SAMJ Vol 105, No 4 (2015)

APRIL 2015

VOL. 105 NO. 4

Basic and comprehensive emergency obstetric and neonatal care

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Optimal staffing to ensure safe maternity units

261

Food insecurity in urban South Africa

268

Management of obstetric haemorrhage

271

MMed supervision – a path out of the swamp

275

Caesarean section and maternal death – latest Saving Mothers report

287

Intrapartum asphyxia and hypoxic encephalopathy

298

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APRIL 2015

GUEST EDITORIAL

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Medical ethics and human rights in wartime G J Annas

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EDITOR’S CHOICE

VOL. 105 NO. 4

EDITOR Janet Seggie, BSc (Hons), MD (Birm), FRCP (Lond), FCP (SA) EDITOR EMERITUS Daniel J Ncayiyana, MD (Groningen), FACOG, MD (Hon), FCM (Hon)

CORRESPONDENCE 243

Community paediatrics and child health A E Goga, U Feucht, M Hendricks, A Westwood, H Saloojee, G Swingler, N McKerrow, D Sanders

IZINDABA

CONSULTING EDITOR JP de V van Niekerk, MD, FRCR DEPUTY EDITOR Bridget Farham, BSc (Hons), PhD, MB ChB SCIENTIFIC EDITOR Ingrid Nye, BSc

244 245 247 248 250 251

Another law change prevents proper healthcare delivery The ‘axe man’ departs, offering hard-won lessons Saving our newborns by doing the basics right – and keeping it simple Turning nutrition on its head – Noakes gets his day Basson slapped down by committee World’s first successful penis transplant at Tygerberg Hospital

TECHNICAL EDITORS Emma Buchanan, BA Paula van der Bijl, BA, HDipLib

253 254

OBITUARIES Stephen Hough Max Klein

HEAD OF PUBLISHING Robert Arendse

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BOOK REVIEW Malignant: How Cancer Becomes Us

NEWS EDITOR Chris Bateman | Email: chrisb@hmpg.co.za CEO AND PUBLISHER Hannah Kikaya

PRODUCTION MANAGER Emma Jane Couzens ART DIRECTOR Brent Meder

SAMJ FORUM

256

HEALTHCARE DELIVERY Basic and comprehensive emergency obstetric and neonatal care in 12 South African health districts R C Pattinson, J D Makin, Y Pillay, N van den Broek, J Moodley

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Safety versus accessibility in maternal and perinatal care R C Pattinson

266

Women’s willingness to use emergency contraception: Experience at Chris Hani Baragwanath Academic Hospital, Johannesburg, South Africa* T A Lukhaimane, Y Adam

268

ISSUES IN PUBLIC HEALTH Food insecurity in households in informal settlements in urban South Africa* N Naicker, A Mathee, J Teare

271

MANAGEMENT OF OBSTETRIC HAEMORRHAGE Oxytocin – ensuring appropriate use and balancing efficacy with safety Z Farina, S Fawcus

275

MEDICAL EDUCATION MMed cohort supervision: A path out of the swamp?

C Rout, T Sommerville, C Aldous

277

OPINION Resuscitating an ethical climate in the health system: The role of healthcare workers* P Pillay

279

Traditional health practitioners and the authority to issue medical certificates* B Tshehla

281

EDITORIALS The HIV/HBV co-infected patient: Time for proactive management M I Andersson, W Preiser, C van Rensburg, J Taljaard, C J Hoffmann

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April 2015, Vol. 105, No. 4

DTP & DESIGN Carl Sampson ONLINE MANAGER Gertrude Fani DISTRIBUTION MANAGER Edward Macdonald | Tel. 021-681-7085 HEAD OF SALES AND MARKETING Diane Smith | Tel. 012-481-2069 Email: dianes@samedical.org PROFESSIONAL ADVERTISING Bronlyne Granger | Tel. 021-681-7000 E-mail: bronlyne.granger@hmpg.co.za HMPG BOARD OF DIRECTORS Prof. M Lukhele (Chair), Dr M R Abbas, Dr M J Grootboom, Mrs H Kikaya, Adv. Y Lemmer, Prof. E L Mazwai, Dr M Mbokota, Mr G Steyn, Dr G Wolvaardt ASSOCIATE EDITORS Q Abdool Karim, A Dhai, N Khumalo, R C Pattinson, A Rothberg, A A Stulting, J Surka, B Taylor, M Blockman ISSN 0256-9574 Publisher website: www.hmpg.co.za SAMA website: www.samedical.org Journal website: www.samj.org.za

LOSARTAN 50 mg | 100 mg HCTZ 12,5 mg | 25 mg 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 Zartan Co 50/12,5 mg. Each film coated tablet contains 50 mg losartan potassium and 12,5 mg hydrochlorothiazide. Reg. No.: RSA S3 42/7.1.3/1068. NAM NS2 12/7.1.3/0070. Zartan Co 100/25 mg. Each film coated tablet contains 100 mg losartan potassium and 25 mg hydrochlorothiazide. Reg. No.: RSA S3 42/7.1.3/1069. NAM NS2 12/7.1.3/0071. For full prescribing information, refer to the package insert approved by the Medicines Control Council, 05 August 2011. ZNCC92/03/2015.

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Of ambivalence, shame and guilt: Perceptions regarding termination of pregnancy among South African women U Subramaney, G E Wyatt, J K Williams

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Abuse in South African maternity settings is a disgrace: Potential solutions to the problem S Honikman, S Fawcus, I Meintjes

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Containing contraceptive costs N D Goldstuck

RESEARCH 287 Maternal death and caesarean section in South Africa: Results from the 2011 - 2013

Saving Mothers Report of the National Committee for Confidential Enquiries into Maternal Deaths

G S Gebhardt, S Fawcus, J Moodley, Z Farina, for the National Committee for Confidential

Enquiries into Maternal Deaths in South Africa 292

Utility of the Robson Ten Group Classification System to determine appropriateness of caesarean section at a rural regional hospital in KwaZulu-Natal, South Africa V Makhanya, L Govender, J Moodley

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Office-based sperm concentration: A simplified method for intrauterine insemination therapy* D R Franken

298

Intrapartum asphyxia and hypoxic ischaemic encephalopathy in a public hospital: Incidence and predictors of poor outcome* E K Bruckmann, S Velaphi

304

Early sexual debut: Voluntary or coerced? Evidence from longitudinal data in South Africa – the Birth to Twenty Plus study* L Richter, M Mabaso, J Ramjith, S A Norris

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Pathological findings in reduction mammoplasty specimens: A South African perspective* C Sofianos, R J Zinn, D A Geoffreys, D Kruger

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Comparison of findings using ultrasonography and cystoscopy in urogenital schistosomiasis in a public health centre in rural Angola* J Santos, J Chaves, H Araújo, N Vale, J M Costa, P J Brindley, C Lopes, J Naples, C Shiff, J Dupret, L L Santos

CONTINUING MEDICAL EDUCATION

GUEST EDITORIAL Chronic kidney disease† A Motsoaledi

REVIEW 316 Paediatric chronic kidney disease

I van Biljon, A M Meyers

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Subscriptions: Tel. 012-481-2071 E-mail: 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. Suites 9 & 10, Lonsdale Building, Gardner Way, Pinelands, 7405 Tel. 021-681-7200 E-mail: publishing@hmpg.co.za Website: www.samedical.org 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 – Noncommercial Works License. http://creativecommons.org/licenses/bync/3.0 Plagiarism is defined as the use of another’s work, words or ideas without attribution or permission, and representation of them as one’s own original work. Manuscripts containing plagiarism will not be considered for publication in the SAMJ. For more information on our plagiarism policy, please visit http://www.samj.org.za/ index.php/samj/about/editorialPolicies Printed by Creda Communications

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ARTICLES Important causes of chronic kidney disease in South Africa* M R Moosa, I van der Walt, S Naicker, A M Meyers

321

Important complications of chronic kidney disease* I van der Walt, C R Swanepoel, B Mahala, A M Meyers

322

Drugs and the kidney* S Naidoo, A M Meyers

List of contributors to the articles and information compiled by the National Kidney Foundation of South Africa† F du Toit

*Full article available online only.

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April 2015, Vol. 105, No. 4

GUEST EDITORIAL

Medical ethics and human rights in wartime The ethical obligations of physicians to respect and protect the human rights of all people are well articulated in international medical ethics statements.

For example, the World Medical Association (WMA)’s Declaration of Geneva (1948) obligates physicians to swear that ‘I will not use my medical knowledge contrary to the laws of humanity.’

Dr Wouter Basson was charged with violating this medical ethics norm during the time he was in the military working with Project Coast and Delta G, specifically by ‘leading a process where chemical substances for warfare were manufactured, weaponized and provided for use in combat, kidnapping and suicide’. The Professional Conduct Committee (PCC), charged with deciding whether he should retain his licence to practise medicine, relied primarily on the Declaration of Geneva, the WMA’s Regulations in Time of Armed Conflict (1956, 1983), to identify medical norms of conduct that he violated (‘Medical ethics in the time of armed conflict is identical to medical ethics in the time of peace …’), and the United Nations Convention on Biological and Toxin Weapons (1972) (prohibiting the development or production of any biological agents or toxins). The PCC was also powerfully aided in its careful articulation of medical ethics norms by the testimony of an international expert on wartime medical ethics from the USA, Dr Steven Miles. The PCC described Miles as ‘the outstanding expert on the conventions and medical ethics’ and as ‘fair’ and ‘highly professional’.

Basson defended himself by arguing that he was not bound by medical ethics during wartime or when under military orders, that he was acting as a soldier not a doctor, that he was not in a doctorpatient relationship, that he did not know that there were medical ethics codes that prohibited his actions, and that the medical ethics of the 1980s was different from today’s medical ethics. While the PCC did not cite the precedent, these arguments were substantially identical to those that were used by the Nazi doctors to defend their conduct at the 1946 - 1947 Nuremberg Doctors’ Trial (which was a criminal trial, with a higher standard of proof than a civil trial for licensure revocation) and that were rejected by the US judges presiding over that trial. The PCC specifically held, among other things, that ‘in South Africa, the medical ethics during war and peace are identical’; that a doctor is responsible for his own actions and cannot escape responsibility by relying on a military order; that as long as a doctor retains his licence he is required to follow medical ethics; and that the absence of a doctor-patient relationship does not relieve the physician of his ethics obligations to the public.

I find all these conclusions reasonable and responsible, but in my opinion the most important and instructive conclusion of the PCC is that if a military physician wants to put military actions before his or her medical obliation to do no harm, he or she must resign from being a physician. In the PCC’s words, only after the physician ‘de-register[s] from the council ... will [he or she] be relieved of the privileges and responsibilities of a doctor’. The PCC did not add, but I think it is implicit, that there is no returning to the practice of medicine after this decision has been made.

Outside of South America, it has been relatively rare for licensing boards to charge physicians with war crimes or crimes against humanity.

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The UK has taken action against a military physician who acted as an accessory to torture in Iraq (under Saddam Hussein), and another who failed to report suspected torture of prisoners while serv­ing with the UK military in Afghanistan. No state licensing body in the USA has taken any action against US military or CIA physicians who have participated in torture or inhuman treatment of prisoners at CIA black sites and Guantanamo Bay. This is shameful, although somewhat understandable as the US government has done all it can to keep the identities of the physicians working for and with the CIA and the US military a secret. Even with the release of the US Senate Intelligence Committee Report on Torture[1] in late 2014, which describes torture committed by US physicians and other health professionals at the 9/11 CIA black sites in excruciating detail, the identities of all but two contract psychologists remain secret. This is unacceptable. As the UN High Commissioner for Human Rights said in commenting on the report before the UN Human Rights Council in March 2015, the report is ‘courageous and commendable’ but must be ‘followed through with real accountability … torture cannot be amnestied’.[2] For most Americans it is especially painful to recall Archbishop Desmond Tutu’s words shortly after 9/11 when Guantanamo Bay prison was opened: ‘I never imagined I would live to see the day that the USA and its satellites would use precisely the same arguments that the apartheid government used for detention without trial. It’s disgraceful.’ Archbishop Tutu was and is correct; and it is just as disturbing to see Basson using the same excuses for his actions that the Nazi physicians used to justify theirs. Americans always knew we had much to learn from Archbishop Tutu; now we know we have more yet to learn from South Africa’s PCC. Restricting physicians who have engaged in crimes against human­ ity from practising medicine is done not to punish them (that is the purpose of a criminal trial), but to protect the public and the medical profession. Physicians are licensed by the state to practise medicine for the benefit of the public and individual patients, and we must all trust ourselves and our health to them. When that trust is betrayed and physicians use their skills to harm at the direction of the state, it is a matter of protecting the integrity of the medical profession, as well as a form of selfdefence for potential patients, that their privilege to practise a healing profession be revoked or restricted.

George J Annas Warren Distinguished Professor and Chair of the Department of Health Law, Bioethics and Human Rights, Boston University School of Public Health, Mass, USA annasgj@bu.edu 1. Report of the US Senate Intelligence Committee on Torture (released December 2014). http://www. intelligence.senate.gov/study2014/sscistudy1.pdf (accessed 9 March 2015).

2. United Nations Human Rights. Opening Statement, Item 2, High Commissioner’s Annual Report. http://www.ohchr.org/EN/NewsEvents/Pages/DisplayNews.aspx?NewsID=15642&LangID=E (accessed 9 March 2015).

S Afr Med J 2015;105(4):240. DOI:10.7196/SAMJ.9529

April 2015, Vol. 105, No. 4

EDITOR’S CHOICE

Matters obstetric (and gynaecological) and neonatal

Much of this month’s SAMJ deals with the above. South Africa (SA)’s current level of maternal mortality is far higher than the 2015 Millennium Development Goal (MDG) 5 target of 38 maternal deaths per 100 000 live births,[1] meaning that this country has failed to fully meet the MDG 5 maternal health goal – to reduce the maternal mortality rate by threequarters and achieve universal access to reproductive health. But the good news is that over 90% of women are receiving antenatal care, and there is a relatively high contraceptive prevalence rate of over 60%.[1] Giving birth is risky in Africa, where most women deliver without skilled care and inequalities in care during pregnancy remain real.

Progress in reducing the number of teenage pregnancies has stalled, putting more young mothers at risk; poverty and lack of education perpetuate high adolescent birth rates; and progress in expanding the use of contraceptives by women has slowed, use of contraception being lowest among the poorest and least-educated women.

It is self-evident that ‘maternal mortality is both a multidimensional health and broader developmental challenge, and that improved sexual and reproductive health is also dependent on a range of other factors including education, decent work, safety, clean water and sanitation, and adequate transport facilities’.[1] The United Nations (UN) is focusing now on Sustainable Development Goals (SDGs) – 2015 is the Time for Global Action.[2] In this context, The Lancet has suggested that the UN’s Open Working Group, with its proposed 17 SDGs for the post2015 era, beginning with: ‘End poverty in all its forms everywhere’, seek Utopia … these 17 SDGs ‘are fairy tales, dressed in the bureaucratese of intergovernmental narcissism, adorned with the robes of multilateral paralysis, and poisoned by the acid of nation-state failure’.[3] At the recent World Economic Forum meeting in Davos,[4] the call was made for the perfectly real possibility of avoiding 40% of premature deaths between 2010 and 2030. This quantitative target for a 2015 SDG was broken down by cause of death: two-thirds of child, maternal and infectious disease deaths averted, together with onethird of premature deaths from non-communicable diseases (NCDs) and injuries. More recently, The Lancet pointed out that ‘In all major countries, except where the effects of HIV or political disturbances predominated, the risk of premature death has been decreasing in recent decades, and it will fall even faster over the next few decades if the new SDGs get the big causes of death taken even more seriously.’

To appreciate SA’s current obstetric status, the two Forum articles by Pattinson, who heads the South African Medical Research Council’s Maternal and Infant Health Care Strategies Unit, are required reading.

Safety versus accessibility in maternal and perinatal care

Pattinson[5] asserts that the starting point is the staff required to provide a safe maternity unit in the community health centres (CHCs) where most women deliver. Assuming that the appropriate equipment is available and the facility is open 24 hours a day, 7 days a week, at a minimum there need to be 10 professional nurses with midwifery/ advanced midwives to ensure safety for mother and baby in every maternity unit. Two norms are used that represent two extremes: the World Health Organization (WHO) norm, being the minimum number of professional nurses required to provide a maternity service, and the Greenfield norm, developed with SA circumstances in mind and viewed as the ideal, even if unattainable at present. Happily most of SA’s maternity units fall some way in between the two. To be cost-effective, safe units should do a minimum of 500 - 1 200 deliveries per year.

Pattinson insists that the solution to making maternity units both safer and more cost-effective is to realign services, so that all are properly functioning and are open 24 hours a day, 7 days a week. This will,

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however, make maternity services less accessible unless there is a system for the efficient and rapid transfer of emergency cases. Realignment of services and most of all improved emergency transport are not impossible to achieve, as demonstrated by the example of the Free State Province, where maternal mortality was halved by providing dedicated maternity care ambulances to expedite interfacility transport and by consolidating the caesarean section (CS) services.[6]

Basic and comprehensive emergency obstetric and neonatal care in 12 SA health districts

Pattinson and colleagues[7] found that the ability of CHCs and district hospitals to perform the lifesaving services of basic and comprehensive emergency obstetric and neonatal care (EmONC) in many of the districts was not consistently available. The three essential components of EmONC are: • Healthcare providers with sufficient knowledge and skills to recognise, stabilise and treat or refer the patient • Healthcare facilities with the essential lifesaving services available, such as capacity to perform CS • An efficient interfacility transfer system.

If these were universally in place in SA, they would prevent approximately 9 000 maternal and perinatal deaths.

Maternal death and CS in SA

In the latest (2011 - 2013) Saving Mothers report, the National Committee for Confidential Enquiries into Maternal Deaths (NCCEMD) highlights the large number of maternal deaths associated with CS.[8] The most serious issue remains bleeding during or after CS – of all the mothers who died during or after a CS, onethird suffered hypovolaemic shock (as a final cause of death).

The risk of a pregnant woman dying as a result of CS during the 2011 - 2013 triennium was almost three times that for vaginal delivery: the case fatality rate, expressed as the number of fatalities per 10 000 causally related to mode of delivery, was 6.7/10 000 for vaginal births and 18.9/10 000 for delivery by CS. The greatest problem was at district hospital level.

Of the 1 243 mothers who died during or after a CS, 42 (3.38% of all CS deaths) died as a result of bleeding problems during the procedure, and 180 (14.5% of all CS deaths) died from haemorrhage following the procedure. Deaths were assessed as clearly avoidable in 70% of cases of bleeding during CS and in 72% of cases of bleeding after CS; only 1.8% of women who died were assessed as having no suboptimal care.

Additional deaths of patients undergoing CS occurred in relation to preeclampsia and eclampsia (six times increased risk of dying), anaesthesia, pregnancy-related sepsis (three times increased risk of dying), and acute collapse and embolism (combined, a five times increased risk of dying).

The authors offer concrete recommendations aimed at reducing deaths from bleeding during or after CS, from CS in hypertensive conditions, from acute collapse, from embolism following CS and from post-CS sepsis.

They conclude by suggesting that everyone involved in surgical delivery should make a concentrated effort to decrease the number of deaths associated with the procedure. Accepting that medical students are ill-equipped to do surgery after graduation, yet are expected to do this major invasive procedure in women ‘with complex, altered physiology where complications that can challenge even a highly skilled doctor can arise within seconds’, they ask: ‘Could CS skills training not be incorporated into the undergraduate medical curriculum?’

In my own opinion the answer should be an emphatic ‘No’. Rather, the realignment of services to which Pattinson refers has to occur to consolidate the CS services while ensuring interfacility transport

April 2015, Vol. 105, No. 4

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EDITOR’S CHOICE

by providing dedicated maternity care ambulances.[6] This is surely reinforced by the findings of the NCCEMD[9] that the following major causes of the 2011 - 2013 deaths from hypovolaemia ascribed to haemorrhage were: • Inadequate utilisation of uterotonic agents • Poor recognition of the severity of blood loss • Inadequate surgical skill • Delays in relaparotomy and/or referral in case of post-CS bleeding.

The recognition and execution of the above are unlikely to be in the skills set of a newly qualified doctor.

Management of obstetric haemorrhage In their Forum article, Farina and Fawcus[9] offer recommendations for the routine prophylactic administration of oxytocin for the medical management of uterine atony at and after CS. These are summarised in the table on p. 273.

The topic for World Health Day 2015 is food safety.[14] Unsafe food is linked to the deaths of an estimated 2 million people annually – including many children. Naicker et al. [15] address the problem of food insecurity in households in informal settlements in urban SA in their Forum article, highlighting, perhaps predictably, the much higher level of food insecurity of our citizens who live in urban informal settlements, where poverty levels dictate the degree of such insecurity. Households with children are more likely to be food insecure. Confirming the well-documented finding that poor socioeconomic status is predictive of food insecurity, lack of full-time employment of the head of the household is significantly associated with an increased risk.

Another outcome of this study, in the context of the epidemic of NCDs, is the increased trend in consumption of fast foods, which climbed by 18% between 2006 and 2009, and has been sustained at this higher level of consumption in subsequent years!

JS

Intrapartum asphyxia and hypoxic ischaemic encephalopathy

A retrospective study at Chris Hani Baragwanath Hospital[10] reveals an incidence of asphyxia of 15/1 000 or 10/1 000 live births respectively, depending on need for assistance with breathing or Apgar score <7 at 5 minutes. Whichever definition is used, the incidence of asphyxia in this study is very high compared with that reported in developed countries, which approximates 1 - 5/1 000 live births. The overall incidence of encephalopathy in these infants was predictably high at 8.5/1 000 live births. Of such infants, 15 - 20% will die in the neonatal period while 25 - 30% of survivors will develop permanent neurodevelopmental abnormalities, including cerebral palsy.

MMed supervision

Food insecurity in informal settlements in urban SA

In my editorial last month,[11] I alluded to a rash of articles offered for publication derived from MMed theses, the mentorship of which is placing considerable strain on academics[12] because potential supervisors meeting all qualifying criteria are a scarce resource in many medical school departments. This month, Rout et al.[13] suggest a ‘path out of the swamp’ for MMed supervision … that of joint supervision. This is required reading for those tasked with having their young mentees succeed!

1. United Nations Development Programme in South Africa. http://www.undp.org/content/south_ africa/en/home/mdgoverview/overview/mdg5/ (accessed 27 February 2015).

2. United Nations. http://www.un.org/millenniumgoals/beyond2015-news.shtml (accessed 27 February 2015).

3. Horton R. Offline: Why the Sustainable Development Goals will fail. Lancet 2014;383(9936):2196. [http://dx.doi.org/10.1016/S0140-6736(14)61046-1] 4. Horton R. Offline: Can one turn an aspiration into reality? Lancet 2015;385(9967):492. [http://dx.doi. org/10.1016/S0140-6736(15)60161-1] 5. Pattinson RC. Safety versus accessibility in maternal and perinatal care. S Afr Med J 2015;105(4):261265. [http://dx.doi.org/10.7196/SAMJ.9182] 6. Schoon M. Impact of inter-facility transport on maternal mortality in the Free State Province. S Afr Med J 2013;103(8):534-537. [http://dx.doi.org/10.7196/SAMJ.6828] 7. Pattinson RC , Makin JD , Pillay Y, van den Broek N, Moodley J. Basic and comprehensive emergency obstetric and neonatal care in 12 South African health districts. S Afr Med J 2015;105(4):256-260. [http://dx.doi.org/10.7196/SAMJ.9181] 8. Gebhardt GS, Fawcus S, Moodley J, Farina Z, for the National Committee for Confidential Enquiries into Maternal Deaths in South Africa. Maternal death and caesarean section in South Africa: Results from the 2011 - 2013 Saving Mothers Report of the National Committee for Confidential Enquiries into Maternal Deaths. S Afr Med J 2015;105(4):287-291. [http://dx.doi.org/10.7196/SAMJ.9351] 9. Farina Z, Fawcus S. Oxytocin – ensuring appropriate use and balancing efficacy with safety. S Afr Med J 2015;105(4):271-274. [http://dx.doi.org/10.7196/SAMJ.9179] 10. Bruckmann EK, Velaphi S. Intrapartum asphyxia and hypoxic ischaemic encephalopathy in a public hospital: Incidence and predictors of poor outcome. S Afr Med J 2015;105(4):298-303. [http://dx.doi.org/10.7196/SAMJ.9140] 11. Seggie J. On getting published in the SAMJ. S Afr Med J 2015;105(2):77-78. [http://dx.doi.org/10.7196/ SAMJ.9348] 12. Aldous CM, Adhikari M, Rout CC. The research component of specialist registration – a question of alligators and swamps? A personal view. S Afr Med J 2015;105(1):21-22. [http://dx.doi.org/10.7196/SAMJ.8732] 13. Rout C, Sommerville T, Aldous CM. MMed cohort supervision: A path out of the swamp? S Afr Med J 2015;105(2):275-276. [http://dx.doi.org/10.7196/SAMJ.9338] 14. World Health Day 2015. http://www.who.int/campaigns/world-health-day/2015/event/en/ (accessed 27 February 2015).

15. Naicker N, Mathee A, Teare J. Food insecurity in households in informal settlements in urban South Africa. S Afr Med J 2015;105(2):268-270. [http://dx.doi.org/10.7196/SAMJ.8927]

Prof. George J Annas,* JD, MPH, is Warren Distinguished Professor and Chair of the Department of Health Law, Bioethics and Human Rights at the Boston University School of Public Health, Mass, USA. He is a leading scholar in the health and human rights field who has been a keen observer and commentator on human rights challenges in South Africa over many years. Former co-chair of the Massachusetts Board of Registration in Medicine, he is author of Worst Case Bioethics. *Annas GJ. Medical ethics and human rights in wartime. S Afr Med J 2015;105(4):240. [http://dx.doi.org/10.7196/SAMJ.9529]

Prof. Bob Pattinson*† is director of the South African Medical Research Council Maternal and Infant Health Care Strategies Research Unit and clinical head of the Department of Obstetrics and Gynaecology at the University of Pretoria. He serves on the National Committee for Confidential Enquiries into Maternal Deaths in South Africa and the National Perinatal Morbidity and Mortality Committee in South Africa, and is also responsible for the perinatal care and child health care surveys in South Africa. His research interests are in obstetrics, medical audits, health systems and effective methods of outreach, and his main research focus is currently on determining the most effective means of implementing new healthcare strategies, improving current programmes and determining the most efficient ways to scale up emergency obstetric care. * Pattinson RC, Makin JD, Pillay Y, van den Broek N, Moodley J. Basic and comprehensive emergency obstetric and neonatal care in 12 South African health districts. S Afr Med J 2015;105(4):256-260. [http://dx.doi.org/10.7196/SAMJ.9181] †

Pattinson RC. Safety versus accessibility in maternal and perinatal care. S Afr Med J 2015;105(4):261-265. [http://dx.doi.org/10.7196/SAMJ.9182]

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April 2015, Vol. 105, No. 4

CORRESPONDENCE

Community paediatrics and child health

To the Editor: In 2012, the Postgraduate Education Committee of the Health Professions Council of South Africa (HPCSA) supported the accreditation of Community Paediatrics and Child Health (CPCH) as a paediatric subspecialty; however, full HPCSA approval is outstanding. Consequently, by February 2015 there had been no visible progress towards implementation. Power and Heese[1] and Swingler et al.[2] highlighted the benefits of CPCH, rendering further debates about CPCH accreditation un­necessary, particularly in a country where: (i) progress towards the fourth Millennium Development Goal is slow; (ii) glaring gaps exist between hospital-based and community care, and between private and public sector care;[3] and (iii) current under- and postgraduate paediatric training emphasises clinical subspecialties (despite reduced public sector posts), yielding graduates with limited knowledge about priority child health conditions. Primary healthcare re-engineering and the establishment of district clinical specialist teams in South Africa have starkly revealed the urgency of CPCH training.[4] CPCH locates child health within a sociocultural-economic-political-environmental-systemic para­digm.[5] Successful community paediatricians share four characteristics:[6] (i) academic collaboration; (ii) finding evidencebased local solutions; (iii) establishing strong community-based partnerships; and (iv) addressing disease outside traditional biomedical models. This suggests that our sometimes narrow approach to under- and postgraduate training needs significant adaptation. The British Association for Community Child Health, affiliated to the Royal College of Paediatricians, is a successful model we can adapt.[7] This custodian of community paediatrics directs traineeships, stipulates requirements and outlines the scope of the discipline.

We suggest six actions to facilitate progress: 1. A pproval of CPCH as a subspecialty 2. Advocacy for CPCH and community paediatricians to create a demand at medical schools and among users in the community 3. Establishment of a pool of CPCH experts at medical schools to facilitate training in community paediatrics 4. A compulsory rotation in CPCH for all undergraduate medical students 5. Development of accredited training sites and posts for paediatricians wanting to subspecialise in CPCH 6. Revision of the paediatric registrar rotation to include a compulsory 6-month regional hospital or similar CPCH rotation.

The examples set by the University of the Witwatersrand (Community Paediatrics Division) and the University of Cape Town (School of Child and Adolescent Health, Postgraduate Diploma in Community

and General Paediatrics) should inspire the launch of similar programmes in other medical schools.

Unless community paediatric training is rapidly expanded and resourced, our current health policies will remain mere statements.

Where is the block, and can we be proactive?

Ameena E Goga

Health Systems Research Unit, South African Medical Research Council, Cape Town, South Africa, and Department of Paediatrics, School of Medicine, Faculty of Health Sciences, University of Pretoria, South Africa ameena.goga@mrc.ac.za

Ute Feucht

Department of Paediatrics, School of Medicine, Faculty of Health Sciences, University of Pretoria, South Africa, and Tshwane District Clinical Specialist Team, Gauteng Department of Health, Johannesburg, South Africa

Michael Hendricks Anthony Westwood

School of Child and Adolescent Health, Faculty of Health Sciences, University of Cape Town, South Africa

Haroon Saloojee

Division of Community Paediatrics, Department of Paediatrics and Child Health, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

George Swingler

School of Child and Adolescent Health, Faculty of Health Sciences, University of Cape Town, South Africa

Neil McKerrow

Department of Paediatrics and Child Health, Nelson R Mandela School of Medicine, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa, and Department of Health, KwaZulu-Natal

David Sanders

School of Child and Adolescent Health, Faculty of Health Sciences, University of Cape Town, South Africa, and School of Public Health, University of the Western Cape, Bellville, Cape Town 1. Power DJ, Heese HdeV. The role of community paediatrics in South Africa. S Afr Med J 1978;53(3):408-410 2. Swingler G, Hendricks M, Hall D, et al. Can a new paediatric sub-specialty improve child health in South Africa? S Afr Med J 2012;102(9):738-739. [http://dx.doi.org/10.7196/SAMJ.5714] 3. Mayosi BM. Benatar SR. Health and health care in South Africa – 20 years after Mandela. N Engl J Med 2014;371(14):1344-1353. [http://dx.doi.org/10.1056/NEJMsr1405012] 4. District Clinical Specialist Teams in South Africa: Ministerial Task Team Report to the Honourable Minister of Health, Dr Aaron Motsoaledi. http://www.rmchsa.org/wp-content/resources/resources_by_type/ DistrictLevelResources/MinisterialTTReport_DCSTInSouthAfrica.pdf (accessed 20 Febru­ary 2015).

5. Council on Community Pediatrics. Community pediatrics: Navigating the intersection of medicine, public health, and social determinants of children’s health. Pediatrics 2013:131(3):623-628. [http:// dx.doi.org/10.1542/peds.2012-3933] 6. Sanders L, Robinson T, Forster L, Plax K, Brosco J, Brito A. Evidence-based community pediatrics: Building a bridge from bedside to neighbourhood. Pediatrics 2005;115(4):1142-1147. [http://dx.doi. org/10.1542/peds.2004-2825H] 7. British Association for Community Child Health. Community child health and the future: A BACCH discussion paper. February 2005. http://www.bacch.org.uk/downloads/briefing_papers/community_ child_health_future.pdf (accessed 9 February 2015).

S Afr Med J 2015;105(4):243. DOI:10.7196/SAMJ.9558

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International Women's Day (IWD) was celebrated on 8 March. The first International Women's Day was held in 1911.

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Another law change prevents proper healthcare delivery[1] A year-old amendment to the Births and Deaths Registration Act, making the cause of death confidential to all but Statistics South Africa (Stats SA) officials, has effectively torpedoed mortality surveillance for public health planning in the Western Cape.

The Western Cape Department of Health (DoH) developed (from 2000 onwards) a sophisticated home-grown mortality data system, working with the City of Cape Town, the University of Cape Town and the South African Medical Research Council (SAMRC) to glean detailed public health information not available from national vital statistics. The province used this vital information not only for statistics but also to develop appropriately placed programmes to reduce diarrhoea deaths among children, and evaluate HIV, antiretroviral therapy (ART) and cervical cancer screening programmes. By January 2014, the City of Cape Town had developed an IT system that was capturing deaths by residential suburb within weeks of the date of death, automatically coding the underlying cause of death (CoD) in 70% of cases. The rapid availability of specific details of where people died and the CoD painted a much richer and clearer picture of the public health action required to address the problems faced by those specific communities. With limited resources and many competing needs, the data gleaned empowered health managers eager to make a difference. That all came to an abrupt end when the Department of Home Affairs (DHA), in an attempt to streamline its processing and maintain individual confidentiality, last February suddenly introduced a new death notification form with the CoD page sealed and only Stats SA legally empowered to open it.

Informed of the objections, StatisticianGeneral Mr Pali Lehohla took a hard line, claiming that what the Western Cape had been doing was ‘illegal’ and citing the media’s controversial accessing of the health records of the late Minister of Health Dr Manto TshablalaMsimang as an example of the violation of the doctor-patient relationship. He said that this ‘sacrosanct principle’ held equally true for the dead. Questioning why it was necessary to wait for a death before interventions were put in place, Lehohla said that stats drawn from health records (i.e. living patient consultations) could help build disease profiles. Anonymity was a ‘fundamental qualifier’ to the aggregates

Drs Pam Groenewald and Debbie Bradshaw of the SAMRC’s Burden of Disease Research Unit.

Stats SA produced on any phenomena of public interest. ‘Even with an application of the most sophisticated algorithm, such aggregates cannot be decomposed [sic] to reveal the specific individual to whom the phenomenon of public interest relates,’ he added. Lehohla cited both the abuse by Nazi Germany of census records to kill Jews during World War II and an alleged raid by Israel on Palestinian census records in order to ‘kill, maim and arrest’ its enemies. He said that Stats SA worked in accordance with the Fundamental Principles of Official Statistics endorsed by the UN General Assembly in January last year, which stated that individual data should remain strictly confidential and be used ‘exclusively for statistical purposes’.

According to Drs Debbie Bradshaw and Pam Groenewald, both highly respected researchers at the SAMRC’s Burden of Disease Research Unit, without a duplicate CoD page to enable a ‘feedback loop’ to health authorities, death notification effec­ tively becomes a one-way data flow, seemingly implying that the information is collected only for statistical purposes and displaying a low appreciation of the nation’s need to take public health action based on such information. The latest CoD report from Stats SA showed that only 48.4% of deaths occurred in healthcare facilities, with 23.2% occurring in homes. ‘It is precisely the deaths that occur without intervention which alert us to failings in our public health system, hence the tremendous value-add of CoD data which are universally sourced, irrespective of health service access,’ they stressed. The Director-General of Home Affairs was within his legal rights to share CoD information

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with the province’s health department – it was only when the Births and Deaths Registration Act was amended last year that this became ‘illegal’ through the death notification form.

The law lacked a stipulation giving health departments access to such information, as was done in the UK. The pair remain convinced that it’s possible to ‘responsibly’ recover this ability without compromising any of the principles highlighted by Lehohla.

Child pneumonia deaths at home – province now unable to respond

Groenewald said that following the signi­ficant reduction in diarrhoea deaths as a result of highly focused efforts informed by the diarrhoea death data, the City of Cape Town was currently on the brink of implementing a childhood pneumonia response after discovering that a significant number of young children were dying of the disease at home. ‘These cases get certified in the forensic morgue, but unless the information from the death notification is available to the health department, they will be unable to respond.’ Western Cape mortality surveillance had illustrated how morgue data and clinical data could be linked to death notification information to examine treatment failures and missed opportunities. She said that HIV and tuberculosis lent themselves to the monitoring of programme outcomes where loss to follow-up was identified as a problem.

Being able to access CoD data and link them with ART registers enabled far more accurate assessment of treatment loss to follow-up, with the possibility of adjusting the programmes accordingly. Said Groenewald: ‘In straight language, the legal amendment has torpedoed

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an essential tool that enabled the provincial DoH to review their programmes.’

The system works like this: somebody dies, a doctor has to (correctly and accurately, it is hoped) certify the medical CoD, and helped by an undertaker the bereaved family files these forms with the local DHA office to register the death. A burial certificate to formally authorise the disposal of the mortal remains is issued after the DHA checks the integrity of the forms and registers the death on the population register. The form is then sent to the DHA’s head office in Pretoria, where it is archived and sent on to Stats SA, who process the information for statistical purposes.

The system developed by the Western Cape DoH together with the City of Cape Town relied on obtaining the information from the regional offices of the DHA to create a surveillance system that was used to provide relevant local-level statistics as well as the opportunity for targeted public health action.

Other provinces: Why monitor causes of death when it’s illegal?

Groenewald laments the closure of the only functional local mortality surveillance system in the country, as a growing

body of evidence suggests that other provinces should be setting up similar systems. Lehohla hit back, saying this would undermine the country’s statistics system and asking ‘How much more will the state expose records of its citizens to unauthorised public display?’

Bradshaw said that DoH participation in mortality surveillance remained ‘key’.

‘It cannot merely be a statistical exercise.

The National Health Act needs to enable Health to have access to identifiable CoD information so that it can be fully utilised to improve the health of the nation. Health handles confidential clinical information all the time and should be well placed to preserve confidentiality of cause-of-death details, but as this law stands only Stats SA may look at individual death records and are not allowed to share it with Health.’

Window of hope

Stats SA is currently leading an evaluation of the civil registration and vital statistics system, providing an opportunity for review of the current legislation. A specific data quality concern that Groenewald believes needs fixing is the collection of information about causes of injury deaths.

Pathologists report the nature of the injury,

but fail to note what caused it. ‘So we don’t know if it’s an accident, homicide or suicide. When this information is coded, the international default is to allocate the unspecified injuries to accidents. Hence we see a lot of gunshot “accidents” in the national injury statistics,’ she said. The solution to this would be an additional space in the death notification form, enabling the pathologist to actually record the cause of the injury (manner of death).

Bradshaw said that the Stats SA evaluation was a great opportunity to ensure that the system of civil registration and vital statistics provided an effective platform for public health action as well as the compilation of national statistics. Both researchers are hoping for a meeting of minds – and that there will be a way to ensure that Health can access the vital data.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2015;105(3):244-245.

DOI:10.7196/SAMJ.9553 1. Bateman C. Zuma’s legal advisors ‘led him astray’, turned health­ care professionals into criminals. S Afr Med J 2015;105(3):196. [http://dx.doi.org/10.7196/SAMJ.9468]

The ‘axe man’ departs, offering hard-won lessons He may be remembered as ‘the axe man’ for his radical fiscal discipline, which included cutting beds in top tertiary hospitals, regulating private work and slashing commuted overtime, but Prof. Craig Househam, who retired as Western Cape health chief in March, was above all a strategist.

Prof. Craig Househam.

He willingly braved collegial umbrage when he believed a greater public good was at stake, and craftily confronted his political masters by deliberately provoking a nearuprising of doctors that made Pretoria so uncomfortable that seemingly threatened specialised Western Cape services were eventually retained.

Househam, 65, earned his ‘hard-core’ reputation while serving as the first health chief of the Free State immediately after the country’s first democratic elections, appointing and mentoring a raw but firstever representative management team and integrating the former homelands of QwaQwa and Bophuthatswana. It was here that he stiffened regulation of the Remuneration for Work Outside the Public Service (RWOPS) and cut commuted overtime, earning the epithet of ‘the butcher’ as he grasped the nettle of limited resource allocation to deliver more care to more people, often at the expense and outrage of high-end specialists.

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Househam joined the ANC in the early 1990s after cutting his medicopolitical teeth in bringing together the skills, academic knowledge and resources of the University of the Free State to better serve Bloemfontein’s majority black population (via a community project in Mangaung still significantly funded by the Kellogg Foundation). Once South Africa (SA)’s first democratic elections were over, the party wasted no time in seconding the Princeton, New Jersey-born and University of Cape Town (UCT)-trained paediatrician to co-ordinate the Free State’s strategic health and welfare management team – and to help advise on the same issues at national level.

Househam was subsequently appointed chief specialist/head of the Free State University’s Department of Paediatrics and Child Health (late 1988 to early 1995), where he had been lecturing for several years. Recalling his early days managing and transforming the Free State health department, Househam said workdays were often 20 hours long

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and ‘weekends became workdays’ – but he quickly learnt the ‘trick of reducing seemingly complex healthcare issues to simplicity by getting the basics right’.

‘Look for the simple in the complex’

Househam described healthcare complexi­ ties as potentially paralysing, particularly for inexperienced managers, and advised: ‘Look for the simple in the complex, because it is there if you look for it and once you have identified the key issues, deal with them.’ Bemoaning the ongoing and now-accelerating healthcare delivery implosion in the Free State, he said that within 3 years of his leaving there in February 2001, everything he’d achieved had been dismantled (his provincial health department had consistently remained within budget and had built up a ‘competent management team’). An analysis of why Free State delivery/management has failed so dramatically and what could have prevented similar situations elsewhere was essential ‘for an effective government in SA, but also for the very future of democracy’, he warned.

When he retired from active public service last month, Househam was the longestserving head of health in the country, the last remaining incumbent from 1995. He openly admits that he owes his initial public service career to the ANC, but stresses that once he became a public servant he deliberately avoided membership of any political party.

Of his unpopular move to the Western Cape, Househam recalls doctors gathered in protest in Groote Schuur Hospital’s Palm Court after his cutting of beds there, and at Tygerberg Hospital, repeated accusations of ‘putting cash before care’ and of ‘destroying a national asset’. He claims the bed reductions were ‘part of a predetermined strategy’ to force the National Department of Health and the National Treasury to review funding to the Western Cape for highly specialised care. ‘The furore created such discomfort nationally that the end result was an increased allocation to the Western Cape and the ability to retain specialised services at these hospitals – in effect, the bed reductions were reversed and funding secured,’ he asserts. Househam thanked his erstwhile opponents, who included top UCT surgeon Prof. Del Kahn and cardiologist and current UCT medicine chief Prof. Bongani Mayosi, for their help in ‘stabilising health funding in the Western Cape’, boasting that he fulfilled his remit, achieving financial stability in the province within 2 years of his appointment, with unqualified audits over the next decade.

Taking on the national health minister

More recently, in 2013, Househam took the unprecedented step (for him) of publicly disagreeing with national health minister Dr Aaron Motsoaledi over the proposed R173 million cut to the Western Cape’s conditional grants for funding highly specialised services and the intended centralisation of management of Groote Schuur and Tygerberg hospitals to Pretoria. Motsoaledi declared that the Western Cape was ‘going to war’ with his department, but reversed the proposed funding cut within a day, perhaps a telling mark of respect for Househam’s track record.

Househam willingly braved collegial umbrage when he believed a greater public good was at stake, and craftily confronted his political masters by deliberately provoking a nearuprising of doctors that made Pretoria so uncomfortable that seemingly threatened specialised Western Cape services were eventually retained.

Philosophising during a valedictory lecture at UCT, Househam said that defining the correct fiscal priorities was essential: ‘If one cannot purchase what one cannot afford, it is also important that what one can afford must be what is essential.’ This no-frills approach to the allocation of resources in the health sector conflicted with the unique doctorpatient relationship in which the doctor would strive at all times to do the best for his or her patient. Having been in clinical practice for 20 years, he was acutely aware of this responsibility, but as a health manager who was also a doctor he had been forced to ‘elevate my view to deal with the greater common good. This … placed me in direct conflict with clinical colleagues,’ he admitted.

Delegating responsibility to the coalface

One tool Househam fashioned to manage this inherent conflict creatively was the hospital ‘functional business unit’, headed by a clinician who was allocated a budget with staff to deliver an agreed amount of service with a suite of data allowing the clinician to measure, monitor and manage the service – for which they then took full responsibility.

While the job was often viewed as a ‘poisoned chalice’, Househam said it allowed doctors to

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be more involved in decisions that affected their practice, given that hospital doctors created expenditure by (for example) ordering X-ray probes and blood tests, prescribing medication and deciding on surgery. ‘I was encouraged by instances where clinicians enthusiastically accepted this responsibility instead of being frustrated by the “pen pushers” in Dorp Street [the Western Cape health department’s headquarters]’, he said.

Turning to the much politically abused truism that the Western Cape is a privileged, well-resourced province that suffers less from the legacies of apartheid than other provinces, Househam said that anyone using this argument to justify the challenges faced in the health sectors in other provinces 20 years into the country’s democratic transition was less than convincing. Many health departments wasted much time sitting in meetings, strategising, writing documents and talking about problems when it was ‘the individual’ who took decisions. ‘My recipe for effective service delivery is empowering people in management to make decisions and then take responsibility for them. Support people if they make a genuine mistake … we all do.

I have an intolerance of incompetence – but a greater intolerance of people who just don’t care.’ Reminiscing on the AIDS denialism days of Mbeki and Tshabalala-Msimang, he said that he sat through numerous presentations of ‘quack’ cures by now-infamous denialists such as Dr David Rasnick, Dr Peter Duesberg and Dr Matthias Rath and his Foundation, not to mention the Presidential Advisory Panel that submitted a highly contentious report to President Mbeki in March 2001. ‘It was surreal to be present at some of these interactions, and some of my academic colleagues sought me out to try and understand what was going on.’ He recalled being confronted by ‘incredulous’ fellow paediatrician Professor Jerry Coovadia, asking for advice on how to approach Tshabalala-Msimang. ‘Needless to say I was not of much assistance – for me the ultimate humiliation as a South African was witnessing the fracas around the SA exhibition at the 2006 World AIDS conference in Toronto when the national health minister taunted the international media with cloves of garlic.’

Working for change ‘from within’

Asked whether he should have resigned, he said he was ‘still troubled’ by having partici­ pated, albeit indirectly, in a system that ‘allowed people to die and babies to be unnecessarily infec­ ted as a result of the unavailability of antiretroviral therapy’. ‘My justification for deciding to stay was that I could do more working within the system then I would have

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been able to achieve outside of it – I leave it to others to pass judgement on the validity of my decision,’ he added, pointing to the Western Cape’s pioneering of antiretrovirals via various trials and non-profit organisations, plus his department’s ground-breaking treatment for prevention of mother-to-child transmission of HIV, despite the political antipathy prevailing at the time. In a fascinating allusion to the oft-cited cause of nationwide dysfunctional healthcare delivery (the federal government system that gives almost complete autonomy to provinces), Househam revealed that this

was the very reason he turned down the job of national health Director-General in 2009.

Despite believing he could do the job, he thought he was the wrong person to ‘manage the political interface’ and that he would have been unable to directly influence healthcare delivery in the provinces. Despite many people accusing him of having let ‘them and the country down’, he still believed it was the correct decision, because he was able to contribute more by remaining the Western Cape health chief.

Househam will be succeeded by Dr Beth Engelbrecht, a previous Director of District

Health Services for the Free State who joined the Western Cape DoH in 2001 as Deputy Director-General. She was effectively Chief of Operations with responsibilities that included specialist health services, emergency services, and district and primary health services.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2015;105(3):245-247.

DOI:10.7196/SAMJ.9589

Saving our newborns by doing the basics right – and keeping it simple Just basic interventions could reduce South Africa (SA)’s neonatal death rate by up to 90%, according to a world-acclaimed innovator in cheap, child-friendly therapies, Prof. Heather Zar, chief of Paediatrics and Child Health at Red Cross War Memorial Children’s Hospital in Cape Town.

In view of the absence of significant reduction in SA’s neonatal mortality rate over the past decade and the country failing dismally to reach this year’s Millennium Development Goal (MDG) of reducing its 1990 child mortality rate by two-thirds, Izindaba quizzed Zar on the most vital interventions required.

Antenatal steroids to mature a baby’s lungs when its mother is in preterm labour, the now world-famous kangaroo care, exclusive breastfeeding, optimal labour and delivery management, neonatal resuscitation and optimal postnatal care including appropriate treatment of neonatal sepsis would, taken together, send the neonatal death rate plummeting, she said.

In preventing preterm delivery, better ante­ natal and obstetric care would also go a long way to ensure safer delivery and effective subse­ quent postnatal care, she added. When it came to reducing under-5 mortality (another MDG SA didn’t achieve), several well-known effective preventive strategies such as immunisation, optimising nutrition, breastfeeding, provision of antiretroviral therapy and prevention of motherto-child transmission (PMTCT) of HIV were required. As neonatal deaths make up almost a third of under-5 deaths, strategies to reduce deaths in the first 28 days of life (and especially in the first 7 days) could have a big impact on the under-5 mortality rate.

Where we have done well …

The above are all areas in which SA has improved by varying degrees, especially PMTCT, where major reductions in HIV infections have for the first time put almost zero transmission within reach, achieving world acclaim. Vaccines for children were a growing local success story, with rates of invasive pneumococcal disease – including cases caused by antibiotic-resistant bacteria – having fallen substantially following the introduction of a pneumococcal conjugate vaccine. The rate of infections resistant to two different antibiotics had declined nearly twice as much as that for infections that could be treated with antibiotics. This proportionately greater effect of vaccination on antibiotic-resistant strains pointed to a very valuable added benefit of immunisation.

Zar said that a maternal influenza vaccine during pregnancy had also recently been shown to substantially reduce influenza in mothers and their babies, and was a strategy that should be strengthened as a matter of urgency. Despite official and scientifically backed recommendations for the influenza vaccine to be prioritised for pregnant women, uptake remained very low.

Zar described as ‘very exciting’ current overseas work on the development of a vaccine for respiratory syncytial virus (RSV), which causes infections of the lungs and respiratory tract. RSV is so common that most children have been infected with it by age 2. In adults and older, healthy children, the symptoms of respiratory syncytial virus are mild and typically mimic the common cold. Self-care measures are usually all that are needed to relieve any discomfort, but

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infection can be severe in in premature babies and infants with underlying health conditions (and in older adults, adults with heart and lung diseases, or anyone with a very weak immune system). Zar said that a major part of her enthusiasm was due to the strategy to immunise pregnant women against RSV as a way of protecting their infants.

Overall, she said, strengthening health systems, reducing poverty and improving the coverage and uptake of these known effective interventions would see SA beginning to make quicker, long-awaited progress in reducing the neonatal mortality and under-5 mortality (and morbidity) rates.

Leading by example with innovation

Zar, a past president of the South African Thoracic Society and president of the Pan African Thoracic Society, currently chairs the Forum of the International Respiratory Societies. She achieved world acclaim with her low-cost plastic cooldrink bottle spacer for asthmatic children, which rendered what used to be expensive inhalers accessible to millions of children in poorer communities. Her invention made the oral alternative therapy, theophylline (a white crystalline alkaloid and vasodilator with several unpleasant side-effects), a thing of the past. The use of cooldrink bottles as asthma spacers is now included in guidelines from the Global Initiative for Asthma and the World Health Organization (WHO). Another surprisingly simple advance that she and her Red Cross War Memorial Hospital team came up with – now also included in WHO guidelines and national recommendations – is the use of

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less invasive sputum induction for rapid tuberculosis (TB) testing in children. A few years ago it was widely believed that children couldn’t provide enough sputum for a TB test. Instead doctors used gastric lavage or stomach pumping, a process that involved starving a child overnight, then sticking a tube down their nostrils or throat into their

stomach, and sucking all the contents out.

Children were subjected to this process three days in a row before doctors could retrieve a specimen large enough for testing. Zar and her team found that by nebulising a child beforehand and suctioning the back of their throat very quickly, it is possible to induce enough sputum for a rapid TB test (using

GeneXpert). This retrieves a better specimen than that from three days of gastric irrigation.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2015;105(3):247-248.

DOI:10.7196/SAMJ.9557

Turning nutrition on its head – Noakes gets his day Indefatigable, with a con­ viction to match his harshest critics, Prof. Tim Noakes took to the scientific trenches in Cape Town in February, fusing the firepower of 15 of the world’s top experts on the low-carbohydrate, high-fat (LCHF) diet at a heavily subscribed R3 million, 4-day ‘health convention’.

Nutritionists, cardiologists, surgeons, family physicians and researchers, many of them best-selling authors, rallied to his side, presenting findings, analyses, arguments on causation, and alarming, undisputed obesity and type 2 diabetes prevalence studies to counter last year’s unprecedented local wave of scientific antipathy towards Noakes – much of it from his own colleagues at the University of Cape Town (UCT)’s Faculty of Health Sciences.

Nearly all the international speakers came at short notice and at their own expense, rounded up by Karen Thomson, granddaughter of heart surgeon Prof.

Chris Barnard, who began a unique sugar/ carbohydrate addiction clinic after winning a battle with alcohol and cocaine addiction.

Thomson wanted to give the charismatic and popular sports scientist a platform to defend himself after what he described to Izindaba as a ‘kangaroo court’ UCT Centenary debate 15 months ago in which he took on fellow UCT graduate and fellow A-rated scientist Prof. Jacques Rossouw, Washington-based epidemiologist, researcher on heart disease prevention, and former director of the South African Medical Research Council’s Institute for Nutritional Diseases. Noakes encountered what he described as a hostile audience there, and saw the debate as ‘a set-up’, declining to engage further after he and his adversary had outlined their initial arguments. A top academic in the chronic disease field, plus a leading professor of endocrinology and diabetic medicine at UCT (Profs Krisela

Prof. Tim Noakes.

Steyn and Dinky Levitt, respectively), later labelled Noakes’ revolutionary approach to nutrition as ‘a public health threat and extremely dangerous’, accusing him of having ‘a superficial understanding of epidemiology’.

UCT’s Faculty of Health Sciences then took the unprecedented step of publicly slamming Noakes’ dietary advice, claiming that he was making ‘outrageous unproven’ claims about disease prevention and ‘maligning the integrity and credibility of peers who criticise his diet for being evidence-deficient and not conforming to the tenets of good and responsible science’.

‘This goes against UCT’s commitment to academic freedom as the prerequisite to fostering responsible and respectful intellectual debate and free enquiry,’ the statement added.

Noakes offered an olive branch in his closing remarks at the February health convention, describing his local colleagues as ‘honest, genuine people who spent their lives trying to help people and speaking out of deep sense of conviction’. However, he remains unyielding: ‘We take the position that they are wrong.’ He said that the health convention was the direct

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result of SAMJ’s coverage of the UCT centen­ ary debate and his critics’ comments there.

Consensual position outlined

The unanimous and urgent viewpoint distilla­ tion in last month’s long-awaited counteroffensive was as simple as it was dramatic: mainstream nutritional and dietary advice has not only failed dismally, it is the immediate cause of the global obesity and diabetes epidemics.

It completely ignores the history of why and how human nutrition developed over the last 3 million years, and more importantly it refuses to acknowledge the presence of insulin resistance (carbohydrate resistance) as the ‘single most prevalent biological state in modern humans eating according to current dietary guidelines promoting low fat and high carbohydrate intakes. People with insulin resistance were at an increased risk of developing a wide range of chronic medical conditions if they ingested high-carbohydrate diets for any length of time (i.e. decades).’ Every speaker at the convention signed this consensual position statement.

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Dr Peter Bond and Prof. Noakes.

Noakes said that conventional scientific enquiry had ‘dropped the bar so low that we came to the point where anything can cause anything’, describing the proponents of conventionally accepted nutrition as ‘want­ ing more funding to do more research – they’re not necessarily interested in getting you healthier’. Parading several formerly obese Capetonians, virtually unrecognisable after their dramatic weight loss on the LCHF diet, Noakes said all their maladies, including atrial fibrillation, type 2 diabetes, sleep apnoea, hypertension, gout and dry flaky skin, had disappeared. One convert, Brian Berkman, a type 2 diabetic, said he was on the verge of undergoing bariatric surgery when he decided to try the Banting diet as a last resort – with spectacular and unexpected success.

Speakers ‘risked their careers’ by taking a stand

Noakes commented: ‘We are surrounded by a population that is full of insulin resistance and we’re not doing anything about it.’ He said that none among his array of highcalibre speakers had any conflict of interests, describing them as ‘having put their careers on the line because they were too honest’.

They were prepared to ‘stand up against the world and say this cannot go on forever’.

American science writer and physicist Gary Taubes, the best-selling author of Why We Get Fat and Good Calories, Bad Calories, told his Cape Town audience that the Cochrane Collaboration research in 2002 showed that weight loss achieved in calorie-restricted diets was ‘so small as to be clinically insignificant’. He added: ‘If we are obese, eat less and end up fat anyway, it’s a pretty good sign that eating less doesn’t work. Clinical trials prove it. Exercising more also doesn’t work.’ Citing the American Heart Association and American College of Sports Medicine physical activity guidelines

of 2007, he continued: ‘It’s reasonable to assume that persons with relatively high daily energy expenditures would be less likely to gain weight, compared with those who have low energy expenditures.

So far, data to support this hypothesis are not particularly compelling.’ He said these 100 - 150-year-old hypotheses had been shown not to work in centuries of testing, thinking and randomised controlled trials.

‘The idea of energy-in minus energy-out, perverted appetite and eating too much with insufficient expenditure is supposedly based on the first law of thermodynamics. It doesn’t tell you anything about why people get fat. It’s nonsensical.’

Obesity ‘a hormonal regulatory disorder’

Taubes’ alternative hypothesis, founded on his research, was that obesity was a hormonal regulatory disorder. Like type 2 diabetes, obesity was fundamentally a disorder of insulin signalling, hence the term ‘diabesity’.

The carbohydrate content of the diet triggered it with the key driver of insulin being the carboyhdrates and sugar in the diet, not fat and not saturated fat. Obesity was shown to be a disorder of excess fat accumulation (not energy balance, not over-eating and not sedentary behaviour). People did not need an excess of food to become obese. Mice made fat out of their food under ‘the most unlikely circumstances, even when half-starved’. Every animal experiment he’d ever found showed that animals did not get fat by over-eating. The degree of insulin resistance or sensitivity was a key factor in the equation of fat accumulation, and explained why diabetes type 2 and obesity went together. More and more research was proving that ‘carbohydrate is driving insulin is driving fat’. Taubes said that the solution to obesity and its associated epidemics was not getting people to move more and eat less, but restricting the causative agent – i.e. refined grains and sugars.

Gary Taubes, best-selling author.

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UK cardiologist Dr Aseem Malhotra.

Tax sugary drinks, subsidise low-carb/ high-fat foods

Cardiologist Dr Aseem Malhotra, from the UK, accused the food industry of ‘spiking’ food with hidden sugar, making it impossible to avoid it. He advocated a tax on sugary drinks and subsidisation of healthy alternatives low in carbs and high in fat. Dr Stephen Phinney, a North American physician/scientist who has spent 35 years studying diet, exercise, fatty acids and inflammation, said it would be in the interests of governments to find a dietary solution for the poor who existed mostly on the ‘two absolute no-no’s of sugar and flour’.

Sweden’s most popular health blogger, family medicine specialist, Dr Andreas Eenfeldt, said it was ‘no coincidence’ that the prevalence of obesity and type 2 diabetes had ‘shot up’ over the past 30 years since the dietary guidelines of the 1980s advocated high-carb, low-fat diets. Swedes’ consumption of butter had doubled over the past two decades, yet heart attacks had dropped over the same period, an anomaly not explained by conventional diet proponents. The Swedish government, after complaints about advocates of LCHF nutrition, had conducted a high-level probe resulting in Sweden becoming the first nation to reject the low-fat diet dogma and adopt the LCHF diet for treatment of people with obesity. Studies across the globe were showing that low-carb diets were not only compatible with the scientific evidence but best practice for overweight or obese patients – with no evidence of harm having emerged. He said that the most popular weight-loss Google searches in Sweden from 2008 to date were LCHF, low glycaemic index, the Paleo diet and Weight Watchers. By the end of 2010

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the LCHF diet was already in ‘a league of its own’, and by 2015 it was more popular than all the other weight-loss diets combined. A recent survey had shown that 23% of the Swedish population was now on some kind of low-carb diet.

The health convention was sponsored by Old Mutual, whose chief medical officer Dr Peter Bond told delegates that the world’s most rapidly spreading and sustained pandemic was not HIV/AIDS but diseases of lifestyle and diet, of which obesity was the most dominant. He said that at current rates the world’s obese population would outnumber those suffering from starvation by 2025. Insurance loadings in South Africa (SA) were increasing all the time, with a 17% deterioration in sub-standard lives over the past 4 years. He estimated that 3.5 million South Africans had type 2 diabetes, and that 5 million were insulin resistant or had impaired fasting glucose or impaired glucose tolerance. Only half of Old Mutual’s clients were aware that

they had these conditions, and people were often only diagnosed during an insurance examination.

Undiagnosed diabetes heralds CVD epidemic

Bond cited a 2012 study in a coloured community in Bellville, Cape Town,[1] showing the prevalence of type 2 diabetes to be 28.2%, with 88% of affected females and 42% of affected males being obese according to waist measurement. A full 55% were undiagnosed, despite nearby healthcare facilities. Bond said this indicated that the prevalence of diabetes had increased hugely in the coloured community. The high prevalence of undiagnosed diabetes ‘portends that cardiovascular diseases might grow to epidemic proportions in the near future in SA’. SA already had the highest overweight and obesity rate in sub-Saharan Africa, with 7 out of 10 women and 4 out of 10 men overweight or obese, double the global rate of nearly 30%. Not a single

country had managed to reduce its obesity rate in the past three decades, he emphasised.

Noakes described the epidemic of obesity and diabetes as ‘the greatest modern threat to human health’, adding that ‘we need to front up and admit that we have been wrong for the past 40 years and must now change’.

He hoped the convention which Chris Barnard had inadvertently inspired would help grant the famous heart surgeon one of his most fervent wishes: that had he focused on preventive medicine earlier he would have saved 150 million lives, rather than the 150 patients via heart transplantation.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2015;105(3):248-250.

DOI:10.7196/SAMJ.9554 1. Erasmus RT, Soita DJ, Hassan MS, et al. High prevalence of diabetes mellitus and metabolic syndrome in a South African coloured popu­ lation: Baseline data of a study in Bellville, Cape Town. S Afr Med J 2012;102(11):841-844. [http://dx.doi.org/10.7196/SAMJ.5670]

Basson slapped down by committee The High Court-approved recusal appli­ c ation by apartheid-era chemical and biological weapons expert Dr Wouter Basson to the two-person Medical and Dental Professions Board Professional Conduct Committee was turned down flat last month.

Dr Wouter Basson.

The latest twist in the 14-year-long hearing, beset by dysfunction in prosecuting the

case by the umbrella complainant body, the Health Professions Council of South Africa (HPCSA), technical postponements and legally skilful delaying High Court applications, may yet deliver more surprises before argument in mitigation of sentence continues on 28 May. Basson’s veteran legal counsel, Jaap Cilliers, SC, submitted that committee chairperson Prof. Jannie Hugo and his deputy Prof. Eddie Mhlanga showed a ‘clear bias’ in failing to disassociate themselves from petitions calling for the strongest possible censure of Basson, drawn up by the South African Medical Association (SAMA) and the Rural Doctors’ Association of South Africa (RUDASA) and filed in aggravation of sentence.

