Cutaneous squamous-cell carcinoma

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Record growth rate, pain, bleeding, ulceration, previous field treatment, scar or ulcer duration, immune state and prior cancers. Measure the lesion and palpate depth, fixation, named nerves and nodes. In darker skin, SCC has a greater proportional association with chronic scars and inflammation and may arise at non-sun-exposed sites; delayed recognition worsens stage.

Clinical recognition cannot reliably establish invasion depth. Urgent specialist biopsy should include adequate dermis and the most indurated area without compromising definitive surgery. Histology records differentiation, depth, level, perineural or lymphovascular invasion, subtype and margins. Pathological high-risk features determine wider excision, Mohs, imaging, nodal evaluation or adjuvant radiotherapy discussion.

Prevention continues after removal. Treat surrounding actinic field change, support sun protection and self-examination and coordinate transplant or haematology teams when immune suppression is modifiable. New neurological symptoms or a draining-basin node after treatment is an urgent recurrence signal, not a routine follow-up issue.

Key points

Suspect SCC in a persistent enlarging tender indurated keratotic, crusted or ulcerated lesion, particularly on chronically sun-exposed skin.
NICE recommends urgent suspected-cancer referral for every lesion clinically suspicious for cutaneous SCC.
High-risk features include lip or ear site, diameter over 2 cm, depth over 6 mm or beyond subcutaneous fat, poor differentiation, perineural invasion, recurrence and immune suppression.
Palpate the relevant nodal basin and document pain, numbness or weakness because clinical perineural and nodal disease alter urgency and staging.
Excision with histological margin assessment is standard; Mohs or wider specialist surgery is considered for high-risk, recurrent or tissue-critical tumours.
Do not curette, freeze or treat with field cream when invasive SCC is plausible; these approaches can delay depth and margin diagnosis.
A cutaneous horn is a reaction pattern, not a diagnosis; assess and sample the indurated base where SCC may be present.
Immune-suppressed patients need a lower biopsy threshold, rapid pathways and multidisciplinary review of prevention and immunosuppression.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Cumulative ultraviolet injury

Long-term ultraviolet exposure produces keratinocyte mutations and field cancerisation, especially on scalp, face, ears, lips and dorsal hands.

Immune suppression

Solid-organ transplantation, haematological malignancy and long-term immunosuppressive medicines greatly increase SCC incidence, multiplicity, recurrence and aggressive behaviour.

Chronic inflammation and scar

Burn scars, non-healing ulcers, draining sinuses, radiation sites and chronic inflammatory dermatoses can develop biologically aggressive SCC.

Oncogenic and chemical exposures

High-risk HPV at selected anogenital or periungual sites, arsenic and occupational carcinogens contribute to particular tumours.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Keratinocyte dysplasia
Accumulating mutations progress from actinic keratosis or in-situ disease to atypical keratinocytes invading through basement membrane.
2
Destructive dermal invasion
Tumour nests produce keratin and infiltrate dermis, creating an indurated scaly, crusted, ulcerated or horn-forming lesion.
3
Perineural spread
Cancer tracks along nerves and causes disproportionate pain, paraesthesia, numbness or motor deficit with increased recurrence risk.
4
Lymphatic metastasis
High-risk tumours spread to regional nodes, with risk shaped by site, diameter, depth, differentiation, nerve invasion and immune state.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Indurated keratotic lesion

A firm tender papule, plaque or nodule has adherent scale, keratin, crust or a central ulcer and progressively enlarges.

Cutaneous horn base

A conical keratin projection with a thick, painful or indurated base raises concern for invasive SCC beneath it.

Lip or ear tumourRed flag

Persistent keratotic ulceration on vermilion lip or pinna carries higher metastatic risk and demands urgent referral.

Perineural symptomsRed flag

Pain, tingling, numbness, facial weakness or other motor loss near a lesion suggests nerve invasion.

Nodal diseaseRed flag

A new firm regional node, parotid mass or in-transit nodule may represent metastasis and requires urgent imaging and sampling.

