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Europace Advance Access originally published online on November 10, 2006
Europace 2006 8(12):1068-1069; doi:10.1093/europace/eul114
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


PACING

Pyoderma gangrenosum complicating pacemaker implant

Francisco G. Cosío1,*, Carlos González Herrada2, Alfonso Monereo3, Agustín Pastor1 and Ambrosio Núñez1

1 Cardiology Service, Hospital Universitario de Getafe, Carretera de Toledo, km 12.5, 28905 Getafe, Madrid, Spain; 2 Dermatology Service, Hospital Universitario de Getafe, Madrid, Spain; 3 Internal Medicine Service, Hospital Universitario de Getafe, Madrid, Spain

Manuscript submitted 23 June 2006. Accepted after revision 5 July 2006.

* Corresponding author. Tel: +34 91 683 078; fax: +34 91 683 9826. E-mail address: fcosio{at}vitanet.nu


    Abstract
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
A 70-year-old lady with diabetes and monoclonal gammopathy underwent pacemaker implant for 2:1 atrioventricular block. Within 7 days, a painful, infiltrating, necrotic lesion involved the implant area. Biopsy was compatible with pyoderma gangrenosum and corticosteroid treatment led to healing in 3 weeks.

Key Words: Pacemaker implant complications, Pyoderma gangrenosum, Pathergy on pacemaker


    Introduction
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 Abstract
 Introduction
 Case report
 Discussion
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Pyoderma gangrenosum (PG) is an inflammatory process of unknown aetiology that can complicate minor trauma, including surgical incisions. We report a case of PG after permanent pacemaker implantation that was controlled with corticosteroids.


    Case report
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 Case report
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A 79-year-old woman with a history of hypertension, diabetes, and monoclonal gammopathy (IgG lambda), without diagnostic criteria for multiple myeloma, underwent a permanent VDD pacemaker implant for 2:1 AV block associated with heart failure. The electrode was advanced through a left subclavian puncture and the generator was placed under the anterior pectoral fascia. Immediate course was uneventful and she was discharged the following day, but fever (38°C) and local pain and swelling developed thereafter. On the seventh day after implant, there was an area of inflammation with deep infiltration and cutaneous blistering, 12 cm in diameter, surrounding the incision. A superficial culture grew Staph epididymis, and cloxacyclin was started. In 3 days, the inflammatory area became dark and coarsely granular in the centre (Figure 1B), and a biopsy showed massive neutrophilic infiltration and extensive necrosis compatible with PG. Systemic corticosteroid therapy was started with 60 mg of prednisone daily. Pain and inflammation subsided rapidly and the lesion healed completely in 3 weeks. Concomitantly, the patient developed progressive heart failure and a severe nephrotic syndrome that led to her death 1 month after admission. Cardiac and renal amyloidosis was suspected, but no biopsy was performed and a post-mortem examination was not authorized.


Figure 1141
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Figure 1 (A) Erythematous, infiltrated plaque with beginning central necrosis and (B) evolving lesion 2 days later. Necrotic ulcer with coarse granulation tissue and bluish borders forming circular segments.

 

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PG is a rare ulcerative process of unknown aetiology, attributed to an immunological reaction, related to a dysfunction of neutrophils.1Go It can involve the skin or internal organs, and in 25% of cases, it is triggered by minor skin injury2Go,3Go or surgery, such as pacemaker implantation,4Go,5Go a phenomenon alluded to as pathergy. It is usually observed between age 20 and 50, but it can occur at any age. In >50% of cases, it is associated with Crohn's disease or ulcerative colitis, rheumatoid arthritis, or haematological diseases, such as leukaemia, or myelofibrosis of monoclonal gammopathy, as in our case.2Go PG starts as a painful erythematous plaque, a nodule, blister, or pustule, evolving rapidly to central necrosis, with bluish circular edges and granulation tissue with the appearance of ‘hamburger meat.’ Healing occurs from the edges, leaving atrophic, cribriform, often-pigmented scars. The diagnosis is made by the clinical and pathological correlation, because the biopsy is non-specific, but it allows ruling out of other processes.1Go Treatment with prednisone, immunosuppressant agents, or necrosis factor inhibitors may allow healing without pacemaker explant, as in our case.6Go Unfortunately, our patient died of comorbid conditions, despite healing of the PG lesions.


    References
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
[1] Su WPD, Davis MDP, Weenig RH, Powell FC, Perry HO. Pyoderma gangrenosum: clinicopathologic correlation and proposed diagnostic criteria. Int J Dermatol 2004; 43: 790–800.[CrossRef][Web of Science][Medline]

[2] Mlika RB, Riahi I, Fenniche S, Mokni M, Dhaoui MR, Dess N, et al. Pyoderma gangrenosum: a report of 21 cases. Intern J Dermatol 2002; 41: 65–8.[CrossRef]

[3] Crowson AN, Magro C, Mih JR. Pyoderma gangrenosum: a review. J Cutan Pathol 2003; 30: 97–107.[CrossRef][Web of Science][Medline]

[4] Lo TSN, Griffith M, Heber ME. Pyoderma gangrenosum presented as a refractory wound infection following permanent pacemaker implantation. Heart 2002; 87: 414.[Free Full Text]

[5] Kaur MR, Gach JE, Marshall H, Lewis HM. Recurrent postoperative pyoderma gangrenosum complicating pacemaker insertion. J Eur Acad Dermatol Venereol 2006; 20: 461–88.[CrossRef][Web of Science][Medline]

[6] Reichrath J, Bens G, Bonowitz A, Tilden W. Treatment recommendations for pyoderma gangrenosum: an evidence-based review of the literature based on more than 350 patients. J Am Acad Dermatol 2005; 53: 273–83.[CrossRef][Web of Science][Medline]


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This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
8/12/1068    most recent
eul114v1
Right arrow Alert me when this article is cited
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