Cilliers marched out of the committee’s December sentencing hearing after Hugo refused to disclose whether he was a member of either organisation, successfully securing a High Court order compelling him to hear an application calling for his and Mhlanga’s recusal. Both highly respected clinicians admitted in papers submitted to the High Court that they were members of the organisations but inactive in management, adding that they would never have contemplated signing such petitions, given the inherent conflict of interest. Cilliers, who was pivotal in securing President Jacob

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Zuma’s rape charge acquittal in 2006 and has represented several right-wingers in other high-profile court cases, told the 13 March recusal hearing that Hugo’s refusal to disclose his membership of the medical bodies was ‘bizarre’. At no stage had Hugo ‘disassociated himself ’ from the stance of these bodies, he contended.

Cilliers argued that the committee granted the complainant (the HPCSA) more than a year to ‘search the world’ for an expert willing to support its stance that Basson acted unethically, yet when he asked for a postponement to probe Prof. Hugo’s involvement with the medical bodies, the committee insisted on continuing the hearing in Basson’s absence, a ‘clear indi­ cation’ of bias. Cilliers called this as ‘an absolute travesty of justice and a disregard of all rules pertaining to a fair trial’, and later labelled the proceedings a ‘Laurel and Hardy show’. He devoted a large part of his argument to the committee’s stance that any medical doctor who joined the defence force in the 1980s was unethical and un­professional.

Hugo responds to recusal application

Hugo responded that the petition was initiated by the People’s Health Movement,

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not SAMA or RUDASA, who nevertheless supported it, like many other organisations.

His and Mhlanga’s association with the two bodies related to their academic and professional work and had no bearing on the matter before them. Basson thus failed to support his claim that the committee was biased, with a vested interest in the outcome.

‘We need to assure Dr Basson that we are acutely aware of our duties in this matter and that he will continue to experience a fair trial,’ he added.

In December 2013 the committee found Basson guilty of unprofessional and un­ethical conduct in that he co-ordinated large-scale production of illegal psychoactive drugs (including Ecstasy), armed mortars with teargas and provided military operatives with disorientating substances to make illegal cross-border kidnappings easier. He also made cyanide capsules available to apartheid-era military spies so that they could commit suicide if captured.

One HPCSA witness said that the Durbanville heart surgeon was unrepentant and failed to show ‘that he even reflected on the possibility’ that he had violated medical ethics, while Hugo said in judgment that medical ethics were ‘especially important’ in times of war and conflict. Basson had defiled the ‘unique and sacred position’ of

trust in doctors by society that impelled them to stay true to the ethical values of ‘beneficence, non-maleficence, justice and autonomy’. Basic medical ethics had not changed since the time of the offences, Hugo stressed.

Hugo responded that the petition was initiated by the People’s Health Movement, not SAMA or RUDASA, who nevertheless supported it, like many other organisations. His and Mhlanga’s association with the two bodies related to their academic and professional work and had no bearing on the matter before them.

Enormous hearing costs hiked by both sides

While the HPCSA will not reveal the cost of the 14-year hearing (in particular Basson’s costs), it has dragged on six times as long as late former police commissioner Jackie Selebi’s corruption trial (late 2009 - 2012), which cost R17 million. The State is footing both bills. Basson has continued to practise between the protracted hearings.

The hearing has helped highlight the general dysfunctionality of the HPCSA, in this case via several belated legal sub­missions, many containing errors that continually gave the upper hand to Basson’s lawyers over the years, dragging out proceedings and push­ ing up costs. National health minister Dr Aaron Motsoaledi last month ordered a full investigation into HPCSA maladministration and the fitness of the body’s managers to lead it. Izindaba has over the past decade repeatedly highlighted HPCSA dys­ function, including the drinking habits of a former president, internal corruption in the registration of foreign-qualified doctors (some inappropriately qualified and let loose on an unsuspecting public), and its accreditation and monitoring of training hospitals.

An independent investigation panel will be chaired by the head of the University of Cape Town’s Department of Medicine, Prof.

Bongani Mayosi, and is due to report back to Motsoaledi at the end of next month (May).

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2015;105(3):250-251.

DOI:10.7196/SAMJ.9601

World’s first successful penis transplant at Tygerberg Hospital A multidisciplinary team at Tygerberg Hospital has performed the first-ever successful penile transplant, giving hope to victims of botched ritual circumcisions and penile cancer and even men with severe erectile dysfunction.

The grateful and delighted 21-year-old recipient, one of 250 known formerly hope­ less penile amputees across the country annually, has been out of hospital for over a month and reports full sexual and urinary function. Nine more candidates are being psychologically and medically prepared for transplantation as part of the globally ground-breaking pilot study. All are victims of failed ritual circumcision – most from the Eastern Cape, with several reported to have contemplated suicide, so powerful is the cultural stigma. The intervention is particularly apt in South Africa (SA), where

Transplant team (l - r) plastic surgeon Prof. Frank Graewe, urologist Prof. André van der Merwe and immunologist Prof. Rafique Moosa. Photo: Chris Bateman.

the prevalence of penile loss is way above the international average, especially in the Xhosa-speaking region of the Eastern Cape.

One snapshot of the only available hospital

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admissions data for life-threatening postritual-circumcision complications in that province stood at 200 patients in December 2001 alone, with 11 mutilations.

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Diligent, careful groundwork

The success is the culmination of 4 years of clinical and ethical preparation, intensive laboratory work on cadavers, frustration in finding willing donors, and careful groundwork to ensure that the procedure and its concomitant lifelong immunesuppressant treatment are replicable and affordable to all.

Dr Dimitri Erasmus, Chief Executive of Tygerberg Hospital, emphasised that the procedure was not an answer to the ongoing loss of life and reproductive organs caused by inexpert ritual male circumcision – a uniquely SA phenomenon. ‘While hugely significant, this is a life-changing, not a lifesaving procedure. The focus should remain on preventive efforts,’ he said.

The 9-hour operation was conducted on 11 December last year by a team led

by Prof. André van der Merwe, head of Stellenbosch University (SU)’s Division of Urology, with his university counterpart in plastic surgery, Prof. Frank Graewe, and SU’s Department of Medicine chief and transplant immunologist, Prof. Rafique Moosa, in attendance. The penis, along with the heart, lungs, kidneys, liver, skin and corneas of an unidentified donor, was removed in a lengthy procedure where each team had to wait their turn to harvest an organ. Van der Merwe said that one of the major obstacles encountered on the long road to success was the reluctance of donor families to bury their loved ones without a penis. By building a look-alike organ using flaps from the forearm, they overcame this and expect a smoother path to donor willingness in future. Asked how they knew their patient had achieved full sexual competence, Graewe said he had recently sent them an identifiable cell-phone picture of an erection, while tumescence had been observed when he was returned to the operating table 4 days after the operation to remove a clot in one of the penile arteries. The penile stump had also been ‘very active’ under anaesthetic.

His recovery included a second return to theatre for drainage of a haematoma and to repair a small fistula of the urethra – but the team has exceeded their greatest expectation, which was that the young man be fully functional at 2 years. Instead this happened at 3 and a half months.

Tygerberg Hospital has a distinguished record in its partnership with SU’s Faculty of Medicine and Health Sciences. This includes SA’s first in vitro fertilisation procedure, resulting in the birth of the country’s first test-tube baby, an innovative microsurgical heart valve, and multiple microsurgical reconstructions after surgery for breast, head and neck cancers.

Van der Merwe said that one of the major obstacles encountered on the long road to success was the reluctance of donor families to bury their loved ones without a penis. By building a lookalike organ using flaps from the forearm, they overcame this and expect a smoother path to donor willingness in future.

Historical precedent unsuccessful

A similar penile transplant procedure was performed in Guangzhou General Hospital in China in 2006, involving a 44-year-old recipient who had lost his penis in an accident, but surgeons had to remove the organ 2 weeks after the operation when skin problems resulted in an aesthetic problem. Graewe said the Chinese used a ‘completely different approach’, warming the donor penis up with an infrared lamp postoperatively, which increased the metabolic requirements, instead of increasing the blood supply as they had.

‘But I think the crucial difference appears to have been inadequate psychological workup,’ he stressed, adding that the recipient’s

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girlfriend had strongly objected to the result. The SA team, which included Dr Nicola Barsdorf, Head of Health Research Ethics at SU, said that because the recipient’s blood vessels that would have matched those of the donor were ‘obliterated’ by the ritual circumcision modus operandi, with excessive fibrosis having occurred, they could only use the local nerve structure.

This meant that they had to reroute a blood vessel from the patient’s lower abdomen to the perineum, where they connected it to the new penis. The surgeons also connected three blood vessels, each between 1 mm and 2 mm in diameter, to ensure sufficient blood flow to the transplanted organ, two dorsal nerves of the same diameter to restore sensation, the urethra, enabling the recipient to urinate through the penis, and the corpus cavernosum, which allowed him to obtain an erection.

Barsdorf said that the research team had addressed the issue of therapeutic misconception (i.e. the risk that a research participant may not fully understand the experimental nature of the treatment) impeccably. The patient had been counselled repeatedly over an extended period about the potential risks and benefits. The transplant team’s partnership with local public health structures also meant that the procedure would be delivered to the people who needed it most by being on offer in state facilities to vulnerable groups that are often unable to afford or access state-of-theart healthcare.

Graewe said the patient has reported that he is enjoying sex ‘at least once a week’, rendering the transplant team somewhat anxious. Van der Merwe revealed that the transplanted organ was not circumcised.

‘We’ve encouraged him to come straight to us for that,’ he added with a smile.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2015;105(3):251-252.

DOI:10.7196/SAMJ.9602

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OBITUARIES Stephen Hough, 1947 - 2014

Stephen Hough and I collided for the first time when we were research fellows in the USA. That encounter in 1980 sowed in me the seed that was to become one of my closest friendships, although at the very beginning I had my doubts. Stephen had hit St Louis about a year before I did and we were to share an office. The potential difficulty lay in putting a slightly ‘left of centre’ Brit in with a South African, and an Afrikaans one at that. This was 1980.

Tricky. Stephen’s opening salvo snuffed out my concerns in a flash – big smile, big handshake, a comment along the lines of ‘welcome to the madhouse’, and a first blast of that window-rattling laugh that was never far from the surface. The politics was not a problem, though it was discussed at length over the years, often facilitated by too little sleep and a certain amount of whisky. Also subject to scrutiny were, in no particular order, the rollercoasters of personalities, sport, academia, clinical medicine, medical politics, food and drink. Stephen loved talking.

The Bone and Mineral Fellowship Pro­ gramme at Washington University in St Louis was quite exceptional at that time, with an enthusiastic group of largely international fellows under the direction of an extraordinarily potent faculty – Avioli, Haddad, Teitelbaum, Whyte, Slatopolsky,

Peck, to name a few. This was a seminal period for Stephen, and one that could easily have ended with him remaining in the USA permanently. There was no shortage of well-supported faculty positions on offer as his reputation grew, and he and I had many a long conversation about the pros and cons of throwing his lot in with the Americans, in many respects an attractive option. Ultimately his sense of duty to family, colleagues, his parent institution and his country trumped all the inducements that were being thrown at him, and it was clear that, with no hint of underlying arrogance, he believed that he should not be a part of the haemorrhage of talent that South Africa was experiencing at the time. In retrospect one can see that the decision was never in doubt.

My family’s experience was common to many of Stephen’s friends. We all thought the world of Stephen – and brightened at the mere mention of his name. My trips to Cape Town have always been immensely enjoyable, largely because of the amount of laughing that always seemed to go on in Stephen’s company, often about very silly things. Stephen really was unquenchable in that respect. One of the most endearing things about him was the fact that this supremely intelligent and able man, even when no longer in the first flush of youth, had a side that was still a boy, and furthermore a boy showing little sign of growing up.

Stephen’s achievements were built on a combination of three A’s – ability, affability and availability. The ability was there for all to see – bright, inquisitive, competitive.

The affability was his hallmark – charm, humour, joie de vivre all served him well, professionally and personally. Availability, so often missing in successful careers, meant that his patients, colleagues and protégés would be very aware of his commitment to them. There was, however, a hard edge as well. He hated posturing and pomposity and was intolerant of anything he perceived as scientific chicanery. He expected from others the high standards that he imposed on himself – Stephen was a man who consistently chose the difficult right path over the easy wrong one.

Although the final grim twist in his story was not anticipated, he tackled it in

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the way he approached everything, with the tenacity that was his hallmark. He knew that he had led a charmed life, enjoying the luxury of a loving family, wonderful friends scattered across the world, and innumerable adventures. That he handled his last illness in the way he did comes as no surprise – a mix of bravery and determination, with a fair sprinkling of obstinacy thrown in for good measure. As the storm clouds gathered he would still toss in the odd gem of dark humour. Even when ill he was determined to live his life as fully as possible. Of course he was always a terrific optimist and remained so virtually to the end – Stephen didn’t do self-pity.

Prof. Sir John Cunningham Professor of Nephrology, Centre for Nephrology, UCL Division of Medicine, School of Life and Medical Sciences, University College London, UK drjohncunningham@gmail.com Stephen Hough was one of the finest clinician-scientists to have emanated from South Africa. In his early thirties and already an established researcher with several degrees in medicine and science, he was earmarked by his mentors for advanced training in the USA. From 1979 to 1981 he worked at Washington University in St Louis, Missouri, while on a 2-year research fellowship in endocrinology and metabolism. This centre was famed for its work in metabolic bone disease and jump-started Stephen’s lifelong passion for this field, osteoporosis in particular.

On his return to the Department of Medicine at Stellenbosch University’s Faculty of Health Sciences, Stephen became head of the newly developed Metabolic Unit (later the Division of Endocrinology) based at Tygerberg Hospital. Over the next 30 years (until retirement) he was pre-eminently responsible for this unit being one of the top training and referral centres in endocrinology in South Africa, as well as the leader in osteoporosis. In 1993 he founded the National Osteoporosis Foundation of South Africa, of which he was President until his death.

From 2001 to 2006 Stephen served as Chairman of the Department of Medicine at Stellenbosch. He retired at the end of

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2012, but was too active and enthusiastic not to stay involved. Besides opening a private practice, as Emeritus Professor he committed one full day a week to his alma mater, which included teaching as well as mentoring five new doctoral candidates.

Not only did Stephen receive numerous local accolades over the past 40 years, but he also held senior positions in the Society for Endocrinology, Metabolism and Diabetes of South Africa (Chairman 1992 - 1994), the Colleges of Medicine of South Africa, the South African Diabetes Association and the South African Medical Research Council, to name a few. Internationally he held high office in many societies, including serving on the Committee of Scientific Advisors of the International Osteoporosis Foundation

(IOF), the International Advisory Panel of the American Paget Foundation and the Membership Committee of the International Bone and Mineral Society.

He was also elected to represent Africa on the IOF Board of Governance. He was the founder editor of the Journal of Endocrinology, Metabolism and Diabetes of South Africa and a reviewer for several prestigious international journals.

I knew Stephen Hough for nearly three decades, at first as a revered elder in our field, later as colleague and good friend. Stephen was always warm to everyone, and was not bothered by ego. He was never pretentious, and never acted superior to even his most junior colleagues. There were no hidden agendas, and he was as honest as the day is long. If he

strongly disagreed with ‘authority’ he was not afraid to tackle it head on. He never harboured prejudice and he abhorred racism, even in an era when it was frequently the norm.

We pay homage to a loving husband and father, a true friend, a national and international icon in his field, a giant of a man, full of gusto, humility and passion. We will never again hear that booming baritone voice filling any room, but we are all so much richer for having known Stephen.

Max Klein, 1941 - 2015

He returned to South Africa in 1974 to establish the paediatric respiratory service at Red Cross Hospital and the first comprehensive intensive care unit. He was a strong opponent of apartheid and discrimination, ensuring that this ICU cared for children of all ethnicities. He was the driving force behind its development, led it for 25 years and trained many of the leading paediatric intensivists in South Africa. As recognition of his contribution, he was presented with a gold medal award by the World Federation of Pediatric Intensive and Critical Care Societies in 2000. As an inaugural gold medallist he was recognised as an international pioneer who established the specialty through clinical and academic excellence, dedication to patients and families, and leadership to colleagues.

Max was a brilliant clinician and teacher.

He conducted many pioneering studies in childhood respiratory illness, including the use of CIPP tubes for upper airway obstruction, use of nasal cannulas for oxygen administration, development of a clinical score for the severity of croup, development of continuous positive airway pressure ventilation, and use of vitamin A for children with measles-associated pneumonia. Among his proudest achievements was the home tracheostomy service he started whereby a whole generation of children with respiratory failure could live at home and have the opportunity to live hopeful lives. In comparing the outcomes of children managed at home with those who were institutionalised, he found the home environment to be much better and wrote: ‘Empowerment is the most important principal in rehabilitation. Mother

is the most sophisticated technology available in the world; love is of more consequence to the child than physical comfort. Intelligence is not related to literacy and best care is not necessarily more costly care.’

Max was the first Extraordinary Professor in the Department of Paediatrics and Child Health at the University of Pretoria. He made an invaluable contribution to starting the Paediatric Pulmonology Fellowship training programme and to teaching, training and research.

Max will be remembered as a fearless opponent of injustice, an outspoken critic for things he believed in, a man of uncompromising integrity, a master clinician and teacher, and an innovator with a real vision for the development of services in paediatric critical care, pulmonology and other areas of child health.

Max Klein passed away suddenly on Tuesday 27 January while doing what he loved, cycling in Stellenbosch. He had made a large contribution to the development of paediatric critical care and paediatric pulmonology in South Africa and beyond.

Max trained as a Wellcome Research Fellow in the first South African neonatal intensive care unit at Groote Schuur Hospital, then as a paediatric registrar at Red Cross War Memorial Children’s Hospital, and then in an adult respiratory unit at Stellenbosch University, where he was subsequently appointed as consultant.

In 1972 he was awarded a Lilly International Fellowship as a fellow to the Cardiovascular Research Unit and the Department of Paediatrics at the University of California Medical Center in San Francisco, USA.

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Prof. Brynne Ascott-Evans Head: Division of Diabetes and Endocrinology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, Cape Town, South Africa bae@sun.ac.za

Heather Zar Department of Paediatrics and Child Health, Red Cross War Memorial Children’s Hospital, Cape Town, and Faculty of Health Sciences, University of Cape Town, South Africa heather.zar@uct.ac.za Robin J Green Department of Paediatrics and Child Health, School of Medicine, Faculty of Health Sciences, University of Pretoria, South Africa robin.green@up.ac.za Eugene Weinberg Emeritus Professor, Paediatrics and Child Health, Faculty of Health Sciences, University of Cape Town weinberg@yebo.co.za

IZINDABA

In his second undergraduate year, Max Klein developed meningococcal meningitis.

Within a few hours he was moribund and pulseless. As the senior house officer on duty, I was obliged to attend to him until expert help could be summoned. After the event, he claimed that his brain had never been clearer! This did not restrain him from admonishing us for perceived lapses in patient care, and throughout his professional life he viewed diagnosis and treatment from a patient perspective and expected his staff to do likewise.

We met again as neonatal research colleagues at Groote Schuur Hospital. Here I got to know the post-meningococcal brain intimately. Its originality of thought was astounding, and I shall be ever grateful for being advised to read The Art of Scientific Investigation by W Beveridge. Research time became playtime, and we pursued numerous exciting ideas in the hope of making discoveries. Now for the sad part.

A discovery does not exist until it is in print, and Max had a writing block. His numer­ous unpublished findings languished for decades – surprising, for later in his career he became a prolific author.

Nevertheless he imparted his treasures to those around him, and his clinical acumen was unsurpassable. He developed special surgical skills, probably as a result of a stint in Chris Barnard’s animal unit in his student years. His simple yet unique methods of tracheostomy and chest drain insertion were adopted by all.

Inevitably our ways parted, as each pursued a subspecialty. After a stint at the Californian Cardiovascular and Pulmonary Institute, Max returned to Red Cross Children’s Hospital where he established a department for lung ailments and an intensive care unit. The latter took its toll, for when he retired, he stated: ‘I have experienced the deaths of 2 200 children, and that’s enough.’ He never tolerated fools or

injustices, but in later years he could be infuriatingly unco-operative. This, I believe, was the result of unrelenting exposure to sick and dying children.

In retirement we were reunited, and each week for ten years we walked the length and breadth of Cape Town and Sydney discussing ideas, books and characters.

Several months before Max’s untimely death he gave up walking because of a knee ailment and concentrated on cycling.

This he enjoyed immensely, and it was during a ride that he quietly and suddenly departed from this world. He was unique, and with his inexplicable creative powers, a genius – the like of which will not be seen again.

V C Harrison 3 Hurley Road, Mowbray, Cape Town, South Africa vincentcostelloharrison@gmail.com

BOOK REVIEW Malignant: How Cancer Becomes Us

By S Lochlann Jain. Berkeley, CA: University of California Press, 2013.

ISBN 9708520276574 Lochlann Jain is a cancer survivor. She is also an anthropologist living in the USA. Malignant is in part the personal

story of what she aptly terms ‘living in prognosis’ after an ordeal of misdiagnosis and subsequent treatment for breast cancer. The book is also her detailed investigation of our profoundly diseased society.

Nearly half of all Americans will be diag­ nosed with an invasive cancer. The time lag between exposure to carcinogens and diagnosis makes pinpointing exact causes difficult, other than overt instances such as smoking and lung cancer, or asbestos exposure and mesothelioma. Many known and unregulated carcinogens are in our food, plastics, dyes and water. Fallout from war, even from medical treatments, adds to risk.

Modern life evolves in a soup of hormones and chemicals, driven by our quest for youth, fertility, fast food, easy travel, gizmos and wealth. There is a massive price to pay, and the cost is often borne by those who do not benefit.

Jain unearths disturbing information, e.g. companies that make both carcinogen-con­ taining products and chemotherapy drugs.

Stating that she doesn’t believe there is evil intent, she remarks that the way to make a fortune is to give cancer to someone who has health insurance, and then test, monitor and treat her for the rest of her life.

Jain’s personal narrative informs and enhances her research. Her ability to present

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her emotional turmoil, vulnerability and even humour, as she finds herself ensnared by the big machine of what she terms ‘the medical industry’, is a thread that holds together an appalling story of the cover-ups and collusion between capital fearful of mass claims, the legal system that is too costly for individuals to seek redress, the health professionals who ask too few questions about causation, and the government agencies that are unwilling to regulate hazards.

There are no easy answers to the questions she poses. Malignant lifts the lid off cancer, showing it to be largely uncontrollable, unknowable, endemic to our culture, and metastasising into every aspect of life on earth, from our economic system to traces of lead found in Arctic ice. We are paying too high a price for our way of life, and we need to know this.

Malignant is essential reading for any­one involved in cancer care, who is affected by cancer, or who might contract the illness.

Going by the stats, that’s pretty much everyone.

Dawn Garisch GP and author of Eloquent Body (Modjaji, 2012) and Dance With Suitcase (Tiber Tree Press, 2013), Cape Town, South Africa dawn.garisch@gmail.com

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HEALTHCARE DELIVERY

Basic and comprehensive emergency obstetric and neonatal care in 12 South African health districts R C Pattinson, J D Makin, Y Pillay, N van den Broek, J Moodley Bob Pattinson is Director of the South African Medical Research Council Maternal and Infant Health Care Strategies Unit, Department of Obstetrics and Gynaecology, Faculty of Health Sciences, University of Pretoria, South Africa, and Jenny Makin is the epidemiologist on the team.

Yogan Pillay is Deputy Director-General for Programmes in the National Department of Health, and Nynke van den Broek is Professor and Head of the Maternal and Child Health Department of the Liverpool School of Tropical Medicine, UK. Jack Moodley is chairman of both the Emergency Obstetric Simulation Training Board and the National Committee for Confidential Enquiries into Maternal Deaths in South Africa.

Corresponding author: R C Pattinson (robert.pattinson@up.ac.za)

Aim. To assess the functionality of healthcare facilities with respect to providing the signal functions of basic and comprehensive emergency obstetric care in 12 districts.

Setting. Twelve districts were selected from the 52 districts in South Africa, based on the number of maternal deaths, the institutional maternal mortality ratio and the stillbirth rate for the district.

Methods. All community health centres (CHCs) and district, regional and tertiary hospitals were visited and detailed information was obtained on the ability of the facility to perform the basic (BEmONC) and comprehensive (CEmONC) emergency obstetric and neonatal care signal functions.

Results. Fifty-three CHCs, 63 district hospitals (DHs), 13 regional hospitals and 4 tertiary hospitals were assessed. None of the CHCs could perform all seven BEmONC signal functions; the majority could not give parenteral antibiotics (68%), perform manual removal of the placenta (58%), do an assisted delivery (98%) or perform manual vacuum aspiration of the uterus in a woman with an uncomplicated incomplete miscarriage (96%). Seventeen per cent of CHCs could not bag-and-mask ventilate a neonate. Less than half (48%) of the DHs could perform all nine CEmONC signal functions (81% could perform eight of the nine functions), 24% could not perform caesarean sections, and 30% could not perform assisted deliveries.

Conclusions. The ability of the CHCs and district hospitals to perform the signal functions (lifesaving services) of basic and comprehensive emergency obstetric care was poor in many of the districts studied. This implies that safe maternity care was not consistently available at many facilities conducting births.

S Afr Med J 2015;105(4):256-260. DOI:10.7196/SAMJ.9181

The South African (SA) Rapid Mortality Surveillance Report of 2012[1] concluded that ‘There is an urgent need to review possible interventions to further reduce maternal and child mortality if the MDG [Millennium Development Goals] targets are to be

met by 2015.’

Complications of HIV infection as reflected in maternal deaths due to non-pregnancy-related infections are the most common underlying cause of maternal death in SA.[2] There has been a massive effort by the National Department of Health (NDoH) to screen and treat pregnant women who are HIV-infected, and this effort is beginning to show signs of success. The institutional maternal mortality ratio (iMMR) has decreased from the 2011 - 2013 sixth Saving Mothers report, mainly due to the drop in maternal deaths due to non-pregnancy-related infections. Ninety-five per cent of these women were HIV-infected.[2] The infant mortality rate has dropped dramatically, as reported by Dorrington et al.[1] Screening and treating pregnant women for HIV infection remains the highest priority; however, although non-pregnancy-related infections accounted for 40% of deaths in 2011 - 2013,[2] other causes still accounted for 60% of maternal deaths. The iMMR for direct causes of maternal death has remained the same for the past decade.[2] This is particularly disappointing given the efforts on the part of the NDoH and the National Committee for Confidential Enquiries into Maternal Deaths in South Africa (NCCEMD) to provide information such as

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guidelines and protocols and to give all healthcare providers involved in maternity care this information.

Complications in pregnancy and labour can occur even in the best of circumstances. Many women who develop complications have one or more detectable risk factors, and complications can be anticipated.

However, the majority of women who have risk factors do not develop a serious problem,[3] i.e. the risk factors are not very specific.

Most importantly, a large proportion of serious complications occur among women with no recognisable risk factors at all,[4] and until the complication occurred they were regarded as having low-risk pregnancies. For these reasons attempts need to be directed to preventing death once the complication has occurred. The sooner a complication is recognised and treated, the better the outcome. Most pregnant women in SA (~60%) give birth at the primary level of care, namely in community health centres (CHCs) and district hospitals (DHs).

If an impact on the iMMR is to be made, recognition, stabilisation and treatment or referral of the obstetric emergency must occur at the site closest to where the complication occurred. There are three essential factors: • Healthcare providers with sufficient knowledge and skills to recognise, stabilise and treat or refer the patient • Healthcare facilities with the essential lifesaving services available, such as being able to perform caesarean sections (CSs) • An efficient interfacility transfer system.

April 2015, Vol. 105, No. 4

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A way to reduce these deaths rapidly is by improving emergency obstetric care.

Kerber,[5] using the Lives Saved Tool,[6] estimated that approximately 9 000 maternal and perinatal deaths in SA could be averted if comprehensive emergency obstetric and neonatal care (CEmONC) was fully implemented.

The emergency obstetric care package is a list of lifesaving services or ‘signal functions’ that define a health facility with regard to its capacity to treat obstetric and neonatal emergencies. Developed by the World Health Organization (WHO) and agreed on internationally by all United Nations organisations, it was first developed and tested in 1992, published as guidelines for monitoring the availability and use of obstetric services issued by UNICEF, the WHO and UNFPA, reviewed and modified in 2006, and published by the WHO as a handbook in 2009.[7] There are seven basic emergency care (BEmONC) signal functions and nine CEmONC signal functions (BEmONC and two others) (Table 1).

A rapid drop in mortality can be achieved by ensuring that these lifesaving services are available, correctly used and accessible to the community.[7] Each lifesaving service, as measured by the signal functions, is important in maternal and neonatal care at facility level. These signal functions, which are easily measured, are markers of these lifesaving services and assessing them gives an indication of the ability of a particular facility to provide emergency obstetric care when complications occur during pregnancy, birth or the postpartum period. This knowledge can be used to identify gaps in availability of essential obstetric care and to catalyse the changes necessary to improve the service.

This survey was undertaken at the start of the Essential Steps in Managing Obstetric Emergencies and Emergency Obstetric Simulation Training (ESMOE-EOST) pro­ grammes to establish the functionality of CHCs and district, regional and tertiary hospitals in 12 health districts in SA with respect to emergency obstetric and neonatal care by assessing these signal functions. The ESMOE-EOST programmes improve the knowledge and skills of healthcare providers in managing obstetric and neonatal emergencies[8] and are being introduced at scale to all the districts in SA.

Methods

This survey was performed between July and October 2012. In all, 133 health institutions were visited (53 CHCs, 63 DHs, 13 regional hospitals (RHs) and 4 provincial tertiary hospitals). A data monitoring team

Table 1. Signal functions used to identify basic and comprehensive emergency obstetric care services[15]* BEmONC services

CEmONC services

1. Administer parenteral antibiotics 2. Administer parenteral uterotonic drugs (i.e. oxytocin) 3. Administer parenteral anticonvulsants for preeclampsia and eclampsia (i.e. magnesium sulphate) 4. Manual removal of retained placenta 5. R emove retained products of conception (e.g. manual vacuum aspiration) 6. P erform assisted vaginal delivery (e.g. vacuum delivery) 7. Perform basic neonatal resuscitation with bag and mask

Perform signal functions 1 - 7, plus: 8. Perform CS 9. Provide blood transfusion

*A BEmONC facility is one in which all functions 1 - 7 are performed. A CEmONC facility is one in which all functions 1 - 9 are performed.

Table 2. Details of scoring system Score MMR

1 = 180 - 230; 2 = 230 - 280; 3 = >280/100 000 live births

Score SBR

1 = 25 - 27; 2 = >27/1 000 births

Score number of MDs

1 = 100 - 150; 2 = 150 - 200; 3 = >200

Score province

2 = highest MMR; 1 = second-highest MMR

MDs = maternal deaths.

Table 3. Distribution of number of signal functions of emergency obstetric care available by type of healthcare facility assessed

Number of signal functions

CHCs (N=53) n (%)

DHs (N=63) n (%)

RHs and tertiary hospitals (N=17) n (%)

CEmONC Perform all 9 functions

NA

30 (47.6)

15 (88.2)

Perform 8 functions

NA

21 (33.3)

2 (11.8)

BEmONC Perform all 7 functions

0 (0.0)

7 (11.1)

-

Perform 6 functions

3 (5.7)

3 (4.8)

-

Perform 5 functions

24 (45.3)

2 (3.2)

-

Perform 4 functions

12 (22.6)

-

-

Perform 3 functions

11 (20.8)

-

-

Perform 2 functions

3 (5.7)

-

-

Perform 1 function

-

-

-

NA = not applicable.

of between three and six members visited each of the sites. The team consisted of members of the data monitoring team of the South African Medical Research Council (MRC) Maternal and Infant Health Care Strategies Unit and various members of the local or provincial maternal and child health units. Before the visit, a planning meeting was held with the district and provincial managers and the purpose and the baseline

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survey form were explained. Each site then completed the form prior to the visit by the data monitoring team. The objective of the baseline survey was to describe each of the sites in terms of their functionality with respect to the signal functions required for basic and comprehensive emergency care. Information on the referral system and resources regarding the signal function was collected at each site.

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The standard programme for the visit, after the team had introduced themselves to the CEO and hospital or CHC management, was a workshop explaining the visit followed by training on the new national birth register and the monthly data sheets and a walk through the site to confirm the data entered on the baseline survey form and ensure that all questions were answered and comments recorded.

The data were entered by two data enterers at the MRC unit. Some survey forms were entered twice for quality assurance. The data were cleaned, and sites where there were incongruences were contacted again to verify the information.

Selection of districts

Twelve districts were selected, using a scoring system developed specifically for this programme and using each districtâ&#x20AC;&#x2122;s iMMR, stillbirth rate (SBR), and number of maternal deaths from 2008 to 2010.

An additional 2 points were given for the worst-performing and 1 point for the second-worst-performing district in the province. This was done to ensure some parity between the provinces. The scoring system is shown in Table 2. Districts scoring â&#x2030;Ľ5 were used. The numbers of births and stillbirths per district were obtained from the District Health Information System and the numbers of maternal deaths per district from the NCCEMD database.

Data from 2008 to 2010 were used. The 12 districts identified contributed to half of all maternal deaths occurring outside districts with medical schools in SA during 2008 2010. Districts with medical schools receive referrals from neighbouring districts, which may contribute to a higher score, and were therefore excluded.

Ethics

The CEO of every site and the district manager of each district gave permission for the survey, which was approved by the Ethics Committee of the Faculty of Health Sciences, University of Pretoria.

Results

Table 3 gives the number of signal functions that the various levels of care could provide and Table 4 the availability and ability of each individual function at the levels of care.

All CHCs were able to give oxytocics and anticonvulsants, but only 32% could give parenteral antibiotics. While all CHCs could give magnesium sulphate, only 48% had a patella hammer available to test reflexes. Nine DHs (14%) similarly lacked a patella hammer but could provide magnesium sulphate.

Table 4. Summary of availability of signal functions of emergency obstetric care CHCs (N=53) n (%)

Perform signal function

RHs and tertiary hospitals (N=17) n (%)

DHs (N=63) n (%)

BEmONC 1. Give parenteral antibiotic

17 (32.1)

63 (100.0)

17 (100.0)

2. Give parenteral uterotonics

53 (100.0)

63 (100.0)

17 (100.0)

3. Give parenteral anticonvulsants

53 (100.0)

63 (100.0)

17 (100.0)

4. Manual removal of retained placenta

37 (69.8)

59 (93.7)

17 (100.0)

5. Manual vacuum aspiration/D&C

1 (1.9)

53 (84.1)

17 (100.0)

6. Assisted delivery

2 (3.8)

44 (69.8)

15 (88.2)

7. Bag-and-mask ventilate a neonate

44 (83.0)

62 (98.4)

17 (100.0)

8. Perform CS

NA

48 (76.2)

17 (100.0)

9. Provide blood transfusion

NA

63 (100.0)

17 (100.0)

CEmONC

D&C = dilatation and curettage.

Table 5. Referral policy CHCs n (%)

DHs n (%)

RHs and tertiary hospitals n (%)

Prescribed referral routes

43 (81.1)

52 (82.5)

16 (94.1)

Prescribed referral criteria

49 (92.5)

57 (90.5)

16 (94.1)

Documented referral policies

37 (69.8)

39 (61.9)

11 (64.7)

Table 6. Ability of CHCs to provide BEmOC, and distance to nearest referral hospital Number of signal functions, n CHCs (%) Distance (km)

2

3

4

5

6

Total

<21

2 (8.0)

4 (16.0)

7 (28.0)

11 (44.0)

1 (4.0)

25

21 - 50

1 (5.6)

4 (22.2)

4 (22.2)

9 (50.0)

-

18

51 - 75

-

2 (22.2)

1 (11.1)

4 (44.4)

2 (22.2)

9

76 - 100

-

1 (100.0)

-

-

-

1

Total

3

11

12

24

3

53

Thirty per cent of CHCs and 6% of DHs could not perform manual removal of a retained placenta at all times, but in some CHCs the ability to manually remove the placenta was patchy, with only 58.5% (31) having midwives capable of manually removing a placenta available at all times. Only 6 CHCs had elbow-length gloves available for manual removal of the placenta. Ninety-eight per cent and 96% of the CHCs could not perform an assisted delivery and manual vacuum aspiration for spontaneous incomplete miscarriage, respectively. Sixteen per cent of the DHs could not manage spontaneous incomplete miscarriages and 30% could not perform assisted deliveries. Surprisingly, 17% of the CHCs could not bag-and-mask ventilate neonates. (This was also the case

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in one DH, but that hospital could intubate a neonate.) Twenty-four per cent of the DHs could not perform CSs, but all had blood available to give blood transfusions.

Table 5 indicates whether the institutions had prescribed referral routes, criteria for referral laid down and a written policy on referral. Most health institutions had clear referral routes and criteria for referral; however, fewer had these documented.

Table 6 shows the ability of CHCs to provide BEmONC and the distance from their referral hospital. Over half (53%) of the CHCs were more than 20 km from their nearest referral hospital, and of these 1 could provide only two signal functions, 7 only three functions and 6 only four functions, i.e. almost a third of CHCs were providing

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Table 7. Ability of DHs to provide CEmONC, and distance to nearest referral hospital Number of signal functions, n DHs (%) Distance (km)

5

6

7

8

9

Total

<21

-

-

1 (14.3)

2 (28.6)

4 (57.1)

7

21 - 50

-

1 (16.7)

2 (33.3)

1 (16.7)

2 (33.3)

6

51 - 75

-

1 (7.7)

2 (15.4)

4 (30.8)

6 (46.2)

13

76 - 100

1 (8.3)

-

2 (16.7)

4 (33.3)

5 (41.7)

12

101 - 150

1 (7.1)

-

-

8 (57.1)

5 (35.7)

14

151 - 200

-

1 (10.0)

-

2 (20.0)

7 (70.0)

10

>250

-

-

-

-

1 (100.0)

1

Total

2

3

7

21

30

63

Table 8. Availability of quality improvement committee and conduct of maternal and perinatal death and clinical audit by type of healthcare facility CHCs n (%)

DHs n (%)

RHs and tertiary hospitals n (%)

Quality improvement committee

35 (66.0)

56 (88.9)

17 (100.0)

Maternal death reviews conducted

37 (69.8)

53 (84.1)

17 (100.0)

Perinatal death reviews conducted

47 (88.7)

62 (98.4)

16 (94.1)

Process clinical audits

33 (62.3)

52 (82.5)

13 76.5

four or fewer signal functions. Table 7 shows that 7 DHs were providing seven or fewer signal functions and were 50 km or more from an RH. Fifteen DHs did not provide a CS service and 14 (93%) were more than 20 km from an RH. The sites were asked to comment on their referral system. The most frequent comment was delays in the ambulance service (25, 40%).

Table 8 gives the performance of quality improvement activities and audits at the various facilities.

Discussion

This survey was undertaken to assess the ability of health facilities in 12 districts to provide emergency obstetric care. It is the first survey of its kind to be undertaken in SA, although similar surveys have been conducted in other countries. Overall no CHC could provide all seven BEmONC signal functions. Forty-nine per cent of the CHCs could perform only four signal functions, and 25% were able to perform only three signal functions. Most CHCs could not perform an assisted delivery or manual vacuum aspiration for a spontaneous incomplete miscarriage, but all had magnesium sulphate and oxytocics. Fortyeight per cent of the DHs could perform all nine of the CEmOC signal functions, and altogether 81% could perform eight of the nine signal functions. The most common signal functions that the DHs were not able

to perform were assisted delivery (30%), CS (24%) and manual vacuum aspiration for a spontaneous incomplete miscarriage (16%).

Surprisingly few (32%) of the CHCs could give parenteral anti­biotics. This could be explained by the earlier versions of the Essential Drugs List not containing intravenous antibiotics for CHCs. This has since changed, and the Essential Drugs List now includes parenteral antibiotics for CHCs. Starting intravenous antibiotics as soon as possible in cases of pregnancy-related sepsis or septic miscarriage improves the chances of women with these complications surviving. Most CHCs had oral antibiotics, but this would be inadequate for initiating treatment in cases of severe sepsis.

Obstetric haemorrhage, especially post­ partum haemorrhage (PPH), is unpredictable and death can occur rapidly. It has been reported that in the absence of any medical intervention the average time to death from a PPH is 2 hours and that for an antepartum haemorrhage 12 hours. In the Birthplace in England Collaborative Group study on birthplaces for women classified as having low-risk pregnancies, 1.2% of women ended up requiring blood transfusion for obstetric haemorrhage.[4] It is essential for all sites conducting births to have the ability (knowledge, skills and resources) to manage PPH. Furthermore, it is important for all sites to practise the active management of the third stage of labour, which includes giving oxytocin to all women in the third stage of

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labour. A retained placenta is a common cause of severe PPH, and the sixth Saving Mothers report indicated that 45 women died of this complication (7% of all maternal deaths due to obstetric haemorrhage).[2] Manual removal of a placenta is an essential skill that all healthcare providers conducting births should have. Thirty per cent of CHCs and 6% of DHs did not have anyone with the ability to perform this function. This indicates a deficit in the health system. Furthermore, in only 31 CHCs (58%) were there midwives capable of manually removing a placenta, suggesting that this skill is not available around the clock in CHCs. The almost total lack of appropriate gloves for the procedure (47/53 CHCs) indicates a lack of knowledge about the appropriate equipment for this procedure.

Administering magnesium sulphate to all women with eclampsia and severe preeclampsia as soon as the condition is recognised is one of the most important ways of reducing deaths due to complications of hypertension.

To administer magnesium sulphate safely and give a repeat dose, the healthcare provider needs to be able to test the patient’s reflexes, and to administer calcium gluconate if there is an overdose of magnesium sulphate.

Left unmanaged, spontaneous incomplete miscarriages (which occur in 15% of women who are clinically pregnant) have a significant risk of becoming infected or resulting in severe blood loss. In 2011 - 2013,[2] 114 and 48 women died of sepsis or haemorrhage following a miscarriage, respectively. Much of this can be prevented if the uterus can be evacuated as soon as possible. The manual vacuum aspirator (MVA) is a simple piece of apparatus that enables a woman with an uncomplicated incomplete miscarriage to undergo evacuation of the uterus as an outpatient. In a randomised trial it was shown to be superior to an evacuation in theatre.[9] It is surprising that use of an MVA was not available at 27 DHs and 5 RHs, and they were almost absent from the CHCs. All doctors should be skilled in the technique.

In SA all midwives with advanced midwifery, and specially trained midwives performing terminations of pregnancy, are trained and legislated to perform this procedure.

In the Birthplace in England Collabora­ tive Group study on perinatal outcomes of low-risk pregnancies,[4] 7.3% and 6.2% of women had vacuum and forceps deliveries, respectively. The perinatal mortality rate (PNMR) in this population was <1/1 000 births. In SA, the PNMR for babies weigh­ ing ≥1 000 g was ~25.6/1 000 births for 2010 - 2011.[11] Intrapartum asphyxia and birth trauma were the major underlying causes of perinatal death, with a rate of 4.87/1 000 births. Our assisted delivery rate

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was 0.52% for vacuum delivery and 0.15% for forceps delivery. The CS rate was 21%. When the intrapartum asphyxia and birth trauma death rates were correlated with the vacuum delivery rate, there was a significant negative correlation of r = –0.307 (p=0.036).[10] A negative correlation means that the fewer vacuum-assisted deliveries there were, the more intrapartum asphyxia and birth trauma deaths occurred. An assisted delivery rate of <1% is too low, and is probably due to the loss of skill in performing assisted delivery.

Even at the tertiary level there is lack of ability to perform assisted delivery. Assisted delivery is a key activity to reduce perinatal deaths by reducing delay in delivery and is an important function for CHCs. All advanced midwives should be able to perform at least a vacuum delivery. The fact that these skills are almost totally absent in the CHCs speaks for itself and must contribute to the high mortality rate due to intrapartum asphyxia and birth trauma.

About 3% of babies born in the Birthplace in England Collaborative Group study required neonatal resuscitation.[4] It is always possible that a neonate will need to be resuscitated, and every healthcare provider conducting births must be able to at least bag-and-mask ventilate a neonate. That 17% of CHCs were not able to do so owing to lack of equipment or skills is very disturbing.

Unexpectedly, 15 (24%) of the DHs in the 12 districts were not performing CSs. The most common reasons were that there were no doctors (11/15) and no functioning theatre (4/15). However, all DHs could give a blood transfusion if necessary. Surprisingly, 16% of DHs did not have maternal death reviews.

Recently Dumont et al.[11] in the QUARITE trial demonstrated that an intervention consisting of emergency obstetric care training and training in conducting maternal mortality review meetings, with monthly meetings, combined with continuing medical education on the problems identified, reduced maternal mortality by 15%. Both these activities (emergency obstetric care training and maternal mortality review meetings) are being scaled up in SA. However, if increased knowledge and skills are not accompanied by increased functionality of the facilities with respect to lifesaving services and effective interfacility transport, the impact of the increased knowledge and skills may be smaller than expected.

The WHO Multicountry Survey on Maternal and Newborn Health analysed the use of the signal function in a random sample of larger hospitals (>1 000 births per year) and found surprisingly high mortality rates.[12] They concluded that having the ability to provide lifesaving services is only useful if healthcare providers are skilled in the management of complicated cases. If the healthcare providers are not skilled in managing a complication the result will be poor, even if the resources are available to manage the case. In the 12 districts studied we do not have good coverage of the basic and comprehensive emergency care signal functions, and the high number of cases that were thought to be possibly or probably avoidable in the Saving Mothers reports would indicate that we also lack the skills to manage complications.

This study concentrates on the 12 most needy districts in SA, so the picture represented here is the worst-case scenario. A survey of other districts needs to be performed to see whether the problems identified in this study are present in all the districts.

A feature not discussed in this paper is the staffing of the various facilities. This is dealt with in a separate paper.[13] A number of recommendations have evolved out of this survey.

The CEOs of the institutions and the district managers must be made aware of the requirements of providing the seven signal functions for BEmONC, and that all DHs should be able to provide the nine signal functions for CEmONC. Currently the scope of practice of a professional nurse with midwifery (the vast majority of nursing staff running maternity units) does not allow them to perform assisted delivery and manual vacuum

260

aspiration. All advanced midwives should have the knowledge and skills to perform vacuum deliveries, manual vacuum aspiration for incomplete miscarriages and manual removal of the placenta. A method must be found to train advanced midwives rapidly to fill the skills gap, especially in CHCs. Special attention needs to be paid to the sites performing CSs. There need to be adequate skills and facilities to provide the service safely.

A concerted effort must be made to ensure that advanced midwives and doctors are skilled in vacuum deliveries, manual removal of the placenta and manual vacuum aspiration of the uterus for incomplete miscarriage.

(Training in these skills is part of the ESMOE-EOST programme.)

CEOs of CHCs and DHs need to ensure that they employ healthcare providers who provide the correct skills mix to ensure that basic and comprehensive emergency care can be effectively provided.

This area is one where task shifting can be fruitfully employed.

Special attention needs to be paid to improving interfacility transport. Use of the Free State model of separating the prehospital and interfacility ambulance service could be a very effective route to follow.[14]

Conclusion

In the 12 districts surveyed, the required level of emergency obstetric care was not available in most CHCs and in a quarter of DHs. If referral of patients to an appropriate level is taken into consideration, less than half the CHCs could possibly get their patients with complications to the appropriate hospital in less than 1 hour.

The ability of the primary level of care (CHCs and DHs) to perform the signal functions (lifesaving services) of basic and comprehensive emergency obstetric care was poor in many of the districts studied.

This implies that safe maternity care was not consistently available at many facilities conducting births.

Acknowledgements. The authors thank Dr Charles Ameh for input on the baseline datasheet. We would also like to thank all the district managers, CEOs of facilities and staff who we interviewed and who helped with the study in the 12 districts.

1. Dorrington RE, Bradshaw D, Laubscher R. Rapid Mortality Surveillance Report 2012. Cape Town: South African Medical Research Council, 2014.

2. Pattinson RC, ed. Saving Mothers 2011-2013: The Sixth Report of the National Committee for Confidential Enquiries into Maternal Deaths in South Africa. Pretoria: Government Printer, 2014.

3. Rooks JP, Weatherby NL, Ernst EK, Stapleton S, Rosen D, Rosenfield A. Outcomes of care in birth centers: The National Birth Center Study. N Engl J Med 1989;321(26):1804-1811. [http://dx.doi. org/10.1056/NEJM198912283212606] 4. Birthplace in England Collaborative Group. Perinatal and maternal outcomes by planned place of birth for healthy women with low risk pregnancies: The Birthplace in England national prospective cohort study. BMJ 2011;343:d7400. [http://dx.doi.org/10.1136/bmj.d7400] 5. Kerber K. Triple return for our rand: How many South African mothers and babies can be saved and what is the cost? Presented at the 30th Annual Priorities in Perinatal Care Conference, Safari Lodge, Polokwane, 8-10 March 2011.

6. Pattinson R, Kerber K, Buchmann E, et al., for The Lancet’s Stillbirths Series steering team. Stillbirths: How can health systems deliver for mothers and babies? Lancet 2011;377(9777):1610-1623. [http:// dx.doi.org/10.1016/S0140-6736(10)62306-9] 7. World Health Organization. Monitoring Emergency Obstetric Care: A Handbook. Geneva: WHO, 2009.

8. Frank K, Lombaard H, Pattinson RC. Does completion of the Essential Steps in Managing Obstetric Emergencies (ESMOE) training package result in improved knowledge and skills in managing obstetric emergencies? S Afr J Obstet Gynaecol 2009;15(3):94-99.

9. De Jonge ETM, Venter CP, de Wet GH, Pattinson RC. Improving care for patients undergoing curettage for incomplete abortion. S Afr Med J 1996;86(9):1172-1174.

10. Pattinson RC. Saving Babies 2010-2011: The Eighth Report on Perinatal Care in South Africa. Pretoria: Tshepesa Press, 2012.

11. Dumont A, Fournier P, Abrahamowicz M, et al. Quality of care, risk management, and technology in obstetrics to reduce hospital-based maternal mortality in Senegal and Mali (QUARITE): A clusterrandomised trial. Lancet 2013;382(9887):146-157. [http://dx.doi.org/10.1016/S0140-6736(13)60593-0] 12. Souza JP, Gülmezoglu AM, Vogel J, et al. Moving beyond essential interventions for reduction of maternal mortality (the WHO Multicountry Survey on Maternal and Newborn Health): A crosssectional study. Lancet 2013;381(9879):1747-1755. [http://dx.doi.org/10.1016/S0140-6736(13)60686-8] 13. Pattinson RC. Safety versus accessibility in maternal and perinatal care. S Afr Med J 2015;105(4):261265. [http://dx.doi.org/10.7196/SAMJ.9182] 14. Schoon M. Impact of inter-facility transport on maternal mortality in the Free State Province. S Afr Med J 2013;103(8):534-537. [http://dx.doi.org/10.7196/samj.6828] 15. World Health Organization. Managing Complications in Pregnancy and Childbirth: A Guide for Midwives and Doctors. (WHO/RHR/00.7). Geneva: WHO, Geneva, 2003.

Accepted 24 November 2014.

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HEALTHCARE DELIVERY

Safety versus accessibility in maternal and perinatal care R C Pattinson Bob Pattinson, MD, FRCOG, FCOG (SA), is Director of the Medical Research Council Maternal and Infant Health Care Strategies Unit, Department of Obstetrics and Gynaecology, Faculty of Health Sciences, University of Pretoria, South Africa. His main interests are in implementing effective healthcare interventions at primary and secondary levels of care.

Corresponding author: R C Pattinson (robert.pattinson@up.ac.za)

This article adds to the debate on appropriate staffing in maternity units. My starting point for assessing staffing norms is the staff required to provide a safe maternity unit. A survey in 12 districts showed that their health facilities were not adequately prepared to perform all the essential emergency services required. Lack of staff was often cited as a reason. To test this notion, two norms (World Health Organization (WHO) and Greenfield) giving the minimum staff required for the provision of safe maternity services were applied to the 12 districts.

Assuming the appropriate equipment is available and the facility is open 24 hours a day 7 days a week, at a minimum there need to be ten professional nurses with midwifery/advanced midwives to ensure safety for mother and baby in every maternity unit. The norms indicate that the units should do a minimum of 500 - 1 200 deliveries per year to be cost-effective. All 12 districts had sufficient staff according to the WHO. When the numbers of facilities with maternity units were compared with Council for Scientific and Industrial Research and WHO norms for number of health facilities per population, a large excess of facilities was found. Per district there were sufficient personnel to perform the number of deliveries for that district using the WHO or Greenfield formulas, but per site there were insufficient personnel. In my view there are sufficient personnel to provide safe maternity services, but too many units are performing deliveries, leading to dilution of staff and unsafe services. A realignment of maternity units must be undertaken to provide safe services, even at the expense of accessibility.

S Afr Med J 2015;105(4):261-265. DOI:10.7196/SAMJ.9182

Complications in pregnancy and labour can occur even in the best of circumstances, and a large proportion of serious complications occur among women with no recognisable risk factors at all.[1,2] Most pregnant women in South Africa (SA) (~60%) give birth at the primary level of care in community health centres (CHCs) and district hospitals (DHs). Most of the unexpected complications will occur at these levels of care.

To reduce maternal deaths, recognition, stabilisation and treatment or referral of the obstetric emergency must occur at the site closest to where the complication occurred. For the majority of women, this means at CHCs and DHs. Three factors must be present at these sites, namely: • Healthcare providers with sufficient knowledge and skills to recognise a complication, stabilise and treat or refer the patient • Healthcare facilities with the essential lifesaving services available, such as in DHs the resources, both human and equipment, to perform caesarean sections (CSs) 24 hours a day, 7 days a week • An efficient emergency transfer system.

A safe maternity unit is one where the healthcare provider has the knowledge and skills to perform all the observations required on a woman in labour and to manage a complication, either by treatment or by stabilisation and referral. Further, the unit should have sufficient staff to ensure that the woman is monitored appropriately and to deal with the immediate management of complications. Since the maternity services are based on a primary healthcare system where the patient is managed at the lowest appropriate level of care, a mechanism of rapid transport must be available should a complication arise.

An accessible maternity unit is one where patients can reach and receive appropriate care quickly. This usually implies that maternity units must be capable of managing normal pregnancies, with a rapid referral mechanism to higher levels of care where required. Ideally, the maternity units for pregnant women with no identified risk factors are close to the women’s homes.

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Michalow et al.[3] using the Lives Saved Tool (LiST) estimated that 11 562 maternal and perinatal deaths could be averted in 2030 if comprehensive emergency obstetric and neonatal care (CEmONC) was fully implemented. LiST is a module in Spectrum, a demographic software package, which preloads national data for health status, mortality rates, and coverage of more than 60 interventions and their effectiveness in relation to specific causes of death.[4] The modelling methods in LiST have been widely reviewed.[5] The basic emergency obstetric and neonatal care (BEmONC) and CEmONC packages are lists of lifesaving services, or ‘signal functions that indicate a health facility’s ability to treat obstetric and neonatal emergencies’ developed by the World Health Organization (WHO).[6] The functionality of 106 CHCs and DHs was assessed with respect to their ability to provide these emergency services. No CHC could provide all seven BEmONC functions, and only 48% of the DHs could provide all nine of the CEmONC services.[7] Shortage of staff was often cited as the reason for this. During this survey, the maternity staffing was also assessed. The number of midwives (defined as professional nurses with midwifery and advanced midwives) that the unit manager reported were working in the labour ward only or, if not applicable, in the maternity unit was used as the figure for the calculations. Where the personnel were not exclusively allocated to the maternity unit, the number of nurses allocated to the unit per day was used.

Staffing norms for maternity units

The Guidelines for Maternity Care in South Africa[8] state that to manage a pregnant woman with no risk factors in the active phase of labour, the fetal heart rate and the woman’s contractions should be observed every half hour; the blood pressure and pulse should be measured every hour; and every 2 hours the urine output should be measured and urine tested for proteins and ketones, and a vaginal examination should be performed to assess cervical dilation and progress of labour. These required observations indicate that every woman in labour is treated the same as a high-care patient in any setting. This is

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Table 1. Allocation of midwives (professional nurses with midwifery and advanced midwives) to maternity units per district District

DHIS births (2011), n

Midwives per district, n

WHO[9] estimates per district, n

Greenfield[10] estimates per district, n

Births/midwife/ year, n

1

25 931

300

148

346

86

2

7 114

59

41

95

121

3

9 522

72

54

127

132

4

13 159

118

75

175

112

5

42 480

263

243

566

162

6

12 895

125

74

172

103

7

16 811

128

96

224

131

8

18 209

170

104

243

107

9

12 383

141

71

165

88

10

16 493

173

94

220

95

11

7 658

61

44

102

126

12

18 569

275

106

248

68

DHIS = District Health Information Service.

Table 2. Structure of maternity staffing at the 12 core district facilities (professional nurses with midwifery and advanced midwives only) Staffing structure

Type of facility

Dedicated labour ward staff n (%)

Rotation of staff through maternity unit but permanently in unit for a while before rotation n (%)

Staff working in all areas of hospital and allocated to maternity on a daily basis n (%)

Rotation of staff through maternity, some permanent, some all areas of facility n (%)

Total N (%)

CHC

0

14 (26.4)

27 (50.9)

12 (22.6)

53 (100.0)

DH

4 (6.3)

39 (61.9)

9 (14.3)

11 (17.5)

63 (100.0)

RH

6 (46.2)

7 (53.8)

0

0

13 (100.0)

PT

4 (100.0)

0

0

0

4

Total

14

60

36

23

133

PT = provincial tertiary hospital.

entirely appropriate, as a pregnancy can only be regarded as low risk after the first 72 hours after birth. Importantly, this implies that the professional nurse with midwifery looking after the patient can do nothing other than monitor that patient, and perhaps another patient in labour in the same area.

Currently most CHCs are staffed by professional nurses with midwifery. Performing an assisted delivery (vacuum delivery) is not in the scope of practice of professional nurses with midwifery, but is part of the skills set of advanced midwives. An attendant skilled in vacuum delivery needs to be available in the maternity unit for every shift. This currently implies that an advanced midwife for a CHC and a doctor or an advanced midwife for a DH must be available all the time in these facilities.

To cover every shift at advanced midwifery level, there need to be five advanced midwives employed at the site (taking off-duty time, vacation, sick leave, etc. into account). If a pregnant woman needs to be referred to a DH, she must to be accompanied by a professional nurse with midwifery. Again, to

ensure proper coverage for 24 hours a day there need to be five such professional nurses.

A safe maternity service in a CHC therefore requires five advanced midwives and five professional nurses with midwifery. I have called this the ideal critical mass of professional nurses, but it is unattainable at present as there are far too few advanced midwives to cover the CHCs. The minimum critical mass of staff, for practical purposes, requires a professional nurse with an assistant nurse or staff nurse always to be present in the maternity unit.

If the ideal critical mass of ten professional nurses is employed, cost-effectiveness requires them to have an adequate workload. Most CHCs and midwife obstetric units (MOUs) refer about a third of women who present to them in labour according to the prescribed referral criteria. The WHO[9] recommends that each midwife should conduct 175 deliveries per year to ensure cost-effectiveness. In terms of CHCs, and given the intrapartum referral rate, a CHC midwife conducting approximately 120 deliveries per year would be cost-effective.

This implies that a CHC operating a maternity

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April 2015, Vol. 105, No. 4

service, or an MOU, must carry out about 1 200 deliveries per year to be safe and costeffective. This is called the ideal minimum births per year – WHO. Greenfield[10] used a formula of 16 midwives per 100 deliveries per month, i.e. 16 midwives per 12 000 births per year or 75 births per midwife per year. (These midwives would also manage the babies in the nursery, and antenatal and any postnatal patients.) Given that approximately a third of pregnant women are referred in labour, the minimum number of births per CHC per year would be about 500. This is called the ideal minimum births per year – Greenfield. If a realistic view is taken, a professional nurse with an assistant nurse or staff nurse should manage 600 births (realistic minimum births – WHO) or 250 births (realistic minimum births – Greenfield) per year.

A similar exercise can be conducted for DHs. They would also require ten professional nurses; five do not have to be advanced midwives, as there are doctors available 24 hours a day.

However, as doctors perform CSs there should be at least two professional nurses and a staff

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Table 3. Distribution of births in CHCs* Births per year, N

n (%)

<250

15 (31.3)

250 - 499

12 (25.0)

500 - 599

3 (6.3)

600 - 1 199

9 (18.8)

>1 200

9 (18.8)

Total

48 (100.0)

*5 CHCs had no data in the District Health Information Service.

Table 4. Distribution of births in DHs Births per year, N

n (%)

<500

11 (17.5)

500 - 1 199

4 (6.3)

>1 200

48 (76.2)

Total

63 (100.0)

Fig. 1 is a scatter plot of the number of mid­ wives (professional nurses with midwifery and advanced midwives) against the number of births per year. Four CHCs have been removed from Fig. 1 because they performed more than 2 000 deliveries per year (namely 2 050, 2 141, 2 198 and 3 544 deliveries). The solid line represents the ideal minimum births per year and the dashed-dotted line the realistic minimum births per year using the WHO norms. The dashed line represents the ideal minimum births per year and the dotted line the realistic minimum births per year using Greenfield’s norms. The ideal critical mass of staff is the number of midwives needed to run a unit safely. The minimum critical mass is the minimum number of midwives (professional nurses with midwifery and advanced midwives) to run a unit safely. In this group, it is assumed that the professional nurse will have a staff nurse or nursing assistant in attendance.

There were 22 CHCs (45.8%) with less than ten midwives in the maternity unit (the ideal

minimum critical mass), making these CHCs theoretically unsafe. If the realistic minimum critical mass of staff (i.e. five midwives and five auxiliary nurses) is used, five CHCs (10.4%) fall below this critical mass. Overall, 20 (41.7%) and 16 (33.3%) CHCs had less than the ideal minimum births and ideal critical mass of midwives using the WHO and Greenfield norms, respectively. Interestingly, 13 of CHCs (27.1%) had more than the ideal critical mass of staff but fewer than the ideal minimum number of births, and 15 (31.3%) had more than the ideal critical mass of staff and ideal minimum of births using Greenfield’s norms. Eighteen CHCs (37.8%) had more than the ideal critical mass of staff but fewer than the ideal minimum number of births, and 10 CHCs (20.1%) had more than the ideal critical mass of staff and ideal minimum of births using the WHO norms.

Fig. 2 is a scatter plot of the number of midwives in maternity units against the number of births in the DHs. One DH,

35 Ideal minimum births (WHO)

Midwives in maternity unit, n

30

Ideal minimum births (Greenfield)

25 20 15

Ideal critical mass

10

Minimum critical mass

5 0

0

200

400

600

800 1 000 1 200 Births per year 2011, n

1 400

1 600

1 800

2 000

Fig. 1. Comparison of midwives in maternity units of CHCs and births per year.

