How do I recognise pyoderma gangrenosum?

The classic presentation is a painful ulcer on the lower limb — often the shin — with a violaceous (purple-red) undermined border and a purulent or necrotic base. The pain is typically described as disproportionate to the size of the ulcer. A characteristic healing scar is described as cribriform or 'wrinkled paper' in appearance. The lesion often starts as a painful papule or pustule and expands over days to weeks. Pathergy — new or worsening lesions at sites of trauma including IV cannula sites, surgical incisions, or even biopsy sites — is a hallmark. The condition is frequently misdiagnosed as infection or necrotising fasciitis, delaying appropriate treatment.

Why should pyoderma gangrenosum not be debrided?

Pyoderma gangrenosum demonstrates a phenomenon called pathergy, where any skin trauma — including surgical debridement — triggers worsening of the existing lesion or creates new ones. Sharp surgical debridement in active pyoderma gangrenosum reliably makes the condition worse, often dramatically so. This is one of the most important clinical principles in dermatology: if a wound ulcerates despite apparently adequate debridement and antibiotics, and especially if the patient has inflammatory bowel disease or rheumatoid arthritis, consider pyoderma gangrenosum before operating further. Gentle wound care with non-adherent dressings is appropriate; sharp debridement is not until the disease is well controlled with immunosuppression.

What conditions are associated with pyoderma gangrenosum?

In approximately 50–70% of cases, pyoderma gangrenosum occurs alongside an underlying systemic disease. Inflammatory bowel disease — particularly Crohn's disease — is the most common association, present in about 30% of cases. Rheumatoid arthritis accounts for around 15%. Haematological malignancies including acute myeloid leukaemia, myelodysplastic syndrome, multiple myeloma, and monoclonal IgA gammopathy are present in 5–10%. Rarer associations include autoinflammatory syndromes. Investigation for an associated condition is important in every case, as identifying and treating the underlying disease often improves the skin condition.

What is the first-line treatment for pyoderma gangrenosum?

For active disease, oral prednisolone at 0.5–1 mg/kg per day is the standard first-line treatment, titrated to response and tapered over several months. Cyclosporine 4–5 mg/kg per day is an alternative or combination agent with comparable efficacy to prednisolone (demonstrated in the STOP-GAP randomised trial). For refractory disease, especially in patients with underlying inflammatory bowel disease, infliximab has phase-3 RCT evidence (the STOP-PG trial) and is PBS-listed with Authority for IBD-associated pyoderma gangrenosum. Mild localised disease may respond to high-potency topical corticosteroids under occlusion or topical tacrolimus.

How quickly does pyoderma gangrenosum need specialist review?

Pyoderma gangrenosum is a serious condition and requires urgent dermatology review. Any ulcer expanding rapidly over days, causing disproportionate pain, worsening after debridement, or occurring in a patient with known inflammatory bowel disease, rheumatoid arthritis, or haematological malignancy should be referred urgently — same-day or within days — rather than being treated empirically as infection. Rapidly progressing disease, new features suggesting sepsis, or severe uncontrolled pain warrant emergency department assessment. In the interim, gentle wound care with non-adherent dressings and adequate analgesia are appropriate while awaiting specialist review.

Pyoderma gangrenosum

Pyoderma gangrenosum: the ulcer that gets worse with debridement

By Dr HB Lo, FACRRM Reviewed 27 October 2026 8 min read

Pyoderma gangrenosum is a serious inflammatory skin condition — not an infection — causing painful ulcers with a characteristic violaceous, undermined border. Around 50–70% of cases occur alongside an underlying disease, most commonly inflammatory bowel disease, rheumatoid arthritis, or a haematological malignancy. The most critical management principle is to avoid surgical debridement: the condition demonstrates pathergy, meaning trauma reliably worsens existing lesions. First-line treatment is systemic immunosuppression; urgent dermatology referral is required in all but the mildest cases.

What pyoderma gangrenosum is

Pyoderma gangrenosum (PG) is an uncommon, painful, ulcerative, neutrophilic dermatosis — a sterile inflammatory condition of the skin driven by a dysregulated immune response, not by infection. Despite its name implying infection (“pyoderma”) and tissue death (“gangrenosum”), it is neither bacterial nor gangrenous in the usual sense. This naming confusion has led to countless misdiagnoses, delayed diagnoses, and — most damagingly — surgical debridements that caused the condition to dramatically worsen.

The incidence is estimated at 3–10 per million people per year worldwide. It predominantly affects adults aged 25–55 with a female to male ratio of approximately 2:1. Australian prevalence data are limited, but the condition is seen regularly in general practice and hospital settings, particularly in patients with inflammatory bowel disease.

