SAMJ Vol 106, No 8 (2016) by HMPG

AUGUST 2016

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GUEST EDITORIAL 2016 National Rheumatic Fever Week CME Functional neurosurgery (part 1) IN PRACTICE Rheumatic heart disease: Chronic conditions and the school health service Lifestyle interventions in type 2 diabetes CASE REPORT Acute functional mitral incompetence RESEARCH Tertiary hypertension screening and management The HIV healthcare transition: Adolescence to adulthood

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AUGUST 2016

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GUEST EDITORIAL

2016 National Rheumatic Fever Week: The status of rheumatic heart disease in South Africa B M Mayosi

EDITOR’S CHOICE

CORRESPONDENCE

Advice to health professionals: Use of lignocaine as a diluent to reduce the pain associated with the administration of benzathine penicillin G G Madeira, A O Mocumbi, B M Mayosi

Haemotoxic snakebite in rural KwaZulu-Natal, South Africa E H Decloedt, G J Müller

Umbilical hernia in children in a developing country: Does the season have an effect on the occurrence of strangulation? G J Ngom, F Gassama, A S Mahomed, O Ndour

Contribution of congenital disorders to under-5 mortality H L Malherbe, C Aldous, A L Christianson, D Woods

ERRATUM Targeting composite treatment of type 2 diabetes in middle-income countries

IZINDABA

12 14 14 16

Emergency medical service workers struggle in violent election climate Médecins Sans Frontières moves to protect refugee healthcare Rape survivor care crisis – mines the worst? HIV treatment under control – now for sexy prevention?

OBITUARY Devanandan Chetty

BOOK REVIEW Beyond the Stethoscope: Casebook of a Township Doctor

CME

GUEST EDITORIAL Functional neurosurgery J M N Enslin

ARTICLES Surgical management of spasticity J M N Enslin, A G Fieggen

Surgical management of epilepsy J M N Enslin, S J Rothemeyer, A G Fieggen

ACTING EDITOR Bridget Farham, BSc (Hons), PhD, MB ChB EDITORS EMERITUS Daniel J Ncayiyana, MD (Groningen), FACOG, MD (Hon), FCM (Hon) JP de V van Niekerk, MD, FRCR ASSOCIATE EDITORS Q Abdool Karim, A Dhai, N Khumalo, R C Pattinson, A Rothberg, A A Stulting, J Surka, B Taylor, M Blockman HMPG CEO AND PUBLISHER Hannah Kikaya | Email: hannahk@hmpg.co.za MANAGING EDITORS Ingrid Nye Claudia Naidu TECHNICAL EDITORS Emma Buchanan Paula van der Bijl NEWS EDITOR Chris Bateman | Email: chrisb@hmpg.co.za PRODUCTION MANAGER Emma Jane Couzens DTP AND DESIGN Carl Sampson CHIEF OPERATING OFFICER Diane Smith | Tel. 012 481 2069 Email: dianes@hmpg.co.za JOURNAL ADVERTISING Charles William Duke Reneé Hinze Ladine van Heerden Azad Yusuf ONLINE SUPPORT Gertrude Fani FINANCE Tshepiso Mokoena HMPG BOARD OF DIRECTORS Prof. M Lukhele (Chair), Dr M R Abbas, Dr M J Grootboom, Mrs H Kikaya, Prof. E L Mazwai, Dr M Mbokota, Dr G Wolvaardt ISSN 0256-9574 SAMA website: www.samedical.org Journal website: www.samj.org.za

IN PRACTICE 30

HEALTHCARE DELIVERY Asymptomatic rheumatic heart disease in South African schoolchildren: Implications for addressing chronic health conditions through a school health service M Shung King, L Zühlke, M E Engel, B M Mayosi

A successful lifestyle intervention model replicated in diverse clinical settings S Mark, S du Toit, T D Noakes, K Nordli, D Coetzee, M Makin, S van der Spuy, J Frey, J Wortman

CLINICAL ALERT Severe hypertension in pregnancy: Using dynamic checklists to save lives J Moodley, N C Ngene

STATEMENT The World Health Organization’s mechanisms for increasing the health sector budget: The South African context F H J Venter, J E Wolvaardt

August 2016, Print edition

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43 Implications of the 2015 World Health Organization isoniazid preventive therapy recommendations on Namibian tuberculosis prevention efforts S A Oloo

ONLINE CONTENTS LISTED IN Index Medicus (Medline) Excerpta Medica (EMBASE) Biological Abstracts (BIOSIS) Science Citation Index (SciSearch) Current Contents/Clinical Medicine

COCHRANE CORNER Antifibrinolytic drugs for acute traumatic injury M McCaul, T Kredo

MEDICINE AND THE LAW When may doctors give nurses telephonic treatment instructions? D J McQuoid-Mason

CASE REPORTS Cardiogenic shock – a look at acute functional mitral incompetence F A Steyn, J Vosloo, H Naude, A J Steyn

Clinical awareness for healthcare professionals: Fatal encephalopathy complicating persistent vomiting in pregnancy N C Ngene, J Moodley

A case of renal cell carcinoma and angiomyolipoma in an adolescent girl J W Rood, K P Mokhobo

RESEARCH Evaluation and management of patients referred to a tertiary-level hypertension clinic in Cape Town, South Africa* M S Moosa, L S Kuttschreuter, B L Rayner

Pan computed tomography for blunt polytrauma: Are we doing too many?* G V Oosthuizen, J L Bruce, W Bekker, N Shangase, G L Laing, D L Clarke

South African healthcare provider perspectives on transitioning adolescents into adult HIV care* T H Kung, M L Wallace, K L Snyder, V K Robson, T S Mabud, C D Kalombo, L-G Bekker

Sialendoscopic treatment of recurrent juvenile parotitis: A South African case series* S Honnet, O Edkins

Please submit all letters and articles for publication online at www.samj.org.za

Attitudes to female genital mutilation/cutting among male adolescents in Ilorin, Nigeria* A S Adeniran, M A Ijaiya, A A Fawole, O R Balogun, K T Adesina, A W O Olatinwo, A O Olarinoye, I P Adeniran

*Full article available online only.

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AUGUST 2016

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GUEST EDITORIAL 2016 National Rheumatic Fever Week

Background photo: Electrocardiogram | funnyangel

CME Functional neurosurgery (part 1) IN PRACTICE Rheumatic heart disease: Chronic conditions and the school health service

Hexagon photos: Lifestyle choice | Central IT Alliance; Open heart surgery | kerale; Computed tomography scanner | zlikovec; Hypertension | JPC-PROD

August 2016, Print edition

Lifestyle interventions in type 2 diabetes CASE REPORT Acute functional mitral incompetence RESEARCH Tertiary hypertension screening and management The HIV healthcare transition: Adolescence to adulthood

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GUEST EDITORIAL

2016 National Rheumatic Fever Week: The status of rheumatic heart disease in South Africa

ARF

RHD

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Fig. 1. Number of cases of ARF and RHD presenting to the Paediatric Cardiology Unit at Chris Hani Baragwanath Hospital, Johannesburg, 1993 2010. 1.6 1.4 RHD mortality, per 100 000 population

Over 25 years ago, the National Department of Health (NDoH) declared the first week of August National Rheumatic Fever Week following the efforts of John Barlow, Budgie van der Merwe and others to focus the attention of the nation on the need to implement proven interventions to reduce the incidence of acute rheumatic fever (ARF) and the prevalence of rheumatic heart disease (RHD).[1,2] It was at this time that ARF was made a notifiable condition, although the uptake of notification was subsequently found to be suboptimal. [3] In October 2005, the NDoH hosted the 1st Pan-African Workshop on Acute Rheumatic Fever and Rheumatic Heart Disease, together with the World Health Organization (Africa Region), the World Heart Federation, the Pan-African Society of Cardiology and the South African Heart and Stroke Foundation, where the Drakensberg Declaration was adopted.[4] The Drakensberg conference issued a clarion call to African governments and their ministries of health to initiate national programmes to eliminate ARF and control RHD by raising awareness among the public and professionals, measurement of the burden of disease through surveillance studies, improvement of medical and surgical care through advocacy, and the widespread use of penicillin in primary and secondary prevention activities (the A.S.A.P. Programme).[5] A.S.A.P. has inspired new research that has provided vital infor mation on the status of ARF and RHD in Africa and the world. [6] South African (SA) studies reveal a changing pattern of disease at hospital and population levels. Hospital-based studies show a high incidence of congestive heart failure caused by RHD (average of 25 cases/100 000/year in Soweto) that is associated with high 60-day and 180-day mortality rates of 24.8% (95% confidence interval (CI) 13.6 - 42.5) and 35.4% (95% CI 21.6 - 54.4), respectively.[7,8] This high burden of heart failure and mortality in adults has to be contrasted with a falling caseload of ARF and RHD in children, as demonstrated in Soweto recently (Fig. 1). Furthermore, there has been a fall in causespecific mortality from RHD over the past 15 years (Fig. 2). These changes are consistent with a transition of ARF/RHD from a condition of childhood to a mature endemic disease of adults. The changes may reflect a ‘Mandela dividend’ associated with the improvement in access to primary healthcare and rising socioeconomic status of South Africans since the advent of the new SA in 1994.[9] The ‘In Practice’ article in this issue of SAMJ on the role of screening echocardiography for RHD in the school health programme by Shung King et al.[10] and the letter describing a regimen for the painless administration of intramuscular penicillin by Madeira et al.[11] address important issues in the quest to end RHD. The commentary by Shung King et al.[10] is a response to an echocardiographic screening study of schoolchildren in Cape Town that showed a prevalence of latent RHD of 20 - 30 per 1 000 among asymptomatic schoolchildren, although about 50% of these cases revert to normal after 5 years of follow-up.[12,13] Screening echocardiography is not recommended as a routine test in the school health programme until studies of its impact on prognosis and cost-effectiveness are conducted.10,14] The advice by Madeira et al.[11] on the use of lignocaine as a diluent for benzathine penicillin is relevant not only to practitioners who use injectable penicillin on a regular basis for the primary and secondary prevention of ARF, but also to those whose patients need penicillin prophylaxis against recurrent infections in sickle cell disease and immune deficiencies.[15,16]

1.2 1 0.8 0.6 0.4 0.2 0

1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 Year

Fig. 2. Cause-specific mortality rate due to RHD in the SA population, 1997 2012. (Dotted lines = the confidence intervals of the estimates of mortality.)

There has been significant progress in the uptake of the A.S.A.P. call by African governments. In June 2015, the heads of state of African countries endorsed the Addis Ababa Communiqué, which sets out seven actions for addressing the barriers to RHD control that were identified in the REMEDY study.[17,18] These are as follows: (i) creation of prospective disease registers at sentinel sites in affected countries to measure disease burden and track progress towards the reduction of mortality by 25% by the year 2025, as mandated by the World Health Organization;[19] (ii) provision of an adequate supply of high-quality benzathine penicillin for primary and secondary prevention; (iii) improvement of access to reproductive health servi ces for women with RHD and other non-communicable diseases (NCDs); (iv) decentralisation of technical expertise and technology for diagnosing and managing ARF and RHD (including ultrasound of the heart); (v) establishment of national and regional centres of

August 2016, Print edition

GUEST EDITORIAL

excellence for essential cardiac surgery for the treatment of affected patients and the training of cardiovascular practitioners of the future; (vi) initiation of national multisectoral RHD programmes within NCD control programmes of affected countries; and (vii) fostering of international partnerships with multinational organisations for resource mobilisation, monitoring and evaluation of the programme to end RHD in Africa.[18] SA has the conditions that are required for success in eradicating ARF and ending RHD. The NDoH has prioritised the prevention of the disease through initiatives such as National Rheumatic Fever Week, the inclusion of ARF among notifiable conditions, and efforts to improve access to primary healthcare. Health practitioners need to play their role by notifying cases of ARF, treating all children with a sore throat with penicillin according to the SA guidelines,[20] and entering all our patients with RHD in the electronic register.[21] These measures, together with other actions outlined in the Addis Ababa Communiqué, if imple mented across the health system, will hasten the demise of ARF and bring RHD under control by the year 2025. Bongani M Mayosi Department of Medicine, Groote Schuur Hospital and Faculty of Health Sciences, University of Cape Town, South Africa bongani.mayosi@uct.ac.za 1. McLaren MJ, Hawkins DM, Koornhof HJ, et al. Epidemiology of rheumatic heart disease in black school children of Soweto, Johannesburg. BMJ 1975;3(5981):474-478. DOI:10.1136/bmj.3.5981.474 2. Lawrenson J. Tribute to Professor Pieter-Luttig van der Merwe. 2015. https://www.saheart.org/ newsletters/viewFile/53 (accessed 2 July 2016). 3. Nkgudi B, Robertson KA, Volmink J, Mayosi BM. Notification of rheumatic fever in South Africa – evidence for underreporting by health care professionals and administrators. S Afr Med J 2006;96(3):206-208. 4. Mayosi B, Robertson K, Volmink J, et al. The Drakensberg declaration on the control of rheumatic fever and rheumatic heart disease in Africa. S Afr Med J 2006;96(3):246.

5. Robertson KA, Volmink JA, Mayosi BM. Towards a uniform plan for the control of rheumatic fever and rheumatic heart disease in Africa – the Awareness Surveillance Advocacy Prevention (A.S.A.P.) Programme. S Afr Med J 2006;96(3):241-245. 6. Mayosi BM, Gamra H, Dangou J-M, Kasonde J. Rheumatic heart disease in Africa: The Mosi-o-Tunya call to action. Lancet Glob Health 2014;2(8):e438-e439. DOI:10.1016/S2214109X(14)70234-7 7. Sliwa K, Carrington M, Mayosi BM, Zigiriadis E, Mvungi R, Stewart S. Incidence and characteristics of newly diagnosed rheumatic heart disease in urban African adults: Insights from the Heart of Soweto Study. Eur Heart J 2010;31(6):719-727. DOI:10.1093/eurheartj/ehp530 8. Zühlke LJ, Engel ME, Watkins D, Mayosi BM. Incidence, prevalence and outcome of rheumatic heart disease in South Africa: A systematic review of contemporary studies. Int J Cardiol 2015;199:375-383. DOI:10.1016/j.ijcard.2015.06.145 9. Mayosi BM, Benatar SR. Health and health care in South Africa – 20 years after Mandela. N Engl J Med 2014;371(14):1344-1353. DOI:10.1056/NEJMsr1405012 10. Shung King M, Engel ME, Zuhlke L, Mayosi BM. Asymptomatic rheumatic heart disease in South African schoolchildren: Implications for addressing chronic health conditions through a school health service. S Afr Med J 2016;106(8):761-762. DOI:10.7196/SAMJ.2016. v106i8.10756 11. Madeira G, Mocumbi AO, Mayosi BM. Advice to health professionals: Use of lignocaine as a diluent to reduce the pain associated with the administration of benzathine penicillin G. S Afr Med J 2016;106(8):742. DOI:10.7196/SAMJ.2016.v106i8.10864 12. Engel ME, Haileamlak A, Zühlke L, et al. Prevalence of rheumatic heart disease in 4720 asymptomatic scholars from South Africa and Ethiopia. Heart 2015;101(17):1389-1394. DOI:10.1136/ heartjnl-2015-307444 13. Zuhlke L, Engel M, Lemmer C, et al. The natural history of latent rheumatic heart disease in a 5 year follow-up study: A prospective observational study. BMC Cardiovasc Disord 2016;16(1):46. DOI:10.1186/s12872-016-0225-3 14. Zühlke L, Mayosi BM. Echocardiographic screening for subclinical rheumatic heart disease remains a research tool pending studies of impact on prognosis. Curr Cardiol Rep 2013;15(3):343. DOI:10.1007/ s11886-012-0343-1 15. Duncan NA, Kronenberger WG, Hampton KC, et al. A validated measure of adherence to antibiotic prophylaxis in children with sickle cell disease. Patient Prefer Adherence 2016;10:983-992. DOI:10.2147/PPA.S103874 16. Owen EP, Leisegang F, Whitelaw A, et al. Complement component C5 and C6 mutation screening indicated in meningococcal disease in South Africa. S Afr Med J 2012;102(6):525-527. 17. Zühlke L, Engel ME, Karthikeyan G, et al. Characteristics, complications, and gaps in evidence-based interventions in rheumatic heart disease: The Global Rheumatic Heart Disease Registry (the REMEDY study). Eur Heart J 2015;36(18):1115-1122. DOI:10.1093/eurheartj/ehu449 18. Watkins D, Zuhlke L, Engel M, et al. Seven key actions to eradicate rheumatic heart disease in Africa: The Addis Ababa Communiqué. Cardiovasc J Afr 2016;27(3):184-187. DOI:10.5830/CVJA-2015-090 19. World Health Organization. Global Action Plan for the Control and Prevention of Noncommunicable Disease 2013-2020. Geneva: WHO, 2013. 20. South African National Department of Health. National Guidelines on the Primary Prevention and Prophylaxis of Rheumatic Fever and Rheumatic Heart Disease for Health Professionals at Primary Level. Pretoria: NDoH, 1997. 21. Van Dam J, Musuku J, Zuhlke LJ, et al. An open-access, mobile compatible, electronic patient register for rheumatic heart disease (‘eRegister’) based on the World Heart Federation’s framework for patient registers. Cardiovasc J Afr 2015;26(6):227-233. DOI:10.5830/CVJA-2015-058

S Afr Med J 2016;106(8):740-741. DOI:10.7196/SAMJ.2016.v106i8.10561

August 2016, Print edition

EDITOR’S CHOICE

CME: Functional neurosurgery

This month’s CME covers part 1 of the topic functional neuro surgery. This is a subdivision of neurosurgery that does not always get the recognition it deserves among general medical practitioners. It is definitely the less ‘sexy’ part of neurosurgery when compared with vascular and skull base neurosurgery, but it is still an important and highly specialised part of the field. At present only one academic unit and about five private sector units perform functional neurosurgical procedures on a regular basis in South Africa (SA). This unfortunately means that many patients and their medical caregivers do not know about the options available to them right here on their doorstep. Patients do not need to leave the country and search for help overseas. Functional neurosurgery consists of four subcategories: epilepsy surgery, spasticity surgery, pain surgery, and surgery for movement disorders. The surgical techniques used are often very specialised and not part of the armamentarium of the general neurosurgeon. It will be clear from this month’s CME, which covers the first two of four articles dedicated to functional neurosurgery topics, that the mere presence of epilepsy or spasticity is not the trigger for surgery. It is only if a patient’s epilepsy is refractory to medical care reviewed by a competent epileptologist that we should consider surgery for epilepsy. Spasticity is often protective and even useful to a patient. But once it leads to pain and deformities and hinders the patient’s function, surgical management becomes an option. Careful discussion with the patient and the family is crucial.

Rheumatic heart disease and the school health service

When new evidence comes to light, it compels us to contemplate the implications of such evidence for health policy and practice. This ‘In Practice’ article[1] examines recent research evidence on the prevalence of asymptomatic rheumatic heart disease (RHD) in SA and considers the implications for the Integrated School Health Programme (ISHP). RHD is still a major burden of disease in developing countries, and elimination of this preventable condition ranks high among the World Heart Federation goals. If left untreated, it becomes a chronic health condition that children have to cope with into their adult lives. The ISHP regards the health needs of children with chronic health conditions, such as RHD, as a key service component. But is the implementation of this chronic health component up to the task? Importantly, the study found a prevalence of RHD of 27 per 1 000 in Langa, Cape Town, compared with 12.5 per 1 000 in Bonteheuwel – arguably close to Langa geographically, but clearly not sociologically. No rural studies are available for comparison from SA, but one from rural Ethiopia gives a prevalence of 30.5 per 1 000, which suggests that a higher prevalence would be expected in rural SA. The current study asked whether some children might have left school as a result of symptoms related to RHD, which would be picked up only through a community-based study, and the extent to which asymptomatic children who remain undiagnosed continue into adulthood with good health and no impact on their schooling. The study team also recognised the controversies that exist around screening for asymptomatic RHD and its prognostic impact. The study convincingly showed that the detection of asymptomatic disease requires an effective, easy-to-administer screening process and tools, with high sensitivity and specificity, in order to appropriately identify children with the condition. Does the availability of such a screening process for RHD merit its automatic inclusion into the mass screening programme of the ISHP? For RHD, improvement in socioeconomic circumstances is core to its eradication. Beyond this, strong and effective primary healthcare services where all children who

require antibiotic treatment for suspected streptococcal sore throat, coupled with appropriate follow-up and secondary prevention, are essential. A well-functioning ISHP has a crucial health-promotion and ongoing monitoring and support role. Simply raising awareness among educators and parents of the need to treat sore throats is an important initial intervention that could lead to greater vigilance and better care of children.

A lifestyle approach to metabolic syndrome and type 2 diabetes

Lifestyle interventions can treat metabolic syndrome and prevent type 2 diabetes mellitus, but they remain under-utilised in routine practice. In 2010, a lifestyle intervention model was created in a rural primary care practice and spread with few resources to four other rural practices.[2] A retrospective chart review evaluated changes in health indicators in two practice environments by following 372 participants; predominantly women, with a mean age of 52 years. At baseline, participants had a body mass index of 37 kg/m2 and lost an average of 12% of their initial body weight from the intervention. Among participants at the first site for which data were available, the prevalence of metabolic syndrome decreased from 58% at baseline to 19% at follow-up. Taken together, this experience suggests that lifestyle interventions are feasible and deliver meaningful results in routine primary care practice.

Male attitudes to female genital mutilation in Nigeria

Men are central to female reproductive health and so are an impor tant group in the fight to eradicate this barbaric and dangerous custom. This article[3] looks at attitudes among male secondary school students aged 14 - 19 years in Ilorin, Nigeria, where female genital mutilation (FGM) is still practised (it was recently made illegal in Nigeria). Most information on the practice came from parents, and of the students 33.5% supported FGM and 27.3% thought it was beneficial to the woman. However, 34.6% were opposed to the practice, and 76.4% would not circumcise a future daughter. Significant predictors of opposition to FGM were seeing a woman who had been subjected to the mutilation, thinking about future daughters, and awareness of government policy on FGM – which is opposed to the practice.

The transition of adolescents into adult HIV care

The first generation of SA children perinatally infected with HIV is entering adulthood, and there is a now a pressing need for systematised transfer of these patients from paediatric to adult care. This study[4] is the first to describe the perspectives of healthcare providers overseeing the transition in resource-limited settings, using government paediatric HIV clinics and hospitals in the Western Cape. A major barrier to the transition identified was the healthcare provider’s difficulty in letting go of their relationships with adolescent patients, as was a lack of structure and effective communication between the paediatric and adult providers. Adolescent support groups were identified as an important approach in adult HIV clinics, as was a later transition age. BF 1. Shung King M, Zühlke L, Engel ME, Mayosi BM. Asymptomatic rheumatic heart disease in South African schoolchildren: Implications for addressing chronic health conditions through a school health service. S Afr Med J 2016;106(8):761-762. DOI:10.7196/SAMJ.2016.v106i8.10756 2. Mark S, du Toit S, Noakes TD, et al. A successful lifestyle intervention model replicated in diverse clinical settings. S Afr Med J 2016;106(8):763-766. DOI:10.7196/SAMJ.2016.v106i8.10136 3. Adeniran AS, Ijaiya MA, Fawole AA, et al. Attitudes to female genital mutilation/cutting among male adolescents in Ilorin, Nigeria. S Afr Med J 2016;106(8):822-823. DOI:10.7196/SAMJ.2016. v106i8.10124 4. Kung TH, Wallace ML, Snyder KL, et al. South African healthcare provider perspectives on transitioning adolescents into adult HIV care. S Afr Med J 2016;106(8):804-808. DOI:10.7196/ SAMJ.2016.v106i8.10496

August 2016, Print edition

CORRESPONDENCE

Advice to health professionals: Use of lignocaine as a diluent to reduce the pain associated with the administration of benzathine penicillin G

To the Editor: Rheumatic heart disease (RHD) is a consequence of untreated group A beta-haemolytic streptococcal pharyngitis in a susceptible individual who is likely to live under social conditions of poverty.[1] There are over 30 million people with the disease, which is associated with over 300 000 deaths per year worldwide. [2] In Mozambique and South Africa, RHD is estimated to affect 20 - 30/1 000 asymptomatic schoolchildren.[3,4] Intramuscular peni cillin is more effective than oral penicillin in the secondary prevention of acute rheumatic fever (ARF), and is highly effective for the primary prevention of ARF in children and young adults with pharyngitis.[5,6] Intramuscular benzathine penicillin G (BPG) is therefore a first-line drug for primary and secondary prevention of ARF and RHD.[5,7] Pain is one of the major problems when intramuscular BPG is given. With this comes fear of the next injection, which is one of the barriers to the primary and secondary prophylaxis of ARF.[8] There is therefore a need to identify effective methods to reduce the pain associated with BPG injection, and to increase adherence to primary and secondary prevention measures for ARF. One of these measures is to use lignocaine (lidocaine) as a diluent of BPG for intramuscular injection. Lignocaine hydrochloride is a local anaesthetic agent which, if added to BPG, reduces the pain of injection and in the first 24 hours after injection, while not significantly affecting serum penicillin concentrations.[7,9] Its effectiveness can be increased by using a vibrating device with a cold pack.[10] A randomised double-blind, crossover trial was carried out in 18 children aged 11 - 19 years who required prophylactic treatment for rheumatic fever.[9] The children were randomly divided into two groups: one received an injection of BPG diluted with 3.2 mL of sterile water, followed 1 month later by an injection of BPG diluted in lignocaine hydrochloride 1%, and the second group received the same regimen in the reverse order. Serum penicillin concentrations and subjective pain sensation were determined after each injection. Peak serum penicillin concentrations at 24 hours after injection were similar for both preparations, as were the other serum values measured throughout the month. The pain score immediately after the injection was significantly lower with the lignocaine than with the sterile water dilution. The data support our recommendation for the use of lignocaine hydrochloride 1% as a diluent for BPG.[7,11] We call upon all health professionals who administer intramuscular BPG on a regular basis to seriously consider using 1% lignocaine hydrochloride as a diluent instead of sterile water in order to mini mise the pain of injection and help to improve adherence to the regimen for secondary prevention of a chronic disease like RHD.

S Afr Med J 2016;106(7):742. DOI:10.7196/SAMJ.2016.v106i7.10864

Haemotoxic snakebite in rural KwaZulu-Natal, South Africa

To the Editor: We would like to comment on the case report published in the May 2016 issue of SAMJ[1] of a suspected boomslang bite presenting with severe haematemesis. We question the diagnosis of a boomslang bite. Firstly, the clinical manifestations as described do not correlate with a boomslang bite. Boomslang bite results in severe consumptive coagulopathy with bleeding from multiple sites and would not be confined to a single organ system as described in the case report. Haemorrhagic gastritis and ulcers also do not fit the clinical picture. These findings may be better explained by chronic heavy alcohol consumption. Secondly, the normal international normalised ratio (INR) does not correlate with a coagulopathy. Furthermore, it should be emphasised that the polyvalent antivenom is not effective in the management of boomslang bite. We recommend the easy-to-perform bedside whole-blood clotting time investigation to diagnose boomslang bite in resource-limited areas.[2] Place 5 mL of whole blood in a clean (preferably new) dry test tube at room temperature. At 20 minutes, tip the tube upside down once. If no clot is seen, the test is positive, indicating abnormal coagulation. If any clot (even very small) is observed, the test is negative. Alternatively, the syringe method can also be used. Draw 5 mL of whole blood in a plastic syringe. Leave the syringe untouched on a flat surface and tilt after 20 minutes to observe whether or not the blood has clotted. The bedside wholeblood clotting time could be repeated 4-hourly after a suspected bite, as the coagulopathy may develop late (12 - 36 hours after boomslang bite). E H Decloedt, G J Müller

Division of Clinical Pharmacology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa ericdecloedt@sun.ac.za 1. Wagener M. Haemotoxic snakebite in rural KwaZulu-Natal, South Africa: A case presenting with haematemesis. S Afr Med J 2016;106(5):459-460. DOI:10.7196/SAMJ.2016.v106i5.9124 2. Punguyire D, Iserson KV, Stolz U, Apanga S. Bedside whole-blood clotting times: Validity after snakebites. J Emerg Med 2013;44(3):663-667. DOI:10.1016/j.jemermed.2012.07.073

Geoffrey Madeira, Ana Olga Mocumbi

Chronic Non-communicable Disease Division, Instituto Nacional de Saúde, Ministério da Saúde, Maputo, Mozambique geogirassol@gmail.com

S Afr Med J 2016;106(8):743. DOI:10.7196/SAMJ.2016.v106i8.11119

Bongani M Mayosi

Department of Medicine, Groote Schuur Hospital and Faculty of Health Sciences, University of Cape Town, South Africa 1. Engel ME, Stander R, Vogel J, Adeyemo AA, Mayosi BM. Genetic susceptibility to acute rheumatic fever: A systematic review and meta-analysis of twin studies. PLoS One 2011;6(9):e25326. DOI:10.1371/journal.pone.0025326 2. Global Burden of Disease Study. Global, regional, and national age-sex specific all-cause and causespecific mortality for 240 causes of death, 1990-2013: A systematic analysis for the Global Burden of Disease Study 2013. Lancet 2015;385(9963):117-171. DOI:10.1016/S0140-6736(14)61682-2 3. Marijon E, Celermajer DS, Tafflet M, et al. Rheumatic heart disease screening by echocardiography: The inadequacy of World Health Organization criteria for optimizing the diagnosis of subclinical disease. Circulation 2009;120(8):663-668. DOI:10.1161/CIRCULATIONAHA.109.849190 4. Engel ME, Haileamlak A, Zühlke L, et al. Prevalence of rheumatic heart disease in 4720 asymptomatic scholars from South Africa and Ethiopia. Heart 2015;101(17):1389-1394. DOI:10.1136/heartjnl-2015-307444

5. Manyemba J, Mayosi BM. Intramuscular penicillin is more effective than oral penicillin in secondary prevention of rheumatic fever: A systematic review. S Afr Med J 2003;93(3):212-218. 6. Robertson KA, Volmink JA, Mayosi BM. Antibiotics for the primary prevention of acute rheumatic fever: A meta-analysis. BMC Cardiovasc Disord 2005;5(1):11. DOI:10.1186/1471-2261-5-11 7. RHD Australia (ARF/RHD writing group), National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand. Australian guideline for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease (2nd edition). 2012. https://www.rhdaustralia. org.au/node/950/attachment (accessed 7 June 2016). 8. Balbaa A, ElGuindy A, Pericak D, Yacoub M, Schwalm J. An evaluation of secondary prophylaxis for rheumatic heart disease in rural Egypt. Glob Cardiol Sci Pract 2015;2015(3):40. DOI:10.5339/gcsp.2015.40 9. Amir J, Ginat S, Cohen YH, et al. Lidocaine as a diluent for administration of benzathine penicillin G. Pediatr Infect Dis J 1998;17(10):890-893. DOI:10.1097/00006454-199810000-00008 10. Russell K, Nicholson R, Naidu R. Reducing the pain of intramuscular benzathine penicillin injections in the rheumatic fever population of Counties Manukau District Health Board. J Paediatr Child Health 2014;50(2):112-117. DOI:10.1111/jpc.12400 11. Zeydi AE, Khezri HD. Can lidocaine be safely used to reduce pain caused by intramuscular penicillin injections? A short literature review. Oman Med J 2012;27(4):337. DOI:10.5001/omj.2012.85

Umbilical hernia in children in a developing country: Does the season have an effect on the occurrence of strangulation?

To the Editor: Umbilical hernia in a child is considered benign in developed countries, as complications seldom occur.[1] In Africa, complications related to umbilical hernia, such as strangulation, are frequent.[2,3] Strangulation often occurs if the hernia has a diameter of 0.5 - 1.5 cm. The theory of a foreign body in the hernial sac

August 2016, Print edition

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CORRESPONDENCE

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Fig. 1. Number of cases of strangulated umbilical hernias during the dry and rainy seasons in Senegal.

was raised by Papagrigoriadis et al.[1] in London, and Brown et al.[4] in South Africa. However, the actual causes of strangulation are unknown. A retrospective study was conducted in the Unit of Paediatric Surgery, University Hospital Aristide Le Dantec, Dakar, Sene gal from 1 May 2006 to 30 April 2009. All patients <16 years of age with a strangulated umbilical hernia were included in the study. Children who presented with an incarcerated hernia were excluded. Incarcerated hernia is characterised by a painful episode, with a momentary irreducibility of the hernia that yields spontaneously. All patients underwent emergency surgery. The study comprised 35 of 305 patients with strangulated hernias operated on during the study period. There were 20 boys and 15 girls (ratio 1.3). The average age was 34 months (range 2 months 9 years). Sixty-five percent of children had rhinitis, asthma or pneumonia. There are two different seasons in Senegal: a dry season (from October to June) and a rainy season (from July to September). During the dry season, we noted 33 cases of strangulated umbilical hernias compared with two cases in the rainy season. Sixty percent of such hernias were seen in April, May and June (Fig. 1), i.e. almost exclusively during the dry season. Dry season in Senegal is marked by the presence of a cold, dry wind, the harmattan, which corresponds to the peak of strangulated hernias during these months. There are many factors, e.g. airborne allergens, which may lead to the onset of rhinitis, pneumonia or asthma. Patients with these respiratory conditions often develop a cough, which is responsible for increased abdominal pressure. The latter promotes visceral protrusion through the collar of the hernia, and causes discomfort. The loop continues to protrude and distend, and its increased volume makes it difficult and consequently impossible for reinsertion into

the abdominal cavity. This promotes strangulation.[5] We conclude that the dry wind in Senegal, which causes a variety of respiratory conditions, is associated with strangulation of umbilical hernias. G Ngom, F Gassama, A S Mohamed, O Ndour

Unit of Paediatric Surgery, University Hospital Aristide Le Dantec, Dakar, Senegal gngom2004@yahoo.fr

1. Papagrigoriadis S, Browse DJ, Howard ER. Incarceration of umbilical hernias in children: A rare but important complication. Pediatr Surg Int 1998;14(3):231-232. DOI:10.1007/ s003830050711 2. Ngom G. Umbilical hernia in African children: Same attitude than that of inguinal hernia. J Indian Assoc Pediatr Surg 2006;11(4):255. DOI:10.4103/0971-9261.29615 3. Chirdan LB, Uba AF, Kidmas AT. Incarcerated umbilical hernia in children. Eur J Pediatr Surg 2006;16(1):45-48. DOI:10.1055/s-2006-923792 4. Brown RA, Numanoglu A, Rode H. Complicated umbilical hernia in childhood. S Afr J Surg 2006;44(4):136-137. 5. Flamant Y, Boudet MJ, Zeitoun G. Hernies et éventrations étranglées. Rev Prat 1993;43:716-721.

