Candida colonisation within a silicone tissue expander

Candida colonisation within a silicone tissue expander open the mouth fully, and should be excluded by clinical and radiological examination. 11'12 In view of the spontaneous disappearance of the adhesions in one baby, there may be justification in managing the situation expectantly, at least for the first few months of the child's life. There are five previous reports in the literature of congenital interalveolar synechiae occurring in conjunction with an isolated cleft palate. This is the first report of this condition arising in siblings. The association of cleft palate and intraoral synechiae in siblings has been postulated to follow an autosomal dominant pattern of inheritance with variable penetration. Whilst drugs have caused similar anomalies in animal models, the absence of any discernible environmental factors in our cases suggests a genetic condition. This may influence counselling. The spontaneous dissolution of the intraoral adhesions in one patient leads us to recommend expectant management for the initial months of life in uncomplicated cases.

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6. 7. 8.

9. 10. 11. 12.

development: comparison with TGF ~ peptide distribution. J Anat 1992; 181: 219-38. Martfnez-Alvarez C, Tudela C, Prrez-Miguelsanz J, O'Kane S, Puerta J, FergusonMWJ. Medial edge epithelialcell fate during palatal fusion.Dev Biol 2000; 220: 343-57. Qiu CX, Ferguson MWJ. The distributionof PDGFs and PDGFreceptors during murine secondary palate development. J Anat 1995; 186: 17-29. Sharpe PM, Brunet CL, FergusonMWJ. Modulationof the epidermal growth factor receptor of mouse embryonic palatal mesenchyme cells in vitro by growth factors. Int J Dev Biol 1992; 36: 275-82. Cohen MM Jr. Syndromes with cleft lip and cleft palate. Cleft Palate J 1978; 15: 306-28. Rao S, Oak S, Wagh M, Kulkarni B. Congenital midline palatomandibular bony fusion with a mandibular cleft and a bifid tongue. Br J Plast Surg 1997; 50: 139-41. Stemberg N, Sagher U, Golan J, Eidelman AI, Ben-Hur N. Congenital fusion of the gums with bilateral fusion of the temporomandibularjoints. Plast Reconstr Surg 1983; 72: 385-7. TraaholtLM. Cleft lip and palate associated with alveolar synechia and filiform palpebral synechia. Plast Reconstr Surg 1990; 86: 337-9.

References 1. Haramis HT, Apesos J. Cleft palate and congenitallateral alveolar synechia syndrome: case presentationand literaturereview.Ann Plast Surg 1995; 34: 424-30. 2. VerdiGD, O'Neal B. Cleft palate and congenitalalveolarsynechia syndrome. Plast ReconstrSurg 1984;74: 684-6. 3. GoodacreTEE, WallaceAF. Congenitalalveolar fusion. Br J Plast Surg 1990;43: 203-9. 4. Dixon MJ, FergusonMWJ. The effects of epidermal growth factor, transforming growth factors alpha and beta and platelet-derived growth factor on murine palatal shelves in organ culture. Arch Oral Biol 1992; 37: 395--410. 5. Ferguson MWJ, Sharpe PM, Thomas BL, Beck F. Differential expression of insulin-likegrowth factors I and II (IGF I and II), mRNA, peptide and binding protein I during mouse palate

The Authors Milind Dalai FRCS, SpecialistRegistrarin Plastic Surgery Paul Davison FRCS(Plast), ConsultantPlastic Surgeon Departmentof Plastic Surgery,North Staffordshire City General Hospital, Newcastle Road, Stoke on Trent ST4 6QG, UK. Correspondenceto Mr MilindDalai, 11 WillowfieldsRoad, Nuneaton,WarwickshireCV 11 6PR, UK. Paper received 17 January 2001. Accepted 11 January2002, after revision.

