FAQ

Quality of life (QoL) in patients with chronic wounds can be assessed using validated tools such as Wound‑QoL (including Wound‑QoL‑17 and Wound‑QoL‑14) and WHOQOL instruments, which capture physical, emotional, and social impact. These questionnaires can be completed by patients or supported by caregivers, with scores used to monitor changes over time and guide clinical decisions. In practice, results should be reviewed with the patient to adjust treatment goals and identify psychosocial or environmental barriers to healing. While these tools help capture less visible issues such as pain or sleep disturbance, they may be limited in patients with severe cognitive impairment.

To improve patients' quality of life (QoL) in wound care, care should follow a patient-centred approach that prioritizes patient and family preferences, treats the whole patient rather than just the wound, and involves patients, caregivers, and the multidisciplinary team (MDT) as active partners while using positive language to support healing. QoL should be assessed using validated tools such as the Wound-QoL questionnaire (e.g., Wound-QoL-14) and by considering psychosocial factors and social determinants of health to guide treatment goals. The “Wound Balance” concept can be applied to manage patients with chronic wounds and improve their QoL by optimizing the wound environment and biomarkers with appropriate therapies such as SAP-containing dressings, enabling early identification of non-healing wounds, and preventing complications. In palliative care, the focus should be on symptom relief, odour management with odour-neutralising agents, and nutritional support, with telehealth used to enhance monitoring and access to care. Consistent patient–clinician relationships, interdisciplinary collaboration, and upskilling of primary care professionals such as GPs are essential to ensure timely and effective care.

Identifying erythema and inflammation requires an inclusive approach, as visual presentation varies across skin tones. In light skin, erythema typically appears as redness, whereas in black, brown, and olive skin it may present as pink, red, purple, or subtle darkening. Assessment should include comparison with unaffected areas, as well as sensory evaluation, since relying on visual signs alone is insufficient. Clinicians should assess skin temperature, for example with an infrared thermometer, and consider non-visible symptoms such as increased pain or general malaise. Establishing a baseline skin tone using appropriate tools also supports earlier detection of changes.

Wound bioburden refers to the presence and quantity of microorganisms in or on a wound, including both planktonic microbes and biofilm. Most wounds carry some bioburden without affecting healing, but infection occurs when the level increases or specific pathogens dominate, which can significantly delay healing.

To prevent wounds at risk from becoming chronic, early identification and intervention are essential. Clinicians should avoid delayed action and recognise early “red flags,” as signs of delayed healing can appear within the first two weeks. High-risk wounds should be actively monitored and managed to address underlying causes and remove barriers.
Key risk factors must be addressed, including patient-related conditions such as diabetes, obesity, poor nutrition, nicotine use, anaemia, impaired circulation, and psychosocial factors, as well as wound-related issues like infection, bioburden, increasing wound size, deteriorating wound bed, and biomarker imbalance such as excessive protease levels. Appropriate wound bed preparation, including debridement, control of inflammation and infection, moisture balance, and optimisation of the wound edge, is critical.
A proactive, holistic approach is required, combining clinician–patient partnership, tailored treatment strategies, and early transition from reactive to healing-focused management, supported by ongoing clinician education and effective communication.

The skin is the largest human organ and performs several essential functions.
It acts as a physical and immunological barrier against microorganisms, chemicals, and ultraviolet (UV) light. It also provides mechanical resistance to pressure and impacts to protect internal organs, and prevents the loss of body fluids.
It helps regulate the body by maintaining a temperature of 37 °C through perspiration and the expansion and contraction of blood vessels (thermoregulation). It facilitates homeostasis and performs excretory functions by eliminating sweat, sebum, water, and dissolved minerals.
It also functions as a sensory organ to perceive temperature, pain, and mechanical stimuli such as touch, pressure, and vibration.
In addition, the skin acts as an immune organ using cells like leukocytes, mast cells, tissue macrophages, and Langerhans cells. It ensures the synthesis of vitamin D, enables the body to move and grow without injury, supports the healing process through unique repair mechanisms, and is capable of absorbing medication.

Skin aging involves progressive changes in skin structure and function, leading to increased fragility, dryness, reduced elasticity, and translucency. These changes are driven by reduced collagen and elastin production, slower epidermal renewal, diminished gland function, decreased melanin synthesis, and overall thinning of the skin. Both endogenous factors, such as reduced cellular activity and impaired nutrient supply, and exogenous factors, including UV exposure, stress, and lifestyle influences, contribute to this process. At the molecular level, mechanisms such as oxidative stress, DNA damage, mitochondrial dysfunction, telomere shortening, hormonal changes, and impaired autophagy play a key role. As a result, the skin loses its mechanical protective properties, significantly increasing the risk of acute and chronic wounds.

Wound odour assessment is not standardised and mainly focuses on intensity. The TELER system (0–5 scale) is commonly used, ranging from odour detectable in the environment to no odour, alongside methods such as estimating the detection distance.

Management of wound odour requires a multimodal approach, including local wound care such as cleansing, debridement, dressing changes, and topical treatments, supported by secondary dressings to manage exudate. Systemic therapies, including antibiotics, may be needed when infection is present, alongside environmental measures to improve air circulation. Silver and metronidazole may help control odour, although the evidence remains limited.

Epithelialization is the process of epithelium re-formation over a denuded surface resulting from an injury.

