Post-inflammatory hyperpigmentation — Viva

Q1: Establish the diagnosis

Examiner: Define PIH and tell me what makes the diagnosis credible. [4][5]

Candidate: PIH is acquired excess epidermal and/or dermal melanin after cutaneous inflammation or injury. I want a plausible precursor, correct chronology and pigment in broadly the same distribution. Brown macules where acne papules healed are typical; skin tone may affect visibility and persistence but does not diagnose PIH.[4][5]

Branch — Examiner: What if the patient cannot recall any preceding eruption? [7][9]

Candidate: I would not force the PIH label. I would reconsider melasma, drug pigmentation, acquired dermal macular hyperpigmentation, contact pigmentation and a pigmented lesion, guided by symmetry, distribution, medicines, products and morphology.[7][9]

Q2: Explain depth without overclaiming

Examiner: How do epidermal and dermal PIH differ? [3][5]

Candidate: Epidermal PIH reflects excess melanin in keratinocytes and is usually brown; it often fades faster and is more topical-responsive. Dermal PIH follows pigment incontinence with melanophages and is often grey-brown or blue-grey; it can persist for years. Mixed lesions contain both components. These are useful tendencies, not guaranteed response or clearance windows.[3][5]

Branch — Examiner: The lesion does not enhance under Wood's lamp. Have you proved dermal PIH? [5][7]

Candidate: No. Wood's lamp may accentuate some epidermal pigment, but it does not confirm or exclude pigment depth and is less useful in deeply pigmented skin. I would integrate colour, history and distribution and reserve biopsy for atypical or consequential diagnostic uncertainty.[5][7]

Q3: Link mechanism to management

Examiner: Give me a concise pathophysiological account. [3]

Candidate: Inflammation changes signalling among keratinocytes, inflammatory cells, fibroblasts and melanocytes, increasing melanogenesis and melanosome transfer. If the dermo-epidermal junction is injured, pigment enters the dermis and is taken up by macrophages. The mediator network is multifactorial and the complete mechanism of persistence is not settled.[3]

Branch — Examiner: Why can treatment make PIH worse? [1][2][6]

Candidate: An irritating topical, peel or energy-based procedure can create new inflammation and therefore new pigment. That is why tolerability, conservative escalation and control of the underlying dermatosis come before aggressive lightening.[1][2][6]

Q4: Perform a focused assessment

Examiner: Assess a patient with acne-associated facial PIH. [4][5][7]

Candidate: I confirm the acne chronology and ask about picking, procedures, medicines and every applied product. I examine for active acne or dermatitis and document whether lesions are flat, their colour and distribution. I look for discordant features: symmetric patches without a precursor, blue-black pigment after prolonged lightener use, generalised or mucosal pigment, or a solitary changing lesion. Typical localised PIH needs no routine laboratory panel; tests or biopsy follow the suspected alternative.[4][5][7]

Branch — Examiner: What would make you investigate urgently rather than prescribe a lightener? [7]

Candidate: A changing solitary lesion, ulceration, generalised pigmentation with oral-mucosal or palmar-crease involvement and systemic symptoms, or blue-black change after prolonged lightener use. These raise a tumour, systemic cause such as adrenal insufficiency, or ochronosis rather than straightforward PIH.[7][10]

Q5: Give a safe first-line plan

Examiner: How would you manage the acne-associated case? [4][6][8]

Candidate: First, I treat active acne with a tolerable regimen and stop any irritating or unlabelled lightener. Second, I recommend broad-spectrum sunscreen, shade and clothing; tinted iron-oxide sunscreen can add visible-light protection if acceptable. Third, after controlling irritation, I discuss one compatible topical option such as clinician-supervised hydroquinone, a topical retinoid that also treats acne, or azelaic acid, starting gently and reviewing response and adverse effects.[4][6][8]

Branch — Examiner: The patient is pregnant. What changes? [6]

Candidate: I prioritise acne control with pregnancy-compatible therapy and photoprotection. I avoid elective hydroquinone and topical retinoids because pregnancy safety evidence is insufficient, and I would discuss an accepted alternative such as azelaic acid with the treating clinician rather than calling any cosmetic regimen risk-free.[6]

