U | Basicmedical Key

U’d pad see Table P1, Figure P1

UKPDS see United Kingdom Prospective Diabetes Study

ulcer non-healing, chronic wound showing concomitant tissue repair and tissue breakdown, chronic inflammation and deposition of fibrous tissue in surrounding/underlying soft tissues, and threat of secondary infection; caused by loss of/breakdown/infection of epidermal/dermal tissues, with subcuticular tissue and deeper structure involvement; characterized by pain (unless in neuropathic tissues), chronic inflammation, fibrosis of underlying and local peripheral tissue, fluid exudation and proneness to infection predisposing factors include arterial, venous, lymphatic, neurological and immune compromise (see Table W1); presence of foreign body (including necrotic material) within the wound, repeated microtrauma, and concurrent systemic disease and drug regimes contribute to non-healing; normal healing events (i.e. healing by secondary intention [inflammation, epithelialization, wound contraction, connective tissue maturation]) are prolonged, disrupted and often non-sequential (Table U1); healing is promoted by addressing the cause of tissue breakdown and concomitant factors that interrupt normal healing, together with measures to promote systemic wellness (Table U2; see Table H14), including rest (e.g. use of a full contact cast to allow non-weight-bearing ambulation), regular wound care (and dressings appropriate to phase of healing to optimize wound environment; see Table D10 and Box D3), antibiotics (to control infection Table A12), pressure bandaging and/or diuretics (to control or reduce foot/limb oedema), vascular surgery (to improve arterial supply/venous return) and tight glycaemic control (see Tables H13, H14 and N5 and Box N2)

complicated ulcer secondarily infected chronic wound penetrating to and involving deeper structures; possibly complicated by osteomyelitis

decubitus ulcer; pressure sore ulcer formation at pressure point (e.g. posterior/plantar margin of heels, sacrum, elbows) in bed-bound patients, caused by compromised local blood supply and reduced tissue viability, relative immobility and general patient debility

gastric ulcer erosion of gastric mucosa due to chronic ingestion of non-steroidal anti-inflammatory drugs or infection with Helicobacter pylori

Marjolin’s ulcer neoplastic deterioration of pre-existing long-standing ulcer

mixed-pathology ulcer chronic wound caused by mixed pathology, e.g. secondary bone infection within a neuroischaemic ulcer

neuroischaemic ulcer ulcer development in neuropathic ischaemic tissue

neuropathic ulcer plantar ulcer induced by relatively minor trauma, in an insensitive foot (see trophic ulcer)

perforating ulcer ulcer whose base penetrates to involve subcuticular structures, e.g. tendon/bone (which may be visible within the lesion base)

rodent ulcer see basal cell carcinoma

trophic ulcer deep plantar ulcer (prone to both aerobic and anaerobic infections) induced by relatively minor trauma and/or tissue stress (e.g. pressure/friction) in a neuropathic (anaesthetic) foot, e.g. in diabetes or leprosy; skin surrounding the ulcer tends to exuberant callous formation (see Box N2 and Table N5)

varicose ulcer; venous ulcer wide, shallow ulcer most commonly found at lower medial one-third of leg in association with poor and prolonged compromised venous return and/or venous stasis; develops within area of oedematous tissue characterized by signs of compromised venous function (e.g. varicose eczema, haemosiderosis, woody tissue fibrosis, scars of healed earlier ulceration, atrophy blanche and varicose veins)

Table U1 Phases in the progression of an ulcer to healing

Ulcer phase	Characteristics	Comment
Active phase	Wound dimensions increase (undermined wound edges) Exudation Formation of slough Periwound oedema and induration of edges	Dissolution and degradation of devitalized tissue ± infection Macrophage and enzyme activity Accumulation of degraded tissue and dead macrophages Chronic, non-resolving inflammation ± collagen deposition
Proliferative phase	Wound begins to infill (wound dimensions reduce) Epithelialization (saucerization) of margins	Formation of granulation tissue Recruitment of fibroblasts; collagen formation Epidermal cells at margins mitose and spread out to begin to close wound
Maturation phase	Wound contraction Wound closure Scar formation	Myofibrils within fibroblasts contract Epithelialization is complete Devascularization of fibrotic tissue that forms scar

