Clinicians often face significant hurdles when managing extensive hidradenitis suppurativa in patients who exhibit both severe active inflammation and irreversible structural damage. Medical treatment alone rarely clears chronic scarred sinus tracts. Conversely, surgical excision without systemic disease control frequently precipitates wound breakdown and perioperative disease flares. Therefore, establishing a unified multimodal regimen is essential. By intentionally sequencing targeted biologics alongside staged surgical reconstruction, multidisciplinary teams can suppress cutaneous inflammatory cascades and excise debilitating fibrotic tunnels. A landmark clinical report demonstrates this integrated concept in Hurley stage III disease. This article reviews the clinical strategies, surgical considerations, and therapeutic reasoning needed to optimize treatment outcomes in severe disease.

The Dual Pathology of Extensive Hidradenitis Suppurativa

Patients with Hurley stage III hidradenitis suppurativa present with two distinct yet overlapping pathological components. Specifically, persistent follicular occlusion triggers severe neutrophilic inflammation, painful nodules, and purulent abscesses. Over time, recurring tissue destruction leads to subcutaneous sinus tract formation, deep epithelialized tunnels, and dense dermal fibrosis. Unfortunately, biologic therapies, while remarkably effective against inflammatory cytokines, cannot reverse mature epithelialized tracts or established scar tissue.

Consequently, clinicians cannot rely solely on biologic escalation when structural tunnels continue to drain foul-smelling exudate. Persistent architectural deformities foster chronic microbial colonization, which in turn fuels recurring regional inflammation. Therefore, surgical intervention becomes mandatory to eliminate irreversible anatomical changes and restore tissue function. However, operating in the middle of uncontrolled systemic inflammation increases surgical morbidity, operative bleeding, and the risk of graft failure. Thus, clinicians must carefully dissect the inflammatory burden from irreversible structural damage before planning definitive interventions. By recognizing these dual pathologies, dermatologists and surgeons can time their therapies effectively and achieve long-term functional recovery.

First-Line Biologic Therapy and Regional Staged Excision

In severe multi-regional disease, initiating therapy with a tumor necrosis factor inhibitor like adalimumab serves as a standard first-line approach. Systemic biologic therapy rapidly reduces tissue edema, suppresses circulating inflammatory mediators, and decreases acute pain. However, when patients present with severe, localized structural tunnels that cause intractable drainage, waiting months for complete medical clearance is impractical. Therefore, surgeons must coordinate targeted regional excisions while maintaining biologic therapy.

In clinical practice, continuing adalimumab throughout the perioperative period prevents severe rebound flares and stabilizes distant anatomic sites. Specifically, surgeons perform wide radical excision of scarred fibrotic beds down to healthy subcutaneous fascia. Subsequently, clinicians apply staged split-thickness skin grafting to reconstruct extensive soft tissue defects. Negative pressure wound therapy frequently secures the skin graft, enhances dermal adherence, and minimizes seroma accumulation. Because the patient continues systemic biologic coverage, the surgical wound bed heals smoothly without secondary infection or graft necrosis. Consequently, this targeted regional intervention delivers immediate symptom relief in high-priority zones while the patient maintains systemic biologic therapy for generalized disease control.

Biologic Switching: From TNF Inhibitors to Dual IL-17 Blockade

Although initial biologic treatment offers substantial local benefits, secondary loss of response remains a widespread clinical reality. When adalimumab fails to suppress active inflammatory nodules across distant anatomical zones, clinicians must evaluate a targeted switch in therapeutic mechanism. Recently, dual inhibition of interleukin-17A and interleukin-17F using bimekizumab has emerged as a potent second-line therapeutic strategy. Both IL-17A and IL-17F drive intense neutrophilic recruitment and stimulate keratinocyte activation, fueling chronic tissue destruction.

Therefore, transitioning non-responsive patients to bimekizumab effectively arrests persistent systemic cytokine cascades. Following this transition, clinicians regularly observe marked reductions in active inflammatory lesion counts and erythema. Nevertheless, clinicians must remember that stubborn epithelialized tracts and deep dermal fibrosis will persist despite achieving cytokine neutralization. For example, clinical trial metrics like the Hidradenitis Suppurativa Clinical Response evaluate inflammatory nodule reduction rather than tunnel resolution. Thus, failure to achieve complete response criteria often reflects remaining structural disease rather than medication failure. Recognizing this fundamental distinction prevents premature discontinuation of a highly efficacious biologic agent and clarifies the urgent indication for complementary surgical excision.

Staged Gluteal Excision and Split-Thickness Skin Grafting

When extensive gluteal tunnels and fibrotic bridges resist systemic medical therapy, definitive surgical excision is necessary. Operating on the gluteal and perianal regions presents distinct anatomical challenges, including shearing forces and heightened bacterial contamination. Therefore, meticulous operative sequencing and robust reconstructive techniques are vital for surgical success. Surgeons perform radical wide local excision of all diseased subcutaneous tissue, ensuring that no epithelialized sinuses remain behind.