The most important clinical message is simple: a painful ulcer with a violaceous undermined border that is getting worse despite antibiotics and debridement is pyoderma gangrenosum until proven otherwise.

A. Core clinical — the AU general-practice framework

Variants and clinical subtypes

Per the Maverakis JAAD 2018 Delphi consensus criteria, pyoderma gangrenosum has several recognised clinical variants:

Ulcerative (classical) — approximately 85% of cases. One or more painful ulcers, typically on the lower limbs. Violaceous, undermined, irregular border with a purulent or haemorrhagic base. Pain disproportionate to lesion size is characteristic.

Bullous — superficial bullae that rapidly erode; strongly associated with haematological malignancy. Requires prompt investigation for acute myeloid leukaemia, myelodysplastic syndrome, and paraproteinaemia.

Pustular — sterile pustules without frank ulceration; often associated with inflammatory bowel disease, particularly during flares.

Vegetative (superficial) — a milder variant with less aggressive course; usually on the trunk; responds more readily to topical treatment.

Peristomal PG — around stomas (ileostomy, colostomy) in patients who have had bowel surgery for inflammatory bowel disease. Frequently missed because stomal nurses and surgeons may not consider it.

History

Lesion progression — rapid onset of painful papule or pustule, spreading centrifugally over days to weeks into a necrotic ulcer with violaceous border.
Pain — characteristically “exquisitely tender” and out of proportion to lesion size. This history alone should raise the diagnosis.
Pathergy — has the ulcer appeared at a site of trauma such as an IV cannula, biopsy, or surgical incision?
Past medical history — known inflammatory bowel disease, rheumatoid arthritis, haematological disease.
Drug history — propylthiouracil, hydralazine, isotretinoin, and levamisole-adulterated cocaine have been associated with drug-induced PG.
Recent changes — a new biologic medication, change in immunosuppression, or recent surgery as a potential trigger.

Examination

The key examination findings are:

Ulcer border — violaceous (purple-red), undermined, and irregular. The undermined edge is pathognomonic: you can insert a probe under the edge of the ulcer.
Ulcer base — purulent, necrotic, or haemorrhagic.
Pain — palpation of the border produces pain disproportionate to what would be expected.
Healing scar — the characteristic cribriform (“wrinkled paper”) scar from resolved lesions is highly characteristic when present.
Size — often rapidly progressive over days.
Location — lower limbs most common, but may occur anywhere including the trunk, face, and peristomal skin.
Pathergy — look for new ulcers at sites of recent skin trauma.
Systemic features — examine for abdominal tenderness or perianal disease (Crohn’s), joint swelling (rheumatoid arthritis), and lymphadenopathy.

Diagnostic criteria

Two validated diagnostic tools are available:

Maverakis Delphi 2018 criteria (JAAD 2018) — 1 major criterion (biopsy of ulcer edge showing neutrophilic infiltrate) plus at least 4 of 8 minor criteria (exclusion of infection; pathergy; history of IBD, RA, or malignancy; ulceration from papule or pustule within 4 days; erythematous border with tenderness; multiple ulcers; cribriform scarring; response to immunosuppression). Sensitivity 86%, specificity 90%.

PARACELSUS score — a 10-item scoring tool that achieves approximately 89% sensitivity and better discriminates PG from venous leg ulcers.

Both tools are useful in practice, particularly in uncertain cases. No tool replaces biopsy and a high index of clinical suspicion.

Investigations

Wound swab — will typically be sterile in PG, or may grow commensals without indicating true infection. Important to exclude concurrent secondary infection.
Skin biopsy (perilesional and ulcer edge) — histology shows neutrophilic infiltrate and ulceration without identifiable organisms, vasculitis, or autoimmune blistering on immunofluorescence. Send tissue culture (bacterial, fungal, mycobacterial) and special stains.
Bloods for associated disease workup — FBC and film (cytopenias or blasts suggesting haematological malignancy); ESR and CRP; UEC and LFT; serum protein electrophoresis, immunofixation, and serum free light chains (monoclonal gammopathy or myeloma); ANA, ENA, ANCA; HIV; hepatitis B and C; syphilis; QuantiFERON-TB Gold (if systemic immunosuppression is planned); faecal calprotectin (IBD); HbA1c.
Colonoscopy — if any gastrointestinal symptoms are present.
CT chest, abdomen, and pelvis — if haematological malignancy is suspected.
Bone marrow biopsy — if cytopenias or blasts are present on FBC.

