wisdom teeth - A major problem in young generation, study on the basis of types and associated complications.

Journal of College of Medical Sciences-Nepal 2010; 6(3):24–28.

3. Mansour MH, Cox SC. Patients presenting to the general practitioner with pain of dental origin. Med J Aust 2006; 185 (2): 64–67.

4. Dodson TB, Susarla SM. Impacted wisdom teeth. Clin Evid (Online). 2010; 2010: 1302.

5. American Association of Oral and

Consult Magazine | Summer 2013

has occurred and then re-assessed three months later to ascertain if it requires removal before any infection occurs.

Tooth involved in tumour resection.5 The impacted wisdom tooth may be associated with both benign and malignant tumours and is surgically removed as part as the surgical resection of the tumour.4,5 Tooth interfering with orthognathic and/or reconstructive jaw surgery.5 When orthognathic surgery is planned to correct skeletal discrepancies, the impacted wisdom teeth may be removed three to six months ahead of such major jaw surgery.8 This ensures the teeth do not provide interference to the surgery when the osteotomy cuts are performed, and also allows for sufficient bone healing to have occurred, thus facilitating plating techniques.

Evidence for extraction The most compelling evidence that careful assessment of wisdom teeth in Maxillofacial Surgeons. Parameters of Care: Clinical Practice Guidelines for Oral and Maxillofacial Surgery (AAOMS ParCare 2012) Version 5.0. Supplement to the Journal of Oral and Maxillofacial Surgery. 2012.

6. Miloro M, Antonia Kolokythas A. Management of Complications in Oral and Maxillofacial Surgery. Wiley-Blackwell; 1 edition (February 21, 2012). ISBN-10: 0813820529.

7. Stanley HR, Alattar M, Collett WK, Stringfellow HR Jr, Spiegel EH. Pathological sequelae of “neglected” impacted third molars.

J Oral Pathol. 1988; 17(3): 113–7.

8. Kandasamy S, Rinchuse DJ, Rinchuse DJ. The wisdom behind third molar extractions.

Australian Dental Journal 2009; 54 (4): 284– 292.

a young patient, and the evidence to support their removal, has been produced by the American Association of Oral and Maxillofacial Surgery who began collecting data in the mid 1990s as part of their third molar clinical trials. In October 2010, a comprehensive multi-disciplinary conference on third molar science was held which included experts not only from the United States of America, but from around the world.11 They discussed the research findings on third molar extractions, retention, patients’ surveillance, potential risks and attending costs. In addition, they reported on their ground breaking research into the pathologies that afflict even disease free third molars, and the evidence based studies that link the bacteria surrounding third molars to systemic diseases as well as conditions that may be detrimental to patients who decide to retain these teeth.

Conference attendees felt that research findings showed that 80% of young adults who retained previously healthy wisdom teeth would develop problems within seven years, and as such, monitoring retained wisdom teeth over a lifetime may be more expensive than the surgical removal of CM these teeth.

9. Haug RH, Abdul-Majid J, Blakey GH, White RP. Evidenced-based decision making: the third molar. Dent Clin North Am. 2009; 53(1): 77–96.

10. Kumar S, Prabhakar V, Rao K, Brar R. A comparative review of treatment of 80 mandibular angle fracture fixation with miniplates using three different techniques.

Indian J Otolaryngol Head Neck Surg. 2011; 63(2): 190–2.

11. Cheifetz ID, Rafetto LK, Nelson WJ. Preface Proceedings of the Third Molar Multidisciplinary Conference Washington, DC, October 19, 2010. Journal of Oral and Maxillofacial Surgery 2012; 70 (9 supp 1):S1.

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Wise about wisdom teeth

age may then allow normal eruption of the second molar teeth.5 In an older patient, where the impacted wisdom tooth has caused the adjacent second molar tooth to be impacted or submerged in the jawbone, a careful clinical and radiographic assessment is made as to which tooth can be safely removed and how the remaining tooth can be brought into position orthodontically.

Mammography and breast cancer

ONCOLOGY

Do we understand the effect of mammography screens on breast cancer incidence and mortality?

Dr Ashwini L Chand

Mammographic screening is widely used to identify significant breast cancer risk in women. However, the utility of screening in improving breast cancer mortality rates is often an issue for debate. This article provides a snapshot of current opinions regarding this issue.

Dr Ashwini L Chand, PhD, Cancer Drug Discovery, Prince Henry’s Institute, Melbourne, Victoria (ashwini.chand@princehenrys.org)

M

ammography as a breast screening tool

Mammography is the best screening tool for breast cancer used today. With mammographic screening, tumours can be identified at an early stage, thereby increasing chances of survival. The National Cancer Institute and American Cancer Society recommend mammographic screening every year from age 40. Women with higher risk of breast cancer, with a genetic predisposition for the disease or a strong family history need to be screened earlier and more frequently. High mammographic density is also assessed by mammograms and is linked to a six-fold increased risk of breast cancer.1,2 Breast density refers to breast tissue composition: epithelial cells from glandular structures and connective tissue or stroma of glandular and connective tissue in the breast appear light while breast adipose tissue appears dark in mammography screens. Standard mammography using X-ray images and digital mammography are currently used. Ultrasound or magnetic resonance imaging is often used in combination with mammography as a breast cancer screening tool.3,4 Genetic factors,5,6 pregnancy and lactation, age and menopause, and body weight are all factors which can account for changes in mammographic density. The exact cellular mechanisms involved in high mammographic density and its link to

8

tumour incidence are largely unknown but the focus of current research worldwide.

The use of mammographic screening for high breast density identifies a significant risk factor for breast cancer in women.

Mammographic screens and cancerassociated mortality: do we have enough evidence to conclusively understand this relationship?

There are contradicting reports in the literature as to the benefits and harm associated with mammographic screening and over-diagnosis of breast cancer.

Differing opinions on this issue arise from the analysis and interpretation of different datasets.

Data from several randomised trials show a reduction of 25% in breastcancer mortality among women in the screening group as compared with the control group.7-9 Randomised trials of mammographic screens have also reported that this reduction in the risk of death from breast cancer is directly correlated with reductions in the risk of receiving a diagnosis of advanced breast cancer.10 In addition, reduction in breast cancerassociated mortality is also likely to be due to the combined effects of mammographic screening and better treatments.11 A recent epidemiological analysis of

data from the National Health Interview Survey in the United States highlights issues currently surrounding the utility of mammographic screens in terms of reduction in cancer-related deaths and the harm of over-diagnosis.11 Since the first introduction of mammography screens, the reported cases for early-stage cancer has increased from 112 to 234 cancers per 100,000 women; and a decrease in late-stage cancer (including ductal carcinoma in situ) from 102 to 94 cases per 100,000 women.11 The authors discuss that 8 of the 122 additional early diagnoses are potentially destined to progress to advanced disease; and conclude that breast-cancer screening involved substantial harm of excess detection of early-stage cancers that was not matched by reduction in late-stage cancers. Similar findings are reported in studies in other populations.12,13 It is important to understand why such discrepancies occur, in particular between randomised trials and general population screening datasets. Closer assessment of confounding factors must be taken into consideration when assessing epidemiological data. Some confounding factors, such as improvements in treatment and heightened awareness of breast cancer, may be associated with a reduction in breast-cancer mortality. Breast screening is designed to improve prospects of early detection of cancers and decrease mortality.

Summer 2013 | Consult Magazine

References 1. Boyd NF, Martin LJ, Yaffe MJ, Minkin S. Mammographic density and breast cancer risk: current understanding and future prospects.

Breast Cancer Res. 2011;13(6):223. [Abstract | Full text] 2. Boyd NF, O’Sullivan B, Fishell E, et al.

Mammographic patterns and breast cancer risk: methodologic standards and contradictory results. J Natl Cancer Inst. 1984;72(6):1253-9.

[Abstract] 3. Pinsky RW, Helvie MA. Mammographic breast density: effect on imaging and breast cancer risk. J Natl Compr Canc Netw.

2010;8(10):1157-64. [Abstract] 4. Eng-Wong J, Orzano-Birgani J, Chow CK, et al.

Effect of raloxifene on mammographic density and breast magnetic resonance imaging in premenopausal women at increased risk for breast cancer. Cancer Epidemiol Biomarkers Prev. 2008;17(7):1696-701. [Abstract | Full text] 5. Vachon CM, Scott CG, Fasching PA, et al.

Common breast cancer susceptibility variants in LSP1 and RAD51L1 are associated with mammographic density measures that

predict breast cancer risk. Cancer Epidemiol Biomarkers Prev. 2012;21(7):1156-66.

6. Varghese JS, Thompson DJ, Michailidou K, et al. Mammographic breast density and breast cancer: evidence of a shared genetic basis.

Cancer Res. 2012;72(6):1478-84. [Abstract | Full text] 7. Chu KC, Smart CR, Tarone RE. Analysis of breast cancer mortality and stage distribution by age for the Health Insurance Plan clinical trial. J Natl Cancer Inst. 1988;80(14):1125-32.

8. Gøtzsche PC, Nielsen M. Screening for breast cancer with mammography. Cochrane Database Syst Rev. 2006;(4):CD001877.

[Abstract | Full text] 9. Nyström L, Rutqvist LE, Wall S, et al. Breast cancer screening with mammography: overview of Swedish randomised trials. Lancet.

1993;341(8851):973-8. [Abstract] 10. Autier P, Héry C, Haukka J, et al. Advanced breast cancer and breast cancer mortality in randomized controlled trials on mammography screening. J Clin Oncol. 2009;27(35):5919-23.

[Abstract | Full text] 11. Bleyer A, Welch HG. Effect of three decades of screening mammography on breast-cancer

Summary

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cancer that would not have otherwise been diagnosed during the woman’s lifetime.

As the future possibility of disease cannot be predicted with certainty, it is not possible to determine to which category of women this might apply. Therefore, continued evaluation of breast-cancer screening programs is warranted in order to better quantify outcomes. To date breast screens have proven to be useful in the early detection of breast tumours and in establishing breast cancer risk in women.

CM

incidence. N Engl J Med. 2012;367(21):19982005. [Abstract] 12. Nederend J, Duijm LE, Voogd AC, et al. Trends in incidence and detection of advanced breast cancer at biennial screening mammography in The Netherlands: a population based study.

Breast Cancer Res. 2012;14(1):R10. [Abstract | Full text] 13. Autier P, Boniol M. The incidence of advanced breast cancer in the West Midlands, United Kingdom. Eur J Cancer Prev. 2012;21(3):21721.

14. Taylor R, Morrell S, Estoesta J, Brassil A. Mammography screening and breast cancer mortality in New South Wales, Australia.

Cancer Causes Control. 2004;15(6):543-50.

[Abstract] 15. Roder D, Houssami N, Farshid G, et al.

Population screening and intensity of screening are associated with reduced breast cancer mortality: evidence of efficacy of mammography screening in Australia.

Breast Cancer Res Treat. 2008;108(3):409-16 [Abstract]

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Mammography and breast cancer

The use of screening mammography

is often debated, and it is important to realise that this debate occurs primarily due to methodology limitations in the epidemiology studies. In addition, the overall benefits of mammography screening programs remain poorly quantified and we should be thinking of alternate ways to address this. To date, the majority of the literature globally and in Australia14,15 indicate that mammographic screening does result in decreased cancerrelated deaths in women. The phrase “over-diagnosis” refers to a diagnosis of

The term “over-diagnosis” includes all scenarios where women with screendetected cancers are destined to die earlier due to other causes before development of their breast tumours. In addition, disease progression cannot be predicted with diagnosis and hence may not be reflected in numbers assessed as cancer-associated mortality.

