Keloids: Causes, Symptoms, Treatment & Prevention

A keloid is a benign, fibroproliferative scar that arises after a wound-healing response runs unchecked in the reticular dermis. Where ordinary wound healing transitions through inflammation, fibroblast proliferation and maturation phases, the keloid pathway stalls in an aberrant fibroblastic phase: dermal fibroblasts proliferate excessively, resist apoptosis, and deposit thickened bundles of disorganised collagen at roughly twenty times the rate of normal skin and three times the rate of a hypertrophic scar. The result is a firm, rubbery dermal nodule that projects above the original wound and—definitionally—extends beyond its margin into surrounding healthy skin.

The biology behind that picture is increasingly understood as a localised, chronic inflammatory disorder of the reticular dermis rather than a simple over-healed scar. Transforming growth factor-β (TGF-β1 and TGF-β2 in particular), platelet-derived growth factor, connective tissue growth factor and interleukin-6 dominate the keloid-forming microenvironment; vascular abnormalities, mast-cell hyper-reactivity and prolonged tension on the wound bed reinforce the loop. Genetic susceptibility is real—familial clustering is common, several HLA associations have been described, and rare syndromes (Rubinstein–Taybi, Goeminne) confer markedly increased risk—but no single causative gene has been identified.

Clinically, keloids matter because they cause real morbidity even though they never metastasise: pruritus, burning, tenderness and pain are reported by most patients, and large lesions can restrict joint movement, distort cosmetically prominent sites (earlobes, chest, mandible) and carry a measurable psychological burden. They also matter because every clinician who handles a needle, a scalpel, a laser or a piercing gun in keloid-prone skin needs to know how to minimise the risk before it crystallises—prevention is far more effective than any current treatment.

Both are aberrant dermal scars; both follow trauma; both are commoner in patients with darker skin tones. The two diverge in behaviour, prognosis and management. The single most useful distinguishing question at the bedside is whether the scar respects the original wound margin.

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Keloids do not have a single internationally agreed grading system, but practical bedside descriptors used in trials and clinical practice include lesion height, surface area, the number of separate lesions, symptom score (pain and itch on a 0–10 scale) and the Patient and Observer Scar Assessment Scale (POSAS). Documenting these consistently makes it possible to demonstrate response—or its absence—objectively.

Patients usually present some weeks to many months after a triggering injury, although a small proportion describe spontaneous lesions where the inciting event was simply too trivial to recall. The lesion is firm, rubbery and frequently tender; the colour ranges from erythematous through dusky purple to flesh-coloured to hyperpigmented depending on Fitzpatrick type and lesion age.

Common presentations

• Smooth, shiny, raised scar that crosses the line of the original wound or piercing track.
• Persistent itching, burning or stinging—reported by approximately 86% of patients in case-series.
• Pain or tenderness on palpation in roughly 46%—often worse at night or under tight clothing.
• Pedunculated earlobe nodule after piercing, classically on the helix or lobe in adolescents.
• Linear keloid along a sternotomy or caesarean scar, especially under tension.
• “Acne keloidalis nuchae” pattern: firm papules and plaques along the occipital hairline in young Black men.
• Post-inflammatory hyperpigmentation haloing the lesion in skin of color.

Pattern-recognition clues

• Helix or earlobe nodule after a 6–12 week-old piercing—almost always keloid in keloid-prone skin; small lesions respond best to early intralesional steroid.
• Sternal “rope” scar after CABG or cardiac surgery—high tension and skin of color combine; layered silicone and pressure prophylaxis are worthwhile from week 2 of healing.
• Painful nodules along the upper back and shoulders in a patient with a history of severe nodulocystic acne—post-acne keloids are often misread as residual acne and over-treated with antibiotics.
• Restricted joint movement from a large pre-sternal, scapular or shoulder keloid—document range of motion at every visit.
• Dyspareunia or perineal discomfort after caesarean section, episiotomy or perineal surgery—uncommon but distressing keloid sites.

