Dental work as a cause of acute inflammation of a lymphoedematous limb
Identifieur interne : 005062 ( Istex/Corpus ); précédent : 005061; suivant : 005063Dental work as a cause of acute inflammation of a lymphoedematous limb
Auteurs : John Chambers ; Katie McgovernSource :
- Palliative Medicine [ 0269-2163 ] ; 2004-10.
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DOI: 10.1177/026921630401800717
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<title-group><article-title>Dental work as a cause of acute inflammation of a lymphoedematous limb</article-title>
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<contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Chambers</surname>
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<aff>Lymphoedema Nurse Specialist, Katharine House Hospice, East End, Adderbury, Oxon OX17 3NL, UK <email xlink:type="simple">dr.ch@mbers.info</email>
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<meta-value> Letters to the editor 667 allow a brief, cheap and timely communication to be made with minimum additional time required by clinical staff to complete this. P Sarah Galbraith and Sara Booth Addenbrooke's Palliative Care Team Addenbrooke's Hospital, Cambridge, UK. References 1 Higginson I. Palliative care services in the community: what do family doctors want? J Palliat Care 1999; 15; 21- 25. 2 Todd J, Edmonds P, Lillie G, Charman F, Chamberlain J. Use of a discharge letter to improve communication between a hospital palliative care team and the primary health care team. Palliat Med 1998; 12: 476-77. Dental work as a cause of acute inflammation of a lymphoedematous limb Sir - The chronic morbidity of lymphoedema typically worsens with successive acute inflammatory episodes (AlEs), yet little is known about their aetiology. We present two case histories that apparently link dental procedures with AIEs. A 90-year-old woman with cancer of the left breast, treated by mastectomy and radiotherapy to the axilla, had a two-year history of stable lymphoedema of the left arm with no AlEs. Three weeks after a triple tooth extraction, she had an AIE. Arm volume increased from 1840 to 2230 mL, associated with warmth and redness. There was no concurrent history of trauma, infection or physical overexertion. Being allergic to penicillin, she was given cephalexin. It took six months for the arm volume to reduce back to 1990 mL. A 55-year-old woman with cancer of the left breast treated by mastectomy, axillary node excision and radio- therapy to the axilla had a 20-year history of stable lymphoedema of the left arm with no AlEs. Following root canal work, her left arm volume increased over six weeks from 1422 to 1750 mL. There was no concurrent history of trauma, infection or physical overexertion. The swelling gradually subsided with a compression sleeve, only to reappear in exactly the same manner following further dental work. If a legitimate link exists between dental work and AlEs, it could have a microbiological basis. The potential role of streptococci in AlEs has been debated for many years. Streptococci were first isolated from AIE sites in 1892.1 In 1954 it was reported that recurrent AlEs could be associated with isolation of exactly the same strain of streptococcus from the inflamed site even when the interval between AlEs exceeded 12 months,2 suggesting that some patients with recurrent AlEs were subject to reinfection from a protected streptococcal reservoir. However, the true situation might be less straightforward. First, it is notoriously difficult to isolate pathogens from infected skin that has not been breached. Secondly, it has been suggested that AlEs might be the result of an immune response to microbial antigen in lymphoedema- tous tissue rather than infection.3 Thirdly, other plausible pathogens for AlEs include fungi and anaerobes, the latter being penicillin-sensitive like streptococci. Regardless of how microbes might be implicated in AlEs, our case histories are compatible with the orophar- ynx serving as a microbial reservoir that can release inflammatory mediators when dental procedures are performed. Streptococci, anaerobes and fungi are all commonly isolated from the oropharyngeal flora and the prevalence of bacteraemia following dental work can range between 10% and 100%, depending upon the procedure performed. Based on the idea that people considered high risk for bacterial endocarditis should receive prophylactic anti- biotic to cover dental procedures, it is tempting to speculate that patients with lymphoedema should receive prophylactic antibiotic to prevent AlEs attributable to dental procedures. However, the use of prophylactic antibiotics to prevent bacterial endocarditis is conten- tious. Whilst 7% of bacterial endocarditis is attributable to dental procedures,4 the absolute risk of any single procedure is very low in high-risk patients. Furthermore, antibiotic prophylaxis does not prevent bacteraemia,5 and anyway, we are all subject to frequent spontaneous episodes of bacteraemia in our daily lives. Therefore we conclude that dental work might be responsible for a small proportion of AlEs in lymphoe- dematous tissue and this would not be incompatible with a streptococcal or alternative microbial aetiology. How- ever, until our understanding of bacteraemias and AIEs improves, it is hard to confidently suggest ways of reducing the apparent risk. The breakthrough in our understanding might come from polymerase chain reac- tion analysis of saline aspirates from sites of AIE to elucidate the nature of any microbial involvement.6 John Chambers Macmillan Consultant and Medical Director, Katharine House Hospice, East End, Adderbury, Oxon OXJ 7 3NL, UK Katie McGovern Lymphoedema Nurse Specialist, Katharine House Hospice, East End, Adderbury, Oxon OX] 7 3NL, UK E-mail: dr. ch@mbers. info 668 Letters to the editor References 1 Sabouraud R. Sur la parasitologie de l'elephantiasis nostras. Ann Derm Syph (Paris) 1892; 3: 592. 2 Stevens FA. Behaviour of local foci causing recurrent streptococcal infections of skin, subcutaneous tissues and lymphatics. Surg Gynec Obstet 1954; 99: 268-72. 3 Mortimer PS. Managing lymphoedema. Clin Exp Derma- tol 1995; 20: 98-106. 4 Tomas Carmona T, Diz Dios D, Limeres Posse J, Gonzalez Quintela A, Martinez Vanquez C, Castro Iglesias A. An update on infective endocarditis of dental origin. J Dent 2002; 30: 37-40. 5 Pallasch TJ. Antibiotic prophylaxis: problems in paradise. Dent Clin North Am 2003; 47: 665-79. 6 Harris KA, Hartley JC. Development of broad-range 16S rDNA PCR for use in the routine diagnostic clinical microbiology service. J Med Microbiol 2003; 52: 685-91.</meta-value>
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