Erythema ab igne

Meet the patient

A 24-year-old software engineer is referred to dermatology for a "bruise" on both anterior thighs that will not fade. It is net-like, brownish-purple, and fixed — press a glass slide to it and it does not blanch. She has spent the last four months with a gaming laptop on her lap for six hours a day, and she is worried it is cancer.[4]

The two questions that settle this consult are the two that settle every erythema ab igne: what is the heat source? (the history answers it in thirty seconds) and is there a new nodule or ulcer inside it? (your eyes and a biopsy answer it). Hold those two and the condition practically diagnoses itself.[1]

The thermal window — 43 to 47 degrees, the danger zone

Erythema ab igne is what happens in the narrow band between harmless warmth and an outright burn. Skin held at roughly 43 to 47 degrees Celsius for hours, day after day, injures the endothelium of the subpapillary venous plexus and the basal keratinocytes — but never coagulates tissue wholesale, which is why it does not blister the way a thermal burn does.[1]

The name is the diagnosis: Latin erythema (redness), ab (from), igne (fire) — "redness from fire." It also travels as toasted skin syndrome, fire stains, and, once it turns keratotic, thermal keratosis.[3]

The classic trap: reaching for the burn pathway when there is no blister. The rare bullae of advanced EAI are an atrophic epidermis peeling off a devitalised base, not acute coagulative necrosis — treat the heat source, not the burn.[1]

From the hearth to the laptop — a disease that never left

EAI was the dermatological signature of the pre-central-heating era, and it came back with the laptop. Before central heating it marked elderly women, tuberculosis and chronic-arthritis sufferers who huddled for hours beside open fires, pot-bellied stoves and hot brick walls. Central heating nearly retired it — then the laptop, the heating pad and the heated car seat brought it roaring back.[1]

Why the clinician cares is a list of three, and the third is the one that kills:[1]

• It is a sentinel. Find the heat source, then find the reason the patient is seeking heat — chronic pain, hypothyroidism, malignancy with cachexia, neurological disease, fuel poverty.
• It can turn malignant. Late thermal keratosis is a histological mimic of actinic keratosis and carries a small but real risk of squamous cell carcinoma.
• The pigment is permanent. The early lesion reverses; the late atrophy and pigmentation do not, so prevention is the only effective intervention.[1]

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Three stages — reversible, sticky, permanent

Stage predicts everything worth predicting: whether the lesion will fade, and whether you need to biopsy. Classify along two axes — clinical stage, which predicts reversibility, and heat source, which directs prevention — and use both.[1]

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Stage 1 is essentially invisible to history — the patient does not notice it. Stage 2 is when most present, alarmed by the cosmetic change. Stage 3 is when the condition stops being a curiosity and becomes a premalignant dermatosis.[1]

Name the source — the HEAT mnemonic

The distribution always matches the heat source, so naming the source names the diagnosis.[1]

[1] [1]

In practice the four buckets collapse to two demographics: young adults with laptops, and the elderly in pain.[4]

A careful history of everyday heat exposure is the single most important diagnostic step — ask specifically about lap-use hours and vent position, heating-pad setting and duration, hot water bottles and the symptom they treat, heated car seats, occupational proximity to ovens and furnaces, and sitting close to fires and radiators.[1]

Who seeks the heat — the sentinel sign

EAI is often a cutaneous clue to a treatable underlying condition, and missing the driver is the bigger error.[1]

The demographics fall into four clean groups:[1]

• Young adults (15 to 35) — laptop-induced, anterior thighs, often bilateral. Students, software professionals, gamers; slightly more women.
• Elderly (over 65) — pain- and cold-intolerance-driven, lower back. Heating pads and radiators; elderly women living alone are over-represented.
• Children and adolescents — rising with gaming laptops, tablets and heated blankets; often misdiagnosed as bruising, Mongolian spot or child abuse.[5]
• Occupational — middle-aged foundry, glass, bakery and kitchen workers; forearms, dorsal hands, face and neck, often bilateral and symmetric.