Atypical and easy-to-miss patterns

Spontaneous keloids—lesions appearing without recalled trauma—are well described, particularly on the pre-sternal chest. They are easily mistaken for fibrous papules, dermatofibromas or nodular acne. Conversely, a “keloid” that ulcerates, develops a heaped indurated edge, or grows rapidly without preceding trauma should prompt a biopsy to exclude dermatofibrosarcoma protuberans, lobomycosis (where geography fits), keloidal scleroderma, morphoea, or rarely cutaneous lymphoma. In children and adolescents, occipital keloids after head-louse treatment or vaccination scars are easily overlooked beneath the hairline; pull the hair forward and inspect the nape of the neck.

Two factors must usually align for a keloid to form: a susceptible host and a trigger that disturbs the dermis. Either alone is rarely enough.

Host (patient) factors

• Heritage: markedly higher prevalence in patients of African, Black Caribbean, Asian and Hispanic descent (4.5–16% in case-series), low in non-Hispanic White and very low in albino populations.
• Age: peak incidence between ages 10 and 30; uncommon at extremes of age.
• Family history: first-degree relatives with keloids confer significant risk; familial clustering is well described.
• Hormonal milieu: incidence rises during puberty and pregnancy, suggesting endocrine modulation of dermal fibroblasts.
• Rare syndromes: Rubinstein–Taybi, Goeminne, Bethlem myopathy and certain HLA-DR / HLA-DQ associations carry increased risk.
• Comorbid skin disease: nodulocystic acne, recurrent folliculitis, ingrown hairs along the beard line, hidradenitis suppurativa and chronic eczema with repeated excoriation.

Triggers (the dermal insult)

• Surgical wounds under tension—sternotomy, caesarean section, shoulder and scapular surgery, mastoid and earlobe procedures.
• Piercings, especially helical/cartilage and earlobe piercings; nipple, navel and lip piercings next.
• Tattoos, particularly large outlines and dark inks; symptomatic keloids may emerge months to years later.
• Acne and folliculitis on the upper trunk, deltoid, shoulders and beard area.
• Burns, abrasions and lacerations, especially when healing is delayed by infection or tension.
• Vaccination scars (BCG in particular) and bite wounds.
• Chickenpox and shingles craters, healed cutaneous infections, and impetigo-affected skin.
• Mechanical tension across the wound—shared by all of the above; tension-relieving sutures, taping and silicone reduce risk.

Modifiable risk levers

The first three levers a clinician genuinely controls are wound tension, choice of elective procedure and prompt management of the early scar. Tension-relieving closure (subcuticular plus deep dermal sutures, paper tape or silicone strips for 2–3 months), avoidance of elective piercings on the helix and elective surgery on tension-prone sites in known keloid-formers, and early use of silicone gel sheeting once the wound is fully epithelialised together account for most of the practically achievable risk reduction.

Diagnosis is overwhelmingly clinical. The workup focuses on confirming the lesion is a keloid, ruling out the small but important list of mimics, and stratifying the patient for treatment intensity.

Bedside history checklist

• Timeline: triggering trauma (surgery, piercing, acne, burn, vaccination), onset of the scar, growth pattern.
• Personal and family history of keloids; previous treatments and outcomes; prior steroid response.
• Comorbid acne, folliculitis or hidradenitis; smoking, diabetes, immunosuppression and current medications.
• Symptom inventory: itch, burning, pain, dyspareunia, restricted joint movement, sleep impact.
• Cosmetic and psychosocial impact; goal of treatment (symptom relief vs cosmetic flattening vs both).
• Pregnancy or breastfeeding status (modifies steroid and 5-fluorouracil decisions).

Clinical examination

Inspect with good light and use a structured skin assessment covering the whole body, not just the presenting site—patients often have additional lesions they have stopped mentioning. Pair it with a head-to-toe assessment to look for scleroderma features, the “dimple sign” of dermatofibroma, lipodystrophy, lymphadenopathy and joint range-of-motion limitation overlying scarring.

• Measure each lesion (length × width × height in millimetres) and photograph at baseline with consent.
• Document Fitzpatrick skin type, distribution, colour, induration, tenderness and any ulceration.
• Score symptoms on a 0–10 scale (pain, itch separately) at every visit.
• Examine drainage to a cervical or axillary nodal basin if any concern about a malignant mimic.