Pulmonary Embolism

PE

Long-term outcomes following acute pulmonary embolism

Dr Austin Chin Chwan Ng

Acute pulmonary embolism (PE) represents the most severe manifestation of venous thromboembolic disease. Recent long-term studies reported ongoing increased risk of death among survivors of acute PE, and identified predictors that may guide long-term management.

Dr Austin Chin Chwan Ng, MBBS, BSc(Med), MMed, FRACP, FCSANZ, Senior Staff Cardiologist, Concord Hospital, NSW (chin.ng@sydney.edu.au)

V

enous thromboembolic disease is a worldwide problem, with acute pulmonary embolism (PE) its most severe manifestation.1 The former has an estimated incidence of 1 in 1000 per year,2 and PE has an annual incidence of 0.31 per 1000.3 The outcome of patients with acute PE is only partly (and to a small extent) determined by the size and extent of thrombus burden, and much more by the presence and extent of right ventricular dysfunction.4 Symptomatic PE can cause death within one hour of onset in up to 10% of cases,5 and is the third largest cause of cardiovascular death after coronary artery disease and stroke,6 occurring in up to 7-30% of all autopsy series.1 Predictors of acute mortality following acute PE are well established and include age greater than 70 years, coexistent malignancy, heart failure, pulmonary disease, systemic hypotension, right ventricular dysfunction, and biomarkers

such as troponin T, B-type natriuretic peptide and elevated D-dimer.7-11 In contrast to the abundant data regarding acute outcome, predictors of long-term mortality have until recently been poorly defined due to the rarity of large cohort studies. The few studies that extended beyond 6 months indicated an increased one-year mortality rate after PE, which may be as high as 25%.12-14 Increased long-term risk of recurrent PE, cancer and cardiovascular events have been reported in patients presenting with acute PE.15-17 Almost all of these earlier studies excluded patients with baseline cardiovascular disease, or did not report this and other baseline comorbidities, making risk stratification for long-term outcome in contemporary, more elderly populations difficult.

We

recently

reported

substantially

increased long-term mortality in a large contemporary adult population hospitalised with acute PE.18 During a mean follow-up of nearly four years, 363 out of a total cohort of 1023 patients died (35.5%), of whom only 31 (3.0%) died inhospital during the index PE admission.

Miniati et al similarly reported that in patients with PE, there was a progressive decline in survival during a median followup of 2.1 years through non-PE related deaths,19 supporting our findings of increased long-term mortality. Older age and underlying comorbidities, including cardiovascular disease, malignancy, neurodegenerative disease and chronic renal disease, were all independent predictors of all-cause mortality during long-term follow-up in our study.

Approximately 36% of post-discharge mortality was attributed to cardiovascular causes and only 5% of deaths were due to recurrent PE. This is consistent with other

Table: Mortality outcome between different chronic cardiovascular diseases

Cohort

Mortality Outcome

Recommended Long-term Follow-up

Outpatients with stable coronary artery disease28 Patients with ST-elevation myocardial infarction30

Annual rate 1.4% 1-yr cumulative rate 8.0%

4 – 12 monthly review29

Annual rate 10.9%

3 – 6 monthly review32

Chronic heart failure31 Current PE cohort Total cohort * With cardiovascular disease

Annual rate 8.5% 12.7%

1-yr cumulative rate 13.2% 14.5%

No recommendation4

* All-cause mortality rate (excluded in-hospital deaths)

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Summer 2013 | Consult Magazine

However, direct association between baseline disease and the cause-specific mortality after PE has, to our knowledge, not been shown. In addition to finding poor long-term outcome in a contemporary cohort of patients admitted with acute PE, we found that baseline characteristics could predict all-cause mortality.12,14 While most cardiovascular and malignant deaths occurred in patients with these diseases at baseline, a substantial number of deaths also occurred in those without these baseline comorbidities at the time of their index PE presentation. Notably, even in patients with no known comorbidities there was a 13% overall mortality and most of these deaths were cardiovascular.

Douketis et al also examined the longterm risk of malignancy in a cohort of patients with a first episode of venous thromboembolism and found an annual risk of malignancy of 1.32 (95% confidence interval, 1.09–1.60) per 100 person-years.20 Our observation confirmed a similarly high mortality rate after acute PE with most deaths occurring post discharge, and that some patients without known malignancy at presentation developed overt malignancy after PE. However, cardiovascular death was at least as common as malignant death during long-term follow-up of our cohort. We also observed that although baseline cardiovascular disease anticipated subsequent cardiovascular death, the absence of baseline cardiovascular disease did not preclude later cardiovascular death in patients with PE. Our study supports References 1. White RH. The epidemiology of venous thromboembolism. Circulation 2003;107(23 Suppl 1):I4-8.

2. Goldhaber SZ. Pulmonary embolism. N Engl J Med 1998;339(2):93-104.

3. Ho WK, Hankey GJ, Eikelboom JW. The incidence of venous thromboembolism: a prospective, community-based study in Perth, Western Australia. Med J Aust 2008;189(3):144-7.

4. Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galie N, Pruszczyk P, et al. Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC).

Eur Heart J 2008;29(18):2276-315.

5. Kearon C. Natural history of venous thromboembolism. Circulation 2003;107(23 Suppl 1):I22-30.

Consult Magazine | Summer 2013

and confirms those of others who had suggested increased cardiac-related morbidity16 and mortality15 after acute PE. There is currently no risk model for predicting long-term outcome for patients who experienced an acute PE event. The Charlson Comorbidity Index score (CCI) is a measure of the burden of disease arising from multiple comorbidities.21,22 It is a summary score based on the presence or absence of 17 medical conditions that include cardiovascular disorders, malignancies, chronic pulmonary and neurological diseases, connective tissue diseases, and others. The index has been shown to be useful in prognosticating the outcome of patients suffering from diseases including heart failure,23 endocarditis24 and cancer.25 We showed that not only was the CCI useful in predicting in-hospital and short-term outcome post acute PE, it can also be incorporated into long-term mortality risk modeling.26 This observation had since been validated by others.27 The long-term mortality of patients with PE compares unfavourably with other chronic cardiovascular disease patients, most of which, unlike patients with PE, have clear guidelines for long-term follow-up (Table). In outpatients with stable coronary artery disease, Jabbour et al reported an annual mortality rate of 1.4%.28 In the Australian ACACIA registry, patients with ST-elevation myocardial infarction 6. Giuntini C, Di Ricco G, Marini C, Melillo E, Palla A. Pulmonary embolism: epidemiology.

Chest 1995;107(1 Suppl):3S-9S. 7. Paneesha S, Cheyne E, French K, Bacchu S, Borg A, Rose P. High D-dimer levels at presentation in patients with venous thromboembolism is a marker of adverse clinical outcomes. Br J Haematol 2006;135(1):85-90.

8. Scridon T, Scridon C, Skali H, Alvarez A, Goldhaber SZ, Solomon SD. Prognostic significance of troponin elevation and right ventricular enlargement in acute pulmonary embolism. Am J Cardiol 2005;96(2):303-5.

9. Becattini C, Agnelli G. Risk factors for adverse short-term outcome in patients with pulmonary embolism. Thromb Res 2001;103(6):V239-44.

10. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet

Pulmonary Embolism

studies reported to date suggesting possible increased cardiovascular events in patients presenting with acute PE.15, 16

had a cumulative one-year mortality rate of 8%,30 whilst in community-based chronic heart failure patients, Roger et al reported an annual mortality rate approaching 11%.31 By comparison, we found an annual mortality rate of 12.7% (cumulative one-year mortality rate of 14.5%) in patients with PE who had underlying cardiovascular disease. Hence, the prognosis of patients with PE is clearly worse than many patients with stable or unstable coronary disease, and at best similar to those with stable chronic heart failure. Formal exclusion of unrecognised cardiovascular disease after treatment of patients with acute PE may need to be considered, especially in light of the high proportion of cardiovascular mortality reported in ours and other studies to date.

Recent studies on the clinical benefits of aspirin given to those patients who completed their anticoagulation treatment for an acute PE episode further support the need for long-term treatment strategy for CM these patients.33, 34

1999;353(9162):1386-9.

11. Klok FA, Mos IC, Huisman MV. Brain-type natriuretic peptide levels in the prediction of adverse outcome in patients with pulmonary embolism: a systematic review and meta-analysis. Am J Respir Crit Care Med 2008;178(4):425-30.

12. Heit JA, Silverstein MD, Mohr DN, Petterson TM, O’Fallon WM, Melton LJ, 3rd. Predictors of survival after deep vein thrombosis and pulmonary embolism: a populationbased, cohort study. Arch Intern Med 1999;159(5):445-53.

13. Pengo V, Lensing AW, Prins MH, Marchiori A, Davidson BL, Tiozzo F, et al. Incidence of chronic thromboembolic pulmonary hypertension after pulmonary embolism. N Engl J Med 2004;350(22):2257-64.

14. Spencer FA, Gore JM, Lessard D, Douketis JD, Emery C, Goldberg RJ. Patient outcomes after deep vein thrombosis and

11

Pulmonary Embolism

pulmonary embolism: the Worcester Venous Thromboembolism Study. Arch Intern Med 2008;168(4):425-30.

15. Becattini C, Agnelli G, Prandoni P, Silingardi M, Salvi R, Taliani MR, et al. A prospective study on cardiovascular events after acute pulmonary embolism. Eur Heart J 2005;26(1):77-83.

16. Sorensen HT, Horvath-Puho E, Pedersen L, Baron JA, Prandoni P. Venous thromboembolism and subsequent hospitalisation due to acute arterial cardiovascular events: a 20-year cohort study.

Lancet 2007;370(9601):1773-9.

17. Klok FA, Mos IC, Broek L, Tamsma JT, Rosendaal FR, de Roos A, et al. Risk of arterial cardiovascular events in patients after pulmonary embolism.

Blood 2009;114(8):1484-8.

18. Ng AC, Chung T, Yong AS, Wong HS, Chow V, Celermajer DS, et al. Long-term cardiovascular and noncardiovascular mortality of 1023 patients with confirmed acute pulmonary embolism. Circ Cardiovasc Qual Outcomes 2011;4(1):122-8.

19. Miniati M, Monti S, Bottai M, Scoscia E, Bauleo C, Tonelli L, et al. Survival and restoration of pulmonary perfusion in a long-term follow-up of patients after acute pulmonary embolism.

Medicine (Baltimore) 2006;85(5):253-62.

20. Douketis JD, Gu C, Piccioli A, Ghirarduzzi A, Pengo V, Prandoni P. The long-term risk of cancer in patients with a first episode of venous thromboembolism. J Thromb Haemost 2009;7(4):546-51.

21. Charlson ME, Pompei P, Ales KL, MacKenzie CR. A new method of classifying prognostic comorbidity in longitudinal studies: development and validation. J Chronic Dis 1987;40(5):373-83.

22. Hall WH, Ramachandran R, Narayan S, Jani

12

AB, Vijayakumar S. An electronic application for rapidly calculating Charlson comorbidity score. BMC Cancer 2004;4:94.

23. Clarke B, Howlett J, Sapp J, Andreou P, Parkash R. The effect of comorbidity on the competing risk of sudden and nonsudden death in an ambulatory heart failure population. Can J Cardiol 2011;27(2):254-61.

24. Sy RW, Chawantanpipat C, Richmond DR, Kritharides L. Development and validation of a time-dependent risk model for predicting mortality in infective endocarditis. Eur Heart J 2009;32(16):2016-26.

25. Albertsen PC, Moore DF, Shih W, Lin Y, Li H, Lu-Yao GL. Impact of comorbidity on survival among men with localized prostate cancer. J Clin Oncol 2011;29(10):1335-41.

26. Ng AC, Chow V, Yong AS, Chung T, Kritharides L. Prognostic Impact of the Charlson Comorbidity Index on Mortality following Acute Pulmonary Embolism. Respiration 2012;85(5):408-16.