When there is no obvious external source, the skin is pointing at the patient:[1]

[1]

The injury cascade — why a net appears under the skin

The net-like pattern is the anatomy of the subpapillary venous plexus made visible by injury. Unlike ultraviolet light, which damages DNA directly, infrared heat damages tissue thermally — denaturing proteins, destabilising membranes and lighting a chronic low-grade inflammatory fire. The plexus absorbs the brunt, and the pigment traces its geometry.[1]

Five steps take a warm thigh to a permanent stain:[1]

1. Endothelial injury. Repeated vasodilation of the subpapillary venous plexus brings endothelial swelling, a perivascular lymphocytic infiltrate and red-cell extravasation. The earliest change is purely vascular — transient, blanching, reticular erythema, reversible within days.
2. Haemosiderin deposition. Extravasated red cells are phagocytosed by dermal macrophages and broken down to haemosiderin — a golden-brown iron complex that persists indefinitely and stains Prussian blue positive. This is the reddish-brown component of the net.
3. Melanin incontinence. Heat-damaged basal keratinocytes lose their grip on melanin; granules spill into the upper dermis and are engulfed by melanophages — the same mechanism as lichen planus and fixed drug eruption, and the reason the brown pigment is so stubborn.
4. Thermal keratosis. The basal layer grows atypical, hyperchromatic keratinocytes — histologically indistinguishable from actinic keratosis — and over years can climb through SCC in situ (Bowen disease) to invasive SCC.[2]
5. Late atrophy and telangiectasia. Epidermis thins, dermis shows elastosis, telangiectasia appears, and the whole picture becomes poikiloderma — atrophy plus telangiectasia plus pigmentation — the same pattern as chronic radiation dermatitis.[1]

The net itself is the dermatological fingerprint: each ring is the watershed around a dermal papilla, and heat damages the venous ends preferentially, so the pigment traces the venous pattern.[1]

Livedo reticularis shares the anatomy but not the disease. Livedo is vascular and reversible — constricted venules holding deoxygenated blood; EAI is pigmentary and fixed — haemosiderin and melanin welded into the dermis. Diascopy is the discriminator: livedo blanches, EAI does not.[1]

Spot it from across the room — the clinical triad

EAI is one of the few diagnoses you can call from the end of the bed. The triad is reticular brownish-purple hyperpigmentation, a distribution that matches a recognisable heat source, and a history of chronic moderate heat exposure.[3]

The lesion is always sharply demarcated to the heat-exposed area — there is no gradual fade into surrounding skin. A clear geometric border is diagnostic gold: the rectangular imprint of a laptop base, the curved edge of a heating pad.[1]

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Asymptomatic is the rule — most notice the cosmetic change and feel nothing. Mild burning, pruritus or paraesthesia can occur; a developing SCC turns tender, bleeding or non-healing.[1]

The timeline an examiner wants verbatim: onset over weeks to months (laptop EAI after roughly 2 to 6 months of daily use for several hours); stage 1 fades in days to weeks; stage 2 lightens over months but may stain permanently; stage 3 is permanent. Malignant transformation needs years — SCC is reported in lesions present over 5 years, often over 10 to 30.[2]

The differential — blanch it, then think

One bedside test, the blanching test, splits the net-like lesions into two families. Press a glass slide to the lesion. Livedo reticularis blanches because it is vascular; EAI does not because the pigment is fixed in the dermis. With that single move the differential collapses.[1]

The mimics, by category:[1]

• Livedo reticularis and cutis marmorata — the big one. Violaceous, blue-purple, blanches on warming. Physiological cutis marmorata in infants and children resolves within minutes of warming and is never pigmented. Secondary livedo points at antiphospholipid syndrome, polyarteritis nodosa, Sneddon syndrome or cryoglobulinaemia.
• Livedoid vasculopathy — painful, ulcerative, thrombo-occlusive, often with prothrombotic states; heals with white atrophie blanche scars. The pain and the scars are absent in EAI.
• Cutaneous small-vessel vasculitis — palpable purpura on the dependent lower legs, non-blanching but papular and palpable, often with systemic symptoms. Not strictly reticular.
• Erythema multiforme — target lesions, three concentric zones, palms, soles and mucosa; acute over 24 to 48 hours. Not reticular.
• Contact dermatitis — eczematous, pruritic, sharply demarcated to the contact area but with no net pattern.
• Poikiloderma — atrophy plus telangiectasia plus mottled pigment; late EAI essentially is a heat-induced poikiloderma. Distinguish by the heat history and the early reticular phase before atrophy dominates.
• Post-inflammatory hyperpigmentation — diffuse or patchy, not reticular, following a preceding rash.
• Fixed drug eruption — round, well-demarcated, recurs at the same site with each dose (NSAIDs, sulfonamides, paracetamol).
• Solar lentigo and actinic keratosis — sun-exposed, single papule or macule, not reticular.
• Addison disease — diffuse generalised hyperpigmentation, palmar creases, oral mucosa; not reticular.[1]

