Intralesional therapy

Meet the patient

A 24-year-old woman is back in clinic six months after a shoulder laceration, pointing to a firm, raised, itchy purple nodule that has spilled past the original scar edge onto normal skin — a keloid. Two doors down, a 30-year-old man shows you three smooth, hairless circles in his beard — limited patchy alopecia areata. Both are booked for the same five-minute procedure: a fine-needle injection that delivers a high local drug concentration with minimal systemic spillover.[1]

Two questions decide whether either visit ends well: what concentration belongs in this syringe for this site? and what is my stopping point? Get those right and the signature complications never appear; get them wrong and you trade a keloid for an atrophic dent that will not recover.[1]

A procedure, not a casual steroid shot

IL therapy is the direct injection of a drug into diseased skin or scar to achieve a high local concentration with relatively little systemic exposure compared with an oral dose of the same class. The dominant agent is triamcinolone acetonide (TAC), a particulate corticosteroid suspension that settles into a slow-release depot. A handful of other injectables — 5-fluorouracil (5-FU), bleomycin, and Candida antigen — extend the platform beyond steroids for scars and warts.[1][3][4]

The trap juniors fall into: treating it as "a steroid shot." It is a procedure whose four variables — concentration, depth, volume per puncture, and interval — entirely determine both its efficacy and its complications. The patient who gets a face full of 40 mg per mL gets atrophy; the one whose keloid is under-dosed gets recurrence. Discipline, not the drug, is the variable you control.[1]

Meet the injectable toolkit

The agent is chosen for the lesion. TAC is first-line for the two indications you will inject most; the others are reserved for the recalcitrant case.[1][3]

[1]

Why a steroid depot works in scar and in hair loss

The mechanism is different in the two flagship indications, and a candidate who can state both earns the marks.[1][6]

In keloid and hypertrophic scar, the lesion is a fibroblast running hot — excessive collagen deposition that outstrips remodelling. Corticosteroid suppresses that fibroblast: it curtails collagen and glycosaminoglycan synthesis and dampens the inflammatory drive, so the raised tissue softens and flattens over serial sessions. 5-FU attacks the same target from the other side, poisoning proliferating fibroblasts, which is why the two are combined in recalcitrant keloids.[1][4][5]

In alopecia areata, the follicle is under autoimmune attack. Perifollicular T-cell inflammation drives the hair out of anagen; local immunosuppression around the follicle can lift that attack and permit regrowth — but only in limited patchy disease, where the surface area is small enough for injection to be practical and effective.[7][9]

How atrophy happens — and how to prevent it

Understand the mechanism of the signature harm and you will never cause it. Atrophy follows oversuppression of the dermal matrix — fibroblast collagen and fat are literally dissolved away, leaving a permanent dent.[1]

The four triggers, in the order juniors commit them:[1]

• Concentration too high — a 40 mg per mL bolus into thin facial skin melts the dermis. Dilute for the face.
• Placement too superficial — a subepidermal bleb concentrates steroid where the matrix is thinnest. Seat the needle in the mid-dermis or scar substance.
• Volume too large — spread beyond the lesion pools into surrounding normal skin and dents it. Inject only to blanch the lesion.
• Interval too short — stacking sessions before the prior depot has cleared compounds the injury. Keep to 3 to 6 weeks.[1]

Everyone forgets: the atrophy you cause today is largely irreversible. The keloid you under-treat can be re-injected; the dent you over-treat is the patient's to keep. When in doubt, dilute, deepen, and defer.[1]

The indications that earn marks — and the ones that do not

IL TAC is first-line for two indications and a useful adjunct for a short list of others. It is emphatically not the answer for extensive disease.[1][7]

• Keloid and hypertrophic scar — the first-line injection in a multimodal plan, layered with silicone, pressure, and (for keloid) planned surgery with postoperative IL steroid.[3][6]
• Limited patchy alopecia areata — for circumscribed scalp or beard patches in a cooperative patient; regrowth over months, with relapse possible after cessation.[7][8][9]
• Other classic uses — hypertrophic lichen planus plaques, prurigo nodularis nodules, acne cysts after drainage, selected granulomatous lesions. Always diagnosis-first.[1]

