C O R R E S P O N D E N C E 1017

found that a number of women who have been asymptomatic (but with abnormalities on examination) when first seen in the clinic have come back of their own accord when they started to develop symptoms.

The ventouse extractor has been used increasingly in the latter part of the study period and subsequently. We are now seeing a number of patients who have sustained a third-degree tear when forceps have been used after a failed ventouse extraction, and a small number after ventouse extraction alone.

The initial repair of third-degree tears is frequently carried by obstetricians in training. During this study one of us visited the labour ward to witness a primary repair of a third-degree tear. The disruptive nature of the injury made precise reconstruction of the individual components of the sphincter impossible, and simple reapproximation of the visible muscle was performed. It would have been impossible to perform the overlapping technique used by coloproctologists in delayed repair. One could speculate that a patient presenting with a similar injury as a result of a road traffic accident would most likely be treated by defunctioning colostomy.

During the study period we recommended that obstetricians change from chromic catgut to longer-lasting absorbable sutures and they now use Maxon (Davis and Geck, Gosport, UK). It is our impression that the incidence of poor outcome has diminished since this change in practice, and this matter will be the subject of a further study. We routinely use antibiotics (a single intravenous dose of cefuroxime and metronidazole) at the time of delayed repair, and it would seem reasonable to use similar prophylaxis at the time of primary repair. Stool softeners are also appropriate. In our assessment clinic we do consider the subject of further deliveries. Patients having a delayed repair for frank incontinence are advised to have a caesarian section to avoid damage to the repair. Those with physical signs and low anal canal pressures are advised to consider seriously caesarian section, and those who have a normal examination are advised to have a further vaginal delivery but to remind all taking part in their obstetric care that they have previously sustained a third- degree tear.

R. W. Motson C. J. Walsh

D. Khoo G. Upton*

Department of Surgery Colchester General Hospital and *Department of Mathematics University of Essex Colchester UK

Mammary duct ectasia-periductal mastitis complex

Sir I was surprised by a number of statements in the recent review by Mr Webb (Br J Surg 1995; 82: 1300-2).

If periductal mastitis and duct ectasia are connected, and present evidence indicates they might not be', then periductal mastitis precedes mammary duct ectasia2, and it would have been more appropriate for the title of the article to be periductal mastitis-duct ectasia.

The first sentence states that it is the second commonest benign disease; as far as symptoms are concerned, it certainly is not2.

There is now general agreement that periductal mastitis affects mainly young women and is associated with the development of non-lactating abscesses and mammary duct fistula^^-^, whereas mammary duct ectasia affects an older age group, is present in over 50 per cent of women after the age of 60 years and is likely merely to represent a feature of breast invol~t ion~,~.

Both aerobic and anaerobic bacteria have been isolated from periareolar absces~es*~~ and mammary duct fistulas4,'" associated

with periductal mastitis. The current antibiotic of choice is co- arnoxyclav"~'* and not, as stated, flucloxacillin and metronidazole combined.

Mr Webb listed a few simple practical points, most of which I would take issue with. I would support all the points raised by Mr Bundred in his recent corre~pondence'~. I would also like to raise further concerns specifically.

(1) In relation to his third practical point, non-lactating breast abscesses can be divided into those that occur in the central periareolar region and those in the periphery of the breast". If pus is obtained on aspiration the correct treatment is aspiration of all the pus combined with appropriate antibiotic therapy, or mini-incision and drainage following application of local anaesthetic cream''. Only in recurrent periareolar abscesses is more extensive surgery likely to be necessary. It has not been my experience that peripheral abscesses recur unless associated with granulomatous lobular mastitis, and few of these peripheral abscesses need any surgical intervention following aspiration or mini-incision and drainage.

(2) It is no longer appropriate to suggest that abscesses should be treated with drainage and packing. Both lactating and non- lactating abscesses can be treated either by aspiration, combined with oral antibiotics, or limited incision and drainage without p a ~ k i n g " ~ ' ~ ~ ' ~ .

(3) Mr Webb suggests that it is more appropriate in meno- pausal and postmenopausal women than in younger women to perform total duct excision. Experience demonstrates that most patients with recurrent sepsis are young premenopausal women and that abscess formation decreases with age. Young patients with recurrent infection often have nipple inversion, so breast- feeding from the affected breast is not possible. It is illogical, therefore, to treat older patients in a different way to younger patients. Our own and other published data do not support his view that, after major duct excision, the success rate of this procedure is modestlh. We have recently sent a questionnaire to 88 patients who underwent total duct excision. Some 94 per cent were satisfied with the outcome of the operation and only six patients required any further surgery: four for cosmetic reasons and two because of further infections. Repeat operation is, therefore, rarely necessary if the procedure is carried out correctly under appropriate antibiotic cove^^^.^^. From the last 30000 patients who were seen in the Edinburgh Breast Unit, there has been no patient who has required mastectomy for recurrent sepsis. In three patients we removed the nipple and areola complex, and I am surprised that mastectomy is ever necessary.

