Synopsis
Diagnose cutaneous small-vessel vasculitis through lesion chronology and clinicopathological correlation, protect ulcerated skin, identify removable triggers, and recognise when the eruption is a marker of systemic disease.
- Cutaneous small-vessel vasculitis is a clinicopathological pattern of inflamed superficial dermal vessels, most often presenting as symmetrical palpable purpura on dependent legs.
- Describe crops, age, elevation, blistering, pustules, ulcers and residual pigment; confluent angular necrosis suggests an occlusive vasculopathy or deeper-vessel process instead.
- A dermatology assessment links each visible lesion to the sample required: a newly developed intact papule for full-depth H&E and a separate very early lesion for direct immunofluorescence.
- Histological leukocytoclasis confirms damaged small vessels but cannot by itself identify medicine, infection, IgA, connective-tissue, clonal or idiopathic causation.
- At presentation measure blood pressure and obtain urine, FBC, renal and liver profiles and inflammatory markers; organ symptoms or recurrent disease justify a broader directed screen.
- Review every medicine and intermittent exposure against the eruption date, but do not stop an essential treatment without agreeing an alternative and recording the suspected reaction precisely.
- First-line care for a mild skin-restricted episode is removal or treatment of the driver, temporary reduction in dependency, elevation, emollient, non-adherent dressings and safe analgesia.
- Compression may help hydrostatic recurrence only after arterial sufficiency and acute inflammation are assessed; antibiotics are for clinical infection, not a positive swab from a colonised ulcer.
- Repeated, painful or ulcerative crops need dermatology-led steroid-sparing treatment; systemic immune therapy belongs to severe skin disease or a defined organ vasculitis pathway.
Key red flags
Toxic illness, rapidly advancing purpura, severe pain, necrosis, haemorrhagic bullae, proteinuria or haematuria, rising creatinine, haemoptysis, breathlessness, abdominal bleeding, focal weakness or constitutional loss demands expedited systemic investigation.
Haemoptysis, renal decline, bowel ischaemia or bleeding, mononeuritis, fever and weight loss indicate disease beyond cutaneous venules.
Cold intensely painful skin, broken livedoid networks and angular black infarction are discordant with uncomplicated superficial leukocytoclastic disease.
Investigation priorities
Confirm inflammatory small-vessel damage and assess depth and competing pathology.
Management branches
New palpable purpura is stable enough for an outpatient or ward diagnostic pathway.
- Map lesion crops and organ symptoms, record blood pressure and urine and photograph representative early, established and ulcerated lesions with consent.
- Select one recent intact raised papule for formalin histology and a separate freshest appropriate lesion for DIF, confirming medium and courier timing with the laboratory.
- Submit exact lesion ages, sites, medicines, prior corticosteroid, systemic findings and differential and review pathology beside the evolving photographs rather than in isolation.
Initial testing is reassuring, lesions are non-necrotic and no organ syndrome is present.
- Treat a confirmed infection or other driver and agree safe withdrawal or substitution of a plausible new medicine with its prescriber.
- During painful crops use leg elevation, reduced prolonged standing, emollient, non-adherent absorbent dressings and analgesia that respects renal, gastrointestinal and bleeding risk.
- Assess arterial circulation and inflammation before graduated compression, then review new-lesion count, wounds, urine and renal function rather than promising immediate permanent resolution.