40 Ideal minimum births (WHO)

35 Midwives in maternity unit, n

nurse per shift. Since the DH performs CSs, its referral out to regional or tertiary hospitals will be less frequent. Hence, to be safe and cost-effective, DHs would need to per­form between 500 (Greenfield)[10] and 1 200 (WHO)[9] deliveries per year. There should also always be a minimum of two doctors on call (one for anaesthesia and one for the surgery), so that CSs may be performed on a 24-hours-a-day, 7-days-a-week basis. The first assistant would need to be a professional nurse or a clinical associate.

These staffing norms were applied to the 12 districts in the baseline survey.[7] The total professional nurse personnel per district allocated to maternity care was in excess of the WHO[9] norm of 175 births per midwife per year in all districts (Table 1); however, when Greenfield’s[10] estimates were used, all districts except one had a shortage of midwives.

The staffing structure for the various levels of care is shown in Table 2. The allocation of staff differed per level of care and within each level of care. In the CHCs all staff rotated, some being allocated to maternity for a day only, and others for a longer period.

Tables 3 and 4 give the distribution of births in the 53 CHCs and 63 DHs. Only nine CHCs (18.8%) performed more than the minimum number of deliveries using the ideal minimum births – WHO norm, while 21 (45.7%) performed more deliveries than the ideal minimum births – Greenfield norm. If a realistic approach is taken with one midwife and one auxiliary nurse, 18 CHCs (37.6%) met the WHO norm and 33 (68.7%) met the Greenfield norm.

Seventy-six per cent of the DHs met the ideal minimum number of births with regard to the ideal minimum births – WHO norm and 82.5% met the ideal minimum births – Greenfield norm.

30 Ideal minimum births (Greenfield)

25 20 15

Minimum critical mass

10 5 0

0

500

1 000

1 500

2 000 2 500 3 000 Births per year 2011, n

3 500

Fig. 2. Comparison of midwives in maternity units of DHs and births per year.

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4 000

4 500

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having 5 827 births and 28 midwives, was excluded from the scatter plot in Fig. 2. The solid vertical line represents the ideal minimum births per DH using the WHO norm and the dashed line the ideal minimum births per DH using Greenfield’s norm. Thirty-one DHs (49.2%) had less than the minimum critical mass of midwives to run their maternity unit safely.

Twenty-two (34.9%) and 10 (15.9%) DHs had less than the ideal minimum number of births using the WHO and Greenfield norms, respectively. Six DHs (1.0%) had a more than minimum critical mass of midwives but less than the ideal minimum number of births, and 18 DHs (28.6%) had more than the minimum critical mass of midwives and the ideal minimum number of births using the WHO norm. If the Greenfield norms are used, no DH had less than the ideal minimum number of births and more than the minimum critical mass of midwives, whereas 26 DHs (41.3%) had both more than the minimum critical mass of midwives and the ideal minimum number of births.

Healthcare facilities and the population

The Council for Scientific and Industrial Research (CSIR) Guidelines for the Provision of Social Facilities in South African Settlements[11] is a guideline document that ‘seeks to provide a quantitative and rational framework for the provision of key social facilities for various levels of settlements to support the planning process and provide support to the social facility investment plans’. The norms given in this guideline are a level 3 hospital per 2.4 million population, a regional hospital (RH) per 1.77 million population (level 2), a DH per 300 000 900 000 population with an access distance of 30 km (level 1), a CHC for every 60 000 140 000 population with 90% access distance of 5 km, and a primary healthcare clinic for every 40 000 population with an access distance of 5 km. Using these figures and those of mid-year Stats SA population estimates for 2013,[12] it can be suggested that SA should have: • 22 tertiary hospitals – level 3 (we have 22) • 30 RHs – level 2 (we have 42) • Between 59 and 177 DHs – level 1 (we have 188).

The number of CHCs and hospitals in each district was counted and an estimation made of the theoretical population based on the United Nations (UN) formula[6] that could be served by that number of institutions. This is similar to the CSIR report.[11] In all 12 districts there was an excess of maternity units for the population served (Table 5).

Table 5. Healthcare facilities, population and UN recommendations for emergency obstetric care

District

RH

PT

District population

Total

Population that could be served*

‘Excess capacity’

CHC

DH

1

9

12

1

1

23

1 806 831

6 000 000

4 193 169

2

0

4

1

0

5

499 875

2 000 000

1 500 125

3

0

5

1

0

6

694 198

2 500 000

1 805 802

4

1

10

1

0

12

767 678

5 000 000

4 232 322

5

7

1

4

1

13

2 965 602

3 000 000

34 398

6

3

3

1

0

7

760 648

2 000 000

1 239 352

7

4

2

1

1

8

1 058 086

2 000 000

941 914

8

3

6

1

0

10

965 950

3 500 000

2 534 050

9

2

8

0

0

10

666 664

4 000 000

3 333 336

10

6

8

1

0

15

943 137

4 500 000

3 556 863

11

4

2

0

1

7

375 167

1 500 000

1 124 833

12

16

3

1

0

20

1 400 000

2 000 000

600 000

55

64

13

4

136

PT = provincial tertiary hospital. * For every 500 000 population, there should be at least one comprehensive and four basic emergency obstetric care facilities.[6]

Table 6. Estimated number of deliveries per year according to birth-weight categories and levels of care CHC

DH

RH

PT

NC

500 - 999 g

748

3 108

4 087

2 027

2 660 3 239

All births, n 1 000 - 1 499 g

1 122

4 663

5 529

2 962

1 500 - 1 999 g

2 431

9 325

9 616

4 365

4 338

2 000 - 2 499 g

13 091

31 084

23 318

8 652

7 172

≥2 500 g

169 616

34 0373

197 842

59 861

40 427

Total

187 007

388 554

240 392

77 867

57 835

460

2 509

3 083

1 362

1 461

Perinatal deaths, n 500 - 999 g 1 000 - 1 499 g

284

2 159

1 863

819

731

1 500 - 1 999 g

260

1 728

1 377

655

506

2 000 - 2 499 g

255

1 551

1 252

504

360

≥2 500 g

560

3948

2 730

952

663

Total

1 819

11 896

10 305

4 292

3 721

PT = provincial tertiary hospital; NC = national central hospital.

Deliveries per site per level of care in SA

The numbers of births per birth-weight category and level of care were calculated using the number of births recorded per level of care in the District Health Information Service for 2012 - 2013 and annualised.[13] This is shown in Table 6.

The Regulation Gazette of 2011[14] listed 188 DHs, 42 RHs, 12 provincial tertiary hospitals and 10 national central hospitals.

Table 7 gives the estimated average number of births and early neonatal deaths (ENNDs) per institution.

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April 2015, Vol. 105, No. 4

Most deaths occur in DHs, as do most births. The mortality rates in the DHs are the highest, but one DH delivering an average of 2 000 babies per year will deliver a liveborn baby weighing between 1 000 g and 1 999 g once every 5 days, and 12% (one in eight) will be an ENND. If the hospital delivery rate is 500 births per year, a liveborn baby weighing between 1 000 g and 1 999 g will be delivered every 20 days and two will die. This analysis raises the question of what resources should be available in each institution and how many deliveries per year will make the institution cost-effective,

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Table 7. Average number of births, stillbirths, live births, stillbirths and ENNDs per level of care and birth-weight category DH

RH

PT

NC

188

42

12

10

500 - 999 g

17

97

169

266

1 000 - 1 499 g

25

132

247

324

1 500 - 1 999 g

50

229

364

434

2 000 - 2 499 g

165

555

721

717

≥2 500 g

1 810

4 711

4 988

4 043

Total

2 067

5 724

6 489

5 784

500 - 999 g

8

46

72

95

1 000 - 1 499 g

7

29

47

48

1 500 - 1 999 g

7

26

43

38

2 000 - 2 499 g

6

23

34

27

≥2 500 g

13

49

58

41

Total

42

173

254

248

500 - 999 g

16

94

162

255

1 000 - 1 499 g

24

128

237

310

1 500 - 1 999 g

49

222

349

415

2 000 - 2 499 g

162

538

693

686

≥2 500 g

1 774

4 568

4 793

3 869

Total

2 025

5 551

6 234

5 536

500 - 999 g

10

50

70

76

1 000 - 1 499 g

6

19

25

29

1 500 - 1 999 g

3

8

13

13

2 000 - 2 499 g

2

7

8

9

≥2 500 g

7

16

20

24

Total

28

99

136

152

South Africa – hospitals per level of care, n Average births per year per hospital, n

Average stillbirths per hospital per year, n

Average live births per hospital per year, n

Average ENNDs per hospital per year, n

PT = provincial tertiary hospital; NC = national central hospital.

while at the same time keeping healthcare accessible to the population.

Discussion

Part of the explanation for the poor functionality with respect to emergency obstetric care in the CHCs and DHs relates to the number of facilities and the staffing of these facilities: (i) according to the UN norms[6] and CSIR norms,[11] there are too many healthcare facilities for the population served, yet there is sufficient staff to manage the births in the district; (ii) there are some maternity units that are clearly unsafe given the number of staff allocated to the unit (less than the ideal minimum critical mass or realistic minimum critical mass of midwives in the case of CHCs); and (iii) there are a number of maternity units that perform fewer than the minimum number of deliveries, making them both unsafe and not cost-effective.

To maintain skills, a midwife needs to perform deliveries regu­larly – doing one delivery a month is insufficient. The Guidelines for Maternity Care in South Africa[8] clearly stipulate the observations required for a ‘lowrisk’ woman in labour, and these are such that during the active phase of labour the woman must be observed at least every half hour. This implies that the professional nurse cannot do anything else during that labour, other than perhaps monitor another woman in labour.

In essence, a woman in labour requires monitoring at the same level as any patient in a high-care setting. This is appropriate, as there is not the knowledge to predict accurately before labour begins which woman or fetus will develop complications during the labour. However, given human resources limitations and the multiple tasks required of professional nurses in many CHCs and

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DHs, it is impossible for them to fulfil these requirements in their maternity units. Such maternity units then become unsafe.

The two norms used, namely the WHO[9] and Greenfield[10] norms, are two extremes, and happily most of SA’s maternity units fall somewhere in between. The WHO norm[9] is the minimum number of professional nurses required to provide a maternity service.

Greenfield’s norms[10] have been developed with SA circumstances in mind and are viewed as the ideal, even if unattainable at present.

The solution to making maternity units safer and more cost-effective is to realign services, which implies reorganisation of services so that there are properly functioning, safe maternity units open 24 hours a day, 7 days a week. However, this will make the maternity services less accessible unless there is a system for the efficient and rapid transfer of emergency cases. The maternity waiting areas could become a valuable mechanism for ensuring that the woman is at a safe maternity unit at the time of her labour.

Realignment of services and improved emergency transport are not impossible to achieve, as demonstrated by the example of the Free State Province, where maternal mortality was halved by improving the province’s interfacility transport by providing dedicated maternity care ambulances, improving the knowledge and skills of the provincial staff and consolidating the CS services.[15] 1. Rosenfield A, Maine D. Maternal mortality – a neglected tragedy: Where is the M in MCH? Lancet 1985;2(8446):83-85. [http://dx.doi.org/10.1016/S0140-6736(85)90188-6] 2. Birthplace in England Collaborative Group. Perinatal and maternal outcomes by planned place of birth for healthy women with low risk pregnancies: The Birthplace in England national prospective cohort study. BMJ 2011;343:d7400. [http://dx.doi.org/10.1136/bmj.d7400] 3. Michalow J, Chola L, McGee S, et al. Triple return on investment: The cost and impact of 13 interventions that could prevent stillbirths and save the lives of mothers and babies in South Africa. BMC Pregnancy Childbirth 2015;15:9. [http://dx.doi.org/10.1186/s12884-015-0456-9] 4. LiST: The Lives Saved Tool. An evidence-based tool for estimating intervention impact. http://www.jhsph.edu/dept/ih/ IIP/list/index.html (accessed 26 February 2015).

5. Boschi-Pinto C, Black RE. Development and use of the Lives Saved Tool: A model to estimate the impact of scaling up proven interventions on maternal, neonatal and child mortality. Int J Epidemiol 2011:40(2):520-521. [http://dx.doi.org/10.1093/ije/dyq171] 6. UNICEF, WHO, UNFPA. Guidelines for Monitoring the Availability and Use of Obstetric Services. New York: United Nations Children’s Fund, 1997.

7. Pattinson RC, Makin JD, Pillay Y, van den Broek N, Moodley J. Basic and comprehensive emergency obstetric and neonatal care in 12 South African health districts. S Afr Med J 2015;105(4):256-260. [http://dx.doi.org/10.7196/SAMJ.9181] 8. Guidelines for Maternity Care in South Africa. http://www. health.gov.za/policies.php (accessed 17 June 2014).

9. Newborns: No longer going unnoticed. In: The World Health Report: 2005: Make Every Mother and Child Count. Geneva: WHO Press, 2005:79-102.

10. Greenfield DH. Midwifery staffing needs in a maternity ward.

Presented at the 25th Conference on Priorities in Perinatal Care in South Africa, Drakensberg, KwaZulu-Natal, 7-10 March 2006.

11. Council for Scientific and Industrial Research. CSIR Guidelines for the Provision of Social Facilities in South African Settlements. 1st ed. Pretoria: CSIR, 2012.

12. Statistical Release P0302. Mid-year population estimates 2013.

Statistics South Africa, May 2013.

13. Pattinson RC, Rhoda N. Saving Babies 2012-2013: Ninth Report on Perinatal Care in South Africa. Pretoria: Tsephega Press, 2014.

14. Regulation Gazette No. 34521 of 12 August 2011, vol. 553, No 9570[1].

15. Schoon M. Impact of inter-facility transport on maternal mortality in the Free State Province. S Afr Med J 2013;103(8):534537. [http://dx.doi.org/10.7196/SAMJ.6828]

Accepted 24 November 2014.

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HEALTHCARE DELIVERY

Women’s willingness to use emergency contraception: Experience at Chris Hani Baragwanath Academic Hospital, Johannesburg, South Africa T A Lukhaimane, Y Adam Tshimangadzo Lukhaimane, MB ChB, FCOG (SA), MMed, has a particular interest in diabetes and other endocrinopathies in pregnancy, and Yasmin Adam, BSc, MB BCh, FCOG (SA), MSc (Biostatistics and Epidemiology), an interest in the prevention of cervical cancer and in contraception.

They are specialists in the Department of Obstetrics and Gynaecology, Chris Hani Baragwanath Academic Hospital, Johannesburg, South Africa.

Corresponding author: Y Adam (yasminadam@gmail.com)

Access to emergency contraception (EC) has little restriction in South Africa. EC is a contraceptive method that can be used by women up to 7 days after unprotected intercourse. It can be used in the following situations: when no contraceptive has been used; for condom accidents; after intrauterine contraceptive device expulsion; when a contraceptive method has been incorrectly used, or contraceptive pills missed; if there has been a >3-hour delay in taking the progestogen-only pill, a >2-week delay for intramuscular depot medroxyprogesterone acetate or a >1-week delay for intramuscular norethisterone enanthate; or after delayed placement or early removal or dislodgement of a contraceptive transdermal patch or vaginal ring.

S Afr Med J 2015;105(4):266-267. DOI:10.7196/SAMJ.9411

Emergency contraception (EC) is available from healthcare provi­ders in South Africa (SA) without a prescription. However, awareness of EC is as low as 35.5% in SA (while being as high as 94% in a UK population).[1,2] Women younger than 20 years of age, with a higher level of education and who spoke either English or Afrikaans were more aware of EC.[1,3] Uptake of EC has been seen to increase when dedicated products are available, as seen in France and Nigeria.[4] Knowledge of EC among healthcare providers may also impact on use of the method. In Durban only a third of pharma­cists and doctors could correctly initiate an EC regimen.[5] There were misconceptions that EC was an abortifacient, or an agent that might promote promiscuity, HIV and sexually transmitted infections.[5,6] One hundred women who had delivered at Chris Hani Baragwanath Academic Hospital, Johannesburg, SA, were interviewed to explore their awareness and knowledge of and willingness to use EC. Ethics approval was obtained from the Human Research Ethics Committee at the University of the Witwatersrand, Johannesburg (ethics clearance certificate No. M120354).

Awareness and knowledge of EC

Forty-four women were aware of EC. Most (28, 63.6%) had heard of EC from friends or peers, 9 (20.5%) at a local clinic, 2 (4.5%) from educators, 2 (4.5%) from family, 1 (2.3%) from a pharmacy, and 2 (4.5%) from multiple sources. Awareness of EC was significantly associated with being single, having a senior secondary or tertiary education, being employed and being born in SA. Of those who were aware, 34 (77.3%) knew the correct time that EC could be used, 42 (95.5%) knew where it could be obtained, and 30 (68.2%) knew that it was available over the counter from a healthcare provider. Two women (4.5%) believed that a prescription was required, and the remaining 12 (27.3%) were not sure. Repeated use of EC was reported as being possible by 11 women (25.0%), and 23 (52.3%) were not sure.

Four women (9.1%) correctly identified side-effects of EC, 24 (54.5%) believed that there were no side-effects, and 15 (34.1%) were unsure

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whether there were side-effects (1 woman did not give an answer).

Only 1 woman (2.3%) was aware that an intrauterine contraceptive device could be used as EC. The other 43 (97.7%) knew of EC as a pill formulation.

Willingness to use EC

The 44 women were given a leaflet on EC that explained when and how it can be taken, how to access it, the time at which it should be taken, the types of EC available, where it can be accessed, the mechanism of action and the side-effects. Their willingness to use EC was then assessed. Thirty-five (79.5%) of the women reported that they had not recognised an opportunity to use EC in the past, while 9 (20.4%) had recognised an opportunity to utilise EC and had done so.

The initial sample of 100 women were asked about their willingness to use EC. The majority (85 women) expressed a willingness to use EC, while 14 were not willing and 1 was unsure. The concerns that women raised were personal and related to stigma and religion. Four women had no preference regarding where they would obtain EC, 63 cited the local clinic, 30 would use a private pharmacy, 1 would go to a general practitioner and 2 would approach either a pharmacy or a general practitioner.

The 100 women were then asked whether or not the concept of an advance supply of EC was something that they considered favourable, and whether they had any concerns regarding an advance supply: 70 supported an advance supply of EC, while 29 were against it and 1 was undecided.

Twenty-four of the women expressed concerns with the concept of an advance supply, citing potential for abuse, promotion of promiscuity (especially by the youth), incorrect use, absence of medical advice, wastage of unused medication, and deliberate misuse of regular contraception. A larger proportion (43 women) had positive comments regarding an advance supply of EC, such as convenience of access, no need to queue or worry that a health facility would be closed, privacy and anonymity, no need to face negative staff attitudes, promotion of responsible behaviour,

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control over reproductive choice, and affordability. Thirty-three women did not give an answer.

Most respondents (63 women) said they would prefer to obtain EC from their local clinic for reasons of convenience and afforda­ bility. Those who preferred a doctor or pharmacy highlighted issues such as stigmatisation by clinic staff, long queues, healthcare clinics being closed over weekends or limited access as reasons for opting for sources that they acknowledged would incur a cost.

Discussion

The low awareness of EC among the women surveyed is a concern, particularly as most of them had booked antenatally (98.0%) and had therefore had some interaction with the health services. Of those who were aware, at least two-thirds knew the correct source of access, the correct timing of use and the fact that EC is available without a prescription. Other studies in SA have shown a 7% awareness of EC in HIV-infected women on antiretroviral therapy,[7] 22.8% awareness among women attending clinics in Gauteng,[8] and 35 - 60% awareness among women in a termination of pregnancy clinic.[1,8] In developed countries where EC awareness is high, a lack of knowledge of the potential risk of pregnancy after condom slippage or missed contraceptive pills[9] accounts for underutilisation. Willingness to use the method was high (85.0%) once women were given the knowledge, highlighting the need for better access to information.

Women’s concerns about an advance supply of EC are relevant and would have to be considered in SA, especially as a randomised control trial of an advance supply v. none in advance among postpartum women in the USA showed that an advance supply increased use of EC (relative risk 4.0).[10] Significantly, only 20.4% of the women who were aware of EC had learned about it at a public healthcare facility, and none had heard of it during antenatal visits. Rather, knowledge of EC was gained from non-healthcare sources, which may explain women’s poor depth of knowledge.

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Conclusion

We have identified that EC awareness is lacking and knowledge is poor among women accessing the public sector. If it is freely available but underutilised, EC is unable to make a positive impact on women’s health and fertility regulation. All contraceptive counselling should include a discussion of EC, incorporating advice on an advance supply.

Disclosure of interests. This article was submitted to the University of the Witwatersrand by TAL as part of her MMed dissertation.

Authorship. TAL conceived the study on which the article is based, wrote the protocol and submitted it to the ethics committee. She also performed all the interviews, entered the data into an Excel spreadsheet and wrote the dissertation for her MMed. YA supervised the project from protocol to dissertation and analysed the data.

Funding. No funding was required.

1. Moodley J, Morroni C. Emergency contraception – lack of awareness among women presenting for termination of pregnancy. S Afr Med J 2007;97(8):584-585. [http://www.ncbi.nlm.nih.gov/pubmed/17952213] 2. Lakha F, Glasier A. Unintended pregnancy and use of emergency contraception among a large cohort of women attending for antenatal care or abortion in Scotland. Lancet 2006;368(9549):1782-1787. [http://dx.doi.org/10.1016/ S0140-6736(06)69737-7] 3. Roberts C, Moodley J, Esterhuizen T. Emergency contraception: Knowledge and practices of tertiary students in Durban, South Africa. J Obstet Gynaecol 2004;24(4):441-445. [http://dx.doi.org/10.1080/01443610410001685619 ] 4. Marston C, Cleland J. Do unintended pregnancies carried to term lead to adverse outcomes for mother and child? An assessment in five developing countries. Popul Stud (Camb) 2003;57(1):77-93. [http://dx.doi.org/ 10.1080/0032472032000061749] 5. Blanchard K, Harrison T, Sello M. Pharmacists’ knowledge and perceptions of emergency contraceptive pills in Soweto and the Johannesburg Central Business District, South Africa. Int Fam Plan Perspect 2005;31(4):172-178. [http://www.guttmacher.org/pubs/journals/3117205.html] 6. Golden NH, Seigel WM, Fisher M, et al. Emergency contraception: Pediatricians’ knowledge, attitudes, and opinions. Pediatrics 2001;107(2):287-292. [http://pediatrics.aappublications.org/content/107/2/287.long] 7. Myer L, Rebe K, Morroni C. Missed opportunities to address reproductive health care needs among HIVinfected women in antiretroviral therapy programmes. Trop Med Int Health 2007;12(12):1484-1489. [http:// dx.doi.org/10.1111/j.1365-3156.2007.01955.x] 8. Siebert I, Steyn PS. Knowledge and use of emergency contraception in a tertiary referral unit in a developing country. Eur J Contracept Reprod Health Care 2002;7(3):137-143. [http://dx.doi.org/10.1080/ejc.7.3.137.143] 9. Ibisomi LDG, Odimegwu C. Predictors of unintended pregnancy among South African youth. East Afr Soc Sci Res Rev 2007;23(1):61-80.

10. Jackson R, Schwarz EB, Freedman L, Darney P. Knowledge and willingness to use emergency contraception among low-income post-partum women. Contraception 2000;61(6):351-357. [http://dx.doi.org/10.1016/ S0010-7824(00)00117-7]

Accepted 2 February 2015.

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ISSUES IN PUBLIC HEALTH

Food insecurity in households in informal settlements in urban South Africa N Naicker, A Mathee, J Teare Dr Nisha Naicker, MB BCh, FCPHM, PhD, is based at the Environment and Health Research Unit, South African Medical Research Council, and is an honorary lecturer at the School of Public Health, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa.

Prof. Angela Mathee, PhD, is the Director of the Environment and Health Research Unit, and holds honorary professorial positions in the Wits School of Public Health and the Faculty of Health Sciences, University of Johannesburg. June Teare, MSc (Med), is a senior scientist at the Environment and Health Research Unit, currently based at Nelson Mandela Metropolitan University, Port Elizabeth, South Africa.

Corresponding author: N Naicker (nisha.naicker@mrc.ac.za)

Food insecurity in the urban poor is a major public health challenge. The Health, Environment and Development study assessed trends in food insecurity and food consumption over a period of 7 years in an informal settlement in Johannesburg, South Africa (SA). Annual cross-sectional surveys were conducted in the informal settlement (Hospital Hill). The degree of household food insecurity decreased significantly from 2006 (85%) to 2012 (70%). There was a spike in 2009 (91%), possibly owing to global food price increases. Childhood food insecurity followed the same trend as household food insecurity. During the first 3 study years, consumption of protein, vegetables and fruit decreased by 10 - 20%, but had returned to previous levels by 2012. In this study, although declining, food insecurity remains unacceptably high. Hunger relief and poverty alleviation need to be more aggressively implemented in order to improve the quality of life in poor urban communities in SA. S Afr Med J 2015;105(4)268-270. DOI:10.7196/SAMJ.8927

Food security is a basic human right. However, during the period 2010 - 2012, 852 million people in developing countries remained food insecure.[1,2] Of these 852 million people, 234 million lived in sub-Saharan Africa.[1] The First Millennium Development Goal endeavoured to reduce hunger by half from 1990 to 2015. Reports produced by the United Nations Food and Agriculture Organisation (FAO) indicate that progress towards this goal has been slow, and declined after 2009.[1] In South Africa (SA), three national surveys showed a decrease (from 52.3% to 25.9%) in food insecurity over the 10-year period 1999 - 2008.[3] In urban areas, food insecurity decreased from 42% to 20.5%. In 2009, a study conducted in three impoverished communities in Johannesburg, SA, showed that 56% of all households surveyed were food insecure and 60% of households in an informal settlement were food insecure.[4] Food insecurity has been linked to detrimental health out­comes such as obesity, chronic diseases and mental health disorders in adults.[5-9] In children, research has established a relationship between food insecurity and stunting, poor development and decreased aca­demic ability.[10-13] The literature contains numerous publications pointing to a variety of factors that increase the risk of being food insecure, such as poverty, lower levels of maternal education, unemployment, larger household size, and households that experience events that place an added demand on their budgets.[14,15] Cities, especially in developing countries, are highly heterogeneous, with communities ranging from extremely wealthy to impoverished.

National surveys are limited and provide an overview, but often do not reflect the degree of food insecurity faced by very poor, marginalised communities such as those residing in informal settlements.

Case study

The Health, Environment and Development study was conducted in an informal settlement (Hospital Hill) in Johannesburg to assess

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trends in food security from 2006 to 2012. The main predictors of food insecurity in this community and associated health outcomes were determined. Hospital Hill is located on the south-western outskirts of Johannesburg. A convenience sample of 188 dwellings was initially drawn for inclusion in the study. The response rate ranged from 55% in 2006 to 73% in 2012.

At the selected dwellings, after written, informed consent had been obtained, a prestructured questionnaire was administered to a household member at least 18 years of age to obtain information on sociodemographic status, perceptions of housing and neighbourhood conditions, food security and health status. The Radimer/Cornell Questionnaire Rating Scale[16] was modified to assess food security in households (Table 1). This scale normally assesses food security in individuals. Modified versions of this tool have been validated in developing countries such as Indonesia.[17] For the purpose of analysis the households were grouped into three categories: • Food secure: if the interviewee answered ‘never’ to all questions • Household food insecure: if they answered ‘sometimes’, ‘often’ or ‘always’ to one or more questions related to household food security (questions 1 - 7) • Child food insecure: if they answered ‘sometimes’, ‘often’ or ‘always’ to one or more questions related to childhood food security (questions 8 - 10).

The categories ‘sometimes’, ‘often’ and ‘always’ were combined and a binary variable produced.

Food security and related socioeconomic factors

The results of this study showed a high degree of household food insecurity in the Hospital Hill community. In 2006, 85% of households were food insecure. This increased and peaked at 91% in 2009. Between 2009 and 2012, the number of food-insecure

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Table 1. Modified Radimer/Cornell Questionnaire Question

Never

Sometimes

Often

Always

1. W e worry whether our food will run out before we get money to buy more 2. T he food that we bought just didn’t last and we didn’t have money to get more 3. W e ran out of the foods that we needed to put together a meal and we didn’t have money to get more food 4. W e eat the same thing for several days in a row because we only have a few different kinds of food on hand and don’t have money to buy more 5. W e can’t afford to eat properly (we cannot eat in the way we would like to) 6. W e are often hungry, but we don’t eat because we can’t afford enough food 7. W e eat less than we think we should because we don’t have enough money for food 8. W e cannot give our child(ren) a balanced meal because we can’t afford that 9. O ur child(ren) is/are not eating enough because we just can’t afford enough food 10. We know our child(ren) is/are hungry sometimes, but we just can’t afford more food

Table 2. Food consumed by household at least three times per week, and expenditure on food 2006 (N=104)

2009 (N=74)

Change over 3 years 2006 - 2009

2012 (N=138)

Change over 3 years 2009 - 2012

Dairy products

55 (52.9)

43 (58.1)

↑

80 (58.0)

↔

Carbohydrates

102 (98.1)

70 (94.6)

↓

131 (94.9)

↔

Proteins

89 (85.6)

49 (66.2)

↓

119 (86.2)

↑

Vegetables

97 (93.3)

60 (81.1)

↓

121 (87.7)

↑

Fruit

92 (88.5)

50 (67.6)

↓

110 (79.7)

↑

Sweets

36 (34.6)

36 (48,6)

↑

69 (50.0)

↑

Fast foods

28 (26.9)

35 (47.3)

↑

62 (44.9)

↓

Food expenditure (ZAR), mean/month

378.10

633.64

↑

753.61

↑

Food item, n (%)

households decreased by 21%. These results are indicative of the effects of the 2007 - 2009 food price increases experienced globally, and confirm the vulnerability of the very poor.[1] In households with children, 67% were food insecure. Households with children were therefore more likely to be food insecure, but the association was not statistically significant (p=0.1). However, there was a significant risk of child food insecurity if the whole household was food insecure (p<0.01) (Fig. 1).

The degree of food security has been shown, in this study and in the literature, to vary within and between households in the same community over time, owing to economic and other stressors such as illness or unexpected expenses.[1,18] Compared with national levels of food insecurity (estimated at 48%),[3] residents of this urban informal settlement face a much higher level of food insecurity (70%). The same is likely to apply to other urban informal settlement communities in SA. Factors such as very low income (<ZAR1 000 per month; 1.00 ZAR = 0.09 USD at the time of writing) (p=0.01; crude odds ratio (OR) 3.46; 95% confidence interval (CI) 2.13 - 5.62), low asset ownership (p<0.01; crude OR 4.11; 95% CI 2.31 - 7.32), having a higher number of major problems with the dwelling (p<0.01; crude OR 3.48; 95% CI 2.19 - 5.54) and lack of full-time employment of the head of the household (p=0.01; crude OR 2.81; 95% CI 1.21 6.53) were significantly associated with an increased risk of having a food-insecure household. This study confirms the well-documented

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finding that indicators of poor socioeconomic status are predictive of food insecurity.[3,19,20] Monthly food expenditure was significantly lower in food-insecure relative to food-secure households (p=0.04), indicating the degree of poverty faced by food-insecure households.

According to Bonti-Ankomah,[21] an average household of four members in 2001 needed at least R1 146 per month to obtain a healthy diet for all members. Owing to inflation, higher monthly food expenditure would be expected in 2012. In this Hospital Hill community, households spent on average only R753.61 on food, an increase of R119.97 from 2009 to 2012.

Household food consumption from 2006 to 2012

From 2006 to 2009, there was a 10 - 20% decrease in the consumption of vegetables, protein foods and fruit. However this increased steadily from 2009 to 2012 to approximately the same levels as in 2006, indicating that in periods of food stress or economic downturn, consumption of vegetables, fruit and protein decreased (Table 2). Another finding of this study is the increased trend in the consumption of fast foods, which climbed by 18% between 2006 and 2009, and was sustained at the higher level of consumption in subsequent years. Undernutrition or malnutrition, i.e. a lack of adequate micronutrients, is a major consequence of chronic food insecurity.[18,20] Coping strategies during periods of food insecurity such as decreasing the variety of foods eaten, limiting portion sizes

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Food insecurity and health outcomes

Levels of chronic disease in this community were relatively low, with only 24% being affected with any type of chronic disease (diabetes mellitus, hypertension or heart disease). Twenty per cent of households with a member who had a chronic disease were food insecure. Thirteen per cent of respondents in food-insecure households screened positive for common mental health disorders (anxiety or depression) using the World Health Organization self-reporting questionnaire,[23] compared with 1% in food-secure households; however, this difference was not significant (p=0.34). While we did not find a significant association with health outcomes, chronic illness has been shown to be a predictor and a consequence of food insecurity, and in some cases the hungry are forced to choose between food and medi­ cine.[24] Sorsdahl et al.[5] showed in a national survey that after controlling for socioeconomic data, food insecurity was significantly related to having a 12-month and lifetime Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV)-confirmed diagnosis of an anxiety disorder. A possible

100 90 80 70 60 %

and eating cheaper fast foods will affect nutritional status negatively.[19,22] The 2012 FAO report showed that worldwide, more than 2.5 million children die each year from malnutrition as a consequence of food insecurity.[1] Sub-Saharan Africa has the highest rates of child underweight and infant and child mortality in the world.[1] Underweight and stunting are common among undernourished children, although at a global level the percentage of stunting and underweight in children has de­creased.[1] In SA, this decrease may be attri­ buted to interventions such as the Child Support Grant or school food programmes.[1,3] However, such national or provincial programmes may not be enough to mitigate the effects of high levels of food insecurity (70% in 2012) in very poor urban households.[18] The study by OldewageTheron et al.[19] in an SA informal settlement showed that 31% of boys and 30% of girls were stunted. The review by Labadarios et al.[3] on the national surveys in SA indicated that the diet consumed by poor SA children was inadequate and did not meet nutritional requirements. These national surveys also confirmed the limited variety of foods consumed.[3] Therefore, although hunger and food insecurity may not be widespread in SA in general, there are communities that are particularly vulnerable.[19]

Household food insecurity

50 Child food insecurity in households with children

40 30 20 10 0 2006 2007 2008 2009 2010 2011 2012 Year

Fig. 1. Trends in household and child food insecurity from 2006 to 2012.

reason for the low levels of chronic ill health or common mental disorders may be the sociodemographic profile of the Hospital Hill community.

Conclusion

This study highlights the plight of South Africans living in urban informal settlements where poverty levels dictate the degree of food insecurity. As an immediate solution, social grants may help to alleviate deprivation by increasing household income, but medium- and long-term strategies such as increased employment opportunities, education and the empowerment of women are required.

1. FAO, WFP and IFAD. The State of Food Insecurity in the World 2012. Economic Growth Is Necessary But Not Sufficient To Accelerate Reduction of Hunger and Malnutrition. Rome: Food and Agricultural Organization of the United Nations, 2012. http://www. fao.org/docrep/016/i3027e/i3027e.pdf (accessed 10 March 2014).

2. De Weerdt J, Beegl K, Friedman J, Gibson J. The Challenge of Measuring Hunger. Policy Research Working Paper No. WPS 6736. Washington, DC: World Bank Group, 2014. http:// documents.worldbank.org/curated/en/2014/01/18741920/ challenge-measuring-hunger (accessed 15 February 2014).

3. Labadarios D, Mchiza ZJ-R, Steyn NP, et al. Food security in South Africa: A review of national surveys. Bull World Health Organ 2011;89:891-899. [http://dx.doi.org/10.2471/ BLT.11.089243] 4. Rudolph M, Kroll F, Ruysenaar S, Dlamini T. The State of Food Insecurity in Johannesburg. Urban Food Security Series No. 12.

Kingston and Cape Town: Queen’s University and AFSUN, 2012.

5. Sorsdahl K, Slopen N, Siefert K, Seedat S, Stein DJ, Williams DR. Household food insufficiency and mental health in South Africa.

J Epidemiol Community Health 2011;65(5):426-431. [http:// dx.doi.org/10.1136/jech.2009.091462] 6. Stuff JE, Casey PH, Szeto KL, et al. Household food insecurity is associated with adult health status. J Nutr 2004;134(9):2330-2335.

7. Heflin C, Ziliak J. Food insufficiency, food stamp participation and mental health. Soc Sci Q 2008;89(3):706-727. [http://dx.doi. org/10.1111/j.1540-6237.2008.00556.x] 8. Adams EJ, Grummer-Strawn L, Chavez G. Food insecurity is associated with increased risk of obesity in California women.

J Nutr 2003;133(4):1070-1074.

9. Ford ES. Food security and cardiovascular disease risk among adults in the United States: Findings from the National Health

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and Nutrition Examination Survey, 2003-2008. Prev Chronic Dis 2013;10:130244. [http://dx.doi.org/10.5888/pcd10.130244] 10. Casey PH, Szeto KL, Robbins JM, et al. Child health-related quality of life and household food security. Arch Pediatr Adolesc Med 2005;159(1):51-56.

11. Matheson DM, Varady J, Varady A, Killen JD. Household food security and nutritional status of Hispanic children in the fifth grade. Am J Clin Nutr 2002;76(1):210-217.

12. Alaimo K, Olson CM, Frongillo EA jr. Food insufficiency and American school-aged children’s cognitive, academic, and psychosocial development. Pediatrics 2001;108(1):44-53. Erratum in: Pediatrics 2001;108(3):824. [http://dx.doi.org/10.1542/peds.108.3.824b] 13. Jyoti DF, Frongillo EA, Jones SJ. Food insecurity affects school children’s academic performance, weight gain, and social skills. J Nutr 2005;135(12):2831-2839.

14. Ben-Davies ME, Kinlaw A, Estrada del Campo Y, Bentley ME, Siega-Riz AM. Risk factors associated with the presence and severity of food insecurity in rural Honduras. Public Health Nutr 2014;17(1):5-13. [http://dx.doi.org/10.1017/S1368980013002048] 15. Rose D. Economic determinants and dietary consequences of food insecurity in the United States. J Nutr 1999;129(2 Suppl):517S-520S. 16. Radimer KL, Olson CM, Campbell CC. Development of indicators to assess hunger. J Nutr 1990;120(11 Suppl):1544-1548 17. Studdert LJ, Frongillo EA jr, Valois P. Household food insecurity was prevalent in Java during Indonesia’s economic crisis. J Nutr 2001;131(10):2685-2691.

18. Altman M, Hart TGB, Jacobs PT. Household food security status in South Africa. Agrekon 2009;48(4):345-361. [http://dx.doi.org /10.1080/03031853.2009.9523831] 19. Oldewage-Theron WH, Dicks EG, Napier CE. Poverty, household food insecurity and nutrition: Coping strategies in an informal settlement in the Vaal Triangle, South Africa. Public Health 2006;120(9):795-804. [http://dx.doi.org/10.1016/j. puhe.2006.02.009] 20. Bhattacharya J, Currie J, Haider S. Poverty, food insecurity, and nutritional outcomes in children and adults. J Health Econ 2004;23(4):839-862. [http://dx.doi.org/10.1016/j.jhealeco.2003.12.008] 21. Bonti-Ankomah S. Addressing Food Insecurity in South Africa. Pretoria: National Institute for Economic Policy, 2001. http://www.sarpn.org.za/EventPpers/ Land/20010605Bonti.pdf (accessed 10 April 2014).

22. Battersby J, McLachlan. Urban food insecurity: A neglected public health challenge. S Afr Med J 2013;103(10):716-717. [http://dx.doi.org/10.7196/SAMJ.7463] 23. Beusenberg M, Orley JH. A User’s Guide to the Self Reporting Questionnaire (SRQ). World Health Organisation 1994.

Geneva: World Health Organization. http://www.who.int/ iris/handle/10665/61113#sthash.XudX8GOM.dpuf (accessed 10 March 2014).

24. Biros MH, Hoffman PL, Resch K. The prevalence and perceived health consequences of hunger in emergency department patient populations. Acad Emerg Med 2005;12(4):310-317. [http://dx.doi.org/10.1197/j.aem.2004.12.006]

Accepted 13 February 2015.

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MANAGEMENT OF OBSTETRIC HAEMORRHAGE

Oxytocin – ensuring appropriate use and balancing efficacy with safety Z Farina, S Fawcus Zane Farina, MB ChB, DA (SA), FCA (SA), is National Anaesthetic Assessor for the National Committee for Confidential Enquiries into Maternal Deaths in South Africa (NCCEMD), Chief Specialist in the Pietermaritzburg Metropolitan Department of Anaesthesia, and an honorary lecturer in anaesthesia at the College of Health Sciences, School of Clinical Medicine, University of KwaZulu-Natal, Durban, South Africa.

Sue Fawcus, MA, MB ChB, FRCOG, is an obstetric assessor for the NCCEMD and a professor in the Department of Obstetrics and Gynaecology, Faculty of Health Sciences, University of Cape Town, South Africa, and heads the Obstetric Unit at Mowbray Maternity Hospital, Cape Town.

Corresponding author: Z Farina (zane.farina@kznhealth.gov.za)

Maternal deaths due to haemorrhage continue to increase in South Africa (SA). It appears that oxytocin and other uterotonics are not being used optimally, even though they are an essential part of managing maternal haemorrhage. Oxytocin should be administered to every mother delivering in SA. Awareness is required of the side-effects that can occur and the appropriate measures to avoid harm from these.

Second-line uterotonics should also be available and utilised in conjunction with mechanical and surgical means to arrest haemorrhage in women who continue to bleed after the appropriate administration of oxytocin.

S Afr Med J 2015;105(4):271-274. DOI:10.7196/SAMJ.9179

The National Committee for Confidential Enquiries into Maternal Deaths in South Africa (NCCEMD) has issued an alert regarding the continuing high levels of maternal deaths due to obstetric haemorrhage, the majority of which are judged to be preventable.

This is especially noted for haemorrhage during and after caesarean section (CS).

The preliminary data of the 2011 - 2013 Saving Mothers triennial report reveal that obstetric haemorrhage accounted for 684 maternal deaths, making it the second most common cause of maternal death.[1] There were 221 deaths (32.3%) ascribed to haemorrhage associated with CS. This bleeding was detected intraoperatively or postoperatively, or was intra-abdominal. Frequently bleeding was due to uterine atony secondary to prolonged labour, other causes being traumatic extensions of the uterine incision or placental site bleeding. Maternal death assessors found over 85% of these deaths to be clearly avoidable.

• Insufficient prophylactic dose of oxytocin at CS (e.g. several cases when only a 10 IU oxytocin infusion was given, and several where no uterotonic agent was given at all) • Excessive intravenous (IV) boluses of oxytocin (e.g. 10 IU IV bolus) • Inadequate dosages of therapeutic oxytocin for treatment of established intraoperative bleeding due to an atonic uterus (e.g. a repeat 2 - 3 IU IV bolus not given, or infusion containing a toolow concentration of oxytocin administered; 10 IU instead of the recommended 20 - 40 IU infusion) • Infrequent use of ergometrine or oxytocin/ergometrine (Synto­ metrine) as treatment for uterine atony at CS, even in women with no contraindication to ergot alkaloids. These agents are of similar efficacy to oxytocin and therefore would be expected by inference to have superior efficacy to misoprostol.[2] Ergometrine has a longer duration of action than oxytocin.[3]

Issues contributing to these deaths

A key step in avoiding postpartum haemorrhage (PPH) is ensuring adequate uterine contraction, as this serves to control bleeding from the placental bed naturally.

The mainstay of uterotonic drugs in obstetric practice has been oxytocin. However, recently this drug has become a cause for concern among anaesthesiologists. The 1997 - 1999 triennial report of the Confidential Enquiries into Maternal Deaths in the UK cited the administration of 10 IU oxytocin as an IV bolus as the precipitating cause of death in two hypovolaemic patients and as contributing to the deaths of a number of other patients.[4] This problem was noted as contributory in two deaths in the 2005 - 2007 NCCEMD report[5] in South Africa (SA) and in another three cases in the 2008 2010 report.[6] A preliminary review of the 2011 - 2013 NCCEMD anaesthesia data reveals that the problem is still occurring.

The following major causes have been identified among the cohort of the 2011 - 2013 deaths ascribed to haemorrhage: • Inadequate utilisation of uterotonic agents • Poor recognition of the severity of the blood loss causing hypovolaemia • Inadequate surgical skill • Delays in relaparotomy and/or referral in case of post-CS bleeding.

Specific problems with uterotonics

• Poor documentation of whether prophylactic oxytocin was given, by what route and in what dosage (there is no designated space on the recommended anaesthetic form, the recommended surgery form or the anaesthetic assessment tool used by the NCCEMD to record oxytocin use) • Poor documentation of additional uterotonic agents given to treat uterine atony, both by the anaesthetist during the surgery and by the obstetrician or nurses postoperatively

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Oxytocin

Over-reaction to adverse reports

Anecdotally, there appears to have been a marked over-reaction to this information, with a number of medical practitioners avoiding

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the use of oxytocin entirely. There has been much discussion of the NCCEMD findings concerning bleeding at CS in obstetric and anaesthetic forums. There is evidence of differences of opinion about the use of oxytocin at CS in situations of hypovolaemia and hypotension, especially when this situation has arisen as a result of bleeding from uterine atony at CS. Obstetricians appear to request higher doses of oxytocin to contract the uterus, but anaesthetists express reluctance to administer oxytocin because of concern about worsening the hypotension. The conflict seems more pronounced among junior obstetric doctors and anaesthetists.

An over-reaction to the information of potential harm is inappropriate. Oxytocin is still highly beneficial, and administration of this drug needs to continue, both intraoperatively and postoperatively. Obviously protocol adaptations need to be made to ensure that the reported adverse events do not impact on the patient.

In the situation of hypovolaemic shock, a rapid high-dose IV bolus of oxytocin is contraindicated, but an infusion is essential to contract the uterus. This should be provided in addition to active fluid, colloid and red blood cell concentrate resuscitation, and the concomitant use of vasopressors. The obstetric surgeon needs to have the expertise to perform surgical measures to reduce bleeding, such as uterine compression sutures, if all medical therapy is unsuccessful.

Vasodilation caused by oxytocin

The main adverse effect of oxytocin is hypotension secondary to vasodilation. This appears to be mediated by calcium-dependent stimulation of nitric oxide release.[3] In animal studies coronary vasoconstriction has been demonstrated.[7] Of concern is the repeated finding of significant reproducible ST depression on the electrocardiogram in pregnant women receiving IV oxytocin boluses.[8] The adverse effects appear to be more marked at higher bolus doses and with more rapid administration. The cardiovascular effects of oxytocin have been well documented and produce a clinical picture of peripheral vasodilation, hypotension and increased pulmonary artery pressures. Cardiac output is increased by an increase in both heart rate and stroke volume.[3] The increase in heart rate and stroke volume protects the majority of women from adverse outcomes, but clearly points to a group who will be especially vulnerable to cardiovascular collapse: those women who cannot achieve an increase in cardiac output. This problem is especially marked in patients who are already hypovolaemic.

It has been determined that the ED90 effect for uterine myocyte stimulation (the dose that can be expected to confer 90% maximal contraction) is 0.35 IU in oxytocin-naïve patients at CS[9] and 3.0 IU in patients who have previously been augmented with oxytocin during labour.[10] Another important finding is that the magnitude of the hypotensive effect of oxytocin appears to be reduced with the administration of repeated doses.[3] In common with all short-acting drugs (oxytocin has a plasma halflife of 3 - 20 minutes[11]), administration of larger IV boluses of oxytocin to try to prolong effects leads to excessive peaks in concentration, but little increase in the duration of action. The solution to this effect is repeated smaller boluses, and/or a constant infusion of the drug.

Suggested dosing of oxytocin

These observations suggest that the use of the lowest effective dose of oxytocin that produces adequate uterine contraction will improve the risk/benefit profile. In the event of inadequate uterine contraction after delivery of the baby, the obstetric surgeon should undertake the usual physical manoeuvres such as removal of any remaining products of conception and manual rubbing up the uterus while the anaesthetist administers a repeat bolus of oxytocin (2.5 IU over

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30 seconds). The infusion rate of the oxytocin should be increased simultaneously. It is important to ensure that the postoperative infusion of oxytocin should not be interrupted in any manner.

It has also been noted that the vasodilatory effect of an oxytocin bolus can be countered by administration of a concurrent dose of phenylephrine.[12] When administering oxytocin to a hypotensive hypovolaemic woman, in addition to the normal resuscitative measures of rapid fluid administration it would be appropriate to administer phenylephrine 50 - 100 µg as an intravenous infusion (IVI).

Prophylactic use of oxytocin at CS

Recommendations for the routine prophylactic administration of oxytocin at CS have previously been issued in SA.[13] These can be summarised as prophylactic administration of 2.5 IU oxytocin as an IVI over 1 minute, followed by 20 IU in 1 L clear fluid over 8 hours. In the situation where haemorrhage is occurring, judicious administration of increased doses of oxytocin is required. The oxytocin infusion regimen may be increased up to the equivalent of 10 IU/h (80 IU in 1 000 mL fluid at 125 mL/h). Where there is access to a syringe driver, this can be achieved by placing 100 IU oxytocin in 50 mL saline and running it at 5 mL/h.

Controlled postoperative infusion of oxytocin for at least 8 hours is the gold standard for the pharmacological prevention of PPH after CS. This is especially important if the obstetrician is inexperienced.[14] However, it may be difficult to achieve in some hospital environments, where care in the wards is erratic and there is limited access to labour-saving devices such as rate controllers.

Mechanical rate controllers (Dial-A-Flo) have been utilised, but are dependent on a functioning IVI line and a specific height of the attached IVI fluid, while flow rates are not constant when other fluids are ‘piggy backed’ onto the IVI line.

Medical practitioners should motivate for mechanical ratecontrolling devices (infusion pumps and syringe drivers) where possible. When it is not possible to achieve reliable oxytocin infusion for at least 8 hours after CS, the intramuscular administration of oxytocin 10 IU 4-hourly or oxytocin/ergometrine 5 IU/0.5 µg 8-hourly may provide a satisfactory alternative.

Ergometrine

Ergometrine is a uterotonic drug that has received bad publicity, firstly because ergometrine is contraindicated when vasoconstriction is a major concern (hypertension and cardiac disease), and secondly because it has pronounced side-effects such as nausea and emesis.

However, ergometrine has an alternative mechanism of action to either oxytocin or misoprostol, and represents a useful second-line agent. The vasoconstrictive action of ergometrine counterbalances the vasodilation of oxytocin. Small IV doses of 0.2 mg, building up to a maximum total of 0.6 mg, are beneficial. Ergometrine has a long duration of action (half-life 120 minutes).[3]

Misoprostol

Misoprostol (Cytotec) has become a popular means of causing uterine contraction. It is easy to administer orally, rectally or sublingually, and appears benign. However, concerning data have been published about adverse effects and worsening outcomes at higher doses.[2] While side-effects of pyrexia and tachycardia are well documented, misoprostol may be a useful adjunct when used in appropriate doses. Since many patients will have received prior doses of misoprostol, it is important to check carefully on the total dose already administered; sufficient drug should be given to bring the total dose up to 600 mg. Anaesthetists find that misoprostol is often most conveniently administered sublingually. The fact that it

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does not require refrigeration is an advantage in the resource-poor environment.

Prostaglandin F2-alpha

Prostaglandin F2-alpha is often used as a ‘last line’ of pharma­ cological action. It is very potent, and severe hypertension and bronchospasm have been recorded after IV use.[15] Off-label intramyometrial injection has been described,[16] but its use should be confined to institutions with specialist skills and experience.

Guidance for use of uterotonics

The NCCEMD has produced guidelines on the prevention and treatment of blood loss at CS adapted from World Health Organi­ zation guidelines, Royal College of Obstetricians and Gynaecologists guidelines and recommendations from obstetric anaesthetic experts.[3,17,18] These are found in the monograph of management of PPH in SA, which contains algorithms outlining use of uterotonic agents.[19] Of note, most international guidelines on prevention and treatment of PPH focus on vaginal delivery and do not separately specify routes and dosages for CS. There is a need to strengthen guidance for use of uterotonics at CS, globally and in SA. The SA guidelines have been described in a number of publi­ cations,[19,20] and wall posters for use in operating theatres have been developed.

The NCCEMD advocates that the problem of mat­er­nal death be approached under the ‘5Cs’: 1. C are – a Commitment to quality 2. C overage – ensuring that all woman receive the care they deserve

3. C aesarean section safety 4. C ontraception 5. C ommunity involvement.

The suggestions in this article encompass three of these important principles.

Commitment to quality

Implement and enforce recognised protocols. Hitherto, the uptake of these guidelines and algorithms has not been widespread.

Implement methods of monitoring uteronic administration. The recommended monitoring tools have been added to the maternity case record charts and the assessment tools used by the confidential enquiry processes. Documentation needs to be improved in SA hospitals.

Coverage

Effective rollout of guidelines at district level must occur, and familiarity with them among the anaesthetic fraternity must increase.

Managers of health facilities conducting CS need to ensure availability of the appropriate drugs, and facilities for administration of these drugs.

Caesarean section safety

It is very important that anaesthetists, obstetricians and midwives achieve consensus on the use of oxytocin and other uterotonics at CS, so that uterine atony at CS can be prevented and treated adequately.

Renewed emphasis on these issues needs to be encouraged via medical schools, the district clinical specialist teams, the Essential

Table 1. A stepwise approach to the administration of uterotonics after CS Stage

Option 1 (suitable for units equipped with volumetric pumps, syringe drivers and trained anaesthetists)

Option 2 (suitable for resource-constrained units)

Step 1: All cases

1. O xytocin 2.5 IU IVI slow bolus (over 30 s) 2. O xytocin 7.5 IU in remaining IVI fluid running in 3. Oxytocin

infusion 20 IU/1 000 mL at 125 mL/h for 8 h (125 mL/h is equivalent to 42 drops/min from a ‘20 dropper’ administration set)

1. S yntometrine 1 amp IMI in left deltoid after delivery of baby (be aware of CIs) If CI: Oxytocin 10 IU IMI in left deltoid after delivery of baby (repeat at 4 hours in ward) 2. O xytocin 20 IU/1 000 mL IVI at 125 mL/h

Step 2: Ongoing uterine atony at 3 minutes

1. R epeat oxytocin 2.5 IU IVI slow bolus (over 30 s) 2. O xytocin infusion 20 IU/1 000 mL at 125 mL/h

Oxytocin 20 IU/1 000 mL IVI at125 mL/h

Step 3: Actively bleeding cases

1. E rgometrine 0.2 mg IVI slow bolus repeated up to 0.6 mg or Syntometrine 0.1 mg/L IU IVI slow bolus (over 30 s) repeated up to 0.5 mg/5 IU or Misoprostol 400 - 600 µg sublingual or rectal (if CI to ergometrine) 2. O xytocin infusion 40 IU/1 000 mL at 125 mL/h 3. T ranexamic acid 1 g IVI (may be considered)

1. S yntometrine 1 amp IMI or ergometrine 1.0 mg IMI in deltoid (if not already administered) or Misoprostol 400 - 600 µg sublingual or rectal (if CI to ergometrine) 2. Continue oxytocin infusion 3. T ranexamic acid 1 g IVI (may be considered if available)

Step 4: Resistant bleeding cases

Consider intramyometrial prostaglandin F2- alpha (dilute 5 mg in 10 mL and give 1 mL intramyometrially, can be repeated × 1)

NB: This table focuses on the use of uterotonic agents for medical management of uterine atony at and after CS. It does not describe the concurrent resuscitative measures required for women with excessive bleeding, nor does it cover surgical measures that must be performed following failed medical management of uterine atony associated with CS. IVI = intravenous infusion; IMI = intramuscular injection; CI = contraindication.

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Steps in the Management of Obstetric Emergencies programme and the national anaesthesiology and obstetric societies.

Table 1 presents a guideline for a stepwise approach to use of uterotonics at CS that has been mutually agreed on between obstet­ ricians and anaesthetists of the NCCEMD and is evidence based.

Conclusion

We strongly recommend roll-out and implementation of these guidelines at all SA facilities conducting CS. The continued increase in deaths from maternal haemorrhage, particularly after CS, is unacceptable. It is the responsibility of the doctors giving the anaesthetic, the doctors performing the surgery and the nurses performing postoperative monitoring to reduce these deaths.

Acknowledgement. The authors thank Prof. J Moodley, Prof. J Hofmeyer and Dr D G Bishop for constructive advice and comments on this article.

1. Pattinson RC, ed. Saving Mothers 2011-2013: The Sixth Report of the National Committee for Confidential Enquiries into Maternal Deaths in South Africa. Pretoria: Government Printer, 2014.

2. Tunçalp Ö, Hofmeyr GJ, Gülmezoglu AM. Prostaglandins for preventing postpartum haemorrhage.

Cochrane Database Syst Rev 2011, Issue 3. Art. No.: CD000494. [http://dx.doi.org/10.1002/14651858.

CD000494.pub4] 3. Dyer RA, van Dyk D, Dresner A. The use of uterotonic drugs during caesarean section. Int J Obst Anesth 2010;19(3):313-319. [http://dx.doi.org/10.1016/j.ijoa.2010.04.011] 4. Royal College of Obstetricians and Gynaecologists. Why Mothers Die. Report on Confidential Enquiries into Maternal Deaths, 1997-9. London: RCOG, 2001.

5. Pattinson RC, ed. Saving Mothers: Fourth Report on Confidential Enquiries into Maternal Deaths in South Africa 2005 - 2007. Pretoria: National Department of Health, 2010.

6. Pattinson RC, ed. Saving Mothers: Fifth Report on Confidential Enquiries into Maternal Deaths in South Africa 2008 - 2010. Pretoria: National Department of Health, 2012.

7. Fortner CL. Effects of synthetic oxytocin with and without preservatives upon coronary blood flow in the dog. J Pharmacol Exp Ther 1969;165(2):258-266.

8. Jonsson M, Hanson U, Lidell C, Norde´n-Lindeberg S. ST depression at caesarean section and the relation to oxytocin dose: A randomised controlled trial. BJOG 2010;117(1):76-83. [http://dx.doi. org/10.1111/j.1471-0528.2009.02356.x] 9. Carvalho JC, Balki M, Kingdom J, Windrim R. Oxytocin requirements at elective caesarean delivery: A dose-finding study. Obstet Gynecol 2004;104(5):1005-1010. [http://dx.doi.org/10.1097/01.

AOG.0000142709.04450.bd] 10. Balki M, Ronayne M, Davies S, et al. Minimum oxytocin dose requirement after cesarean delivery for labor arrest. Obstet Gynecol 2006;107(1):45-50. [http://dx.doi.org/10.1097/01.

AOG.0000191529.52596.c0] 11. Syntocinon® [package insert]. Novartis Pharmaceuticals Australia Pty. Ltd., 12 March 2009.

12. Dyer RA, Reed AR, van Dyk D, et al. Hemodynamic effects of ephedrine, phenylephrine, and the coadministration of phenylephrine with oxytocin during spinal anesthesia for elective cesarean delivery. Anesthesiology 2009;111(4):753-765. [http://dx.doi.org/10.1097/ ALN. 0b013e3181b437e0] 13. Farina Z, Rout C. Anaesthesia for caesarean section In: Moodley J, ed. A Monograph on Caesarean Section. Pretoria: National Department of Health, 2013:9-29. http://www.hst.org.za/publications/ saving-mothers-caesarean-section-monograph-2013 (accessed 6 February 2015).

14. Sheehan SR, Montgomery AA, Carey M, et al. Oxytocin bolus versus oxytocin bolus and infusion for control of blood loss at elective caesarean section: Double blind, placebo controlled, randomised trial.

BMJ 2011;343:d4661. [http://dx.doi.org/10.1136/bmj.d4661] 15. Harber C, Levy D, Chidambaram S, Macpherson M. Case report: Life-threatening bronchospasm after intramuscular carboprost for postpartum haemorrhage. BJOG 2007;114(3):366-368. [http://dx.doi. org/10.1111/j.1471-0528.2006.01227.x] 16. Chou MM, MacKenzie IZ. A prospective, double-blind, randomized comparison of prophylactic intramyometrial 15-methyl prostaglandin F sub 2alpha, 125 micrograms, and intravenous oxytocin, 20 units, for the control of blood loss at elective cesarean section. Am J Obstet Gynecol 1994;171(5):13561360. [http://dx.doi.org/10.1016/0002-9378(94)90160-0] 17. World Health Organization. WHO Guidelines for the Management of Postpartum Haemorrhage and Retained Placenta. Geneva: WHO, 2012.

18. Royal College of Obstetricians and Gynaecologists. Postpartum Haemorrhage, Prevention and Management (Green-top Guideline No. 52). London: RCOG, May 2009. https://www.rcog.org.uk/en/ guidelines-research-services/guidelines/gtg52/ (accessed 26 February 2015).

19. South African National Committee for Confidential Enquiries into Maternal Deaths. A Monograph of the Management of Postpartum Haemorrhage. Pretoria: National Department of Health, 2010.

20. Fawcus S, Moodley J. Postpartum haemorrhage associated with caesarean section and caesarean hysterectomy. Best Pract Res Clin Obstet Gynaecol 2013; 27(2):233-249. [http://dx.doi.org/10.1016/j. bpobgyn.2012.08.018]

Accepted 24 November 2014.

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MEDICAL EDUCATION

MMed cohort supervision: A path out of the swamp?

C Rout, T Sommerville, C Aldous Chris Rout, MB BS, FFARCS, FCA (SA), erstwhile Research Professor and currently a sessional specialist in the Department of Anaesthetics, Nelson Mandela School of Medicine, College of Health Sciences, University of KwaZulu-Natal (UKZN), Durban, South Africa, is in private anaesthetic practice in Durban. He maintains a research interest in obstetric anaesthesia and is developing interests in clinical skills transfer, clinical support needs of medical officers in rural district hospitals, and the influence of Plato on 15th century Florentine art. Ted Sommerville, MB ChB, BSc (Med), DA, FFA, PhD (Higher Education), previously Director and Head of Department, School of Undergraduate Medical Education, UKZN, is currently semi-retired, facilitating research, tending bonsai and teaching at the local primary school. Colleen Aldous is a senior lecturer in the School of Clinical Medicine at UKZN. She is a medical scientist with a PhD in science education and is involved in postgraduate research mentorship across several medical disciplines including surgery, orthopaedics, dermatology, paediatrics, opthalmology, general medicine and psychology. Her own research interest is human genetics, and she is a member of the national steering committee and working group reviewing National Department of Health policy guidelines for human genetics services.

Corresponding author: C Rout (rout@ukzn.ac.za)

The authors present the case for collaborative cohort supervision (CCM), including both master’s students and novice supervisors, as a possible way to rapidly increase the number of supervisors needed to address the recent implementation of a compulsory research component to specialist registration with the Health Professions Council of South Africa. Different models of CCM are discussed and possible pitfalls highlighted.

S Afr Med J 2015;105(4):275-276. DOI:10.7196/SAMJ.9338

The problems currently facing many clinical departments in providing appropriate supervision for the research component of the MMed degree have been highlighted in the SAMJ.[1,2] The most pressing issues are the inadequate numbers of potential supervisors available and time allocation for research activities. Clearly the traditional apprentice-master model (AMM) of one supervisor to one student will not meet the throughput demands of the Health Professions Council of South Africa, the Colleges of Medicine of South Africa and clinical departments, and the one-supervisor-multiplestudents model has two problems. Firstly the supervisor is not likely to have enough time to take on several students and ensure thorough supervision for all, and secondly many potential clinical supervisors may not yet have developed the skills and experience to supervise students in the research process as well as the clinical discipline.