BritishJournalofPlasticSurgery(2002),55 9 2002The BritishAssociationof PlasticSurgeons doi:10.1054fojps.2002.3796

Candida colonisation within a silicone tissue expander A. Saray, S. Kaygusuz*, U. Kisat and D. Kilic*

Departments of Plastic Surgery, *Infectious Diseases and Clinical Microbiology, and tBiochemistry, Ktrtkkale University Medical School, Klrtkkale, Turkey SUMMARY.

The fungal contamination of tissue expanders is rarely reported. There are, however, occasional reports of fungi in association with inflatable mammary implants. We describe the colonisation of a tissue expander with Candida albicans, resulting in the fluid becoming a turbid brown colour. The possible modes of inoculation and survival of the microorganism within the expander shell were investigated by means of biochemical and microbiological analyses of the fluid. The colonisation of silicone implants by opportunistic fungi is probably more common than has been reported, and precautions that can be taken to avoid this complication are emphasised. 9 2002 The British Association of Plastic Surgeons

Keywords: Candida albicans, tissue expander, implant.

Fungal infections around alloplastic implants are a wellknown clinical entity. This phenomenon, however, is a rare complication of augmentation mammaplasty. Previously, fungal infection has been diagnosed and reported in five patients who have undergone breast augmentation using silicone mammary implants. 1-3 Candida

albicans and Aspergillus niger have been identified as infecting organisms in inflatable silicone implants.2 To date, only one case of fungal contamination within a tissue expander has been reported. 4 We present a case in which C. albicans colonised the supposedly sterile saline filler of a silicone tissue

258 expander used for post-mastectomy breast reconstruction. This case is unique in that the C. albicans colonisation was detected in the silicone tissue expander in the absence of any clinical signs of infection around the implant. The fluid inside the implant was analysed to determine whether the fungus could have been sustained by the influx of nutrients from the external milieu.

Case report A 45-year-old woman presented for reconstruction of her left breast 5 years after undergoing a modified radical mastectomy and radiotherapy. She had a horizontal scar with no excess skin. Reconstruction was planned as a two-stage procedure of tissue expansion and subsequent replacement of the expander with a saline-filled breast implant. In the first stage, the lateral half of the mastectomy scar was incised and a 650ml round tissue expander (McGhan, USA) was inserted deep to the pectoralis major muscle. The injection port was placed laterally on the chest, and 100ml of normal saline (Soro Fisiologico 0.9% NaCI, Paracelsia, Industria Farmaceutica, Portugal) was drawn from a bowl on the operating room trolley and immediately injected into the expander. Thereafter, expansion was performed at biweekly intervals, and completed 5 months postoperatively. The expansion period was uneventful, and every expansion was performed under sterile conditions using sterile saline. In the second stage, 9 months after the first, the tissue expander was replaced by a 300ml saline-filled prosthesis; a vertical reduction mammaplasty was performed on the contralateral normal breast. A satisfactory cosmetic result was achieved. When the tissue expander was removed during the second operation, it was seen to contain a turbid brown fluid (Fig. 1). Biopsy of the fibrous capsule surrounding the tissue expander was submitted for culture and histopathological evaluation. The turbid dark brown fluid within the implant was also submitted for biochemical evaluation. Analysis of the fluid that was withdrawn from the tissue expander revealed a glucose content of 10mgd1-1, a protein content of 1.1 gdl 1, a urea content of 2 mg dl-1, a cholesterol content of 14mgdl 1, a triglyceride content of 6mgdl -I, a very-low-density tipoprotein content of 1 mgdl 1, a sodium content of 157.5 mEq 1-1 and a potassium content of 0.86 mEq 1-1. Calcium, phosphorus and uric acid were also present in low quantities. Fluid cultures from the tissue expander grew in Sabaroud dextrose agar (SDA) and automated blood culture bottle (Bactec, Becton Dickenson, USA) mediums at 48h.

Figure 1--The tissue expander and the connected port, showing the dark brown and turbid fluid within the shell.

