Keloid and Hypertrophic Scar — Viva

Q1: Diagnose and define

Examiner: What is the diagnosis, and what is the pivotal distinction from a hypertrophic scar?[1][3]

Candidate: This is a keloid because the raised scar extends beyond the original acne-wound boundary into adjacent skin and persists. A hypertrophic scar remains within the wound and may flatten with time. Symptoms such as itch and pain occur in either lesion and do not define the boundary.[1][3]

Examiner: Can you diagnose it from ancestry or skin colour?[3][4]

Candidate: No. Some studies report higher prevalence in certain darker-phototype or ancestry populations, but estimates are heterogeneous and affected by definitions and ascertainment. I diagnose the lesion clinically and individualise care by scar history, site, treatment response and patient priorities—not race.[3][4]

Q2: Explain the biology without overclaiming

Examiner: What goes wrong in wound repair?[2][3][13]

Candidate: Normal haemostasis, inflammation, proliferation and remodelling overlap. Pathological scarring is associated with persistent inflammation, dysregulated TGF-beta/SMAD signalling, fibroblast heterogeneity, altered extracellular-matrix turnover and mechanotransduction. These form an interacting network; there is no proven single “remodelling switch” that is necessary and sufficient in every keloid or hypertrophic scar.[2][3][13]

Examiner: Why does the family history matter?[4]

Candidate: Familial clustering supports susceptibility, but the genetics are heterogeneous. I would not promise a simple autosomal-dominant recurrence pattern or use a p53 claim as the explanation. Family history changes risk counselling; it does not replace the clinical boundary test.[4]

Q3: Decide when tissue is needed

Examiner: Do all keloids need biopsy?[1][3]

Candidate: No. A typical keloid is a clinical diagnosis. I biopsy when the diagnosis is uncertain or the lesion is ulcerated, fixed, destructive, unexpectedly changing, unexplained by the history, or suspicious for a malignant, inflammatory or infectious mimic.[1][3]

Examiner: Name the important mimics.[1][3]

Candidate: Dermatofibrosarcoma protuberans, scar-associated squamous cell carcinoma, scar sarcoidosis, dermatofibroma, a deeper desmoid-type lesion, infection and cutaneous metastasis. DFSP is an indurated progressive spindle-cell tumour, typically CD34-positive; SCC raises concern with ulceration, bleeding or destructive change. I would not attach an unsourced treatment margin to a differential answer.[1][3]

Examiner: What histology distinguishes the scars?[3][13]

Candidate: Keloids classically have broad, glassy, hyalinised eosinophilic “keloidal” collagen. Hypertrophic scars more often have relatively aligned or nodular collagen with myofibroblastic activity. There is overlap, and histology cannot reconstruct the original clinical wound boundary.[3][13]

Q4: Assess and score safely

Examiner: What will you measure before treatment?[2][3]

Candidate: Symptoms, sleep, function, patient priority, original wound boundary, length, width, elevation, colour, pliability, fixation, ulceration and joint movement. I take standardised photographs with consent and document prior treatments and adverse effects.[2][3]

Examiner: Describe POSAS.[5]

Candidate: The original Patient and Observer Scar Assessment Scale has six patient items and six observer items, each scored 1–10. Each six-item subscale totals 6–60; the overall-opinion item is recorded separately. Later versions differ, so I document the version rather than combining everything into a falsely universal 12–120 total.[5]

Examiner: And VSS?[3]

Candidate: The Vancouver Scar Scale records vascularity, pigmentation, pliability and height. It was developed for burn scars and versions vary, so I name the version used instead of claiming one universal maximum.[3]

Q5: Build a treatment hierarchy

Examiner: How will you treat this symptomatic chest keloid?[1][2][6]

Candidate: First I agree whether pain, itch, flattening or appearance is the main goal and document a baseline. Silicone can be used only on intact, epithelialised skin, but the evidence is limited by high-risk-of-bias trials. I would offer intralesional triamcinolone and then reassess response and adverse effects.[1][2][6]

Examiner: Give a sourced triamcinolone regimen.[7]

Candidate: The 2024 KECORT e-Delphi preferred 40 mg/mL, a four-week interval, and a maximum 80 mg per month, while also reporting no complete dosing consensus. I would call this expert-consensus practice, individualise injected volume, keep injection intralesional rather than subcutaneous, and counsel about pain, atrophy, telangiectasia and dyspigmentation.[7]

Examiner: What if response is inadequate?[2][9]

Candidate: I refer to an experienced scar service for combination intralesional treatment such as 5-fluorouracil, cryotherapy or another specialist option; the exact recipe is protocol-specific because results are mixed. Laser is an adjunct, not a proven standard: a Cochrane review of 15 randomised trials with 604 participants found low- or very-low-certainty evidence for most comparisons.[2][9]

Q6: Defend surgery and radiotherapy

Examiner: Why not simply excise it?[1][2]

Candidate: Excision creates another wound and recurrence is high when surgery is used alone. Before operating, I agree the indication, tension-reducing closure, postoperative adjuvant and follow-up. I avoid the absolute claim that every lesion will recur, but I do not perform an unplanned stand-alone excision.[1][2]

Examiner: What radiotherapy dose and timing will you prescribe?[10][11][12]

Candidate: I will not prescribe a universal dermatology regimen. In selected adults with recurrent or refractory keloids, the radiation oncologist individualises modality, dose, fractionation, timing and shielding. A 2017 meta-analysis reported 22% overall postoperative recurrence, with subgroup estimates of 15% after brachytherapy, 23% after x-ray therapy and 23% after electron therapy; these pooled data were heterogeneous and chest lesions did worse.[10]

Prompt postoperative treatment is common, but a timing meta-analysis did not show a significant recurrence advantage for immediate over delayed radiotherapy. Modern reviews judge secondary malignancy risk low with careful planning and organ protection, not zero. Avoid radiotherapy in pregnancy and generally defer it in children.[11][12]

Q7: Prevention, special groups and follow-up

Examiner: How do you reduce risk around necessary surgery?[6][8]

Candidate: Discuss the patient's own scar history and whether the procedure is necessary; minimise tissue trauma, inflammation and wound tension; and wait for complete epithelialisation before silicone. If a hypertrophic burn scar needs pressure therapy, use a specialist-fitted protocol. A 2023 systematic review suggested at least 20–25 mmHg, started within two months and continued at least 12 months, preferably 18–24 months, but these are review-derived suggestions rather than a universal prescription.[6][8]

Examiner: What changes in a child or during pregnancy?[2][12]

Candidate: In children I prioritise conservative and function-preserving care, provide an age-appropriate pain plan for injections and generally defer radiotherapy. During pregnancy I defer elective procedures, avoid radiotherapy and seek obstetric/pharmacy advice before intralesional cytotoxic or systemic treatment. I will not label an unsourced low dose as automatically safe.[2][12]

Examiner: How long will you follow her?[2][10]

Candidate: Follow-up matches the intervention and recurrence risk. I review during active treatment according to that protocol, use the same photographs and score version, and continue long enough to detect clinically meaningful recurrence. Because study follow-up is inconsistent, there is no evidence-based universal three-monthly, annual or 12–24-month schedule for every patient.[2][10]

Viva closer

Examiner: Give me the safe one-line management answer.[1][2][3]

Candidate: Confirm the boundary-based diagnosis, biopsy atypical behaviour, agree a measurable patient-centred goal, start with the least harmful conservative or intralesional option, and never create a new wound without an individualized adjuvant and follow-up plan.[1][2][3]