SAMJ Vol 106, No 7 (2016)

JULY 2016

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GUEST EDITORIAL Childhood pneumonia – the Drakenstein Child Health Study CME Adolescent health (part 2) IN PRACTICE The role of ward-based outreach in ending child deaths The Expanded Programme on Immunisation in SA CASE REPORT Rigid cervical collar resolves rheumatoid pannus mass RESEARCH Risk factors and outcomes in contrast-induced nephropathy Malaria success story in Comoros

INNOVATION IN DRY EYE THERAPY

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NEW

Caring for the 3 layers between your eyes and the world1 Lipid deficiencies Aqueous tear-deficiencies Mucin deficiencies

References: 1. Liposic Product Monograph. Data on file, Bausch&Lomb Inc. Scheduling status: S0 Proprietary name and dosage form: Liposic Eye Gel. Composition: Each 1 g contains: 2 mg carbomer, triglycerides – medium chain, sorbitol, sodium hydroxide and purified water, Cetrimide 0,01 % m/m (preservative).

Pharmacological classification: A 15.4 Ophthalmic preparations - Other. Indications: Substitution of tear fluid for management of dry eye conditions such as symptomatic treatment of keratoconjunctivitis sicca. Registration number: 37/15.4/0224. © 2003 Bausch & Lomb Incorporated. ®/™ denote trademarks of Bausch & Lomb Incorporated. Applicant: SofLens (Pty) Ltd. Reg. No.: 1968/11787/07. Marketed by: Bausch & Lomb (SA) (Pty) Ltd. Reg. No.: 1996/003931/07. 15E Riley Road, Bedfordview, Gauteng, South Africa, 2008. Tel: +27 11 087 0000 www.bausch.co.za BL94/15

JULY 2016

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GUEST EDITORIAL

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Childhood pneumonia: The Drakenstein Child Health Study H J Zar, W Barnett, L Myer, M P Nicol

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EDITOR’S CHOICE

CORRESPONDENCE

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Topic reviews need to be robust E Klug; response from N A B Ntusi, S M Kraus, G Ogunbanjo, K Sliwa

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Hydroxyethyl starches in burns A D Rogers; response from D den Hollander

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

HMPG

12 Knowledge of multidrug-resistant tuberculosis in the Thabo Mofutsanyana District, Free State, South Africa: A Grade 10 learner’s project

L Ntsutle, N Mofolo 14 14 14

ERRATA Peter Beighton Festschrift Chronic diseases in the Western world: Increasing incidence or increasing overdiagnosis?

May 2016 CPD question 2

IZINDABA

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HPV: Hope in 15 years for unvaccinated women Chris Bateman wins award Zika – a wake-up call for continuous fetal monitoring Restoring hope for terminal cancer patients – a ‘St Jude’ legacy Alarming rate of COPD in SA

EDITORIAL

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Overview of the 2016 South African Health Review A Padarath, J King, E-L Mackie, J Casciola

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

CME 28

ASSOCIATE EDITORS Q Abdool Karim, A Dhai, N Khumalo, R C Pattinson, A Rothberg, A A Stulting, J Surka, B Taylor, M Blockman

GUEST EDITORIAL Colliding epidemics of communicable and non-communicable diseases during adolescence in South Africa Q Abdool Karim

ARTICLES 29

Adolescence: The age of Proteus H Coovadia, Y Jugnundan, A Ramkissoon

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A weighty matter: Identification and management of overweight and obesity in adolescents N Peer, Y N Ganie

IN PRACTICE 36

CLINICAL PRACTICE The impact of HIV infection on the presentation of lung cancer in South Africa C F N Koegelenberg, T van der Made, J J Taljaard, E M Irusen

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ISSUES IN PUBLIC HEALTH Review of the 2015 Guidelines for Maternity Care with relevance to congenital disorders H L Malherbe, D L Woods, C Aldous, A L Christianson

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Ending preventable child deaths in South Africa: What role can ward-based outreach teams play?

T Doherty, M Kroon, N Rhoda, D Sanders

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HEALTHCARE DELIVERY The Expanded Programme on Immunisation in South Africa: A story yet to be told N R Dlamini, P Maja

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MEDICINE AND THE LAW Social justice and research using human biological material: A response to Mahomed, Nöthling-Slabbert and Pepper D W Jordaan

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July 2016, Print edition

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 van der Ryst 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

A Lupin Group Company

Slower onset for consistent flow Carzin XL, the extended release doxazosin offers: A slower onset of action vs IR formulations to allow fewer titration steps and to minimize side-effects2.

Effective treatment for urinary outflow obstruction and BPH symptoms3.

Safe BPH treatment for normotensive and hypertensive patients3.

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For further product information contact PHARMA DYNAMICS P O Box 30958 Tokai Cape Town 7966 Tel 021 707 7000 Fax 021 701 5898 Email info@pharmadynamics.co.za CUSTOMER CARE LINE 0860 PHARMA (742 762) www.pharmadynamics.co.za Carzin XL. Each film coated tablet contains 4 mg doxazosin. Reg. No.: RSA S3 41/7.1/0557. NAM NS2 10/34/0376. For full prescribing information, refer to the package insert approved by the Medicines Control Council, July 2009.

1) Pompeo ACL, et al. A randomised, double blind study comparing the efficacy and tolerability of controlled release Doxazosin and tamsulosin in the treatment of benign prostatic hyperplasia. Int J. Clin Pract Oct 2006;60(10):11721177. 2) Kirby RS, et al. A Combined analysis of double-blind trials of the efficacy and tolerability of doxazosin-gastrointestinal therapeutic system, doxazosin standard and placebo in patients with benign prostatic hyperplasia. British Journal of Urology International 2001 Feb;87(3):192-200. 3) Carzin XL package insert. 4) Vs. Doxazosin XL originator 4 mg modified release formulation. Department of Health website.http://www.mpr.gov.za - Accessed 21/05/2015.

CLXC73/01/2015

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Public health officials and MECs should be held liable for harm caused to patients through incompetence, indifference, maladministration or negligence regarding the availability of hospital equipment D J McQuoid-Mason

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CASE REPORTS Burkitt’s lymphoma patients in Northwest Cameroon have a lower incidence of sickle cell trait (Hb AS) than healthy controls P B Hesseling, D T Jam, D D Palmer, P Wharin, G S Tuh, R Bardin, M Kidd

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Resolution of a periodontoid rheumatoid pannus mass in an elderly patient treated with a rigid cervical collar: A case report and literature review A Oseni, G Kakavas, M Scholz, A Petridis

54 A case of refractory thrombotic thrombocytopenic purpura treated with plasmapheresis and rituximab

N Kirui, A Sokwala 56

Schwannoma extending from the umbilical region to the mid-thigh, compressing the major vessels of the right leg: A case report and review of the literature J Yorke, B M Duduyemi, A C Yifieyeh, P K S Fiifi-Yankson, C Appiah, D Afful-Yorke, M O Adinku, D Ahulu

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RESEARCH Analysis of 5 years of morbidity and mortality conferences in a metropolitan South African trauma service* V Y Kong, D L Clarke

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Risk factors and outcomes of contrast-induced nephropathy in hospitalised South Africans* J Banda, R Duarte, C Dickens, T Dix-Peek, M Muteba, G Paget, V Mngomezulu, P Manga, S Naicker

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Major decline in malaria morbidity and mortality in the Union of Comoros between 2010 and 2014: The effect of a combination of prevention and control measures* S A Kassim, P B James, R N Alolga, A G Assanhou, A Bacar, R Silai, L Tian, H Li, A Ma

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Measles outbreak reveals measles susceptibility among adults in Namibia, 2009 - 2011* I U Ogbuanu, C Muroua, M Allies, K Chitala, S Gerber, P Shilunga, P Mhata, J L Kriss, L Caparos, S B Smit, R J de Wee, J L Goodson

*Full article available online only.

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CPD QUESTIONS

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Subscriptions: Tel. 012 481 2071 Email: members@samedical.org The SAMJ is published monthly by the Health and Medical Publishing Group (Pty) Ltd, Co. registration 2004/0220 32/07, a subsidiary of SAMA. HEAD OFFICE Health and Medical Publishing Group (Pty) Ltd Block F, Castle Walk Corporate Park, Nossob Street, Erasmuskloof Ext. 3, Pretoria, 0181 Tel. 012 481 2069 Email: dianes@hmpg.co.za EDITORIAL OFFICE Suites 9 & 10, Lonsdale Building, Gardener Way, Pinelands, 7405 Tel. 021 532 1281 | Cell. 072 635 9825 Email: publishing@hmpg.co.za Please submit all letters and articles for publication online at www.samj.org.za © Copyright: Health and Medical Publishing Group (Pty) Ltd, a subsidiary of the South African Medical Association Use of editorial material is subject to the Creative Commons Attribution – Non-commercial Works Licence. http://creativecommons.org/licenses/by-nc/3.0 Printed by TANDYM PRINT

JULY 2016

Background photo: Elderly man behind X-ray machine | Blend Images Hexagon photos: Mosquito on a mosquito net | Birute Vijeikiene; Rheumatoid pannus reduction 1 month after rigid cervical collar immobilisation | Teenage boy using weight scales; Moodboard | Digital vision; Drakenstein Mbekweni | Heather Zar

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July 2016, Print edition

PRINT EDITION

GUEST EDITORIAL Childhood pneumonia – the Drakenstein Child Health Study CME Adolescent health (part 2) IN PRACTICE The role of ward-based outreach in ending child deaths The Expanded Programme on Immunisation in SA CASE REPORT Rigid cervical collar resolves rheumatoid pannus mass RESEARCH Risk factors and outcomes in contrast-induced nephropathy Malaria success story in Comoros

GUEST EDITORIAL

Childhood pneumonia: The Drakenstein Child Health Study Advances in immunisation, improvements in socioeconomic status and effective HIV prevention and treatment strategies have reduced the population burden of childhood pneumonia and severe disease. [1] However, pneumonia remains the major single cause of death in children outside the neonatal period, causing approximately around 1 million deaths annually, or 15% of an estimated 6.3 million deaths in children aged <5 years.[2,3] This burden is disproportionately high in low- and middle-income countries (LMICs) and in Africa, where almost 50% of deaths in children aged <5 years occur, despite African children comprising only 25% of live births globally.[3,4] The incidence and severity of pneumonia are highest in the first year of life, especially in the first 6 months.[2,5] New conjugate vaccines against Haemophilus influenzae type b (Hib) and Streptococcus pneumoniae (PCV) can substantially reduce the burden of childhood pneumonia in vaccinated children. Data from six studies of the effectiveness of Hib conjugate vaccine in LMICs reported reductions of 18% in radiological pneumonia, 6% in severe pneumonia and 7% in pneumonia-associated mortality.[6] The impact of PCV in reducing pneumonia hospitalisation, mortality, bacteraemic disease and clinical disease in children has been reported in several studies.[7-11] PCV immunisation of children has also led to a decline in hospitalisation and death due to pneumonia in adults as a result of indirect protection through reduction in circulating vaccinetype pneumococcal serotypes.[7] Defining pneumonia epidemiology and aetiology in the context of strong immunisation programmes is an ongoing priority for child health. South Africa (SA) was the first African country to implement PCV immunisation in the national immunisation programme; 7-valent PCV was introduced for infants at 6 and 10 weeks and 9 months in 2009 and replaced with 13-valent PCV (PCV13) in 2011. In the context of relatively strong immunisation and primary healthcare programmes, it is important to understand the changing epidemiology and aetiology of childhood pneumonia.

The Drakenstein Child Health Study is an SA birth cohort study of 1 000 mother-child pairs that investigates the epidemiology, aetio­logy, risk factors and long-term outcome of childhood pneumonia and determinants of child health.[12] This study takes place at two primary healthcare clinics and one hospital in the Drakenstein subdistrict in Paarl, a periurban area outside Cape Town. Women enrolled during pregnancy are followed through childbirth, and mother-child pairs are followed until children are at least 5 years of age. Children receive primary healthcare and immunisation at clinics. Continuous pneumonia surveillance is undertaken.[13] Although the prevalence of HIV infection in pregnant women in the cohort was around 25%, only 2 children were HIV-infected, a reflection of the strong mother-to-child HIVprevention programme. To assess pneumonia aetiology, a nested casecontrol study was done and respiratory specimens (nasopharyngeal swabs and induced sputum) were tested using a multiplex polymerase chain reaction to identify up to 33 potential respiratory organisms.[14] We found that pneumonia remains a major cause of illness (inci­ dence 0.27 episodes per child year) and hospitalisation, particularly in the first 6 months of life, despite excellent immunisation coverage including PCV13.[14] Several viruses, most strikingly respiratory syncytical virus (RSV, the most frequently detected pathogen), were strongly associated with pneumonia.[14] Bordetella pertussis was strongly associated with pneumonia, but occurred in a small number of children; H. influenzae (other than type b) was less strongly associated with pneumonia, but was common. Multiple potential

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pathogens were identified at each pneumonia episode, adding to evidence that childhood pneumonia may be due to infection with multiple organisms, particularly in the case of severe disease.

Induced sputum provided an increased yield for potential pathogens compared with nasopharyngeal specimens, notably for B. pertussis and several viruses, suggesting that induced sputum can be used to improve diagnostic strategies even in very young infants.[14] The high burden of childhood pneumonia may partly reflect high exposure to potential pathogens and to risk factors that may make a child vulnerable to pneumonia. Smoke exposure, lack of breastfeeding, prematurity or low birth weight, low socioeconomic status, crowded living conditions, or HIV infection or exposure are important risk factors for childhood pneumonia that were common in this setting and in LMIC settings generally.[2,4] Despite the high incidence of pneumonia and of severe disease, there was a low case fatality rate, attesting to good access to care and a strong primary healthcare programme including use of case management guidelines, antibiotics, oxygen, timely referral and access to hospital.[14] With increasing uptake of PCV in LMICs, the proportion of lower respiratory tract infections (LRTIs) due to viruses, particularly RSV, may be expected to increase.[15,16] RSV was the commonest identifiable organism, and was associated with severe disease but not with mortality. This is consistent with global and African data preceding PCV that reported RSV to be the commonest pathogen in children with LRTI.[17] Globally RSV was estimated to cause approximately 34 million episodes of acute lower respiratory tract infections (ALRIs) in children aged <5 years, or 22% of all ALRIs; 10% of episodes resulted in severe illness and hospitalisation, and 99% of deaths occurred in LMICs. Further studies in African children preceding the availability of PCV,[18,19] and several recent case-control studies in children well vaccinated with PCV13, mostly from high-income countries, have reported RSV to be a predominant pathogen in children hospitalised with pneumonia.[20,21] Consistent with other studies, RSV occurred in young infants with the peak incidence under 6 months.[22] Maternal immunisation against RSV during late pregnancy may therefore be an attractive novel strategy to prevent disease in young infants.[23] In addition, B. pertussis occurred in young infants, and mostly before completion of the primary series of three immunisations; in turn, immunisation of pregnant women with B. pertussis may also be an effective strategy to prevent this burden.[24] As health systems are strengthened, it is crucial to consider the impact of childhood pneumonia beyond acute disease in childhood or mortality. This is especially relevant as health systems are challenged to address the Sustainable Development Goals for 2030. Chronic sequelae from early childhood pneumonia such as bronchiectasis are increasingly recognised; one review reported chronic sequelae following severe pneumonia to occur in ~15% of children.[25] Early childhood pneumonia has increasingly been associated with the development of chronic non-communicable respiratory diseases into childhood and adulthood, such as asthma or chronic obstructive airways disease (COPD),[26] of which SA has one of the highest global prevalences. Accumulating evidence from several cohort studies has shown that lung health is established early in life and that lung function follows a set trajectory into adulthood, implying that the roots of adult lung disease such as COPD lie in early exposures including childhood pneumonia.[27] For many African countries or LMICs, challenges remain in imple­ menting available effective, preventive and management strategies

July 2016, Print edition

GUEST EDITORIAL

for childhood pneumonia.[28] However, the Drakenstein Child Health Study shows that even in LMIC settings with strong health pro­ grammes, pneumonia remains a major concern for child health. The strengthening and implementation of available effective preventive and management interventions, such as available immunisations and use of case management, have the potential to substantially reduce pneumonia burden and under-5 mortality. [6] Strategies to reduce risk factors, such as optimising nutrition, promoting breastfeeding, preventing HIV transmission through mother-to-child prevention programmes and reducing exposure to biomass or cigarette smoke, must be strengthened, particularly in Africa. However, our findings show that despite good application of these in this area and the low prevalence of HIV in children, there is a large residual burden of pneumonia, for which novel strategies are required.

While attention to reducing risk factors and strengthening health systems to deliver effective preventive and management strategies are a priority in LMICs, novel strategies are needed to reduce pneumonia incidence, especially looking beyond pneumonia mortality to the considerable associated morbidity and development of chronic disease. This is a key lesson from the Drakenstein Child Health Study, where despite good primary healthcare, high coverage with vaccines contained in the SA national immunisation programme, very low prevalence of HIV infection in children and good access to care, pneumonia remains a major cause of childhood illness.[14] Given the considerable burden of LRTI due to RSV and the young age of infants most vulnerable to disease and to developing severe LRTI, the development of several new RSV vaccine candidates is a promising development.[23] A novel strategy to immunise pregnant women in the third trimester of pregnancy to protect against RSV disease in their infants in the first few months of life has recently been developed.[23] This will probably need to be coupled with additional vaccination of infants to provide extended protection until children are 2 years of age. The challenge for African and other LMICs will be to ensure that such new strategies are accessible and affordable, if effective.

Heather J Zar Department of Paediatrics and Child Health, Red Cross War Memorial Children’s Hospital, and Medical Research Council Unit on Child and Adolescent Health, Faculty of Health Sciences, University of Cape Town, South Africa heather.zar@uct.ac.za Whitney Barnett Medical Research Council Unit on Child and Adolescent Health, Faculty of Health Sciences, University of Cape Town, South Africa Landon Myer Division of Epidemiology and Biostatistics, School of Public Health and Family Medicine, Faculty of Health Sciences, University of Cape Town, South Africa Mark P Nicol Division of Medical Microbiology, Department of Pathology, Faculty of Health Sciences, University of Cape Town and National Health Laboratory Service, Cape Town, South Africa Funding. Prof. Zar acknowledges funding for the Drakenstein Study from the Bill & Melinda Gates Foundation (OPP 1017641), the National Institutes of Health, USA (H3Africa 1U01AI110466-

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01A1), the SA Medical Research Council and the National Research Foundation, SA. Acknowledgements. We thank the Drakenstein Child Health Study staff in Paarl, the data and lab teams, Dr Breslau Kruger, CEO of Paarl Hospital, Dr Eckhart von Delft, Head of Paediatrics at Paarl Hospital, and Sandra Theron, Janine Bosch, and Cathy Solomons, primary healthcare area managers for the district. We thank the clinical and administrative staff of the Western Cape Health Department at Paarl Hospital and at the clinics for supporting the study. We acknowledge advice from members of the study International Advisory Board and thank our collaborators. We thank the families and children who participate in this study.

1. Campbell H, Nair H. Child pneumonia at a time of epidemiological transition. Lancet Glob Health 2015;3(2):e65-e66. DOI:10.1016/S2214-109X(14)70308-0 2. Rudan I, O’Brien KL, Nair H, et al. Epidemiology and etiology of childhood pneumonia in 2010: Estimates of incidence, severe morbidity, mortality, underlying risk factors and causative pathogens for 192 countries. J Glob Health 2013;3(1):010401. DOI:10.7189/jogh.03.010401 3. Liu L, Oza S, Hogan D, et al. Global, regional, and national causes of child mortality in 2000-13, with projections to inform post-2015 priorities: An updated systematic analysis. Lancet 2015;385(9966):430440. DOI:10.1016/S0140-6736(14)61698-6 4. Zar HJ, Madhi SA, Aston SJ, Gordon SB. Pneumonia in low and middle income countries: Progress and challenges. Thorax 2013;68(11):1052-1056. DOI:10.1136/thoraxjnl-2013-204247 5. Nair H, Simoes EA, Rudan I, et al. Global and regional burden of hospital admissions for severe acute lower respiratory infections in young children in 2010: A systematic analysis. Lancet 2013;381(9875):1380-1390. DOI:10.1016/S0140-6736(12)61901-1 6. Bhutta ZA, Das JK, Walker N, et al. Interventions to address deaths from childhood pneumonia and diarrhoea equitably: What works and at what cost? Lancet 2013;381(9875):1417-1429. DOI:10.1016/ S0140-6736(13)60648-0 7. Simonsen L, Taylor RJ, Schuck-Paim C, Lustig R, Haber M, Klugman KP. Effect of 13-valent pneumococcal conjugate vaccine on admissions to hospital 2 years after its introduction in the USA: A time series analysis. Lancet Respir Med 2014;2(5):387-394. DOI:10.1016/S2213-2600(14)70032-3 8. Scotta MC, Veras TN, Klein PC, et al. Impact of 10-valent pneumococcal non-typeable Haemophilus influenzae protein D conjugate vaccine (PHiD-CV) on childhood pneumonia hospitalizations in Brazil two years after introduction. Vaccine 2014;32(35):4495-4499. DOI:10.1016/j.vaccine.2014.06.042 9. Griffin MR, Mitchel E, Moore MR, et al. Declines in pneumonia hospitalizations of children aged <2 years associated with the use of pneumococcal conjugate vaccines – Tennessee, 1998-2012. MMWR Morb Mortal Wkly Rep 2014;63(44):995-998.

10. Becker-Dreps S, Amaya E, Liu L, et al. Changes in childhood pneumonia and infant mortality rates following introduction of the 13-valent pneumococcal conjugate vaccine in Nicaragua. Pediatr Infect Dis J 2014;33(6):637-642. DOI:10.1097/INF.0000000000000269 11. Madhi SA, Groome MJ, Zar HJ, et al. Effectiveness of pneumococcal conjugate vaccine against presumed bacterial pneumonia hospitalisation in HIV-uninfected South African children: A casecontrol study. Thorax 2015;70(12):1149-1155. DOI:10.1136/thoraxjnl-2014-206593 12. Zar HJ, Barnett W, Myer L, Stein DJ, Nicol MP. Investigating the early-life determinants of illness in Africa: The Drakenstein Child Health Study. Thorax 2015;70(6):592-594. DOI:10.1136/ thoraxjnl-2014-206242 13. Le Roux DM, Myer L, Nicol MP, Zar HJ. Incidence of childhood pneumonia: Facility-based surveillance estimate compared to measured incidence in a South African birth cohort study. BMJ Open 2015;5(12):e009111. DOI:10.1136/thoraxjnl-2014-206242 14. Zar HJ, Barnett W, Stadler A, Gardner-Lubbe S, Myer L, Nicol MP. Aetiology of childhood pneumonia in a well vaccinated South African birth cohort: A nested case-control study of the Drakenstein Child Health Study. Lancet Respir Med 2016, April 21. Manuscript ID: THELANCET-D-15-06271.

15. Zar HJ, Polack FP. Childhood pneumonia: The role of viruses. Thorax 2015;70(9):811-812.

DOI:10.1136/thoraxjnl-2015-207320 16. Shi T, McLean K, Campbell H, Nair H. Aetiological role of common respiratory viruses in acute lower respiratory infections in children under five years: A systematic review and meta-analysis. J Glob Health 2015;5(1):010408. DOI:10.7189/jogh.05.010408 17. Nair H, Nokes DJ, Gessner BD, et al. Global burden of acute lower respiratory infections due to respiratory syncytial virus in young children: A systematic review and meta-analysis. Lancet 2010;375(9725):1545-1555. DOI:10.1016/S0140-6736(10)60206-1 18. Howie SR, Morris GA, Tokarz R, et al. Etiology of severe childhood pneumonia in The Gambia, West Africa, determined by conventional and molecular microbiological analyses of lung and pleural aspirate samples. Clin Infect Dis 2014;59(5):682-685. DOI:10.1093/cid/ciu384 19. Hammitt LL, Kazungu S, Morpeth SC, et al. A preliminary study of pneumonia etiology among hospitalized children in Kenya. Clin Infect Dis 2012;54(Suppl 2):S190-S199. DOI:10.1093/cid/cir1071 20. Jain S, Finelli L, Team CES. Community-acquired pneumonia among U.S. children. N Engl J Med 2015;372(22):2167-2168. DOI:10.1056/NEJMc1504028 21. Rhedin S, Lindstrand A, Hjelmgren A, et al. Respiratory viruses associated with community-acquired pneumonia in children: Matched case-control study. Thorax 2015;70(9):847-853. DOI:10.1136/thoraxjnl-2015-206933 22. Shi T, Balsells E, Wastnedge E, et al. Risk factors for respiratory syncytial virus associated with acute lower respiratory infection in children under five years: Systematic review and meta-analysis. J Glob Health 2015;5(2):020416. DOI:10.7189/jogh.05.020416 23. Mazur NI, Martinon-Torres F, Baraldi E, et al. Lower respiratory tract infection caused by respiratory syncytial virus: Current management and new therapeutics. Lancet Respir Med 2015;3(11):888-900.

DOI:10.1016/S2213-2600(15)00255-6 24. Swamy GK, Heine RP. Vaccinations for pregnant women. Obstet Gynecol 2015;125(1):212-226.

DOI:10.1097/AOG.0000000000000581 25. Edmond K, Scott S, Korczak V, et al. Long term sequelae from childhood pneumonia: Systematic review and meta-analysis. PloS One 2012;7(2):e31239. DOI:10.1371/journal.pone.0031239 26. Svanes C, Sunyer J, Plana E, et al. Early life origins of chronic obstructive pulmonary disease. Thorax 2010;65(1):14-20. DOI:10.1136/thx.2008.112136 27. Lange P, Celli B, Agusti A, et al. Lung-function trajectories leading to chronic obstructive pulmonary disease. N Engl J Med 2015;373(2):111-22. DOI:10.1056/NEJMoa1411532 28. Zar HJ, Ferkol TW. The global burden of respiratory disease – impact on child health. Pediatr Pulmonol 2014;49(5):430-434. DOI:10.1002/ppul.23030

S Afr Med J 2016;106(7):642-643. DOI:10.7196/SAMJ.2016.v106i7.11108

July 2016, Print edition

EDITOR’S CHOICE

CME: Adolescent health (part 2)

This second issue of CME focusing on adolescent health issues addresses the colliding epidemics of communicable and noncommunicable diseases (NCDs) during adolescence in South Africa (SA). Adolescence has not typically been associated with ill health, but this picture is changing rapidly, with the present generation of adolescents encountering diverse challenges with biosocial and neurocognitive responses different from those in their parents and grandparents. These transitions are influenced by geographical, cultural, economic and genetic contexts. The two articles in this issue of CME highlight the epidemiological transitions from a predominance of infectious diseases and complications of malnutrition to the convergence with NCDs, and the problem of overweight and obesity in adolescence.

Ending preventable child deaths in SA

SA has emerged from the Millennium Development Goal (MDG) era with a mixture of success and failure.[1] MDG4 aimed to reduce the under-5 mortality rate (U5MR) by two-thirds between 1990 and 2015. SA’s MDG baseline of 60 under-5 deaths per 1 000 live births meant a target of 20. Estimates from rapid mortality surveillance placed the U5MR in 2014 at 39. Much of this reduction has been due to the successful national scale-up of prevention of mother-tochild transmission of HIV services. As a result, HIV/AIDS is no longer the leading cause of under-5 mortality – it has been surpassed by neonatal deaths (25%), gastroenteritis (15%) and suspected pneumonia (13%). However, although no current data are available, over the past few decades, including during the height of the HIV/ AIDS epidemic, there appears to have been no progress in coverage of high-impact interventions for pneumonia and diarrhoea. A recent review of child deaths in two medicolegal mortuaries in Cape Town and Durban found that lower respiratory tract infections and diarrhoea were the most common causes of sudden unexpected natural deaths among children aged <5 at both sites. Furthermore, the study reported that 11% of the natural deaths were associated with possible health systems failures where a child was taken to a health facility within 48 hours of death and medical management was suspected to be lacking. This study highlights that even in the metropolitan areas of Durban and Cape Town, access to care is poor, and the situation in other less well-resourced provinces is likely to be significantly worse – hence the importance of community health workers (CHWs) trained to diagnose and treat diarrhoea, malaria and pneumonia in children aged 2 - 59 months in communities where access to health services is poor. SA embarked on a strategy to re-engineer the primary healthcare system in 2011, which includes the creation of ward-based outreach teams consisting of around 6 CHWs supervised by one nurse. However, this ratio of CHWs to population is too small. Added to this, the role of CHWs is narrow, with no curative functions. More needs to be done in this area of practice to counter the failure in MGD4.

Follow-up of elderly breast cancer patients after diagnosis (online only)

The impact of breast cancer in the elderly is generally not well characterised. There is a real lack of data regarding disease burden, post-treatment surveillance and breast cancer relapse, which poses a challenge in the provision of care for this group of patients. In this single-centre review of patients in KwaZulu-Natal,[2] the incidence of breast cancer among patients aged >65 was 26.7%, and of these a significant proportion (56.3%) presented with advanced disease. Of 46.9% who had surveillance mammograms, only 6.3% received these

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in accordance with international recommendations, and there were new mammographic findings in 26.7% of these patients during 5-year follow-up. Of all the patients in the study, 15.6% presented with disease recurrence, and 80% of these were detected clinically. Overall 5-year survival was 65.6%. This indicates many patients with advanced disease at diagnosis, poor compliance with internationally recommended posttreatment surveillance mammograms, and low 5-year survival.

Staff recruitment and retention challenges at the University of Botswana medical school (online only)

Botswana, like many similar countries, is failing to successfully recruit and retain academic staff at its medical school. Using records of the numbers and countries of origin of staff recruited and on post each year since 2008, Kebaetse et al.[3] looked at net staff gain or loss per year. A major multilevel change in university governance in 2011 could potentially have affected recruitment and retention.

They considered curriculum decisions that the school made during its initial 5 years of existence, to see whether staff availability had influenced those decisions. They also recorded the numbers of new students enrolled each year since 2009 and the number of students as of December 2013, again calculating net loss or gain. During the 5 years of the study, the new medical school recruited 74 academics (84% of its staff requirement), with good variation in specialty and including experience in establishing new medical schools. Before April 2011, about 50% of the staff came from outside Africa. After this, a similar proportion came from other parts of Africa, mainly East Africa. Local staff members remained at 25% throughout the study. The recruitment and retention challenges are severe, with retention a greater problem than recruitment. While salaries and other factors were likely contributors, the widespread, multilevel change in management may have been destabilising and excessive for the medical school, adversely affecting recruitment and retention.

Decline in malaria morbidity and mortality in Comoros

Between them, the World Health Assembly and the Roll Back Malaria Partnership have set a target of a 75% decline in malaria incidence across those countries affected by the disease. Between 2010 and 2014, Kassim et al.[4] assessed trends in malaria morbidity and mortality in the three islands of the Comoros Archipelago, using a retrospective study. They found a substantial decline in the incidence of malaria for each island and a general reduction in malaria case fatality. Similar trends were seen in pregnant women and in children aged <5 years – two important groups in malaria morbidity and mortality. The authors describe ‘a cocktail of interventions’ that include insecticide-treated bed nets, rapid diagnostic services, and increased access to artemisinin-combination therapy. This study is important in its demonstration that these interventions – relatively inexpensive and easy to implement – can have major impacts in developing world countries.

BF 1. Doherty T, Kroon M, Rhoda N, Sanders D. Ending preventable child deaths in South Africa: What role can ward-based outreach teams play? S Afr Med J 2016;106(7):669-671. DOI:10.7196/SAMJ.2016. v106i7.10790 2. Parag Y, Buccimazza I. How long are elderly patients followed up with mammography after the diagnosis of breast cancer? A single-centre experience in a developing country. S Afr Med J 2016;106(7):721-723. DOI:10.7196/SAMJ.2016.v106i7.10405 3. Kebaetse M, Mokone GG, Badlangana L, Mazhan L. Academic staff recruitment and retention challenges at the University of Botswana medical school. S Afr Med J 2016;106(7):730-734.

DOI:10.7196/SAMJ.2016.v106i7.10482 4. Kassim SA, James PB, Alolga RN, et al. Major decline in malaria morbidity and mortality in the Union of Comoros between 2010 and 2014: The effect of a combination of prevention and control measures.

S Afr Med J 2016;106(7):709-714. DOI:10.7196/SAMJ.2016.v106i7.10902

July 2016, Print edition

CORRESPONDENCE

Topic reviews need to be robust

To the Editor: I note with interest the review entitled ‘Heart failure in sub-Saharan Africa: A clinical approach’.[1] It is very concerning that the only heart failure guideline published in Africa was not referenced in this review.[2] The Heart Failure Society of South Africa (HeFSSA) is the only official heart failure society in Africa. The HeFSSA guideline was published as a modification of the European Society of Cardiology guideline that is quoted in the review,[3] specifically to impart a ‘sub-Saharan’ perspective.

If the HeFSSA guideline was included in this review then I’m sure the significant omission of the hydralazine-nitrate oral combination as a crucial arm of chronic heart failure therapy would not have occurred. Considering the demographics of sub-Saharan Africa, omitting a therapy that has proven to significantly improve survival, reduce hospitalisations and improve quality of life in black Africans,[4] is most unfortunate.

The review also includes perindopril 2 - 4 mg in their list of suggested angiotensin-converting enzyme (ACE) inhibitors. The HeFSSA guideline excluded this particular drug as no large randomised data exist for the efficacy of this drug in heart failure, not to mention the recommended dose. Perindopril 4 mg as a single drug had no benefit on reducing stroke,[5] and perindopril 8 mg was needed to reduce events in high-risk cardiovascular patients.[6] The effective dose in heart failure is unknown. Telmisartan is also included in this review. No heart failure end point and effective dose data exist for this drug either and it is not listed in the HeFSSA guideline.

The comments in the review on a heart rate target of <75 beats/ minute with beta-blocker therapy are confusing and ill advised for the heart failure practitioner. No large, randomised beta-blocker trial that showed improved survival and reduced hospitalisations in chronic heart failure therapy has used heart rate as a target in therapy. Target beta-blocker doses were aimed for in the trials and should be aimed for in clinical therapy. The statement in this review confuses the systolic heart failure treatment (SHIFT)[7] trial and extrapolates inappropriately the heart rate data to beta-blocker therapy with no randomised evidence to support this advice. This advice in the review will also result in underdosing of beta-blocker therapy. If this review[1] is to be used as a reference for doctors to guide their heart failure therapy, then I strongly suggest corrections should be published in a revised review.

Eric Klug

President of the Heart Failure Society of South Africa, Heart Failure Clinic, Charlotte Maxeke Johannesburg Academic Hospital, and Sunninghill Hospital, Johannesburg, South Africa eklug@global.co.za 1. Kraus S, Ogunbanjo G, Sliwa K, Ntusi NA. Heart failure in sub-Saharan Africa: A clinical approach. S Afr Med J 2016;106(1):23-31.DOI:10.7196/SAMJ.2016.v106i1.10325 2. Mpe, MT, Klug, EQ, Sliwa, KS, et al. Heart Failure Society of South Africa (HeFSSA) perspective on the European Society of Cardiology (ESC) 2012 chronic heart failure guideline. S Afr Med J 2013;103(9 Suppl 2):661-667. DOI:10.7196/SAMJ.7319 3. McMurray JJ, Adamopoulos S, Anker SD, et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Eur Heart J 2012;33(14):1787-1847. DOI:10.1093/ eurheartj/ehs104 4. Taylor, AL, Ziesche S, Yancy C, et al. Combination of isosorbide dinitrate and hydralazine in blacks with heart failure. N Engl J Med 2004;351(20):2049-2057.

5. PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack. Lancet 2001;358(9287):1033-1041. DOI:10.1016/S0140-6736(01)06178-5 6. Fox KM, EURopean trial On reduction of cardiac events with Perindopril in stable coronary Artery disease Investigators. Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomised, double-blind, placebo-controlled, multicentre trial (the EUROPA study). Lancet 2003;362(9386):782-788. DOI:10.1016/S0140-6736(03)14286-9 7. Swedberg K, Komajda M, Böhm M, et al. Ivabradine and outcomes in chronic heart failure (SHIFT): A randomised placebo-controlled study. Lancet 2010;376(9744):875-885. DOI:10.1016/S01406736(10)61198-1

Ntusi et al. respond: We are grateful for the opportunity to respond to the comments made by Dr Klug in reference to our article titled

8

‘Heart Failure in sub-Saharan Africa: A clinical approach’,[1] which formed part of the recent cardiovascular disease (CVD) continuing medical education (CME) in the Journal. Indeed, the heart failure (HF) guideline[2] published under the auspices of the Heart Failure Society of South Africa (HeFSSA) was not cited in this review.

We admit this was an important omission. However, our review liberally cited the European Society of Cardiology (ESC) guideline on the management of HF,[3] upon which the HeFSSA guideline is also heavily premised.

While we acknowledge the importance of the HeFSSA guideline and its place in the management of HF in South Africa (SA), the HF review, which was not meant to replace the current treatment recommendations of HeFSSA, like all the articles that formed the CVD CME, focused on simple, pragmatic clinical approaches to common cardiovascular challenges encountered at the primary level of healthcare, with the aim of not being overly complex. As such, in this successful collaboration, the CME articles were jointly produced by SA cardiologists and family physicians with the dual objectives of empowering doctors who manage these conditions in primary care settings in SA and improving the care of CVD patients in such settings. In the first issue, HF,[1] dyspnoea,[4] hypertension in the young[5] and valvular heart disease[6] were reviewed. In the second issue, infective endocarditis[7] and pericardial disease[8] were discussed. The final edition provided an evidence-based and pragmatic approach to chest pain and acute coronary syndromes[9] and suspected tachyarrhythmias in the emergency room.[10] Upon this background, the main goals of the HF review were to: (i) emphasise how to make the diagnosis of HF; (ii) highlight clues for recognition of the underlying aetiology of HF; (iii) review the pathophysiology of HF; and (iv) provide a simplified approach to management of HF. The lack of recommendations relating to use of hydralazinenitrate oral combination in our HF review, in particular for black African patients, are indeed a notable omission. In the SA public sector, particularly at the primary healthcare level, the availability of hydralazine is haphazard. Further, while this combination therapy is associated with improved survival, reduced hospitalisation and improved quality of life in black African patients, compared with placebo, it is comparable with the mortality benefit of angiotensin converting enzyme (ACE) inhibitors, which are much more freely available and accessible in primary health centres around SA. Moreover, this combination therapy should be used with caution in certain patients.[11] In addition, the recently performed Bi treatment with hydralazine/nitrates v. placebo in black Africans admitted with acute HF (BA-HEF) study had to be terminated prematurely due to poor recruitment and was neutral. [12] One of the main reasons for poor recruitment was hypotension.

Even though perindopril does not have randomised trial data supporting its specific use in HF, in certain provinces within SA such as the Eastern Cape, it has been the only ACE inhibitor available within the state sector, and it is still included (at the doses stated in our HF review) in the ESC guidelines.[3] We have opted to adopt a pragmatic approach that is relevant to primary healthcare practitioners in SA. The comments relating to target heart rate with beta-blockers are noted and we share the same views as Dr Klug. Indeed, there is no evidence of improved outcomes with beta-blockers titrated to a specific target heart rate. However, there is strong evidence that heart rate reduction in HF is associated with improved survival,[13,14] although the optimal heart rate target has not been established.

July 2016, Print edition

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CORRESPONDENCE

It is our hope that our review will provide a simple and pragmatic clinical approach to the management of HF at the primary healthcare level in SA in order to improve the lives of SA HF patients.

Ntobeko A B Ntusi

Lecturer and Fellow, Division of Cardiology, Department of Medicine, Faculty of Health Sciences, University of Cape Town and Groote Schuur Hospital, Cape Town, South Africa ntobekontusi@gmail.com

Sarah M Kraus

PhD Candidate, Division of Cardiology, Department of Medicine, Faculty of Health Sciences, University of Cape Town and Groote Schuur Hospital, Cape Town, South Africa

Gboyega Ogunbanjo

Head, Department of Family Medicine and Primary Health Care, Sefako Makgatho Health Sciences University, Pretoria, South Africa

Karen Sliwa

Professor of Cardiology, Division of Cardiology, Department of Medicine, Faculty of Health Sciences, University of Cape Town and Groote Schuur Hospital, Cape Town; and Director, Hatter Institute for Cardiovascular Research in Africa, Department of Medicine, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa 1. Kraus S, Ogunbanjo G, Sliwa K, Ntusi NA. Heart failure in sub-Saharan Africa: A clinical approach. S Afr Med J 2016;106(1):23-31. DOI:10.7196/samj.2016.v106i1.10325 2. Mpe MT, Klug EQ, Silwa KS, Hitzeroth J, Smith DA. Heart Failure Society of South Africa (HeFSSA) perspective on the European Society of Cardiology (ESC) 2012 chronic heart failure guideline. S Afr Med J 2013;103(9, Suppl 2):660-667. DOI:10.7196/samj.7319 3. McMurray JJ, Adamopoulos S, Anker SD, et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Eur Heart J 2012;33(14):1787-1847. DOI:10.1093/ eurheartj/ehs104 4. Coccia CB, Palkowski GH, Schweitzer B, Motsohi T, Ntusi NA. Dyspnoea: Pathophysiology and a clinical approach. S Afr Med J 2016;106(1):32-36. DOI:10.7196/samj.2016.v106i1.10324 5. Mangena P, Saban S, Hlabyago KE, Rayner B. An approach to the young hypertensive patient. S Afr Med J 2016;106(1):36-38. DOI:10.7196/samj.2016.v106i1.10329 6. Cupido BJ, Peters F, Ntusi NA. An approach to the diagnosis and management of valvular heart disease.

S Afr Med J 2016;106(1):39-42. DOI:10.7196/samj.2016.v106i1.10326 7. Hitzeroth J, Beckett N, Ntuli P. An approach to a patient with infective endocarditis. S Afr Med J 2016;106(2):145-150. DOI:10.7196/SAMJ.2016.v106i2.10327 8. Kyriakakis CG, Mayosi BM, de Vries E, Isaacs A, Doubell AF. An approach to the patient with suspected pericardial disease. S Afr Med J 2016;106(2):151-155. DOI: 10.7196/SAMJ.2016.v106i2.10328 9. Pandie S, Hellenberg D, Hellig F, Ntsekhe M. An approach to chest pain and acute myocardial infarction. S Afr Med J 2016;106(3):239-245. DOI:10.7196/SAMJ.2016.v106i3.10323 10. Chin A, Vezi B, Namane M, Weich H, Scott-Millar R. An approach to the patient with suspected tachycardia in the emergency department. S Afr Med J 2016;106(3):246-250. DOI:10.7196/SAMJ.2016. v106i3.10322 11. Elkayam U, Bitar F. Effects of nitrates and hydralazine in heart failure: Clinical evidence before the African American Heart Failure Trial. Am J Cardiol 2005; 96(7B):37i-43i. DOI:10.1016/j. amjcard.2005.07.031 12. Sliwa K, Damasceno A, Davison BA, et al. Bi treatment with hydralizine/nitrtaes versus placebo in Africans admitted with acute heart failure (BA-HEF). Eur J Heart Fail 2016(in press).

13. Swedberg K, Komajda M, Böhm M, et al. Ivabradine and outcomes in chronic heart failure (SHIFT): A randomised placebo-controlled study. Lancet 2010;376(9744):875-885. DOI:10.1016/S01406736(10)61198-1 14. McAlister FA, Wiebe N, Ezekowitz JA, et al. Meta-analysis: Beta-blocker dose, heart rate reduction, and death in patients with heart failure. Ann Intern Med 2009;150(11):784-794. DOI:10.7326/0003-4819150-11-200906020-00006

S Afr Med J 2016;106(7):644-645. DOI:10.7196/SAMJ.2016v106i7.10903

Hydroxyethyl starches in burns

To the Editor: Den Hollander[1] argues that ‘the exclusion of severe burns from the indications for the use of colloids, as well as the exclusion of consultant surgeons and emergency specialists from those who will be allowed to prescribe HES-containing products, indicates little insight into the evidence and the clinical situation “at the coalface”.’

The author places considerable emphasis on the value of starch in light of its volume sparing effect,[1] and there is some support for this assertion,[2] but he also quotes a randomised controlled double blind trial which shows no such effect.[3] Of more concern, however, is the fact that although large randomised controlled trials are clearly lacking in the context of fluid resuscitation in major burns, evidence

10

demonstrating actual harm with hydroxyethyl starches (HESs), albeit from the general critical care literature, should be acknowledged. [4,5] Haase and Perner[6] stated that there is ‘no clear evidence for an overall beneficial effect of HES in any subgroup of critically-ill patients, but there are clear signs of harm’. These include adverse effects on renal and haemostatic function, with trends towards increased mortality.

They recommended that its use be discontinued in these patients.

An international survey revealed that a considerable percentage of burn surgeons introduce albumin to their initially crystalloidbased resuscitation within the 1st 24 hours post burn.[7] Albumin facilitates adequate resuscitation with significantly less fluid in the initial 24 hours after burn injury. While unlikely to reduce the initial extravasation of fluid into the interstitium, as a result of the capillary permeability in the burn wound itself, albumin does appear to ameliorate the impact of the reduced colloid osmotic pressure in unburnt tissues and notably in the lung, manifesting as reduced ‘fluid creep’, ventilatory requirements, and ultimately, mortality.[8,9] In light of the best available evidence, I encourage the author to reconsider his staunch advocacy for synthetic colloids, and especially HESs, and instead make use of 5% albumin as a ‘rescue’ measure in the specific context of major burn resuscitation.

Alan D Rogers

Attending Burn Surgeon, Ross Tilley Burn Centre, Sunnybrook Health Sciences Centre, Toronto; and Assistant Professor, Division of Plastic and Reconstructive Surgery, University of Toronto, Canada alandavid.rogers@sunnybrook.ca 1. Den Hollander D. Hydroxyethyl starches in severe burns. S Afr Med J 2014;104(10):650-651.

DOI:10.7196/SAMJ.8808 2. Waters LM, Christenson MA, Sato RM. Hetastarch: An alternative colloid in burn shock management.

J Burn Care and Rehabil 1989;10(1):11-16.

3. Béchir M, Puhan MA, Faasshauer M, Schuepbach RA, Stocker R, Neff TA. Early fluid resuscitation with hydroxyl starch 200/0.5 (10%) in severe burn injury: A randomized controlled double blind clinical trial. Crit Care 2013;17(6):R299. DOI:10.1186/cc13168 4. Vlachou E, Gosling P, Moiemen NS. Hydroxyethylstarch supplementation in burn resuscitation – a prospective randomized controlled trial. Burns 2010;36(7):984-991. DOI:10.1016/j.burns.2010.04.001 5. Myburgh JA, Finfer S, Bellomo, et al. Hydroxyethyl starch or saline for fluid resuscitation in intensive care. New Engl J Med 2012;367(20):1901-1911. DOI:10.1056/NEJMoa1209759 6. Haase N, Perner A. Hydroxyethyl starch for resuscitation. Curr Opin Crit Care 2013;19 (4):321-325.

DOI:10.1097/MCC.0b013e3283632de6 7. Greenhalgh DG. Burn resuscitation: The results of the ISBI/ABA survey. Burns 2010 Mar;36(2):176182. DOI: 10.1016/j.burns.2009.09.004 8. Demling RH, Smith M, Bodai B, et al. Comparison of postburn capillary permeability in soft tissue and lung. J Burn Care Rehabil 1981;15:86-92.

9. Navickis RJ, Greenhalgh DG, Wilkes MM. Albumin in burn shock resuscitation: A meta-analysis of controlled clinical studies. J Burn Care Res 2016;37(3):e268-278. DOI:10.1097/BCR.0000000000000201

Den Hollander responds: Many thanks for allowing me to res­pond to the above letter. The conclusion of my original letter was that although the scales are starting to tip in favor of hydroxyethyl starches (HESs), there is very little level 1 evidence for its effectiveness in burns, and until such evidence is available, decisions regarding its use should be left to the experts who regularly care for such complex cases.[1] Too often, decisions are forced onto them by those with little insight into the evidence and Roger’s argument is no exception.

The study by Béchir et al..[2] is, despite its title, not a randomised controlled trial (RCT) but – as I pointed out in my letter – a posthoc analysis 10 years later of the 30 burn patients included in the Volume Substitution and Insulin Therapy in Severe Sepsis (VISEP) study. [3] The latter was indeed an RCT, but a post-hoc analysis of an RCT is not itself an RCT. Although the Béchir study showed no effect of HESs over saline, there are major methodological problems with this study, not least of which the fact that the HES-treated group was more severely injured than the saline group. Rogers subsequently advised me to ‘acknowledge evidence demonstrating actual harm with HES’, quoting in support the crystalloid v. HES CHEST study and Vlachou’s work, both of which were referenced in my letter. The CHEST study,[4] like the VISEP study,[3] has been severely criticised, recently again by Weisskopf and James,[5] who

July 2016, Print edition

CORRESPONDENCE

concluded that they both contain ‘important methodological and interpretative flaws’. They also contained mainly patients in septic shock, and results could not be applied to other patient populations.

In these studies, the HES was administered not as a resuscitation fluid but as a daily supplement for several weeks. There are now 59 RCTs in surgical patients, totaling nearly 5 000 patients, showing a benefit in blood loss and transfusion requirements without any reported increase in adverse effects.[6-8] A single RCT in trauma showed a more rapid lactate clearance and a lower incidence of renal injury in patients resuscitated by HESs.[9] Rogers would do well to remember recent history. It was not so long ago that albumin was blamed for the same adverse events as HESs are now – renal failure and an increased mortality – until the Saline v. Albumin Fluid Evaluation (SAFE) study[10] demon­ strated otherwise. It is also good to remember that the SAFE study reported no survival benefit of albumin over saline in their study population. A recent meta-analysis of albumin use in burns[11] concluded that albumin administration was associated with lower mortality and decreased risk of abdominal compartment syndrome than resuscitation with crystalloids only. However, this study cannot be used to justify a preference of albumin over HESs. Indeed, Vlachou[12] in a small RCT (26 patients) reached the same conclusions regarding HESs. These benefits seem to be rather effects of colloid over crystalloid resuscitation than evidence on which to base a choice between colloids. Other reviews of the use of albumin in burns and trauma resuscitation have confirmed the lack of untoward effects, but evidence of benefit has been harder to come by.[13-19] In the basic science literature, our understanding of the microcirculation and the mechanisms responsible for oedema formation are radically changing, centreing on the role of the glycocalyx.[20] That colloid osmotic pressure does not play the role it was assigned by Ernest Starling is known to many burn surgeons, as burn oedema usually resolves in the face of dropping albumin levels. The mechanism responsible for ‘leaky capillaries’ seems to be not so much gaps that occur between endothelial cells, but rather a defective glycocalyx. One aim of resuscitation should be maintenance and restoration of the glycocalyx. The effects of various resuscitation fluids on the glycocalyx are still being worked out. Although albumin is an important constituent of the glycocalyx, experimental work has revealed that this structure is saturated with albumin at a plasmaalbumin level of as little as a quarter of physiological levels.[21] It may turn out that that plasma would be the ideal resuscitation fluid, as it has been shown to restore damaged glycocalyx in rats,[22] probably as a result of its ability to replenish glycosaminoglycans, an essential component of the glycocalyx. These studies are, however, still very much in the preclinical stage. Furthermore, plasma is expensive and carries risks. Under these circumstances the choice of which colloid to use should be left to the clinician. If Rogers prefers albumin for burns resuscitation, he may, as long as he realises that it is just that, a preference.

Daan den Hollander

Clinical Director, Burns Centre, Inkosi Albert Luthuli Central Hospital, Durban; and Honorary Lecturer, University of KwaZulu-Natal, Durban, South Africa daanhol@ialch.co.za 1. Den Hollander D. Hydroxyethyl starches in severe burns. S Afr Med J 2014;104(10):650-651.

DOI:10.7196/samj.8897 2. Béchir M, Puhan MA, Faasshauer M, Schuepbach RA, Stocker R, Neff TA. Early fluid resuscitation with hydroxyl starch 200/0.5 (10%) in severe burn injury; A randomized controlled double blind clinical trial. Crit Care 2013;17(6):R299. DOI:10.1186/cc13168 3. Brunkhorst FM, Engel C, Blood E, et al. Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med 2008;358(2):125-139. DOI: 10.1056/NEJMoa070716 4. Myburg JA, Finfer S, Bellodomo, et al. Hydroxyethyl starches or saline for fluid resuscitation in intensive care. N Engl J Med 2012;367(20);1901-1911. DOI:10.1056/NEJMao1209759

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5. Weisskopf RB, James MF. Update on use of hydroxyethyl starches in surgery and trauma. J Trauma Acute Care Surg 2015;78(6 Suppl 1):S54-S59. DOI:10.1097/TA.0000000000000636 6. Van Der Linden P, James M, Mythen M, Weiskopf RB. Safety of modern starches used during surgery.

Anesth Analg 2013;116:35-48. DOI:10.1213/ANE.0b013e31827175da 7. Martin C, Jacob M, Vicaut E, Guidet B, Van Aken H, Kurz A. Effect of waxy maize-derived hydroxyethyl starch 130/0.4 on renal function in surgical patients. Anesthesiology 2013;118(2);387394. DOI:10.1097/ALN.0b013e31827e5569 8. Gillies MA, Habicher M, Sander JM, Mythen M, Hamilton M, Pearse RM. Incidence of postoperative death and acute kidney injury associated with IV 6% hydroxyethyl starch use: Systematic review and meta-analysis. Br J Anaesth 2013;112(1):25-34. DOI:10.1097/bja/aet383 9. James MFM, Michelle WL, Joubert A, et al. Resuscitation with hydroxyethyl starch improves renal function and lactate clearance in penetrating trauma in a randomized controlled study: The FIRST Trial (Fluids in Resuscitation of Severe Trauma). Br J Anaesth 2011;107(5):693-702. DOI:10.1093/bja/aer229 10. Finfer S, Bellomo R, Boyce N, et al. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004;350(22):2247-2256. DOI:10.1056/NEJMoa040232 11. Navickis R, Greenhalgh DG, Wilkes MM. Albumin in burn shock resuscitation: A meta-analysis of controlled clinical studies. J Burn Care Res 2016;37(3):e268-78. DOI:10.1097/BCR.0000000000000201.

12. Vlachou E, Gosling P, Moiemen NS. Hydroxyethyl starch supplementation in burn resuscitation – A prospective randomized controlled trial. Burns 2010;36(7):984-991. DOI:10.1016/j.burns.2010.04.001 13. Carotti R, Callum J. A review of the use of human albumin in burn patients. J Burn Care Res 2012;33(6):702-717. DOI:10.1097/BCR.0b013e318251b1cf6 14. Huwer C. Are colloid solutions essential for the treatment of pediatric trauma or burn patients? Review for the Expert Committee on the Selection and Use of Essential Medicines.

15. Geneva: World Health Organization, 2012. http://www.who.int/selection_medicines/committees/ expert/19/applications/Colloidstrauma_11_1_C_R.pdf (accessed 3 May 2016).

16. James MF. Place of the colloids in fluid resuscitation of the traumatized patient. Curr Opin Anesthesiol 2012;25(2):248-252. DOI:10.1097/ACO.0b013e3283fcede 17. Finfer S. Reappraising the role of albumin for resuscitation. Curr Opin Crit Care 2013;19(4):351-320.

DOI:10.1097/MCC.0b013e3283632e42 18. Cairont P, Langer T, Gattinoni L. Albumin in critically ill patients: The ideal colloid? Curr Opin Crit Care 2015;21(4):302-308. DOI:10.1097/MCC.0000000000000223 19. Muller Dittrich MH, Brunow de Carvalho W, Lopes Lavado E. Evaluation of the ‘early’ use of albumin in children with extensive burns: A randomized controlled trial. Pediatr Crit Care Med 2016. Published ahead of print. DOI:10.1097/PCC.0000000000000728 20. Alphonsus CS, Rodseth RN. The endothelial glycocalyx: A review of the vascular barrier. Anaesthesia 2014;69(7):777-784. DOI:10.1111/anae.12661 21. Jacob M, Chappell D. Reappraising Starling: The physiology of the microcirculation. Curr Opin Crit Care 2013;19(4):282-289. DOI:10.1097/MCC.0b013e3283632d5e 22. Torres LN, Sondeen JL, Ji L, Dubick MA, Filho IT. Evaluation of resuscitation fluids on endothelial glycocalyx, venular blood flow, and coagulation function after hemorrhagic shock in rats. J Trauma Acute Care Surg 2013;75(4):759-766. DOI:10.1097/TA.0b013e3182a92514

S Afr Med J 2016;106(7):646-647. DOI:10.7196/SAMJ.2016v106i7.10906

Knowledge of multidrug-resistant tuberculosis in the Thabo Mofutsan­ yana District, Free State, South Africa: A Grade 10 learner’s project

To the Editor: Tuberculosis (TB) remains one of the leading causes of mortality in the world.[1] South Africa (SA) has the third highest incidence of TB, largely fuelled by the HIV epidemic and poor TB management.[1-3] The incidence of multidrug-resistant (MDR)-TB is also increasing, with SA among the five countries contributing to 60% of new cases.[4] The reported number of deaths in SA due to MDR-TB has increased by 16.6% between 2013 and 2014.[2] Thabo Mofutsanyana District, a rural area in the Free State Prov­ ince, has one of the highest provincial TB death rates (9.3%). [2] The learner’s hypothesis was that the people in the Thabo Mofutsanyana District have limited knowledge of TB and MDR-TB, which could relate to the high disease burden and defaulter rate. A questionnaire to test the knowledge of MDR-TB was designed and translated to all local languages in the area. The questionnaire was distributed to high school learners at five district schools as well as to nursing personnel working at the local clinics and hospitals. Of the 550 questionnaires handed out, 500 were returned and analysed (response rate of 90.9%). Learners accounted for 57.2% of the participants. The results showed that 67.2% of people in the district had no knowledge of MDR-TB. Possible reasons given were lack of posters, posters not in their local language, illiteracy, and not being informed by healthcare facilities. Participants with knowledge of MDR-TB indicated that they gained information from local clinics (45.7%), the media (33.5%) and other sources including family members, friends and schools (20.7%). Only 44.5% of the knowledgeable participants knew that the duration of MDR-TB treatment is 24 months. It was encouraging to see that 93.3% of the

July 2016, Print edition

CORRESPONDENCE

knowledgeable participants knew the main symptoms of MDR-TB. With the results showing a severe lack of knowledge in an area with a high TB burden, the learner designed and produced pamphlets with information on TB and MDR-TB and distributed these to schools and clinics in the district. The pamphlets included a list of TB symptoms and an explanation of TB, stating that it is curable.

Furthermore, she organised workshops to educate people. To reach the youth, she initiated a project on social media, by successfully distributing information via Instagram and other social media platforms.

Lerato Ntsutle

Grade 10 learner, Witteberg High School, Bethlehem, Dihlabeng District, Free State, South Africa

Nathaniel Mofolo

Head of Department: Family Medicine, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa mofolon@ufs.ac.za 1. World Health Organization. World Health Statistics 2011. Geneva: World Health Organization, 2011. http://www.who.int/gho/publications/world_health_statistics/EN_WHS2011_Full.pdf?ua=1 (accessed 6 April 2016).

2. Statistics South Africa. Mortality and Causes of Death in South Africa, 2014: Findings from Death Notification. Pretoria: Statistics South Africa, 2015. http://www.statssa.gov.za/publications/P03093/ P030932014.pdf (accessed 06 April 2016).

3. National Department of Health, South Africa. National Strategic Plan on HIV, STIs and TB, 2012 - 2016.

Pretoria: DoH, 2011. http://www.gov.za/sites/www.gov.za/files/national%20strategic%20plan%20on%20 hiv%20stis%20and%20tb_0.pdf (accessed 06 April 2016).

4. National Department of Health, South Africa. Multi-drug Resistant Tuberculosis: A Policy Framework on Decentralised and Deinstitutionalised Management for South Africa. Pretoria: DoH, 2011. http:// www.tbfacts.org/wp-content/uploads/2015/08/SA-MDR-TB-Policy.pdf (accessed 06 April 2016).

S Afr Med J 2016;106(7):648. DOI:10.7196/SAMJ.2016v106i7.10882

Errata Peter Beighton Festschrift In the Peter Beighton Festschrift (supplement to the June 2016 SAMJ, Vol. 106, No. 6), the following errors occurred: Text was missing from the end of the tribute by Peter Bonafede on p. S62, the final paragraph and last two lines of which should have read: It is now 38 years since I worked in the Department of Human Genetics, UCT, and it was a most productive and enjoyable time in my practice of medicine. I have many wonderful memories and could recount numerous additional anecdotes. I can truly say that PB was a major leader in the development of the field of human genetics in SA and his influence is felt worldwide. I was very fortunate to be able to learn and work under him and am proud to have played a very small role in his department in the early days.

Thank you, Prof. Beighton.

Thank you Janet Bonafede and Caroline McCulley, MD, for critical review of the manuscript.

In the tribute by George Gericke starting on the same page, the first paragraph should have read as follows: Who is Peter Beighton? A man’s man, characterised by honesty, integrity, humility, diligence and a love of exuberant laughter; highly adventurous and of great courage, racing the death-defying Isle of Man motorcycle event; walking across the Sahara with a Taureg, recording urine osmolality along the trip; and being a military medical officer with the UN in the (then) Belgian Congo.

Paragraph 3 of the same tribute (p. S63) should have read as follows: He had an exceptional lecturing talent, interlaced with humour. Once, at Tygerberg Hospital, where, in his last slide, an orthopaedic surgeon stood next to a man with a skeletal dysplasia, he asked, ‘Is the Professor of Orthopaedics a giant, or is the patient a dwarf?’

The online version of the supplement was corrected on 31 May 2016.

S Afr Med J 2016;106(7):735. DOI:10.7196/SAMJ.2016.v106i7.11156

Chronic diseases in the Western world: Increasing incidence or increasing overdiagnosis?

In the editorial entitled ‘Chronic diseases in the Western world: Increasing incidence or increasing overdiagnosis?’, which appeared in the May 2016 SAMJ (Vol. 106, No. 5, p. 422), reference 1 should have read as follows: Nojilana B, Bradshaw D, Pillay-van Wyk V, et al., on behalf of the South African National Burden of Disease team. Emerging trends in non-communicable disease mortality in South Africa, 1997 2010. S Afr Med J 2016;106(5):477-484. DOI:10.7196/SAMJ.2016.v106i4.10674. The online version of the article (http://dx.doi.org/10.7196/ SAMJ.2016.v106i5.10875) was corrected on 8 June 2016.

S Afr Med J 2016;106(7):736. DOI:10.7196/SAMJ.2016.v106i7.11158

May 2016 CPD question 2 CPD question 2 in the May 2015 SAMJ (Vol. 106, No. 5) should have read as follows: ‘Women who die from bleeding associated with CD would be expected to have lost more than 2 500 mL of blood.’ The online version of the CPD (http://dx.doi.org/10.7196/SAMJ.2016. v106i5.10929) was corrected on 8 June 2016.

S Afr Med J 2016;106(7):737. DOI:10.7196/SAMJ.2016.v106i7.11157

14

July 2016, Print edition

Dual impact on functional and social limitations results in greater improvement in quality of life for Heart Failure patients.* 1 •

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* vs furosemide ** Observed in one large trial † Compared to furosemide, characteristics demonstrated that were not found in furosemide NYHA – New York Heart Association References: 1. Wargo K, Banta W. A Comprehensive Review of the Loop Diuretics: Should Furosemide Be First Line? Ann Pharmacother 2009;43:1836-47. 2. Muller K, Gamba G, Jaquet F, Hess B. Torasemide vs. furosemide in primary care patients with chronic heart failure NYHA II to IV—efficacy and quality of life. The European Journal of Heart Failure 2003;5:793-801. 3. Cosin J, Diez J, on behalf of the TORIC investigators. Torasemide in chronic heart failure: results of the TORIC study.

The European Journal of Heart Failure 2002;4:507–513. 4. Murray M, Deer M, Ferguson J, Dexter P, Bennett S, Perkins S, et al. Openlabel Randomized Trial of Torsemide Compared with Furosemide Therapy for Patients with Heart Failure. Am J Med 2001;111:513–520. 5. Yamato M, Sasaki T, Honda K, Fukuda M, Akutagawa O, Okamoto M, et al. Effects of Torasemide on Left Ventricular Function and Neurohumoral Factors in Patients With Chronic Heart Failure. Circ J 2003;67:384-390 3Unat® 2,5, Torasemide 2,5 mg, Reg. No: 28/18.1/0292. 3Unat® 5, Torasemide 5 mg, Reg. No.: 28/18.1/0293. 3Unat® 10, Torasemide 10 mg, Reg. No: 28/18.1/0294.

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HPV: Hope in 15 years for un­vaccinated women The deadly cervical cancer-causing human papillomavirus (HPV) could be eliminated in South Africa (SA) within 15 years if ground-breaking new ‘test-and-treat’ technology for women can be successfully introduced to supplement nationwide vaccination of primary schoolgirls.

This was said last month by Prof. Lynette Denny, Head of the Department of Obstetrics and Gynaecology at the University of Cape Town’s Faculty of Health Sciences and Principal Specialist at Groote Schuur Hospital. Creator of the ‘test-and-treat’ HPV-detecting technology, which uses the GeneXpert machine (currently diagnosing tuberculosis and rifampicin resistance), Denny was asked what overall impact this would have when added to the current HPV vaccination being offered at all primary schools. Dr Yogan Pillay, Deputy DirectorGeneral of Strategic Health Programmes in the National Department of Health (NDoH), said that 659 330 grade 4 girls aged 9 years and older completed the required two doses of HPV vaccination at schools across the country in 2014/2015. The goal is eventually to cover all 18 000 primary schools.

Cancer of the cervix is the most common cancer among women in SA, with 6 000 new cases diagnosed annually, half of whom eventually die and most of whom are black.

The vaccine cannot help the millions of already infected women, so the 1-hour ‘test-and-treat’ intervention, the outcome of Denny’s life’s work so far, will help reduce this suffering via early detection and highly successful treatment. There are currently 250

Dr Yogan Pillay, Deputy Director-General of Strategic Health Programmes in the NDoH.

GeneXpert machines in the country, which can take cartridges from 32 analysts, one of which is high-risk HPV. Denny said there is a ‘bit more scientific work to do to make it slightly more accurate – we don’t want to waste resources as we’re already overtreating a small proportion of women’. In 5 years her team would be ready to ‘go with infrastructure for point-of-care screen and treat’ to prevent cervical cancer. ‘I reckon

Prof. Lynette Denny, Head of the Department of Obstetrics and Gynaecology at the University of Cape Town’s Faculty of Health Sciences and Principal Specialist at Groote Schuur Hospital.

we’ll pick up 90% of existing disease – and if we can combine it with the HPV vaccine we’ll drastically reduce if not eliminate it within the next 10 - 15 years,’ she added.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(7):649.

DOI:10.7196/SAMJ.2016.v106i7.11093

Chris Bateman wins award Izindaba News Editor and Healthcare Gazette Editor Chris Bateman last month won the Commentary and Analysis category in the annual Discovery Health Journalism awards for his story entitled ‘Mental health under-budgeting undermining SA’s economy’.[1] The citation read, in part: ‘In presenting analysis together with a well-chosen personal narrative, Bateman made a persuasive and indispensable case for proper care.’ Chris has won the category three times previously and ‘Best Trade Publication’ twice since 2008.

1. Bateman, C. Mental health under-budgeting undermining SA’s economy. S Afr Med J 2015;105(1):7-8. DOI:10.7196/SAMJ.9166

S Afr Med J 2016;106(7):650.

DOI:10.7196/SAMJ.2016.v106i7.11120

16

July 2016, Print edition

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S3 FLIXOTIDE® 50/125/250 INHALER CFC-FREE. Reg No.: 35/21.5.1/0377-0082/3. Delivers 50/125/250 µg of fluticasone propionate per actuation. INDICATIONS: Prophylactic management of atopic asthma in adults and children of 6 years and older. CONTRA-INDICATIONS: History of allergy to any of its components.

PREGNANCY AND LACTATION: Safety not established. DOSAGE AND DIRECTIONS FOR USE: For inhalation use only. Should be taken regularly even when asymptomatic. The onset of therapeutic effect is 4 to 7 days. Should not be used for relief in acute attacks but for routine long term management. Patients will require a fast- and short-acting inhaled bronchodilator to relieve acute symptoms. If patients find that relief with short-acting bronchodilator treatment becomes less effective or they need more inhalations than usual, medical attention must be sought. Adults and children over 16 years of age: 100-1000 µg twice daily.

Starting dose should be appropriate for severity of the disease. Dose may be adjusted until control is achieved or reduced to the minimum effective dose, according to the individual response. Children over 6 years of age: 50-100 µg twice daily. The dose may be adjusted until control is achieved and should be reduced to the minimum effective dose according to the individual response. Special patient groups: No dose adjustment in elderly patients. For the transfer of patients being treated with oral corticosteroids: Patients treated with systemic steroids for long periods of time or at a high dose may have adrenocortical suppression and adrenocortical function should be monitored regularly and their dose of systemic steroid reduced cautiously. After approximately a week, gradual withdrawal of the systemic steroid may be commenced. Decrements in dosages should be appropriate to the level of maintenance systemic steroid, and introduced at not less than weekly intervals. In some patients on oral corticosteroids the dose reduction or replacement with inhaled corticosteroids may not be possible. Some patients feel unwell in a non-specific way during the withdrawal phase despite maintenance or even improvement of the respiratory function. They should be encouraged to persevere with inhaled fluticasone propionate and to continue withdrawal of systemic steroid, unless there are objective signs of adrenal insufficiency. SIDE EFFECTS AND SPECIAL PRECAUTIONS: Treatment should not be stopped abruptly as adrenal insufficiency may be precipitated. Candidiasis of the mouth and throat (thrush) may occur. May be helpful to rinse out mouth with water after use. Symptomatic candidiasis can be treated with topical anti-fungal therapy whilst continuing treatment. Hoarsenes. Paradoxical bronchospasm with an immediate increase in wheezing. Treat immediately with a fast-acting inhaled bronchodilator.