27. Golpe R, Perez-de-Llano LA, Castro-Anon O. Prognostic value of the Charlson comorbidity index in pulmonary embolism. Respiration 2013;85(5):438.

28. Jabbour S, Young-Xu Y, Graboys TB, Blatt CM, Goldberg RJ, Bedell SE, et al. Long-term outcomes of optimized medical management of outpatients with stable coronary artery disease. Am J Cardiol 2004;93(3):294-9.

29. Gibbons RJ, Abrams J, Chatterjee K, Daley J, Deedwania PC, Douglas JS, et al. ACC/AHA 2002 guideline update for the management of patients with chronic stable angina--summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Chronic Stable Angina). Circulation 2003;107(1):149-

58.

30. Chew DP, Amerena JV, Coverdale SG, Rankin JM, Astley CM, Soman A, et al. Invasive management and late clinical outcomes in contemporary Australian management of acute coronary syndromes: observations from the ACACIA registry. Med J Aust 2008;188(12):691-7.

31. Roger VL, Weston SA, Redfield MM, Hellermann-Homan JP, Killian J, Yawn BP, et al. Trends in heart failure incidence and survival in a community-based population.

Jama 2004;292(3):344-50.

32. Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult--Summary Article: A Report of the American College of Cardiology/American CM Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration With the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: Endorsed by the Heart Rhythm Society. Circulation 2005;112(12):1825-1852.

33. Becattini C, Agnelli G, Schenone A, Eichinger S, Bucherini E, Silingardi M, et al. Aspirin for preventing the recurrence of venous thromboembolism. N Engl J Med 2012;366(21):1959-67.

34. Brighton TA, Eikelboom JW, Mann K, Mister R, Gallus A, Ockelford P, et al.

Low-dose aspirin for preventing recurrent venous thromboembolism. N Engl J Med 2012;367(21):1979-87.

Summer 2013 | Consult Magazine

for all the wrong reasons?

Dr Joe Kosterich - M.B.B.S, author, speaker, doctor and health industry consultant, medical spokesperson: Virtual Medical Centre (www.drjoe.net.au)

We are all used to the usual CPD in areas of medicine where we can learn more or improve our skills. A recent court case suggests that traditional medical skills are not what is needed and that new skills will have to be acquired.

I

am going to get some different CPD this year. It will be practical “hands on” type training in an area where I am clearly deficient.

It is not suturing or other minor procedures.

I am going to work with babies and toddlers but not in a neonatal or paediatric ward. Interestingly the experience gained will not actually be applied to treating babies or toddlers.

The skill that I am totally deficient in but one that I clearly need according to a recent court finding is that of the full time nanny.

No longer is taking a history, performing an examination, ordering investigations (where appropriate), forming a diagnosis and recommending treatment enough.

A man in Sydney has successfully sued his GP because the GP “failed”

Consult Magazine | Summer 2013

13

OPINION

Different CPD

OPINION

to refer him “proactively” for gastric surgery.1 The verdict is being appealed.

The man was significantly obese. He also had liver problems and developed liver cancer. The man’s case is sad.

However the judge was of the view that surgery would have made all the difference. In reality some people benefit from gastric banding or other forms of bariatric surgery. Others do not and lose no weight or put it back on.

This is much the same with any form of weight management. Furthermore he could potentially have died from complications of surgery. This is rare but not unprecedented.

A long term US study 2 tracked patients post bariatric surgery and found that over the subsequent six years there was no difference in their “cost” to the health system. Some may well have improved quality of life. Whilst medical costs are not exactly the same as disease References 1. Kaye B. Obese man sues GP and wins $364k.

Medical Observer. 05 February 2013. Available from URL

14

prevalence it is a reasonable proxy.

Remember, bariatric surgery has been claimed to reduce future health costs.

There are also multiple factors involved in the development of liver cancer. If it was just obesity then it would not be a rare form of cancer.

The key point in the Sydney case is who is responsible for the decisions made by a competent adult. If someone chooses to eat too much then they are free to do so. Nobody can claim that they are not aware or could not easily find out about possible health complications of being morbidly obese (BMI over 40).

The fact that people know this but choose not to make any changes is their right. The consequences are also their responsibility.

If doctors are to be responsible for weight management by adults then the

next logical step is that doctors will need to do the shopping and meal preparation for patients. Indeed they will need to be there at meal times too as supervisor.

And probably through the day too so that no chocolate bars are snuck in.

In other words be a full time nanny.

This may be the ultimate dystopian fantasy of those who promote the nanny state.

As doctors we need to be very careful as often we are drawn into supporting measures, which seek to reduce the onus on the individual to be responsible for their actions.

So it is time to get in early. I reckon training, as a nanny will put me ahead of the curve. Who cares if I can practice medicine so long as I can nanny people?

CM

2. Healy M. Study disputes long-term medical savings from bariatric surgery. Chicago Tribune Health. 20 February 2013. Available from URL

Summer 2013 | Consult Magazine

We are proud to announce the launch of our new VMC patient website!

Coming soon in January 2014

Coronary imaging 2013

CARDIOLOGY

Which imaging test for coronary disease in 2013?

Dr Kenneth Lee

How should the plethora of new tests for coronary disease be used? Do stress testing and nuclear imaging still have a role? This article provides guidelines for contemporary clinical use.

Dr Kenneth Lee, FRACP, FCSANZ, FAANMS, Cardiologist and Nuclear Medicines Specialist, MIA Victoria, Warringal Private Hospital, Heidelberg (kenneth.lee@i-med.com.au)

S

creening for Coronary artery disease in asymptomatic subjects

Coronary Calcium Scoring (CCS) has the best current evidence base in the asymptomatic population for males 45 years and older and females from 50-55 years old.1 It has been shown to improve upon traditional risk factor assessment across all coronary risk groups, particularly the intermediate risk group (10-20% ten year event rate), where 52% are reclassified as low or high risk. A zero score signifies an excellent prognosis (less than 1% mortality risk at 12 years) and generally contraindicates further investigations. CCS detects mild preclinical coronary artery disease (CAD) as calcium deposition occurs early in plaque development.

The calcium score increases as disease progresses and correlates well with both the severity of CAD and prognosis. CCS is not

a Medicare Benefits Schedule (MBS) listed item in Australia but is widely available at $50-$200. It involves a five second scan, low radiation and no contrast.

Functional ischaemia tests (treadmill exercise ECG with or without imaging) are not suited for screening the asymptomatic, as the low prevalence of severe disease results in a high false positive rate. These tests should only be considered when there is other evidence of coronary disease, such as resting ECG changes or an ischaemic equivalent presentation (left ventricular systolic dysfunction, ventricular tachycardia or elevated troponin).

Current imaging guidelines2 do not recommend coronary CT angiography, in addition to CCS, purely for risk stratification in asymptomatic subjects.

Table 1: Tests for ischaemic heart disease 1.

2.

3.

4.

5.

6.

7.

Treadmill exercise ECG test* Stress echocardiogram* Nuclear myocardial perfusion scan (SPECT*, PET) CT coronary calcium score Coronary CT angiography* (see table 3) Cardiac magnetic resonance imaging Coronary angiography* +/- flow reserve calculation +/- intra-coronary imaging *MBS item (Australia)

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Investigation of stable symptomatic patients Treadmill exercise ECG testing is performed less frequently in 2013 due to suboptimal accuracy. It is now more often combined with imaging, as part of either a stress echocardiogram (SE) or nuclear myocardial perfusion imaging (MPI).3 Stress testing alone still has a role in providing rapid confirmatory evidence for or against angina, in those with a normal resting ECG, who can exercise adequately.

In Australia, SE is now more widely used than MPI, which is the opposite situation to the US and most developed countries.3 This partly relates to the place of SE within cardiology practices in this country, whereas MPI requires referral to an imaging department (in the USA most MPI is cardiology controlled). SE has advantages of lower cost, shorter procedure duration, and absence of administered radiation. Recently progress has been made in reducing radiation doses from MPI; by using low dose stress-only studies when possible, Tc-99m perfusion tracers rather than thallium-201 and new imaging software and scanners which facilitate high quality, low-dose images. There is a widespread belief that SE and MPI are interchangeable based on similar accuracies in small published series. Indeed, which test is more accurate in the average patient may depend on local expertise, as both are highly dependent on interpreting specialist skills. However, there are pros and cons

Summer 2013 | Consult Magazine

Coronary imaging 2013

of both techniques and certain clinical scenarios may favour one test over the other. It is generally acknowledged that MPI has a greater sensitivity for detection of myocardial ischaemia than SE. Thus, it may detect milder ischaemia, and better delineate the extent of ischaemia than SE. In comparative studies,4,5 SE has demonstrated greater specificity, largely due to the positive reporting of artefacts on MPI. If there is good local expertise in both SE and MPI, SE may be preferred in younger, thinner patients, who can exercise adequately. SE may provide important additional data regarding structural heart disease and pulmonary artery pressures in patients in whom exertional dyspnoea (rather than chest pain) is the dominant symptom. In Australia, progressively more patients being investigated for CAD are older, poorly mobile or obese and thus not suitable for treadmill SE.6 In those who cannot perform adequate exercise, MPI is easily combined with pharmacological stress (using coronary vasodilators such as adenosine or dipyridamole) whereas SE is limited to the inotropic agent dobutamine.

Diagnostic quality MPI studies can also be obtained in virtually all patients, including the non-echogenic obese. In patients who have had previous myocardial infarctions or revascularisation procedures, MPI often provides a better assessment of areas of recurrent or residual ischaemia, and myocardial viability, allowing the interventional cardiologist to better target treatment.

A simplified version of the current

Consult Magazine | Summer 2013

US “appropriate use criteria” for MPI is provided in table 2.

requires specialist referral for relatively narrow indications.

The recently published indications for SE and the new technique of coronary computed tomographic angiography (CCTA) are similar with considerable overlap.8,9 The Cardiac Society of Australia and New Zealand also published clinical indications in 2010.2 MBS billing for CCTA in Australia

CCTA is beginning to make its way into diagnostic algorithms, but its precise place in clinical use remains somewhat uncertain and controversial. It should not be used in those with known CAD or a high pre-test likelihood. The current trend is to use CCTA in lower risk cases with stable chest pain and stress imaging

Table 2: Appropriate use of criteria for myocardial perfusion imaging7 1.

CAD Detection • Stable chest pain: when intermediate-high risk; resting ECG changes; • Unable to exercise adequately • Acute chest pain: when normal ECG, LBBB, pacing or normal/equivocal troponin. In elderly or presence of co-morbid conditions that contra-indicate coronary angiography • Other presentations (ischaemic equivalents): LV systolic dysfunction, ventricular tachycardia, elevated troponin, syncope with high risk

2.

Known CAD patients • New/worsening symptoms • Angiographic coronary stenosis of uncertain functional significance • High CCS esp.> 400 • Intermediate-high risk exercise treadmill test

3.

Risk assessment prior to non-cardiac surgery • For high risk surgery (vascular, thoracic) in high risk patients • Prior to major orthopaedic surgery in high risk patients unable to exercise

4.

Post-Myocardial Infarction/Acute Coronary Syndrome • After patient stable and in cases where coronary angiography avoided

5.

Post-Coronary Stent • For follow-up when incomplete revascularisation or presentation atypical

6.

Assessment of Myocardial Viability • When severe LV systolic dysfunction and eligibility for revascularisation

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Coronary imaging 2013

Table 3: CCTA Medicare item requirements Computed tomography of the coronary arteries performed on a minimum of a 64 slice (or equivalent) scanner if: a) the request is made by a specialist or consultant physician, and b) one of the following applies to the patient: I.… …the patient has stable symptoms consistent with coronary ischaemia, is at low to intermediate risk of coronary artery disease and would have been considered for coronary angiography; II.… …the patient requires exclusion of coronary artery anomaly or fistula; III.… …the patient will be undergoing non-coronary cardiac surgery is preferred in patients more likely to have ischaemia. CCTA is promising for the emergency department rapid triage of low risk acute chest pain as it has a high negative predictive value for ruling out disease, however, more study is required before it becomes routine in Australia.