The classic trap: reaching for IL steroid in extensive alopecia areata — more than half the scalp, ophiasis pattern, or progressing rapidly. Intralesional injection cannot cover that surface and delays the systemic or advanced therapy the patient actually needs. Network meta-analysis places IL steroid as one node among many in a broad efficacy landscape, not the whole algorithm for severe disease.[7][9]

When not to inject

Half of safe injecting is knowing when to put the syringe down. These are the situations where another modality comes first.[1]

[1]

Bedside technique — the four variables you control

Preparation is where the complications are prevented. Confirm the diagnosis and exclude infection, photograph the baseline for scars and alopecia, and counsel the patient on pain, the need for multiple sessions, atrophy and pigment-change risk, and realistic goals — flattening and softening, not erasure. Then choose the working concentration by site and thickness.[1]

The injection principles that follow are the ones a viva examiner wants heard in order:[1][9]

[1]

Concentration follows site — the one rule that prevents most harm

If you remember a single pattern from this page, make it this. Low for the face and for alopecia; high for a thick truncal keloid. The face and the scalp cannot forgive a strong solution; the dense collagen of a chest keloid will barely register a weak one.[1][6]

A consultant confession: the 40 mg per mL vial is for the keloid, not the face. Diluting TAC with saline or lidocaine to a face-appropriate concentration feels like a chore in a busy clinic, and that is exactly when the permanent dent happens. Dilute first, inject second, every time.[1]

The same discipline governs the cumulative dose. Across a large keloid burden, injected in many sessions over months, the totals can climb high enough to rarely produce genuine systemic glucocorticoid effects — Cushingoid features and hypothalamic-pituitary-adrenal suppression. This is a documented, board-level safety fact, not a curiosity, and it is the reason you track the running total and space the sessions.[2]

Combination strategies for the recalcitrant keloid

A keloid treated with IL steroid alone recurs often enough that multimodal care is the standard, not the exception. Evidence syntheses converge on the same backbone.[3][6]

• IL steroid remains the foundation, softened and flattened over serial sessions.[1]
• IL 5-FU, alone or combined with TAC, is added for stubborn keloids, with two systematic reviews behind it.[4][5]
• Silicone gel sheeting and pressure are layered on as adjuvants between sessions.[3]
• Planned excision with postoperative IL steroid is reserved for selected lesions, because excision alone recurs worse than the original.[3][6]

The complications — common, less common, and rare

The harms cluster cleanly into three tiers, and a candidate should be able to name all three.[1][2]

[2]

Anaphylaxis after IL TAC is rare but reported, and it is the reason every injecting clinic needs an emergency protocol and adrenaline to hand — a "minor" procedure is not exempt from resuscitation readiness. Systemic steroid toxicity is uncommon relative to the volume of practice, but documented enough that cumulative-dose discipline matters, especially across a large keloid burden.[2][10]

Special populations

These are the groups where the risk-benefit shifts and the consent conversation changes.[1]

• Children — limit sessions by pain tolerance; use topical anaesthetic adjuncts and lower total doses, because a frightened child will not return.[9]
• Pregnancy — avoid non-essential cytotoxic IL agents such as 5-FU and bleomycin; individualise any steroid use.[4]
• Skin of colour — hypopigmentation and atrophy are highly visible and may be long-lasting; obtain explicit, documented consent and favour conservative concentrations.[6]
• Periocular skin — extra caution around local steroid effects; never fire a casual high-dose periocular injection.[1]

Prognosis and follow-up

Set the expectation honestly at the first visit, and the follow-up is straightforward.[3][7]

Keloids usually need serial injections and may still recur without a multimodal plan, so counsel for a programme of care rather than a cure. Patchy alopecia areata may show regrowth over months, with relapse possible after cessation — stop when response plateaus. In both, escalate when the disease outgrows the injection strategy: extensive alopecia to systemic therapy, recurrent keloid to excision plus adjuvants.[3][7][9]

The mantra, and the memory device

[1]

The mantra: concentration to site, inject to blanch, watch for atrophy.[1]