Treatment should be discontinued immediately, the patient assessed, and if necessary alternative therapy instituted. Cutaneous hypersensitivity. Systemic corticosteroid effects may occur. Patients transferred from other inhaled steroids or oral steroids remain at risk of impaired adrenal reserve for a considerable time after transferring to inhaled fluticasone propionate. Increasing use to control symptoms indicates deterioration of asthma control and patient should be reassessed. Sudden and progressive deterioration in asthma control is potentially life-threatening and may have several causes. Consideration should be given to increasing corticosteroid dosage if not caused by otherwise treatable causes of deterioration. Severe asthma requires regular medical assessment as death may occur. Sudden worsening of symptoms may require increased corticosteroid dosage which should be administered under urgent medical supervision. Patients weaned off oral steroids whose adrenocortical function is still impaired should carry a steroid warning card indicating that they may need supplementary systemic steroid during periods of stress, e.g. worsening asthma attacks, chest infections, major intercurrent illness, surgery, trauma, etc. Inhaled therapy may unmask underlying eosinophilic conditions (e.g. Churg Strauss syndrome). These cases have usually been associated with reduction or withdrawal of oral corticosteroid therapy. Similarly replacement of systemic steroid treatment with inhaled therapy may unmask allergies such as allergic rhinitis or eczema previously controlled by the systemic drug. These allergies should be symptomatically treated with antihistamine and/or topical preparations, including topical steroids. Patients in a medical or surgical emergency, who require high doses of inhaled steroids and/or intermittent treatment with oral steroids, are at risk of impaired adrenal reserve. The extent of the adrenal impairment may require specialist advice before elective procedures. The possibility of residual impaired adrenal response and elective situations likely to produce stress and appropriate corticosteroid treatment must be considered. Lack of response or severe exacerbations of asthma should be treated by increasing the dose of inhaled fluticasone propionate or by giving a systemic steroid and/or an antibiotic if there is an infection. Special care is necessary in patients with active or quiescent pulmonary tuberculosis. Patients on corticosteroid therapy may have adrenocortical suppression. MANAGEMENT OF OVERDOSAGE: Monitoring of adrenal reserve may be indicated. Treatment with inhaled fluticasone propionate should be continued at a dose sufficient to control asthma. APPLICANT: GlaxoSmithKline South Africa (Pty) Ltd; (Co. reg. no.1948/030135/07). 39 Hawkins Avenue, Epping Industria 1, Cape Town, 7460.

Reference: 1. Laube BL, Janssens HM, de Jongh FHC, et al. What the pulmonary specialist should know about the new inhalation therapies. Eur Respir J 2011;37:1308-1331. 2. VORTEX® package insert.

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IZINDABA

Zika – a wake-up call for continuous fetal monitoring A medical ethicist from the University of KwaZulu-Natal (UKZN), Prof. Sylvester Chima, warned maternal health workers attending the Africa Health Exhibition/ Congress in Gauteng this June to be especially vigilant in monitoring for fetal abnormalities.

The Zika outbreak in Catholic South America, which set global alarm bells ringing, with pregnant women warned against travelling there, represented the ‘perfect storm’ and highlighted medicolegal and ethical issues around termination of pregnancy. Although the chances of a Zika-infected woman arriving in South Africa (SA) were relatively slim, the now-confirmed link between the virus and fetal microcephaly emphasised the vital need for continuous fetal monitoring. Many SA doctors did not appreciate the importance of continuous monitoring (to term), with three cases of physician negligence proven in the Supreme Court after babies were born with congenital abnormalities, the latest in 2010. ‘It can be caused by anything from fetal alcohol

syndrome [FAS] to intrauterine infections or genetic abnormalities. Zika reminds us of the importance of ultrasound or magnetic resonance imaging.’ In several SA communities, the FAS rate is higher than the HIV/AIDS rate, and further research will indicate just how widespread the syndrome is. SA has one of the world’s highest per capita alcohol consumption rates.

SA’s liberal termination of pregnancy laws did not mirror the tragic situation in 11 other African countries where abortion was illegal, leaving physicians in an ethical quagmire.

Chima, a professor of medical ethics in the Faculty of Health Sciences, UKZN, said that SA’s liberal termination of pregnancy (TOP) laws did not mirror the tragic situation in 11 other African countries where abortion was

illegal, leaving physicians in an ethical quag­ mire. In SA, the Choice on Termination of Pregnancy Amendment Act of 2008 allowed for termin­ation in the first trimester for ‘almost any reason’ (often socioeconomic), while in the second trimester a reason was required (e.g. rape, congenital abnormality) to show that continued pregnancy would be harmful to the mother or baby. TOP in the third trimester required two doctors to confirm severe congenital abnormality. In spite of continuing professional development and education in medical ethics being a central recommendation of the Truth and Reconciliation Commission, low awareness by doctors of their ethical duties persisted. ‘Doctors are not properly trained and many remain unaware – which can have dire consequences all round,’ he warned.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(7):651 DOI:10.7196/SAMJ.2016.v106i7.11094

Restoring hope for terminal cancer patients – a ‘St Jude’ legacy Were it not for 80-year-old Prof. Ernette du Toit’s unceasing efforts to get South Africa (SA) and its donors on the global stem cell registry map, more than 100 of her compatriots would not be alive and fulfilling their dreams and ambitions today.

The unique work, which requires exact donor matching to replace diseased bone marrow after a terminally ill prospective recipient has been subjected to lethal chemotherapy to destroy it, demands nerves of steel from all involved – especially those heading their country’s stem cell donor registry. Du Toit, who retired as Medical Director of the South African Bone Marrow Registry (SABMR) in April this year after a 25-year stint with the registry, was able to translate her early work in Groote Schuur Hospital’s Laboratory for Tissue Immunology (LTI) into a bone marrow registry that today has international life-

saving reach for patients suffering from certain end-stage haematological disorders.

These include leukaemia, lymph node cancers, certain anaemias and SCIDS (severe combined immune deficiency syn­ drome, a rare genetic disorder in which affected children have no resistance to disease and must be kept isolated from infection after birth). Like many of life’s pivotal game-changers, she was, to use her own self-effacing description, ‘in the right place at the right time’ – and she grabbed the golden opportunity presented by her role in Prof. Chris Barnard’s first-ever heart transplant. In early December 1967, the LTI tissue-matched the heart donor for Louis Washkansky, who survived for 16 days, making history.

Over the ensuing months and years, the LTI moved from matching tissue for hearts to kidneys and then livers, its staff in the process touring the world with Barnard,

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July 2016, Print edition

Prof. Ernette du Toit.

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giving them direct access to the world’s top haematologists and immunologists. The late Prof. Peter Jacobs had in the meantime broken new immunological ground in SA with stem cell transplants, first in rabbits and later in humans. While the chance of a genetic match in family members – hugely reducing the chance of immunological transplant rejection – was as high as 25%, the net needed to be thrown far wider. The obvious next step was to set up a tissue typing registry – stimulated by feedback by Dutch haematologist Prof. Jon van Rood of the Haematology Department at the University of Leiden, who ran the Netherlands blood bank and co-ordinated the registration of unrelated potential stem cell donors worldwide. Explains du Toit: ‘Peter [Jacobs] said he’d do the transplant side and I was told by the international community [read Van Rood] that you cannot get donors from a global source unless you have a competent donor registry yourself – a kind of a quid pro quo and quality assurance set-up.’ She set to work to comply.

There are 76 bone marrow donor regis­ tries worldwide with 28 million registered donors, of whom just 71 000 are South Africans – the biggest ongoing issue being the tragically few black (global and local) donors and the gap between SA’s funded private transplant funding and unfunded state sector transplants. Add to this SA’s genetic diversity, in contrast to a more homogenous society like Japan, and you quickly realise how miraculous are the continued lives of the SA recipients, one now an around-the-world sailor and another, 5 years old at the time of the transplant, now a healthy teenager.

For over 70% of patients, their only hope is to find a donor via the SABMR, with the chances of finding a compatible unrelated donor standing at about one in 100 000.

The therapy itself, while risky because of the varying degrees of logistical complexity in the global donor cell retrieval (and ‘sell your house’ costly for the recipient and/or medical aid), has a 60 - 70% success rate, with 380 unrelated (i.e. non-family) bone marrow transplants conducted in SA since 1991 after the SABMR was set up.

All of which makes the reference to St Jude – patron saint of hope and impossible causes – so pertinent in Du Toit’s case.

She says, with undiminished enthusiasm,

‘It’s miraculous and magical what we can achieve. You’re actually destroying an individual’s whole immunological system and replacing it with one from somebody who’s like an identical twin, but found in the general population.’ Finding the donor is merely the first hurdle. The next is transporting the stem cells, mostly from overseas (Germany being a frequent go-to country, because of its efficiency and healthy registry), with European countries preferred because of the shorter travel time and a 72-hour stem cell expiry window. Du Toit tells stories of dedicated couriers (they carry a special cold-box at their feet, and even take it to the toilet with them) being delayed due to severe weather conditions, volcanic eruption clouds or technical flight hitches and having to catch a prebooked backup flight, some arriving at the recipient’s bedside with just hours to spare. The drama and tension involved (the harvesting being done after the recipient’s immune system has already been destroyed several thousand kilometres away) are enough to give anyone grey hair. Du Toit, who speaks in strong, assertive but deeply empathic tones, reveals that international registry protocols prevent donors and reci­ pients from meeting for between 1 and 5 years (SA is 5 years) after the transplant – for very good reasons. ‘You can’t afford for them to get emotionally involved. Bone marrow transplants are not infallible and the recipient might relapse, requiring a top-up from the same donor or a full second transplant. If they met, the donor would not have the freedom to make an independent choice and consent a second time. We’ve had donors changing their minds. When it works, it’s actually one of the most amazing things that can happen between two people.’

This miraculous exchange happens some 12 500 times a year worldwide, according to Terry Schlaphoff, deputy director of the SABMR. Schlaphoff says that the setting up of the only internationally accredited tissue typing laboratory in Africa, introducing formal paternity testing in SA, hosting the World Marrow Donor Association conference in Cape Town in 2006 and helping discover a unique globally lowfrequency HLA antigen called A43 (a rare genetic marker found mainly in Khoisan people) will remain lasting strains in her former boss’s sonata. Asked about how she

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July 2016, Print edition

sees the future of stem cell transplants, Du Toit replies: ‘You don’t know today. I think stem cell transplant is probably pretty crude. There must be a development in the future where medication or some other intervention will be the answer. There’s hope somewhere in the future and stem cell registries may go out of fashion.’ She points to the ‘haplo’ transplants already taking place in SA, where recipients are ‘halfidentical’ to the donor, making it cheaper and easier to find a match.

Du Toit tried to take early retirement 16 years ago (nobody could be found to replace her), and has just retired, with her medical doctor husband Len Anstey, to Century City outside Cape Town. It’s a far cry from her rural origins on a farm near Montagu, but she’s stayed a Capetonian, having graduated from the University of Cape Town in 1960, where Chris Barnard was one of her final-year lecturers. As a Groote Schuur house surgeon, she can remember his dedication in pitching up at a patient’s bedside at 3 a.m. ‘He’d look at the monitors, all normal, and then say, ‘But the blood pressure’s going up!’ – he could work very intuitively, yet he also put together the first heart pumps. One day when the electricity went off he was able to instruct staff on how to keep it going manually,’ she said. Asked about Barnard’s reputation as a ladies’ man, she laughed. ‘I was always wary of getting too near him – he was not an easy man to work with, but I was fortunate in being a young woman (which softened his interactions).’

Now able to enjoy going to the theatre, indulge in some charity work and read – all things she seldom did ‘because I wanted to get up early to work’ – she sometimes drives her husband mad, indulging in her love for classical music and lieder (German music of the Romantic period with solo voice and piano accompaniment). It’s not that surprising; she counts one of the high points of her career as having performed the Alto Solo in Handel’s Messiah at the Cape Town City Hall during her early working career.

Her ‘voice’, it seems, will linger on well beyond that historic hall.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(7):652-653.

DOI:10.7196/SAMJ.2016.v106i7.11092

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Alarming rate of COPD in SA Urgent research is needed to understand the massive potential burden of nontobacco-related chronic obstructive pul­ mon­ ary disease (COPD) in Cape Town and South Africa (SA), both of which have among the world’s worst COPD burdens, Prof. Richard van Zyl, Associate Professor and Head of the Lung Clinical Research Unit at the University of Cape Town, said last month.

Van Zyl was responding on 6 June to the global Burden of Lung Disease (BOLD) 2007 findings debated at the May 2016 Cipla Respiratory Congress in Cape Town.

These showed Ravensmead in Cape Town to have the highest prevalence of COPD among 47 towns and cities globally (19%),

and SA the highest incidence of COPD among 24 countries surveyed. He cautioned against extrapolating the Ravensmead findings (the only suburb surveyed in Cape Town) to the entire metro, saying that the prevalence in the Cape Town areas and nationally was probably between 10% and 15% – still among the world’s worst. He stressed that the global study examined only smokers.

Greater Cape Town has some of the high­ est tuberculosis (TB) rates in the country, while the prevalence of cigarette smoking among coloured people (who comprise the majority of the city’s population) stands at a record 40.1%, with 34.4% of these being women (five times the rate for all SA

women), according to Stats SA. SA has one of the most serious global TB epidemics.

Van Zyl said there was a glaring absence of COPD data on dagga, biomass fuel indoor pollution, post-TB obstructive lung disease, HIV and early childhood and intrauterine issues that impaired lung development. ‘We have a confluence of all these in SA, so healthcare workers must look out for other potential causes besides tobacco,’ he warned.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2016;106(7):654.

DOI:10.7196/SAMJ.2016.v106i7.11147

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.

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EDITORIAL

Overview of the 2016 South African Health Review The Global Report on Urban Health: Equitable, Healthier Cities for Sustainable Development, issued in March 2016 by the World Health Organization (WHO) and the United Nations Human Settlements Programme (UN-Habitat),[1] emphasises the need for enhanced governance and leadership to achieve universal health coverage and the Sustainable Development Goals (SDGs). Noting that a healthy population forms the foundation for ‘sustainable economic growth, social stability, and full realisation of human potential’, the report presents ‘practical, proven solutions for working across sectors to tackle these … health challenges’, and includes examples of such successes in South Africa (SA).

The 20 chapters that make up the 2016 edition of the South African Health Review[2] mirror this global health and development agenda in a local context and offer evidence-based recommendations for resolving our country’s health challenges. Binding this content is the aspiration for an accessible, high-performing public health (PH) system that ameliorates health disparities and provides quality healthcare that is bolstered by multisectoral mobilisation under adept management, leadership and governance.

The urgency of evolutionary interventions to achieve this ideal is heightened by the rapidly growing burden of non-communicable disease (NCD) in tandem with prevailing infectious disease conditions, the imminently devastating effects of climate change, and the unrelenting vulnerability of economically deprived and socially unprotected members of our communities. It has never been more important to abandon vertical and fragmented approaches and opt for an inclusive coalition of roleplayers to holistically address the inherently interdependent factors that benefit human health, the environment and the economy.

The chapters in the Review are grouped in the following focus areas: leadership and governance; human resources for health; service delivery; financing and medical products; and information.

Section 1. Leadership and governance

In chapter 1, Andy Gray and Yousuf Vawda describe milestones in SA’s health policy and legislation over the past year, and the delays and challenges beleaguering the development and application thereof. They point out that although the long-awaited National Health Insurance (NHI) White Paper was released, related funding and policy issues lack detail and finalisation, while the Office of Health Standards Compliance and the South African Health Products Regulatory Authority are yet to be fully operationalised. They note that the development of secondary and tertiary legislation for the Medicines and Related Substances Amendment Acts (Act No. 72 of 2008 and Act No. 14 of 2015) is needed for promulgation, and that there is no movement on the proposed redesign of the Health Professions Council of South Africa. They also note that while draft bills to amend the National Health Laboratory Service Act (No. 37 of 2000) and to create a new National Public Health Institute of South Africa have been prepared, neither bill has yet been tabled in Parliament.

Laetitia Rispel contributes a powerful perspective on PH sector transformation in chapter 2, noting that although singularly progressive measures in health policy, legislation and resource allocation have been taken since the advent of democracy in SA, three key fault lines in implementation underpin the relatively poor performance of our health system and are impeding realisation of improved health for the nation. In her analysis, tolerance of ineptitude and failures in leadership, management and governance,

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a district health system that does not adequately drive the delivery of primary healthcare, and the unsolved health workforce crisis constitute a conjoined threat to the feasibility of NHI. With the South African Medical Association warning[3] in Novem­ ber 2015 that climate change will produce a surge in waterborne diseases, David Hemson’s research on water, sanitation and health in SA, presented in chapter 3, portrays the factors indicating a need for improved water and health management, with greater surveillance of water quality – particularly in vulnerable communities – and the delivery of universal water services to ensure health and prevent disease outbreaks. His recommendations include regular review and routine public reporting of water quality management, and further research into the development and sustainability of sanitation services.

In chapter 4, Mark Spires, David Sanders, Philipp Hoelzel, Peter Delobelle, Thandi Puoane and Rina Swart focus on evidence relating to a change from a diet of traditional foods to one of highly processed and animal-origin foods with more added sugar, salt and fat being implicated in the rise of NCDs in SA. They note that positive policy steps in this regard have been made at the national level, but consequent action has been lacking, and a sustained PH effort is required to address the environmental factors and knowledge, attitudes and behaviours that aggravate the NCD burden.

A co-ordinated plan is needed to make healthy foods more available, acceptable and affordable.

Section 2. Human resources for health

Virginia Zweigenthal, Leslie London and William Pick contend in chapter 5 that several of SA’s key transformative health policies make scant mention of the skilled PH workforce that is required to monitor the progress of NHI and the SDGs, identify health service priorities and implement effective delivery strategies. Historically, PH training was reserved for doctors. However, since 1994, graduate PH programmes have expanded to include other health professionals and social scientists who can apply their broad and versatile skills base in technical and service roles at district, provincial and national levels. The authors suggest that existing PH units in the Western Cape and Gauteng provinces staffed with multidisciplinary teams of PH medical specialists and other PH professionals could be replicated across the country as a resource for health system development and restructuring.

In chapter 6, Rajen Naidoo, Saloshni Naidoo and Sujatha Hari­ parsad provide a review and critique of the current approaches to managing ill-health among healthcare workers and assessing their ability to work. Healthcare workers experience a significant burden of disease caused by a range of workplace hazards, and inadequate institutional management of sickness absence results in a high number of lost workdays, translating into massive costs. The authors propose that institutional responsibility for a work-focused approach be adopted to address the health of healthcare workers, and thereby improve productivity and patient care; this would entail involvement of the Employee Health Service for periods of 5 days of absence, or of the occupational medical practitioner for repeated short-term absences and assessment of fitness to work.

In the focus of chapter 7, on addressing language barriers in SA health through trained interpreters, Ereshia Benjamin, Leslie Swartz, Linda Hering and Bonginkosi Chiliza identify themes emerging from mentor sessions in a pilot project conducted in Western Cape hospitals. Community interpreters were found to experience

July 2016, Print edition

EDITORIAL

their work as challenging on practical and emotional levels, and to be uncertain about their location and role in the health system.

Highlighting the potential to develop a multilingual health service for SA’s culturally and linguistically diverse population, the authors argue for the promotion of language access in health services, the professionalisation of health interpreters, and areas for further research.

Mosa Moshabela, Thembelihle Zuma and Bernhard Gaede contri­ bute a compelling chapter on the need for respectful engagement between biomedical and traditional health practitioners, following the promulgation of the Traditional Health Practitioners Act (No. 22 of 2007) (chapter 8). In foregrounding the resilience of indigenous knowledge, practice and experience, they advocate for the ‘reclamation’ of traditional medicine and healing through policy, legislation and research that will resolve continuing tensions between the two paradigms of healthcare and, through the lens of mutuality rather than opposition, prioritise the needs of the large proportion of SA’s patient population. A merged, complementary system of plural healthcare would benefit both arms of healthcare practice, the patients themselves, and other countries in the African region that seek to institutionalise traditional healing.

Section 3. Service delivery

Chapter 9, crafted by Naomi Lince-Deroche et al., acknowledges SA’s progressive and comprehensive laws, policies and guidelines on contraceptive service provision in the public sector and the country’s commitment to integrated, rights-based service delivery in the con­ text of the SDGs and the Family Planning 2020 initiative. However, scarce resources and SA’s HIV epidemic, and their impact on delivery of contraceptive services, are health systems constraints that demand accountability for related budgeting and dispensing methods. The authors suggest that shifting and scale-up of contraceptive use in SA requires ongoing assessment of the couple year protection rate and unmet need, along with counselling, education and supportive interactions with the healthcare system for all women, in order to optimise improved contraceptive uptake.

Knowledge and evidence, politics and governance, and capacity and resources are the three linked elements of an enabling environ­ment for breastfeeding. In chapter 10, Lisanne du Plessis, Nazia Peer, Simone Honikman and René English observe that enhancing and broadening breastfeeding interventions at all levels of impact will contribute extensively to the achievement of the health, food security, education, equity, development and environmental SDG targets. To support breastfeeding through a multilayered approach across the various levels of government and society, the authors urge for dissemination of evidence to promote a culture of breastfeeding, political will, removal of societal and structural barriers to breastfeeding, regulation of the breastmilk substitute industry, interventions tailored to local needs, appropriate capacity and resources, good-quality data, standardised messages, and explicit guidelines.

MomConnect – a national digital maternal health programme that implements the SA mHealth Strategy and the National Health Normative Standards Framework (HNSF) for Interoperability in eHealth – has drawn global attention because of its innovative features and its avoidance of many of the common pitfalls of implementing digital health projects at scale in low-resource settings.

Enrolment of more than half a million women from all regions of the country in the first year of operation (representing approximately half the number of pregnancies in the PH sector) has generated a national register of pregnant individuals and set up a national feedback system to clients. In chapter 11, Christopher Seebregts, Peter Barron, Gaurang Tanna, Peter Benjamin and Thomas Fogwill focus on the

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design and development of the technical infrastructure supporting MomConnect, and offer evidence-based recommendations for the future development of the MomConnect technical infrastructure and related projects as part of the HNSF implementation, several of which are already being investigated or developed by the National Department of Health.

Chapter 12, written by Helen Malherbe, Colleen Aldous, Dave Woods and Arnold Christianson, explores the virtually hidden disease burden of congenital disorders (CDs) as a cause of child mortality in SA. As mortality from communicable diseases drops, the proportion of deaths from undiagnosed or misdiagnosed CDs is increasing in SA, and inaccurate data for CDs as the cause of death mask the true scale of the role of CDs in child mortality and morbidity. The authors note that the re-engineering of the healthcare service and the NHI initiative provide opportunities for the rebirth of medical genetic services for the prevention and care of CDs, specifically through integration into services for women’s, maternal and child health, throughout the continuum of care in all appropriate stages of life.

In order to improve national and global health, similar integration into health policy and practice is required for mental, neurological and substance use disorders. Chapter 13 demonstrates that integration of mental health into primary care in SA, while challenging, can be both efficient and cost-effective, and that not doing so will result in mental health continuing to be underfunded and marginalised.

Marguerite Schneider et al. provide an overview of existing policies and services in place for mental healthcare in SA, describe current research on effective strategies for providing such services, and identify key barriers and facilitators in implementing and scaling up mental health services.

The rights and health issues of SA’s sex workers form the focus of chapter 14, authored by Andrew Scheibe, Marlise Richter and Jo Vearey, who assert that SA will not reach the United Nations Joint Programme on HIV and AIDS (UNAIDS) 90-90-90 targets unless adequate attention and political will are invested in sensitive, appropriate and evidence-based responses to sex worker health. The South African National AIDS Council’s Sex Worker Programme 2016 - 2019 represents limited but important progress in expanding appropriate programmes for sex workers in SA, but this requires rapid implementation, and much more is needed to reach and empower sex workers to keep themselves safe, safeguard PH, and achieve health-related sustainable development goals. Delays in addressing data gaps, implementing global recommendations on sex work law reform and a lack of evidence-based interventions continue to impact negatively on sex worker morbidity and mortality, and have wide-ranging implications for PH and related expenditure.

Another aspect of PH requiring urgent attention in order for NHI to succeed is SA’s extensive injury burden. Addressing the causes and treatment of trauma requires specialist services and multidisciplinary care. Chapter 15 presents data from numerous studies giving insight into the options for establishing systems of quality trauma care and accreditation programmes for hospitals. The authors – Timothy Hardcastle, George Oosthuizen, Damien Clarke and Elizabeth Lutge – address current and optimal staffing of trauma care facilities, compliance with minimum equipment standards, and the potential for patient harm, and call for the establishment of a national trauma databank. They emphasise the need for prevention programmes and the cost implications of trauma care, noting the cost-benefit ratio of good trauma care compared with the litigation risk to government when such care cannot be provided.

The last chapter in the section related to health service delivery speaks to clinical quality of care and client satisfaction (chapter 16).

July 2016, Print edition

EDITORIAL

Ronelle Burger, Shivani Ranchod, Laura Roussouw and Anja Smith propose that measuring quality of care will be strengthened by complementing current approaches with alternatives such as standar­ dised clients and vignettes, health worker knowledge tests, direct observation, and gathering client feedback on the clinical dimensions of client-provider interaction. Measuring quality and its improvement is pivotal for the planned health-system reforms to be effective in promoting health, ensuring client safety and saving lives. Continued critical reflection and debate on how best to measure quality in the public sector should be centred on the affordability, feasibility, reliability, credibility and relevance of current and alternative approaches.

Section 4. Financing and medical products

Chapter 17, contributed by Mark Blecher et al., investigates HIV financing in SA. The authors probe whether there is sufficient fiscal space to afford and sustain the expanded and rapid roll-out of antiretroviral treatment and prevention interventions needed to reach the UNAIDS 90-90-90 targets in the context of declining economic growth, the monetary constraints announced in Budget 2016, and diminishing donor funding. Their analysis uses the results of the recent HIV investment case, which includes the most recent national costing, cost-effectiveness and allocative efficiency modelling of the epidemic, and information from recent national budgets. Overall, there are indications that introducing the HIV 90-90-90 targets will be hard to achieve, but that they are likely to be affordable and cost-effective if implemented in a phased way and if annual increments to government AIDS budgets are sustained.

Bearing in mind that spending more now will lead to a decrease in total spend, the total cost of the national HIV and AIDS programme will increase, notwithstanding the mix of interventions chosen, because of SA’s generalised epidemic and government’s pre-existing commitment to fund lifelong ART to existing patients.

In Chapter 18, Varsha Bangalee and Fatima Suleman discuss SA’s pharmaceutical pricing dynamics and related transparency issues.

As more countries look to SA for lessons from its pricing policies, an understanding of the manufacturer’s price, logistics fees and the relationship between the two has become increasingly necessary to support the principle that the single exit price (SEP) – which clarifies the price at which a manufacturer may sell a medicine to logistic service providers or medicine dispensers – leads to more transparent prices. Their findings reveal that prices reflected in SA medicine price registries may not be a true reflection of those negotiated between manufacturers and distributors/wholesalers. To guide further policy decisions, gauge market changes in response to the various policies, and ensure transparent pricing, more robust information on medicine pricing in the SA pharmaceutical sector, gleaned from larger, in-depth pharmacoeconomic evaluations, is needed.

Section 5. Information

Chapter 19 reviews the concept of health research observatories as globally recognised proactive institutions that provide appro­ priate evidence-based information to guide policy-making decisions for improving a country’s healthcare. It describes the vision, mandate, purpose, scope and benefits of, as well as key challenges to, SA’s proposed National Health Research Observatory (NHRO).

26

Nobelungu Mekwa et al. identify the NHRO as a comprehensive infor­mation and translation system designed to enable the national co-ordination and integration of research and health information from the country’s multiple research platforms, driven by the National Health Research Committee’s commitment to elevating health research that is aligned with both SA’s National Development Plan 2030 and the WHO’s global interest in research for health. This synopsis serves to stimulate local awareness among and participation by the health research community and relevant stakeholders for sectoral adoption and support of the NHRO. The final chapter – presenting health and related indicators – is the long-established ballast of the Review compiled by Candy Day and Andy Gray. Casting their statistical analyses against the backdrop of the SDGs that catalyse efforts to tackle NCDs alongside major communicable diseases, the authors note that although the SDGs pose extended data and monitoring challenges, they also yield more opportunities for productive engagement between researchers and operational actors. This year’s indicators chapter offers its characteristically wide range of information, with a specific focus on the data needed to monitor NCDs. The scope covers demographic, socioeconomic and risk factor indicators, health services indicators (health facilities and health personnel), and health financing indicators. Health status data on mortality, disability, tuberculosis, HIV and AIDS, infectious disease and malaria are reported, as are reproductive health statistics featuring contraception, sexual behaviour, sexually transmitted infections, termination of pregnancy and maternal health. The remaining categories are child health, nutrition, NCDs, injuries, risk behaviour and determinants of health.

It is said that a river cuts through a rock not because of its power but because of its persistence, and as the momentum towards universal health coverage in SA gathers pace, and our national contribution to achieving the SDGs is gradually consolidated, we offer this edition of the South African Health Review to inform policy and enhance service delivery and holistically address the inherently interdependent factors that benefit human health, the environment and the economy.

This overview was adapted from our editorial in the 2016 South African Health Review.[2]

Ashnie Padarath, Judith King, Emma-Louise Mackie Health Systems Trust, Durban, South Africa Julia Casciola Independent consultant, Cape Town, South Africa Corresponding author: E-L Mackie (emma.mackie@hst.org.za) 1. World Health Organization, United Nations Human Settlements Programme (UN-Habitat). Global Report on Urban Health: Equitable, Healthier Cities for Sustainable Development. http://www.who. int/kobe_centre/measuring/urban-global-report/en/ (accessed 23 May 2016).

2. Padarath A, King J, Mackie E, Casciola J, eds. South African Health Review 2016. Durban: Health Systems Trust, 2016. http://www.hst.org.za/publications/south-african-health-review-2016 (accessed 11 May 2016).

3. South African Medical Association. Media Release: SA’s doctors brace for wave of climate change disease. 23 November 2015. https://www.samedical.org/cms_uploader/viewArticle/185) (accessed 11 May 2016).

S Afr Med J 2016;106(7):655-657. DOI:10.7196/SAMJ.2016.v106i7.11033

July 2016, Print edition

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CSIR INTERNATIONAL CONVENTION CENTRE • PRETORIA

INTERNATIONAL VISITORS

Sunday 7 August Continued

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Barrett’s Oesophagus Colorectal Twilight Symposium IBD, iron deficiency & GI bleeding Monday 8 August Gastro Foundation Hepatocellular Carcinoma a Festschrift Symposium in honour of Prof Michael Kew Invited Speakers: Prof Adrian Di Bisceglie – United States Prof Geoff Dusheiko – United Kingdom Dr Jay Hoofnagle – United States Prof Massimo Pinzani – United Kingdom Dr Lewis Roberts – United States

Friday 5 August 2016: Academic Day Saturday 6 – Monday 8 August 2016: Congress

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CME

GUEST EDITORIAL

Colliding epidemics of communicable and non-communicable diseases during adolescence in South Africa Over the past 50 years, the improvement of health outcomes in infants and young children has received more attention than that in adolescents, primarily because adolescence is not typically associated with ill health. However, this picture is rapidly changing, with the present generation of adolescents already encountering diverse challenges, with different biosocial and neurocognitive responses compared with their parents and grandparents. These transitions are influenced by geographical, cultural, economic and genetic contexts.

This issue of CME includes the final two articles on the topic of adolescent health.

Coovadia et al.[1] highlight the epidemiological transitions taking place in South Africa (SA) during adolescence, from a predominance of infectious diseases and complications of malnutrition to a growth of and convergence with non-communicable disorders (NCDs). The health and economic implications of NCDs are increasing, and they are initiated by early-life malnutrition and later-life obesity. The most common NCDs are those related to obesity, diabetes, hypertension and mental disorders. The article underscores the importance of early events during adolescence that lay the foundations for and are predictive of chronic conditions during adulthood, and highlights the opportunity to prevent this by addressing issues during the early stage of susceptibility. Factors that contribute to adolescent NCDs include early sexual exposure, unprotected sex, multiple sex partners, indoor open stoves, allergies, substance abuse, violence, exposure to pollutants, lack of exercise and diet. The article alerts health practitioners to the importance of paying attention to a pattern of diseases that predict the development of NCDs later in life.

Peer and Ganie[2] highlight the fact that we are already facing an NCD crisis in SA. The severity of the obesity epidemic in this country can be illustrated by the fact that nearly one in every five SA boys and one in every four girls is obese. This has major consequences for cardiometabolic disease (type 2 diabetes mellitus, high blood pressure, dyslipidaemia), respiratory conditions

28

(obstructive sleep apnoea), gastrointestinal disease, musculoskeletal disease, psychological problems (depression) and social difficulties (stigmatisation), and has huge cost implications for healthcare delivery and the quality of life of the next generation of adults.

A key contributor to overweight/obesity in adolescents is a more sedentary lifestyle, in parallel with the overconsumption of highdensity refined foods. Early diagnosis and interventions to reduce obesity during adolescence can have a huge impact on improving adult health outcomes. Creating healthier environments, an increase in physical activity, and increasing awareness of healthy food choices during adolescence can make a big difference in containing the obesity epidemic, and minimise the need the need for weight loss medications or bariatric surgery and avert the serious long-term consequences.

The growing epidemic of NCDs in SA, together with the current high burden of communicable diseases, including HIV, and high teenage pregnancy rates, underscores the urgent need for innovative prevention interventions and access to treatment programmes to ensure that adolescents grow up to be healthy and productive adults.

Quarraisha Abdool Karim Guest editor Centre for the AIDS Programme of Research in South Africa, Durban, South Africa quarraisha.abdoolkarim@caprisa.org 1. Coovadia H, Jugnandan Y, Ramkissoon A. Adolescence: The age of Proteus. S Afr Med J 2016;106(7):659-661. DOI:10.7196/SAMJ.2016.v106i7.10945 2. Peer N, Ganie YN. A weighty matter: Identification and management of overweight and obesity in adolescents. S Afr Med J 2016;106(7):662-665. DOI:10.7196/SAMJ.2016.v106i7.10946

S Afr Med J 2016;106(7):658. DOI:10.7196/SAMJ.2016.v106i7.11130

July 2016, Print edition

CME

Adolescence: The age of Proteus H Coovadia, MBBS, FC Paed (SA), MSc, MD; Y Jugnundan, MB ChB; A Ramkissoon, PhD, MBA Maternal, Adolescent and Child Health Systems (MatCH), School of Public Health, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Corresponding author: H Coovadia (hcoovadia@match.org.za)

This article focuses on adolescents as a group, who are exposed to major changes in their near future, with the key transformation being the epidemiological transition from the age of infectious and nutritional problems to that of the non-communicable disorders (NCDs). The major NCDs are: obesity, diabetes, maternal, newborn and child, hypertension and mental health disorders. We also dis­cuss allergies, exposure to pollutants, indoor open stoves, and behavioural factors, such as lack of exercise, unhealthy diet, substance abuse, injuries and violence, and sexually transmitted diseases, which contribute to a risky environment. We particularly emphasise the continuum from birth to old age, during which early events may produce lifelong diseases, and which requires serious attention with regard to preventive measures during the earliest period of susceptibility. Some indicators of disease can serve as diagnostic markers and help healthcare workers to avoid complications and manage a disorder efficiently.

S Afr Med J 2016;106(7):659-661. DOI:10.7196/SAMJ.2016.v106i7.10945

I n Greek mythology, Proteus is god of ‘elusive sea change’ and will change his shape to avoid certain situations. ‘Protean has positive connotations of flexibility, versatility and adaptability.’ (Wikipedia)[1]

Definitions

Adolescence marks a period of transition in both physical and psycho­ logical growth, which intervenes between childhood and adult­hood.

Socially, it serves as a point of evolution into the maturity of acquiring an adult role with the appropriate privileges and related responsibilities.

This transition is driven by biological processes, such as the onset of puberty, which subsequently terminates in sexual and physical matura­ tion. The duration of this transition varies owing to geographical, cul­ tural, economic and genetic contexts, although it has been defined by the World Health Organization (WHO)[2] as being in the 10 - 19-year age group. Furthermore, a youth has been defined as someone in the 15 - 24-year age group. This overlap encompasses all persons between the ages of 10 and 24 years – referred to as young people.

Health: Key issues

The following paragraph on key issues in adolescent health is sum­ marised from articles in The Lancet.[3-5] There are 1.8 billion adolescents (between 10 and 24 years of age) worldwide, who account for more than a quarter of the global population.

Adolescent health has lagged behind improvements in the healthcare of younger children over the past 50 years. It is evident that this generation of adolescents encounters different challenges from those of their prede­ cessors, with dissimilar biosocial and probably neurocog­nitive responses.