When to investigate further

Most keloids need no investigations beyond a careful examination. A skin biopsy is reserved for atypical lesions: rapid growth without preceding trauma, ulceration or bleeding, irregular borders, lesions failing to respond as expected to standard therapy, or any clinical suspicion of dermatofibrosarcoma protuberans, scleroderma, lobomycosis or carcinoma. Histopathology in a true keloid shows broad bands of hyalinised eosinophilic “keloidal” collagen, a tongue-like advancing edge below the papillary dermis, a horizontal fibrous band in the upper reticular dermis, and a prominent deep fascial-like band; vertically oriented vessels are characteristically scarce.

A complete blood count and inflammatory markers are useful only if superinfection is suspected, while a wound swab and culture is appropriate for any draining or ulcerated lesion. Imaging (high-frequency ultrasound or MRI) is not routine but can occasionally help map deep extent before excision of a large pre-sternal lesion.

Common interpretation traps

• “Hypertrophic scar” that is steadily growing months later. If extension beyond the wound margin is present, it is a keloid; treat accordingly.
• Earlobe nodule “granuloma” after metal piercing. A true allergic granuloma is doughy and resolves on jewellery change; a hard, tender mass after 6–12 weeks is almost always a keloid.
• “Failed acne” on the chest and shoulders. Persistent firm nodules along acne scars are usually keloids—antibiotics will not help.
• Steroid “failure” after one injection. Most keloids need 3–6 sessions at 4–6 week intervals; do not abandon the protocol prematurely.
• Cryotherapy first in dark skin. Risks long-lasting hypopigmentation; combine with steroid or use other modalities first in Fitzpatrick IV–VI.

A pragmatic chain that ward, primary-care and outpatient teams can apply on first contact:

1. Confirm the diagnosis at the wound margin. Extension beyond the original injury and a typical site or risk profile makes a keloid the working diagnosis; biopsy only when atypical features are present.
2. Stage the lesion and the patient. Size, height, symptoms, location, joint involvement, Fitzpatrick type, family history and previous treatments determine the intensity of the plan.
3. Set realistic goals together. Symptom relief, cosmetic flattening, regaining the ability to wear earrings, restoring joint movement—each goal demands different combinations of therapy.
4. Start the universal foundation. Daily silicone gel sheeting over the lesion (once skin is intact), pressure where feasible (earring, garment), trigger removal (avoid further piercings, manage acne), and wound-tension reduction at any new healing site.
5. Layer first-line therapy. Intralesional triamcinolone 10–40 mg/mL every 4–6 weeks for 3–6 sessions for symptomatic, small to moderate lesions; pressure and silicone in parallel.
6. Escalate when needed. Refractory or large lesions: combine triamcinolone with 5-fluorouracil, add cryotherapy or laser, consider intralesional verapamil or bleomycin in specialist hands.
7. Consider excision only with adjuvant therapy. Reserve for large pedunculated lesions, functional impairment or failed conservative therapy; pair with intralesional steroid (within 2–3 weeks post-op, then every 4–6 weeks for 6 months), silicone, pressure, and—if appropriate—superficial radiation therapy within 24–48 hours.
8. Plan structured follow-up. Review at 4–6 weeks after the last injection, then at 3, 6 and 12 months; most recurrences appear in the first year. Re-treat early at the first sign of regrowth.
9. Refer urgently for atypical lesions, suspected DFSP or carcinoma, refractory symptoms, paediatric facial keloids, large radiation-candidate lesions or significant psychological distress.

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No single therapy reliably eradicates a keloid. The clinical reality is that combination treatment, layered over months, delivers the best symptom relief and the lowest recurrence rates. The ladder runs three rails simultaneously: prevent further injury to the lesion or any new wound, repair and protect the dermis with silicone and pressure, and modulate the abnormal fibroblast response with intralesional and adjuvant agents.