B. Evidence — what the trials say

The landmark STOP-GAP RCT (BMJ 2015) compared oral prednisolone with cyclosporine as first-line treatment for PG and found them equally effective, with comparable three-month response rates. This established that either agent is an acceptable first-line choice, with the selection guided by the individual patient’s comorbidities, contraindications, and tolerability.

For refractory disease, particularly with an underlying IBD association, infliximab has the best evidence. The Brooklyn STOP-PG trial demonstrated infliximab superior to placebo in PG, particularly in IBD-associated cases. PBS Authority listing exists for IBD-associated PG.

The critical clinical message is avoid surgical debridement in active disease. Multiple case series document catastrophic worsening following debridement. The pathergy phenomenon means surgery reliably creates new areas of active disease. This principle is supported across the Maverakis criteria paper, eTG, and the Australasian College of Dermatologists position.

Topical therapy (clobetasol propionate under occlusion or topical tacrolimus) is reasonable for mild, localised, or early-stage disease as part of a specialist-supervised approach.

C. Dressings, wound care, and analgesia

Wound care in pyoderma gangrenosum is as important as systemic treatment:

Non-adherent dressings — silicone or hydrogel dressings that do not traumatise the wound surface. Avoid adhesive dressings and gauze that require soaking to remove.
Saline or hydrogel for wound cleansing — no sharp debridement, no vigorous scrubbing.
Pain management — pyoderma gangrenosum ulcers are intensely painful. Paracetamol, NSAIDs (with appropriate precautions), and short-term opioids for breakthrough pain are appropriate while systemic immunosuppression takes effect. Document opioid prescribing per the RACGP SafeScript guidance.
Topical anaesthetics — EMLA or lignocaine gel before dressing changes can make an enormous difference to patient experience.

Once systemic immunosuppression achieves disease control and the wound is entering a healing phase, skin grafting under specialist supervision may be considered for large defects. Surgery is only appropriate in stable, well-controlled disease.

D. Australian operations

MBS items

Standard GP consultations — MBS items 23 / 36 / 44.
Skin biopsy — MBS item 30196 (excision biopsy); histopathology rebatable.
GP Chronic Condition Management Plan — MBS items 965 / 967 for chronic disease management when associated comorbidity is present.
Mental Health Care Plan — MBS items 2715 / 2717 for chronic illness adjustment.
Telehealth — items 91890 / 91891.
ATSI health assessment — item 715.

PBS medicines

Prednisolone — PBS general schedule; multiple dose strengths available.
Cyclosporine (Sandimmun, Neoral) — PBS Authority Required for autoimmune conditions; renal function, blood pressure, and cyclosporine levels require monitoring.
Infliximab — PBS Section 100 HSDP with Authority Required; specialist initiation; IBD-associated PG has a specific indication pathway.
Adalimumab — PBS Section 100 HSDP alternative biologic.
Dapsone — PBS general; pre-treatment G6PD screen required; methaemoglobinaemia risk.
Azathioprine, mycophenolate — PBS Authority for autoimmune conditions; used as steroid-sparing agents.
Topical tacrolimus — PBS Authority for atopic dermatitis only; off-label for PG (private script).
IVIG — Section 100 NBA criteria for qualifying conditions.

Aboriginal and Torres Strait Islander considerations

Closing the Gap PBS co-payment applies to eligible patients. Coordinate care through Aboriginal Community Controlled Health Organisations when appropriate. Culturally safe communication about chronic immunosuppression and wound care is essential.

E. Special populations

Inflammatory bowel disease — PG is one of the most significant extraintestinal manifestations of IBD. Managing the bowel disease with appropriate therapy, including biological agents, frequently results in concurrent improvement of the skin. Crohn’s and Colitis Australia is a valuable consumer resource for patients.

Post-operative and peristomal PG — patients with stomas who develop peristomal ulcers should be assessed for PG before any revision surgery is undertaken. Peristomal PG can be easily missed or attributed to stomal complications. Stomal nurses should be familiar with the clinical appearance.

Haematological malignancy — PG occurring in the context of AML, MDS, or myeloma should prompt urgent haematology review. Treating the underlying malignancy may lead to resolution of the skin condition.

Pregnancy — pyoderma gangrenosum in pregnancy is rare but serious. Systemic corticosteroids are generally preferred over cyclosporine or biologics in this context; specialist input from a multidisciplinary team including dermatology and maternal-fetal medicine is essential.

