Reviving island pedicle flaps: Tackling superficial necrosis in basal cell carcinoma surgery with recombinant epidermal growth factor

INTRODUCTION

Basal cell carcinoma (BCC) is a commonly encountered malignancy in dermatology outpatient departments. Depending on its location and size, various treatment modalities are employed. Here, we present a seemingly straightforward case that presented unexpected challenges during management, specifically due to superficial flap necrosis following surgical excision of a 1.8 cm BCC, which was reconstructed using an island pedicle flap.

CASE REPORT

A 69-year-old diabetic male presented with a gradually enlarging, pigmented, ulcerated plaque over the right infraorbital area for 2 months [Figure 1a]. On clinical examination, the 1.8 cm lesion was located in a low-risk anatomical area. Dermoscopy revealed large blue–gray ovoid nests/blotches, multiple blue – gray globules, and ulceration, features suggestive of BCC. The clinical and dermoscopic diagnosis was subsequently confirmed on histopathological examination.

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Figure 1: (a) Well-defined basal cell carcinoma plaque with markings indicating planned island pedicle flap. (b) Immediate post-operative view of island pedicle flap reconstruction.

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A detailed history was revisited in light of the patient’s diabetes. Additional considerations included hypertension, ischemic heart disease, history of previous surgeries (particularly under local anesthesia), current medications (aspirin, statins), and known drug allergies. Smoking history was specifically noted due to its relevance in flap viability. Pre-operative investigations included routine blood work along with prothrombin time (PT), activated partial thromboplastin time (APTT), and international normalized ratio (INR).

Surgical management was planned in accordance with standard guidelines, employing a V-to-Y advancement flap, also known as an island pedicle flap. The flap was designed such that the donor site scar would align with the relaxed skin tension lines (RSTLs). Local anesthesia was administered 15 min before the procedure. Wide excision with a 5 mm margin was performed, followed by reconstruction with an island pedicle flap [Figure 1b]. Subdermal undermining was carried out carefully to preserve the rich dermal vascular plexus. The excised specimen was handled gently using nontoothed forceps to prevent crushing.

Intraoperatively, the patient experienced excessive bleeding, which was controlled using adrenaline-soaked gauze. Hemostasis was achieved, and the flap was secured using simple interrupted 5-0 Prolene sutures. Aspirin was discontinued postoperatively, and the patient was started on broad-spectrum antibiotics.

However, by the 2^nd post-operative day, approximately 70% of the flap developed black discoloration, indicating superficial necrosis [Figure 2]. The central portion showed epidermal denudation. Notably, there was no evidence of hematoma, edema, tension along suture lines, or signs of infection or inflammation. The necrotic tissue was debrided, and daily dressings with recombinant epidermal growth factor (EGF) were initiated. Over the course of 21 days, the patient achieved complete re-epithelialization [Figure 3].

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Figure 2: Second post-operative day showing superficial necrosis involving more than 70% of the island pedicle flap.

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Figure 3: Complete re-epithelialization achieved by day 21 postoperatively.

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Contributing factors included diabetes mellitus, which impairs microvascular circulation and wound perfusion, alongside hypertension, ischemic heart disease, and intraoperative excessive bleeding.

Healing solely by secondary intention in superficial flap necrosis typically takes 4–8 weeks for complete re-epithelialization, involving granulation, contraction, and epithelial migration. In this case, complete healing occurred in just 21 days following timely debridement, standard wound care, and daily recombinant EGF application, suggesting EGF’s role in accelerating epidermal turnover, fibroblast proliferation, and collagen synthesis beyond natural processes. EGF’s documented effects in reducing wound healing time in dermatological wounds and ulcers support this attribution, especially in a diabetic patient prone to delayed healing.

DISCUSSION

Flap necrosis can be classified as either superficial or full thickness. Superficial necrosis is typically identified by black discoloration of the flap surface, whereas full-thickness necrosis, which carries a higher risk of tissue loss, presents as a pale or white flap due to compromised arterial perfusion.