S Afr Med J 2016;106(8):744. DOI:10.7196/SAMJ.2016.v106i8.10947

Contribution of congenital disorders to under-5 mortality

To the Editor: The article ‘Where do children die and what are the causes?’, which appeared in the April 2016 issue of the SAMJ,[1] provides an overview of the causes of death in under-5 children in the Metro West geographical service area of the Western Cape for 2011. It highlights the proportion of under-5 deaths from conge nital abnormalities (obvious structural abnormalities), which are particularly prevalent in early neonatal mortality − a close third (9.6%) of in-hospital deaths after hypoxia (10.0%) and immaturity (40.6%) according to the Perinatal Problem Identification Programme (PPIP) data.[1] In the Local Mortality Surveillance System in-hospital

August 2016, Print edition

data, congenital abnormalities are ranked as the second (13.5%) cause of early neonatal death after prematurity (35.8%).[1] Although already prominent as a cause of death, congenital disorders (CDs) may collectively contribute to a greater proportion of child deaths than reported. In the study, congenital abnormalities relate to chapter XVII: Congenital malformations, deformities and chromosomal abnormalities in the Inter national Classification of Diseases (ICD-10) and are aggregated to the Burden of Disease list of causes.[1-3] Limited to developmental structural abnormalities only, this excludes a significant portion of CDs found elsewhere in the ICD-10 system (e.g. congenital syphilis A50; haemophilia D66 - 68; oculocutaneous albinism E70.310).[3] This ICD- 10 coding fragmentation has exacerbated global con fusion around terminology related to CDs.[4] In 2006, international agreement was reached on the synonymous use of the terms CDs and birth defects, defined as abnormalities of structure or function, including metabolism, present from birth and manifesting at birth or later in life.[5] However, use of inequiva lent terms, such as congenital abnormality, continues. Consequently, data for subsets of CDs are often interpreted as the totality of CDs when it is not the case. If singlegene disorders, accounting for 30.0% of CDs (B Modell − personal communication, 2016), were pooled with congenital abnormalities in the study by Reid et al.,[1] a greater proportion of under-5 deaths may be attributed to CDs. CDs are also significantly underestimated, as many remain undiagnosed or are misdiagnosed, with the incorrect cause of death due to the lack of trained clinicians,[6-8] as acknowledged by the Child Healthcare Problem Identification Programme.[4,9] Undiag nosed CDs may be the underlying cause of death in a number of cases assigned to other causes (including ‘ill-defined’) or comorbidity in the study, as infants born with CDs, such as congenital heart defects, may be more susceptible to infection. Honein et al.[10] reported that CDs are more than five times as likely to occur among very preterm infants (24 - 31 weeks) compared with term infants (37 - 41 weeks), resulting in 16.0% of preterm infants having a CD. A significant portion of deaths assigned to ‘prematurity’ in early neonatal deaths in the study may therefore be undiagnosed CDs, which are predisposed to preterm birth. The relative frequency of CDs should be noted and investigated in light of the above mentioned factors contributing to their under reporting, particularly as the majority of CD-related deaths occur during the first 5 years of life. As the proportion of deaths from CDs increases along with

CORRESPONDENCE

epidemiological transition − seen in the dramatic decrease in HIV- related deaths − the challenge of CDs will continue. [11] Possible areas for further study include comparison with other provincial populations, analyses of preventable CDs (e.g. fetal alcohol spec trum disorder) and prenatal diagnosis of serious CDs. H L Malherbe, C Aldous

School of Clinical Medicine, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa helen@hmconsult.co.za

A L Christianson

Wits Centre for Ethics (WiCE), Faculty of Humanities, University of the Witwatersrand, Johannesburg, South Africa

D Woods

Division of Neonatal Medicine, School of Child and Adolescent Health, Faculty of Health Sciences, University of Cape Town, South Africa 1. Reid AE, Hendricks MK, Groenewald P, Bradshaw D. Where do children die and what are the causes? Under-5 deaths in the Metro West geographical service area of the Western Cape, South Africa, 2011. S Afr Med J 2016;106(4):359-364. DOI:10.7196/SAMJ.2016.v106i4.10521

2. Pillay-Van Wyk V, Laubscher R, Msemburi W, et al. Second South African National Burden of Disease Study: Data Cleaning, Validation and South African National Burden of Disease List. Cape Town: Burden of Disease Research Unit, South African Medical Research Council, 2014:1-51. 3. World Health Organization. International Statistical Classification of Diseases and Related Health Problems. 10th revision. Geneva: WHO, 1992. http://apps.who.int/classifications/icd10/browse/2015/en (accessed 1 June 2016). 4. Malherbe H, Aldous C, Woods D, Christianson A. The contribution of congenital disorders to child mortality in South Africa. In: Padarath A, King J, Mackie E, Casciola J, eds. South African Health Review. Durban: Health Systems Trust, 2016:137-152. 5. World Health Organization. Management of Birth Defects and Haemoglobin Disorders. Report of a Joint WHO/March of Dimes Meeting. Geneva, Switzerland, 17 - 19 May 2006. Geneva: WHO, 2006:1-27. 6. World Health Organization. Prevention and Management of Genetic Disorders and Birth Defects in Developing Countries. Report of a joint WHO/WAOPBD meeting, The Hague, 5 - 7 January 1999. Geneva: WHO, 1999. http://www.who.int/genomics/publications/reports/en/ (accessed 27 February 2016). 7. Christianson A, Modell B. Medical genetics in developing countries. Ann Rev Genomics Hum Genet 2004;5:219-265. DOI:10.1146/annurev.genom.5.061903.175935 8. Christianson A, Howson CP, Modell B. March of Dimes: Global Report on Birth Defects, the Hidden Toll of Dying and Disabled Children. White Plains: March of Dimes, 2006. 9. Patrick ME, Stephen CR. Saving children: 2005. A survey of child healthcare in South Africa. Child Healthcare Problem Identification Programme and Medical Research Council, 2005. http://www. childpip.org.za/documents/report_saving_children_2005.pdf (accessed 23 March 2016). 10. Honein MA, Kirby RS, Meyer RE, et al. The association between major birth defects and preterm birth. Matern Child Health J 2009;13(2):164-175. DOI:10.1007/s10995-008-0348-y 11. Malherbe H, Christianson A, Aldous C. Need for services for the care and prevention of congenital disorders in South Africa as the country’s epidemiological transition evolves. S Afr Med J 2015;105(3):186-188. DOI:10.7196/SAMJ.9136

S Afr Med J 2016;106(8):745. DOI:10.7196/SAMJ.2016.v106i8.11129

Erratum Targeting composite treatment of type 2 diabetes in middle-income countries

In the article entitled ‘Targeting composite treatment of type 2 diabetes in middle-income countries – walking a tightrope between hyperglycaemia and the dangers of hypoglycaemia’, which appeared in the January 2016 SAMJ (106(1):57-61), J Wing’s qualifications on the title page should have read MB BCh, FCP (SA). The online version of the article (http://dx.doi.org/10.7196/SAMJ.2016.v106i1.10284) was corrected on 15 June 2016. S Afr Med J 2016;106(8):829. DOI:10.7196/SAMJ.2016.v106i8.11183

Conﬁdence Through Clinical and Real World Experience1-3 #1 NOAC prescribed by Cardiologists* Millions of Patients Treated Across Multiple Indications4 References: 1. Patel M.R., Mahaffey K.W., Garg J. et al. Rivaroxaban versus warfarin in non-valvular atrial fibrillation. N Engl J Med. 2011;365(10):883–91. 2. Tamayo S., Peacock W.F., Patel M.R., et al. Characterizing major bleeding in patients with nonvalvular atrial fibrillation: A pharmacovigilance study of 27 467 patients taking rivaroxaban. Clin Cardiol. 2015;38(2):63–8. 3. Camm A.J., Amarenco P., Haas S. et al. XANTUS: A Real-World, Prospective, Observational Study. 4. Calculation based on IMS Health MIDAS, Database: Monthly Sales December 2015. For full prescribing information, refer to the package insert approved by the Medicines Regulatory Authority (MCC). S4 XARELTO ® 10 (Film-coated tablets). Reg. No.: 42/8.2/1046. Each film-coated tablet contains rivaroxaban 10 mg. PHARMACOLOGICAL CLASSIFICATION: A.8.2 Anticoagulants. INDICATION: Prevention of venous thromboembolism (VTE) in patients undergoing major orthopaedic surgery of the lower limbs. S4 XARELTO ® 15 and XARELTO ® 20 (Film-coated tablets). Reg. No.: XARELTO ® 15: 46/8.2/0111; XARELTO ® 20: 46/8.2/0112. Each film-coated tablet contains rivaroxaban 15 mg (XARELTO ® 15) or 20 mg (XARELTO ® 20). PHARMACOLOGICAL CLASSIFICATION: A.8.2 Anticoagulants. INDICATIONS: (1) Prevention of stroke and systemic embolism in patients with non-valvular atrial fibrillation (SPAF); (2) Treatment of deep vein thrombosis (DVT) and for the prevention of recurrent deep vein thrombosis (DVT) and pulmonary embolism (PE); (3) Treatment of pulmonary embolism (PE) and for the prevention of recurrent pulmonary embolism (PE) and deep vein thrombosis (DVT). HCR: Bayer (Pty) Ltd, Reg. No.: 1968/011192/07, 27 Wrench Road, Isando, 1609. Tel: 011 921 5044 Fax: 011 921 5041. L.ZA.MKT.GM.01.2016.1265 *Impact RX Data Oct - Dec 2015 NOAC: Non Vitamin K Oral Anticoagulant

August 2016, Print edition

IZINDABA

Emergency medical service workers struggle in violent election climate Two of South Africa’s leading emerg ency medical service (EMS) chiefs and govern ment advisors last month backed the Gauteng Department of Health’s call to protesting communities to allow emer gency rescuers into volatile environments to save lives and treat injured people. Mr Raveen Naidoo, National Director of EMS and Disaster Management, and Prof. Lee Wallis, also a senior government disaster/ EMS advisor (and EMS chief in the Western Cape), said that their staff were frequently endangered and ambulances or other rescue vehicles hijacked or damaged during civil unrest such as protests over lack of service delivery. Their appeal came in mid-June as civic protests, many of them related to the upcoming municipal elections, erupted in Pretoria, East London, Port Elizabeth and Bronkhorstpruit with civilian killings, buses burnt, major roads barricaded and civilian vehicles stoned. While neither EMS advisor had any reports of staff injuries at the time, both said that in some provinces the hijacking of ambulances was more frequent, with denial of access to township areas widespread. Wallis said that the hijacking of rescue vehicles and ambulances, in order to strip them for vehicle parts, and protestors blocking emergency crews were common and ‘bother us on a weekly basis’. This ‘stressed out’ their crews and affected service delivery. In late May, in KwaZakhele township, Port Elizabeth, protests turned violent when residents learnt that their party list candidates had not made the cut, while widespread protests over taxi operating permits a fortnight later blocked major roads around all major Eastern Cape metropolitan areas, with dozens of people arrested and injured and vehicles damaged and/or burnt. On 14 June at Zithobenia township near Bronkhorstspruit, some 45 km from Pretoria, EMS staff were blocked from reaching a diabetic patient during protests over alleged election list nominations. Also, a resident with a rubber bullet wound could not be helped immediately. Roads in and around Pretoria were blocked, causing traffic mayhem. Neither patient outcome is known to Izindaba. Gauteng MEC for Health Qedani Mah langu urged members of the public not to attack and block EMS staff from access

ing and exiting from communities or locations during protests. This not only endangered the lives of EMS personnel but also deprived members of the community of critical services. She added: ‘At all times there is a need to minimise loss of lives and prevent long-term complications due to emergency care being delayed unnecessarily.’ She implored members of the community to allow staff to do their work without hindrance. With much of the civic hostility directed at ‘imposed’ candidates for the up com ing August municipal elections, the Inde pendent Electoral Commission (IEC) expressed grave concern at the rising levels of violence and intimidation character ising political and campaign activities. It said that incidents of what appeared to be politically motivated murders, assaults and other forms of intimidation of candidates were reported across a number of provinces, including Gauteng, KwaZuluNatal, Mpumalanga and North West, over the last weeks of June. Condemning the violence, intimidation, destruction of property and intolerance, the IEC said they had no place in a country with a constitution based on respect for human rights, the rule of law and democracy. That some of the acts were carried out under the guise of ‘defending democratic processes’ was ‘all the more shameful and incongruent with our democracy’, it added, calling on political leaders and candidates to speak out strongly against any conduct that undermined conditions conducive to free and fair elections. It singled out the involvement of party members and supporters in such actions, saying that political leaders were ‘ultimately responsible’. Naidoo said that EMS staff country wide had guidelines on how to manage situations during endemic civil strife. To reduce loss of life and mitigate health complications, they trained community members in first aid, liaised with community leaders and police and set up perimeter pick-up points. They also had standing instructions to withdraw from volatile environments if there were any signs of danger. ‘Going in is an informed decision based on the stability of the situation and police presence. Quick response by the community and timely

August 2016, Print edition

Prof. Lee Wallis, head of EMS in the Western Cape.

response and treatment by EMS are critical factors that influence patient outcomes,’ added Naidoo. He said that staff sometimes entered highly volatile areas without SAPS escorts. EMS management had also engaged with ward councillors and the communities in an attempt to address the unfortunate spate of attacks on EMS personnel. ‘We want them to take ownership of these ambulances, as they serve the very communities that will be adversely affected by the delay in response times to calls in the affected areas,’ he said. The Eastern Cape EMS went as far as notifying all radio stations and local newspapers of the incidents in order to raise awareness, and appealed for help from all stakeholders in protecting EMS personnel. All staff who been subjected to ‘these heinous crimes’ had been debriefed through the Employee Assistance Prog ramme, he added. Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(8):746. DOI:10.7196/SAMJ.2016.v106i8.11227

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IZINDABA

Médecins Sans Frontières moves to protect refugee healthcare As Médecins Sans Frontières (MSF) spurned all European Union (EU) fund ing for its projects worldwide after a series of cynical EU-country moves to choke inward refugee flow, South African (SA) activists in Johannesburg this June protested the proposed stiffening of local refugee laws. The People’s Coalition Against Xeno phobia, consisting of MSF, the Africa Dias pora Forum, Lawyers for Human Rights, Section 27 and a host of other related NGOs, intervened in various xenophobic crises that erupted across the country in 2008 and 2015, providing emergency healthcare and successfully improving healthcare access. Explaining the Coalition’s 18 June protest, Dr Borrie le Grange, MSF’s SA communications chief, said that the proposed Refugees Act Amendment Bill wanted to move refugee centres closer to the country’s borders and reduce the time they had to apply for refugee status by nearly two-thirds (14 days to 5 days) from when they entered the country. Asylum applications would be based on a refugee’s ability to sustain him- or herself and any dependants with the help of family or friends for at least 4 months, while limiting or prohibiting him or her from working. This rolled back the rights of refugees, who MSF

April 22, 2015 – fugitives of xenophobia. Malawians line up to catch buses home from displacement camps around Durban. Source: MSF.

had learnt from working with them at the Central Methodist Church in Johannesburg (2008 - 2013) were reluctant to seek official healthcare, with provincial healthcare staff demanding ‘green ID books’ before treating anyone. ‘They’ve often been attacked or raped in getting here and finding food, shelter and employment take precedence over medical care,’ he explained. MSF, through its primary healthcare interventions and accompanied referrals, had compelled health authorities in Johannesburg to change

staff attitudes and care to comply with basic human rights. SA has 1 096 063 pending cases of asy lum seekers, an increase from the 463 900 reported previously by government, says the United Nations Commission for Refugees. Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(8):747. DOI:10.7196/SAMJ.2016.v106i8.11229

Rape survivor care crisis – mines the worst? The dire need for better healthcare worker training in rape forensics and safe survivor care has never been better illustrated than by the horrifying rape statistics Médecins Sans Frontières (MSF) presented last month from the platinum-mining boom town of Rustenburg. Promising to increase its rape survivor care and forensic support beyond the 120 nurses it has just trained there, MSF revealed that a quarter of all women reported being raped during their lifetimes. Dr Sarah-Jane Steele, an epidemiologist who led the rape and intimate partner violence survey of 2 530 households (900 women) in November and December last year, was answering questions at an MSF Scientific Day held at the University of the Witwatersrand on 9 June. She said that one of the MSF recomm endations following the probe into sexual

violence (with its implications for service provision and prevention in Rustenburg) was that the low healthcare worker awareness on how to handle rape survivors be ‘urgently quantified’. Her main concern, however, was the low reporting of patients to relevant support structures. Steele was asked what the levels of rape survivor referral and linkage were outside of the relatively few local Thutuzela and Rape Crisis-staffed healthcare facilities. A fuller MSF analysis would be available this August, but the 120 nurses they trained would be assessed for knowledge gain, while more training was planned. ‘We want to get away from just one-day training to building around forensics and survivor care,’ she added. Not only had 25% of all woman surveyed been raped: if this was generalised to the 247 780 women living in the entire Rusten burg municipality, it would mean that 48 217

August 2016, Print edition

women were raped (including forced sexual acts). The specific survey found 28% of women were raped by their sexual partner – with a fifth of them telling nobody about it until her team came along. Steele said that these represented some of the highest estimates for both partner and non-partner sexual violence in sub-Saharan Africa. A full 75% of survivors had been forced to have sex, while the rest of the victims felt scared or degraded, but were not forced. Tragically few women and girls knew what their treatment options were, and only 50% knew that HIV infection could be prevented. The findings have led to the study being described as a potential ‘canary in a coalmine’ given the lack of similar studies in migrantworker mining towns elsewhere, pointing to a dire need for training of healthcare workers in prevention and treatment in similar settings.

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The average age of the women surveyed was 32 years, and the antenatal HIV prevalence was 35%. Rustenburg has a predominantly migrant labour force and is uniquely male in South African mining town terms (65% male), women usually outnumbering men. The municipal population, currently estimated at

550 000, grew by 80% between 1996 and 2011. A total of 11 113 women per year were raped by a partner, the survey found. Steele said that for the purposes of the survey, rape was defined in World Health Organization terms, i.e. forced to have sexual intercourse or perform unwanted sexual act/s with a nonpartner, prior sexual partner or current part-

ner. ‘Current’ was defined as in the previous 12 months and ‘prior’ as prior to that period. Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(8):748. DOI:10.7196/SAMJ.2016.v106i8.11231

HIV treatment under control – now for sexy prevention? The South African (SA) government launched a ZAR2 billion HIV prevention and young women empowerment pro gramme, the biggest this country has ever seen, at the Pietermaritzburg Showgrounds on 24 June – and healthcare workers may soon start selling sexual pleasure as a prevention tool. The multisector, 3-year overseas-funded campaign, to be supple mented by an as-yet-undisclosed Treasury amount, also aims to reduce teenage pregnancies and gender-based violence, keep girls in school, and create economic opportunities. Speaking to Izindaba before the launch, Dr Fareed Abdullah, CEO of the South African National AIDS Council, embraced

the ‘pleasure principle’ as part of a multi pronged strategy to promote the poorly used female condom. Knowledge of Femidoms among 15-year-old girls is measured at 78%, but use at just 7%. ‘It’s a great way to think about it because it’s the most effective women-controlled HIV prevention method. We’d like to increase its attractiveness to both sexes,’ he added. Asked why the strategy was being considered so belatedly, he responded: ‘In all honesty, we haven’t embraced it. We talk about HIV a lot, but not about sex and pleasure and how they drive new infections. I’m very open to those making the case and who have the expertise.’ SA increased the distribution of condoms from 353 million in 2013 to 723 million in

2015, and of Femidoms from 7.6 million in 2013 to 20.7 million last year. While the treatment push has reaped rich rewards, paradoxically contributing to an HIV preva lence hike (10 - 12% from 2008 to 2012, i.e. more people surviving), an increasing incidence, especially among younger women, is now the big worry. Studies estimate that 1 700 women between the ages of 18 and 24 years are being infected with HIV every week (latest incidence 2.8%). Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(8):749. DOI:10.7196/SAMJ.2016.v106i8.11232

OBITUARY

Devanandan Chetty (1935 - 2015)

Deva Chetty’s life vividly brings to mind the effects of apartheid and discrimination that

he suffered, namely restriction of bursary funds, a separate graduation ceremony, salary discrepancies, and being appointed part-time head of an Indians-only hospital and not being allowed to examine white patients. Deva matriculated in 1952 at the age of 16 years with a first-class pass. Coming from a very poor background, he applied for a bursary to do medicine at the University of Natal medical school. He was told by the Dean of the medical school that prefer ence was given to black students regarding bursaries/loans, and that colonial Indians were given last preference. However, fortu nately he was offered a bursary of £40 by the late V K Pillay Trust, which covered the cost of fees and books. In his 3rd year of medicine he was offered and accepted a government loan, which he had to pay

August 2016, Print edition

back on qualifying as a doctor, on condition that he would never examine or treat white patients. Deva qualified as a doctor in 1959, but did not attend the graduation because whites and non-whites had separate ceremonies. He specialised in obstetrics and gynaecology at the University of Natal and passed the MRCOG exams in London in 1966. He then took up the post of consultant lecturer in the department, and many well-known obstetricians and gynaecologists passed through his hands. In 1968 there was a ‘go-slow strike’ because of salary discrepancies between white and non-white doctors. As a result, Deva resigned from government service with the intention of commencing private practice in Lorne Street, Durban, in 1969. He was told that he needed 3 months’ notice to

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The progestin in ZOELY TM , nomegestrol acetate, has an elimination half-life of 46 hours.1 REFERENCES: 1. ZoelyTM Package Insert, October 2014. 2. Mansour D, Verhoeven C, Sommer W, et al. Efficacy and tolerability of a monophasic combined oral contraceptive containing nomegestroll acetate and 17ß-oestradiol 1 in a 24/4 regimen, in comparison to an oral contraceptive containing ethinylestradiol and drospirenone in a 21/7 regimen. Eur J Contracept Reprod Health Care. 2011;16(6):430-443. 3. Duijkers IJM, Klipping C, Grob P, Korver T. Effects of a monophasic combined oral contraceptive containing nomegestrol onoph acetate and 17ß-oestradiol on ovarian function in comparison to a monophasic combined oral contraceptive containing drospirenone and ethinylestradiol. Eur J Contracept Reprod Health Care. 2010;15:314-325. 4. Data on file. 5. Schindler AE, Campagnoli C, Druckmann R, Huber J, Pasqualini JR, et al. (2008) Classification and pharmacology of progestins. Maturitas 61:171-180. 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WARNINGS AND SPECIAL PRECAUTIONS: If any of the conditions/risk factors mentioned below are present, the benefits of the use of ZOELYTM should be weighed against the possible risks for each individual woman and discussed with the woman before she decides to start using ZOELYTM. Circulatory Disorders: The use of any combined oral contraceptive (COC) carries an increased risk of venous thromboembolism (VTE) compared with no use. The excess risk of VTE is highest during the first year a woman ever uses a combined oral contraceptive. Thrombosis has also been reported to occur in the other blood vessels, e.g. hepatic, mesenteric, renal, cerebral or retinal veins and arteries, in COC users. The risk of venous thromboembolic events increases with: increasing age, a positive family history of thromboembolism, prolonged immobilisation, major surgery, any surgery to the legs, or major trauma, obesity (body mass index over 30 kg/m2), smoking. The risk of arterial thromboembolic complications or of a cerebrovascular accident increases with: increasing age, smoking, (with heavier smoking and increasing age the risk further increases, especially in women over 35 years of age), dyslipoproteinaemia, obesity (body mass index over 30 kg/m2), hypertension, migraine, valvular heart disease, atrial fibrillation, a positive family history of arterial thrombosis. An increase in frequency or severity of migraine during ZOELYTM use may be a reason for immediate discontinuation of ZOELYTM use. Tumours: The most important risk factor for cervical cancer is persistent human papilloma virus (HPV) infection. Long-term use of ethinylestradiol-containing COCs may contribute to this increased risk of cervical cancer. With the use of the higher-dosed COCs (50 μg ethinylestradiol) the risk of endometrial and ovarian cancer is reduced. Whether this also applies to ZOELYTM remains to be confirmed. A meta-analysis from 54 epidemiological studies reported that there is an increased relative risk (RR = 1,24) of having breast cancer diagnosed in women who are currently using oestrogen-containing COCs. Benign and even more rarely, malignant liver tumours have been reported in users of COCs such as ZOELYTM. In isolated cases, these tumours have led to life-threatening intra-abdominal haemorrhages. Other Conditions: Women with hypertriglyceridaemia, In women with hereditary angioedema, exogenous oestrogens contained in COCs may induce or exacerbate symptoms of angioedema, worsening of depression, Crohn’s disease and ulcerative colitis have been associated with COC use, chloasma may occur, especially in women with a history of chloasma gravidarum. Reduced efficacy: The efficacy of ZOELYTM may be reduced in the event of e.g. missed tablets, gastrointestinal disturbances during active tablet taking, or use of concomitant medication. 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SIDE EFFECTS: Possibly related undesirable effects that have been reported in users are: Very common (≥1/10): acne and abnormal withdrawal bleeding; Common (≥1/100 to <1/10): Decreased libido, depression/ depressed or altered mood, headache, migraine, nausea, metrorrhagia, menorrhagia, breast pain, pelvic pain and weight increase.

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leave, as he was a lecturer, and not 1 month’s notice. This condition would be waived if he accepted the post of part-time head of the Department of Obstetrics and Gynaecology at RK Khan Hospital, which had been built for the Indian community. He accepted this post, and served there until his retirement. Deva was admitted as FRCOG in 1982. In 2009 he was given an award in recognition of his pioneering dedication and ethical contri bution to the field of medicine by the Private Hospital Group (Joint Medical Holdings).

On his retirement at the age of 75 years, his contribution to obstetrics and gynaecology was acknowledged and felici tated by the Durban Obstetricians and Gynaecologists Society, in recognition of his honesty and integrity and the assistance he had given to colleagues over the years. We will always remember him, especially for his humility, modesty, compassion and ethical practice of medicine. Deva passed away peacefully on 28 Nov em ber 2015. Our sincere condolences go

to his family, especially his wife Mani, a retired radiographer, and his three children Theyagaraj, Krishnan and Kalesvaran. May his soul rest in peace, and memories of him live on. Siva Moodley Chairman, Durban Obstetricians and Gynaecologists Society, and Council Member, South African Society of Obstetricans and Gynaecologists siva@ispace.co.za

BOOK REVIEW Beyond the Stethoscope: Casebook of a Township Doctor By Neelan Govender. Durban, South Africa: Rebel Rabble, 2015. 308 pages. ISBN 978-0-620-45640-1

Notwithstanding its subtitle of ‘Caseb ook’, this delightful collection has nothing to do with clinical medicine per se. Rather, it is a collection of human-interest stories about individual patients and their families ten ded by a caring and involved general practitioner during a career spanning over 50 years. The author, Neelan Govender, fondly known as PN among his medical colleagues, is a longstanding activist in medical and liberat ion politics. PN is well known for his participation and leadership in various medical societies, including the South African Medical Association. His medical practice is located in an apartheid-designated ‘Indian’ township, the residents of which are descendants of the indentured labourers brought in from India in 1860 and the following years to work in the sugarcane plantations of what was then the Natal Colony. Restricted to legally segregated townships, these working-class communities have retained many of the religious and cultural ways of life of the old country. This book provides a fascinating peek into the daily vicissitudes of the lives of their people – family intrigues, religious

August 2016, Print edition

rituals, superstition, love and marriage, the challenges of Western assimilation, and even murder. As a township GP who regularly made house calls and was routinely relied upon for counsel, PN inevitably became em broiled in numerous, often humorous but sometimes quite dramatic, life events of his patients. The stories unfold in flowing prose, with the occasional Victorian English turn of phrase. When was the last time you packed a portmanteau? The KwaZulu-Natal reader will also be delighted by the typical Durban Indian-English vernacular from the patients’ mouths, and the roundabout manner of providing a history. The reader will learn Hindi-derived words in the local vernacular: charro (Indian), witou (white man), aka (sister). All in all, the book is a marvellous read and a worthy archive of the kind of community general medical practice that is fast becoming extinct. Daniel J Ncayiyana Editor Emeritus, SAMJ profdjn@gmail.com

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CME

GUEST EDITORIAL

Functional neurosurgery It is a great honour to write the editorial for this month’s CME component of the SAMJ. Functional neurosurgery is a subdivision of neurosurgery that does not always receive the recognition we feel that it deserves among general medical practitioners. It is definitely the less ‘sexy’ component of neurosurgery compared with vascular and skull base neurosurgery, but it is an important and highly specialised part of our field. There are currently only one academic unit and about five private sector units that perform functional neurosurgery procedures on a regular basis in South Africa. This, unfortunately, leads to many patients and their medical caregivers not knowing about the options available to them on their doorstep. Patients do not need to leave the country to search for help in other countries. Functional neurosurgery consists of four subcategories: epilepsy surgery, spasticity surgery, pain surgery and surgery for movement disorders. The surgical techniques used are often very specialised and not part of the armamentarium of the general neurosurgeon. The specialised equipment used in the evaluation of the patient before and during surgery is very expensive. This equates to functional neurosurgery being performed in centres of excellence worldwide, where expertise and funding are clustered together, thereby ensuring the most reliable and safest outcomes in patients who are affected by functional neurosurgical problems. Surgery for epilepsy, pain, spasticity and movement disorders is definitely not something an isolated neurosurgeon should be performing. The functional neurosurgical unit consists of neurologists with an interest in these conditions, a developmental paediatrician, a neuropsychologist, social workers, neurophysiologists and, often, a psychiatrist. A multi disciplinary approach to decision-making and therapy is crucial. Surgery has high associated risks, as the patients are often ‘well’. They still function, although they are impaired by their condition. Surgery therefore has a high risk of causing significant morbidity to the patient if things go awry. It is clear from this month’s CME that the mere presence of epilepsy or spasticity is not a trigger for surgery. Only if a patient’s epilepsy is

refractory to medical care and reviewed by a competent epileptologist, should one consider surgery. Spasticity is often protective and even useful to a patient, but when it leads to pain and deformities and hinders the patient’s functioning, surgical management becomes an option. Lengthy discussion with the patient and the family is crucial. A common opinion held by medical care funders and especially by state health departments is that functional neurosurgery procedures are too highly specialised and expensive for developing countries to be spending time and finances on. Readers of the August and September CME articles will observe that intelligent use of resources and longterm saving of money are the reasons why developing countries should be investing in functional neurosurgery units. Surgery for medical refractory epilepsy can save large amounts of money in the long run if one considers the cost of second- and third-line anti-epileptic drugs and the associated morbidity of uncontrolled epilepsy. The same argument holds for pain, spasticity, and movement disorder surgery. It is important that healthcare funders on our continent develop long-term management strategies that are not penny wise, pound foolish. This month’s CME covers the first two[1,2] of four articles that are dedicated to functional neurosurgery topics. J M N Enslin Division of Neurosurgery, Red Cross War Memorial Children’s Hospital, and Constantiaberg Mediclinic, Cape Town, South Africa enslin@functionalneurosurgery.co.za 1. Enslin JMN, Fieggen AG. Surgical management of spasticity. S Afr Med J 2016;106(8):753-756. DOI:10.7196/SAMJ.2016.v106i8.11225 2. Enslin JMN, Rothemeyer SJ, Fieggen AG. Surgical management of epilepsy. S Afr Med J 2016;106(8):757-760. DOI:10.7196/SAMJ.2016.v106i8.11194

S Afr Med J 2016;106(8):752. DOI:10.7196/SAMJ.2016.v106i8.11195

August 2016, Print edition

CME

Surgical management of spasticity J M N Enslin,1 BPhysT, MB ChB, FCNeurosurgery (SA), MMed (Neurosurg); A G Fieggen,2 MB ChB, MSc, MD, FCNeurosurgery (SA) 1 2

ivision of Neurosurgery, Red Cross War Memorial Children’s Hospital, and Constantiaberg Mediclinic, Cape Town, South Africa D Department of Neurosurgery, Faculty of Health Sciences, University of Cape Town, and Division of Neurosurgery, Red Cross War Memorial Children’s Hospital, Cape Town, South Africa

Corresponding author: J M N Enslin (enslin@functionalneurosurgery.co.za)

The management of patients with cerebral palsy and other causes of spasticity is a challenge to an entire rehabilitation team and to caregivers. In South Africa, neurosurgeons have had limited involvement in this field owing to a perceived lack of options, leaving the care of these patients largely in the hands of paediatric neurologists and orthopaedic surgeons. A committed team-based approach, where a neurosurgeon is part of the decision-making process, can however significantly improve functional outcomes in patients with spasticity. Key to the evaluation and therapeutic decision-making is the focus on function – not only the range of movement or the presence of spasticity. Some techniques can completely remove spasticity and contractures, but these mostly leave a patient with more functional impairment than they had before the surgery. With the careful combination of botulinum toxin injections and oral baclofen, these patients, who may benefit from further orthopaedic and neurosurgical procedures, can be identified and helped in reducing the function-limiting spasticity. With the emphasis on function as an individualising factor, significant improvements may follow minor interventions, e.g. performing a surgical procedure to allow reduced hip adductor spasticity, thereby allowing improved hygiene and less pain in a child in whom it was previously not possible to abduct the hips enough to change a nappy. Functional improvement does not necessarily equate to walking. We describe the process of evaluating patients with spasticity and outline the surgical decision-making process that helps towards an individualised therapeutic strategy in managing this challenging group of patients. S Afr Med J 2016;106(8):753-756. DOI:10.7196/SAMJ.2016.v106i8.11225

Spasticity is defined as an increase in muscle tone that is elicited by a velocity-dependent stretching of the muscles. It is part of the upper motor neuron syndrome of muscle weakness and is worst in antigravity muscles.[1,2] The most common causes of spasticity are: • cerebral palsy (spasticity is a dominant feature in 80% of all patients with cerebral palsy)[3] • stroke • traumatic brain injury • spinal cord injury • multiple sclerosis • hereditary spastic paraparesis • degenerative neuromuscular diseases. Management of spasticity should follow a planned, stepwise process of gradual escalation of therapy; only when the preceding step is shown to be ineffective, should more invasive options be considered. It is especially important to remember that the presence of spasticity in itself is not an indication for surgical management − only when spasticity becomes troublesome does surgery become an option. Criteria used to consider surgical management options are: • spasticity that impairs function in a patient, e.g. difficulty with walking owing to spastic hamstring muscle group and triceps surae muscles • spasticity that causes significant pain to the patient • spasticity that makes caring for the patient troublesome, e.g. adductor spasticity, which makes it difficult to change a child’s nappy; or a debilitated stroke patient • spasticity may lead to irreversible deformities of the skeletal system, such as hip dislocations or abnormal degeneration of hip and knee joints owing to asymmetrical weight-bearing on the joints.

