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Pyoderma gangrenosum mimicking an infected foot Pyoderma gangrenosum (PG) is a rare skin disease characterized by pustule formation, which rapidly develops into an area of necrosis. Most cases of PG occur in patients with underlying systemic diseases, including inflammatory bowel disease, rheumatoid arthritis and neoplastic disease. We present a case of a lady with inflammatory bowel disease, who presented with erythema and pustule formation on her foot. Clinically, this was difficult to differentiate from infection. This case underlines the pitfalls in diagnosis and management of PG. A 28-year-old lady with a past medical history of ulcerative colitis presented with a 2-week history of painful, spreading erythema on the dorsal aspect of her right foot. She had seen her general practitioner prior to admission, who had prescribed flucloxacillin 500 mg QDS, without effect. Her blood results on admission showed a high-normal white cell count (8.3) and a slightly raised C-reactive protein (CRP) (43); all other results were within normal range. On the basis of the raised inflammatory markers and appearance of the foot, a diagnosis of partially treated cellulitis was made and the patient was given a course of flucloxacillin 2 g IV QDS. After 1 day of this antibiotic regimen, the patient felt that she had improved and the erythema had appeared to subside. She was discharged to complete the course of antibiotics at home. However, 2 days later she re-presented, complaining the lesion was becoming more painful. Clinically, the lesion was fluctuant, had a purplish discolouration and the patient was pyrexial (Fig. 1). CRP
was significantly raised (254). On the basis of the poor response to antibiotics and fluctuant nature of the lesion, an abscess was diagnosed and this was incised and drained. Intra-operatively, there was 5 mL of purulent material within the lesion, which was sent for culture and sensitivities. Post-operatively she was restarted on IV antibiotics (flucloxacillin and clindamycin) but continued to deteriorate. Forty-eight hours post-op, the clinical appearance of the lesion was much worse than the preoperative picture (Fig. 2) and she had pain out of proportion to the appearance of the lesion. Her CRP had also further risen to 346. By virtue of a rapidly worsening picture and extreme pain, she was diagnosed with necrotizing fasciitis and booked for further debridement. At this point, the culture and sensitivities of the pus found at operation returned as no growth. Given the poor response to antibiotic therapy, surgical intervention and the patient’s history of ulcerative colitis, a diagnosis of PG was considered. A dermatology opinion was requested urgently prior to any further surgery. A dermatologist reviewed the patient that evening, and PG was confirmed. Further management was medical. Antibiotics were stopped, steroids were started and patient had no further surgery. At follow-up 3 months later, her wound had significantly improved (Fig. 3).
Fig. 1. Arrow denotes ‘bogginess’, which led to an abscess being diagnosed.
Fig. 2. Worsening appearance post-debridement. Note violet hue to borders.
© 2015 Royal Australasian College of Surgeons
ANZ J Surg •• (2015) ••–••
2
Images for surgeons
the Köbner phenomenon seen in psoriasis in that it appears at sites of trauma, and is well described in post-surgical wounds.10 PG is a rare and difficult-to-diagnose condition that requires a high clinical index of suspicion. Failing to do so can lead to needless operations that can lead to increased morbidity and even mortality, with a significant cost burden. Given the above case report, it is crucial to reconsider the initial working diagnosis if the expected clinical response is not observed.
References
Fig. 3. Much improved picture after course of steroids.
