Wound healing — Viva

Q1: Definition and phases (2 min)

How does adult skin heal, and how does Wang frame the phases?^[2][6]

• Werner: blood clotting, inflammation, new tissue formation, then tissue remodeling; exogenous growth factors are in most cases beneficial.^[6]
• Wang: three successive overlapping phases — hemostasis/inflammatory, proliferative, remodeling. Excessive healing = hypertrophic scar/keloid; failure = chronic ulcer.^[2]
• Classical teaching splits haemostasis from inflammation; do not quote unsourced tensile-strength percentages.^[2]

Q2: TIME and aetiology (3 min)

What local factors delay healing, and how do you classify a chronic leg ulcer?^[8][11]

• Wound-bed preparation: diagnose the cause, patient-centred concerns, correct systemic and local factors. TIME: tissue debridement, infection or inflammation, moisture balance, edge effect.^[8]
• Venous (Kantor 40–70% of LE chronic wounds; Bonkemeyer Millan 1–3% US) vs arterial (Nelson: 20% of people with leg ulcers have arterial disease) vs neuropathic DFU (Singh 4–10% prevalence in diabetes).^[10][11][14]

Q3: Investigations (2 min)

What must you assess before compressing a gaiter ulcer? How do you screen a diabetic foot?^[10][14]

• Perfusion before compression — arterial disease is a poor prognostic sign; 20% of leg ulcers have arterial disease.^[11][14]
• DFU: brief history + Semmes-Weinstein monofilament in primary care; specialist clinics may add Doppler ultrasound and ankle-brachial indices.^[10]

Q4: Management (3 min)

Venous ulcer, diabetic foot, pyoderma gangrenosum, necrotising infection — first steps?^{[14][18][17][15]}

• VLU: compression, exercise, dressings, pentoxifylline, tissue products; early ablation of superficial reflux can improve healing and decrease recurrence.^[14]
• DFU: off-loading to reduce plantar pressure; invasive infection beneath fascia → inpatient systemic antibiotics, vascular laboratory testing, surgical debridement; with PAD this is critical limb ischaemia.^[18]
• PG: systemic corticosteroids, cyclosporine, or TNF-α inhibitors; do not surgically debride (pathergy).^[17]
• SSTI/necrotising fasciitis: prompt diagnosis, identify the pathogen, timely effective treatment (IDSA 2014).^[15]

Q5: Complications and prognosis (2 min)

• Severe venous-ulcer complications: infection and malignant change — biopsy a changing chronic wound.^[14]
• Kantor: week-4 % area change predicts 24-week healing (PPV 68.2%, NPV 74.7%, ROC 0.75).^[13]
• Singh: DFU is the usual first step to lower-extremity amputation.^[10]

References10ShowHide

1. [2]Wang PH, Huang BS, Horng HC, Yeh CC, Chen YJ. Wound healing. J Chin Med Assoc, 2018.PMID 29169897
2. [6]Werner S, Grose R. Regulation of wound healing by growth factors and cytokines. Physiol Rev, 2003.PMID 12843410
3. [8]Sibbald RG, Orsted H, Schultz GS, Coutts P, Keast D. Preparing the wound bed 2003: focus on infection and inflammation. Ostomy Wound Manage, 2003.PMID 14652411
4. [10]Singh N, Armstrong DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. JAMA, 2005.PMID 15644549
5. [11]Nelson EA Venous leg ulcers. BMJ Clin Evid, 2011.PMID 22189344
6. [13]Kantor J, Margolis DJ A multicentre study of percentage change in venous leg ulcer area as a prognostic index of healing at 24 weeks. Br J Dermatol, 2000.PMID 10809855
7. [14]Bonkemeyer Millan S, Gan R, Townsend PE. Venous Ulcers: Diagnosis and Treatment. Am Fam Physician, 2019.PMID 31478635
8. [15]Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis, 2014.PMID 24947530
9. [17]Tan MG, Tolkachjov SN. Treatment of Pyoderma Gangrenosum. Dermatol Clin, 2024.PMID 38423680
10. [18]Bandyk DF. The diabetic foot: Pathophysiology, evaluation, and treatment. Semin Vasc Surg, 2018.PMID 30876640