It is likely to have an increasing role in References 1. Aroney C. A suggested paradigm for coronary risk screening in asymptomatic persons assessment of total coronary atheromatous burden. Heart, Lung and Circ, 2012: 21; 449454.

2. The Cardiac Society of Australia and New Zealand. Non-invasive coronary artery imaging: current clinical applications.

Available from URL 3. Levin D, Rao V, Parker L, Frangos A, Intenzo C. Recent payment and utilization trends in radionuclide myocardial perfusion imaging. J

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evaluating patients with new-onset heart failure, dilated cardiomyopathy and left bundle branch block for underlying CAD. CCTA requires a stable slow heart rate and generally cannot be performed when there are frequent ectopic beats or atrial fibrillation. Patients should be Am Coll Radiol 2009 June; 6(6):437-41 4. Fleischman K, Hunnik M, Kuntz, Douglas P. Exercise echocardiography or exercise SPECT imaging? A meta-analysis of test performance.

JAMA 1998; 280:913-920 5. Rai M, Baker W, Parker M, Heller G. Metaanalysis of optimal risk stratification in patients > 65 years of age. Am J Cardiol 2012 Oct 15; 110 (8):1092-9 6. Miyamoto M, Vernotico S, Majmundar H, Thomas G. Pharmacologic stress myocardial perfusion imaging: A practical approach. J Nucl Cardiol 2007; 14:250-5

able to tolerate beta-blockade before the procedure and should have no worse than mild renal dysfunction, as potentially nephrotoxic intra-venous contrast is required. Radiation doses from CCTA have fallen to acceptable levels with current technology, such that most patients are studied with the equivalent of 1-2 years of background radiation. CCTA accurately detects both calcified and non-calcified coronary atheroma, correlates well with invasive angiography, may identify high risk plaque characteristics, and has recently shown excellent prognostic capability.

When moderate disease is present, CCTA often over-estimates the lesion severity necessitating correlative stress imaging to determine whether it is flow limiting.

CM

7. Hendel RC, Berman DS, Di Carli MF, Heidenreich PA, Kenkin RE, Pellikka PA, Pohost GM, Williams KA. Appropriate use criteria for cardiac radionuclide imaging. J Am Coll Cardiol 2009; 53(23): 2201-2229 8. Douglas PS, Khandheria B, Stainback RF, Weissman NJ. Appropriateness criteria for stress echocardiography. J Am Coll Cardiol 2008; 51(11): 1127-1147 9. Taylor AJ, Cerqueira M, Hodgson JM, Mark D, Min J, O’Gara P, Rubin GD. Appropriate use criteria for cardiac computed tomography. J Am Coll Cardiol 2010; 56(22): 1864-1894

Summer 2013 | Consult Magazine

INFECTION DENGUE F E V ER

Dengue Fever Prof John McBride

Dengue fever epidemics are becoming more frequent worldwide (including north Queensland). Whether your patient is a returned traveller or a local person, you should know the basics of how to diagnose and prevent the spread of this disease.

Prof John McBride, Professor of Medicine, School of Medicine and Dentistry, James Cook University, Cairns Base Hospital, Cairns, Queensland (john.mcbride@theiddoctor.com)

D

ENGUE and dengue haemorrhagic fever are caused by any of the four serotypes of dengue viruses (designated DEN 1-4).1 In Australia, dengue viruses are transmitted by the Aedes aegypti mosquito; this mosquito is a highly domesticated, urban mosquito found in association with people throughout the tropics and subtropics.

Uncomplicated dengue is rarely serious.

The reason for concern is the less common, and occasionally, fatal form of the disease known as dengue haemorrhagic fever (DHF). Second and subsequent infections with differing serotypes of dengue increase the risk of DHF. Dengue fever has caused frequent epidemics in the north Queensland cities of Cairns and Townsville, as well as population centres in the Torres Strait Islands. Infection is introduced by travellers and transmitted by the local A. aegypti mosquitoes.2

Virology The dengue viruses belong to the genus Flavivirus. Other viruses that belong to this genus include Japanese encephalitis virus, Murray Valley encephalitis virus and yellow fever virus.

The virus is composed of ribonucleic acid which is transcribed into three structural proteins and five non-structural proteins [NS1-5), including NS1, and it is released into the bloodstream from infected cells. While its exact function is

Consult Magazine | Summer 2013

not known, its detection is a specific and sensitive way to diagnose dengue.1

The mosquito vector A. aegypti usually breeds in artificial

containers in and around dwellings in urban areas. The flight range of A.aegypti is up to 300 metres from its breeding site and it may have frequent, incomplete blood meals; a single dengue virusinfected female can infect several people in a house in a short period.3 Female A. aegypti mosquitoes acquire the dengue virus by biting an infected person during the viraemic phase of the illness, which usually lasts for 4-5 days.

An extrinsic incubation in the mosquito of 8-10 days passes before the virus can be subsequently transmitted on to other humans. After this incubation, the mosquito may transmit the virus during every subsequent feed of its life (every 2-3 days). The incubation period is typically about 4-5 days.4 A. aegypti is located throughout the equatorial regions of the world. In Australia it is found throughout north Queensland but not in the Northern Territory or Western Australia.

Clinical findings Infection with a dengue virus causes a spectrum of illness from a mild nonspecific febrile illness (classic dengue fever) through to life-threatening DHF. The diagnosis of dengue in non-travellers

indicates that dengue transmission is occurring locally and, from a public health perspective, this is extremely important. Several epidemics in north Queensland have escaped early detection because dengue has not been considered in local residents with fever.

Classic dengue fever is generally observed in older children and adults.

Typically the onset is sudden, with a high fever (up to 40°C) accompanied by: • • •

Headache (typically retro-orbital).

Rash (macular, widespread and may be petechial, figure 1) Muscle, bone and joint pains (‘breakbone fever’).

Plus other less specific symptoms.

There may also be minor haemorrhagic manifestations, such as epistaxis, menorrhagia and gingival bleeding. Blood test abnormalities include a low white cell count with neutropenia, lymphopenia and thrombocytopenia. Elevated hepatic transaminase levels are common, with aspartate aminotransferase often higher than alanine aminotransferase.

Complications, which include severe haemorrhage, hepatitis or encephalitis, are rare. The illness usually lasts for about seven days. Some patients may take several weeks to completely recover from classic dengue fever. Although the disease can be incapacitating acutely, death is extremely rare.

A small number of patients progress to DHF; typically occurring on the fourth

19

DENGUE F E V ER

M (IgM - which reacts with dengue virus) in someone with symptoms compatible with dengue infection. The test can rarely be falsely positive or negative. Immunoglobulin G (IgG) denotes infection at some stage in the past.

Treatment In the first few days of illness, it is not possible to predict which patients will develop DHF. Patients who have had dengue before have a higher risk, but in most cases it is not known whether patients have had dengue or not. DHF can still occur in primary infections, so all dengue cases should be managed as if there is a risk of DHF. Treatment of dengue fever is the same as for other acute uncomplicated viral infections: Figure 1: This picture shows a typical rash seen in uncomplicated dengue.

The rash is widespread and has a maculopapular appearance.

or fifth day of illness, the main pathology of which is capillary leaking, resulting in intravascular fluid loss. Warning signs include abdominal pain or tenderness, persistent vomiting, clinical fluid accumulation, mucosal bleeding, lethargy, restlessness and liver enlargement. An increasing haematocrit, in association with a falling platelet count, are laboratory clues.4

Diagnosis A clinical diagnosis of dengue can be confirmed either by detection of the virus (from the blood) or by using serological tests (see figure 2).5 The virus can be detected during the first five days (and up to ten days in some cases) using: • • •

• •

• Plenty of oral fluids.

• Paracetamol (not aspirin).

No intramuscular injections.

Instruction to seek further medical advice if there are any of the warning signs (listed above) for DHF.

The critical phase of dengue occurs in the 24-48-hour period around fever defervescence (3-7 days after illness onset): in uncomplicated dengue fever, this is associated with clinical improvement, but in DHF it is associated with deterioration.

If you are not sure about home supports, or warning signs are present, it is reasonable

to admit to hospital for observation until the patient has been afebrile for 24 hours. Observations every 1-2 hours and haematocrit every 4-6 hours should be ordered for all patients being assessed for DHF. Patients who have been admitted for observation, but have not yet met the criteria for DHF, can continue to be managed in the same way as those with uncomplicated dengue fever. Overzealous administration of intravenous fluids is to be avoided.4

Management of DHF Intravenous therapy is fundamental to the treatment of DHF. The type of fluid used has been evaluated in trials, with crystalloid solutions (sodium chloride 0.9% w/v and sodium lactate [also known as Hartmann’s solution]) being as effective as colloid solutions. The rate of fluid administration in adults is 10 millilitres/ kilogram/hour, up to a maximum of 500 millilitres per hour.7 With appropriate management the mortality rate in DHF is less than 1%. The best results are obtained when there is a dedicated and experienced team managing the condition.

Research Significant progress is being made with candidate dengue vaccines.8 Exciting research with the bacterium Wolbachia, a life-shortening bacterial parasite of A. aegypti, is also being conducted in Brisbane and Cairns. This bacterium has also been shown to interfere with the replication of the dengue virus in the mosquito.9 CM

Reverse transcription PCR (RTPCR).

Virus culture.

Detection of the non-structural protein 1 (NS1).

The NS1 protein test is more widely available than other virus detection tests.

In studies performed to date, this assay is at least as sensitive as the RT-PCR assay and specificity is high. The virus serotype cannot be identified by the NS1 assay.6 After the viraemic period, a presumptive diagnosis of dengue can be made on the basis of detection of immunoglobulin

20

Figure 2: This figure demonstrates the kinetics of dengue viral markers and antibodies seen in primary and secondary infections.

Summer 2013 | Consult Magazine

Consult Magazine | Summer 2013

Programme for Research and Training in Tropical Diseases. Dengue : guidelines for diagnosis, treatment, prevention, and control.

Geneva: World Health Organization 2009.

5. Peeling RW, Artsob H, Pelegrino JL, et al.

Evaluation of diagnostic tests: dengue. Nat Rev Microbiol. 2010;8(12 Suppl):S30-38.

6. McBride WJ. Evaluation of dengue NS1 test kits for the diagnosis of dengue fever. Diagn Microbiol Infect Dis. 2009;64(1):31-36.

7. Wills BA, Nguyen MD, Ha TL, et al.

Comparison of three fluid solutions for

resuscitation in dengue shock syndrome. N Engl J Med. 2005;353(9):877-889.

8. Webster DP, Farrar J, Rowland-Jones S. Progress towards a dengue vaccine. Lancet Infect Dis. 2009;9(11):678-687.

9. Hoffmann AA, Montgomery BL, Popovici J, et al. Successful establishment of Wolbachia in Aedes populations to suppress dengue transmission. Nature. 2011;476(7361):454457.

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DENGUE F E V ER

References 1. Guzman MG, Halstead SB, Artsob H, et al.

Dengue: a continuing global threat. Nat Rev Microbiol. 2010;8(12 Suppl):S7-16.

2. McBride WJ. Dengue fever: is it endemic in Australia? Internal Medicine Journal.

2010;40(4):247-249.

3. Platt KB, Linthicum KJ, Myint KS, et al.

Impact of dengue virus infection on feeding behavior of Aedes aegypti. Am J Trop Med Hyg. 1997;57(2):119-125.