It involves the migration and proliferation of keratinocytes to re-surface the denuded area of the wound. The process is driven by growth factors and complex interactions among cells, including keratinocytes, fibroblasts, endothelial cells, and inflammatory cells.

The skin is the largest human organ and is primarily composed of three main layers. The epidermis is the outermost, avascular layer that acts as a protective barrier. It is composed of five layers: Stratum corneum (horny layer), Stratum lucidum (translucent layer), Stratum granulosum (granular layer), Stratum spinosum (prickle cell layer), and Stratum basale (basale layer). The primary cells in this layer are keratinocytes and melanocytes.

The dermis is the thickest layer, located beneath the epidermis. It contains connective tissue, blood vessels, nerves, hair follicles, and sweat and oil (sebum) glands. It is divided into the Stratum papillare (papillary layer), which contains capillary loops and sensory receptors, and the Stratum reticulare (reticular layer), which contains collagen fiber bundles that provide elasticity.

The subcutaneous tissue, or hypodermis, is the deepest layer and consists of fat and connective tissue. Additionally, the skin includes appendages such as hair, nails, and sebaceous, sweat, and scent glands.

Dermatoporosis, or chronic cutaneous insufficiency, describes age-related skin fragility with loss of mechanical protection, resulting in dry, less elastic, and translucent skin. It is characterized by skin atrophy, senile purpura, and stellate pseudo scars due to degeneration of collagen and elastic fibres. The condition is worsened by factors such as sun exposure, prolonged corticosteroid use, anticoagulant therapy, malnutrition, and dehydration. As a result, patients have an increased risk of trauma-related wounds, skin tears from mechanical forces such as adhesive removal, and severe complications like deep dissecting haematoma associated with fragile vessels and skin atrophy.

Skin ageing significantly affects skin integrity and wound healing. Structural changes make the skin more fragile and susceptible to breakdown, increasing the risk of skin tears and both acute and chronic wounds. The healing process is also impaired, with a prolonged inflammatory phase, increased production of inhibitory factors, and reduced cellular proliferation due to senescence, which contributes to hard-to-heal wounds. In addition, age-related conditions such as dermatoporosis, arteriosclerosis, and sarcopenia further increase the risk of pressure ulcers and delay healing. Fragile perilesional skin in elderly patients is particularly vulnerable to damage from inappropriate bandaging, frequent dressing changes, or excessive cleansing.

Systemic conditions and factors that impair wound healing include medical conditions such as diabetes mellitus, metabolic syndrome, dyslipidaemia, venous and arterial insufficiency, ischaemia, critical limb ischaemia, lymphatic insufficiency, autoimmune and chronic inflammatory disorders, immunosuppression, cancer, connective tissue disorders, and arterial hypertension. These are further influenced by physiological factors including ageing, nutritional deficiency, malnutrition, malabsorption, anaemia, obesity, and genetic predisposition. Lifestyle and psychosocial factors such as smoking, alcohol or substance dependency, poor compliance, and psychological stress also contribute. In addition, medical interventions such as immunosuppressants, corticosteroids, anticoagulants, and radiotherapy can further impair wound healing.

Local conditions and factors that impair wound healing include tissue and physical factors such as devitalized tissue, slough, larger initial incisions, and ongoing mechanical stress or trauma, as well as vascular and oxygenation factors like hypoxia and ischaemia. Infection and bioburden, including contamination, high bioburden, and biofilm, further delay healing. In addition, inflammatory conditions with aberrant local inflammation, oxidative stress, excessive protease levels such as MMPs and PMN elastase, growth factor inactivation, and matrix destruction disrupt the wound environment, while excessive exudate production also impairs healing.

Improving patient concordance in wound care relies on building a strong, patient-centered relationship through respectful communication and trust, and understanding the patient’s personal context. Shared decision-making is essential, aligning treatment goals with the patient’s priorities and using motivational techniques to support adherence. Clear, multimodal education and confirmation of understanding help ensure engagement. A holistic, tailored approach that addresses individual barriers, such as pain, psychosocial factors, or lifestyle, combined with effective symptom management and support for daily activities, further strengthens concordance.

Acute wounds are disruptions of skin integrity that heal in a predictable and orderly manner through normal wound healing phases, typically within 4–6 weeks, with an identifiable external cause, minimal underlying pathophysiology, and a controlled inflammatory response.

In contrast, chronic wounds fail to progress in a timely manner, often persisting beyond 6–12 weeks, and are typically stalled in the inflammatory phase. They are associated with underlying pathophysiology, persistent inflammation, and an unpredictable healing trajectory, often leading to complications during the healing process.

Compression therapy is contraindicated in severe arterial disease or critical limb ischaemia, decompensated chronic heart failure, septic phlebitis, and phlegmasia. It should also be avoided in patients with severe exuding dermatosis, intolerance to compression materials, marked sensory disorders of the extremities, advanced peripheral neuropathy, or significant joint conditions such as primary chronic polyarthritis.

Compression systems are classified by material and configuration. Short‑stretch (inelastic) bandages have high stiffness, low extensibility (<100%), low resting pressure, and high working pressure, making them suitable for chronic oedema and nighttime use. Long‑stretch (elastic) bandages show higher extensibility (>100%), higher resting pressure, and lower working pressure, which may reduce tolerance overnight. Multi‑layer systems are more effective than single‑component systems; they often combine elastic and inelastic properties, with the four‑layer bandage (4LB) considered a standard. Two‑component systems provide similar efficacy with easier application, while hosiery and wraps offer simpler alternatives.

