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SAMJ: South African Medical Journal

versão On-line ISSN 2078-5135
versão impressa ISSN 0256-9574

SAMJ, S. Afr. med. j. vol.102 no.6 Pretoria Jun. 2012


Chairman of the South African Society of Clinical and Radiation Oncology


Raymond Abratt
Michiel Botha
Robbie De Muellenaere
Leon Gouws
Greg Hart
Amo Jordaan
Waldek Szpak ^rND^1A01^nDerek^sRaghavan^rND^1A02^nMichael^sSteinberg^rND^1A03^nHoward^sSandler^rND^1A01^nDerek^sRaghavan^rND^1A02^nMichael^sSteinberg^rND^1A03^nHoward^sSandler^rND^1A01^nDerek^sRaghavan^rND^1A02^nMichael^sSteinberg^rND^1A03^nHoward^sSandler



Neutron radiotherapy: Abratt supported



To the Editor: We write, with some unease, given that much of this matter is internal to the medical affairs of South Africa (SA), to lend support to the stance of Prof Abratt,1,2 regarding closure of the neutron facility in SA.

We recognise clearly the limitations of participating in this debate when we are not South African and do not practise medicine in the African continent. That said, there are points of illogic in the criticisms of Prof Abratt's stand that must be challenged.

Firstly, the rhetoric supporting the purported importance of recent research on neutron therapy, and the charge that Prof Abratt's view of neutron therapy is outdated, are simply unreasonable. The whole issue of the utility of neutron therapy remains highly controversial internationally after more than 25 years of research and clinical practice. The issues remain unchanged: lack of proven benefit, narrow spectrum of clinical indications, offset by excessive toxicity demonstrated in the majority of published studies. While we recognise the difficulty of completing randomised clinical trials in this setting, it is important to note the absence of high-quality data to support this expensive technology.

Despite the claims of the proponents of such research on the topic of neutron therapy, we note a paucity of well-structured published research on the role of this treatment modality. It appears that the majority of use of available equipment has been for routine clinical practice, despite the absence of significant, recent published data to support such therapy; one might have hoped that investigational equipment might have been used to produce new data.

Perhaps of more importance, in a continent that is challenged by a shortage of costly medical resources, it seems importune to make a case for maintenance of an expensive, controversial, unproven therapy with so few indications, and to criticise an earnest and honest attempt to bring reason to the debate. We support Prof Abratt's view, based on logic, fiscal pragmatism, and recognise his presence as a leader in academic radiation oncology with several decades of carefully structured published data.


Derek Raghavan
Levine Cancer Institute, Carolinas HealthCare System Charlotte, NC, USA

Michael Steinberg
IRadiation Oncology, David Geffen School of Medicine UCLA, USA

Howard Sandler
Radiation Oncology, Cedars-Sinai Medical Center Los Angeles, CA, USA


1. Abratt RP. The fast neutron therapy programme for patients in South Africa should come to an end. S Afr Med J 2012;102(2):58.        [ Links ]

2. Abratt RP. Neutron radiotherapy in South Africa: Abratt replies. S Afr Med J 2012;102(5):270-271.        [ Links ]^rND^sAbratt^nRP^rND^sAbratt^nRP^rND^1A01^nD L^sSkinner^rND^1A01^nD L^sSkinner^rND^1A01^nD L^sSkinner



Traumatic rhabdomyolysis (crush syndrome) in the rural setting



To the Editor: I read with interest the article entitled 'Traumatic rhabdomyolysis (crush syndrome) in the rural setting'.1 Crush syndrome from sjambok injury is a uniquely southern African experience.2 It is unfortunately commonplace, making treatment guidelines essential to prevent the progression of acute kidney injury (AKI) and subsequent need for renal replacement therapy. The advent of the RIFLE and AKIN criteria in the description and risk stratification of AKI provides a framework from which strategies to prevent ongoing injury can be implemented.3 Their use has become commonplace in critical care and should be implemented in the emergency department.

