Pressure Injuries

Etiology references

1. 1. Farage MA, Miller KW, Elsner P, Maibach HI: Characteristics of the aging skin. Adv Wound Care (New Rochelle) 2(1):5–10, 2013. doi: 10.1089/wound.2011.0356

2. 2. Qaseem A, Mir TP, Starkey M, Denberg TD; Clinical Guidelines Committee of the American College of Physicians. Risk assessment and prevention of pressure ulcers: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2015;162(5):359-369. doi:10.7326/M14-1567

3. 3. Bergstrom N, Braden BJ, Laguzza A, Holman V: The Braden scale for predicting pressure sore risk. Nurs Res 36(4):205–210, 1987.

Pathophysiology References

1. 1. Gefen A. The complex interplay between mechanical forces, tissue response and individual susceptibility to pressure ulcers. J Wound Care. 2024;33(9):620-628. doi:10.12968/jowc.2024.0023

2. 2. Van Damme N, Van Hecke A, Remue E, et al. Physiological processes of inflammation and edema initiated by sustained mechanical loading in subcutaneous tissues: A scoping review. Wound Repair Regen. 2020;28(2):242-265. doi:10.1111/wrr.12777

3. 3. Sree VD, Rausch MK, Tepole AB. Linking microvascular collapse to tissue hypoxia in a multiscale model of pressure ulcer initiation. Biomech Model Mechanobiol. 2019;18(6):1947-1964. doi:10.1007/s10237-019-01187-5

4. 4. de Bengy AF, Lamartine J, Sigaudo-Roussel D, et al. Newborn and elderly skin: two fragile skins at higher risk of pressure injury. Biol Rev Camb Philos Soc. 2022;97(3):874-895. doi:10.1111/brv.12827

Staging systems

Several staging systems exist. The most widely used system is from the National Pressure Injury Advisory Panel (NPIAP), which classifies pressure injuries into four stages (1 to 4) according to the depth of tissue damage. However, the numerical staging does not imply linear progression of pressure injuries. That is, pressure injuries do not always manifest as stage 1 and then progress to higher stages. Sometimes, the first sign is a deep, necrotic stage 3 or 4 injury. In a rapidly developing pressure injury, subcutaneous tissue can become necrotic before the epidermis erodes. Thus, a small injury may in fact represent extensive subcutaneous necrosis and damage. Similarly, the scale does not imply that healing progresses from stage 4 through stage 1. The updated NPIAP staging system also includes definitions for unstageable, deep-tissue, medical device-related, and mucosal membrane pressure injuries (1).

Stage 1 pressure injuries manifest as intact skin with nonblanchable erythema, usually over a bony prominence. Color changes may not be as visible in dark skin. The lesion may also be warmer, cooler, firmer, softer, or more tender than adjacent or contralateral tissue. An actual ulcer (a defect of skin into the dermis) is not yet present. However, ulceration may occur with continued pressure, shear, friction, and/or moisture.

Stage 2 pressure injuries are characterized by partial-thickness skin loss, with loss of epidermis (erosion or blister) with or without true ulceration (defect beyond the level of the epidermis); subcutaneous tissue is not exposed. The injury is shallow with a pink to red base. No necrotic tissue is present in the base. Stage 2 also includes intact or partially ruptured blisters secondary to pressure. (NOTE: Non–pressure-related causes of erosion, ulceration, or blistering, such as skin tears, tape burns, maceration, and excoriation, are excluded from stage 2.)

Stage 3 pressure injuries manifest as full-thickness skin loss with involvement of subcutaneous tissue extending down to (but not including) the underlying fascia. The ulcers are crater-like but without underlying muscle or bone exposure.

Stage 4 pressure injuries manifest as full-thickness skin loss with extensive destruction, tissue necrosis, and exposure of underlying muscle, tendon, or bone.

Unstageable pressure injuries are characterized by full-thickness skin loss in which the extent of tissue damage cannot be determined because it is obscured by debris, slough, or eschar. If the slough or eschar is removed, a stage 3 or stage 4 pressure injury is revealed. However, stable, nonfluctuant lesions with dry eschar should never be debrided solely for the sake of staging.