Red flags requiring action

Rapid growth, severe pain, numbness, fixation, recurrent tumour, lip or ear site, diameter over 2 cm, immune suppression, palpable nodes or chronic-scar ulceration requires urgent suspected-cancer referral and high-risk staging.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Deep representative biopsyFirst step
Why
Confirm SCC and measure invasive and pathological risk features.
Interpretation and limitations
Include sufficient dermis from the indurated component; a superficial shave may show dysplasia but miss invasion.
02
Histopathological risk report
Why
Record diameter, depth, differentiation, invasion plane, nerves, vessels and margins.
Interpretation and limitations
High-risk features are combined rather than judged from one item and should trigger multidisciplinary management.
03
Regional-node examination and ultrasound
Why
Detect nodal spread in high-risk or clinically suspicious disease.
Interpretation and limitations
Ultrasound-guided cytology or core biopsy confirms suspicious nodes; normal palpation does not exclude microscopic disease.
04
MRI or CT
Why
Assess clinical perineural, bone, deep soft-tissue or nodal extension.
Interpretation and limitations
Choose imaging by anatomy and multidisciplinary advice; MRI is particularly useful for named-nerve spread.
05
Immune and field-risk review
Why
Identify transplant, haematological, medicine and chronic-wound factors that change surveillance.
Interpretation and limitations
Do not independently reduce essential immunosuppression; coordinate risk modification with the treating specialty.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Keratoacanthoma

A rapidly growing symmetrical crateriform nodule may regress, but cannot be reliably separated from SCC and is managed as malignant until histology.

Actinic keratosis and Bowen disease

Rough macules and well-demarcated in-situ plaques lack proven dermal invasion but may harbour or progress to invasive SCC.

Basal-cell carcinoma

A pearly rolled border with arborising vessels suggests BCC, while keratin, tenderness and faster growth favour SCC.

Inflamed seborrhoeic keratosis

A stuck-on lesion can crust and itch, but persistent induration, ulceration or growth requires biopsy rather than reassurance.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Suspected SCCRefer every invasive suspicion urgentlyFirst stepA persistent indurated keratotic, ulcerated or rapidly growing lesion could represent invasive SCC.

1Measure and document morphology, growth, site, immune status, neurological symptoms and regional nodes.
2DefinitiveMake an urgent suspected-cancer referral, leaving the lesion available for appropriately deep biopsy and definitive planning.
3Safety-net accelerated growth, bleeding, pain, numbness or nodes and track attendance and pathology outcome.

02Confirmed high-risk SCCStage and control marginsHistology or clinical context shows high-risk site, size, depth, subtype, nerve involvement, recurrence or immune suppression.

1Discuss in the specialist multidisciplinary team and image nerves, bone or nodes where indicated.
2Use margin-controlled or specialist excision and assess need for nodal treatment or adjuvant radiotherapy.
3Coordinate immune-risk modification and establish more intensive scar, node and whole-skin surveillance.

03Possible recurrence or metastasisEscalate scar, nerve and node changeEscalationA treated patient develops scar induration, ulceration, neurological symptoms or a draining-basin mass.

1Arrange urgent examination of scar, nerves, in-transit skin and nodes and retrieve prior pathology and margins.
2Biopsy the suspicious lesion or node and obtain anatomy-directed imaging.
3Return confirmed disease to the skin-cancer multidisciplinary team for surgery, radiotherapy, systemic treatment and supportive care.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Local tissue destruction

Invasion of cartilage, bone, lip, ear, eyelid or digit can impair function and require major reconstructive surgery.

Regional nodal metastasis

Firm nodes in parotid, cervical, axillary, epitrochlear or inguinal basins may represent spread and change stage and treatment.

Perineural disease

Clinical or microscopic nerve invasion increases local recurrence and can extend toward skull base with pain or cranial neuropathy.

Multiple future tumours

Field cancerisation and ongoing immune or ultraviolet risk lead to additional SCC, BCC and actinic keratoses.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Confirm that pathology documents depth, differentiation, perineural or lymphovascular invasion and margin status.
At follow-up examine scar, in-transit pathway and nodal basin and ask about pain, numbness and weakness.
Perform whole-skin surveillance proportional to immune status, tumour burden and field cancerisation.
Teach rapid self-referral for a new growing keratotic lesion, non-healing ulcer, scar nodule or lymph node.
Coordinate transplant, haematology or rheumatology teams before any immunosuppression change.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Tenderness is informative

Pain in a keratotic lesion raises invasive and perineural concern rather than proving simple inflammation.

The horn hides histology

Risk resides in the lesion beneath a keratin horn, so the base needs diagnostic assessment.

Depth beats surface

A modest-looking lesion invading beyond subcutaneous fat can be higher risk than a broad in-situ plaque.

Nodes follow anatomy

Scalp and facial tumours may drain to parotid or cervical nodes, while limbs use axillary, epitrochlear or inguinal basins.

11Common pitfallsFrequent interpretation and management errors.

01
Using a routine referral because the lesion resembles a keratoacanthoma despite inability to exclude SCC.
02
Taking a superficial sample that cannot assess invasion depth.
03
Failing to palpate regional nodes or ask about sensory change.
04
Treating a cutaneous horn with cryotherapy without diagnosing its base.
05
Assuming SCC in darker skin must be on sun-exposed skin and missing a chronic-scar lesion.