Critical temporal factors, such as early childhood events, puberty and, later, social determinants, influence health and development. Social media accelerate sociocultural change. The health and economic burden of non-communicable disorders (NCDs) is significant and increasing.

It is propagated by early-life under-nutrition and later-life adiposity, decreasing physical activity, increasing sedentary behaviour, poor dietary diversity, and intergenerational factors. The NCD burden falls heavily on low- and middle-income countries (LMICs). Sub-Saharan Africa is the only region worldwide where the number of adolescents is predicted to grow, despite having the worst adolescent health profile.

A life course

The concept of a life course in the origins and development of disorders, when precursor events during early-age periods predict

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later-onset disease, is discussed below, e.g. adolescents along the pathway to NCDs in South Africa (SA).

The NCDs of importance in SA and globally

The NCDs, i.e. obesity, diabetes, hypertension, and mental disorders, are the new epidemic in SA and are especially important for public policy and innovative prevention and treatment programmes. The factors mentioned below are also important because of their biomedi­ cal significance and for establishing the injurious environment in which they develop along the causal pathway to NCDs. Furthermore, the prevalence of early sexual debut, unprotected sex, allergies, exposure to pollutants, indoor open stoves, and behavioural factors such as lack of exercise and diet, contribute to a risky environment.

Substance abuse, injuries and violence, and sexually transmitted dis­ eases are also likely to be on this trajectory to NCDs.[6,7] The basic (non-epidemiological) mechanisms of the transition from infectious diseases to NCDs are poorly understood, but the concept that there are critical periods in early life and during the life course that affect subsequent health and disease, is supported by a growing body of evidence.[8-10] The objective of this article is to introduce the emergence of this epidemic to practitioners, and to assist health professionals to recog­ nise, in clinical practice, a constellation of diseases that is a harbinger for the development of NCDs. We discuss a number of common predisposing factors that exist along this pathway and a profile of biomarkers during puberty and adolescence, which are predictive of risk for the most frequently reported NCDs in SA.[8,9,11,12]

Risk factors for NCDs

The SA National Health and Nutrition Examination Survey (SANHANES)-1 data[13] and Statistics SA[14] provide more detail on NCDs. The risk factors are already prevalent in late adolescence and young adulthood. The significance of including a background of HIV and antiretroviral (ARV) treatment is unarguable, as SA is at the epicentre of the global pandemic, with the largest national programme of ARV treatment.

Health practitioners must pay particular attention to the clinical features of puberty in the assessment of health and disease. Pubertyassociated changes, a critical segment of the life course, probably create conditions for the subsequent development of NCDs. The fundamental changes during puberty, and the multiple vulnerabilities to ill-health

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throughout adolescence, may constitute critical periods in the genesis of NCDs. The combination of these two contiguous and probably continuous sets of factors could influence the subsequent progression to NCDs in adulthood. The mechanisms of this process are not clearly understood, but possibly include the hormonal, psychological and socioeconomic disturbances during puberty and adolescence, which, when added to the formative elements in childhood, cumulatively impact on the development of NCDs in later life. Ninety-five percent of SA children between 12 and 15 years of age attend school.[15] Therefore, secondary schools and youth centres are the most likely public sites where adolescents gather and socialise, and thus become susceptible to disorders leading to NCDs and targets for interventions.

Clinical risk factors: The example of pregnancy

Clinical factors such as lack of exercise, diet, obesity and substance abuse are already of relevance to public health. While the extreme dangers of teenage pregnancies, such as deaths, are well known, the moderate to severe effects of this period may be less well recognised, despite being protean and clinically identifiable. A recent large study,[9] which is of considerable relevance to developing countries, including SA, has shown that pregnancy in young mothers identifies a critical period for NCDs, during which interventions could success­ fully be applied. The key findings, derived from outcomes from ~17 000 birth samples, ~13 000 children samples and ~10 000 adult samples, indicate that there are dif­ ferences in risk to these offspring according to extremes of maternal age (<19 years; >35 years) compared with mothers 20 - 24 years of age. The COHORTS Collaboration,[9] which includes 19 403 participants located in five birth cohorts in Brazil, Guatemala, India, the Philippines, and SA, was established to investigate risk factors for NCDs in pregnant women and outcomes in their infants. The findings revealed an increased risk of low birth weight, preterm birth, stunting at 2 years, failure to complete secondary schooling, and lower adult height in children of young moth­ ers (≤19 years) compared with mothers aged 20 - 24 years. Although mothers aged ≥35 years had an increased risk of preterm birth, their chil­ dren had less stunting, better school progression and adult height attain­ ment, the latter two being novel findings in LMICs. Adult fasting glucose concentrations were increased in offspring of young and old mothers,[9] but adult blood pressure was unrelated to maternal age. Children of women <19 years and >35 years may benefit from focused public health endeavours to offset their risks of abnormal glucose metabolism, with its attendant disorders.

These findings suggest that in addition to the well-recognised temporal thresholds of greatest risk for morbidity and mortality in children in LMICs, which rightly concentrate on young age groups (perinatal, infancy, first 1 000 days, and under-5s), there is a strong case to be made for continued vigilance throughout the adolescent years. Policymakers and clinicians need this evidence.

Interventions to reduce NCDs

A recent systematic review, specifically examining LMICs, identified various interventions aimed at reducing adolescent fertility, includ­ ing improved communication, peer education and school-based programmes.[16] Young women in LMICs should be exposed to programmes that discourage early marriage. Allowing for cultural constraints, marriageable age legislation may be introduced for this purpose. It is well recognised that early marriage transgresses human rights conventions and inhibits social integration and educational progress; interventions to promote delayed child-bearing are impor­ tant. Health-related and social support for teenage pregnancies to minimise adverse effects of young age, is essential. It is of major importance to improve child nutrition and invest in early child­ hood education. We suggest standardisation of definitions for rapid growth, overweight and obesity in children.

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As indicated above, nutrition, obesity, diabetes, hypertension, mental disorders, early sexual debut, unprotected sex, allergies, exposure to pollutants, indoor open stoves, and behavioural factors such as lack of exercise and diet, substance abuse, injuries and violence, and sexually transmitted diseases, are especially important for public policy and innovative prevention and treatment programmes. The interventions to minimise these risk factors are available from a number of articles,[2,3] and others are mentioned below.

To provide the wider context for these necessarily focused bio­medical indicators, a number of relevant biosocial factors detected during puberty and adolescence must be assessed to determine the strength of their association along the pathway to development of NCDs later in life. There remains a gap in the scientific evidence linking clinical entities to the subsequent development of specific NCDs. The NCDs in SA and other high-prevalence countries should be placed in the context of the prevailing HIV epidemic. It is possible that ARV treatment also has a bearing on NCDs. A range of problems, including prevalence of anaemia, early sexual debut and unprotected sex, allergies, exposure to pollutants and indoor open stoves, should be included in the assessment.

Useful investigations to diagnose the common risk factors for NCDs

Clinicians should routinely screen adolescents for NCD risk factors and should ask questions relating to substance use, sexual behaviour, diet, level of physical activity and mental health status. Healthcare providers should be alert to mental health problems and behaviours. Counselling and information should be provided on reducing the risk of developing NCDs in adulthood. This should include information on healthy lifestyles, i.e. increasing physical activity, a nutritious diet, and reducing intake of salt, sugar, trans fats and junk food. Effective communication with adolescents requires confidentiality, consulting the patient alone, tailoring the discus­ sion to the individual, and understanding the role of parents/caregivers.

Clinical assessments and blood samples will be needed, such as weight and height, waist circumference and blood pressure measure­ ments. Abdominal ultrasound for subcutaneous and visceral fat determination is useful for establishing overweight and obesity (set out below). Samples should be assayed for the following biomarkers: fasting insulin, fasting blood glucose, highly sensitive C-reactive protein, and a lipogram. If these pathways are identified, and it is assumed they indicate an individual on the pathway to the NCDs of interest, prevention and therapy can be addressed.

The list of biomarkers is given below. The choice of NCDs pos­ sibly prevalent in SA can be gauged from the burden of disease in this country. There is emerging evidence that exposure to various chal­ lenges, especially environmental and nutritional ones, but possibly also infection and other factors during fetal life, are associated with health outcomes later in life.[10] However, less is known about the evolution of exact biomarkers and specific NCDs. Pre- and postnatal growth patterns should be ascertained, as these are associated with the timing of the menarche.[11] As there are well-established interactions between nutrition and immune responses, these interactions should form part of the investigations. These factors have implications for interventions and behavioural change, and may even extend to healthy ageing.

Established criteria may be used to select specific biomarkers to define risk, and describe clinical and biochemical characteristics to diagnose individual NCDs. Puberty is determined by a validated self-assessment protocol (from birth-to-10 study, using Tanner’s stages to assess pubertal development).[17] Predetermined, established clinical and biochem­ ical criteria are used to diagnose the individual NCDs. Methods used for the different aspects of adolescence are the following: mood disorders; household socioeconomic status; education/employment/ household relationships; and the Snyder’s trait hope scale, which can

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be adapted from the Life Course, Developmental Pathways for Health Research Unit, University of the Witwatersrand, Johannesburg, SA.[18] Blood samples to establish the presence and trends of biomark­ ers over this critical segment of the life course should be taken after permission has been obtained, around the onset of puberty and again 2 - 3 years later, and during early and late adolescence (at about 14 and 19 years of age). Mobile technology can be employed to ensure reliable collection and retrieval of blood samples, and analysis of the results.

Biomarkers of NCDs

• Diabetes mellitus: fasting blood sugar; urine Dipstix for glycosuria • Hypertension: urine Dipstix for albuminuria • Mental health (psychological) disorders: history, including sub­ stance abuse, depression and suicidal tendencies; clinical examina­ tion; and psychological tests, if indicated • Obesity: height, weight, body mass index and waist circumference; questionnaire on physical activity; fasting insulin; lipogram; highly sensitive C-reactive protein • Chronic lung disease: history; chest radiograph, if indicated • Cancer: full blood count; erythrocyte sedimentation rate; exclusion of haematological cancers and chronic anaemias.

Acknowledgements. We are grateful to our colleagues, who wrote a joint document (not published in a journal or other public or private document), for allowing us to use some of their data: Profs M S Norris, M L Newell, M Hanson, D Moodley, Q Abdool Karim and A Stein, and Ms C Searle.

References 1. Wikipedia. https://en.wikipedia.org/wiki/Proteus (accessed 10 May 2016).

2. World Health Organization. Global Status Report on NCDs. WHO: Geneva, 2010. http://www.who. int/chp/ncd_global_status_report/en/ (accessed 8 September 2015).

3. Sawyer SM, Afifi RA, Bearinger LH, et al. Adolescence: A foundation for future health. Lancet 2012;379:1630-1640. DOI:10.1016/S0140-6736(12)60072-5 4. Gore F, Bloem P, Patton G, et al. Global burden of disease in young people aged 10 - 24 years: A systematic analysis. Lancet 2011;377:2093-2102.

5. The Lancet series on adolescent health. Adolescent health 2007. Lancet 26 March 2007. http://www. thelancet.com/series/adolescent-health (accessed 17 May 2016).

6. Coovadia H, Jewkes R, Barron P, Sanders D, McIntyre D. The health and health system of South Africa: Historical roots of current public health challenges. Lancet 2009;374:817-834. DOI:10.1016/S0140-6736(09)60951-X 7. Mayosi BM, Lawn JE, van Niekerk A, Bradshaw D, Abdool Karim SSA, Coovadia HM. Health in South Africa: Changes and challenges since 2009. Lancet 2013;381:269-271. DOI:10.1016/S0140-6736(12)61814-5 8. Power C, Kuh D, Morton S. From developmental origins of adult disease to life course research on adult disease and aging: Insights from birth cohort studies. Annu Rev Public Health 2013;34:7-28.

DOI:10.1146/annurev-publhealth-031912-114423 9. Fall CHD, Sachdev HS, Osmond C, et al., and the COHORTS investigators. Association between maternal age at childbirth and child and adult outcomes in the offspring: A prospective study in five lowincome and middle-income countries (COHORTS collaboration). Lancet Glob Health 2015;3:e366-e377.

10. Barker DJP. Mothers, Babies and Health in Later Life. 2nd ed. London: Churchill Livingstone, 1998.

11. Bradshaw D, Nannan N, Laubscher R, et al. South African National Burden of Disease Study 2000.

Estimates of Provincial Mortality: Summary Report. Cape Town: SA Medical Research Council, 2006.

12. Norman R, Bradshaw D, Schneider M, et al. A comparative risk assessment for South Africa in 2000: Towards promoting health and preventing disease. S Afr Med J 2007;97:637-641.

13. SANHANES Team. South African National Health and Nutrition Examination Survey. SANHANES-1 Report. 2013. http://www.hsrc.ac.za/en/research-areas/Research_Areas_PHHSI/sanhanes-health-andnutrition (accessed 10 May 2016).

14. Statistics South Africa. Mortality and causes of death in South Africa. Findings from death notification.

2008. www.statssa.gov.za/publications/.../P030932008.pdf (accessed 10 September 2015).

15. Lloyd CB. Progress towards ‘education for all’: Trends and current challenges for sub-Saharan Africa.

In: Lloyd CB, Behrman J, Stromquist NP, Cohen B, eds. The Changing Transitions to Adulthood in Developing Countries: Selected Studies. Washington, DC: National Academies Press, 2005:84-117.

16. McQueston K, Silverman R, Glassman A. The efficacy of reduced adolescent child-bearing in low- and middle-income countries: A systematic review. Stud Fam Plann 2013;44:369-388.

17. Norris S, Richter L. Usefulness and reliability of Tanner pubertal self-rating to urban black adolescents in South Africa. J Res Adolesc 2005;15(4):609- 624. DOI:10.1111/j.1532-7795.2005.00113.x 18. MRC/Wits Developmental Pathways for Health Research Unit, University of the Witwaters­ rand, Johannesburg, South Africa. www.ncbi.nlm.nih.gov/pubmed/23876525 (accessed 17 May 2016).

A weighty matter: Identification and management of overweight and obesity in adolescents N Peer,1 MB ChB, MBA, MPH, PhD; Y N Ganie,2 MB ChB, DCH, FC Paed (SA), Cert Endocrinology and Metabolism (SA) Paed Non-communicable Diseases Research Unit, South African Medical Research Council, Durban; and Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa 2 Division of Paediatric Endocrinology and Metabolic Diseases, Inkosi Albert Luthuli Central Hospital, Durban; and Department of Paediatrics and Child Health, Faculty of Health Sciences, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa 1

Corresponding author: N Peer (nasheeta.peer@mrc.ac.za)

Overweight and obesity are common in South African boys (18.8%) and girls (26.3%). Considering the potential serious consequences of these conditions, clinicians need to identify overweight and obese adolescents to enable early diagnosis and treatment. The key contributor in adolescents is increased intake of unhealthy foods and lower levels of physical activity. The consequences of overweight and obesity in adolescence are multisystemic and include cardiometa­bolic (type 2 diabetes mellitus, high blood pressure, dyslipidaemia), respiratory (obstructive sleep apnoea), gastrointestinal (non-alcoholic fatty liver disease), musculoskeletal, psychological (depression) and social (stigmatisation) effects.

Body mass index (BMI) is calculated to determine overweight and obesity in adolescents. Numerous expert committees, despite using different methods, classify overweight and obesity in children by age- and gender-specific cut points for BMI. After a diagnosis of overweight and obesity, secondary causes must be excluded, and a history of dietary intake, physical activity and sedentary behaviour obtained. This will identify modifiable behaviours that promote energy imbalance. All obese adolescents should undergo cardiometabolic assessments comprising fasting glucose, lipid and blood pressure measurements every 2 years. Inter­ventions should focus on creating healthier home environments that provide easy access to healthy foods, encourage physical activity and discourage sedentary behaviour. Medication for weight loss or bariatric surgery may be considered for severely obese adolescents who do not respond to other strategies.

S Afr Med J 2016;106(7):662-665. DOI:10.7196/SAMJ.2016.v106i7.10946

Overweight and obesity Prevalence

Over the past few decades, the prevalence of overweight and obesity in children and adolescents has increased rapidly.[1] In 2013, the

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prevalence in South African (SA) boys and girls <20 years of age was 18.8% and 26.3%, respectively.[2] With almost 1 in 5 boys and a quarter of girls in SA being overweight and obese, this represents a major burden of a serious and preventable disease in children and adolescents.

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In view of the potentially serious conse­ quences, it is vital for the clinician to identify overweight and obese adolescents timeously to ensure an early diagnosis, screening for comorbidities and the implementation of appropriate management strategies.

Determinants

The development of overweight and obe­ sity is a complex and multi­faceted inter­play between genetic, epigenetic, environ­mental and behavioural factors. Individual differ­ ences determine the degree of susceptibility to overweight and obesity.[1] Although weight regula­ tion is influenced by immunologi­ cal, neural, hormonal, metabolic and other mechanisms, genetic factors and geneticenvironmental interactions are thought to be among the more important ones.[3] Factors that influence susceptibility to an obesityconducive environment include environmental dynamics, lifestyle choices, and cultural and sociological factors, in addition to a genetic predisposition.

The key contributor to overweight and obesity in adolescents, similar to that in adults, is the emergence of the ‘obesogenic’ environment.[1] There have been alterations in adolescents’ dietary and physical activ­ ity patterns, with the overconsumption of food, particularly calorie-dense foods, and

decreases in physical activity with increas­ es in sedentary behaviours, such as more ‘screen time’ (television, computer and video games). This has led to an energy imbal­ ance between calories consumed and calo­ ries expended, with more calories consumed than expended. The subsequent accumula­ tion of abnormal or excessive fat presents a risk to health and is the hallmark of over­ weight and obesity.

Comorbidities

Overweight and obesity in adolescence are multisystem diseases with potentially devas­ tating consequences that affect both physi­ ological and psychosocial wellbeing. Chronic conditions that were once considered diseases of middle age are now prevalent in adolescents because of the rise in childhood obesity.[1] The onset of these conditions in childhood implies greater life-years lost than if the onset was in adulthood.

Obesity in adolescents, as in adults, is associated with a higher risk of the devel­ opment of insulin resistance and type 2 diabetes mellitus. The latter accounts for almost 50% of diabetes in children and adoles­cents.[4,5] Most of the major risk fac­ tors for cardiovascular diseases, e.g. high systolic and diastolic blood pressure (BP), manifest during this period, although the

Table 1. Some comorbidities associated with overweight and obesity [1,3-5] Category

Comorbidity

Psychological

Lack of confidence, low self-esteem, anxiety and depression, behavioural disorders

Social

Stereotyping, stigmatisation, discrimination, social rejection and isolation, loneliness, school avoidance and poor academic performance, victim or perpetrator of bullying behaviour, substance abuse

Disordered eating

Overeating, binge eating, bulimia nervosa, night-eating syndrome

Respiratory

Asthma, obstructive sleep apnoea, obesity hypoventilation syndrome

Orthopaedic

Hip, knee and ankle pain from musculoskeletal stress, slipped capital femoral epiphysis, Blount’s disease

Gastrointestinal

Non-alcoholic fatty liver disease, gastro-oesophageal reflux disease, constipation, gallbladder disease

Gynaecological

Oligomenorrhoea or amenorrhoea due to polycystic ovarian syndrome, early onset of puberty in girls

Neurological

Headaches due to pseudotumour cerebri

endpoints, such as ischaemic heart disease and stroke, are not necessarily evident in adolescence. Overweight is probably the most significant factor associated with ele­ vated BP in childhood, responsible for >50% of the risk of developing hypertension.[6] About 13% and 9% of overweight children have raised systolic and diastolic BP, respec­ tively.[5] Dyslipidaemia (raised low-density lipoprotein cholesterol (LDL-C), increased triglycerides, and low high-density lipopro­ tein cholesterol (HDL-C)) is one of the most common medical abnormalities in over­ weight adolescents.[3,5] It is a causal factor in the development of atherosclerotic vascular lesions by late adolescence.[4] Moreover, overweight and obesity have wide and far-reaching consequences involv­ ing multiple systems, such as the respiratory and gastrointestinal systems, and orthopae­ dic problems.[1,3-5] Importantly, overweight and obesity in adolescents are associated with nume­rous adverse psychosocial effects (Table 1).

Identification

Numerous techniques may be used to deter­ mine adiposity in adolescents. The common­ ly used measure is the calculation of body mass index (BMI), where the person’s weight in kilograms is divided by their height in metres squared (kg/m²). BMI is a good proxy to measure adiposity in adolescents because it correlates with body fat and denotes an increased risk of adverse health outcomes, particularly cardiometabolic diseases.[5] The BMI guidelines to diagnose overweight and obesity in childhood are those of the International Obesity Task Force (IOTF) standards, described by Cole et al.,[7] the World Health Organization (WHO), and the Centers for Disease Control and Prevention (CDC) (2000) (Table 2).[8] The IOTF method uses age- and genderspecific cut points in 2 - 17-year-old children to predict a BMI of ≥25 kg/m2 (overweight) and ≥30 kg/m2 (obesity) at 18 years of age.

Children defined as obese are also included in the overweight category. The international age- and gender-specific child BMI cut points

Table 2. Methods for determining overweight and obesity in adolescents using BMI[7,9,10] Cut points Adiposity indicator

Calculation method

Overweight

Obesity

International Obesity Task Force

Age- and gender-specific cut points predict BMI at 18 years

BMI ≥25 kg/m2

BMI ≥30 kg/m2

World Health Organization

Software used to obtain z-scores; equivalent to BMI at 19 years

z-score ≥1 SD; corresponds to BMI ≥25 kg/m2

z-score ≥2 SD; corresponds to BMI ≥30 kg/m2

Centers for Disease Control and Prevention

Age- and gender-specific charts

BMI ≥85th centile

BMI ≥95th centile

SD = standard deviation.

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were derived from a large international sample that used regression techniques by passing a line through the health-related adult cut points at 18 years.[7] The WHO has child growth references for 5 - 19-year-olds where z-score values for BMI-for-age are calculated using WHO soft­ ware. [9] Overweight and obesity are defined as ≥1 standard deviation (SD) and ≥2 SD, respectively.

The CDC (2000) uses charts to identify overweight and obese children and adoles­ cents,[8] where BMI levels are compared with those of their peers of the same sex and age.

National survey data collected from 1963 1965 to 1988 - 1994 were used to determine the overweight and obesity percentiles for each age and sex. Clinical overweight corre­ lates with BMI >85th centile and obesity with BMI >95th centile.[10] Table 3. Some secondary causes of adolescent overweight and obesity[12] Category

Cause

Endocrine

Hypothyroidism Growth hormone deficiency Cushing’s syndrome Pseudohypoparathyroidism

Syndromes

Down syndrome Prader-Willi syndrome Bardet-Biedl syndrome

Drug induced

Steroid treatment Secondary to sodium valproate

Genetic/ monogenic obesity

Leptin deficiency

There are other measures of overweight and obesity that do not use weight and height in adolescents, which may add value in defining visceral fat and body composition; however, few have paediatric norms while others are expensive or impractical in clin­ [4,8] ical practice.

Although BMI and waist circumference are highly correlated and the associations with visceral adiposity are of similar magni­tudes,[11] reference cut points for waist circumference in adolescents that identify risk beyond that provided by BMI category are not available.[5] The cheapest but least reproducible is the measurement of skinfold thickness using calipers; this is therefore not recommended in routine clinical care.[5] Other measures, generally limited to the research setting, include electrical impedance techniques, hydrodensitometry (underwater weighing), computed tomography, magnetic resonance imaging, and dual-energy X-ray absorptiometry.[4,8]

Clinical assessment

Once overweight and obesity have been diagnosed, it is imperative to determine the aetiology and associated morbidities. A thorough medical examination, followed by a nutritional assessment, is required. The medical examination should include screening for signs of secondary causes of obesity, some of which are listed in Table 3.[12] These may be excluded clinically; an endocrine cause is particularly unlikely if there has been no delay in linear growth.[4,5] In the absence of dysmorphic features and developmental delays, a genetic cause is unlikely. If a secondary cause is not probable, the adolescent and the parents, who often seek a medical cause, should be reassured that no further workup is necessary.

Nevertheless, they must be made aware of the need to screen for comorbidities and to initiate treatment without delay.

Following the exclusion of a secondary cause of obesity, obtaining a dietary, physical activity and sedentary behavioural history is important.[4,5] The purpose is twofold: (i) to identify the behaviours that promote energy imbalance and are modifiable; and (ii) to assess the capacity of the adolescent and their family to change these behaviours.[5] A dietary history includes an assessment of the frequency of intake of sugared beverages and fast foods, and the contents of school lunches. [4] However, cognizance must be taken of the limitations associated with selfreported food intake. A history of risky eating behaviours, such as purging or diet pill use, binge eating and late-night eating, should also be determined, as these frequently coexist with obesity.

The time spent on physical activity and sedentary behaviours, such as watching televi­ sion and playing computer games, needs to be documented. Decreased physical activity has been related to overweight in early ado­ lescence,[4] while television viewing time, as a proxy for sedentary behaviour, correlated with rising BMI and the development of diabetes.[4] The presence of comorbidities, particularly obstructive sleep apnoea, orthopaedic and psychosocial problems, should be elicited on history and examination of overweight and obese adolescents (Table 1).[4] Polycystic ovarian syndrome, with its increased future risk of diabetes and dyslipidaemia, is common in obese adolescent girls and needs to be considered in the assessment.

The American Academy of Pediatrics recommends that all obese adolescents undergo

Table 4. Diagnosis of cardiometabolic abnormalities in adolescents[4,5,11] Condition

Symptoms and signs

Investigation

Diagnosis

Management

Diabetes

Asymptomatic, polyuria, polydipsia, weight loss, acanthosis nigricans

Fasting glucose 2-h glucose post OGTT Random glucose

≥7.0 mmol/L ≥11.1 mmol/L ≥11.1 mmol/L

Diet and lifestyle modification, metformin

Hypertension

Asymptomatic, headaches, dyspnoea, sweating

BP reading taken with appropriate cuff size on ≥3 separate occasions

Systolic and/or diastolic BP ≥95th percentile for age, gender and height

Diet and lifestyle modification, pharmacological agents if symptomatic

Dyslipidaemia

Xanthomata

Fasting lipid screen – total cholesterol LDL-C HDL-C Triglycerides

>4.7 - 5.2 mmol/L

Diet and exercise, pharmacological agents if LDL-C >4.9 mmol/L

Waist circumference, triglycerides, HDL-C, BP, fasting glucose

Abdominal obesity plus ≥2 of the following: high triglycerides, low HDL-C, high BP, high fasting glucose

Metabolic syndrome*

Specific to each condition of the syndrome

>3.4 - 4.1 mmol/L <1.0 mmol/L >1.7 - 2.3 mmol/L

OGTT = oral glucose tolerance test; BP = blood pressure; LDL-C = low-density lipoprotein cholesterol; HDL-C = high-density lipoprotein cholesterol. *No consensus with regard to cut points in adolescents.

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Medication for weight loss may only be considered for severely obese adolescents who have not responded to other strategies.

However, a recent systematic review and meta-analysis of treatment of overweight and obese children and youth reported no difference in reductions in BMI and BMI z-scores between those on behavioural interventions alone compared with those on pharmacological plus behavioural interventions.[15] Notably, most weight-loss drugs have not been studied in the adolescent population and should be used with caution. Another modality of treatment to consider for severe refractory obesity in adolescents is bariatric surgery, either gastric bypass or gastric banding.[4,5] However, there is a dearth of data on the long-term effects of such surgery, as longitudinal studies conducted in large samples are not available.[4] Obesity intervention, apart from a positive change in body composition, has beneficial effects on the cardiometabolic profile of adolescents. Even with small changes in BMI, improvements in lipid profile, BP and insulin resistance have been noted.[13] Therefore, weight loss, healthier dietary habits and increased physical activity are mandatory for the improvement of cardiometabolic disorders in adolescents. However, pharmacotherapy should be considered for hypertension >99th percentile, LDL-C >4.9 mmol/L and diabetes not responding to lifestyle changes.[4]

Table 5. Some recommended lifestyle changes[1,12] Reduce energy intake – diet Keep to regular meal times and eat small snacks Eat more low-energy snacks, such as fruits and vegetables Eat dinner as a family 5 - 6 times per week Avoid eating while watching television Avoid eating away from home, especially fast foods Avoid high-energy foods, such as chips, chocolate, sweets Avoid ‘grazing’ Avoid sugary juices/sweetened drinks/soft drinks Reduce portion sizes Increase energy consumption – activity Do more moderate to vigorous physical activity for 1 h/day Do more walking/cycling instead of travelling by car or bus Increase active leisure and weekend activities Use stairs not lifts Be more active around the home/garden, e.g. helping with domestic activities Watch less television – limit to 2 h/day and no television viewing in the bedroom Sit less – spend less time on computer-related leisure activities

Conclusion

cardiometabolic assessments every 2 years, com­prising fasting glucose, lipid and BP measurements.[4,11] Cardiometabolic abnormalities and the metabolic syndrome are common with overweight and obesity, even during adolescence, and the appropriate cut points for diagnosis in the adolescent population are presented in Table 4.

The metabolic syndrome, comprising dysglycaemia, dyslipidaemia, raised BP and obesity, increases the risk of cardiovascular disease and diabetes and appears to be common in obese adolescents. Although three or more criteria (Table 4) are required for a diagnosis, there is currently no consensus on age-specific cut points for a diagnosis in adolescents.[4]

Management

Obesity should be considered a disease per se that warrants inter­ vention, even in the absence of comorbidities.[13] However, owing to the multiple pathways involved in its development, i.e. environmental, social, behavioural, and biological roots, manage­ment of the disorder is extremely challenging, particularly in children and adolescents.[1] A critical factor for success is motivation, which may be achieved through the use of motivational interviewing techniques.[1] This involves employing the four primary skills of asking, informing, advising and listening. Adolescents or parents are allowed to arrive at their own insights and decisions, rather than these being imposed on them. A recent randomised controlled trial by Resnicow et al.[14] demonstrated significant reductions in BMI using motivational interviewing techniques.[14] Interventions should focus on creating healthier environments by providing opportunities for fun physical activities and easy access to healthy meals.[13] Parental involvement is considered critical in supporting change to the adolescent’s lifestyle behaviours. This is achieved by creating an enabling home environment by providing easy access to healthy foods, encouraging physical activity and discouraging sedentary behaviour such as television viewing. Some recommended lifestyle changes are described in Table 5. To achieve and sustain such adjustments, obese adolescents require high levels of social support from family, friends and healthcare professionals.[5,13] In addition to diet and activity, there is a third key component for successful obesity management, which is the psychology of the adolescent.

Among the techniques to reinforce compliance and positive thinking are goal setting, self-monitoring, reinforcements, rewards, and peer mentoring.[1]

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Overweight and obesity in adolescents have serious long-term conse­ quences and are highly likely to track into adulthood.[1] However, obese adolescents who revert to normal adiposity have the same risk of developing diabetes, hypertension and dyslipidaemia in adulthood as those who were never obese.[11] Therefore, it is essential that this condition be diagnosed early and managed holistically to ensure a successful outcome. This is particularly relevant in view of the increasing prevalence of adolescent obesity in SA.[3] Overweight and obesity in adolescence are difficult to manage.

Therefore, healthcare professionals need to have a thorough scientific background and understanding of the obese adolescent with regard to the physical, emotional, cognitive and physiological barriers facing them.[13] Furthermore, the primary care clinician plays a central role in preventing the development of overweight and obesity by promoting healthy lifestyle behaviours in all children and adolescents.

References 1. Murray R, Battista M. Managing the risk of childhood overweight and obesity in primary care practice.

Curr Probl Pediatr Adolesc Health Care 2009;39(6):146-165. DOI:10.1016/j.cppeds.2009.03.002 2. Ng M, Fleming T, Robinson M, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980 - 2013: A systematic analysis for the Global Burden of Disease Study 2013. Lancet 2014;384(9945):766-781. DOI:10.1016/S0140-6736(14)60460-8.

3. Rossouw HA, Grant CC, Viljoen M. Overweight and obesity in children and adolescents: The South African problem. S Afr J Sci 2012;108(5/6). DOI:10.4102/sajs.v108i5/6.907 4. Peebles R. Adolescent obesity: Etiology, office evaluation, and treatment. Adolesc Med 2008;19(3):380405.

5. Barlow SE. Expert committee recommendations regarding the prevention, assessment, and treatment of child and adolescent overweight and obesity: Summary report. Pediatrics 2007;120(Suppl 4):S164-S192. DOI:10.1542/peds.2007-2329C 6. Lurbe E, Cifkova R, Cruickshank JK, et al. Management of high blood pressure in children and adolescents: Recommendations of the European Society of Hypertension. J Hypertens 2009;27(9):17191742. DOI:10.1097/HJH.0b013e32832f4f6b 7. Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing a standard definition for child overweight and obesity worldwide: International survey. BMJ 2000;320(7244):1240-1243. DOI:10.1136/bmj.320.7244.1240 8. Sweeting HN. Measurement and definitions of obesity in childhood and adolescence: A field guide for the uninitiated. Nutr J 2007;6:32. DOI:10.1186/1475-2891-6-32 9. World Health Organization. Growth Reference 5 - 19 years. Geneva: WHO, 2007. http://www.who.int/ growthref/en/ (accessed 28 August 2015).

10. Centers for Disease Control and Prevention. About child and teen BMI. http://www.cdc.gov/ healthyweight/assessing/bmi/childrens_bmi/about_childrens_bmi.html (accessed 28 August 2015).

11. Morandi A, Maffeis C. Predictors of metabolic risk in childhood obesity. Horm Res Paediatr 2014;82(1):3-11. DOI:10.1159/000362237 12. Poskitt EM. Defining childhood obesity: The relative body mass index (BMI). European Childhood Obesity group. Acta Paediatr 1995;84(8):961-963.

13. Pienaar AE, Strydom GL. Childhood obesity: The need for practice based solutions – a South African perspective. In: Yuca SA, ed. Childhood Obesity. Potchefstroom: North-West University, 2012.

14. Resnicow K, McMaster F, Bocian A, et al. Motivational interviewing and dietary counseling for obesity in primary care: An RCT. Pediatrics 2015;135(4):649-657. DOI:10.1542/peds.2014-1880 15. Peirson L, Fitzpatrick-Lewis D, Morrison K, Warren R, Usman Ali M, Raina P. Treatment of overweight and obesity in children and youth: A systematic review and meta-analysis. CMAJ Open 2015;3(1):E35-E46. DOI:10.9778/cmajo.20140047

July 2016, Print edition

SAMA CONFERENCE,EXHIBITION & ANNUAL DOCTORâ&#x20AC;&#x2122;S AWARDS 21-23 OCTOBER 2016 Sandton Convention Centre

Universal Access to Healthcare

For further information: www.samedical.org/events | Registration opens 1 March 2016

IN PRACTICE

CLINICAL PRACTICE

The impact of HIV infection on the presentation of lung cancer in South Africa C F N Koegelenberg,1 MB ChB, MMed (Int), FCP (SA), FRCP (UK), Cert Pulm (SA), PhD; T van der Made,1 MB ChB; J J Taljaard,2 MB ChB, MMed (Int); E M Irusen,1 MB ChB, FCP (SA), PhD 1 2

ivision of Pulmonology, Department of Medicine, Stellenbosch University and Tygerberg Hospital, Cape Town, South Africa D Division of Infectious Diseases, Department of Medicine, Stellenbosch University and Tygerberg Hospital, Cape Town, South Africa

Corresponding author: C F N Koegelenberg (coeniefn@sun.ac.za)

Background. Despite the very high background prevalence of HIV and smoking-related diseases in sub-Saharan Africa, very little is known about the presentation of lung cancer in HIV-infected individuals.