4. World Health Organization., Special

S u d d e n d e at h i n t h e Yo u n g

CARDIOLOGY

The family practitioner and preventing sudden death from inherited heart disease

Dr Jonathan R Skinner

Sudden unexpected death in young people is always a terrible tragedy. While newspaper articles may write headlines such as “adult cot death mystery”, in fact for many cases the cause can be found and the death could have been prevented.

Dr Jonathan R Skinner, MB ChB, DCH, MRCP(UK), FRACP, MD, Paediatric Cardiologist/electrophysiologist, Greenlane Paediatric and Congenital Cardiac Services, Starship Children’s Hospital, Park Road, Grafton, Auckland, 1030, New Zealand Chair Cardiac Inherited Disease Group New Zealand (www.cidg.org), Honorary Associate Professor in Child Health University of Auckland, New Zealand (jskinner@adhb.govt.nz)

I

nherited heart conditions are usually concealed in outwardly healthy people, often right up until the day they die suddenly and unexpectedly.

The vigilant family practitioner can be the one who makes the difference.

Consider three cases:* 1. A 21 year old woman who died suddenly and was found to have hypertrophic cardiomyopathy on autopsy.

2. A 10 year old boy treated for epilepsy who had a near drowning 3. A 35 year old who was found to have idiopathic dilated cardiomyopathy by his cardiologist Errors were made in the management of these cases which have resulted ultimately in loss of life. Some useful lessons may be learned. This article describes what happened, and then what should have happened.

Case 1 A 21 year old woman collapsed and died running for a bus. Hypertrophic cardiomyopathy (HCM) was found on autopsy. The pathologist recommended family screening to the GP.

22

The GP knew the woman had an older brother of 24. He sent a referral for an outpatient echocardiogram for him to the cardiology department. The report came back as normal, the GP let him know and no further action was taken.

of presymptomatic individuals is thus imperative, and depends on thorough screening of family members of anyone identified with the condition, even if they are deceased.

Five years later the young woman’s mother, aged 54, was found dead in the garden. Autopsy revealed severe HCM. Her husband demanded full investigation of the family. His GP (a different GP) referred them to a clinical genetic service which discovered a history of several young deaths in the extended family, including a 21 year old with a defibrillator for HCM. Genetic testing helped find five further presymptomatic individuals, two of whom ultimately went on to receive intracardiac defibrillators for severe HCM.

Learning points in this case Any of the clinicians involved in this story should have made a referral to a genetic service to ensure other family members were traced; the pathologist, the deceased woman’s GP, the cardiologist triaging the echo request, and the cardiologist implanting the defibrillator.

Hypertrophic Cardiomyopathy (HCM) HCM is quite common at 1 in 500 people.1 Like most inherited heart diseases, it is inherited in an autosomal dominant fashion. Thus 50% of first degree relatives carry the at risk gene. Gene carriers have variable clinical expression of the disease, and need to be followed by expert cardiology for life, from childhood. Sudden death is a common first presentation, but can be prevented by the use of intracardiac defibrillators.2 Detection

Case 2 A 10 year old boy treated for epilepsy was swimming in a race at school when he suddenly stopped moving. He was limp and when he was pulled out but he came round quickly. His seizures were usually related to exercise of some sort.

His GP referred him back to his neurologist who changed his antiepileptic medication. He had no seizures for two years. He collapsed suddenly warming up for a school hockey game, witnessed by his parents. Attempts at resuscitation failed.

The autopsy was uninformative.

Death was put down to epilepsy initially

Summer 2013 | Consult Magazine

Long QT syndrome (LQTS) LQTS is the commonest of the cardiac ion channelopathies (about 1 in 2000 people).4 These are disorders of the cardiac potassium and sodium ion channels regulating the cardiac action potential.

Others include Brugada syndrome and CPVT (catecholaminergic polymorphic ventricular tachycardia). All are autosomal dominant and cause sudden death in otherwise healthy people who have hearts which appear normal. A family history of young sudden death is common.

In LQTS death can be prevented by beta blockers and avoidance of some medications (www.qtdrugs.org). There are two common types. LQTS type 1 is the commonest; worst in boys mostly, and collapse whilst swimming or during or after exercise is typical.5 LQTS type 2 affects women mostly and death during sleep or after a sudden startle is typical; “nocturnal seizures” may be present.6 Learning points in this case LQTS, CPVT and Brugada are commonly mistaken for epilepsy in nonReferences 1. Maron BJ, Maron MS, Semsarian C. Genetics of hypertrophic cardiomyopathy after 20 years: clinical perspectives. J Am Coll Cardiol 2012 Aug 21;60(8):705-15.

2. Jayatilleke I, Doolan A, Ingles J, McGuire M, Booth V, Richmond DR, et al. Longterm follow-up of implantable cardioverter defibrillator therapy for hypertrophic cardiomyopathy. American Journal of Cardiology 2004 1;93(9):1192-4.

3. Gladding PA, Evans CA, Crawford J, Chung SK, Vaughan A, Webster D, et al. Posthumous diagnosis of long QT syndrome from neonatal screening cards. Heart Rhythm 2010 Jan 4.

4. Earle N, Crawford J, Smith W, Hayes I, Shelling A, Hood M, et al. Community detection of long QT syndrome with a clinical registry: an alternative to ECG screening programs? Heart Rhythm 2013 Feb;10(2):233-8.

5. Goldenberg I, Moss AJ, Peterson DR, McNitt S, Zareba W, Andrews ML, et al. Risk factors

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fatal attacks, since during an attack of rapid ventricular tachycardia there is zero cardiac output, and hypoxic seizures can occur.7 Once a misdiagnosis of epilepsy is made- it tends to stick for many years.8 The neurologist and the GP had several opportunities to revise this diagnosis prior to his death. The clinical history is absolutely classical for LQTS type 1.9,10 An ECG is an easy and cheap test and would have been abnormal. An ECG should always be done after the first afebrile seizure when there is no obvious cerebral pathology.

After sudden unexplained death in a young person, the pathologist should have saved DNA and initiated family screening by referral to a cardiac genetic service.11-13

Case 3 A 31 year old father of three children presented with palpitations and was found to have a dilated cardiomyopathy (DCM) of unknown cause by the investigating cardiologist. The GP assisted in his management over the subsequent ten years, but he did not refer the family for cardiac assessment.

The man’s father then died suddenly aged 59 whilst working on his car. At autopsy, he had severe DCM.

DCM, and the other two were normal and are under surveillance.

Dilated Cardiomyopathy (DCM) DCM has many causes. Most cases beyond childhood are secondary to coronary artery disease and alcohol for example. However, when no cause is apparent, familial DCM must be considered, and accounts for about a third of those where no overt cause is found.

Clinical management can be effective; particularly beta blockers and ACE inhibitors, and cardiac re-synchronisation and defibrillator pacemakers can be lifesaving.

Learning points in this case A thorough family history and full cardiac investigation of at least all first degree relatives is mandatory in all cases of CM “idiopathic” DCM.

*The cases are real but some details have been changed to protect the identity of the families concerned Acknowledgements Dr Skinner is part funded by Cure Kids.

The original patient, now aged 41, had three children who were then referred for cardiological assessment. One has severe

6.

7.

8.

9.

for aborted cardiac arrest and sudden cardiac death in children with the congenital long-QT syndrome. Circulation 2008 Apr 29;117(17):2184-91.

Sauer AJ, Moss AJ, McNitt S, Peterson DR, Zareba W, Robinson JL, et al. Long QT syndrome in adults. J Am Coll Cardiol 2007 Jan 23;49(3):329-37.

MacCormick JM, Crawford JR, Chung SK, Shelling AN, Evans CA, Rees MI, et al. Symptoms and signs associated with syncope in young people with primary cardiac arrhythmias. Heart Lung Circ 2011 Sep;20(9):593-8.

MacCormick JM, McAlister H, Crawford J, French JK, Crozier I, Shelling AN, et al.

Misdiagnosis of long QT syndrome as epilepsy at first presentation. Ann Emerg Med 2009 Jul;54(1):26-32.

Albertella L, Crawford J, Skinner JR. Presentation and outcome of water-related events in children with long QT syndrome.

Arch Dis Child 2011 Aug;96(8):704-7.

10. Skinner JR. Detection of Dangerous Arrhythmias. Paediatrics and Child Health 2011;21(8):369-77.

11. Behr ER, Dalageorgou C, Christiansen M, Syrris P, Hughes S, Tome Esteban MT, et al.

Sudden arrhythmic death syndrome: familial evaluation identifies inheritable heart disease in the majority of families. Eur Heart J 2008 Jul;29(13):1670-80.

12. Skinner JR, Crawford J, Smith W, Aitken A, Heaven D, Evans CA, et al. Prospective, population-based long QT molecular autopsy study of postmortem negative sudden death in 1 to 40 year olds. Heart Rhythm 2011 Mar;8(3):412-9.

13. Skinner JR, Duflou JA, Semsarian C. Reducing sudden death in young people in Australia and New Zealand: the TRAGADY initiative. Med J Aust 2008 Nov 17;189(10):539-40.

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S u d d e n d e at h i n t h e Yo u n g

(“SUDEP”- sudden unexpected death in epilepsy), until a family friend, a paediatrician, referred the family to an arrhythmia specialist. The mother had a long QT interval on her ECG, and subsequent molecular genetic testing of DNA extracted from the deceased boy’s neonatal screening (Guthrie) card revealed long QT type 1.3

Cancer in pregnancy

ONCOLOGY

Gynaecological cancers in pregnancy

Dr Padmaj Kulkarni

Management of cancer in a pregnant woman involves careful consideration of the well-being of the mother as well as of the foetus. In particular, curative treatment of gynaecological cancers generally involves removing the uterus and ovaries. The woman’s wish to conserve the pregnancy needs to be scientifically weighed against the risks due to cancer progression and toxicities of oncological management. The present review considers the various physiological and oncological principles of treating this special class of gynaecological cancers.

Dr Padmaj Kulkarni MD, DM; Consultant and Head of Oncology, Noble Hospital, Pune, India; Consultant Medical Oncologist, Deenanath Mangeshkar Hospital, Pune, India (padmaj.kulkarni@gmail.com)

G

ynaecological cancers form 19% of estimated newly diagnosed cancer cases worldwide.1 Cancer is the second leading cause of death in women of reproductive age, with a reported incidence of 1:1000 maternities.2 The definition of a pregnancy-associated cancer is when the initial cancer diagnosis is made during pregnancy or within 12 months of delivery.

The most common malignancies in pregnancy are listed in order of decreasing frequency:3 • • • • • •

Melanoma (1:350); Cervical cancer (1:2250); Hodgkin’s lymphoma (1:3000); Breast cancer (1:7500); Ovarian cancer (1:18,000); and Leukaemia (1:75,000).

In Australia, the crude incidence rate of pregnancy-associated cancer increased from 112.3 (in 1994) to 191.5 (in 2007) per 100,000 maternities (P < 0.001).2 Although maternal age was a strong risk factor for cancer, improved diagnostic techniques, detection and increased interaction with health services during pregnancy may also

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have contributed to the increase in numbers.

Over two-thirds of pregnancy-associated cancers were diagnosed in the twelve months after pregnancy. In this review, we will consider only gynaecological cancers associated with pregnancy.

reproductive capacity as a result of cancer therapy.

The age-adjusted incidence rates of cervical, ovarian, and endometrial cancer are 8.1, 12.9, and 23.5 per 100,000 women per year, respectively.4-6 Only 3.5% of ovarian cancers and 1.6% of uterine cancers are diagnosed between the ages of 20 and 34,5 with other gynaecological cancers (such as vulvar and vaginal cancers) being extremely rare in this young population.3 Because of this, the evidence available to manage gynaecological cancers during pregnancy is largely based on case reports, small case series, and pooled reviews. Recently though, guidelines of an international consensus meeting have become available.7

Depending on the stage of pregnancy, management of gynaecological cancers can involve surgery, chemotherapy and radiotherapy in various combinations.