In practice, immobile patients are typically treated with elastic multi‑layer systems, except in chronic oedema where inelastic systems are preferred, while mobile patients can use either. Compression improves ulcer healing, particularly with multi‑layer systems. Selection depends on wound characteristics, patient factors, and clinician expertise. Full compression requires prior assessment, including ABPI, and must be applied correctly in dorsal flexion, as insufficient or excessive pressure can lead to oedema, venous congestion, thrombosis, nerve damage, or necrosis.

Compression therapy works by applying external pressure to the limb, which promotes ulcer healing through several mechanisms.
It improves venous haemodynamics by reducing the diameter of major veins and venous reflux, redistributes blood toward the central parts of the body, increases blood flow velocity, supports the calf muscle pump, and improves microcirculation and arterial inflow.

It controls oedema by increasing local tissue pressure, counteracting the loss of capillary fluid, reinforcing the absorption of fluid into the veins and lymph vessels, and improving lymphatic drainage. It also helps reduce inflammatory mediators.

Negative Pressure Wound Therapy (NPWT) is considered a standard approach for managing open abdominal wounds and dehisced sternal wounds after cardiac surgery, and is effective in complex surgical wounds. For closed incisions, closed incision NPWT (ciNPT) can improve healing outcomes and reduce the risk of infection and complications. In acute traumatology, NPWT supports the management of traumatic wounds and temporary closure of dermatofasciotomy wounds prior to definitive surgical treatment.

Closed incision negative pressure therapy (ciNPT) is the application of negative pressure over closed surgical incisions. It can improve surgical outcomes, reduces infection risk, and may lower the incidence of surgical site infections.

Common risk factors for Surgical Site Infection (SSI) include patient‑related factors such as age, body mass index, diabetes mellitus, severe comorbidities, trauma‑related procedures, and wound contamination level. Procedure‑related factors include operation duration, emergency setting, surgical expertise, hospital type, and use of minimally invasive techniques. Additional contributors include multiple procedures, prolonged ICU stay, and postoperative care factors.

Contraindications for Negative Pressure Wound Therapy (NPWT) include bleeding risk, such as in patients with clotting disorders or active bleeding after injury or debridement; exposed organs, blood vessels, or vascular anastomoses; necrotic wound bed; untreated osteomyelitis; and the presence of neoplastic tissue in the wound area.

Virtual reality (VR) can support wound care by providing an interactive and immersive way for healthcare professionals to train and refine their skills. It allows clinicians to practice procedures and wound management in a realistic but risk-free environment, using lifelike patient scenarios without exposing real patients to harm.

At the same time, VR makes training more efficient and flexible by reducing the need for physical resources and allowing learning to take place at convenient locations. It can also be applied through educational tools such as serious games for wound assessment and documentation, as well as simulations that help users practise dressing application and develop surgical skills in a more intuitive and engaging way.

Wound debridement is the removal of devitalised or contaminated tissue from a wound or its surrounding area, including slough, necrotic tissue, debris, foreign material, microorganisms, biofilm, eschar, pus, haematomas, senescent cells, and bone fragments.

Its main goals are to promote wound healing, restore a balanced wound environment, and reduce bacterial burden by disrupting biofilm.

Debridement is different from cleansing, which only removes dirt or loose metabolic waste.

The main methods of wound debridement include surgical and sharp debridement, autolytic debridement, mechanical debridement, enzymatic debridement, biological debridement, technical debridement, and other approaches such as oxidative and osmotic debridement.

Surgical and sharp debridement are effective for removing biofilm and devitalised tissue but require specialist training and experience to avoid damage to vessels, nerves, and tendons. In contrast, autolytic debridement is easy to use and relies on endogenous enzymes to remove devitalised tissue. Mechanical debridement uses pads, ultrasound, or irrigation, enzymatic debridement applies topical agents, and biological debridement involves larval therapy. Technical debridement includes hydrosurgical methods, ultrasonic techniques, and NPWTi-d, while oxidative and osmotic methods are typically used as adjuncts. An emerging concept, integral debridement, refers to combining complementary methods on the same wound to optimise outcomes.

Autolytic debridement is a natural process that uses the body’s own moisture and proteolytic enzymes produced by phagocytic cells and leucocytes to rehydrate, soften, and liquefy devitalised tissue, slough, and eschar, leading to its gradual separation from the wound bed. It is safe, atraumatic, and easy to use without specialist training, promotes granulation and epithelialization, and selectively targets devitalised tissue while preserving healthy tissue. It also supports infection management by removing bacteria within necrotic tissue and can be facilitated by wound dressings, enabling self-care and potentially reducing hospital stay. This “softer” method is suitable for most clinicians and is particularly useful in immunological wounds such as pyoderma gangrenosum or when surgical debridement carries increased risk, for example in patients receiving anticoagulants.

Hydro-responsive wound dressings are non-medicated dressings that manage moisture and infection risk through physical mechanisms. They can donate moisture to dry wounds or absorb exudate from wet wounds, helping maintain fluid balance. They reduce bacterial load by removing devitalised tissue and disrupting biofilm without using antimicrobial agents, thereby avoiding resistance risks. In addition, they support wound bed preparation by promoting cleansing, debridement, and granulation tissue formation. These dressings typically consist of a soft pad with superabsorbent polyacrylate (SAP) particles pre-activated with Ringer’s solution and are designed as a safe, first-line option that can be easily used by non-specialist practitioners.