Sherrington[4] in his Nobel prize-winning work in 1932 still hold true today. Sherrington described the concept of reciprocal innervation and noted that the muscle is under inhibitory and excitatory control of the central nervous system. Key to his understanding of spasticity was loss of this control owing to injury to the spinal cord or brain. Loss of inhibitory control from the brain via the spinal cord leads to uninhibited excitation of the monosynaptic spinal reflex arc.[5] The muscles, therefore, fire on their own, which causes spasticity. A basic representation of this reflex arc is shown in Fig. 1. Inhibition of the corticospinal tract is generally thought to cause spasticity, but over the years it has been noted that there are many examples of corticospinal tract injuries where patients do not present with spasticity, but reduced tone. It is thought that the reticulospinal tract, which has a modulation effect via interneurons on the afferent signal to muscles, may play a more significant role

Dorsal nerve root Spinal cord

Pathophysiology of spasticity

Over the past century there has been little progress in the under standing of the pathogenesis of spasticity. Concepts developed by

Skeletal muscle

Ventral nerve root

Fig. 1. Schematic illustration of monosynaptic spinal reflex.

August 2016, Print edition

CME

in the pathogenesis of spasticity, and loss of reciprocal inhibition after spinal cord injuries or cerebral injuries may lead to spasticity.[5] From the many theories of the causes of spasticity in humans, it is clear that we do not completely understand the condition. As diagnostic tests and more qualitative evaluation techniques become available, we may get closer to the answers.

Evaluation of spasticity for surgical management

The surgical management of spasticity should focus on the functional evaluation of the patient. Meticulous questioning and evaluation of the patient during their daily activities and of their lifestyle is much more revealing than the most thorough neurological examination. The approach to taking the history and examining the patient should reflect this. It is invaluable to evaluate a patient in their home environment. A video recording taken by a relative of the patient sitting in a chair, lying on the bed, standing and walking is also of great benefit. This allows one to assess function in a familiar environment. Careful observation of the patient while the family, or the patient, recounts the history is often much more beneficial than a physical examination. The following points are important to observe in the history: • antenatal events and maternal health • perinatal events, such as hypoxia, prolonged labour, premature rupture of the membranes, HIV exposure, Apgar scores • family history of neurological diseases • trauma • previous operations for spasticity or orthopaedic deformities or corrections • current and previous medications • intervals of botulinum toxin injections and splinting, if any. A detailed systemic history with specific attention to bladder and bowel habits is also important. One needs to enquire about respiratory tract infections, as patients with cerebral palsy are more prone to such infections. Throughout the examination, careful attention should be paid to determine whether the problematic spasticity is focal or diffuse, and whether there are dystonic features associated with or underlying the spasticity. The latter has significant therapeutic implications. Physical examination of patients with spasticity should be inititated by evaluating function: • eating or drinking, dressing and communicating while sitting • standing upright from a seated position on own wheelchair, a chair or a bed • balancing in standing and sitting positions • gait with and without support or frames • gait and standing with and without an orthosis • ability to climb stairs • running and jumping (if possible). Once these functional activities have been evaluated, the focus should move towards more specific aspects of spasticity: • Posture when lying, sitting and standing is important – note pelvic alignment and spinal deformities. • Trunk and neck tone while sitting and standing. • Muscle power in a functional motion, such as kneeling, sitting, squatting, and climbing a step. Traditional measures of power are not reliable in a patient with abnormal tone. • Range of motion in all joints, especially around the hips and ankles. • Evaluation of muscle tone, as spasticity is a velocity-dependent increase in tone. Pay attention to the difference between active and passive movements and tone.

• With regard to deep tendon reflexes, pay specific attention to crossing over of reflexes to other limbs as well as spreading of reflexes in the same limb. • Presence of pathological reflexes, such as clonus and the Babinski sign. • A good screening sensory examination that focuses on proprio ception and light touch is important for future surgical inter ventions. • Establish whether the spinal deformity has been corrected or is correctable.

Management of spasticity

Spasticity in itself is not a problem; its presence may be protective in preventing the patient from further injuring a limb or joint, especially in focal spasticity, which occurs after a stroke in an upper limb. The presence of spasticity may increase the functional abilities in some patients, e.g. children with spastic diplegia may be able to stand, because they may use their hip adductor spasticity to increase truncal tone, which forms a stable base for them to stay erect. Once spasticity leads to pain and deformities or it starts to impair function, treatment to reduce it becomes important. In the evaluation of spasticity the clinician must decide whether it is focal or diffuse/ global. Fig. 2 demonstrates how this important differentiation is used to decide which therapeutic modality is potentially useful. There is, for example, no place for the use of intrathecal baclofen in patients with focal hand spasticity. It is also not possible to administer botulinum toxin injections or perform a peripheral neurotomy on every muscle involved in diffuse spasticity, such as in a child with spastic quadriplegia. Physical and occupational therapy remain at the core of any good rehabilitation and care programme for all patients with spasticity. Speech therapists and psychology services also have an important role in the holistic care plan. The entire team must understand the functional goals of surgery, and often training that starts ahead of surgery is extremely beneficial in optimising the patient for the procedure, but also in learning new exercises that follow the surgery. The various surgical treatments for patients with function-limiting spasticity are listed in Table 1. As a rule, most patients with spasticity should be on oral baclofen as an empiric antispasticity medication. If pain forms a major part of the spasticity, either as an exacerbation factor or owing to the spasticity, pain-modulating medications that also have an effect on spasticity, such as gabapentin, may be added. Once these non-surgical management options have been exhausted, with no improvement in the function of the patient, surgical manage ment may become relevant. Focal spasticity

Botulinum toxin injections

Selective peripheral neurotomy/dorsal rhizotomy

Reversible therapy

Permanent therapy Intrathecal baclofen therapy

Dorsal root entry zone lesioning

Global spasticity Fig. 2. Spasticity management diagram.

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Table 1. Surgical options in patients with spasticity Neurosurgical

Other surgical

Selective peripheral neurotomy

Tendon-lengthening procedures

Intrathecal baclofen therapy

Bony anatomy correction/ rotation osteotomies

Selective dorsal rhizotomy

Intravesicular botulinum toxin injections

Dorsal root entry zone lesioning

Intramuscular botulinum toxin injections

Selective peripheral neurotomy. The peripheral nerve is dissected free and the motor branches are mapped out with the use of a nerve stimulator. Once absence of a sensory branch of the nerve is confirmed, about 80% of the nerve to the spastic muscle is sectioned and 5 mm are resected. The goal is to restore the balance between the agonist and antagonist muscles around a joint. It is therefore only appropriate for focal spasticity around one or two joints, e.g. a hemiplegic patient after a stroke, who is starting to stand but cannot stand on a flat foot owing to inversion of the foot, resulting in pain. Performing a peripheral neurotomy on the posterior tibial nerve, targeting the branches to the tibialis posterior muscle, can allow the patient to stand on a flat foot with less pain. The muscle is usually not perceived to be weaker, as the number of motor units innervated by the remaining nerve fascicles increases significantly within a few weeks and there should not be any discernable sensory deficit after the procedure. Baclofen. This acts as a gamma-aminobutyric acid (GABA) β-receptor agonist, leading to a reduction in calcium inflow to nerve terminals and a reduction in excitation in neurotransmitters that are released in the spinal cord.[6] While baclofen can be administered orally, the side-effects are often not tolerated and an attractive alternative is direct administration. Intrathecal baclofen (ITB). This is provided by an implanted pump. A small catheter is placed into the thecal space (subarachnoid spinal canal), with the tip placed in the high cervical area to treat dystonia or spastic quadriplegia, or in the low thoracic area to treat spastic diplegia. Baclofen can then be administered in a slow continuous infusion at a much lower dose than oral baclofen. This leads to better bioavailability at the receptors in the spinal canal and fewer systemic effects. A key benefit of ITB is that it is reversible and very effective in patients with dystonia and spasticity. Selective dorsal rhizotomy. This is a surgical procedure that is well proven in children with spastic diplegia and was adopted worldwide following Warwick Peacock’s work in Cape Town in the 1980s. During this procedure, a multilevel laminotomy is performed from the L2 - S1 level, the cauda equina is exposed and the dorsal root is separated from the ventral root. The dorsal root is then split, typically into 3 - 4 fascicles, and guided by intraoperative neurophysiology, between 30% and 60% of the dorsal root being sectioned. With the use of this technique the monosynaptic reflex arc is interrupted, which reduces the spasticity. Key to this operation is good strength and postural stability in the child before surgery is considered. Pelvic control and strength of hip extension and abduction with good knee extension are very important in rehabilitation and improving gait in these patients. Dorsal root entry zone lesioning (DREZotomy). During this procedure the point where the dorsal nerve roots enter the spinal cord is cauterised up to a specific depth. This interupts the interneurons for muscle tone in the Rexed laminar levels. The great benefit of this

procedure is that it can be done selectively and for multiple levels, depending on the individual’s need. DREZotomy is also an excellent operation for pain; with the correct technique a patient with severe pain due to uncontrolled spasticity may obtain significant relief of both. The techniques discussed above are mostly irreversible (Fig. 2). It is therefore very important to determine what the expected functional effect of a procedure will be. Muscle tone is lower after surgery, but one also needs to have a concept of the patient’s function afterwards. For example, it is not helpful to have improved leg tone but be unable to stand or walk if one could do this before the procedure. The expected effect can be tested by using botulinum toxin in selective muscles, temporarily administering ITB via an infusion pump, or performing a peripheral nerve block with a long-acting neural anaesthetic agent. Functional activity can now be evaluated with the temporary reduction in muscle tone. Reliable intraoperative neurophysiology is mandatory during surgical techniques for spasticity. These techniques are used to preserve bladder and bowel function and to guide fascicular dissection. Surgery forms a small part of the entire process involved in managing patients with spasticity. As illustrated in Fig. 3, careful evaluation and appropriate surgical procedures, performed with the correct goal in mind, need to be followed by active patient and family participation in a structured rehabilitation programme that starts as soon as possible after surgery. The goals of the patient, therapist, relatives, caregivers and surgeon all need to be aligned and specific functional activities developed that will improve certain aspects of the recovery and rehabilitation process. There is no one recipe that fits all patients.

Outcomes of surgery for spasticity

Clear goals need to be discussed with the family and the management team before surgery. Expectations need to be tailored to what is achievable. It is not possible, for example, for a child who is completely dependent for all daily activities (gross motor function classification system (GMFCS) level 5) to walk independently after any form of surgical therapy. Any surgeon claiming this possibility is headed for a disaster. The goal of surgical therapy may not necessarily be for the patient to walk independently. A realistic goal for a 65-year-old woman with left hemiplegia after a stroke may be to be able to hold a glass of water with her left hand again, or to stand with a flat foot while using a walking stick. A surgical goal in a spastic quadriplegic child who is wheelchair bound, may be for the child to be able to lie down flat on his back in bed while asleep, without hips and knees pulling up into flexion continuously. This reduction in spasticity around the hips may allow improved personal care and reduced bladder infection,

Evaluation

Rehabilitation Surgery

Fig. 3. The importance of evaluation and rehabilitation in spasticity manage ment.

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as the hips can now be abducted to allow easier nappy changes and cleaning. Improving the ability for a wheelchair-bound child to sit more easily in a wheelchair with comfortable knee and hip flexion is also a great achievement in a severely spastic child who has difficulty being placed in a wheelchair owing to severe hip and knee spasticity. At the same time, it is possible for a child with spastic diplegia to walk unaided after a selective dorsal rhizotomy if he has good trunk and hip strength. Small improvements on a rating scale may lead to large functional gains in a patient. The preoperative goals of surgery should be clearly defined by the family and the rehabilitation team. The outcome should be functional; this same function should be targeted in personalising the therapeutic strategy and the postoperative outcomes evaluation. ITB shows very good reduction in spasticity and painful deformities caused by this condition in 80 - 97% of cases.[7] The reduction in spasticity is documented with a 2 - 3-point improvement in the 5-point Ashworth scale, and tolerance is generally very good.[7] Peripheral neurotomies have an 80 - 85% success rate in reducing painful deformities and spasticity in focal conditions.[7] This leads to improved functional activity and prevents worsening of deformities caused by increased tone. DREZotomy leads to a 70 - 82% decrease in spasticity, while at the same time relieving pain in paraplegic patients in up to 91% of cases.[7] A 20-year follow-up by the Cape Town group[8] shows very good long-term outcomes in patients after selective dorsal rhizotomy. In a group of 14 patients, all but one had long-term control of their spasticity and good functional improvement that lasted into adulthood.

Complications of surgery for spasticity

As the purpose of the surgical treatment of spasticity is to improve function, possible complications must be carefully considered. It is particularly important that a wheelchair-bound patient does not have ‘useless hypotonia’ after surgery. Concerns about impaired bladder and bowel control, as well as spinal deformities, are also frequently raised. Tsirikos[9] reviewed reports on the incidence of spinal deformities in the cerebral palsy population and found an incidence of 20 - 25%. Some studies report up to a 74% incidence in spastic quadriplegic patients;[10] it is important to keep this natural history in mind when considering surgical management of spasticity and its influence on spinal deformity. In the 20-year study by Langerak et al.[8] − to date the study with the longest duration − no patients experienced spinal deformity that required further surgery. Urological dysfunction among patients with spasticity, and especially the cerebral palsy group, is much more common than

previously thought. Mobility, age, communication problems and spasticity of the detrusor muscle all play a role.[10] Murphy et al.[11] have an interest in cerebral palsy patients and bladder function; 16.4% of their cohort showed spastic, hyperreflexic bladders on urodynamic testing. There were no bladder or bowel complications reported in the selective dorsal rhizotomy cohort in the Cape Town study.[8] Specific enquiry and examination, often with invasive urodynamic testing, are important in patients with cerebral palsy, as resultant recurrent urinary tract infections may lead to renal injury in the long run. Major leaps in surgical techniques, but more importantly in intraoperative neurophysiological monitoring, have allowed surgeons to reduce the incidence of all these complications.

Summary

Surgery plays an important role in the multimodal management of spasticity. While every patient with spasticity can be helped, not all require an operation. In cases where an operation may benefit the patient, it is not a one-procedure-for-all scenario. Only a team, which consists of a neurosurgeon, orthopaedic surgeon, developmental paediatrician and rehabilitation therapists, can offer each patient an objective opinion on therapeutic options. Thorough examination and multiple visits are key to planning a management strategy. The distribution of spasticity is important, as this has implications with regard to surgical management options, and every patient should be carefully screened for the presence of dystonia. Patients who do not respond well to surgical procedures for spasticity are often those in whom a coexistence of dystonia was missed. The role of the family and video analysis of the patient in their home and work environment are important in determining the patient’s functional impairment. These impairments have to be incorporated in the surgical and rehabilitation goals of the patient, as individualisation of the therapeutic plan is crucial. References 1. Lance JW. Symposium synopsis. In: Feldman RG, Young RR, Koella WP, eds. Spasticity: Disordered Control. Chicago: Yearbook Medical, 1980:485-494. 2. Young RR. Spasticity: A review. Neurology 1994;44:512-520. 3. Odding E, Roebroeck ME, Stam HJ. The epidemiology of cerebral palsy: Incidence, impairments and risk factors. Disabil Rehabil 2006;28(4):183-191. 4. Sherrington CS. Nobel lecture: Inhibition as a coordinative factor. http://www.nobelprize.org/nobel_ prizes/medicine/laureates/1932/sherrington-lecture.html (accessed 29 June 2016). 5. Nielsen JB, Crone C, Hultborn H. The spinal pathophysiology of spasticity – from a basic science point of view. Acta Physiol (Oxf) 2007;189(2):171-180. 6. Scherkenbach LA, Coles LD, Patterson EE, et al. Pharmacokinetics and pharmacodynamics of intravenous baclofen in dogs: A preliminary study. J Pharm Pharmacol 2014;66(7):935-942. DOI:10.1111/jphp.12221 7. Sindou M, Georgoulis G, Mertens P, eds. Neurosurgery for Spasticity: A Practical Guide for Treating Children and Adults. Vienna: Springer, 2014. 8. Langerak NG, Lamberts RP, Fieggen AG, et al. Selective dorsal rhizotomy: Long-term experience from Cape Town. Childs Nerv Syst 2007;23(9):1003-1006. 9. Tsirikos AI. Development and treatment of spinal deformity in patients with cerebral palsy. Indian J Orthop 2010;44(2):148-158. DOI:10.4103/0019-5413.62052 10. Borzyskowski M. Cerebral palsy and the bladder. Dev Med Child Neurol 1989;31:687-689. 11. Murphy KP, Boutin SA, Ide KR. Cerebral palsy, neurogenic bladder, and outcomes of lifetime care. Dev Med Child Neurol 2012;54(10):945-950. DOI:10.1111/j.1469-8749.2012.04360

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Surgical management of epilepsy J M N Enslin,1 BPhysT, MB ChB, FCNeurosurgery (SA), MMed (Neurosurg); S J Rothemeyer,2 MB ChB, FCNeurosurgery (SA); A G Fieggen,3 MB ChB, MSc, MD, FCNeurosurgery (SA) ivision of Neurosurgery, Red Cross War Memorial Children’s Hospital, and Constantiaberg Mediclinic, Cape Town, South Africa D Department of Neurosurgery, Faculty of Health Sciences, Groote Schuur Hospital and University of Cape Town, South Africa 3 Department of Neurosurgery, Faculty of Health Sciences, University of Cape Town, and Division of Neurosurgery, Red Cross War Memorial Children’s Hospital, Cape Town, South Africa 1 2

Corresponding author: J M N Enslin (enslin@functionalneurosurgery.co.za)

The fact that epilepsy can be cured or ameliorated with surgery is an often neglected and overlooked aspect of modern management. Epilepsy affects almost 50 million people worldwide. One-third of people who suffer from epilepsy are refractory to medication alone. It is this group of patients who may benefit from epilepsy surgery, which can be divided into three main categories, i.e. resection procedures, disconnection procedures, and neuromodulation procedures. The goal of surgery in epilepsy is to remove the epileptogenic region from the brain, or to disconnect it and thereby prevent spread to other parts of the brain. In cases where this is not possible owing to the location of the epileptic focus, certain neuromodulation techniques may benefit the patient. Successful outcomes of epilepsy surgery techniques vary from 50% to 80% in rendering patients free of their epilepsy; many more patients can expect improvement in the severity or frequency of their disabling seizures. The outcome depends on factors such as age, location of the epileptogenic zone, histology and cause of the seizures. Patients undergo a detailed and prolonged work-up to determine candidacy and to decide on the safest technique that will lead to the best outcomes. An experienced team should perform the surgery. This team should consist of multiple members who can attend to the medical, social, psychological and reintegration needs of the patient before and after surgery. S Afr Med J 2016;106(8):757-760. DOI:10.7196/SAMJ.2016.v106i8.11194

Epilepsy is the fourth most common disorder that affects the nervous system, with only migraine, cerebrovascular incidents and Alzheimer’s disease being more common. Epilepsy affects ~50 million people worldwide.[1] In Africa, epilepsy affects ~10 million people.[2] Global statistics show that about one-third of patients with epilepsy are refractory to anti-epileptic medication.[3] This translates into ~2.5 million people in Africa with devastating epilepsy, who may require alternative treatment to control or cure their epilepsy. Since 1886, neurosurgeons such as Horsley, Penfield and Krause have been interested in the surgical treatment of epilepsy in both adults and children.[4] From these early days, doctors understood that epilepsy is caused by abnormal electrical discharges in a specific part of the brain. This led to the premise that if that abnormal part of the brain can be resected, the epilepsy will be controlled.

Indications for surgery

Surgery should be the main therapeutic option in refractory epilepsy if a clear cause has been identified. This is the case in patients with focal cortical developmental or migrational abnormalities, and in patients in whom epilepsy is associated with a tumour or lesion in the brain. Undertaking surgery is a much more difficult decision in patients with cryptogenic epilepsy, i.e. where there is no anatomical abnormality demonstrable on a magnetic resonance imaging (MRI) scan. At this point, the role of the functional neurosurgeon specialising in epilepsy surgery and working in conjunction with an experienced epileptologist (neurologist with a special interest in epilepsy) becomes vital. Surgery for epilepsy is never an emergency, except in rare cases of rapidly enlarging brain tumours, but then the focus is on tumour surgery and not treating the epilepsy. The timing of surgery in the course of the disease also needs some consideration, with the benefit of earlier surgery becoming more evident from recent data. It has been demonstrated that earlier control of seizures (at a younger age) leads to better long-term outcomes in patients with epilepsy.[5,6]

For a patient with epilepsy to be considered for work-up for surgery, the following criteria must be met: • The patient must be refractory to medical treatment, i.e. the patient must be on adequate medical therapy with at least two drugs, one of which is a newer-generation agent that is monitored and prescribed by an experienced epileptologist, and have lifeimpairing seizures.[7] There is no time duration to this definition. • There must be correlation shown between semiology (clinical presentation, e.g. posturing, during an attack), anatomy (imaging findings on an MRI scan) and electrical (findings on an electroencephalogram (EEG) tracing) abnormalities.

Work-up for surgery

The work-up in a patient with epilepsy, who is a potential candidate for surgery, requires a multidisciplinary approach. Patients with significant epilepsy are usually managed by an epileptologist (a paediatric neurologist, or an adult neurologist with a special interest and experience in treating patients with epilepsy). The team must be convinced that the patient is on optimal medication to prove refractoriness before surgery is considered. Pre-operative neuropsychological testing can help in determining the side of dominance of speech and memory and the psychological impairment, and prepare the family for significant changes if the surgery is successful. It seems odd to be concerned about this, but for a family with a patient with a chronic illness such as epilepsy, the patient not having epilepsy often leads to greater anxiety and is a challenge. Therefore, meticulous psychological follow-up and preparation are of the utmost importance. The neurosurgeon takes part in the counselling and evaluation of the patient and the interpretation of the multimodality imaging and telemetry to plan the surgery. Careful telemetry is needed, while the patient is kept in a unit with constant 24-hour per day video surveillance and is connected to the EEG monitor for the entire period, sometimes for a few days. This allows accurate correlation between the ictus (seizure event), clinical presentation (semiology) and EEG of the patient during the

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event. The patient undergoes neuro-imaging to illustrate the cortical abnormality that may be associated with the epileptiform area. Currently, 3 Tesla MRI scanning is becoming the gold standard for the imaging of patients with epilepsy, as it allows the epilepsy surgery team to evaluate for subtle cortical abnormalities that were previously left undetected by 1.5 Tesla scanners. Special sequencing, such as diffusion tractography imaging and functional MRI, can be used to determine the association between eloquent brain areas and the epileptogenic area, thereby allowing preservation of function in patients who undergo resection of the epileptiform area. Some epilepsy surgery units have access to positron emission tomography (PET) scanning that allows visualisation of abnormal activity or active lesions in cases of multiple lesions, e.g. patients with tuberous sclerosis, hereby determining which lesion is responsible for the seizures. Combining pre-ictal and ictal single-photon emission computed tomography (SPECT) scans can also be very helpful in localising the epileptiform cortex, especially in patients in whom there is no structural abnormality detectable on MRI. The intracarotid injection of amobarbital (Wada test) has mostly been replaced by functional MRI, which offers a non-invasive way to determine lateralisation of functions such as speech and memory. This is especially important in temporal lobectomies. A CT scan has limited use in the work-up of refractory epilepsy, but is often still the first imaging modality employed owing to the cost associated with MRI scanning.

Surgical procedures

The goal of surgery is always maximal resection of the epileptiform focus, tempered by the need to respect and preserve functional areas, venous drainage, arterial supply and white matter connecting tracts. Surgery for epilepsy is divided into three major categories: • anatomical resection procedures, e.g. resection of the frontal lobe or temporal lobe • disconnection procedures (disconnecting the epileptiform cortex from the rest of the brain by sectioning white matter tracts) • neuromodulation (placing of vagal nerve stimulator or deep brain stimulation for epilepsy).

It is important to stress the difference between tumour surgery and epilepsy surgery. In tumour surgery the focus is on removing the lesion and the malignant infiltrates in the surrounding tissue, which are often not visible under a microscope. Various techniques are used to allow visualisation of this infiltrated area, e.g. amino-acid PET masking. Traditionally, this approach is used in epilepsy surgery associated with lesions, such as developmental neuro-ectodermal tumours. The belief is that the lesion is epileptogenic; therefore, performing a lesionectomy is all that is required to control the seizures. However, epilepsy surgeons are aware that, in some cases, this does not control the epilepsy (Figs 1 and 2 illustrate this principle). Part of the work-up for epilepsy surgery takes this into account and great effort is made to search for the epileptiform cortex, even more distant from the lesion. This is why in epilepsy surgery the term topectomy is preferred rather than lesionectomy.

Disconnection techniques

In patients in whom the focus of the epileptiform activity is restricted to an area that does not allow resection owing to its eloquence, another approach is to ‘disconnect’ that part of the brain from the rest, thereby in effect isolating the epileptic activity to a focal portion of the brain and preventing secondary generalisation. An example of this is a functional hemispherectomy, where the diseased hemisphere is disconnected from the rest of the brain and the patient does not have dangerous progression of focal seizures to generalised seizures. This procedure is a variation of the older technique of anatomical hemispherectomy, where one half of the brain was removed. This led to significant morbidity and mortality.

Neuromodulation techniques

Neuromodulation for epilepsy is being investigated, as it is seen as the next great frontier in epilepsy surgery. In the same manner that deep brain stimulation has been shown to have a significant effect in patients with Epileptogenic zone Resection to control seizures

Resection techniques

The choice of resection techniques, or combinations thereof, depends on the location of the epileptiform focus, eloquent tissue, vascular supply, and venous drainage patterns. Surgical planning is also informed by only grey matter (cerebral cortex) having epileptogenic potential; however, seizure activity can propagate via white matter tracts. Resective techniques remove the offending area or lesion, often also with a subcortical bank of tissue, whereas disconnective techniques tend to leave the area of epileptogenic grey matter as an isolated island in the brain. Certain types of epilepsy are better controlled with specific tech niques, e.g. atonic seizures (drop attacks) are ideal cases for corpus callosotomy, as this prevents generalisation to the contralateral cortex. Patients continue to have unilateral seizure activity, but not the dangerous atonic seizure that often leads to falling into a fire or in front of a moving vehicle. In eloquent areas the surgeon uses a subpial dissection technique, where the pial bank is preserved against blood vessels and nerves, while the grey matter is dissected out and away from the white matter tracts, often using an ultrasonic aspirating device on very low suction and fractionation settings. An area of white matter network, which is free of the electrically active grey matter, is left behind. Electrical mapping techniques are used during the procedure to preserve eloquent brain matter. In this way the delicate border between eloquent tissue and epileptiform tissue is delineated, allowing safe resection.

Lesion

Fig. 1. Relationship between lesion and resection margins that may be required to control seizures.

Tumour/ lesion

Epileptogenic zone

Fig. 2. Resecting of a lesion may not always cure epilepsy.

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Parkinson’s disease, dystonia and tremor, certain targets in the thalamus show promise in treating medication- and surgery-refractory epilepsy. Vagal nerve stimulation is a surgical procedure in which a small wraparound electrode is placed on the left vagal nerve in its cervical course. This electrode is then connected to an implanted pulse generator, similar to a cardiac pacemaker, which stimulates the vagal nerve at a predetermined frequency and amplitude. The mechanism of action is as yet unsure, but it does show at least a 50% improvement in 50% of patients who have the device implanted.[5] It seems as though only a small number of patients benefit, but it is important to remember that this group of patients suffer tremendously and that medication and other surgical options have failed or are not possible. Therefore, even such small odds are worthwhile and can lead to great improvement in quality of life. Some of the more recent trials are related to deep brain stimulation (DBS) for drug-resistant epilepsy.[8] In this procedure a DBS electrode is placed into the anterior nucleus of the thalamus via a stereotactic technique and an implanted pulse generator produces a constant pulse at a predetermined frequency, which modulates abnormal electrical activity in the brain. More recently, promising work has been done, where a subdural or depth electrode and a thalamic electrode are implanted into the epileptic zone in the brain. As soon as abnormal electrical activity is detected in a closed loop system, the pulse generator stimulates the thalamus and the abnormal electrical activity is aborted.[9] This technique is still in its infancy as a treatment for medical refractory epilepsy, but holds great potential, especially for non-lesional epilepsy or epilepsy with seizure foci that are in non-resectable areas.

Surgical risks for epilepsy

Surgery for epilepsy is a major decision and there are significant asso ciated risks. Therefore, strict criteria need to be met before surgery can be considered in the treatment of medical refractory epilepsy. Surgery can lead to memory impairment after temporal lobectomies, and motor weakness or aphasia in hemispheric procedures. Occipital lobe surgery and damage to the optic tract in medial temporal lobe resections can lead to blindness. Disturbances in the flow of cerebrospinal fluid can lead to hydrocephalus that will require shunt procedures, with associated risks. These risk factors need to be weighed up against those associated with the long-term use of anti-epileptic medication. Females, especially, have to consider the teratogenic effect of most first-line antiepileptic medication during pregnancy. Untreated epilepsy carries significant morbidity and even mortality. Sudden unexpected death in epilepsy is a rare, but real threat to patients with the condition. There are therefore certain conditions, such as focal cortical dys plasia and dysembryoplastic neuro-epithelial tumours, which are known to be mostly refractory to anti-epileptic drugs, where an argument can be made to perform the respective surgery as soon as a diagnosis is made, especially if the lesion is in a non-eloquent area, such as the medial temporal lobe in the right hemisphere.

Outcomes of epilepsy surgery

In the follow-up of patients after epilepsy surgery it is important to enquire about seizures and their frequency. For many years the emphasis of epilepsy surgery outcomes has focused on these aspects,

but increasingly units are publishing their data on patients with regard to their memory, school performance, and psychological and emotional wellbeing.[10] Fewer seizures is only half of the problem solved, as 45 - 50%[10] of patients suffer from depression and anxiety after surgery and careful evaluation is needed to determine sequelae of the resected cortical tissue and its effect on mood, memory and personality, with school and work performance being sensitive surrogates to evaluate this. In the absence of seizures, patients have difficulty in dealing with these new feelings of depression and emotional lability. The treating team need to be aware of this and pre-empt these factors during counselling. Freedom of seizures after surgery is the primary goal, though. The outcome is dependent on the aetiology of the seizure, location of the epileptiform region, degree of resection done and type of procedure performed. Some published epilepsy surgery outcomes are summarised in Table 1.[11-13] There are some factors that have been identified to yield better long-term seizure freedom after surgery, e.g. presence of hippocampal atrophy and absence of generalised tonic-clonic seizures. Spencer et al.[14] found that 25% of patients relapse after 2 years of seizure freedom in cases of temporal lobe resections. Patients with medial temporal lobe epilepsy, who are operated on later in life, also show a worse seizure freedom rate after surgery.[15] This is yet another motivation for earlier surgery in patients who are medically refractory to epilepsy treatment. Children with epilepsy and a specific lesion on MRI are also increasingly free of seizures after surgery compared with those with no identifiable lesion – only an electrically localisable focus (70% v. 56% in a temporal focus). The seizure freedom rate in non-lesional epilepsy is about 62%, independent of the presence of a lesion.[16] In a study by the University of California, Los Angeles (UCLA) group[17] it was shown that children with cortical dysplasia have a slightly higher recurrence rate than other patients with epilepsy, but it is clear that early surgery, before 3 years of age, makes a significant difference and leads to lower seizure recurrence rates. In a comparison of children with cortical dysplasia and surgery before 3 years of age v. older children, the younger group showed 65% seizure freedom compared with 38% in the older group at 5 years after epilepsy surgery follow-up.[17] Even though more than half of patients remain seizure free after surgery, the trend in our unit and most of the rest of the world is to taper the anti-epileptic medication slowly 6 months after surgery. Most patients (95%) who are seizure free at 6 months after surgery remain seizure free thereafter.[18] Table 2 summarises possible causes of seizure recurrence after successful surgery.[19,20] Careful multidisciplinary follow-up and counselling is an ongoing process and the patient is never completely discharged – support and motivation continue life-long.