Management of gynaecological cancers during pregnancy needs careful consideration of principles of oncology along with obstetrics. Foetal preservation (where possible) needs to be weighed against the potential loss of the patient’s

Foetal growth and risks from treatment

Surgery during pregnancy In approximately 1–2% of pregnancies an operation is needed. Anaesthesia is safe during pregnancy provided physiologic adaptations are considered. Foetal effects after anaesthesia are more related to maternal hypotension or hypoxia, altered glucose metabolism or hypothermia, rather than the use of anaesthetic drugs.

Adequate post-operative analgesia is important as pain can induce premature contractions. Thrombosis prophylaxis also needs to be considered. Of the women who undergo surgery during pregnancy, 2% will deliver prematurely.7

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Cancer in pregnancy

Chemotherapy during pregnancy During the first ten days following conception, the cells are subjected to an “all or nothing” phenomenon, such that if injury should occur, cell death ensues with the loss of the early blastocyst without the opportunity to develop into abnormal structures.7 Organogenesis occurs during weeks three to eight and is generally completed by week 13 (i.e. the first trimester).

As chemotherapy and radiation are known to be teratogenic, chemotherapy and radiation should be avoided during this trimester, where possible.3,7,8 During the second and third trimesters, chemotherapy and radiotherapy can be administered safely to the upper part of the body and the limbs.9,10 Administration of chemotherapy three weeks before delivery is not recommended due to the risk of cytopenia, bleeding, infection and death, particularly around the time of delivery. Additionally, active metabolites are not cleared well by the neonate’s hepatic and renal system.7

Physiological changes of pregnancy and chemotherapy The following physiological changes that occur during pregnancy may interfere with the pharmacodynamics and

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pharmacokinetics of chemotherapy: •

•

• • • •

Plasma volume and total body water increase by 50%: increases the distribution volume for watersoluble drugs.11 Increase in renal plasma flow and glomerular filtration rate: increased excretion rates of chemotherapeutic agents.

Reduced serum albumin: may increase concentrations of unbound drugs.

Increased hepatic metabolism and oxidation: increased drug clearance from the body.

Increased enterohepatic circulation: leads to absorption of active metabolites excreted in the colon.

Reduced gastrointestinal motility in the third trimester of pregnancy: affects the absorption of oral chemotherapeutic regimens.3,11,12

Chemotherapy agents may also cross into the placental circulation and affect the foetus. Factors that affect drug transplacental circulation include lipid and water solubility, foetal blood pH, and the molecular weight of the drug. The foetal gastrointestinal tract absorbs chemotherapy agents swallowed from the amniotic fluid.

The placental exchange of molecules is not equivalent in both directions. The quantum and speed of transfer between can lead to more drug being transferred to the foetus, as compared to from the foetus to the mother. This results in an accumulation of

the drug in the amniotic fluid.

There is very limited information available about the efficacy and toxicity of chemotherapy drugs in pregnancy. Taking into account a background risk of foetal malformation of 3%, the use of cytotoxic drugs during organogenesis is associated with an overall risk of 17%. If you exclude folate antagonists, the risk is reduced to 6%.

Consequently, the dosing of chemotherapy agents during pregnancy remains the same as for the non-pregnant patient.3,7,11,12

Neonatal and long-term outcomes Respiratory problems are the most important neonatal complication. Twodimensional echo monitoring of the left and right foetal ventricles, assessed using fractional shortening, showed no significant differences between exposed and unexposed foetuses in systolic function. However, a trend towards a lower wall thickness and left ventricular mass was found.13 In an Australian population-based study,2 women with cancer diagnosed during pregnancy were found to be more likely to deliver at a tertiary hospital, and to have had an induced labour or a pre-labour caesarean section. The mean gestational age at delivery was 37.7 weeks (SD = 3.2 weeks) for women with cancer diagnosed during pregnancy, 38.8 weeks (SD = 2.3 weeks) for women with cancer diagnosed postpartum and 39.0 weeks (SD = 2.2 weeks) for women

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Cancer in pregnancy

without cancer. Antenatal hospitalisations were more frequent for women with cancer diagnosed during pregnancy. After adjusting for other risk factors, cancer during pregnancy was associated with a significantly increased risk of caesarean section, planned preterm birth and large for gestational age (LGA) infants.2 Recognised cancer complications, such as the risks of thromboembolic events, sepsis and severe morbidity, were higher among women with cancer diagnosed during pregnancy.2 Limited retrospective data does not show an increased risk for congenital malformations after intra-uterine exposure to chemotherapy during the second and third trimester. Long-term follow up is, however, needed to provide more safety data on cognitive and cardiac function, fertility and the occurrence of secondary malignancies or germ cell mutations.12,14-16

Radiotherapy during pregnancy Radiotherapy should be planned and executed carefully as leakage radiation and collimator scatter can damage the foetus.

Prenatal irradiation with a foetal dose of 100 milligray (mGy) will increase the risk for childhood cancer and leukaemia (stochastic effect) from a background risk of 2–3/1000 to 3–4/1000.12 Foetal malformations mainly occur during organogenesis and when the foetal exposure exceeds 100–200 mGy.12 Adequate treatment of cancers in the pelvis involves radiation to the pelvis and always results in loss of foetal life as a result of severe foetal damage. Alternatives, such as administration of neoadjuvant chemotherapy or postponed radiotherapy until delivery, should be considered.

Staging investigations Diagnostic imaging of body parts at a distance from the foetus can be executed safely since the foetal dose is lower than 1 mGy. The sentinel lymph node procedure with technetium-99m (99mTc) can safely be performed during pregnancy. Computed tomography (CT) of the pelvis exposes the foetus to 10–40 mGy; therefore, alternatives such as sonography or magnetic resonance imaging should be preferred. PET-CT exposes the foetus to 19 mGy and may be done if considered absolutely essential.

Organ pathology Cervical neoplasms The incidence of abnormal cervical cytology is about 1–5% of all pregnancies

26

and the reported rate of cervical cancers ranges between 1 and 12 per 10,000 pregnancies.17 All pregnant women should undergo a cervical (Pap) test at the time of their initial prenatal examination.18,19 The interpretation of the cytology in pregnant patients is more difficult due to large ectropion, frequent inflammation and the presence of confusing decidual cells that can be mistaken for atypia (Arias-Stella reaction).

Diagnostic procedures after abnormal cervical screening should be the same as in non-pregnant women. Colposcopy with a biopsy has a sensitivity of 73– 95% while endocervical curettage is contraindicated.20,21 The majority of lowgrade lesions regress while about 30% remain unchanged. Progression to more severe lesions is rare. For high-grade lesions (cervical intraepithelial neoplasia (CIN) grade 3 or CIN 3), the regression rate is low (about 30%) and progression occurs in about 5%.12,22-24 If there is no sign of invasive carcinoma, no treatment is needed during pregnancy and management can be delayed to the post-partum period. However colposcopic follow-up every trimester is recommended for women without invasive lesions along with repeated biopsies in cases of suspected progression.

If microinvasive or invasive disease is suspected, conisation or a large-loop excision procedure should be done early in the pregnancy; the choice between these procedures depends on the size of the cervix, the clinical team’s preference, and the degree of suspicion.17 Invasive cervical cancer The management of cervical cancer mainly depends on four criteria: 1.

2.

3.

4.

Extent of local spread; Nodal status; Term of pregnancy; and Histological subtype.

Traditionally, cervical cancers diagnosed before 20 weeks would inevitably end with termination of the pregnancy as the only treatment option. If the diagnosis was made after 20 weeks of pregnancy, pregnancy is continued until the foetus reaches maturity. At that stage, caesarean section followed by definitive treatment of the cervical cancer (dictated by the cancer stage at that time).12 Currently, the trend is to preserve the pregnancy, particularly in patients with early stage disease and no nodal involvement.17

In case of any doubt on the diagnosis of cervical cancer, or as a treatment for stage IA disease, conisation is indicated; a flat cone is usually sufficient since the exocervix is more visible during pregnancy.

The gold standard to accurately calculate nodal status is still the histopathological assessment of lymph nodes. A laparoscopic lymphadenectomy is feasible up to 20 weeks gestation. Pelvic lymphadenectomy seems to be a valid diagnostic procedure during the first or second trimester for patients with early stage cervical cancer.17,25 The documentation of a negative nodal status is necessary to accept a conservative approach. Positive nodes would characterise high risk disease, necessitating standard treatment for cervical cancer at the cost of pregnancy.12 70% of cervical cancers during pregnancy are diagnosed at stage I.26,27 The node negative disease can be followed up carefully, both clinically and radiologically. The definitive treatment of the cervical tumour is done after delivery.

Delayed treatment until foetal maturation for patients with stage IA disease has an excellent prognosis and is now the standard of care.17 The second option is conservative surgical treatment of the cervical tumour with fertility preserving surgery, namely, conisation, cervical amputation (large cone) and radical trachelectomy. Conisation is the standard treatment for stage IA1 cervical cancer. The most frequent complications of a conisation during pregnancy are haemorrhage (5–10%), miscarriage (25%), preterm labour and delivery as well as infection.33 To minimise the risk of miscarriage and blood loss, the optimal time for cervical conisation is the second trimester, preferably between 14 and 20 weeks of gestation. For lesions less than IB1, radical trachelectomy can be offered.

However, it is technically hazardous, is associated with large blood loss volumes, and the risk of pregnancy loss is still considerable. For management of locally advanced disease, the main treatment choice is either neoadjuvant chemotherapy or concurrent chemoradiation.

Neoadjuvant chemotherapy can stabilise or reduce cervical cancer until foetal maturation has been reached. Then caesarean section followed by final treatment can be planned.12,28 For chemoradiation, the pregnancy must be ended before the initiation of therapy. But in exceptional cases in which surgery to end the pregnancy is not technically feasible (i.e. a bulky cervical tumour), radiation therapy

Summer 2013 | Consult Magazine

Vulvar pathology Intra-epithelial neoplasia This is the most common oncological vulvar pathology in pregnancy. It is common in young women and is associated with HPV infection. It may be treated with laser vaporisation, laser skinning and surgical excision, using the same guidelines for non-pregnant women.7,12 Invasive vulvar cancer Invasive vulvar cancer (> 1 mm) is uncommon during pregnancy.12 Its management depends on the nodal status and the pregnancy trimester. Node negative disease is treated as in a non-pregnant woman, with hemi/total vulvectomy with unilateral/ bilateral inguinofemoral lymphadenectomy or sentinel lymph node procedure.7 For node positive disease, termination of pregnancy with immediate definitive treatment is warranted in the first and second trimesters. During the third trimester, delivery should precede standard treatment.7,12 Pregnancy and cancer combined lead to a higher risk of thrombotic episodes; therefore, adequate prophylaxis is needed.

