Abstract
Keloids are challenging fibroproliferative scars with high recurrence rates following monotherapy. We report the successful management of bilateral ear lobule keloids in a 50-year-old woman using a multidisciplinary treatment protocol incorporating preoperative intralesional triamcinolone injections and mechanical compression, surgical excision with acellular dermal matrix reconstruction, postoperative radiotherapy (16 Gy), and long-term silicone compression therapy. At 18 months of follow-up, there was no clinical recurrence, the Vancouver Scar Scale score was 1, and the patient reported excellent cosmetic satisfaction with pain-free healing. This case highlights the value of combining mechanical, biological, surgical, and radiotherapeutic strategies to reduce recurrence and emphasizes the importance of interdisciplinary collaboration in keloid management.
Introduction
Keloids are a pathological manifestation of aberrant wound healing, resulting in excessive collagen deposition and scar tissue proliferation beyond the original injury boundaries. Unlike hypertrophic scars, which remain confined to the wound site, keloids exhibit aggressive growth patterns, often causing functional impairment, pain, pruritus and significant psychosocial distress. 1 Common triggers include trauma (e.g., piercings, burns, surgical incisions), infections and inflammatory skin conditions, with high-tension anatomical regions ear lobules, sternum, and deltoid regions are particularly vulnerable.2,3 Their development is influenced by both genetic and environmental factors. The incidence of keloids is disproportionately higher in individuals with darker skin types (Fitzpatrick IV-VI), with genetic predisposition accounting for up to 50%–80% of susceptibility.4,5
Pathologically, keloid formation is driven by a dysregulated crosstalk between fibroblasts, immune cells, extracellular matrix components and dysregulated transforming growth factor-beta (TGF-β) signalling.
TGF-β/Smad pathway hyperactivation, driving excessive collagen I/III synthesis. 6
Reduced apoptosis of myofibroblasts, perpetuating fibrosis. 7
Mechanical stress-induced YAP/TAZ signalling, amplifying profibrotic gene expression. 2
These molecular abnormalities lead to prolonged inflammation, aberrant wound healing, and uncontrolled fibrosis.
Despite the availability of multiple therapeutic interventions, keloid management remains fraught with >50% recurrence rates after monotherapy. 8 Intralesional corticosteroids (e.g., triamcinolone) suppress inflammation but fail to address mechanical tension, while surgery alone triggers rebound fibrosis. 9 Therefore, multimodal strategies combining excision, intralesional steroids, compression therapy, acellular dermal matrices (ADMs) and radiotherapy have emerged as promising approaches to improving long-term outcomes.
Case Presentation
A 50-year-old healthy female presented with bilateral ear lobule keloids that developed over 5 years following second ear piercing. Right ear keloid measured 5cm in largest dimension, while the left lesion was significantly smaller (1.5 cm). Despite being asymptomatic, the lesions caused significant cosmetic distress and social discomfort. The patient had Fitzpatrick type IV skin and had not received prior interventions for her keloids.
Clinical examination revealed well-demarcated, raised, firm masses with irregular borders. Given the chronic nature of her lesions, a stepwise management approach integrating preoperative optimisation, surgical excision, ADM grafting and adjuvant therapy was formulated.
Management Plan
Preoperative Optimisation
The preoperative phase focused on keloid regression, mechanical modulation and skin conditioning:
Intralesional triamcinolone acetonide (40 mg/mL, monthly for 6 months):
Triamcinolone was administered to suppress fibroblast activity, reduce vascularity and induce apoptosis in keloid tissue. This approach aimed to inhibit further growth and facilitate excision.
Customised pressure clips with incremental weights:
Mechanical compression therapy was used to improve dermal remodelling and tissue pliability. By delivering sustained pressure to the keloid, this mechanomodulatory approach disrupted excessive collagen deposition and promoted adaptive skin remodelling. An acrylic clip with an attachment for adding weights was employed. The patient began by wearing the pressure clip alone, followed by the sequential addition of incremental weights, 2 g, 5 g, 10 g and 20 g, applied during day and increased weekly over a period of 5 weeks.