Summary

Surgery for medical refractory epilepsy requires a multidisciplinary approach that involves neurosurgeons, epileptologists, neuropsychologists and a keen team of nursing and social worker staff. With the premise that about 2.5 million people in Africa have medically refractory epilepsy that may be treated with surgery, a great deal of awareness needs to be spread among physicians, nursing personnel and families of patients with severe epilepsy. Early surgery in patients with localisable seizure foci in non-

Table 1. Summary of epilepsy surgery outcomes[11-13] Adults

Temporal epilepsy

Extratemporal epilepsy

Extratemporal lesion

Frontal seizures

Seizure free after 1 year, %

Significant improvement, %

Seizure free at 1 year

Temporal epilepsy

Extratemporal epilepsy

Hemispherectomy

All surgeries

Children, %

Adolescents, %

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Table 2. Early and late seizure recurrence causes

[19,20]

Early

Late

Incomplete resection of epileptogenic zone

Acute AED level changes

Gliosis of the resection margins

Electrolyte disturbances/hypoglycaemia

Progression of underlying disease or tumour

Fever/pain/sleep deprivation

Withdrawal of AEDs in multifocal epilepsy

Surgery-related cortical irritation AED = anti-epileptic drug.

eloquent areas such as the medial temporal lobe leads to significant reductions (>70%) in epilepsy. Epilepsy is one of the most disabling chronic diseases; if help is possible, it must be made available to those who need it. With the increasing amount of knowledge, imaging methods and surgical techniques gained every year, surgery for epilepsy can be done safely and produce reliable results. Ultimately, the quality of life of patients with this devastating disease can be greatly improved. Timely referral to specialist epilepsy surgery units is mandatory if we want to decrease this disease burden on patients and their families.

References 1. Dua T, de Boer HM, Prilipko LL, Saxena S. Epilepsy care in the world: Results of an ILAE/IBE/WHO global campaign against epilepsy survey. Epilepsia 2006;47(7):1225-1231. DOI:10.1111/ j.1528-1167.2006.00595.x 2. World Health Organization. The Global Campaign Against Epilepsy. Epilepsy in the African Region: Bridging the Gap. Geneva: WHO, 2004. 3. Schuele SU, Lüders HO. Intractable epilepsy: Management and therapeutic alternatives. Lancet Neurol 2008;7(6):514-524. DOI:10.1016/S1474-4422(08)70108-X 4. Magiorkinis E, Diamantis A, Sidiropoulou K, Panteliadis C. Highights in the history of epilepsy: The last 200 years. Epilepsy Res Treat 2014;2014:1-13. DOI:10.1155/2014/582039 5. Mapstone TB. Vagus nerve stimulation: Current concepts. Neuro surg Focus 2008;25(3):E9. DOI:10.3171/FOC/2008/25/9/E9 6. Chen H-H, Chen C, Hung S-C, et al. Cognitive and epilepsy outcomes after epilepsy surgery caused by focal cortical dysplasia in children: Early intervention may be better. Child’s Nervous System 2014;30(11):1885-1895. DOI:10.1007/s00381-014-2463-y 7. Engel J, Wiebe S, French J, et al. Practice parameter: Temporal lobe and localized neocortical resections for epilepsy. Neurology 2003;60(4):538-547. DOI:10.1212/01.WNL.0000055086.35806.2D

8. Fisher R, Salanova V, Witt T, et al; SANTE Study Group. Electrical stimulation of the anterior nucleus of thalamus for treatment of refractory epilepsy. Epilepsia 2010;51(5):899-908. DOI:10.1111/j.1528-1167.2010.02536.x 9. Sun FT, Morrell MJ, Wharen RE. Responsive cortical stimulation for the treatment of epilepsy. Neurotherapeutics 2008;5(1):6874. DOI:10.1016/j.nurt.2007.10.069 10. Ring HA, Moriarty J, Trimble MR. A prospective study of the early postsurgical psychiatric associations of epilepsy surgery. J Neurol Neurosurg Psychiatry 1998;64(5):601-604. DOI:10.1136/jnnp.64.5.601 11. Rasmussen T. Surgery for frontal lobe epilepsy. Adv Neurol 1975;8:197-205. 12. Engel J Jr. Update on the surgical treatment of the epilepsies. Neurology 1993;43(8):1612-1617. DOI:10.1212/WNL.43.8.1612 13. Wyllie E, Comair Y, Kotaga P, et al. Seizure outcome after epilepsy surgery in children and adolescents. Ann Neurol 1998;44(5):740-748. DOI:10.1002/ana.410440507 14. Spencer SS, Berg AT, Vickrey BG, et al. Predicting longterm seizure outcome after resective epilepsy surgery: The multicenter study. Neurology 2005;65:912-918. DOI:10.1212/01. wnl.0000176055.45774.71 15. Schwartz TH, Jeha L, Tanner A, Bingaman W, Sperling MR. Late seizures in patients initially seizure free after epilepsy surgery. Epilepsia 2006;47(3):567-573. DOI:10.1111/j.1528-1167.2006.00469.x 16. Paolicchi JM, Jayakar P, Dean P, et al. Predictors of outcome in pediatric epilepsy surgery. Neurology 2000;54(3):642-647. DOI:10.1212/WNL.54.3.642 17. Mathern GW, Giza CC, Yudovin S, et al. Postoperative seizure control and antiepileptic drug use in pediatric epilepsy surgery patients: The UCLA experience, 1986 - 1997. Epilepsia 1999;40(12):1740-1749. DOI: 10.1111/j.1528-1157.1999.tb01592.x 18. Menon R, Rathore C, Sarma SP, Radhakrishnan K. Feasibility of antiepileptic drug withdrawal following extratemporal resective epilepsy surgery. Neurology 2012;79(8):770-776. DOI:10.1212/ WNL.0b013e3182644f7d 19. Schmidt D, Baumgartner C, Löscher W. Seizure recurrence after planned discontinuation of antiepileptic drugs in seizure-free patients after epilepsy surgery: A review of current clinical experience. Epilepsia 2004;45(2):179-186. DOI:10.1111/j.0013-9580.2004.37803.x 20. Mani J, Gupta A, Mascha E, et al. Postoperative seizures after extratemporal resections and hemispherectomy in pediatric epilepsy. Neurology 2006;66(7):1038-1043. DOI:10.1212/01.wnl.0000204236.96232.1c

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Asymptomatic rheumatic heart disease in South African schoolchildren: Implications for addressing chronic health conditions through a school health service M Shung King,1 DPhil; L Zühlke,2,3 PhD; M E Engel,2 PhD; B M Mayosi,2 DPhil ealth Policy and Systems Division, School of Public Health and Family Medicine, Faculty of Health Sciences, University of Cape Town, H South Africa 2 Department of Medicine, Groote Schuur Hospital and Faculty of Health Sciences, University of Cape Town, South Africa 3 Department of Paediatrics and Child Health, Red Cross War Memorial Children’s Hospital and Faculty of Health Sciences, University of Cape Town, South Africa 1

Corresponding author: M Shung-King (maylene.shungking@uct.ac.za)

When new evidence comes to light, it compels us to contemplate the implications of such evidence for health policy and practice. This article examines recent research evidence on the prevalence of asymptomatic rheumatic heart disease (RHD) in South Africa and considers the implications for the Integrated School Health Programme (ISHP). RHD is still a major burden of disease in developing countries, and elimination of this preventable condition ranks high among World Heart Federation goals. If left untreated, it becomes a chronic health condition that individuals have to cope with into their adult lives. The ISHP regards the health needs of children with chronic health conditions, which include conditions such as RHD, as a key service component. However, the chronic health component of the ISHP is still poorly developed and can benefit from good evidence to guide implementation. A recent study to ascertain the prevalence of RHD in asymptomatic schoolchildren through mass screening affords an opportunity to reflect on whether, and how, asymptomatic chronic health conditions in schoolchildren could be addressed, and what the implications would be if this were done through a school-based programme such as the ISHP. S Afr Med J 2016;106(8):761-762. DOI:10.7196/SAMJ.2016.v106i8.10756

Strategies on how to address the health needs of children with chronic health conditions are increasingly receiving international attention as the global focus on non-communicable diseases escalates.[1] A recent study on the prevalence of rheumatic heart disease (RHD) in asymptomatic children, conducted in South Africa (SA) and Ethiopia,[2] presents interesting lessons for conceptualising and addressing the needs of children with chronic health conditions through a school health programme such as the Integrated School Health Programme (ISHP) in SA.[3] An important component of the wide range of health needs that the ISHP in SA aims to address is the identification and support of children with chronic health conditions throughout their school years. However, the ISHP provides little practical guidance on how this should be done.[4,5] The findings of a study identifying the presence of RHD in a cohort of asymptomatic and undiagnosed schoolchildren present an opportunity to contemplate what these findings mean for addressing the needs of schoolgoing children with chronic health conditions in the context of the ISHP.

Study findings and implications

The study established the prevalence of RHD by screening randomly selected schoolchildren from 4 through to 24 years of age.[2] It employed the standardised echocardiographic diagnostic criteria of the World Heart Federation (WHF).[6] The study spanned two study settings: the Bonteheuwel and Langa communities of Cape Town, SA, and Jimma, Ethiopia. The varying socioeconomic gradient across the study sites increased the applicability of the findings to a range of socioeconomic contexts.

A total of 2 720 schoolchildren (mean age 12.2 (standard deviation (SD) 4.2) years) were screened in SA, of whom the greater proportion (58.9%) were female. In Ethiopia (N=2 000) the sex distribution was equal, with a younger mean age of 10.7 (SD 2.5) years. The mean prevalence in the SA arm of the study was 20.2/1 000, with the prevalence of 27/1 000 in Langa, double the 12.5/1 000 in Bonteheuwel, demonstrating an important socioeconomic gradient, even in two geographically contiguous urban communities. The even higher prevalence of 30.5/1 000 in Jimma, Ethiopia, where circumstances are more akin to those in rural SA, suggests that a similar higher prevalence can be expected in poorer rural areas. Key study conclusions are summarised in Table 1. Two subsequent questions that emerged for the study team were: (i) whether some children may have left school as a result of symptoms related to RHD, which would be picked up only through a community-based study; and (ii) the extent to which asymptomatic children who remain undiagnosed continue into adulthood with good health and no impact on their schooling. The study team also recognised the controversies that exist around: (i) the method of screening for asymptomatic RHD; (ii) the borderline disease entity; and (iii) the prognostic impact of asymptomatic RHD. [8] The WHF criteria, which represent the only evidence-based standardised guideline for the diagnosis of asymptomatic RHD and have been applied to both high- and low-risk populations,[9] are not without criticisms, particularly with regard to their high specificity and low sensitivity. [10] The practical implications for longer-term screening are still unclear.[11] Recent publications of long-term follow-up have divergent recommendations for repeat screening in endemic populations,[10] including those in which previous

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Table 1. Key study findings[2] 1. A high prevalence of RHD in asymptomatic schoolchildren. The prevalence of echocardiographic RHD of 20.2/1 000 in Cape Town was much higher than the 6.9/1 000 previously estimated using clinical auscultation over 30 years ago,[7] meaning that the new standardised echocardiographic method is more sensitive and likely to identify larger numbers of undetected children than previous techniques. 2. T he differing odds of detecting echocardiographic RHD between countries and between adjacent communities in SA points to the pronounced gradient across differential socioeconomic conditions, with increasing prevalence occurring with increasing levels of poverty. 3. T his socioeconomic gradient between countries and communities also manifested in the severity of asymptomatic RHD. Schoolchildren from Ethiopia had the more severe variant, followed by Langa and then Bonteheuwel. 4. B ased on these findings, there appears to be a substantial pool of schoolchildren in SA and Ethiopia with definite and borderline RHD that remains undetected. How to respond to these findings in the context of a school health programme requires consideration.

screening was negative, as well as for follow-up at regular intervals (including borderline disease) to monitor clinical progression.[12] However, pending more definitive studies of impact on prognosis, echocardiographic screening for asymptomatic RHD remains, for now, more of a research tool.[13]

Some key lessons and considerations

The study convincingly showed that the detection of asymptomatic disease requires a screening process and tools that are effective and easy to administer, with high sensitivity and specificity, to appropriately identify children with the condition of interest. Does the availability of such a screening process for RHD merit its automatic inclusion into the mass screening programme of the ISHP? Recent debates on the implementation of the current ISHP point to the need to reduce, rather than increase, mass screening.[4,5] In these debates, task-shifting of mass screening activities to a well-trained lower cadre of health workers is further proposed, in contrast to the method used in the study, where professional echocardiographers were required to do the screening. This points to a need for careful contemplation of the implementation context, despite meritorious evidence. Further considerations from the study, that are in line with international screening criteria considerations and have implications for similar chronic health conditions, are: (i) the large numbers of screens that are required to identify a small number of cases; (ii) the unclear longterm prognosis of asymptomatic and borderline RHD in children; and (iii) the current capacity of health services to respond adequately to children who may need further testing, follow-up or surgery.[14,15] In a school setting, children with chronic health conditions fall into one of the following main categories: (i) asymptomatic children, such as in this study; (ii) symptomatic children who are as yet undiagnosed; and (iii) children with confirmed diagnoses, who may be on treatment but are not identified in the school and school health service systems as needing support. This study prompts us to consider how to approach children who fall within these categories. As already indicated, mass screening to detect disease in asymptomatic children is not necessarily a viable option for RHD or for any other chronic health condition. An alternative is to focus targeted screening on other easily accessible asymptomatic groups at risk of complications, such as adolescent girls who attend antenatal services – this merits further debate. Children who are symptomatic, and in particular those who have symptoms severe enough to impact on their general wellbeing and schooling, urgently require mechanisms to identify and fully support them. Equally important are considerations of how to follow up and monitor children with early, as yet uncomplicated conditions, where early identification can prevent progression and complications. It is here that the ISHP in partnership with schools can play a crucial role. Current research into potential models of early identification and support for children with mental health conditions is in progress, and

may help in informing a broader service model covering all children with chronic health conditions. For RHD, improvement in socioeconomic circumstances is the core to eradication. Beyond this, having strong and effective primary healthcare services is essential, where all children who require anti biotic treatment for suspected streptococcal sore throat are appropri ately treated and followed up, and where secondary prevention measures are available.[16] A well-functioning ISHP has a crucial health promotion and ongoing monitoring and support role. Simply raising awareness among educators and parents of the need to treat sore throats is an important initial intervention that could lead to greater vigilance and care of children.[17,18] While policy makers and practitioners grapple with how to appropriately respond to the now confirmed population of children with asymptomatic RHD, and the yet unknown population of children with other undiagnosed chronic health conditions, there is an opportunity to equip educators, parents and caregivers with simple guidelines on how to identify children who display signs of difficulty, whether physical or mental, while working towards strengthening the ISHP and school system capacity. 1. Proimos J, Klein JD. Noncommunicable diseases in children and adolescents. Pediatrics 2012;130(3):379-381. DOI:10.1542/peds.2012-1475 2. Engel ME, Haileamlak A, Zuhlke L, et al. Prevalence of rheumatic heart disease in 4720 asymptomatic scholars from South Africa and Ethiopia. Heart 2015;101(17):1389-1394. DOI:10.1136/heartjnl-2015-307444 3. National Department of Health, South Africa. Integrated School Health Policy. Pretoria: NDoH, 2012. 4. Shung-King M. From ‘stepchild of primary healthcare’ to priority programme: Lessons for the implementation of the National Integrated School Health Policy in South Africa. S Afr Med J 2013;103(12):895-898. DOI:10.7196/SAMJ.7550 5. Shung-King M, Orgill M, Slemming W. School health in South Africa: Reflections on the past and prospects for the future. In: Padarath A, English R, eds. South African Health Review. Durban: Health Systems Trust, 2014:59-72. 6. Reményi B, Wilson N, Steer A, et al. World Heart Federation criteria for echocardiographic diagnosis of rheumatic heart disease – an evidence-based guideline. Nat Rev Cardiol 2012;9(5):297-309. DOI:10.1038/nrcardio.2012.7 7. McLaren MJ, Hawkins DM, Koornhof HJ, et al. Epidemiology of rheumatic heart disease in black schoolchildren of Soweto, Johannesburg. BMJ 1975;3(3755):474-478. 8. Roberts K, Colquhoun S, Steer A, Remenyi B, Carapetis J. Screening for rheumatic heart disease: Current approaches and controversies. Nat Rev Cardiol 2013;10(1):49-58. DOI:10.1038/nrcardio.2012.157 9. Roberts K, Maguire G, Brown A, et al. Echocardiographic screening for rheumatic heart disease in high and low risk Australian children. Circulation 2014;129(19):1953-1961. DOI:10.1161/ CIRCULATIONAHA.113.003495 10. Tani LY. Echocardiographic screening for rheumatic heart disease. Circulation 2014;129(19):19121913. DOI:10.1161/CIRCULATIONAHA.114.009406 11. Zühlke L, Engel ME, Lemmer CE, et al. The natural history of latent rheumatic heart disease in a 5 year follow-up study: A prospective observational study. BMC Cardiovasc Disord 2016;16(1):46. DOI:10.1186/s12872-016-0225-3. 12. Mirabel M, Fauchier T, Bacquelin R, et al. Echocardiography screening to detect rheumatic heart disease: A cohort study of schoolchildren in French Pacific Islands. Int J Cardiol 2015;188:89-95. DOI:10.1016/j.ijcard.2015.04.007 13. Zühlke L, Mayosi BM. Echocardiographic screening for subclinical rheumatic heart disease remains a research tool pending studies of impact on prognosis. Curr Cardiol Rep 2013;15(3):343. DOI:10.1007/ s11886-012-0343-1 14. Andermann A, Blancquaert I, Beauchamp S, Déry V. Revisiting Wilson and Jungner in the genomic age: A review of screening criteria over the past 40 years. Bull World Health Organ 2008;86(4):317-319. 15. Wilson J, Jungner G. Principles and practice of screening for disease. Arch Intern Med 1969;123(3):349. 16. Irlam JH, Mayosi BM, Engel ME, Gaziano TA. A cost-effective strategy for primary prevention of acute rheumatic fever and rheumatic heart disease in children with pharyngitis. S Afr Med J 2013;103(12):894-895. DOI:10.7196/SAMJ.7244 17. Nordet P, Lopez R, Duenas A, Sarmiento L. Prevention and control of rheumatic fever and rheumatic heart disease: The Cuban experience (1986-1996-2002). Cardiovasc J Afr 2008;19(3):135-140. 18. Robertson KA, Volmink JA, Mayosi BM. Towards a uniform plan for the control of rheumatic fever and rheumatic heart disease in Africa – the Awareness Surveillance Advocacy Prevention (A.S.A.P.) Programme. S Afr Med J 2006;96(3):241-245.

Accepted 16 March 2016.

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A successful lifestyle intervention model replicated in diverse clinical settings S Mark,1 MSc, PhD; S du Toit,2 MD; T D Noakes,3 MD, DSc; K Nordli;2 D Coetzee,4 MD; M Makin,4 MD; S van der Spuy,4 MD; J Frey,4 MD; J Wortman,5 MD pproach Analytics, Nanaimo, British Columbia, Canada A Valemount Health Center, British Columbia, Canada 3 Department of Human Biology, Faculty of Health Sciences, University of Cape Town; Sports Science Institute of South Africa, Cape Town, South Africa 4 Omineca Medical Clinic, Vanderhoof, British Columbia, Canada 5 Department of Family Practice, Faculty of Medicine, University of British Columbia, Vancouver, Canada 1 2

Corresponding author: S Mark (sean@approachanalytics.com)

Lifestyle interventions (LIs) can treat metabolic syndrome and prevent type 2 diabetes mellitus, but they remain underutilised in routine practice. In 2010, an LI model was created in a rural primary care practice and spread with few resources to four other rural practices. A retrospective chart review evaluated changes in health indicators in two practice environments by following 372 participants, mainly women (mean age 52 years). Participants had a mean body mass index of 37 kg/m2 at baseline and lost an average of 12% of their initial body weight as a result of the intervention. Among participants at the first intervention site for whom cardiometabolic data were available, the prevalence of metabolic syndrome decreased from 58% at baseline to 19% at follow-up. Taken as a whole, our experience suggests that LIs are feasible and deliver meaningful results in routine primary care practice. S Afr Med J 2016;106(8):763-766. DOI:10.7196/SAMJ.2016.v106i8.10136

Lifestyle interventions (LIs) can treat metabolic syndrome and reduce the incidence of type 2 diabetes mellitus (T2DM) in high-risk individuals.[1] However, realising the health benefits of LIs in routine clinical practice remains elusive.[2] In January 2010, an LI model was created in a rural primary care practice and spread to four other rural communities. We present changes in health indicators among participants in two physician-led interventions.

Methods

Ethics approval was obtained from the Northern Health Authority and the University of British Columbia (Ref. no. H10-02573), Canada. The intervention was open to both individuals wanting to lose weight and those interested in a non-pharmacological approach to managing insulin resistance. The foundation of the intervention model was group medical visits, with 15 - 25 participants overseen by a clinical facilitator. The clinically facilitated meetings featured a presentation germane to living a healthier lifestyle, such as sugar addiction, medication management, maintaining adherence while on vacation, etc. The remainder of the meeting time was used to answer participants’ questions and address experiences relating to living a healthier lifestyle. At the first site (S1), programme length was determined by participants’ progress towards their health goals. At the second site (S2), the intervention was 3 months in length. Individuals requiring additional support were encouraged to form peer-led support groups on their own initiative. A quality improvement process whereby various lifestyle pre scriptions were tested with different groups was used to refine the intervention at S1. Results from these non-randomised ‘trials’ were tracked using local electronic medical record data. The outcome of this process was an intervention featuring a two-stage diet programme. The weight-loss diet restricted calories to approximately 1 100 and 1 500 kcal/day for women and men, respectively; participants were

instructed to avoid foods containing sugar and other refined carbo hydrates, in addition to restricting the consumption of dietary fat. To assist in appetite control, participants were instructed not to undertake moderate or vigorous physical activity until they had reached their weight-loss goal. After reaching their target weight, a high-fat diet was used for weight maintenance. The use of a high-fat diet was predicated on the high prevalence of insulin resistance in the patient population and favourable changes in multiple health indicators in randomised trials of up to 2 years’ duration in such populations.[3] Foods consumed on the maintenance diet included beef, poultry, fish, eggs, oils, moderate amounts of hard cheeses, and small amounts of nuts, nut butters, seeds and berries.

Measurements

Height was measured using a stadiometer, with participants wearing no shoes. Waist circumference was measured with a flexible tape measure and with the help of another participant. Weight was measured at every group visit with participants wearing light indoor clothing. Participants completed the PHQ-9 questionnaires to assess their mood. Scores on the PHQ-9 range from 0 (absence of depressive symptoms) to 27 (severe depressive symptoms). A score of ≥10 on the PHQ-9 was used to indicate depression.

Evaluation rationale, data extraction and statistical analyses

Following the success of the intervention at S1, the intervention model spread to four other rural communities. The intervention was created in 2010 by a physician (SDT) working in a service contract environment and was adopted into the practices of four fee-for-service physicians, a nurse practitioner and two registered nurses. The initial evaluation was planned to document health changes at S1, but owing to the unanticipated spread of the intervention, weight-loss results were included in the evaluation from four fee-for-service physicians.

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Results

This study documented the creation and replication of a successful LI in rural British Columbia (BC). We evaluated health imp rovements among 372 participants at two physician-led interventions in a service contract (S1) and a fee-for-service practice context (S2); 139 participants were evaluated at S1 and 233 at S2, which began 2 years after the creation of the LI model at S1 (Tables 1 and 2). Participants at both sites were mainly women (~80%), with a mean age of 52 (standard deviation (SD) 13) years and 51 (SD 14) years for S1 and S2, respectively. Participants ranged in age from 16 to 85 years. Additional measures were available from participants at S1, including cardiometabolic indicators (n=119) and mood scores (n=111). More than 90% of participants had a high waist circumference, while the average baseline BMI was 37 kg/ m2. Consistent with the high prevalence

45 39.2

40 35 Participants, %

The clinical and community observations from the other sites, which have not been formally evaluated, were consistent with the health improvements reported here. Data were extracted from an electronic medical system during the most active periods of the interventions; this was early 2010 to 2011 for S1, while for S2 anthropometric data were retrieved beginning in early 2012. For S1, where cardiometabolic data were available, baseline data were sought no earlier than January 2008. The time between the first and last weighing was used to define the time spent in the LI by participants at S1, as participants were weighed at each meeting. Intensity of participation in the LI was calculated by dividing the months in the programme by the number of visits. We used International Diabetes Federation criteria[4] to classify participants as having metabolic syndrome (MetS). A haemoglobin A1c (HbA1c) measurement was used to indicate the presence of diabetes, in accordance with local clinical protocols. Differences between anthropometric and biochemical variables were calculated, and paired t-tests were used to assess whether baseline values were statistically different to those at follow-up. Owing to the small sample size of individuals with HbA1c measurements (n=18), the Wilcoxon signedrank test was used to test whether followup values were significantly different from baseline. We used multivariable analysis to examine the predictors of changes in body mass index (BMI) between baseline and follow-up in participants at S1. All statistical analyses were conducted on SAS version 9.2 (SAS Institute, USA).

29.8

30 25 20

16.9

15 10

7.3 4.0

5 0

0.0

0.3

0.0

1.1

−4

−10

−16

−22

−28

0.5

0.3

−34

−40

−46

Weight loss, %

Fig. 1. Weight loss (%) among participants in LIs in two primary care practices in rural British Columbia, Canada (N=372).

Table 1. Characteristics at baseline and follow-up of participants at S1 in a service contract primary care practice in rural BC, Canada (N=139) Characteristic

Baseline

Follow-up

Change

p-value

Age (years), mean (SD)

52.4 (13.1)

Sex, % female

80.4

Height (m), mean (SD)

1.7 (0.1)

Weight (kg), mean (SD)

97.2 (22.6)

84.2 (20.6)

–12.8 (8.9)

<0.0001

BMI (kg/m ), mean (SD)

35.4 (7.0)

30.7 (6.4)

–4.7 (3.2)

<0.0001

% with elevated waist circumference

90.7

66.2

–24.5

<0.0001

% with metabolic syndrome

57.6

19.4

–38.2

<0.0001

% with PHQ-9 score ≥10

23.7

7.9

–15.8

<0.0001

PHQ-9 score (n=111), mean (SD)

7.0 (5.2)

3.4 (4.6)

–3.6 (4.6)

<0.0001

Blood pressure (mmHg, n=119), mean (SD)

136.6/85.4

122.5/77.0

–14.1/8.4

<0.0001

HDL-C (mmol/L, n=119), mean (SD)

1.34 (0.35)

1.42 (0.35)

0.08 (0.27)

0.0019

LDL-C (mmol/L), mean (SD)

3.31 (1.04)

2.90 (0.88)

–0.41 (0.97)

<0.0001

Triglyceride concentration (mmol/L), mean (SD)

1.63 (0.80)

1.08 (0.59)

–0.56 (0.64)

<0.0001

Triglyceride/HDL-C ratio, mean (SD)

1.36 (0.91)

0.84 (0.73)

–0.52 (0.77)

<0.0001

Fasting blood glucose concentration (mmol/L, n=111), mean (SD)

5.91 (1.74)

5.32 (1.17)

–0.59 (1.47)

<0.0001

HbA1c concentration (%, n=18), mean (SD)

7.47 (1.64)

6.95 (1.09)

–0.52 (1.91)

0.089

HDL-C = high-density lipoprotein cholesterol; LDL-C = low-density lipoprotein cholesterol.

of obesity, 57.6% (80/139) of participants began the intervention at S1 with MetS while 12.9% (18/139) had T2DM. Participants in these LIs had unusually large improvements in health, particularly given the real-world contexts of the interventions. For example, 372 participants had weight loss of >12% (Fig. 1), while in the Diabetes Prevention Program, a wellresourced trial, the weight-loss goal was 7% of initial body weight. Among other studies examining LIs in routine practice, average weight loss was 3 - 5% at year 1.[2] Consistent with the considerable weight loss, participants at S1 showed marked

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improvements in their cardiometabolic profile. For example, blood triglyceride concen trations, measured among 119 participants at S1, decreased by 34%, probably a reflection of the reduced intake of starches and sugars.[3] Among the 18 individuals with T2DM in the LI at S1, there was a mean decrease in HbA1c of 0.5%, a figure that fails to account for any reductions in pharmacotherapy, which were not documented in this report. The extent of the changes in cardiometabolic indicators that were measured in this study are therefore a conservative estimate of the health improvements, as participants experienced reductions in the use of

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Table 2. Characteristics at baseline and follow-up of participants at S2 in a rural feefor-service primary care practice in BC, Canada (N=233) Characteristic

Baseline

Follow-up

Change

p-value

Age (years), mean (SD)

51.3 (14.1)

Sex, % female

81.6

Height (m), mean (SD)

1.6 (0.1)

Weight (kg), mean (SD)

101.0 (21.4)

89.5 (19.4)

–11.4 (6.4)

<0.0001

BMI (kg/m2), mean (SD)

37.2 (6.6)

33.0 (6.2)

–4.3 (2.5)

<0.0001

% with elevated waist circumference

98.3

83.3

–15.0

<0.0001

Table 3. Predictors of change in BMI among participants in an LI in rural BC, Canada (N=132) Parameter

Change in BMI

Standard error

p-value

R2 (full model = 0.23)

Sex (women referent)

–0.236

0.646

0.7151

0.000

Age of participants (years)

0.036

0.019

0.0618

0.024

Baseline BMI (kg)

0.179

0.035

<0.0001

0.151

Months in programme

0.138

0.065

0.0347

0.018

No. of visits/month

0.721

0.254

0.0045

0.033

insulin and oral hypoglycaemic, antihypertensive and cholesterol-lowering agents. To the intervention participants, the reductions in pharmacotherapy were an empowering ‘side-effect’ of the intervention, and for the clinicians administering the intervention, use of this therapeutic approach improved control of hyperglycaemia, hypertension and dyslipidaemias. Similar to the findings of others,[5,6] we documented improvements in mood among participants in the intervention at S1 (n=111). Among the 32 participants with mood scores indicative of depression (PHQ-9 score ≥10), the mean decrease in score was 7.0 (SD 5.2). It was not possible to separate the effect of participating in group sessions from the physiological effects of the LI, as both these exposures are probably associated with improvements in mood. The mood improvements associated with weight loss may be attributable to reductions in pathophysiological processes such as inflammation and hypothalamic-pituitary-adrenal axis activation that are common to both insulin resistance and mood disorders.[7] We examined the predictors of weight change among participants at S1 using multivariable analysis (Table 3). We found that each visit per month increase in the LI was associated with a 0.7 kg/m2 greater loss in BMI after controlling for sex, age, baseline BMI and time spent in the programme. The importance of intensity of participation was reaffirmed in regression analysis by using change in weight per month as the

dependent variable. These findings highlight the importance of group support in achieving therapeutic goals. Moreover, the clinical observation prior to the creation of the LI model was that one-on-one lifestyle counselling was less effective in producing lifestyle changes than participation in support groups. The effectiveness of support groups in the context of LIs has been documented previously[8] and may indicate the contribution of food addictions to these conditions.[9]

Conclusions

We documented the creation of an LI model and the replication of this intervention in different rural practices. This intervention was a powerful wellness tool, empowering not only patients[10] and physicians but the rural communities, which can be burdened with a high prevalence of chronic disease. The intervention model documented in this study differed from the consensus prescription for LIs. For example, participants in this intervention were counselled to restrict moderate to vigorous physical activity while on the weight-loss diet; in contrast, in two highly cited randomised trials, participants were encouraged to undertake 150[1] and 175[11] minutes per week of moderate physical activity, respectively. More controversially, our intervention used a high-fat diet for weight maintenance, while in the Diabetes Prevention Program and the Look AHEAD trials, participants were counselled to avoid consuming foods rich in

August 2016, Print edition

dietary fat. These conflicting prescriptions allude to a state of uncertainty that exists with regard to the optimal prescription for LIs for individuals with insulin resistance. This situation persists despite decades-old findings by Reaven (Garg et al.[12]) showing that insulin resistance is fundamentally a disorder of carbohydrate metabolism. Given the magnitude of the obesity and diabetes pandemics, there is a public health imperative to provide practitioners with evi dence that supports effective interventions. While well-resourced randomised trials are powerful analytical tools, rigorous trials take decades to yield results and are argu [13] ably prohibitively expensive. Moreover, study results often lack generalisability to [14] routine practice. In contrast, the quality improvement process used in this study was not only powerful, as evidenced by the replication of the intervention model at four different practice sites, but offers a more expeditious way to spread effective interventions for obesity and insulin resistance. Despite the rigour of our quality improvement process, our efforts to communicate the merits of this intervention to health system administrators met with a frustrating lack of uptake. This is not surprising, given that the research literature has many competing ‘solutions’ for the epidemics of obesity and diabetes,[15] many of which are difficult to falsify.[16] To support health administrators in making evidence-based decisions, a broader set of data sources could be used to evaluate health system interventions such as that documented here. For example, the Institute of Health Improvement recommends using indicators that measure patient satisfaction, health system cost and population health status,[17] complementing data from physician records. A broader set of health system indicators combined with longer-term follow-up of intervention participants would enable evidence-based health system decision-making in a climate of fiscal restraint. Taken as a whole, our evidence suggests that a timely response to the obesity and diabetes pandemics requires a critical rethink not only of the current evidence base underpinning LIs, but also of the systems with which evidence is generated and integrated into health system practice. Conflicts of interest. SDT, KN, DC, MM, SVDS and JF have no conflicts of interest to declare. SM is the founder of a sole proprietorship, Approach Analytics, providing analytical support to clinical and public health initiatives. JW is on the Scientific Advisory

IN PRACTICE

Board for Atkins Nutritionals Inc. and has accepted honoraria and travel expenses to attend meetings. TN is the author of the books Lore of Running and Waterlogged and co-author of The Real Meal Revolution, Raising Superheroes and Challenging Beliefs. All royalties from the sales of The Real Meal Revolution and Raising Superheroes and related activities are donated to the Noakes Foundation, of which he is the chairman and which funds research on insulin resistance, diabetes and nutrition as directed by its Board of Directors. Money from the sale of other books is donated to the Tim and Marilyn Noakes Sports Science Research Trust, which funds the salary of a senior researcher at the University of Cape Town, South Africa. The research focuses on the study of skeletal muscle in African mammals with some overlap to the study of type 2 diabetes in carnivorous mammals and of the effects of (scavenged) sugar consumption on freeliving (wild) baboons. 1. Orchard TJ, Temprosa M, Goldberg, R, et al. The effect of metformin and intensive lifestyle intervention on the metabolic syndrome: The Diabetes Prevention Program Randomized Trial. Ann Intern Med 2005;142(8):611-619. DOI:10.7326/0003-4819-142-8-200504190-00009 2. Kahn R, Davidson MB. The reality of type 2 diabetes prevention. Diabetes Care 2014;37(4):943-949. DOI:10.2337/dc13-1954 3. Shai I, Schwarzfuchs D, Henkin Y, et al. Weight loss with a low-carbohydrate, Mediterranean, or lowfat diet. N Engl J Med 2008;359(3):229-241. DOI:10.1056/NEJMoa0708681 4. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the metabolic syndrome: A joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention;

National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 2009;120(16):1640-1645. DOI:10.1161/circulationAHA.109.192644 5. McClernon FJ, Yancy WS, Eberstein JA, Atkins RC, Westman EC. The effects of a low-carbohydrate ketogenic diet and a low-fat diet on mood, hunger, and other self-reported symptoms. Obesity (Silver Spring) 2007;15(1):182-187. DOI:10.1038/oby.2007.516 6. Brinkworth GD, Noakes M, Buckley JD, Keogh JB, Clifton PM. Long-term effects of a very-lowcarbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo. Am J Clin Nutr 2009;90(1):23-32. DOI:10.3945/ajcn.2008.27326 7. McIntyre RS, Soczynska JK, Konarski JZ, et al. Should depressive syndromes be reclassified as ‘metabolic syndrome type II’? Ann Clin Psychiatry 2007;19(4):257- 264. DOI:10.1080/10401230701653377 8. Jaber R, Braksmajer A, Trilling JS. Group visits: A qualitative review of current research. J Am Board Fam Med 2006;19(3):276-290. DOI:10.3122/jabfm.19.3.276 9. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev 2008;32(1):20-39. DOI:10.1016/j. neubiorev.2007.04.019 10. Lavoie C. Gestational diabetes: Poke, pee, and eat your carbs. Can Fam Physician 2011;57(7):756-757. 11. Look AHEAD Research Group, Wing RR, Bolin P, Brancati FL, et al. Cardiovascular effects of intensive lifestyle intervention in type 2 diabetes. N Engl J Med 2013;369(2):145-154. DOI:10.1056/NEJMoa1212914 12. Garg A, Bantle JP, Henry RR, et al. Effects of varying carbohydrate content of diet in patients with non-insulin-dependent diabetes mellitus. JAMA 1994;271(18):1421-1428. DOI:10.1001/ jama.1994.03510420053034 13. Howard BV, van Horn L, Manson JE, et al. Low-fat dietary pattern and risk of cardiovascular disease: The Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA 2006;295(6):655-666. DOI:10.1001/jama.295.6.655 14. Rothwell PM. External validity of randomised controlled trials: ‘To whom do the results of this trial apply?’ Lancet 2005;365(9453):82-93. DOI:10.1016/S0140-6736(04)17670-8 15. Taubes G. Prosperity’s plague. Science 2009;325(5938):256-260. DOI:10.1126/science.325_256 16. Ioannidis JP. Why most published research findings are false. PLoS Med 2005;2(8):e124. DOI:10.1371/ journal.pmed.0020124 17. Berwick DM, Nolan TW, Whittington J. The triple aim: Care, health and cost. Health Aff 2008;27(3):759-769. DOI:10.1377/hlthaff.27.3.759

Accepted 6 June 2016.

