Discussion

Sweet syndrome was initially described as an acute inflammatory disorder characterized by painful cutaneous lesions associated with fever and a dense neutrophilic dermal infiltrate.1 Although it is classically considered an acute condition that responds favorably to systemic corticosteroid therapy, several studies have shown that its course may be associated with cutaneous and systemic sequelae, particularly in severe or untreated forms.

From a cutaneous perspective, post-inflammatory dyschromia, atrophic or hypertrophic scarring, and ulceronecrotic lesions have been reported, especially in bullous or necrotic variants associated with intense neutrophilic infiltration and sometimes secondary vasculitis.6,7 Most patients heal without scarring; however, chronic or recurrent forms may occur.6 Cohen and Kurzrock also described recurrences in a significant proportion of cases, which may lead to persistent cutaneous morbidity and impaired quality of life.7,8

Extracutaneous involvement represents another potential source of sequelae. Ocular, pulmonary, neurologic, and articular manifestations have been described and may compromise functional prognosis in the absence of prompt treatment.7,9 These systemic manifestations are likely related to widespread neutrophil activation and increased production of pro-inflammatory cytokines such as Interleukin-1 beta, Interleukin-6, and Granulocyte colony-stimulating factor, which are thought to play a central role in the pathophysiology of the disease.9

Furthermore, association with an underlying disorder, particularly hematologic disease or malignancy, constitutes a major indirect prognostic concern and justifies prolonged surveillance. Hematologic malignancies, especially Acute myeloid leukemia and

Myelodysplastic syndromes, are the most frequently reported associations, supporting the role of Sweet syndrome as a potential paraneoplastic syndrome.

In the context of plastic surgery, Sweet syndrome represents a major diagnostic challenge.

Particular attention should be paid to the differential diagnosis with postoperative PPG, another rare neutrophilic dermatosis that may occur after surgical procedures and closely mimic surgical site infection. While Sweet syndrome typically presents with painful erythematous plaques, fever, and a dense neutrophilic dermal infiltrate without vasculitis, PPG is characterized by rapidly progressive ulcerative lesions with violaceous undermined borders and tissue necrosis. Distinguishing between these conditions is of major clinical importance because surgical debridement, often performed when infection is suspected, may trigger pathergy and dramatic lesion worsening in patients with PPG. Conversely, Sweet syndrome generally presents with non-ulcerative inflammatory plaques and responds rapidly to systemic corticosteroids. In both conditions, negative microbiological cultures, lack of response to antibiotics, and early dermatologic assessment should prompt consideration of a neutrophilic dermatosis. Awareness of these entities is crucial for plastic surgeons, as delayed diagnosis may result in unnecessary surgical procedures, prolonged hospitalization, impaired aesthetic outcomes, and increased morbidity.

Several postoperative cases have been reported following thoracic, spinal, or breast reconstructive surgery, highlighting the diagnostic difficulty in the surgical setting and the importance of early recognition.

These observations support the systematic inclusion of Sweet syndrome in the differential diagnosis of postoperative cutaneous complications, particularly in cases of atypical progression or failure of well-conducted antibiotic therapy. Early skin biopsy and prompt initiation of systemic corticosteroid therapy are key elements of management in order to limit cutaneous and functional sequelae.

The current literature is mainly based on observational studies, case series, and case reports, limiting the level of evidence regarding the true frequency of sequelae and prognostic factors. Few prospective or randomized studies are available, and the pathophysiology remains only partially understood. Future studies may help identify predictive biomarkers of severity and recurrence, as well as assess the comparative efficacy of emerging immunomodulatory therapies, particularly IL-1 inhibitors.

Thus, Sweet syndrome represents a rare but potentially severe dermatologic complication in plastic surgery, whose early recognition is essential to prevent cutaneous and systemic sequelae and optimize therapeutic management.