(4) I am not clear what Mr Webb means by 'underpinning the residual ectatic ducts following total duct excision'. It is not something I ever do after total duct excision and, as stated above, a recent audit demonstrates that our results for this procedure are satisfactory. It is disappointing that Mr Webb does not outline the current optimal method of surgical treatment of mammary duct fistulas and/or recurrent periareolar sepsis. Fistulas and recurrent periareolar sepsis are best treated by total duct excision or occasionally by excision of the diseased duct alone, combined with excision of any fistula tract if present, with primary closure of the wound under appropriate antibiotic

(5) I am not clear what the author means by a 'tender para- areolar breast cyst'.

There is now clear evidence that smoking has a major role in the aetiology of periductal mastitis, but recent evidence indicates that patients with duct ectasia are not more likely to smoke than the general population'.

J. M. Dixon Department of Surgery The University of Edinburgh Royal Infirmary Lauriston Place Edinburgh EH3 9YW UK

c0ver4s.1 1,1R,

1 Dixon JM, RaviSekar I, Chetty U, Anderson TJ. Periductal mastitis and duct ectasia: different conditions with different

0 1996 Blackwell Science Ltd, British Journal of Surgery 1996,83, 1010-1019

1018 C O R R E S P O N D E N C E

aetiologies. Br J Surg 1996; 83: 820-2. 2 Dixon JM, Anderson TJ, Lumsden AB, Elton RA, Roberts

MM, Forest APM. Mammary duct ectasia. Br .f Surg 1983; 70:

3 Hughes LE, Mansel RE, Webster DJT. Abberations of normal development and involvement (ANDI): a new perspective on the pathogenesis and nomenclature of benign breast disorders. Lancet 1987; ii: 1316-19.

4 Bundred NJ, Dixon JM, Chetty U, Forrest APM. Mammillary fistula. Br J Surg 1987; 74: 466-8.

5 Dixon JM, Thompson AM. Effective surgical treatment for mammillary fistula. Br J Surg 1991; 78: 1185-6.

6 Dixon JM. Periductal mastitis/duct ectasia. World J Surg 1989;

7 Frantz VK, Pickren JW, Melcher GM, Auchincloss H. Incidence of chronic cystic disease in so-called normal breasts. Cancer 19.51; 47: 62-83.

8 Leach RD, Eykyn S, Philips I, Corrin B. Anaerobic subareolar breast abscesses. Lancef 1979; i: 3.5-7.

9 Ingam IHR, Freeman R, Wilson RG. Anaerobic breast abscesses. Lancet 1979; i: 164-9.

10 Bundred NJ, Dixon JM, Lumsden AB et al. Are the lesions of duct ectasia sterile? Br J Surg 198.5; 72: 844-5.

11 Dixon JM. ABC of Breast Diseases: breast infection. BMJ

12 Dixon JM. Breast surgery. In: Taylor EW, ed. Infection and Surgical Practice. Oxford: Oxford University Press, 1992:

13 Bundred NJ. Mammary duct ectasia-periductal mastitis complex. Br J Surg 1996; 83: 872-3 (Letter).

14 Dixon JM. Repeated aspiration of breast abscesses in lactating women. BMJ 1988; 297: 1517-18.

1.5 Dixon JM. Out-patient treatment of non-lactating breast abscesses. Br J Surg 1992; 79: 56-7.

16 Lambert ME, Betts CD, Cellwood RA. Mammillary fistula. Br J Surg 1986; 73: 367-8.

17 Dixon JM, Chetty U, Forrest APM. Wound infections after breast biopsy. Br J Surg 1988; 75: 918-19.

18 Bundred NJ, Webster DJT, Mansel RE. Management of mammillary fistulae. J R Coll Surg Edinb 1991; 36: 381-3.

601-3.

13: 71.5-20.

1994; 309: 946-9.

187-96.

Author’s reply

Sir I am grateful for the opportunity to reply to Mr Dixon’s criticisms. Some of his comments will have been addressed coincidentally in my reply to Mr Bundred.

Regarding the title, I have no strong feelings; periductal mastitis-duct ectasia complex is quite acceptable. However, the possible distinction between these components is not yet established, and it is common knowledge from published illustrations1 and countless histopathological specimens that they are associated. Clinically, uncomplicated palpable duct thickening is equally evident in women under 40years of age as in those above. In his paper with others*, Mr Dixon comments on a possible sequence of events: ‘Periductal inflammation, which then resolves, leads on to secondary duct fibrosis and dilatation’. Yet so often gross duct dilatation and periductal inflammation in all stages of activity are seen to coexist. The other theory of causation3 is equally tenable.