CLINICAL ALERT

Severe hypertension in pregnancy: Using dynamic checklists to save lives J Moodley,1 MB ChB, FRCOG, FCOG, MD; N C Ngene,2 Dip Obst, Dip HIV Man, MMed (Fam Med), FCOG, MMed (O&G) omen’s Health and HIV Research Group, Department of Obstetrics and Gynaecology, School of Clinical Medicine, College of Health Sciences, W Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa 2 Department of Obstetrics and Gynaecology, School of Clinical Medicine, College of Health Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa 1

Corresponding author: J Moodley (jmog@ukzn.ac.za)

Severe hypertension is a major cause of morbidity and mortality. The South African Saving Mothers report (2011 - 2013) indicates that cerebral injury due to severe hypertension is resulting in avoidable maternal deaths. This demands that management of severe hypertension in pregnancy needs to be improved. A rapid-acting antihypertensive is recommended for the initial management of severe hypertension during pregnancy. A single dose of a rapid-acting agent may be ineffective, in which case incremental doses of the same medication or another antihypertensive may be required for adequate blood pressure control. To ensure that appropriate antihypertensives at the correct doses are administered, the use of a guideline in a dynamic checklist format is advocated and discussed in this article. It is envisaged that the use of dynamic checklists will be valuable to all healthcare professionals providing care during pregnancy and the puerperium. S Afr Med J 2016;106(8):767-770. DOI:10.7196/SAMJ.2016.v106i8.10908

Hypertensive disorders of pregnancy (gestational hypertension, preeclampsia, eclampsia and chronic hypertension) are a major cause of maternal mortality in South Africa (SA) and worldwide. The most recent Saving Mothers report (2011 - 2013)[1] indicates that 14.8% of all maternal deaths were due to hypertensive disorders of pregnancy (HDP). This publication, which is the triennial report of the National Committee for Confidential Enquiries into Maternal Deaths (NCCEMD) in SA, also indicates that the final cause of death in >50% of hypertensive maternal mortality was probably associated with cerebral injury, particularly in cases of severe pre-eclampsia and eclampsia. In addition, the majority of deaths occurred in young

women in their first pregnancies and a large proportion (>60%) were avoidable.[1] Although severe HDP may cause other target organ damage such as renal impairment and pulmonary oedema, the authors have chosen to elaborate on cerebral injury, given the Saving Mothers report on the association between untreated severe hypertension and cerebral haemorrhage.[1] Moreover, in the authors’ clinical experience and according to findings in recent reports, severe hypertension often precedes other cerebral manifestations such as blindness in pregnancy, stroke, altered mental state and the posterior reversible encephalopathy syndrome (PRES).[2-6]

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PRES and severe hypertension in pregnancy

A known maternal cerebral complication of severe pre-eclampsia is PRES.[2] This syndrome is a clinico-neuroimaging entity and is hypothesised to be related to impaired cerebral blood flow autoregulation that leads to either over- or under-perfusion of the brain. On magnetic resonance imaging and computed tomography scans of the brain, oedema is seen mainly in the subcortical white matter and occasionally in the cortex of the occipital and parietal lobes.[3] Recently, Van Veen et al.[4] investigated cerebral blood flow autoregulation by measuring cerebral artery blood flow velocity using transcranial Doppler ultrasound and found impaired autoregulation in women with pre-eclampsia when compared with those who had gestational hypertension or normal pregnancies. There is therefore increasing evidence that impaired cerebral blood flow autoregulation plays a central pathological role in cerebral manifestations associated with pre-eclampsia/eclampsia syndrome. Symptoms of PRES include persistent headache, nausea, vomiting, visual disturbances, confusion and seizures. These clinical signs are well known by obstetricians to herald seizures and other features of cerebral dysfunction. Eclampsia is reported to be one of the most important causes of PRES, and although most patients have severe hypertension, some have mildly elevated or even normal blood pressure (BP).[2,4] It has been reported that PRES is reversible and that initiating early treatment of severe hypertension leads to cure, while delayed recognition of symptoms and cognisance of the need to lower high BP judiciously but immediately leads to cerebral injury.[2,3] The Saving Mothers report (2011 - 2013)[1] indicates that one of the avoidable health professional factors leading to maternal mortality is failure to institute appropriate and prompt management of severe systolic and diastolic hypertension in the ante-, intra- and postpartum periods.

Immediate treatment of severe hypertension in pregnancy

Standardised clinical protocols for the management of severe preeclampsia and eclampsia have been shown to reduce complications associated with this hypertensive disorder.[7-9] In pregnancy, acuteonset severe hypertension that is accurately measured using standard techniques and persistent for ≥15 minutes is regarded as a hypertensive emergency.[7-9] If not adequately treated, severe hypertension can cause cerebral injury. A systolic BP of >160 mmHg is included in the definition of severe hypertension in pregnancy. Severe diastolic hypertension of ≥110 mmHg is also regarded as a hypertensive emergency.[7-10] Pregnant women with acute-onset, severe systolic and/or diastolic BPs in the ante-, intra-, or immediate postpartum periods therefore warrant antihypertensive treatment. The goal should be to lower high BP levels to a range of 140 - 150/90 - 100 mmHg in order to prevent repeated prolonged exposure of the patient to severe systolic hypertension with subsequent loss of cerebral vasculature autoregulation.[10]

Some case scenarios and the ‘5 Rs’ in severe hypertension in pregnancy

If health professionals are aware that severe hypertension in preg nancy may result in cerebral injury, what should they do when they are faced with such clinical situations in an SA setting? Health professionals must be aware of the 5 Rs: 1. Recognition that acute-onset severe hypertension (≥160 mmHg systolic or ≥110 mmHg diastolic BP) in pregnant women is a MAJOR ALERT 2. Responding by notifying a specialist or seeking advice from the most appropriate health professional 3. Responsibility: taking responsibility to initiate early anti hypertensive therapy and provide close monitoring until the patient is stabilised

4. Reviewing the clinical situation once high BP is stabilised 5. Realising that effective high BP control is merely a surrogate marker of maternal and neonatal outcome; components such as fetal assessment, prevention of seizures (eclampsia), expeditious delivery and post-delivery care must therefore be considered.[1-10]

Case scenarios

Health professionals may be faced with women with acute-onset severe hypertension in varying clinical scenarios. These include: • In the antenatal period. When hypertension occurs in this setting, the patient should be admitted to hospital immediately and the high BP should be stabilised before delivery, even in urgent situations.[1] Lowering of the high BP should occur in a high-care area, or a dedicated bed selected for this purpose. • If transfer from a district health facility to a regional/tertiary centre is required, the high BP should be stabilised and other measures such as the administration of magnesium (in cases of severe preeclampsia and/or eclampsia) started before transfer. Monitoring must continue while awaiting an ambulance for the transfer. • When the diagnosis of acute-onset severe pre-eclampsia is made in an office setting, available emergency treatment should be initiated and the patient expeditiously sent to a regional/tertiary hospital for treatment and further management. • If any hospitalised patient with pre-eclampsia has either a systolic BP of 160 mmHg or a diastolic BP of 110 mmHg, the automatic response should be initiating a rapid-acting antihypertensive agent such as nifedipine 10 mg orally, labetalol 20 mg intravenously (IV) or hydralazine 5 - 10 mg IV.[9,10] • Induction of anaesthesia and intubation. In a setting in which the patient may require endotracheal intubation in a labour ward (high-care bed), an operating theatre or an intensive care unit, it should be recognised that endotracheal intubation increases the BP and should therefore not be undertaken without prior measures to prevent or minimise the hypertensive response to intubation. • Acute-onset severe hypertension in the postpartum period. Onset may occur for the first time after delivery, or it may be superimposed on women with chronic hypertension, gestational hypertension and those with mild to moderate pre-eclampsia. In women with such diagnoses, long-acting antihypertensive therapy must therefore be maintained after delivery and not stopped abruptly. In the clinical setting of postpartum acute-onset severe hypertension, the same treatment, viz. rapid-acting antihypertensive agents, must be used to stabilise systolic and/or diastolic hypertension. In general terms, healthcare professionals must provide close maternofetal monitoring during the stabilisation of acute-onset severe hypertension. Judicious fluid administration is recommended, especially in the oedematous pre-eclamptic patient with oliguria and laboratory signs of renal dysfunction. Fluid balance and signs of early pulmonary oedema must therefore be given careful attention. After initial BP stabilisation, close monitoring should be carried out and a maintenance dose of antihypertensive(s) given. Over the past decade, the use of clinical protocols and dynamic checklists has become a standard approach to ensure patient safety and improve the care provided to mothers and their newborns.[11] The clinical management of severe acute-onset pregnancy hypertension lends itself to dynamic checklists.

First-line antihypertensive therapy for acute-onset severe hypertension

IV labetalol, IV dihydralazine and oral nifedipine are the commonly used antihypertensive agents. The contraindications to and

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Severe hypertension in pregnancy Regard as a MAJOR ALERT BP ≥160 mmHg systolic, or ≥110 mmHg diastolic; therefore inform the most senior/experienced obstetrician/medical officer/fetomaternal specialist. Institute fetal surveillance if the fetus is viable. Aim to achieve a goal BP of 140 - 150/90 - 100 mmHg. Is patient conscious and able to tolerate oral medication? Yes

If severe hypertension persists for ≥15 minutes, administer nifedipine tablet (10 mg orally).

If the high BP persists for ≥15 minutes or if there are symptoms of impending eclampsia (nausea and vomiting, severe headache, epigastric pain, visual disturbances), administer labetalol 20 mg IV slowly over 2 minutes.

Re-check BP after 20 minutes.

Check BP after 10 minutes. If there is still severe hypertension, administer nifedipine tablets (20 mg orally). If the BP is successfully reduced below the severe hypertension threshold, continue BP monitoring closely.

If there is still severe hypertension, administer IV labetalol 40 mg over 2 minutes. Should the BP be successfully reduced below the severe hypertension threshold, continue BP monitoring closely.

Re-check BP after 20 minutes. If there is still severe hypertension, administer nifedipine tablets (20 mg orally). If the BP is successfully reduced below the severe hypertension threshold, continue BP monitoring closely.

Check BP after 10 minutes. If there is still severe hypertension, administer IV labetalol 80 mg over 2 minutes. If the BP is successfully reduced below severe hypertension threshold, continue BP monitoring closely. Check BP after 10 minutes. If there is still severe hypertension, obtain emergency consultation from one of the following: fetomaternal specialist, internal medicine specialist, obstetric anaesthetist or critical care specialist.

Re-check BP after 20 minutes.

Administer additional antihypertensive drug as per specific order (in SA this is usually methyldopa 500 mg 6-hourly). Administer additional antihypertensive therapy as per specific order. Once the desired BP is achieved: • re-check BP every 10 minutes for the next 1 hour • then re-check BP every 15 minutes for the next 1 hour • then re-check BP every 30 minutes for the next 1 hour • then re-check BP every 1 hour for the next 4 hours.

Once the desired BP is achieved: • re-check BP every 10 minutes for the next 1 hour • then re-check BP every 15 minutes for the next 1 hour • then re-check BP every 30 minutes for the next 1 hour • then re-check BP every 1 hour for the next 4 hours • then re-check BP every 4 hours. Commence additional antihypertensive therapy per specific order.

Note: Hydralazine (5 mg or 10 mg IV over 2 minutes) may be the initial antihypertensive administered. After 20 minutes, an additional 10 mg may be administered. In the next 20 minutes, 20 mg may be administered. Then re-check BP after 10 minutes; if there is still severe hypertension, request emergency consultation and commence labetalol 40 mg IV over 2 minutes. Fig. 1. Algorithm for the initial control of BP in severe hypertension in pregnancy.

compelling indications for the available rapid-acting agents must be considered when choosing a particular drug. Magnesium sulphate

is not recommended as an antihypertensive agent, but remains the drug of choice for seizure prophylaxis in severe pre-eclampsia

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Table 1. Common contraindications of the rapid-acting antihypertensive agents Cautions

Contraindications

Nifedipine

Hypertrophic obstructive cardiomyopathy, aortic stenosis. The capsules cause a reflex increase in sympathetic tone which should be avoided in women with increased myocardial oxygen demands, e.g. fixed valvular obstruction.

Unstable angina, congestive heart failure, myocardial infarction

Labetalol

Controlled heart failure, hepatic disorder. Best avoided in women with asthma. Parenteral labetalol may cause neonatal bradycardia, but is not a major problem in clinical practice.

Heart failure with symptoms, 2nd and 3rd degree atrioventricular block, severe bronchospasm, asthma, sinus bradycardia

Hydralazine

Renal or hepatic impairment, porphyria, angina. It causes a reflex increase in sympathetic tone and should therefore be avoided for women in whom increased myocardial oxygen demands could be dangerous, e.g. coronary artery disease, mitral stenosis.

Systemic lupus erythematosus, aortic stenosis, tachycardia, hypertrophic obstructive cardiomyopathy

and for controlling seizures in eclampsia.[12] Nifedipine may be the more appropriate antihypertensive agent in a setting of primary healthcare clinics and midwifery obstetric units because it can be given orally. [13,14] Intravenous agents (labetalol or dihydralazine if available) are preferable if the patient is restless or semiconscious or in a hospital setting. Fig. 1 outlines the steps for the use of rapid-acting antihypertensive agents for acute-onset severe hypertension during pregnancy and the postpartum period. It should be noted that dihydralazine is not available in most provinces of SA. Oral nifedipine and/or labetalol should therefore be a ‘stock item’ for all hospitals providing healthcare for pregnant women. Both of these drugs are available in public sector hospitals in SA. The common contraindications of rapid-acting antihypertensive agents are shown in Table 1. All the agents listed may cause severe hypotension, but these events are rare. It is suggested that where possible fetal heart rate monitoring should be done at the same time as the lowering of very high BP.

Key points

• There is consensus that sustained severe hypertension in pregnancy should be lowered immediately in a controlled manner to reduce the risk of cerebral complications. • A systolic BP of 160 mmHg is suggested as the most appropriate threshold for defining severe maternal hypertension. • If threshold systolic BP levels are sustained or occur with a combination of symptoms suggesting maternal cerebral compli cations, immediate use of rapid-acting antihypertensive agents is essential. • The goal of rapid-acting antihypertensive agents should be to achieve a BP of 140 - 150/90 - 100 mmHg. • Use of dynamic checklists is essential for the management of acuteonset severe pregnancy hypertension.

Conclusion

Severe hypertension in pregnancy is an emergency (major alert) that requires immediate attention. An inappropriately managed severe hypertensive condition may result in cerebral haemorrhage. Timely action to reduce sustained systolic hypertension judiciously by means of a rapid-acting antihypertensive drug will reduce maternal and neonatal mortality and morbidity. 1. National Committee on the Confidential Enquiries into Maternal Deaths. Saving Mothers 20112013: Sixth Report on the Confidential Enquiries into Maternal Deaths in South Africa. Short report. Pretoria: NDoH, 2015. http://www.kznhealth.gov.za/mcwh/Maternal/Saving-Mothers-2011-2013short-report.pdf (accessed 28 August 2015). 2. Mayama M, Uno K, Tano S, et al. Incidence of posterior reversible encephalopathy in eclamptic and patients with preeclampsia with neurologic symptoms. Am J Obstet Gynecol 2016; Feb 20. pii: S00029378(16)00339-2. DOI:10.1016/j.ajog.2016.02.039 [Epub ahead of print] 3. Naidu K, Moodley J, Corr P, Hoffmann M. Single photon emission and cerebral computerised tomographic scan and TCD in eclampsia. BJOG 1997;104(10):1165-1172. DOI:10.1111/j.1471-0528.1997.tb10941.x 4. Van Veen TR, Panerai RB, Haeri S, et al. Cerebral autoregulation in different hypertensive disorders of pregnancy. Am J Obstet Gynecol 2015;513:e3. DOI:10.1016/j.ajog.2014.11.003 5. Crovetto F, Somalglaiana E, Peguero A, Figueras F. Stroke during pregnancy and pre-eclampsia. Curr Opin Obstet Gynecol 2013;25(6):425-432. DOI:10.1097/GCO.0000000000000024 6. Bushnell C, Chireau M. Pre-eclampsia and stroke. Stroke Res Treat 2011 (2011), Article ID 858134. DOI:10.4061/2011/858134 7. Von Dadelszen P, Sawchuck D, McMaster R, et al. The active implementation of pregnancy hypertension guidelines in British Columbia. Obstet Gynecol 2010;116(3):659-666. DOI:10.1097/ AOG.0b013e3181eb669d. 8. American College of Obstetricians and Gynecologists. Emergent therapy for acute-onset, severe hypertension during pregnancy and the postpartum period. Committee opinion No. 623. Obstet Gynecol 2015;125(2):521-525. DOI:10.1097/01.AOG.0000460762.59152.d7 9. Magee LA, Abalos E, von Dadelszen P, et al., for the CHIPS Study Group. How to manage hypertension in pregnancy effectively. Br J Clin Pharmacol 2011;72(3):394-401. DOI:10.1111/j.1365-2125.2011.04002.x 10. Clark SL, Christmas JL, Frye DR, Meyers JA, Perlin JR. Maternal mortality in the United States: Predictability and the impact of protocols on fatal post caesarean pulmonary embolism and hypertension-related intracranial haemorrhage. Am J Obstet Gynecol 2014;211(1):32.e1-32e9. DOI:10.1016/j.ajog.2014.03.031 11. Fausett MB, Propst A, von Doren K, Clark BT. How to develop an effective obstetric checklist. Am J Obstet Gynecol 2011;205(3):165-170. DOI:10.1016/j.ajog.2011.06.003. 12. Altman D, Carroli G, Duley L, et al., for Magpie Trial Collaboration Group. Do women with preeclampsia and their babies benefit from magnesium sulphate? The Magpie Trial: A randomised placebo-controlled trial. Lancet 2002;359(9321):1877-1890. DOI:10.1016/S0140-6736(02)908778-0. 13. Shekhar S, Gupta S, Kirubakaran R, Pareek P. Oral nifedipine versus intravenous labetalol for severe hypertension during pregnancy: A systematic review and meta-analysis. BJOG 2016;123(1):40-47. DOI:10.1111/1471-0528.13463. 14. Duley L, Meher S, Jones L. Drugs for treatment of very high blood pressure during pregnancy. Cochrane Database Syst Rev 2013, Issue 7. Art. No.: CD001449. DOI:10.1002/14651858.cd001449.pub3

Accepted 13 April 2016.

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STATEMENT

The World Health Organization’s mechanisms for increasing the health sector budget: The South African context F H J Venter, MCom (Economics), DPH; J E Wolvaardt, BCur, MPH, PGCHE, PhD School of Health Systems and Public Health, Faculty of Health Sciences, University of Pretoria, South Africa Corresponding author: F H J Venter (fouche.venter@dnaeconomics.com)

South Africa (SA) has limited scope for raising income taxes, and the proposed National Health Insurance (NHI) scheme will necessitate growth in the health sector budget. The NHI White Paper suggests five funding scenarios to meet the expected shortfall. These scenarios are a mixture of a surcharge on taxable income, an increase in value-added tax and a payroll tax. Five alternative options, suggested by the World Health Organization, are interrogated as ways to decrease the general taxation proposed in the White Paper. The five mechanisms (corporate tax, financial transaction levy, and taxes on tobacco, alcohol and unhealthy foods) were chosen based on their fund-raising potential and their mandatory element. A literature review provides the information for a discussion of the potential costs of each mechanism. Within specific assumptions, potential budgetary contribution is compared with the requirement. First, raising corporate tax rates could raise enough funds, but the losses due to capital flight might be too much for the local economy to bear. Second, a levy on currency transactions is unlikely to raise the required resources, even without a probable decrease in the number of transactions. Third, the increase in the tax on tobacco and alcohol would need to be very large, even assuming that consumption patterns would remain unchanged. Lastly, a tax on unhealthy food products is a new idea and could be explored as an option – especially as the SA Treasury has announced its future implementation. Implementing only one of the mechanisms is unlikely to increase available funding sufficiently, but if they are implemented together the welfare-maximising tax rate for each mechanism may be high enough to fulfil the NHI scheme’s budgetary requirement, moderating the increases in the tax burden of the SA population. S Afr Med J 2016;106(8):771-774. DOI:10.7196/SAMJ.2016.v106i8.10654

The World Health Organization (WHO)’s 2010 report on health systems financing for universal health coverage[1] proposed various innovative mechanisms for raising additional resources for health. These proposals were primarily based on a background paper by Stenberg et al.[2] on the same topic, in which each of the options was ranked according to its fund-raising potential. South Africa (SA) is currently in the process of implementing a National Health Insurance (NHI) scheme. The resource requirement for implementation of this scheme is substantial, and the NHI White Paper (hereinafter referred to as ‘the White Paper’) outlines five scenarios to meet the middle-ground projected shortfall of ZAR71.9 billion (2010 prices) by 2025/26.[3] Very little information about the factors and assumptions that were taken into account, such as medical inflation and changes in disease profile, is provided in the White Paper. Scenario A includes the introduction of a payroll tax, a surcharge on taxable income and increases in the rate of value-added tax (VAT). Scenario B utilises a combination of the surcharge with a payroll tax, while scenario C is a combination of a surcharge on taxable income with an increase in VAT. Scenario D is a payroll tax with a surcharge on taxable income, while scenario E is a surcharge on taxable income only. Four of the five scenarios include a surcharge on taxable income, and all five scenarios include percentage increases spread over the time period.[3] However, these are not the only options available. The White Paper also elaborates on excise duties on alcohol and tobacco products, reallocation of medical scheme funding and the proposed carbon tax as potential sources of NHI funding. This article considers excise duties on alcohol and tobacco products along with the various other low-medium, medium, mediumhigh and high potential fund-raising options, without a voluntary

element, as defined and proposed by the WHO, and reviews each in the SA context. Stenberg et al.[2] used various methods to calculate the potential of each option to generate additional resources for the health system. Where possible, this article uses these methods or methods of its own to estimate the increase in the health budget that could potentially result from the implementation of the mechanisms. These elementary calculations assume no change in economic or social behaviour. The result of the calculations is compared with the average yearly increase required by the NHI. The comparison is based on the assumption that the mechanism was implemented in 2010 and that the proceeds from the mechanism are earmarked for the health sector. Possible costs or negative effects of the mechanism’s implementation in SA are extrapolated from the literature.

Health sector funding requirement

The White Paper states that the requirements for health (in real 2010 financial terms) will increase from ZAR109.8 billion in 2010 to ZAR255.8 billion in 2025/26, the proposed roll-out period of the scheme.[3] In addition to this estimation, McIntyre[4] modelled the resource requirements for three health financing reforms, one of which involves pursuing universal health coverage through an NHI scheme. Estimations varied widely depending on assumptions, but her ‘best guess’ scenario increased health resource requirements from state funding to ZAR295 billion by 2025 (2010 prices).[4] Fig. 1 illustrates the gap between the funding requirement necessi tated by NHI implementation (solid line) and the projected funding (dashed line). The projected funding assumes that the budget allocated to the health sector increases at the White Paper’s middle-ground funding scenario rate of 3.5% between 2010 and 2025. Even though

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280 000 260 000 240 000 220 000 ZARm

200 000 180 000 160 000 140 000 120 000 /2 6

/2 5

/2 4

24 20

/2 3

23 20

/2 2

/2 1

/2 0

/1 9

19 20

/1 8

18 20

/1 7

/1 6

16 20

/1 5

/1 4

/1 3

13 20

/1 2

12 20

/1 1

100 000 20

the White Paper assumes that this is its most likely scenario, a GDP growth rate of 3.5% seems optimistic. In the recently pub lished statement by the South African Reserve Bank’s Monetary Policy Committee, it is stated that GDP growth in 2015 was a mere 1.3% and that growth of only 0.8%, 1.4% and 1.8% is expected for 2016, 2017 and 2018, respectively.[5] Given this weak economic outlook, it is possible that even the White Paper’s most pessimistic annual fund ing growth scenario, in which funding to the health sector grows by only 2%, could be a challenge to achieve. Nevertheless, given the information currently available, we thought it was most appropriate to remain in line with the White Paper and base our calculations on its middle-ground scenario of 3.5%. All calculations in this article have been adjusted for inflation using 2010 as the base year. For the funding requirement, the predic tion provided by the White Paper is used. This is a conservative estimate when com pared with that of McIntyre,[4] and is that the SA health budget should grow to ZAR255.8 billion by 2025.[3] The White Paper predicts various short falls in 2025/26 based on various specific health funding growth over the period – ZAR71.9 billion if the baseline resources increase by 3.5% per year (Fig. 1), ZAR27.6 billion if baseline resources increase by 5.0% per year, and finally ZAR108 billion if baseline resources grow by 2.0% per year. Rather than looking at the shortfall in 2025/26, this article calculates the cumulative shortfall under the 3.5% growth scenario over the 15-year period between 2010/11 and 2025/26, the NHI implementation period. This allowed us to calculate an average percentage shortfall for each year within the period and compare this value with the potential funding contribution for each of the instruments under review. The shortfall, represented by the space between the solid and dashed lines in Fig. 1, aggregates to ZAR378.5 billion over the 15 years. This cumulative shortfall represents 16.4% of the cumulative funding projection over the same period, implying that if the funding, as projected by the 3.5% growth scenario, was and is increased by a further 16.4% each year between 2010 and 2025, the cumulative funding would equal the required cumulative expenditure over the implementation period. The five tax scenarios outlined by the White Paper are an attempt to address the shortfall, and this article explores the feasibility of using innovative finance mechanisms to moderate the size of the probable surcharge on taxable income – an inclusion in four of the five tax scenarios.

NHI funding requirement Projection of funding (annual increase of 3.5% in baseline expenditure)

Fig. 1. Projected funding gap (2010 prices).[2]

The options

Recognising the additional resources requ ired for universal healthcare, the WHO proposed 13 options for increasing funding for health. For this article, the options categorised as having a low fundraising potential as well as those with a voluntary or charity element have been disregarded.[2] Only increasing corporate taxes, imposing sectorspecific corporate taxes, imposing a levy on currency transactions, increasing excise duties on alcohol and tobacco products and imposing excise duties on unhealthy foods will therefore be discussed.

Corporate tax

Corporate tax differentials, or a country’s corporate tax rate relative to countries with which it competes for investment, are more important than the absolute level.[6,7] SA’s top marginal corporate income tax rate is currently 28%, with lower rates applying to smaller businesses.[8] When compared with Brazil, Russia, China and India, SA’s corporate income tax rate is in the middle of the range (Table 1). Diamond et al.[7] point out the negative economic effects of a relatively high corporate tax rate in the USA compared with other developed countries, i.e. an outflow of capital and a consequent reduction in productive capacity. In a study on the Organisation for Economic Co-operation and Development countries, Johansson et al.[9] label corporate income taxes as more harmful to economic growth than any other tax. Compared with the other BRICS (Brazil, Russia, China, India and SA) countries, SA may have some space for an increase in corporate taxation. However, following the abolishment of the Secondary Tax on Companies on 1 April 2012,[10] it is unlikely that government would have an appetite for

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Table 1. Corporate tax rates for BRICS member countries (current on 1 January 2015)[10] Country

Top marginal corporate income tax rate

India

34%

Brazil

34%

28%

China

25%

Russia

20%

BRICS = Brazil, Russia, China, India and SA.

such a policy move. In the 2013/14 financial year, corporate tax revenue in SA amounted to ZAR177.3 billion,[11] or ZAR151.3 billion at constant 2010 prices.[12] Covering the NHI shortfall (16.4%) during that year would have required a 13.2% increase in total revenue from corporate income taxation. The WHO report does not suggest an increase in the taxation rate for all companies, but rather for the most profitable. If the shortfall is to be financed by an increase in the corporate tax rate of specific industries instead of all industries, the magnitude of the increase per company would have to be greater. The economic effects resulting from higher relative corporate tax rates that Diamond et al.[7] discuss could be magnified or diminished in these industries. Because of their higher profits, such companies might be able to absorb a greater tax shock, resulting in a subsequent smaller macroeconomic impact. However, if tax rate increases are too severe, capital flight from these profitable industries would lead to comparatively worse economic effects. Further research should be done to estimate the corporate tax rate threshold of SA’s most profitable industries and determine whether this could

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be high enough to significantly affect the NHI budget shortfall without leading to severe macroeconomic consequences.