Immunosuppressed patients — patients on biological therapies for IBD or RA are at baseline increased infection risk. Adding systemic corticosteroids or cyclosporine for PG requires careful infection risk assessment, up-to-date vaccinations, and close monitoring.

When to escalate

Refer or escalate when:

Any suspected PG — urgent dermatology referral for biopsy, diagnostic confirmation, and treatment initiation.
Rapidly progressing disease — same-day assessment or emergency department if the ulcer is expanding over hours, sepsis features are present, or pain is uncontrolled.
New or worsening haematological abnormalities — haematology referral for investigation of AML, MDS, or paraproteinaemia.
Gastrointestinal symptoms — gastroenterology referral for colonoscopy and IBD assessment.
New joint or systemic autoimmune features — rheumatology referral.
Mental health impact of chronic painful illness — Mental Health Care Plan with psychology.

What this article is and is not

This is general health information drawn from current dermatology guidelines and evidence — Maverakis JAAD 2018, STOP-GAP RCT, Frontiers in Medicine 2023 review, eTG, and the Australasian College of Dermatologists. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about investigation, treatment, and specialist referral are made with your own GP and treating clinicians.

For Australian consumer-friendly resources: HealthDirect, Better Health Channel, and Crohn’s and Colitis Australia for those with underlying IBD.

Sources cited

Frequently asked questions

How do I recognise pyoderma gangrenosum?

The classic presentation is a painful ulcer on the lower limb — often the shin — with a violaceous (purple-red) undermined border and a purulent or necrotic base. The pain is typically described as disproportionate to the size of the ulcer. A characteristic healing scar is described as cribriform or 'wrinkled paper' in appearance. The lesion often starts as a painful papule or pustule and expands over days to weeks. Pathergy — new or worsening lesions at sites of trauma including IV cannula sites, surgical incisions, or even biopsy sites — is a hallmark. The condition is frequently misdiagnosed as infection or necrotising fasciitis, delaying appropriate treatment.
Why should pyoderma gangrenosum not be debrided?

Pyoderma gangrenosum demonstrates a phenomenon called pathergy, where any skin trauma — including surgical debridement — triggers worsening of the existing lesion or creates new ones. Sharp surgical debridement in active pyoderma gangrenosum reliably makes the condition worse, often dramatically so. This is one of the most important clinical principles in dermatology: if a wound ulcerates despite apparently adequate debridement and antibiotics, and especially if the patient has inflammatory bowel disease or rheumatoid arthritis, consider pyoderma gangrenosum before operating further. Gentle wound care with non-adherent dressings is appropriate; sharp debridement is not until the disease is well controlled with immunosuppression.
What conditions are associated with pyoderma gangrenosum?

In approximately 50–70% of cases, pyoderma gangrenosum occurs alongside an underlying systemic disease. Inflammatory bowel disease — particularly Crohn's disease — is the most common association, present in about 30% of cases. Rheumatoid arthritis accounts for around 15%. Haematological malignancies including acute myeloid leukaemia, myelodysplastic syndrome, multiple myeloma, and monoclonal IgA gammopathy are present in 5–10%. Rarer associations include autoinflammatory syndromes. Investigation for an associated condition is important in every case, as identifying and treating the underlying disease often improves the skin condition.
What is the first-line treatment for pyoderma gangrenosum?

For active disease, oral prednisolone at 0.5–1 mg/kg per day is the standard first-line treatment, titrated to response and tapered over several months. Cyclosporine 4–5 mg/kg per day is an alternative or combination agent with comparable efficacy to prednisolone (demonstrated in the STOP-GAP randomised trial). For refractory disease, especially in patients with underlying inflammatory bowel disease, infliximab has phase-3 RCT evidence (the STOP-PG trial) and is PBS-listed with Authority for IBD-associated pyoderma gangrenosum. Mild localised disease may respond to high-potency topical corticosteroids under occlusion or topical tacrolimus.
How quickly does pyoderma gangrenosum need specialist review?

Pyoderma gangrenosum is a serious condition and requires urgent dermatology review. Any ulcer expanding rapidly over days, causing disproportionate pain, worsening after debridement, or occurring in a patient with known inflammatory bowel disease, rheumatoid arthritis, or haematological malignancy should be referred urgently — same-day or within days — rather than being treated empirically as infection. Rapidly progressing disease, new features suggesting sepsis, or severe uncontrolled pain warrant emergency department assessment. In the interim, gentle wound care with non-adherent dressings and adequate analgesia are appropriate while awaiting specialist review.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.

T1 AU primary 5 sources
T3 Named-author reconstruction 3 sources