Blackwell Science, LtdOxford, UKBJUBJU International1464-4096BJU InternationalMarch 2003 914 Letters
March 2003 914 Letters CORRESPONDENCE
W R I T E TO T H E E D I TO R AT B J U I N T E R N AT I O N A L , 4 7 E C C L E S S T R E E T, D U B L I N 7 , I R E L A N D
INTRA-URETERIC CAPSAICIN IN LOIN PAIN HAEMATURIA SYNDROME: EFFICACY AND COMPLICATIONS Sir, I read with interest this article by Playford et al. [1] on intra-ureteric capsaicin in loin pain haematuria syndrome (LPHS), and commend the authors for reporting its inefficacy and complications. All medical and surgical therapies previously tried and failed were mentioned. Renal atrophy and mesangial proliferative glomerulonephritis are important, but whether they cause LPHS, or another overlooked factor is responsible merits discussion. Recent reports suggest another cause of LPHS, i.e. symptomatic nephroptosis (SN) [2–4], which may help to direct the search for a successful therapy, saving the efforts, expense and disappointments of researching ineffective methods. I prospectively studied 190 patients presenting with loin pain with or without haematuria over a decade. The results confirmed that all patients had SN, on repeated IVU with the patient standing. The natural history of the features of SN and the causes of its complications were reported for 36 (19%) patients with LPHS and four (2%) with renal atrophy [2,3]. Renal pain was heterogeneous, difficult to resolve and elusive both for stages of reversible SN and irreversible LPHS. ‘Disparaged SN’ [4] is impossible to detect on any supine imaging and neither is LPHS pathology undetectable using current protocols. The many associated splanchnic symptoms of SN and LPHS confuse the diagnosis of pain, and differential diagnoses, making the disease appear illusory and doubtful [2,4]. In addition to ‘auto-nephropexy’ affecting 12 of 36 (33%) and ‘auto-nephrectomy’ or renal atrophy affecting four (11%) patients, ‘sympathetic nephroplegia’ of the
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CIRCUMCISION AND NEWBORN UTIS: WINBERG'S SOLUTION Sir, UTIs of the newborn are very easy to cure, but in the USA proponents of the removal of the foreskin support it as a major prophylactic measure. Winberg (and others) countered this view in 1989 [1]: ‘it is suggested that the effects of one unphysiological intervention are counterbalancing those of another, i.e. colonization of the baby’s gastrointestinal tract and genitals in maternity units by Escherichia coli strains of non-maternal origin, to which the baby has no passive immunity. As an alternative to circumcision to prevent early infantile male UTI, more natural colonization could be promoted by strict roomingin of mother and baby or by active colonization of the baby with his mother's anaerobic gut flora' [1]. Other authors [2–4] highlighted this proposal, but the views were published in either an English review [2] or in relatively obscure American or French publications [3,4]. Winberg's proposal has not been properly considered in the USA; it was not even cited in the last policy statement of the American Academy of Pediatricians [5], which seems to be reticent on this major scientific issue. It is time that this view was given more attention worldwide. Winberg and his supporters are unexpectedly in agreement with Leboyer's cause for the sake of nature; the mother and her baby must never be separated [6]. ‘SIGISMOND’ Paris e-mail:
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Winberg J, Bollgren I, Gothefors L, Herthelius M, Tullus K. The prepuce: a mistake of nature? Lancet 1989; i: 598–9 Thomson RS. Is routine circumcision indicated in the newborn? An opposing view. J Fam Pract 1990; 31: 189–96 Zwang G. Quel avenir pour la circoncision? Contraception, fertilité, sexualité 1995; 23: 350 Dritsas LS. Below the belt: doctors, debate, and the ongoing American discussion of routine neonatal male circumcision. Bull Sci Technol Soc 2001; 21: 297–311 Anonymous. Circumcision policy statement. American Academy of Pediatrics. Task Force on Circumcision. Pediatrics 1999; 103: 686–93 Leboyer F. Birth Without Violence. Rochester: Inner Traditions Ltd, 1995
contralateral left kidney, either mobile or not (akin to that in the eye or testis) affected about a third of those with LPHS, further camouflaging the cause [2]. Successful therapy [2–4] was a combination of ‘nephropexy [5] and renal sympathetic denervation (RSD)’ of the renal pedicle [6]. Although surgical [7] and chemical [1] sympathectomy were previously reported to be ineffective, the new aetiopathology explains this paradox.
