Case
All patients were female and the mean age at diagnosis was 37.9 ± 7.6 years (range: 25–51 years). Endometriosis (
n
= 2) was the most frequent comorbidity. Regarding chronic medication use, combined oral contraceptives (
n
= 2) were the most commonly used (
Table 1
).
A history of previous cesarean section was the most frequently reported prior surgery (
n
= 4), followed by laparoscopic cholecystectomy (
n
= 2). One patient had a history of abnormal postoperative wound healing after cesarean section, requiring surgical re-intervention. A family history of autoimmune disease was present in only one case (systemic lupus erythematosus in a third-degree relative). None of the patients had a personal history of autoimmune disorders (
Table 1
).
Among the surgeries triggering PPG, breast augmentation with implants (
n
= 4) and reduction mammoplasty (
n
= 4) were most commonly associated (
Table 2
). Clinical findings included erythematous papules progressing to plaques and ulcerations (
n
= 10) along the surgical wound, which were painful (
n
= 5), purulent-draining (
n
= 3), or necrotic (
n
= 1). Lesions appeared on average 11.4 ± 5.7 days postoperatively (range: 5–21 days;
Figs. 1
2
3
). Only one patient presented systemic symptoms, such as fever (
Table 2
). Bilateral breast involvement occurred in 75% of patients undergoing breast surgery, and one patient experienced implant extrusion (
Fig. 4
). The nipple–areolar complex was spared in all cases.
Abbreviations: ESR/CRP, erythrocyte sedimentation rate/C-reactive protein; RF, rheumatoid factor.
Purulent ulcers along the surgical wound, sparing the nipple, in a 39-year-old patient with PPG, appearing 10 days after reduction mammoplasty. PPG, Post-surgical pyoderma gangrenosum.
Ulcers along the surgical wound, with violaceous edges, sparing the nipple, in a healthy 25-year-old patient with PPG, 10 days after reduction mammoplasty. PPG, post-surgical pyoderma gangrenosum.
Ulcers along the surgical wound, with violaceous and undermined edges, sparing the nipple, in a 35-year-old patient, 7 days after reduction mammoplasty. The arrow represents Gulliver's sign: epithelial growth at the edge of the ulcer toward the center, leaving cribriform scars.
Breast implant extrusion.
All patients underwent laboratory testing after lesion onset, including viral serologies, autoimmune screening (antinuclear antibody, rheumatoid factor [RF], and thyroid function), and wound/secretion cultures. The most common laboratory finding was leukocytosis (WBC > 10,000/µL) without immature forms (
n
= 4), followed by elevated inflammatory markers (
n
= 3). RF was reactive in two patients, with values of 10 and 48 IU/mL (nonreactive < 8 IU/mL). Culture results were negative in all cases. Only one patient did not receive antibiotics prior to PPG diagnosis, and half of the patients (
n
= 5) underwent surgical reintervention, such as resuturing or debridement, which led to worsening of the condition (
Table 2
).
The diagnosis of PPG was primarily clinical and was established on average 36.7 days (range: 7–150 days) after the surgical procedure. Skin biopsies were performed in 50% of cases (
n
= 5), mainly to exclude differential diagnoses (
Table 2
).
Following diagnosis, systemic corticosteroids were the mainstay of treatment (prednisone,
n
= 9), with intravenous methylprednisolone pulses administered in two cases. In 8 of 10 cases, immunosuppressive agents were added to corticosteroids, and two patients required a combination of three medications for disease control. Adjunctive agents included dapsone (
n
= 4), cyclosporine (
n
= 4), azathioprine (
n
= 2), and methotrexate (
n
= 1). One patient achieved remission with topical therapy alone (clobetasol propionate and tacrolimus). Adjunctive therapies included HBOT, with a mean of 37 sessions (range: 20–60), and low-level laser therapy in one case (6 sessions;
Table 3
). As the procedure was performed at an external facility, detailed technical parameters of the laser device are not available.
Abbreviation: HBOT, hyperbaric oxygen therapy.
The mean time to complete wound healing, followed by tapering and discontinuation of therapy, was 5.7 ± 2.6 months (range: 2–10 months). At the time of this publication, one patient remained under treatment with a gradual corticosteroid taper and good clinical response (
Table 3
).
Conclusion
This case series reinforces that PPG is a diagnostic and therapeutic challenge requiring clinical vigilance and multidisciplinary coordinated care. Prompt initiation of immunosuppressive therapy, careful surgical planning, and adjunctive modalities such as HBOT contribute to improved healing and reduced recurrence. Further studies are warranted to refine treatment protocols and better understand the immunopathogenesis of this serious complication.
Discussion
PPG represents a diagnostic challenge, particularly following elective surgeries. The appearance of rapidly progressing ulcerative lesions with purulent discharge post-surgery is frequently mistaken for common bacterial infection. However, the hallmark violaceous undermined borders, rapid progression despite antibiotics, absence of bacterial growth in cultures, and worsening after surgical debridement should raise suspicion, which requires a markedly different therapeutic approach.