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The one-line discriminator: blanching points to vascular (livedo); fixed pigment points to EAI; palpable purpura points to vasculitis; a target points to erythema multiforme.[1]

The bedside — find the source, find the why

EAI is a clinical diagnosis; the history does the work and the skin points at the patient. Two goals at the bedside — confirm the diagnosis by naming the heat source, and hunt for the reason the patient is seeking heat.[1]

The heat-source question is the single most important one you will ask. Cover lap-use hours and vent position, heating-pad setting and duration, hot water bottles and the symptom they treat, heated car seats, occupational heat, and proximity to fires and radiators. Then run the system review — weight loss, cold intolerance, constipation and dry skin for hypothyroidism; night pain and cachexia for malignancy.[1]

Diascopy is the key bedside manoeuvre: livedo blanches, EAI does not. Combined with the heat history, it usually confirms the call.[1]

On examination, match the morphology to the stage, check the geometric border, palpate for induration (the sign of SCC), and never skip the general exam — bradycardia and slow-relaxing reflexes for hypothyroidism, cachexia for malignancy, joint deformity for the pain driving the heat-seeking.[1]

Investigations — usually none, sometimes a biopsy

In the typical case you investigate nothing; the triad is enough. Reach for tests only when the presentation is atypical, when you suspect a systemic driver, or when a chronic lesion grows a nodule.[1]

Biopsy is the one investigation that matters, and its histology tracks the stage:[2]

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The biopsy pearl: Prussian blue stains the haemosiderin positive and the melanin negative — the single stain that separates the two pigments welding the net together. Thermal keratosis is histologically indistinguishable from actinic keratosis, which is exactly why a keratotic plaque in an EAI field is managed like an actinic keratosis.[2]

When EAI appears without a source, investigate the driver — TSH and free T4 for hypothyroidism, full blood count and ferritin for anaemia, an autoimmune screen if poikiloderma suggests lupus or dermatomyositis, a thrombophilia screen if livedoid vasculopathy is in play, and imaging if cachexia or night pain suggests occult malignancy.[1]

Kill the heat — the one intervention that matters

Eliminate the heat source. It is both the resuscitative and the definitive treatment, and there is no pharmacological substitute. The earlier the heat goes, the more likely the lesion resolves completely.[1]

Counsel to the source, specifically:[1]

• Laptop — desk or lap desk, never on bare skin, breaks every hour; gaming laptops run hottest, so counsel explicitly.
• Heating pad — lower setting, no overnight use, a towel between pad and skin; treat the underlying pain or the pad comes straight back.
• Hot water bottle — wrapped in cloth, 15 to 20 minutes per session, never applied directly to skin.
• Heated car seat — lowest setting, off periodically on long drives.
• Space heater or fire — at least one metre of distance; sit to the side rather than face-on.[1]

For acute symptoms, a cool compress and an emollient suffice while the heat source goes. Topical corticosteroids are not indicated for EAI itself: they do not help, and they can mask an early SCC.[1]

The classic trap: missing a coexisting full-thickness burn in the neuropathic, paraplegic or demented patient who cannot report early discomfort. Examine for blistering and eschar before you reassure.[1]

If the EAI field turns warm, swollen, spreading and febrile, that is secondary cellulitis — treat with oral flucloxacillin 500 mg four times daily for 5 to 7 days (or cephalexin 500 mg four times daily; clindamycin if penicillin-allergic; add MRSA cover with doxycycline or vancomycin if risk factors).[1]