British Journal of Plastic Surgery Evaluation of the smooth and creamy colonies revealed Grampositive ovoid cells. The yeast was identified as C. albicans by using carbohydrate assimilation and fermentation reactions, nitrate utilisation, urea production and germ-tube formation. Histological examination revealed a capsule lined with one-layer flat epithelium with congested and dilated vessels surrounded by mononuclear phagocytic cells, scattered macrophage infiltrations and fibrosis.

Discussion Fungal infections around alloplastic implants and prostheses are a well-recognised clinical entity. The cardiovascular and otorhinolaryngological literature are replete with reports of fungal infections involving silicone prostheses or devices. Fungal contamination, however, is a rare complication of augmentation mammaplasty. There have been few reports of fungal infections in and around breast implants, and only A. niger, C. albicans, Curvilaria sp., Penicillium sp. and Paecilomyces variotii have been shown to grow in fungal culturesJ -3 Contamination of a tissue expander has only been previously reported once, by Coady et al.4 In their case report, colonisation of a tissue expander by A. niger resulted in mechanical obstruction of the device.4 Candida is the most common fungal pathogen to cause a wide spectrum of opportunistic diseases. The past few decades have seen increasing numbers of candida infections, including both community-acquired and nosocomial infections, reflecting, among other things, the use of broad-spectrum antibiotics, the use of intravascular devices and the growing population of immunosuppressed patients. The many clinical symptoms associated with candida infection are most frequently caused by C. albicans. The organisms are normal commensals of humans and are commonly found on the skin, throughout the entire gastrointestinal tract, in the female genital tract and in the urine of patients with indwelling Foley catheters. There is a relatively high incidence of carriage on the skin of healthcare workers. 5 The expander used in this case was assumed to be sterile when the package was opened. It was a single-use implant, which was supplied empty, in a sealed gammairradiated package. Yeast forms of C. albicans could only have contaminated it either during the first operation when it was inserted or during the biweekly expansion involving percutaneous saline injection. The saline solutions were used meticulously during the operations, and a new and sterile solution was used in every case. However, the saline-containing sterile plastic containers, either in the operating theatre or in a neighbouring storage room, could have already been colonised by C. albicans. The 100ml of normal saline used for the initial expansion was retrieved from a sterile container that, although used only for this purpose, had been lying on the theatre trolley for some time. The saline for expansion was drawn up using a sterile 5 0 m l needle and syringe from single-use sterile plastic containers with twist-off caps. The fungus could also have originated from the patient's skin. Although the skin is cleaned with povidone iodine (10%) and draped in every patient, C. albicans might have survived, despite the antifungal effect of disinfectant. There is a relatively high incidence of carriage on the skin of healthcare workers. 5 It is most

The butterfly design: coverage of a large sacral defect likely that the contamination occurred during the biweekly outpatient visits. Before each transcutaneous injection of normal saline into the expander, the patient's skin overlying the port was cleansed with povidone iodine (10%). This agent is very effective against most microorganisms, including fungi. 6 However, complete antisepsis is hard to achieve because of the brief contact time of the iodine-containing solution with the skin. Biochemical evaluation of the fluid withdrawn from the implant revealed several clues as to how the fungus was able to grow and survive. C. albicans grows rapidly at 25-37 ~ on simple media as oval budding cells. It has minimal growth requirements and can assimilate and ferment glucose to produce gas. Furthermore, C. albicans has been shown to proliferate rapidly in lipid-containing admixtures such as total parenteral nutrition solutions. 7 It has been reported to grow in total nutrient admixtures containing 17.6% glucose, 5% amino acids and 4% lipids with a pH of 5.6. 8 In this case, the composition of the fluid within the tissue expander seems to have facilitated the growth and survival of C. albicans colonies. The expander, inflated solely by saline injections, was eventually found to contain a growth medium consisting of glucose, protein and lipid, which served as nutrients for C. albicans. Silicone rubbers act as semipermeable membranes, allowing the passage of electrolytes as well as a whole variety of other substances, including drugs, Silicones are variously permeable to many drugs, and their use as implantable or skin-surface drug-delivery systems is increasing. 9 Therefore, the exchange of ions and the influx of proteins and lipids through the silicone shell is not a surprise. The silicone shell is also permeable to gas and has been shown to permit the diffusion of oxygen and carbon dioxide across the envelope of a tissue expander. 4 Thus, sufficient quantities of gas may have diffused through the membrane of the silicone tissue expander to sustain the favourable medium for the microorganism. The colonisation of silicone implants by fungi is probably more common than has hitherto been suspected. Regardless of the source of the contamination, it is interesting that fungi were able to colonise the supposedly sterile implant without giving rise to significant clinical signs. Infection associated with fungi in and around an implant has previously been reported twice. 1-3 Our case is the first in which an expander has been colonised with C. albicans without any signs of peri-implant infection. Both internal and external contamination of tissue expanders by pathogenic organisms must be prevented, and every measure should be taken to perform expander inflations under sterile conditions. During every expansion episode, the surgeon should be meticulous about retrieving the saline by direct needle puncture from a sterile container. The saline should be opened immediately