Joint supervision

One possible path to be explored is that of joint supervision. There are four options by which joint supervision can be achieved: 1. T wo supervisors to one student 2. T wo supervisors to a cohort of students within a single discipline 3. Two or more disciplinary and research process supervisors to a cohort of students from different disciplines 4. One or more supervisors to a cohort of students and a cohort of novice supervisors.

Clearly option 1 is numerically inappropriate for a department that is battling to find supervisors, and differs little from the traditional AMM. However, this model may be suitable in a department where a specialist with the requisite qualifications but lacking supervision experience is paired with an experienced supervisor. This is the purpose of the Council for Higher Education recommendation: ‘In the case of inexperienced or new supervisors, there is ongoing staff development and support, and joint supervision is explored as an option.’[3]

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However, some centres are using this form of joint supervision to compensate for the absence of a supervisor with ‘… a qualification in a relevant field of study higher than, or at least at the same level as, the exit level of the postgraduate programme he/she is supervising’.[3].

While it could be argued that the latter is the least important of the regulations, this practice is effectively ignoring their purpose, but is applied by academic administrators as a way of complying with the regulations without any thought.

Options 2, 3 and 4, all collaborative cohort models (CCMs), provide effective gearing for student research within a limited population of supervisors, but only option 4 addresses the immediate need for more supervisors. Disciplinary supervisors, who may be relatively research-naive, focus on discipline-specific aspects of the research; the research process supervisors, who may be unfamiliar with the disciplinary contexts, enhance the scientific process within the accepted canon and enrich it by introducing possible alternative approaches. In this article we explore the advantages and possible pitfalls of cohort supervision.

Cohort supervision

CCMs have been evolving in postgraduate supervision for over 50 years as part of the debate surrounding solutions for poor completion rates for postgraduate degrees.[4] Option 2 may be feasible for larger departments, and may be preferable to two (or more) staff members separately being allocated groups of students. Option 3 may make more efficient use of resources from several departments, but risks becoming too elaborate and labour-intensive. Furthermore, if a faculty is simultaneously to develop the supervisory skills of its staff, the obvious solution of pairing experienced and inexperienced supervisors would throw a double mentoring load on the experienced supervisor in options 1 - 3.

Option 4 has the advantage of combining the benefits accruing to students participating in multimember groups[5] with modelling the supervisor’s role for the benefit of disciplinary specialists

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Define research question Literature review Monitor literature and add to review Protocol-in-a-day workshop Refine protocol with supervisor Submit protocol for postgraduate and ethics approval Await study approval Data collection Finalisation of data collection and cleaning of data Data analysis Paper-in-a-day workshop Refine article with supervisors Submit article for publication Article resubmission

Year 1 Year 2 Year 3 Year 4 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16

Fig. 1. Gant chart for MMed research project process through 16 year-quarters.

unaccustomed to that role. Postgraduate students need to be inducted into the functional elements of proposal writing, data gathering and reporting, enculturated into a community of scholarly practice, encouraged to think critically about what they are doing and why, emancipated to the point that the student rather than the supervisor owns the research, and given sufficient pastoral care to see them through the inevitable tough times.[6] Similarly, novice supervisors need to see these elements of the research process enacted by those more experienced than themselves.

For the purposes of the MMed, we believe that the CCM model must include both students and supervisors. This avoids the possibility of the CCM group contradicting a student’s own supervisor. If the group is large enough, more homogeneous subgroups (based upon either discipline or research design) may separate within the process to discuss matters of specific relevance, thereby also affording more individualised guidance of students. Effectively, students belong to two cohorts: disciplinary and research method.

There is a danger that the process may adopt a linear seminar-based approach, which is not the intention. One way to avoid this is to use a goal-directed model where the objectives of each group meeting are planned in advance, based upon milestones within the research process; Gant charts can be particularly useful in this regard.

An example of a chart applied at the Grey’s Hospital Department of Surgery is shown in Fig. 1.

A more open ‘rolling entry’ model, such as that used by Burnett,[4] is better suited to MMedSci and PhD students, who are more familiar with the research process than MMed students and do not have the same time constraints. Above all, the students must take ownership of the meetings, presenting their projects, defending their work and contributing to the work of others as part of a peer review process. Novice supervisors, if option 4 is applied, acquire skills in mentorship, group supervision, supervisory advice and positive critique.[7] Meetings must not devolve into a session of talking heads and passive audience.

The main drawbacks of any cohort model in the context of clinical medicine are logistical. Firstly, whatever the timetable for the sessions, both trainees and disciplinary specialists would be removed simultaneously from clinical service. The chances are that both students and novice supervisors will be from the same discipline, exacerbating the problem, particularly in small clinical departments.

Secondly, different disciplines may focus on the research component of professional training at different times during the 4-year programme, and examination timetables have to be considered. Thirdly, particularly in disciplines with scant undergraduate exposure, trainees may be unfamiliar with possible areas within the specialty in which they might find a research interest. While the latter applies to all supervision models, it presents a particular problem with CCM in terms of when to commence the programme.

How these issues are surmounted will vary between institutions, and no general

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recommendation is possible other than that research time has to be provided for trainees and their supervisors, as has been highlighted previously,[1] whatever the super­ vision model.

Compulsory research programmes as part of professional registration differ from those discussed in the literature in three ways: the research is generally viewed by postgraduate students/trainees not as inher­ently desirable but as a necessary evil on the path to specialisation; the clinical service load must continue to be borne by the postgraduate students/trainees; and at present in South Africa many institutions have to grow their own supervisor wood while cultivating the MMed crop. We argue that setting a systematic supervision process in place would mitigate the first two challenges.

Finding time for scholarship in the face of a growing clinical load is a matter that must also be addressed.

The introduction of a system that is costly both in time and personnel must be appropriately monitored to ensure that it meets the needs of specialist disciplines, students and supervisors and is timed to the convenience of all groups, not that of university calendars.

Any feedback from questionnaire data must be actively processed and used to modify the programme in successive years to ensure mutual benefit.[8] This is particularly important with an externally motivated process such as compulsory research.

The lack of literature specific to super­ vision of compulsory research means that we are heading into uncharted territory.

Any method of potential value must be approached with an open mind and em­bedded quality assurance programmes.

1. Aldous C, Adhikari M, Rout C. The research component of specialist registration – a question of alligators and swamps?

A personal view. S Afr Med J 2015;105(1):21-22. [http://dx.doi. org/10.7196/SAMJ.8732] 2. Seggie J. On getting published in the SAMJ. S Afr Med J 2015;105(2):77-78. [http://dx.doi.org/10.7196/SAMJ.9348] 3. Council for Higher Education criteria for programme accreditation, November 2004. 3.1.8 Postgraduate policies, procedures and regulations: Criterion 9. (ii). http:/nr-online.che. ac.za/html_documents/CHE_accreditation_criteria_Nov2004. pdf (accessed 28 July 2014).

4. Burnett P. The supervision of doctoral dissertations using a collaborative cohort model. Counselor Education and Supervision 1999;39(1):46-52. [http://dx.doi.org/10.1002/j.1556-6978.1999. tb01789.x] 5. Samuel M, Vithal R. Emergent frameworks of research teaching and learning in a cohort-based doctoral programme. Perspectives in Education 2011;29(3):76-87.

6. Lee A. How are doctoral students supervised? Concepts of doctoral research supervision. Studies in Higher Education 2008;33(3):267-281. [http://dx.doi.org/10.1080/030750708020 49202] 7. De Lange N, Pillay G, Chikoko V. Doctoral learning: A case for a cohort model of supervision and support. South African Journal of Education 2011;31(1):15-30.

8. Stalmeijer R, Whttingham J, de Grave W, Dolmans D. Strengthening internal quality assurance processes: Facilitating student evaluation committees to contribute. Assessment and Evaluation in Higher Education 2014. [http://dx.doi.org/10.108 0/02602938.2014.976760]

Accepted 12 January 2015.

FORUM

OPINION

Resuscitating an ethical climate in the health system: The role of healthcare workers P Pillay Dr Prinitha Pillay, BSc (Hons), MB BCh, MSc Infectious Diseases, works for the Rural Health Advocacy Project and has extensive experience working in difficult and remote settings in rural South Africa, and with the humanitarian organisation Médecins Sans Frontières/Doctors Without Borders in Lesotho, Darfur, South Sudan, Sierra Leone, Libya and India.

Corresponding author: P Pillay (prinitha@rhap.org.za)

South Africa boasts a proud tradition of healthcare professionals speaking out against injustice in line with the medical doctrine of beneficence (to do good) and maleficence (do no harm). There are many who play a part in making the health system better, including the state, managers, patients and healthcare workers (HCWs). This article looks at the role of HCWs beyond providing medical care to individual patients. HCWs often face a lack of resources enabling them to adequately provide care and treatment and respond to lifethreatening emergencies. As a result, they are forced to make difficult decisions when it comes to allocating those scarce resources. These decisions are not purely fiscal in nature, but also ethical. Deciding who to bump off a theatre list because there is no linen is a choice most HCWs did not imagine they would ever have to make. In order to circumvent a sense of hopelessness, HCWs need to empower and motivate themselves (and others) with knowledge of how to make things better.

S Afr Med J 2015;105(4):277-278. DOI:10.7196/SAMJ.9397

Witnessing the state of healthcare

Despite steps to improve access to healthcare for all since 1994, South Africa’s healthcare system remains highly inequitable. According to the latest South African Health Review,[1] the 17% of the population who access private healthcare is served by about 70% of the country’s medical practitioners, 60% of its specialists and half of its professional nurses.

The private sector commands 52% of the total health budget. The remainder is devoted to serving the majority who use the public sector. The situation is worst in the rural areas. Rural populations carry a double burden – beyond the human resource shortages, they tend to have higher out-of-pocket expenditure accessing public services, such as transport costs when ambulances are not available.[2] As healthcare workers (HCWs), we are confronted with this reality of inequity daily. We are often left deeply frustrated by alltoo-common problems including shortages of medicine, equipment and staff. Many of us work in poorly maintained facilities backed by inadequate budgeting and planning and without access to timely emergency services. It is front-line workers who are often confronted first by the symptoms of an ailing health system struggling to survive.

Perhaps even more worryingly, it has becoming increasingly difficult to speak out about problems like these and violations of patient rights without fear of reprisal. Victimisation, vilification and even death threats in the workplace force HCWs to keep quiet.

However, there is a hidden cost of silence and inaction – it can perpetuate the culture of fear and breathes life into the very failure to provide clinical leadership.

There will always be conflicts in healthcare. Within ourselves, we have to uphold the ideals and value system of medicine, and demonstrate this consistently in how we work and live. Externally, conflicts may arise with those to whom we report. HCWs may experience split loyalties, pitting the profession’s ethics and duties to patients against those to the state or the employer. However, working

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within services that impact not only on patients but on their families and communities as well makes the welfare of citizens our primary responsibility.

HCWs are not merely passive employees but active, independent practitioners. When confronted with limited resources and other health system ailments, they have a right to feel frustrated. Indeed, the duty is upon the state to create the enabling conditions for them to deliver the constitutional right to health. Yet, when the state is failing or not making progress fast enough, this does not negate the duty of HCWs to work towards improving the public health system.

HCWs respond in different ways to a health system in crisis – some withdraw, others resign, while others continue their patient advocacy, sometimes behind the scenes and sometimes boldly and openly. So what to do if one wants to do good, but not lose hope or one’s job?

Making your voice heard

There is an array of constructive responses at the disposal of HCWs. They should use the available complaint mechanisms as laid out in the National Management of Complaints Protocol (NMCP) at facility, district and provincial levels that have been created for the very purpose of improving the health system.[3] Write and talk to your colleagues, managers, internal clinic or quality improvement committees, or hospital board to advocate for improvements. Start at your facility and escalate to district or provincial level if your concerns haven’t been addressed effectively. Familiarise yourself with, and make use of, the Office of Health Standards Compliance and independent bodies such as the South African Human Rights Commission and the Public Protector, as well as independent legal or advocacy organisations.

HCWs need to know that they are entitled to go beyond their manager if they need to, as documented in the NMCP. If workers experience hostility in the workplace, stemming from the reporting of problems in the public interest, they can be protected by the Protected Disclosures Act.[4] Keeping a paper trail, e.g. documenting

April 2015, Vol. 105, No. 4

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steps taken to resolve problems and responses received, is critical not only in holding those responsible to account but also for personal protection. However, there is power in numbers and HCWs should work together with others and with patients, to amplify their voices.

The challenge is not only to HCWs to empower themselves with this knowledge, but to students who witness healthcare failures, to those who teach and supervise them and to those developing medical curricula, so that all contribute to acting in their patients’ interest in an ethical and humanistic manner.[5] There is no getting away from it – it takes hard work to make things work. There is no one-size-fits-all approach to every problem, and the trick is knowing which is the best tool and strategy for a particular context and place. Everyone involved in the health system needs to work continuously and relentlessly in order to create the ethical climate we wish to work within.

Unless we act, and support those who do act, we risk allowing the unacceptable to become acceptable. It is more imperative now than ever before that HCWs remain engaged in monitoring the rights afforded to South Africans by the Constitution, because if we want a different healthcare system, we cannot afford indifference.

‘There’s really no such thing as the “voiceless”. There are only the deliberately silenced and the preferably unheard.’ (Arundhati Roy)

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This article is a publication of the VOICE Project, co-ordinated by the Rural Health Advocacy Project in partnership with the Rural Doctors Association of South Africa, Rural Rehab Association of South Africa, Professional Association of Clinical Associates in South Africa, Médecins Sans Frontières/Doctors Without Borders, Southern African HIV Clinicians Society and SECTION27. A healthcare provider’s guide to reporting healthcare challenges is available at http://rhap.org.za/voiceproject-manual/ 1. Padarath A, English R, eds. South African Health Review 2012/2013. Durban: Health Systems Trust, 2013. http://www.hst.org.za/publications/south-african-health-review-2012/13 (accessed 24 February 2015).

2. Harris B, Goudge J, Ataguba JE, et al. Inequities in access to health care in South Africa. J Public Health Policy 2011;32:S102-S123. [http://dx.doi.org/10.1057/jphp.2011.35] 3. National Department of Health Office of Standard Compliance Directorate: Quality Assurance.

National Complaints Management Protocol for the Public Health Sector of South Africa. Pretoria, 2013. http://www.rhap.org.za/national-complaints-management-protocol-for-the-public-health-sector/ (accessed 24 February 2015).

4. Department of Justice and Constitutional Development. Practical Guidelines for Employees in Terms of Section 10(4)(a) of the Protected Disclosures Act 26 of 2000. Pretoria, 31 August 2011. http://www. justice.gov.za/legislation/notices/2011/20110831_gg34572_n702-disclosure-guidelines.pdf (accessed 24 February 2015).

5. Benatar S. The humanistic side to medical education. S Afr Med J 2015;105(1):3. [http://dx.doi. org/10.7196/SAMJ.9043]

Accepted 2 February 2015.

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OPINION

Traditional health practitioners and the authority to issue medical certificates B Tshehla Boyane Tshehla is a lecturer in the Faculty of Law at North-West University (Mafikeng Campus), North West Province, South Africa. His research interests include the interaction between legal theory and practice. He focuses on the application, relevance and practicalities of the law in a social context.

Corresponding author: B Tshehla (boyane.tshehla@nwu.ac.za)

The Interim Traditional Health Practitioners Council was inaugurated in February 2013, and in May 2014 the sections of the Traditional Health Practitioners Act that give it full powers came into effect. The Council, as a professional body established by Parliament, gives traditional health practitioners registered with it the authority to issue medical certificates in line with the provisions of the Basic Conditions of Employment Act. However, the Council does not seem to be in a position to perform this function yet. Moreover, the field itself seems almost impossible to regulate because the practitioners cannot be subjected to objective assessment measures. While registered traditional health practitioners have the authority to issue medical certificates, it remains a moot point whether the certificates should be given full credibility before specific requirements for registration have been formulated and are implementable, and the envisaged code of conduct is in force.

S Afr Med J 2015;105(4):279-280. DOI:10.7196/SAMJ.9217

The Traditional Health Practitioners Act[1] (the Act) was legislated in 2007 and has been progressively activated, with the result that the majority of its sections are in effect (sections 7, 10, 11(3), 12, 13, 14, 15, 47, 48 and 50 came into effect on 30 April 2008 (Proc. No. 17, GG 31020), and sections 4, 5, 6, 8, 9, 16, 17, 18-46, 49 and 51 on 1 May 2014 (Proc. No. 29 GG 37600). The sections promulgated so far include section 4 (see the speech by the Deputy Minister of Health on the day[2]), which establishes the Interim Traditional Health Practitioners Council (the Council). The Council, duly established and inaugurated at the beginning of 2013, has the status of a professional regulatory body. Chapter 2 of the Act[1] stipulates the functions of the Council, which has the powers to register practitioners who qualify, investigate complaints laid against them, remove such practitioners from the register, and perform many other related functions in the field of traditional health practice.

The Council was inaugurated in February 2013, and in May 2014 the sections of the Traditional Health Practitioners Act that give it full powers came into effect. The Council, as a professional body established by Parliament, gives traditional health practitioners registered with it the authority to issue medical certificates in line with the provisions of the Basic Conditions of Employment Act.[3] However, the Council does not seem to be in a position to perform this function yet. Moreover, the field itself seems almost impossible to regulate because the practitioners cannot be subjected to objective assessment measures. While registered traditional health practitioners have the authority to issue medical certificates, it remains a moot point whether the certificates should be given full credibility before specific requirements for registration have been formulated and are implementable, and the envisaged code of conduct is in force.

This is an important development in the health sector of South Africa, given that the non-regulation of the traditional health sector created a lot of problems in the past. One of the obvious consequences of a non-regulated profession was that practitioners could not effectively be held accountable for their wrongful acts

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or omissions. One of the immediate effects of the establishment of the Council is the authority of traditional health practitioners to issue medical certificates for an employee who has been absent from work due to injury or sickness. This is a positive development, given that this particular issue has been a source of controversy for a considerable time.[4] On the one hand, employees who preferred to consult traditional health practitioners found themselves in an untenable situation because some employers would not accept certificates issued by traditional health practitioners. On the other hand, employers found themselves in a situation where they had no mechanisms of establishing the authenticity of the certificate even if they were prepared to accept it, as there was no official body or council that could verify traditional health practitioners’ credentials.

The establishment of the Council fills this vacuum.

However, the Council does not seem capacitated to deliver satisfactorily on its mandate yet. There are a number of reasons for this, but prominent among them is the difficulty the Council is likely to face in selecting the credible practitioners from the bogus ones for registration purposes.

Who is a traditional health practitioner?

Section 1 of the Act[1] defines a traditional health practitioner as a person who is ‘registered under this Act in one or more of the categories of traditional health practitioners’. The categories of traditional health practitioners include ‘diviners, herbalists, traditional birth attendants and traditional surgeons’ (section 47(f)(i)). From the wording of the Act, it is evident that the Council has the responsibility of determining who is to be registered as a traditional health practitioner, and section 47 of the Act gives the Minister of Health the powers to issue regulations that deal with issues of qualification for registration. It is clear that the definition of a traditional health practitioner is wide enough to include almost anyone who has some ability to heal by traditional methods. Any person who engages in traditional health practice without first registering commits an offence.

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However, this provision is suspended for a period of a year after the promulgation of the Act. Given that the section that contains this provision came into effect on 1 May 2014, traditional health practitioners who are not registered have a grace period of a year from that date to practise.

The traditional health practitioner’s medical certificate and potential problems

The absence of an employee from work is regulated by the provisions of the Basic Conditions of Employment Act.[3] Section 23(1) of this Act states that ‘[a]n employer is not required to pay an employee in terms of section 22 if the employee has been absent from work for more than two consecutive days or on more than two occasions during an 8-week period and, on request by the employer, does not produce a medical certificate stating that the employee was unable to work for the duration of the employee’s absence on account of sickness or injury’. Section 23(2) requires that ‘the medical certificate must be issued and signed by a medical practitioner or any other person who is certified to diagnose and treat patients and who is registered with a professional council established by an Act of Parliament’.

By virtue of the Council being a professional body established in terms of an Act of Parliament, an employer will be obliged to accept a certificate from a registered traditional health practitioner.

In theory that is sensible and equitable because, after all, people have a right to use health practitioners of their choice. The practical problem, however, is that this provision has come into effect before the measures according to which credible traditional health practitioners will be registered have been perfected. There are already reports that the process of registering traditional health practitioners seems subjective and biased in some instances.[5] The problem is two-fold. Firstly, it is almost impossible to formulate an objective set of assessment measures to verify whether a person is a genuine traditional healer or not. Secondly, the Council has not yet perfected measures to conduct this assessment for registration purposes.

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Conclusion

The establishment of a regulatory body dedicated to the traditional health practitioners’ profession is long overdue and ought to be welcomed. It goes a long way in acknowledging that many South Africans rely on this profession for their medical needs and, in an employment situation, should not be disadvantaged because of their choice of medical practitioner.

Notwithstanding the appropriateness of the regulatory body, it seems that the establishment of the Council and its implications regarding the requirements of a valid medical certificate as contained in the Basic Conditions of Employment Act[3] may create a lot of confusion and difficulties in the employment environment. An example of the problems a medical certificate and its validity can bring about came sharply to the fore in Kievits Kroon Country Estate (Pty) Ltd v Mmoledi,[4] where an employer and employee were at odds regarding the validity of a certificate issued by a traditional healer. The case started at the Commission for Conciliation, Mediation and Arbitration, went to the Labour Court and then the Labour Appeal Court, and was eventually finalised in the Supreme Court of Appeal. While the Supreme Court of Appeal found in favour of the employee in this case, it did not make a finding on the validity or otherwise of a medical certificate issued by a traditional health practitioner.

Until the envisaged code of conduct is introduced and enforced, there is ample space for the abuse of this authority, and this will not only create difficulties in the employment environment but do serious damage to the credibility of traditional health practice.

1. Traditional Health Practitioners Act 22 of 2007. http://www.polity.org.za/article/traditional-healthpractitioners-act-no-22-of-2007-2008-01-31 (accessed 24 February 2015).

2. Architect Africa News Network. Speech by Deputy Minister Gwen Ramokgopa at the inauguration of the Interim Traditional Health Practitioners Council of South Africa. http://architectafrica. com/NETWORK/SA/content/speech-deputy-minister-gwen-ramokgopa-inauguration-interimtraditional-health-practitioners- (accessed 1 December 2014).

3. Basic Conditions of Employment Act 75 of 1997. http://www.polity.org.za/article/basicconditions-of-employment-act-751997-determination-earrings-threshold-gazette-no-35404notice-422-2012-06-01 (accessed 24 February 2015).

4. Kievits Kroon Country Estate (Pty) Ltd v Mmoledi 2014 (1) SA 585 (SCA).

5. Summerton J. The incorporation of African traditional health practitioners into the South African health care system. Acta Academica 2006;38(1):143-169.

Accepted 13 February 2015.

April 2015, Vol. 105, No. 4

EDITORIAL

The HIV/HBV co-infected patient: Time for proactive management Worldwide an estimated 240 million people are chronically infected with chronic hepatitis B virus (CHB), of whom an estimated 3.4 million are co-​ infected with HIV.[1] Chronic liver disease has emerged as an important cause of morbidity in the HIV-infected population. It is, after opportunistic infections, the second most common cause of death among some populations of HIV-infected patients on antiretroviral therapy (ART).[2] In resource-limited settings (RLSs), infection with HIV and hepatitis B virus (HBV) is associated with poorer outcomes than HBV mono-infection. Co-infection is associated with higher rates of HBV persistence after acute infection, and among individuals with CHB, higher HBV DNA levels, a higher prevalence of HBV e antigenaemia, and an increased risk of progression to fibrosis, cirrhosis and possibly hepatocellular carcinoma (HCC).[2,3] Identifying patients who are chronically infected and providing specific management improves outcomes.[4] However, screening for active HBV infection before starting ART is not currently part of HIV guidelines in many countries in sub-Saharan Africa (SSA).

Epidemiology

Much of SSA has been considered to have high endemicity of CHB (≥8%). In Zimbabwe prevalence rates as high as 25% in an antenatal cohort, and rates of 13% in Malawi, 10.6% in Botswana and 17.3% in HIV-infected adults in Tanzania, have been reported. However, more recent data suggest that the prevalence in SSA may be lower than previously thought, probably owing to wide variations in prevalence across countries; for example, in South Africa (SA) the prevalence of hepatitis B surface antigen (HBsAg) as a marker of active HBV infection ranges from 3.5% to 23%.[5-7] Nevertheless, the morbidity coupled with the overall high endemicity of CHB is reason to screen for this infection and initiate optimal management for those found to be infected.

Goals of treatment and drug therapy

The primary goal of treating CHB is to reduce the risk of progressive liver disease, cirrhosis and HCC by suppressing HBV replication. The management cascade starts with diagnosing CHB by testing for HBsAg. This can be done by rapid point-of-care assays. If HBsAg is persistently detectable in the blood for >6 months, the patient is diagnosed with CHB. In patients positive for HBsAg, additional testing may include hepatitis B e antigen (HBeAg), antibody to hepatitis B e antigen (anti-HBe), and HBV DNA qualitatively and quantitatively. Intermediate goals and markers of treatment success are suppression of HBV replication as measured by the HBV viral load, HBeAg/anti-HBe seroconversion (in HBeAg-positive patients), HBsAg/anti-HBs seroconversion (preceded by a reduction in HBsAg titre), alanine aminotransferase normalisation and improvement of liver histological features. Viral eradication is not currently a goal of therapy, as none of the available therapeutic agents clear the highly stable covalently closed circular DNA (cccDNA) from hepatocytes.

A number of agents are available for the treatment of CHB, of which some also have HIV activity. A reverse transcriptase step in the HBV lifecycle, whereby pregenomic HBV RNA is transcribed to viral DNA, is the explanation for this. Screening for HIV in the HBV-infected patient before starting ART is therefore critical to avoid inadequate HIV therapy.

Tenofovir is among the most potent and effective agents for treating CHB. Lamivudine also has activity against HBV, but is less potent and has a high rate of failure and resistance development when used as a single HBV-active agent.[8] Entecavir also has potent activity against HBV but minimal activity against HIV. It is generally the treatment of choice when renal impairment makes tenofovir use problematic. Although available

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in SA, it is prohibitively expensive. Other HBV-specific agents have been developed (telbivudine, adefovir), but they are expensive, have a poorer resistance profile and are not widely available. Daily interferon (IFN) or weekly pegylated IFN therapy to treat and potentially clear HBsAg (but not cccDNA) is a treatment option in the mono-infected patient. However, it achieves lower rates of HBeAg seroconversion among co-infected patients, especially in the HBV genotypes common in SA, and is poorly tolerated.

Risks and benefits of treating CHB should be assessed before initiating therapy. Among co-infected patients who are eligible for ART, ART should always include HBV-active agents – ideally tenofovir. There is probably a subset of CHB patients with a low risk of progressive liver disease. Patients who are HBeAg-negative, have low HBV viral loads and lack evidence of liver fibrosis may not benefit from treatment. It is notable that the use of transaminases for monitoring liver disease, which assists in assessing treatment need among HIV-uninfected individuals, may have limited value in HIV infection because of lower transaminase values despite ongoing necroinflammatory disease and fibrosis. Any HBV-infected patient with cirrhosis or stigmata of chronic liver disease should receive antiviral therapy. All HIV/HBV co-infected patients with any evidence of liver disease (elevated transaminase levels, elevated HBV DNA titres, necroinflammation and fibrosis on biopsy) should be started on HBV-active therapy irrespective of CD4 count.[9] The most recent SA HIV treatment guidelines (December 2014) include known HBV infection as an indication to start ART, irrespective of CD4 count.

Addressing other risks

Lifestyle modifications such as reducing or curtailing alcohol intake will minimise the additional risk of cirrhosis. Advice about avoiding over-thecounter herbal remedies and traditional medications is important. The metabolic syndrome is associated with both HIV and the development of non-alcoholic steatohepatitis (NASH). NASH may lead to cirrhosis and HCC. Risk factors for NASH and advanced fibrosis in the HBV mono-infected patient are age, diabetes, obesity, exposure to stavudine, and the metabolic syndrome. Vaccination against hepatitis A is indicated in those who are non-immune. The cirrhotic patient requires additional intervention and surveillance, e.g. gastroscopy.

Monitoring, managing and stopping HBV therapy

After initiation of agents active against HBV in the HIV/HBV co-infected patient, HBV DNA levels decline far more gradually than HIV RNA levels. If HBV DNA monitoring is available, it is reasonable to perform a test after 12 months of therapy. If there is failure to achieve HBV suppression by 12 months despite good adherence suggested by undetectable HIV RNA, entecavir added to tenofovir-containing therapy may result in better HBV control. Costeffective and practical methods for monitoring HBV DNA that will be valuable in RLSs, such as point-of-care HBV viral load tests and testing of dried blood spots, are under development.

Following initiation of ART, transaminase levels commonly increase transiently among co-infected patients. This is usually attributed to druginduced hepatotoxicity, but other causes should be considered (Table 1).

The reported incidence of ART-related hepatotoxicity is between 5% and 10% in the HIV-infected population, with a higher rate in co-infected patients.[9] Some agents, particularly nevirapine, are more likely to cause hepatotoxicity than others and should be avoided in patients with liver disease. Lopinavir/ritonavir given at higher doses in the presence of rifampicin-containing antituberculosis medication may induce mild to moderate hepatotoxicity. Most episodes are brief, lasting around 2 - 4

April 2015, Vol. 105, No. 4

EDITORIAL

The commencement of routine infant HBV vaccination, currently at 6 weeks of age, should be shifted to closer to the time of birth in order to prevent mother-to-child transmission (MTCT) of HBV.

Table 1. Causes of liver enzyme elevation during ART Drug effects – ART related and non-ART related Poor adherence Inadvertent stopping of anti-HBV agents, e.g. changing from first- to second-line ART Infection with another agent, e.g. TB, HAV, HEV Hepatic steatosis (associated with chronic ART use and the metabolic syndrome) Toxins, e.g. alcohol and herbal medicines Worsening of underlying liver disease, e.g. autoimmune liver disease Emergence of HBV resistance TB = tuberculosis; HAV = hepatitis A virus; HEV = hepatitis E virus.

weeks, and resolve without intervention. Discontinuation of ART may be another cause of liver inflammation, either as part of a regimen change or through a lapse in adherence. Stopping HBV-active ART can lead to a rapid rise in HBV replication, leading to symptoms that can range from subclinical to fulminant hepatitis, and may mimic acute HBV infection.

This syndrome generally occurs several weeks to months after stopping therapy, but may occasionally occur within days. Drug resistance rarely emerges in patients on potent therapy such as tenofovir.[10]

Screening for HCC

Routine CHB management in resource-rich settings includes regular screening for HCC. American Association for the Study of Liver Diseases (AASLD) guidelines recommend an ultrasound scan of the liver every 6 - 12 months for those at risk of developing HCC.[11] Alpha-fetoprotein screening at 6-monthly intervals lacks sensitivity for early HCC.[12] Studies on optimal screening methods, intervals and evaluations of costeffectiveness in HIV/HBV co-infected populations in RLSs are needed.

Occult HBV infection

Occult HBV infection is partially controlled HBV infection, usually associated with low levels of HBV DNA (<104 IU/mL) and an HBsAgnegative serological profile. Antibodies to HBV core (anti-HBc) may or may not be present. Estimates of the prevalence of occult HBV infection among HIV-infected patients in Africa vary between 2% and 85%, depending on population, study design and extent of immune deficiency.[13] Recovery of CD4 counts, as occurs with ART, can lead to the resolution of occult HBV infection. The overall clinical importance of occult HBV infection is unclear, and there are currently no guidelines that recommend screening for this condition.

HBV vaccination

HBV vaccination is routinely provided in many high-income countries for adults in high-risk groups. Cost, and perhaps a lack of appreciation of the frequency of adult HBV transmission, have discouraged implementation of similar programmes in many RLSs, including SA. Although there are few data on acute HBV infection among adults in most of SSA, infection can and does occur, especially among higher-risk populations. One study from SA reported an annual incidence of newly acquired HBV infection of 2.5% among young women at high risk for HIV.[14] Only approximately a quarter of these women had evidence of prior exposure (anti-HBc antibodies), leaving the majority of the population at risk of infection. Given this incidence of HBV, the practice of vaccinating nonimmune HIV-infected individuals would seem reasonable.

Because individuals with CD4 counts <200 cells/μL have a poor immune response to vaccination, vaccinating adults with higher CD4 counts is likely to have greater public health impact. Data are needed to better understand the cost-effectiveness of HBV vaccination in HIV-infected adults in RLSs.

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Conclusion

With the roll-out of ART in RLSs, the emphasis of care is shifting to maintaining quality of life and managing chronic conditions.

Given the high prevalence of HBV infection in SSA and the risk of HIV/HBV co-infected patients developing liver complications, the management of HBV/HIV should be prioritised. In SSA efforts need to be focused on screening for chronic viral hepatitis, early institution of effective antiviral therapy, vaccinating those who are most at risk of infection, and the prevention of HBV MTCT. M I Andersson W Preiser Division of Medical Virology, Department of Pathology, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, Cape Town, South Africa, and National Health Laboratory Service Tygerberg, Cape Town C van Rensburg Division of Gastroenterology and Hepatology, Department of Internal Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, Cape Town, South Africa J Taljaard Division of Infectious Diseases, Department of Internal Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, Cape Town, South Africa C J Hoffmann Johns Hopkins University, Baltimore, MD, USA, and Aurum Institute, Johannesburg, South Africa Corresponding author: M I Andersson (andersson_m@sun.ac.za) 1. Puoti M, Airoldi M, Bruno R, et al. Hepatitis B virus co-infection in human immunodeficiency virusinfected subjects. AIDS Rev 2002;4(1):27-35 PMID 11998781.

2. Thio CL, Seaberg EC, Skolasky R, et al. HIV-1, hepatitis B virus, and risk of liver-related mortality in the Multicenter Cohort Study (MACS). Lancet 2002;360(9349):1921-1926. [http://dx.doi.org/10.1016/ S0140-6736(02)11913-1] 3. Salmon-Ceron D, Rosenthal E, Lewden C, et al. Emerging role of hepatocellular carcinoma among liver-related causes of deaths in HIV-infected patients: The French national Mortalité 2005 study. J Hepatol 2009;50(4):736-745. [http://dx.doi.org/10.1016/j.jhep.2008.11.018] 4. Chen C-J, Yang H-I. Natural history of chronic hepatitis B REVEALed. J Gastroenterol Hepatol 2011;26(4):628-338. [http://dx.doi.org/10.1111/j.1440-1746.2011.06695.x] 5. Ott JJ, Stevens GA, Groeger J, Wiersma ST. Global epidemiology of hepatitis B virus infection: New estimates of age-specific HBsAg seroprevalence and endemicity. Vaccine 2012;30(12):2212-2219. [http://dx.doi.org/10.1016/j.vaccine.2011.12.116] 6. Andersson MI, Maponga TG, Ijaz S, et al. The epidemiology of hepatitis B virus infection in HIV-infected and HIV-uninfected pregnant women in the Western Cape, South Africa. Vaccine 2013;31(47):5579-5584. [http://dx.doi.org/10.1016/j.vaccine.2013.08.028] 7. Lukhwareni A, Burnett RJ, Selabe SG, Mzileni MO, Mphahlele MJ. Increased detection of HBV DNA in HBsAgpositive and HBsAg-negative South African HIV/AIDS patients enrolling for highly active antiretroviral therapy at a tertiary hospital. J Med Virol 2009;81(3):406-412. [http://dx.doi.org/10.1002/jmv.21418] 8. Benhamou Y, Bochet M, Thibault V, et al. Long-term incidence of hepatitis B virus resistance to lamivudine in human immunodeficiency virus-infected patients. Hepatology 1999;30(5):1302-1306. [http://dx.doi.org/10.1002/hep.510300525] 9. Soriano V, Puoti M, Bonacini M, et al. Care of patients with chronic hepatitis B and HIV co-infection: Recommendations from an HIV-HBV International Panel. AIDS 2005;19(3):221-240. [http://dx.doi. org/10.1097/01.aids.0000163948.62176.e7] 10. Audsley J, Arrifin N, Yuen LK, et al. Prolonged use of tenofovir in HIV/hepatitis B virus (HBV)coinfected individuals does not lead to HBV polymerase mutations and is associated with persistence of lamivudine HBV polymerase mutations. HIV Med 2009;10(4):229-235. [http://dx.doi.org/10.1111/ j.1468-1293.2008.00675.x] 11. Lok ASF, McMahon BJ. Chronic hepatitis B: Update 2009. Hepatology 2009;50(3):661-662. [http:// dx.doi.org/10.1002/hep.23190] 12. Aghoram R, Cai P, Dickinson JA. Alpha-foetoprotein and/or liver ultrasonography for screening of hepatocellular carcinoma in patients with chronic hepatitis B. Cochrane Database Syst Rev 2012, Issue 9. Art. No.: CD002799. [http://dx.doi.org/10.1002/14651858.CD002799.pub2] 13. Cohen Stuart JW, Velema M, Schuurman R, Boucher CA, Hoepelman AI. Occult hepatitis B in persons infected with HIV is associated with low CD4 counts and resolves during antiretroviral therapy. J Med Virol 2009;81(3):441-445. [http://dx.doi.org/10.1002/jmv.21422] 14. Baxter C, Yende-Zuma N, Tshabalala P, Abdool Karim Q, Abdool Karim SS. Safety of coitally administered tenofovir 1% gel, a vaginal microbicide, in chronic hepatitis B virus carriers: Results from the CAPRISA 004 trial. Antiviral Res 2013;99(3):405-408. [http://dx.doi.org/10.1016/j.antiviral.2013.06.019]

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Of ambivalence, shame and guilt: Perceptions regarding termination of pregnancy among South African women Termination of pregnancy (TOP) for health or other reasons is an emotive and contentious issue, steeped in the context of a political, moral and religious climate.

For most women, the decision to have a TOP is not easy, regardless of the reason. While early literature[1-3] supported the notion that that there is little in the way of negative sequelae following TOP, more recent long-term studies[4-6] have suggested that negative sequelae may be more common than was previously thought. Risk factors for the development of negative sequelae include the attitude projected by those providing the procedure (negative attitudes of providers tend to promote emotional sequelae in women undergoing TOP), previous psychological/psychiatric history (associated with higher rates of post-traumatic stress disorder (PTSD) and depression[6] following TOP), and low income (with women from low-income groups having higher admission rates for depression and PTSD after TOP[4]).

A recent survey involved 102 women undergoing TOP at two clinics in Johannesburg, SA (51 from each), one serving women with few economic resources (site 1) and the other serving women with adequate resources (site 2). The women were recruited and followed up for 3 months. At baseline, biographical data were obtained and there were no significant demographic differences between women recruited from the two sites.

The Beck Depression Inventory (BDI),[7] a 21-item self-rating scale that is a validated and reliable instrument to assess depression, was administered to all the women.

To explore the meaning that the decision to undergo TOP had for women, the consensual qualitative research method[8] was used to analyse the transcripts of 22 women, 13 from site 1 and 9 from site 2, 1 month after the procedure. The women were administered a short questionnaire during a semistructured interview that sought to capture: (i) their reasons for TOP; (ii) their thoughts and feelings before the procedure; (iii) their thoughts and feelings after the procedure; and (iv) their experiences of the procedure (any positive and/or negative feelings about the actual procedure). To elicit symptoms of PTSD, together with the BDI, the revised version of the Impact of Events Scale (IES-R)[9] was administered to assess women’s subjective experience, including intrusive thoughts, re-experiencing and avoidance reactions, each on a severity rating of 0 - 5.

The women who willingly answered the question ‘What was the reason for the TOP?’ were generally younger, better educated and more likely to be employed than those who did not answer the question.

There were no differences in scores for depression and PTSD in those who answered the question compared with those who did not. There were also no differences between the responses of women of lower socioeconomic status (site 1) and higher socioeconomic status (site 2).

Major themes and subthemes were identified independently by three reviewers, and consensus was obtained to ensure credibility and reliability of the interpretations made by the primary researcher. The following themes emerged related to personal characteristics (timing and readiness, e.g. not old enough; not ready for the responsibility; medical/health problems) and the women’s circumstances, such as relationship with their partners (including partner coercion), financial worries and desire to continue education: • Ambivalence was a common theme, e.g. ‘I am relieved it’s over but I feel really guilty’, together with mixtures of • Emotional distress (guilt, shame, regret, anxiety, depression, desperation/feeling compelled) and • Fear and thoughts of death (should she go through with the procedure, or should she not terminate the pregnancy?).

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With regard to the question ‘What were your thoughts after the procedure?’, ambivalence was again a common theme. Regarding respondents’ experience of the actual procedure, the theme of ambivalence was once again prominent. Negative feelings about the experience were mainly personal feelings of guilt and shame and pain. Many women expressed surprise that there was so much pain, and wished that they could have been offered more pain relief, while others believed that they ‘deserved’ to be experiencing pain. Positive feelings were those of relief, feeling supported and happy, and feeling that they were treated well in a non-judgemental environment. It was important that they were managed in a safe environment, that the treating person was sympathetic and that they were told what to expect and how to relax.

While this survey 1 month after TOP did not allow for longer-term follow-up with regard to PTSD and depressive symptoms, it offers insight into the subjective feelings experienced by the women. Of note was the universality of the responses, regardless of socioeconomic, religious and cultural standing. Ambivalence and anxiety before the procedure has been reported in previous studies. Indeed, Lemkau[10] claims that ambivalence is the norm for a woman who has an abortion, despite liberalisation of abortion laws, and that it is conceptualised in intrapsychic terms as ‘personal conflict’, her decision being in conflict with her personal values.[11,12] The fact that women in this survey seemed relieved and objectively euthymic (as revealed by the completed PTSD and depression screening instruments), yet admitted to depressed mood/suicidal ideation/ conflicted emotions, emphasises the subjective experience of the TOP.

Conclusion

Our findings suggest that despite legislative changes and the promotion of non-judgemental attitudes among healthcare providers and indeed society as a whole, the experience of TOP remains contentious and difficult to study. Psychiatric sequelae such as depression and PTSD are not common, certainly not in the short term, but ambivalence with feelings of relief, guilt and anxiety before and after the procedure are common. Service providers should be alert to this and promote an empathic, safe and secure environment.

Ethics approval for the survey reported here was obtained from the South General Institutional Review Board at the University of California, Los Angeles (No. G07-06-057-01) and from the Human Research and Ethics Committee (HREC) of the University of the Witwatersrand (ethics clearance No. M070624).

Ugash Subramaney Department of Psychiatry, School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Gail Elizabeth Wyatt John K Williams Semel Institute, Department of Biobehavioural Sciences, University of California, Los Angeles, USA Corresponding author: U Subramaney (ugasvaree.subramaney@wits.ac.za) 1. Belsey EM, Greer HS, Lal S, Lewis SC, Beard RW. Predictive factors in the emotional response to abortion: King’s Termination Study-IV. Soc Sci Med 1977;11(2):71-82. [http://dx.doi.org/10.1016/0037-7856(77)90002-6] 2. Adler NE. Emotional responses of women following therapeutic abortion. Am J Orthopsychiatry 1975;45(3):446-454. [http://dx.doi.org/10.1111/j.1939-0025.1975.tb02555.x] 3. Cohen L, Roth S. Coping with abortion. J Human Stress 1984;10(3):140-145. [http://dx.doi.org/10.10 80/0097840X.1984.9934968]

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4. Reardon DC, Cougle JR, Rue VM, Shuping MW, Coleman PK, Ney PG. Psychiatric admissions of lowincome women following abortion and childbirth. CMAJ 2003;168(10):1253-1256.

5. Fergusson DM. Abortion and mental health. Psychiatr Bull 2008;32(9):321-324. [http://dx.doi. org/10.1192/pb.bp.108.021022] 6. Fergusson DM, Horwood LJ, Boden JM. Abortion and mental health disorders: Evidence from a 30-year longitudinal study. Br J Psychiatry 2008;193(6):444-451. [http://dx.doi.org/10.1192/bjp.bp.108.056499] 7. Beck AT, Beamesderfer A. Assessment of depression: The Depression Inventory. In: Pichot P, ed.

Psychological Measurements in Psychopharmacology. Basel: S Karger, 1974:151-159.

8. Hill CE, Knox S, Thompson BJ, Hess SA, Williams EN, Ladanay N. Consensual qualitative research: An update.

Journal of Counselling Psychology 2005;52(2):196-205. [http://dx.doi.org/10.1037/0022-0167.52.2.196]

9. Weiss DS, Marmar CL. The Impact of Event Scale – revised. In: Keane JPWTM, ed. Assessing Psychological Trauma and PTSD. New York: Guilford Press, 1996:339-411.

10. Lemkau JP. Emotional sequelae of abortion: Implications for clinical practice. Psychol Women Q 1988;​ 12(4):461-472. [http://dx.doi.org/10.1111/j.1471-6402.1988.tb00978.x] 11. Adler NE, David HP, Major BN, Roth SH, Russo NF, Wyatt GE. Psychological responses after abortion.

Science 1990;248(4951):41-44. [http://dx.doi.org/10.1126/science.2181664] 12. Major B, Cozzarelli C. Psychosocial predictors of adjustment to abortion. J Soc Issues 1992;48(3):121142. [http://dx.doi.org/10.1111/j.1540-4560.1992.tb00900.x]

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Abuse in South African maternity settings is a disgrace: Potential solutions to the problem Abuse of patients by healthcare staff in maternity settings has been reported globally, in high- and lowincome settings.[1] Such behaviours include verbal abuse, physical abuse, non-consensual care, non-confidential care, neglect, abandonment of care and bribery.

Review articles suggest that the causes are multifactorial, including lack of professional support for healthcare workers, hierarchical work relationships, excessive workload, inadequate staffing levels and poor infrastructure.[1] A World Health Organization statement in 2014 emphasised that the problem of disrespect and abuse of women during facility-based childbirth is a global phenomenon requiring urgent attention.[2] In South Africa (SA) the problem has been documented and studied over many decades[3-5] and was described by Prof. Lynette Denny, Head of the Department of Obstetrics and Gynaecology at the University of Cape Town, as ‘one of the world’s great disgraces’ (personal communication). Studies in maternity facilities have documented staff rudeness, arbitrary acts of unkindness, clinical neglect, verbal abuse, psychological abuse, physical assault and sexual violence.[6-8] Studies in community-based maternity care facilities found that many women express expectations of being ‘shouted at, beaten or neglected’.[6]

The context of maternity services in SA

Healthcare workers’ working environments are influenced by physical, social and psychological factors that result in a range of occupational stressors[9,10] and affect the staff-patient relationship and the quality of care provided. SA public sector facilities serve 85% of the popu­lation.[11] An unequal healthcare system, inherited from the apartheid era,[12] is characterised by maldistribution of health workers and resources,[11,13] poorly funded facilities and a lack of mentorship and leadership,[14,15] demoralisation and a lack of motivation,[6,12,16,17] high responsibility, excessive overtime demands, task overload and an ever-burgeoning demand for health services.[15] Abusive behaviour in this context may result from staff ’s perceived sense of powerlessness to intervene.

Studies documenting the prevalence of diagnosed antenatal and postnatal depression in SA have shown rates of 47%[18] and 34%,[19] respectively. Despite this, primary healthcare providers are not trained to detect mental illness,[20] and their working environment does not provide the resources or support structures that they need in order to offer the appropriate care.[21] The additional emotional burden imposed by mental illness in this setting can compound exhaustion, burnout and compassion fatigue among staff.[11] This may contribute to the development of common mental disorders among staff themselves, which in turn may further exacerbate their disengagement from or abuse of their patients.[22] The dysfunctional relationship between healthcare worker and patient can be exaggerated by the vulnerability of being in labour[7,23] and the fact that for a range of reasons many women in the SA setting have no birthing companion.[6,24-26]

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Solutions: Global and national initiatives to address abuse of women in labour

The rights-based approach provides an important framework to address the problem of abuse of maternity patients and seeks to ensure accountability of health professionals and managers for poor quality of care.[27] There are two critical components of quality of care: firstly, evidence-based effective care to reduce adverse maternal and perinatal outcomes, and secondly, patientcentred care in which women are treated with respect and dignity. Care for health workers themselves is a vital element of the latter.[28] There are examples of initiatives at global and country level to address abuse of women in labour and promote effective care. These include the Humanising Childbirth Movement (predominantly South America),[29] the Better Births Initiative (SA),[30] and more recently the Respectful Maternity Care Movement (Mozambique, Ethiopia)[31-34] and the Heshima Project (Kenya).[34]

The Patient-Centred Maternity Care Code in the Cape Metro

This was introduced in 2013 in response to complaints from women about their care and widespread observations by 4th-year medical students of disrespectful behaviour by maternity health staff. A meeting was convened by the head of the Cape Town Metro District Health Services and senior academics from the departments of Public Health and Obstetrics and Gynaecology of the University of Cape Town, and a task team was established.

A code for patient-centred maternity care was developed that includes zero tolerance for abusive or disrespectful behaviour, but also addresses health system problems which may contribute to such behaviours.

The objectives of the code are as follows: • Every woman or every couple seeking maternity care has the right to effective healthcare and the right to be treated with respect and dignity.

• Every woman or every couple has the right to information about pregnancy and the necessary obstetric care.

• Every woman to have a chosen personal and/or facility-provided companion while in labour.

• Maternity facilities to be responsive to the communities they serve.

Each objective includes a list of specific actions, for example friendly reception, a respectful approach by the health worker to the woman in labour, and supply chain/infrastructure improvements. Monitoring and implementation tools have been developed. Educational and information pamphlets about maternity care, companions and the code have been produced.

The code, which has been formally adopted as Western Cape Health policy, coheres with Western Cape Health’s strategy of ‘patientcentred care’, the core values of which are Caring, Competence, Accountability, Integrity, Responsiveness and Respect (C2AIR2).

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The process has been slow to implement, with many challenges identified by an initial participatory action research evaluation (J Rucell, School of Politics and International Studies, University of Leeds, UK – personal communication to the Metro task team, December 2013). It was difficult to get ‘buy-in’ from all staff, and there was fear of disciplinary action or suspension. There were challenges in providing proper debriefing mechanisms and adequate training, and in addressing infrastructural and procurement problems.

The programme has now been decentralised to the substructure level, where there will be a multidisciplinary approach to promoting patient-centred maternity care with inputs from medical and nursing schools, managers and healthcare staff in maternity facilities.

Birth companions as a method for improving women’s experience of care in labour

One maternity care practice for which there is considerable evidence of benefit is that of providing companions and emotional support for women in labour. This can be in the form of a personal companion (partner, mother, aunt, etc.), or a lay supporter or ‘doula’ (a woman who cares for other women). A Cochrane review in 2011 of 22 randomised controlled trials involving 15 000 women and investigating ‘continuous support for women during childbirth’ showed the following significant benefits: women were more likely to have spontaneous birth, less likely to require intrapartum analgesia, and less likely to report dissatisfaction; their labours were slightly shorter; they were less likely to require caesarean section, instrumental delivery or regional analgesia; and they were less likely to have a baby with a low 5-minute Apgar score.[35] Despite there being more evidence for this practice than for many other interventions in labour, its implementation in public sector maternity wards is often impeded by infrastructural problems such as poor security, lack of privacy and a lack of enabling policies.

Healthcare worker training and emotional support: The Secret History method

The Perinatal Mental Health Project[36] at the University of Cape Town developed the Secret History training method in 2004. The project has used this approach in a wide variety of settings with a range of healthcare workers, and the training has undergone qualitative internal and external evaluation. The aim is to improve empathic engagement skills of healthcare staff working with mothers.

The group role-play facilitates an enactment of typical dysfunctional responses between healthcare worker and patient through a case story unfolding between them, over the course of pregnancy and labour, and postnatally. The secret history of each character is revealed in stages. Participants have a chance to ‘play’ one of the two roles and are then asked to switch roles half way through the story. At each phase of the story, the players are asked to identify their feelings and needs, both as the healthcare worker and as the mother.

Identifying with ‘the other’ is a critical element of the training and allows for dissolution or reframing of unhelpful cognitions. A process of reintegration of self and ‘other’ follows. This allows participants to engage with a wider context of maternal care, one which encourages empathy for the ‘other’ and validates sympathy for the ‘self ’. Participants are then able to develop their own solutions to address difficulties in the workplace and interpersonal challenges with colleagues and patients, and to be more supportive of the needs of patients and each other.

Conclusions

Disrespect and abuse of women during childbirth is an infringement of women’s human rights and a deterrent to seeking care, thus resulting in adverse pregnancy outcomes. It is therefore each healthcare

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worker’s professional and ethical obligation to report observed abuses to senior management.

The promotion of respectful maternity care requires attitudinal changes by staff, staff support mechanisms, adequate training, appropriate infrastructure, functioning procurement processes, and effective clinical and managerial governance.

Simone Honikman Perinatal Mental Health Project, Alan J Flisher Centre for Public Mental Health, University of Cape Town, South Africa, and Professional Standards Committee, University of Cape Town Sue Fawcus Department of Obstetrics and Gynaecology, University of Cape Town, South Africa, and Head of Obstetric Services, Mowbray Maternity Hospital, Cape Town Ingrid Meintjes Perinatal Mental Health Project, Alan J Flisher Centre for Public Mental Health, University of Cape Town, South Africa Corresponding author: S Honikman (simone.honikman@uct.ac.za) 1. Bowser D, Hill K. Exploring Evidence for Disrespect and Abuse in Facility-based Childbirth. USAID, 2010. http://wordpress.sph.harvard.edu/mhtf-2/wp-content/uploads/sites/32/2014/08/RespectfulCareatBirth920-101Final.pdf (accessed 27 February 2015).

2. World Health Organization Human Reproduction Programme Statement. The Prevention and Elimination of Disrespect and Abuse during Facility Based Childbirth. Geneva: WHO, 2014.

3. Abrahams N, Jewkes R, Mvo Z. Health care-seeking practices of pregnant women and the role of the midwife in Cape Town, South Africa. J Midwifery Womens Health 2001;46(4):240-247. [http://dx.doi. org/10.1016/S1526-9523(01)00138-6] 4. Farrell E, Pattinson RC. Out of the mouths of babes – innocent reporting of harmful labour ward practices. S Afr Med J 2004;94(11):896-897.

5. Human Rights Watch. ‘Stop Making Excuses’: Accountability for Maternal Health Care in South Africa. http://www.hrw.org/reports/2011/08/08/stop-making-excuses-0 (accessed 10 March 2014).

6. Jewkes R, Abrahams N, Mvo Z. Why do nurses abuse patients? Reflections from South African obstetric services. Soc Sci Med 1998;47(11):1781-1795. [http://dx.doi.org/10.1016/S0277-9536(98)00240-8] 7. Kruger L, Schoombee C. The other side of caring: Abuse in a South African maternity ward. J Reprod Infant Psychol 2010;28(1):84-101. [http://dx.doi.org/10.1080/02646830903294979] 8. Khalil D. Public hospitals. Nurs Forum 2009;44(3):207-217. [http://dx.doi.org/10.1111/j.1744-6198.2009.00144] 9. Chan AOM, Huak CY. Influence of work environment on emotional health in a health care setting.

Occup Med 2004;54(3):207-212. [http://dx.doi.org/10.1093/occmed/kqh062] 10. Klopper HC, Coetzee SK, Pretorius R, Bester P. Practice environment, job satisfaction and burnout of critical care nurses in South Africa. J Nurs Manag 2012;20(5):685-695. [http://dx.doi.org/10.1111/j.1365-2834.2011.01350.x] 11. Breier M, Wildschut A, Mgqolozana T. Nursing in a New Era: The Profession and Education of Nurses in South Africa. Cape Town: Human Sciences Research Council, 2009.

12. 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. [http://dx.doi. org/10.1016/S0140-6736(09)60951-X] 13. Zachariah R, Ford N, Philips M, et al. Task shifting in HIV/AIDS: Opportunities, challenges and proposed actions for sub-Saharan Africa. Trans R Soc Trop Med Hyg 2009;103(6):549-558. [http:// dx.doi.org/10.1016/j.trstmh.2008.09.019] 14. Saxena S, Thornicroft G, Knapp M, Whiteford H. Resources for mental health: Scarcity, inequity, and inefficiency. Lancet 2007;370(9590):878-889. [http://dx.doi.org/10.1016/S0140-6736(07)61239-2] 15. Pillay R. Retention strategies for professional nurses in South Africa. Leadersh Health Serv 2009;22(1):39-57. [http://dx.doi.org/10.1108/17511870910928010] 16. Kim J, Motsei M. ‘Women enjoy punishment’: Attitudes and experiences of gender-based violence among PHC nurses in rural South Africa. Soc Sci Med 2002;54(8):1243-1254. [http://dx.doi.org/10.1016/S0277-9536(01)00093-4] 17. Chopra M, Lawn JE, Sanders D, et al. Achieving the health Millennium Development Goals for South Africa: Challenges and priorities. Lancet 2009;374(9694):1023-1031. [http://dx.doi.org/10.1016/S0140-6736(09)61122-3] 18. Rochat TJ, Tomlinson M, Bärnighausen T, Newell M-L, Stein A. The prevalence and clinical presentation of antenatal depression in rural South Africa. J Affect Disord 2011;135(1):362-373. [http://dx.doi.org/10.1016/j.jad.2011.08.011] 19. Cooper PJ, Tomlinson M, Swartz L, Woolgar M, Murray L, Molteno C. Post-partum depression and the mother-infant relationship in a South African peri-urban settlement. Br J Psychiatry 1999;175(6):554558. [http://dx.doi.org/10.1111/j.1365-2214.2006.00598.x] 20. Hamad R, Fernald LCH, Karlan DS, Zinman J. Social and economic correlates of depressive symptoms and perceived stress in South African adults. J Epidemiol Community Health 2008;62(6):538-544. [http://dx.doi.org/10.1136/jech.2007.066191] 21. Moyle W. Nurse-patient relationship: A dichotomy of expectations. Int J Ment Health Nurs 2003;12(2):103-109. [http://dx.doi.org/10.1046/j.1440-0979.2003.00276.x] 22. Van der Colff J, Rothmann S. Occupational stress, sense of coherence, coping, burnout and work engagement of registered nurses in South Africa. South African Journal of Industrial Psychology 2009;35(1):1-10. [http://dx.doi.org/10.4102/sajip.v35i1.423] 23. Hodges S. Abuse in hospital-based birth settings? J Perinat Educ 2009;18(4):8-11. [http://dx.doi. org/10.1624/105812409X474663] 24. Gilson L, Daire J. Leadership and governance within the South African health system. In: Padarath A, English R, eds. South African Heath Review. Durban: Health Systems Trust, 2011:66-80.

25. Tomlinson M, Cooper P, Stein A, Swartz L, Molteno C. Post-partum depression and infant growth in a South African peri-urban settlement. Child Care Health Dev 2006;32(1):81-86. [http://dx.doi. org/10.1111/j.1365-2214.2006.00598.x] 26. Kaibe NV. The knowledge of the registration of the role of the doula in the facilitation of natural child birth. Master’s thesis (Nursing Science). Tygerberg, Cape Town: Department of Interdisciplinary Health Sciences, Stellenbosch University, 2011.

27. United Nations General Assembly Human Rights Council. Technical guidance on the application of a human-rights based approach to the implementation of policies and programmes to reduce preventable maternal morbidity and mortality. July 2012. http://www.who.int/pmnch/media/news/2012/20120910_ humanrightscouncil/en/ (accessed 9 March 2015).

April 2015, Vol. 105, No. 4

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28. Brodie P. ‘Midwifing the midwives’: Addressing the empowerment, safety of, and respect for, the world’s midwives. Midwifery 2013;29(10):1075-1076. [http://dx.doi.org/10.1016/j.midw.2013.06.012] 29. Goer H. Humanizing birth: A global grassroots movement. Birth 2004;31(4):308-314. [http://dx.doi. org/10.1111/j.0730-7659.2004.00324.x] 30. Smith H, Brown H, Hofmeyr GJ, Garner P. Evidence-based obstetric care in South Africa – influencing practice through the ‘Better Births Initiative’. S Afr Med J 2004;94(2):117-120.

31. Reis V, Deller B, Carr C, Smith J. Respectful Maternity Care. 2012. https://www.k4health.org/sites/ default/files/RMC Survey Report.pdf (accessed 27 February 2015).

32. Snow J. MCHIP Year Four Annual Report. Baltimore, MD: Johns Hopkins University Press, 2013.

33. K4Health. Respectful maternity care toolkit. http://www.k4health.org/toolkits/rmc (accessed 27 February 2015).

34. Warren C, Njuki R, Abuya T, et al. Study protocol for promoting respectful maternity care initiative to assess, measure and design interventions to reduce disrespect and abuse during childbirth in Kenya.

BMC Pregnancy Childbirth 2013;13(1):21-29. [http://dx.doi.org/10.1186/1471-2393-13-21] 35. Hodnett ED, Gates S, Hofmeyr GJ, Sakala C, Weston J. Continuous support for women during childbirth. Cochrane Database Syst Rev 2013, Issue 7. Art. No.: CD003766. [http://dx.doi.org/10.1002/14651858.CD003766.pub5] 36. Field S, Baron E, Meintjes I, van Heyningen T, Honikman S. Maternal mental health care: refining the components in a South African setting. In: Okpaku SO, ed. Essentials of Global Mental Health. Cambridge: Cambridge University Press, 2014:173-186.

S Afr Med J 2015;105(4):284-286. DOI:10.7196/SAMJ.9582

Containing contraceptive costs There are about 7 billion people living on our planet.

In many countries resources are strained and we seek to slow down the rate of population growth. There are obviously many factors that lead to rapid population growth. Contraceptive methods are an important means of slowing population growth by helping people limit and/or space their families. While the cost of older methods such as the oral contraceptive pill, injectable progestogens and copper intrauterine contraceptive devices (IUCDs) has come down considerably, the cost of the newer hormone-based long-acting reversible contraceptive (LARC) methods has not.

It is now generally accepted that LARC methods are most effective in preventing unwanted pregnancy, because their use does not demand daily compliance.[1] While the copper-based IUCDs remain effective and are very cost-effective, they generally have more side-effects (including excessive bleeding) than the subdermal etonogestrel-based implant (Implanon) and levonorgestrel-based Norplant, and the levonorgestrel intrauterine systems (IUSs) Mirena and Skyla/Jaydess (the latter not currently available in South Africa).

Use of the Implanon and Mirena is increasing and bringing with it increased costs to both government and third party and individual payers. Are we paying too much – not because the manufacturer is overcharging, but because we are not fully utilising the lifetime of these products?