PG is a rare but often serious, ulcerative skin condition that can lead to significant complications if missed in diagnosis and thus wrongly managed.1,2 The condition was first described in 1930 by Brunsting et al.3 who described it as ‘a chronic, recurring, destructive ulcerations of the skin in association with ulcerative colitis’. The pathogenesis of PG is still poorly understood; however, the most widely accepted theory is related to defects in humoral and cellmediated immunity.4 Epidemiologically, PG has never been formally assessed; thus, the stated epidemiology is based on case reports and series.5 This state PG is more common in women (3.8:1), with 75% of cases having associated systemic disease and 80% of lesions located in the lower extremities.6 The described appearance of PG is usually one that begins with a pustule or nodule that rapidly develops into a cutaneous necrotic lesion, the border of which is undermined and has a characteristic violet hue.7 PG has been described not only in conjunction with ulcerative colitis but also alongside chronic disease, namely autoimmune mediated and neoplastic.8,9 As well as these associations, PG elicits a pathognomonic effect called pathergy, which is similar to
1. Lê Huu S, Spertini F, Roggero P, Egloff DV, Raffoul W. Pyoderma gangrenosum: a rare pathology or an omitted diagnosis? Ann. Chir. Plast. Esthét. 2009; 54: 82–7. 2. Bisarya K, Azzopardi S, Lye G, Drew PJ. Necrotizing fasciitis versus pyoderma gangrenosum: securing the correct diagnosis! A case report and literature review. Eplasty 2011; 11: e24. 3. Brunsting LA, Goerckerman WH, O’Leary PA. Pyoderma (ecthyema) gangrenosum: clinical and experimental observations in five cases occurring in adults. Arch. Dermatol. Syph. 1930; 22: 655–68. 4. Bennet CR, Brage ME, Mass DP. Pyoderma gangrenosum mimicking postoperative infection in the extremities. J. Bone Joint Surg. Am. 1999; 81 (A): 1013–8. 5. Langan SM, Groves RW, Card TR, Gulliford MC. Incidence, mortality, and disease associations of pyoderma gangrenosum in the United Kingdom: a retrospective cohort study. J. Invest. Dermatol. 2012; 132: 2166–70. 6. Pereira N, Brites MM, Gonçalo M, Tellechea O, Figueiredo A. Pyoderma gangrenosum – a review of 24 cases observed over 10 years. Int. J. Dermatol. 2013; 52: 938–45. 7. Brooklyn T, Dunnill G, Probert C. Diagnosis and treatment of pyoderma gangrenosum. BMJ 2006; 2006: 181–184. 8. Yayli S, Bahadir S, Alpay K, Cims¸it G, Cobanog˘lu U, Tosun M. Pyoderma gangrenosum in association with juvenile rheumatoid arthritis. J. Dermatol. 2005; 32: 827–30. 9. Duchnowska R, Ziajka E, Góralska A, Grala B. Recurrent pyoderma gangrenosum precipitated by breast cancer: a case report and review of the literature. J. Med. Case Rep. 2014; 8: 226. 10. Ogon M, Sepp NT, Wimmer C, Behensky H. Case report: a surgical wound infection? Lancet 2000; 356: 1652.
Samuel Haines, MBBCh Ben Hickey, BM, MRCS Christopher Wilson, MBBS, FRCS (Orth) Trauma and Orthopaedics, University Hospital of Wales, Cardiff, UK doi: 10.1111/ans.13042
© 2015 Royal Australasian College of Surgeons
Pyoderma gangrenosum mimicking an infected foot Pyoderma gangrenosum (PG) is a rare skin disease characterized by pustule formation, which rapidly develops into an area of necrosis. Most cases of PG occur in patients with underlying systemic diseases, including inflammatory bowel disease, rheumatoid arthritis and neoplastic disease. We present a case of a lady with inflammatory bowel disease, who presented with erythema and pustule formation on her foot. Clinically, this was difficult to differentiate from infection. This case underlines the pitfalls in diagnosis and management of PG. A 28-year-old lady with a past medical history of ulcerative colitis presented with a 2-week history of painful, spreading erythema on the dorsal aspect of her right foot. She had seen her general practitioner prior to admission, who had prescribed flucloxacillin 500 mg QDS, without effect. Her blood results on admission showed a high-normal white cell count (8.3) and a slightly raised C-reactive protein (CRP) (43); all other results were within normal range. On the basis of the raised inflammatory markers and appearance of the foot, a diagnosis of partially treated cellulitis was made and the patient was given a course of flucloxacillin 2 g IV QDS. After 1 day of this antibiotic regimen, the patient felt that she had improved and the erythema had appeared to subside. She was discharged to complete the course of antibiotics at home. However, 2 days later she re-presented, complaining the lesion was becoming more painful. Clinically, the lesion was fluctuant, had a purplish discolouration and the patient was pyrexial (Fig. 1). CRP
was significantly raised (254). On the basis of the poor response to antibiotics and fluctuant nature of the lesion, an abscess was diagnosed and this was incised and drained. Intra-operatively, there was 5 mL of purulent material within the lesion, which was sent for culture and sensitivities. Post-operatively she was restarted on IV antibiotics (flucloxacillin and clindamycin) but continued to deteriorate. Forty-eight hours post-op, the clinical appearance of the lesion was much worse than the preoperative picture (Fig. 2) and she had pain out of proportion to the appearance of the lesion. Her CRP had also further risen to 346. By virtue of a rapidly worsening picture and extreme pain, she was diagnosed with necrotizing fasciitis and booked for further debridement. At this point, the culture and sensitivities of the pus found at operation returned as no growth. Given the poor response to antibiotic therapy, surgical intervention and the patient’s history of ulcerative colitis, a diagnosis of PG was considered. A dermatology opinion was requested urgently prior to any further surgery. A dermatologist reviewed the patient that evening, and PG was confirmed. Further management was medical. Antibiotics were stopped, steroids were started and patient had no further surgery. At follow-up 3 months later, her wound had significantly improved (Fig. 3).
