Postoperative Pyoderma Gangrenosum: Rare Infection Mimic and Diagnostic Challenge – A Case Report

Abstract

Background

Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis that can occur in the postoperative period, often mimicking surgical site infections (SSIs). The clinical overlap between PG and SSIs – including erythema, wound dehiscence, and purulent discharge – makes timely diagnosis challenging.

Case Presentation

A 61-year-old female with a history of ovarian cancer and metachronous liver metastasis underwent an open left hemihepatectomy. On the fifth postoperative day, she developed erythema, wound dehiscence, and necrosis unresponsive to broad-spectrum antibiotics. Wound cultures remained sterile. Dermatologic consultation and histopathology confirmed the diagnosis of PG, characterized by dense neutrophilic infiltration and pyogenic folliculitis. High-dose corticosteroid therapy led to marked clinical improvement within 5 days, with full wound healing achieved by discharge.

Conclusion

Postoperative PG should be considered in non-resolving postoperative wound complications with negative cultures and antibiotic failure. In this context, prior exposure to PARP inhibitors may be a biologically plausible cofactor through immune modulation; however, a causal link remains unproven. Early dermatology consultation and biopsy are essential to avoid harmful debridement and expedite immunosuppression.

Introduction

Pyoderma gangrenosum (PG) is an uncommon neutrophilic dermatosis characterized by rapidly progressive, painful ulcers with undermined, violaceous borders. Although often associated with systemic diseases (e.g., inflammatory bowel disease, rheumatoid arthritis, hematologic disorders), PG may also arise postsurgically, where it is frequently misdiagnosed as SSI. Postsurgical PG (PSPG) typically manifests within the first postoperative week and presents with erythema, purulent drainage, and dehiscence despite sterile cultures and antibiotic non-response [1–4]. We report a case of PSPG following left hemihepatectomy. The novelty lies in the potential – yet unproven – contribution of PARP inhibitor exposure (niraparib) to the inflammatory milieu that predisposes to neutrophilic dermatoses. We pair the case with a focused review comparing PSPG across surgery types and time-to-diagnosis, and we discuss biological plausibility for PARP inhibitor-related neutrophilic dermatoses.

Case Presentation

A 61-year-old woman with high-grade serous ovarian carcinoma previously treated with cytoreductive surgery and hyperthermic intraperitoneal chemotherapy presented with three metachronous liver metastases on imaging. She had been on niraparib maintenance; the last dose was taken 14 days prior to surgery per institutional protocol. She underwent open left hemihepatectomy via a midline upper abdominal laparotomy without intraoperative complications.

On the fifth postoperative day, the patient developed intense incisional erythema, warmth, swelling, and partial dehiscence with necrotic edges. An SSI was suspected and broad-spectrum intravenous antibiotics were initiated. Despite therapy, the wound deteriorated with undermined violaceous borders and seropurulent exudate (Fig. 1a, b). Blood tests showed elevated inflammatory parameters; repeated wound and blood cultures remained negative. Contrast-enhanced CT showed no intra-abdominal-related complication or sepsis.

Fig. 1.

Sequential clinical photographs of the laparotomy wound illustrating the clinical course and therapeutic response in postoperative pyoderma gangrenosum. a Postoperative day 8: rapidly worsening erythema, undermined violaceous borders, and necrosis despite local wound care and broad-spectrum antibiotics. b Postoperative day 10: continued progression with extension of necrosis and dehiscence despite ongoing continued local wound management. c Marked improvement 5 days after initiation of high-dose systemic corticosteroids, with reduction of erythema and arrest of necrosis. d Healed scar on postoperative day 30.

Dermatology was consulted. Punch biopsy from the ulcer edge demonstrated dense neutrophilic dermal infiltrates with folliculitis and the absence of vasculitis or microorganisms on special stains – findings consistent with PG. Systemic high-dose corticosteroids were started (methylprednisolone equivalent), along with gentle, nontraumatic wound care. The lesion improved rapidly with decreased erythema and halted necrosis within 5 days (Fig. 1c). Antibiotics were discontinued once infection was excluded. The patient completed a slow steroid taper as an outpatient; the wound re-epithelialized fully without grafting. Written informed consent for publication of clinical details and images was obtained.