Superabsorbent polymer (SAP) dressings are designed for moderate to highly exuding wounds.

They contain superabsorbent polymers with very high absorption capacity, able to take up large amounts of fluid and lock it within the dressing. At the same time, they can bind microorganisms and excess proteases, helping to reduce factors that delay healing. Some products also include a silicone contact layer to improve comfort during dressing changes.

Clinically, SAP dressings control exudate, reduce maceration, and support wound healing, while improving patient comfort and potentially reducing dressing change frequency. They are particularly useful for highly exuding wounds, such as venous leg ulcers or other complex lower limb wounds.

Non-medicated wound dressings (NMWDs) do not contain active pharmaceutical ingredients. They help reduce bacterial load and wound bioburden through physical and non-antimicrobial mechanisms rather than chemical antimicrobial action.

They are commonly used as an alternative to antimicrobial dressings for managing bioburden in both acute and chronic wounds, supporting antibiotic stewardship and helping address antimicrobial resistance (AMR). Examples include hydrogels, hydrocolloids, super-absorbent dressings, carboxymethylcellulose (CMC) dressings, hydro-responsive wound dressings (HRWDs), and DACC-coated dressings.

Their effect is mainly based on physical mechanisms, such as promoting autolytic debridement, absorbing exudate along with microorganisms and their by-products, and sequestering or retaining microorganisms within the dressing structure, thereby reducing their presence in the wound bed.

Antimicrobial stewardship (AMS) is the organised and supervised use of antimicrobial agents to reduce multidrug-resistant infections and improve clinical outcomes through appropriate use. In wound care, it promotes responsible prescribing, monitoring, and clinician-led infection assessment to minimise resistance, toxicity, and costs. It also includes antiseptic stewardship, which supports the judicious use of antiseptics to prevent infection and disrupt biofilm. AMS is typically managed by dedicated healthcare teams to ensure the correct therapy is selected while minimising harm and limiting future resistance.

Wound infection is recognised through a combination of local signs, systemic features, and more subtle clinical changes. Local signs include erythema, warmth, swelling, purulent exudate, new or increasing pain, and malodour. In chronic wounds, infection may present less obviously, with features such as delayed healing, friable or bleeding granulation tissue, pocketing at the base of the wound, increased serous drainage, or discolouration of granulation tissue, and any progressive wound breakdown or enlargement should raise concern. In surgical wounds, additional indicators include wound dehiscence, increased exudate, and early systemic signs such as raised heart rate or elevated temperature. Systemic features of wound infection include fatigue, chills, malaise, lymphadenopathy, and elevated inflammatory markers such as CRP and leukocyte count.

Antimicrobial dressings should be used under specific circumstances, primarily guided by a confirmed diagnosis and specialist recommendation. Antimicrobial dressings are indicated when there are clinical signs of local wound infection or when biofilm is suspected or confirmed. Their use may also be considered in wounds at high risk of infection, for example in immunocompromised patients or following high-risk surgical procedures.

Treatment should be reviewed regularly, with reassessment after around two weeks to ensure adequate control of bacterial load. Routine or prolonged prophylactic use is not recommended and should be avoided unless there are exceptional circumstances.

The risk of wound infection is influenced by a combination of wound-related, individual (host), and environmental factors. Wound-related risk factors include contaminated or dirty acute wounds, traumatic injuries, contaminated or dirty surgical procedures, large or long-standing chronic wounds, and wounds located near sites of potential contamination, such as the sacrum or perineum. Additional factors include the presence of foreign bodies (e.g., sutures, drains, or dressing fragments), necrotic or sloughy tissue, haematomas, impaired tissue perfusion, involvement of deeper structures such as bone, joints, muscle, or tendon, wounds over bony prominences or those probing to bone, and poorly managed exudate or oedema. Individual risk factors include poorly controlled diabetes (hyperglycaemia), obesity, peripheral neuropathy, malnutrition, immunosuppression, and conditions associated with hypoxia or poor tissue perfusion, such as cardiac or respiratory disease and anaemia. Smoking, alcohol or illicit drug use, age over 65 years, and treatments such as corticosteroids, chemotherapy, or radiotherapy also increase the risk of infection. Environmental and treatment-related factors include unhygienic environments, hospitalisation with exposure to antibiotic-resistant microorganisms, inadequate hand hygiene or aseptic technique, prolonged surgical procedures, intra-operative hypothermia, inadequate surgical closure, and poor management of perspiration, incontinence, or wound exudate.

Antimicrobial wound dressings are used to reduce bioburden, manage bacterial load, and support wound healing. They can be classified into two broad categories based on their mechanism of action.

Medicated antimicrobial dressings contain active antimicrobial agents, such as silver, iodine, honey, or polyhexamethylene biguanide (PHMB). Depending on the agent and its concentration, they may exert bactericidal effects by killing microorganisms or bacteriostatic effects by inhibiting bacterial growth. These dressings provide antimicrobial activity against a broad spectrum of wound pathogens.