Methods. We prospectively compared HIV-positive (n=44) and HIV-negative lung cancer patients (n=425) with regard to demographics, cell type, performance status and tumour node metastasis staging at initial presentation.

Results. HIV-positive patients were found to be younger than HIV-negative (mean 54.1 (standard deviation 8.4) years v. 60.5 (10) years, p<0.01), more likely to have squamous cell carcinoma (43.2% v. 30.1%, p=0.07) and significantly more likely to have a poor Eastern Cooperative Oncology Group (ECOG) performance status of ≥3 (47.7% v. 29.4%, p=0.02). In the case of non-small cell-lung cancer, they were also significantly less likely to have early stage lung cancer (0% v. 10.3%, p=0.02) compared with HIV-negative patients.

Conclusions. HIV-positive lung cancer patients were younger, significantly more likely to have a poor performance status at presentation and significantly less likely to have early stage lung cancer when compared with HIV-negative patients.

S Afr Med J 2016;106(7):666-668. DOI:10.7196/SAMJ.2016v106i7.10737

The South African (SA) healthcare system has to deal with the largest HIV burden in the world, one of the highest incidences of TB, and a very high prevalence of smoking-related diseases.[1] In fact, there is currently renewed interest in what has been termed the ‘colliding epidemics’ of HIV, tobacco smoking and TB.[1] Two recent studies from SA showed similar changes in the pre­ dominant tissue type of lung cancer to that observed in other parts of the world, with adenocarcinoma being the most common form.[2,3] Despite the very high background prevalence of HIV and smoking-related diseases in sub-Saharan Africa, and the fact the lung cancer has become the most common non-AIDS-defining cancer among HIV-positive individuals on antiretroviral (ARV) therapy, surprisingly little is known about the presentation of lung cancer in HIV-infected individuals in SA.[4] Therefore, our objective was to compare HIV-positive and HIV-negative lung cancer patients with regard to demographics, cell type, performance status and umour node metastasis (TNM) staging at initial presentation.

Methods

We prospectively identified all cases of primary lung cancer presen­ ted at our weekly combined multidisciplinary chest oncology meeting from August 2013 to September 2015. Tygerberg Hospital is a 1 380-bed tertiary facility in Cape Town, SA. It is one of two referral centres in the city and renders a tertiary service to a population of about 1.5 million, of whom 5.2% (95% confidence interval (CI) 3.4 - 7.8%) are currently HIVinfected. This is considerably lower than the national average of 12.2%.[5] We collected data on all patients with a known HIV status who had a tissue diagnosis of primary lung cancer and who underwent a staging computed tomography (CT) scan. Routine demographic and clinical data were collected, including the smoking status (to qualify as a smoker a patient had to have smoked at least 10 packyears per lifetime) and performance status according to the Eastern Cooperative Oncology Group (ECOG).

36

All patients were advised and counselled to undergo HIV testing, but the test was only performed on those who provided written informed consent. The CD4 count value recorded closest to time of lung cancer diagnosis was documented in all HIV-positive patients.

All patients had access to positron emission tomography-CT, bronchoscopy with endobronchial ultrasound, guided transbronchial needle aspiration with rapid onsite evaluation, transthoracic imageguided biopsy (ultrasound or CT) and related diagnostic techniques that were performed at the discretion of the treating physicians as per standard operating procedures. A combined panel of at least a pulmonologist, thoracic radiologist, thoracic surgeon, specialist onco­ logist and pathologist staged all patients as per the 2009 International Association for the Study of Lung Cancer TNM staging system.

Chi-square or Fisher’s exact tests (where indicated) were performed on dichotomous categorical variables, and t-testing on continuous data.

Results

During the 2-year period, 467 of 609 (76.7%) patients with lung cancer consented to an HIV test or were known to be HIVpositive at presentation. In total, 44 of 467 (9.4%) were HIV-positive (Table 1). The CD4 count of HIV-positive patients ranged from 9 to 790 cells/ mL (mean 385 cells/mL).

HIV-positive patients (mean age 54.1 (standard deviation (SD) 8.4) years) were younger than HIV-negative patients (60.5 (10.0) years, p<0.001), with no significant difference in gender distribution or smoking prevalence (Table 1). Overall, adenocarcinoma was the most frequent form of lung cancer (48.9%), followed by squamous cell carcinoma (29.7%). In HIV-positive patients, however, squamous cell carcinoma was more common than adenocarcinoma (43.2% v.

30.1%, p=0.07).

Fifty-five of the 532 patients (10.3%) with non-small-cell lung cancer (NSCLC) were staged as early stage disease (up to stage IIIA).

July 2016, Print edition

IN PRACTICE

Not a single HIV-positive patient had early stage lung cancer, compared with 38 of 369 confirmed HIV-negative patients with NSCLC (0% v. 10.3%, p=0.02).

HIV-positive patients were also more likely to have a poor performance status (ECOG 3 and 4) at presentation (47.7% v.

29.4%, p=0.02).

Discussion

In this prospective, observational study in patients with lung cancer, we found that HIV-positive patients were younger, more likely to have squamous cell carcinoma and significantly more likely to have a poor ECOG performance status of ≥3 at presentation. Moreover, in the case of NSCLC, they were significantly less likely to have early stage lung cancer at presentation when compared with HIV-negative patients.

Although lung cancer is currently the most common non-AIDS-defining cancer among HIV-positive individuals, the exact role of the virus in the pathogenesis of lung cancer remains uncertain.[4] It has been postulated that HIV may have a direct oncogenic role.[6] Some experimental data suggest that the HIV trans-activator of transcription (tat) gene product may modu­ late expression of growth-related genes. Other potential mechanisms include accelerated lung damage associated with HIV-related infections and an increase in susceptibility to tobacco carcinogens through genomic instability.[7] Sigel et al.[4] analysed data from large US registries to calculate incidence rates of lung cancer in order to determine incidence rate ratios (IRRs), adjusting for age, sex, race/ethnicity, smoking prevalence, previous bacterial pneumonia and chronic obstructive pulmonary disease. The inci­ dence rate of lung cancer in HIV-positive patients was 204 v. 119 cases per 100 000 person-years in uninfected patients, with an IRR of 1.7 (95% CI 1.5 - 1.9), arguably providing the strongest epidemiological evidence to date in favour of HIV infection being viewed as an independent risk factor for lung cancer.[4] In an earlier study, also performed on large US registries, Shiels et al.[7] found that the proportion of person-time contributed by older persons was far smaller in the AIDS population (1.5%) than in the general popu­ lation (12.5%). As a result, the ages at diagnosis for most types of cancer were ~20 years younger among persons with AIDS. However, after adjustment for differ­ ences in the populations at risk, the median ages at diagnosis in the AIDS and general populations did not differ for most types of

Table 1. Demographics, cell types, stage and performance status for all lung cancer patients (n=610) All (N=610)*

HIV-negative (n=425)

HIV-positive (n=44)

p-value†

Age (years), mean (SD)

59.9 (10.1)

60.5 (10.0)

54.1 (8.4)

<0.001

Gender (male), n (%)

372 (61.0)

252 (59.3)

29 (65.9)

0.42

Smokers, n (%)

557 (91.3)

389 (91.5)

40 (90.9)

1

CD4 count (cells/mm ), mean (SD)

-

-

385 (207)

-

AIDS, n (%)

9 (1.5)

0 (0)

9 (20.5)

-

Adenocarcinoma

298 (48.9)

210 (49.4)

17 (38.7)

0.21

Squamous cell carcinoma

181 (29.7)

128 (30.1)

19 (43.2)

0.07

Poorly differentiated

28 (4.6)

18 (4.2)

2 (4.5)

1

Other

25 (4.1)

13 (3.1)

2 (4.5)

0.64

78 (12.8)

56 (13.2)

4 (9.1)

0.64

I

7 (1.3)

6 (1.6)

0 (0)

II

15 (2.8)

9 (2.4)

0 (0)

IIIA

33 (6.2)

23 (6.2)

0 (0)

IIIB

115 (21.6)

85 (23)

8 (80)

IV

362 (59.3)

246 (66.7)

32 (20)

Limited

10 (12.8)

6 (10.7)

1 (25)

Extensive

68 (87.2)

50 (89.3)

3 (75)

0-2

411 (67.4)

300 (70.6)

23 (52.3)

3-4

199 (32.6)

125 (29.4)

21 (47.7)

Demographics

3

Cell type, n (%) NSCLC

SCLC Stage, n (%) NSCLC

0.02‡

SCLC -

ECOG performance status 0.02

SCLC = small-cell lung cancer. *HIV status was unknown in 141 patients. † HIV positive v. negative. ‡ Stages I-IIIA v. stages IIIB-IV NSCLC.

cancer, with the exceptions of lung (median 50 v. 54 years) and anal cancer (median 42 v. 45 years).[6] Although earlier reports have suggested that that a higher prevalence of smoking may be to blame for the increased incidence of lung cancer in HIV-positive individuals, there are currently very few data to support this.[4] We found no difference in smoking status between HIV-positive and negative participants.

We observed statistically significant and clinically relevant differences between HIV-​ positive and HIV-negative patients with regard to their performance status and stage at presentation. All patients with NSCLC presented with advanced cancer, and approximately half had a poor ECOG performance status of ≥3, suggesting that the

37

July 2016, Print edition

HIV infection adversely affected the prognosis of lung cancer.

Contrary to most published series, we observed a trend towards squamous cell carcinoma as the most common tissue type in HIV-positive patients. Unlike anal cancer, where an identifiable infection such as human papillomavirus is involved in carcinogenesis, no co-infective contributor has been identified in lung cancer, making this observation difficult to elucidate.[6] Our data also confirmed previous observations that the degree of immunosuppression (as judged by viral load or CD4 count) seems to have little or no impact on the risk for lung cancer.[4,6] A limitation of our study is the fact that we did not specifically document socio­ economic status, level of education and

IN PRACTICE

substance abuse, all of which may be viewed as potential confounders that may have influenced the perceived late presentation and poor prognosis of the HIV-positive cohort.

Conclusion

We found HIV-positive lung cancer patients were younger, significantly more likely to have a poor ECOG performance status of ≥3 at presentation and significantly less likely to have early stage lung cancer when compared with HIV-negative patients. The numbers of HIV-positive patients with lung cancer will most likely rise considerably over the next 2 decades owing to improved survival of patients on combination ARV therapy, resulting in an aging HIVpositive population with a relatively higher risk for lung cancer. This highlights the importance of further research on lung cancer in HIV, especially in the setting of ‘colliding epidemics’.

1. Van Zyl Smit RN, Pai M, Yew WW, et al. Global lung health: The colliding epidemics of tuberculosis, tobacco smoking, HIV and COPD. Eur Respir J 2010;35(1):27-33.

DOI:10.1183/09031936.00072909 2. Nanguzgambo AB, Aubeelack K, von Groote-Bidlingmaier F, et al. Radiologic features, staging, and operability of primary lung cancer in the Western Cape, South Africa: A 1-year retrospective study.

J Thorac Oncol 2011;6(2):343-350. DOI:10.1097/JTO.0b013e3181fd40ec 3. Koegelenberg CF, Aubeelack K, Nanguzgambo AB, et al. Adenocarcinoma the most common cell type in patients presenting with primary lung cancer in the Western Cape. S Afr Med J 2011;101(5):321.

DOI:10.7196/SAMJ.4554 4. Sigel K, Wisnivesky J, Gordon K, et al. HIV as an independent risk factor for incident lung cancer.

AIDS 2012;26(8):1017-1025. DOI:10.1097/QAD.0b013e328352d1ad 5. Shisana, O, Rehle, T, Simbayi LC, et al. South African National HIV Prevalence, Incidence and Behaviour Survey, 2012. Cape Town: Human Sciences Research Council Press, 2014. http://www.hsrc. ac.za/en/research-data/view/6871 (accessed 8 December 2015).

6. Kirk GD, Merlo CA, Lung HIV Study. HIV infection in the etiology of lung cancer: Confounding, causality, and consequences. Proc Am Thorac Soc 2011;8(3):326-332. DOI:10.1513/pats.201009-061WR 7. Shiels MS, Pfeiffer RM, Engels EA. Age at cancer diagnosis among persons with AIDS in the United States. Ann Intern Med 2010;153(7):452-460. DOI:10.7326/0003-4819-153-7-201010050-00008

Accepted 7 March 2016.

ISSUES IN PUBLIC HEALTH

Review of the 2015 Guidelines for Maternity Care with relevance to congenital disorders H L Malherbe,1 MSc; D L Woods,2 FRCP; C Aldous,1 PhD; A L Christianson,3 FRCP S chool of Clinical Medicine, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa School of Child and Adolescent Health, University of Cape Town, South Africa 3 Wits Centre for Ethics (WiCE), University of the Witwatersrand, Johannesburg, South Africa 1 2

Corresponding author: H L Malherbe (helen@hmconsult.co.za)

The 4th edition of the Guidelines for Maternal Care in South Africa published by the National Department of Health in 2015 was evaluated with relevance to the care and prevention of congenital disorders (CDs). Disparate terminology is used for CDs throughout the guidelines, and overall less detail is included on CDs compared with the previous edition. This demonstrates a lack of awareness around the growing health need and contribution of CDs to the disease burden in South Africa (SA). Referrals to medical genetic services in the guidelines for mothers of advanced maternal age and other high-risk categories do not take into account the insufficient capacity available for screening and diagnosis of CDs. This highlights the lack of consultation with the medical genetics sector during the development of the guidelines. To respond to the Sustainable Development Goals by 2030, CDs must be integrated comprehensively at all levels of healthcare in SA. S Afr Med J 2016;106(7):669-671. DOI:10.7196/SAMJ.2016.v106i7.10813

In 2015, the 4th edition of the Guidelines for Maternity Care in South Africa was published by the National Department of Health (NDoH). [1] A manual for clinics, community health centres and district hospitals, these replaced the previous 2007 edition.[2] The guidelines provide, among other things, a practical approach for primary healthcare to manage pregnancy, labour and delivery in South Africa (SA) with the ultimate aim of reducing maternal mortality (deaths during pregnancy or within 42 days of delivery).

With the maternal mortality ratio (MMR) estimated as having quadrupled in SA due to the HIV/AIDS epidemic, the need for such guidelines is clear.[3] At 154 maternal deaths per 100 000 live births in 2011 - 2013, the MMR was reduced to almost pre-HIV epidemic levels, but the Millennium Development Goal target of 38/100 000 live births was not achieved.[4,5] Sights are now set on the Sustainable Development Goal of a global MMR of less than 70/100 000 by 2030.[6] Owing to the inextricable link between mother and child, poor maternal health and maternal death are more likely to lead to death of the newborn.[7] With 40% of under-5 deaths occurring during the

38

neonatal period in SA, and 75% of these occurring as early neonatal deaths, the benefits of quality prenatal care for the child are obvious. [8] In SA, deaths in infants and children under-5 decreased rapidly between 2008 and 2011, with a more modest improvement in neonatal deaths from 2009 to 2011, after which all these rates stagnated.[9] Efforts to combat communicable diseases – including HIV/AIDS – continue, and interventions are underway such as those identified in the report by Chola et al.,[10] the childhood Expanded Program of Immunization, and improving social determinants of health; these will contribute to further reducing childhood deaths. However, for significant further reductions in childhood mortality and morbidity, including neonatal deaths, the contribution of congenital disorders (CDs) must be addressed.[11,12]

The growing burden of congenital disorders

Data from the Perinatal Problem Identification Program (PPIP) in 2014 indicated that congenital abnormalities have overtaken infection as the third leading cause of early neonatal deaths, after hypoxia and

July 2016, Print edition

IN PRACTICE

immaturity.[12,13] Since congenital abnormalities (obvious structural CDs identified at birth) are a sub-group of CDs, the true death toll from CDs is likely to be much higher. CDs, which are abnormalities of structure or function present from birth – although they may only manifest later in life[14] – are estimated to affect one in 15 live births in SA.[11] CDs have not been prioritised as a healthcare issue in SA, despite World Health Assembly Resolution 63.17 of 2010 recognising their contribution to neonatal deaths and calling member states to action.[11,15] The lack of accurate, empirical data has led to an underestimate of the true contribution of CDs to the burden of disease.[16,17] The purpose of this article is to evaluate the 2015 Guidelines on Maternity Care with relevance to the care and prevention of CDs. [1] Where appropriate, these will be compared with the previous edition of the guidelines within the current epidemiological context in SA.[1,2]

to CDs, whereas the 2007 edition consistently used the term ‘birth defects and genetic disorders’. [2] The internationally agreed term ‘congenital disorders’ itself is not used in the document, although the synonym ‘birth defects’ is used several times.[14] Unsupported by a glossary, the terms used include: congenital anomalies; congenital abnormality; congenital infection; chromosomal and congenital defect; abnormalities; structural and chromosomal fetal anomalies; birth defect; genetic or chromosomal defects; genetic disorder; genetic anomalies; genetic disease; familial and genetic disorder; fetal abnormalities; and fetal anomaly. Except for birth defects, these all refer to subsets of CDs, and some categories of CDs are excluded (personal communication, Bernadette Modell, November 2015).[14] This inconsistent use of disparate terms for CDs is of concern and causes confusion around this healthcare issue.

What is the aim of the Guidelines for Maternity Care?

Teratogens

Prepared by the National Maternity Guidelines Committee at the NDoH, the guidelines are for health workers (doctors and midwives) providing obstetric, surgical and anaesthetic services for pregnant women in primary healthcare facilities where specialist care is not normally available.[1] Clinics, community health centres and district hospitals are encouraged to use the guidelines to develop protocols tailored to their specific needs, for identifying, diagnosing and managing common and serious pregnancy and delivery problems. Both editions of the guidelines respond to report recommendations by the National Committee on the Confidential Enquiry into Maternal Deaths, with the overall aim to improve clinical management and referral to reduce pregnancyrelated deaths and ill health.[5] While the 2015 guidelines follow a similar format to that of the previous edition, they also include some new chapters and omit others. [1,2] Content of relevance to CDs is included in chapters 2: Levels of care; 4: Antenatal care; 9: Problems in pregnancy; 10: Management of intra-uterine deaths, stillborn babies and neonatal deaths; and 15: Basic ultrasound at district level and routine postnatal care.

Additional chapters in the 2015 edition do not include new content relevant to CDs; rather, the level of detail and quality of information on CDs has been decreased.

Confusion in terminology

The most notable difference in the 2015 edition is the use of 14 different terms to refer

In the 2015 edition, teratogens including alcohol, recreational drug use, maternal infections (rubella and syphilis), and the use of teratogenic medications during pregnancy are listed under ‘risks for genetic disease’. The risks associated with poorly controlled medical conditions are also listed, but diabetes mellitus is add­ ressed elsewhere in the guidelines and hypothyroidism and iodine deficiency are not mentioned. With teratogens accounting for almost 20% of CDs in SA and affecting 14 000 births annually, these need to be contextualised correctly, with greater emphasis placed on these preventable CDs.[11]

Surveillance

An exclusion from the 2015 guidelines is the regular compilation of data on the number of babies born with genetic disorders and major birth defects, as specified in the 2007 edition.

In contrast, the 2015 edition refers only to the recording of mortalities, and recommends

the PPIP format for data collation. This sole focus on deaths omits morbidity and the opportunity to provide vital data into national surveillance of CDs.

Other content relevant to CDs

The majority of content relevant to CDs is included in chapters 4: Antenatal care and 10: Management of intra-uterine deaths, stillborn babies and neonatal deaths. In chapter 4, the importance of history taking for familial and genetic disorders to assess risk factors at the first antenatal visit is emphasised, as is 5 mg of folic acid daily 3 months prior to and throughout pregnancy for the prevention of neural tube defects. A concise section entitled ‘Risk of genetic disease’ lists categories of women of childbearing age potentially at risk of having a child with a ‘birth defect or genetic disorder’, but includes non-genetic CDs. It recommends the provision of essential information to all pregnant women on specific topics including the avoidance of alcohol, tobacco and recreational drugs, the use of medication (self-care) and genetic disorders and birth defects relevant to newborn and infant care.

Capacity constraints in medical genetic services

In chapter 10: Management of intra-uterine deaths, stillborn babies and neonatal deaths, genetic counselling and relevant referral should be provided as part of postpartum care when CDs are suspected, prior to another pregnancy in case of reoccurrence. Steps outlined to obtain a diagnosis when a CD is suspected as the cause of death include undertaking a history and a basic external examination. When a diagnosis cannot be made, a postmortem or whole body X-ray/ digital photography for referral to a geneticist is recommended. This does not take into account the limited capacity available in SA due to there being only 12 practising medical geneticists, clustered around academic centres in urban areas (Table 1).[12]

Table 1. A comparison of medical genetics services capacity in 2001 and 2015[12] 2001

2015

Recommended (2003)[18]

Category

n (ratio) (N=46.13m)[19]

n[20]

Ratio (N=44.82m)[19]

n

Medical geneticists

20 (1 per 2m)

4

1 per 11.2m

12*

1 per 4.6m

Genetic counsellors

80 (1 per 580 000)

<20

1 per 2.2m

9†

1 per 6.1m

Medical scientists/ technologists

100 (1 per 450 000)

50

1 per 900 000

26‡

1 per 2.1m

Ratio (N=54.96m)[21]

*No medical geneticists are employed by the state in Gauteng. Personal communication, A Krause, 11 February 2016. † This figure increased to 9 in April 2016, plus 6 in private practice. Personal communication, T Wessels, 25 February 2016. ‡ NHLS academic medical scientists only. Personal communication, H Soodyall, 27 July 2015.

39

July 2016, Print edition

IN PRACTICE

Capacity in the medical genetic services sector is further underestimated in chapter 15: Basic ultrasound at the district level. While acknowledging that routine screening for structural and fetal anomalies is ‘not yet practical in the public sector’, all women of advanced maternal age (specified as over 37 years) are referred to a specialist health facility or a maternal fetal ultrasound unit. This includes referral to a genetics clinic where consenting women should be routinely offered a scan, genetic counselling and invasive testing to rule out Down syndrome. It does not specify that genetic counselling should be undertaken prior to the scan and repeated afterwards in the case of abnormal findings. Women with a previous history or family history of structural, chromosomal or genetic disorders are also referred to specialist hospitals for structural screening and management decision. Analysis of recorded live births in 2013 indicates that 84 260 births (8.5%) were to women over 37 years. [22] As outlined in Table 1, current capacity falls far short of recommended levels, with only 12 practising medical geneticists, fewer than 9 genetic counsellors and compromised laboratory services operating almost entirely from academic medical genetic departments countrywide.

This available capacity makes it impossible for this number of referrals of women of advanced maternal age to be implemented. Medical genetic services relating to the care and prevention of CDs are in a state of decline and at a lower base today than prior to the HIV/AIDS epidemic.[11,12]

Genetic counselling

In addition to referring high-risk women to regional and tertiary hospitals, genetic screen­ing and counselling services are specified as a function of district hospitals in chapter 2: Levels of care. A significant contribution to the care of newborns is undertaken by nurses in these low-resourced primary healthcare settings, particularly in rural areas. These nurses, and general medical officers, are in the main not equipped with genetic counselling skills, and the nurses who are trained are in short supply. SA is also experiencing a severe shortage of doctors, with only 60 per 100 000 population in 2013 compared with the global average of 152/100 000, and even fewer specialists (including medical geneticists).[23] This places a huge strain upon the system and medical practitioners are overworked and often unsupported. This general lack of capacity of healthcare professionals at all levels must be rectified before such an under-resourced system can respond to additional demands.

Conclusion

As management guidelines, the 2015 edition responds to the policy directive to reduce maternal mortality by offering principles from which detailed institutional protocols can be developed. However, the guidelines are not cognisant of the limited infrastructure, capacity and resources available in the medical genetic services sector. The lack of investment in medical genetic services, largely due to competing health priorities, make it impossible for referrals in the guidelines to be implemented.

Consultation with the medical genetics community during the development of the 2015 edition could have prevented this disjoint and would have benefited from the ongoing review of the 2001 Policy Guidelines for the Management and Prevention of Genetic Disorders, Birth Defects and Disabilities.[20] With SA once again in positive epidemiological transition, the proportion of neonatal, infant and child deaths from CDs will

40

continue to increase as the country develops and communicable diseases are better controlled.[11,12] Relevant, accessible and effective medical genetic services can prevent, cure and ameliorate CDs by up to 70% and may be the only way to significantly reduce child mortality further. [11,12,16,17,24] If SA is to respond to Sustainable Development Goal 3 to end preventable deaths in newborns and reduce premature mortality from non-communicable diseases by two-thirds by 2030, CDs must be addressed comprehensively and funding allocated to build capacity and infrastructure in the sector. [6,12] This response must permeate every level of implementation, to ensure no child is left behind.

Acknowledgements. Thanks to Prof. Eckhart Buchmann, National Maternity Guidelines Committee, for his feedback on the article.

1. National Department of Health, South Africa. Guidelines for Maternity Care in South Africa. A Manual for Clinics, Community Health Centres and District Hospitals. 4th ed. Pretoria: NDoH, 2015:172. http:// www.health.gov.za/index.php/2014-03-17-09-09-38/policies-and-guidelines/category/230-2015p# (accessed 15 June 2015).

2. National Department of Health, South Africa. Guidelines for Maternity Care in South Africa. A Manual for Clinics, Community Health Centres and District Hospitals. 3rd ed. Pretoria: NDoH, 2007:171.

3. Burton R. Maternal health: There is a cause for optimism. S Afr Med J. 2013;103(8):520-521.

DOI:10.7196/SAMJ.7237 4. United Nations. United Nations General Assembly, Resolution 55/2. United Nations Millennium Declaration, A/RES/55/2 18 September 2000. http://www.un.org/millennium/declaration/ares552e. htm (accessed 13 January 2016).

5. National Committee for Confidential Enquiry into Maternal Death. Saving Mothers 2011 - 2013: Sixth Report on the Confidential Enquiry into Maternal Deaths in South Africa. Short Report. Pretoria: NDoH, 2014:79.

6. United Nations. Sustainable Development Goal 3: Ensure Healthy Lives and Promote Wellbeing for All and at All Ages. http://www.un.org/sustainabledevelopment/health/ (accessed 1 February 2016).

7. Sines E, Tinker A, Ruben J. The Maternal–Newborn–Child Health Continuum of Care: A Collective Effort to Save Lives. Washington DC: Save the Children and Population Reference Bureau, 2006. http:// www.prb.org/pdf06/snl-contofcare_eng.pdf (accessed 20 January 2016).

8. Lloyd LG, de Witt TW. Neonatal mortality in South Africa: How are we doing and can we do better?

S Afr Med J 2013;103(8):518-519. DOI:10.7196/SAMJ.7200 9. Dorrington R, Bradshaw D, Laubscher, R, Nannan N. Rapid Mortality Surveillance Report 2014. Cape Town: South African Medical Research Council, 2015. http://www.mrc.ac.za/bod/ RapidMortalitySurveillanceReport2014.pdf (accessed 26 January 2016).

10. Chola L, Pillay Y, Barron P, Tugendhaft A, Kerber K, Hofman K. Cost and impact of scaling up interventions to save lives of mothers and children: Taking South Africa closer to MDGs 4 and 5. Glob Health Action 2015;8:27265. DOI:10.3402/gha.v8.27265 11. Malherbe HL, Christianson AL, 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 12. 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 2016, Chapter 12. 19th ed. Durban: Health Systems Trust, 2016:137-152.

13. Pattison R, Rhoda N. Saving Babies 2012 - 2013: Ninth Report on perinatal care in South Africa. Pretoria: Tshepesa Press, 2014:35. http://www.ppip.co.za/wp-content/uploads/Saving-Babies-2012-2013.pdf (accessed 1 October 2014).

14. World Health Organization, March of Dimes. Management of Birth Defects and Haemoglobin Disorders. Report of a Joint WHO-March of Dimes Meeting, Geneva, Switzerland, 17 - 19 May 2006. Geneva: World Health Organization, 2006. http://www.who.int/genomics/publications/WHOMODreport-final.pdf (accessed 10 May 2014).

15. World Health Assembly. Resolution 63.17. Birth Defects, WHA63.17 (21 May 2010). http://apps.who. int/gb/ebwha/pdf_files/WHA63/A63_R17-en.pdf (accessed 2 September 2014).

16. Christianson CL, Modell B. Medical genetics in developing countries. Annu Rev Genomics Hum Genet 2004;5:219-265. DOI:10.1146/annurev.genom.5.061903.175935 17. Christianson A, Howson CP, Modell B. March of Dimes: Global Report on Birth Defects, the Hidden Toll of Dying and Disabled Children. New York: March of Dimes Birth Defects Foundation, 2006:85.

18. National Department of Health, South Africa. Strategic Framework for the Modernisation of Tertiary Hospital Services. Discussion Document. Pretoria: NDoH, 2003:86.

19. Statistics South Africa. South African Statistics 2014. Pretoria: Statistics South Africa, 2014.

20. National Department of Health, South Africa. Policy Guidelines for the Management and Prevention of Genetic Disorders, Birth Defects and Disabilities. Pretoria: NDoH, 2001.

21. Statistics South Africa. Mid-year Population Estimates 2015. Pretoria: Statistics South Africa, 2015.

22. Statistics South Africa. Recorded Live Births 2013 (dataset). Pretoria: Statistics South Africa, 2015.

23. Econex. Identifying the determinants of and solutions to the shortage of doctors in South Africa: Is there a role for the private sector in medical education? Hospital Association of South Africa, 2015. http://econex.co.za/wp-content/uploads/2015/08/ECONEX_Doctor-shortages-and-training_FINAL1. pdf (accessed 1 Feb 2016).

24. Czeizel AE, Intôdy Z, Modell B. What proportion of congenital abnormalities can be prevented? BMJ 1993;306(6876):499-503.

Accepted 4 April 2016.

July 2016, Print edition

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ISSUES IN PUBLIC HEALTH

Ending preventable child deaths in South Africa: What role can ward-based outreach teams play?

T Doherty,1 MPH, PhD; M Kroon,2 MB ChB, FC (Paed); N Rhoda,3 MB ChB, FC (Paed); D Sanders,4 MB ChB, MRCP, DTPH ealth Systems Research Unit, South African Medical Research Council, Cape Town; and School of Public Health, University of the H Western Cape, Cape Town, South Africa 2 Department of Neonatology, University of Cape Town and Mowbray Maternity Hospital, Cape Town, South Africa 3 Department of Neonatology, University of Cape Town and Groote Schuur Hospital, Cape Town, South Africa 4 School of Public Health, University of the Western Cape; School of Child and Adolescent Health, Faculty of Health Sciences, University of Cape Town, South Africa 1

Corresponding author: T Doherty (tanya.doherty@mrc.ac.za)

South Africa (SA) has emerged from the Millennium Development Goal era with a mixture of success and failure. The successful national scale-up of prevention of mother-to-child transmission of HIV services with increasingly efficacious antiretroviral regimens has reduced the mother-to-child transmission rate dramatically; however, over the same period there appears to have been no progress in coverage of high-impact interventions for pneumonia and diarrhoea, which are now leading causes of under-5 mortality. SA embarked on a strategy to re-engineer the primary healthcare system in 2011, which included the creation of ward-based outreach teams consisting of community health workers (CHWs). In this article we argue that the proposed ratio of CHWs to population is too low for public health impact and that the role and scope of CHWs should be extended beyond giving of health information to include assessment and treatment of childhood illnesses (particularly diarrhoea and suspected pneumonia). Evidence and experience amply demonstrate that CHWs in sufficient density can have a rapid and positive impact on neonatal and young child mortality, especially when they are allowed to treat common acute conditions. SA’s mediocre performance in child survival could be dramatically improved if there were more CHWs who were allowed to do more.

S Afr Med J 2016;106(7):672-674. DOI:10.7196/SAMJ.2016.v106i7.10790

South Africa (SA) has emerged from the Millennium Development Goal (MDG) era with a mixture of success and failure. MDG4 aimed to reduce the under-5 mortality rate (U5MR) by two-thirds between 1990 and 2015. SA’s MDG baseline (1990) of 60 under-5 deaths per 1 000 live births meant a target of 20.[1] Estimates from rapid mortality surveillance placed the U5MR in 2014 at 39[2] (Fig. 1).

Much of this reduction has been due to the successful national scale-up of prevention of mother-to-child transmission (PMTCT) of HIV services with increasingly efficacious antiretroviral regimens reducing the mother-to-child transmission rate at 4 - 8 weeks of infant age to around 2.6%.[3] As a result, HIV/AIDS is no longer the leading cause of under-5 mortality – it has been surpassed by neonatal deaths (25%), gastroenteritis (15%) and suspected pneu­ monia (13%).[4] Although no current data are available, over the past few dec­ ades – including during the height of the HIV/AIDS epidemic – there appears to have been no progress in coverage of high-impact interventions for pneumonia and diarrhoea. The proportion of children <5 years old with symptoms of pneumonia taken to an appropriate healthcare provider declined from 75% in 1998 to 65% in 2003 (the most recent Demographic and Health Survey); similarly, coverage of oral rehydration solution (ORS) for children with diarrhoea declined from 51% in 1998 to 40% in 2003.[5] A recent review[6] of child deaths in two medicolegal mortuaries in Cape Town and Durban found that lower respiratory tract infections (LRTIs) and diarrhoea were the most common causes of sudden, unexpected natural deaths among children under-5 at both sites. Of the natural deaths, LRTIs accounted for 65% of infant deaths and 56% of 1 - 4-year-old deaths, respectively. Deaths due

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to diarrhoea accounted for 12% of infant and 26% of 1 - 4-yearold natural deaths, respectively. Importantly, the majority of these deaths occurred outside healthcare facilities. Almost half (44%) of the LRTI deaths were among infants born prematurely, with many of these deaths occurring soon after babies were discharged from hospital.

Furthermore, the study reported that 11% of the natural deaths were associated with possible health systems failures where a child was taken to a health facility within 48 hours of death and medical management was suspected to be lacking. This study highlights that even in the metropolitan areas of Durban and Cape Town, access to care is poor. The situation in other less well-resourced provinces is likely to be significantly worse.

As a strategy to complement facility-based integrated management of childhood illness (IMCI) and in conjunction with broader efforts to address the major causes of child mortality, integrated community case management (iCCM) was endorsed by the World Health Organization (WHO) and the United Nations Children’s Fund (UNICEF) in 2012 as an equity-focused strategy to train, supply and supervise community health workers (CHWs) to diagnose and treat diarrhoea, malaria and pneumonia among children aged 2 59 months in communities where access to health services is poor. [7] In some settings, the package of treatment services includes severe acute malnutrition and antibiotics for neonatal sepsis. The joint statement by the WHO and UNICEF was based on accumulated evidence of the effectiveness of CHWs in increasing uptake of highimpact child survival interventions,[8] reducing child mortality[9] and reducing both early and late neonatal mortality[10] through a package of community-based interventions including treatment. The

July 2016, Print edition

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NMR (VR)

IMR (VR)

U5MR (VR)

NMR (DHIS)

IMR (RMS)

U5MR (RMS)

IMR (direct)

NMR (direct VR)

NMR (direct DHIS)

90 80

Deaths per 1 000 live births, n

70 60 50 40 30 20 10 0 2000

2001

2002

2003

2004

2005

2006

2007

2008

2009

2010

2011

2012

2013

2014

Fig. 1. U5MR and infant mortality rate (IMR) from vital registration (VR) and rapid mortality surveillance (RMS) and neonatal mortality rate (NMR) from VR/DHIS (District Health Information System), 2000 - 2014 (after adjusting for incompleteness). Reproduced with permission from Dorrington et al.[2]

uptake of iCCM by national governments in Africa has been rapid, increasing from a total of 7 countries with iCCM policies in 2005 to 28 countries by 2013.[11] The scale-up of community-based delivery platforms, including treatment of the common causes of child deaths, has contributed to the achievement of MDG4 in several countries in Africa, including Malawi and Niger.[12,13] SA embarked on a strategy to re-engineer the primary healthcare (PHC) system in 2011, including the creation of ward-based out­reach teams (WBOTs), comprising approximately six CHWs supervised by one nurse.[14] According to national guidelines, each ward should have one or more PHC outreach teams serving a population of ~7 660 people (1 CHW to 1 276 people). Given the quadruple burden of disease in SA[15] and the important role of social determinants of health, this ratio of CHWs to population is unlikely to achieve the desired health improvements, and compares unfavourably with Brazil (1 CHW to 800 people) or Rwanda (1 CHW to 255 people).