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The previous failure of sympathectomy is related to how, when and where it is done. The link of LPHS with SN was unknown [2,3], and thus the value of nephropexy added to RSD was unrealised. The intermittent effects of time and gravity on the ‘renal pedicle stretch’ of SN and its mechanism inducing ischaemia and sympathetic over-activity remain overlooked. Ischaemia and sympathetic neuropathy have a vital role in the cause of LPHS [7] and in its curability. Sympathectomy 429
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was ineffective when used too long after the intermittent ischaemia of SN had caused the permanent ischaemic renal damage of LPHS, and sympathetic overactivity became neuropathy [7]. The scattered bilateral nature of sympathetic innervation synapse at the coeliac plexus [8] may explain the failure of the dorsal division of T10–12 nerves and chemical sympathectomy. As there is now an adequate follow up, the results of prospective observational [2] and interventional studies [4] are being objectively analysed, but many data are already available for appraisal. The observations on renal atrophy in LPHS [1] are affirmed, but it complicates underlying SN spontaneously and insidiously and may be acutely precipitated by any therapy [2,3]. Mesangial proliferative glomerulonephritis may also complicate LPHS. A.N. GHANEM, MD (Urol), FRCS(Ed), Consultant Urological Surgeon, King Khalid Hospital, Najran, Saudi Arabia (currently PO Box 213, Mansoura 35511, Egypt) 1
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Playford D, Kulkarni H, Thomas M et al. Intra-ureteric capsaicin in loin pain haematuria syndrome. efficacy and complications. BJU Int 2002; 90: 518–21 Ghanem AN. Features and complications of nephroptosis causing the loin pain and haematuria syndrome. A preliminary report. Saudi Med J 2002; 23: 447–55 Ghanem AN. Early experience of intraureteric capsaicin infusion in loin pain haematuria syndrome. BJU Int 2000; 86: 911–4 Ghanem AN. ‘Disparaged’ nephroptosis. Urology 2000; 56: 183–4 Hahn E. Die operative Behandlung der beweglichen Niere Durch fixation. Zintralbl Chir 1881; 29: 449–52 Blalock AR. Renal denervation with releasing renal capsule incision in the loin pain haematuria syndrome. Br J Urol 1989; 62: 203–4
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Andrews BT, Jones NF, Browse NL. The use of surgical sympathectomy in the treatment of chronic renal pain. Br J Urol 1997; 80: 6–10 Williams PL, Warwick R, Dyson M, Bannister LH eds, Gray's Anatomy 37th edn. Edinburgh: Churchill Livingstone, 1989: 1165–8
technique. There are currently at least four UK centres offering urodynamics courses, all of which have a fairly standard approach as they have all, to varying extents, developed from the Bristol Urodynamics courses. We do not think it is the role of the ICS to police the quality of individual units' technique or results; perhaps mandatory certification of training in urodynamics is the best way forward.
AN AUDIT OF URODYNAMIC STANDARDIZATION IN THE WEST MIDLANDS, UK Sir, We were interested to read the audit by Sriram et al. [1] showing poor adherence to standardized methods in urodynamics. We have had similar experience reviewing traces for international trials [2], particularly with incorrect zeroing of transducers and inaccurate baseline pressures. Our impression from teaching urodynamics is more encouraging; most delegates are now aware of, and report that they adhere to, zeroing to atmospheric pressure. There is a serious error in the article; the 1988 ICS standardization report quoted [3] does not, as stated in the article, give any threshold contraction amplitude for the diagnosis of detrusor instability. The most recent ICS report [4] has changed the term to detrusor overactivity, states that phasic detrusor contractions are not always accompanied by any sensation, and again gives no threshold amplitude for the diagnosis of detrusor overactivity. Sriram et al. suggested that the ICS is not doing enough to publicise guidelines or ensure best practice. The ICS standardization reports are available to all, on the ICS website at http://www.icsoffice.org. (under ‘documents’, then ‘standardization reports’) and in peer-reviewed journals [3,4]. The recent report on Good Urodynamic Practice [5] gives detailed advice on good urodynamic
J. SULLIVAN SpR in Urology, Gloucester Royal Hospital L. SWITHINBANK Director, Urodynamic Unit P. ABRAMS Professor of Urology and Secretary, ICS, Southmead Hospital Bristol, UK 1
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Sriram R, Ojha H, Farrar DJ. An audit of urodynamic standardization in the West Midlands, UK. BJU Int 2002; 90: 537–9 Lewis P, Howell S, Shepherd A, Abrams P. Urodynamic interpretation: guidance not guesswork. Proceedings of the International Continence Society, 1998: 71–72 Abrams P, Blaivas JG, Stanton SL, Andersen JT. The standardisation of terminology of lower urinary tract function. The International Continence Society Committee on Standardisation of Terminology. Scand J Urol Nephrol 1988; Suppl 114: 5–19 Abrams P, Cardozo L, Fall M et al. The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society. Am J Obstet Gynecol 2002; 187: 116–26 Schafer W, Abrams P, Liao L et al. Good urodynamic practices: uroflowmetry, filling cystometry, and pressure-flow studies. Neurourol Urodynam 2002; 21: 261–74
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2003 BJU INTERNATIONAL