Table U2 Examples of ulcer classification systems

Classification system	Details	Comments
Wagner	Grade 0: local deformity or callosity but no open lesions Grade 1: partial or full skin thickness, superficial ulcer Grade 2: deep ulcer without osteomyelitis, but extending to ligament, tendon, bone, joint capsule or deep fascia Grade 3: deep ulcer with associated cellulitis, abscess formation and/or osteomyelitis and/or joint sepsis Grade 4: gangrene localized to the forefoot or heel Grade 5: extensive gangrene	Widely recognized and used system Rather generalist and non-specific Ignores neuropathy and lesion size, and thus their effects of choice of treatment/lesion management
S SAD	S = size of lesion (area; depth) S = sepsis (presence/absence) A = arteriopathy (ischaemia) D = denervation (sensory/autonomic/motor neuropathy)	Builds on from the Wagner system (above), introducing additional categories, each awarded 0 (normal), 1 (mild change), 2 (moderate change), 3 (severe change) subclassification
RYB	R = red wound (pale pink–beefy red ulcer base, proliferating/inflammatory ulcer) Y = yellow wound (moist, exudating ivory/ green/brownish sloughy wound) B = black wound (dry wound with black/ brown/tan hard eschar)	Wound assigned colour grading A limited classification that focuses solely on wound appearance and ignores other factors (e.g. distal sensory neuropathy, peripheral ischaemia, cellulitis, size/depth of lesion, phase of progression of lesion)
PEDIS	P = perfusion of limb/foot E = extent of wound (size of lesion) D = depth of lesion/tissue loss I = infection S = sensation (perception of light touch, vibration, contact of 10 g monofilament, hot/cold discrimination)	Each subcategory is graded 1–4, where 1 = normal/absence and 4 = severe Useful research tool allowing indepth assessment of lesion progression over time, and comparison of lesions subjected to varying treatment modalities
DEPA	D = depth of lesion E = extent of bacterial colonization P = phase of ulcer (Table U1) A = associated aetiology (e.g. trauma, neuropathy, ischaemia, infection, diabetes mellitus) DEPA <6 = low-grade wound (i.e. local debridement, oral antibiosis as necessary, glycaemic control measures) DEPA 7–9 = moderate-grade wound (i.e. debridement, parenteral antibiosis, insulin therapy, wound-healing promotion agents, pressure relief) DEPA 10–12 = high-grade wounds (i.e. parenteral antibiosis, insulin therapy, wound-healing promotion agents, vascular reconstruction)	Each subcategorization is graded 1–3 to reflect increasing levels of severity Validated system Score 6 = wound likely to heal in time Score 10: great difficulty in healing Score 11–12 (especially heel wounds): prognostic of lower-limb amputation
University of Texas system	Tier 1 Wound graded 0–3 according to wound depth/tissue involvement: 0 = pre-/postulcer with intact epithelium 1 = superficial ulcer not involving bone/tendon 2 = ulcer penetrates to tendon/joint capsule 3 = ulcer penetrates to bone/joint Tier 2 Wound graded A–D according to wound burden/tissue status A = non-infected/non-ischaemic B = infected/non-ischaemic C = non-infected/ischaemic D = infected/ischaemic	Multisite validated system Two-tier wound classification (tier 1 = ulcer; tier 2 = wound burden/tissue status, e.g. 1C = no current ulcer; ischaemic foot) gives risk assessment Useful wound management ‘road map’ Should be used in conjunction with other markers of limb status (e.g. degree of sensory neuropathy, autonomic function; ankle–brachial pressure index, Buerger’s test, presence of critical ischaemia, skin condition, local foot/toes deformity, subtalar joint range of motion)