Universal foundation (every patient)

• Silicone gel sheeting or topical silicone gel for at least 12–24 hours per day for ≥2–3 months on intact, healed skin. Suitable for both established keloids and prevention after high-risk wounds.
• Pressure therapy at 15–45 mmHg for >23 hours per day for at least 6 months on amenable sites: pressure earrings for earlobe lesions, custom garments for chest, shoulder and limb lesions.
• Trigger control: avoid further piercings (especially helical), treat acne early and aggressively, manage folliculitis and ingrown hairs, and reduce wound tension with subcuticular closure and paper-tape stabilisation in any new wound.
• Symptom relief: bland emollients, soap substitutes and (rarely) short courses of second-generation antihistamines such as cetirizine, loratadine or fexofenadine for prominent itch.
• Patient and family education about realistic expectations, lifelong susceptibility and the value of early re-treatment.

First-line systemic dermal therapy

• Intralesional triamcinolone acetonide: 10 mg/mL for small or facial lesions, 20–40 mg/mL for thicker body lesions, every 4–6 weeks for 3–6 sessions; expect symptom relief by injection 2 and visible flattening by injection 3–4.
• Topical mid-to-high potency corticosteroids (mometasone, betamethasone valerate or clobetasol for short pulses) under occlusion can ease itch and inflammation between injections; hydrocortisone 1% is suitable for face, eyelids and intertriginous sites.
• Steroid-impregnated tape (e.g. flurandrenolide tape) is useful as a continuous low-dose alternative on small lesions.

Second-line and combination intralesional therapy

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Surgical excision and adjuvant therapy

Surgery alone recurs in 45–100% of keloids, often regrowing larger and more symptomatic than the original lesion. Combine excision with one or more of:

• Post-operative intralesional triamcinolone starting 2–3 weeks after suture removal, repeated every 4–6 weeks for 6 months; widely available and cost-effective.
• Adjuvant superficial radiation therapy (SRT) delivered within 24–48 hours of excision (10–20 Gy in fractionated doses), which can reduce recurrence to ~10–20%; counsel about peeling, pigment change and rare radiation-induced malignancy, and avoid near breast, thyroid or salivary glands when alternatives exist.
• Pressure earring or compression garment for 6–12 months post-excision.
• Silicone gel sheeting from the moment the wound is fully epithelialised.
• Suture choice and closure technique: tension-relieving deep dermal sutures, subcuticular monofilament closure, layered repair to minimise wound tension.

Refractory and special situations

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Intralesional steroid injection is the workhorse of keloid management. The technique is straightforward but unforgiving—getting it right protects the patient from atrophy, hypopigmentation and disappointing outcomes.

Pre-procedure (nursing role)

• Confirm patient identity, lesion site, planned drug (triamcinolone acetonide), dilution and volume; check allergy status and pregnancy/breastfeeding status.
• Exclude active infection over the lesion; defer if any cellulitis, weeping or drainage is present.
• Review systemic conditions that complicate steroid use—uncontrolled diabetes, recent live vaccine, severe immunosuppression—and discuss with the clinician.
• Photograph the lesion with consent, measure dimensions and record symptom scores (pain and itch on 0–10 scales).
• Set out 27–30G needles with Luer-lock syringes (keloid tissue is dense and will leak under high back-pressure with slip-tip syringes), chlorhexidine or alcohol skin wipes, gauze and sharps disposal.
• Position the patient comfortably—supine for chest, prone for upper back, head supported on a pillow for ear lesions; warn about transient burning during injection and offer topical lidocaine or a cold pack first.

During the procedure

• Verify drug, dose and concentration with the prescribing clinician using a structured medication administration check.
• Stabilise the skin around the keloid; the injection plane is intralesional (into the dense scar), not subcutaneous.
• Aspirate before injecting in vascular sites (helix, glabella, alar rim, temple) to avoid intra-arterial steroid.
• Inject slowly until visible blanching is achieved across the lesion; a typical small earlobe lesion takes 0.1–0.3 mL of 10–20 mg/mL triamcinolone, larger chest lesions 0.5–2 mL of 20–40 mg/mL.
• Apply gentle pressure with gauze afterwards; document the volume injected, the concentration and the actual site.
• Monitor for vasovagal pre-syncope, particularly in adolescents; lower the head, raise the legs and reassess vital signs as needed.