Non-medicated antimicrobial wound dressings do not contain active antimicrobial agents but reduce the microbial burden through physical or biochemical mechanisms. These mechanisms include absorbing and sequestering microorganisms within the dressing, retaining them until they are removed during dressing changes, or reducing microbial adherence through biochemical interactions. Examples include dialkylcarbamoyl chloride (DACC)-coated dressings, as well as certain superabsorbent and hydro-responsive wound dressings that sequester microorganisms.

Differentiating wound infection from inflammation requires careful assessment of local and systemic findings. Inflammation is a normal part of wound healing and is characterised by erythema, oedema, increased local temperature, and pain. These signs are expected during the inflammatory phase and may be associated with exudate without necessarily indicating infection. Wound infection, in contrast, involves microbial invasion with associated tissue damage. Local signs include purulent exudate, malodour, induration, spreading erythema beyond the wound margin, abscess formation, and crepitus. Systemic features may include fever, chills, malaise, tachycardia, tachypnoea, and elevated inflammatory markers such as CRP and leukocytosis. Subtle signs may include delayed healing, friable or bleeding granulation tissue, pocketing at the base of the wound, and increased serous drainage.

In practice, differentiation can be difficult, particularly in chronic wounds where classical signs may be less pronounced. Inflammation alone does not confirm infection, and some conditions, such as autoimmune-related wounds, may show similar features due to an exaggerated inflammatory response rather than bacterial involvement. Clinicians need to distinguish between normal healing-related inflammation and abnormal changes associated with infection or non-healing wounds.

Managing wound biofilms requires a structured approach targeting both planktonic and biofilm bacteria to reduce chronic inflammation and delayed healing. The biofilm pathway involves early aggressive debridement and topical antiseptics, followed by reassessment, personalised antimicrobial therapy, and a four-week review to guide maintenance debridement and further treatment, with advanced therapies introduced if healing remains insufficient.

Key actions include disrupting and removing biofilm through cleansing and debridement, preventing reformation with appropriate dressings, and controlling bioburden using topical antiseptics, antimicrobial or bacterial-binding dressings, NMWDs, and biofilm-disrupting technologies, alongside systemic antibiotics when needed. Management should also address underlying pathology. Biofilms remain challenging due to their high tolerance to antimicrobials and reduced susceptibility to single-agent antibiotic therapy.

Matrix metalloproteinases (MMPs), also known as matrix metallopeptidases or matrixins, are calcium‑dependent, zinc‑containing enzymes that break down proteins such as collagen in the extracellular matrix (ECM).

During wound healing, MMPs are secreted by inflammatory cells and fibroblasts, and are involved in debridement, angiogenesis, and epithelialization. When their activity is balanced, they help cleanse the wound of damaged tissue and ECM, modify the wound matrix to support cell migration and tissue remodeling, and enable keratinocytes to migrate and cover the wound.

For successful healing, MMP activity must be balanced by tissue inhibitors of metalloproteinases (TIMPs). If this balance is lost and MMP activity becomes excessive, it can damage growth factors, cells, and newly formed ECM, leading to chronic, non‑healing wounds.

SAP‑containing dressings can help by absorbing and retaining MMPs, supporting a better balance of MMP activity and shifting the wound toward a more normal healing trajectory.

Wounds become non‑healing when the normal healing phases, haemostasis, inflammation, proliferation, and remodelling, are disrupted, most commonly due to persistence of the inflammatory phase.

This is driven by prolonged inflammation, with increased levels of pro‑inflammatory cytokines and proteolytic enzymes such as MMPs and elastase, leading to ongoing tissue breakdown and impaired repair. Oxidative stress and reduced growth factor activity further limit healing.

In addition, systemic factors such as diabetes, peripheral vascular disease, malnutrition, and certain medications contribute to impaired healing capacity, while local factors including biofilm, devitalized tissue, hypoxia or ischaemia, excessive exudate, and repeated mechanical stress further delay wound progression.
Overall, non‑healing wounds reflect an imbalance between tissue destruction and tissue repair.

Clinical evidence in wound care is organised as a hierarchy of evidence often illustrated as a pyramid, where higher-quality and more valid evidence is positioned at the top and lower-quality evidence forms the base. At the top are systematic reviews and meta-analyses, which combine results from multiple studies and provide the most reliable evidence, followed by randomized controlled trials that are considered the gold standard for evaluating interventions. Below these are non-randomized controlled trials and observational studies. Further down are case series and case reports, which describe individual or small groups of patients without comparison, while at the base are expert opinions, which rely mainly on clinical experience rather than structured research.

Consensus documents in wound care integrate evidence from systematic reviews as part of their methodology. In addition, recommendations are developed through expert consensus, combining clinical experience, published research, and evidence‑based literature.

Palliative wound care is a person- and family-centered, holistic, interdisciplinary approach for wounds that may heal, may not heal, or may be too burdensome to treat. It focuses on symptom management, including pain, odor, exudate, bleeding, and infection, while prioritizing quality of life, comfort, and dignity for patients and caregivers. It also supports skin integrity and addresses physical, emotional, and social needs, with an emphasis on relieving suffering rather than solely achieving healing

Malignant fungating wounds (MCWs) arise from primary, secondary, or recurrent cancers and typically present as cauliflower-like lesions with protruding tissue and irregular, uneven surfaces. They most commonly occur in the breast, neck, chest, extremities, genitalia, and head. These wounds are associated with significant clinical challenges, including bleeding due to fragile tumour vasculature, as well as pain, odour, exudate, and ulceration.