A higher CHW-to-population ratio would increase the frequency of contact with community members and thus increase the potential impact on behaviour change and coverage of health interventions.

In Ethiopia, there is a two-tier community-based delivery platform with trained health extension workers (HEWs), who operate out of static health posts. They are supported by a volunteer cadre known as the health development army, who are mainly responsible for promoting essential family practices. [16] An evaluation of the nutrition support programme concluded that volunteers most likely contributed to a drop in stunting levels and underweight children and that the high ratio of volunteers to households (1 volunteer to 10 15 households and 10 volunteers to 1 full-time CHW) was central to this success.[17] The evaluation report noted that the support volunteers received from CHWs was key to their effectiveness. The ratio of volunteers to population is close to the volunteer-to-child

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population ratio of 1:10 – the WHO-recommended optimal density for effective preventive healthcare. [18] In SA, ~24% of children under 5 are moderately or severely stunted; a prevalence rate that has not shifted significantly over the past few decades.[5] Furthermore, SA has one of the lowest exclusive breastfeeding rates in Africa (8% in infants under 6 months of age). [19] There is evidence from lowand middle-income countries,[8] including SA,[20] of the impact of CHWs undertaking breastfeeding promotion and counselling on improving exclusive breastfeeding.

In addition to concerns over the low CHW-to-population ratio, the proposed role for CHWs in SA is extremely narrow, focusing primarily on counselling around prevention activities and adherence support. There are no curative functions included in their scope of work. We welcome the recent policy shift enabling CHWs in SA to administer biannual mebendazole and vitamin A to children aged 1 - 5 years in their catchment areas.[21] This is hopefully the first step towards an enlarged scope that should also include community-based support for premature babies in the critical few weeks following discharge and treatment of neonatal sepsis, diarrhoea, suspected pneumonia and acute malnutrition.

The high coverage of PMTCT services needs to be maintained; however, limited additional mortality reduction is likely unless the prevention and treatment of the current leading causes of child deaths – most notably pneumonia, diarrhoea and neonatal deaths – are tackled in an integrated manner, including increasing access to care through community-based delivery.

Evidence and experience amply demonstrate that CHWs in sufficient density can have a rapid and positive impact on neonatal and young child mortality, especially when allowed to treat common acute conditions. SA’s mediocre performance in child survival could be dramatically improved if there were more CHWs who were allowed to do more.

July 2016, Print edition

IN PRACTICE

1. United Nations Children’s Fund. Levels and Trends in Child Mortality: Report 2015. New York: UNICEF, 2015.

2. Dorrington R, Bradshaw D, Laubscher R, Nannan N. Rapid mortality surveillance report 2014. Cape Town: South African Medical Research Council, 2015.

3. Goga AE, Jackson DJ, Singh M, Lombard C, SAPMTCTE study group. Early (4 - 8 weeks post-delivery) Population-level Effectiveness of WHO PMTCT Option A, South Africa, 2012 - 2013. Pretoria: South African Medical Research Council and National Department of Health of South Africa, 2014.

4. National Department of Health, South Africa. 2nd Triennial Report of the Committee on Morbidity and Mortality in Children under 5 Years (CoMMiC): Triennium 2011 - 2013. Pretoria: NDoH, 2014.

5. United Nations Children’s Fund. Countdown to 2015 Maternal Newborn and Child Survival. A Decade of Tracking Progress for Maternal, Newborn and Child Survival: The 2015 Report. New York: UNICEF, 2015.

6. Mathews S, Martin L, Scott C, Coetzee D, Lake L. Every Child Counts: Lessons Learned from the South African Child Death Review Pilot. A Research Brief. Cape Town: Children’s Institute, University of Cape Town, 2015.

7. World Health Organization/United Nations Children’s Fund. Joint Statement Integrated Community Case Management. An Equity-focused Strategy to Improve Access to Essential Treatment Services for Children. New York: UNICEF, 2012.

8. Lewin S, Munabi-Babigumira S, Glenton C, et al. Lay health workers in primary and community health care for maternal and child health and the management of infectious diseases. Cochrane Database Syst Rev 2010;(3):CD004015. DOI:10.1002/14651858.CD004015.pub3 9. Sazawal S, Black RE. Effect of pneumonia case management on mortality in neonates, infants, and preschool children: A meta-analysis of community-based trials. Lancet Infect Dis 2003;3(9):547-56.

DOI:10.1016/s1473-3099(03)00737-0 10. Lassi ZS, Haider BA, Bhutta ZA. Community-based intervention packages for reducing maternal and neonatal morbidity and mortality and improving neonatal outcomes. Cochrane Database Syst Rev 2010;(11):CD007754. DOI:10.1002/14651858.CD007754.pub2 11. Rasanathan K, Muniz M, Bakshi S, et al. Community case management of childhood illness in subSaharan Africa – findings from a cross-sectional survey on policy and implementation. J Glob Health 2014;4(2):020401. DOI:10.7189/jogh.04.020401

12. Doherty T, Zembe W, Ngandu N, et al. Assessment of Malawi’s success in child mortality reduction through the lens of the Catalytic Initiative Integrated Health Systems Strengthening programme: Retrospective evaluation. J Glob Health 2015;5(2):020412.

13. Besada D, Kerber K, Leon N, et al. Niger’s child survival success, contributing factors and challenges to sustainability: A retrospective analysis. PloS One 2016;11(1):e0146945. DOI:10.1371/journal. pone.0146945 14. National Department of Health, South Africa. Provincial Guidelines for the Implemention of the Three Streams of PHC Re-engineering. Pretoria: NDoH, 2011.

15. Coovadia H, Jewkes R, Barron P, Sanders D, McIntyre D. The health and health system of South Africa: Historical roots of current public health challenges. Lancet 2009;374(9692):817-834. DOI:10.1016/ S0140-6736(09)60951-X 16. Leon N, Sanders D, van Damme W, et al. The role of ‘hidden’ community volunteers in communitybased health service delivery platforms: Examples from sub-Saharan Africa. Glob Health Action 2015;8:27214. DOI:10.3402/gha.v8.27214 17. White J, Mason J. Assessing the impact on child nutrition of the Ethiopia community-based nutrition programme. New Orleans: Tulane University, 2012.

18. World Health Organization. Essential Nutrition Actions: Improving maternal-newborn-infant and Young Child Health and Nutrition. Geneva: WHO, 2012.

19. National Department of Health, South Africa and Measure Demographic and Health Survey. South Africa Demographic and Health Survey 2003: Full report. Pretoria: NDoH, 2004.

20. Tomlinson M, Doherty T, Ijumba P, et al. Goodstart: A cluster randomised effectiveness trial of an integrated, community-based package for maternal and newborn care, with prevention of motherto-child transmission of HIV in a South African township. Trop Med Int Health 2014;19(3):256-266.

DOI:10.1111/tmi.12257 21. National Department of Health, South Africa. Circular Minute Number 3 of 2014. Pretoria: NDoH, 2014.

Accepted 22 March 2016.

HEALTHCARE DELIVERY

The Expanded Programme on Immunisation in South Africa: A story yet to be told N R Dlamini,1 BSc, MB ChB, MMed (Paed); P Maja,2 BA Hons Child, Youth and School Health: National Department of Health, Pretoria, South Africa Communication and Stakeholder Engagement: National Department of Health, Pretoria, South Africa

1 2

Corresponding author: P Maja (majap@health.gov.za)

During the past two decades, immunisation has saved millions of lives and prevented countless illnesses and disabilities in South Africa (SA). However, vaccine-preventable diseases are still a threat. A vaccine-preventable disease that might lead to a 1- or 2-week illness in an adult, could prove deadly for infants, children or elderly people. Vaccination protects oneself and one’s family. For example, adults are the most common source of pertussis (whooping cough) infection in infants, which can be deadly for the latter. This article demonstrates the commitment of the SA government to immunisation, highlights key milestones of the Expanded Programme on Immunisation (EPI) and dispels the myth that the EPI in SA is in shambles.

S Afr Med J 2016;106(7):675-677. DOI:10.7196/SAMJ.2016.v106i7.10956

Recently, the South African Medical Journal published an article entitled ‘Vaccines: SA’s immunisation programme debunked’.[1] The article extensively quotes someone who has resigned from the Department, and to give credence to the avalanche of negativity about the country’s Expanded Programme on Immunisation (EPI), the former employees of the Department are posted as the top National Department of Health (NDoH) EPI managers with substantial years of experience and, supposedly, expertise.

When a journalist publishes a story of the views of the former employees and does not seek the voice of those who are still serving, one will not be able to know whether what is reported is fact or sour grapes.

Good journalism is balanced journalism – giving the protagonists, so to speak, equal opportunity to tell their versions of the story.

The resignation of the two employees did not create a crisis for the EPI for two reasons: (i) the implementation of EPI is done

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at provincial level, and the NDoH’s responsibility is to develop policies and monitor their implementation; and (ii) the supervisors of these two former employees have years of experience, not only in immunisation but child health as a whole, which is more than just basic EPI. This is of paramount importance because integration is needed for efficiencies and cost-effectiveness in the delivery of health programmes. Their years of experience certainly contribute to institutional memory.

Staffing of the EPI unit at the national office has been priori­ tised. Posts were advertised following the resignation of the two employees, interviews have been conducted and the process of appointment is being finalised. Some of the incumbents have taken up the posts and others are still going through the process. All the posts will be filled, including that of the medi­ cal officer.

July 2016, Print edition

IN PRACTICE

Human resources for health

With the Sustainable Development Goals (SDGs), the global commu­ nity sees greater than ever consensus about the crucial role that the health workforce plays in realising goals to achieve universal health coverage. Qualified health workers, trained to work in effective teams within and across professional cadres to address the biomedical and social determinants of health, are critical to achieving health goals. While great progress has been made in maternal and child health and HIV/AIDS, continued shortages of adequately trained health workers raise the question of whether health professional education (HPE) systems are producing the health workforce needed to meet outstanding and emerging global health challenges.

There is recognition by the World Health Organization (WHO) and other health scientists across the world that the train­ing of health professionals does not meet the health needs of the 21st century.[2,3] Training of health professionals is based on outdated, fragmented, and content-oriented curricula that produce graduates with narrow contextual understanding and insufficient knowledge, skills, and competencies to understand social and other determinants of health and burden of disease. This outdated training has led to: poor teamwork and inadequate colla­boration within and across health professional cadres; episodic encounters with patient illnesses rather than continuous and holistic healthcare; a predominant hospital orientation at the expense of primary care; an imbalance between health workforces and health needs; and weak leadership in improving health system performance.[4] The achievement of the health-related objectives of the National Development Plan (NDP) and SDGs is contingent on a skilled, compet­ent, multiprofessional and interprofessional health workforce working synergistically to address the quadruple burden of disease.[5] The NDoH is working towards a health workforce that has the right skills, and works in the right place at the right time to provide the right services to the right people.[4] Above all, the Department is encouraging integrated teams that are comprised of team players.

Persons who elevate themselves beyond team work often find it difficult to fit into the new culture.

The effectiveness of the EPI in South Africa (SA)

Scientific literature on the effectiveness of EPI in SA is prolific and includes reports of studies done by independent researchers.[6-8] Madhi[9] has reported that in SA under-5 childhood deaths increased from 74 753 in 2000, peaked at 89 418 in 2005 and declined to 47 409 in 2013. He attributes this to the introduction of the EPI. Immunisation averts some 2.5 million premature deaths a year according to estimates and protects millions of children from illness and disability. Parents and children attending a clinic in SA are among those today who will reap the benefits of routine immunisation from the first days of life.[9] South Africa now has 11 antigens in the EPI schedule, including the most recently introduced human papillomavirus (HPV) vaccine for protection of young girls against cancer of the cervix that may affect them later in life. The immunisation programme has come a long way since it was launched in 1974, when there were only six vaccines in the schedule: diphtheria, pertussis and tetanus (DPT), measles, polio and Bacillus Calmette-Guérin (BCG) for protection against tuberculosis.[6] The EPI in SA has made significant achievements in the last few decades, including: • Polio has been eliminated in SA, with a last case found in 1989.

• Other conditions that are under control are diphtheria and pertussis, commonly known as whooping cough.

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• SA has been in the forefront of introducing new vaccines. In 1995 the country introduced hepatitis B (hep B) vaccine. In 1999 Haemophilus influenzae type b (Hib) vaccine was introduced. 2009 saw the introduction of pneumococcal vaccine (PCV) and rotavirus vaccine (RV), and most recently in 2014 HPV to prevent cervical cancer. On the continent, SA has been one of the first countries to introduce these vaccines – all fully funded by government. The programme continues to improve as evidenced by the fact that early in 2015 pentavalent vaccine was phased out and replaced by the more baby-friendly hexavalent so that the baby is only pricked once to receive six antigens.

When SA introduced the PCV and RV, the Department asked the National Institute for Communicable Diseases (NICD) to establish a surveillance system and to study the impact of these new vaccines on incidence of pneumonia and diarrhoea. The NICD reports that there has been a >40% reduction in pneumococcal diseases across all ages. The greatest decline is among children <2 years of age, the age group that carries the highest levels of the disease. In addition the NICD found that there was a 34% decline in pneumococcal disease in people ≥45 years old. Besides the impact of vaccine on pneumonia, the NICD reported that the vaccine has an effect on antimicrobial resistance – which is a global problem and if not urgently addressed can reduce the effectiveness of the antibiotics that are currently used.

The pneumococcus vaccine contributes to a significant decline in penicillin, ceftriaxone (Rocephin) and multidrug-resistant strains of pneumococcus.[7,10] Similar surveillance on the impact of the RV shows that the vaccine has resulted in a 40% reduction in the hospitalisation of children with diarrhoea (attributable to all causes) and 60% reduction in hospitalisations from diarrhoea that is caused by rotavirus.

In 2014 the Department of Health introduced the HPV for all girls in grade 4 who are ≥9 years old. The HPV vaccine protects from cancer of the cervix when they are older women. It is known that cancer of the cervix is the most common cancer among women in SA and predominantly affects black women, at an increasingly younger age. Cancer of the cervix has debilitating complications and often severely compromises the quality of life of those affected before they eventually succumb to it. It is estimated that 6 000 women a year in SA contract cervical cancer and about half of them die from the disease.

SA was the first country on the African continent to introduce the two new vaccines. PCV has now been introduced in other countries in Africa such as Kenya and Rwanda that are supported by the Global Alliance for Vaccines and Immunisation (GAVI).

SA remains the only country in the WHO Africa region that selffinances vaccines.[9] The introduction of PCV and RV is a significant public health milestone for the country and the continent. Furthermore, it points to the leadership role that SA has taken on the continent with the introduction of new and underutilised vaccines, dating back to 1995 with the introduction of hep B and, in 1999, Hib vaccines.

Sound decision-making process

Given the complexity of the introduction of new vaccines and that such decisions relate to an important public health programme, it is crucial that these decisions which establish immunisation policies are well informed, unbiased, evidence based and locally relevant. This has been the basis of the formation of national immunisation technical advisory groups (NITAGs) in many countries, particularly in developed countries where these groups are well established. SA has a functional NITAG, referred to as the National Advisory Group on Immunisation (NAGI). NAGI is

July 2016, Print edition

IN PRACTICE

effective as a source of information and an advisory body to the NDoH. This is evidenced by its major role in the introduction of PCV and RV into the EPI.[8] When there is an intention to add vaccines to the EPI, several factors need to be taken into consideration. These include the burden and significance of the disease within the country, whether there is a safe and effective vaccine available, what the cost-benefit of the vaccine would be and whether the country could afford to implement it, and finally, whether the vaccine could be incorporated practically into the national EPI programme.

Political stewardship

Political leadership in the public health sector became more pro­ nounced in April 2008 when there was a spike in child deaths in the rural Ukhahlamba District (currently Joe Gqabi) of the Eastern Cape Province, with 70% of 140 deaths reportedly due to gastroenteritis, pneumonia and malnutrition. Rather than any specific disease outbreak, the deaths were mainly attributable to weaknesses in the health system.

Widespread media coverage prompted the Ministry of Health to travel to the Ukhahlamba District to attend to the crisis and offer support. Propelled by the Ukhahlamba deaths, public concern and advocacy efforts to get government to financially and politically commit to the introduction of the vaccines, the Health Minister announced to the 61st World Health Assembly in May 2008 in Geneva, that the vaccines against pneumococcal and rotavirus disease would be introduced within 3 months. Instead of a 2-year lead in, the plan had to be fast-tracked to meet the deadlines, and this had huge financial and programmatic implications as both vaccines would be introduced sooner and simultaneously with the new pentavalent vaccine.

To this day, political commitment is steadfast in all priority programmes.

Programme performance

The programme indicators are routinely monitored using District Health Information Software (DHIS), whereby the denominators are the Statistics South Africa (StatsSA) mid-year estimates. The denominators for the HPV vaccine are obtained from the Department of Basic Education.

Currently the country has embarked on the Demographic and Health Survey, which will provide immunisation coverage data as one of its deliverables.

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Milestones in EPI in SA

Several milestones have been reached in the history of the EPI in SA: • 1995: hep B vaccine was introduced • 1999: Hib vaccine was introduced • 2000: converted from percutaneous to intradermal route for BCG vaccine • 2002: neonatal tetanus was eliminated • 2006: SA was declared polio-free; last reported case was in 1989 • 2008: CPV and RV vaccines were introduced • 2009: SA first African country and middle-income country to introduce PCV into public immunisation programme, in April (USD20 per dose = ZAR600 million annually)[9] • 2009: SA first African country to introduce RV vaccine into public immunisation programme, in August (USD7.5 per dose = ZAR150 million annually)[9] • 2009: SA switched from whole-cell pertussis vaccine to acellular pertussis vaccine with the introduction of the pentavalent vaccine (5-in-1) • 2015: SA became the first country in Africa to introduce a fully liquid hexavalent vaccine (6-in-1) by replacing the pentavalent (5-in-1) and hep B vaccines.[9] The EPI is a priority programme of government. It is not going to die because one or two of its officials have resigned from the national office.

1. Bateman C. Vaccines: SA’s immunisation programme debunked. S Afr Med J 2016;106(4):318-319.

DOI:10.7196/SAMJ.2016.v106i4.10765 2. World Health Organization. Maximising Positive Synergies Collaborative Group: An assessment of interactions between global health initiatives and country health systems. Lancet 2009;373:2137-2169.

3. Cailhol J, Craveiro I, Madede T, et al. Analysis of human resources for health strategies and policies in 5 countries in sub-Saharan Africa, in response to GFATM and PEPFAR-funded HIV-activities.

Globalization Health 2013;9:52.

4. Frenk J, Chen L, Bhutta ZA, et al. Health professionals for a new century: Transforming education to strengthen health systems in an interdependent world. Lancet 2010;376:1923-1958.

5. Essack S. Human Resources for Health – Challenges and Solutions. Public Health Association of South Africa, 2013. https://www.phasa.org.za/human-resources-for-health-challenges-and-solutions/ (accessed 4 May 2016).

6. Human Resources for Health South Africa: HRH Strategy 2012 to 2017. Pretoria: National Department of Health, 2012.

7. Schoub BD, Mphahlele MJ, Ngcobo NJ, Hoosen AA, Meheus A. Introducing new vaccines into the South African national immunisation programme – a case study. Vaccine 2012;30(Suppl 3):C1-C2.

DOI:10.1016/j.vaccine.2012.06.094 8. Baker L. The face of South Africa’s Expanded Programme on Immunisation (EPI) schedule. SA Pharmaceutical Journal 2010;Jan/Feb:18-21.

9. Madhi SA. From Vaccine Clinical Trials to Realising Public Health Benefit in South Africa.

Presentation to Vaccinology Scientific Congress, National Institute of Communicable Diseases (NICD), Johannesburg, 19 - 20 October 2015.

10. Von Gottberg A, de Gouveia L, Tempia S, et al. Effects of vaccination on invasive pneumococcal disease in South Africa. N Engl J Med 2014;371:1889-1899. DOI:10.1056/NEJMoa1401914

Accepted 26 April 2016.

July 2016, Print edition

IN PRACTICE

MEDICINE AND THE LAW

Social justice and research using human biological material: A response to Mahomed, Nöthling-Slabbert and Pepper D W Jordaan, PhD Department of Jurisprudence, College of Law, University of South Africa Corresponding author: D W Jordaan (mail@donrichjordaan.law.za)

Social justice in the context of research using human biological material is an important contemporary legal-ethical issue. A question at the heart of this issue is the following: Is it fair to expect a research participant (a person who participates in such research by, among others, making available biological material from his or her body) to participate on an altruistic basis, while the researchers and the investors in the research can gain commercially from the research? In a recent article, Mahomed, Nöthling-Slabbert and Pepper proposed that research participants should be entitled to share in the profits emanating from such research via a proposed new statutory right to the intellectual property emanating from such research. In order to stimulate debate on this important issue of social justice, this article responds to the position of Mahomed et al. by focusing on two main points: Firstly, I contend that Mahomed et al. fail to make a convincing argument in favour of shifting away from altruism; secondly, I caution against framing the debate in terms of the binary poles of altruism v. profitsharing, and suggest that should healthcare public policy ever move away from altruism, various non-monetary forms of benefit-sharing by research participants should be considered.

S Afr Med J 2016;106(7):678-680. DOI:10.7196/SAMJ.2016.v106i7.10552

The broad theme of this article is social justice in the context of commercial medical research that uses human biological material, such as blood samples or other tissue samples that may have been removed during a medical procedure on a patient. Within this broad theme, the following question is germane: Is it fair that the researchers and the investors in the research can commercially gain from the research, while the research participants – persons who participate in such medical research by, among others, making available biological material from their bodies – are expected to do so altruistically?

Current healthcare public policy answers this question in the affirmative: In March 2012, the South African (SA) Minister of Health made the Regulations Relating to the Use of Human Biological Material[1] in terms of the National Health Act.[2] These Regulations deal with the use of human biological material for research purposes, and provide that a person from whose body human biological material is withdrawn for research purposes may only be reimbursed for reasonable expenses incurred by him or her.[1,reg11] Accordingly, our law as it currently stands upholds an altruistic paradigm for participation in research and effectively outlaws any form of remuneration of the research participant over and above reimbursement for reasonable expenses.

In a recent article, Mahomed et al.[3] explore the subject of commercial medical research that uses human biological material, and take an opposing position to the current healthcare public policy of altruism, suggesting that research participants should be entitled to share in the profits emanating from the research to which they contributed. As a vehicle for such entitlement, Mahomed et al. propose that research participants should have a statutory right regarding the information generated from research to which they contributed; therefore, in effect a new type of intellectual property right.

In an open society, which SA aspires to be, no aspect of public policy should be sacrosanct and beyond critical, rational analysis. As such, the

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challenge to the current altruistic paradigm by Mahomed et al. should be welcomed. Moreover, I suggest that the issue of social justice in the context of commercial medical research that uses human biological material is an important legal-ethical issue in contemporary society, and deserves more critical analysis. To stimulate academic dis­course on this issue, this article briefly responds to the article by Mahomed et al. This article is not intended to provide arguments for or against current healthcare public policy, but is intended to highlight the weaknesses in the challenge to current healthcare public policy mounted

by Mahomed et al. In particular, I contend that the position regarding (non-)ownership of human biological material is not as vague as suggested by Mahomed et al., but is in fact well established. I subsequently highlight that the only purported support that Mahomed et al. proffer for their proposed shift away from altruism in fact lends no support to such proposed shift. Lastly, accepting for the sake of argument that healthcare public policy may move away from altruism, I point out that profit-sharing as proposed by Mahomed et al. is not the only alternative to altruism, and suggest that other forms of community-based benefitsharing may be more appropriate alternatives.

A note on terminology

Mahomed et al. employ the terms ‘human tissue’ and ‘tissue donors’.

Instead of these terms, I use ‘human biological material’ and ‘research participant’. My reasons are as follows: The Regulations Relating to the Use of Human Biological Mater­ial[1, reg1] define ‘biological material’ as: ‘material from a human being including DNA, RNA, blastomeres, polar bodies, cultured cells, embryos, gametes, progenitor stem cells, small tissue biopsies and growth factors from the same.’

I suggest that ‘human biological material’ is therefore a more suitable term than ‘human tissue’ in the context of research using human biological material.

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The Regulations Relating to the Use of Human Biological Material[1] employ the term ‘donor’. However, given that ‘donor’ has a legaltechnical meaning that implies ownership, I suggest that this term may as such cause confusion. I rather employ the term ‘research participant’. The term ‘research participant’ is defined by the Department of Health[4,p59] as follows: ‘A living individual (or group of living individuals) about whom a researcher conducting research obtains data through intervention or interaction with the person or identifiable private information.’

The term is sufficiently wide to include – and therefore acknowledge – activities by the research participant that go beyond allowing biological material to be withdrawn from her or his body, such as regularly completing questionnaires for the research, participating in the planning and conducting of the research project, and involvement in patient advocacy groups that may play an oversight role regarding the research.

The issue of ownership of human biological material

Mahomed et al. suggest that there are no firm ‘rules’ regarding ownership of human biological material and, with reference to two landmark US cases, suggest that each situation will have to be determined on its own facts.[3,p18] It is against this background of purported legal uncertainty that Mahomed et al. propose the legislative intervention to create legal certainty in the form of a new statutory intellectual property right to ensure profit-sharing by research participants.

However, I differ from the position of Mahomed et al. that there are no firm ‘rules’ regarding ownership of human biological material for three reasons: Firstly, the common law position in SA is clear, namely that the human body is not a proper object of ownership: Grotius,[5] a leading Roman-Dutch law authority, defines property as all useful things excluding or external to humans (my translation of: ‘Zaken noemen wy hier al wat daer is buiten den mensch, den mensch eenichsints nut zijnde.’); this definition by Grotius must be read with the provision in the Corpus Iuris Civilis[6] (a codification of Roman Law) that no-one is to be regarded as the owner of his own limbs (my translation of: ‘quoniam dominus membrorum suorum nemo videtur’). As Mahomed et al. point out, this general common law rule has been changed through secondary legislation – the Regulations Relating to Artificial Fertilisation of Persons[7] – in the specific case of gametes and embryos in the context of artificial reproduction.

However, this exception created by these Regulations is specific to gametes and embryos in the context of artificial reproduction, and does not amount to general uncertainty regarding ownership of human biological material that calls for a case-by-case approach. In the absence of more legislation in this field, the courts will apply the rule that human biological material (except gametes and embryos in the context of artificial reproduction) cannot be owned.

Secondly, US case law must be contextualised and cannot simply be applied to the SA context. For instance, one of the US cases discussed

by Mahomed et al., Washington University v Catalona,[8] was decided in the jurisdiction of the state of Missouri, where – in contradistinction from SA – human biological material is a proper object of ownership.

In other words, in Missouri ownership of human biological material can contractually be transferred from a research participant as original owner to another person, such as a research institution, that will then become the new legal owner. Such a transaction would be a legal impossibility in SA (arguably with the possible exception of gametes and embryos in the context of artificial reproduction).

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Thirdly, I do not agree with the interpretation by Mahomed et al. of the other landmark US case that they discuss in their article, Moore v Regents of the University of California.[9] In particular, Mahomed et al. state that the California Supreme Court found that ‘an individual has a tangible property right in his or her own tissue.’[3,p18] This is incorrect. In Moore v Regents of the University of California, the research participant indeed argued that withdrawn human biological material should be legally perceived as a species of tangible personal property, but although a lower court accepted this argument, the majority of the California Supreme Court held the argument to be ‘problematic’.[9] The majority ruled that withdrawn human biological material is a legal object sui generis and that it cannot be assumed that the residual right to control the use of withdrawn human biological material amounts to ‘property’.[9] The statement by Mahomed et al. on this core issue is therefore the exact opposite of what was in fact decided by the California Supreme Court.

Accordingly, the position taken by Mahomed et al. that there are no firm ‘rules’ regarding ownership of human biological material in SA, and that each situation will have to be determined on its own facts, does not hold water. As I state above, the SA common law position is clear, and approximates to the position set out by the California Supreme Court in Moore v Regents of the University of California.

Profit-sharing by research participants

Mahomed et al. propose that the current altruistic paradigm be replaced by profit-sharing by research participants.[3,p19] The only purported support that Mahomed et al. proffer for such a major shift in healthcare public policy is a single article by Truog et al.[10] However, contrary to the statements by Mahomed et al. that they attribute to Truog et al., Truog et al. do not propose profit-sharing. In fact, Truog et al. conclude their article as follows: ‘While the intuition that tissue donors should be financially compensated for their donation is commendable, as a policy matter this approach is ethically and practically problematic.

Except in those situations where the tissue’s market value can be estimated beforehand, investigators should adopt a practice of accepting tissue donations only when patients have freely agreed to give the donation as a gift, without expectation of monetary compensation. However, the altruism of patients to donate tissue to medical research must be met by similar generosity on the part of investigators and institutions. This could be accomplished through legislative mandates that promote the sharing of research findings and products with other scientists, or by voluntary efforts of investigators and institutions to do the same.’ (My emphasis) Accordingly, the only purported support that Mahomed et al. proffer for their proposed shift away from the current altruistic paradigm, in fact lends no support to such proposed shift.

Profit-sharing as a species of benefit-sharing

Should society’s changing sense of social justice ever demand that research participants can no longer be expected to contribute biological material altruistically to commercial medical research, but are morally entitled to some benefit (beyond reimbursement for costs incurred), such benefit could take various forms, such as immediate payment, free products or healthcare services provided by the research organisation or its affiliates, or community-based benefits, such as building a new clinic or school. Mahomed et al. frame the benefit that they propose exclusively in monetary language and make it dependent on the eventual success of both the research and the commercialisation effort. (Mahomed et al. refer to the ‘distribution’

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and ‘apportionment’ of ‘proceeds’ and ‘profit’.[3,pp18-19]) The question should be posed as to whether this is the most appropriate form of benefit-sharing with research participants. Mahomed et al. do not provide a rationale for preferring their particular form of profitsharing over other forms of benefit-sharing. Should our country’s healthcare public policy ever move away from altruism and embrace benefit-sharing with research participants, there is a variety of benefit-sharing options available, and the proponent of one (or a certain combination) would have to put forward convincing reasons for favouring a specific one (or a specific combination) of benefitsharing options above the rest.

Conclusion

Truog et al. – on whom Mahomed et al. purportedly rely – are clearly of the opinion that although not without its practical challenges, social justice can in principle be served within the altruistic paradigm. If Truog et al. are wrong, and social justice demands a new paradigm of benefit-sharing by research participants, the following ramifications must be considered: If research participants are entitled to benefit directly from their contribution of human biological material, why not also organ donors and blood donors? Is there a moral difference between having a blood sample taken for purposes of medical research, and

having blood taken for purposes of blood transfusion; and if the answer is affirmative, does such moral difference warrant the right to a benefit in the former case but not the latter? These are just some of the ramifications that require consideration if one intends to mount a challenge to the current altruistic paradigm. In the absence of an exhaustive and convincing rationale for replacing the existing altruistic paradigm with a paradigm of benefitsharing by research participants, any discussion of benefits for research participants is driftwood in the legal-ethical ocean.

1. Regulations Relating to the Use of Human Biological Material GN R177/2012.

2. National Health Act, No. 61 of 2003.

3. Mahomed S, Nöthling-Slabbert M, Pepper MS. The legal position on the classification of human tissue in South Africa: Can tissues be owned? S Afr J BL 2013;6(1):16-20. DOI:10.7196/SAJBL.258 4. National Department of Health, South Africa. Ethics in Health Research: Principles, Structures, and Processes. Pretoria: DoH, 2004.

5. Grotius. Inleidinge tot de Hollandsche Rechts-Geleerdheid. 2.1.3.

6. Digesta 9.2.13 pr.

7. Regulations Relating to Artificial Fertilisation of Persons GN R175/2012.

8. Washington University v Catalona 490 F 3d 667 - Court of Appeals, 8th Circuit 2007.

9. Moore v Regents of the University of California 51 Cal. 3d 120; 271 Cal. Rptr. 146; 793 P.2d 479, 15 U.S.P.Q.2d 1753 (1990).

10. Truog RD, Kesselheim AS, Joffe S. Paying tissue donors: The legacy of Henrietta Lacks. Science 2012;337(6090):37-38. DOI:10.1126/science.1216888

Accepted 11 May 2016.

MEDICINE AND THE LAW

Public health officials and MECs should be held liable for harm caused to patients through incompetence, indifference, maladministration or negligence regarding the availability of hospital equipment 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)

There have been several reports of state hospitals not having functional equipment such as radiological equipment. Where these are due to incompetence, indifference, maladministration or negligence by the public officials concerned, they may be held personally liable for the resulting harm to patients. However, the courts have often observed that where the State has been sued vicariously for the wrongs of public officials, it has not obtained reimbursement from the offending official. It has therefore been suggested that irresponsible public servants should be sued in their personal capacity (in addition to the State), to prevent taxpayers always having to pay for their misdeeds. If an individual public official cannot afford to pay all the damages awarded, the injured party can recover the balance from the State by citing it as a vicarious joint wrongdoer.

S Afr Med J 2016;106(7):681-683. DOI:10.7196/SAMJ.2016.v106i7.10722

Shortages of radiology equipment machines in the South African (SA) public health sector, resulting in harm to patients, have been reported, which undermines the public’s confidence in the public sector health facilities and its ability to host a national health insurance scheme.

In Gauteng Province in 2014, a broken X-ray machine at the country’s largest hospital resulted in ‘many botched operations in the orthopaedics department’.[1] Furthermore, a broken computed

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tomography (CT) scanner – one of two that could not be repaired because previous repair bills had not been paid – resulted in urgent cases not being attended to because there were too many patients for one scanner.[1] In KwaZulu-Natal Province in 2015, in several hospitals vital CT scanner machines were not serviced, had broken down or had not been acquired.[2] The problems began in 2011 at the province’s

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premier hospital, but were not addressed. The ‘waiting time for a CT scan for inpatients increased from the usual 24 - 48 hours to an unacceptable 5 - 10 days’, while outpatients had to wait for 4.5 months. The situation was ‘catastrophic for patients whose health depended on early detection of disease through CT scans’.[2] Similar problems occurred at other hospitals across the province. There were no service contracts for broken machines, CT scanners broke down regularly and promises to replace them had come to nothing.[2] In the Western Cape Province in 2016, ‘a shortage of radiologists and radiological equipment was negatively affecting the quality of healthcare services in the public sector’.[3] The public sector was ‘chronically understaffed and under-equipped [and] … Old CT scanners in provincial public hospitals – which performed nearly four times as many scans a year per machine as in the private sector – took longer to operate than the new multi-detector machines in the private sector which could scan a patient in 30 seconds’.[3] It must be considered whether, if the harm caused to patients is the result of incompetence, indifference, maladministration or negligence by hospital administrators and/or provincial authorities, they should be held personally liable to compensate such patients, or whether the relevant Department of Health (i.e. the taxpayers) should pay compensation. The answer will depend on whether: (i) public servants have immunity against being personally sued for harm caused through incompetence, indifference, maladministration or negligence; (ii) vicarious liability by the State excuses public officials from personal liability; and (iii) the courts are prepared to impose personal liability on public servants acting in the course and scope of their employment.

