2. Comparison of pressure ulcer classification systems.

NPUAP/EPUAP/PPPIA Classification System (2014, 2009)		NPUAP (1989)		The UK Consensus (Stirling) Classification of Pressure Sore Severity (1994)		The Torrence Classification System (1983)
Category/Stage	Definition	Category/Stage	Definition	Category/Stage	Definition	Category/Stage	Definition
Quoted directly fromNPUAP/EPUAP/PPPIA 2014		Quoted directly from NPUAP 1989		Quoted directly fromReid 1994		Quoted directly fromHarker 2000
Category/Stage I: Nonblanchable Erythema	Intact skin with non‐blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its colour may differ from the surrounding area. The area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue. Category/Stage I may be difficult to detect in individuals with dark skin tones. May indicate “at risk” individuals (a heralding sign of risk).	Stage I	Non‐blanchable erythema of intact skin: the heralding lesion of skin ulceration. Identification of Stage I pressure ulcers may be difficult in patients with darkly pigmented skin.	Stage 1	Discoloration of intact skin (light finger pressure applied to the site does not alter the discolouration) 1.1 Non‐blanchable erythema with increased local heat 1.2 Blue/purple/black discolouration	Stage 1	Blanching hyperaemia: Reactive hyperaemia is a temporary dilation of the capillaries which bring oxygen to the area and remove accumulated carbon dioxide and other waste products. It causes a distinct erythema after pressure is released. Light finger pressure is said to cause blanching of this erythema, indicating that the microcirculation is intact.
Category/Stage II: Partial Thickness Skin Loss	Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising.* This Category/Stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation. *Bruising indicates suspected deep tissue injury.	Stage II	Partial thickness skin loss involving epidermis and/or dermis. The ulcer is superficial and presents clinically as an abrasion, blister or shallow crater.	Stage 2	Partial thickness skin loss or damage involving epidermis and/or dermis 2.1 Blister 2.2 Abrasion 2.3 Shallow ulcer, without undermining of adjacent tissue 2.4 Any of these with underlying blue/purple/black discolouration or induration.	Stage 2	Non‐blanching hyperaemia: the erythema remains when light pressure is applied indicating a degree of microcirculatory disruption and inflammation. Oedema distorts and thickens all tissues compressed between the bone and the support surface. Superficial damage may present as swelling, induration, blistering or epidermal ulceration, which might expose the dermis.
Category/Stage III: Full Thickness Skin Loss	Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunnelling. The depth of a Category/Stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and Category/Stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep Category/Stage III pressure ulcers. Bone/tendon is not visible or directly palpable.	Stage III	Full thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia. The ulcer presents clinically as a deep crater with or without undermining of adjacent tissue.	Stage 3	Full‐thickness skin loss involving damage or necrosis of subcutaneous tissues but not extending to underlying bone, tendon or joint capsule 3.1 Crater, without undermining of adjacent tissue 3.2 Crater, with undermining of adjacent tissue 3.3 Sinus, the full extent of which is not certain 3.4 Full‐thickness skin loss but wound bed covered with necrotic tissue (hard or leathery black/brown tissue or softer yellow/cream/grey slough) which masks the true extent of tissue damage. Until debrided it is not possible to observe whether damage extends into the muscle or involves damage to bone or supporting structures.	Stage 3	Ulceration progresses through the dermis to the junction with subcutaneous tissue. The ulcer edges are distinct but it is surrounded by erythema and induration. At this stage the damage is still reversible.
Category/Stage IV: Full Thickness Tissue Loss	Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunnelling. The depth of a Category/Stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and these ulcers can be shallow. Category/Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis possible. Exposed bone/tendon is visible or directly palpable. The depth of a Category/Stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and these ulcers can be shallow. Category/Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis possible. Exposed bone/tendon is visible or directly palpable.	Stage IV	Full thickness skin loss with extensive destruction, tissue necrosis or damage to muscle, bone, or supporting structures (for example, tendon or joint capsule). Note: undermining and sinus tracts may also be associated with Stage IV pressure ulcers.	Stage 4	Full‐thickness skin loss with extensive destruction and tissue necrosis extending to underlying bone, tendon or joint capsule 4.1 Visible exposure of bone, tendon or capsule 4.2 Sinus assesses as extending to bone, tendon or capsule.	Stage 4	Ulceration extends into the subcutaneous fat. Small‐vessel thrombosis and infection compound fat necrosis. Underlying muscle is swollen and inflamed, and undergoes pathological changes. The relative avascular deep fascia temporarily impedes downward progress of the damage but promotes lateral extension, causing undermining of the skins. Epidermal thickening creates a distinct ulcer margin but inflammation, fibrosis and retraction distort the deeper areas of the sore.
Unstageable: Depth Unknown	Full thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, grey, green or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore Category/Stage, cannot be determined. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels serves as ‘the body’s natural (biological) cover’ and should not be removed.	Unstageable	When eschar is present, accurate staging of the pressure ulcer is not possible until the eschar has sloughed or the wound has been debrided.			Stage 5	Infective necrosis penetrates the deep fascia, and muscle destruction progresses rapidly. The wound spreads along the fascial planes and bursae, and may even reach the joints and body cavities. Osteomyelitis can easily develop. Multiple pressure ulcers may join, resulting in massive areas of tissue destruction.
Suspected Deep Tissue Injury: Depth Unknown	Purple or maroon localized area of discoloured intact skin or blood‐filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.