Effective dressings should conform closely to the cancer wounds, be soft and pliable to adapt to fungating tissue, and maintain intimate contact to prevent leakage and pooling of exudate. Silicone superabsorbent polymer (SAP) dressings can improve patient comfort and outcomes in management of cancer wounds. The choice between adhesive and non-adhesive silicone SAP dressings depends on wound topography, particularly the presence of protruding, cauliflower-like tissue, and bordered dressings are generally avoided. Additional dressings or agents may be required to help control bleeding.

Wound biomarkers are objective substances such as enzymes, cytokines, and metabolites found in wound tissue or fluid that reflect the biological state of a wound. They are used to assess disease status, monitor treatment response, track healing, and identify factors that may delay recovery.
Examples include enzymes such as matrix metalloproteinases (MMP-2, MMP-9), serine proteinases like neutrophil elastase, and peroxidases; pro-inflammatory proteins such as calprotectin (S100A8/A9) and procalcitonin; molecular mediators including growth factors, cytokines, and chemokines; enzyme inhibitors like tissue inhibitors of metalloproteinases (TIMPs); reactive metabolites such as reactive oxygen species and nitric oxide; extracellular matrix proteins including type I collagen and fibronectin; as well as factors related to local nutrition and oxygen.

All patients with diabetes are at risk of developing diabetic foot syndrome, which includes neuropathy, ulceration, Charcot foot, infection, and peripheral arterial disease (PAD).

Diabetic foot ulcers arise from a combination of peripheral neuropathy, impaired blood flow, and repeated pressure or trauma. Neuropathy leads to loss of protective sensation, so minor injuries often go unnoticed, while PAD reduces tissue perfusion and delays healing. The risk is further increased by factors such as older age, long duration of diabetes, obesity, smoking, hypertension, and poor glycaemic control, which all contribute to nerve and vascular damage. Local mechanical factors also play an important role, including foot deformities, high plantar pressure, callus formation, and inappropriate footwear, all of which promote skin breakdown under repetitive stress.

Charcot foot (also called Charcot neuroarthropathy) is a serious complication of diabetes-related neuropathy that affects the bones, joints, and soft tissues of the foot. It develops when loss of protective sensation due to neuropathy means that repetitive minor injuries or fractures go unnoticed. As patients continue to walk on the injured foot, this leads to progressive bone destruction, joint dislocation, and deformity. Over time, the foot can collapse and change shape, often resulting in a “rocker-bottom” deformity, which increases the risk of pressure points, ulceration, and infection.

In simple terms, Charcot foot is a destructive process of the foot caused by neuropathy, where unrecognized trauma and continuous weight-bearing lead to severe structural damage.

Wound bed preparation (WBP) is the management of a wound to promote endogenous healing and enhance the effectiveness of therapeutic interventions, particularly in wounds with devitalised tissue. It aims to create optimal healing conditions by removing barriers such as necrosis, slough, and biofilm, which can increase infection risk. WBP is commonly guided by structured frameworks such as TIME and TIMERS, focusing on tissue debridement, control of infection and inflammation, moisture balance, and optimisation of the wound edge, combined with appropriate clinical interventions to support healing progression.

Skin tears are traumatic wounds caused by mechanical forces such as shear, friction, blunt force, or adhesive removal, leading to separation of skin layers without extending beyond the subcutaneous tissue. Skin tears can be partial-thickness, defined as separation of the epidermis from the dermis, or full-thickness, defined as separation of both the epidermis and dermis from underlying structures such as the hypodermis or subcutaneous tissue.

The STAR (Skin Tear Audit Research) classification categorizes skin tears based on flap viability and edge alignment. Category 1A refers to wounds where the edges can be realigned to the normal anatomical position and the skin is not pale, dusky, or darkened, while Category 1B also allows realignment but the skin appears pale, dusky, or darkened. In Category 2A, the edges cannot be realigned, although the skin is not pale, dusky, or darkened, whereas Category 2B describes wounds with non-realignable edges and skin that is pale, dusky, or darkened. Category 3 indicates that the skin flap is completely absent.

The management of skin tears involves prompt first aid, appropriate dressing, and ongoing skin protection. Initial care focuses on bleeding control, gentle cleansing, and careful realignment of any skin flap without overstretching, followed by protection of the affected area. Wound dressings, such as silicone-based dressings that enable atraumatic removal, can be used to prevent further skin damage and effectively manage exudate. Ongoing care aims to protect and maintain skin integrity. Attention should be given to risk factors such as skin frailty, comorbidities, and exposure to friction or shear. Continuous monitoring is essential, and wounds showing deterioration or delayed healing should be reassessed and referred for further medical review if necessary.

Wound exudate is a biological fluid composed of serum, white blood cells, proteins, and other components that leak from capillaries into the wound during inflammation. It is a normal and important part of the healing process, particularly during the inflammatory and proliferative phases. It consists predominantly of water but also contains electrolytes, proteins, nutrients, pro-inflammatory cytokines, proteolytic enzymes (such as matrix metalloproteinases, MMPs), growth factors, metabolic byproducts, and cellular components such as neutrophils, macrophages, and platelets.

Exudate plays a key role in maintaining a moist wound environment, transporting immune mediators and nutrients, and supporting autolytic debridement. However, when exudate becomes excessive or unbalanced, particularly in chronic wounds, it can lead to complications such as maceration of the surrounding skin, delayed healing, and an increased risk of infection.

