Short notes

Br. J. Surg. 1988, Vol. 75, September, 918-919

Wound infection after breast biopsy

J. M. Dixon, U. Chetty and A. P. M. Forrest

University Department of Surgery, Longmore Breast Unit, Edinb ugh, UK Correspondence to; Mr J. M. Dixon, University Department of Surgery, Royal Infirmary, Edinburgh EH3 9YW, U K

Breast biopsy is a 'clean' operation normally associated with a low incidence of wound infection. We have presented evidence that the lesions of periductal mastitis/duct ectasia' are not ~ t e r i l e ~ . ~ and, ifthis is so, breast biopsy for this condition should be associated with an increased frequency of wound infection. In this study we have compared wound infection rates in more than 300 patients undergoing breast biopsy with the histology of the excised specimen.

Patients and methods The study was performed on 338 patients having a breast biopsy, 148 under general and 190 under local anaesthesia. Most were included in a controlled trial of adrenaline in breast surgery4. All wounds were examined 8-13 days after operation by the same group of surgical staff and wound complications were noted. Patients with wound problems were reviewed at weekly intervals until these resolved. A wound infection was recorded only if there was a discharge of pus from the wound in the postoperative period.

Bacteriology Dry swabs from all but one infected wound were submitted to the laboratory and cultured on blood agar (Columbia agar base CM33 1, Oxoid Ltd., Basingstoke, UK) and MacConkey agar (CM109, Oxoid Ltd.) and incubated aerobically in 10 per cent oxygen. Blood agar plates were also incubated anaerobically in 10 per cent carbon dioxide. Identification of organisms was by routine laboratory methods.

Pathology The histology of the excised specimen was that reported by routine examination, except for the biopsies diagnosed as periductal mastitis or duct ectasia. These were reviewed and if the diagnosis was confirmed the degree of periductal inflammation and duct dilatation was graded as previously described'.

Periductal inflammation: I, acute inflammation or severe chronic inflammation with granuloma formation; 11, moderate chronic inflammation; 111, minor chronic inflammation.

Duct dilatation: I , no ducts dilated; 11, occasional ducts dilated; 111, many ducts dilated.

All patients with histologically proven periductal mastitis/duct ectasia presented with either breast pain, a mass with or without overlying skin inflammation, nipple discharge or nipple retraction. Comparison of the frequency of wound infection in differentr groups was performed by either the x 2 or Wilcoxon rank sum tests.

Results There were 14 wound infections in the 338 patients, an incidence of 4 per cent. Acomparison of the frequency of wound infection and the histopathological diagnosis is given in Table I . Nine wound infections occurred in the eighty-eight (10.2 per cent) patients with a histological diagnosis of periductal mastitis/duct ectasia compared with 5 in the 250 (2.0 per cent) patients with

other pathologies. This difference was highly significant ( P < 0.001).

The organisms isolated are shown in Table I . Enterococci and Bacteroides sp. were seen only in the periductal mastitis/duct ectasia group.

The use of adrenaline did not appear to influence wound infection rates (Table 2). Wound haematomas and bruising were also unrelated to the use of adrenaline'. Infection developed in 2 of the 15 wounds with (13 per cent) and 12 of 323 wounds without (3.7 per cent) haematomas. This difference was not significant and did not account for the difference in infection rates.

Patients with periductal mastitislduct ectasia The rates of wound infection in patients with varying degrees of periductal inflammation and duct dilatation are shown in Table 3. There appeared to be a direct correlation between the frequency of wound infection and the histological features of active inflammation and non-dilated ducts. Because of the small numbers in each group the differences reached statistical significance only when the group with either acute/severe chronic periductal mastitis or no dilated ducts were compared with the other two groups combined.

The relationship between clinical features and wound infection is presented in Table 4 . Patients presenting with inflammatory masses were most likely to develop postoperative infection.

Table 1 infections with the histopathology in patients undergoing breast biopsy

Comparison of the frequency and bacteriology of wound

Number Number Histological of with diagnosis patients infection :< Carcinoma 17 Benign 133

2.0

1

1

Fibro-adenoma 48

Other 52

Periductal 88 9 I 10.2

mammary dysplasia

benign*

mastitis/ duct ectasia

Organisms isolated

Staphylococcus aureus

Staphylococcus albus N o growth

Not sent

No growth

No growth x 2 Staphylococcus alhus Staphylococcus aureus Enterococci x 2 Bacteroides x 3

* Other benign includes normal breast, papillomas, sclerosing lesions and fat necrosis

Table 2 Injluence of adrenaline on wound infection rate in patients whose breast biopsies showed evidence ofperiductal rnastitislduct ectaria or other pathologies