Levies on financial transactions/instruments

Stenberg et al.[2] provide several examples of how financial transactions can be utilised to raise more revenue for health, e.g. Argentina taxes current account debits and credits, Brazil taxes bank withdrawals and earmarks the revenue for its public health sector, and Zambia has a levy on all gross interest earned on any savings or deposit accounts, treasury bills, government bonds or other financial instruments. In addition, the issuing of diaspora bonds in some countries such as India, Israel and Sri Lanka is mentioned as a mechanism to raise revenue for health.[2] This article reviews the possibility of raising additional funds in SA through a levy imposed on currency transactions. Currency transactions are any transactions in which the buying and/or selling of foreign currency for domestic currency are involved. Stenberg et al.[2] mention that most discussions involving the imposition of a currency transaction levy have focused on imposing such a levy in high-income countries, and then distributing these funds to lowerincome countries. The number of these transactions is relatively low in lower-income countries compared with high-income countries, and the assumption is that the costs might outweigh the benefits when such levies are imposed in lower-income countries. The associated costs include increased market volatility, increased economic uncertainty,[13] and a decrease in the number of transactions due to the levy,[14] a pivotal element of any economy. [2] There is also significant debate around the technical and political feasibility of such a tax, as it has been posited that it is relatively easy to evade through market migration to offshore tax havens or to avoid through asset substitution.[15] Schmidt[16] used an increase in the spread between the bid and ask price in the dollar/yen currency market between 1986 and 2006 as a proxy for the imposition of such a tax. It was found that a 1% increase in the spread caused a 0.43% decrease in the volume of currency transactions.[16] The methodology applied to India described by Stenberg et al.[2] is now applied to SA. SA, although a smaller economy, still managed USD21 billion daily turnover (current prices) from currency transactions in 2013.[17] If the WHO’s High Level Taskforce for Innovative International Financing suggestion of a 0.005% levy on annual turnover[18] had been accepted in SA, ZAR2.9 billion worth of revenue (2010 prices and average 2013 exchange rate of ZAR9.65[19] per USD) could have been added to the SA revenue pool in 2013. It can, however, be expected that this amount would be slightly lower, as the imposition of the tax would also lead to fewer daily currency transactions and therefore less daily turnover. Even if there was, unrealistically, no decrease in the number of transactions and the entire amount of revenue raised by the levy had been earmarked for the health sector in 2013, the levy would have been able to decrease the shortfall by 14.5% from ZAR20 billion to ZAR17.1 billion.[20] It is clear that that even under the best circumstances, a tax on currency transaction would only be able to reduce the shortfall marginally on its own.

Excise taxes on products harmful to health

The harmful side-effects of tobacco consumption (e.g. neoplastic, vascular and respiratory diseases,[21] cancer, abdominal aortic aneurysms and cataracts[22]) and excessive alcohol consumption (e.g. infectious diseases, stroke, cancer, diabetes, neuropsychiatric diseases, liver and pancreatic disease[23,24]) are well documented. In fact, research has shown that tobacco and alcohol are the second and third largest contributors, respectively, to the global disease burden and together cause nearly 12% of the world’s disability-adjusted lifeyears. There is therefore a rational reason for the widespread advocacy

for the imposition of excise duties on alcohol and tobacco products, as it has been shown that these duties can decrease consumption and subsequently decrease the disease burden.[25,26] In SA, specific excise duties on alcohol and tobacco contributed 3.2% to total tax revenue in 2013/14, or approximately ZAR24.7 billion (constant 2010 prices).[12] If SA had increased the revenue generated from these taxes and earmarked the increased revenue to the health sector to cover the NHI shortfall in 2013/14, it would have had to increase tax revenue from excise duties on alcohol and tobacco by 80.8%.[6] Given the effect that an increase in the tax rates would have on demand in the formal market for these goods, on average, the tax rates themselves would have had to be increased by even more than 80.8%. Stenberg et al.[2] also suggest a tax on unhealthy food. This can be done through increased VAT on foods that are high in fat or sugar, or a specific tax per unit on unhealthy products such as carbonated sugary beverages, sweets, ice cream, etc.[2] The most widely advocated instrument, which SA is in the process of implementing, is a specific tax on sugar-sweetened beverages. Similar to alcohol and tobacco, the side-effects of excessive consumption of these products can be severe and include obesity, diabetes, coronary heart events and strokes.[27,28] The rationale for excise duties on unhealthy products is therefore similar for all products. The price elasticity of demand for alcohol[29-31] and tobacco[29,31] is traditionally relatively low,[31,32] meaning that the imposition of a tax can contribute substantially to the total revenue pool.[2] The price elasticity of demand for unhealthy food products varies more widely, depending on the substitutability of the product. [31] If the tax is high enough to affect consumption, the health benefits from decreased consumption are able to decrease the health budget requirement.[31] The tax rate should therefore be set in such a way that this twofold benefit maximises societal welfare.[2] The imposition of specific excise taxes on harmful products has two major counter-arguments. The first of these relates to their potential to increase smuggling and the size of the illicit market.[33,34] This argument is specifically related to tobacco, although research shows that the size of this market and the effects of the tax are often overstated by the tobacco industry.[33,35,36] Nevertheless, commenting on the illicit cigarette market in SA, Van Walbeek[37] states that the ‘Illicit tobacco trade is a problem and should be taken seriously’. Research shows that until 2010 there was no evidence that the market for illicit cigarettes had increased,[33] despite a significant increase in the real tax per cigarette packet in SA from 1993 onwards.[33] The alcohol sector industries in SA have often argued against increases in excise taxes by noting the potential for increased illicit liquor consumption.[38,39] Even though taxes on unhealthy foods will not lead to an increase in illicit trade, the regressivity of excise taxes on these foods along with alcohol and tobacco[40-44] is worth debate. With an ever-increas ing Gini coefficient (0.66 in 1993 and 0.7 in 2008), SA is one of the most economically unequal societies in the world.[45] For this reason, special caution is necessary when considering a tax with regressive effects. In terms of the tax on unhealthy food, there are ways of circumventing the regressive effects of the tax by subsidising healthier options.[41] It must be kept in mind, however, that the revenue raised by the tax on unhealthy food can be negated by the subsidy on healthier options.

Discussion

The White Paper has a specific focus on payroll taxes, surcharges on taxable income and increases in VAT as fiscal instruments that could cover the funding shortfall caused by the implementation of NHI. It also provides some discussion on current employer contributions to medical

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schemes being reallocated to the NHI fund, the current tax credit for medical scheme membership being scaled down, and the potential utilisation of the carbon tax in the health sector. No specific estimation of the size of the effect that these actions might have on the shortfall is provided, and further research into this area is strongly recommended. This article reviewed various funding options, other than those already under consideration, that are available to the SA government to raise additional resources for its health sector. Raising corporate taxation could raise enough funds, but the losses due to capital flight might be too much for the SA economy to bear. The increase would therefore have to be moderate, and it is unlikely that a welfare-maximising corporate tax rate could raise sufficient government income, especially if only specific companies or industries are targeted. A financial transaction tax, specifically a levy on currency transactions, is also unlikely to raise the required resources on its own, even without a likely decrease in the number of transactions. Finally, the required increase in the tax on tobacco and alcohol would have to be very large, even when assuming that consumption patterns would remain unchanged. The imposition of a tax on unhealthy food products is a very new idea and something that could be explored further as an option for SA. Nevertheless, the problem with excise duties is their regressivity which is a specific problem for a country as economically unequal as SA. Yates[46] has identified progressive taxes as key to financing a health system’s striving towards universal health coverage. The premise would therefore promote increases in corporate taxes[46] and levies on financial transactions,[47] and discount taxes on tobacco, alcohol and unhealthy foods. Nevertheless, regressivity is not the only cost associated with the imposition of these fund-raising mechanisms, and the increase in the tax revenue would have to be weighed against these costs for each mechanism. The White Paper clearly outlines five scenarios for revenue generation, all of which are combinations of more than a single source. If more mechanisms are used, less tax will have to be collected from each one, increasing the possibility that SA will be able to collect more tax revenue for the health sector without compromising the rest of the economy. All tax mechanisms have associated administrative costs,[48,49] which also have to be taken into account when deciding on how many mechanisms should be implemented.

Conclusion

The calculations in this article make very strong assumptions and should by no means be confused with modelling. They are merely utilised as devices to illustrate to the reader the massive task that is set before the SA National Treasury to finance the implementation of the NHI scheme. The current scenario that makes use of the most sources of income (surcharge on taxable income, VAT increase and a payroll tax) has implications for the working population, the poor and employers. This article has outlined additional mechanisms to modify the burden on the average South African. 1. World Health Organization. Health Systems Financing: The Path to Universal Coverage. Geneva: World Health Organization, 2010. 2. Stenberg K, Elovainio R, Chisholm D, et al. Responding to the Challenge of Resource Mobilization – Mechanisms for Raising Additional Domestic Resources for Health. Geneva: World Health Organization, 2010. http://www.who.int/healthsystems/topics/financing/healthreport/13Innovatived omfinancing.pdf (accessed 4 February 2016). 3. National Department of Health, South Africa. National Health Insurance for South Africa: Towards Universal Health Coverage. Version 40. Pretoria: NDoH, 2015. 4. McIntyre D. Health Service Financing for Universal Coverage in East and Southern Africa. EQUINET Discussion Paper 95. Cape Town: Health Economics Unit, University of Cape Town, 2012. 5. South African Reserve Bank: Monetary Policy Committee. Press Statement Embargo Delivery. Statement of the Monetary Policy Committee. 2016. https://www.resbank.co.za/Lists/News%20and%20Publications/ Attachments/7223/MPC%20Statement%2017%20March%202016%20.pdf (accessed 5 June 2016). 6. Bénassy-Quéré A, Fontagné L, Lahrèche-Révil A. How does FDI react to corporate taxation? Int Tax Public Finance 2005;12(5):583-603. DOI:10.1007/s10797-005-2652-4 7. Diamond J, Zodrow G, Carroll R. Macroeconomic Effects of Lower Corporate Income Tax Rates Recently Enacted Abroad: Report Prepared for the Reforming America’s Taxes Equitably (RATE) Coalition. Washington, DC: Ernst & Young, 2013. http://ratecoalition.com/wp-content/uploads/2013/04/EY_ TPA_RATE_Coalition_Macroanalysis_2013_03_04_FINAL.pdf (accessed 2 September 2015).

8. South African Revenue Services. Tax Pocket Guide. Pretoria: National Treasury, 2015. http://www. treasury.gov.za/documents/national%20budget/2015/default.aspx (accessed 15 July 2015). 9. Johansson Å, Heady C, Arnold J, et al. Taxation and Economic Growth. OECD Economics Department Working Papers, No. 620. Paris: OECD Publishing, 2008. DOI:10.3386/w5826 10. Ernst and Young. Worldwide Corporate Tax Guide. London: Ernst & Young, 2015:175, 256, 586, 1184, 1284. http://www.ey.com/Publication/vwLUAssets/Worldwide_corporate_tax_guide_2015/$FILE/ Worldwide%20Corporate%20Tax%20Guide%202015.pdf (accessed 20 July 2015). 11. National Treasury. Budget Review. Pretoria: National Treasury, 2015. http://www.treasury.gov.za/ documents/national%20budget/2015/review/default.aspx (accessed 10 June 2015). 12. Statistics South Africa. P0141 – Consumer Price Index (CPI). Pretoria: SSA, 2015:4. http://www. statssa.gov.za/?page_id=1854&PPN=P0141&SCH=6037 (accessed 1 August 2015). 13. McCulloch N, Pacillo G. The Tobin tax: A review of the evidence. IDS Research Reports 2011;2011(68):1-77. DOI:10.1111/j.2040-0217.2011.00068_2.x 14. Wang GHK, Yau J. Would a Financial Transaction Tax Affect Financial Market Activity? Insights from Future Markets (July 9, 2012). Washington, DC: Cato Institute Policy Analysis, 2012. http://ssrn.com/ abstract=2226961 (accessed 3 February 2016). 15. Nissanke M. Revenue potential of the currency transaction tax for development finance: A critical appraisal. WIDER Discussion Papers/World Institute for Development Economics (UNU-WIDER), No. 2003/81, 2003. http://hdl.handle.net/10419/53109 (accessed 3 February 2016). 16. Schmidt R. The Currency Transaction Tax: Rate and Revenue Estimates. Ottawa: North-South Institute, 2007. 17. Bank for International Settlements: Monetary and Economic Department. Triennial Central Bank Survey. Basle: Bank for International Settlements, 2013:14. http://www.bis.org/publ/rpfx13fx.pdf (accessed 15 July 2015). 18. World Health Organization. Constraints to Scaling up the Health Millennium Development Goals: Costing and Financial Gap Analysis. Background Document for the Taskforce on Innovative International Financing for Health Systems. Geneva: WHO, 2010. 19. Nedbank Group. Exchange rates – annual averages from 1995. Nedbank Group, 2015. http://www.nedbankgroup. co.za/pdfs/economic/exchangeRates/Annual_Average_for_Knet_2015.pdf (accessed 27 August 2015). 20. National Treasury. National Budget Review. Pretoria: National Treasury, 2014. http://www.treasury. gov.za/documents/national%20budget/2014/default.aspx (accessed 10 June 2015). 21. Jha P, Ramasundarahettige C, Landsman V, et al. 21st-century hazards of smoking and benefits of cessation in the United States. N Engl J Med 2013;368(4):341-350. DOI:10.3410/f.717973072.793473561 22. US Department of Health and Human Services. The Health Consequences of Smoking: A Report of the Surgeon General. Atlanta, Ga: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. 23. Rehm J. The risks associated with alcohol use and alcoholism. Alcohol Res Health 2011;34(2):135-143. 24. World Health Organization. Global Status Report on Alcohol and Health. Geneva: WHO, 2014. 25. Salti N, Chaaban J, Nakkash R, Alaouie H. The effect of taxation on tobacco consumption and public revenues in Lebanon. Tob Control 2015;24(1):77-81. DOI:10.1136/tobaccocontrol-2012-050703 26. Xu X, Chaloupka FJ. The effects of prices on alcohol use and its consequences. Alcohol Res Health 2011;34(2):236. 27. Wang YC, Coxson P, Shen YM, Goldman L, Bibbins-Domingo K. A penny-per-ounce tax on sugarsweetened beverages would cut health and cost burdens of diabetes. Health Aff 2012;31(1):199-207. DOI:10.1377/hlthaff.2011.0410 28. Blecher E. Taxes on tobacco, alcohol and sugar sweetened beverages: Linkages and lessons learned. Soc Sci Med 2015;136:175-179. DOI:10.1016/j.socscimed.2015.05.022 29. Diaz MC, Chaloupka FJ, Jernigan DH. The Effects of Alcohol Excise Tax Increases on Public Health and Safety in Texas. Texans Standing Tall, 2 March 2015. http://texansstandingtall.org/pdfs/15_ Alcohol_ExciseReport.pdf (accessed 4 July 2016). 30. Daley JI, Stahre MA, Chaloupka FJ, Naimi TS. The impact of a 25-cent-per-drink alcohol tax increase. Am J Prev Med 2012;42(4):382-389. DOI:10.1016/j.amepre.2011.12.008 31. Sassi F, Belloni A, Capobianco C, Alemanno A. Taxation and Economic Incentives on Health-Related Commodities: Alcohol, Tobacco and Food. HEC Paris Research Paper No. LAW-2014-1038. Cambridge: Cambridge University Press, 2014. http://ssrn.com/abstract=2400930 (accessed 4 February 2016). 32. Chaloupka FJ, Yurekli A, Fong GT. Tobacco taxes as a tobacco control strategy. Tob Control 2012;21(2):172-180. DOI:10.1136/tobaccocontrol-2011-050417 33. Van Walbeek C, Shai L. Are the tobacco industry’s claims about the size of the illicit cigarette market credible? The case of South Africa. Tob Control 2015;24(e2):e142-e146. DOI:10.1136/ tobaccocontrol-2013-051441 34. Cooper A, Witt D. The linkage between tax burden and illicit trade of excisable products: The example of tobacco. World Customs J 2012;6(2):41-58. 35. Chen J, McGhee SM, Townsend J, Lam TH, Hedley AJ. Did the tobacco industry inflate estimates of illicit cigarette consumption in Asia? An empirical analysis. Tob Control 2015;24(e2):e161-e167. DOI:10.1136/tobaccocontrol-2014-051937 36. Stoklosa M, Ross H. Contrasting academic and tobacco industry estimates of illicit cigarette trade: Evidence from Warsaw, Poland. Tob Control 2014;23(e1):e30-e34. DOI:10.1136/tobaccocontrol-2013-051099 37. Van Walbeek C. Measuring changes in the illicit cigarette market using government revenue data: The example of South Africa. Tob Control 2014;23(e1):e69-e74. DOI:10.1136/tobaccocontrol-2013-051178 38. Babor TF, Robaina K, Jernigan D. The influence of industry actions on the availability of alcoholic beverages in the African Region. Addiction 2015;110(4):561-571. DOI:10.1111/add.12832 39. Parry C, London L, Myers B. Delays in South Africa’s plans to ban alcohol advertising. Lancet 2014;383(9933):1972. DOI:10.1016/s0140-6736(14)60954-5 40. Monkan N, Woolard I, Ajam T. The tax system and inclusive growth in South Africa: Towards an analytical framework for the Davis Tax Committee. Pretoria: Davis Tax Committee, 2015. http:// www.taxcom.org.za/docs/20150605%20DTC%20Macro%20Analysis%20Framework%20First%20 Interim%20Report%20(Full)%20%20for%20public%20comment.pdf (accessed 1 August 2015). 41. López-Casasnovas G, Gil J, Mora T. Taxation of unhealthy consumption of food and drinks: An updated literature review. Hacienda Pública Española/Review of Public Economics 2013;207(4/2013):119-140. DOI:10.7866/hpe-rpe.13.4.5 42. Hoffer A, Gvillo R, Shughart II WF, Thomas MD. Regressive Effects: Causes and Consequences of Selective Consumption Taxation. Arlington, Va: Mercatus Center at George Mason University, 2015. 43. Ataguba JE. Alcohol policy and taxation in South Africa. Applied Health Econ Health Policy 2012;10(1):65-76. DOI:10.2165/11594860-000000000-00000 44. Mytton OT, Clarke D, Rayner M. Taxing unhealthy food and drinks to improve health. BMJ 2012;344:e2931. DOI:10.1136/bmj.e2931 45. Hvistendahl M. While emerging economies boom, equality goes bust. Science 2014;344(6186):832835. DOI:10.1126/science.344.6186.832 46. Yates R. Universal health coverage: Progressive taxes are key. Lancet 2015;386(9990):227-229. DOI:10.1016/s0140-6736(15)60868-6 47. Schäfer D, Schulmeister S, Vella J, Masciandaro D, Passarelli F, Buckley RP. The financial transaction tax – boon or bane? Intereconomics 2012;47(2):76-103. DOI:10.1007/s10272-012-0409-8 48. Auriol E, Warlters M. The marginal cost of public funds and tax reform in Africa. J Dev Econ 2012;97(1):58-72. DOI:10.1016/j.jdeveco.2011.01.003 49. Dharmapala D, Slemrod J, Wilson JD. Tax policy and the missing middle: Optimal tax remittance with firm-level administrative costs. J Public Econ 2011;95(9):1036-1047. DOI:10.2139/ssrn.1138015

Accepted 2 June 2016.

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STATEMENT

Implications of the 2015 World Health Organization isoniazid preventive therapy recommendations on tuberculosis prevention efforts in Namibia S A Oloo, MB ChB, MMed Department of Internal Medicine, School of Medicine, University of Namibia, Windhoek, Namibia Corresponding author: S Oloo (adikini84@yahoo.com)

The World Health Organization recently released guidelines recommending 36-month use of isoniazid preventive therapy in adults and adolescents living with HIV in resource-limited settings. Namibia continues to grapple with one of the highest incidences of tuberculosis (TB) worldwide. Implementation of these guidelines requires considerations of TB epidemiology, health infrastructure, programmatic priorities and patient adherence. This article explores the challenges Namibia currently faces in its fight against TB and the implications of the new guidelines on Namibian TB prevention efforts. S Afr Med J 2016;106(8):775-776. DOI:10.7196/SAMJ.2016.v106i8.10787

Isoniazid preventive therapy (IPT) is a key strategy recommended by the World Health Organization (WHO) for the prevention of tuberculosis (TB) in patients infected with HIV. The WHO recently updated its guidelines and now recommends IPT for a duration of at least 36 months for adults and adolescents living with HIV in resource-limited settings.[1] The WHO notes that the implementation of continuous IPT requires considerations of: (i) TB epidemiology; (ii) health infrastructure; (iii) programmatic priorities; and (iv) patient adherence. Individuals with HIV are at an increased risk of developing active TB infection, with studies[2] showing that the incidence of TB doubles within the first year of HIV seroconversion and increases fourfold after 2 years. This article discusses some of the challenges Namibia currently faces in its ongoing fight against TB and the implications of the new WHO IPT recommendations.

Discussion

Namibia, an upper-middle-income sub-Saharan African country, continues to grapple with what are among the highest prevalences of both HIV and TB worldwide. This, coupled with a sparsely distributed population, presents a great challenge in terms of healthcare delivery. The incidence of TB in Namibia remains one of the highest in the world, with a case notification rate of 589 cases per 100 000 population. [3] In its continued effort to attain its vision of a Namibia where TB is no longer a health threat,[4] the Ministry of Health and Social Services (MoHSS) works very closely with both primary healthcare providers and public health services at national, regional and district levels to ensure the success of the WHO directly observed therapy, short-course (DOTS) strategy in the treatment of TB patients, and to create public awareness of practical interventions for the prevention of TB, especially in people living with HIV. According to the 2012/2013[5] MoHSS report, the TB and HIV co-infection rate at the time stood at 47%. A 2014 - 2015 MoHSS report[6] indicates that there has been a small decline in case numbers of TB, suggesting a declining incidence of the disease burden in the country. Significant improvements in TB/HIV service coverage are exemplified by: (i) improved HIV testing for TB patients, currently at 92% compared with 76% in 2010; and (ii) improved coverage of antiretroviral therapy (ART) among TB/HIV patients, up to 84% from 43% in 2010.

The overall prevalence of HIV in the country is currently estimated at 13.1% in the general population although there is wide variation in different regions. Despite government efforts to improve ART coverage, Namibia remains one of the top ten countries in the world worst affected by HIV, which in turn continues to fuel the rise of TB in the country. Over 230 000 people aged >15 years are living with HIV.[7] The number of people living with HIV is expected to increase as ART coverage increases, reducing the numbers of AIDS-related deaths.

Health infrastructure and cost implications

The structure of the health sector in Namibia aims to decentralise health services as much as possible while integrating public health strategies in service delivery. The continued collaboration of the Namibia TB Leprosy Program with the National Institute of Pathology and the Division of Pharmaceutical Services has demonstrated outstanding success in ensuring the timely provision of quality laboratory services, as well as uninterrupted supply of TB drugs to the TB treatment centres in both the capital city and remote clinics in the rural areas. However, in health facilities in the peripheral regions, including the border towns, services are still grossly inadequate, especially in terms of human resources. Studies[8] in the Omaheke region show that more service-related factors than community-related factors influenced the successful implementation of community-based TB care. According to the MoHSS,[6] the TB delivery programme in this region was inadequate, with a 51.4% defaulter rate. In its health budget planning, the government of Namibia needs to consider the projected cost implications of adopting the new 36-month IPT strategy as opposed to a 6-month IPT strategy. Smith et al.[9] examined the cost of implementation of IPT in Botswana, where ART is readily available, and found that a 36-month IPT strategy for HIV-positive individuals was more cost-effective for reducing both TB and death than individual costs of: (i) providing IPT without tuberculin skin testing (TST); (ii) providing only 6 months of IPT; or (iii) expanding ART eligibility without IPT. Gupta et al.[10] also showed that models providing ART coverage to 90%, TB infection control and 36-month IPT strategy averted most

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TB cases and were more cost-effective than models that provided less ART coverage.

Possible adverse events and the balance between benefit and harm

The key outcome of interest in the development of the new recommendations was progression to active TB. Other outcomes of interest include adverse effects and adherence. In the formulation of the new guidelines, a meta-analysis of adverse events was not performed because of the heterogeneity of the definition of sideeffects by the different studies that were considered by the WHO. The study by Swaminathan et al.[11] did not report information on adherence, while Martinson et al.’s[12] recorded adherence of 60.4% in the 36-month IPT group compared with 83.8% in the 6-month IPT group. There is also currently insufficient evidence to indicate whether continuous IPT use increases the risk of development of isoniazid resistance. According to Swaminathan et al.[11] and Samandari et al.,[13] the observed proportion of resistance cases among TB cases was similar to the expected rate. However, resistance patterns are known to vary vastly from region to region.

Conclusion

Implementation of the new IPT strategy in HIV-positive patients would be likely to record success alongside ART strategies, as patients can be counselled for drug adherence and monitored on therapy at the same time. However, this will require a renewed commitment from the government of Namibia and its collaborators to implement

the intervention, finance the additional costs associated with drug supply and increase the human resources capacity. 1. World Health Organization. Update 2015 - Recommendations on 36 Months on Isoniazid Preventive Therapy to Adults and Adolescents Living with HIV in Resource-constrained and High TB- and HIVprevalence Settings. Geneva: WHO, 2015. http://www.who.int/tb/publications/2015_ipt_update/en/ (accessed 11 May 2016). 2. Sonnenberg P, Glynn JR, Fielding K, Murray J, Godfrey-Faussett P, Shearer S. How soon after infection with HIV does the risk of tuberculosis start to increase? A retrospective cohort study in South African gold miners. J Infect Dis 2005;15:191(2):150-158. DOI:10.1086/426827 3. Ministry of Health and Social Services, Namibia. Organisation and programme management. In: National Guidelines for the Management of Tuberculosis. 3rd ed. Windhoek: MoHSS, 2012:3-5. 4. Ministry of Health and Social Services, Namibia. Second Medium-Term Strategic Plan for Tuberculosis and Leprosy (2010 - 2015). Windhoek: MoHSS, 2010. 5. Ministry of Health and Social Services, Namibia. The Namibia AIDS Response Progress Report 2015; Reporting Period: 2013 - 2014. Windhoek: MoHSS, 2015. 6. Ministry of Health and Social Services, Namibia. National Tuberculosis and Leprosy Programme (2014 - 2015). Windhoek: MoHSS, 2015. 7. UNAIDS. Namibia HIV and AIDS estimate. http://www.unaids.org/sites/default/files/epidocuments/ NAM.pdf (accessed 12 May 2016). 8. Zvavamwe S, Ehlers VJ. Factors associated with community-based TB care in the Omaheke region, Namibia. Afr J Nurs Midwifery 2007;9(1):59-72. 9. Smith T, Samandari T, Abimbola T, Marston B, Sangrujee N. Implementation and operational research: Cost-effectiveness of antiretroviral therapy and isoniazid prophylaxis to reduce tuberculosis and death in people living with HIV in Botswana. J Acquir Immune Defic Syndr 2015;70(3):e84-e93. DOI:10.1097/QAI.0000000000000783 10. Gupta S, Abimbola T, Date A, et al. Cost effectiveness of the three I’s for HIV/TB and ART to prevent TB among people living with HIV. Int J Tuberc Lung Dis 2014;18(10):1159-1165. DOI:10.5588/ ijtld.13.0571 11. Swaminathan S, Menon PA, Gopala N, et al. Efficacy of a 6-month versus a 36-month regimen for prevention of tuberculosis in HIV-infected persons in India: A randomised clinical trial. PloS One 2012;7(12):e47400. DOI:10.1371/journal.pone.0047400 12. Martinson NA, Barnes GL, Moulton LH, et al. New regimens to prevent tuberculosis in adults with HIV infection. N Engl J Med 2011;365(1):11-20. DOI:10.1056/NEJMoa1005136 13. Samandari T, Agizew TB, Nyirenda S, et al. 6-month versus 36-month isoniazid preventive treatment for tuberculosis in adults with HIV infection in Botswana: A randomised, double-blind, placebocontrolled trial. Lancet 2011;377(9777):1588-1598. DOI:10.1016/S0140-6736(11)60204-3

Accepted 30 May 2016.

COCHRANE CORNER

Antifibrinolytic drugs for acute traumatic injury M McCaul,1 MSc (Clin Epi); T Kredo,2 MB ChB, MMed (Clin Pharm), Dip HIV Man (SA) 1 2

entre for Evidence-Based Health Care, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa C Cochrane South Africa, South African Medical Research Council, Cape Town, South Africa

Corresponding author: M McCaul (mmccaul@sun.ac.za)

In South Africa, trauma is a major concern, with violence and road traffic accidents being the fifth and seventh leading causes of death, respectively. Antifibrinolytic agents have been used in trauma and major surgery to prevent fibrinolysis and reduce blood loss. We highlight an updated Cochrane review investigating the effect of antifibrinolytic drugs in patients with acute traumatic injury. The review authors conducted comprehensive literature searches in January 2015 with regard to all randomised controlled trials comparing antifibrinolytic agents after acute traumatic injury. Three randomised controlled trials, of which two (n=20 451) assessed the effect of tranexamic acid (TXA), were included. The authors concluded that TXA safely reduces mortality in trauma with bleeding without increasing the risk of adverse events. TXA should be administered as early as possible, and within 3 hours of injury. There is still uncertainty with regard to the effect of TXA on patients with traumatic brain injury; however, ongoing randomised controlled trials should shed more light on this. S Afr Med J 2016;106(8):777-778. DOI:10.7196/SAMJ.2016.v106i8.11042

Injuries are responsible for more deaths per year than HIV/AIDS, tuberculosis and malaria combined.[1] Furthermore, each year ~4 million people die as a result of traumatic injuries and violence worldwide. In South Africa, trauma is a major concern, with violence and road traffic accidents being the fifth and seventh leading causes of death respectively.[2] Antifibrinolytic agents have been used in trauma and major surgery to prevent fibrinolysis and reduce blood loss.

We summarise the evidence from an updated Cochrane review[3] investigating the effect of antifibrinolytic drugs in patients with acute traumatic injury.

Methods

The review authors conducted comprehen sive literature searches in January 2015. All randomised controlled trials comparing antifibrinolytic agents (aprotinin, tranexamic acid (TXA), epsilon aminocaproic acid

August 2016, Print edition

IN PRACTICE

and aminomethylbenzoic acid) administered after acute traumatic injury were included. No restrictions were made with regard to language, date or publication status. Standard Cochrane methods for independent data screening and eligibility assessment, data extraction and riskof-bias evaluation were followed.

Results

Three randomised controlled trials were inclu ded, of which two (n=20 451) assessed the effect of TXA. The Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage (CRASH)-2 trial (n=20 211),[4] the larger of the two, was conducted in 40 countries and included patients with a variety of trauma types; the other specifically investigated patients with traumatic brain injury (TBI) (n=240). The third trial assessed aprotinin in participants with major bony trauma and shock. All three trials[3] provided data for meta-analysis. Antifibrinolytics reduced the risk of death by 10% (relative risk (RR) 0.90, 95% confidence interval (CI) 0.85 - 0.96; three trials, high-quality evidence) compared with placebo. It should be noted that this estimate was largely based on the results of CRASH-2, a metho dologically rigorously conducted trial. The authors found that antifibrinolytics do not have adverse effects on the risk of vascular occlusive events, such as deep vein thrombosis, stroke or pulmonary embolism (moderate-quality evidence). TXA reduced the risk of myocardial infarction by 39% (RR 0.61, 95% CI 0.40 - 0.92; two trials, moderate-quality evidence). Further results are shown in Table 1. The TBI subgroup of patients who received TXA may be less likely to die (all-cause mortality) compared with patients who received placebo (RR 0.63, 95% CI 0.40 - 0.99; two trials, n=510, low-quality evidence); the low number of events and relative imprecision resulted in the downgrading of overall confidence in the results. Stronger evidence exists for the reduced

Table 1. Summary of findings*† Relative effect (95% CI)

Study participants, n (RCT, n)

Quality of the evidence, grade‡

Mortality

RR 0.90 (0.85 - 0.96)

20 437 (3)

Surgical intervention

RR 1.00 (0.97 - 1.03)

20 437 (3)

⊕⊕⊕⊕ High

Blood transfusion

RR 0.98 (0.96 - 1.01)

20 367 (2)

Myocardial infarction

RR 0.61 (0.40 - 0.92)

20 367 (2)

Deep vein thrombosis

RR 0.95 (0.62 - 1.47)

20 367 (2)

Stroke

RR 0.86 (0.61 - 1.23)

20 367 (2)

Pulmonary embolism

RR 1.01 (0.73 - 1.41)

20 367 (2)

Outcomes

⊕⊕⊕⊕ High

⊕⊕⊕⊝ Moderate§ ⊕⊕⊕⊝ Moderate§ ⊕⊕⊕⊝ Moderate§ ⊕⊕⊕⊝ Moderate§

CI = confidence interval; RR = risk ratio; RCT = randomised controlled trial. *Adapted from Ker K, et al.,[3 ] with permission. † Population: treating bleeding trauma patients; settings: hospital settings in 40 countries;[4] intervention/comparison: antifibrinolytic drugs v. placebo. ‡ Grade = working group grades of evidence; high quality = further research is very unlikely to change our confidence in the estimate of effect; moderate quality = further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate; low quality = further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate; very low quality = we are very uncertain about the estimate. § Downgraded one level for imprecision: estimate based on few events and wide CIs.

risk of volume of intracranial bleeding with TXA in TBI patients compared with placebo (RR 0.75, 95% CI 0.58 - 0.98; subgroup n=478, high-quality evidence).

Conclusion

The review authors concluded that TXA safely reduces mortality in trauma with bleeding, without increasing the risk of adverse events. TXA should be given as early as possible and within 3 hours of injury. There is still uncertainty with regard to the effect of TXA on patients with TBI; however, ongoing randomised controlled trials should shed more light on this. Evidence from this review has been incorporated into trauma clinical practice guidelines[5] by the National Institute for Health and Care Excellence (NICE) in the

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UK, which has made recommendations for TXA use in both in-hospital and prehospital settings. 1. World Health Organization. Injuries and Violence: The Facts. Geneva: WHO, 2010:2-18. http://scholar.google.com/scholar?h l=en&btnG=Search&q=intitle:Injuries+and+Violence:+The+Fac ts#0 (accessed 22 June 2016). 2. Naghavi M, Wang H, Lozano R, et al. Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990 - 2013: A systematic analysis for the Global Burden of Disease Study 2013. Lancet 2015;385(9963):117-171. DOI:10.1016/S0140-6736(14)61682-2 3. Ker K, Roberts I, Shakur H, Coats T. Antifibrinolytic drugs for acute traumatic injury. Cochrane Database Syst Rev 2015;(5):CD004896. DOI:10.1002/14651858.CD004896.pub4. 4. CRASH-2. The use of tranexamic acid. http://www.crash2.lshtm. ac.uk/ (accessed 27 June 2016). 5. National Institute for Health and Care Excellence. Major Trauma: Assessment and Initial Management. UK: NICE, 2016. https:// www.nice.org.uk (accessed 22 June 2016).