Careful monitoring of fluid balance is essential, and a paper discussing the ATN and RENAL trial results shows that avoiding a positive fluid balance improves renal recovery times.4 Therefore I  urge caution in trying to force a diuresis with resuscitation fluids if patients present with anuria/oliguria and do not respond to initial fluid therapy as they can be pushed into fluid overload with subsequent need for ventilatory support.

Alkalinisation of the urine with bicarbonate has been challenged as the standard of care. Evidence for this practice is weak; in 2083 trauma ICU admissions, Velmahos' group failed to show improvement in outcomes despite urinary alkalinisation.5

The use of diuretics in AKI does not improve mortality outcomes and the use of renal replacement therapy.6 Mannitol has also been implicated as a cause of AKI in head-injured patients and should be used with caution.7

At present, measuring serum creatinine and urine output remain the two best indicators of renal function that are easily available to the clinician. These remain our renal biomarkers of choice until the use of newer renal biomarkers, such as neutrophil gelatinase associated lipocalin and cystatin C, becomes commonplace.8

Patient therapy must be individualised, with haemodynamic optimisation and careful monitoring of fluid balance, specifically concentrating on urine output. Care must be taken to avoid nephrotoxic agents such as intravenous contrast and aminoglycosides. Early referral for renal replacement therapy is essential in those not responding to conventional fluid therapy.


D L Skinner
Level 1 Trauma Unit and Trauma ICU Inkosi Albert Luthuli Central Hospital Durban


1. Rosedale KH, Wood D. Traumatic rhabdomyolysis (crush syndrome) in the rural setting. S Afr Med J 2012;102:37-39.        [ Links ]

2. Muckart DJ, Abdool-Carrim AT. Pigment-induced nephropathy after sjambok injuries. S Afr J Surg 1991:29(1):21-24.        [ Links ]

3. Bellomo R, Ronco C, Kellum JA, et al Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference ofthe Acute Dialysis Quality Initiative (ADQI) Group. Critical Care 2004:8(4):204-212.        [ Links ]

4. Glassford NJ, Bellomo R. Acute kidney injury: how can we facilitate recovery? Curr Opin Crit Care 2011:17(6):562-568.        [ Links ]

5. Brown CV, Rhee P, Chan L, et al. Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference? J Trauma 2004:56(6):1191-1196.        [ Links ]

6. Karajala V, Mansour W, Kellum JA. Diuretics in acute kidney injury. Minerva Anestesiol 2009:75(5):251-257.        [ Links ]

7. Fang L, You H, Chen B, Xu Z. Mannitol is an independent risk factor of acute kidney injury after cerebral trauma: a case-control study. Ren Fail 2010:32(6):673-679.        [ Links ]

8. Smith WA, Hardcastle TC. A crushing experience: The spectrum and outcome of soft tissue injury and myonephropathic syndrome at an urban South African university hospital. African Journal of Emergency Medicine 2011:1(1): 17-24.        [ Links ]



Wood replies: Traumatic rhabdomyolysis is often a result of natural disasters such as earthquakes where patients are crushed by debris. However, rhabdomyolysis associated with interpersonal violence such as sjambok injuries and community beatings is endemic to South Africa. Most of these patients present to district or regional hospitals with limited diagnostic capabilities and no renal replacement therapies such as renal dialysis. Our study1 suggests that early diagnosis of rhabdomyolysis using clinical examination and blood on urine Dipstix as a surrogate marker are critical in preventing ensuing myoglobin-associated acute renal failure. Key to management is early and aggressive fluid management (a target of 200 - 300 ml/h urine output)2 to prevent renal tubule damage. A low urine pH augments myoglobin cast sedimentation3 and renal tubular damage. Some guidelines2,3 suggest the use of bicarbonate, with a target urine pH >6.5, to reduce this effect. Caution is advised with bicarbonate therapy since hypocalcaemia, hypernatraemia, systemic alkalosis and potential tetany are potential adverse effects. Most guidelines also recommend the use of mannitol in oliguric patients.2,3 Theoretical advantages of mannitol include osmotic diuresis, free radical scavenging and stimulating the release of vasodilatory prostaglandins, enhancing glomerular filtration. The use of mannitol and bicarbonate is controversial, with new evidence suggesting that their use is of no benefit in rhabdomyolysis.