Post-procedure and follow-up

• Counsel that mild burning and tenderness can persist for 24–48 hours; cool packs help.
• Possible side effects: skin atrophy, telangiectasia, hypopigmentation in dark skin, menstrual irregularity (rare) and very rarely adrenal suppression with high cumulative doses (e.g. >40 mg/week long-term).
• Schedule the next session in 4–6 weeks; advise the patient to contact the clinic if signs of infection, blistering or rapidly increasing pain develop in the interim.
• Continue silicone and pressure between sessions; document symptom and size response at every visit.
• Plan to step down to topical or longer-interval injections once symptoms resolve and the lesion plateaus.

Pregnancy and lactation

Keloids commonly become more pruritic and may enlarge slightly during pregnancy under hormonal influence. Defer elective intralesional therapy until after delivery and the early breastfeeding phase if possible. Silicone gel sheeting, pressure garments and short-term low-potency topical steroids are generally considered safe in pregnancy. Avoid 5-fluorouracil, bleomycin and methotrexate. Re-stage and re-plan in the early postpartum period; lesions that grew in pregnancy may regress modestly but rarely return fully to their pre-pregnancy size without intervention.

Paediatric considerations

Children and adolescents present unique challenges: they are in the peak-incidence age window, lesion sites (face, ears, anterior chest) are cosmetically prominent, and procedural tolerance is variable. Use lower triamcinolone concentrations (5–10 mg/mL) at smaller volumes, prioritise non-pharmacological measures (silicone, pressure earrings) and involve play specialists where injections are needed. Avoid radiation in patients under 18 years where alternatives exist. Active acne control in adolescence is one of the highest-yield prevention measures available.

Skin of color (Fitzpatrick IV–VI)

Patients of African, Asian, Hispanic and Black Caribbean heritage shoulder the bulk of keloid prevalence and bear the greatest risk of adverse cosmetic effects from treatment. Practical adaptations include: starting at lower triamcinolone concentrations (10–20 mg/mL) and stepping up only as needed; using verapamil or 5-FU when steroid atrophy or hypopigmentation is becoming a problem; preferring Nd:YAG over pulsed-dye laser to limit pigment alteration; using cryotherapy cautiously and combining it with intralesional steroid to limit hypopigmentation; and counselling explicitly on lifelong susceptibility, with practical guidance on avoiding helical piercings, treating acne early and protecting any new wound with silicone and tension-relieving closure.

• Document objectively at every visit. Use length × width × height in millimetres, photographs (with consent), pain and itch on 0–10 scales, and POSAS scores where the unit uses them. Trends matter more than single snapshots.
• Confirm the plan before each injection. Drug, concentration, total volume, allergy status, infection status, pregnancy status; a structured medication-administration check eliminates most preventable errors.
• Choose the right injection equipment. 27–30G needles with Luer-lock syringes—dense scar tissue will pop slip-tip syringes apart. Pre-filled cartridges reduce dose-calculation errors when available.
• Coach the silicone routine. Patients commonly under-use silicone (sub-therapeutic 4–6 hours/day). Teach a 12–24 hour daily target on intact, healed skin, with rotation breaks to prevent maceration; an explicit wound care teach with a written schedule improves adherence.
• Reassess pressure devices. Pressure earrings stretch and lose force; garments lose elasticity after 2–3 months of laundering. Re-fit and replace as needed to maintain 15–45 mmHg.
• Use a structured nursing handoff at each clinic transition: lesion size, current therapy step, last injection dose and date, planned next session, and any psychosocial flags.
• Track pain assessment trends. A rising pain score between sessions can flag superinfection, rapid growth or psychosocial decompensation—not just “waiting for the next injection”.
• Coordinate elective surgery proactively. Flag any keloid-prone patient on the pre-operative checklist; offer prophylactic silicone and pressure planning at discharge after sternotomy, caesarean section, mastoid or earlobe procedures.
• Mind infection control for intralesional procedures—single-dose vials where possible, sterile technique, never re-cap needles, and document every sharps event.
• Refer early when red flags appear. Atypical lesions, paediatric facial keloids, refractory symptoms, suspected DFSP and significant psychological distress all warrant same-week specialist contact.