Accepted 30 May 2016.

IN PRACTICE

MEDICINE AND THE LAW

When may doctors give nurses telephonic treatment instructions? D J McQuoid-Mason, BComm, LLB, LLM, PhD Centre for Socio-Legal Studies, University of KwaZulu-Natal, Durban, South Africa Corresponding author: D J McQuoid-Mason (mcquoidm@ukzn.ac.za)

Doctors are expected to examine their patients before issuing telephonic instructions to nurses. However, in emergencies or when they are aware of the health status of their patients, it may be justified for a doctor to issue telephonic instructions to nurses without examining the patient. Doctors on call owe a special duty to patients, who they may have to examine or arrange for another doctor to do so before issuing telephonic instructions. In deciding whether doctors acted reasonably in issuing telephonic instructions to nurses, the courts will decide whether they exercised the same degree of skill and care as reasonably competent practitioners in their branch of the profession. Suggestions are made concerning doctors giving telephonic instructions to nurses regarding patients they have not examined. S Afr Med J 2016;106(8):787-788. DOI:10.7196/SAMJ.2016.v106i8.10830

When is it legal for doctors to give nurses telephonic treatment instructions? Common sense indicates that good medical practice expects doctors to have examined the patient beforehand, except in emergencies or when they know the patient’s health history. To answer whether these assumptions are consistent with the law we must consider: (i) whether it makes a difference legally if telephonic instructions are regarded as telemedicine or not; (ii) what constitutes a medical emergency justifying telephonic instructions; (iii) whether a personal examination by the doctor is necessary; (iv) whether the situation changes if the doctor is ‘on call’; and (v) whether it is sufficient for doctors to issue instructions to nurses based on their patients’ health histories.

Does it make a legal difference if telephonic instructions constitute telemedicine?

Telemedicine is defined as ‘the practice of medicine, from a distance, in which interventions, diagnostic and treatment decisions and recommendations are based on clinical data, documents and other information transmitted through telecommunication systems’.[1] This definition which refers to ‘other information transmitted through telecommunication systems’ seems to cover telephonic treatment instructions to nurses by doctors. However, the HPCSA’s Draft General Ethical Guidelines for Good Practice in Telemedicine state that ‘Telemedicine generally does not include audio-only mechanisms, telephone conversations, e-mail, instant messaging conversations or faxes’.[2] Thus the HPCSA regards audio-only telephonic instructions such as those to nurses as falling outside the scope of the HPCSA Guidelines for Telemedicine. However, presumably face-to-face Skype-type conversations where the parties, including patients, are visible to each other might fall under the Guidelines for Telemedicine. I submit that the courts will not dwell on whether audio-only mechanisms fall under the definition of telemedicine or not, but will consider what ought to be regarded as good medical practice for treatment instructions given over the telephone to nurses. The test will be whether the treating doctors have exercised the same degree of skill and care as reasonably competent practitioners in their branch of the profession when giving the telephonic instructions.[3] Judges

will then usually follow what the medical profession regards as good medical practice,[4] but are not obliged to do so.[3]

What constitutes an emergency justifying telephonic instructions?

The Constitutional Court has defined a medical emergency as ‘a dramatic, sudden situation or event which is of passing nature in terms of time’[5] that can be cured through medical treatment. Therefore emergency medical treatment refers to conditions that can be rectified through medical treatment – unlike chronic illnesses that cannot be cured.[5] Emergency medical treatment is needed when patients are faced with the possibility of death, serious bodily injury or deterioration in health.[6] Therefore, if in such circumstances the doctors cannot reach the patients in time for an examination, it is reasonable for them to issue telephonic instructions to the relevant nurses to stabilise the patients until examined by the instructing doctor or another doctor. If the patient is mentally able to give consent or a proxy is available to do so in terms of a court order or the provisions of the National Health Act,[7] emergency medical treatment should be given after obtaining such consent. The following may act as proxies in order of preference: a court-appointed curator, or the spouse or partner, parent, grandparent, adult child or sibling of the patient. [7] Alternatively, persons appointed by patients in writing before becoming mentally incapacitated may be authorised to give consent.[7] If the patient or a legal proxy cannot give consent, emergency treatment may be given without consent – provided it is not against a previous directive issued by a patient refusing treatment, e.g. a refusal to accept a blood transfusion for religious reasons.[8] Before issuing telephonic instructions doctors should consider whether telephone management is appropriate in the situation concerned, and reflect on this throughout the call.[9] To issue telephonic instructions to nurses in emergencies, a doctor should: (i) request and record the name and surname of the nurse; (ii) obtain a detailed history of the patient’s health and condition from the nurse; (iii) paraphrase and reflect back to the nurse the nurse’s description of the patient’s condition; (iv) give the nurse the instructions and ensure that they are understood; (v) get the nurse to repeat the instructions; (vi) repeat the instructions to another nurse if available and record

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IN PRACTICE

her or his name and surname; and (vii) if a second nurse is not available repeat the instructions to the first nurse and get her or him to repeat them. This protocol is based on suggested guidelines for when doctors telephonically give instructions to patients,[9] which I have adapted to apply to telephonic instructions to nurses.

Is a personal examination by the doctor necessary before issuing telephonic instructions to nurses?

Doctors should always consider whether issuing telephonic instructions without examining the patient is appropriate in the circumstances concerned, and should review their decision through out.[9] Doctors must be satisfied that it is in the patient’s best interests to issue treatment instructions to nurses without having examined the patient. The UK General Medical Council (GMC) has stated that it may not be appropriate to issue telephonic instructions where: (i) the patient is not previously known to the doctor; (ii) the assessment may be helped by examination of the patient; and (iii) there is no provision for appropriate monitoring of the patient or follow-up care.[10] Although the GMC later withdrew this statement, the South African courts may find that it is in line with common sense and good medical practice, and provides useful guidelines for local doctors when deciding whether or not to issue telephonic instructions to nurses.

Does the situation regarding telephonic treatment instructions change if the doctor is ‘on call’?

May doctors issue instructions to nurses based on their patients’ health histories?

Before issuing telephonic instructions a doctor should always consider whether telephone management is appropriate in the situation concerned, and reflect on this throughout the call.[9]

Despite doctors being aware of their patients’ health histories, where they are mentally competent it may be necessary to clarify their condition by telephonically speaking with the patient before issuing instructions to the nurses. When able to speak telephonically to the patient before instructing the nurses the doctor should: (i) obtain and record a history of the patient’s condition since last examined

Mentally incompetent patients

Where the patient is mentally incompetent and a legal proxy is available in terms of the National Health Act,[7] and has knowledge of the patient’s condition since the doctor last examined the patient, the steps applied to a telephonic consultation with a mentally competent patient could be applied to the proxy – save that the first step should be to record the name, identity number and telephone number of the proxy and the basis on which he or she is acting as a proxy. Where the patient is not mentally competent and no proxy is available, the same steps should be followed as in the case of emer gency medical treatment.

Conclusion

Whether or not ‘on call’ will make no difference to doctors’ legal liability should they have failed to act as a reasonably competent doctor ought to have acted under similar circumstances.[3] Doctors ‘on call’ should follow the proposed protocols when issuing telephonic instructions. However, if the nurses’ information indicates that patients must be examined by a doctor before instructions are issued, the doctor ‘on call’ must either examine the patient personally or arrange for another medical practitioner to do so.[10] This applies whether the doctor ‘on call’ is on or off the premises of the health institution concerned at the time the nurses seek treatment guidance. The test for legal liability will be whether a reasonably competent doctor ‘on call’ would have examined the patient, or have arranged for another doctor to do so, before issuing the telephonic instructions; or whether a reasonably competent doctor would have considered it reasonable to issue treatment instructions to the nurses without examining the patient.[3]

Mentally competent patients

by the doctor; (ii) give the patient treatment options; (iii) obtain an informed consent regarding the treatment; (iv) give specific advice on follow-up; and (v) ask the patient to repeat the advice given to check that the consent is informed.[9] As in emergencies, the doctor should then instruct the nurse regarding the treatment of the patient and: (i) request and record the name of the nurse; (ii) give the nurse the instructions and ensure that they are understood; (iii) get the nurse to repeat the instructions; (iv) repeat the instructions to another nurse, whose name and surname should be recorded; and (v) if another nurse is not available repeat the instructions to the first nurse and get her or him to repeat them.[9]

Nurses may sometimes fail to carry out the directions of doctors accurately or effectively. Therefore, doctors should be cautious about issuing telephonic instructions and ensure that they are clearly understood. Accurate records of the instructions given must be kept by the doctors and nurses to prevent ambiguities arising should patients exposed to telephonic instructions suffer harm as a result of these not being properly carried out. Provided doctors are satisfied that telephonic instructions to nurses are appropriate in a particular situation without examining the patient, they should follow the proposed protocols for emergency and non-emergency treatment of patients. The law courts will decide whether the doctor in a particular situation has exercised the degree of skill and care of a reasonable medical practitioner in their field of expertise. Although the courts will generally follow what the medical profession regards as good medical practice they are not bound to do so. Hopefully these protocols will assist doctors and nurses to avoid unprofessional conduct that may harm their patients when doctors give, and nurses receive, telephonic instructions. 1. World Health Organization. Statement on Accountability, Responsibility and Ethical Guidelines in the Practice of Telemedicine. Geneva: WHO, 2005:Preamble para 1. 2. Health Professions Council of South Africa. Draft General Ethical Guidelines for Good Practice in Telemedicine. Pretoria: HPCSA, 2014:para 3. 3. Cf. Castell v De Greef 1993 (3) SA 501 (C). 4. Van Wyk v Lewis 1924 AD 438. 5. Soobramoney v Minister of Health, KwaZulu-Natal 1998 (1) SA 765 (CC) 778. 6. Strauss SA. Doctor, Patient and the Law. 3rd ed. Pretoria: JL van Schaik, 1991:93. 7. Republic of South Africa. Section 7(1) of the National Health Act No. 61 of 2004. Pretoria: Government Gazette, 2004. 8. ES v AC [2015] NASC 11. www.saflii.org/na/cases/NASC/2015/11.html (accessed 20 March 2016). 9. Cf. Chloe Borton. Telephone Consultations, 12 June 2009. http://patient.info/doctor/telephone -consultations (accessed 17 March 2016). 10. General Medical Council. Providing Advice and Medical Services Online or by Telephone, 1998 2004. London: General Medical Council, 1998-2004. www://gmc-uk.org/providing_advice_nov1998. pdf_25416215.pdf (accessed 17 March 2016).

Accepted 4 April 2016.

August 2016, Print edition

IN PRACTICE

CASE REPORT

Cardiogenic shock – a look at acute functional mitral incompetence F A Steyn,1 MB ChB, DA (SA); J Vosloo,2 MB ChB, Cert Crit Care (Surg), FCS (SA), FCS (SA); H Naude,3 MB ChB, MMed (Thor); A J Steyn,4 MB ChB, FCA epartment of Anaesthesiology, Rob Ferreira Hospital, Nelspruit, South Africa D Intensive Care Unit, Rob Ferreira Hospital, Nelspruit, South Africa 3 Rob Ferreira Hospital, Nelspruit, South Africa 4 Private Practice, Nelspruit, South Africa 1 2

Corresponding author: J Vosloo (joann.vosloo@gmail.com)

A 44-year-old man presented with cardiogenic shock secondary to acute functional mitral incompetence as well as septic shock related to pneumonia. The patient deteriorated haemodynamically despite adequate medical therapy. An echocardiogram revealed a massive mitral incompetence and an ejection fraction of 32%. An intra-aortic balloon pump was placed and the patient improved dramatically. On day 6 after admission the echocardiogram was repeated, revealing a mild mitral incompetence and an ejection fraction of 58%. S Afr Med J 2016;106(8):789-791. DOI:10.7196/SAMJ.2016.v106i8.10283

Case report

A 44-year-old man presented to an emerg ency room, complaining of acute breathlessness that had started that day. Further questioning revealed a 3-day history of diarrhoea and a 7-month history of a productive cough with bloodstained sputum. The patient reported having had fevers and night sweats for an uncertain period of time. He was a known hypertensive, for which he was on treatment. He had never been tested for HIV and had no known allergies. In terms of social habits, he reported being a casual smoker for the past 20 years. The only previous surgical exposure was an explorative laparotomy for a stabbed abdomen. The general examination revealed an acutely ill patient. His fingers were clubbed; he was not pale but perspiration was noted on the face and chest. The vital signs on presentation were a heart rate of a 160 bpm, a blood pressure of 88/41 mmHg and a respiratory rate of 40 breaths per minute. Pulse oximetry readings showed a saturation of 88% on room air. The cardiovascular system examination revealed a rapid, weak pulse that appeared regular. There was no parasternal heave and the apex was not displaced. The jugular venous pressure was elevated. Auscultation revealed a gallop rhythm, but no murmur could be identified. The respiratory system examination showed diffuse crepitation on the left and amphoric breathing over the right lower lobe. The differential diagnosis was given as pneumonia, pulmonary embolus or ruptured pulmonary abscess with a pneumothorax.

The possibility of an acute myocardial infarction was also considered. A chest radiograph (Fig. 1) revealed right lower lobe consolidation and an electro cardiogram (ECG) showed an atrial flutter. No ECG changes suggestive of ischaemia, such as ST-segment abnormalities or T-wave inversions, were present. A 6 mg dose of adenosine was administered with no effect, followed by a 12 mg bolus, which led to a 5-second asystole. The asystole converted to sinus rhythm, which became a supraventri cular tachycardia of 140 bpm. The blood pressure remained low at 78/60 mmHg. The biochemical work-up did not reveal any abnormalities except low magnesium levels and raised inflammatory markers. The patient was intubated and admitted to the intensive care unit (ICU). Despite admini stration of a dobutamine and phenylephrine infusion, the blood pressure remained low at 80/60 mmHg and perfusion was inadequate, the lactate level increasing from 2.2 to 3.3 mmol/L. An amiodarone infusion was started, as it was reasoned that the fast heart rate was contributing to the poor perfusion. The blood pressure improved marginally, but the patient started sweating profusely as the pulse slowed. Empirical antibiotic cover with ceftriaxone was started in response to raised C-reactive protein (CRP) markers (52 mg/L) and the clinical and radiological evidence of pneu monia. An echocardiogram revealed massive mitral regurgitation and a left ventricular

August 2016, Print edition

Fig. 1. Chest radiograph showing right lower lobe consolidation (arrow).

ejection fraction of 32%. Decreased move ment of the posterior wall of the left ven tricle and the interventricular septum was noted. The left atrium was dilated, with a left atrial aortic outflow tract ratio of 2.1:1. The left ventricle was normal in size, while the right atrium and ventricle were also dilated. Right ventricular and right atrial dilatation were present with a normal-sized left ventricle. The vena cava collapsibility index was <5%. Furosemide at a dose of 1 mg/h was started, to reduce the preload. The serum lactate level had increased to 4.4 mmol/L and urine output had dropped below 0.5 mL/kg. The pulse pressures remained low and the patient continued sweating. In consultation with the cardiothoracic specialist, it was decided to place an intra-aortic balloon pump (IABP). The decision was based on the poor tissue perfusion despite optimal inotropes (dobutamine). The IABP was placed on day 1 of ICU care.

IN PRACTICE

The IABP was started on a 1:1 ratio and the haemodynamics improved immediately. The blood pressure improved to 105/70 mmHg and the pulse rate varied between 100 and 115 bpm. The lactate levels started to decrease, urine output increased and the patient stopped sweating. The dobutamine was weaned to a quarter of the pre-IABP dose within 24 hours and the phenylephrine stopped. On the morning of day 3, the anti biotic treatment was upscaled to include imipenem, as the inflammatory markers had deteriorated (procalcitonin 100 ng/mL and CRP 336 mg/L). The dose of furosemide was decreased to 0.5 mg/h. Power, generator and equipment failures meant that the IABP had to be urgently removed on the evening of day 3. Fortunately, the patient could be maintained on low-dose dobutamine. He was extubated the next day (day 4), and his haemodynamic measurements and perfusion parameters were normal. He was kept in the ICU until the following day, when he was discharged to the ward. An echocardiogram was repeated 5 days after the initial one, which was 1 day after discharge from the ICU, and revealed minimal mitral regurgitation and improvement in the ejection fraction to 58%, with normal septal and posterior wall movement. From a cardiovascular perspective, the patient was stable and out of danger. Further more, it was established that he was HIVpositive with a CD4 count of 129 cells/µL. The work-up for pneumonia was disappointing, with negative results from cultures, for acidfast bacilli and from GeneXpert. Initial blood cultures contained a Clostridium species, but follow-up blood cultures had no growth after a week. The septic markers (Table 1) dropped dramatically with the change of antibiotics to imipenem.

treated surgically and functional causes can be managed supportively, with medication and the use of an IABP while the underlying cause is addressed.[1]

Pathophysiology of acute mitral incompetence

Acute mitral incompetence differs from chronic incompetence in that there is no time for remodelling.[1,3] The stroke volume is decreased, which can be due to ventricular dysfunction as well as retrograde flow from the left ventricle into the left atrium.[1-3] The decreased stroke volume is compensated for by tachycardia in an effort to maintain cardiac output. When compensation fails, the patient will present with hypotension and end-organ failure presenting as cardiogenic shock.[1,2] The regurgitation into the left atrium results in raised left atrial pressures and pul monary wedge pressures that lead to pulmonary oedema.[1-3] Numerous cases have been reported presenting with unilateral pulmonary oedema, usually on the right side and confined to the upper lobe.[3,4]

This is often confused with pneumonia. [4] Symptoms are related to the fraction of the stroke volume that is regurgitated. Regurgitation of <30% of the stroke volume usuallypresents with mild symptoms, 30 60% regurgitation with moderate symptoms, and regurgitation of >60% with severe symptoms.

Differentiating between acute and chronic mitral incompetence

A combination of pulmonary cardiac cathe ter measurements and ultrasonography is used to differentiate between acute and chronic mitral regurgitation. The difference in findings is based on the time for compensation. Table 3 summarises the basic differences.[1]

Clinical presentation

The usual triad of dyspnoea, haemodynamic instability and shock is not always present in patients with acute mitral incompetence. [1] Auscultation can be misleading, as the new murmur may be subtle and masked by the compensatory tachycardia.[1] However, the

Table 1. Blood results White cell count (×109/L)

10/2/15

11/2/15

12/2/15

13/2/15

14/2/15

15/2/15

17/2/15

5.5

11.9

9.9

10.7

9.6

7.6

CRP (mg/L)

227

336

200

120

Procalcitonin (ng/mL)

100

Table 2. Causes of acute mitral incompetence[1,2] Organic causes of acute mitral incompetence

Functional causes of acute mitral incompetence

Leaflet perforation or chordae tendineae rupture from endocarditis

Dilated cardiomyopathy leads to leaflet tethering

Discussion

Chordal rupture in myxomatous valvular disease

Acute ischaemic akinesis of wall segments and papillary muscle dysfunction

Acute mitral incompetence in patients with cardiogenic shock has an observed mortality of 55%, which is marginally improved to 39% in patients selected for emergency surgery. Severe mitral incompetence affects about 7% of patients with cardiogenic shock.[1,2] Acute mitral incompetence can be classi fied as organic or functional. Organic causes result in physical disruption of the valve, while functional incompetence results from abnormalities of the left ventricle. The causes of acute mitral incompetence are listed in Table 2. Differentiation between the two groups is very important, as organic causes are usually

Papillary muscle rupture due to myocardial infarction

Takotsubo’s cardiomyopathy

Acute severe mitral incompetence

Prosthetic valve dysfunction due to endocarditis

Table 3. Differentiating between acute and chronic mitral regurgitation Chronic mitral regurgitation

Acute mitral regurgitation

Cardiac output

Normal

Decreased

Ejection fraction

Increased

Normal or decreased

Left ventricular size

Increased

Normal

Left atrial compliance

Normal

Left ventricular end-diastolic pressure

Normal

Markedly increased

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IN PRACTICE

Table 4. Echocardiographic findings in acute mitral regurgitation[2] Mild

Moderate

Severe

Regurgitant volume (mL/beat)

<30

30 - 59

≥60

Regurgitant fraction (%)

<30

30 - 49

≥50

0.20 - 0.39

≥0.40

Effective regurgitant orifice area (cm ) <0.20 2

Vena contracta width (cm)

<0.30

≥0.70

murmur, when identified, is pansystolic and best heard at the apex of the heart with the patient in the lateral decubitus position.[2] When the afterload is increased, for example by strong hand grip or squatting, the murmur is accentuated. Using similar logic, the intensity of the murmur is decreased by standing and the valsalva manoeuvre.[2] Tachypnoea and associated pulmonary oedema can further increase the difficulty of auscultation. Any signs that could suggest myocardial infarction should prompt thorough investigation, as this remains the most common cause of acute mitral regurgitation. [1] Patients presenting with fever in association with the above signs should be worked up for infective endocarditis. As the clinical signs of acute valvular pathology are not always obvious, a high index of suspicion should be maintained. If acute valvular pathology is suspected, the patient should receive an ECG, chest radiograph and echocardiography.[1,2] The echocardiographic findings that determine the severity of mitral regurgitation are summarised in Table 4. Transoesophageal echocardiography (TEE) provides a more detailed view and should be used if endocarditis or valvular thrombi are suspected.[2] The use of TEE has become increasingly important in the assessment of mitral incompetence as it is highly specific and sensitive for numerous causes and helps to localise the problem area with more precision. It is essential in the planning of surgical intervention.[1,2] In patients with pulmonary artery catheters in situ, moderate and severe mitral incompetence can be recognised by a large v wave and a rapid y descent.[2] The routine blood tests should include a full blood count, electrolyte profile and urea, and creatinine should be tested together with troponin and B-type natriuretic peptide (BNP) levels.[1,5]

Management of acute mitral incompetence

The general management of acute mitral incompetence includes reducing afterload and maintaining a fast-normal heart rate (80 100 bpm). Care should be taken to prevent sudden increases in afterload, for example, during intubation and surgical stimulus, as this will increase the regurgitation fraction. In the management of acute mitral incompetence with an organic cause, supportive therapy can stabilise patients long enough to prepare the operating suite. Medical therapy is not a substitute for surgical intervention in these patients. Valve repair or replacement is the definitive treatment, while the use of dobutamine, nitroprusside and nitroglycerine are temporary measures. The use of an IABP may be beneficial in these patients. Surgical treatment is reserved

for patients with a regurgitant fraction >30%. Whenever possible, valve repair is preferred to replacement as the prognosis is better and anticoagulants are not needed.[1,3] In the management of acute mitral incompetence with functional causes, supportive therapy may be sufficient and surgical intervention not required unless initial supportive measures fail. The aim is to optimise the perfusion of the heart and thus the affected area. The use of an IABP is effective in all cases of functional mitral incompetence, and this is especially true for cases of myocardial ischaemia or cardiomyopathy.[1,3]

Prognosis

There are limited studies on the prognosis of patients with acute mitral incompetence. Numerous studies have been done on increased mortality from ischaemic mitral incompetence following myocardial infarction and the presence of mitral incompetence post-infarction is a poor prognostic sign.[6] Studies on the prognosis of acute functional mitral incompetence are few and none have ventured to assign values to mortality. Studies have shown that the degree of left ventricular dysfunction is not proportionate to the severity of the mitral incompetence and it is therefore impossible to draw accurate correlations between severity and outcome.[7] Functional mitral regurgitation is a poor prognostic sign in left ventricular dysfunction caused by cardiomyopathy or ischaemic disease.[7] BNP measurement is being used increasingly as a prognostic tool. Its use in relation to functional mitral incompetence has not been specifically studied. A correlation between a raised BNP level and an increased number of adverse events under conservative management has been observed. BNP measurement should be used in conjunction with other risk stratification tools and clinical evaluation.[5] Aggressive early surgical management of patients with acute organic mitral incompetence has been shown to decrease mortality.[1]

Conclusion

The incidence of acute functional mitral incompetence is dwarfed by the incidence of acute organic mitral incompetence. However, it is important to exclude acute functional mitral incompetence, which has markedly different management to and much lower morbidity and mortality than acute organic mitral incompetence. 1. Mokadam NA, Stout KK, Verrier ED. Management of acute regurgitation in left-sided cardiac valves. Tex Heart Inst J 2011;38(1):9-19 2. Armstrong GP. Cardiovascular disorders: Mitral regurgitation. The Merck Manual Professional Edition [internet homepage]. 2014. http://www.merckmanuals.com/professional/cardiovascular_ disorders/valvular_disorder/mitral_regurgitation.html (accessed 21 March 2015). 3. Mitral regurgitation. 2015. http://www.openanesthesia.org/mitral_regurgitation/ (accessed 18 March 2015). 4. Roach JM, Stajduhar KC, Torrington KG. Right upper lobe pulmonary edema caused by acute mitral regurgitation. Diagnosis by transesophageal echocardiology. Chest 1993;103(4):1286-1288. 5. Detaint D, Messika-Zeitoun D, Avierinos JF, et al. B-type natriuretic peptide in organic mitral regurgitation. Circulation 2005;111(18):2391-2397. DOI:10.1161/01.cir.0000164269.80908.9d 6. Trichon BH, Felker GM, Shaw LK, Cabell CH, O’Connor CM. Relation of frequency and severity of mitral regurgitation to survival among patients with left ventricular dysfunction and heart failure. Am J Cardiol 2003;91(5):538-543. DOI:10.1016/s0002-9149(02)03301-5 7. Yiu SF, Enriquez-Sarano M, Tribouilloy C, Seward JB, Tajik AJ. Determinants of the degree of functional mitral regurgitation in patients with systolic left ventricular dysfunction. Circulation 2000;102(12):1400-1406. DOI:10.1161/01.cir.102.12.1400

Accepted 9 November 2015.

August 2016, Print edition

IN PRACTICE

CASE REPORT

Fatal encephalopathy complicating persistent vomiting in pregnancy: Importance of clinical awareness on the part of healthcare professionals N C Ngene, MBBS, Dip Obst (SA), Dip HIV Man (SA), MMed (Fam Med), FCOG (SA), MMed (O&G); J Moodley, MB ChB, FCOG (SA), FRCOG (UK), MD Department of Obstetrics and Gynaecology, School of Clinical Medicine, College of Health Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa Corresponding author: N C Ngene (ngenenc@gmail.com)

Women with persistent vomiting during pregnancy need early referral to appropriate health facilities. Delayed referral and inappropriate management may lead to metabolic encephalopathy from a variety of causes, including electrolyte derangements or thiamine deficiency (Wernicke’s encephalopathy) (WE). We present a case of persistent vomiting in pregnancy in which there was delayed referral, inappropriate treatment and failure to associate neurological signs such as terminal neck stiffness with WE, resulting in poor fetomaternal outcomes. In this report, we discuss the following lessons: (i) the need for early transfer of a patient with persistent vomiting and enigmatic clinical features to a higher healthcare facility; (ii) failure to associate neurological signs with complications of hyperemesis gravidarum/WE; (iii) lack of thiamine supplementation; and (iv) the advantages of magnetic resonance imaging over a computed tomography scan in the diagnosis of WE. S Afr Med J 2016;106(8):792-794. DOI:10.7196/SAMJ.2016.v106i8.10909

Hyperemesis gravidarum (HEG) is persistent vomiting in preg nancy that results in dehydration, electrolyte imbalance, ketosis and loss of more than 5% of prepregnancy weight or 3 kg.[1,2] HEG resulted in five in-hospital maternal deaths in South Africa between 2011 and 2013.[3] Because vomiting and nausea are the most common symptoms in pregnancy, affecting 50 - 90% of mothers,[1] some cases of vomiting are erroneously considered to be minor ailments. To assess the severity of vomiting and identify patients with HEG, the PUQE (Pregnancy-Unique Quantification of Emesis and Nausea) scoring system may be used.[4-6] HEG may result in neurological complications such as Wernicke’s encephalopathy (WE), Korsakoff syndrome and osmotic demyelination (central pontine myelinolysis). [2,7,8] Wernicke’s encephalopathy is an acute thiamine deficiency classically characterised by the triad of eye signs, an altered mental state and ataxia.[9] The prevalence of WE among alcoholics and non-alcoholics is 12.5% and 0.04 - 0.13%, respectively.[10] We report a case in which non-provision of appropriate medical care to a patient with persistent HEG resulted in a fatal metabolic encephalopathy with neurological signs probably in keeping with a diagnosis of WE. The gaps in management are discussed so as to provide clinical lessons to all medical practitioners.

Case report

A 28-year-old woman, gravida 3, para 2, who had had two previous normal vaginal births, presented to a district hospital (DH) at 6 weeks’ gestation with a history of persistent vomiting. She was diagnosed as having HEG, admitted and treated with an antiemetic, metoclopramide, for 6 days. She was not alcoholic. At 8 weeks’ gestation, she was readmitted to the same hospital with HEG and again treated with metoclopramide and intravenous (IV) fluids for 7 days. During this admission, the medical officer managing the patient obtained advice from a doctor at a regional hospital (RH). They agreed that the patient should be reviewed in the RH in 9 days’

time. The patient was not transferred on the agreed date for unknown reasons. At 11 weeks’ gestation, she presented to the DH again and was referred to the regional facility. The serum electrolytes were not assessed at the DH. When seen in the emergency obstetric unit at the RH, the patient had persistent vomiting, headache, photophobia, generalised body weakness and dehydration. Physical examination showed a Glasgow Coma Score (GCS) of 14 (motor response 5, eye opening 5, verbal response 4), abducent nerve palsy, terminal neck stiffness, a blood pressure of 102/79 mmHg, a pulse rate of 90 bpm and a temperature of 35.3oC. The serum sodium level was 146 mmol/L and the potassium level 2.5 mmol/L. She was reviewed by the internal medicine team, who made a provisional diagnosis of meningitis, prescribed ceftriazone and requested a computed tomography (CT) brain scan prior to performing a lumbar puncture. On the 3rd day after admission to the RH, the patient was found to have renal impairment (serum creatinine level 435 μmol/L), hypokal aemia, horizontal nystagmus and an offensive vaginal discharge. She was resuscitated with a normal saline infusion and potassium replacement therapy. On the 7th day, the CT brain scan showed no abnormalities; the planned lumbar puncture was performed, and analysis showed the cerebrospinal fluid (CSF) to be normal. At this stage, the beta human chorionic gonadotrophin (hCG) level was 71 109 IU/L, the blood urea nitrogen (BUN) level had improved from 27.5 to 3.1 mmol/L, the serum creatinine level had decreased from 435 to 41 μmol/L and the potassium level had increased from 1.8 to 2.8 mmol/L. An HIV test was negative, and thyroid dysfunction, malaria, autoimmune disorders and urinary tract infection were excluded. An ultrasound scan of the uterus revealed a live fetus of ~12 weeks’ gestational age with no gross abnormalities and a normal placenta. The hCG levels were in keeping with the gestational age. On the 9th day after admission, the patient was still vomiting and had a GCS of 8 (motor response 3, eye opening 3, verbal response 2),

August 2016, Print edition

IN PRACTICE

hypernatraemia (sodium level 164 mmol/L), hypokalaemia (potass ium level 3.1 mmol/L), hypomagnesaemia (magnesium level 0.51 mmol/L) and a blood glucose level of 5.3 mmol/L. She was not polyuric. The clotting profiles were all within normal limits, and a chest radiograph and liver function tests did not show any abnormality. Thromboprophylaxis was commenced and correction of electrolyte imbalance was continued. Among the IV fluids administered during this period was 5% dextrose. A repeat obstetric scan revealed intrauterine death of the fetus. The patient was subsequently admitted to the intensive care unit (ICU) because of inability to correct her electrolyte imbalance, especially the hypernatraemia. She received the following IV fluids in the ICU: magnesium sulphate, potassium phosphate, 5% dextrose infusion, and 0.45% saline mixed with 5% dextrose. The sodium level decreased from 164 to 158 mmol/L over a 3-day period. Because of concern about possible chorioamnionitis, misoprostol was administered to expel the products of the conception. The patient later had manual vacuum aspiration for an incomplete miscarriage. She subsequently developed respiratory failure and was mechanically ventilated. On day 3 after ICU admission (day 13 post admission), the patient’s condition in the previous 24 hours suggested that recovery was unlikely. The clinical conditions were: fixed and dilated pupils, no corneal reflex, GCS 2T, no response to pain stimulus and inability to trigger the ventilator. The ventilator was switched off after informed consent had been obtained from the patient’s family, and she died. WE was thought to be the most probable cause of death, based on the presence of a metabolic encephalopathy with transient abducent nerve palsy and nystagmus in the context of prolonged vomiting. An autopsy was not performed.