In addition, there may be more preoperative blood loss due to increased vascularity. Caesarean section is usually the preferred route of delivery to avoid scar or

episiotomy recurrence. As post-operative radiotherapy is contraindicated during pregnancy, positive surgical margins should be avoided.12 Chemotherapy has a limited role in this disease. Vulvar melanoma is treated similar to that in nonpregnant patients. It is associated with a risk of placental involvement as well as foetal metastases.29 Endometrial cancer Endometrial carcinoma is very rare in pregnancy, and is usually diagnosed after miscarriage or after a successful pregnancy during investigation of postpartum haemorrhage. Hence, curettings should be examined properly in such situations to rule out endometrial carcinoma. A welldifferentiated lesion with minimal invasion is most common and is managed as per usual guidelines.12,30 Adnexal masses Modern antenatal care involves frequent obstetric examinations, especially in asymptomatic women. This has led to the increased detection of adnexal masses in the first trimester, about 90% of which disappear spontaneously. Most of these lesions are benign and include teratoma, cystadenoma, endometrioma, ovarian cysts or leiomyomas.12 The diagnosis and characterisation of the adnexal lesions is mainly based on sonar findings since tumour markers during pregnancy are less specific.12,17 MRI is the preferred investigation as pelvic CT scan is contraindicated.7,17 In practice, however, a malignancy in an adnexal mass is suspected on sonographic criteria: size of more than

5 cm, complex solid-cystic nature and presence of extra-ovarian disease.17 Simple ovarian cysts may resolve spontaneously and do not need any intervention, while complex masses generally need surgical intervention (1:600 to 1:1500 pregnancies).17,31 Malignant and borderline ovarian tumours constitute 3-6% of cancer cases during pregnancy. Non-epithelial tumours (germ-cell and sex cord tumours) are the most common, followed by ovarian tumours of low malignant potential, while the epithelial ovarian carcinoma is the rarest.31

Ovarian pathology Ovarian tumours of low malignant potential These tumours in pregnancy are generally found in stage I and have, in general, an excellent prognosis. This disease is managed similarly to that in non-pregnant women, with some exceptions. The treatment usually involves resection of the affected cyst, all macroscopic disease with frozen section as well as routine peritoneal staging, but the macroscopically normal ovary can be left in place.32 If an ovarian tumour of low malignant potential is not diagnosed on the frozen section, restaging surgery should be offered. Restaging surgery could be postponed until after delivery if the tumour is diagnosed after 20â&#x20AC;&#x201C;24 weeksâ&#x20AC;&#x2122; gestation.17,32 Malignant ovarian cancers The malignant ovarian masses are frequently detected early due to modern antenatal care. These tumours are aggressive and most of them need chemotherapy, neoadjuvant or adjuvant, for their treatment. Preservation of pregnancy may be feasible and will depend on histology, nodal status, tumour stage and trimester of pregnancy.

Non-epithelial ovarian cancer These tumours (i.e. germ cell and sex cord stromal tumours) often present with bulky masses and are therefore more likely to have early symptoms. Indeed, more than 90% are detected in stage I. Fertility preserving surgery with complete peritoneal staging and excision of suspicious pelvic lymph nodes is the standard of care.7,12,17 Adjuvant chemotherapy is indicated in all patients as per standard indication, except FIGO stage I grade I immature teratoma and FIGO stage I dysgerminoma.7 BEP (bleomycin, etoposide, platinum) as per standard guidelines or paclitaxel-carboplatin 6 cycles are used as adjuvant treatment regimens.

Restaging post-delivery may be considered depending on the imaging findings and tumour markers.7,17

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Cancer in pregnancy

can be administered with the foetus in utero, resulting in a spontaneous abortion in about three weeks.17

Cancer in pregnancy

Epithelial ovarian cancers This cancer is the rarest ovarian cancer and the most difficult to treat. Peritoneal and nodal spread occur in more than two thirds of patients; most patients need neoadjuvant or adjuvant chemotherapy.17 Preservation of pregnancy is possible as long as the cancer is caught in the early stages and is a low grade tumour.

For stage IA, grade I tumours, surgical staging similar to borderline tumour is offered, with post-delivery restaging.

For stages IA grade 2-3, IB, IC and IIA, lymphadenectomy and adjuvant platinum References 1. Sankaranarayanan R, Ferlay J. Worldwide burden of gynaecological cancer: the size of the problem. Best Pract Res Clin Obstet Gynaecol. 2006;20(2):207-25. [Abstract] 2. Lee YY, Roberts CL, Dobbins T, et al.

Incidence and outcomes of pregnancyassociated cancer in Australia, 1994-2008: a population-based linkage study. BJOG. 2012;119(13):1572-82. [Abstract | Full text] 3. Ko EM, Van Le L. Chemotherapy for gynecologic cancers occurring during pregnancy.

Obstet Gynecol Surv.

2011;66(5):291-8. [Abstract] 4. SEER STAT fact sheets: Cervix uteri [online].

Rockville, MD: National Cancer Institute; November 2012 [cited 20 May 2013]. [URL] 5. SEER STAT fact sheets: Corpus and uterus, NOS [online]. Rockville, MD: National Cancer Institute; November 2012 [cited 20 May 2013]. [URL] 6. SEER STAT fact sheets: Ovary [online].

Rockville, MD: National Cancer Institute; November 2012 [cited 20 May 2013]. [URL] 7. Amant F, Van Calsteren K, Halaska MJ, et al.

Gynecologic cancers in pregnancy: guidelines of an international consensus meeting. Int J Gynecol Cancer. 2009;19(Suppl 1):S1-12.

[Abstract] 8. Tewari K. Cancer in pregnancy. In: Disaia PJ, Creasman WT (eds). Clinical Gynecologic Oncology (7th edition). New York: Mosby Elsevier; 2007: 467-531. [Book] 9. Cardonick E, Iacobucci A. Use of chemotherapy during human pregnancy.

Lancet Oncol. 2004;5(5):283-91. [Abstract] 10. Kal HB, Struikmans H. Radiotherapy during pregnancy: fact and fiction. Lancet Oncol.

2005;6(5):328-33. [Abstract] 11. Shahab N, Doll D. Chapter 27: Chemotherapy in pregnancy. In: Perry M (ed). Chemotherapy Source Book. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:273-82. [Book] 12. Amant F, Van Calsteren K, Vergote I, Ottevanger N. Gynecologic oncology in pregnancy. Crit Rev Oncol Hematol.

2008;67(3):187-95. [Abstract | Full text] 13. Cardonick E, Iacobucci A. Use of chemotherapy during human pregnancy.

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based chemotherapy are needed as well.

If the patient is upstaged post-surgery, chemotherapy during pregnancy and final surgery post-delivery are planned. As expected, true debulking surgery during pregnancy is not feasible as a hysterectomy is needed.7 Advanced stage ovarian cancers are the most difficult to treat. The management depends on the fitness of patient, the duration of pregnancy and the wish to preserve the pregnancy. With a pregnancy of less than 20 weeks duration, its preservation is not feasible. In such cases, Lancet Oncol. 2004;5(5):283-91. [Abstract] 14. Van Calsteren K, Berteloot P, Hanssens M, et al. In utero exposure to chemotherapy: effect on cardiac and neurologic outcome. J Clin Oncol. 2006;24(12):e16-7. [Full text] 15. Ring AE, Smith IE, Jones A, et al.

Chemotherapy for breast cancer during pregnancy: an 18-year experience from five London teaching hospitals. J Clin Oncol.

2005;23(18):4192-7. [Abstract | Full text] 16. Hahn KM, Johnson PH, Gordon N, et al. Treatment of pregnant breast cancer patients and outcomes of children exposed to chemotherapy in utero. Cancer.

2006;107(6):1219-26. [Abstract | Full text] 17. Morice P, Uzan C, Gouy S, et al.

Gynaecological cancers in pregnancy.

Lancet. 2012;379(9815):558-69. [Abstract] 18. Wright TC Jr, Massad LS, Dunton CJ, et al. 2006 consensus guidelines for the management of women with cervical intraepithelial neoplasia or adenocarcinoma in situ. Am J Obstet Gynecol.

2007;197(4):340-5. [Abstract | Full text] 19. Selleret L, Mathevet P. Precancerous cervical lesions during pregnancy: diagnostic and treatment. J Gynecol Obstet Biol Reprod (Paris). 2008;37(Suppl 1):S131-8. [Abstract] 20. Economos K, Perez Veridiano N, Delke I, et al. Abnormal cervical cytology in pregnancy: a 17-year experience. Obstet Gynecol.

1993;81(6):915-8. [Abstract] 21. Jain AG, Higgins RV, Boyle MJ. Management of low-grade squamous intraepithelial lesions during pregnancy. Am J Obstet Gynecol. 1997;177(2):298-302. [Abstract] 22. Vlahos G, Rodolakis A, Diakomanolis E, et al. Conservative management of cervical intraepithelial neoplasia (CIN(2-3)) in pregnant women. Gynecol Obstet Invest.

2002;54(2):78-81. [Abstract] 23. Robova H, Rob L, Pluta M, et al. Squamous intraepithelial lesion-microinvasive carcinoma of the cervix during pregnancy.

Eur J Gynaecol Oncol. 2005;26(6):611-4.

[Abstract] 24. Kaplan KJ, Dainty LA, Dolinsky B, et al.

Prognosis and recurrence risk for patients with cervical squamous intraepithelial

standard debulking surgery, with removal of the foetus, and adjuvant chemotherapy are recommended. After 20 weeks of pregnancy, preservation may be tried, though this is still considered experimental.

In such cases, the role of surgery is limited to establish the diagnosis. Less than optimal debulking is to be avoided as it exposes the foetus to unnecessary risk. Paclitaxelcarboplatin chemotherapy until foetal maturity is the standard treatment. Either planned caesarean delivery followed by debulking, or vaginal delivery (if feasible) followed by final surgery in the postpartum period are acceptable options.7,17 CM

lesions diagnosed during pregnancy. Cancer.

2004;102(4):228-32. [Abstract | Full text] 25. Guidelines Committee of the Society of American Gastrointestinal and Endoscopic Surgeons, Yumi H. Guidelines for diagnosis, treatment, and use of laparoscopy for surgical problems during pregnancy. Surg Endosc. 2008;22(4):849-61. [Abstract] 26. Lee RB, Neglia W, Park RC. Cervical carcinoma in pregnancy. Obstet Gynecol.

1981;58(5):584-9. [Abstract] 27. Takushi M, Moromizato H, Sakumoto K, Kanazawa K. Management of invasive carcinoma of the uterine cervix associated with pregnancy: outcome of intentional delay in treatment. Gynecol Oncol.

2002;87(2):185-9. [Abstract] 28. Bader AA, Petru E, Winter R. Long-term follow-up after neoadjuvant chemotherapy for high-risk cervical cancer during pregnancy. Gynecol Oncol. 2007;105(1):26972. [Abstract] 29. Alexander A, Samlowski WE, Grossman D, et al. Metastatic melanoma in pregnancy: risk of transplacental metastases in the infant. J Clin Oncol. 2003;21(11):2179-86.

[Abstract | Full text] 30. Vaccarello L, Apte SM, Copeland LJ, et al.

Endometrial carcinoma associated with pregnancy: A report of three cases and review of the literature. Gynecol Oncol.

1999;74(1):118-22. [Abstract] 31. Whitecar MP, Turner S, Higby MK. Adnexal masses in pregnancy: a review of 130 cases undergoing surgical management.

Am J Obstet Gynecol. 1999;181(1):19-24.

[Abstract] 32. Camatte S, Morice P, Thoury A, et al.

Impact of surgical staging in patients with macroscopic â&#x20AC;&#x153;stage Iâ&#x20AC;? ovarian borderline tumours: analysis of a continuous series of 101 cases. Eur J Cancer. 2004;40(12):1842-9.

[Abstract] 33. Van Calsteren K, Hanssens M, et al. Successful conservative treatment of endocervical adenocarcinoma stage Ib1 diagnosed early in pregnancy. Acta Obstetricia et Gynecologica.

2008;87:250-3. [Abstract]

Summer 2013 | Consult Magazine

INFORMED CONSENT Informed consent

Informed consentthe important conversation

Dr Jocelyne Benatar

Informed consent is an effective way to protect patients’ rights and should enhance the doctor- patient relationship. Unfortunately, the process is increasingly used to mitigate risk rather than reflecting respect for the patient’s autonomy.