Fade the pigment, burn the keratosis

After the heat goes, treatment splits into two jobs: cosmetic for the pigment, premalignant for the keratosis. Residual hyperpigmentation takes months to fade and may never fully resolve; thermal keratosis needs field therapy identical to actinic keratosis.[1]

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Sun protection is non-negotiable — UV deepens any residual pigment, so daily broad-spectrum sunscreen SPF 30 or higher, cloudy days included.[1]

If biopsy confirms thermal keratosis, field-treat it exactly as you would an actinic keratosis:[2]

• 5-fluorouracil 5 per cent cream twice daily for 2 to 4 weeks — the standard; expect inflammation, erosion and crusting as the dysplastic keratinocytes die, then healing over 2 to 4 weeks after cessation.
• Imiquimod 5 per cent two to three times weekly for 4 to 16 weeks as an alternative immune modifier.
• Cryotherapy with liquid nitrogen for isolated focal keratoses.
• Photodynamic therapy with aminolaevulinic acid or methyl aminolaevulinate for field therapy of multiple keratoses.[1]

When SCC moves in — cut it out

A new nodule, ulcer, induration or non-healing erosion inside a longstanding EAI field is SCC until proven otherwise — biopsy, do not watch.[2]

• Incisional or excisional biopsy of the suspicious area to confirm invasive atypical squamous epithelium infiltrating the dermis.
• Surgical excision with a 4 to 6 mm margin for low-risk SCC (under 2 cm diameter, well-differentiated, under 2 mm depth).
• Mohs micrographic surgery for high-risk SCC — face, ears, periocular, perinasal, large, deeply invasive, poorly differentiated or recurrent.
• Regional node dissection if nodal disease is suspected; radiotherapy for inoperable tumours or patients unfit for surgery.[1]

Treat the why — the skin is pointing at the patient

EAI is frequently a clue to a treatable underlying condition; the lesion fades only when the reason for the heat-seeking is addressed.[1]

• Chronic pain (osteoarthritis, low back pain, fibromyalgia, endometriosis) — refer to pain management, rheumatology or gynaecology; optimise analgesia, physiotherapy, intra-articular steroids or surgery.
• Hypothyroidism — check TSH and free T4; treat with levothyroxine (typical starting dose 1.6 micrograms per kg daily, titrated to TSH). The EAI fades only once euthyroid and the heat-seeking stops.
• Cachexia or weight loss — imaging, tumour markers and tissue diagnosis; refer to oncology; the EAI may be an early clue to occult cancer.
• Neurological disease — occupational therapy for positioning and protective devices.
• Fuel poverty — refer to social services.[1]

The five faces of EAI

The same disease wears five demographic masks; the mask decides the counselling and the surveillance intensity.[1]

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The paediatric trap deserves its own line: a fixed, reticular, brownish-purple patch on a child's thigh is EAI from a gaming device, not a bruise — but if the heat history is inconsistent, escalate to multidisciplinary review for non-accidental injury.[5]

Special populations — the ones who need different rules

Pregnancy and immunosuppression change the drug list and the surveillance interval.[1]

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The trap door — pitfalls that cost patients

Six complications, and the first is the only one that kills.[2]

1. Squamous cell carcinoma — arises in thermal keratosis in longstanding (over 5 years, often 10 to 30) lesions; small but real risk; any new nodule, ulcer or induration must be biopsied.
2. Permanent hyperpigmentation and atrophy — stage 3 changes do not improve with treatment.
3. Thermal burn — coexisting full-thickness injury in the neuropathic or demented patient.
4. Cellulitis — fissured atrophic skin is a portal for staphylococci and streptococci.
5. Psychological distress — the cosmetic change, especially in young women with thigh EAI, can be significant; address it explicitly.
6. Missed underlying disease — EAI is a sentinel; failing to investigate the driver is the recurring error.[1]

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Consultant confession: the patient who returns with advanced EAI is almost always the one whose pain was never controlled. Treat the joint, the thyroid, the malignancy — or the pad comes back, and so eventually does the SCC.[1]

Prognosis — stage decides everything

The prognosis is decided entirely by the stage at which the heat source is eliminated.[3]