One study showed that bicarbonate and mannitol therapy had no advantage in preventing renal failure over saline diuresis alone.4 However, the study was not randomised and patients in the mannitol/bicarbonate group had an overall higher average creatine kinase, suggesting a more severe pathology. The study indicated that patients with a creatine kinase >30 000 U/l may benefit from mannitol/bicarbonate therapy.4,5 The use of mannitol and bicarbonate in this setting should be revisited.

In settings with limited or no renal support such as renal dialysis, preventing renal failure in traumatic rhabdomyolysis is critical. Early detection of rhabdomyolysis and fluid therapy is the cornerstone of renal saving. Patients who do not respond to fluid resuscitation and show an increasing trend toward renal failure as indicated by a climbing serum creatinine may need additional treatment strategies when dialysis services are not an option. They should have their intravascular volume monitored, which in most settings is limited to central venous pressure monitoring, before the use of diuretics such as mannitol is considered. Strict monitoring of urine and serum pH when considering the use of bicarbonate is recommended. Our small observational study in a rural regional hospital showed that patients with suspected rhabdomyolysis can be effectively treated using recommended guidelines where resources are not adequate for renal replacement treatments. Serious clinical dilemmas exist when patients don't respond to fluid therapy alone and show worsening renal functions, and where there is no recourse to services such as renal dialysis.

Large prospective randomised controlled trials are required to provide clarity on the most effective treatment strategies in trauma-associated rhabdomyolysis, especially in the resource-challenged areas to which most patients present.



1. Rosedale KH, Wood D. Traumatic rhabdomyolysis (crush syndrome) in the rural setting. S Afr Med J 2012:102: 37-39.        [ Links ]

2. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009:361:62-72.        [ Links ]

3. Jagodzinsky NA, Weerasinghe C, Porter K. Crush injuries and crush syndrome - a review. Part1: the systemic injury. Trauma 2010:12:69-88.        [ Links ]

4. Brown CVR, Rhee P, Chan L, et al. Preventing renal failure in patients with rhabdomyolysis: Do bicarbonate and mannitol make a difference? J Trauma 2004:56(6):1191-1196.        [ Links ]

5. Thomas R. Rhabdomyolysis and the use of sodium bicarbonate and/or mannitol. Best Bets 2010:ApriL        [ Links ]^rND^sRosedale^nKH^rND^sWood^nD^rND^sMuckart^nDJ^rND^sAbdool-Carrim^nAT^rND^sBellomo^nR^rND^sRonco^nC^rND^sKellum^nJA^rND^sGlassford^nNJ^rND^sBellomo^nR^rND^sBrown^nCV^rND^sRhee^nP^rND^sChan^nL^rND^sKarajala^nV^rND^sMansour^nW^rND^sKellum^nJA^rND^sFang^nL^rND^sYou^nH^rND^sChen^nB^rND^sXu^nZ^rND^sSmith^nWA^rND^sHardcastle^nTC^rND^sRosedale^nKH^rND^sWood^nD^rND^sBosch^nX^rND^sPoch^nE^rND^sGrau^nJM^rND^sJagodzinsky^nNA^rND^sWeerasinghe^nC^rND^sPorter^nK^rND^sBrown^nCVR^rND^sRhee^nP^rND^sChan^nL^rND^sThomas^nR^rND^1A01^nViroj^sWiwanitkit^rND^1A01^nViroj^sWiwanitkit^rND^1A01^nViroj^sWiwanitkit