Dr Jocelyne Benatar, Senior Research Doctor, Cardiovascular Research Unit, Auckland City Hospital, Park Rd, Grafton, Auckland 1030 (Jbenatar@adhb.govt.nz), Virtual Medical Centre Editorial Advisory Board member

T

he importance of informed consent is relatively new to the practice of medicine. In ancient Greece, patient participation in decision making for medical treatment was considered undesirable and this attitude prevailed until the first half of the last century.1

This changed when the horrors perpetuated by the Nazis in the name of medical experiments were revealed. As a consequence, the Nuremberg Code forged in 19492 , declared the voluntary consent of human subjects to be ‘absolutely essential’.

Lack of informed consent and unethical research continued despite publications in 19663 detailing unethical research; however the issue of informed consent was truly brought to public attention with the exposure of the Tuskegee Syphilis Study in 1972.4 Informed consent has since become one of the most important facets of bioethics.5 Doctors are obligated to make sure that a patient understands the risks and benefits of any medical procedure. In medical research, which is done largely for the benefit of people other than participants in clinical trials, and where the anticipated benefits to participants are usually less certain than in other medical contexts, the process is especially important.

What is informed consent?

By definition informed consent is a

Consult Magazine | Summer 2013

process of information sharing in which professionals provide information so that individuals can make an informed decision about their healthcare. A signature on a consent form does not necessarily equate to informed consent. It is incumbent on the doctor to document the process as this is what will be used to demonstrate the consent process. Informed consent originates from the legal and ethical right the patient has to direct what happens to their body, and from the ethical duty of the physician to involve the patient in their health care. Inadequately informed consent makes certain intrusions impermissible.

For consent to be genuinely informed, a number of conditions have to be met.5,6 The individual with whom the conversation is taking place needs to be competent to make a decision. In medicine, competence is presumed unless there are reasonable grounds to assume the patient is not competent.7,8 The information presented, whether it is verbal or oral, needs be easily understood by the patient and should not be jargonistic or legalistic. In addition to discussing the risks and benefits of any proposed treatment, the patient has the right to know of alternative treatments and their risks and benefits. Consent needs to be voluntary and free of coercion and deception.9

If a competent adult does not give sufficiently informed and voluntary consent to intervention in their body or private sphere, then, at least when the

intervention is substantial, not trivial the intervention is impermissible. Lack of informed consent can be used to establish negligence (and hence malpractice and torts), or battery and assault.

Issues with informed consent Most of the problems related to informed consent arise from fear of complaints in an increasingly litigious society. The oft-cited case of medico-legal risk exposure in the area of informed consent is the doctor who fails to disclose a rare risk to a patient, who then consents to a procedure and is injured when the risk materialises. This has resulted in more information being relayed with an increasing use of legalistic language, which may be more confusing to patients.10 Patients frequently misconstrue the purpose of informed consent, perceiving it to be for the protection of the doctor, rather than for their own benefit.

The emphasis on risk rather than benefit may lead to the misconception that the treatment does more harm than good.

Doctors grapple with how much needs to be said to patients to fulfill the obligation to ‘full disclosure’. Most of the literature and law in this area suggest that the most reasoned approach is to give information to a reasonable patient standard.11 The doctor is expected to tailor information to the patient needs and consider the ability for the patient to understand the information. The difficulty is applying this in situations when critically unwell

29

Informed consent

patients may not have the time consider, ask questions and have all concerns addressed.

In that situation, it may be necessary to focus on the most important aspects of the treatment (risks, benefits), including possible alternatives and return later to address any concerns.

Some patients may waive the right to discuss the details of a treatment.

Sometimes patients maintain that they do not want a lot of detail about possible complications from the proposed treatment. In this situation, the doctor must record this decision and decide whether or not the patient has in fact received sufficient relevant information to References 1. Murray PM. The History of Informed Consent. The Iowa Orthopaedic Journal.

1990;10:104–9.

2. Code. N. Trials of War Criminals before the Nuremberg Military Tribunals under Control Council Law: U.S. Government Printing Office; 1949.

3. Beecher HK. Ethics and clinical research.

The New England Journal of Medicine.

1966;274(24):1354-60. Epub 1966/06/16.

4. Kampmeier RH. The Tuskegee study of untreated syphilis. South Med J. 1972;65(10):1247-51.

5. Beauchamp TLaC, James F Principles

30

make an informed choice. If not, then the doctor may need to consider declining to perform the procedure under discussion.

In such circumstances, it is vital to seek collegial support and / or refer the patient to another doctor.12 Another less cited issue is the role of the patient in the process. Informed consent is considered a right for patients but no responsibilities are attached to this.13,14 This imbalance may leave the physician vulnerable to complaints if an adverse outcome occurs even when this may be exacerbated by the patient’s action. For example, the patient who does not inform the doctor of over-the-counter remedies

6.

7.

8.

9.

of Biomedical Ethics. New York: Oxford University Press; 1994.

Faden RR, & Beauchamp, T. L. . A History and Theory of Informed Consent. New York: Oxford University Press.; 1986.

Farnsworth MG. Competency evaluations in a general hospital. Psychosomatics.

1990;31(1):60-6.

RJ. G. Psychological testing: History, principles and applications. 5th ed. Boston: Pearson Education 2007.

Protection of human subjects; Belmont Report: notice of report for public comment.

Federal register. 1979;44(76):23191-7. Epub 1979/03/30.

which may interact with treatment.

Considering informed consent solely as a right when medicine is patriarchal and patients have little access to information is justified, especially in vulnerable populations. However, in the developed world, patients have increasingly unprecedented access to a wealth of information at a touch of a button, and the relationship between doctor and patient has shifted and is less unbalanced. The debate on informed consent may need to include the rights and responsibilities of both patients and doctor in this circumstance.

CM

10. Benatar JR, Mortimer J, Stretton M, Stewart RA. A booklet on participants’ rights to improve consent for clinical research: a randomized trial. PloS One. 2012;7(10):e47023. Epub 2012/10/25.

11. Kottow M. The battering of informed consent.

Journal of Medical Ethics. 2004;30(6):565-9.

12. Hull RT. Informed consent: patient’s right or patient’s duty? The Journal of Medicine and Philosophy. 1985;10(2):183-97. Epub 1985/05/01.

13. Kant I. Religion within the Limits of Reason Alone,1793.

14. Hume D. An Enquiry Concerning the Principles of Morals, 1777.

Summer 2013 | Consult Magazine

It’s only Champagne.

Prof Rod Underwood

T

here is much more to sparkling wines than just Champagne.

The French, of course, have established themselves as the benchmark for the Champagne style of sparkling wines. However, we ignore the sparkling wines of Spain and Italy, as well as Australia, to our cost.

French Bubbles If the bubbles in your bottle come from a region located about 140 kilometres east of Paris, around the city of Rheims and stretching along the Marne River to Epernay, then you are drinking Champagne.

Today, the vineyards cover some 34,000 hectares and produce 25 million bottles annually. All 300 Champagne villages scattered around the district are rated for the grape quality potential, and the top 17 are designated as “Grand Cru” vineyards.

Champagne is typically produced from a blend of two black grapes – pinot noir and pinot meunier – and a white grape – chardonnay. Most of the Champagne produced today is “non-vintage”, meaning that it is a blended product of grapes from multiple vintages. If the conditions of a particular vintage are favourable, some producers will make a “Vintage” wine that must be composed of at least 85% of the grapes from that vintage year.

Blanc de Noirs is a French term for a white wine produced entirely from black grapes. It may be encountered in Champagne where the wine has been made from either pinot noir, pinot meunier or a blend of both.

Consult Magazine | Summer 2013

31

LI F ESTYLE - CHAMPAGNE

What’s in a Name?

LI F ESTYLE - CHAMPAGNE

Blanc de Blancs is the term used to designate Champagnes made exclusively from chardonnay grapes.

The rose wines of Champagne (also known as Pink Champagne) are produced either by leaving the clear juice of black grapes to macerate on its skins for a short time or, more commonly, by adding a small amount of still pinot noir red wine to the sparkling wine cuvée – vat or tank.

If the bubbles in your bottle are French, but not from the Champagne region, you have a Crémant sparkler. There are just two major differences between Crémant and Champagne: first, only wines made in the eponymous geographical appellation rightly can be called ‘Champagne’. Crémants hail from other parts of France. And second, Crémants can be made from grapes other than the Champagne standards of pinot noir, pinot meunier and chardonnay.

Traditionally, Champagne has been served with oysters, foie gras, lightly dressed salads, lobster in white sauce or sharply flavoured cheeses such as chèvre and Maroilles. Its acidity cuts through salt very well, so a partnership with caviar is perfect, and that same crispness makes it a good foil for smoked salmon. Champagne is one of the few wines that can pair with your gravlax.

Spanish Bubbles Cava, the Spanish sparkling wine, is produced in the north-east region of Catalonia. If you are in Barcelona you are in Cava territory. Cava may be white (blanc) or rose (anta). Macabeu, parellada and xarello are the most popular and traditional grape varieties for producing Cava. Only wines produced in the traditional method (méthode champenoise) may be labelled Cava. Bubbles produced by other processes are called vinos espumonos (sparkling wines). The two major producers of Cava

32

are Codorníu and Freixenet.

Sparkling wines tend to have a higher acidity and lower sugar levels than table wines. These two extremes complement elements in almost any food, from smoked fish to spicy Asian take-away.

Cava is ideal with Spanish tapas and all kinds of seafoods. Cava can also handle the fiery qualities of some Indian dishes, and it is delicious with a broad range of Asian cuisines.

Italian Bubbles If your bubbles have an Italian accent they are likely to have come from northern Italy. Asti is a picturesque town set in the rolling hills of Piedmont in the northwestern corner of Italy. In addition to the eponymous sparkler, the wine region of Asti also produces Moscato d’Asti as well as a red sparkling wine called Bracchetto. Asti is a light, slightly off-dry, vaguely peachy wine made from 100 per cent Moscato (Muscat grapes). It has a high-acidity, which helps to balance its sweetness. Asti is a non-vintage wine best consumed within a couple years after bottling.

Moscato is technically a fizzante, a fizzy or light sparkling wine. The wine is light and crisp and relatively low in alcohol, about 5-7%, making it an ideal wine for lunch on a hot summer’s day. A number of Australian wineries are now producing a Moscato style of bubbles (e.g., Brown Brothers, Two Hands).

Prosecco is the name of the grape that is used to produce this sparkling wine from Veneto in north-eastern Italy. As this grape is prized for its delicate flavours and aromatics, the wine is made by the Charmat method where the second fermentation occurs in steel tanks rather than in the bottle thus ensuring its freshness.

Asti is ideal paired with gorgonzola

cheese (another specialty of Piedmont) or by itself as an aperitivo. Prosecco is excellent paired with calamari, a green salad or a plate of pasta; the acidity will cut through any cream sauce or cheese.

Australian Bubbles Australian sparkling wines are being made increasingly from cold climate grapes grown in Tasmania and high altitude parts of southern Victoria. Australian sparklers are typically produced from Chardonnay and Pinot Noir in the style of Champagne, although more wine makers are experimenting with other varieties.

Sparkling Shiraz is unique to Australia and is altogether different, though no less enjoyable than a sparkling white wine.

Italian lambrusco is of similar style, but unlike Australian red sparkling wine, uses no oak. Seppelt’s Sparkling Shiraz has defined this style of wine over many years.

Most of the Australian sparkling red wines are made from Shiraz because its smoky flavours lend themselves to effervescence. Sparkling Shiraz is quite a versatile variety and tends to go well with desserts, light foods like fois gras, pâté and curry puffs, a variety of oriental food, as well as duck and grilled meat, such as pork spare ribs.

And the last word on the subject of bubbles is left to Oscar Wilde who observed that:

Pleasure without Champagne is purely artificial.

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Summer 2013 | Consult Magazine

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