Case Report Eur Surg (2013) 45:306–309 DOI 10.1007/s10353-013-0234-8 Pyoderma gangrenosum after ventral hernia repair: a pitfall and how to avoid it C. Augschöll · C. Nawara · M. Lechner · F. Mayer · S. Reich-Weinberger · T. Jäger · D. Öfner Received: 24 January 2013 / Accepted: 10 September 2013 / Published online: 9 November 2013 © Springer-Verlag Wien 2013 Summary Background In case of large ventral hernias, the avoidance of a mesh infection caused by a surgical site infection (SSI) is crucial, as surgical options are limited. Pyoderma gangrenosum (PG) is a rare condition that mimics SSI, and is therefore often identified with significant delay. Mechanical alteration is known to maintain the progress of PG, outlining the importance of early discrimination against SSI. Methods We report our recent clinical experience with PG in a 73-year-old patient after ventral hernia repair. Results We present our experience, based on the case of a 73-year-old woman with postoperative PG. Conclusions By a systematic approach, we provide indicators to contribute to an earlier diagnosis and adequate treatment in future cases. To the best of our knowledge, this is the first to-the-point checklist in the published literature so far. Keywords Pyoderma gangrenosum · Ventral hernia · Hernioplasty · Surgical site infection · Checklist Introduction Pyoderma gangrenosum (PG) is a rare disease of the skin, which presents with painful centrifugal necrosis. It is encountered worldwide, usually in adults and without gender prevalence. PG is mostly seen on the surface of the torso and the extremities but can also appear in extra- Dr. C. Augschöll ( ) · C. Nawara, MD · M. Lechner, MD · F. Mayer, MD · S. Reich-Weinberger, MD · T. Jäger, MD · D. Öfner, MD Department of Surgery, Paracelsus Private Medical University of Salzburg, Müllner Haupstrasse 48, 5020 Salzburg, Austria e-mail: [email protected] 306 cutaneous manifestations in lungs, heart, and central nervous system, where it is usually associated with poor prognosis. Etiology and pathogenesis remain unclear— an overactivation of leukocytes for unknown reasons leads to local formation of microabscesses, necrosis, and exquisitely painful destruction of soft tissue. Blood vessels are not directly affected, and because PG is not an actual form of vasculitis, the typical histopathological signs are not found on examination. The condition has been known to be associated with malignant neoplasms, underlying medical conditions like chronic inflammatory bowel disease, rheumatoid, or seronegative arthritis, and other disorders of the immune system. PG can also be observed as a complication in postoperative wound healing. Among the known types of the condition, from a surgical point of view, the postoperative progressive gangrene of the skin is the most significant one: after the initial trauma, a formation of necrotic ulcers with a tendency toward rapid centrifugal growth is observed. The lesions frequently show a smeared background, can spread at a rate of one or more centimeters a day, and show typical soft, undermined, bluish-red margins. Patients’ blood samples often reveal leucocytosis, mildly elevated C-reactive protein (CRP), and discrete anemia. Tests for antibodies like c-ANCA and antinuclear antibodies are negative, which is useful with regard to Wegener’s granulomatosis as a differential diagnosis. Pathergy is a typical sign found in approximately 20 % of patients at risk of developing PG, with an onset after localized trauma of the skin and resembling an active state of the condition, potentially without other clinical manifestations at the time of testing. During time of positive pathergy, all surgical wounds are at particular risk of being affected by PG. It is worth noting that pathergy is not entirely specific of PG but can also occur in Wegener’s and Behçet’s disease. Pyoderma gangrenosum after ventral hernia repair: a pitfall and how to avoid it 13 Case Report Treatment is traditionally based on high doses of glucocorticoids and cyclosporin A. TNF-α antagonists, azathioprine, and cyclophosphamide have, among others, proven to be effective. Topical application of glucocorticoids and disinfectants can be used. Antibiotics are not indicated unless in case of bacterial superinfection. Further surgical trauma at the site of occurrence must be avoided. Without treatment, PG has been known to continue for months before the lesions slowly heal, leaving behind an almost pathognomic type of scar. However, fulminant courses of the disease with shock and fatal outcome have occurred [1–2]. Literature provides only occasional case reports of PG after mesh implantation, where the diagnosis is frequently missed or, at best, made with significant delay [3–6]. We report a manifestation in a 73-year-old woman after mesh-augmented ventral hernia repair, explain our path of eventual successful management that allowed us to save the implanted mesh, and present a line-up of indicators to contribute to earlier