Etymology for viva gold: triamcinolone is a tri-substituted synthetic corticosteroid; acetonide marks the cyclic acetal that makes the molecule insoluble enough to sit as a depot in the dermis rather than dissolving away. The chemistry is the pharmacology — the depot is the point.[1]

Ward-round test — three stems, thirty seconds each

Stem 1 — the facial keloid that got 40 mg per mL (answer)

A registrar injects a small cheek keloid with undiluted 40 mg per mL triamcinolone. Six weeks later the keloid is flatter, but a pale, depressed, finely telangiectatic patch sits where normal cheek was. What happened, and what was the error? Model: This is steroid-induced dermal atrophy with telangiectasia and hypopigmentation — the signature harm of a high concentration placed in thin facial skin. The lesion flattened, but the surrounding dermis was dissolved. The error was concentration: facial skin demands a dilute TAC solution, seated in the mid-dermis, injected only to blanch. Prevention is diluting before drawing up, every time. The dent will not fully recover.[1]

Stem 2 — extensive alopecia areata booked for IL steroid (answer)

A woman has lost 70 percent of her scalp hair over three months, with an ophiasis band at the occipital hairline. The plan is serial intralesional triamcinolone across the scalp. What is wrong with this plan? Model: This is extensive, rapidly progressive alopecia areata in an ophiasis pattern — a poor prognosis for local therapy. Intralesional injection cannot practically cover this surface area, and it delays the systemic or advanced therapy the patient needs. The Cochrane network meta-analysis places IL steroid as one node among many, not the answer for severe disease. Escalate to systemic or advanced therapy; reserve IL steroid for limited patchy disease.[7][9]

Stem 3 — collapse minutes after a keloid injection (answer)

A patient becomes breathless, flushed, and hypotensive within minutes of an intralesional triamcinolone injection. What is the diagnosis, and what is the immediate response? Model: This is anaphylaxis following intralesional triamcinolone — rare but documented. Stop the procedure, call for help, give intramuscular adrenaline, secure the airway and give high-flow oxygen and fluid, and position the patient flat. The lesson is procedural: a "minor" injection is not exempt from resuscitation readiness — adrenaline and an emergency protocol must be immediately available in every injecting clinic.[10]

References

1. [1]Richards RN. Update on intralesional steroid: focus on dermatoses J Cutan Med Surg, 2010.PMID 20128986
2. [2]Fredman R, Tenenhaus M. Cushing's syndrome after intralesional triamcinolone acetonide: a systematic review of the literature and multinational survey Burns, 2013.PMID 23092701
3. [3]Walsh LA, Wu E, Pontes D, et al. Keloid treatments: an evidence-based systematic review of recent advances Syst Rev, 2023.PMID 36918908
4. [4]Bijlard E, Steltenpool S, Niessen FB. Intralesional 5-fluorouracil in keloid treatment: a systematic review Acta Derm Venereol, 2015.PMID 25805099
5. [5]King A, Guirguis M, Satkunanathan S, et al. Intralesional 5-Fluorouracil for Keloids: A Systematic Review J Cutan Med Surg, 2024.PMID 38807454
6. [6]Ekstein SF, Wyles SP, Moran SL, et al. Keloids: a review of therapeutic management Int J Dermatol, 2021.PMID 32905614
7. [7]Mateos-Haro M, Novoa-Candia M, Sánchez Vanegas G, et al. Treatments for alopecia areata: a network meta-analysis Cochrane Database Syst Rev, 2023.PMID 37870096
8. [8]Liu YC, Chuang KW, Chang HC. Intralesional Corticosteroid Versus Cryotherapy for Alopecia Areata: A Systematic Review and Meta-analysis Acta Derm Venereol, 2025.PMID 40908758
9. [9]Dakkak M, Forde KM, Lanney H. Hair Loss: Diagnosis and Treatment Am Fam Physician, 2024.PMID 39283847
10. [10]Laisuan W, Wongsa C, Dchapaphapeaktak N, et al. Anaphylaxis following intralesional triamcinolone acetonide (Kenacort) injection Asia Pac Allergy, 2017.PMID 28487843