• Stage 1 — fully reversible within days to weeks; no residual pigment.
• Stage 2 — improves over months; may leave permanent pigment, particularly in darker-skinned individuals.
• Stage 3 — permanent; thermal keratosis needs active treatment (5-FU, cryotherapy, PDT) and lifelong SCC surveillance.[1]

The predictors of malignant transformation are duration over 5 years, thermal keratosis on biopsy, late atrophic changes, immunosuppression and coexisting UV damage (additive carcinogenesis). Patients with any of these are reviewed every 6 to 12 months indefinitely, with education on self-examination and the red-flag features that mandate urgent review.[2]

Evidence and regional differences

There is no single international guideline for EAI; practice follows narrative reviews and the actinic-keratosis playbook applied to thermal keratosis.[1]

The evidence base is limited — case reports, case series and narrative reviews, with no randomised trials. Harview and Krenitsky (2023) is the modern clinical synthesis; Wilder and colleagues (2021) anchored the malignant-transformation risk; Kucuktas and colleagues (2010) established the laptop epidemiology; and Poddighe and colleagues (2023) mapped the paediatric rise and its diagnostic pitfalls.[1]

[1]

The open questions: no RCTs back the retinoids (use is empirical); laser therapy (Q-switched ruby, intense pulsed light, fractional) appears only in small case series for refractory pigment; there is no consensus on the SCC surveillance interval (most use 6 to 12 monthly); and opinion divides over whether all thermal keratoses warrant prophylactic 5-FU or only biopsy-confirmed dysplasia.[1]

Exam pearls

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Ward-round test — three stems, thirty seconds each

Stem 1 — the bruise that will not fade (answer)

A 22-year-old student has a fixed, brownish-purple, net-like patch on both anterior thighs for three months. It does not blanch. What is the diagnosis, the bedside test, and the first treatment? Model: This is classic erythema ab igne from laptop use on the lap — reticular, fixed, non-blanching hyperpigmentation in the heat-exposed distribution. The bedside test is diascopy: livedo reticularis blanches, EAI does not. The first treatment is to eliminate the heat source — move the laptop to a desk or lap desk. No drug works without this.[4]

Stem 2 — the nodule in the old stain (answer)

A 78-year-old with a 12-year history of heating-pad EAI on the lower back presents with a new, tender, non-healing nodule inside the pigmented field. What do you do, and why? Model: This is SCC until proven otherwise — a new nodule or ulcer in a longstanding (over 5 years) EAI field arising in thermal keratosis. Arrange urgent incisional or excisional biopsy, then surgical excision with a 4 to 6 mm margin for low-risk SCC or Mohs for a high-risk site. Do not watch and wait.[2]

Stem 3 — the net without a heat source (answer)

A 68-year-old woman has bilateral reticular brownish-purple pigmentation on her shins but denies any heat source. She is tired, cold, constipated and gaining weight. What is the next investigation? Model: The EAI is a sentinel for an underlying driver — her fatigue, cold intolerance, constipation and weight gain point straight at hypothyroidism driving heat-seeking behaviour. Check TSH and free T4 and treat with levothyroxine. The EAI fades only once euthyroid and the heat-seeking ceases; also screen for anaemia and occult malignancy if the picture does not fit.[1]

References

1. [1]Harview CL, Krenitsky A. Erythema Ab Igne: A Clinical Review Cutis, 2023.PMID 37289686
2. [2]Wilder EG, Frieder JH, Menter MA. Erythema Ab Igne and Malignant Transformation to Squamous Cell Carcinoma Cutis, 2021.PMID 33651859
3. [3]Miller K, Hunt R, Chu J, et al. Erythema ab igne Dermatol Online J, 2011.PMID 22031654
4. [4]Küçüktaş M, Demirkesen C, Aslan C, Aydemir EH. Laptop-induced erythema ab igne Clin Exp Dermatol, 2010.PMID 20089079
5. [5]Poddighe D, Assylbekova M, Almukhamedova Z, Aman A, Mukusheva Z. Pediatric erythema ab igne: clinical aspects and diagnostic issues Eur J Pediatr, 2023.PMID 37661206