discrimination against surgical site infections (SSIs). Case report We report the case of a 73-year-old woman who was scheduled for the repair of a large ventral hernia, which had existed for many years. Patient history revealed an open cholecystectomy 20 years and a hysterectomy for myomatosis 30 years earlier. Comorbidities included hypertension, hyperthyreosis, varicosis of the lower legs, and recurrent herpes simplex infection of the left eye. Eight years earlier, the patient had suffered a bursitis olecrani on the right arm after a minor trauma. After ineffective topic therapy, initial treatment included incision and lavage, accompanied by an antibiosis with cefazolin (1.5 g thrice daily). A microbiological analysis showed β-hemolyzing streptococci. A revision 4 days later with necrosectomy was performed due to deterioration of the local condition, with a lesional size of 6–3 cm. In addition, negative pressure therapy (NPT) was applied. After referral to a plastic surgeon, the patient was scheduled for a flexor carpi radialis myocutaneous flap plastic surgery, after an angiopathy had been ruled out. The further course remained uneventful. On August 20, 2011, the patient presented with large bleeding ulcers on the site of the hernia and abdominal pain. A computed tomography suggested a herniation of wide parts of the right hemicolon and small intestine, without signs of incarceration (Fig. 1). Due to the immanent risk of a rupture of the hernia sac and the reported symptoms, we opted for immediate surgical treatment. On August 30, herniotomy was performed. The intraoperative findings revealed a complete herniation of the right-sided hemicolon, approximately half of the small intestine, and the omentum majus, with a defect diameter of 11 cm. Therefore, the hernia was graded M2-3W3 following the EHS classification of primary and incisional abdominal wall hernias [7]. To allow for a safe and tension-free closure of the abdominal wall, particularly with regard to the indispensable wide excision of the ulcerous skin, we opted for an extensive approach including a right-sided hemicolectomy with side-to-side ileotransversostomy, an omentectomy, a minimally invasive component separation, and a sublay patch plastic surgery using a macroporous polypropylene mesh (ParieteneTM, Covidien, Ireland) of 20–18 cm. The immediate postoperative course was uneventful; the wound showed no signs of infection; and the patient recovered well. On day 5, the infection parameters began to rise, and fevers with temperatures up to 39 °C occurred. Intravenous antibiotic therapy with piperacillin/tazobactam, 4.5 g thrice daily, was initiated, and a computed tomography was performed, delineating only minor signs of infection. Microbiological cultures were sterile so far. Day 8 onward, the wound altered, starting with livid discoloration and leading to necrosis of 2 cm in diameter on the following day. We removed some of the skin clamps and applied NPT after debridement. Under this Fig. 1 Preoperative computed tomography showing the extent of the hernia with partial loss of domain 13 Pyoderma gangrenosum after ventral hernia repair: a pitfall and how to avoid it 307 Case Report Fig. 2 Extensive polycyclic ulceration with necrosis and livid margin (14th postoperative day) treatment, infection parameters were steadily rising, accompanied by septic fever despite adapted antibiotic treatment. On day 12, the NPT wound dressing was renewed, and again debridement and necrosectomy were performed. The mesh was still covered by fascia, and the infection was limited to the subcutis. After this intervention, a transfer to the intensive care unit was necessary due to septic fever. The patient required intubation and catecholamine support. Blood samples revealed a CRP level of 30 mg/dl (< 0.6 mg/dl), interleukin 6 level of 266 pg/ml (< 0.5 pg/ml), procalcitonin level of 1.8 µg/l (< 0.5 μg/l), and a leukocytosis count of 32.9 g/l (3.5–9.8 g/l). Another wound revision on day 14 led to lavage, emptying of a subcutaneous retention, and partial resection of the fascia. Yet, we found no purulent infection of the mesh (Fig. 2), and microbiological cultures were still without any pathological finding. The first assessment by a dermatologist was on the 15th postoperative day, on which the suspicion of PG arose. On this day, we detected an infection with Staphylococcus epidermidis and Staphylococcus haemolyticus, both methicillin-resistant. According to the antibiogram, therapy was expanded with vancomycin in addition to clindamycin and ciprofloxacin. The still-progressive lesion hardened the suspicion of a pyoderma, with polycyclic superficial ulcers and a livid margin. This led us to start a high-dose cortisone treatment with prednisolone, 250 mg twice daily, and a local wound treatment with moist swabs only. Under these measures, we observed a rapid decrease of the infection parameters, and the local wound stabilized. The following days showed a diminishment of the lesion area, and prednisolone dose was lowered stepwise. The wound was then only treated by rinsing with fresh water and with sulfadiazine ointment. Prednisolone was continued until the 44th postoperative day, when we first discussed a reconstruction by split-skin graft. With further improvement of the local wound, we decided against reconstruction to prevent recurrence of PG, especially because the patient did not mind a suboptimal esthetic outcome. 