259 before expansion, not drawn from a bottle left for any length of time or from a bottle that has been previously unsealed. Before percutaneous injection, the skin should be cleansed with a disinfectant of known mycocidal activity. Also, the disinfectant chosen for skin preparation should be rapidly active. After the disinfectant agent has been applied, it should be left for 5-7 min for maximum effect. 6-8 References 1. Truppman ES, Ellenby JD, Schwartz BM. Fungi in and around implants after augmentation mammaplasty. Plast Reconstr Surg 1979; 64: 804-6. 2. Williams K, Walton RL, Bunkis J. Aspergillus colonization associated with bilateral silicone mammary implants. Plast Reconstr Surg 1983; 71: 260-1. 3. Niazi ZBM, Salzberg CA, Montecalvo M. Candida albicans infection of bilateral polyurethane-coated silicone gel breast implants. Ann Plast Surg 1996; 37: 91-3. 4. Coady MSE, Gaylor J, Knight SL. Fungal growth within a silicone tissue expander: case report. Br J Plast Surg 1995; 48: 428-30. 5. Edwards JE Jr. Candida species. In Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases. Philadelphia: Churchill Livingstone, 2000: 2656-7. 6. Pi6rard GE, Pidrard-Franchimont C, Arrese JE. Povidone-iodine wash solutions in the prevention of superficial fungal infections; predictive evaluation using the corneofungimetry bioassay. Eur J Clin Pharmacol 1997; 53: 101-4. 7. Goldmann DA, Martin WT, Worthington JW. Growth of bacteria and fungi in total parenteral nutrition solutions. Am J Surg 1973; 126: 314-18. 8. Didier ME, Fischer S, Maki DG. Total nutrient admixtures appear safer than lipid emulsion alone as regards microbial contamination: growth properties of microbial pathogens at room temperature. J Parenter Enteral Nutr 1998; 22: 291-6. 9. Brody GS. Silicone technology for the plastic surgeon. Clin Plast Surg 1988; 15: 517-20.

The Authors Aydin Saray MD, Assistant Professor of Plastic Surgery Plastik ve Rekonstriiktif Cerrahi AD, Sedat Kaygusuz MD, Assistant Professor in Infectious Diseases and Clinical Microbiology Dilek Kilic MD, Assistant Professor in Infectious Diseases and Clinical Microbiology Infeksiyon Hastaliklari AD, Ucler Kisa PhD, Assistant Professor in Biochemistry Biokimya AD, Ktrtkkale Universitesi, Tip Fakfiltesi, Fabrikalar Mahallesi, Saglik Caddesi, 71100 Ktrtkkale, Turkey. Correspondence to Aydin Saray MD. Paper received 10 October 2001. Accepted 12 December 2001.