Discussion

Diagnostic Considerations and Mimics

PSPG is primarily a clinical-pathologic diagnosis. The Delphi consensus diagnostic criteria for ulcerative PG require one major criterion (biopsy showing a neutrophilic infiltrate) plus minor criteria such as exclusion of infection, pathergy, peripheral erythema/undermined border, rapid progression, and response to immunosuppression [5]. In our patient, the combination of sterile cultures, early postoperative onset, rapid progression with violaceous undermined borders, compatible histology, and brisk steroid response supported PSPG over SSI. Early dermatology input and avoidance of surgical debridement are critical because pathergy can exacerbate lesions [2–4].

Frequency by Surgical Category and Time to Onset

Two large syntheses provide helpful context. In a 220-case systematic review, PSPG most commonly followed breast (25%), cardiothoracic (14%), abdominal (14%), and obstetric (13%) procedures; early signs appeared on average postoperative day 7 [1]. In a Mayo Clinic series of 18 postoperative PG patients, involvement was breast 38% and abdomen 38% (with other sites less frequent), and the mean time to symptoms was ∼11 days [3]. Breast surgery-focused reviews have corroborated the dominance of breast procedures but also underscore that combined breast-abdominal operations may present with multisite involvement and typical onset within 4 days–6 weeks [6] (see Table 1).

Table 1.

Postsurgical pyoderma gangrenosum across key series/reviews

Source	N (PSPG)	Common surgical categories	Time to onset	Notable outcomes/notes
Zuo et al. [1] (2015)	220	Breast 25%; cardiothoracic 14%; abdominal 14%; obstetric 13%	Mean 7 days	Avoid debridement; consider peri-op steroids in high-risk breast cases
Tolkachjov et al. [3] (2016)	18	Breast 38%; abdomen 38%; others 24%	Mean ∼11 days	Often misdiagnosed as SSI; antibiotics common before recognition
Ehrl et al. [6] (2018)	67 (breast)	Reduction mammoplasty predominant	4 days–6 weeks	Rapid deterioration post-op; steroid-responsive

Drug-Induced PG and Neutrophilic Dermatoses

Drug-induced PG is rare but recognized, while related neutrophilic dermatoses – especially Sweet’s syndrome – are more commonly reported and share overlapping cytokine pathways (IL-1, IL-8, TNF-α) and pathergy [7].

Biological Plausibility for PARP Inhibitor Involvement

While no direct, indexed case of PG from a PARP inhibitor has been published to date, there is a peer-reviewed report of niraparib-induced Sweet’s syndrome – closely related to PG – necessitating drug discontinuation [8]. PARP1 functions as a transcriptional cofactor for NF-κB, and experimental PARP1 perturbation alters innate-immune gene expression, including IL1B and TNF; PARP inhibition also interfaces with cGAS-STING/IFN pathways and can modulate myeloid cell phenotypes [9–11]. Clinically, PARP inhibitors have documented cutaneous immune adverse events, including vasculitis and erythema nodosum [12–14]. Together, these observations support a mechanistic plausibility that prior PARP inhibitor exposure could, in predisposed hosts and in the setting of surgical pathergy, tilt cutaneous immunity toward a neutrophil-dominant flare manifesting as PG. In our case, niraparib discontinuation 2 weeks pre-op reduces the likelihood of a direct temporal trigger but does not exclude an immune-priming contribution; we therefore frame the association as hypothesis-generating rather than causal.

Conclusion

PSPG is an uncommon but high-impact mimic of SSI. In patients with non-resolving postoperative wounds, sterile cultures, and antibiotic non-response, clinicians should seek early dermatology consultation and perform a biopsy to confirm PG and initiate immunosuppression. Prior or current PARP inhibitor exposure may be a biologically plausible cofactor for neutrophilic dermatoses; this warrants further study and careful pharmacovigilance, but causation remains unproven.

Acknowledgment

We sincerely thank the patient for granting permission to share this clinical case and its associated images, thereby contributing to medical education and awareness of this rare condition.

Statement of Ethics

Ethical approval was obtained from the Ethics Committee of the University Medical Faculty of Rostock (Approval No. A 2025-0160). All authors confirm that the patient provided written informed consent for publication of this case. The CARE Checklist has been completed by the authors for this case report and is attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000550349).

Conflict of Interest Statement

The authors declare no conflicts of interest.

Funding Sources

No funding was received for this study.

Author Contributions

S.A. reviewed the literature and participated in the study design and manuscript drafting. S.H. and C.S. critically revised the manuscript. All authors read and approved the final manuscript.

Funding Statement

No funding was received for this study.

Data Availability Statement

All data generated or analyzed during this work are included in this article and its online supplementary material files. Further inquiries can be directed to the corresponding author.