Excessive or poorly managed wound exudate can lead to both clinical and psychosocial complications. Clinically, prolonged exposure to exudate can damage the periwound skin, causing maceration, excoriation, and erosion, which may further weaken the skin barrier and lead to wound enlargement. It also increases the risk of infection and biofilm formation, while high levels of proteolytic enzymes such as matrix metalloproteinases (MMPs) can contribute to tissue degradation and delayed healing. Patients may also experience pain, discomfort, and malodour.

Beyond the physical impact, exudate can significantly affect quality of life. Uncontrolled leakage may cause embarrassment, anxiety, and emotional distress, and the visible and odorous nature of exudate can lead to social withdrawal. It can also interfere with daily life, for example through soiling of clothing or bedding. In addition, poor exudate management may increase treatment costs due to more frequent dressing changes and greater demand on healthcare resources.

Sequestration is an important mechanism by which superabsorbent polymer (SAP) wound dressings support wound healing. SAP dressings bind and trap excess wound exudate together with harmful components, including microorganisms and proteases such as elastase and matrix metalloproteinases (MMP-2 and MMP-9), within the core of the dressing. This prevents these substances from causing further tissue damage or delaying healing, helping to restore a more favourable wound environment and support the normal wound healing process.

To manage wounds with stalled inflammation, the focus is on wound bed preparation and correction of underlying factors that prevent progression into the proliferative phase, with overall management often guided by structured wound bed preparation frameworks such as TIMERS, and holistic, patient-centred wound management frameworks such as the Wound Balance concept. This includes management of underlying pathology such as vascular disease or diabetes that contributes to persistent inflammation. Maintenance debridement is used to remove non-viable or devitalised tissue and reduce ongoing inflammatory stimulus. Infection and elevated bioburden should be controlled using appropriate antimicrobial strategies where indicated. Moisture balance is also essential, as excess exudate can contain inflammatory mediators and contribute to maceration, further delaying healing. Advanced therapies may be considered to help shift the wound environment from a pro-inflammatory to a pro-reparative state by modulating cytokine activity. Patient-related factors such as nutrition, obesity, and smoking should also be addressed to optimise healing potential.

The wound balance concept is a multifactorial approach that integrates key parameters to support individualized, patient-centered care and clinical decision-making. It represents a shift in focus from merely managing wounds to actively pursuing healing as early as possible. It balances the wound microenvironment (including biomarkers, exudate, moisture, and early signs of chronicity), patient-related factors such as quality of life and treatment engagement, and consistency in clinical practice to reduce overall burden. Its goal is to guide the wound microenvironment towards healing, identify barriers to progression, and enable early recognition of wounds at risk of non-healing through improved knowledge and training.

Clinical and knowledge gaps remain one of major key challenges. Expertise discrepancies exist between expert clinicians and primary care nurses, who often have limited access to advanced training, and in residential aged care most nurses are generalists without specialized wound management expertise. These gaps lead to practice inconsistencies in wound assessment, treatment selection, and the use of evidence‑based practices, and some patients receive poor assessments and inaccurate diagnoses. Access to specialists is also limited globally, and routine surgical or sharp debridement is often not achievable.

Resource and systemic constraints further impact care. Clinicians face workforce and time pressure due to limited time, understaffing, and shortages. Resource limitations can hinder adequate care and comprehensive assessment, while financial and administrative hurdles, including high treatment costs and complex health insurance systems, complicate management.

Patient and treatment challenges are also significant. The complexity of wounds, especially “hard‑to‑heal” and malignant wounds, creates a major burden, with issues such as undulating tissue, high exudate, and malodour. Symptom management, particularly pain, odour, and exudate, remains difficult, especially in palliative care. In addition, patient engagement and communication barriers, such as language or limited capacity, can affect adherence and clarity about whether the goal is dressing, managing, or healing the wound.

Common clinical classification systems for diabetic foot ulcers (DFUs) include Wagner, which consists of six grades based on ulcer depth, presence of gangrene, and perfusion; the University of Texas system, which combines grade and stage; PEDIS, which assesses perfusion, extent, depth, infection, and sensation; SINBAD, which evaluates site, ischaemia, neuropathy, bacterial infection, area, and depth; and WIfI, which focuses on wound, ischaemia, and foot infection.

The recommended approach to managing diabetic foot ulcers is holistic and multidisciplinary, addressing both the wound and the underlying causes.
It starts with optimizing overall health, including good glycaemic control and management of comorbidities, while tailoring care to the individual patient. Adequate blood supply is essential, so any ischemia should be identified and treated, including revascularization if needed, and infections must be managed promptly.

At the same time, pressure offloading is critical to reduce mechanical stress on the ulcer, typically using devices such as casts or specialized footwear. Locally, the wound requires regular assessment, appropriate debridement, and dressings that maintain a moist environment and control exudate.
Long-term management focuses on prevention through patient education, proper foot care, suitable footwear, and regular follow-up, including vascular and neurological assessment.

Early signs of pressure injury can be identified using the following methods: Physical assessment involves regular visual inspection combined with palpation, including evaluation of persistent erythema, skin temperature, and tissue consistency, rather than relying on appearance alone. This is particularly important in patients with darker skin tones, where colour changes may be less visible and early damage can be missed. Subepidermal moisture (SEM) measurement uses a device to detect localised increases in extravascular fluid (oedema), which may indicate early tissue damage before visible skin changes appear.