Do public servants have immunity from being sued personally?

Public officials in SA who are incompetent, indifferent or negligent, and who cause harm to others, have no immunity. They can be held personally liable provided that the injured person can prove that their conduct was either negligent or intentional. Where several public officials have caused the harm, all of them may be held personally liable.[4]

Negligent conduct

Incompetence and maladministration are often the result of negligence. Negligent conduct means that a reasonable person in the position of the wrongdoer ought to have foreseen the likelihood of harm and would have taken steps to guard against it.[5] For example, where hospital managers ought reasonably to foresee that patients will be harmed if they do not have working radiological equipment and do not take reasonable steps to prevent such harm by ensuring that broken machines are fixed or replaced, they may be held personally liable for harm caused to patients. The State may also be held vicariously liable for their misconduct.[6] In such situations healthcare managers could be held liable for negligently failing to arrange for the repair or replacement of medical equipment – unless they have to rely on the relevant department of health official or member of the executive committee (MEC) for health to procure the items. In the latter case, the public health official or MEC would be liable if they ought to have foreseen that a failure to fix or replace defective equipment would harm patients, and there are sufficient resources to purchase them.

If, however, available resources have been negligently wasted or squandered through incompetence or maladministration, the responsible public officials may also be held personally liable for the foreseeable harm caused to patients. Public officials who negligently harm patients may be sued for damages such as loss of income,

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medical expenses, pain and suffering, reduced life expectancy and loss of support for dependents of patients.[6]

Intentional misconduct

Intentional misconduct may occur where as a result of indifference persons deliberately refrain from acting because they do not care, or intentionally engage in malpractice which harms patients, and when their will is directed to do or not to do things which they know are unlawful.[6] For example, where hospital managers, public officials or MECs for health are informed of the likely harm to patients should radiological equipment not be repaired or replaced and they fail to rectify the situation – despite having available resources – they may be held personally liable for harm caused to patients.[6] Liability depends on who has the authority to enter into the procurement arrangements, whether they wilfully refrained from doing so, or knowingly enter into procurement arrangements with inadequately qualified persons.

If hospital managers, public health officials and MECs responsible for health have intentionally depleted resources allocated for repairs to, or replacement of, medical equipment through wasteful expenditure, they too may be held liable for the resultant harm suffered by patients.

Public officials who intentionally harm patients will be liable for damages that can be measured in monetary terms and ‘sentimental’ damages (i.e. damages for hurt feelings).[6]

Misconduct by more than one public official

If several public officials (e.g. the public hospital manager, procurement officer and chief executive officer of the relevant department of health) are found personally liable for harming a patient, the damages may be apportioned among them and each will be liable for a proportion of the damages to the patient.[4] The courts usually hold joint wrongdoers ‘jointly and severally liable’ which means that any one of them can be made to pay all the compensation, and the person paying may then claim a contribution from the others in proportion to their fault.[4] If a public health official who is held personally liable by the court cannot afford to compensate the harmed patient in full, the patient may always cite the relevant provincial MEC for health or Minister of Health as a joint wrongdoer vicariously liable to pay the balance. The parties will be ‘jointly and severally liable’ but the court may order each to pay a proportion of the damages.[7]

Vicarious liability

In common law vicarious liability refers to situations where one person is liable for another’s unlawful conduct irrespective of fault by the first person.[8] Vicarious liability usually refers to the employeremployee relationship. An employer will be held liable for the harmful negligent or intentional wrongful acts or omissions of their employees if: (i) there was an employer-employee relationship; (ii) the employee committed an unlawful act or omission; and (iii) the employees acted in the course and scope of their employment, even if this was in an improper way.[8] These principles apply to the public and private sectors.[6] The State is in the same position as private employers, and the State Liability Act provides that the State is vicariously liable for the wrongful acts or omissions of State employees.[9] Thus the MECs for health and provincial Departments of Health may be held vicariously liable for the wrongful acts of their employees committed within the course and scope of their employment,[10] even if they intentionally failed to carry out or obey instructions.

It has been said that where there is a shortage of resources, a Health Department or hospital cannot be expected to exercise a standard of care that is beyond its financial resources.[11] However, where the

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shortage has arisen because of intentional or negligent harmful acts or omissions by public health officials or hospital management, patients would have a valid claim against them for any harm suffered. The State would be vicariously liable for such conduct by the public health officials or hospital administrators. However, even where the State is vicariously liable for the conduct of its public officials, the latter may still be held personally liable.[12] Such public officials may be personally sued, or may be cited as joint wrongdoers together with the State. Where the State has been held vicariously liable for the conduct of such public officials, the latter may be required to reimburse the State for any damages paid out to injured or harmed patients.

Are the courts prepared to impose personal liability on public servants?

The courts have realised that shaming of public officials ‘no longer works’, and that ‘[e]ven the strongest exhortation of our highest courts’ for public officials to be held accountable has fallen ‘on deaf ears’.[13] It has been suggested that: ‘Individual public responsibility, in contrast to nominal responsibility, could be enhanced by forcing individual public officials to explain and account for their own actions, as parties to the litigation.’[14] The individual responsibility of public servants could be improved if they were sued in their personal capacity in addition to the State’s being sued vicariously. Several cases have made public servants personally liable for wasted costs incurred in indefensible matters,[13] but the same principles apply to holding them personally liable for harming patients.

In deciding whether or not to impose personal liability on public servants acting in the course and scope of their employment, the courts have recognised that ‘to err is human’, but ‘indifference’, ‘incompetence’ and ‘not caring’ have been sanctioned by the courts, for instance by awarding costs against public officials in their personal capacity. The courts have observed that ‘[T]he public should not have to suffer this complete indifference and incompetence at the hands of public servants.’[15] The State is bound to ‘respect, protect, promote and fulfil the rights in the Bill of Rights’.[16] The State must act so that their fundamental

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rights are realised and the Constitution requires constitutional obligations to ‘be performed diligently and without delay’.[17] ‘[I] ncompetence undermines the Constitution and with it the social contract underlying it … If personal accountability among public officials does not come naturally it must be inculcated. Somehow these officials must be taught that their actions (or lack thereof) have consequences’.[18] The courts have observed further that ‘the taxpayer also has an interest in these matters, as public funds are at risk in matters where damages against the Minister are claimed’.[19] MECs of provinces have been held individually liable where they have been personally involved in decisions and have also been held vicariously liable in their representative capacity for the wrongs of their employees.[10] 1. Green A. Broken machines and shortages vex Baragwanath Hospital. Mail and Guardian. 3 January 2014. http://mg.co.za/article/2014-01-02-broken-machines-and-shortages-vex-baragwanath-hospital (accessed 18 February 2016).

2. Attwood V. CT scanner shortage puts lives at risk. Sunday Tribune. 21 June 2015. http://www.iol.co.za/ news/south-africa/kwazulu-natal/ct-scanner-shortage-puts-lives-at-risk-1874242 (accessed 18 Feb­ ruary 2016).

3. Staff writer. Shortage has a negative effect on health care. Independent Online. 18 February 2016. http://www.iol.co.za/news/south-africa/shortage-has-negative-effect-on-health-care-294075 (accessed 18 February 2016).

4. Apportionment of Damages Act No. 34 of 1956, Sections 1(1)(a) and 2(13). www.saflii.org/za/legis/ consol_act/aoda1956/246.pdf (accessed 18 February 2016).

5. Cf. Kruger v Coetzee 1966 (2) SA 428 (A).

6. McQuoid-Mason D. Practising medicine in a resource-starved environment: Who is liable for harm caused to patients – the health care administrators or the clinicians? S Afr Med J 2010;100(9):573575.

7. Lushaba v MEC for Health, Gauteng 2015 (3) SA 616 (GJ) para 102.

8. Minister of Police v Rabie 1986 (1) SA 117 (A).

9. State Liability Act 20 of 1957, Section 1. www.justice.gov.za/legislation/acts/1957-020.pdf (accessed 26 February 2016).

10. South African Liquor Traders’ Association v Chairperson, Gauteng Liquor Board 2009 (1) SA 565 (CC) paras 47, 49.

11. Cf. Collins v Administrator, Cape 1995 (4) SA 73 (C).

12. Cf. Feldman (Pty) Ltd. v Mall 1945 AD 733.

13. Lushaba v MEC for Health, Gauteng 2015 (3) SA 616 (GJ) para 90.

14. Kate v MEC for Department of Welfare, Eastern Cape 2005 (10) SA 141 (SE) para 11.

15. Lushaba v MEC for Health, Gauteng 2015 (3) SA 616 (GJ) paras 70, 71.

16. Constitution of the Republic of South Africa 1996, Section 7(2).

17. Mlatsheni v The Road Accident Fund 2009 (2) SA 401 (E) para 14.

18. Lushaba v MEC for Health, Gauteng 2015 (3) SA 616 (GJ) para 88.

19. The Minister of Safety and Security v G45 International UK Ltd. Case 07/12735 South Gauteng High Court, para 14. www.saflii.org/za/cases/ZAGPPH/2015/844.pdf (accessed 26 February 2016).

Accepted 11 March 2016.

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CASE REPORT

Burkitt’s lymphoma patients in Northwest Cameroon have a lower incidence of sickle cell trait (Hb AS) than healthy controls P B Hesseling,1 MD; D T Jam,2 MD; D D Palmer,2 MD; P Wharin,3 MD; G S Tuh,2 Dip Tech; R Bardin,2 MD; M Kidd,4 PhD epartment of Paediatrics and Child Health, Tygerberg Children’s Hospital, Stellenbosch University, Cape Town, South Africa D Mbingo Baptist Hospital, Mbingo, Northwest region, Cameroon 3 Beryl Thyer Memorial Africa Trust, Warkton, UK 4 Department of Biostatistics, Stellenbosch University, Cape Town, South Africa 1 2

Corresponding author: P B Hesseling (pbh@sun.ac.za)

Contradictory findings have been reported from Africa with regard to the risk of developing Burkitt’s lymphoma (BL) in sickle cell trait (AS) carriers. Haemoglobin electrophoresis was performed in 78 BL patients in the Northwest region of Cameroon, and in 78 nearest-neighbour controls of the same age, sex and tribe from the same village. AS was confirmed in 4 of 78 (5.13%) BL patients and in 11 of 78 (14.10%) controls (χ2, p=0.052; Fisher’s exact, one-tailed, p=0.050). Sickle cell trait carriers had a marginal statistically reduced risk of developing BL. S Afr Med J 2016;106(7):686. DOI:10.7196/SAMJ.2016.v106i7.10693

Burkitt’s lymphoma (BL), the most common childhood cancer in sub-Saharan Africa, occurs mainly in areas with holo-endemic malaria.[1] Young children with haemoglobin (Hb) AS (sickle cell trait) are largely protected against severe Plasmodium falciparum mala­ ria.[2} The prevalence of AS in the Northwest region of Cameroon, a holo-endemic malaria area, is between 10% and 30%.[2] The annual incidence of BL between 2003 and 2010 was 2.58/100 000 children <15 years of age, and the monthly average of malaria cases was 10 938 in the dry season and 11 499 in the rainy season.[3] It is hypothesised that the AS trait lowers the risk of developing BL. One hundred Nigerian Yoruba children with BL had a significantly lower incidence of the AS genotype than hospital controls. No difference in frequency of AS was, however, subsequently observed between 306 Kenyan children with BL and age-, ethnically and geo­ graphically matched controls.[4,5] We observed an AS incidence of 7% in 167 BL patients treated in Cameroon,[6] and subsequently conducted a prospective study in surviving BL patients resident in the Northwest region.

Methods

Seventy-nine BL patients in the Northwest region of Cameroon were visited at home, where a nearest-neighbour control of the same tribe, age and sex was identified. One parent of a patient with BL refused consent.

An ethylenediaminetetra-acetic acid (EDTA) venous blood sample was obtained from the

index patients and controls, and paper electrophoresis was performed at pH 8.9 in boric and trisaminomethane (TRIS) buffer. Institutional review board appro­ val and informed parental consent were obtained.

Results

The 79 BL patients included 41 girls and 38 boys aged 4 - 17 (mean 9.9) years.

Controls had a similar age and gender distribution. Four (5.13%) BL patients had AS compared with 11 (14.10%) controls (χ2 (df=1)=3.74, p=0.052; Fisher’s exact, one-tailed, p=0.050) (Table 1).

Table 1. Observed frequencies of Hb AA and Hb AS Subjects

Hb AA

Hb AS

Total

Patients, n

74

4

78

Patients, %

94.87

5.13

Controls, n

67

11

Controls, %

85.9

14.10

Total

141

15

78 156

χ2 (df=1)=3.74, p=0.052; Fisher’s exact, one-tailed, p=0.050.

Discussion

The validity of the Nigerian study[4] was later questioned because controls were not from the same tribe, region and village. It is not clear whether controls in the Kenyan study[5] were carefully matched for age and if they

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July 2016, Print edition

were indeed nearest-neighbour controls.

This is of critical importance because of large differences in the distribution of the AS gene.

Conclusion

The relatively small number of patients studied limits the statistical significance of our findings. This study of confirmed BL patients and very well-matched controls did, however, demonstrate that AS carriers in Cameroon probably have a reduced risk of developing BL. Further studies in this regard are justified.

Acknowledgement. We acknowledge laboratory support from the Came­roon Baptist Convention Health Board.

1. Rainey JJ, Mwando WO, Wairiumu P, Morman AMM, Wilson ML, Rochford R. Spatial distribution of Burkitt’s lymphoma in Kenya and association with malaria risk. Trop Med Int Health 2007;12:936-943.

2. Tchana Sinou M. Antenatal screening of sickle cell disease. 8th Postgraduate Course for Training in Reproductive Medicine and Reproductive Biology. Geneva: Geneva Foundation for Medical Education and Research, 2008. http:www.gfmer.ch/ENDO/ PGC_ network/antenatal_ screening_sickle_ cell_Tchana.htm (accessed 17 May 2016).

3. Lewis N, Young J, Hesseling PB, McCormick P, Wright N. Epidemiology of Burkitt’s lymphoma in Northwest Province Cameroon 2003 - 2010. Paediatr Int Child Health 2012;32:8285. DOI:10.1179/2046905511Y.0000000016 4. Williams AO. Haemoglobin genotypes, ABO blood groups, and Burkitt’s tumour. J Med Genet 1966;3:177-179.

5. Mulama DH, Bailey JA, Foley J, et al. Sickle cell trait is not associated with endemic Burkitt lymphoma: An ethnicity and malaria endemicity-matched case-control study suggests factors controlling EBV may serve as a predictive biomarker for this pediatric cancer.

Int J Cancer 2014;134(3):645-653. DOI:10.1002/ijc.28378 6. Hesseling PB. Wharin. Poster presentation at the Africa International Society of Paediatric Oncology (SIOP) Conference, Cape Town, South Africa, 21 - 23 March 2012.

Accepted 24 February 2016.

IN PRACTICE

CASE REPORT

Resolution of a periodontoid rheumatoid pannus mass in an elderly patient treated with a rigid cervical collar: A case report and literature review A Oseni,1,3 MD, MSc; G Kakavas,2 MD; M Scholz,2 MD; A Petridis,2 MD 1 2

ivision of Neurosurgery, Department of Surgery, Lagos University Teaching Hospital, Nigeria D Department of Neurosurgery, Sana Kliniken Duisburg, Duisburg, Germany

Corresponding author: A Oseni (oseniabidemi@yahoo.com)

In patients with C2 rheumatoid pannus with spinal cord compression the treatment of choice is extensive surgery either through a transoral resection of the dens axis or a dorsal stabilisation, or both. We present a case of an 11-mm rheumatoid pannus with significant compression of the spinal cord, which failed surgical treatment with respect to dorsal stabilisation. Therefore, rigid cervical collar for 8 weeks followed by soft collar for another 4 weeks was chosen as a treatment option. During the follow-up period of 1 year, the pannus reduced significantly and the spinal cord decompressed. In cases where surgery is not an option or is technically very demanding, the alternative of cervical collar immobilisation is a satisfying option.

S Afr Med J 2016;106(7):687-688. DOI:10.7196/SAMJ.2016.v106i7.9861

Rheumatoid arthritis (RA) is a multisystemic, chronic inflammatory disease that afflicts the metacarpophalangeal and metatarsophalan­ geal joints. The primary pathology involves the synovium, which is thickened as a result of chronic inflammatory cell proliferation and surface cell hyperplasia. With progression of the disease, articular cartilage and bone destruction follow. This invariably manifests clinically as symmetrical peripheral polyarthritis. Involvement of the cervical spine is a highly characteristic component of RA as well as other chronic inflammatory rheumatic diseases.[1] Cervical spine involvement is common in advanced RA.[1,2] Anterior atlantoaxial subluxation and atlantoaxial impaction are the most characteristic cervical spine disease in RA, occurring in 13 - 70% and 4 - 35% of patients, respectively, worldwide.[2] The spinal cord compression caused by the subluxation at the craniocervical junction may lead to the formation of periodontoid pannus, compromising the anteroposterior diameter of the spinal canal and causing neurological deficits.[3] Cervical spine involvement, although characteristic, is often missed by the treating physician because of problems related to the hands and feet. Non-infectious, non-tumorous retro-odontoid masses are rare, and have not been reported to compress the spinal cord extensively.[4] Transoral transpharyngeal excision of the pannus is sometimes feasible for anterior decompression of the spinal cord; however, posterior fusion and instrumentation have been known to result in spontaneous regression of the pannus mass and symptomatic relief.[3,5] This case report illustrates that severe atlantoaxial vertical subluxation and posterior subluxation of the axis associated with RA can be managed satisfactorily with minimal surgical manipulation and prolonged immobilisation with a rigid cervical collar, thus avoiding extensive surgery in high-risk patients.

Case report

A 73-year-old woman was referred to the Department of Neurosurgery, Sana Kliniken with an already non-operative treated pannus behind C2 with seronegative polyarthritis, and clinical and radiological signs of myelopathy. She had a history of long-term

52

cortisone use due to chronic obstructive pulmonary disease (COPD).

Her symptoms dated back 2 years prior to presentation, with mild headaches, nuchalgia and burning paraesthesias in both arms – right more than left – with no associated dermatome. Paraesthesias were also noted in the upper body down to the mammary region, with no further neurological deficits.

Initial care was given by our rheumatologists, owing to chronic neck pain syndrome around a crowded dens and seronegative polyarthritis. The initial visit to neurosurgical outpatient clinic confirmed the clinical findings, with radiological findings of a 11-mm pannus behind the dens, with associated compression of the medulla and a syrinx (Fig. 1). The patient was prepared for surgical decompression with preoperative planning for a C1 laminectomy and dorsal C1/ C2 fusion. She underwent cervical decompression C1 laminectomy, but the planned C1/C2 fusion was not feasible due to weak pedicle bone substance found intraoperatively. Transarticular screw fixation, i.e. Magerl technique, was considered but also dropped owing to prominent vertebral artery curvature elongation and the risk of injury to the artery. With the intraoperative difficulties, it was decided to make a bone graft transplant from the dorsal iliac crest directly between C2 and the nuchal area. Fixation was achieved with non-resorbable material around C2.

Immediate postoperative computed tomography (CT) scan of the cervical spine showed a well-fixed bone graft still located at the point of fixation. According to the patient, the pain subsided, and a rigid cervical collar was applied to be maintained for 8 weeks, day and night, whereupon the patient was discharged. In the subsequent months, the patient reported every month to the outpatient clinics.

She had CT scans performed every month in order to follow the progress or dislocation of the bone graft. After 8 weeks, the rigid cervical collar was changed to a soft neck brace, which allowed certain but minimal range of motion. This was maintained for 4 weeks, whereafter it was removed and the patient was allowed free range of motion. The CT scan at this point showed the bone graft no longer attached to C2, suspected to be owing to bone absorption. No dislocation was measured. A C2-to-nuchal-area distance of 5 mm was

July 2016, Print edition

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A

B

C

Fig. 1. Rheumatoid pannus reduction after rigid cervical collar immobilisation over 1 year: (A) Pre-intervention T2 weighted sagittal MRI of the cervical spine showing an 11-mm pannus behind C2 with significant compression of the spinal cord; (B) 1-month follow-up after rigid collar immobilisation and interposition of a C0 - C2 bone graft, which was fixed by sutures only, i.e. no screw fixation was performed; (C) 1-year follow-up shows a reduction of the pannus with decompression of the spinal cord.

evident in all consecutive CTs. A significant decrease in the size of the pannus was noticed, from 11 mm to 5 mm, with associated reduced pain according to the patient. In subsequent CT scans, the medulla reached a normal width and myelopathy signs subsided; the patient still had burning sensation in both arms but with no measurable neurological deficit (at follow-up after 1 year). There was improved neck motion, with a postoperative rotation of 15º.

Discussion

The erosion of the ligamentous support for the odontoid peg due to rheumatoid synovitis causes atlantoaxial instability leading to compression of the upper cervical cord and brainstem. Pannus is located ventrally to the bulbomedullary junction, and can produce a severe myelopathy and even sudden death.[6] According to some studies, this is an inflammatory granulation process, whereas in others this tissue is a reactive fibrous tissue secondary to the mechanical stress, rather than secondary to an inflammatory process. [1,2,6] The instability leads to forward subluxation, producing neuro­ logical damage. Patients with rheumatoid cervical spine involvement may have no symptoms, but more often have some nonspecific neck pain or C2 neuralgia and stiffness.[6] The symptoms of nuchal pain, and lancinating sensation with loss of power of upper and lower limb muscles indicate atlantoaxial joint disease with bursitis and subluxation of joint due to RA.[1,6] Transoral transpharyngeal excision of the pannus is thought necessary for anterior decompression of the spinal cord by some authors;[3,5,7] however, occasional reports of spontaneous resolution of the periodontoid pannus after posterior atlantoaxial fusion and fixation have been documented.[3] Evidence suggests that atlantoaxial instability is the de facto reason for the formation of periodontoid

53

pannus,[1,3,4,7] and as such, interventions to reduce the instability lead to spontaneous resolution of the pannus mass.[3,6,8] Posterior atlantoaxial fixation is a viable option especially in older patients with significant myelopathy from soft-tissue compression, and may prevent the need for removal of the panus through the transoral route. However, there are no reports of strictly conservative treatment with only cervical collar immobilisation showing such a significant reduction of the pannus, as in the present case report. In cases were surgery is not an option or is technically very demanding, the alternative of cervical collar immobilisation with a rigid collar for 8 weeks followed by a soft collar for another 4 weeks is a satisfying option. Monthly follow-up with CT scanning every month for the first 3 months and thereafter every 2 months for the first year should also be done.

1. Prakash P, Srivastava S, Sharma SC, et al. Cervical complications of rheumatoid arthritis. JIACM 2006;7(2):161-164.

2. Daoud L, Kochbati S. Magnetic resonance imaging evaluation of the cervical spine in patients with rheumatoid arthritis. Report of 30 cases. La Tunisie Medicale 2009;87(6):375-379.

3. Lu K, Lee TC. Spontaneous regression of periodontoid pannus mass in psoriatic atlantoaxial subluxation. Case report. Spine 1999;15;24(6):578-581.

4. Takuechi M, Yasuda M, Takahashi E. A large retro-odontoid cystic mass caused by transverse ligament degeneration with atlantoaxial subluxation leading to granuloma formation and chronic recurrent microbleeding. Case report. Spine J 2011;11(12):1152-1156. DOI:10.1016/j. spinee.2011.11.007 5. Jun BY. Complete reduction of retro-odontoid soft tissue mass in os odontoideum following the posterior C1-C2 transarticular screw fixation. Spine 1999;15:24(18);1961-1964.

6. Lagares A, Arrese I, Pascual B, et al. Pannus resolution after occipitocervical fusion in a nonrheumatoid atlanto-axial instability. Eur Spine J 2006;15(3):366-369. DOI:10.1007/s00586-005-0969-4 7. Isono M, Ishii K, Kamida T, et al. Retro-odontoid soft tissue mass associated with atlantoaxial subluxation in an elderly patient: A case report. Surg Neurol 2001;55(4):223-227.

8. Sasaki T, Miyamoto K, Hosoe H, Shimizu K. Transoral anterior approach for extensive anterior decompression at the C3 vertebra level in a patient with severe atlantoaxial vertical subluxation and rheumatoid arthritis. Spinal Cord 2006;44(1):52-55.

Accepted 4 May 2016.

July 2016, Print edition

IN PRACTICE

CASE REPORT

A case of refractory thrombotic thrombocytopenic purpura treated with plasmapheresis and rituximab N Kirui,1,2 MB ChB, MMed; A Sokwala,2 MD, MMed 1 2

epartment of Internal Medicine, School of Medicine, College of Health Sciences, Moi University, Eldoret, Kenya D Aga Khan University Hospital, Nairobi, Kenya

Corresponding author: A Sokwala (drsokwala@gmail.com)

Thrombotic thrombocytopenic purpura (TTP) is a rare, life-threatening disorder with no prevalence or incidence studies in sub-Saharan Africa. Acquired TTP has several causes, all of which lead to decreased activity of von Willebrand factor cleaving protease (ADAMTS13) due to autoantibodies that are directed towards ADAMTS13. We report a case of a 46-year-old man who presented with most of the classic clinical manifestations of TTP. S Afr Med J 2016;106(7):689-691. DOI:10.7196/SAMJ.2016.v106i7.9856

Background

Thrombotic thrombocytopenic purpura (TTP) is a rare, life-threaten­ ing disorder that occurs due to deficiency of ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13), which is a von Willebrand factor (VWF) cleaving protein.[1] The absent or severely reduced activity of ADAMTS13 in patients with TTP prevents timely cleavage of unusually large multimers of VWF as they are secreted by endothelial cells, resulting in adhesion and aggregation of platelets in flowing blood, with formation of microvascular thrombi, which are responsible for most of the clinical features.[2] Both congenital and acquired forms of TTP have been described. There are no prevalence or incidence studies on TTP in sub-Saharan Africa (SSA), but several case reports are available in literature. Scully et al.[3] in the UK reported a TTP incidence rate of six cases per million people in 2008.

There are several causes of acquired TTP, all of which lead to decreased activity of ADAMTS13 due to autoantibodies that are directed towards ADAMTS13.[4] The classic presentation of TTP is that which follows postinfectious intestinal infection with either shigatoxin-producing Escherichia coli or Shigella dysenteriae.[5] HIV infection has been directly associated with TTP,[6] and a case series

by Gunther et al.,[7] in South Africa in 2007, demonstrated that HIVassociated TTP was the most common form of TTP. Postinfectious TTP is therefore the most common cause of TTP in SSA, where there is still a high incidence of infectious diseases.

TTP was originally characterised by a pentad of thrombocytopenia, microangiopathic haemolytic anaemia, fluctuating neurological deficits, renal impairment and fever, often with insidious onset.[8] However, TTP can present without the full pentad. Up to 35% of patients do not have neurological signs at presentation, and renal abnormalities and fever are not always prominent features.[9] Galbusera et al.[9] in 2006 described revised diagnostic criteria for TTP in which the diagnosis can be made upon identification of the presence of thrombocytopenia and microangiopathic haemolytic anaemia (MAHA) only. Other atypical manifestations of TTP that have been described include non-occlusive mesenteric ischaemia, pancreatitis, hepatitis, acute respiratory distress syndrome and peripheral digital ischaemia.[10,11] TTP is a severe illness and, if untreated, >90% of patients die from the syndrome.[12] Plasmapheresis is the treatment of choice for TTP, in addition to steroids, which are initiated immediately after start of

54

plasma exchange therapy (PEX).[8] Rituximab is effective and safe in acute idiopathic TTP and in patients with immune TTP who have failed to respond to PEX and steroids.[13] The poor outcome of untreated patients is a big challenge particularly in SSA, where there are poor health systems and poor access to quality healthcare.

We report a case of a 46-year-old man who presented with most of the classic clinical manifestations TTP.

Case presentation

A 46-year-old male patient born deaf and dumb presented to the Aga Khan University Hospital as a referral from a peripheral facility, with a 2-week history of severe headache, abdominal pains, diarrhoea and vomiting. He had been fine prior to the onset of symptoms and there was no history of travel to a malaria endemic region. The headache was occipital, of sudden onset, severe (scale 8 - 10/10), nonradiating, worsened with activity and was temporarily relieved by use of analgesics. There was no associated fever or neck stiffness. He had visual hallucinations with no other visual symptoms. Diarrhoea was watery and not blood stained, and the vomiting was mostly postprandial with associated epigastric abdominal pain. There was no history of decreased urine output, lower-limb swelling and facial swelling, and no respiratory symptoms. His past medical history and family history were non-significant. He worked as a tailor and was married with three children. Physical examination showed a well-developed, middle-aged black African male patient of good nutritional status and with stable vital signs. He had mild pallor, was not jaundiced, had no lymphadenopathy and no oedema, and skin examination was normal. He communicated by sign language, his neck was supple and the rest of the neurological examination findings were unremarkable. Abdominal, respiratory and cardiovascular examinations were unremarkable. Laboratory findings showed severe anaemia (haemoglobin 5.8 mg/dL), thrombocytopenia (platelet counts 9 × 109), increased lactate dehydrogenase activity (517 IU/L) and schistocyte count was 3%. Renal and liver function tests were normal with a negative direct Coombs test. HIV antibody, hepatitis B surface antigen and hepatitis C virus antibody tests were negative.

Blood and stool cultures were negative, while renal and liver function tests were normal; it is important to note that he had been on intravenous antibiotics in the referring facility. His blood slide for malaria parasites was also negative.

July 2016, Print edition

IN PRACTICE

TTP was suspected because of the haemolytic anaemia, thrombocytopenia, schistocytes on the peripheral blood film and the neurological manifestations. The patient was started on PEX at a dose of one volume PEX daily, and the efficacy of the plasma exchange was monitored using daily thrombocyte levels. Despite being on daily PEX, his thrombocytes did not improve until after 5 days of therapy. After 1 week in the hospital, undergoing PEX, he was noted to have declining mental status, and increased aggressiveness and disorientation.

Magnetic resonance imaging was not done because of the need for sedation. Computed tomography scan of the brain showed small bilateral subdural haematomas with no pressure effects; the patient was put on conservative management with continued monitoring of neurological status. He improved and there was no need for neurosurgical intervention.

After seven sessions of PEX, the thrombo­ cytes improved to 157 × 109/L. PEX was stopped after the thrombocyte levels remained above 150 × 109/L for 2 consecutive days. Three days after PEX had been stopped, the thrombocytes dropped to 47 × 109/L, and a diagnosis of refractory TTP was made. Finan­ cial constraints limited subsequent PEX to one more session, and only one dose of rituximab (375 mg/m2 body weight) for refractory TTP was given. The thrombocytes improved and the patient’s clinical condition improved tremendously, and he was discharged 4 days after the dose of rituximab. The thrombocyte count improved to 160 × 109/L on starting rituximab and to 198 × 109/L on review in a clinic 2 weeks later.

The patient was discharged on prednisolone, tapered over 3 months. He was doing very well 3 months post discharge, with no symptoms, and he had returned to work. He had a platelet count of 253 × 109/L and 233 × 109/L on review 2 and 3 months post discharge, respectively (Fig. 1).

Discussion

TTP was diagnosed in this patient owing to the presence of thrombocytopenia, MAHA with schistocytes of 3% and neurological manifestations.[9] Systemic bacterial and fungal infections were excluded with several negative blood cultures, as severe sepsis is one of the differentials for schistocytosis and thrombocytopenia.[14] Patients with severe sepsis may also present with disseminated intravascular coagulation with a subsequent lack of procoagulant proteins, causing bleeding diathesis and anaemia.

TTP is a life-threatening condition, espe­ cially in SSA, where optimal treatment facilities are not available. PEX was initiated owing to a presumptive diagnosis of TTP because of the associated high mortality of up to 90% in untreated patients.[12] PEX is the mainstay of treatment in TTP as it reduces mortality from 90% to 10 - 20%. [8] This moda­lity of treatment depletes the circulating antibodies against ADAMTS13 and the very high molecular weight von Willebrand factor multimers. PEX also replaces the missing von Willebrand cleav­ing protease. [15] Although the mortality of TTP has been reduced in most European countries and in America, we postulate that TTP still has a high mortality in SSA owing to lack of PEX. Management of refractory TTP is a bigger challenge owing to the need for more prolonged duration of treatment. However, more intensive PEX may be required in resis­ tant cases with new-onset symptoms while on therapy.[16] Our patient improved tremendously but deteriorated 2 days postPEX, with thrombocytes dropping to 47.

Owing to financial constraints, only one additional session of PEX was done for refractory TTP and one dose of rituximab was given. Fakhouri et al.[13] showed that rituximab is effective and safe in immune TTP for patients who have failed PEX and Platelet counts

300

Platelet count, n

250 200 150 100 50

1s

Ad m

iss i St on a t s rt 2n essi PP o d se n P 3r ssio P d se n P 4t ssio P h se n P 5t ssi P o h se n P 6t ssio P h se n P 7t ssio P h St s n op ess PP pe ion d P 8t PP P h d Ri ses ay 3 tu sio xim n ab PP Po da st y 0 R Po day st 2 Po R 2 st wk R Po 1 m st R o 3 m o

0

Intervention

Fig. 1. Platelet counts against intervention. (R = rituximab; wk = weeks; mo = months.)

55

July 2016, Print edition

methylprednisone treatment and in acute relapsed TTP. Rituximab is the current treatment of choice for refractory TTP and should be given once weekly for 4 weeks;[3,8] our patient was started on rituximab early because of the challenges of PEX in our setting. Rituximab in combination with predni­sone is effective and can be used with­ out concurrent plasma exchange in patients without neurological or renal impairment. [17] Long-term consequences of TTP are not well known, but it has been postulated that some patients may go on to develop longterm renal dysfunction and neurocognitive deficits.[15] This case report demonstrates both the poss­ ibilities and challenges of managing TTP. Diagnosis and initiation of appropriate therapy according to international guidelines was possible for this patient and a relatively good response was demonstrated. However, our patient did not receive optimal care owing to financial constraints; this is a common scenario in SSA. Our patient responded well to one dose of rituximab.

Further studies are necessary to explore the viability of use of rituximab alone in settings where PEX is not possible.

Conclusions

TTP can present without the full pentad of the classic clinical presentation. There should be increased suspicion of TTP in patients who present with MAHA, especially in a population that has a high prevalence of HIV infection. This is the first reported case of TTP that was relatively appropriately managed with plasma exchange and rituxi­ mab in this part of the developing world.

Rituximab has been used for patients with resistant and relapsed TTP with successful results in other regions of the world; these results can be replicated in our setting.

Further studies to assess the feasibility and viability of the use of rituximab alone in settings where PEX is not possible are necessary.

1. Fujikawa K, Suzuki H, McMullen B, Chung D. Purification of human von Willebrand factor-cleaving protease and its identification as a new member of the metalloproteinase family. Blood 2001;98(6):1662-1666. DOI:10.1182/blood. v98.6.1662 2. Maoke J. Thrombotic microangiopathies. N Engl J Med 2002;347(8):589-600. DOI:10.1056/NEJMra020528 3. Scully M, Yarranton H, Liesner R, et al. Regional UK TTP registry: Correlation with laboratory ADAMTS13 analysis and clinical features. Br J Haem 2008;142(5):819-826. DOI:10.1111/ j.1365-2141.2008.07276.x 4. Furlan M, Robles R, Galbusera M, et al. Von Willebrand factor-cleaving protease in thrombotic thrombocytopenic purpura and the hemolytic-uremic syndrome. N Engl J Med 1998;339(22):1578-1584. DOI:10.1056/NEJM199811263392202 5. Bitzan M, Schaefer F, Reymond D. Treatment of typical (enteropathic) hemolytic uremic syndrome. Semin Thromb Hemost 2010;36(6):594-610. DOI:10.1055/s-0030-1262881 6. Novitzky N, Thomson J, Abrahams L, du Toit C, McDonald A. Thrombotic thrombocytopenic purpura in patients with retroviral infection is highly responsive to plasma infusion therapy. Br J Haem 2005;128(3):373-379. DOI:10.1111/j.1365-2141.2004.05325.x

IN PRACTICE

7. Gunther K, Garizio D, Nesara P. ADAMTS13 activity and the presence of acquired inhibitors in human immunodeficiency virus-related thrombotic thrombocytopenic purpura. Transfusion 2007;47(9):1710-1716. DOI:10.1111/j.1537-2995.2007.01346.x 8. Scully M, Hunt BJ, Benjamin S, et al. Guidelines on the diagnosis and management of thrombotic thrombocytopenic purpura and other thrombotic microangiopathies. Br J Haem 2012;158(3):323-335.