Following radical excision, reconstructive surgeons utilize staged split-thickness skin grafting to achieve functional closure. Maintaining bimekizumab throughout the operative window actively suppresses local tissue inflammation, thereby promoting rapid neo-vascularization of the graft bed. In addition, surgeons avoid tension-prone primary closures that frequently lead to dehiscence and recurrence. By placing split-thickness grafts onto clean, well-vascularized beds, surgical teams achieve excellent graft take without major bleeding, hematoma, or wound infection. Furthermore, prolonged postoperative monitoring confirms that stabilizing systemic inflammation allows donor and recipient sites to heal without complication. Consequently, combining deep surgical clearance with ongoing dual IL-17 blockade produces durable regional control and prevents painful postoperative breakdowns.

Long-Term Remission and Multidisciplinary Clinical Synergy

Achieving durable clinical control in advanced hidradenitis suppurativa requires continuous collaboration between dermatologists and reconstructive surgeons. When clinicians evaluate post-surgical outcomes using objective measures like the International Hidradenitis Suppurativa Severity Score System, the synergy of combined therapy becomes evident. Radical surgical excision permanently eradicates structural tunnels, while modern biologics like bimekizumab eliminate microscopic inflammatory activity. As a direct result, patients experience precipitous drops in severity scores and achieve lasting symptom remission.

Moreover, sustained biologic therapy prevents new inflammatory lesions from developing around surgical margins or in distant, untouched apocrine fields. Real-world follow-up demonstrates that patients maintain disease control and graft stability well past fifteen months when managed with this combined protocol. Additionally, multidisciplinary teams should actively manage common metabolic comorbidities, including obesity, metabolic syndrome, and tobacco dependence, to optimize long-term health. Ultimately, this comprehensive management model transforms a previously intractable disease into a controllable condition. By viewing systemic biologics and radical reconstructive surgery as complementary partners rather than competing strategies, clinicians can restore functional independence and significantly enhance their patients' overall quality of life.

Why must clinicians combine surgery with biologic therapy in advanced hidradenitis suppurativa?

Clinicians must combine both modalities because advanced disease features two distinct pathological components. Biologic therapies effectively reduce circulating inflammatory cytokines and clear active inflammatory nodules. However, medications cannot resolve mature fibrotic scars or epithelialized draining sinus tracts. Therefore, radical surgical excision is required to eliminate persistent architectural damage, while continuous biologic therapy prevents recurring inflammatory flares, minimizes surgical site breakdown, and protects distant apocrine glands from developing new disease lesions.

Is it safe to continue biologic therapy during major reconstructive surgery for hidradenitis suppurativa?

Recent surgical evidence indicates that continuing biologic agents during major excisions and split-thickness skin grafting is safe and beneficial. Uncontrolled systemic inflammation poses a greater risk for wound dehiscence, disease flares, and graft loss than biologic immunosuppression. Furthermore, continuing agents such as adalimumab or bimekizumab does not significantly elevate perioperative bleeding, wound infection, or graft failure rates when surgeons operate in sterile conditions and implement diligent postoperative wound care protocols.

When should clinicians consider switching from adalimumab to dual IL-17 inhibitors like bimekizumab?

Clinicians should consider switching when patients demonstrate inadequate clinical response, secondary loss of efficacy, or intolerable adverse effects while receiving anti-TNF therapy. Dual inhibition of interleukin-17A and interleukin-17F blocks key downstream inflammatory drivers of tissue damage and neutrophilic recruitment. Therefore, switching to bimekizumab provides superior anti-inflammatory suppression for refractory lesions. However, clinicians must remember to surgically excise residual scarred tunnels rather than assuming persistent drainage indicates primary drug failure.

Disclaimer: This content is for informational and educational purposes only. It is not intended to provide medical advice, diagnosis, or treatment. Refer to the latest local and national guidelines for clinical practice.

References

1. Hashizumi S et al. Treatment Sequencing With Biologic Switching, Staged Excision, and Split-Thickness Skin Grafting for Extensive Hidradenitis Suppurativa. J Dermatol. 2026 Oct 14. doi: 10.1111/1346-8138.70538. PMID: 42875379.
2. Alikhan A, Sayed C, Alavi A, et al. North American clinical management guidelines for hidradenitis suppurativa: A publication from the United States and Canadian Hidradenitis Suppurativa Foundations: Part II: Topical, intralesional, and systemic medical management. J Am Acad Dermatol. 2019;81(1):91-101.
3. Zouboulis CC, Bechara FG, Dickinson-Blok JL, et al. S2k guideline for the treatment of hidradenitis suppurativa/acne inversa. J Eur Acad Dermatol Venereol. 2019;33(1):19-40.
4. Kimball AB, Jemec GBE, Armstrong AW, et al. Dual neutralization of IL-17A and IL-17F with bimekizumab in moderate to severe hidradenitis suppurativa: results from the BE HEARD I and BE HEARD II phase 3 randomized trials. Lancet. 2024;403(10443):2504-2517.