My editorial in no way contradicted the accepted fact that periductal sepsis is common in younger women and discharge more likely in those over 40 years of age, but there is an overlap, especially with nipple discharge. All I stated - in company with others4 - is that in some younger women there is a place for conservative duct excision. For obvious widespread duct disease total excision is indicated (sections 4 and 5 of the article).

My experience with microbiological cultures is less convincing than that of Mr Dixon. I have used flucloxacillin and metronidazole, also various cephalosporins and erythromycin, in patients who were sensitive to penicillins. I would be reluctant to

reject metronidazole. Used alone in possible minor inflammatory breast situations, it has coincided with excellent and rapid resolution.

Regarding his comments on practical points. (1) For non-lactating breast abscesses I am less conservative

than Mr Dixon and confess to being heavily influenced by the teaching of G. J. Hadfield; I have found it eminently sound and sensible. Over a lifetime of surgical experience with breast disease, his messages appear unchanged’~~.~.

Even with adequate drainage and liberal antibiotics I have needed to re-explore and drain further abscesses. A few have been associated with florid granulomatous disease (much more than lobulitis), but other patients have shown no such tissue changes.

(2) I am sceptical of Mr Dixon’s assertions, and surgeons will have to decide from their own experience.

(3) I did not intend to indicate from sections 4 and 5 of the article that total duct excision should not be performed in younger women. I apologize if I caused a misunderstanding. Mr Dixon’s good results from total duct excision, contrasting with the results quoted from BristoP, may possibly relate to case selection. However, experience since then and from referred patients still leads me to express caution. Hadfield5, in 1990, highlights the complexity of recurrent periareolar sepsis and sets in perspective his use of antibiotics. I suspect that this surgical problem is under-reported. Our patients underwent mastectomy over 10 years ago and I know of one other patient since then in whom mastectomy should have been advised as disease was so extensive and the clinical course protracted.

(4) Regarding the surgical technique, I refer Mr Dixon to the original descriptions by Hadfield3.’ and Urban*. The latter advocates far more breast excision than the former. Hadfield3 recommends ligating the larger breast ducts emerging from the breast tissue with fine catgut. I have tended to excise a shallow disc of breast tissue with the ducts to ensure complete clearance. Herewith residual ducts cannot be ligated, and the logical procedure is ‘underpinning’ on the breast surface. I have no problem with ‘pouting the papilla’ but it must be done without damaging the blood supply. The so-called ‘dead space’ is difficult.

The infolding manoeuvre reported by Preece9 is sometimes possible but may distort the nipple.

The current optimal method for mammary duct sepsis and fistula formation is included in section 7 of the article.

(5) A ‘tender para-areolar cyst’ is a discrete breast swelling within or around (in the average breast) a 5-cm circle centred on the papilla. In my experience it is a distinct entity, but a tender cyst may also arise elsewhere in the breast. Fine-needle aspiration cytology yields turbid fluid but not pus. The cytology shows many polymorphs, foamy histiocytes, ‘round’ cells and atypical cyst-lining cells, commonly apocrine in type. It is an important source of reported cytological atypia.

I was surprised that Mr Dixon, in his report with others on breast cyst morphologylO, did not include ‘inflammatory’ cysts. They differ from the simple apocrine variety.

The association of smoking and periductal inflammation I have mentioned. In those aged over 40years, I suspect that symptomatic nodularity and nipple discharge is more likely in cigarette smokers, but my data are immature.

7 Percival Road Bristol BS8 3LE UK

A. J. Webb

1 Hadfield GJ. The pathological lesions underlying discharges from the nipple in women. Ann R Coll Surg Engl 1969; 44:

2 Dixon JM, Anderson TJ, Lumsden AB, Elton RA, Roberts MM, Forrest APM. Mammary duct ectasia. Br J Sue 1983; 70: 601-3.

3 Hadfield GJ. Excision of major duct system of breast. Br J

4 Hughes LE, Mansel RE, Webster DJT. Benign disorders and diseases of the breast. London: Baillibre Tindall, 1989: 125-9.

323-33.

SUT 1960; 47: 472-7.

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5 Hadfield GJ. Benign diseases of the breast. In: Hadfield GJ, Hobsley M, Treasure T, eds. Current Surgical Practice. Volume 5. London: Edward Arnold, 1990: 208-18.

6 Thomas WG, Williamson RCN, Davies JD, Webb AJ. The clinical syndrome of mammary duct ectasia. Br J Surg 1982;

7 Hadfield GJ. Further experience of the operation for excision of the major duct system of the breast. Br J Surg 1968; 5 5 :

69: 423-5.

530-5. 8 Urban JA. Excision of the major duct system. Cancer 1963;

9 Preece P. How I do a subareolar duct excision. Breast News

10 Dixon JM, Miller WR, Scott WN, Forrest APM. The morphological basis of human breast cyst populations. Br J

16: 516-20.

1987/88; 2: 9-12.

SUT 1983; 70: 604-6.

0 1996 Blackwell Science Ltd, British Journal of Surgery 1996,83, 1010-1019