Discussion

The management of HEG involves resuscitation, identification and treatment of any cause of the vomiting,[11] correction of electrolyte imbalance, symptomatic support such as rehydration, administration of antiemetics, thiamine supplementation, and nutritional as well as psychological support. It is not certain why the serum electrolytes were not assessed in the DH despite the availability of a functional laboratory. Health professionals must recognise the need to correct electrolyte imbalance and fully resuscitate pregnant women with a history of persistent vomiting. The patient was also managed in a standard hospital ward for some days. In such cases, correction of electrolyte imbalance must be carried out in a high-care area or an ICU setting. Persistent vomiting causes hyponatraemia, dehydration, increased thirst and prerenal impairment. Inadequate resuscitation and poor oral intake in our patient, who had a low GCS, may have caused the hypernatraemia. The return of the BUN and serum creatinine to normal levels following fluid therapy was consistent with prerenal failure. Rapid correction of hypernatraemia may lead to central myelinosis, and it is an alternative cause of neurological deterioration. In our patient, the correction of hypernatraemia was gradual, but not resolved prior to death. Early referral to an ICU or a high-care area is certainly recommended in cases such as ours. Acquisition of such knowledge on maternal resuscitation should begin during undergraduate education and continue after qualification by taking part in continuing education programmes dealing with obstetric emergencies, such as the Essential Steps in the Management of Obstetric Emergencies training or other similar programmes for medical practitioners. Delayed arrival of the patient to the RH affected the outcome. Such a delay may be preventable if healthcare workers endeavour to transfer patients with non-remitting/enigmatic clinical features

early enough to a higher level of care or seek appropriate advice from specialists. It may also be preventable if dedicated health workers are assigned to keep track of referred patients to ensure that they are reviewed at the referral centre. An acute confusion state (encephalopathy) is a medical emergency that requires structured evaluation. In an encephalopathic patient, normal findings on brain imaging and CSF analysis in the absence of head trauma, recent seizures, sepsis or cardiorespiratory instability suggest metabolic encephalopathy. Causes include electrolyte and glucose abnormalities, vitamin deficiencies, and drug or alcohol withdrawal. In this case, diagnostic considerations were not expanded to include vitamin deficiencies in a patient who was unable to eat. In a previous report, loss of appetite and persistent vomiting were associated symptoms in a case of WE resulting from gastroparesis after a partial antrectomy.[12] The body’s thiamine reserve is depleted in HEG and WE, especially in tissues with a high metabolic rate such as the brain.[13] It is therefore recommended that serum thiamine be assessed and supplemented.[9] Given that the diagnosis of WE was not considered, thiamine was not administered. Furthermore, the use of dextrose-containing IV fluid could have worsened the neurological condition, as glucose infusion precipitates WE in patients who are thiamine depleted.[9] The protocol in the RH recommends against routine use of dextrose-containing fluid at the inception of management in HEG. This is regardless of a research finding that suggests that the administration of dextrosecontaining IV fluids may not cause harm.[14] Nonetheless, a recent case series supports thiamine therapy before administration of glucose in any patient with altered consciousness of unknown causation. [15] To ensure appropriate management of WE or persistent HEG, a neurologist or an experienced medical practi tioner should be involved early on. In a pregnant woman with persistent vomiting, dehydration and neurological signs, health professionals must consider WE. Since assessment of serum thia mine levels is not routinely available, the diagnosis of WE can be made clinically by demonstrating response to thiamine supple mentation. Where facilities exist, patients with persistent vomiting may need magnetic resonance imaging (MRI) for evaluation. The MRI features of WE include hypersignal intensity at the thalamus.[12,13] A CT scan of the brain is not a reliable diagnostic test for WE,[9] and use of a CT scan of the brain to evaluate a patient with prolonged vomiting in pregnancy may therefore delay the diagnosis of WE. An MRI scan of the brain may reveal complications such as central pontine myelinolysis. Its use is also important in atypical cases of acute nonalcoholic WE.[12,16] Although an MRI scan was not performed, the patient did not have pseudobulbar paralysis or spastic quadriparesis, which are classic features of myelinolysis.[7]

Conclusion

The management of HEG (Table 1) requires prompt, proper resusci tation and exclusion of other causes of vomiting. In a DH, this will mean obtaining advice from a specialist and timely referral; investigations must include a full blood count, urine dipstick testing, urine culture, blood glucose, liver function tests, hCG levels, obstetric ultrasound, thyroid function tests, serum urea, creatinine and electrolytes. Where the facilities exist, assessment of serum thiamine and evaluation of the brain with an MRI are valuable if there is an encephalopathy. Given the poor prognosis associated with undiagnosed WE, we strongly recommend routine thiamine supplementation in patients with persistent vomiting in pregnancy.

August 2016, Print edition

IN PRACTICE

Table 1. Management of persistent vomiting in pregnancy Resuscitate Admit the patient to a high-care area or ICU Take detailed history, determine PUQE score and perform physical examination Always assess serum electrolytes Judiciously correct electrolyte imbalance Supplement with thiamine Avoid routine administration of dextrose-containing fluid prior to thiamine supplementation Exclude other causes of vomiting and consider administration of appropriate antiemetic(s) Discuss the patient with an experienced medical practitioner, preferably an obstetrician or fetomaternal medicine specialist In the absence of clinical improvement, refer the patient to a higher level of care and involve a specialist physician Be aware that neurological signs may suggest WE If neurological signs develop, and facilities exist, perform MRI of the brain Cases with non-remitting/enigmatic clinical features should be discussed in scheduled multidisciplinary clinical meetings. During the discussion, the opinion of each clinical discipline must be given due consideration 1. Jarvis S, Nelson-Piercy C. Management of nausea and vomiting in pregnancy. BMJ 2011;324:d3606 DOI:10.1136/bmj.d3606 2. Sonkusare S. The clinical management of hyperemesis gravidarum. Arch Gynecol Obstet 2011;283(6):1183-1192. DOI:10.1007/s00404-011-1877-y

3. National Committee on the Confidential Enquiries into Maternal Deaths. Saving Mothers 2011 - 2013: Sixth report on the confidential enquiries into maternal deaths in South Africa. Pretoria: National Department of Health, 2015. http://www.kznhealth.gov.za/mcwh/Maternal/Saving-Mothers-20112013-short-report.pdf (accessed 12 July 2015). 4. Birkeland E, Stokke G, Tangvik RJ, et al. Norwegian PUQE (Pregnancy-Unique Quantification of Emesis and Nausea) identifies patients with hyperemesis gravidarum and poor nutritional intake: A prospective cohort validation study. PLoS One 2015;10(4):e0119962. DOI:10.1371/journal. pone.0119962 5. Ebrahimi N, Maltepe C, Bournissen FG, Koren G. Nausea and vomiting of pregnancy: Using the 24-hour Pregnancy-Unique Quantification of Emesis (PUQE-24) scale. J Obstet Gynaecol Can 2009;31(9):803-807. DOI:10.1016/s1701-2163(16)34298-0 6. Koren G, Boskovic R, Hard M, Maltepe C, Navioz Y, Einarson A. Motherisk-PUQE (Pregnancy-Unique Quantification of Emesis and Nausea) scoring system for nausea and vomiting of pregnancy. Am J Obstet Gynecol 2002;186(5, Suppl 2):S228-S231. DOI:10.1067/ mob.2002.123054 7. Zara G, Codemo V, Palmieri A, et al. Neurological complications in hyperemesis gravidarum. Neurol Sci 2012;33(1):133-135. DOI:10.1007/s10072-011-0660-y 8. Kotha VK, de Souza A. Wernicke’s encephalopathy following hyperemesis gravidarum. A report of three cases. Neuroradiol J 2013;26(1):35-40. DOI:10.1177/197140091302600106 9. Galvin R, Brathen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. Eur J Neurol 2010;17(10):1408-1418. DOI:10.1111/j.1468-1331.2010.03153.x 10. Kantor S, Prakash S, Chandwani J, Gokhale A, Sarma K, Albahrani MJ. Wernicke’s encephalopathy following hyperemesis gravidarum. Indian J Crit Care Med 2014;18(3):164-166. DOI:10.4103/09725229.128706 11. Jueckstock JK, Kaestner R, Mylonas I. Managing hyperemesis gravidarum: A multimodal challenge. BMC Med 2010;8:46. DOI:10.1186/1741-7015-8-46 12. Ganie NS, Janse van Rensburg E. Wernicke’s encephalopathy as a complication of gastroparesis after emergency partial antrectomy. S Afr Med J 2015;105(2):157. DOI:10.7196/SAMJ.9271 13. Sutamnartpong P, Muengtaweepongsa S, Kulkantrakorn K. Wernicke’s encephalopathy and central pontine myelinolysis in hyperemesis gravidarum. J Neurosci Rural Pract 2013;4(1):39-41. DOI:10.4103/0976-3147.105608 14. Tan PC, Norazilah MJ, Omar SZ. Dextrose saline compared with normal saline rehydration of hyperemesis gravidarum: A randomized controlled trial. Obstet Gynecol 2013;121(2):291-298. DOI:10.1097/aog.0b013e31827c5e99 15. Antel K, Singh N, Chisholm B, Heckmann JM. Encephalopathy after persistent vomiting: Three cases of non-alcohol-related Wernicke’s encephalopathy. S Afr Med J 2015;105(6):442-443. DOI:10.7196/ SAMJ.9299 16. Elefante A, Puoti G, Senese R, et al. Non-alcoholic acute Wernicke’s encephalopathy: Role of MRI in non typical cases. Eur J Radiol 2012;81(12):4009-4104. DOI:10.1016/j. ejrad.2012.08.006

Accepted 13 April 2016.

August 2016, Print edition

IN PRACTICE

CASE REPORT

A case of renal cell carcinoma and angiomyolipoma in an adolescent girl J W Rood,1 MB ChB, Dip HIV Man; K P Mokhobo,2 MB ChB, DPH, DTM&H, FCPSA, Dip Cardiol (Copenhagen) 1 2

epartment of Internal Medicine, Tygerberg Hospital, Cape Town, South Africa D Department of Internal Medicine, Potchefstroom Provincial Hospital, North West Province, South Africa

Corresponding author: J W Rood (jacquesrood@gmail.com)

We describe a case of renal cell carcinoma in the right kidney together with an angiomyolipoma in the left kidney, encountered in an adolescent girl at Potchefstroom Provincial Hospital, North West Province, South Africa. S Afr Med J 2016;106(8):795-796. DOI:10.7196/SAMJ.2016.v106i8.10519

Renal cell carcinoma is the most common cancer involving the kidneys. It is reported to occur in 3% of all malignancies in adults and accounts for 90 - 95% of all cancers involving the kidneys. The peak age of diagnosis is between 50 and 70 years; in recent years the median age has been given as 64. There is also a slight predominance in males, with a ratio of 2:1.[1] Renal cell carcinoma has been attributed primarily to smoking, but other risk factors include conditions such as acquired cystic diseases of the kidneys, tuberous sclerosis and von Hippel Lindau (VHL) syndrome. Approximately 35% of patients with VHL disease develop clear renal cell carcinoma.[1] Only 10% of patients present with the classic triad of flank pain, haematuria and a flank mass. The 5-year survival rate for stage 4 renal cell carcinoma is between 0% and 20%.[1] We present a rare case of dual pathologies, renal cell carcinoma in the right kidney and angiomyolipoma in the left, which is still more unusual because the patient was a 17-year-old girl. Verbal consent for the study and publication of material was obtained on initial presentation from the patient as well as the parent.

Case report

A 17-year-old girl of mixed race was referred to Potchefstroom Provincial Hospital, North West Province, South Africa, from the local clinic with what was thought to be spleno megaly. On arrival at the secondary hospital, the abdominal mass was confirmed and was reported probably to be of splenic origin. The history confirmed that the mass had been present for 5 months but had not caused problems until now. She had left-sided flank pain and dysuria, with no

frank haematuria. Urine dipsticks showed microscopic haematuria (blood 4+, protein 1+). She also complained of arthralgia, espe cially in the lower region of the back. There was intermittent nausea but rarely vomiting. She had developed a rash/freckles (pale reddish-brown soft small papules) on the face 8 months prior to initial presentation and was referred from the clinic with a query of angiofibroma (Fig. 1). Subsequent work-up for systemic lupus erythematosus was reported to be negative. The rash was reviewed and labelled as papulosa nigra, a normal variant of pigmented skin without any pathological features. No biopsy was done. The patient had no vaginal bleeding or discharge and reported normal bowel function; urine output was normal. She was not coughing and had no complaints of any neurological or cardiovascular symptoms, and reported no smoking or alcohol use. She reported not being sexually active, and a pregnancy test confirmed that she was not pregnant. Menstruation was reported as normal. She had no travel history, medical comorbidities or allergies. She was not using any form of contraception. There was a family history of malignancy in her brother, but the family did not know what type it was. She had no history of tuberculosis and had tested negative for HIV in the weeks preceding presentation.

Physical findings

The physical findings were unremarkable considering the underlying pathology. The patient was slightly underweight with a body mass index of 19 kg/m2. She was not pale or oedematous and no rash was seen. The findings on cardiovascular, respiratory and neurological examination were essentially normal apart from a slightly elevated blood

August 2016, Print edition

Fig. 1. Possible angiofibromas indicative of tuber ous sclerosis.

pressure of 145/89 mmHg and a persis tent mild tachycardia of 106 bpm. She had a slight fever of 37.8°C and maintained saturation of 98% on room air. Abdominal examination revealed an abdominal mass on the left side measuring ~10 cm below the costal margin that moved inferiorly on inspiration. A notch was felt which at that time led the examiner to believe it was a massive spleen. The abdomen was soft and only mildly tender over the mass with no guarding or rebound tenderness. Bowel sounds were present and the liver was not palpable.

IN PRACTICE

Side-room investigations showed microscopic haematuria (4+) and proteinuria (1+). The haemoglobin concentration was 11.5 g/ dL and a pregnancy test was negative. Blood samples were taken for spleno megaly work-up at the time and revealed nothing further to indicate the origin of the mass. Kidney function (urea 2.4 mmol/L, creatinine 51 µmol/L, estimated glomerular filtration rate >60 mL/min/1.73 m2 and electrolyte levels were normal, as was liver function (alkaline phosphatase 96 U/L, gamma-glutamyl transpeptidase 16 U/L, alanine aminotransferase 10 U/L, aspartate aminotransferase 18 U/L, total bilirubin 4 µmol/L, albumin 42 g/L, total protein 85 g/L). A full blood count (white cell count 6.31 × 109/L, haemoglobin 11.6 g/dL, platelets 264 × 109/L) was normal. A malaria screen, enzyme-linked immunosorbent assay for HIV and antinuclear antibody were negative. The C-reactive protein level was 32 mg/L. The erythrocyte sedimentation rate (ESR) was raised at 105 mm/h. The high ESR together with the presence of the mass alerted the clinician to serious pathology. The patient was sent for an urgent ultrasound scan, which revealed kidneys of normal size but with increased echogenicity. No hydronephrosis was observed, but a hypoechoic mass of 5 × 5 cm in the midpole of the right kidney and a tiny cyst on the lower pole of the left kidney were seen. The bladder, liver, gallbladder, spleen, pancreas and uterus were reported to be normal. The ovaries were not visualised owing to gas dilating the bowel. The patient was sent for an urgent computed tomography (CT) scan of the abdomen with contrast. The following day, the clinician was called to assess the CT scan together with the radiologist. The radiologist reported a hypodense mass with hyperdense vessels inside the lower part of the left kidney; it also consisted of fatty density and appeared hypervascularised after administration of contrast medium. On first glance, the mass measured 63 × 126 mm but on review it was 150 × 90 mm (Fig. 2). This mass was compressing the collecting system of the upper part of the left kidney as well as the aorta and some small bowel loops. Another enhancing solid mass was present in the middle part of the right kidney, measuring 51 × 58 mm in diameter (Fig. 3). Neither ureter was dilated and there was good excretion of the contrast medium by both kidneys. No enlarged retroperitoneal lymph nodes were seen. There were some small sclerotic lesions in the thoracic and lumbosacral vertebral bodies and both iliac bones, suggestive of bone metastases. The patient was referred to a tertiary setting for a nephrologist to perform a confirmative biopsy of the renal masses and provide further management.

Discussion

A search of the literature revealed articles describing these dual pathologies in one individual.[2-4] One of them had a unifying diagnosis of tuberous sclerosis.[3] These articles suggest that one should look for renal involvement in patients with tuberous sclerosis complex (TSC).[2-4] Could this patient have TSC, or could the angiomyolipoma be unusual renal metastases presenting radiologically as angiomyolipoma?[5] Could her freckles be mistaken for angiofibromas, which would support the diagnosis of tuberous sclerosis? These are important considerations in this case that may offer some treatment options. For example, she could receive treatment with everolimus (Afinitor), which is used for TSC and has been proven to have a 42% response rate in double-blind, placebocontrolled phase III trial studies.[6,7]

Conclusion

This is an uncommon case of dual renal malignancies in a young girl, with a suspicion of TSC as the underlying cause.

Fig. 2. Angiomyolipoma in the left kidney (arrow).

Fig. 3. Right kidney showing clear solid mass (black arrow) and left kidney deformed due to angiomyolipoma (white arrow).

The patient was referred to a tertiary setting for biopsy and further management. In the referral letter it was suggested that a diagnosis of TSC be considered. Acknowledgement. Dr M J Kleynhans and Dr M Radebe are acknow ledged for their critical evaluation of the manuscript. 1. Scher HI, Rosenberg JE, Motzer RJ. Bladder and renal cell carcinoma. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 19th ed. New York: McGraw-Hill, 2015. 2. Korula S, Ekbote A, Kumar N, Danda S, Agarwal I, Chaturvedi S. Renal manifestation of tuberous sclerosis among children: An Indian experience and review of literature. Clin Kidney J 2014;7(2):134137. DOI: 10.1093/ckj/sft162 3. Kakkar A, Vallonthaiel AG, Sharma MC, Bora G, Panda A, Seth A. Composite renal cell carcinoma and angiomyolipoma in a patient with tuberous sclerosis: A diagnostic dilemma. Can Urol Assoc J 2015;9(7-8):E507-E510. DOI:10.5489/cuaj.2532 4. Mei M, Rosen LE, Reddy V, Cimbaluk DJ, Gattuso P. Concurrent angiomyolipomas and renal cell neoplasms in patients without tuberous sclerosis: A retrospective study. Int J Surg Pathol 2015;23(4):265-270. DOI:10.1177/1066896915569914 5. Sung CK, Kim SY, Woo S, et al. Angiomyolipoma with minimal fat: Differentiation of morphological and enhancement features from renal cell carcinoma at CT imaging. Acta Radiol 2015; Dec 11 [Epub ahead of print]. DOI:10.1177/0284185115618547 6. Bissler JJ, Kingswood JC, Radzikowska E, et al. Everolimus for angiomyolipoma associated with tuberous sclerosis complex or sporadic lymphangioleiomyomatosis (EXIST-2): A multicentre, randomised, double-blind, placebo-controlled trial. Lancet 2013;381(9869):817-824. DOI:10.1016/ S0140-6736(12)61767-X 7. Everolimus reduces kidney tumors in tuberous sclerosis complex. Medscape Medical News, 11 Jan 2013.

Accepted 14 January 2016.

August 2016, Print edition

November 8-12, 2016

Held in conjunction with the South African Urological Association (SAUA) Meeting • November 8 – 9, 2016

RESEARCH

Evaluation and management of patients referred to a tertiary-level hypertension clinic in Cape Town, South Africa M S Moosa,1 MB ChB, FCP (SA); L S Kuttschreuter,2 MB ChB; B L Rayner,3 MB ChB, FCP (SA), MMed, PhD epartment of Medicine, New Somerset Hospital, Cape Town, South Africa D Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa 3 Division of Nephrology and Hypertension, Department of Medicine, Groote Schuur Hospital, Cape Town, South Africa 1 2

Corresponding author: M S Moosa (shiraz.moosa@gmail.com)

Background. Hypertension remains a global health burden, with a high incidence of long-term morbidity and mortality. Objectives. To evaluate blood pressure (BP) control, factors associated with poor BP control, target organ damage (TOD), whitecoat hypertension, treatment-resistant hypertension and secondary hypertension in patients referred to a tertiary-level hypertension clinic. Method. This was a prospective case-control study of patients referred for specialist hypertension management. Patient parameters recorded included age, gender, body mass index, uric acid, cholesterol, screening BP, follow-up BP, TOD and medications. We also recorded causes of secondary hypertension. Net BP change and the percentage achieving target BP were calculated in all patients followed up. Results. A total of 175 patients were sampled (72 males and 103 females, mean age 46.5 years). Of the patients 16.6% had a normal screening BP; 62.9% of patients were followed up, and 43.6% of these achieved BP control. After intervention, there was a net drop of 13.2 mmHg (range 7.9 - 18.4) in systolic BP and of 3.8 mmHg (4.4 - 12.0) in diastolic BP. Of all the patients, 12.6% had resistant hypertension, 49.1% had evidence of left ventricular hypertrophy and 18.3% had microalbuminuria; 13.1% of the patients were diagnosed with secondary hypertension. Conclusion. Specialist intervention was useful in identifying patients with white-coat and secondary hypertension, as well as in improving hypertension control in patients with apparent treatment-resistant hypertension. However, a significant percentage of patients did not reach target BP, and further efforts are required to identify the underlying causes for this. S Afr Med J 2016;106(8):797-800. DOI:10.7196/SAMJ.2016.v106i8.9610

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i8.9610

Pan computed tomography for blunt polytrauma: Are we doing too many? G V Oosthuizen, FCS (SA); J L Bruce, FCS (SA); W Bekker, FCS (SA); N Shangase, FCS (SA); G L Laing, FCS (SA), PhD; D L Clarke, FCS (SA), PhD Pietermaritzburg Metropolitan Trauma Service, Department of Surgery, School of Clinical Medicine, College of Health Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Pietermaritzburg, South Africa Corresponding author: G V Oosthuizen (george.oost@gmail.com)

Background. Pan computed tomography (CT) is widely used in the evaluation of patients with blunt polytrauma, but there is growing concern about the radiation risks imposed. Objectives. To ascertain whether we were possibly overutilising pan CT in our trauma service, and whether we could safely cut down on scans without missing significant injuries. Methods. We audited all pan scans performed in the Metropolitan Trauma Service, Pietermaritzburg, South Africa, during the 12-monthÂ period 1Â January - 31 December 2012. An analysis was done to determine what injuries were identified and how these findings influenced our management.

August 2016, Print edition

RESEARCH

Results. Of the 140 pan scans, 108 (77.1%) influenced management. These included the following components: 62 brain scans (44.3%), 16 cervical spine scans (11.4%), 50 chest scans (35.7%) and 31 abdominal scans (22.1%). The remaining 32 pan scans (22.9%) did not influence management. However, it turned out that many of these ‘clinically negative’ scans were in fact clinically important, ruling out injury in patients in whom clinical assessment was regarded as unreliable: 3 patients (2.1%) were hypoxic and had to be sedated, intubated and ventilated; 14 (10.0%) had a Glasgow Coma Score (GCS) of <15; and 9 (6.4%) had major distracting injuries. This left only 6 pan scans (4.3%) that were not regarded as clinically helpful. Conclusion. In our setting, the majority of pan scans influence management. By ruling out significant injuries, clinically negative scans are valuable in patients who are obtunded, intubated and ventilated, or have major distracting injuries. In patients with a GCS of 15, not sedated and ventilated and with no major distracting injuries, clinical assessment and alternative imaging modalities may suffice. S Afr Med J 2016;106(8):801-803. DOI:10.7196/SAMJ.2016.v106i8.10376

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i8.10376

South African healthcare provider perspectives on transitioning adolescents into adult HIV care T H Kung,1,2 BA; M L Wallace,1 MSc, PhD; K L Snyder,1 MSc; V K Robson,1,3 BS; T S Mabud,2 MSc; C D Kalombo,1,4 MB ChB; L-G Bekker,1 MB ChB, DTMH, DCH, PhD esmond Tutu HIV Centre, Faculty of Health Sciences, University of Cape Town, South Africa D School of Medicine, Stanford University, Stanford, CA, USA 3 School of Medicine, Harvard University, Boston, MA, USA 4 Metro-District Health Services, Gugulethu, Cape Town, South Africa 1 2

Corresponding author: T H Kung (tkung@stanford.edu)

Background. The first generation of South African (SA) children perinatally infected with HIV is entering adulthood, and there is now a pressing need for systematised transfer of these patients from paediatric to adult care. Objectives. Previous research has investigated the HIV healthcare transition in North America and Europe, yet none has been conducted in SA. Our study is the first to describe the perspectives of healthcare providers overseeing the transition in resource-limited settings. Methods. We approached healthcare providers working in government paediatric HIV clinics and hospitals in the Western Cape Province, SA. Seven physicians and counsellors in adolescent/paediatric care, representing five clinics, were interviewed, and 43 completed a written survey. Interviews addressed the current state of the transition, barriers and facilitators, and model components. Interviews were assessed for major themes using framework analysis, while logistic regression was applied to survey responses to identify associations with measured covariates. Results. Analysis of interview transcripts revealed several overarching perspectives that were corroborated by survey responses. One barrier identified was the healthcare providers’ difficulty in letting go of their relationships with the adolescent patients. Since healthcare providers regarded their patients as particularly vulnerable, they felt a strong and protective attachment towards them. A second barrier identified was a lack of structure and effective communication between adult and paediatric providers; accordingly, healthcare providers feared that they were transferring their adolescents unprepared, to a judgemental, depersonalised and overburdened environment. All interviewees and a majority of survey respondents (>80%) agreed that the formation of adolescent support groups in adult care clinics as well as a later transition age would improve the transition process. Conclusion. This study highlights the need for a systematic healthcare transition for HIV-positive adolescents cared for in the Western Cape, while acknowledging the limitations of the current healthcare infrastructure. Several feasible recommendations have been identified, including forming support groups and greater involvement of adolescent healthcare providers to facilitate the transition. S Afr Med J 2016;106(8):804-808. DOI:10.7196/SAMJ.2016.v106i8.10496

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i8.10496

August 2016, Print edition

RESEARCH

Sialendoscopic treatment of recurrent juvenile parotitis: A South African case series S Honnet,1 BSc, MB BCh; O Edkins,1,2 MB BCh, FCORL (SA), MMed (Otol) 1 2

epartment of Otorhinolaryngology, New Somerset Hospital, Cape Town, South Africa D Department of Otorhinolaryngology, Faculty of Health Sciences, University of Cape Town, South Africa

Corresponding author: S Honnet (simonhonnet@yahoo.com)

Background. Recurrent juvenile parotitis (RJP) is a well-recognised cause of parotitis in childhood. Sialendoscopy has been extensively used for the investigation and treatment of many benign salivary disorders, and now offers a minimally invasive approach to RJP. Objectives. To investigate the epidemiology and disease profile of RJP, and review the efficacy of sialendoscopy for its investigation and treatment. Methods. The relevant literature on RJP was reviewed, and a retrospective folder review was performed for all patients who had undergone sialendoscopy for RJP at two South African (SA) hospitals between April 2013 and September 2015. Patients’ epidemiological and clinical data were recorded, as well as the findings and outcomes of ultrasonography and sialendoscopy. In particular, the time following treatment without any further recurrences was recorded as a measure of success. Results. Five children underwent sialendoscopic investigation and treatment for RJP. Their demographic and disease profiles and the results of investigations and treatments were in keeping with published literature. No surgical complications occurred, and no patients reported any further symptoms postoperatively, with an average follow-up of 22 months. Conclusion. Although small in sample size, this is the first reported case series in the SA literature on the use of sialendoscopy for RJP, and the results are consistent with internationally published data. Sialendoscopy is regarded as safe and effective for the diagnosis and management of RJP, and should be considered for patients who remain symptomatic after conservative management. S Afr Med J 2016;106(8):899-812. DOI:10.7196/SAMJ.2016.v106i8.10561

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i8.10561

Feasibility of Pulse Oximetry Pre-discharge Screening Implementation for detecting Critical Congenital heart Lesions in newborns in a secondary-level maternity hospital in the Western Cape, South Africa: The ‘POPSICLe’ study A M van Niekerk,1 BSc, MB ChB, DCH (SA), FCPaed (SA), Cert Cardiol Paed (SA); R M Cullis,1 MB ChB, DCH (SA), FCPaed (SA); L L Linley,1 MB ChB, FCPaed (SA), Reg Neon (SA); L Zühlke,2 MB BCh, DCH, FCPaed (SA), Cert Cardiol Paed (SA), MPH, FESC, PhD (Paed) ivision of Neonatal Medicine, School of Child and Adolescent Health, Faculty of Health Sciences, University of Cape Town; Mowbray D Maternity Hospital, Cape Town, South Africa 2 Department of Paediatrics, Red Cross War Memorial Children’s Hospital and Faculty of Health Sciences, University of Cape Town, South Africa 1

Corresponding author: A M van Niekerk (anika.vanniekerk@westerncape.gov.za)

Background. Early detection of critical congenital heart disease (CCHD) through newborn pulse oximetry (POx) screening is an effective strategy for reducing paediatric morbidity and mortality rates and has been adopted by much of the developed world. Objectives. To document the feasibility of implementing pre-discharge POx screening in well babies born at Mowbray Maternity Hospital, a busy government hospital in Cape Town, South Africa. Parent and staff acceptance was assessed.

August 2016, Print edition

RESEARCH

Methods. We conducted a prospective study of predischarge POx screening in one postnatal ward, following informed parental consent. Results. During the 4-month study period, 1 017 of 2 256 babies discharged (45.1%) were offered POx screening and 1 001 were screened; 94.0% of tests took <3 minutes to perform, 4.3% 3 - 5 minutes and 1.7% >5 minutes. Eighteen patients needed second screens and three required third screens. Only 3.1% protocol errors were made, all without consequence. The vast majority (91.6%) of nursing staff reported insufficient time to perform the study screening in addition to their daily tasks, but ~75% felt that with a full nursing staff complement and if done routinely (not part of a study), pre-discharge POx screening could be successfully instituted at our facility. Over 98% of the mothers had positive comments. Two babies failed screening and required echocardiograms; one was diagnosed with CCHD and the other with neonatal sepsis. The sensitivity and specificity were 50% (95% confidence interval (CI) 1.3 - 98.7%) and 99.9% (95% CI 99.4 - 100%), respectively, with a percentage correct of 99.8%. Conclusions. POx screening was supported and accepted by staff and parents. If there are no nursing staff shortages and if it is done routinely before discharge, not as part of a study, we conclude that POx screening could be implemented successfully without excessive false positives or errors, or any additional burden to cardiology services. S Afr Med J 2016;106(8):817-821. DOI:10.7196/SAMJ.2016.v106i8.10071

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i8.10071

Attitudes to female genital mutilation/cutting among male adolescents in Ilorin, Nigeria A S Adeniran,1 FWACS, FMCOG; M A Ijaiya,1 FWACS; A A Fawole,1 FWACS; O R Balogun,1 FWACS; K T Adesina,1 FWACS, FMCOG; A W O Olatinwo,1 FWACS; A O Olarinoye,1 FWACS; I P Adeniran,2 RPN 1 2

epartment of Obstetrics and Gynecology, University of Ilorin and University of Ilorin Teaching Hospital, Ilorin, Kwara State, Nigeria D Nursing Services Department, University of Ilorin Teaching Hospital, Ilorin, Kwara State, Nigeria

Corresponding author: A S Adeniran (acrowncord@hotmail.com)

Background. The central role of males in female reproductive health issues in patriarchal societies makes them an important group in the eradication of female genital mutilation/cutting (FGM/C). Objectives. To determine knowledge about and attitudes to FGM/C among male adolescents, and their preparedness to protect their future daughters from it. Methods. A cross-sectional survey among male adolescent students in Ilorin, Nigeria. Participants completed a self-administered questionnaire after consent had been obtained from them or their parents. Statistical analysis was with SPSS version 20.0 (IBM, USA). A p-value of <0.05 was taken as significant. Results. Of 1 536 male adolescents (mean age 15.09 (standard deviation 1.84) years, range 14 - 19), 1 184 (77.1%) were aware of FGM/C, 514 (33.5%) supported female circumcision, 362 (23.6%) would circumcise their future daughters, 420 (27.3%) were of the opinion that FGM/C had benefits, mostly as a necessity for womanhood (109, 7.1%), and 627 (40.8%) perceived it as wickedness against females; 546 (35.5%) were aware of efforts to eradicate FGM/C, and 42.2% recommended education as the most important intervention to achieve this. Conclusion. Education and involvement in advocacy may transform male adolescents into agents for eradication of FGM/C. S Afr Med J 2016;106(8):822-823. DOI:10.7196/SAMJ.2016.v106i8.10124

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i8.10124

August 2016, Print edition

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Feasibility of Pulse Oximetry Pre-discharge Screening Implemen tation for detecting Critical Congenital heart Lesions in newborns in a secondary level maternity hospital in the Western Cape, South Africa: The ‘POPSICLe’ study 9. The incidences of congenital heart disease (CHD) are constant worldwide, across geographical and ethnic backgrounds and in spite of variations in socioeconomic conditions. 10. Without an early diagnosis and appropriate treatment, half of those born with significant CHD will die in infancy or early childhood, a third of them within the first month of life. CME Surgical management of spasticity 11. Spasticity is a dominant feature in 80% of all patients with cerebral palsy. 12. Evaluation of a patient for surgery for spasticity focuses on functional evaluation of the patient. 13. Spasticity that leads to pain and deformities starts to impair function. 14. After surgery, physical and occupational therapy are no longer required for patients with spasticity. 15. The goal of surgical therapy may not always be for the patient to walk independently. Surgical management of epilepsy 16. About one-third of patients with epilepsy are refractory to antiepileptic medication. 17. To be considered for surgery, the patient must be refractory to medical treatment and must show a correlation between semiology, anatomy and electrical abnormality. 18. Psychological counselling is not required before surgery for epilepsy. 19. When planning surgery for epilepsy, the fact that it is only grey matter that has epileptogenic potential, but seizure activity can propagate via white matter tracts, is important. 20. Functional hemispherectomy is an example of a disconnection technique.

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