The evidence that copper IUCDs can be used well beyond their registered lifetimes is not new.[2] While there are practical costs associated with changing these products at the specified intervals, and attendant clinical risks, it is with the hormone-based LARC methods that the potential savings are greatest. Unlike copper IUCDs, which in some countries are very cheap, the hormone-based LARCs are universally expensive. A new study from St Louis, USA, has evalua­ ted using the Mirena for an extra year beyond its recommended life­time.[3] A total of 263 women completed an additional 197.7 woman-years of follow-up. There was one pregnancy, giving a failure rate of 0.51% (95% confidence interval 0.01 - 2.82). The etonogestrel implant was also evaluated for an additional year by measuring serum etonogestrel levels. The median and range of etonogestrel levels were 188.8 pg/ml (63.8 - 806.6) at 3 years of use, and 177.0 pg/ ml (67.9 - 470.5) at 4 years. Etonogestrel levels were unrelated to body mass index. This supplements a previous clinical study of the etonogestrel implant beyond 3 years of use.[4] The situation with the Mirena is interesting in that it contains 52 mg of levonorgestrel. Initially the release rate of levonorgestrel is ~20 µg/d, declining to ~10 µg/d at the end of its 5-year lifespan. The Skyla/Jaydess contains 13.5 mg of levonorgestrel, which is initially released at the rate of ~10 µg/d, declining to ~5 µg/d at the end of its 3-year lifespan. In the USA the Skyla is promoted as a ‘low-dose’ IUS for women and healthcare providers who think that the Mirena is capable of producing side-effects such as weight gain, depression, mood swings, acne and fluid retention. In reality, its narrow presenting diameter allows it to negotiate the nulliparous cervix easily and its

286

smaller frame fits the smaller nulliparous uterine cavity.[5] If the Skyla IUS remains effective at a release rate of 5 µg/d, it is logical to assume that the Mirena would as well. This suggests that the Mirena may be fully effective well beyond its current 5-year lifespan. The good news is that women who delay or fail to return for follow-up are likely to be protected against pregnancy for a considerable time, and that if they desire a pregnancy they will present for removal of the device.

The dilemma remains for the clinician who sees users who return timeously. She/he is trapped between the Scylla of wanting to save the patient or the third-party payer a substantial sum of money, and the Charybdis of complying with the licence specifics of the product.

How do we explain to our method users that the lifespan of these products is really fairly arbitrary, and that the manufacturer evaluates safety and efficacy for a certain timespan that seems reasonable? The process of testing to find the near limit of any medical products utility would be time consuming, expensive and unethical. When independent evidence emerges that a product lifespan is indeed longer than the licence dictates, manufacturers rarely go to the expense of getting a new licence, especially if it is against their financial interests. Wu and Pickle[2] provide some controversial guidelines for the extended use of IUCDs. In the end, as always, clinicians have to use their clinical judgement. We should replace the device for users who seem concerned, and support users who request extended use either because they have heard about it elsewhere or because it is suggested to them. Some will be natural candidates for extended use, either because they are older and have declining fertility or because they are considering the use of another method or sterilisation.

While existing manufacturers are unlikely to make changes to their existing products, if the experience of the copper-based IUCDs over the past 40 years is repeated, new and generic manufacturers will use these new data in order to capture market share. Cheaper and longeracting hormonal LARC methods are on the way.

Norman David Goldstuck Department of Obstetrics and Gynaecology, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Hospital, Cape Town, South Africa Corresponding author: N D Goldstuck (nahumzh@yahoo.com) 1. Winner B, Peipert J, Qiuhong Zhao MS, et al. Effectiveness of long-acting reversible contraception. N Engl J Med 2012;366(21):1998-2007. [http://dx.doi.org/10.1056/NEJMoa1110855].

2. Wu J, Pickle S. Extended use of the intrauterine device: A literature review and recommendations for clinical practice. Contraception 2014;89(6):495-501. [http://dx.doi.org/10.1016/j.contra­ ception.2014.02.011] 3. McNicholas C, Maddipati R, Qiuhong Zhao MS, Swor E, Peipert JF. Use of the etonogestrel implant and levonorgestrel intrauterine device beyond the U.S. Food and Drug Administration-approved duration.

Obstet Gynecol 2015;125(3):599-604. [http://dx.doi.org/10.1097/AOG.0000000000000690] 4. Affandi B, Korver T, Paul-Guerts TB, Bennink HJT. A pilot study with a single rod implant (Implanon®1) in 200 Indonesian women treated for 4 years. Contraception 1999;59(3):167-174.

5. Steyn PS, Goldstuck ND. Contraceptive needs of the adolescent. Best Pract Res Clin Obstet Gynaecol 2014;28(6);891-901. [http://dx.doi.org/10.1016/j.bpobgyn.2014.04.012]

S Afr Med J 2015;105(4):286. DOI:10.7196/SAMJ.9480

April 2015, Vol. 105, No. 4

RESEARCH

Maternal death and caesarean section in South Africa: Results from the 2011 - 2013 Saving Mothers Report of the National Committee for Confidential Enquiries into Maternal Deaths G S Gebhardt,1MB ChB, MSc (Med Sci), MMed (O&G), FCOG (SA); S Fawcus,2 MA, MB BCh, FRCOG; J Moodley,3 MB ChB, FCOG, FRCOG, MD; Z Farina,4 MB ChB, DA (SA), FCA (SA); for the National Committee for Confidential Enquiries into Maternal Deaths in South Africa Department of Obstetrics and Gynaecology, Faculty of Medicine and Health Sciences, Stellenbosch University and Tygerberg Hospital, Tygerberg, Cape Town, South Africa 2 Department of Obstetrics and Gynaecology, Faculty of Health Sciences, University of Cape Town and Mowbray Hospital, Cape Town, South Africa 3 Department of Obstetrics and Gynaecology, Nelson Mandela School of Medicine, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa 4 Department of Anaesthesia, Nelson Mandela School of Medicine, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa, and Greyâ&#x20AC;&#x2122;s Hospital, Pietermaritzburg, South Africa 1

Corresponding author: S Gebhardt (gsgeb@sun.ac.za)

Background. In the latest (2011 - 2013) Saving Mothers report, the National Committee for Confidential Enquiries into Maternal Deaths in South Africa (SA) (NCCEMD) highlights the large number of maternal deaths associated with caesarean section (CS). The risk of a woman dying as a result of CS during the past triennium was almost three times that for vaginal delivery. Of all the mothers who died during or after a CS, 3.4% died during the procedure and 14.5% from haemorrhage afterwards. Including all cases of death from obstetric haemorrhage where a CS was done, there were 5.5 deaths from haemorrhage for every 10 000 CSs performed.

Objective. To scrutinise the contribution or effect of the surgical procedure on the ultimate cause of death by a cross-cutting analysis of the 2011 - 2013 national data.

Methods. Data from the 2011 - 2013 triennial review were entered into an Excel database and analysed on a national and provincial basis.

Results. There were 1 243 maternal deaths where a CS was the mode of delivery and 1 471 deaths after vaginal delivery. More mothers died as a result of CS in the provinces where there is a low overall CS rate. The following CS categories were identified as specific problems: bleeding during or after CS, pre-eclampsia and eclampsia, anaesthesia-related deaths, pregnancy-related sepsis and acute collapse and embolism.

Conclusion. This is an area of concern, and a concentrated effort should be done to make CS in SA safer. Several recommendations are made to this effect.

S Afr Med J 2015;105(4):287-291. DOI:10.7196/SAMJ.9351

Worldwide, haemorrhage during pregnancy remains the most important cause of maternal death.[1] As there are established practices and protocols to manage antepartum and postpartum haemorrhage (PPH), failure to reduce deaths may in part be attributed to a rise in caesarean section (CS) rates with its increased surgical risks for bleeding. Major obstetric intervention by skilled healthcare workers should reduce maternal deaths.[2] The National Committee for Confidential Enquiries into Maternal Deaths in South Africa (SA) (NCCEMD) has published triennial reports of maternal deaths[3] since its inception in 1998. In the previous report, concern was raised about the increasing rate of haemorrhage during and after CS.[4] An extensive campaign to reduce these deaths was launched, with increased awareness, training and protocols.[5] A monograph on management of PPH[6] as well as a manual of recommended techniques for safe CS[7] were also produced. Despite this, in the latest report[8] the NCCEMD again highlights the alarming rate of maternal deaths associated with CS. The most serious issue identified remains bleeding during or after

287

CS. Of all the deaths during or after a CS, one-third were due to hypovolaemic shock (as a final cause).

The risk of a woman dying during the past triennium as a result of CS was almost three times that for vaginal delivery: the case fatality rate (CFR), expressed as the number of deaths per 10 000 causally related to mode of delivery, was 2.8 times higher for operative delivery (6.7/10 000 for vaginal births and 18.9/10Â 000 for CS).

There are limitations in using fatality rates for CS, as it is difficult to separate the inherent risk of the condition for which the surgery was done (such as eclampsia or life-threatening bleeding from placenta praevia) from the risk associated with the procedure itself (surgical, anaesthesia or postoperative care). During 2011 - 2013, of all the CSs performed in public sector facilities, 35% took place at district hospitals, 40% at regional hospitals and 25% at tertiary or central hospitals, which is similar to previous years.

Of the 1 243 mothers who died during or after a CS, 42 (3.4% of all CS deaths) died as a result of bleeding problems during the procedure, and 180 (14.5% of all CS deaths) from haemorrhage following the procedure. Including all other cases of death from

April 2015, Vol. 105, No. 4

RESEARCH

Objectives

The triennial data are analysed and organised into categories according to the major causes of maternal deaths; each category is reviewed by an expert in the field. As there were CS deliveries in all these separate clusters, the aim of this cross-cutting analysis of the 2011 - 2013 national data was to scrutinise the contribution or effect of the surgical procedure on the ultimate cause of death.

70 60 50

Deliveries* CS rate

20 10 0

g

n te

u Ga

po

Lim

e

e

po

N

KZ

rn ste

Ea

p Ca

rn ste

e W

p Ca

th or

m

M

t

a

ng

ala

pu

es W

ee Fr

N

e at St

e

n er

p Ca

rth

No

Fig. 1. CS rates per province (%), 2011 - 2013, with the total number of deliveries (*deliveries presented as total number × 10 000).

35

Results

30 25

%

There were 2 831 066 deliveries in SA during the past triennium (2011 - 2013), of which 655 686 were by CS, amounting to a national CS rate of 23.1%. There were 1 243 maternal deaths where a CS was the mode of delivery and 1 471 deaths after vaginal delivery. Most deliveries took place in Gauteng Province, and most CSs (in terms of actual numbers) were done in KwaZulu-Natal Province (KZN).

There was a striking difference in CS rates between the provinces, with the highest CS rate (28.8%) in KZN and the lowest (15.4%) in Limpopo (Fig. 1).

The CS CFR compared with the number of CS deaths per province is shown in Table 1. There were five provinces (Eastern Cape, Free State, North West, Mpumalanga and Limpopo) in which the CFR was higher than the national average.

When the CS rate for each province was compared with its CFR from CS, more mothers died from CS in the provinces with a low overall CS rate. The provinces with a CS rate of >23% all had a CS CFR of <20, and those with a CS rate of <17% had the worst CFR (Fig. 2). The negative correlation between the CS rate and the CFR is shown in Fig. 3.

Table 2 shows the relationship between primary obstetric cause of death and route of delivery, and includes those patients undelivered at time of death. It includes the delivery type-specific CFR and separates

40 30

Methods

Data from the completed 2011 - 2013 triennial review were entered into an Excel database and analysed on a national and provincial basis. Data are anonymous and collected as part of the NCCEMD process.

Permission to publish the information was obtained from the National Department of Health.

As a final cause of death, hypovolaemic shock was associated with one-third of all CS deaths; this risk was almost five times higher than for vaginal delivery. Likewise, the risk of dying from acute collapse due to embolism was 4.5 times increased after CS.

patients identified as bleeding during or after CS (BDACS) from the overall haemorrhage group to show its rank in terms of the other deaths (sorted in descending order).

It also shows the relative risk (RR) of dying according to type of delivery.

%

obstetric haemorrhage (e.g. abruptio placen­ tae and placenta praevia) where a CS was done (N=363), the haemorrhage CFR equates to 5.5 deaths from haemorrhage for every 10 000 CSs performed.

20 15

CFR CS rate

10 5 0 g

n te

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po

Lim

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po

N

KZ

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Ea

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rn ste

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No

rth

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Fig. 2. Comparison of CS rate (%) and CFR (/10 000 CSs) from CS per province, 2011 - 2013.

Table 1. Comparison of CS deaths per province, 2011 - 2013, proportion of the total deaths in each province, and CFRs Province

Deaths during or after CS, n

Proportion of total deaths for the province, %

CFR, /10 000 CSs

Western Cape

73

34.1

10.1

Gauteng

253

29.8

16.4

KZN

273

28.3

16.4

Northern Cape

20

18.2

16.5

South Africa

1 243

27.9

18.9

Eastern Cape

174

29.3

19.5

Free State

74

26.3

21.6

North West

71

24.3

23.5

Mpumalanga

117

29.3

30.5

Limpopo

188

25.1

31.9

288

April 2015, Vol. 105, No. 4

RESEARCH

As can be deduced from the data in Table 2, death of patients with CS as route of delivery was a specific problem in the following categories: • Bleeding during or after CS

• Pre-eclampsia and eclampsia (six times increased risk of dying) • Anaesthesia-related deaths • Pregnancy-related sepsis (three times increased risk)

35

Even though the indication for the CS may have been an attempt to save a life, this is an area of concern and a concentrated effort is necessary to make these CSs safer.

Bleeding during or after CS

30 CFRs, /10 000 CSs

• Acute collapse and embolism (combined, a five times increased risk).

25 20

CFR

15

Log. (CFR)

10 5 0 0

5

10

15

20

25

30

CS rates, %

Fig. 3. Graphical presentation of negative correlation between CS rates (%) and CFRs (/10 000 CSs) in provinces, 2011 - 2013.

BDACS was linked to 222 deaths in 2011 2013. In previous reports it was linked to 78 deaths in 2002 - 2004, 141 deaths in 2005 2007, and 180 deaths in 2008 - 2010. Since the 2008 - 2010 report, the category ‘other uterine trauma’ (which was used in previous years, and was a composite of bleeding with CS as well as vaginal/cervical trauma) was changed so that BDACS is measured separately. This category excludes deaths from haemorrhage attributed to other pathology (placenta praevia, abruptio placentae, cervical tears, bowel perforation during CS, etc.) of patients also delivered by CS. There may be some

Table 2. Relationship between primary obstetric cause of death and route of delivery Vaginal deliveries, n

CFR for vaginal delivery only, /10 000 vaginal deliveries

CSs, n

CFR for CS delivery only, /10 000 CSs

Non-pregnancy-related infections

646

2.9

166

2.5

Hypertension

RR (for CS delivery, if RR for vaginal delivery = 1)

Primary obstetric cause of death 154

0.7

272

4.1

5.9

Pre-eclampsia

39

0.18

68

1

5.8

Eclampsia

78

0.36

146

2.2

6.2

HELLP syndrome

27

0.4

44

0.67

1.6

Medical and surgical disorders

165

0.76

125

1.9

2.5

Obstetric haemorrhage (excludes BDACS)

250

1.1

147

2.2

1.9

Pregnancy-related sepsis

112

0.5

100

1.5

2.96

222

3.3

Miscarriage

6

0.027

1

0.01

Unknown

72

0.3

41

0.6

Coincidental cause

14

0.06

20

0.03

Anaesthetic complications

5

0.02

79

1.2

Embolism

23

0.1

44

0.6

6.3

Acute collapse – cause unknown

24

0.1

27

0.4

3.7

Bleeding – CS (BDACS)

Final cause of death Circulatory system

486

567

Hypovolaemic shock

279

407

Septic shock

207

160

Respiratory failure

595

282

Cardiac failure

298

363

Pulmonary oedema

113

133

Cardiac arrest

185

230

38

52

Acute collapse due to embolism

289

April 2015, Vol. 105, No. 4

4.8

4.5

RESEARCH

• Referral for post-CS bleeding was arranged, rather than a relook laparotomy.

• Internal bleeding was common in post-CS bleeding deaths, but there was a delay in recognition.

• Poor use of uterine compression sutures, balloon tamponade and uterine tourniquets.

• Hospital managers should ensure that a continuous stock of emergency blood and freeze-dried plasma be available at district hospitals.

• Implement the use of standard protocols for the use of uterotonics for prevention and/or management of bleeding after CS. • Training to focus on problem recognition and skills training of doctors performing CS, and anaesthetics for obstetric patients at district hospitals.

• Women with abnormal vital signs after CS should not leave the recovery area and should not be transferred to a postnatal ward in an unstable condition; a doctor should come and assess such a patient immediately.

• There should be a clear plan for regular planned reassessment of at-risk women who are deemed suitable for transfer to the postoperative ward, and written instructions should be sent to the ward with regard to targets at which earlier medical review should be requested.

• All women with blood loss after CS need to be resuscitated immediately and a doctor called to assess them, with immediate return to theatre if response to uterotonics is poor.

• Direct telephonic links should be provided for 24-hour specialist support to district hospital doctors.

• Emergency transport to be onsite for transfers from district hospitals.

• Essential skill competencies to include: district hospitals – safe CS, safe anaesthesia, balloon tamponade, uterine compression sutures and uterine tourniquet; and regional/tertiary hospitals – all the above plus hysterectomy.

• For second-stage CS, with the head impacted in the pelvis, the risk of lateral tears and blood loss is lower with the reverse breech extraction method of delivery of the baby.[9]

Anaesthesia deaths and frequency of CS

The percentages of women dying from anaesthetic complications per province, and the CS rate per province, are shown in Fig. 4. It can again be deduced that the anaesthetic death rate is negatively correlated with the CS rate – the risk of dying from anaesthetic complications is higher when the CS rate is lower. Most deaths arising from complications from anaesthesia were in Limpopo, Mpumalanga and the Eastern Cape.

The deaths from haemorrhage in particular reveal the issue of poor interaction with the surgical and anaesthetic teams, where volumes of blood loss, severity of hypotension and degree of compromise of the patient were not appreciated across the entire surgical team. Patients were transferred to the ward from the recovery room in a compromised state with no clear plan of monitoring or intervention.

Discussion and recommendations

Based on the data, the following recommendations are made: A. To reduce deaths from bleeding during or after CS: • Prevent anaemia, prolonged labour and second-stage CS as far as possible.

35 30 25 20

CS rate

%

overlap, as death from an atonic uterus during CS may be classified under atony or under BDACS. The BDACS group is (in terms of numbers) as important a cause of death as pregnancy-related sepsis.

There were 363 deaths associated with haemorrhage and CS, of which 222 were directly associated with the procedure; a further 54 CS-related deaths in the haemorrhage group were attributed to abruptio placentae and 26 to complications arising from placenta praevia or placenta accreta. A total of 110 deaths (for any method of delivery) were attributed to abruptio placentae, with the risk of dying from abruptio placentae being relatively low (1/25 736 deliveries), but more than eight times increased when abruptio placentae was managed with a CS (RR 8.8; 95% confidence interval 5.5 - 13; p<0.0001).

Deaths were assessed as clearly avoidable in 70% of cases of bleeding during CS and in 72% of cases of bleeding after CS; only 1.8% of women who died were assessed as having no suboptimal care. The greatest problem was at district hospital level.

The following themes arose from the folder assessments of the BDACS cases: • The source of the BDACS was not always specified in the patient folder, i.e. whether it was due to uterine atony, traumatic extension of uterine incision or tears, or placental site bleeding.

• Many women died in the ambulance before during or after referral. This reflected reluctance to perform necessary surgery at the district hospitals (due to lack of sufficient blood products and lack of surgical competence), but also ambulance delays.

• Better monitoring by nurses was observed compared with previous years, but there was poor response to deteriorating vital signs by nurses and doctors, and the latter frequently gave telephonic advice rather than assessing the patient. Colour-coded early-warning charts were not found in the folders.

• Poor use of uterotonics, especially ergometrine to prevent and treat uterine atony at CS • Poor surgical skills at initial CS • Poor interaction between the surgical and anaesthetic teams at all stages of the operative process: • Preoperative evaluation of the patient and anticipation of potential problems • Communication during the surgical procedure with regard to changes in the condition of the patient and the operative situation • Postoperative management and care plans.

15

% of deaths Log. (CS rate)

10

Log. (% of deaths) 5 0 po

M

a

ng

po

Lim

pu

m

ala

ste

Ea

e

p Ca rn

N

KZ

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No

Fig. 4. Percentage of women dying from anaesthetic complications per province, and CS rate (%) per province. A logarithmic trend line was added.

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RESEARCH

B. To reduce deaths from CS in hypertensive conditions: • All women with eclampsia, irrespective of type, must be managed at regional/tertiary levels of care. Aim for a vaginal delivery as far as possible.

• Eclamptic women with a Glasgow Coma Score (GCS) of 13 - 15/15 generally do well, and if a CS is required, regional anaesthesia can be considered as long as: • This is carried out by an experienced anaesthetist or supervised by such a person • The high blood pressure is stabilised (with several readings) prior to anaesthesia • There is no coagulation problem, the platelet count is >70 × 109/L, and there is no evidence (clinical or biochemical) of the haemolysis/ elevated liver enzymes/low platelets (HELLP) syndrome • Preventive measures are taken against PPH and the patient is observed after the procedure in a high-care bed or one dedicated for this purpose for at least 24 hours after the initiation of magnesium sulphate.

• In the case of eclamptic women with a GCS of 10 - 12/15, if a CS is required, this should be done under general anaesthesia by an experienced anaesthetist or under his/her supervision.

• The oedematous eclamptic may have a swollen airway. In addition, if such patients have an elevated serum urate level, they may be in danger of pulmonary oedema. Careful attention must be given to fluid balance management.

• The restless eclamptic – these patients may be hypoxic and/or have cerebral oedema.

• Strong consideration must be given to ventilate such patients (oedematous or restless eclamptics) for at least 24 hours follow­ ing delivery.

• Patients with a GCS ≤9 should be ventilated for at least 24 hours after the procedure.

• The pressor response to intubation can be exacerbated in preeclamptic patients. High blood pressure should be controlled, even in the operating theatre before intubation. An expert familiar with the use of agents (such as magnesium sulphate and alfentanil) to facilitate safe intubation should be contacted.

• Post-delivery care is mandatory in all pre-eclamptics, and a stepwise decrease in the dosage of antihypertensives may prevent readmission due to hypertensive complications.

• All CSs should be performed by experienced persons and steps taken to minimise bleeding.

Administer prophylactic antibiotics (a first-generation cephalosporin, e.g. 1 g cefazolin intravenously (IV)) to EVERY woman who has a CS, whether elective or emergency. Administer 30 - 60 minutes before surgery (as premedication). For women with severe penicillin allergy, clindamycin or erythromycin can be used instead.

• Give a higher dose (2 g) when the BMI is >30 (or the patient weighs >100 kg).[12] • Although there is no good evidence from randomised trials, the following women may benefit from a prolonged course (3 days) of antibiotics (e.g. ampicillin 2 g 6-hourly, gentamycin 240 mg IV daily, and metronidazole 400 mg 8-hourly orally): • HIV-positive patients • Blood transfusion during surgery • Blood loss >1 000 mL during surgery • Second-stage emergency CS • Prolonged (>12 hours) rupture of membranes • >5 vaginal examinations during labour • When a birth attendant had to push up the head vaginally during difficult delivery of the head.

• Anticipate difficult surgery (specifically two or more previous CSs, BMI >40, previous CS with septic wound, second-stage CS) and request the most experienced surgeon to operate. Do a longitudinal abdominal incision for CS in patients with two or more previous Pfannenstiel incisions, especially for an emergency CS, to prevent accidental bowel or bladder injury.

C. To reduce deaths from acute collapse and embolism following CS: • Measure the body mass index (BMI, kg/m2) at booking. Women with a booking BMI of ≥40 should preferably be managed at a specialist/ regional hospital level owing to the increased risk of thrombosis, diabetes, macrosomic babies, difficult CS (both anaesthesia and surgery) and PPH. Women with a booking BMI of ≥50 should preferably deliver at a tertiary hospital owing to increased anaesthetic risks, including difficult airway and postoperative difficulty in breathing.

• The Saving Mothers report of 2005 - 2007[10] included protocols on the risk stratification of pregnant women for thromboembolism.

This (or Green-top Guideline No. 37a from the Royal College of Obstetricians and Gynaecologists[11]) should be used to identify women at risk of thromboembolism, and provide effective thromboprophylaxis until 7 days after delivery.

1. Say L, Chou D, Gemmill A, Tunçalp Ö, et al. Global causes of maternal death: A WHO systematic analysis. Lancet Glob Health 2014;2(6):e323-e333. [http://dx.doi.org/10.1016/S2214109X(14)70227-X] 2. Weil O, Fernandez H. Is safe motherhood an orphan initiative? Lancet 1999;354(9182):940-943. [http://dx.doi.org/10.1016/S0140-6736(99)02369-7] 3. Moodley J, Pattinson RC, Fawcus S, et al. The confidential enquiry into maternal deaths in South Africa: A case study. BJOG 2014;121(Suppl 4):53-60. [http://dx.doi.org/10.1111/1471-0528.12869] 4. Pattinson RC, ed. Saving Mothers: Fifth Report on Confidential Enquiries into Maternal Deaths in South Africa 2008 - 2010. Pretoria: National Department of Health, 2012.

5. Fawcus S, Moodley J. Haemorrhage associated with caesarean section in South Africa – be aware. S Afr Med J 2011;101(5):306,308-309.

6. Fawcus S, Moodley J. A Monograph of the Management of Postpartum Haemorrhage. Pretoria: Department of Health, 2011.

7. Moodley J, ed., National Department of Health. A Monograph on Caesarean Section. Pretoria: Department of Health, 2013.

8. Pattinson RC, ed. Saving Mothers 2011-2013: The Sixth Report of the National Committee for Confidential Enquiries into Maternal Deaths in South Africa. Pretoria: Government Printer, 2014.

9. Berhan Y, Berhan A. A meta-analysis of reverse breech extraction to deliver a deeply impacted head during cesarean delivery. Int J Gynaecol Obstet 2014;124(2):99-105. [http://dx.doi.org/10.1016/j. ijgo.2013.08.014] 10. Pattinson RC, ed. Saving Mothers: Fourth Report on Confidential Enquiries into Maternal Deaths in South Africa 2005 - 2007. Pretoria: National Department of Health, 2010.

11. Royal College of Obstetricians and Gynaecologists. Thrombosis and Embolism during Pregnancy and the Puerperium, Reducing the Risk (Green-top Guideline No. 37a). London: RCOG, 2010. https:// www.rcog.org.uk/en/guidelines-research-services/guidelines/gtg37a/ (assessed 5 January 2015).

12. American College of Obstetricians and Gynecologists. Use of prophylactic antibiotics in labor and delivery. Practice Bulletin No. 120. Obstet Gynecol 2011;117(6):1472-1483. [http://dx.doi.org/10.1097/ aog.0b013e3182238c31

D. To reduce deaths from post-CS sepsis: • Adhere to the accepted antisepsis strategies during surgery.

• Use the World Health Organization surgical safety checklist (maternity version) as published in the 5th Saving Mothers report.[4]

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Conclusion

The inverse relationship between CS deaths and the CS rate in specific provinces could be attributed to a variety of reasons, including lack of easy access to safe CS, long waiting times to get to theatre and retention of skills when a reasonable CS rate is maintained. What it does argue is that doing more CSs does not necessarily lead to more surgically related deaths.

A concentrated effort should be made by everyone involved in all the various aspects of surgical delivery to decrease the number of deaths associated with the procedure. Medical students are illequipped to do surgery after graduation, yet they are expected to do a major invasive procedure in women with complex, altered physiology where complications that can challenge even a highly skilled doctor can arise within seconds. Could CS skills training not be incorporated into the undergraduate medical curriculum?

References

Accepted 15 January 2015.

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Utility of the Robson Ten Group Classification System to determine appropriateness of caesarean section at a rural regional hospital in KwaZulu-Natal, South Africa V Makhanya,1 MB ChB; L Govender,1 MB ChB, FCOG; J Moodley,1,2 MB ChB, FRCOG, FCOG, MD epartment of Obstetrics and Gynaecology, Nelson Mandela School of Medicine, College of Health Sciences, University of KwaZulu-Natal, D Durban, South Africa 2 Womenâ&#x20AC;&#x2122;s Health and HIV Research Group, Department of Obstetrics and Gynaecology, Nelson Mandela School of Medicine, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa 1

Corresponding author: V Makhanya (vuyo.makhanya@ymail.com)

Background. High caesarean section (CS) rates are not only costly but associated with significant perinatal and maternal morbidity and mortality. It has recently been suggested that structured auditing of CSs may identify those groups in the obstetric population that contribute substantially to the high rates and for which focused interventions may bring about change.

Objective. To evaluate the utility of the Robson Ten Group Classification System (RTGCS) in determining appropriateness of CS at a regional rural hospital in KwaZulu-Natal Province, South Africa.

Methods. A retrospective review of the hospital records of women delivered by CS over a 3-month period was performed. The RTGCS was used to categorise women according to parity, age, past obstetric history, singleton or multiple pregnancy, fetal presentation, gestational age and mode of onset of labour/delivery.

Results. There were 2 553 hospital births over the 3-month study period. The CS rate was 42.4% (1 082/2 553). According to the RTGCS, groups 1 (n=296, 27.4%), 5 (n=186, 17.2%) and 10 (n=253, 23.4%) were substantial contributors to the overall CS rate. The main indications for CS were fetal distress (36.5%) and cephalopelvic disproportion (26.8%).

Conclusion. The RTGCS is a useful tool with which to identify patient groups warranting interventions to reduce high CS rates in a rural regional hospital setting. Group 1 (nullipara: single cephalic term pregnancy; spontaneous labour) warrants the most attention. Applying stricter criteria and due diligence in decision-making for primary CS may decrease the high CS rates.

S Afr Med J 2015;105(4):292-295. DOI:10.7196/SAMJ.9405

Caesarean section (CS) rates continue to increase globally. The current CS rate at our institution (Lower Umfolozi War Memorial District Hospital, KwaZulu-Natal Province (KZN), South Africa (SA)) in a low- and middle-income country (LMIC) approaches 50% (institutional statistics) and has been increasing steadily over time. There is concern about increasing numbers of women with a history of previous CS undergoing CS with subsequent pregnancies. Reducing the CS rate would decrease maternal morbidity without affecting perinatal mortality rates.

Marked differences in CS rates between district, regional and tertiary public sector hospitals in SA have been documented, largely reflecting the effect of high-risk pregnancies on the rate. [1] In a tertiary hospital in Durban, CS rates of >30% have been reported, the explanation being the large numbers of highrisk patients.[2] The World Health Organization (WHO) states that CS rates should be between 10% and 15%.[3] It has been reported that if the CS rate were reduced to 15%, there would be worldwide cost savings of around USD2.32 billion.[4] However, others argue that reasons for CS should be assessed to evaluate whether high rates are appropriate or not, rather than focusing on the rates themselves. [5] Rates can be affected by the population of patients served and the expertise of the attending clinician. Auditing of events prior to CS, indications for CS and outcomes can provide insight into the appropriateness of abdominal deliveries.[5]

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The Robson Ten Group Classification System (RTCGS) is a struc­ tured auditing method that has been used for monitoring CS rates in Europe.[5,6] This ten-category classification system is based on the following obstetric concepts: category of the pregnancy; previous obstetric record; course of labour and delivery; and gestational age.

The system is said to be easily reproducible and is not dependent on whether the population is at low or high risk.[5,6] Although promoted by a Pretoria research group that has reported on the use of RTGCS in urban health facilities,[1,7] our impression is that such auditing methods are limited in rural health facilities in SA.

Objective

To use the RTGCS to identify the leading patient categories contributing to high CS rates in a rural regional hospital.

Methods

This was a retrospective chart review of all patients who had a CS over a 3-month period at Lower Umfolozi War Memorial District Hospital, a regional hospital in northern KZN. Most of the decisions for emergency CS at the study site were made and the procedures carried out by medical officers. Specialist obstetricians performed or supervised those CSs that were expected to be surgically difficult. In general, obstetric management followed that described in the maternity care guidelines of SA.[8] Fetal heart rate monitoring was carried out by intermittent fetal cardiography, and labour management included the use of the partogram (labour graph).[8]

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Institutional ethical approval to conduct the study was obtained (BE: 308/13, Biomedical Research Ethics Committee, University of KwaZulu-Natal).

Data collection followed a structured format and included all relevant clinical information. Data were entered into a computer database using Microsoft Excel software. Windows SPSS version 21 was used for analysis. Results were presented as percentages, means and frequencies.

Results

There were 2 553 deliveries during the study period. The total number of CSs was 1 085; 1 082 files were analysed as three files were missing, giving a CS rate of 42.4%.

Table 1 shows the demographic characteristics of all patients who had a CS, and Table 2 shows RTGCs of all patients who had CSs and the percentage contribution by each group to the overall CS rate.

Table 3 shows the indications for CS per RTGC group. Group 1 was the leading group, with the combination of fetal distress, cephalopelvic disproportion, hypertensive disorders of pregnancy (HDP) and abruptio placentae being the commonest indications.

Group 10 (singleton pregnancies ≤37 weeks’ gestational age) was the second leading group, with the additional indication of failed induction of labour.

RTGC group 5, totalling 186 patients with a scarred uterus, contributed 17.2% to the overall CS rate (Table 4). The majority of

Table 1. Demographic characteristics of the study population Variables Age (years), median, mean (SD), range

24, 25.3 (6.2), 15 - 48

Parity, mean (SD), range

1 (1), 0 - 7

Gestational age (weeks), mean (SD), range

37.5 (3.3), 22 - 43

HIV status Infected (positive), n (%)

377 (38.4)

CD4 count (cells/µL), mean (SD), range

369.8 (198.8), 29 - 1 045

Uninfected (negative), n (%)

690 (63.8)

Result unknown or untested, n (%)

15 (1.4)

SD = standard deviation.

Table 2. RTGC and percentage contribution by each group to the overall CS rate[5,6]

RTGC

n

Contribution to overall CS rate (%)

Group 1. Nullipara: single cephalic term pregnancy*; spontaneous labour

296

27.4

Group 2. Nullipara: single cephalic at term; planned CS or induced labour

85

7.9

Group 3. Multipara without uterine scar: single cephalic at term*; spontaneous labour

164

15.2

Group 4. Multipara without uterine scar: single cephalic term pregnancy*; planned CS or induced labour

66

6.1

Group 5. Multipara with a scarred uterus: single cephalic term pregnancy*

186

17.2

Group 6. Multipara: singleton breech presentation

10

9

Group 7. Multipara: singleton breech presentation (including women with a scarred uterus )

5

5

Group 8. All multiple pregnancies (including women with a scarred uterus)

17

1.6

Group 9. All women with single oblique or transverse pregnancy (including women with a scarred uterus )

0

0

Group 10. All women with a singleton cephalic preterm pregnancy <37 weeks’ gestational age at delivery

253

23.4

*At least 37 completed weeks of pregnancy.

Table 3. Indications for CS as per the RTGCS Indications RTGC group

FD

CPD

Failed IOL

Bx

HDP

Prev. CS

Abruptio

Twin

Total

1

155

130

0

1

6

0

4

0

296

2

44

18

13

1

9

0

0

0

85

3

48

101

13

0

0

0

2

0

164

4

9

31

14

0

7

0

5

0

66

5

0

0

0

0

0

186

0

0

186

6

0

0

0

10

0

0

0

0

10

7

0

0

0

5

0

0

0

0

5

8

0

0

0

0

0

0

0

17

17

9

0

0

0

0

0

0

0

0

0

10

152

12

16

4

22

0

23

24

253

Total

408

292

56

24

44

186

34

38

1 082

FD = fetal distress; IOL = induction of labour; Bx = breech; Abruptio = abruptio placentae.

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Table 4. Indications for CS, categorised as elective and emergency, in RTGC group 5 (N=186) Indications for CS

Table 5. Neonatal and perinatal outcomes, N=1 120 births Outcomes

n (%)

Singleton pregnancies (N=1 044)

Elective CS (N=147) Prev. CS (declined VBAC)

78 (53.1)

Prev. CS × 2

39 (26.5)

Prev. CS × 3

6 (4.1)

Estimated fetal weight >3 500 g

8 (5.4)

HDP

6 (4.1)

Post dates

8 (5.4)

Other

2 (1.4)

Alive, n (%)

1 025 (98.2)

Stillbirths, n (%)

19 (1.8)

eonatal birth weight (g), mean N (SD), range

2 902 (745), 1 120 - 4 980

Twin pregnancies (N=38) Alive

Emergency CS (N=39)

Twin 1

38

Twin 2

36

Stillbirths (fresh stillbirth, twin 2)

2

Fetal distress

11 (28.2)

CPD

17 (43.6)

Abruptio placentae

2 (5.1)

Twin 1

2 270.8 (524.2), 1 140 - 3 350

HDP

6 (15.4)

Twin 2

2 125.5 (545.7), 1 000 - 2 960

Other

eonatal birth weight (g), mean N (SD), range

SD = standard deviation.

3 (7.7)

these CSs were elective (n=147, 79.0%), and of these patients 53.1% qualified for vaginal birth after their previous CS, but declined.

Emergency CSs made a very small proportion of group 5 (n=39, 21.0%). Of the emergency CSs, 43.6% were due to cephalopelvic disproportion (CPD) and 28.2% to fetal distress (Table 4).

Neonatal and perinatal outcomes are shown in Table 5. There were 1 120 births; 1 099 were live births, which included 1 025 singletons and 74 twins. There were 21 stillbirths (1.9%).

Discussion

Our findings show a CS rate of 42.4% over the study period. This is almost three times higher than the 15% recommended by the WHO.[3] However, it is in keeping with the high CS rate of 40.2% reported for the whole of KZN.[9] Our study site was a referral centre for 17 district hospitals and local clinics, and the fact that all high-risk cases were referred to this hospital may explain the high CS rate. It is important to note that we calculated the CS rate for deliveries at the study site alone and not for the entire geographical population within the hospital’s referral area.

In our study, 53.1% of women who qualified for vaginal birth after CS (VBAC) ended up having an elective CS. Offering and carrying out VBAC is one way of decreasing CS rates, especially as a number of studies have shown VBAC success rates of ≥50% without increasing perinatal and maternal morbidity.[10] Our study highlights the fact that RTGC group 5 (repeat CS) contributes significantly to the high CS rates. Our impression is that insufficient counselling for VBAC occurs at the study site, meriting greater emphasis in offering VBAC and counselling all women with a previous CS to consider it if indicated.

The main contributors to the overall CS rate in our study were RTGC group 1 (n=296, 27.4%), group 5 (n=186, 17.2%) and group 10 (n=253, 23.4%). Of note, we found a high CS rate in group 10 (<37 weeks’ gestation), the main indications for CS in this group being fetal distress, HDP and abruptio placentae. The high rate of CS in group 10 could reflect the many complications secondary to hypertension in our population. The indication of CPD is difficult to explain, as these pregnancies were <37 weeks. Further attention needs to be given to group 10 patients, for whom better decision-making may be possible at the hands of more experienced doctors and bettersupervised juniors.

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Studies evaluating CS using the RTGCS in LMICs are very limited.

Suliman et al.[7] reported that groups 1, 3 and 5 were major contributors to CS (15.3%, 9.3% and 83.8%, respectively), accounting for 67.9% of CSs overall. These authors conducted their study in central and eastern Tshwane municipality, which is in an urban area with teaching hospitals.

Group 5 was their biggest contributor to the CS rate (83.5%), which could be explained by the high-risk nature of their patients, among whom there was an overall CS rate of 58.2%.[7] This contrasts with our findings that group 5 contributed only 17.2% to the CS rate, of which 79% were elective CS, and among whom 53.1% qualified for VBAC but ended up with an elective CS. Only 21% of CSs in our group 5 were emergencies, of which 43.6% were due to CPD and 28.2% to fetal distress.

Recently Litorp et al.,[11] whose study was carried out in a large teaching hospital in a major city in Tanzania, reported a CS rate of 27%, with groups 1, 3 and 5 contributing 12%, 12% and 14%, respectively.[11] All the decisions regarding CS involved specialists, in contrast to our study setting where the majority of these decisions were made by non-specialist medical officers.

Our findings are similar to those of the above studies in that RTGC groups 1 and 5 were major contributors to overall CS rates.

Group 1 is amenable to corrective measures during labour. Given the fact that fetal distress and CPD were the major indications for CS in group 1, close attention needs to be given to these factors, possibly ensuring strict criteria for CS and including training on interpretation of fetal cardiotocographic recordings, and proper use and interpretation of partograms. Such measures may be expected to play a role in reducing primary CSs. Furthermore, it is known that in KZN a significant proportion of women giving birth at regional hospitals are under the age of 24 years. As many of these pregnancies are unplanned, there is a clear need to improve contraceptive services, which would result in planned pregnancies and a probable reduction in primary CS rates and subsequent repeat abdominal deliveries.

In group 10, most of the indications for CS were fetal distress, HDP and abruptio placentae. This group must be investigated further, particularly as these findings are not in keeping with those of Suliman et al.[7] and Litorp et al.[11] However, since these authors’ studies were undertaken in urban populations, it is possible that in the rural KZN setting late booking for antenatal care, delayed referral and poor transport systems resulted in a greater number of ‘emergency cases’ requiring CS.

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We found that 106 (9.6%) of the infants born alive were admitted to the neonatal intensive care unit (NICU), compared with the 13.9% reported by Geller et al.[12] Prematurity complicated by birth asphyxia and transient tachypnoea of the newborn was the major indicator for admission. This is in keeping with the large number of preterm babies in group 10, which accounted for 23.4% of our overall CS rate.

Although fetal distress was the leading indication for CS in our study, birth asphyxia was not the leading cause of admissions to the NICU, reflecting either timeous intervention by staff in the labour ward or unwarranted intervention due to lack of definitive diagnostic tests for fetal distress such as fetal scalp pH and lactate levels. A study from Tanzania revealed that many CSs were done on the basis of reliance on the CTG alone to diagnose fetal distress, without ready availability of invasive techniques such as fetal scalp pH and lactate levels to limit false-positive diagnoses.[13] There is also a risk that the habit of easy resort to CS, especially in low-resource settings, may act as a barrier to other more effective improvements in obstetric care.[13] Our results confirm that use of the RTGCS is feasible for auditing CS rates in a rural regional health facility and results in findings different to those in an urban setting, potentially leading to target setting relevant to the local population. This work should encourage local rural health authorities to adopt the RTGCS in an endeavour to reduce high CS rates and improve child and maternal outcomes.

References 1. Pattinson RC. Overview. In: Pattinson RC, ed. Saving Babies 2008-2009. Seventh Perinatal Care Survey of South Africa. Pretoria: Tshepesa Press, 2011.

2. Naidoo R, Moodley J. Rising rates of CSs: An audit of CSs in a specialist private practice. S Afr Fam Pract 2009;51(3):254-258. [http://dx.doi.org/10.1080/20786204.2009.10873857] 3. Villar J, Valladares E, Wojdyla D, et al. Caesarean delivery rates and pregnancy outcomes: The 2005 WHO global survey on maternal and perinatal health in Latin America. Lancet 2005;367(9525):18191829. [http://dx.doi.org/10.1016/S0140-6736(06)68704-7] 4. Gibbons JMB, Lauer JA, Betrán AP, Althabe F. The Global Numbers and Costs of Additionally Needed and Unnecessary Caesarean Sections Performed Per Year: Overuse as a Barrier to Universal Coverage.

Background paper 30. Geneva: World Health Organization, 2010.

5. Robson MS, Scudamore IW, Walsh SM. Using the medical audit cycle to reduce caesarean section rates. Am J Obstet Gynecol 1996;174(1):199-205. [http://dx.doi.org/10.1016/S0002-9378(96)70394-0] 6. Robson MS. Can we reduce the caesarean section rate? Best Pract Res Clin Obstet Gynaecol 2001;15(1):179-194. [http://dx.doi.org/10.1053/beog.2000.0156] 7. Suliman S, Soma-Pillay P, McDonald AP, Pattinson RC. Factors associated with caesarean section using the Robson Ten Group Classification System. Presented at the 29th Priorities in Perinatal Care Conference, Goudini Spa, Western Cape, 9-12 March 2010.

8. National Department of Health. Maternity Care Guidelines in South Africa. 3rd ed. Pretoria: NDoH, 2007.

9. Day C, Monticelli F, Barron P, Haynes R, Smith J, Sello E. District Health Barometer 2008-2009: Health Systems Trust Technical Report. Durban: Health Systems Trust, 2010.

10. Tahseen S, Griffiths M. Vaginal birth after 2 caesarean sections (VBAC-2) – a systematic review with meta-analysis of success rate and adverse outcomes of VBAC-2 versus VBAC-1 and repeat (third) caesarean sections. BJOG 2010;117(1):5-19. [http://dx.doi.org/10.1111/j.1471-0528.2009.02351.x] 11. Litorp H, Kidanto HL, Nystrom L, Darj E, Essén B. Increasing caesarean section rates among low-risk groups: A panel study classifying deliveries according to Robson at a university hospital in Tanzania.

BMC Pregnancy Childbirth 2013;13(107):1-10. [http://dx.doi.org/10.1186/1471-2393-13-107] 12. Geller EJ, Wu JM, Jannelli ML, Nguyen TV, Visco AG. Maternal outcomes associated with planned vaginal versus planned primary caesarean delivery. Am J Perinatol 2010;27(9):675-683. [http://dx.doi. org/10.1055/s-0030-1249765] 13. Maaløe N, Sorensen BL, Onesmo R, Secher NJ, Bygbjerg IC. Prolonged labour as indication for emergency caesarean section: A quality assurance analysis by criterion-based audit at two Tanzanian rural hospitals. BJOG 2012;119(5):605-613. [http://dx.doi.org/10.1111/j.1471-0528.2012.03284.x]

Accepted 2 February 2015.

Office-based sperm concentration: A simplified method for intrauterine insemination therapy D R Franken, PhD Department of Obstetrics and Gynaecology, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa Corresponding author: D R Franken (frankendr@ufs.ac.za)

Background. Intrauterine insemination (IUI) could become preferred to more invasive and expensive techniques of assisted reproduction therapy (ART) and should be offered as the first choice in cases with no female factors and mild male factor subfertility. However, developing countries and especially their rural areas often lack the necessary equipment and laboratory facilities.

Objective. To describe a simplified one-step method to determine the sperm concentration range for IUI therapy.

Methods. Semen samples from 51 sperm donors were used. Following swim-up separation, the sperm concentration of the retrieved motile fraction was counted, as well as progressive motile sperm using a standardised wet preparation. The number of sperm in a 10 µL droplet covered with a 22 × 22 mm coverslip was counted under 400 × total magnification. The observed numbers of retrieved motile sperm were divided into three groups: <40, 40 - 100 and >101 spermatozoa as recorded per intial estimation on the wet preparation.

Results. The mean (standard deviation) estimated sperm concentration for each group compared with actual counts per Neubauer counting chamber were: estimated <40 sperm (n=14), mean 20 (8), Neubauer count 2.5 × 106/mL; estimated 40 - 100 sperm (n=14), mean 71 (15), Neubauer count 16 × 106/mL; and estimated >100 sperm (n=23), Neubauer count 48.3 (21.7) × 106/mL. Conclusion. The results with IUI in male subfertility cases reported by Ombelet et al. in 1995 support the concept of first-line treatment of infertility by three to four cycles of IUI therapy in selected cases.

S Afr Med J 2015;105(4):295-297. DOI:10.7196/SAMJ.8944

Three levels of reproductive healthcare are currently available: (i) a large number of primary centres/clinics performing initial inexpensive diagnostic fertility assessments, including a basic semen analysis; (ii) a smaller number of intermediary practices that offer screening and essential reproductive healthcare treatments; and (iii) tertiary care centres and private institutions providing advanced

295

assisted reproductive technologies in an established academic setting.[1] Treatment for the infertile couple in a First-World setting developed rapidly through access to high-technology procedures and equipment, ready-made culture media and the finest monitoring systems in a controlled environment. However, a very different scenario exists in developing countries where clinicians manage

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Table 1. Comparison between estimated sperm count and Neubauer counting chamber recordings Group 1, estimated count <40 sperm (N=14)

Group 2, estimated count 40 - 100 sperm (N=14)

Group 3, estimated count >101 sperm (N=23)

Estimated count

Neubauer count, × 106/mL

Estimated count

Neubauer count, × 106/mL

Estimated count

Neubauer count, × 106/mL

Mean

20.0

2.5

71

16.0

100.0

48.3

SD

8.0

1.2

15.3

10.4

0.0

21.7

Range

8.0 - 34

1-4

15 - 90

6 - 34

100

21 - 98

Table 2. Semen parameters of andrology referrals classified according to the initial estimated sperm count Estimated count

Neubauer count × 106/mL

Progressive motility

Morphology, % normal

Mean

20.0

2.5

46.8

3.7

SD

8.0

1.2

12.0

2.6

Range

8 - 34

1-4

30 - 65

1-8

Mean

69.6

14.2

48.2

7.9

SD

14.9

9.4

9.7

3.1

Range

40 - 89

6 - 34

40 - 70

3 - 15

Mean

99.6

48.0

58.7

11.1

SD

2.1

22.1

11.1

2.4

Range

90 - 100

21 - 98

40 - 80

7 - 15

Group 1: Estimated count <40 sperm

Group 2: Estimated count 40 - 100 sperm

Group 3: Estimated count >100 sperm

an office-based infertility counselling service. In the rural regions the consulting clinician often has only the most basic equipment available to assist with diagnostic and therapeutic procedures.

As part of a ‘basic fertility’ work-up, a simple semen analysis is therefore mandatory for couples seeking fertility treatment in a developing country.[2] Many cases can be resolved with intrauterine insemination (IUI), as the infertility is often due to treatable reproductive tract infections.[3-5] The interesting question arises as to whether it is possible to simplify the laboratory environment and procedures without substantially compromising the results.[2] In cases where IUI therapy is advised as a first line of treatment, the consulting clinician can determine its feasibility by obtaining the sperm concentration and progressive motility values of the semen sample after a sperm preparation process. Ombelet et al.[6] concluded that >300 × 105 sperm with 10% progressive motility after preparation is sufficient to be used successfully in IUI cycles. The percentage of normal sperm did not play a role during their observations.

This study aimed to develop a simplified method to evaluate the sperm concentration using an office-based microscope to record sperm concentration by estimating the number of sperm on a standardised wet preparation.

Methods

Semen samples from 51 sperm donors were used in the study.

Institutional review board approval was obtained. Following liquefaction, all samples were analysed according to the 2010 World Health Organization (WHO) semen analysis manual.[7] Motile fractions were retrieved from all samples using the direct swimup technique. One ml of semen was placed in a sterile 15 ml conical centrifuge tube and gently layered with 1 ml Ham’s F1-10 culture medium

296

(supplemented with 0.3% g bovine serum albumin). The tube was placed at an angle of 45o at 37oC for 1 hour, after which the uppermost 1 ml of medium, which contains the motile fraction, was removed.

Wet preparations of the motile fractions were prepared by removing a 10 µl aliquot, which was placed onto a clean glass slide and covered with a 22 × 22 mm coverslip. The semen drop was allowed to settle out of suspension for 5 minutes. Motility was recorded as follows: progressive motility – spermatozoa moving actively, either linearly or in a large circle, regardless of speed; non-progressive motility – all other patterns of motility with an absence of progression, e.g. swimming in small circles, the flagellar force hardly displacing the head, or if only a flagellar beat could be observed; and immotile – no movement.

Following the motility evaluation, the sperm concentration was estimated on the same slide under 400 × total magnification according to the WHO guidelines to determine the dilution factor before counting with a Neubauer counting chamber. The semen samples were then diluted and loaded into the Neubauer counting chamber. In cases where >40 - 100 and >100 sperm were observed on the wet preparation, a 1:20 dilution was used, while a 1:2 dilution was used for counts ≤40. The prepared dilutions were loaded onto the two counting chambers on the Neubauer chamber. Both chambers were counted according to WHO guidelines.

The estimated sperm counts and motility values of each sample were subdivided into three groups: <40 sperm (group 1), 40 - 100 sperm (group 2), and >101 sperm (group 3). The estimated counts were compared with the counts recorded with the Neubauer counting chamber.

Results

The mean values (standard deviation (SD)) of the estimated sperm concentration as determined on the wet preparation, and the actual

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sperm concentration per Neubauer counting chamber, are presented in Table 1.

The mean values (SD) of the estimated Neubauer counts, progressive motility and morphology are set out in Table 2. In all three estimated categories, the progressive motility was >30% with mean concentrations >1 × 106/mL.

Discussion

The success and usefulness of ART techniques in treating infertility are well established, but the high cost of ART and lack of health insurance subsidies place a heavy burden on the couple seeking treatment for infertility. The cost of in vitro fertilisation (IVF) and intracytoplasmic sperm injection is significantly higher than the cost of a single ovarian stimulation/IUI cycle.

[4,8] Affordable low-cost office-based infertility treatment has become a field of interest among clinicians.[9] Recent results from a pilot study reported the first pregnancies using a simplified laboratory method for human IVF.[10,11] In the case of unexplained moderate male factor infertility, provided tubal patency has been documented, IUI with the husband’s semen in natural cycles or after clomiphene citrate (CC) stimulation can be promoted as a first-line treatment without major costs or expensive infrastructure.[6,12] The results of IUI in male subfertility cases reported by Ombelet et al.[6] support the concept of first-line treatment, namely three to four cycles of IUI therapy.

The method described allows the consulting clinician to establish the concentration and motility of semen to ascertain whether the sample is adequate to be used in IUI. He or she does not need expensive laboratory equipment, as a microscope, microscope glass slides, coverslips and a micropipette suffice. However, this only holds true in cases where no female factors are present. Estimating the sperm concentration should never be regarded as replacement of the standardised method prescribed in the 2010 WHO manual.[7] The above method is recommended to clinicians in rural areas of developing countries who are confronted by childless couples who are not able to travel to distant fertility centres or cannot afford the expensive treatment that ART typically involves.

The results of this study underline that cost-effective semen analysis is possible. The mean sperm concentrations per Neubauer counting chamber were >1 × 106/mL with progressive motility of >30% in all three estimated categories, indicating that these samples could theoretically be suitable for three to four IUI cycles. In a large retrospective analysis

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of patients with normal ovarian response to CC stimulation, Ombelet et al.[13] showed overall cycle fecundity and a baby take-home rate of 14.6% and 9.9%, respectively, provided the insemination motile concentration of sperm was >1 million. IUI remains successful in cases with <1 million motile spermatozoa, provided the sperm morphology score using strict criteria is ≥4% (cumulative pregnancy rate of 21.9% after three IUI cycles).[13] The development of low-cost ART which is associated with a low complication rate is needed if institutions in developing countries are to be convinced to fund infertility clinics. IVF procedures can be modified to make them affordable. Studies on simplified, low-cost diagnostic procedures and ART techniques are urgently required in a low-cost setting.[14] References 1. Huyser C. Affordable ART services in Africa: Synthesis and adaptation of laboratory services. ESHRE Monographs 2008;2008(1):77-84. [http://dx.doi.org/10.1093/humrep/den139] 2. Ombelet W, Campo R. Affordable IVF for developing countries. Reprod Biomed Online 2007;15(3):257265. [http://dx.doi.org/10.1016/S1472-6483(10)60337-9] 3. Leke RJ. The prevalence of infertility and its preventive measures in sub-Saharan Africa. In: SekaddeKigondu C, Chikamata D, Franken D, eds. Management of Infertility in AFRO & EMRO Countries.

Geneva: World Health Organization, 2002:79-91.

4. Comhaire F. Economic strategies in modern male subfertility treatment. Hum Reprod 1995;10(Suppl 1):103-106. [http://dx.doi.org/10.1093/humrep/10.suppl_1.103] 5. Nygren K, Zegers-Hochschild FZ. Documentation of infertility prevalence, treatment access and treatment outcomes in developing countries. ESHRE Monographs 2008;2008(1):5-7. [http://dx.doi. org/10.1093/humrep/den218] 6. Ombelet W, Puttermans P, Bosman E. Intrauterine insemination: A first-step procedure in the algorithm of male subfertility treatment. Hum Reprod 1995;10(Suppl 1):90-102. [http://dx.doi. org/10.1093/humrep/10.suppl_1.9] 7. World Hwealth Organization. WHO Laboratory Manual for the Examination and Processing of Human Semen. 5th ed. Geneva: WHO, 2010.

8. Peterson CM, Hatasaka HH, Jones KP, et al. Ovulation induction with gonadotropins and intrauterine insemination compared with in vitro fertilization and no therapy: A prospective nonrandomized cohort study and meta-analysis. Fertil Steril 1994;62(3):535-544.

9. Gentis RK, Siebert I, Kruger TF, de Beer ML. Implementation of an office based semen preparation method (SEP-D kit) for intra-uterine insemination (IUI): A controlled randomized study to compare the IUI pregnancy outcome between a routine (swim-up) and SEP-D Kit method. S Afr J Obstet Gynaecol 2012;18(2):54-55.

10. Pilcher H. Fertility on a shoestring. Nature 2006;442:976-977. [http://dx.doi.org/10.1038/442975a] 11. Van Blerkom J, Ombelet W, Klerkx E, et al. First births with a simplified culture system for clinical IVF and embryo transfer. Reprod Biomed Online 2014;28(3):310-320. [http://dx.doi.org/10.1016/j. rbmo.2013.11.012] 12. Ombelet W, Deblaere K, Bosmans E, et al. Semen quality and intrauterine insemination. Reprod Biomed Online 2003;7(4):485-492. [http://dx.doi.org/10.1016/S1472-6483(10)61894-9] 13. Ombelet W, Vandeput H, van de Putte G, et al. Intrauterine insemination after ovarian stimulation with clomiphene citrate: Predictive potential of inseminating motile count and sperm morphology? Hum Reprod 1997;12(7):1458-1463. [http://dx.doi.org/10.1093/humrep/12.7.1458] 14. Ombelet W, Cooke I, Dyer S, Serour G, Devroey P. Infertility and the provision of infertility medical services in developing countries. Hum Reprod Update 2008;14(6):605-621. [http://dx.doi.org/10.1093/ humupd/dmn042]

Accepted 13 February 2015.

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Intrapartum asphyxia and hypoxic ischaemic encephalopathy in a public hospital: Incidence and predictors of poor outcome E K Bruckmann, MB ChB; S Velaphi, MB ChB, FCPaed Department of Paediatrics, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa, and Chris Hani Baragwanath Academic Hospital, Johannesburg Corresponding author: E Bruckmann (eduard.bruckmann@wits.ac.za) Objective. To determine the incidence of asphyxia and hypoxic ischaemic encephalopathy (HIE) and predictors of poor outcome in a hospital in a developing country.

Methods. Neonates of birth weight ≥2 000 g who required bag-and-mask ventilation and were admitted with a primary diagnosis of asphyxia from January to December 2011 were included. Medical records were retrieved and maternal and infant data collected and analysed. Infants who had severe HIE and/or died were compared with those who survived to hospital discharge with no or mild to moderate HIE. Results. There were 21 086 liveborn infants with a birth weight of ≥2 000 g over the study period. The incidence of asphyxia ranged from 8.7 to 15.2/1 000 live births and that of HIE from 8.5 to 13.3/1 000, based on the definition of asphyxia used. In 60% of patients with HIE it was moderate to severe. The overall mortality rate was 7.8%. The mortality rate in infants with moderate and severe HIE was 7.1% and 62.5%, respectively. The odds of severe HIE and/or death were high if the Apgar score was <5 at 10 minutes (odds ratio (OR) 19.1; 95% confidence interval (CI) 5.7 - 66.9) and if there was no spontaneous respiration at 20 minutes (OR 27.2; 95% CI 6.9 - 117.4), a need for adrenaline (OR 81.2; 95% CI 13.2 - 647.7) and a pH of <7 (OR 5.33; 95% CI 1.31 - 25.16). Predictors of poor outcome were Apgar score at 10 minutes (p=0.004), need for adrenaline (p=0.034) and low serum bicarbonate (p=0.028).

Conclusion. The incidence of asphyxia in term and near-term infants is higher than that reported in developed countries. Apgar score at 10 minutes and need for adrenaline remain important factors in predicting poor outcome in infants with asphyxia.

S Afr Med J 2015;105(4):298-303. DOI:10.7196/SAMJ.9140

Asphyxia is defined biochemically as a condition of impaired respiratory gaseous exchange that leads to hypoxaemia, hypercapnia and metabolic acidosis.

Metabolic acidaemia, defined as a base deficit of >12 mmol/L, has been associated with episodes of intrapartum asphyxia and has therefore been used to define asphyxia biochemically.[1] The problem with this definition is that a number of normal babies have metabolic acidosis, and if it is used on its own there is a risk that the incidence of asphyxia may be over­estimated.[2] Clinically, the need for bag-and-mask ventilation (BMV) at birth and/or an Apgar score <7 have been used to define intrapartum asphyxia.[3] Since in many developing countries there are no facilities to do blood gas measurement, base deficit is not used as part of the definition and only the clinical definition is used. Using the clinical definition alone to describe the incidence of asphyxia may also overestimate the incidence, as infants who do not initiate respiration are not always asphyxiated intrapartum. Assessing the incidence of asphyxia using a combination of clinical definition of need for BMV, Apgar score <7 at 5 minutes and metabolic acidaemia (base deficit >12 mmol/L) is therefore more likely to provide information on the true incidence of asphyxia in any population.

Neonates with asphyxia often have ongoing respiratory depression requiring respiratory support in a neonatal intensive care unit (NICU). Where resources are limited, there is competition for these interventions, resulting in rationing and their being offered to infants who are more likely to survive with minimal morbidity. It is therefore important to determine factors that are associated with severe morbidity and mortality, as they could assist in decision-making on who should be offered these limited resources.

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In this study we sought to assess the incidence of asphyxia and hypoxic ischaemic encephalopathy (HIE) according to the presence of signs that define HIE 1, 2 and 3 in Sarnat staging (Table 1),[4] infant characteristics and factors associated with severe HIE and mortality in term and near-term neonates diagnosed with asphyxia in a setting where there is a high patient load and resources are limited.

Methods

Study design. A retrospective, descriptive study of neonates born at term or near term (defined as birth weight ≥2 000 g) and admitted with a diagnosis of asphyxia.

Study setting. Chris Hani Baragwanath Academic Hospital (CHBAH), Johannesburg, South Africa, a public government hospital.

This hospital serves the population of Soweto and the surrounding areas. Until April 2014, it was the only hospital in Soweto. It is also a referral centre for all clinics conducting births in Soweto and surrounding areas. These clinics conduct about 8 000 births per year and the hospital about 23 000 births per year, with a total of just over 30 000 births per year for the cluster. In 2011, the hospital had two operating theatres for obstetric surgery including caesarean sections (CSs), and 12 NICU beds.

Study population. Infants who were born weighing ≥2 000 g, required resuscitation with at least BMV and were admitted with a diagnosis of asphyxia were included. The study period was from 1 January to 31 December 2011. Infants who died in the labour ward soon after birth were excluded, as their records were either missing or had incomplete information. Infants born before arrival to hospital, twins and infants with severe congenital abnormalities were also excluded.