False-positive HIV DNA PCR testing of infants



To the Editor: I would like to share ideas on the report by Feucht et al. who concluded that 'Decreasing mother-to-child HIV transmission rates reduce the positive predictive value of a single HIV DNA PCR test result, necessitating adaptations to diagnostic algorithms to avoid misdiagnosis and inappropriate treatment, especially with early initiation of antiretroviral therapy in asymptomatic infants.'1

False positivity is basic in laboratory medicine and can result from any tests, including molecular diagnoses. The basic concept to consider when discussing the diagnostic property of a test is that prevalence is the main factor determining sensitivity, specificity and predictive values, which can be reflected in their report. The authors' conclusions are based on a single centre with retrospective data review, which cannot control for the confounding factors and quality of the laboratory test.

Despite the use of molecular testing for HIV diagnosis, practitioners must be concerned about the possibility of false positivity, as available commercial kits for HIV molecular testing differ in their false-positive rates.2 The information on the false-positive rate of each diagnostic test should be available for interpretation of the results. There should also be a focus on the quality of the diagnostic test, as poor quality of some locally available in-house HIV molecular testing owing to contamination has been reported.3


Viroj Wiwanitkit
Wiwanitkit House Bangkhae Bangkok, Thailand; Visiting Professor Hainan Medical University, China; Adjunct Professor Joseph Ayobabalola University, Nigeria


1. Feucht U, Forsyth B, Kruger M. False-positive HIV DNA PCR testing of infants: Implications in a changing epidemic. S Afr Med J 2012;102:149-152.        [ Links ]

2. Maritz J, Preiser W, van Zyl GU. Establishing diagnostic cut-off criteria for the COBAS AmpliPrep/ COBAS TaqMan HIV-1 Qualitative test through validation against the Amplicor DNA test v1.5 for infant diagnosis using dried blood spots. J Clin Virol 2012;53(2):106-109.        [ Links ]

3. Monleau M, Plantier JC, Peeters M. HIV contamination of commercial PCR enzymes raises the importance of quality control of low-cost in-house genotypic HIV drug resistance tests. Antivir Ther 2010;15(1):121-126.        [ Links ]



Feucht replies, on behalf of the authors: We thank Professor Wiwanitkit for sharing ideas on our paper and highlighting the importance of the laboratory quality control matters, including knowledge on false-positivity rates of different test kits and use of test kits of highest quality. During our study, the great majority of HIV DNA PCR tests were done using the Amplicor HIV-1 DNA test, version 1.5 (Roche Molecular Systems), while during the last year of our study the Cobas AmpliPrep/Cobas TaqMan ('CAP/CTM') HIV-1 Qual test (Roche Molecular Systems) was introduced, which is less labour-intensive and has a shorter turnaround time. The report from Maritz et at.1 on the comparison between the Amplicor and the CAP/CTM tests is of concern, owing to reported lower specificity of the CAP/CTM test. As shown in our study, any decrease in test specificity would greatly decrease the positive predictive value of any one positive HIV DNA PCR test result in the context of the rapidly decreasing prevalence of HIV infection in babies on whom routine testing is done as part of prevention of mother-to-child transmission (PMTCT) programmes.

We acknowledge the concern that our study was a retrospective review from a single centre. Our intention was to study how well the HIV DNA PCR test performs in an everyday clinical setting within a large-scale HIV programme. Our conclusion was that the false positivity rates that clinicians were experiencing can be explained by the test specificity combined with the epidemiological changes of the rapidly decreasing HIV prevalence in babies undergoing routine testing as part of the PMTCT programme.


1. Maritz J, Preiser W, van Zyl GU. Establishing diagnostic cut-off criteria for the COBAS AmpliPrep/ COBAS TaqMan HIV-1 Qualitative test through validation against the Amplicor DNA test v1.5 for infant diagnosis using dried blood spots. J Clin Virol 2012;53(2):106-109.        [ Links ]^rND^sFeucht^nU^rND^sForsyth^nB^rND^sKruger^nM

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