308 Fig. 3 The same lesion 6 months later Following this, the case was managed in our outpatient department, and the lesion diminished continuously (Fig. 3). Discussion SSIs appear in approximately 25 % of patients after open ventral repair in case of large incisional hernias [8, 9]. A major threat is the infection of the mesh graft, which occurs in 1–2 % of cases [8]. Therapeutical strategies in case of mesh infection are limited to intravenous antibiotics combined with complete or partial mesh excision or application of an NPT [8, 10]. Mesh removal naturally leads to a hernia recurrence, which requires further surgical treatment [8]. In case of large ventral hernia, the avoidance of a mesh infection is crucial, as surgical options are limited. Early stages of PG are often mistaken for an SSI. Yet, surgical interventions maintain the progress of PG, which makes quick discrimination against common SSI essential. Similar to SSI, besides the lesion itself, elevation of infection parameters and fever occur. If PG therefore is mistaken as an SSI and “aggressive” treatment with NPT is started to prevent mesh from secondary infection, the opposite effect of what was intended is achieved due to the mechanical alteration. There are, however, almost pathognomic signs of PG: at first, the affected area often shows a pustule, turning into a necrotic ulcer with fast centrifugal growth up to 2 cm per day and a bluish-red margin. Any physical manipulation leads to further enlargement. Microbiological culture is initially negative, but may show staphylococcal or streptococcal superinfection later. The use of antibiotics shows no effect on the progression. Histological findings are often non-specific at an early stage, but later, abscess-forming inflammatory reaction with infiltration of the epidermis by neutrophilic granulocytes can be observed. In the case presented, we did not observe any of the frequently associated conditions like malignant neoplasm, chronic inflammatory bowel disease, or arthritis. Yet, the patient had suffered a superficial infection after a Pyoderma gangrenosum after ventral hernia repair: a pitfall and how to avoid it 13 Case Report Table 1 Checklist for discrimination of pyoderma gangrenosum against surgical site infection History of Complicated wound infection Arthritis Chronic inflammatory bowel disease Malignant neoplasm Immunological disorder Hematologic disease PG. As reported by several authors and in line with our own experience, recognition is difficult due to the similarity to SSI, the non-specific histopatholocial findings in the beginning, and simply the low incidence of PG. Yet, therapy of PG is completely contrary to the treatment of SSI, which highlights the importance of early and correct diagnosis. Table 1 provides a systematic approach. To the best of our knowledge, this is the first to-the-point checklist in the published literature so far. Conflict of interest The authors declare that there is no conflict of interest. Clinical presentation Pustule with inflammatory halo (initially) Necrotic ulcer Rapid centrifugal a/o polycyclic growth References Bluish-red margins Microbiological findings Negative Use of antibiotics No improvement Mechanical manipulation Further enlargement minor trauma, which had led to necrosectomy and application of NPT and ended in a radialis flap plastic surgery in 2004. Whether this complication had been due to PG could not be cleared in retrospect. Initially, we also mistook the lesion for SSI. Due to the exceptionally big ventral hernia, we applied NPT in combination with antibiotics in an attempt to save the mesh graft from infection. Due to the associated mechanical alteration, this was of course not effective. Finally, the progression of the polycyclic lesion, which did not react to antibiotics and showed no bacterial growth over the course of 2 weeks, made us suspect PG. Under adequate therapy with high-dose glucocorticoids, we observed rapid recovery. In accordance with published literature and our own experience, we define indicators that allow the discrimination of PG against SSI. The more these conditions occur, the likelier is that PG is the underlying cause of the lesion in question (Table 1). Conclusion Whenever a fast growing necrotic ulcer with sterile microbiological findings is observed, one has to consider 13 1. Ruocco E, Sangiuliano S, Gravina AG, et al. Pyoderma gangrenosum: an updated review. J Eur Acad Dermatol Venereol. 2009;23:1008–17. 2. Fritsch P. 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