Multiple factors contribute to flap necrosis, with inadequate vascular supply and venous congestion being the primary culprits. Lifestyle habits such as smoking and tobacco use significantly impair microvascular circulation and are known to adversely affect flap viability. Hence, cessation of tobacco products is strongly recommended at least 2 weeks before and after flap surgery.¹

Proper flap design plays a crucial role in optimizing flap survival. Designing a flap that is too small for the defect increases tension, particularly at the distal end, thereby jeopardizing its vascular supply. A broad pedicle is essential to maintain adequate inflow and outflow. During flap elevation, meticulous care must be taken to preserve the subdermal vascular plexus. Flap thickness should be appropriate; excessively thin flaps risk vascular injury, while overly thick flaps may not conform well to the defect. Elevating the flap in the appropriate surgical plane, such as the subcutaneous (facelift) plane, helps preserve vascular integrity. Technical errors, including failure to observe optimal length-to-width ratios, inappropriate arc of rotation, or violation of the flap base, can also precipitate necrosis.²

Additional intraoperative factors, such as excessive tension along suture lines, inadequate hemostasis, formation of hematomas, and direct trauma to the subepidermal plexus, further compromise flap viability. Meticulous hemostasis is critical before closure. Early signs of hematoma formation include dusky erythema or a bluish hue along with underlying swelling. While small hematomas beneath large flaps may resolve without consequence, larger hematomas can release free radicals, contributing to tissue damage. Prompt evacuation, often requiring partial suture removal, is necessary to prevent necrosis.¹

In lesions with high malignant potential or a risk of recurrence, excision with wide margins is mandated. In such cases, local tissue rearrangement using flap reconstruction necessitates careful evaluation of surrounding tissue characteristics, including skin laxity, anatomical landmarks, nearby vital structures, and (RSTL). A tension-free closure remains paramount. Elderly patients with lax skin are typically favorable candidates for flap procedures, whereas in younger individuals with tight adjacent skin, alternative options such as skin grafts or tissue expansion may be preferred. For anatomically challenging regions, such as periarticular areas with reduced laxity and significant mobility, keystone flaps offer a reliable reconstructive alternative.³

Other risk factors for flap necrosis include infection, anatomic locations with compromised perfusion, periarticular areas, diabetes mellitus, and delayed wound healing. Early recognition of impending necrosis, manifested by changes in flap color, is critical. Hematomas should be addressed promptly, as outlined above.

Management of superficial flap necrosis involves identifying and addressing the underlying etiology, followed by debridement of nonviable tissue and regular wound care. Preventing secondary infection is essential. Residual defects can be treated using skin grafts, alternate flap designs, or allowed to heal by secondary intention. Adjunctive use of biologics such as platelet-rich plasma (PRP) and platelet-rich fibrin has been shown to accelerate healing and improve scar quality.

In cases of full-thickness necrosis, commonly indicated by a pale or white flap resulting from critical ischemia due to excessive tension, management includes releasing sutures to relieve pressure and reassessing perfusion. The pinprick test remains a valuable intraoperative tool for evaluating flap vascularity. Healing in such cases often proceeds slowly and may result in hypertrophic or cosmetically unacceptable scarring.¹

Advances in molecular biology and tissue engineering have introduced several growth factors with potent regenerative properties for surgical applications. These include platelet-derived growth factor (PDGF), vascular endothelial growth factor, fibroblast growth factors, EGF, keratinocyte growth factor, transforming growth factor-beta, and granulocyte-macrophage colony-stimulating factor, among others.⁴

EGF protein, human recombinant EGF is a polypeptide growth factor that stimulates the proliferation of a wide range of epidermal and epithelial cells. Human EGF is a 6.2 kDa protein containing 53 amino acid residues. It enhances epidermal cell turnover and promotes faster wound contraction through increased myofibroblast activity and collagen synthesis. By boosting fibroblast proliferation and acting as an antioxidant, it helps neutralize harmful oxidative byproducts. These combined effects support quicker epithelialization, reduce wound size and healing time, and help relieve pain, inflammation, and ulcer-related discomfort.⁵ It is used for burns, non-healing ulcers, and diabetic ulcers.

Recombinant EGF appears promising for wound healing, though current evidence is still mostly anecdotal or from small-scale trials. In a study by Shin et al., topical recombinant EGF outperformed standard antibiotic ointment by significantly reducing wound area and accelerating epithelialization in various dermatological wounds.⁵

In contrast, standard-of-care approaches, such as antibiotic dressings, debridement, and clinically approved growth factors such as platelet-derived growth factors have broader high-quality evidence and regulatory approval. For instance, platelet-derived growth factors are FDA-approved, and PRP is widely used, most commonly for diabetic foot ulcers.

While some meta-analyses suggest recombinant growth factors may outperform standard of care in healing rates and time (especially in diabetic foot ulcers), groups such as the International Working Group on the Diabetic Foot regard the overall evidence as insufficient for routine use.⁶

In this case, the superficial necrosis was managed through timely recognition, by extending the antibiotic coverage, removal of necrotic tissue, and daily dressing with recombinant EGF.

CONCLUSION

Recombinant epidermal growth factor may be a useful adjunct in the management of flap necrosis following flap reconstruction for basal cell carcinoma, contributing to accelerated wound healing and favorable functional and cosmetic outcomes.