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Table 1. Sarnat and Sarnat[4] classification of HIE

Stage 1

Stage 2

Stage 3

Level of consciousness

Hyperalert

Lethargic or obtunded

Stuporous

Muscle tone

Normal

Mild hypotonia

Flaccid

Posture

Mild distal flexion

Strong distal flexion

Intermittent decerebration

Stretch reflexes

Overactive

Overactive

Decreased or absent

Segmental myoclonus

Present

Present

Absent

Suck

Weak

Weak or absent

Absent

Moro

Strong; low threshold

Weak; incomplete; high threshold

Absent

Oculovestibular

Normal

Overactive

Weak or absent

Tonic neck

Slight

Strong

Absent

Generalised sympathetic

Generalised parasympathetic

Both systems depressed

Pupils

Mydriasis

Miosis

Variable; often unequal; poor light reflex

Heart rate

Tachycardia

Bradycardia

Variable

Bronchial and salivary secretions

Sparse

Profuse

Variable

Gastrointestinal motility

Normal or decreased

Increased; diarrhoea

Variable

Seizures

None

Common; focal or multifocal

Uncommon (excluding decerebration)

Neuromuscular control

Complex reflexes

Autonomic function

Table 2. Incidence of asphyxia according to different definitions of asphyxia (N=21 086 live births) Definition

Infants with asphyxia, n

Incidence /1 000 live births

Need for BMV at birth

321

15.2

BMV + base deficit >12 mmol/L

261

12.4

BMV + Apgar score <7 at 5 min

218

10.3

BMV, Apgar score <7 at 5 min + base deficit >12 mmol/L

183

8.7

Study procedure. Hospital records of new­ born infants who met the inclusion criteria were retrieved and the following data were collected: birth weight, gender, gestational age, growth, Apgar score, resuscitation required, time to spontaneous respiration, arterial blood gas done within the first hour of birth, and the diagnosis of HIE. Maternal records were also reviewed for maternal age, parity, maternal HIV results, antenatal care, maternal disease, mode of delivery, presence of fetal distress or meconium-stained amniotic fluid and cardiotocographic records. Means, standard deviations (SDs), medians and ranges were used to describe continuous variables, while frequencies and percentages were used to describe categorical variables. The χ2 test or Fisher’s exact test and Student’s t-test were used to compare the categorical variables and continuous variables, respectively, between infants with no or mild to moderate HIE and those with severe HIE or who died. Differences between the two groups were considered statistically significant at a p-value of <0.05.

The extent of association of different varia­ bles with severe HIE or death was reported using odds ratios (ORs) and the precision using 95% confidence intervals (CIs). In order to determine predictors of severe HIE or death, variables with p-values <0.05 on the univariate logistic regression were included in the multivariate logistic regression. STATA version 10.0. was used to perform the statistical analysis.

Approval to conduct the study was obtained from the hospital protocol review committee and the University of the Witwatersrand Human Research Ethics Committee.

Results

Incidence of asphyxia

Of a total of 23 035 liveborn infants, 21 086 weighed ≥2 000 g at birth. Of those weighing ≥2 000 g, 357 had a diagnosis of asphyxia, of whom 321 were admitted and 36 died in the labour ward before admission; since records of the latter were either missing or had incomplete information, they were excluded.

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The incidence of asphyxia ranged from 8.7 to 15.2/1 000 deliveries, depending on the definition of asphyxia used (Table 2). Using the definition combining need for BMV, Apgar score <7 at 5 minutes and base deficit >12 mmol/L (representing a truer reflection of intrapartum asphyxia) the incidence was 8.7/1 000 live births, compared with 15.2/1 000 using need for BMV alone.

Maternal characteristics

Demographic and clinical characteristics of mothers giving birth to infants diagnosed with asphyxia are shown in Table 3. Most of the mothers (95.6%) had attended antenatal care. The average maternal age was just over 25 years, and 57.6% were pregnant for the first time. Just over a quarter of mothers (25.9%) were positive for HIV. Among the mothers who had maternal illness recorded, the most common diagnosis was pregnancyinduced hypertension, accounting for 75.9% of mothers with recorded illness and 19.6% of mothers giving birth to infants with a diagnosis of asphyxia. Of babies with asphyxia, 34.3% were born to mothers with meconium-stained amniotic fluid. The mode of delivery was CS in 38.0% of cases, with only 8.7% of deliveries being assisted vaginal deliveries. The most common reason for performing CS in mothers of asphyxiated infants was fetal distress (68.9%) followed by prolonged second stage of labour (7.3%), cephalopelvic disproportion (6.3%) and cord prolapse (4.1%). Electronic monitoring with a

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Table 3. Characteristics of mothers who gave birth to infants with asphyxia (N=321)

Table 4. Characteristics of infants diagnosed with asphyxia (N=321) Variables

Variables Maternal age (years), mean (SD)

25.17 (6.4)

First pregnancies, n (%)

185 (57.6)

Positive HIV test, n (%)

83 (25.9)

Received antenatal care, n (%)

307 (95.6)

Hypertension

63 (19.6) 20 (6.2) 122 (38.0)

Vaginal delivery

171 (43.2)

Assisted vaginal delivery

28 (8.7)

Meconium-stained amniotic fluid, n (%) Documented electronic monitoring during labour (CTG), n (%)

249 (77.6)

No

72 (22.4)

Male

192 (59.8)

Female

129 (40.2)

<5

75 (23.4)

5-7

143 (44.6)

≥7

101 (31.5)

Recorded

233 (72.6)

<5

19/233 (8.2)

5-7

50/233 (21.5)

≥7

164/233 (70.3)

Not recorded, n (%)

88 (27.4)

Resuscitation required, n (%)

Normal CTG in monitored patients, n (%)

132/249 (53)

Abnormal CTG in monitored patients, n (%)

117/249 (47)

Late decelerations

90/117 (76.9)

Early decelerations

8/117 (6.8)

Fetal bradycardia

8/117 (6.8)

Beat-to-beat variability

3/117 (2.6)

Suspicious tracing

8/117 (6.8)

cardiotocograph (CTG) was performed in 77.6% of cases; tracings were normal in 53% and abnormal in 47%. In mothers with an abnormal CTG, the common abnormality was late deceleration (76.9%), followed by early deceleration (6.8%) and fetal bradycardia (6.8%).

Infant characteristics (Table 4)

Apgar scores The average birth weight was 3 084 g and the average gestation 38.5 weeks. Apgar scores were done at 1 and 5 minutes in 99.5% of the infants and at 10 minutes in 72.6%. At 5 minutes 68.0% had an Apgar score of <7. Of infants with a documented Apgar score at 10 minutes, 29.7% had a score of <7.

Resuscitation and time to spontaneous respiration During resuscitation, the majority (89.7%) of infants diagnosed with asphyxia responded to BMV only, while just over 10% required extensive resuscitation in the form of chest compressions (7.2%) and adrenaline (3.1%). Of the infants who had time to spontaneous respiration recorded, 50.0% took >5 minutes to attain spontaneous respiration.

Blood gases All infants were resuscitated with 100% oxygen. The majority of infants had blood gas analysis performed within an hour after delivery. The mean partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2) were 145.6 mmHg and 36.6 mmHg, respectively, suggesting overzealous BMV. Only 24.0% of infants had a pH of <7.00, 57.9% had a PaO2 of >100 mmHg, 53.0%

300

38.5 (2.2)

Apgar score at 10 min, n (%)

110 (34.3)

Yes

Gestational age (weeks), mean (SD)

Apgar score at 5 min, n (%)

Mode of delivery, n (%) CS

3 084 (448)

Gender, n (%)

Maternal illness, n (%) Other medical conditions

Birth weight (g), mean (SD)

BMV only

288 (89.7)

BMV + CC

23 (7.2)

BMV + CC + adrenaline

10 (3.1)

Time to spontaneous breathing (min), n (%) <5

105 (32.7)

5 - 10

89 (27.7)

10 - 20

42 (13.1)

>20

27 (8.4)

Not recorded

58 (18.1)

pH, mean (SD)

7.09 (0.16)

pH <7.00 , n (%)

77 (24.0)

pH 7.00 - 7.25, n (%)

182 (56.7)

pH >7.25, n (%)

38 (11.8)

PaO2 (mmHg), mean (SD)

145.63 (79.92)

PaO2 <50, n (%)

16 (5)

PaO2 50 - 100, n (%)

92 (28.7)

PaO2 >100, n (%) PaCO2 (mmHg), mean (SD)

186 (57.9) 36.66 (16.71)

PaCO2 <35, n (%)

170 (53.0)

PaCO2 35 - 45, n (%)

64 (19.9)

Base deficit (mmol/L), mean (SD)

18.09 (5.26)

Base deficit ≤12, n (%)

35 (10.9)

Base deficit >12, n (%)

261 (81.3)

CC = chest compressions.

had hypocarbia (PaCO2 <35 mmHg), and 81.3% had a base deficit of >12 mmol/L. The lactate level, which is a good indicator of tissue hypoxia, was found to be >7.5 mmol/L in 97.4% of cases in which it was documented.

Incidence of HIE and mortality

The incidence of HIE ranged from 8.5 to 13.3/1 000 live births, depending on the definition of asphyxia used (Table 5). Defining

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asphyxia as an Apgar score of <7 at 5 minutes and base deficit of >12 mmol/L, 179 patients (97.8%) developed signs of HIE (according to Sarnat and Sarnat staging[4]), giving an incidence of 8.5/1 000 live births, compared with 13.3/1 000 live births when asphyxia was defined as need for BMV. Among those who developed HIE, 59.0% had moderate to severe HIE. The overall mortality rate was 7.8%, with the rates in infants with HIE ranging from 8.9% to 12.3%, depending on the definition of asphyxia. Only 1.4% of infants with HIE 1 died, as opposed to 7.1% and 62.5% of those with HIE 2 and 3 respectively, defining asphyxia with inclusion of metabolic acidaemia. There were no deaths among those who did not develop HIE. Sixty-four per cent of the deaths were primarily due to HIE, and 16.0% were due to HIE and meconium aspiration syndrome, with or without persistent pulmonary hypertension of the newborn; 24.0% were due to sepsis. Comorbidities in patients with asphyxia included renal

dysfunction in 31.2%, clinically presumed sepsis in 24.6% and positive blood culture in 13.9%.

Comparison of mild to moderate HIE with severe HIE and/or death

Comparison was made between the above two groups for all patients with asphyxia defined as need for BMV. On univariate analysis, there were no statistically significant differences in maternal charac­ teristics and CTG readings between those with no HIE or mild to moderate HIE compared with those with severe HIE or who died. The infant factors that were associated with poor outcome (severe HIE or death) were low Apgar scores at 5 and 10 minutes, need for adrenaline, delay in time to spontaneous respiration, low pH, high base deficit and low bicarbonate.

The median Apgar score was lower at 5 minutes (4 v. 6; p<0.01) and 10 minutes (5 v. 8; p<0.01), time to spontaneous respi­ ration was longer (15.4 minutes v. 6.2

Table 5. Incidence of HIE and mortality rate in patients with asphyxia, depending on definition used Need for BMV

No HIE

Apgar score <7 + base deficit >12 mmol/L

Total N (%)

Incidence /1 000 live births

Died n (%)

Total N (%)

Incidence /1 000 live births

Died n (%)

40 (12.5)

-

0 (0)

4 (2.2)

-

0 (0)

HIE 1

131 (40.8)

6.2

2 (1.5)

71 (38.8)

3.4

1 (1.4)

HIE 2

122 (38.0)

5.8

7 (5.7)

84 (45.9)

4.0

6 (7.1)

HIE 3

28 (8.7)

1.3

16 (57.1)

24 (13.1)

1.1

15 (62.5)

All HIEs

281 (87.5)

13.3

25 (8.9)

179 (97.8)

8.5

22 (12.3)

minutes; p<0.01), pH was lower (6.9 v. 7.1; p<0.01), base excess was higher (22.8 v.

17.5 mmol/L) and bicarbonate was lower (8.9 v. 11.6 mmol/L) in infants with severe HIE and/or who died compared with those with either no HIE or mild to moderate HIE who survived to hospital discharge (Table 6). Factors showing statistically significant differences in univariate analysis were included in a multivariate analysis to determine factors that could predict severity of HIE or death. Only Apgar score at 10 minutes (p=0.004), need for adrenaline (p=0.034) and bicarbonate levels in the first hour after birth (p=0.02) were found to be predictors of severe HIE and/or death.

Severity of different variables and odds of developing severe HIE or death

The odds of having severe HIE or death increased if the Apgar score at 5 minutes was <5 (OR 9.33; 95% CI 2.83 - 34.03); if the Apgar score at 10 minutes was 5 - 7 (OR 3.05; 95% CI 1.08 - 8.62) or <5 (OR 19.1; 95% CI 5.66 - 66.9) compared with a score of >7; if chest compressions were required (OR 4.51; 95% CI 1.06 - 18.0); if adrenaline was required (OR 81.2; 95% CI 13.2 - 647.7); and if time to spontaneous respiration was >20 minutes (OR 27.2; 95% CI 6.89 - 117.4). When arterial blood gas was measured within the first hour of life, the odds of having severe HIE and/or death were increased if the pH was <7 (OR 5.33; 95% CI 1.31 - 25.16); if the PaO2 was <60 mmHg (OR 9.65; 95% CI 1.87 - 55.12); and if the PaCO2 was >45 mmHg (OR 3.98; 95% CI 1.11 - 15.56) (Table 7).

Table 6. Factors associated with severe HIE or death in infants with asphyxia p-value No HIE or HIE 1 - 2 (N=256)

HIE 3 and/or death (N=37)

Univariate

Multivariate

Median Apgar at 5 min

6

4

<0.001

0.99

Median Apgar at 10 min

8

5

<0.001

0.004

Need for CCs, n (%)

19/256 (7.4)

4/37 (10.8)

0.36

N/A

Need for adrenaline, n (%)

1/256 (0.4)

9/37 (24.3)

<0.001

0.03

Time to spontaneous respiration (min), mean (SD)

6.17 (5.71)

15.36 (11.93)

<0.001

0.69

pH, mean (SD)

7.11 (0.14)

6.92 (0.18)

<0.001

0.54

PaO2 (mmHg), mean (SD)

145.25 (76.00)

148.75 (108.35)

0.82

N/A

PaCO2 (mmHg), mean (SD)

34.94 (13.89)

49.91 (27.69)

<0.001

0.33

Bicarbonate (mmol/L), mean (SD)

11.59 (2.84)

8.91 (2.72)

<0.001

0.03

Base deficit (mmol/L), mean (SD)

17.48 (4.88)

22.74 (5.79)

<0.001

0.30

Lactate (mmol/L), mean (SD)

15.90 (4.34)

18.26 (3.68)

0.008

0.61

Glucose (mmol/L), mean (SD)

6.79 (2.30)

6.93 (4.48)

0.82

N/A

CCs = chest compressions; N/A = not applicable.

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Table 7. ORs for developing severe hypoxic ischaemic encephalopathy and/or death according to severity of different variables Variables

OR (95% CI)

Apgar score at 5 min

>7

Reference

5-7

1.79 (0.50 - 7.01)

<5

9.33 (2.83 - 34.03)

Apgar score at 10 min >7

Reference

5-7

3.05 (1.08 - 8.62)

<5

19.13 (5.66 - 66.89)

Extent of resuscitation BMV only

Reference

CCs

4.51 (1.06 - 17.98)

Adrenaline

81.2 (13.17 - 647.7)

Time to spontaneous respiration (min) <5

Reference

5 - 10

2.18 (0.55 - 9.24)

10 - 20

3.41 (0.74 - 16.20)

>20

27.19 (6.89 - 117.38)

pH >7.25

Reference

7.0 - 7.2

1.48 (0.35 - 7.13)

<7.0

5.33 (1.31 - 25.16)

PaO2 (mmHg) 60 - 100

Reference

>100

2.40 (0.63 - 10.74)

<60

9.65 (1.87 - 55.12)

PaCO2 (mmHg) 35 - 45

Reference

>45

3.98 (1.11 - 15.56)

<35

0.75 (0.19 - 3.07)

CCs = chest compressions.

Discussion

The recent development of induced hypothermia having been reported to reduce the risk of mortality and disability in infants with asphyxia prompted this study to assess the burden of asphyxia (incidence of asphyxia) and the numbers of infants who might require cooling (incidence of moderate to severe HIE) in a setting where there is a high patient load but limited resources. Defining asphyxia as need for BMV, Apgar score <7 at 5 minutes and base deficit >12 mmol/L within an hour after delivery, the incidence of asphyxia was 8.7/1 000 live births. Most studies reporting on the incidence of birth asphyxia in developing countries do not include blood gases, and use only need for assistance with respiration and/or Apgar score <7 at 5 minutes.

Using the definition of need for assistance with breathing or Apgar score <7 at 5 minutes, our incidence of asphyxia was 15.2/1 000 or 10.3/1 000 live births, respectively. Whichever definition is used, the incidence of asphyxia in this study is very high compared with that reported in developed countries (~1 - 5/1 000 live births.[5,6] We did not collect data on modifiable factors that may have contributed to

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this high incidence. A perinatal care survey conducted in South Africa in 2008/9 reported that delay in seeking medical care, inadequate monitoring during labour and lack of facilities were modifiable factors identified in neonates who died from asphyxia.[7] We postulate that these same factors contribute to our high incidence of asphyxia.

The overall incidence of encephalopathy in infants with Apgar scores <7 and base deficit >12 mmol/L was 8.5/1 000 live births, with 60% of cases being due to HIE 2 and 3. The overall incidence reported in this study was higher than the incidences reported from Sweden, a developed country, and Kathmandu in Nepal, a developing country (1.8 and 6.4/1 000 live births, respectively[8.9]), but lower than the 28.1/1 000 reported for Sarlahi, Nepal.[10] It has been reported that of infants diagnosed with HIE, 15 - 20% will die in the neonatal period and 25 - 30% of survivors will develop permanent neurodevelopmental abnormalities including cerebral palsy.[6] In our study, 62% and 7% of infants with HIE 3 and HIE 2, respectively, died before hospital discharge. Some infants with HIE 2 and most of those with HIE 3 who survive to hospital discharge will have a poor neurological outcome.

The high incidence of HIE in this report is a major concern and highlights the need for improvements in the healthcare system to reduce the incidence of asphyxia and HIE. It is also important to treat infants with moderate to severe HIE with induced hypothermia to reduce neurological disability and mortality.

Predictors of severe HIE and/or death were low Apgar score at 10 minutes, need for adrenaline and low bicarbonate. Shah et al.[11] reported similar findings, and that need for chest compressions, high base deficit and delay in onset of respiration beyond 20 minutes in infants with asphyxia were associated with poor outcome; rates of severe adverse effects were 64% if one predictor was present, 76% if two were present and 93% if all three were present. The finding that Apgar score at 10 minutes is a predictor of poor outcome is helpful, as the Apgar score is easy to perform and widely used in labour and delivery rooms in both developed and developing countries. Although the Apgar score has not been helpful in predicting which infants will develop cerebral palsy, especially in the era of induced hypothermia for asphyxia,[12] it has been shown to be very useful in predicting survival in both preterm and term infants. Laptook et al.[13] reported that each point decrease in Apgar score at 10 minutes was associated with a 45% increase in the odds of death or disability, and concluded that Apgar score at 10 minutes provided useful prognostic information before other evaluations are available.

The presence of metabolic acidaemia or low bicarbonate is of additional value to the Apgar score in predicting poor outcome, as the Apgar score is often not done in real time and can therefore be unreliable. A base deficit of >16 mmol/L has previously been reported to be a predictor of poor outcome.[10] Casey et al.[14] also reported that a combination of low Apgar score (0 - 3) and cord pH of <7.0 increased the risk of mortality in both preterm and term infants, whereas Sehdev et al.[15] reported that a base deficit of >16 and a 5-minute Apgar score of <7 together identified 79% of neonates who would develop complications.

Study limitations

The chief limitation of this study is that it is retrospective. The diagnoses of asphyxia and encephalopathy were therefore mainly based on what was recorded in the patient’s hospital file. This may have led to overestimation of the true incidence of HIE, especially as some clinical findings could be affected by the experience of a person conducting the examination, e.g. junior doctors commonly labelling infants with asphyxia as having HIE. Our study nevertheless serves to highlight the burden of asphyxia and encephalopathy at CHBAH, which possibly reflects the incidence in other public sector hospitals in South Africa.

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Conclusion

The incidences of both asphyxia and HIE are very high at CHBAH. As moderate to severe HIE is likely to be associated with abnormal neurodevelopmental outcomes and disability, factors that contribute to a high incidence of asphyxia must be avoided. Infants at risk of developing encephalopathy must be offered neuroprotective treatment, i.e. induced hypothermia.

Where arterial blood gas analysis, NICU facilities and induced hypothermia are not available or are limited, an Apgar score of <5 at 10 minutes and the need for adrenaline can be of assistance in predicting poor outcome.

References 1. Low JA, Lindsay BG, Derrick EJ. Threshold of metabolic acidosis associated with newborn complications. Am J Obstet Gynecol 1997;177(6):1391-1394. [http://dx.doi.org/10.1016/S00029378(97)70080-2] 2. Josten BE, Johnson TR, Nelson JP. Umbilical cord blood pH and Apgar scores as an index of neonatal health. Am J Obstet Gynecol 1987;157(4):843-848. [http://dx.doi.org/10.1016/S0002-9378(87)80069-8] 3. Ersdal HL, Mduma E, Svensen E, Perlman J. Birth asphyxia: A major cause of early neonatal mortality in a Tanzanian rural hospital. Pediatrics 2012;129(5):e1238-e1243. [http://dx.doi.org/10.1542/ peds.2011-3134] 4. Sarnat HB, Sarnat MS. Neonatal encephalopathy following fetal distress: A clinical and electroencephalographic study. Arch Neurol 1976;33(10):696-705. [http://dx.doi.org/10.1001/ archneur.1976.00500100030012] 5. Wu YW, Backstrand KH, Zhao S, Fullerton HJ, Johnston SC. Declining diagnosis of birth asphyxia in California: 1991-2000. Pediatrics 2004;114(6):1584-1590. [http://dx.doi.org/10.1542/peds.2004-0708]

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6. Tomashek KM, Crouse CJ, Iyasu S, Johnson CH, Flowers LM. A comparison of morbidity rates attributable to conditions originating in the perinatal period among newborns discharged from United States hospitals, 1989-90 and 1999-2000. Paediatr Perinat Epidemiol 2006;20(1):24-34. [http://dx.doi. org/10.1111/j.1365-3016.2006.00690.x] 7. Pattinson R, ed. Saving Babies 2008-2009: Seventh Report on Perinatal Care in South Africa. Pretoria: Tshepesa Press, 2011:28.

8. Thornberg E, Thiringer K, Odeback A, Milsom I. Birth asphyxia: Incidence, clinical course and outcome in a Swedish population. Acta Paediatr 1995;84(8):927-932. [http://dx.doi. org/10.1111/j.1651-2227.1995.tb13794.x] 9. Ellis M, Manandhar N, Manandhar DS, Costello AM. Risk factors for neonatal encephalopathy in Kathmandu, Nepal, a developing country: Unmatched case-control study. BMJ 2000;320(7244):12291236. [http://dx.doi.org/10.1136/bmj.320.7244.1229] 10. Lee AC, Mullany LC, Tielsch JM, et al. Incidence of and risk factors for neonatal respiratory depression and encephalopathy in rural Sarlahi, Nepal. Pediatrics 2011;128(4):e915-24 [http://dx.doi.org/10.1542/ peds.2010-3590] 11. Shah PS, Beyene J, To T, Ohlsson A, Perlman M. Postasphyxial hypoxic-ischemic encephalopathy in neonates: Outcome prediction rule within 4 hours of birth. Arch Pediatr Adolesc Med 2006;160(7):729736. [http://dx.doi.org/10.1001/archpedi.160.7.729] 12. Apgar V. A proposal for a new method of evaluation of the newborn infant. Curr Res Anesth Analg 1953;32(4):260-267.

13. Laptook AR, Shankaran S, Ambalavanan N, et al. Outcome of term infants using Apgar scores at 10 minutes following hypoxic-ischemic encephalopathy. Pediatrics 2009;124(6):1619-26 [http://dx.doi. org/10.1542/peds.2009-0934] 14. Casey BM, McIntire DD, Leveno KJ. The continuing value of the Apgar score for the assessment of newborn infants. N Engl J Med 2001;344(7):467-471. [http://dx.doi.org/10.1056/ NEJM200102153440701] 15. Sehdev HM, Stamilio DM, Macones GA, Graham E, Morgan MA. Predictive factors for neonatal morbidity in neonates with an umbilical arterial cord pH less than 7.00. Am J Obstet Gynecol 1997;177(5):1030-1034. [http://dx.doi.org/10.1016/S0002-9378(97)70008-5]

Accepted 13 February 2015.

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Early sexual debut: Voluntary or coerced?

Evidence from longitudinal data in South Africa – the Birth to Twenty Plus study L Richter,1,2 BA, BA Hons, PhD; M Mabaso,2 BSc, BSc Hons, MSc, PhD; J Ramjith,3 BSc, BSc Hons, MSc; S A Norris,1 BSc, BSc Hons, BA Hons, PhD ST-NRF Centre of Excellence in Human Development, University of the Witwatersrand, Johannesburg, South Africa D HIV/AIDS, STIs and TB, Human Sciences Research Council, Durban, South Africa 3 School of Public Health and Family Medicine, Centre for Infectious Disease Epidemiology and Research, University of Cape Town, South Africa 1 2

Corresponding author: L Richter (lrichter@hsrc.ac.za)

Background. Early sexual debut, voluntary or coerced, increases risks to sexual and reproductive health. Sexual coercion is increasingly receiving attention as an important public health issue owing to its association with adverse health and social outcomes.

Objective. To describe voluntary and coerced experience at sexual debut.

Methods. A longitudinal perspective among 2 216 adolescents (1 149 females, 1 067 males) in a birth cohort study in South Africa, analysing data collected on six occasions between 11 and 18 years.

Results. The median age of sexual debut was 16 years for females and 15 for males. Reported coerced sexual debut included children <11 years of age.

Males reported earlier sexual debut, with both voluntary and coerced sexual experience, than females (p<0.0001). Sexual coercion at early sexual debut among both male and female adolescents occurred mostly through sexual intercourse with older adolescents and partners of the same age.

Conclusion. The identified time periods and age groups need to be targeted for interventions to delay sexual debut and prevent sexual coercion among young people. More research is needed to understand underlying predisposing risk factors for sexual coercion at sexual debut, both early and not early.

S Afr Med J 2015;105(4):304-307. DOI:10.7196/SAMJ.8925

Early sexual debut among young women and men (commonly defined as having had first sexual intercourse at or before age 14 years) is associated with risks to sexual and reproductive health. These include risky sexual behaviours such as multiple partners, sex under the influence of alcohol or drugs, unplanned pregnancy and sexually transmitted infections (STIs), including HIV.[1-3] Early sexual debut not only increases risks to sexual and reproductive health but is also associated with experiences of sexual coercion.[4-6] Sexual coercion has been defined as the act of forcing (or attempting to force) another individual, through violence, threats, verbal insistence, deception, cultural expectations or economic circumstances, to engage in sexual behaviour against his or her will.[4,7] Sexual coercion, which is associated with childhood sexual abuse, is increasingly receiving attention as an important public health issue owing to its association with adverse health and social out­ comes.[5-8] Adverse health consequences of sexual coercion among young people have been reported from diverse settings in Latin America, Africa and South Asia; these include self-destructive behaviours such as unprotected sex, non-use of condoms and early non-consensual sexual intercourse.[7-9] In severe cases sexual coercion culminates in prostitution and psychological problems (depression, post-traumatic stress disorder and suicidal ideation), and low self-esteem leading to inability to avoid or refuse unwanted sexual advances and/or negotiate safe sexual behaviours.[9,10] Social outcomes include acceptance of violence, especially towards women, adherence to traditional gender roles such as male dominance, poor educational achievement as a result of withdrawal from school, and inability to build adult partnerships with loss of marriage prospects.[9]

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In many low- and middle-income countries including South Africa (SA), there is evidence that sexual encounters at a young age are frequently coerced.[4,7] Data from nationally representative cross-sectional surveys indicate that the median age of sexual debut in SA is approximately 16 years for males and 17 years for females.[11-13] Data from four rounds of a prospective population-based survey (conducted from 2003 to 2007) in a rural part of KwaZulu-Natal Province among youths 15 years and older found that the median age at first sexual inter­course was 18.5 and 19.2 years for women and men, respectively.[14] How­ever, studies linking early sexual debut and sexual coercion are scant.[6] This paper describes voluntary or coerced sexual experience at sexual debut from a longitudinal perspective among a large sample of young South Africans participating in the Birth to Twenty Plus cohort.

Methods

Age at first sexual intercourse was examined in an analysis of data from a prospective longitudinal birth cohort in Soweto, Johannesburg, SA, using information gathered on six occasions from young people between the ages of 11 and 18 years.

The Birth to Twenty cohort (Bt20)

From 1990 the Bt20 cohort, described in detail elsewhere,[15] enrolled women in their second and third trimesters of pregnancy through public health facilities and interviewed them regarding their health, social history and current circumstances. The children born to these women, together with their families, have been followed up more than 18 times between birth and 23 years of age, with approximately 2 300 children and their families remaining in contact with the study.[15] Data for the present study

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came from a sample of 2 216 adolescents (1 149 females, 1 067 males) between 11 and 18 years of age.

Measures

Demographic measures used included race and maternal education. Socioeconomic status was determined by a list of household assets and amenities.[16] Sexual behaviour measures (age at first foreplay, oral, anal and/or vaginal intercourse, age and gender of partner, coerced or voluntary) were collected from age 11 years at six subsequent time points (11 - 12 years, 13 years, 14 years, 15 years, 16 years and 17 - 18 years). Self-reported responses were submitted through the method of secret ballot. Questions remained standard and included reports of the first time a young person experienced foreplay, oral sex and sexual intercourse, whether the experience was coerced or not, and characteristics of the first-time partner.

The first-time vaginal or anal intercourse was recorded as the age of sexual debut.

Sexual activity prior to 11 years was retrospectively reported. Reports of either foreplay or oral sex were classified as first sexual experience. Tanner staging of pubertal status was determined from adolescent selfassessment using a locally validated scale.[17]

the level of statistical significance at p<0.05.

Median age of sexual debut was determined by survival analysis. Data were processed using Stata statistical software (version 12).[18]

Results

Table 1 shows summary statistics for the study participants. Female and male participants were similar in terms of their demographic and socioeconomic characteristics. Girls were ahead of boys in terms of Tanner pubertal self-reports,[17] and more girls than boys reported sexual experience by age 13.

Age of sexual debut and sexual experience

The median age of sexual debut was 16 years for females and 15 for males. Fig. 1 shows that irrespective of type of first sexual intercourse, males engaged in sexual intercourse earlier than females (p<0.0001). By 15 years of age, 14.2% of females and 38.2% of males had engaged in sexual intercourse. By age 18, 42.9% of females and 59.5% of males had engaged in intercourse. There was a dramatic increase in sexual debut among females, and to some extent among males, between the ages of 14 and 17 years. The majority

Table 1. Characteristics of the study participants (N=2 216), according to gender Females (N=1 149, 52%) n (%)

Males (N=1 067, 48%) n (%)

Black

934 (81.3)

866 (81.2)

Coloured

151 (13.1)

137 (12.8)

White

35 (3.0)

35 (3.3)

Asian

29 (2.5)

29 (2.7)

Low

386 (33.6)

383 (35.9)

Middle

229 (19.9)

168 (15.7)

High

194 (16.9)

168 (15.7)

Primary/less

132 (11.5)

126 (11.8)

Secondary

820 (71.4)

754 (70.7)

Post-school training

99 (8.6)

98 (9.2)

Prepubertal

60 (5.2)

177 (16.6)

Early puberty

636 (55.4)

628 (58.9)

Mid puberty

261 (22.7)

81 (7.6)

Late puberty

29 (2.5)

81 (7.6)

922 (80.2)

787 (73.8)

Race

Socioeconomic status (asset index)

Maternal education

Ethics

Each round of data collection in the Bt20 research programme has ethics approval from the Committee for Research on Human Subjects at the University of the Witwatersrand, Johannesburg (M010556), and counselling services were available to all young people who participated in the study.

Pubertal stage (Tanner self-rating)[17] at age 13 years

Data analysis

Frequencies and cross-tabulations were calculated to describe the data. Analyses were run separately for males and females, and a two-sample t-test was used to assess

Sexual experience by age 13 years Foreplay or oral sex

Table 2. Adolescent males and females who had not and those who had engaged in sexual intercourse and their first sexual experience (voluntary or coerced) by the end of the 18-year wave Females 1 149 (51.9%), n (%) Age (years)

Not yet engaged in sex

Engaged in sex

Voluntary

Males 1 067 (48.1%), n (%) Coerced

Not yet engaged in sex

Engaged in sex

Voluntary

Coerced

≤12

1 136 (98.9)

13 (1.2)

3 (0.3)

10 (0.9)

958 (89.8)

109 (10.2)

66 (6.2)

43 (4.0)

≤13

1 118 (98.1)

22 (1.9)

6 (0.5)

16 (1.4)

887 (83.8)

171 (16.2)

114 (10.8)

57 (5.4)

≤14

1 075 (94.9)

58 (5.1)

30 (2.6)

28 (2.5)

772 (73.6)

277 (26.4)

197 (18.8)

80 (7.6)

≤15

963 (85.8)

160 (14.2)

107 (9.5)

53 (4.7)

641 (61.8)

396 (38.2)

285 (27.5)

111 (10.7)

≤16

815 (73.4)

296 (26.4)

222 (20.0)

74 (6.6)

529 (51.7)

495 (48.3)

362 (35.3)

133 (13.0)

≤17

672 (61.5)

420 (38.5)

331 (30.3)

89 (8.2)

447 (44.3)

561 (55.7)

415 (41.2)

146 (14.5)

≤18

585 (57.1)

440 (42.9)

349 (34.0)

91 (8.9)

387 (40.5)

568 (59.5)

419 (43.9)

149 (15.6)

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Discussion

Nearly half of all the participants followed prospectively had not engaged in sexual intercourse by the age of 18 years. Males engaged in sexual intercourse earlier than females, irrespective of whether the first sexual experience was voluntary or coerced.

Furthermore, more males than females reported both voluntary and coerced sexual debut across all ages. The results draw attention to high rates of sexual coercion of young men, a phenomenon little studied in sub-Saharan Africa.[19] First sexual intercourse was reported at a very young age by some young people, especially girls younger than 13 years.

Rates of childhood sexual abuse are reported to be high in SA, with high levels of penetrative sexual abuse before age 12, especially among

girls.[20] There is evidence that girls experiencing sexual abuse are more likely to engage in riskier sexual behaviours, including early sexual debut, than their peers.[4,20] Sex involving children younger than 16 years of age is illegal in SA, and children reporting oral sex or sexual intercourse before this age were referred to the study counsellor, who made further referrals.

Very few studies have looked at the sexual coercion experiences of adolescents in subSaharan Africa at their sexual debut.[7] Those that have indicate that coercion is common, affecting between 15% and 38% of adolescent girls.[21] In our study, sexual coercion tended to involve older sexual partners, although among older girls, only 9% of coerced sex was reported to have taken place with a partner 4 years or more older. In another SA study, sexual coercion was associated with significantly older partners.[4] However, our data also suggest that sexual coercion between same-aged groups is prevalent in SA, especially among those aged 15 - 17 years. These observations are in line

with the findings of previous studies in the country.[12-14] Interventions to counter coerced sexual intercourse therefore need to target both adolescents and young adults.

This is one of very few prospective studies of sexual debut, and has collected data on both voluntary and coerced first sexual experience; it is the only study in SA that has collected prospective data from the preteen years. While the data are limited by the unknown validity of self-reports of sexual behaviour, every effort was made to enhance the validity of reported sexual behaviour through use of the method of secret ballot.

Nonetheless, topic sensitivity and social desirability effects could have contributed to a well-known tendency towards female underreporting and male over-reporting of sexual experiences.[22] The objective of this study was mainly descriptive in nature. A more detailed analysis of the determinants of coercion at first sexual experience will be able to throw more light on the underlying risk factors.

40

Cumulative frequency, %

of females reported experiencing their first sexual intercourse between 15 and 17 years of age, peaking at 16. There was a less dramatic increase among males, with the majority experiencing sexual debut at a younger age, 14 - 16 years, peaking at age 16.

Table 2 shows the cumulative frequency distribution for adolescent males and females (and both groups combined) who had, and those who had not, engaged in sexual intercourse by the end of the 18-year wave, and whether their first sexual experience was coerced. Reported sexual intercourse before age 12 was ten times higher among boys than girls. However, more females, and especially those younger than 14 years, reported their first sexual intercourse as coerced.

Table 3 shows reported age differences between young people and their first sexual partners. Except for two girls and two boys, all reported partners tended to be within a 4-year age difference. Irrespective of coerced or voluntary sexual debut, significantly (p<0.05) more males had partners with no age difference or who were 1 - 4 years younger than themselves, and a significantly higher proportion of females had partners who were 1 year or more older.

30

20

10

0 12

13

14

15 Age, years

16

17

Females engaged in voluntary sex

Females coerced into sex

Males engaged in voluntary sex

Males coerced into sex

18

Fig. 1. Sexual debut for males and females by age from the first retrospective report of sexual intercourse, starting before 12 years of age.

Table 3. Partner age differences and sexual experience (voluntary or coerced) at first sexual intercourse by gender Voluntary

Coerced

Age difference

Females (N=348) n (%)

Males (N=419) n (%)

Females (N=91) n (%)

Males (N=149) n (%)

Partner ≥5 years younger

1 (0.3)

2 (0.5)

0 (0%)

0 (%)

Partner 1 - 4 years younger

3 (0.9)

115 (27.4)*

1 (1.1)

45 (30.2)*

Partner same age

42 (12.1)

143 (34.1)*

15 (16.5)

53 (35.6)*

Partner 1 - 4 years older

239 (68.7)*

115 (27.4)

55 (60.4)*

30 (20.1)

Partner ≥5 years older

45 (12.9)*

2 (0.5)

10 (11.0)*

2 (1.3)

*Significant at p<0.05.

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Conclusion

This study found that coerced sexual debut among young ado­ les­cents occurred mostly through sexual intercourse with peers, older adolescents and young adults, rather than with older adults.

These time periods and age groups therefore also need to be targeted for interventions to delay sexual debut and prevent sexual coercion. Targeted interventions aimed at delaying sexual debut and sexual coercion will help to prevent adolescent sexual risk behaviour, unwanted pregnancy and STIs, including HIV. More research is needed on the predisposing risk factors for sexual coercion as it relates to early sexual debut among youth, in order to inform existing and new prevention programmes targeted at intervening during childhood and adolescence.

Acknowledgements. We are grateful for funding received from the Wellcome Trust, the University of the Witwatersrand, the South African Medical Research Council and the South African Human Sciences Research Council. We acknowledge the input of Nuala McGrath, Clare Schur and Rashmika Singh to an earlier analysis plan.

References 1. Harrison A, Cleland J, Gouws E, Frohlich J. Early sexual debut among young men in rural South Africa: Heightened vulnerability to sexual risk? Sex Transm Dis 2005;81(3);259-261. [http://dx.doi. org/10.1136/sti.2004.011486] 2. Pettifor A, O’Brien K, MacPhail C, Miller W, Rees H. Early coital debut and associated HIV risk factors among young women and men in South Africa. Int Perspect Sex Reprod Health 2009;35(2):82-90. [http://dx.doi.org/10.1363/3508209] 3. Stöckl H, Kalra N, Jacobi J, Watts C. Is early sexual debut a risk factor for HIV infection among women in Sub-Saharan Africa? A systematic review. Am J Reprod Immunol 2013;69(Suppl 1):27-40. [http:// dx.doi.org/10.1111/aji.12043] 4. Jewkes R, Abrahams N. The epidemiology of rape and sexual coercion in South Africa: An overview.

Soc Sci Med 2002;55(7):1231-1244. [http://dx.doi.org/10.1016/S0277-9536(01)00242-8] 5. Erulkar AS. The experience of sexual coercion among young people in Kenya. Int Fam Plan Perspect 2004;30(4):182-189. [http://dx.doi.org/10.1363/3018204]

307

6. Maharaj P, Munthree C. Coerced first sexual intercourse and selected reproductive health outcomes among young women in KwaZulu-Natal, South Africa. J Biosoc Sci 2007;39(2):231-244. [http://dx.doi. org/10.1017/S0021932006001325] 7. Koenig M, Lutalo T, Zhao F, et al. Coercive sex in rural Uganda: Prevalence and associated risk factors.

Soc Sci Med 2004;58(4):787-798. [http://dx.doi.org/10.1016/S0277-9536(03)00244-2] 8. Noell J, Rohde P, Seeley J, Ochs L. Childhood sexual abuse, adolescent sexual coercion and sexually transmitted infection acquisition among homeless female adolescents. Child Abuse and Neglect 2001;25(1):137-148. [http://dx.doi.org/10.1016/S0145-2134(00)00223-4] 9. Jejeebhoy SJ, Bott S. Non-consensual Sexual Experiences of Young People: A Review of the Evidence from Developing Countries. South and East Asia Regional Working Paper No. 16. New Delhi: India Population Council, 2003.

10. Agardh A, Tumwine G, Asamoah BO, Cantor-Graae E. The invisible suffering: Sexual coercion, interpersonal violence, and mental health – a cross-sectional study among university students in southwestern Uganda. PLoS One 2012;7(12):e51424. [http://dx.doi.org/10.1371/journal.pone.0051424] 11. Pettifor AE, Rees HV, Kleinscmidt I, et al. Young people’s sexual health in South Africa: HIV prevalence and sexual behaviours from a nationally representative household survey. AIDS 2005;19(14):15251534. [http://dx.doi.org/10.1097/01.aids.0000183129.16830.06] 12. Shisana O, Rehle T, Simbayi L, et al. South African National HIV Prevalence, HIV Incidence, Behaviour and Communication Survey. Cape Town, HSRC Press, 2005.

13. Zuma K, Setswe G, Ketye T, Mzolo T, Rehle T, Mbelle N. Age at sexual debut: A determinant of multiple partnerships among South African youth. Afr J Reprod Health 2010;14(2):47-54.

14. McGrath N, Nyirenda M, Hosegood V, Newell M-L. Age of first sex in rural South Africa. Sex Transm Dis 2009;85(Suppl 1):S49-S55. [http://dx.doi.org/10.1136/sti.2008.033324] 15. Richter L, Norris S, Pettifor J, Yach D, Cameron, N. Mandela’s children: The 1990 Birth to Twenty study in South Africa. Int J Epidemiol 2007;36(6):504-511. [http://dx.doi.org/10.1093/ije/dym016] 16. Filmer D, Scott K. Assessing Asset Indices. Washington, DC: World Bank, 2008. [http://dx.doi. org/10.1596/1813-9450-4605] 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. [http://dx.doi.org/10.1111/j.15327795.2005.00113.x] 18. StataCorp. Stata Statistical Software: Release 12. College Station, TX: StataCorp LP, 2011.

19. Richter L, Komárek A, Desmond C, et al. Reported physical and sexual abuse in childhood and adult HIV risk behaviour in three African countries: Findings from Project Accept (HPTN-043). AIDS Behav 2014;18(2):381-389. [http://dx.doi.org/ 10.1007/s10461-013-0439-7] 20. Jewkes R. Non-consensual sex among South African youth: Prevalence of coerced sex and discourses of control and desire. In: Jejeebhoy S, Shah I, Thapa S, eds. Sex without Consent: Young People in Developing Countries. New York: Zed Press, 2005.

21. Moore AM, Awusabo-Asare K, Nyovani Madise N, John-Langba J, Kumi-Kyereme A. Coerced first sex among adolescent girls in sub-Saharan Africa: Prevalence and context. Afr J Reprod Health 2007;11(3):62-82. [http://dx.doi.org/10.2307/25549732] 22. Nnko S, Boerma T, Urassa M, Mwaluko J, Zaba B. Secretive females or swaggering males? An assessment of the quality of sexual partnership reporting in rural Tanzania. Soc Sci Med 2004;59(2):299-310. [http://dx.doi.org/10.1016/j.socscimed.2003.10.031]

Accepted 13 February 2015.

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Pathological findings in reduction mammoplasty specimens: A South African perspective C Sofianos, MB BCh, MRCS (Eng); R J Zinn, MB ChB, FC Plast Surg (SA), MMed; D A Geoffreys, MB ChB, FC Plast Surg (SA); D Kruger, BSc, PGCHE, PhD Department of Surgery, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa Corresponding author: C Sofianos (sofianosc@gmail.com)

Background. Preoperative, intraoperative and follow-up guidelines for managing occult carcinoma in reduction mammoplasty specimens are scant.

Methods. We retrospectively analysed the records and pathology reports of 200 patients who had undergone reduction mammoplasty at two major public hospitals in Johannesburg, South Africa, during 2009 - 2014. Demographic data, their history of breast cancer and preoperative screening, the surgical techniques used and pathological reports were included. In all cases preoperative screening for breast cancer had been negative.

Results. All the patients were female, mean age 37.1 years, range 20 - 84 (standard deviation 11.9). All reductions were performed using standard techniques. Benign pathology was observed in 98 patients (49%) and malignant pathology in four (2%). The most common benign pathology observed was fibrocystic disease, and the most common malignant pathology ductal carcinoma in situ. Patient age correlated significantly with benign or malignant disease.

Conclusions. Reduction mammoplasty produces tissue that should always be sent for pathological assessment. Patients should be stratified by risk, as doing so helps in selecting both the surgical setting and the approach to pathological analysis of the specimen. While the incidence of occult carcinoma in reduction mammoplasty specimens is low, all patients undergoing the procedure should be informed that tissue will be sent for pathological examination, allowing them to prepare to receive possible news of breast cancer and be adequately equipped for subsequent decision-making.

S Afr Med J 2015;105(4):308-311. DOI:10.7196/SAMJ.9108

Breast reduction (reduction mammoplasty) is fre­ quently performed by plastic and breast surgeons to relieve macromastia symptoms.[1] In the USA, a 97% increase in the number of reduction mammoplas­ ty procedures has been observed.[2] The procedure increases both physical and psychological wellbeing and improves quality of life for many patients.[3] Crikelair and Malton[4] published the first reported case of occult carcinoma discovered during reduction mammoplasty in 1959. They described the presence of ductal carcinoma seen on microscopic examination of surgical specimens. Interestingly, they then published an addendum to their initial report when the patient developed another primary tumour in the other breast. Since then, as detailed below, many studies have attempted to investigate the incidence of occult carcinoma in reduction mammoplasty specimens.

Snyderman and Lizardo[5] performed a landmark study investi­ gating the presence of occult carcinoma in reduction mammoplasty specimens. They examined 5 008 cases and demonstrated an incidence of 0.38%. In 1997, Jansen et al.[6] found an incidence of 0.16% in their series of 2 576 patients; however, the study design made use of a postal questionnaire sent out to consultant plastic surgeons, so it was susceptible to sampling bias. A population-based series study in Ontario, Canada, found a significantly lower inci­dence (0.06%) of breast cancer at the time of reduction mammo­ plasty.[7] While older studies such as this are possibly outdated, given the improved awareness of breast malignancy and enhanced clinical and radiological techniques used in its detection, in the above series, patients diagnosed with breast cancer at the time of reduction mammoplasty were less likely to have advanced cancer than the general population and had a better 5-year survival rate. Preoperative screening featured both a clinical breast examination and mammography.[7]

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In South Africa (SA), from which our data are drawn, the latest available statistics from the SA National Cancer Registry are from 2006 and show that the incidence of breast cancer in SA is 0.029%.[8] Macromastia is in itself a factor predisposing to breast cancer.[9] The increased prevalence of carcinoma of the breast in these women suggests that they may ultimately develop breast cancer following breast reduction.[10] Surgeons should be mindful of this fact, and undertake preoperative screening.[11] If a lesion is detected, the recommended triple breast evaluation steps outlined in Table 1 must be followed.

Diagnosis of breast cancer prior to reduction mammoplasty is vital, as management and treatment options may change signifi­ cantly.[12] A woman would be unlikely to opt to proceed with reduction mammoplasty without having both a biopsy and a multidisciplinary team decision on the management of malignancy. The diagnosis of breast cancer during reduction mammoplasty reduces the number of appropriate surgical options available and also complicates further treatment of the cancer.[2]

Methods

The worldwide incidence of occult carcinoma in reduction mammoplasty specimens is low. No study examining these patho­ logical findings has been performed in SA. As discussed, studies have been conducted in developed countries, but this information may not be accurately extrapolated to developing countries such as SA.

Study area

Chris Hani Baragwanath Academic Hospital (CHBAH) is a public hospital situated in Soweto, Johannesburg, South Africa. It serves a mostly black African, lower-income population of 2.5 million. Mammoplasty procedures are performed at CHBAH free of charge to the patient.

Helen Joseph Hospital (HJH) is a public hospital situated in Westdene,

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Table 1. Triple breast evaluation History

Carefully gather a patient history, with the aim of identifying any personal or family history of breast cancer, or any predisposing factors[9]

Clinical examination

Undertake a physical examination (including breast and nodal basin examination)[2]

Imaging

Undertake imaging, by either a mammogram or breast ultrasound[2,11]

Johannesburg, and serves a population of approximately 198 000 of mixed socioeconomic status. Mammoplasty procedures are not provided free of charge at HJH, but the cost is lower than that at a private hospital.

Table 2. Specific benign and malignant lesions Pathological diagnosis

n

Benign lesions (N=98)

Study design

A retrospective record review was performed of all patients who had undergone reduction mammoplasty procedures at CHBAH or HJH between January 2009 and January 2014, inclusive. Along with demographic data, patient histories of breast cancer, findings on preoperative screening, surgical techniques and pathological reports were recorded.

Inclusion criteria

To be included in the study sample, each patient had to meet the following three inclusion criteria: no preoperative history or examination suggestive of any breast disease; reduction mammoplasty performed on one or both breasts, using standard surgical techniques; and surgical specimens submitted for pathological review.

Preoperative screening

A detailed history was obtained, and aimed to identify previous or current breast disease and personal or family risk factors for breast disease. Screening further included clinical examination of the breasts as well as imaging â&#x20AC;&#x201C; specifically, breast ultrasound for patients <35 years of age, and mammography for those aged â&#x2030;Ľ35 years.

Preoperative imaging not only enabled significant breast disorders to be identified before surgery, but provided a control for detection of abnormalities after surgery had been performed.[13]

Pathological assessment

Pathological findings were categorised into two broad groups: benign lesions and malignant lesions. Fibrocystic disease was included under benign pathology. Malignant pathology included carcinoma in situ. Only cases with at least two random blocks per breast were included. All specimens had been submitted to the SA National Health Laboratory Service.

Statistical analysis

The Statistical Package for the Social Sciences (SPSS) 20.0 (SPSS Inc., USA) software program for Macintosh was used in data analysis.

Descriptive results were expressed as means and standard deviations (SDs). Statistical evaluations were performed using the non-parametric Mann-Whitney U-test. The level of significance was set at p<0.05.

Ethical approval

Ethical approval was obtained from the Human Research Ethics Committee of the University of the Witwatersrand (clearance No. M140239).

Results

A total of 209 patients were identified for inclusion in the study.

Nine were excluded because their operative specimens had not been submitted for pathological analysis. The 200 patients included were all female, with a mean (SD) age of 37.1 (11.9) years. The

309

Atypical ductal hyperplasia

1

Phyllodes

1

Ductal ectasia

2

Lipoid necrosis

2

Ductal hyperplasia

8

Fibroadenoma

14

Sclerosing adenosis

20

Fibrocystic change

50

Malignant lesions (N=4) Ductal carcinoma in situ

3

Invasive lobular carcinoma

1

youngest patient was 20 years of age, and the oldest 84. All patients had undergone a preoperative work-up including history-taking, clinical examination and imaging. All reductions were performed using standard techniques, with 195 procedures being bilateral and five unilateral. The mean (SD) weight of specimens submitted for pathological review was 1 002.8 (652.1) g.

Benign pathology was observed in 98/200 patients (49%) and malignant pathology in four (2%). Specific pathological findings are listed in Table 2. Benign pathology was observed at a mean age of 46.5 years and malignant pathology at a mean of 50.2 years.

The Shapiro-Wilk test of normality revealed that the age and average specimen weight variables were not normally distributed. A Mann-Whitney U-test showed that age was a variable significantly associated with the presence of both benign disease (p<0.0001) and malignant disease (p=0.012). No significant difference was found when the presence of benign or malignant disease was correlated with specimen weight. Furthermore, there was no significant difference when specific malignant lesions were compared, probably owing to the small sample number.

Discussion

Reduction mammoplasty produces a variable amount of tissue that should always be sent for pathological examination.[14] The procedure is of both cosmetic and oncological significance.[15] Its oncological significance is based primarily on the observation that breast cancer risk is reduced proportionate to the amount of breast tissue removed during the procedure.[16] Additionally, breast cancer encountered before, during, or after reduction mammoplasty requires a multidisciplinary approach to treatment, like any other breast cancer.

Malignant pathology was observed in 2% (n=4) of the 200 patients in this study. The incidence of occult breast carcinoma in other series ranges from 0.06% to 4.6%, with the most recent study in 2013 reporting a 0.56% rate of malignant pathology (including both invasive carcinoma and carcinoma in situ).[17] Differences in incidence

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Table 3. Risk stratification for reduction mammoplasty patients[14] Setting in which surgery should take place

Risk group

Features

High risk

Personal history of breast cancer BRCA1 or BRCA2 mutations Previous radiation to the chest Personal history of cancer syndromes

Pathology and surgical oncology services should be available

Margins should be inked and specimens orientated and divided into individual containers per segment resected

Intermediate risk

Family history of breast cancer Proliferative benign breast lesions

Pathology and surgical oncology services should be available

Inking of margins may be omitted

Low risk

Age <30 years No family history of breast cancer

Surgery may be performed at an outpatient centre

Specimen may be sent in two containers: left and right breast

arise because some studies include patients with previous or current breast disease, while in others, carcinoma in situ was not included. In addition, the pick-up of abnormal pathology increases in proportion to the degree of the pathological analysis.[18] In 1984, Nielsen et al.[19] showed through intensive pathological scrutiny of breast specimens obtained from autopsy (200 or more blocks per specimen) that 14 16% of these specimens had occult carcinoma or carcinoma in situ.

A future direction for our study would be a prospective investigation including a higher number of blocks per specimen to increase the rate of pick-up of pathological lesions.

Freedman et al.[20] found that the incidence of both premalignant and malignant lesions increased with increasing patient age; this trend was also seen in the current study, the significance extending to benign lesions as well as premalignant and malignant lesions.

The malignant conditions encountered were largely (75%) of the ductal carcinoma in situ variety. The most common benign lesion encountered was fibrocystic change, followed by sclerosing adenosis.

We found fibroadenoma, classically a condition encountered in younger individuals, to be more common among older patients. The weight of the specimen was not found to influence the presence of benign or malignant disease.

Patients who undergo reduction mammoplasty at CHBAH or HJH are followed up at 6 and 12 months. They are given advice regarding further screening, and are also followed up as part of SA’s standard breast cancer screening programmes. Long-term follow-up of these patients would be of value to ascertain the incidence of breast cancer in the remaining breast tissue. Furthermore, in countries with a high prevalence of HIV/AIDS, variables such as HIV positivity and CD4 count would be useful data to capture and examine in future research.

These data were not available for our retrospective review, but could be included in future prospective studies.

Every patient in the current study had had preoperative screening, despite the scant availability of universal guidelines for preoperative assessment and pathological assessment.

All methods of breast reduction allow for good exposure of breast parenchyma, and for direct visualisation and palpation of other segments; theoretically, any palpable tumour therefore can and should be detected at that time.[1] Titley et al.[21] suggested in 1996 that surgical specimens be separated clearly into left and right, and that a marker stitch be placed in the main specimen, possibly separating tissues into quadrants. Since the majority of reduction mammoplasty specimens do not have occult carcinoma, it would be difficult to convince all surgeons to ink the margins of surgical specimens; however, it is reasonable to insist that specimens from women at an increased risk of developing breast cancer be inked for orientation.[2] More recently it has been suggested that patients undergoing reduction mammoplasty be stratified according to risk; doing so

310

Approach to specimen

would dictate the setting in which surgery should take place and the approach to pathological analysis of the specimen.[15] Table 3 outlines the approach to risk stratification and in what settings surgery should be done.

Patients diagnosed with breast cancer at the time of reduc­tion mammoplasty are likely to be treated with a completion mastec­ tomy.[7] The basis of this decision is the rearrangement of tissue during the procedure, as well as the possibility of tumour seeding in the normal breast. Discovery of a breast carcinoma during or after a reduction mammoplasty poses a number of technical challenges: a large field of dissection, including a breach of pectoral fascia in certain areas; a larger skin incision; and possible contamination of the other breast during bilateral procedures.[12] The suggested technique, if breast cancer is discovered in pathological examination of surgical specimens from reduction mammoplasty, is a completion mastectomy that includes pre-existing incisions from the reduction mammoplasty procedure.[22] Reduction mammoplasty should not be considered a contraindication to sentinel lymph node biopsy, as many lymphatic channels remain intact and most breast reduction techniques involve incisions on the inferior aspect of the breast.[23] Many philosophical debates on ethics and informed consent have arisen in recent years. In the UK, screening for breast cancer is not recommended for any woman under the age of 50.[24] Furthermore, the US Preventive Services Task Force’s breast screening recom­ mendations recently indicated that mammography is of no benefit for patients under the age of 50.[25] Given these recommendations, many young women worldwide who are undergoing reduction mam­ moplasty are in effect undergoing a ‘screening procedure’ without their informed consent.[26] Although the incidence of occult carci­ noma among reduction mammoplasty specimens is low, all patients undergoing the procedure should be fully informed that the tissue will be sent for pathological examination, as doing so allows them to prepare for the possibility of receiving news of breast cancer, and to be adequately equipped for the decision-making that will follow.[26] Indeed, ‘The primary intent of mammoplasty is cosmetic, but it is a medical procedure, taking place in a medical setting, and those per­ forming it have a fiduciary obligation towards their patients’ health and wellbeing.’[26]

Conclusion

It has been demonstrated that, even in developing countries, it is of vital importance that surgeons aim to adequately investigate reduction mammoplasty candidates preoperatively and ensure that all tissue is submitted for pathological analysis. During the informed consent process for the procedure, patients should be fully informed of the potential consequences of the pathological analysis of surgical specimens obtained. Multidisciplinary approaches to

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breast cancer treatment should always be included for patients undergoing reduction mammoplasty who are diagnosed with breast cancer. Age was found to correlate significantly with the presence of benign or malignant disease in reduction mammoplasty specimens.

Further areas of study exist, and the results thereof could increase our understanding of the various pathological lesions found in reduction mammoplasty specimens.

References 1. Viana GA, Pitanguy I, Torres E. Histopathological findings in surgical specimens obtained from reduction mammaplasties. Breast 2005;14(3):242-248. [http://dx.doi.org/10.1016/j.breast.2004.12.006] 2. Keleher AJ, Langstein HN, Ames FC, et al. Breast cancer in reduction mammaplasty specimens: Case reports and guidelines. Breast J 2003;9(2):120-125. [http://dx.doi.org/10.1046/j.15244741.2003.09216.x] 3. Goyal A, Coulson SG, Wu JM, et al. Occult breast carcinoma in breast reduction specimens in European women. Breast Cancer Res Treat 2011;128(3):749-753. [http://dx.doi.org/10.1007/s10549011-1589-9] 4. Crikelair GF, Malton SD. Mammaplasty and occult breast malignancy: Case report. Plast Reconstr Surg Transplant Bull 1959;23(6):601-606. [http://dx.doi.org/10.1097/00006534-195906000-00006] 5. Snyderman RK, Lizardo JG. Statistical study of malignancies found before, during, or after routine breast plastic operations. Plast Reconstr Surg Transplant Bull 1960;25(3):253-256. [http://dx.doi. org/10.1097/00006534-196003000-00006] 6. Jansen DA, Murphy M, Kind GM, et al. Breast cancer in reduction mammoplasty: Case reports and a survey of plastic surgeons. Plast Reconstr Surg 1998;101(2):361-364. [http://dx.doi. org/10.1097/00006534-199802000-00014] 7. Tang CL, Brown MH, Levine R, et al. Breast cancer found at the time of breast reduction. Plast Reconstr Surg 1999;103(6):1682-1686. [http://dx.doi.org/10.1097/00006534-199905000-00016] 8. National Health Laboratory Service. National Cancer Registry of South Africa. http://www.nioh.ac.za/ assets/files/NCR_2006_TABLES_FINAL.pdf (accessed 29 April 2014).

9. Dotto J, Kluk M, Geramizadeh B, et al. Frequency of clinically occult intraepithelial and invasive neoplasia in reduction mammoplasty specimens: A study of 516 cases. Int J Surg Pathol 2008;16(1):2530. [http://dx.doi.org/10.1177/1066896907307176] 10. Rees TD, Coburn R. Breast reduction: Is it an aid to cancer detection? Br J Plast Surg 1972;25(2):144146. [http://dx.doi.org/10.1016/S0007-1226(72)80036-5]

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11. Van der Torre PM, Butzelaar RM. Breast cancer and reduction mammoplasty: The role of routine pre-operative mammography. Eur J Surg Oncol 1997;23(4):341-342. [http://dx.doi.org/10.1016/S07487983(97)90885-4] 12. Gottlieb JR, McKinney P, Walkinshaw MD, et al. Occult breast carcinoma in patients undergoing reduction mammaplasty. Aesthetic Plast Surg 1989;13(4):279-283. [http://dx.doi.org/10.1007/ BF01570361] 13. Shiffman MA. Mammograms in cosmetic breast surgery. In: Shiffman MA, ed. Mastopexy and Breast Reduction: Principles and Practice. 1st ed. Heidelberg: Springer, 2009:37-40.

14. Ishag MT, Bashinsky DY, Beliaeva IV, et al. Pathologic findings in reduction mammaplasty specimens.

Am J Clin Pathol 2003;120(3):377-380. [http://dx.doi.org/10.1309/4KD652HN739XTLM3] 15. Jansen DA, Ghere MC, Lee M, et al. Breast cancer and reduction mammaplasty. In: Shiffman MA, ed.

Mastopexy and Breast Reduction: Principles and Practice. 1st ed. Heidelberg: Springer, 2009:657-670.

16. Brinton LA, Persson I, Boice JD jr, et al. Breast cancer risk in relation to amount of tissue removed during breast reduction operations in Sweden. Cancer 2001;91(3):478-483. [http://dx.doi. org/10.1002/1097-0142(20010201)91:3%3C478::AID-CNCR1025%3E3.3.CO;2-X] 17. Aytac B, Sahsine T, Erturk FY, et al. Evaluation of incidence and histolopathological findings of breast lesions in reduction mammoplasty specimens: Uludag University experience. J Pak Med Assoc 2013;63(7):878-881.

18. Kerrigan CL, Slezak SS. Evidence-based medicine: Reduction mammaplasty. Plast Reconstr Surg 2013;132(6):1670-1683. [http://dx.doi.org/10.1097/PRS.0b013e3182a807ec] 19. Nielsen M, Jensen J, Andersen J. Precancerous and cancerous breast lesions during lifetime and at autopsy: A study of 83 women. Cancer 1984;54(4):612-615. [http://dx.doi.org/10.1002/10970142(1984)54:4%3C612::AID-CNCR2820540403%3E3.0.CO;2-B] 20. Freedman BC, Smith SM, Estabrook A, et al. Incidence of occult carcinoma and high-risk lesions in mammaplasty specimens. Int J Breast Cancer 2012;2012:145630. [http://dx.doi. org/10.1155/2012/145630] 21. Titley OG, Armstrong AP, Christie JL, et al. Pathological findings in breast reduction surgery. Br J Plast Surg 1996;49(7):447-451. [http://dx.doi.org/10.1016/S0007-1226(96)90028-4] 22. Rudolph R, Niedbala AR. Surgical management of the patient with invasive carcinoma discovered at reduction mammoplasty. Am Surg 2003;69(11):1003-1005.