Surgical Excision and Reconstruction
Following preoperative optimisation, complete surgical excision was performed with preservation of surrounding normal tissue to minimise tension:
Total keloid excision with margin clearance:
The lesions were excised en bloc to ensure removal of all hypertrophic scar tissue. Hemostasis was meticulously achieved using bipolar electrocautery.
ADM grafting (Integra→ Bi-layered Matrix):
To avoid donor-site morbidity and secondary keloid formation, an ADM was placed over the excised defect. The ADM provided a biological scaffold conducive to controlled healing, minimising fibrosis and excessive collagen accumulation. 10
Adjuvant Therapy
To further reduce recurrence risk and enhance cosmetic outcomes, a multimodal postoperative regimen was instituted:
Single-dose radiotherapy (16 Gy-8 Gy/side, within 48 hours post-op):
Radiotherapy was initiated within the critical time window to suppress fibroblast proliferation and mitigate early inflammatory cascades with a appropriate shielding of the adjacent structures. By targeting rapidly dividing cells, radiotherapy helped disrupt pathways that drive keloid recurrence.11,12
Silicone gel sheets and compression therapy:
Silicone dressings were applied postoperatively to modulate hydration and reduce mechanical stress. Continuous compression therapy was maintained for 6 weeks to stabilise dermal architecture and prevent collagen hyperplasia.
Outcome Assessment
Short-term results (3 weeks)
Complete wound epithelialisation achieved. Patient reported pain score: 0–1/10. No signs of infection or delayed healing.
Long-term results (18 months)
No clinical recurrence or hypertrophic regrowth. Vancouver Scar Scale score: 1 (indicating minimal scarring). Excellent patient satisfaction with improved cosmesis.
Photographic documentation confirmed progressive scar remodelling and subjective feedback reinforced the psychological benefits of aesthetic restoration.
Discussion
Multimodal Therapy Superiority
A single-treatment modality often fails to address the multifactorial pathogenesis of keloids, leading to unsatisfactory outcomes. Combining surgery with steroids, ADM and radiotherapy generates a synergistic effect by targeting different aspects of keloid formation:
Steroids reduce inflammation and inhibit fibroblast proliferation. Mechanical modulation influences fibroblast behaviour by reducing cellular proliferation.
2
Biological intervention: ADM provides a structured healing matrix, optimising scar architecture.
10
Radiation therapy: Timely irradiation directly inhibits fibroblast overactivity, preventing recurrence.11,12
ADM’s Role in Preventing Secondary Scarring
ADM serves as a bioengineered scaffold that mitigates excessive scar formation. By eliminating the need for autologous graft harvest, ADM prevents donor-site fibrosis and enhances controlled tissue integration. 10
Optimal Radiotherapy Timing
Early postoperative irradiation (within 48 hours) halts fibroblast hyperproliferation. 12 Studies have demonstrated superior efficacy when radiotherapy is administered within this critical window, reinforcing the necessity of precise scheduling
Conclusion
This case highlights the need for a personalised, stepwise protocol for keloid management, integrating mechanical, biological and radiation therapies to break the cycle of recurrence. Interdisciplinary collaboration, incorporating surgical innovation, prosthetic expertise and radiation oncology, is fundamental to achieving optimal patient outcomes.
By combining advanced therapeutic approaches with precision-driven planning, keloid management can transition from traditional excision alone to a structured, precision-based multidisciplinary treatment strategy.
Footnotes
Data Availability Statement
The datasets generated and/or analysed during the current study are available from the corresponding author on reasonable request.
Declaration of Conflicting Interests
The authors declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article.
Ethical Approval and Informed Consent
Written informed consent for publication of clinical details and photographs was obtained from the patient in accordance with the Declaration of Helsinki.
Funding
The authors received no financial support for the research, authorship and/or publication of this article.