1
2
The pathergy phenomenon is well-documented and can be triggered by minor injuries, including biopsies.
4
9
This risk likely contributed to the low rate of biopsy in our series and underscores the importance of clinical diagnosis and exclusion of infection.
The etiopathogenesis of PG is still not fully elucidated, but growing evidence supports its classification within the spectrum of autoinflammatory neutrophilic syndromes.
10
Genetic predisposition, dysregulated neutrophil function, and the release of inflammatory cytokines—particularly IL-17, IL-1β, TNF-α, and IL-8—promote excessive neutrophilic infiltration and tissue necrosis.
3
Aberrant activation of inflammasomes and the JAK-STAT pathway have been described, providing a rationale for emerging targeted therapies with JAK inhibitors.
11
These mechanisms explain why local trauma, including surgical incisions or debridement, may trigger or exacerbate lesions through the pathergy phenomenon.
Among elective plastic surgeries, breast procedures are the most common triggers for PPG, though the reasons remain unclear. Bilateral breast involvement was observed in 75% of cases, with nipple sparing noted in all patients, a potentially useful diagnostic clue. Fever and leukocytosis were uncommon, which aligns with the understanding that systemic inflammatory signs may be mild or absent in PPG.
12
13
Management requires prompt immunosuppression to control inflammation and prevent tissue destruction. Systemic corticosteroids are considered the first-line treatment, alone or combined with other immunosuppressants like cyclosporine, azathioprine, and dapsone, as applied in our series.
2
6
Our results align with existing literature demonstrating that combination therapy often yields better control of refractory cases.
4
When corticosteroid monotherapy proved insufficient, additional immunosuppressants were selected based on clinical profile, comorbidities, and drug tolerance: cyclosporine was chosen in cases requiring rapid disease control or corticosteroid-sparing effect, given its potent inhibition of T cell activation and cytokine release
14
; dapsone was used for its anti-neutrophilic and anti-oxidative properties, making it suitable for milder or localized lesions and as an adjunct to corticosteroids
15
; azathioprine served as a maintenance agent in chronic or relapsing cases, particularly when tapering corticosteroids
3
; and methotrexate was reserved for refractory disease and in patients intolerant to cyclosporine or dapsone.
10
Adjunct therapies such as HBOT have shown promise in enhancing wound healing by improving tissue oxygenation, modulating immune responses, and promoting angiogenesis, without provoking pathergy, making it a safe and effective complement to systemic immunosuppression.
6
8
HBOT, administered to several patients in our study, was associated with lesion resolution and good tolerance, echoing findings from earlier case series and reviews (
Fig. 5
).
7
12
A 40-year-old patient, before (
A
) and after (
B
) 48 HBOT sessions associated with pulse therapy with methylprednisolone (500 mg/day for 3 days), followed by prednisone (2 mg/kg/day), cyclosporine (200 mg/day), and azathioprine (100 mg/day), gradually reduced over 6 months. Extensive, but not deep, ulceration along the flank liposuction wound. HBOT, hyperbaric oxygen therapy.
Newer biologic and small-molecule agents, including anti-TNF, anti-IL-1, and JAK-STAT inhibitors, have shown promise in refractory cases, particularly in patients with underlying systemic inflammatory diseases.
11
However, randomized controlled trials remain lacking, and therapeutic choices currently rely on clinician expertise and individual response.
Introduction
Post-surgical pyoderma gangrenosum (PPG) is an uncommon and often misdiagnosed variant of neutrophilic dermatosis that occurs following surgical trauma, typically in previously healthy individuals. Clinically, it presents as rapidly progressive, painful ulcers at surgical sites, often mistaken for wound infections, which may lead to unnecessary antibiotic use or surgical debridement, ultimately worsening the condition.
1
2
Although its pathogenesis remains poorly understood, PPG is considered to result from an abnormal immune response in genetically predisposed individuals. The dysregulation of neutrophilic chemotaxis, coupled with aberrant T cell activation, leads to an overproduction of interleukin-17 (IL-17) and subsequent release of proinflammatory cytokines such as IL-1β, IL-8, and tumor necrosis factor-α (TNF-α). These mediators amplify neutrophilic infiltration and tissue destruction.
3
A phenomenon known as pathergy—the development or worsening of lesions after minor trauma or surgery—is characteristic of pyoderma gangrenosum (PG) and particularly relevant in the postoperative setting.
4
Some patients have associated systemic diseases, especially inflammatory bowel disease.
5
6
The diagnosis is primarily clinical, based on exclusion of infections and other ulcerative dermatoses, and it is supported by compatible histopathological findings in selected cases.
7
Treatment usually involves systemic corticosteroids and/or immunosuppressive agents. Adjunctive therapies such as hyperbaric oxygen therapy (HBOT) may be considered, as it promotes tissue healing by increasing oxygen availability in ischemic or inflamed areas.
8
We report a case series of 10 women diagnosed with PPG after elective aesthetic surgeries, highlighting their clinical characteristics, management, and outcomes.
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