Q6: Handle apparent failure and procedures

Examiner: The marks remain distressing after an initial topical plan. Is laser now mandatory? [1][2]

Candidate: No. I first reassess diagnosis, active inflammation, adherence, irritation and expectations. If a procedure is considered, dermatology review should individualise the device or peel, use conservative parameters and discuss dyspigmentation. Systematic reviews show partial response is much commoner than complete clearance, and some laser or energy-based treatments worsen PIH.[1][2]

Branch — Examiner: Quote the evidence boundary. [2]

Candidate: In the 2024 review of 41 studies and 877 patients, complete response was 18.1% with laser or energy-based devices and 5.4% with topicals; 2.6% worsened after laser or energy-based therapy. Most included PIH was acne-associated and outcomes were heterogeneous, so those pooled results cannot predict an individual response.[2]

Q7: Counsel on prognosis and unsafe extrapolation

Examiner: What do you tell the patient about time course and oral tranexamic acid? [1][2][11]

Candidate: I say improvement is gradual: epidermal pigment often improves over months, while dermal pigment may persist for years. I avoid fixed clearance promises. Oral tranexamic acid has reported efficacy in melasma, but that evidence does not establish routine PIH treatment; systemic use also carries potential thromboembolic risk.[1][2][11]

Branch — Examiner: Give three safety-net instructions. [6][7]

Candidate: Return earlier for a changing solitary lesion, generalised or mucosal pigmentation with systemic symptoms, or blue-black change after prolonged lightener use. Also report treatment-induced burning, itch or scale because dermatitis can create further PIH.[6][7][10]

References

1. [1]Mar K, Khalid B, Maazi M, et al. Treatment of Post-Inflammatory Hyperpigmentation in Skin of Colour: A Systematic Review. J Cutan Med Surg, 2024.PMID 39075672
2. [2]Kashetsky N, Feschuk A, Pratt ME. Post-inflammatory hyperpigmentation: A systematic review of treatment outcomes. J Eur Acad Dermatol Venereol, 2024.PMID 37843491
3. [3]Maghfour J, Olayinka J, Hamzavi IH, et al. A Focused review on the pathophysiology of post-inflammatory hyperpigmentation. Pigment Cell Melanoma Res, 2022.PMID 35306737
4. [4]Elbuluk N, Grimes P, Chien A, et al. The Pathogenesis and Management of Acne-Induced Post-inflammatory Hyperpigmentation. Am J Clin Dermatol, 2021.PMID 34468934
5. [5]Silpa-Archa N, Kohli I, Chaowattanapanit S, et al. Postinflammatory hyperpigmentation: A comprehensive overview: Epidemiology, pathogenesis, clinical presentation, and noninvasive assessment technique. J Am Acad Dermatol, 2017.PMID 28917451
6. [6]Chaowattanapanit S, Silpa-Archa N, Kohli I, et al. Postinflammatory hyperpigmentation: A comprehensive overview: Treatment options and prevention. J Am Acad Dermatol, 2017.PMID 28917452
7. [7]Wang RF, Ko D, Friedman BJ, et al. Disorders of hyperpigmentation. Part I. Pathogenesis and clinical features of common pigmentary disorders. J Am Acad Dermatol, 2023.PMID 35151757
8. [8]Lyons AB, Trullas C, Kohli I, et al. Photoprotection beyond ultraviolet radiation: A review of tinted sunscreens. J Am Acad Dermatol, 2021.PMID 32335182
9. [9]Narayan R V, Thakur V, Bishnoi A, et al. Acquired dermal macular hyperpigmentation: a unified spectrum of dermal pigmentary dermatoses. Clin Exp Dermatol, 2026.PMID 41700520
10. [10]Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and Treatment of Primary Adrenal Insufficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab, 2016.PMID 26760044
11. [11]Sheu SL. Treatment of melasma using tranexamic acid: what's known and what's next. Cutis, 2018.PMID 29554171