Wound management in general practice: diagnose before you dress, crack biofilms, and when to rethink atypical ulcers

Burden and the GP reality

Globally, roughly 2.5 per 1,000 people live with a wound each year; by 2024 estimates were approaching 13 million wounds annually. In Australia about 460,000 people live with a wound every year, at a treatment cost near $3 billion.

In general practice the mismatch is stark: Medicare-timed consults are short, yet wound care can take up to an hour. Product choice is overwhelming — on the order of ~27,000 wound-care products on the Australian market — and continuity across nurses, podiatrists, and specialists is often confusing. There is now a Chronic Wound Consumable Scheme (more below), but diagnosis still has to come before the dressing trolley.

Hard-to-heal — stuck in inflammation

Older labels split wounds into acute, chronic, and complex. Newer framing prefers hard-to-heal: any of those categories can stall. Classic “chronic” meant failure to heal in four to six weeks, but the biology matters more than the calendar.

Healing phases run haemostasis → inflammation → proliferation → remodelling. Hard-to-heal wounds typically get stuck in inflammation. That inflammatory phase starts within the first three days of injury — so there is roughly a three-day window to assess well, get diagnostics right, and choose products that put the wound on a healing track. Reality check: many patients present months or years late. The speaker described a lower-leg venous ulcer lasting 54 years that was eventually healed — patients should not have to live a lifetime with these wounds.

Why wounds fail to heal

• Misdiagnosis is the biggest recurring theme in the literature — documentation that only says “left leg ulcer” without venous/arterial/pressure etiology leads to wrong treatment.
• Poor perfusion — less oxygen, nutrients, and immune cells at the cellular level; diabetes and other chronic disease amplify this.
• Biofilms — bacteria glued into every nook of the wound bed with a protective matrix that saline-and-gauze does not shift.
• A smaller share: non-concordance / treatment hesitancy.

Biofilms — crack them, keep cracking them

Molecular imaging shows traditional normal saline and gauze do little against biofilms. Advanced cleansers (examples spoken as microdacyn / “microdasin”, granudacyn / “granadasin”, and hypochlorous-type agents) raise the cleansing game — but research is clear: the reliable way to remove biofilm is debridement.

• Mechanical debridement at every dressing change (microfibre cloths such as Debrisoft / AllPrep if available).
• Sharp debridement (curette or scalpel) on average roughly weekly for most wounds needing it.
• Biofilms regrow in about 48–72 hours — so one “big clean” is not enough; keep cracking the biofilm head.

Six steps to clarity

A pocket checklist for everyday wound reviews:

1. What caused the wound? (etiology, not just “ulcer”)
2. Is perfusion adequate? (Doppler ABPI/TBPI; duplex when needed — interpret carefully in diabetes, CKD, rheumatoid disease)
3. Is pressure contributing?
4. Are there clinical signs of infection?
5. Could this be atypical? (especially if no budge by about four weeks)
6. Can this patient heal? (challenge nihilism — most wounds can heal with the right plan)

When healing stalls, widen investigations: ABPI/TBPI or duplex; systemic bloods including iron studies and HbA1c in diabetes; X-ray / probe-to-bone when osteomyelitis is possible even without florid cellulitis.

Treat the patient, not the swab (AMS)

All wounds are colonised; not all are infected. The speaker rarely recommends a swab unless the patient is systemically unwell. Local infection → antimicrobial dressings; systemic infection → systemic antibiotics, under antimicrobial stewardship.

Knowing if you are on track

• >30% surface-area improvement in 4 weeks predicts you are on a healing trajectory.
• If there is no change by 2 weeks, go back to assessment, diagnostics, and the plan — something is missing.
• Waiting too long without rethinking diagnosis, perfusion, offloading, or infection is itself a failure mode.

Atypical wounds — about 1 in 5

Research suggests around 20% of chronic wounds are atypical — inflammatory disease, infection, malignancy, chronic illness, genetic disorders. Two patterns highlighted:

Diabetic foot ulcers — three types

Hallmark across many DFUs: callus rim with shearing and haemorrhage underneath before breakdown.

Keep it simple — cleansers, antimicrobials, barrier cream, scheme

• Reserve normal saline mainly for acute wounds; for longer-standing hard-to-heal wounds prefer advanced cleansers (microdacyn / granudacyn and similar as spoken).
• Local infection signs → antimicrobial options such as cadexomer iodine and silver dressings.
• Barrier cream around the wound edge is a high-yield tip: copious exudate spills, macerates, and enlarges the wound if unprotected.
• Debride, debride, debride — mechanical every change; sharp when indicated.

Tissue-type cheat sheets (slough × exudate × infection → numbered dressing pathways such as alginates / gelling fibres / hypertonic saline) were promoted from the stand — useful when product choice feels paralysing.

Five takeaways

1. Diagnose before you dress.
2. Assess perfusion before compression.
3. Treat clinical infection, not colonisation.
4. If it is not progressing, reconsider the diagnosis (and atypical causes).
5. Keep wound care simple, evidence-based, and affordable.

Bottom line: hard-to-heal wounds are stuck in inflammation; biofilms need repeated debridement; dressings without diagnosis waste time and money; and about one in five “chronic” wounds may be atypical — rethink early rather than escalate antibiotics alone.

All Dr Kotha CPD pages · wound-management.drkotha.com · ochre theme