23. Golshan M, Lesnikoski BA, Lester S. Sentinel lymph node biopsy for occult breast cancer detected during breast reduction surgery. Am Surg 2006;72(5):397-400.

24. McPherson K. Screening for breast cancer â&#x20AC;&#x201C; balancing the debate. BMJ 2010;340:c3106. [http://dx.doi. org/10.1136/bmj.c3106] 25. Screening for breast cancer: US Preventive Services Task Force recommendation statement. Ann Intern Med 2009;151(10):716-736. [http://dx.doi.org/10.7326/0003-4819-151-10-200911170-00008] 26. Keshtgar M, Hamidian Jahromi A, Davidson T, et al. Tissue screening after breast reduction. BMJ 2009;338:b630. [http://dx.doi.org/10.1136/bmj.b630]

Accepted 13 February 2015.

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Comparison of findings using ultrasonography and cystoscopy in urogenital schistosomiasis in a public health centre in rural Angola J Santos,1,2,9 MD; J Chaves,1,2,9 MD, PhD; H Araújo,2,9 MD; N Vale,3 ChemD, PhD; J M Costa,4 PhD; P J Brindley,5 PhD; C Lopes,6 MD, PhD; J Naples,7 MD, PhD; C Shiff,7 MD, PhD; J Dupret,8 MD; L L Santos,6 MD, PhD rology Unit, Americo Boavida Hospital, Luanda, Angola U Urology Unit, Sagrada Esperança Clinic, Luanda, Angola 3 Centro de Investigação em Química da Universidade do Porto (CIQUP), Chemistry and Biochemistry Department, Faculty of Sciences, University of Porto, Porto, Portugal 4 Centre for the Study of Animal Science, University of Porto, Portugal 5 Department of Microbiology, Immunology and Tropical Medicine, School of Medicine and Health Sciences, George Washington University, Washington, DC, USA 6 Experimental Pathology and Therapeutics Group, Research Centre of the Portuguese Institute of Oncology, Porto, Portugal, and Oncocir – Education and Care in Oncology and National Cancer Centre, Angola 7 Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA 8 Ministry of Health, Angola 9 Agostinho Neto University, Luanda, Angola 1 2

Corresponding author: L L Santos (llarasantos@gmail.com)

Background. Schistosomiasis is a chronic disease caused by infection with parasitic worms of the genus Schistosoma. In sub-Saharan Africa, infections with S. haematobium are most common. Cystoscopic examination (CE) has been accepted as the gold-standard test for detecting the late manifestations of schistosomiasis, including urothelial cancer of the bladder. However, this procedure is invasive and 10 - 40% of tumours may remain undetected. A non-invasive examination and a new generation of biomarkers are needed for better monitoring of the disease.

Objective. To assess the usefulness of ultrasound (US) scans for monitoring of structural urinary tract disease by local public health services in areas of Angola in which urogenital schistosomiasis is endemic.

Methods. A cohort of 80 S. haematobium-infected patients was selected in order to compare changes in the bladder wall detected by US with those observed on CE. Results. There was a notable correlation between the findings observed on CE and US. Patients with lesions of the bladder mucosa such as neoplasms, ulcers or granulomas detected by CE also had changes in bladder wall thickness on US. The results support increased use of portable US machines for non-invasive examination of the bladder by local general practitioners.

Conclusion. US examination should be an integral part of the investigation of haematuria and used in all S. haematobium control programmes. General practitioners may find it useful for more accurate diagnosis of haematuria and to identify bladder wall alterations in both adults and children in schistosomiasis-endemic regions.

S Afr Med J 2015;105(4):312-315. DOI:10.7196/SAMJ.8564

Anthropophilic species of Schistosoma currently infect more than 200 million people in 77 countries in the endemic areas of Africa, the Caribbean, Central America, South America, East Asia and the Middle East.[1] More than 90% of these cases occur in Africa, and of these approximately two-thirds are caused by S. haematobium.[2] Recently King[3] suggested that the number of cases of S. haematobium infection may be greater than was previ­ously believed. If this is confirmed, urogenital schistosomiasis may represent the most common infection in sub-Saharan Africa.[3] Many infections with S. haematobium result in minimal symptoms or cause haematuria, dysuria, anaemia and inflammation of the urinary tract. However, a significant proportion of infected patients, ranging from 25% to 50%, experience moderate to severe morbidity. Late manifestations include kidney dysfunction, ureteric obstruction and squamous cell carcinoma of the bladder. Cystoscopic examination (CE) is accepted as the gold standard for the detection of disorders of chronic schistosomiasis.[4] However, this procedure is invasive and 10 - 40% of malignancies may be undetected. Microscopic examination of the

312

urine remains the gold-standard test for the diagnosis of urogenital schistosomiasis, although it has some limitations. Detection of specific antibodies and/or antigens by serological assays can be useful in specific circumstances in endemic areas, but their application is limited[5] beyond diagnosis of the disease in travellers from non-endemic areas.[6] Schistosomiasis can be controlled with safe and effective drug therapy.

Other components of management include the provision of potable water, adequate sanitation, hygiene education and snail control.[6-7] In a resource-poor setting with numerous limitations, what can general practitioners, other healthcare professionals and local health services do for populations in their care in regions endemic for schistosomiasis? Lesions caused by infection with S. haematobium can be detected readily on ultrasound (US) examination. King[3] reported that US-based population surveys enabled effective assessment of reversibility of structural changes in a range of age groups, and provided data assisting choice of treatment protocols.

The present study assessed the performance of US detection of bladder wall changes in a group of patients in a schistosomiasisendemic area (Pita, Angola; Fig. 1) referred to a public clinic with

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nonspecific haematuria, comparing and contrasting changes in the bladder wall detected by US with those observed at CE. To our knowledge, this is the first time such an assessment has been done.

Methods

Study sites and participants

Ethical approval for the study was granted by the ethics committee of Agostinho Neto University, Luanda, Angola. Parental consent in the case of children and consent from participating adults was obtained.

Eighty people were recruited into the study between December 2011 and September 2012. Of these, 70 were consecutive patients with macroscopic haematuria who attended a rural public clinic (PitaMuxima) in Luanda Province (municipality of Quissama). An additional 10 were admitted to the Department of Urology at Américo Boavida Hospital (ABH), Luanda, with haematuria and suspected bladder cancer. All participants had bladder US scans with subsequent CE and mucosal biopsy.

Urine

Urine samples were collected from the 80 patients. They were tested for haematuria using reagent strips (Hemastix, Bayer, UK). Parasi­ tological examination for detection of S. haematobium eggs was done by filtering a 10 ml aliquot through a polycarbonate filter with a pore size of 12 μm diameter (Millipore, UK). The slides were examined at × 100 under a compound light microscope, according to World Health Organization (WHO) guidelines.[8]

Ultrasound examination

Fluid was given to each patient 30 minutes to 1 hour before US examination to ensure adequate filling of the bladder to assess its shape and any wall irregularity. A portable US apparatus (Siemens portable ultrasound with a 3.5 MHz curvilinear probe, WA 980297002, USA) was used. The scans were done by medically qualified persons, particular attention being paid to abnormalities of bladder shape, irregularities or thickening of the bladder wall, discernible masses and presence of polyps, calcification and/ or hydronephrosis. Findings were recorded photographically. WHO criteria were used to classify any bladder damage detected.[9]

Cystoscopic examination

Patients underwent CE in the Department of Urology at ABH. CE was performed after the US scan, and particular attention was given to major bladder mucosa alterations such as ulcers, schistosome eggs, granulomas and tumours (14 patients had schistosome eggs and other mucosal changes). A Karl

Fig. 1. Pita, Luanda Province, Angola.

Storz cystoscope, 20-Fr (adults) and 11.5-Fr (children), with a 30o eyepiece was used.

Treatment

Prazinquantel 40 mg/kg was offered to patients diagnosed with schistosomiasis, according to WHO guidelines.[10] Those who were diagnosed with bladder cancer were admitted to the urology service of ABH for specific treatment.

a

Statistical analysis

Statistical analysis was performed using SPSS 17 statistics software (SPSS Inc. for Windows). Demographic, bladder US and cystoscopy data were recorded. χ2 analysis using Fisher’s exact test (two-tailed) was performed for categorical data, with a p-value of ≤0.05 considered statistically significant.

Results

The median age of the patients was 41 years (range 3 - 75); 62 (77.5%) were males. All had macroscopic haematuria, and the reagent strips were positive for the presence of blood.

A parasite egg count was positive in 36 patients (45.0%). All the paediatric patients were treated for the first time during this study. Bladder wall irregularities detected by US are described in Table 1. In brief, 60 (75.0%) of the participants had distortion of the bladder shape and 29 (36.3%) had bladder masses (Fig. 2). Major findings on CE are set out in Tables 1 and 2.

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b Fig. 2. (a) US bladder wall irregularities and (b) appearance on CE in a patient with haematuria (arrows = granuloma).

Here, 54 patients (67.5%) had only schistosome eggs, granulomas being present in 14 (17.5%).

Neoplasms were seen in 10 patients (12.5%) and ulcerations in 2 (2.5%), both of whom were <19 years of age. The median age of patients with tumours was 51 years (range 10 - 68).

There was a notable correlation between the findings on CE and US. Patients with lesions in the bladder mucosa such as neoplasms, ulcers or granulomas detected by

RESEARCH

Table 1. Gender, presence of haematuria, bladder US and CE features and findings on examination of the urine Variables

Patients n (%)

Gender Female

18 (22.5)

Male

62 (77.5)

Haematuria

80 (100.0)

US bladder shape Normal

20 (25.0)

Abnormal

60 (75.0)

US bladder wall irregularities <5 mm normal

1 (1.3)

≥5 mm focal

40 (50.0)

5 mm multifocal or ≥ diffuse

39 (48.7)

Table 2. Dominant features on bladder CE according to age group Patients, n Age group (years)

S. haematobium eggs

Granuloma

Ulcer

Neoplasm

Total

≤19

4

8

2

1

15

20 - 29

12

1

0

1

14

30 - 39

4

3

0

1

8

40 - 49

18

1

0

1

20

50 - 59

8

0

0

4

12

60 - 69

6

0

0

2

8

≥70

2

1

0

0

3

Total

54

14

2

10

80

Table 3. Dominant features on bladder CE and irregularities noted on bladder US US discernible masses, n Cystoscopy features

US bladder wall irregularities

None

Single

Multiple

Total, n

S. haematobium eggs

<5 mm – normal

1

-

-

1

US discernible masses None

51 (63.7)

Single

13 (16.3)

Multiple

16 (20.0)

Granuloma

US presence of pseudopolyps Yes

6 (7.5)

No

74 (92.5)

Ulcer

US calcification Yes

75 (93.7)

No

5 (6.3)

Neoplasm

≥5 mm focal

29

3

-

32

≥5 mm multifocal or diffuse

18

2

1

21

<5 mm – normal

-

-

-

-

≥5 mm focal

1

-

1

2

≥5 mm multifocal or diffuse

1

2

9

12

<5 mm – normal

-

-

-

-

≥5 mm focal

1

-

-

1

≥5 mm multifocal or diffuse

1

-

-

1

≥5 mm focal

-

5

-

5

≥5 mm multifocal or diffuse

-

-

5

5

Hydronephrosis Yes

3 (3.7)

No

77 (96.3)

CE S. haematobium eggs

54 (67.5)

Granuloma

14 (17.5)

Ulcer

2 (2.5)

Neoplasm

10 (12.5)

Urine S. haematobium eggs

36 (45.0)

CE also had changes in bladder thickness on US. Only one patient in whom CE showed the presence of eggs in the mucosa had a normal US scan (Table 3). Residual urine was observed in 17 patients (21.3%), and bilateral hydronephrosis was found in 3 (3.8%). One patient had an associated kidney neoplasm.

The outcomes achieved by the two diagnostic approaches supported an acceptable correlation for the detection of bladder changes by US and CE. While bladder wall distortion or bladder masses in urogenital schistosomiasis were detected by US, it was not possible to obtain meaningful information about bladder thickness (Fig. 3).

Discussion

US is suitable for monitoring schistoso­ miasis-related pathology of the urinary tract, and is particularly useful in assessing its evolution after therapy. Bladder alterations observed by US have been associated with known biomarkers of bladder cancer in adults with chronic S. haematobium infection.[11] The importance of US examination in monitoring structural disorders in urogenital schistosomiasis has long been established. US provides clear evidence of ureteric wall abnormalities causing strictures and ureterocelelike lesions of the ureteric ostia, and demonstrates resolution of bladder lesions after treatment, including in paediatric patients.[12] A recent report indicates that general practitioners can learn to carry out a simple US examination for accurate diagnosis and followup of S. haematobium infection-related bladder lesions within a few sessions.[13] The aim of the present study was to verify the reproducibility of the bladder changes detected by US and bladder mucosa lesions observed by CE in order to teach general doctors to perform bladder US as an additional tool in the diagnosis of haematuria in areas endemic for S. haematobium.

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April 2015, Vol. 105, No. 4

Our results support other observations on S. haematobium-infected patients >30 years of age, in whom severe bladder damage was evident on US examination but no S. haematobium eggs were present in their urine samples.[14] The optimal imaging modality for patients with haematuria remains controversial, particularly given developments in computed tomography urography and magnetic resonance urography.[15] However, the European Society of Urogenital Radiology guidelines for the investigation of painless haematuria recommend the use of US.[16] Our results confirm that in patients with haematuria, the changes seen on US examination of the bladder correlated significantly with the presence of eggs of S. haematobium, ulcers or granulomas in the bladder mucosa observed at CE. We consider that a training programme for general practitioners in US for this purpose would be valuable in developing countries. Portable US devices are also useful for the evaluation of breast, gynaecological and urological pathology, and should be among the tools employed for routine examinations by the general doctor in resource-poor settings.[17]

RESEARCH

a

Bladder shape Normal Distorted

40

Patients, n

30

20

References

10

0

S. haematobium eggs

Granuloma

Ulcer

Neoplasm

Cystoscopy

b

Discernible bladder masses None Single Multiple

50

Patients, n

40

30

20

10

0

ABH and Sagrada Esperança Clinic, and the Dean of the Faculty of Medicine of Agostinho Neto University, Prof. Miguel Betencourt Mateus.

Author contributions. JS and LLS conceived and designed the experiments, JS, JC and HA performed the experiments, JS, CL, JMC and LLS analysed the data, and JS, CS, JD, JN, NV, CL, PJB, JMC and LLS wrote the paper.

S. haematobium eggs

Granuloma

Ulcer

Neoplasm

Cystoscopy

Fig. 3. Correlation between CE features and bladder changes on US: (a) bladder shape on US (p=0.005); (b) masses detected on US (p=0.0001).

Infection with S. haematobium has been detected in 64.8% of adults examined in the north of Angola.[18] At the 2014 International Congress of Angolan Physicians in Luanda, Pintar et al.[19] presented their finding that 83% of 149 children with S. haematobium infection had bladder wall changes that were evident on US. Angola has a programme of prevention, control and elimination of neglected diseases such as schistosomiasis that includes the training of general practitioners in US to help achieve early diagnosis of urogenital schistosomiasis and to monitor the results of chemotherapy. The introduction of

tests of high sensitivity and specificity, such as detection of parasite-specific DNA in urine,[11,20] will be of added value in monitoring elimination programmes.

Conclusions

US examination should be an integral component of the diagnosis of haematuria and should be performed in all S. haematobium control programmes in schistosomiasisendemic regions, including in paediatric populations.

Acknowledgments. The authors thank the team of Pita Public Clinic, the urological services of

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April 2015, Vol. 105, No. 4

1. Mostafa MH, Sheweita SA, O’Connor PJ. Relationship between schistosomiasis and bladder cancer. Clin Microbiol Rev 1999;12(1):97-111.

2. Brindley PJ, Hotez PJ. Break out: Urogenital schistosomiasis and Schistosoma haematobium in the post-genomic era. PLoS Negl Trop Dis 2013;7(3):e196. [http://dx.doi.org/10.1371/journal.pntd.0001961] 3. King CH. Ultrasound monitoring of structural urinary tract disease in Schistosoma haematobium infection. Mem Inst Oswaldo Cruz 2002;97(1):149-152. [http://dx.doi.org/10.1590/ S0074-02762002000900028] 4. Devidas A, Lamothe F, Develoux M, Gakwaya I, Ravisse P, Sellin B. [Morbidity due to bilharziasis caused by S. haematobium: Relationship between the bladder lesions observed by ultrasonography and the cystoscopic and anatomo-pathologic lesions]. Acta Trop 1988;45(3):277-287.

5. Nausch N, Dawson EM, Midzi N, Mduluza T, Mutapi F, Doenhoff MJ. Field evaluation of a new antibody-based diagnostic for Schistosoma haematobium and S. mansoni at the point-of-care in northeast Zimbabwe. BMC Infect Dis 2014;14(3):165-173. [http:// dx.doi.org/10.1186/1471-2334-14-165] 6. Pardo J, Carranza C, Turrientes MC, et al. Utility of Schistosoma bovis adult worm antigens for diagnosis of human schistosomiasis by enzyme-linked immunosorbent assay and electroimmunotransfer blot techniques. Clin Diagn Lab Immunol 2004;11(6):1165-1170. [http://dx.doi.org/10.1128/CDLI.11.6.1165-1170.2004] 7. Engles D, Chitsulo L, Montresor A, Savioli L. The global epidemiological situation of schistosomiasis and new approaches to control and research. Acta Trop 2002;82(2):139-146.

8. Montresor A, Crompton DWT, Bundy DAP, Hall A, Savoli L. Guidelines for the Evaluation of Soil-transmitted Helminthiasis and Schistosomaisis at Community Level: A Guide for Managers of Control Programmes. Geneva: WHO, 1998.

9. Richter J, Hatz C, Campagne G, Bergquist NR, Jenkins JM. Ultrasound in Schistosomiasis: A Practical Guide to the Standardized Use of Ultrasonography for the Assessment of Schistosomiasisrelated Morbidity. Geneva: World Health Organization, 2000.

10. World Health Organization, Prevention and control of schistosomiasis and soil-transmitted helminthiasis. WHO Technical Reports Series No. 912. Geneva: WHO, 2002.

11. Shiff C, Veltri R, Naples J, et al. Ultrasound verification of bladder damage is associated with known biomarkers of bladder cancer in adults chronically infected with Schistosoma haematobium in Ghana. Trans R Soc Trop Med Hyg 2006;100(9):847-854. [http:// dx.doi.org/10.1016/j.trstmh.2005.10.010] 12. Kardorff R, Traoré M, Doehring-Schwerdtfeger E, Vester U, Ehrich JH. Ultrasonography of ureteric abnormalities induced

by Schistosoma haematobium infection before and after praziquantel treatment. Br J Urol 1994;74(6):703-709.

13. Bonnard P, Boutouaba S, Diakhate I, Seck M, Dompnier JP, Riveau G. Learning curve of vesico-urinary ultrasonography in Schistosoma haematobium infection with WHO practical guide: A ‘simple to learn’ examination. Am J Trop Med Hyg 2011;85(6):10711074. [http://dx.doi.org/10.4269/ajtmh.2011.11-0282] 14. Shiff C. The importance of definitive diagnosis in chronic schistosomiasis, with reference to Schistosoma haematobium. J Parasitol Res 2012;2012:761269. [http://dx.doi.org/10.1155/2012/761269] 15. O’Connor OJ, McSweeney SE, Maher MM. Imaging of hematuria. Radiol Clin North Am 2008;46 (1):113-132. [http:// dx.doi.org/10.1016/j.rcl.2008.01.007] 16. Van der Molen AJ, Cowan NC, Mueller-Lisse UG, NolteErnsting CC, Takahashi S, Cohan RH, CT Urography Working Group of the European Society of Urogenital Radiology (ESUR).

CT urography: Definition, indications and techniques: A guideline for clinical practice. Eur Radiol 2008;18(1):4-17.

17. Shetty M, Longatto-Filho A. Early detection of breast, cervical, ovarian and endometrial cancers in low resource countries: An integrated approach. Indian J Surg Oncol 2011;2(3):165-171. [http://dx.doi.org/10.1007/s13193-011-0082-6] 18. Sousa-Figueiredo JC, Gamboa D, Pedro JM, et al. Epidemiology of malaria, schistosomiasis, geohelminths, anemia and malnutrition in the context of a demographic surveillance system in northern Angola. PLoS One 2012;7(4):e33189. [http:// dx.doi.org/10.1371/journal.pone.0033189] 19. Pintar Z, Bocanegra C, Molina I, Moreno M, Salvador F, Serres X. Ultrasonographic findings in Schistosoma haematobium infection in paediatrics (Poster). Presented at the International Congress of the Order of Physicians, Luanda, Angola, 24-25 January 2014.

20. Shiff C, Naples JM, Isharwal S, Bosompem KM, Veltri RW. Noninvasive methods to detect schistosome-based bladder cancer: Is the association sufficient for epidemiological use? Trans R Soc Trop Med Hyg 2010;104(1):3-5. [http://dx.doi.org/10.1016/j.trstmh.2009.05.013]

Accepted 13 February 2015.

GUEST EDITORIAL

Chronic kidney disease In his review article in the March 2015 edition of CME, Prof. A M Meyers refers to chronic kidney disease as ‘an important disease group that threatens health’. I fully concur with this observation and wish to go a step further and assert that kidney disease, together with other related non­-communicable diseases (NCDs), poses not only a threat to health but also to the overall development of South Africa (SA). It is now almost 4 years since the adoption of the Political Declaration of the High-level Meeting of the General Assembly on the Prevention and Control of Non­-communicable Diseases (September 2011), where it was emphatically stated that member States that have signed the Declaration (including SA) ‘Acknowledge that the global burden and threat of non-communicable diseases constitutes one of the major challenges for development in the twenty-first century, which undermines social and economic development throughout the world, and threatens the achievement of internationally agreed development goals’.

This means that we have to act decisively to prevent and combat NCDs (including kidney diseases), based on interventions informed by best evidence and cost-effectiveness. We need to do this not just for the sake of better health, which of course as Minister of Health is fundamental to me, but because if we do not act against NCDs we will also be increasing individual and household impoverishment and hindering social and economic development.

In the SA Strategic Plan for the Prevention and Control of NonCommunicable Diseases 2013 - 2017, kidney disease is specifically included as an additional priority to what are often referred to as the ‘main’ NCDs, i.e. cardiovascular diseases, diabetes, chronic respiratory diseases and cancer. This is in recognition and acknowledgement that kidney disease is a major health burden in SA, leading to very significant morbidity and mortality, significant interrelationships between other NCDs and kidney disease, and the fact that risk factors are common. Although comprehensive studies on national prevalence of kidney disease are still lacking, statistics presented in the March and April articles in CME are certainly a compelling call to action. It is clear that end-stage kidney disease is to a large extent driven by hypertension and diabetes, which are rising in incidence as globalisation and industrialisation increase. Many NCDs occur much earlier in local populations than in highly developed countries and mortality is much higher in low- and middle-income countries. Nearly 30% of NCD-related deaths in low-income countries occur in people <60 years of age, whereas in high-­income countries the proportion is only 13%.

SA is committed to providing universal health coverage and we will support the inclusion of this goal when the United Nations meet later this year to decide on the post-Millennium Development Goals – now usually referred to as the Sustainable Development Goals for 2030. To achieve this objective, we know that we must keep our population healthy, diagnose potential health problems as early as possible and ensure cost containment and cost-effectiveness in all health services. We must also provide care based on evidence of good practice and healthcare must be provided by sufficient, skilled and well-trained practitioners at each level of the health system.

We must also reach towards achieving equity in healthcare so that socioeconomic status does not determine whether a person receives care or the type of care. These principles are particularly important with regard to kidney disease.

In the first instance all concerned, including government and nonstate actors, must put more effort into prevention. Some progress is being made, but much more is needed. Sodium is one of the key risk factors for kidney disease and from 2016 food manufacturers will have to comply with regulatory targets, which will have to be further reduced to meet 2019 targets, when a Department of Health strategy to reduce obesity will be finalised and implemented. We realise though that combating obesity cannot be achieved through interventions from the Department of Health alone, and that other sectors such as Agriculture, Trade and Industry, Basic Education, and Sport and Recreation Communications will need to contribute, as will industry, non-governmental organisations and healthcare practitioners.

Guidelines on screening and treatment of kidney disease such as those contained in these editions of CME are most welcome as we move towards affordable and ethical care and treatment of kidney disease and end-stage kidney failure. I am personally facilitating consultations between the Department of Health and major stakeholders in kidney disease to ensure that all of us improve our preventive efforts, care and treatment interventions so that we have the best possible interventions that SA can afford. I do this in the knowledge that better health is essential for our growth and development as a country.

Dr Aaron Motsoaledi Minister of Health, South Africa S Afr Med J 2015;105(4). DOI:10.7196/SAMJ.9620

April 2015, Vol. 105, No. 4

CONTINUING MEDICAL EDUCATION

REVIEW

Paediatric chronic kidney disease I van Biljon,1 MMed (Paed), FC Paed (SA), Cert Nephrology (SA) Paed; A M Meyers,2 MB BCh, FCP (SA), Cert Nephrology (SA), FRCP (Lond) 1 2

epartment of Paediatrics, Faculty of Health Sciences, University of Pretoria, South Africa D Donald Gordon Medical Centre, Klerksdorp Hospital, and National Kidney Foundation of South Africa, Johannesburg, South Africa

Corresponding author: A M Meyers (nkfsa@mweb.co.za)

Doctors use various guidelines on paediatric chronic kidney disease (CKD) for managing their patients according to the availability of resources. As with adolescent and adult patients, CKD in children can also progress to end-stage renal failure – the time course being influenced by several modifiable factors. Decline in renal failure is best categorised in stages, which determine management and prognosis.

Staging is based on three categories, i.e. cause, glomerular filtration rate and proteinuria. Early diagnosis of CKD allows for the institution of renoprotective treatment of modifiable factors and treatment to prevent the development of complications. The two most important modifiable factors that can be treated successfully are hypertension and proteinuria.

The objective of this article is to provide information on the diagnosis and treatment of CKD in children. Early identification and treatment of modifiable risk factors of CKD decreases the burden of disease and delays or prevents the need for renal replacement therapy.

S Afr Med J 2015;105(4):316-319. DOI:10.7196/SAMJ.9532

Nephrology is a subspecialty often associated with expensive and technologically advanced therapies. Furthermore, paed­ iatric nephrology services are limited as there are only a few registered paediatric nephrologists in South Africa (SA), almost all of whom practise in tertiary academic hospitals distributed unevenly across the country. The objective of this article is to provide information to general practitioners and paediatricians caring for children with chronic kidney disease (CKD).

The Kidney Disease Improving Global Outcomes guideline proposes the following definition of CKD: • Abnormalities of kidney structure or function that have been present >3 months, with implications for the health of the patient, and either of the following: • decreased glomerular filtration rate (GFR) <60 mL/min/1.73 m2, and/or • presence of markers of kidney damage.

• Markers of kidney disease include any of the following: • proteinuria (urine dipstick ≥2+ or urine protein:creatinine ratio 5 × the upper limit of normal) • urine sediment abnormalities • electrolyte and other abnormalities caused by tubular disorders • histological abnormalities • structural abnormalities detected by imaging • history of renal transplantation.

The aforementioned definition does not apply to children <2 years of age in whom an appropriate age-adjusted GFR value should be used instead of GFR <60 mL/min/1.73 m2.

Mature adult renal function is only achieved at 2 years of age. In infants ≤3 months old, a duration of >3 months does not apply.

Causes of CKD in children

Causes of CKD can be primary, i.e. no systemic disease present, or secondary, i.e. systemic disease affecting the kidney.

The most common causes of CKD in children are: • congenital abnormalities of the kidney and urogenital tract (CAKUT), e.g. obstructive uropathy and reflux nephropathy • hypoplastic/dysplastic kidneys • primary focal and segmental glomerulo­ sclerosis (nephrotic syndrome) • haemolytic uraemic syndrome • immune complex glomerulonephritis/ chronic glomerulonephritis • hereditary nephropathies, e.g. polycystic kidney disease • other rarer causes, e.g. drug/toxin-related renal disease.

Glomerular filtration rate category

In children the estimated GFR (eGFR) is calculated using the modified Schwartz formula: [40 × height (cm)] ÷ serum creatinine (µmol/L) (ml/min/1.73 m2).

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Table 1. GFR categories GFR category*

GFR (mL/min/1.73 m2)

G1

≥90

G2

60 - 89

G3a

45 - 59

G3b

30 - 44

G4

15 - 29

G5

<15

*Applicable to all children >2 years of age.

Table 1 lists the GFR categories.

Proteinuria category

A positive urine dipstick test for proteinuria should be confirmed with quantitative proteinuria measurement (measured as urine:protein:creatinine ratio (g/mmol) on a spot urine sample). Table 2 shows the proteinuria categories applicable to children.

Proteinuria is influenced by age, e.g. infants usually have a higher urinary loss of both glomerular and tubular protein, underlying pathology, and stage of CKD. Proteinuria eventually develops in all patients with CKD and is both a marker and a risk factor for the progression of this condition.

Symptoms and signs of CKD

Acquired CKD is generally a silent disease, which may only become symptomatic in its

CONTINUING MEDICAL EDUCATION

Table 2. Proteinuria categories applicable to children Category

Protein:creatinine ratio (g/mmol)

Terms

P1

<0.02

Normal

P2

>0.02 - <0.2

Moderate increase, non-nephrotic range

P3

≥0.2

Nephrotic range proteinuria

more advanced stages. Symptoms are often nonspecific, e.g. infants usually present with feeding-related complaints. Poor growth is the single most common, and almost universal, feature in all children.

In infants with CAKUT, the disease may be discovered by routine antenatal ultrasound scanning during pregnancy. In older children, the diagnosis may come as a complete surprise when a pathological condition is discovered co-incidentally.

Medical history

This should start with the antenatal history and include the perinatal and infant periods and other preceding illnesses and investigations, and concentrate on current symptoms of all the major organ systems.

Of importance is the history of the antenatal period with regard to CAKUT in the fetus, including oligohydramnios, maternal disease (e.g. hypertension (HT), infections, diabetes mellitus), and drug exposure (e.g. nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitors).

Routine antenatal ultrasound scanning in the maternal and fetal unit is the most important diagnostic tool to diagnose CAKUT before the infant becomes symp­ tomatic. Ideally, every woman should have at least one antenatal ultrasound scan during pregnancy, which is the practice in developed countries.

Kidney disease presents with nonspecific complaints, which contributes to a delay in making the diagnosis. Parents are often unable to recall the onset of symptoms because of the insidious nature of the disease.

A family history of kidney disease or specific pathology in other systems associated with inherited kidney disease, such as deafness, ear and eye abnormalities and HT, may give an indication of the diagnosis.

Examination

Clinical features associated with CKD

Longitudinal assessment of weight, length/ height and skull circum­ference plotted on an appropriate growth chart, is most important when evaluating a child’s health. A complete physical examination should be done, including measurement of blood pressure

•

of dysmorphic red blood cells and red cell casts, which are diagnostic for glomerulonephritis.

Serum urea, creatinine and electrolytes.

Serum creatinine is necessary to calculate GFR. Serum urea is a poor tool to evaluate renal function, as it is influenced by hydration, nutritional status and protein intake.

Urine volume may be normal or increased (polyuria) (>4 mL/kg/hour), or decreased (oliguria) (<1.0 mL/kg/hour).

Serum calcium, phosphate, alkaline phosphatase and plasma parathyroid hormone should be determined to assess bone mineral disease and secondary hyperparathyroidism.

Renal ultrasound is necessary to demonstrate kidney size (small shrunken kidneys are characteristic of CKD) and exclude urinary tract obstruction.

There is no place for renal biopsy in patients with end-stage renal failure (ESRF).

(BP). HT in children is defined as systolic and/or diastolic BP ≥95th percentile for age, gender and height percentile. Ideally, one should use a BP percentile chart to interpret the BP level. Alternatively, a formula may be used, which provides a value corresponding to the 95th percentile BP for children of both sexes falling on the 50th percentile for height: • systolic BP (95th percentile) – 1 - 17 years old: 100+ (age in years × 2) • diastolic BP (95th percentile) – 1 - 10 years old: 60+ (age in years × 2) • diastolic BP (95th percentile) – 11 - 17 years old: 70+ (age in years).

•

Other presenting features include: • dysmorphic features typical of a syndrome associated with CAKUT, e.g. Eagle-Barrett syndrome • tachypnoea mimicking acute ‘respiratory distress’ to compensate for metabolic acidosis • chronic anaemia • bone mineral disease, i.e. bone pain and skeletal deformities • volume overload: oedema, HT, heart failure, pulmonary oedema • uraemic symptoms and signs: nausea, vomiting, pruritus, brownish skin pig­ mentation, uraemic frost • bleeding tendency (mucosa) • convulsions due to HT, hyponatraemia, hypernatraemia, hypo­calcaemia or uraemia.

Treatment

Special investigations

• A urine dipstick test is an invaluable tool for the diagnosis of glomerular disease.

• A urine dipstick test does not detect tubular proteinuria, in which case urine amino acids or the β2-microglobulin:creatinine ratio should be measured.

• If proteinuria is present, the protein:creatinine ratio should be measured in an early-morning urine sample (normal <0.02 g/mmol).

• If a urine dipstick test reveals leucocytes and nitrites, a sterile sample of urine should be obtained for microscopy, culture and sensitivity.

• Twenty-four-hour urine or timed urine collection for creatinine clearance is impractical in children.

• Microscopy done on urine sediment provides information on the presence

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April 2015, Vol. 105, No. 4

•

•

•

The principal renoprotective strategies with regard to modifiable risk factors for progression of CKD are the following: • Treat and control HT and fluid overload.

HT and cardiovascular disease are the two most common causes of death in children with CKD. • Treat proteinuria with an ACE inhibitor, even in the absence of HT. Minimise proteinuria, using maximum tolerable doses of ACE inhibitors.

• Control hyperphosphataemia and hyper­ parathyroidism and avoid hyper­calcaemia.

• Treat anaemia.

• Treat dyslipidaemia.

• Investigate and treat infections.

• Provide a balanced nutritious diet to allow for optimal growth.

Monitoring and followup of children with CKD

Intervals between follow-up visits depend on the age of the child, staging of CKD and presence of complications. Children with stage 1 and 2 CKD are best followed up once every 6 months. Those with stage 3 and 4 CKD need to be followed up every 2 - 3 months.

Physical assessment at each visit should include: • A complete physical examination. Monitor for end-organ damage of CKD. • Monitor anthropometry and assess nutritional status.

• Monitor BP and cardiovascular system for volume overload, left ventricular hypertrophy/dilatation.

CONTINUING MEDICAL EDUCATION

• Monitor mineral and bone disorder, looking for muscle weakness, delayed closure of the anterior fontanelle, bowing or deformities of the long bones.

• Assess neurodevelopment, especially in infants and children <5 years old.

• Fundoscopic examination must be done in all children with HT.

HT

The degree of HT correlates with severity of the underlying renal disease.

• Use long-acting drugs, preferably once daily.

• Evening administration may be more beneficial.

• Control BP to <90th BP percentile.

• In children with proteinuria, lower-target BP is recommended: 50 - 75th BP percentile as long as the child does not have symp­ toms of hypotension.

ACE inhibitors

• When proteinuria is present, an ACE inhibitor is the drug of choice for the treatment of HT. • Beneficial effects include: decreasing BP, decreasing proteinuria independent of its effect on systemic BP, and slowing down the progression of CKD. • ACE inhibitors should be administered over a run-in period.

• Enalapril 0.1 mg/kg/dose should be administered once daily.

• The dose may be increased to 0.5 mg/kg/day as a single dose or two divided doses.

• ACE inhibitor treatment is also indicated in all children with persistent nephrotic range proteinuria and a GFR >30 mL/min/1.73 m2, even in absence of HT.

Monitoring treatment

• ACE inhibitors may cause hyperkalaemia, worsen metabolic acidosis or cause decline in renal function.

• It is obligatory to confirm tolerability and monitor serum potassium, bicarbonate, and renal function within 5 - 7 days after the start of treatment, and regularly thereafter as indicated by the level of renal function.

• If the serum creatinine increases by >25%, hydration status should be checked, diuretics discontinued and dose of ACE inhibitor halved.

• If renal function does not improve, or hyperkalaemia of >5.5 mmol/L persists, discontinue ACE inhibitors.

Calcium channel blockers (CCBs)

• CCBs do not have renoprotective effects other than controlling BP. • They can increase proteinuria, and are best used in non-proteinuric patients or in combination with ACE inhibitor/angiotensin II receptor blocker treatment.

• Amlodipine 0.1 - 0.3 mg/kg/day as a single daily dose (maximum dose 10 mg/day).

β-blockers

• β-blockers decrease pulse rate, cardiac output, afterload and renin release.

• Administer atenolol 1 - 2 mg/kg as a single daily dose or in two divided doses per day.

Other antihypertensive drugs

If the BP remains uncontrolled, review treatment compliance. In most cases uncontrolled HT is caused by volume overload, a direct consequence of non-compliance relating to a low salt diet and drug treatment.

318

CKD – bone and mineral disorder

CKD is associated with progressive phosphate retention, secondary hyperparathyroidism and development of bone mineral disease.

Management

Management includes dietary restriction of phosphate, phosphate binders and activated vitamin D. Phosphate binders • These should be used in combination with dietary phosphate restriction.

• Most of dietary phosphate originates from protein-containing foods.

• Restrict intake of dairy, grains and cereals, soft drinks, and food containing baking powder.

• Start phosphate binders early when the eGFR <70 mL/min/1.73 m2 or serum phosphate >1.8 mmol/L. • Maintain parathyroid levels within the normal range.

Types of phosphate binders These include: • calcium carbonate, calcium acetate and sevelamer • calcium carbonate (Titralac) 1 - 4 tablets three times daily with meals • calcium acetate and sevelamer (Renagel) are more expensive and not commonly used in children.

Hydroxylated vitamin D (1α-hydroxycholecalciferol or 1,25 dihydroxycholecalciferol) therapy • CKD is associated with a decreased production of activated vitamin D. • Activated vitamin D should be given to all children with CKD with hypocalcaemia (serum calcium <2.2 mmol/L).

• If the serum phosphate is >2.5 mmol/L, hyperphosphataemia should be treated first to decrease serum phosphate to <1.8 mmol/L to prevent calcification of vascular and soft tissues.

• Start with α-calcidiol 0.25 µg/dose initially twice weekly.

• Increase the dose as necessary to maintain serum calcium in the upper normal range.

• Doses as high as 0.5 µg twice daily may be required.

Anaemia

Anaemia is defined as a haemoglobin (Hb) level of <11 g/dL in children 6 months - 5 years, <11.5 g/dL in those 5 - 12 years and <12 g/dL in those 12 - 15 years.

Investigations

• Complete blood count, including Hb, red cell indices, white cell count, differential count and platelet count.

• Absolute reticulocyte count.

• Serum ferritin level.

• Serum transferrin saturation.

• Serum B12 level.

• Serum folate level.

Management

• Maintain optimal nutrition.

• Exclude other factors that may contribute to anaemia, e.g. infections.

• Current available investigations are unreliable for the monitoring of iron status. Ferritin is an acute-phase reactant that may be elevated in malnutrition and systemic inflammation. The target serum ferritin level in the absence of inflammation is >100 ng/mL or 100 µg/L, and the target transferrin saturation (TSAT) is >20%.

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• If iron deficiency is present, treat with an oral iron supplement 6 mg/kg elemental iron/day administered before eating or taking phosphate binders.

• Intravenous iron may be more practical for patients on haemodialysis.

• All children with CKD who are on erythropoietin-stimulating agents (ESA) should be treated with iron (oral or parenteral) to maintain TSAT >20% and a ferritin level >100 ng/mL. • Consider treatment with ESA when anaemia is persistent despite correction of iron, folate and vitamin B2 deficiencies.

• BP must be controlled before starting ESA treatment.

• Start with 100 U/kg/week subcutaneously in two divided doses.

• Measure Hb, reticulocyte count and ferritin every 4 weeks.

• If the Hb increases <1 g/dL/month, exclude occult infection, blood loss or vitamin B12 or folate deficiency.

• If no cause is found, increase the ESA dose by 25 U/kg/week.

• Continue monitoring the Hb level every 4 weeks and adapt the dose.

• The maximum ESA dose is 300 U/kg/week.

• The target Hb is 10 - 12 g/dL. • Once the target Hb level of 12 g/dL has been reached, continue with this dose.

• If the Hb increases >12 g/dL, discontinue erythropoietin for one week, and continue with 25 U/kg less per week.

Dyslipidaemia

Dyslipidaemia is an independent risk factor for cardiovascular disease and progression of CKD.

Management

• Prevent malnutrition.

• Treat anaemia, correct metabolic acidosis and manage hyper­ parathyroidism.

• Lifestyle modification does not have impressive effects in children with dyslipidaemia.

• Consider treatment with a statin (hydroxymethylglutaryl co-enzyme A reductase inhibitor) in children >8 years of age with persistent total cholesterol levels >7 mmol/L. • Administer simvastatin 10 mg at night (maximum dose 40 mg at night).

• Investigate for rhabdomyolysis if the child complains of muscle cramps.

Fluid and electrolyte balance Sodium

• Infants with salt-losing CKD (obstructive uropathy and renal hypodysplasia) require NaCl supplementation. A starting dose of NaCl is 1 - 2 mmol/kg/day in divided doses. The dose is guided by serum sodium and chloride levels.

• Salt intake is restricted in patients with oedema, volume overload and HT. • No salt should be added to food during preparation. Avoid saltpreserved foods.

Water intake is not restricted and should be taken as desired.

319

Potassium

• Hyperkalaemia often occurs in association with catabolism and metabolic acidosis.

• Limit potassium intake if serum potassium >5.5 mmol/L. • Restrict potassium-rich foods (fruit juices, fresh fruits and vegetables).

• Soak vegetables for 24 hours before cooking or decant water twice during cooking.

• Discontinue drugs that can cause hyperkalaemia (e.g. ACE inhibitors, β-blockers, spironolactone).

• If serum potassium remains >5.5 mmol/L, treat with sodium polystyrene sulphonate (Kexelate) 1 g/kg/dose dissolved in dex­ trose water administered orally once or twice daily.

Acid-base status

• Chronic metabolic acidosis causes anorexia and is associated with protein wasting.

• Correction of acidosis improves growth, prevents bone demineralisation and helps to manage hyperkalaemia.

• Treat with NaHCO3- – starting dose 2 mmol/kg/day in 2 - 3 divided doses.

• Maintain serum HCO3- between 18 and 24 mmol/L.

Nutrition and diet

• Protein restriction has no beneficial effects on the progression of CKD in children.

• It is associated with poor growth and the development of malnutrition.

• Children with CKD need a high-calorie and normal protein diet for optimal growth.

• Nasogastric tube feeds/gastrostomy feeds should be given if indicated.

Vitamins and minerals

• Multivitamin 5 mL daily, including vitamins B1, B6, B12 and C. • Folic acid 2.5 mg daily.

Immunisation

• All children must complete routine immunisations according to the Expanded Programme of Immunisation schedule.

• Pneumovax (23 strain) 0.5 mL intramuscularly is given to children >2 years.

• Varicella zoster virus vaccine, 2 000 pfu/0.5 mL subcutaneously, reconstituted to 3 mL; two doses given with a 6-week dose interval.

• Check immunity against hepatitis B. In the absence of immunity, vaccinate as for any non-immune individual.

• Hepatitis B vaccine 1 mL (3 µg) intramuscular injection, three doses at monthly intervals.

• If the antibody level is considered non-protective or insufficient, give two booster doses one month apart.

Final recommendation

Once a child reaches stage 3 CKD, referral to a paediatric nephrologist is necessary to discuss and/or start planning the potential future need of renal replacement therapy with the parents.

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ARTICLE

Important causes of chronic kidney disease in South Africa M R Moosa,1 MB ChB, FCP (SA), MD, FRCP (Lond); I van der Walt,2 MB ChB, MMed (Int), Cert Nephrology (SA); S Naicker,3 MB ChB, MRCP, FRCP (Lond), FCP (SA), PhD; A M Meyers,4 MB BCh, FCP (SA), Cert Nephrology (SA), FRCP (Lond) Division of Nephrology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa Netcare Jakaranda Hospital, Pretoria, South Africa 3 School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa 4 Donald Gordon Medical Centre, Klerksdorp Hospital, and National Kidney Foundation of South Africa, Johannesburg, South Africa 1 2

Corresponding author: A M Meyers (nkfsa@mweb.co.za)

In hypertensive patients without chronic kidney disease (CKD) the goal is to keep blood pressure (BP) at ≤140/90 mmHg. When CKD is present, especially where there is proteinuria of ≥0.5 g/day, the goal is a BP of ≤130/80 mmHg. Lifestyle measures are mandatory, especially limitation of salt intake, ingestion of adequate quantities of potassium, and weight control. Patients with stages 4 - 5 CKD must be carefully monitored for hyperkalaemia and deteriorating kidney function if angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) are used, especially in patients >60 years of age with diabetes or atherosclerosis. BP should be regularly monitored and, where possible, home BP-measuring devices are recommended for optimal control.

Guidelines on the use of antidiabetic agents in CKD are presented, with the warning that metformin is contraindicated in patients with stages 4 - 5 CKD. There is a wide clinical spectrum of renal disease in the course of HIV infection, including acute kidney injury, electrolyte and acid-base disturbances, HIV-associated glomerular disease, acute-on-chronic renal disease and side-effects related to the treatment of HIV. S Afr Med J 2015;105(4):320. DOI:10.7196/SAMJ.9535

Blood pressure and chronic kidney disease

From 1999 to 2006 South Africa (SA) has seen a 67% rise in deaths owing to chronic kidney disease (CKD), and the prevention of this condition remains an important priority. Although accurate statistics are not available in SA, hypertension and type 2 diabetes mellitus (in line with worldwide trends) are the dominant diseases associated with end-stage kidney disease (ESKD), particularly in black ethnic groups. Levels of systolic and diastolic blood pressure (BP) are directly linked to the prevalence of CKD and the components of the metabolic syndrome.

Prevention of CKD at the population level requires interventions that improve lifestyles that lead to a reduction in BP, obesity, type 2 diabetes mellitus (DM) and smoking. At the primary practitioner level, it is mandatory to measure BP in all adult patients and, if the patient has hypertension, to routinely screen for evidence of CKD (urine dipsticks, and serum creatinine (with calculate glomerular filtration rate (GFR)) and associated comorbidities, such as type 2 DM.

Treatment of hypertension without overt CKD

• Patients with established hypertension should be treated in accordance with the South African Hypertension Society guidelines.

• The goal BP is <140/90 mmHg.[1] • It is particularly important to recognise patients at greatest risk for the development of malignant hypertension and progression to ESKD. These patients usually have severe hypertension (BP >180/100 mmHg) and are often young, lean black males without other major risk factors. It is important to initiate combination therapy with at least two antihypertensive agents, and patients should be followed up within 7 days to assess BP response.

Treatment of hypertension in patients with established CKD

• Hypertension is a cause of CKD and aggravates existing CKD, resulting in a vicious cycle. Antihypertensive therapy has been proven to disrupt this cycle.

• Hypertension is also a potent risk factor for cardiovascular disease (CVD). Control of hypertension prevents cardiovascular morbidity and mortality, especially in CKD. • It is important to understand that the pathogenesis of hypertension in CKD is related to overactivity of the renin-angiotensinaldosterone and sympathetic nervous systems, and volume overload. Angiotension II also plays an important role in the progression of CKD. These basic facts underlie the rationale for antihypertensive therapy.

• The most important objective of antihypertensive treatment is to achieve a BP of <130/80 mmHg; the secondary objective being to reduce proteinuria to at least 0.5 g/24 hours or <0.05 g/mmol on spot urine.

• Lifestyle changes are an essential adjunct to antihypertensive drugs. Smoking cessation, exercise and weight loss are encouraged and sodium content of the diet reduced to <100 mmol/day.

The latter can be checked by 24-hour urinary sodium analysis. Nonsteroidal anti-inflammatory drugs (NSAIDs) and other drugs that raise BP or worsen renal function must be avoided.

• In the absence of contraindications (bilateral renal artery stenosis, planned pregnancy or history of angioedema (angiotensinconverting enzyme (ACE) inhibitor only)), ACE inhibitors or angiotensin II receptor blockers (ARBs) are the preferred first-line drugs of choice, especially if proteinuria is present.

The agents should be titrated to their maximum recommended dosages.

• Treatment with ACE inhibitors and ARBs must be carefully monitored, especially in patients with stages 3 and 4 CKD who are prone to develop hyperkalaemia and deterioration in renal function, particularly if there is prerenal failure owing to overuse of diuretics

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•

•

•

•

or inter-current illnesses. However, from a physiological perspective, reninangiotensin system (RAS) inhibitors cause a rise in creatinine owing to a reduction in intraglomerular pressure – a 20% or less rise in creatinine is acceptable. The RAS inhibitor may be continued provided there is no further deterioration in renal function and the serum K+ remains <5.6 mmol/L. However, any greater rise should prompt the physician to withdraw the RAS inhibitor after excluding dietary contributions.

In the majority of patients combination therapy is required, often with ≥3 anti­ hypertensive drugs to reach the target BP. The next antihypertensive added to the RAS inhibitor is either a calcium channel blocker or a diuretic or both. Both enhance the activity of RAS inhibitors, and calcium channel blockers avoid the metabolic sideeffects of diuretics. However, diuretics are preferred when volume overload is present.

Thiazide or thiazide-like diuretics should be used in patients with normal renal function, and loop diuretics if renal function is impaired. Hydrochlorothiazide can be titrated to a dose of 25 mg/day. Furosemide should be given in divided doses because of its short duration of action.

If BP control is not achieved, review drug adherence; sodium restriction is warranted and BP control outside the office with either home or 24-hour BP monitoring should be assessed to exclude the white coat effect.

If after this the BP remains at >130/80 mmHg, there are two options: add low-dose spironlactone 25 - 50 mg/day, provided renal function is normal and K+ is carefully monitored, or introduce agents that block the sympathetic nervous system. A β-blocker

followed by a long-acting α-blocker or a centrally acting sympatholytic-like moxo­ nidine is a rational strategy.

• In recalcitrant patients consider minoxidil, but avoid long-term use in females and be aware of possible pericardial effusion in stages 4 and 5 CKD.

Summary

Control of hypertension is the most important factor in the primary prevention and progression of CKD. In patients with CKD, the goal BP is <130/80 mmHg and first-line therapy is the administration of an RAS inhibitor. However, multiple agents are often required to achieve the BP target.

Diabetic patients[2]

• DM is the most common cause of CKD worldwide.

• Both type 1 and 2 DM are on the increase.

• The incidence of CVDs is increased in diabetic patients.

Diagnosis of diabetic nephropathy

• It normally develops after DM duration of >10 years.

The clinical stages of diabetic nephropathy are given in Table 1.

Preservation of renal function

• Strict glycaemic control. HbA1c <6.5%.

• BP control. Aim for <130/80 mmHg. Avoid systolic BP <110 mmHg. • Use ACE inhibitors or ARBs as first-line therapy.

• Add other classes of BP medications to achieve the target BP. • Reduce proteinuria. Administer ACE inhibitors or ARBs for an antiproteinuric effect.

• Restrict salt intake (4 - 6 g/24 hours).

• Prevention of acute kidney injury. Avoid nephrotoxins (NSAIDs, aminoglycosides, X-ray contrast media).

• Attention to CVD risk. Most patients with DM and CKD do not reach stage 5 CKD, as they die early owing to CVD. • Lifestyle and nutrition.[4] Aerobic exercise daily for approximately 30 minutes is recommended. Smoking should be discontinued. Weight should be reduced.

Patients should be on a protein-restricted diet (0.6 - 0.8 g/kg/day predialysis; 1.2 g/kg/day on dialysis).

Table 1. Clinical stages of diabetic nephropathy[3] Stage

GFR

UAE

Blood pressure

Years

1. Hyperfiltration

Super normal

<30 mg/day

Normal

0-5

2. Microalbuminuria

High normal - normal

30 - 300 mg/day

Rising

5 - 15

3. Overt proteinuria

Normal - decreasing

>300 mg/day

Elevated

10 - 20

4. Progressive nephropathy

Decreasing

Increasing

Elevated

15 - 25

5. ESKD

<15 mL/min

Massive

Elevated

20 - 30

ESKD = end-stage renal disease; GFR = glomerular filtration rate; UAE = urinary albumin excretion.

Table 2. Modifications of antidiabetic drugs in patients with type 2 diabetes mellitus (adapted from the Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines) Dosing recommendation stages 3 and 4 CKD or kidney transplant

Dosing recommendation dialysis

Acetohexamide, tolazamide, tolbutamide

Avoid

Avoid

Chlorpropamide

Avoid when GFR <50 mL/min/1.73 m²

Avoid

Glipizide, gliclazide

Preferred sulfonylurea No dose adjustment

Preferred sulfonylurea No dose adjustment

Glyburide

Avoid

Avoid

Glimepiride

Initiate at low dose, 1 mg/day

Avoid

α-glucosidase inhibitors

Acarbose

Not recommended if serum creatinine >180 µmol/L

Avoid

Biguanides

Metformin

See text

Avoid

Meglitinides

Repaglinide

No dose adjustment

Avoid

Nateglinide

Initiate at low dose (60 mg before each meal)

Avoid

Thiazolidinediones

Pioglitazone, rosiglitazone

No dose adjustment

No dose adjustment

Class

Drug

First-generation sulfonylureas Second-generation sulfonylureas

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Pharmacological treatment of DM

Patients with stages 3 - 5 CKD are at risk of hypoglycaemia because of: • decreased renal clearance of insulin and sulfonylureas • impaired renal gluconeogenesis.

Type 1 DM Insulin needs may change with decreasing renal function, as CKD is associated with insulin resistance and there is decreased renal clearance of insulin with advancing CKD. Type 2 DM A number of different oral hypoglycaemic drugs are available (Table 2).

The benefits of intensive therapy are independent of the type of treatment administered.

Metformin Metformin should be used with caution in patients with stages 4 and 5 CKD. Its use in CKD carries a small risk of severe lactic acidosis; the risk increases with decreasing glomerular filtration rate (GFR) and the dose should be adjusted.

The use of metformin should be reviewed when the patient reaches stage 3 CKD and its use is contraindicated in stages 4 and 5 CKD. Sulfonylureas First-generation sulfonylureas should be avoided. Second-generation sulfonylureas may be used in patients who have learnt to avoid

hypoglycaemic episodes, as long as their diabetes is controlled and nutritional status is satisfactory.

Thiazolidinediones These may be used in patients without heart failure. Caution is advised in patients with ischaemic heart disease.

Insulin When insulin therapy is used, care should be taken to avoid hypoglycaemic episodes, as the renal clearance of insulin declines with advancing renal impairment.

Newer antidiabetic drugs • DPP-4 antagonists (vildagliptin, saxagliptin) can be used with dose adjustments. Avoid combination drugs that also contain metformin.

• GLP-1 receptor agonists (exenatide, liraglutide). These should not be used in moderate renal function impairment (creatinine clearance <30 mL/min).

HIV and CKD

Global prevalence of HIV infection

There are an estimated 35 million people infected with HIV, 68% of whom are in sub-Saharan Africa (SSA). Southern Africa is the worst affected, with the national adult HIV prevalence exceeding 15% in eight southern African countries.[5]

Table 3. Spectrum of renal disease in HIV • Electrolyte and acid-base disturbances • Acute kidney injury • CKD • Intrinsic renal disease unrelated to HIV itself (e.g. DM and hypertension) • HIV-associated glomerulonephropathies: may present as acute-on-chronic or chronic renal failure; this group is primarily implicated in the burden of CKD • Acute-on-chronic kidney disease • Side-effects related to treatment of HIV (ART and drugs used to treat complications of HIV) • Long-term metabolic side-effects of ART

Table 4. Spectrum of glomerular disease in HIV Glomerular pattern

Subtypes

HIV-FGS or ‘classic’ HIVAN (HIV-associated nephropathy)

Some have described a mixed variant of HIV-FGS in combination with a proliferative glomerulonephritis

HIV-ICD (this group of patients may have co-infection with hepatitis B or C)

Mesangial proliferative Membranoproliferative (type I and III) Lupus-like Exudative-proliferative Crescentic IgA Membranous

Various glomerulonephropathies (this is a heterogeneous group with different aetiologies)

Minimal change Immunotactoid Amyloidosis

HIV-TTP/HUS

TTP/HUS

Comorbid disease

Diabetic nephropathy Hypertensive nephrosclerosis Auto-immune disease (e.g. lupus nephritis)

FGS = focal glomerulosclerosis; HIV-ICD = HIV immune complex disease; TTP = thrombotic thrombocytopenic purpura; HUS = haemolytic uraemic syndrome.

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Table 5. Dose adjustments for ART in CKD and ESKD[19] Agent

CKD (adjusted according to creatinine clearance, or by eGFR)

Dialysis

Abacavir

No adjustment

No adjustment. HD: dosing independent of dialysis sessions

Azidothymidine/zidovudine (AZT)*

Cr cl ≥15 mL/min: no adjustment Cr cl <15 mL/min: 100 mg po q 6 - 8 h

100 mg po q 6 - 8 h* or 300 mg po qd

Didanosine (ddi)

Weight >60 kg

Weight <60 kg

Cr cl 30 - 59 mL/min: 200 mg po qd Cr cl 10 - 29 mL/min: 125 mg po qd Cr cl <10 mL/min: 125 mg po qd

125 mg po qd 100 mg po qd 75 mg po qd

Nucleoside/ nucleotide analogues

Dose for Cr cl <10 mL/min†

Emtricitabine‡

Cr cl >50 mL/min: no adjustment Cr cl 30 - 49 mL/min: 200 mg po q 48 h Cr cl 15 - 29 mL/min: 200 mg po q 72 h Cr cl <15 mL/min: 200 mg po q 96 h

200 mg po q 96 h† PD: no data

Lamivudine (3TC)*

Cr cl >50 mL/min: no adjustment Cr cl 30 - 49 mL/min: 150 mg po qd Cr cl 15 - 29 mL/min: 150 mg first dose, then 100 mg po qd Cr cl 5 - 14 mL/min: 150 mg first dose, then 50 mg po qd Cr cl <5 mL/min: 150 mg first dose, then 25 mg po qd

150 mg first dose, then 25 mg po qd†

Stavudine (d4T)

Cr cl >50 mL/min: no adjustment Cr cl 26 - 50 mL/min: 15 - 20 mg po bid Cr cl ≤25 mL/min: 15 - 20 mg po qd

20 mg po qd† PD: has been used safely

Tenofovir‡

Cr cl >50 mL/min: no adjustment Cr cl 30 - 49 mL/min: 300 mg q 48 h Cr cl 10 - 29 mL/min: 300 mg q 72 h

300 mg po every 7 days†

Zalcitabine

Cr cl ≥40 mL/min: no adjustment Cr cl 10 - 40 mL/min: 0.75 mg q 12 h Cr cl <10 mL/min: 0.75 mg q 24 h

HD: dose for Cr cl <10 mL/min† PD: no data

Non-nucleoside reverse transcriptase inhibitors

No adjustment

Protease inhibitors

No adjustment

No adjustment

Cr cl ≥35 mL/min: no adjustment Cr cl <35 mL/min: unknown, use with caution

Unknown, use with caution

No dosage recommendations Patients with Cr cl <50 mL/min should only receive maraviroc and CYP3A inhibitor if potential benefit outweighs the risk

No data

No adjustment

No adjustment

Entry/fusion inhibitor Enfuvirtide CCR5 receptor antagonist Maraviroc

Integrase inhibitor Raltegravir

Cr cl = creatinine clearance; HD = haemodialysis; PD = peritoneal dialysis. * Combination AZT/lamivudine tablets (300 mg/150 mg) should be administered separately when eGFR <50 mL/min. † Defer daily dose/s after haemodialysis (extraction of drug occurs on dialysis). ‡ Combination emtricitabine/tenofovir tablets (200 mg/300 mg). If Cr cl 30 - 49 mL/min: 1 tablet po q 48 h; if Cr cl <30 mL/min, the combination tablet should not be prescribed.

Spectrum of kidney disease with HIV infection

There is a wide clinical spectrum of renal disease (Tables 3 and 4) in the course of HIV infection.

Acute kidney injury in HIV

The causes of acute kidney injury (AKI) in hospitalised HIVinfected patients may be community or hospital acquired, the latter being 5 - 10 times more common than the former, with a worse outcome in hospital-acquired AKI.[6] The known causes of AKI are similar in HIV and non-HIV groups, the most common being acute tubular necrosis (ATN), secondary to sepsis, hypotension, dehydration and nephrotoxicity. AKI is

potentially reversible with appropriate medical treatment and, if indicated, dialysis support.[6,7] In studies of hospitalised patients with HIV infection, AKI occurred in up to 20% of cases, and age and ethnicity contributed to mortality. In another study, the short-term prognosis in this group of patients showed mortality of 18% at 2 months, with 80% of patients diagnosed with AIDS at the time of hospital admission. Since the advent of ART (antiretroviral treatment), a prospective study on AKI in ambulatory HIV-infected outpatients with access to ART concluded that more severe immunosuppression (CD4 <200 cells/mm3 and/ or HIV RNA level >10 000 copies/mL) is still the predominant risk factor for AKI.[8]

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Table 6. Common drug-drug interactions with ART[19] Class of drug

Concomitant medication

Effect

PIs

Anticoagulant: warfarin

Variable, check INR

Anticonvulsants: carbamazepine, phenobarbital, phenytoin

Variable, recommend therapeutic drug monitoring

Antifungals: ketoconazole, itraconazole, voriconazole

Levels of antifungals increased

Calcium channel blockers: diltiazem, nifedipine, verapamil, amlodipine, nicardipine, isradipine, felodipine, bepridil

Levels of CCBs increased Life-threatening arrhythmias with bepridil

HMG-CoA reductase inhibitors (statins): lovastatin, simvastatin, atorvastatin

Levels of statins increased â&#x20AC;&#x201C; risk of myopathy/ rhabdomyolysis Preferred: pravastatin, rosuvastatin, fluvastatin

Immunosuppressive drugs: cyclosporine, tacrolimus, sirolimus

Levels of immunosuppressive drugs increased, recommend therapeutic drug monitoring

Opioids: methadone

Levels of methadone may decrease; therefore, may have to increase dose

PDE5 inhibitors: sildenafil, vardenafil, tadalafil

Levels of PDE5 inhibitors increased, decrease dosage and increase dosing interval

Tricyclic antidepressants: amitriptyline, imipramine, desipramine, trazodone

Levels of tricyclic antidepressants increased

NNRTIs

Calcium channel blockers: warfarin, anti-arrhythmics, PDE5 inhibitors, cyclosporine

Plasma concentrations, clinical effects, and toxicities of concomitant medications should be closely monitored NNRTIs have less of an effect than PIs

Delaviridine

Statins*

Levels of statins significantly increased

Anticonvulsants

Carbamazepine, phenobarbital, phenytoin contraindicated due to very low levels of delaviridine

Glucocorticoids

Levels of glucorticoids increased

Immunosuppressives

Levels of sirolimus and tacrolimus increased

Statins

Levels of atorvastatin and simvastatin decreased

Glucocorticoids

Levels of glucocorticoids decreased

Nevirapine

Fluconazole

Fluconazole may double nevirapine levels

Glucocorticoids

Levels of glucocorticoids decreased

NRTIs and fusion inhibitors

Little or no effect on hepatic cytochrome P450 metabolism

Few drug-drug interactions

Efavirenz

PI = protease inhibitor; NNRTI = non-nucleoside reverse transcriptase inhibitor; CCB = calcium channel blocker. *Levels not affected by nevirapine and efavirenz.