At every clinic visit

• Lesion measurements (length × width × height) and high-quality photograph with consent and date stamp.
• Pain and itch scores (0–10) compared with baseline and previous visit.
• Functional impact: joint range of motion, ability to wear earrings, dyspareunia, cosmetic distress.
• Adjuvant adherence: silicone hours/day, pressure garment hours/day, topical regimen.
• Side effects of previous injections: skin thinning, hypopigmentation, telangiectasia, menstrual change.
• Mood and psychosocial status; safety screening when distress is significant.

During an intralesional injection visit

• Vital signs, particularly in adolescents and anxious patients—vasovagal episodes are common at first injection.
• Pre-procedure timeout: drug, dilution, dose, site, allergy and infection check confirmed verbally.
• Observe for blanching of the lesion as injection progresses; stop if blanching extends well beyond the keloid.
• Post-injection: gauze pressure, observation for 5–10 minutes, written aftercare advice, scheduled review date.

Red flags requiring escalation

• Spreading erythema, increasing pain, fever or purulent drainage from an injected or excised lesion—suspect superinfection and start the local cellulitis pathway.
• Rapid lesion growth without preceding trauma, ulceration or bleeding—biopsy to exclude DFSP, carcinoma or aggressive variant.
• New paraesthesia, weakness or restricted joint movement after injection—consider intra-tissue spread or injection-related complication.
• Signs of systemic steroid effect (Cushingoid features, glucose dysregulation, menstrual irregularity, mood change) in patients receiving frequent or high-dose intralesional therapy.
• Recurrence within 3 months of treatment completion—re-treat early; mature recurrences respond far less well.
• Suicidal ideation, severe body-image distress or social withdrawal—refer for psychological support.

Direct from the keloid

• Persistent pruritus and pain—often the dominant patient-reported burden.
• Restricted joint movement when the lesion overlies a joint or major muscle group.
• Cosmetic disfigurement, particularly facial, anterior chest and earlobe lesions; significant psychological impact in adolescents and young adults.
• Secondary bacterial infection of macerated, scratched or ulcerated lesions—staphylococcal cellulitis is the most common downstream event.
• Sleep disturbance and daytime fatigue from pruritus or pressure-related discomfort.

From treatment

• Intralesional steroid: skin atrophy, telangiectasia, hypopigmentation in skin of color, peri-lesional fat atrophy, very rare adrenal suppression with high cumulative dose, vasovagal syncope at injection.
• Cryotherapy: pain, blistering, prolonged hypopigmentation (especially in Fitzpatrick IV–VI), delayed healing.
• Surgical excision: 45–100% recurrence risk if unaided, often regrowing larger; new wound infection; widening of scar.
• Radiation therapy: peeling, prolonged pigment change, telangiectasia, rare reports of radiation-induced malignancy in adjacent tissues over the long term.
• 5-Fluorouracil and bleomycin: local hyperpigmentation, ulceration, transient leucopenia with high cumulative doses; bleomycin carries very rare pulmonary fibrosis risk at much higher systemic doses than used intralesionally.
• Laser: pigmentary changes, blistering and rare scarring at higher fluences.
• Topical agents (steroids, tacrolimus, imiquimod): local irritation, pigment change, infection risk if applied over broken skin.

Prevention has the largest practical impact for keloid-prone patients—every clinical interaction is a chance to reduce future lesion burden. The highest-yield levers are:

• Avoid elective skin trauma in known keloid-formers. Counsel against helical and cartilage piercings, multiple ear piercings, decorative scarification, and elective tattoos in younger keloid-prone patients.
• Treat acne early and effectively. Aggressive management of nodulocystic acne reduces post-acne keloid formation on the chest, shoulders and jawline.
• Engineer surgical wounds for low tension. Place incisions along Langer lines where possible; use deep dermal and subcuticular sutures; tape or silicone strips for 8–12 weeks after suture removal in keloid-prone patients undergoing elective surgery.
• Apply silicone gel sheeting prophylactically over high-risk healed wounds (sternotomy, caesarean section, shoulder and ear surgery) once full re-epithelialisation is confirmed—12–24 hours/day for 2–3 months.
• Use pressure on amenable sites—pressure earrings after lobe surgery, custom garments after thoracic and limb surgery in burn-care pathways.
• Treat early scar warning signs. A red, raised, itchy scar at week 4–8 is the optimum window for a single early intralesional injection or aggressive silicone/pressure use—small, immature lesions respond far better than mature keloids.
• Counsel on re-piercing and re-tattooing. Re-injuring a previously keloid-affected site almost guarantees recurrence; honest conversation before any procedure prevents avoidable harm.
• Manage comorbid skin disease—folliculitis, hidradenitis, ingrown hairs along the beard line and chronic eczema with excoriation all add cumulative dermal trauma.

Prognosis is mixed and honest counselling is critical. Approximately 50–80% of keloids shrink with a series of intralesional triamcinolone injections, but many regrow within five years; combined excision plus adjuvant therapy (intralesional steroid, silicone, pressure or superficial radiation) reduces recurrence to roughly 10–30% in published series. Pure surgical excision recurs in 45–100% of cases and should be reserved for combination strategies. Most recurrences appear within the first year after treatment, with the majority before five years; lifelong susceptibility means new lesions can develop at fresh sites.

Symptom relief usually outpaces cosmetic flattening: pruritus and pain typically improve after the second or third injection, while visible reduction in height and surface area lags by several sessions. A patient who walks out of clinic itch-free but with a still-prominent scar is a treatment success in progress, not a failure. Maturation of any treated scar continues for 12–24 months, and ongoing silicone, pressure and trigger-avoidance support the long arc of remodelling. Set the expectation explicitly that keloid management is a maintenance endeavour rather than a one-shot cure.

Subtle deterioration

The keloid that is quietly worsening rarely complains loudly. Watch for the cluster: a lesion that has crept beyond its previous photo border, a darker peripheral halo, a new pinpoint scab from scratching at night, a patient who has stopped coming back for sessions “because it didn’t help” when in fact symptoms had been improving. A scheduled phone or text follow-up between visits often catches drift before it becomes loss to follow-up.

Communication friction

Keloid patients—particularly skin-of-color patients—often arrive having been told for years that their scarring is “just scarring” or that nothing can be done. Acknowledge the impact, validate the previous experience, and outline a structured plan with realistic milestones. Be honest that complete eradication is rarely possible but that symptom control, slowing growth and modest cosmetic improvement are achievable in most patients with a layered approach. Avoid promising flat skin from a single injection.

Bedside checklist

• Photograph and measure at every visit; trends decide whether the plan is working.
• Confirm silicone hours/day and pressure garment use—numerically, not “yes I’m using it”.
• Re-take the trigger history each visit (new piercings, new acne flare, new tattoos).
• Reconcile medications—new ACE inhibitors, isotretinoin, immunomodulators or chemotherapeutics may modify scarring biology.
• Schedule the next session and the next milestone review at clinic exit—open-ended waiting fuels disengagement.
• Loop in psychological support early when distress is significant; the burden is real and often underestimated.

Initial bundle: ABCDE primary survey if systemically unwell, IV access, vital signs and capillary glucose, paired bloods (FBC, CRP, U&E, glucose) plus blood cultures and a wound swab if infection suspected. Stop the injection schedule, photograph the lesion, document the timeline of symptoms, and escalate to dermatology, plastic surgery or critical care as the picture evolves. Never assume that a tender, erythematous keloid is simply “post-injection inflammation” without ruling out infection.

These NCLEX-style clinical judgment practice items focus on the nursing priorities for this condition — recognise cues, escalate red flags, take safe action and evaluate outcomes (NCSBN Clinical Judgment Measurement Model) — through Priority FIRST, SATA, deterioration trends, multi-patient triage, ordered response, matrix matching and cloze completion on the topic of keloid recognition, intralesional steroid technique, post-excision adjuvant planning and red-flag escalation—matched to Clinical Judgment Measurement Model layering of cues before action.