~~

Number Number of with

Pathology Adrenaline patients infection %

Other No 132 3 2.3 Other Yes 118 2 1.7 PDM/DE No 46 5 10.9 PDM/DE Yes 42 4 9.5

PDM, periductal mastitis; DE, duct ectasia. No significant differences were found between groups

91 8 0007~1323/88/090918~02$3.00 1 1988 Butterworth & Co (Publishers) Ltd

Short notes

Table 3 ectasia related to frequency of’ wound infection

Pathological features of patients with periductal mastitislduct

Pathological features

~ ~~ ~

Number Number of with patients infection :<

Inflammation Acute/severe chronic 24 5 21 Moderate chronic 38 3 8 Minor chronic 26 1 4

None 22 5 23 Occasional 35 3 9

Ducts dilated

Many 31 1 3 ~ ~ -

There was no significant direct correlation between histological factors and the frequency of wound infection A significantly greater rate of wound infection was found in groups with acute inflammation and no dilated ducts when compared with the other two groups combined (P<OO5 in both cases)

Table 4 ectayia related to the frequency of wound infection

Prebenting syrnptomr of patients with periductul mastitislducr

Symptoms

Number Number of with patients infection %

Pain 18 2 11 Mass no inflammation 20 1 5 Mass +inflammation 6 4 67 Nipple discharge 24 2 8 Nipple retraction 20 0 0

There was a significantly greater infection rate in patients with mass +inflammation, P<O~OOOl

Outcome of infections By 3 weeks the wounds of four of the five patients with other pathologies and four of the nine with periductal mastitis had healed. One patient, with a wound infection after a biopsy for cancer, healed at 4 weeks following a course of flucloxacillin. Two of the live patients with periductal mastitis whose wounds had not healed by 3 weeks were treated with metronidazole alone and one received metronidazole and cephradine. These three wounds had healed by 6 weeks. Three wounds did not heal due to the development of a mammillary fistula. Two of these patients were in the group of six who had presented with a periareolar inflammatory mass.

Discussion This study indicates that wound infection after surgery for periductal mastitis/duct ectasia is more common than for other

benign or malignant conditions of the breast. Although the numbers are small, it also suggests that the bacteria associated with this increase in infection rate are enterococci and Bacteroides, the same organisms which we have previously noted to be present in the nipple discharge of patients with periductal mastitis/duct e ~ t a s i a ~ . ~ . Further evidence for the relationship of these organisms to this condition comes from reports that the same bacteria can be isolated from non- lactating breast a b s c e s s e ~ ~ . ~ which occur as a complication of periductal mastitis/duct ectasia2r3.

We believe that periductal mastitis is part of the syndrome which includes duct ectasia, non-lactating breast abscesses and mammillary fistulae’. The finding that wound infections are more frequent in patients with acute or active chronic inflammation and no duct dilatation suggests that bacteria may be the cause of this initial inflammation. Resolution of periareolar inflammation with a combination of metronidazole and flucloxacillin’ supports this suggestion. Thus the theory that the lesions of periductal mastitis/duct ectasia become infected as a result of stasis of secretions may be incorrect.

In view of these findings, the value of perioperative antibiotics in certain patients with periductal mastitis/duct ectasia needs to be investigated.

Acknowledgements We are grateful to our colleagues who reported the histopathology of the specimens in the study through the routine pathological service; and also to our colleagues in the department of microbiology who reported the bacteriology of the wound infections. Thanks are also accorded to Dr R.A. Elton for statistical assistance and to the nursing staff of Longmore Hospital for their care of these patients.

References 1.

2.

Dixon JM, Anderson TJ, Lumsden AB, Elton RA, Roberts MM, Forrest APM. Mammary duct ectasia. Br J Surg 1983; 70: 601-3. Dixon JM, Bundred NJ. Mammary duct ectasia-studies of factors involved in its aetiology and pathogenesis. Breast News

Bundred NJ, Dixon JM, Lumsden AB, Chetty U, Forrest APM. Are lesions of duct ectasia sterile? Br J Surg 1985; 72: 844-5. Dixon JM, Crofts TJ, Armstrong CP, Lee D, Wilson J, Forrest APM. The advantage of adrenaline in local and general anaesthetic breast biopsy. J R Coll Surg Edinb 1983; 28: 2924. Pearson NE. Bacteroides in areolar breast abscesses. Surg Gynecol Obstet 1967; 125: 800-2. Leach RD, Eykyn S, Phillips I , Corrin B. Anaerobic subareolar breast abscesses. Lancet 1979; i : 35-7. Bundred NJ, Dixon JM, Chetty U, Forrest, APM. Mammillary fistula. Br J Surg 1987; 74: 466-7.

1986; 4: 1-5. 3.

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Paper accepted 6 December 1987

Br. J. Surg., Vol. 75, No. 9, September 1988 91 9