Synopsis
Recognise the rapidly painful undermined ulcer of pyoderma gangrenosum, avoid harmful trauma while excluding infection and vascular disease, investigate systemic associations, and coordinate wound and immune treatment.
- Classic pyoderma gangrenosum begins as a tender pustule, papule or nodule and expands into an exquisitely painful ulcer with a dusky violaceous undermined border and purulent-looking sterile base.
- On brown or black skin the active border may look deep purple, grey, brown or black; palpated overhang, warmth, oedema and rapid centrifugal change help when erythema is subtle.
- Pathergy is lesion induction or worsening after minor trauma, cannulation, biopsy, stoma friction or debridement; it supports PG but is neither universal nor unique.
- There is no single confirmatory test. Diagnosis combines characteristic evolution, edge biopsy, exclusion of infection and vascular disease, systemic associations and response to appropriate immune treatment.
- Inflammatory bowel disease, inflammatory arthritis and haematological disorders are important associations; bullous superficial disease should prompt urgent blood count and myeloid-malignancy assessment.
- First-line small localised disease may use a superpotent topical corticosteroid or tacrolimus with atraumatic wound care; rapidly progressive or extensive ulceration needs systemic therapy.
- Prednisolone and ciclosporin had similar healing in the UK STOP GAP trial; choose by infection, diabetes, bone, blood pressure, kidney, malignancy and interaction risk rather than assuming one is universally superior.
- Avoid sharp debridement of active inflammatory borders, but do not use pathergy fear to withhold life-saving drainage of proven deep infection or removal of clearly non-viable tissue after inflammation is controlled.
- Pain, wound exudate, steroid toxicity and the associated disease need parallel management; apparent surface improvement alone is not enough.
Key red flags
Shock, crepitus, spreading deep pain, exposed tendon or bone, critical ischaemia, uncontrolled bleeding, sepsis, ocular disease, stoma breakdown, rapidly expanding bullae, cytopenia or constitutional loss requires same-day multidisciplinary assessment.
Superficial blue-grey bullae and erosions, often on upper limbs or face, are associated with myeloid malignancy and require urgent haematological assessment.
Crepitus, shock, anaesthetic skin, fascial spread or gas is not safely attributed to PG and requires immediate infection and surgical evaluation.
Investigation priorities
Document rate, edge morphology and treatment response while reducing repeated traumatic handling.
Management branches
A painful ulcer is expanding quickly or worsens after a procedure.
- Assess ABCDE, pain, crepitus, perfusion, fascial signs and systemic toxicity and take photographs and cultures without slowing treatment of suspected sepsis.
- Convene surgical, dermatology and infection review early; operate urgently for credible necrotising infection while avoiding serial margin debridement driven only by sterile postoperative expansion.
- Take coordinated viable-edge tissue for histology and bacterial, fungal or mycobacterial studies and record prior antibiotics, corticosteroids and trauma.
PG is localised and slowly progressive without deep exposure or major systemic illness.
- Apply a dermatologist-directed superpotent topical corticosteroid or tacrolimus to the active edge and reassess within days to weeks for pain and expansion.
- Use non-adherent absorbent dressings, gentle cleansing, adequate analgesia and adhesive or stoma modifications that minimise stripping, leakage and pressure.
- Do not sharply debride the inflamed undermined edge; remove loose devitalised material only through an agreed wound plan and escalate if the ulcer continues to enlarge.