DOI:10.1111/j.1365-2141.2012.09167.x 9. Galbusera M, Noris M, Remuzzi G. Thrombotic thrombocytopenic purpura – then and now. Semin Thromb Hemost 2006;32(2):81-89. DOI:10.1055/s-2006-939763 10. Chang JC, Gupta S. Acute respiratory distress syndrome and non-occlusive mesenteric ischemia as major clinical manifestations of thrombotic thrombocytopenic purpura: Complete remission following exchange plasmapheresis. J Clin Apher 1998;13(4):190-192.

11. Chang JC, Kathula SK. Various clinical manifestations in patients with thrombotic microangiopathy.

J Investig Med 2002;50(3):201-206. DOI:10.2310/6650.2002.33434 12. Patschan D, Korsten P, Behlau A, et al. Idiopathic combined, autoantibody-mediated ADAMTS-13/ factor H deficiency in thrombotic thrombocytopenic purpura-hemolytic uremic syndrome in a 17-year-old woman: A case report. J Med Case Rep 2011;5(1):598. DOI:10.1186/1752-1947-5-598

13. Fakhouri F, Vernant JP, Veyradier A, et al. Efficiency of curative and prophylactic treatment with rituximab in ADAMTS13-deficient thrombotic thrombocytopenic purpura: A study of 11 cases.

Blood 2005;106(6):1932-1937. DOI:10.1182/blood-2005-03-0848 14. Irmak K, Sen I, Cöl R, et al. The evaluation of coagulation profiles in calves with suspected septic shock.

Vet Res Commun 2006;30(5):497-503. DOI:10.1007/s11259-006-3258-8 15. See JR, Sabagh T, Barde CJ. Thrombotic thrombocytopenic purpura: A case presenting with acute ischemic colitis. Case Rep Hematol 2013;2013:592930. DOI:10.1155/2013/592930 16. Nguyen L, Li X, Duvall D, Terrell DR, Vesely SK, George JN. Twice-daily plasma exchange for patients with refractory thrombotic thrombocytopenic purpura: The experience of the Oklahoma Registry, 1989 through 2006. Transfusion 2008;48(2):349-357. DOI:10.1111/j.1537-2995.2007.01530.x 17. Ahmad A, Aggarwal A, Sharma D, et al. Rituximab for treatment of refractory/relapsing thrombotic thrombocytopenic purpura (TTP). Am J Hematol 2004;77(2):171-176. DOI:10.1002/ajh.20166

Accepted 17 March 2016.

CASE REPORT

Schwannoma extending from the umbilical region to the mid-thigh, compressing the major vessels of the right leg: A case report and review of the literature J Yorke,1,2 MD; B M Duduyemi,3 FMCPath; A C Yifieyeh,2 FWACS; P K S Fiifi-Yankson,2 MB ChB; C Appiah,2 MB ChB; D Afful-Yorke,2 BSc; M O Adinku,2 FWACS; D Ahulu,2 BSc epartment of Surgery, School of Medical Sciences, College of Health Sciences, Kwame Nkrumah University of Science and Technology, D Kumasi, Ghana 2 Directorate of Surgery, Komfo Anokye Teaching Hospital, Kumasi, Ghana 3 Department of Pathology, Kwame Nkrumah University of Science and Technology, Kumasi, Ghana 1

Corresponding author: B M Duduyemi (babsdudu@yahoo.com)

Schwannomas are benign, usually encapsulated, nerve sheath tumours derived from Schwann cells. They commonly arise from the cranial nerves as acoustic schwannomas and are extremely rare in the pelvis and retroperitoneal area (<0.5% of reported cases) unless they are combined with Von Recklinghausen disease (type 1 neurofibromatosis). We report the case of a 23-year-old woman with a mass extending from the umbilical region in the abdomen to the upper two-thirds of the thigh. As this tumour is so rare, and in order to ensure optimal treatment and survival for our patient, a computed tomography-guided biopsy was performed before en bloc tumour excision. Because of the possibility of malignancy, complete excision of the mass was performed, with pelvic blunt dissection. Histological examination showed a benign neoplasm, originating from the cells of peripheral nerve sheaths; the diagnosis was a schwannoma. Abdominal schwannomas are rare neoplasms that can be misdiagnosed. Laparoscopy is a safe and efficient option for approaching benign pelvic tumours and may offer the advantage of better visualisation of structures owing to the magnification in laparoscopic view, especially in narrow anatomical spaces.

However, in our case laparoscopy was not considered owing to the size and anatomical location of the tumour.

S Afr Med J 2016;106(7):692-694. DOI:10.7196/SAMJ.2016.v106i7.10252

Schwannomas are benign, usually encapsu­ lated, nerve sheath tumours derived from Schwann cells. One of the most common types of benign peripheral nerve sheath tumours, they are common in cranial and peripheral nerves but are rarely located in the pelvis. [1,2] Schwannomas can occur sporadically or as manifestations of genetic conditions such as neurofibromatosis types 1 and 2. Pelvic schwannomas have no specific radiological features and are often considered to be urological diseases or gynaecological masses.[3,4] We report the rare case of a woman with a pelvic schwannoma in the right parametrium and extending into the right thigh.

Case report

A 23-year-old woman was referred to a general surgery outpatient department for management of an abdominal mass of increasing size and sustained pain in the right leg that had been present for 13 years.

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The pain was independent of activity, and the patient had no sign of neurovascular deficit. The swelling had progressively increased in size since it was first noticed and was initially associated with occasional dull intermittent pain that radiated to the right lower limb. Five months before presentation, the mass became extremely painful. The pain was throbbing and stabbing in nature, constant, radiated to the right lower limb, and was exacerbated by movement and relieved by rest. There was associated swelling of the right lower limb on standing for long periods, numbness and paraesthesiae. There was no history of other gastrointestinal or cardiovascular symptoms.

The patient denied any unexplained weight loss and had a negative history for cancer. Her medical, surgical, obstetric and family history was unremarkable.

Physical examination revealed a well-nourished young woman, afebrile, anicteric, not pale and well hydrated, with a dumbbell-

July 2016, Print edition

IN PRACTICE

shaped mass on the right lumbar region of the abdomen extending to the right thigh and measuring 25 × 20 cm (Fig. 1). The mass was smooth and firm with well-defined edges and tender around the femoral region, and was attached to the underlying structures but not to the skin. There were varicosities over the mass at the femoral region but no lymphadenopathy. There was full power in all the muscles, and sensation was normal in the right lower limb. The femoral, popliteal, posterior tibialis and dorsalis pedis pulses were all palpable with adequate capillary refill in all the digits.

The results of routine haematological investigations and urinalysis as well as testing for several tumour markers, including carcinoembryonic antigen, α-fetoprotein and carbohydrate antigen 19.9, were all within normal limits.

Fig. 1. Firm mass extending from the region of the umbilicus to the upper two-thirds of the right thigh.

Fig. 3. Surgically resected well-defined and encapsulated dumbbell-shaped mass measuring 26.5 × 26.3 × 16.3 cm.

Imaging

Imaging studies included plain radiographs, ultrasonography and a computed tomography (CT) scan of the abdomen and thigh.

Radiographs of the right hip and thigh revealed soft-tissue swelling with no bone deformities. A chest radiograph was normal.

Serial axial contrast-enhanced CT images showed a 26.5 × 26.3 × 16.3 cm welldefined dumbbell-shaped heterogeneously enhancing mass arising at the level of L4 on the right and extending inferiorly lateral to the right femoral vessels to the anterior compartment of the proximal right femur, about 7 cm inferior to the pubic symphysis.

The mass had internal calcifications and internal areas of hypodensity suggestive of cystic degeneration. It also exerted a mass effect, displacing bowel loops superiorly, and compressing and displacing the urinary bladder, uterus, distal inferior vena cava and right iliac and femoral vessels to the contralateral side.

The mass was in close proximity to the femoral vessels, but was not seen to infiltrate or spread to adjacent organs. The bones appeared normal, with no remodelling or lytic or sclerotic lesion seen (Fig. 2).

Diagnosis and treatment

A diagnosis of right femoral nerve schwan­ noma was made. Total removal of the mass (Fig. 3) was achieved through laparotomy and extension of the incision to the upper thigh.

Intraoperative findings were a right retro­ peritoneal mass extending from below the right kidney to the upper two-thirds of the right thigh with superficial varicosities. The right kidney, ovary, ureter, femoral artery and vein, liver and bladder were normal.

Fig. 2. Axial contrast-enhanced CT image of the abdomen and upper thigh, showing the dumbbell-shaped mass.

The preoperative findings indicated that we had to deal with a retroperitoneal tumour of unknown pathology in a nulli­ parous woman in her reproductive years.

The abdomen was opened through an exten­ ded lower midline incision. A large retro­ peritoneal mass, measuring 26.5 × 26.3 × 16.3 cm, was noted in the right para­metrium and in close proximity to the internal iliac vessels. Complete excision of the mass was performed. Histological examination showed a benign neoplasm originating from the cells of the peripheral nerve sheath consistent with a schwannoma (Fig. 4). The patient recovered well, was discharged on postoperative day 10 and was seen again for follow-up 2 months after surgery (Fig. 5).

Discussion

Schwannomas are nerve sheath tumours that arise in peripheral, cranial or visceral nerves at any anatomical site in the human body.[5,6] These tumours commonly arise from the cranial nerves as acoustic neuri­ nomas, but they are extremely rare in the pelvis and the retroperitoneal area (<0.5% of reported cases), unless they are combined with Von Recklinghausen disease (type 1 neurofibromatosis).[6] Schwannomas are non-aggressive, slow-growing, soli­tary neo­ plasms with an extremely low possi­bility of malignant transformation or recur­rence after excision.[7] Macro­ scopically, schwannomas

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July 2016, Print edition

Fig. 4. Histological section of a benign spindle cell neoplasm with admixture of cellular areas (Antoni A) and loosely cellular areas (Antoni B) consistent with a schwannoma.

Fig. 5. The patient at follow-up 2 months after surgery.

are solitary, well-circum­scribed and encapsu­ lated tumours.[4] As a result of their slow growth rate and anatomical location, pelvic schwannomas remain asymptomatic and are discovered either incidentally during a medical investigation for unrelated symptoms or when they become sufficiently large to cause a mass effect.[7,9] This mass effect can lead to pain in the pelvic area and lower back and a sense of heaviness accompanied with urinary and digestive symptoms caused by bladder and bowel compression.[9] Pelvic schwannomas are not easily diagnosed. The clinical signs and symptoms are not pathognomonic for this pathological entity.

Our case encouraged us to conduct a literature review and document cases of abdomino­ pelvic schwannomas. The small

IN PRACTICE

number of these cases indicates the rarity of retroperitoneal abdominopelvic schwann­ omas. One case was a retro­ peritoneal pelvic schwannoma located in the right paracolpium,[10] and another was a schwann­oma present at the L5 vertebral body and causing pelvic pain.[11] Takeuchi et al.[12] reported 11 presacral and lateral pelvic region neurilemomas, 8 of which were located in the right or left presacral area and 3 in the lateral extraperitoneal region.

One pelvic schwannoma of the anterior surface of the sacrum mimicking an ovarian cyst was also reported. [13] An additional case of a retroperitoneal schwannoma localised in the pelvic cavity with complete cystic degeneration, mimicking an ovarian carcinoma, was reported,[14] and there was one report of a presacral neurilemoma. [15] One pelvic retroperitoneal neurilemoma arose in the fallopian [17] tube,[16] and one malignant schwannoma arose in the cervix.

[18] Yadav et al. reported one case of neurilemoma located in the right adnexa, and Sinha et al.[9] reported two cases of pelvic schwannomas located in the broad ligament, with the clinical expression of a broadligament myoma. One reported case of neurilemoma of the pelvis mimicked a myoma of the uterus.[19] Pelvic tumours, and specifically pelvic schwannomas, can cause chronic pelvic pain, as was reported in a case of a femoral nerve schwannoma with the clinical expression of chronic pelvic pain.[6] There were two cases of obturator nerve tumours arising from Schwann cells, one expressed as a pelvic tumour and the other as an ovarian tumour.[20] Nine cases of schwannomas mimicking ovarian malignancies have also been reported.[21,22] Pelvic schwannomas, as mentioned above, are easily misdiagnosed owing to the lack of specific symptoms. Treatment is complete excision of the tumour, either laparoscopically or with open abdominal surgery.[23] Because the vast majority of schwannomas are benign tumours, simple tumour enucleation could also be effective. In these surgical approaches it is important that the surgery does not result in neural lesions.[7] The presacral-retrorectal space is considered to be a downward extension of the retroperitoneal space because it communicates superiorly with the latter at the level of peritoneal reflection (S2 - S3 vertebrae); surgical extirpation of presacral and pelvic tumours may therefore present several difficulties owing to limited access and poor visualisation in a narrow pelvis.[23,24] Schwannomas are solitary, well-circumscribed, encapsulated tumours, and do not invade local tissues.[4] Owing to these characteristics they are easily dissected from adjacent tissues, which makes laparoscopic resection possible. Laparoscopy is a safe and efficient option for approaching benign pelvic tumours and may offer the advantage of better visualisation of structures because of the magnification of the laparoscopic view, especially in narrow anatomical spaces.[23] Our literature review indicated that laparo­ scopic excision of these neural tumours is the treatment of choice. We

58

used open surgery in our case because of the large size of the tumour and the extension into the thigh.

Of note is that many pelvic schwannomas were misdiagnosed, and were discovered during an operation that was considered to be the optimal therapy for the initial diagnosis.

Acknowledgment. The patient provided written consent for this case report.

1. Rao W, Wang G, Xiu D. Laparoscopic resection of a retroperitoneal schwannoma adherent to vital vessels. Surg Laparosc Endosc Percutan Tech 2009;19(1):e21-e23. DOI:10.1097/SLE.0b013e3182365a3f 2. Funamizu N, Sasaki A, Matsumoto T, Inomata M, Shiraishi N, Kitano S. Laparoscopic resection of a retroperitoneal schwannoma behind the lesser omental sac. Surg Laparosc Endosc Percutan Tech 2004;14(3):175-177. DOI:10.1097/01.sle.0000129379.96203.66 3. Mehta M, Thurston WA, Merchant N, Murphy KJ. Obturator nerve schwannoma presenting as an adnexal mass: Case report. Can Assoc Radiol J 1999;50(1):20-22.

4. Daneshmand S, Youssefzadeh D, Chamie K, et al. Benign retroperitoneal schwannoma: A case series and review of the literature. Urology 2003;62(6):993-997. DOI:10.1016/S0090-4295(03)00792-1 5. Borghese M, Corigliano N, Gabriele R, et al. Benign schwannoma of the pelvic retroperitoneum: Report of a case and review of the literature. G Chir 2000;21(5):232-238.

6. Dawley B. A retroperitoneal femoral nerve schwannoma as a cause of chronic pelvic pain. J Minim Invasive Gynecol 2008;15(4):491-493. DOI:10.1016/j.jmig.2008.02.007 7. Strauss DC, Qureshi YA, Hayes AJ, Thomas JM. Management of benign retroperitoneal schwannomas: A single-centre experience. Am J Surg 2011;202(2):194-198. DOI:10.1016/j.amjsurg.2010.06.036 8. White W, Shiu MH, Rosenblum MK, Erlandson RA, Woodruff JM. Cellular schwannoma: A clinicopathologic study of 57 patients and 58 tumours. Cancer 1990;66(6):1266-1275.

DOI:10.1002/1097-0142(19900915)66:6%3C1266::AID-CNCR2820660628%3E3.0.CO;2-E 9. Sinha R, Sundaram M, Hegde A, Mahajan C. Pelvic schwannoma masquerading as broad ligament myoma. J Minim Invasive Gynecol 2008;15(2):217-219. DOI:10.1016/j.jmig.2007.09.009 10. Ueda M, Okamoto Y, Ueki M. A pelvic retroperitoneal schwannoma arising in the right paracolpium.

Gynecol Oncol 1996;60(3):480-483. DOI:10.1016/0020-7292(96)81558-X 11. Shoher A, Arbab F, Lucci A, Jr. Giant pelvic schwannoma with ancient change. J Am Coll Surg 2003;197(1):163. DOI:10.1016/S1072-7515(03)00339-9 12. Takeuchi M, Matsuzaki K, Nishitani H, Uehara H. Ancient schwannoma of the female pelvis. Abdom Imaging 2008;33(2):247-252. DOI:10.1007/s00261-007-9228-y 13. Ibraheim M, Ikomi A, Khan F. A pelvic retroperitoneal schwannoma mimicking an ovarian dermoid cyst in pregnancy. J Obstet Gynaecol 2005;25(6):620-621. DOI:10.1080/01443610500243752 14. Aran T, Guven S, Gocer S, Ersoz S, Bozkaya H. Large retroperitoneal schwannoma mimicking ovarian carcinoma: Case report and literature review. Eur J Gynaecol Oncol 2009;30(4):446-448.

15. Song JY, Kim SY, Park EG, et al. Schwannoma in the retroperitoneum. J Obstet Gynaecol Res 2007;33(3):371-375. DOI:10.1111/j.1447-0756.2007.00539.x 16. Duran B, Guvenal T, Yildiz E, Cetin M, Erden O, Demirkoprulu N. An unusual cause of adnexal mass: Fallopian tube schwannoma. Gynecol Oncol 2004;92(1):343-346. DOI:10.1016/j.ygyno.2003.09.032 17. Lallas TA, Mehaffey PC, Lager DJ, Van Voorhis BJ, Sorosky JI. Malignant cervical schwannoma: An unusual pelvic tumour. Gynecol Oncol 1999;72(2):238-242. PMID:10021307 18. Yadav Y, Onon T, Sukumar S. Conservative management of a pelvic Schwannoma presenting as an adnexal mass. J Obstet Gynaecol 2008;28(3):364-365. DOI:10.1080/01443610802066265 19. Chen CH, Jeng CJ, Liu WM, Shen J. Retroperitoneal schwannoma mimicking uterine myoma. Taiwan J Obstet Gynecol 2009;48(2):176-177. DOI:10.1016/S1028-4559(09)60282-5 20. Ningshu L, Min Y, Xieqiao Y, Yuanqing Y, Xiaoqiang M, Rubing L. Laparoscopic management of obturator nerve schwannomas: Experiences with 6 cases and review of the literature. Surg Laparosc Endosc Percutan Tech 2012;22(2):143-147. DOI:10.1097/SLE.0b013e3182478870 21. Ozat M, Altinkaya SO, Gungor T, et al. Extraovarian conditions mimicking ovarian cancer: A single center experience of 15 years. Arch Gynecol Obstet 2011;284(3):713-719. DOI:10.1007/s00404-010-1705-9 22. Korkontzelos I, Tsimoyiannis E, Zagaliki A, Demou A, Karabina E, Antoniou N. Pelvic retroperitoneal schwannoma presenting as a gynecologic mass: Case report. Eur J Gynaecol Oncol 2005;26(1):117-119.

PMID:15755018 23. Konstantinidis K, Theodoropoulos GE, Sambalis G, et al. Laparoscopic resection of presacral schwannomas. Surg Laparosc Endosc Percutan Tech 2005;15(5):302-304. DOI:10.1097/01. sle.0000183252.96808.78 24. Wolpert A, Beer-Gabel M, Lifschitz O, Zbar AP. The management of presacral masses in the adult. Tech Coloproctol 2002;6(1):43-49. DOI:10.1007/s101510200008

Accepted 2 November 2015.

July 2016, Print edition

RESEARCH

Analysis of 5 years of morbidity and mortality conferences in a metropolitan South African trauma service V Y Kong, MB ChB, MSc, PhD, MRCS (Eng); D L Clarke, MMedSci, MBA, MPhil, PhD, FCS (SA) Pietermaritzburg Metropolitan Trauma Service, Department of Surgery, University of KwaZulu-Natal, Pietermaritzburg, South Africa Corresponding author: D L Clarke (damianclar@gmail.com)

Background. Since 2008 the Pietermaritzburg Metropolitan Trauma Service (PMTS) has run a structured, self-reporting, metropolitan morbidity and mortality conference (MMC). In 2012 a hybrid electronic medical registry (HEMR) was introduced to capture routine data and to generate reports on morbidity and mortality. This paper reviews our experience in setting up a metropolitan MMC and compares the quality of the reported morbidity data from the pre- and post-HEMR era.

Methods. We compared data from the MMC before and after the introduction of the HEMR to audit the impact of these meetings on the reporting and analysis of surgical morbidity and mortality in our service.

Results. During the 4-year period from 2008 to 2011, a total of 208 MMCs were held. A total of 10 682 patients were admitted by the PMTS during that period, of whom 87% were males, and the mean age was 26 years. Penetrating trauma accounted for 40.9% (4 344/10 628) of the total workload. A total of 432 (4.1%) morbidities were identified. Of these, 36.6% (158) were related to human error, 32% (138/432) were related to surgical pathologies and the remaining 31.9% (136/432) were related to systemic diseases. There was an exponential increase in the reporting of morbidity each year. The total in-hospital mortality was 3% (358/10 682). Following the introduction of the HEMR, from 2012 to 2014, 6 217 patients were admitted. A total of 1 314 (21.1%) adverse events and 315 (5.1%) deaths were recorded by the HEMR. The adverse events were divided into 875 ‘pathology-related’ morbidities and 439 ‘error-related’ morbidities.

Conclusions. The development of the MMC led to increased reporting of morbidity and mortality. The introduction of the HEMR resulted in a dramatic improvement in the capturing of morbidity and mortality data, suggesting that a paper-based self-reporting system tends to underestimate morbidity. Over one-third of all morbidities were related to human error. Common morbidities have been identified.

S Afr Med J 2016;106(7):695-698. DOI:10.7196/SAMJ.2016.v106i7.10549

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i7.10549

Risk factors and outcomes of contrast-induced nephropathy in hospitalised South Africans J Banda,1,2 MB ChB, MMed; R Duarte,1 MSc, PhD; C Dickens,1 MSc, PhD; T Dix-Peek,1 MSc; M Muteba,3 MB ChB, MSc; G Paget,1,2 FCP, Cert Nephrol, MMed; V Mngomezulu,4 FRCRad; P Manga,1,5 FCP, FRCP, PhD; S Naicker,1,2 FCP, FRCP, PhD Department of Internal Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Division of Nephrology, Charlotte Maxeke Johannesburg Academic Hospital, Johannesburg, South Africa 3 Health Sciences Research Office, University of the Witwatersrand, Johannesburg, South Africa 4 Division of Radiology, Charlotte Maxeke Johannesburg Academic Hospital, Johannesburg, South Africa 5 Division of Cardiology, Charlotte Maxeke Johannesburg Academic Hospital, Johannesburg, South Africa 1 2

Corresponding author: J Banda (katusib@yahoo.co.uk)

Background. Despite ranking third as a cause of hospital-acquired acute kidney injury (AKI), iatrogenic contrast-induced nephropathy (CIN) impacts significantly on morbidity and mortality and is associated with high hospital costs. In sub-Saharan Africa, the rates and risk factors for CIN and patient outcomes remain unexplored.

Methods. We conducted a prospective observational study at the Charlotte Maxeke Johannesburg Academic Hospital, South Africa, from 1 July 2014 to 30 July 2015. Hospitalised patients undergoing computed tomography scan contrast media administration and angiography

59

July 2016, Print edition

RESEARCH

were consecutively recruited to the study and followed up for development of AKI. CIN was defined as an increase in serum creatinine >25% or an absolute increase of >44 µmol/L from baseline at 48 - 72 hours post exposure to contrast media. Outcome variables were the occurrence of CIN, length of hospitalisation and in-hospital mortality.

Results. We recruited 371 hospitalised patients with a mean (standard deviation) age of 49.3 (15.9). The rates of CIN, assessed using an absolute or relative increase in serum creatinine from baseline, were 4.6% and 16.4%, respectively. Anaemia was an independent predictor for the development of CIN (risk ratio (RR) 1.71, 95% confidence interval (CI) 1.01 - 2.87; p=0.04). The median serum albumin was 34 g/L (interquartile range (IQR) 29 - 39.5) and 38 g/L (IQR 31 - 42) in the CIN and control groups, respectively (p=0.01), and showed a significant trend for CIN development (RR 1.68, 95% CI 0.96 - 2.92; p=0.06). Mortality was significantly increased in the CIN group (22.4% v. 6.8%; p<0.001), and CIN together with anaemia increased mortality twofold (RR 2.39, 95% CI 1.20 - 4.75; p=0.01) and threefold (RR 3.32, 95% CI 1.48 - 7.43; p=0.003), respectively.

Conclusions. CIN has a relatively high incidence in sub-Saharan Africa and predicts poorer clinical outcomes. The presence of CIN and anaemia positively predicted mortality. Caution should be exercised in patients with hypoalbuminaemia and anaemia undergoing contrast media administration.

S Afr Med J 2016;106(7):699-703. DOI:10.7196/SAMJ.2016.v106i7.10429

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i7.10429

Major decline in malaria morbidity and mortality in the Union of Comoros between 2010 and 2014: The effect of a combination of prevention and control measures S A Kassim,1,4 PhD; P B James,2 MSc; R N Alolga,3 PhD; A G Assanhou,3 PhD; S M Kassim,4 MD; A Bacar,5 MD; R Silai,5 MSc; L Tian,1 MSc; H Li,1 PhD; A Ma,1 PhD S chool of International Economics and Trade, China Pharmaceutical University, Nanjing, China Department of Social and Administrative Pharmacy, School of International Economics and Trade, China Pharmaceutical University, Nanjing, China 3 School of Pharmacy, China Pharmaceutical University, Nanjing, China 4 Department of Internal Medicine – Gastroenterology, Southern Medical University, Guangzhou, China 5 National Malaria Control Center, Ministry of Health, Moroni, Comoros 1 2

Corresponding author: A Ma (maaixia@cpu.edu.cn)

Background. Malaria remains a public health challenge in sub-Saharan Africa. In response to this, many countries are working towards achieving the World Health Assembly and Roll Back Malaria Partnership target of a 75% decline in malaria incidence.

Objective. To assess trends in malaria morbidity and mortality in the three islands of the Comoros Archipelago from 2010 to 2014.

Methods. This was a retrospective study in which all confirmed malaria cases and deaths recorded between 2010 and 2014 were accessed from the national malaria control database. Trends and comparisons in malaria incidence and case fatality rates for all age groups, including under-5 children and pregnant women, were analysed using Microsoft Excel and SPSS version 16.

Results. A substantial decline in malaria incidence was observed for each island between 2010 and 2014; from 75.98 cases per 1 000 population in 2010 to 0.14 in 2014 in Moheli, 60.60 to 0.02 in Anjouan and 235.36 to 5.47 in Grand Comoro. Additionally, a general reduction in malaria case fatalities was observed. In Moheli, there were no case fatalities between 2010 and 2014, while there was a decline in the case fatality rate in Anjouan (from 1.20 fatalities per 1 000 cases to 0) and Grand Comoros (0.51 to 0). There were also significant differences (p<0.05) in malaria incidence and case fatalities between the three islands. A similar trend was observed for pregnant women and under-5 children.

Conclusions. Our study indicates a significant decline in malaria morbidity and mortality in the islands of Moheli, Anjouan and Grand Comoro from 2010 to 2014. This considerable reduction is attributed to a combination of malaria prevention and control interventions implemented during the study period.

S Afr Med J 2016;106(7):709-714. DOI:10.7196/SAMJ.2016.v106i7.10902

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i7.10902

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July 2016, Print edition

RESEARCH

Measles outbreak reveals measles susceptibility among adults in Namibia, 2009 - 2011 I U Ogbuanu,1,2 MD, PhD, MPH; C Muroua,3 BSN; M Allies,3 BA; K Chitala;4 S Gerber,5 MPH; P Shilunga;3 P Mhata;6 J L Kriss,1 PhD, MPH; L Caparos,7 BSc; S B Smit,8 MSc (Med); R J de Wee,9 MPH; J L Goodson,1 MPH lobal Immunization Division, Center for Global Health, US Centers for Disease Control and Prevention, Atlanta, USA G Department of Immunization, Vaccines and Biologicals, World Health Organization, Geneva, Switzerland 3 Ministry of Health and Social Services, Windhoek, Namibia 4 Inter-country Support Team for Eastern and Southern Africa, World Health Organization, Nairobi, Kenya 5 Namibia Country Office, Center for Global Health, US Centers for Disease Control and Prevention, Windhoek, Namibia 6 World Health Organization Field Office, Oshakati, Namibia 7 Namibia Institute of Pathology, Windhoek, Namibia 8 Centre for Vaccines and Immunology, National Institute for Communicable Diseases, Johannesburg, South Africa 9 Office of the World Health Organization Representative in Namibia, Windhoek, Namibia 1 2

Corresponding author: I Ogbuanu (ogbuanui@who.int)

Background. The World Health Organization, African Region, set the goal of achieving measles elimination by 2020. Namibia was one of seven African countries to implement an accelerated measles control strategy beginning in 1996. Following implementation of this strategy, measles incidence decreased; however, between 2009 and 2011 a major outbreak occurred in Namibia.

Methods. Measles vaccination coverage data were analysed and a descriptive epidemiological analysis of the measles outbreak was conducted using measles case-based surveillance and laboratory data.

Results. During 1989 - 2008, MCV1 (the first routine dose of measles vaccine) coverage increased from 56% to 73% and five supplementary immunisation activities were implemented. During the outbreak (August 2009 - February 2011), 4 605 suspected measles cases were reported; of these, 3 256 were confirmed by laboratory testing or epidemiological linkage. Opuwo, a largely rural district in north-western Namibia with nomadic populations, had the highest confirmed measles incidence (16 427 cases per million). Infants aged â&#x2030;¤11 months had the highest cumulative age-specific incidence (9 252 cases per million) and comprised 22% of all confirmed cases; however, cases occurred across a wide age range, including adults aged â&#x2030;Ľ30 years. Among confirmed cases, 85% were unvaccinated or had unknown vaccination history. The predominantly detected measles virus genotype was B3, circulating in concurrent outbreaks in southern Africa, and B2, previously detected in Angola.

Conclusion. A large-scale measles outbreak with sustained transmission over 18 months occurred in Namibia, probably caused by importation.

The wide age distribution of cases indicated measles-susceptible individuals accumulated over several decades prior to the start of the outbreak.

S Afr Med J 2016;106(7):715-720. DOI:10.7196/SAMJ.2016.v106i7.10651

Full article available online at http://dx.doi.org/10.7196/SAMJ.2016.v106i7.10651

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July 2016, Print edition

CAREERS & CLASSIFIEDS Tel: 012 481 2121 | E-mail: ladinev@hmpg.co.za We accept credit card payments - Visa or MasterCard.

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People feel cared for as individuals Paediatric Au Paedia Audiologist udiologist Our East Kent Children’s Hearing Service are looking for a new Paediatric Audiologist to join their team. Our team is based in Canterbury, a historic city within the garden of England and you will be expected to travel to a number of sites within East Kent.

As part of this role you will work autonomously and as part of a team providing a comprehensive range of services to children from birth to 18 years. You will have responsibility for Audiological assessment and rehabilitation, whilst ensuring the delivery of a high quality service for patients.

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You will also work to support the Consultant Audiovestibular Physician and the Lead Paediatric Audiologist in providing a high quality service.

You will have a BSc in Audiology or equivalent and will be an excellent communicator with an ability to work with a diverse population.

To apply please visit the NHS website at www.jobs.nhs.uk and search reference number 344-3033SDK. Closing date: 22 July 2016.

We are actively encouraging equal opportunities. The Trust operates a complete smoking ban on all sites and grounds.

All posts are subject to a DBS check from the Disclosure and Barring service in the event of the post being offered.

The Trust is committed to safeguarding children and vulnerable adults.

Visit www.ekhuft.nhs.uk

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Please send CV to: Dr Pierre Theron Fax: 0865118317 Email: pdtheron@iafrica.com Sms: 0825701341

Tel: 011 941 3796 Email: blyne@meredalemed.co.za

SAMF

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True (A) or false (B): SAMJ Ending preventable child deaths in South Africa (SA): What role can ward-based outreach teams play?

1. HIV/AIDS is no longer the leading cause of under-5 mortality in SA. 2. Lower respiratory tract infections and diarrhoea were recently found to be the most common causes of sudden unexpected natu­ral deaths among children aged <5 years in Cape Town and Durban.

Analysing 5 years of metropolitan morbidity and mortality confer­­ ences in an SA trauma service identifies common errors and morbidities, which need to be specifically targeted by quality improvement interventions 3. Self-reporting of morbidity is generally believed to result in a significant underestimation of morbidity.

Risk factors and outcomes of contrast-induced nephropathy in hospitalised South Africans 4. Iatrogenic contrast-induced nephropathy ranks third as a cause of hospital-acquired acute kidney injury.

5.

Contrast-induced nephropathy was defined as an increase in serum creatinine of >25% or an absolute increase of >44 µmol/L from baseline 48 - 72 hours after exposure to contrast media.

Major decline in malaria morbidity and mortality in the Union of Comoros between 2010 and 2014: The effect of a combination of prevention and control measures 6. Malaria accounted for 163 million cases and 528 000 deaths in sub-Saharan Africa in 2013.

Measles outbreak reveals measles susceptibility among adults in Namibia, 2009 - 2011 7. The World Health Organization African Region has a goal of elimination of measles in the area by 2020.

8. Seven African countries have implemented an accelerated measles control strategy since 1996.

How long are elderly breast cancer patients followed up with a mammo­gram after the diagnosis of breast cancer? A single-centre experience in a developing country (online only) 9. Increasing age is the largest single risk factor for the development of breast cancer.

10. Women have an overall lifetime risk of developing breast cancer of 1 in 35.

CME Adolescence: The age of Proteus 11. Adolescents make up more than a quarter of the world’s population.

12. Children born to women aged <19 and >35 years may have increased adult fasting glucose concentrations.

13. There is no need to screen adolescents for non-communicable diseases.

14. Abdominal ultrasound measurement for subcutaneous and visc­ eral fat determination is useful for establishing overweight and obesity.

15. There is emerging evidence that exposure to various challenges during fetal life, especially environmental and nutritional factors, but probably also infection and other factors, is associated with later-life health outcomes.

A weighty matter: The identification and management of over­ weight and obesity in adolescents 16. Cardiometabolic abnormalities are common in overweight and obese adolescents.

17. The body mass index is a good proxy for adiposity in adolescents.

18. It is not necessary to screen regularly for cardiometabolic abnor­ malities in overweight adolescents.

19. Intervention in obesity in adolescents is necessary, even in the absence of comorbidities.

20. It is highly likely that an obese adolescent will become an obese adult.

Readers please note: articles may appear in summary/abstract form in the print edition of the Journal, with the full article available online at www.samj.org.za

A maximum of 3 CEUs will be awarded per correctly completed test.

INSTRUCTIONS 1. Read the journal. All the answers will be found there, in print or online.

2. Go to www.mpconsulting.co.za to answer the questions.

Accreditation number: MDB015/038/01/2016

July 2016, Print edition

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