HIV-associated CKD (HIV-CKD)

Screening studies from Africa differ widely in their reported prevalence of kidney disease in HIV. In most studies the prevalence of kidney disease has been assessed on the presence of albuminuria and/or estimated GFR (eGFR) (based on creatinine clearance).

Studies from Africa have shown a variable prevalence of renal disease in HIV, ranging from 6% to 45% (6% in SA, 38% in Nigeria, 26% in Cote dâ&#x20AC;&#x2122;Ivoire, 28% in Tanzania, 25% in Kenya, 20 - 48.5% in Uganda, and 33.5% in Zambia), depending on the populations studied and the criteria for diagnosis of kidney disease. Part of this wide variation may be ascribed to differences in study design, populations studied and definitions used for CKD. Recent literature recommends the CKD-EPI formula as the most reliable in calculating eGFR in this patient population.[9] Very few studies detail the histological pattern

of kidney disease on kidney biopsy and, fewer still, the response to treatment.

HIV-associated nephropathy (HIVAN)

Most African patients with HIVAN present late, with advanced kidney failure. This late detection of HIVAN could be because of a lack of screening for proteinuria and/ or renal dysfunction and the relative absence of overt symptoms and signs, such as peripheral oedema and hypertension.

Patient outcomes with HIVAN have been correlated with the clinical stage of their disease, suggesting that survival improves with earlier detection.[10] There is an increased relative risk of 2.5 - 3.0 for overall mortality with proteinuria after correcting for other risk factors. In one study, 77% of renal abnormalities developed with CD4 counts >200 cells/mm3.[11] This was also seen in a study from SA where the mean

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CD4 count of those with biopsy-proven HIVAN was 232 cells/mm3.[12] HIVAN has been revised by the World Health Organization (WHO) as stage 4 disease, thus emphasising the need for initiation of ART in this condition, irrespective of the CD4 count. The initial description of HIVAN in individuals of African descent has been attributed to the presence of APOL1 genetic variants.[13]

Screening for CKD in HIV

Statistics in the USA estimate the incidence of HIVAN as 3.5 - 12%.[14] If this were to be extrapolated to SSA, where an estimated 22 million are infected with HIV, between 770 000 and 2.64 million people would be predicted to have HIVAN. With the advent of wider access to ART, the epidemiological pattern of HIVAN that evolved in the USA over the last 14 years

CONTINUING MEDICAL EDUCATION

Table 7. Other causes of CKD Age groups Disorder

<45 years

>45 years

Ethnic groups Black

Other

+

++

Congenital/ inherited • ADPKD • RTA

+

Glomerular disease • Primary

+++

• Secondary

+

• PSGN

+ +++

+

++

+

+

+

+

Dosing of ART in CKD

+ +

+

• Malignancies (e.g. myeloma) Viral (not HIV) • Hepatitis B

++

++

+

• Hepatitis C

+/-

+/-

+/-

Renovascular*

+

++

+/-

++

Obstructive uropathy

+

+

+

++†

Chronic pyelonephritis

++

+

+/-

++

Renal calculi

++

+

+/-

+++

Toxicity (medication)

+++

+

+

+++‡

ADPKD = autosomal-dominant polycystic kidney disease; PSGN = post-streptococcal glomerular nephritis; RTA = renal tubular acidosis; SLE = systemic lupus erythematosus; +/-, +, ++, +++ = frequency of diagnosis. *Renovascular disease in young blacks, e.g. Takayasu syndrome (rare), or in older other ethnic groups, i.e. atheromatous. † Prostatic diseases. ‡ Toxicity of therapeutic medicines.

may predict what will happen in SSA. This presents a potentially unprecedented burden of CKD. The Infectious Diseases Society of America published guidelines for the management of CKD in HIV in 2005, with a revision in 2014, which included recommendations for screening,[9] e.g. all individuals should be assessed for kidney disease at the time of diagnosis of HIV infection and annually thereafter, with a screening urinalysis for proteinuria and estimation of renal function. It is important when interpreting the significance of proteinuria that it is persistent, as false positives are common in patients who may have comorbid conditions such as infection. Failing to confirm persistence of proteinuria can significantly impact on the number of referrals in high-prevalence populations. Any patient with persistent proteinuria, persistent haematuria or a GFR <60 mL/min/1.73 m2 should therefore be referred to an institution where a specialist can evaluate the patient. An important caveat is that if no referral system is available, clinicians should initiate ART as early as possible to prevent progression to end-stage kidney diseases (ESKD). Considering the resource limitations in SSA, with particular reference to renal replacement therapy (RRT), it is imperative that screening, early detection and treatment of HIV-CKD

Drugs and HIV-CKD

In addition to ART, patients are treated for opportunistic infections, malignancies, and comorbid chronic illnesses (DM/hypertension) and may be given immunosuppression for kidney transplantation. HIV-CKD is compounded by the nephrotoxic potential of long-term ART.

++ +

• SLE

HIV-infected cadaveric donor organs may be transplanted into HIV-infected recipients with ESKD. Four such transplants have been reported in Cape Town, with good graft and recipient survival, but the data are preliminary. A further >20 such transplants have been performed, with good results.[18]

be a public health priority. A screening algorithm (Fig. 1) is proposed for this purpose, accommodating resource-limited settings.

ESKD due to HIV-CKD

Life expectancy in HIV-infected patients has increased by 10 - 20 years in developed countries with the use of ART; many of these patients are now dying from the complications of ESKD and other chronic diseases, rather than HIV infection.

Currently, HIV-infected patients requiring either haemodialysis or peritoneal dialysis, who are stable on ART, are achieving survival rates comparable with those of dialysis patients without HIV infection. The choice of dialysis modality does not impact on survival.[16] Transplantation has been performed with success in HIV-infected patients. Preliminary short-term data in liver, kidney, and heart transplant recipients suggest that patient survival rates are similar to those in highrisk HIV-uninfected transplant recipients and there has been no increase in the prevalence of opportunistic infections. In spite of high rates of acute graft rejection, survival appears to be similar to high-risk HIV uninfected recipients.[17] In areas with high endemic rates of HIV infection, in view of the shortage of donor organs, it has been proposed that

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Many ARTs are partially or completely eliminated by the kidney and require dose adjustment in CKD; hence the necessity to measure renal function (Table 5).

Certain drug classes, such as the protease inhibitors (PIs) and the non-nucleoside reverse transcriptase inhibitors (NNRTIs), are metabolised by the liver and do not require dose adjustment. Entry/fusion inhibitors, integrase inhibitors, and CCR5 receptor antagonists also do not require dose adjustment.[19] Most of the NRTIs are excreted unchanged in the urine and require dose adjustment, with the exception of zidovudine and abacavir, which have substantial extrarenal biotransformation requiring less or no dose adjustment.

Factors that influence dialysability of ART relate to the properties of the dialysis membrane and molecular weight, degree of protein binding, molecular charge and water solubility of the drug. If removal of a drug occurs during haemodialysis, it should be taken after dialysis. If the drug is removed in peritoneal dialysis effluent, the dose may have to supplemented. Dosing recommendations in both haemo- and peritoneal dialysis are limited by the lack of reliable data. Fixed drug combinations should not be used in patients with an eGFR <30 - 50 mL/min.[19]

Drug interactions

The NNRTIs and PIs are metabolised and eliminated by the hepatic and intestinal cytochrome P450 enzyme system, in particular CYP3A4 and P-glycoprotein. Most interactions are a consequence of enzyme induction or inhibition and there are many drug-drug interactions (Table 6). Certain overthe-counter preparations can affect drug levels, such as St John’s Wort (Hypericum perforatum), which induces enzyme induction, causing lower PI and NNRTI levels. Concomitant use is not recommended.[19]

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Assessment for kidney disease in all HIV Risk factors: black race, family history of CKD, use of nephrotoxic agents (including traditional medicines), diabetes mellitus, hepatitis C, HIV viral load >4 000 copies/mL, CD4 count <200 cells/mL Urine dipstick test for leucocytes If leucocytes and/or nitrites are present: urine microscopy and culture Urinary tract infection (UTI) symptoms: treat empirically, adjust treatment according to culture results if indicated Sterile pyuria: exclude sexually transmitted infection (STI) (including syphilis) and/or tuberculosis -infected individuals at presentation Repeat urine dipstick at follow up visit 000 copies/mL, Urine dipstick test for proteinuria 3 If negative, test for microalbuminuria. If no proteinuria or microalbuminuria, repeat screen Investigations: urine dipstick and serum creatinine, calculate eGFR (CKD-EPI formula) in 12 months for those at risk of development of CKD !

! "#$%&'()*'(+#& ,!-.(#%!/(0&'(12!*#/!&%.-3!1.%*'(#(#%4!1*51-5*'%!%678!9:;< =>0(!?+.3-5*@

Proteinuria or microalbuminuria: exclude potential causes of proteinuria, e.g. fever, infection (UTI, STI, tuberculosis), pregnancy, uncontrolled diabetes, uncontrolled hypertension, cardiac failure Treat comorbid conditions: repeat urine dipstick in 1 month If nephrotic, nephritic or nephritic/nephrotic: refer for investigation and management Start antiretroviral treatment (ART)

At follow-up: persistent proteinuria/microalbuminuria and/or creatinine clearance <60 mL/min/1.73 m2 â&#x20AC;&#x201C; protein:creatine ratio or microalbumin:creatine ratio and investigate with kidney ultrasound scan, serological testing for hepatitis C, B, Plasmodium malariae (if appropriate, depending on infections endemic to the region), auto-immune screen Refer to a nephrologist, if available

If unable to refer: ART â&#x20AC;&#x201C; dose adjust according to eGFR If still proteinuric after 3 months on ART: start antiproteinuric agents + + K <5.0 mmol/L: ACE inhibitor or ARB and check K in one week + K >5.0 mmol/L: potassium-binding resin or non-dihydropyridine calcium channel blocker (verapamil or diltiazem) Manage stage of CKD appropriately Gradual up-titration of dose, depending on tolerance and severity of proteinuria Fig. 1. Management algorithm for screening HIV-infected patients for CKD (adapted from Fabian and Naicker[15]).

Summary

The extent of the HIV epidemic and its associated burden of CKD in SSA, coupled with the cost of RRT in a resource-limited setting, make it a challenging problem. The current stark reality in SA and many developing countries is that most people with ESKD

and HIV die; some have limited access to dialysis. Most clinicians deal with advanced stages of CKD in HIV and prevention or early detection of renal disease in this population is neglected. Primary healthcare practitioners need a working system for screening, early detection and referral. Referral centres require resources for

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appropriate investigation and treatment of those with confirmed CKD.

Other causes of CKD

Other important but less frequently encountered causes of CKD are briefly presented, sub-divided into two divisions based on age and ethnicity (Table 7).

Additional causes of CKD are renal tuberculosis, sarcoidosis and a number of other inherited or acquired but rare conditions. If there is any suspicion of any of the abovementioned disorders, timeous referral to a nephrologist or specialist physician is important.

References 1. Seedat YK, Rayner BL; Southern African Hypertension Society. South African Hypertension Guideline 2011.

S Afr Med J 2011;102(1 Pt 2):57-83.

2. National Kidney Foundation. KDOQAI Clinical Practice Guideline for Diabetes and CKD: 2012 Update. Clin J Kidney Dis 2012;60(5):850-886. [http://dx.doi.org/10.1053/j.ajkd.2012.07.005] 3. Parving H, Mauer M, Ritz E. Diabetic nephropathy. In: Brenner BM, ed. Brenner and Rector’s the Kidney. 7th ed. Philadelphia: WB Saunders, 2004:1777-1818.

4. Phisitkul K, Hezagy K, Chauhirun T, et al. Continued smoking exacerbates but cessation ameliorates progression of early type 2 diabetic nephropathy. Clin J Med Sci 2008;335(4):284-291. [http://dx.doi. org/10.1097/MAJ.0b013e318156b799] 5. UNAIDS Report on the Global AIDS Epidemic 2013. www.unaids.org/en/resources/documents/2013 (accessed 25 February 2015).

6. Lameire N, Van Biesen W, Vanholder R. The changing epidemiology of acute renal failure. Nat Clin Pract Nephrol 2006;2(7):364-377. [http://dx.doi.org/10.1038/ncpneph0218] 7. Vachiat A, Musenge E, Wadee S, Naicker S. Renal failure in HIV-positive patients – a South African experience. Clin Kidney J 2013;0:1-6. [http://dx.doi.org/10.1093/ckj/sft128] 8. Franceschini NS, Napravnik WF, Finn LA, Szczech JJ, Eron JJ Jr. Immunosuppression, hepatitis C infection, and acute renal failure in HIV-infected patients. J Acquir Immune Defic Syndr 2006;42(3):368-372. [http://dx.doi.org/10.1097/01.qai.0000220165.79736.d3] 9. Lucas GM, Ross MJ, Stock PG, et al.; HIV Medicine Association of the Infectious Diseases Society of America. Clinical Practice Guideline for the Management of Chronic Kidney Disease in Patients Infected with HIV: 2014 Update. Clin Infect Dis 2014;59(9):e96-138. [http://dx.doi.org/10.1093/cid/ciu617] 10. Winston JA, Klotman PE. Are we missing an epidemic of HIV-associated nephropathy? J Am Soc Nephrol 1996;7:1-7.

11. Gardner LI, Holmberg SD, Williamson JM, et al. Development of proteinuria or elevated serum creatinine and mortality in HIV-infected women. J Acquir Immune Defic Syndr 2003;32(2):203-209.

12. Han TM, Naicker S, Ramdial PK, Assounga AG. A cross-sectional study of HIV-seropositive patients with varying degrees of proteinuria in South Africa. Kidney Int 2006;69(12):2243-2250. [http://dx.doi. org/10.1038/sj.ki.5000339] 13. Genovese G, Friedman DJ, Ross MD, et al. Association of trypanolytic ApoL1 variants with kidney disease in African Americans. Science 2010;329:841-845. [http://dx.doi.org/0.1681/ASN.2010070730] 14. Ross MJ, Klotman PE. Recent progress in HIV-associated nephropathy. J Am Soc Nephrol 2002;13(12): 2997-3004. [http://dx.doi.org/10.1097/01.ASN.0000040750.40907.99] 15. Fabian J, Naicker S. HIV and kidney disease in sub-Saharan Africa. Nat Rev Nephrol 2009;5(10):591598. [http://dx/doi/org/10.1038/nrneph.2009.141] 16. Soleymanian TS, Raman FN, Shannaq FN, et al. Survival and morbidity of HIV patients on hemodialysis and peritoneal dialysis: One center’s experience and review of the literature. Int Urol Nephrol 2006;38(2):331-338. [http://dx.doi.org/10.1007/s11255-006-0080-8] 17. Stock PG, Roland ME, Carlson L, et al. Kidney and liver transplantation in human immunodeficiency virus-infected patients: A pilot safety and efficacy study. Transplantation 2003;76(2):370-375.

18. Muller E, Kahn D, Mendelsohn M. Renal transplantation between HIV positive donors and recipients.

N Engl J Med 2010;362(24):2336-2337. [http://dx.doi.org/10.1056/NEJMc0900837] 19. Berns JS, Kasbekar JN. Highly active antiretrovial therapy and the kidney: An update on antiretroviral medications for nephrologists. Clin J Am Soc Nephrol 2006;1(1):117-129.

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ARTICLE

Important complications of chronic kidney disease I van der Walt,1 MB ChB, MMed (Int), Cert Nephrology (SA); C R Swanepoel,2 MB ChB, MRCP (UK), FRCP (Edin); B Mahala,3 MB ChB, FCP (SA), MMed, Cert Nephrology (SA); A M Meyers,4 MB BCh, FCP (SA), Cert Nephrology (SA), FRCP (Lond) Netcare Jakaranda Hospital, Pretoria, South Africa Division of Nephrology and Hypertension, Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa 3 Netcare Waterfall City Private Hospital, Johannesburg, South Africa 4 Donald Gordon Medical Centre, Klerksdorp Hospital, and National Kidney Foundation of South Africa, Johannesburg, South Africa 1 2

Corresponding author: A M Meyers (nkfsa@mweb.co.za)

The complications of chronic kidney disease (CKD) are dyslipidaemia, hyperkalaemia, metabolic acidosis, anaemia, and bone and mineral disorders. Dyslipidaemia may be treated with low-density lipoprotein-lowering agents. Statins are ineffective in stages 4 and 5 CKD, but are indicated for preventing the progression of disease in the earlier stages. Chronic acidosis has recently been shown to be a risk factor in the progression of CKD renal dysfunction. Therefore, treatment is mandatory. Practically, this should consist of 1 - 2 heaped teaspoons of sodium bicarbonate 2 - 3 times per day, which is an inexpensive and safe therapy that does not raise the blood pressure in spite of the increased sodium level. Target levels of haemoglobin, according to international guidelines, are between 10 g/dL and 12 g/dL. The serum phosphate level is raised in stage 4 CKD, and especially in stage 5 CKD, which is associated with coronary carotid and other vascular calcifications and may result in ischaemic heart disease, myocardial infarction and stroke. A raised parathyroid hormone level (secondary hyperparathyroidism) is also a major risk factor for cardiovascular disease and is associated with increased hypertension and resistance to the treatment of CKD-associated anaemia.

S Afr Med J 2015;105(4):321. DOI:10.7196/SAMJ.9536

Dyslipidaemia

Chronic kidney disease (CKD) is associated with alterations in lipoprotein structure and function, including: • reduced high-density lipoprotein cholesterol • increased intermediate-density lipoprotein • increased proatherogenic lipid particles.

Significance of dyslipidaemia control

• Successful treatment of dyslipidaemia is known to lower cardio­ vascular disease (CVD) risk and should also retard the decline of kidney function.

• Since statins have been shown to decrease urinary protein or albumin excretion, they are recommended for CKD with proteinuria.

• Remarks on statin use in stages 3 - 5 CKD are given in Table 1.

• Concurrent use of statins and fibrates increases the risk of rhabdomyolysis.

Target for low-density lipoprotein cholesterol

• The Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines recommend the following for dyslipidaemia therapy in CKD: in cases of low-density lipoprotein cholesterol (LDL-C) <3.5 mmol/L, the first step is lifestyle modification; in cases of LDL-C >3.5 mmol/L, drug therapy should be contemplated in addition to lifestyle modification, including diet therapy, weight control and exercise.

• It is essential that LDL-C be lowered to ≤1.8 mmol/L.

KDOQI guidelines for cholesterol lowering in CKD patients (2013):

• Patients >50 years of age should receive a statin.

• Patients 18 - 49 years of age should receive a statin if another comorbidity is present.

• Kidney transplant recipients should receive a statin.

Treatment of hyperkalaemia and metabolic acidosis Hyperkalaemia

• As CKD progresses in stage, acidosis and hyperkalaemia are observed.

Hyperkalaemia is defined as a serum potassium level ≥5.5 mmol/L. Hyperkalaemia >7 mmol/L may potentially cause cardiac arrest; such cases should be treated as emergencies.

• If severe hyperkalaemia is observed, despite the absence of reduced kidney function, pseudohyperkalaemia, an artefact due to haemolysis of the blood specimen, should be considered.

• Hyperkalaemia is a risk factor for arrhythmias. In cases of severe hyperkalaemia, emergency levels should be confirmed by ECG abnormalities such as tenting T-waves, prolongation of PQ-times, followed by disappearance of the P-wave and widening of the QRS complex. Patients with life-threatening ECG findings, bradycardia and hypotension should be treated promptly, followed by treatment in conjunction with a nephrologist.

• Drug-induced hyperkalaemia in CKD is mostly caused by reninangiotensin-aldosterone inhibitors such as ACE inhibitors, angiotensin II receptor blockers (ARBs) and spironolactone or excessive intake of potassium-containing foods. Other causes include the administration of β-blockers, digoxin, nonsteroidal anti-inflammatory drugs (NSAIDs), trimethoprim or pentamidine.

• CKD caused by diabetic nephropathy may be associated with hyporeninaemic hypoaldosteronism, which may cause hyperkalaemia despite relatively well-preserved kidney function.

This is known as type IV renal tubular acidosis.

Emergency treatment • The first step is to stabilise the myocardium. The intravenous administration of calcium gluconate does not change plasma potassium, but transiently improves the ECG. The administration of calcium gluconate 20 mL intravenously over 1 minute can

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Table 1. Drugs for dyslipidaemia available in South Africa and cautionary remarks regarding their use in CKD Class

Generic name

Characteristics

Use in low GFR

3-hydroxy-3-methylglutaryl-CoA reductase enzyme inhibitors (statins)

Pravastatin Simvastatin Fluvastatin Atorvastatin Rosuvastatin

Inhibits cholesterol production in the liver Very effective to decrease TC, LDL-C Adverse reaction: liver damage, rhabdomyolysis Prolongs QT-interval on ECG

Main excretory route is the bile duct, i.e. it can be used in kidney damage (pravastatin is excreted mainly in the urine) Rhabdomyolysis may occur, although there is a low incidence in CKD. In stages 3 and higher CKD, careful follow-up is necessary Cyclosporine, which is often used in resistant nephrotic syndrome, may have adverse effects if used simultaneously

Anion exchange resins

Cholestyramine Colestimide

Inhibits bile acid circulation (intestine-liver) Lowers TC, LDL-C

No problems

Fibrates

Bezafibrate Fenofibrate

Lowers TG (very effective) Increases HDL-C Rhabdomyolysis Do not use with statins

Do not use bezafibrate or fenofibrate in kidney failure or dialysis patients Do not use for stages 4 and 5 CKD

Lowers TG Lowers Lp (a) Rash on face

No problems

Lowers TG Antiplatelet function: antiatherosclerosis Prevents absorption of cholesterol

No problems

Nicotinic acids

Others

Eicosapentaenoic acid Ezetimibe

TC = total cholesterol; TG = triglyceride; HDL-C = high-density lipoprotein cholesterol; LPL = lipoprotein lipase; Lp (a) = lipoprotein (a); GFR = glomerular filtration rate; ECG = electrocardiogram.

be repeated if there is no improvement in the ECG within 3 - 5 minutes.

• The second step is to shift the potassium from the extracellular to the intracellular compartment to try to rapidly decrease the serum potassium level. This can be done in three different ways: • Intravenous insulin combined with glucose. Administer 10 U short-acting insulin combined with 50 mL of 50% dextrose as a bolus, followed by an intravenous infusion of 5% dextrose to prevent hypoglycaemia.

• β2-agonist. Administer 20 mg salbutamol, a β2-agonist, by inhalation over 10 minutes, with onset of action approximately 30 minutes. (This is not usually required.)

• Sodium bicarbonate in CKD patients who are not yet on dialysis. Bicarbonate administration can lower serum potassium by enhancing renal potassium excretion. The effect is very slow and not of use in an acute situation unless the patient has severe metabolic acidosis that needs bicarbonate treatment.

• Once the previous temporary measures have been performed, further interventions are undertaken to remove potassium from the body.

• Loop diuretics are only successful in patients with adequate kidney function.

• The resin exchanger sodium polystyrene sulphonate (Kexelate) removes potassium from the blood into the gut in exchange for an equal amount of sodium. It is slow acting and the plasma potassium only starts decreasing within 1 - 2 hours. It can be given orally or as a retention enema. The amount given varies from 30 g to 60 g. This can be repeated, but tends to cause constipation.

• Haemodialysis is the treatment of choice for patients with advanced CKD and severe hyperkalaemia.

Prevention • Dietary counselling on potassium restriction.

• Avoid medications that interfere with renal excretion of potassium, e.g. potassium-sparing diuretics, NSAIDs, ACE inhibitors, ARBs. • Avoid drugs that interfere with potassium shifts from the intracellular to the extracellular compartments, e.g. non-selective β-blockers.

• In selected patients with sufficient residual kidney function treatment with a loop diuretic may be used to stimulate urinary potassium excretion.

Metabolic acidosis

Metabolic acidosis is characterised by: • low arterial blood pH (acidaemia) (<7.35) • reduced serum HCO3- concentration • decreased pCO2 (from respiratory compensation).

Systemic effects Metabolic acidosis may lead to a variety of changes in tissues and organs, e.g.: • cardiovascular changes such as tachycardia, bradycardia, hypotension and cardiac failure • life-threatening hyperkalaemia • nausea, vomiting and abdominal pain • confusion, with depression of the central nervous system.

The associated symptoms and signs will depend on the rate and magnitude of fall in the pH and of the underlying pathology.

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Uraemic acidosis Metabolic acidosis occurs in renal failure owing to a decreased ability to excrete H+ or an inability to produce ammonia.

In the early stages of CKD (GFR <40 mL/min), metabolic acidosis with a normal anion gap (AG) may become evident. As CKD progresses (GFR <20 mL/min), a high AG metabolic acidosis may result.

In advanced CKD, an increased AG is typical owing to the presence of retained acids such as sulphates, phosphates, urate and hippurate.

anaemia of chronic disease is mediated by inflammatory cytokines through the inhibition of erythropoietin production and efficacy and reduced iron availability.

Hepcidin is the key mediator of iron metabolism. In inflammatory states hepcidin blocks iron absorption in the gut and promotes iron sequestration in macrophages.

Other causes

Treatment principles Patients with metabolic acidosis are often very ill and their condition tends to deteriorate rapidly.

The routine administration of sodium bicarbonate is controversial, although it needs to be done to correct severe acidosis.

The potential complications of sodium bicarbonate administration include volume overload, especially in patients with renal or cardiac function impairment, hypernatraemia, hypokalaemia, hypocalcaemia and alkalosis.

The amount of bicarbonate required (mmol) can be estimated as follows: target plasma HCO3- (mmol/L) − current plasma HCO3- (mmol/L) × 40% body weight (kg).

Anaemia associated with CKD is most likely renal anaemia; however, the differential for other diseases must be considered true for stages 1 - 3 CKD. The evaluation of anaemia in CKD patients should include a complete blood count with red cell indices (mean corpuscular haemoglobin concentration, mean corpuscular volume). Renal anaemia is usually normochromic and normocytic. Vitamin B12 and folate deficiency may lead to macrocytosis, while iron deficiency or inherited disorders of haemoglobin may produce microcytosis. Iron studies should be performed to assess the level of iron in tissue stores or the adequacy of iron supply for erythropoiesis.

Anaemia may signify the presence of malnutrition or systemic illness. It is an independent risk factor for hospitalisation, CVD and mortality. ACE inhibitors can exacerbate anaemia.

Anaemia in CKD

Treatment of anaemia protects the heart

Anaemia is the most common complication of CKD and is associated with greatly reduced quality of life. Successful treatment of anaemia in renal disease may reduce the decline of kidney function. The target haemoglobin levels are 10 - 12 g/dL when treating anaemia in CKD. The treatment is costly and therefore rational consideration is mandatory.

Renal anaemia

Renal anaemia is typically normochromic normocytic. It is caused mainly by the impaired production of erythropoietin by the kidney and partly by uraemic toxins. Other causes that may play a role in CKD, especially in dialysis patients, are: • erythropoietin resistance (most significant) • bone marrow toxins (none has been isolated yet) • bone marrow fibrosis, secondary to hyperparathyroidism • ongoing inflammatory processes, e.g. untreated infections • haematinic deficiency (iron, folate and vitamin B12) • increased red cell destruction • abnormal red cell membranes, causing increased osmotic fragility • increased blood loss from occult gastrointestinal bleeding and blood sampling and during haemodialysis • ACE inhibition.

Erythropoietin is a glycoprotein hormone that stimulates red cell production by binding to erythropoietin receptors, located on early erythroid progenitor cells in the bone marrow.

The binding of erythropoietin to these progenitor cells saves them from apoptosis and therefore permits cell division and maturation into red cells. In CKD, the erythropoietin levels may be normal, but inadequate for the degree of anaemia. The mechanisms impairing erythropoietin production in diseased kidneys remain poorly understood. Inhibition of erythropoiesis by uraemic inhibitors is also possible and may contribute greatly to the anaemia of CKD; such factors have not been identified. Dialysis can improve renal anaemia and the efficacy of erythropoietin-stimulating agents. Patients with renal disease may develop chronic infections and other chronic diseases. Chronic disease contributes to anaemia in such cases. The

Anaemia exacerbates heart failure. Treatment of anaemia is beneficial for life expectancy and can also improve the prognosis of CVD. The quality of life is improved for those with a haemoglobin level within the target range.

Target level of haemoglobin

The Kidney Disease Improving Global Outcome (KDIGO) guidelines state that the haemoglobin level should range from 10.0 g/dL to 12 g/dL in CKD patients on dialysis. Pre-dialysis levels should be at 10 g/dL.

Role-sharing between nephrologists and primary care physicians

Early referral to a nephrologist is advisable. Once the treatment strategy has been decided, nephrologists and primary care physicians continue management in partnership.

Evaluation of iron deficiency

Evaluation of the iron deficit and correct iron supply is important in the treatment of anaemia. Anaemia may improve with the administration of iron supplements, even when the patient is not apparently iron deficient, as the use of recombinant erythropoietin may cause relative iron deficiency.

The KDOQI guidelines for recombinant human erythropoietin in CKD are: • serum ferritin >100 ng/mL before dialysis • serum ferritin >200 ng/mL in dialysis patients • transferrin saturation >20%.

Iron can be given either intravenously or orally. Intravenous iron is more efficacious, especially for dialysis patients and those on erythropoietin treatment.

Use of exogenous erythropoietins

There are currently a number of erythropoietin-stimulating agents available, including older, shorter-acting drugs and new, longer-acting ones. The appropriate agent and dose depend on a number of factors,

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including cost, efficacy and convenience. As these drugs are expensive and have side-effects, their management is best left to a nephrologist.

Bone and mineral disorders

Hyperphosphataemia is the key abnormality that sets off a cascade of metabolic events, resulting in bone mineral density of CKD. Phosphate is retained as renal function deteriorates – much the same as creatinine is retained. This retention becomes obvious as stage 3b CKD is reached. It will progressively worsen as end-stage is approached and must be lowered to within normal limits.

A high phosphate diet stimulates osteocytes to produce fibroblast growth factor 23 which, in turn, inhibits the hydroxylation of vitamin D to active 1,25 vitamin D3. Without vitamin D3, calcium absorption and bone remodelling are decreased. The resultant hypocalcaemia is a major stimulus for parathyroid hormone (PTH) release, with the consequent development of renal bone disease. Serum alkaline phosphatase is a marker of increased bone turnover. Therefore, high blood levels show PTH activity.

Of note, both hyperphosphataemia and vitamin D3 deficiency result in increased PTH secretion.

Initially the stimulus for PTH secretion may be controlled by increasing the serum calcium, reducing the phosphate levels in the blood and prescribing vitamin D3. This is the secondary hyper­ p arathyroidism stage (Table 2). However, with time and uncontrolled, prolonged stimulation of PTH secretion, the parathyroid hormones become autonomous and the stage of autonomous hyper­ p ara­ t hyroidism is reached (Table 3). Parathyroidectomy may now be necessary or expensive calcimimetic drugs must be administered to try to restore the disordered metabolic environment.

There is uncertainty about the interpretation of vitamin D3 level measurements. If they are to be measured, then 25-OH-vitamin D3 levels are recommended for assessment.

Table 2. Diagnosis of secondary hyperparathyroidism* Serum biochemistry

Normal range

Calcium

Below or low normal range

Phosphate

High

*PTH 2 - 9 times the normal range (check with the laboratory which assay and normal range) and low vitamin D3 levels: measure 25-OH-vitamin D3.

Table 3. Autonomous hyperparathyroidism* Serum biochemistry

Normal range

Calcium

Higher or high normal range

Phosphate

High

* PTH >2 - 9 times the normal range (check with the laboratory which assay and normal range).

Therapy

The steps for therapy are shown in Table 4. Non-calcium-containing phosphate binders are recommended when there is significant metastatic calcification and/or when hypercalcaemia is present.

Calcimimetics, which sensitise the parathyroid glands to serum calcium, are useful to prescribe in hyperparathyroidism when the serum PTH levels are high (2 - 9 times above the normal range – check with the laboratory for normal ranges). They have a role to play in diminishing PTH levels in any of the clinical situations that occur in CKD.

Follow-up blood measurements

These are given in Table 5.

These follow-up times are guidelines only and the tests should be performed more frequently if there are significant abnormalities.

Special points to note

• Involve a nephrologist early in the course of CKD. • Avoid over-suppression of the parathyroid glands, as this will lead to dynamic bone disease.

• The exact PTH level at which secondary and autonomous hyperparathyroidism is diagnosed is uncertain, because of vary­ ing assays. The biochemistry, as outlined above (together with radiographs of bones), must then be used to assist in the diagnosis.

• Be aware of trends in serum alkaline phosphatase levels; the level may be in the normal range but may have doubled from the previous reading.

• Osteoporosis accompanies bone disease that occurs in CKD. Bisphosphonates must not be used in stages 3 - 5 CKD patients.

Table 4. Steps for therapy Steps

Stages 3 - 4 CKD

Stages 5 - 5d CKD

Lower the serum phosphate

Calcium carbonate or non-calcium-containing phosphate binders, e.g. lanthanum carbonate or sevelamer carbonate

Calcium carbonate or non-calcium-containing phosphate binders, e.g. lanthanum carbonate or sevelamer carbonate

Increase the serum calcium

First administer calcium carbonate, then vitamin D3

First administer calcium carbonate, then vitamin D3

Table 5. Follow-up blood measurements Stage CKD

3-monthly

6-monthly

3

-

Calcium and phosphate levels

4

Calcium, phosphate and alkaline phosphatase levels

PTH levels 25-OH-vitamin D3

5

Calcium, phosphate and alkaline phosphatase levels

PTH levels 25-OH-vitamin D3

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ARTICLE

Drugs and the kidney S Naidoo,1 MB BCh, FCP (SA), Cert Nephrology (SA), MMed; A M Meyers,2 MB BCh, FCP (SA), Cert Nephrology (SA), FRCP (Lond) S chool of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand; Charlotte Maxeke Johannesburg Academic Hospital; and Wits Donald Gordon Medical Centre, Johannesburg, South Africa 2 Donald Gordon Medical Centre, Klerksdorp Hospital, and National Kidney Foundation of South Africa, Johannesburg, South Africa 1

Corresponding author: A M Meyers (nkfsa@mweb.co.za)

This article on drug nephrotoxicity is detailed, as it is important to be fully aware of renal side-effects of drugs with regard to prevention and early diagnosis in order to manage the condition correctly. Many therapeutic agents are nephrotoxic, particularly when the serum half-life is prolonged and blood levels are raised because of decreased renal excretion. Distal nephrotoxicity is markedly enhanced when the glomerular filtration rate (GFR) is reduced and is a particular threat in elderly patients with so-called ‘normal’ creatinine levels. In patients of 45 - 55 years of age the GFR is reduced by about 1 mL/min/year, so that an otherwise healthy person of 80 may have an estimated GFR (eGFR) of <60 mL/min or <50 mL/min, i.e. stage 2, 3 or 3b chronic kidney disease (CKD). Furthermore, other effects related to kidney dysfunction may be seen, e.g. worsening of hypertension with the use of non-steroidal anti-inflammatory drugs, increased bruising or bleeding tendency with aspirin, and hyponatraemia hypertension acidosis with angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers. Digoxin is contraindicated in stage 3 CKD, even in a reduced dosage. Other drugs can cause the direct formation of kidney stones, e.g. topiramate (used in the prophylaxis of resistant migraine).

Levofloxacin (Tavanic) can cause rupture of the Achilles tendon and other tendons.

Radiocontrast media must be used with care. Occasionally, strategies to prevent acute kidney insufficiency cause irreversible CKD, especially in patients with diabetes and those with myeloma who have stage 4 - 5 CKD. Gadolinium in its many forms (even the newer products) used as contrast medium for magnetic resonance imaging is best avoided in patients with stages 4 and 5 CKD. S Afr Med J 2015;105(4):322. DOI:10.7196/SAMJ.9537

The kidneys are the primary organs for maintaining homoeostasis of extracellular fluid volumes. They receive 20 - 25% of the cardiac out­ put. The nephron (Fig. 1), which is the functional unit of the kidney, determines the pharmacokinetics of various drugs. Each nephron is capable of producing urine and is composed of a glomerulus through which fluid is filtered from the blood and a long tubular system in which the filtered fluid is converted to urine. Surrounding the tubular system is an extensive network of capillaries – the peritubular capillary network – which is supplied with blood from the efferent arteriole,

Table 1. Pathophysiology of drug-induced nephropathy Level of the nephron

Action

Drugs

Preglomerular (afferent arteriole)

Afferent arteriolar constriction

Cyclosporine

Glomerulus

Decreased GFR (prostaglandins) Glomerulonephritis

NSAIDs Gold, NSAIDs Penicillamine, cisplatin

Proximal tubules

Acute tubular necrosis

Aminoglycosides, radiocontrast dyes

Distal tubules

Renal tubular acidosis type 4

ACE inhibitors, cyclosporine

Tubules and ducts

Crystalluria

Acyclovir, sulphonamide

Interstitium

Interstitial nephritis

Penicillin, allopurinol

Renal papilla

Papillary necrosis

NSAIDs, analgesics

Table 2. Diuretics: Mechanism of action and indications Diuretic

Mechanism of action

Indication

Loop

Blocks NaK2Cl (NKCC2) transporter in the thick ascending loop of Henle Blocks NaKCl

Fluid overload Hypertension Hypercalcaemia

Thiazide

Distal convoluted tubule Blocks electroneutral Na/Cl exchanger (NCCT) Reaches site of action in glomerular filtrate – higher doses required in low GFR (ineffective when serum creatinine >200 µmol/L)

Antihypertension, especially in combination with ACE inhibitors/ARBs In combination with loop diuretics for profound oedema

Amiloride

Blocks ENaC (channel for sodium secretion in collecting ducts under the control of aldosterone)

Spironolactone

Aldosterone receptor antagonist Reaches distal collecting tubules via bloodstream (not dependent on GFR)

April 2015, Vol. 105, No. 4

Often combined with loop diuretics or thiazide to capitalise on potassium-sparing action

CONTINUING MEDICAL EDUCATION

blood that has already passed through the glomerulus.

The kidneys perform two major functions.

Firstly, they excrete most of the end-products of the bodily metabolism, and, secondly, they control the concentration of most of the constituents of the body fluids. In normal kidney function the counter current multiplier system, together with the reninangiotensin-aldosterone system (RAAS), involves extracellular fluid volume control, electrolyte balance, waste product excretion, drug and hormone elimination/metabolism, blood pressure (BP) and haematocrit regulation, and calcium/phosphate balance (vitamin D3 metabolism).

Therefore, the kidney is involved in absorption, distribution, metabolism, eli­ mination, secretion and filtration, and the effects of drugs can be idiosyncratic or accu­ mulative (Table 1).

Many drugs and their metabolites are excreted by the kidney by glomerular filtration, by tubular secretion, or in some cases by both. Renal impairment has a significant effect on clearance of these drugs, with important clinical consequences.

The glomerular filtration rate (GFR)/ estimated GFR (eGFR) is an important tool in staging chronic kidney disease (CKD).

Pathophysiology of drug-induced nephropathy

Multiple drugs can affect the same site, e.g. acute tubular necrosis, which is the commonest cause of renal failure in adults, can be caused by aminoglycosides, radiocontrast dyes and many other drugs.

A single drug can affect different sites in the kidney, e.g. non-steroidal antiinflammatory drugs (NSAIDs) can cause acute renal failure, interstitial nephritis and glomerulonephritis (Table 1).

The nephron and electrolyte balance

Overall conclusions

Cumulative event rates from the primary outcome (fatal chronic heart disease (CHD) or non-fatal myocardial infarction (MI)) of the Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) treatment group, have demonstrated that because of the superiority of thiazide-type diuretics in preventing one or more major forms of cardiovascular disease (CVD) and their lower cost, they should be the drugs of choice for first-step antihypertensive drug therapy.

In Table 2 the mechanism of action and indications of diuretics are shown.

Table 3 lists the side-effects and half-life of diuretics.

Specific diuretics are listed in Table 4.

Spironolactone

Spironolactone as a class is a potassiumsparing diuretic. Its mode of action is antagonising the effect of aldosterone at levels of the mineralocorticoid receptor.

The aldosterone complex translocates to the nucleus to effect gene transcription.

Indications include the prevention of hypo­ kalaemia in patients on diuretics or digoxin.

It improves survival in advanced heart failure (Randomised Aldactone Evaluation Study).[1] Spironolactone can be used as an anti­ hypertensive (adjunctive third-line therapy for hypertension) or as a first-line drug (patients with Conn’s syndrome). Another indication is for the treatment of ascites in patients with cirrhosis.

The side-effects of aldactone include antiandrogenic effects through the antagonism of dihydrotestosterone at its binding site.

Drug interactions occur with other potassium-sparing drugs, e.g. angiotensinconverting enzyme (ACE) inhibitors/angio­ tensin II receptor blockers (ARBs) and potassium supplements.

(LoSalt may be used as an NaCl substitute in cooking.)

Table 5 lists diuretic adverse effects and drug interactions.

Table 3. Side-effects and half-life of diuretics Diuretic

Side-effect

Half-life

Loop

• • • •

Oral bioavailability between 10% and 90% Acts at luminal side of the thick ascending limb (NaK2Cl transporter) Highly protein bound Rebound after single dose T½: 4 hours

Thiazide

Metabolic • Hyperuricaemia, impaired glucose tolerance and electrolyte disturbances (hypokalaemia and hyponatraemia) • Volume depletion

Electrolyte imbalance Hypokalaemia Volume depletion (prerenal uraemia) Tinnitus (acts within the cochlea – can synergise with aminoglycoside antibiotics

T½: 3 - 5 hours

Filter plasma Reabsorb good stuff

Fig. 1. The nephron.

April 2015, Vol. 105, No. 4

Reabsorb water as needed

Eliminate waste Acid base Electrolytes Blood volume Calcium balance

Adjust Na, K, H

Keep medulla hypertonic

The different diuretics include the loop diuretics, thiazide diuretics, aldactone and osmotic agents. They can by their effect on the nephron significantly alter electrolyte balance.

The indications for diuretic use include heart failure (acute or chronic), pulmonary oedema, hypertension, nephritic syndrome, hypercalcaemia and hypercalciuria. Diuretic drugs increase urine output by the kidney, i.e. they promote diuresis. This is accomplished by altering the manner in which the kidney handles sodium. If the kidney excretes more sodium, the water excretion will also increase. Most diuretics produce diuresis by inhibiting the reabsorption of sodium

at different segments of the renal tubular system. Sometimes a combination of two diuretics is given as it can be significantly more effective than either compound alone, the reason being that one nephron segment can compensate for altered sodium reabsorption at another nephron segment; therefore, blocking multiple nephron sites significantly enhances efficacy.

CONTINUING MEDICAL EDUCATION

Nephrotoxic drugs

Table 4. Specific diuretics Class

Drug

Thiazide

Chlorothiazide

Comments

Chlorthalidone

Thiazide-like in action, not in structure

Hydrochlorothiazide

Prototypical drug

Hydroflumethiazide Indapamide

Thiazide-like in action, not in structure

NSAIDs

Methyclothiazide Metolazone

Thiazide-like in action, not in structure

Polythiazide Loop

Bumetanide Ethacrynic acid

Furosemide

Torsemide K+-sparing

Carbonic anhydrase inhibitors

Nephrotoxic drugs may have a dose-dependent effect and/or cause idiosyncratic renal damage.

Dose-dependent nephrotoxic drugs include NSAIDs, such as cyclo-oxygenase-2 (COX-2) inhibitors, aminoglycosides and radio-opaque contrast materials. Idiosyncratic renal damage may be secondary to NSAIDs, penicillins, gold and penicillamine.

Amioloride

Distal tubule Na+-channel inhibitor

Eplerenone

Aldosterone receptor antagonist; fewer side-effects than spironolactone

Spironolactone

Aldosterone receptor antagonist; side-effect: gynaecomastia

Triamterene

Distal tubule Na+-channel inhibitor

Acetazolamide

Prototypical drug; not used for treating hypertension or heart failure

Dichlorphenamide

Not used for treating hypertension or heart failure

Methazolamide

Not used for treating hypertension or heart failure

Table 5. Adverse effects and drug interactions of diuretics Class

Adverse side-effects

Drug interactions

Thiazide

Hypokalaemia Metabolic alkalosis Dehydration (hypovolaemia), leading to hypotension Hyponatraemia Hyperglycaemia in diabetics Hypercholesterolaemia, hypertriglyceridaemia Increased low-density lipoproteins Hyperuricaemia (at low doses) Azotaemia (in renal disease)

Hypokalaemia potentiates digitalis toxicity NSAIDs: reduce diuretic efficacy Beta-blockers: potentiate hyperglycaemia, hyperlipidaemias Corticosteroids: enhance hypokalaemia

Loop

Hypokalaemia Metabolic alkalosis Hypomagnesaemia Hyperuricaemia Dehydration (hypovolaemia), leading to hypotension Dose-related hearing loss (ototoxicity)

Hypokalaemia potentiates digitalis toxicity NSAIDs: reduce diuretic efficacy Corticosteroids: enhance hypokalaemia Aminoglycosides: enhance ototoxicity, nephrotoxicity

K+-sparing

Hyperkalaemia Metabolic acidosis Gynaecomastia (aldosterone antagonists) Gastric problems, including peptic ulcer

ACE inhibitors: potentiate hyperkalaemia NSAIDs: reduce diuretic efficacy

Carbonic anhydrase inhibitors

Hypokalaemia Metabolic acidosis

April 2015, Vol. 105, No. 4

The NSAIDs are commonly used and have a wide range of pathological and physiological effects. They interfere with prostaglandin production, disrupt regulation of renal medul­lary blood flow and salt water balance.

With habitual use they can cause chronic renal impairment. Their effect can be exacerbated by other drugs (antihypertensives, ACE inhibitors). They have typical radiological features with advanced renal dysfunction.

The pharmacology of the NSAIDs includes good absorption and hepatic metabolism, they are highly protein bound and are excreted by both enterohepatic and renal routes. Their half-lives vary. They have common therapeutic indications and adverse effects. Even though their pharmacokinetics and potencies differ and they are from different chemical families, their mechanism of action is similar. NSAIDs are cyclooxygenase inhibitors with different levels of selectivity for COX-1 and COX-2 enzymes.

Their similarities are more striking than their differences.

The role of prostaglandins is described in Table 6.

Table 7 lists the functions of COX-1 and COX-2 enzymes.

NSAIDs such as ibuprofen, diclofenac and indomethacin have short half-lives, with a more rapid effect and clearance.

The following NSAIDs have a longer halflife and slower onset and clearance: e.g. naprosyn, celecoxib, rofecoxib, nabumetone and piroxicam.

NSAID toxicity is wide and variable on the gastrointestinal, renal, haematological, central nervous and hepatic systems, as well as on the skin, and causes allergies.

Table 6. Role of prostaglandins Pathological

Physiological

• • • • • • • •

• • • • • •

Asthma Ulcers Diarrhoea Dysmenorrhoea Inflammation Bone erosion Pain Fever

Temperature control Bronchial tone Cytoprotection Intestinal mobility Myometrial tone Semen viability

CONTINUING MEDICAL EDUCATION

Table 7. Functions and location of COX-1 and COX-2 enzymes COX-1

COX-2

• • • • •

• • • • •

Constitutively expressed Housekeeping function Present in every organ Stomach, kidney, intestine, platelets Vascular endothelium

Inducible Inflammatory Necrotic sites Present in the kidney Uterus, ovary, brain, small intestine

Table 8. NSAID classification Non-selective inhibition Acetic acid derivatives • Diclofenac • Etodolac • Indomethacin • Sulindac • Tolmetin

Proprionic acid derivatives • Fenoprofen • Flurbiprofen • Ibuprofen • Ketoprofen • Naproxen • Oxaprozin

Naphthyl alkanone • Nabumetone

Fenamate derivatives • Meclofenamate • Mefenamic acid

Salicylates • Aspirin • Diflunisal • Choline magnesium trisalicylate • Salicylate

Enolic acid derivatives • Piroxicam • Meloxicam Selective COX-2 inhibition • Celecoxib • Rofecoxib

The renal effects are secondary to lowered renal blood flow, with decreased renal prostaglandins. The risk factors are volume depletion, and renal, liver and vascular disease.

The patient with NSAID toxicity typically presents with oedema, high BP and increased creatinine levels. The following may also be present: nephrotic syndrome: interstitial neph­ ritis; electrolyte imbalance: K+; attenuation of BP medication; papillary necrosis; and kidney stones.

The prostaglandin pathway can be seen in Fig. 2.

The classification of NSAIDs is given in Table 8.

These drugs have common drug interactions with antihypertensive treatment, phenytoin, anticoagulants and methotrexate.

NSAID-induced deterioration of renal function depends on the specific drug, the dose, the duration of the pharmacological effect, and particularly the state of health of the recipient.

Renal syndromes associated with the use of NSAIDs are: • vasomotor acute renal failure • nephrotic syndrome associated with interstitial nephritis • CKD • sodium retention • hyponatraemia • hyperkalaemia.

Tissue injury Phospholipids Leukotrienes • Bronchoconstriction

Arachidonic acid

Inhibitors • NSAIDs (non-COX-2) • Aspirin

COX-1 (constitutional)

Cytoprotective prostaglandins • Protect gastric mucosa • Aid platelet aggregation

COX-2 (inducible)

Inducers • Cytokines • Growth factors Inhibitors • COX-2 inhibitors • NSAIDs (non-COX-2) • Aspirin

Inflammatory prostaglandins • Recruit inflammatory cells • Sensitise skin pain receptors • Regulate hypothalamic temperature control

Fig. 2. The prostaglandin pathway.

April 2015, Vol. 105, No. 4

CONTINUING MEDICAL EDUCATION

For risk factors for acute vasomotor renal failure induced by NSAIDs, see Table 9.

COX-2: Renal In knock-out mouse models with renal disease the pathology shows fibrosis, inflammation and papillary changes. Clinical studies have shown oedema that resolves with drug withdrawal.

Drug-induced acute interstitial nephritis

The features are renal impairment with tubular function defect, such as acidosis, increased potassium level, and decreased urinary concentration ability. There may be fever, skin rash, eosinophilia or eosinophiluria (allergic reaction). The kidneys are of normal size (as the condition is acute, there is no time for the kidneys to shrink), with proteinuria of <2 g/day. The condition may occur within hours and is reversible in most cases. There is interstitial oedema with polymorph infiltration and eosinophils.

The drugs that induce acute interstitial nephritis are given in Table 10.

Table 9. Risk factors for acute vasomotor renal failure induced by NSAIDs Decreased EABV

Normal or increased EABV

• • • • • • • •

• • • • • •

Congestive heart failure Cirrhosis Nephrotic syndrome Sepsis Haemorrhage Diuretic therapy Postoperative patients (with third-space fluid loss) Volume depletion/hypotension

Chronic kidney disease Glomerulonephritis The elderly Contrast-induced nephropathy Obstructive uropathy Cyclosporine, tacrolimus use

EABV = effective arterial blood volume.

Table 10. Drug-induced acute interstitial nephritis Classes Antibiotics

Diuretics

Others

Penicillins

Furosemide

Captopril

Cephalosporins

Thiazides

Amphotericin B

Rifampicin

NSAIDs

Sulfonamides Ciprofloxacin

Diagnosis • Reversal of renal failure after discontinuing the drug.

• Renal biopsy (if the cause of acute renal failure is uncertain, or known but a biopsy is taken to ascertain that there are no other causes).

high peak concentration-enhancing efficacy with a long postdose effect. A single daily dose is less nephrotoxic. The dose depends on size and renal function. It is important to measure aminoglycoside levels.

interval may have to be adjusted. The halflife is often prolonged. Therefore, reduce the dose or increase the dosing interval.

Some drugs have active metabolites that are excreted renally, e.g. warfarin and diazepam.

Treatment • Withdrawal of the drug.

• Corticosteroid (30 - 60 mg/day).

• Supportive dialysis if needed (temporarily in acute renal failure).

Intravenous contrast

It is commonly used for computed tomo­ graphy scanning, intravenous urography and angiography. It is unsafe in patients with preexisting renal impairment. The risk increases in diabetic nephropathy, heart failure and dehydration. Contrast can precipitate ESRF. There is a cumulative effect with repeated administration. The risk can be reduced by using acetylcysteine.[2]

Amphotericin

Drug-induced chronic interstitial nephritis Features • Renal impairment that leads to end-stage renal disease (ESRD).

• Small-size kidneys, with proteinuria <2 g/day.

• Tubular function defect.

• Occurs within months or year.

• Not reversible, so if left untreated it will lead to ESRD. • Pathology.

• Tubular atrophy and interstitial fibrosis (there is no eosinophilia).

Possible causes Analgesics, NSAIDs, cisplatin, cyclosporine.

Aminoglycosides

The aminoglycosides are highly effective antimicrobials that are bactericidal, but nephrotoxic and ototoxic, with a narrow thera­ peutic range. When prescribing aminogly­ cosides, a once-daily regimen is recommended in patients with normal kidneys. There is a

Prescribing in kidney disease Patients include those: • with renal impairment • on dialysis • with renal transplants.

Principles

It is important to establish the type of kidney disease. Most patients with kidney failure are taking a number of drugs. Therefore, interactions are common and care needs to be taken to avoid drug toxicity. Patients with renal impairment and renal failure are often also taking antihypertensive drugs and phosphate binders.

Dosing in renal impairment

The loading dose does not usually need to be changed. Maintenance doses or the dosing

April 2015, Vol. 105, No. 4

Amphotericin is an antifungal agent for topical and systemic use. It is a lipid-soluble drug that binds steroid alcohols (ergosterol) in the fungal cell membrane, causing leakage of cellular content and death. It is effective against Candida species and is both fungistatic and fungicidal, depending on the concentration. It has a broad spectrum of activity (Candida, Cryptosporidium).

It is administered intravenously for systemic invasive fungal infections and can be used orally for gastrointestinal mycosis.

Side-effects include local/systemic effects with infusion (fever). It can cause chronic kidney dysfunction, with a decline in GFR with prolonged use. Other effects include tubular dysfunction (membrane permeability), hypokalaemia, renal tubular acidosis (bicarbonate wasting type 1/distal), diabetes insipidus, and hypomagnesaemia.

Caution should be taken with prehydration/ saline loading to avoid problems. Toxicity can be further reduced substantially by liposomal packaging of amphotericin.

Lithium

Lithium carbonate is used for the treatment of bipolar mood disorder. Its toxicity is closely related to serum levels. Symptoms and signs include cardiovascular arrhythmias

CONTINUING MEDICAL EDUCATION

Table 11. Renal toxicity of antiviral therapy Antiretroviral class

Antiretroviral therapy

Renal effect

Clinical recommendations

Protease inhibitors

Indinavir

Nephrolithiasis, crystalluria, dysuria, papillary necrosis, acute kidney injury, interstitial nephritis Ritonavir/lopinavir may increase toxicity of indinavir

Daily fluid intake of >2 L/day

Ritonavir

Reversible acute renal failure (usually in combination with nephrotoxic drugs)

Reverse transcriptase inhibitors

Other

Saquinavir, nelfinavir

Renal calculi (rare)

Increased fluid intake

Tenofovir, abacavir

Renal tubular damage: proximal tubular dysfunction, Fanconi syndrome, nephrogenic diabetes insipidus, acute tubular necrosis, acute renal failure

Patients on tenofovir should be monitored for signs of tubular dysfunction (glycosuria, acidosis, mild increase in plasma creatinine level, and proteinuria)

Didanosine, lamivudine, stavudine

Isolated case reports of tubular dysfunction

Cidofovir, adefovir

Renal tubular damage, proximal tubular dysfunction (cidofovir)

(especially junctional dysarrhythmias) and central nervous system tremor, confusion, coma and neprhrogenic diabetes insipidus.

Treatment is supportive and includes haemodialysis and colonic irrigation for very high levels. There is inadvertent toxicity from interactions with ACE inhibitors, and loop and thiazide diuretics. Carbamazepine and other anti-epileptics increase neurotoxicity.

Digoxin

Digoxin toxicity (high levels) is demonstrated in 10% of patients and toxicity has been reported in 4% of a series of 4 000 digoxin samples assayed.

The pharmacokinetics include a large volume of distribution (reservoir is skeletal muscle). About 30% of stores are excreted in urine per day.

Treatment of digoxin toxicity includes supportive correction of electrolyte imbalance. Atropine should be administered for bradycardia, and stimulants should be avoided because of arrhythmogenicity. Absorption can be limited with the use of charcoal (or cholestyramine) within 8 hours. Specific measures include the use of digoxin immune fab (Digibind and DigiFab) (digoxin-specific antibodies), which binds plasma digoxin, and the complex is eliminated by the kidney. These antibodies are used when serum drug values approach those of an overdose or are near arrest levels. Furthermore, digoxin elimination can be enhanced by using charcoal/cholestyramine to interrupt enterohepatic cycling. Dialysis is ineffective.

Antituberculosis drugs

Tuberculosis can be a difficult therapeutic problem in patients with renal failure. Rifampicin and isoniazid may be given in the normal dosage. Neither is cleared significantly by dialysis. Pyridoxine should be given with isoniazid to prevent peripheral neuropathy.

The plasma half-life of ethambutol is prolonged in renal impairment.

If the GFR is <30 mL/min, the dose should be 10 - 15 mg/kg/day, with a further reduction to 4 mg/kg/day if the GFR is <10 mL/min.

Although 10 mg/kg/day has been used at these levels of GFR, cases of optic atrophy have been reported. Ethambutol is not dialysed to any significant extent. Pyrazinamide should be given at a reduced dose (10 - 15 mg/kg). Capreomycin is a second-line drug, which can be used in isoniazid or streptomycin resistance. It is, however, nephrotoxic and ototoxic, but can be administered in a single dose of 500 mg. In patients receiving multiple transplants, and who are on cyclosporine, rifampicin cannot be used as it reduces the concentration of cyclosporine very substantially as a result of hepatic enzyme induction. The necessity to use more than three agents will be dictated by the nature and severity of the infection.

Treatment may need to be prolonged (9 - 12 months) in uraemic or immunosuppressed patients, in contrast to the shorter courses that are preferred in patients with normal renal function.

Antiretroviral therapy (ART)

Renal toxicity of antiviral therapy is shown in Table 11.

Refer also to the Table on dose adjustments for ART in CKD and ESRD in the HIV and CKD section of the article ‘Important causes of CKD in South Africa’.[3]

Other drugs

Intravenous iodinated radiocontrast agents labelled with gadolinium are used as contrast media in patients undergoing MRI scans.

Gadolinium is contraindicated in patients with stages 4 and 5 CKD, as it can result in a diffuse systemic fibrosis (sclerosis-like syndrome with quadriplegia and eventual death). It is perfectly acceptable to perform an MRI without contrast if indicated.

References 1. Pitt B, Zannad F, Remme W, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. New Engl J Med 1999;341(10):709-717.

2. Tepel M, van der Giet M, Schwarzfeld C, Laufer U, Liermann D, Zidek W. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med 2000;343(3):180-184.

3. Moosa MR, Van der Walt I, Naicker S, Meyers AM. Important causes of chronic kidney disease in South Africa. S Afr Med J 2015;105(4):320. [http://dx.doi.org/10.7196/SAMJ.9535]

April 2015, Vol. 105, No. 4

CONTINUING MEDICAL EDUCATION

Chronic kidney disease List of contributors to the articles and information compiled by the National Kidney Foundation of South Africa Enquiries: Fanie du Toit (email: nkfsa@mweb.co.za; tel. number: 011-4472531)

List of contributors

Prof. A M Meyers Prof. A G Assounga Dr T Gerntholtz Dr P Hsu Dr B Mahala Prof. M R Moosa Prof. S Naicker Dr S Naidoo Dr I P Naiker Dr G Paget Prof. C R Swanepoel Prof. I van Biljon Dr I van der Walt Prof. B van Rensburg

The National Kidney Foundation of South Africa (NKFSA) is most grateful to all the contributors, both from the public and private sectors, who have given so much of their time to make this publication possible.

References

The CME articles on chronic kidney disease (CKD) were inspired by and based on the format used in the Japanese Guidelines for the treatment of CKD. (Japanese Society of Nephrology. Japanese Guidelines. Clin Exp Nephrol 2009;13(3):192-248. [http://dx.doi.org/10.1007/s10157-009-0188-0]) Other references are included in some instances, but any reference not included may be requested by sending an email to nkfsa@mweb.co.za

Other resources and references

South African Renal Society (SARS): www.sa-renalsociety.org/ South African Transplantation Society (SATS): www.sats.org.za/ International Society of Nephrology (ISN): www.theisn.org S Afr Med J 2015;105(4). DOI:10.7196/SAMJ.9598

April 2015, Vol. 105, No. 3

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9.

According to the NCCEMD, deaths ascribed to haemorrhage resulted from inadequate utilisation of uterotonic agents.

Intrapartum asphyxia and hypoxic ischaemic encephalopathy 10. Of infants suffering intrapartum asphyxia, 50% will die in the neonatal period and 50% of survivors will develop permanent neurodevelopmental abnormalities including cerebral palsy.

CME Paediatric chronic kidney disease (CKD) 11. There is no need to confirm a positive urine dipstick test for proteinuria with a quantitative proteinuria measurement.

Important causes of CKD in SA 12. Regarding hypertension, when CKD is present, especially where there is proteinuria of ≥0.5 g/day, the goal is a blood pressure of ≤130/80 mmHg. 13. Metformin is contraindicated in diabetic patients with stages 4 - 5 CKD. 14. Regarding CKD in HIV infection, measurement of kidney function is essential to prescribe appropriate doses of antiretroviral drugs.

Important complications of CKD 15. Regarding the dyslipidaemia associated with CKD, statin therapy is not effective in stages 4 - 5.

16. Chronic acidosis has recently been shown to be a risk factor in the progression of CKD renal dysfunction.

17. A raised serum phosphate level occurs with stage 4 CKD, and especially with stage 5.

Drugs and the kidney 18.

Nephrotoxicity is markedly enhanced when the glomerular filtration rate (GFR) is reduced, as in elderly subjects when socalled ‘normal’ creatinine levels may be found.

19. From the age of 45 - 55 years, the GFR is reduced by about 1 mL/ min/year so that an otherwise healthy person of 80 may have an estimated GFR of <60 mL/min or <50 mL/min, i.e. stage 2, 3 or 3b CKD. 20. An increased bruising or bleeding tendency with aspirin may be a marker of kidney dysfunction.

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April 2015, Vol. 105, No. 4