Pressure injuries occur through a complex interaction of sustained mechanical loading and patient‑related risk factors. Prolonged pressure, shear, friction, and adverse microclimate conditions (such as heat and moisture) lead to deformation of the skin and underlying soft tissues, particularly over bony prominences or under medical devices.

Reduced mobility and impaired sensory perception increase the risk by limiting repositioning and the ability to detect discomfort, while factors such as age and previous wounds further contribute. At a tissue level, these forces cause cell deformation, reduced blood perfusion, impaired lymphatic drainage, and disrupted interstitial transport. This results in inflammation, increased capillary permeability, oedema, and ultimately tissue damage.

Microclimate also plays a key role, as excess moisture or dryness weakens skin integrity and makes it more vulnerable to pressure, shear, and friction.

Chronic lower limb wounds are mainly classified based on their underlying cause.

The most common types are venous leg ulcers, which are linked to poor venous circulation, and arterial leg ulcers, which result from reduced blood flow due to peripheral arterial disease. Some patients have features of both, known as mixed leg ulcers, where venous insufficiency and arterial compromise coexist.

Venous leg ulcers are typically associated with a throbbing, aching, or heavy feeling in the legs, which often improves with rest and elevation. They are usually located on the lower leg or around the ankle, most commonly near the medial malleolus. The surrounding skin often shows features of chronic venous disease, such as oedema, varicose veins, atrophie blanche, hemosiderin deposits, lipodermatosclerosis, and vascular dermatitis, and there is no exposure of deep structures.

Arterial leg ulcers, in contrast, are generally very painful, especially at rest, during exercise, or at night, and the pain may improve when the leg is dependent. These ulcers are typically found on the toes, toe tips, lateral foot, or outer ankle over pressure points. They are often deeper in nature and may extend to underlying structures such as bone, muscle, or tendon.

Mixed venous–arterial leg ulcers combine features of both conditions. They are usually located on the medial or lateral aspects of the leg and can sometimes extend circumferentially. Clinically, they present with overlapping signs of venous insufficiency and arterial compromise, depending on the severity of each component.

A comprehensive assessment of a patient with a leg ulcer should be holistic, covering both the patient and the wound. Patient history, including comorbidities such as diabetes or peripheral vascular disease, along with the ulcer history, should be assessed, followed by a focused clinical examination. It is also important to understand the patient’s overall condition, including mobility and general wellbeing. Pain and signs of infection should be carefully assessed.

The ulcer itself should be evaluated in terms of size, depth, and surrounding skin changes such as oedema or features of chronic venous disease. Vascular assessment is essential, particularly measuring ABPI to rule out arterial disease before starting compression therapy. As wound healing can change over time, reassessment should be performed regularly, especially if progress is delayed.

The BIOMES tool is designed to support early recognition and assessment of chronic and non-healing wounds, allowing clinicians to identify risk factors for delayed healing at an early stage rather than waiting for a wound to become chronic. It focuses on key barriers to healing, including blood flow, infection control, offloading or mechanical stress, metabolic factors and comorbidities, exudate and bioburden, and social or economic factors.

Based on the number of BIOMES factors present, wounds can be stratified into different risk levels. Wounds with no identified factors are considered low risk. When a single factor is present, the wound is regarded as moderate risk, and management should focus on addressing the underlying issue, following best practices in wound care, and considering referral if needed. Wounds with two or more factors are classified as high risk and typically require specialist referral, close monitoring, and a coordinated approach to address multiple barriers to healing.

The BIOMES framework promotes a shift toward earlier intervention and more personalised wound care management, encouraging clinicians to actively identify and manage barriers to healing. It aligns with broader wound care principles, including structured assessment, optimisation of the wound bed, management of comorbidities, and consideration of social and environmental factors that may impact healing outcomes.

Periwound skin maceration is the softening, wetting, wrinkling, or sogginess of the skin immediately adjacent to the wound bed. It is caused by prolonged exposure to excessive moisture such as wound exudate and is often associated with suboptimal moisture control or inadequate exudate management. At a cellular level, the stratum corneum absorbs fluid and swells, and the process is associated with the activity of proteolytic enzymes such as proteases and matrix metalloproteinases (MMPs), which reduce epidermal cell adhesion. Clinically, macerated skin typically appears white or pale, while in darker skin tones it may appear shiny, grey, purple, or as darker discolouration, and may become red if inflamed. Maceration predisposes the skin to breakdown and increases the risk of friction-related damage and infection, including localised tissue infection. It also impairs epidermal migration and can contribute to wound enlargement and delayed healing.

Periwound maceration is managed through appropriate dressing selection and periwound skin protection. Dressings should be chosen based on their exudate-handling capacity to ensure adequate absorption and protection of the surrounding skin. In cases of moderate to high exudate levels, superabsorbent polymer (SAP) dressings can be used to enhance fluid retention and reduce leakage. Low-adherent or silicone dressings are preferred where appropriate, and adhesive tape should be avoided when possible to minimise trauma during dressing removal. Skin protection should be maintained through the regular use of barrier products, skin protectant creams, or barrier films to reduce prolonged exposure of the periwound area to exudate. Advanced barrier systems such as cyanoacrylate-based skin protectants may be considered in pressure ulcers or injured periwound skin, and in selected cases where the periwound skin is inflamed due to irritant exposure, topical corticosteroids may be used.