Fig. 1. Arrow denotes ‘bogginess’, which led to an abscess being diagnosed.
Fig. 2. Worsening appearance post-debridement. Note violet hue to borders.
© 2015 Royal Australasian College of Surgeons
ANZ J Surg •• (2015) ••–••
2
Images for surgeons
the Köbner phenomenon seen in psoriasis in that it appears at sites of trauma, and is well described in post-surgical wounds.10 PG is a rare and difficult-to-diagnose condition that requires a high clinical index of suspicion. Failing to do so can lead to needless operations that can lead to increased morbidity and even mortality, with a significant cost burden. Given the above case report, it is crucial to reconsider the initial working diagnosis if the expected clinical response is not observed.
References
Fig. 3. Much improved picture after course of steroids.
PG is a rare but often serious, ulcerative skin condition that can lead to significant complications if missed in diagnosis and thus wrongly managed.1,2 The condition was first described in 1930 by Brunsting et al.3 who described it as ‘a chronic, recurring, destructive ulcerations of the skin in association with ulcerative colitis’. The pathogenesis of PG is still poorly understood; however, the most widely accepted theory is related to defects in humoral and cellmediated immunity.4 Epidemiologically, PG has never been formally assessed; thus, the stated epidemiology is based on case reports and series.5 This state PG is more common in women (3.8:1), with 75% of cases having associated systemic disease and 80% of lesions located in the lower extremities.6 The described appearance of PG is usually one that begins with a pustule or nodule that rapidly develops into a cutaneous necrotic lesion, the border of which is undermined and has a characteristic violet hue.7 PG has been described not only in conjunction with ulcerative colitis but also alongside chronic disease, namely autoimmune mediated and neoplastic.8,9 As well as these associations, PG elicits a pathognomonic effect called pathergy, which is similar to
1. Lê Huu S, Spertini F, Roggero P, Egloff DV, Raffoul W. Pyoderma gangrenosum: a rare pathology or an omitted diagnosis? Ann. Chir. Plast. Esthét. 2009; 54: 82–7. 2. Bisarya K, Azzopardi S, Lye G, Drew PJ. Necrotizing fasciitis versus pyoderma gangrenosum: securing the correct diagnosis! A case report and literature review. Eplasty 2011; 11: e24. 3. Brunsting LA, Goerckerman WH, O’Leary PA. Pyoderma (ecthyema) gangrenosum: clinical and experimental observations in five cases occurring in adults. Arch. Dermatol. Syph. 1930; 22: 655–68. 4. Bennet CR, Brage ME, Mass DP. Pyoderma gangrenosum mimicking postoperative infection in the extremities. J. Bone Joint Surg. Am. 1999; 81 (A): 1013–8. 5. Langan SM, Groves RW, Card TR, Gulliford MC. Incidence, mortality, and disease associations of pyoderma gangrenosum in the United Kingdom: a retrospective cohort study. J. Invest. Dermatol. 2012; 132: 2166–70. 6. Pereira N, Brites MM, Gonçalo M, Tellechea O, Figueiredo A. Pyoderma gangrenosum – a review of 24 cases observed over 10 years. Int. J. Dermatol. 2013; 52: 938–45. 7. Brooklyn T, Dunnill G, Probert C. Diagnosis and treatment of pyoderma gangrenosum. BMJ 2006; 2006: 181–184. 8. Yayli S, Bahadir S, Alpay K, Cims¸it G, Cobanog˘lu U, Tosun M. Pyoderma gangrenosum in association with juvenile rheumatoid arthritis. J. Dermatol. 2005; 32: 827–30. 9. Duchnowska R, Ziajka E, Góralska A, Grala B. Recurrent pyoderma gangrenosum precipitated by breast cancer: a case report and review of the literature. J. Med. Case Rep. 2014; 8: 226. 10. Ogon M, Sepp NT, Wimmer C, Behensky H. Case report: a surgical wound infection? Lancet 2000; 356: 1652.
Samuel Haines, MBBCh Ben Hickey, BM, MRCS Christopher Wilson, MBBS, FRCS (Orth) Trauma and Orthopaedics, University Hospital of Wales, Cardiff, UK doi: 10.1111/ans.13042
© 2015 Royal Australasian College of Surgeons