Deep-tissue pressure injury is characterized by intact or nonintact skin with a localized area of damage to underlying tissue due to excessive pressure and/or shearing forces at the muscle-bone interface. Findings include persistent, nonblanchable, purple to maroon discoloration of intact skin, and blood-filled vesicles or bullae. The area may feel firmer, boggier, warmer, or cooler compared with surrounding tissue. In this context, the term deep-tissue pressure injury should not be used to describe underlying vascular, traumatic, neuropathic, or dermatologic conditions.

Medical device–related pressure injury results from the use of devices designed and applied for therapeutic purposes (eg, casts, splints). Prolonged use of poorly placed, ill-fitted medical devices can cause pressure injury to skin or mucosal membranes. Injury typically conforms to the pattern or shape of the device. The injury should be staged using the NPIAP staging system. Medical device–related pressure injury has been extended to include injury caused by personal protective equipment (PPE), including face masks, continuous positive airway pressure (CPAP) masks, oxygen tubing, and other devices that are used to prevent or manage respiratory conditions such as COPD or COVID-19.

Mucosal membrane pressure injury appears on mucous membranes where medical devices have been in use (eg, misfitting dentures, endotracheal tubes). Because of the anatomy of the tissue, these injuries cannot be staged.

When estimating the depth of pressure injuries for purposes of staging, it is important to take into account the anatomical location, especially in the case of stage 3 injuries. For example, the bridge of the nose, ear, occiput, and malleolus have minimal subcutaneous tissue and, consequently, pressure injuries in those locations are very shallow. However, they are still graded as stage 3 because they are as significant as deeper stage 3 injuries over locations with significant subcutaneous tissue (eg, the sacral region).

Manifestations of Pressure Injury Stages 1 to 4

Stage 1 Pressure Injury (Buttocks)

This photo of a stage 1 pressure injury shows nonblanchable redness but no break in the skin.

This photo of a stage 1 pressure injury shows nonblanchable redness but no break in the skin.

Photo from Gordian Medical, Inc. dba American Medical Technologies; used with permission.

Stage 2 Pressure Injury

This patient has a stage 2 pressure injury on the upper right buttock (arrow). There is loss of epidermis and an erythematous base. Subcutaneous tissue is not exposed. Note surrounding areas of stage 1 pressure injury (for an example, see arrowhead) with nonblanching erythema over intact epidermis.

This patient has a stage 2 pressure injury on the upper right buttock (arrow). There is loss of epidermis and an erythe

... read more

BOILERSHOT PHOTO/SCIENCE PHOTO LIBRARY

Stage 3 Pressure Injury (Foot)

This photo of a stage 3 pressure injury shows full thickness skin loss but no exposure of muscle or bone.

This photo of a stage 3 pressure injury shows full thickness skin loss but no exposure of muscle or bone.

Roberto A. Penne-Casanova/SCIENCE PHOTO LIBRARY

Stage 3 Pressure Injury (Base of Spine)

This photo of a stage 3 pressure injury shows subcutaneous tissue but no muscle or bone.

This photo of a stage 3 pressure injury shows subcutaneous tissue but no muscle or bone.

DR BARRY SLAVEN/SCIENCE PHOTO LIBRARY

Stage 4 Pressure Injury (Knee)

This photo of a stage 4 pressure injury shows visible deep structures, such as tendon and joint.

This photo of a stage 4 pressure injury shows visible deep structures, such as tendon and joint.

Photo from Gordian Medical, Inc. dba American Medical Technologies; used with permission.

Stage 1 Pressure Injury (Buttocks)

This photo of a stage 1 pressure injury shows nonblanchable redness but no break in the skin.

This photo of a stage 1 pressure injury shows nonblanchable redness but no break in the skin.

Photo from Gordian Medical, Inc. dba American Medical Technologies; used with permission.

Stage 2 Pressure Injury

This patient has a stage 2 pressure injury on the upper right buttock (arrow). There is loss of epidermis and an erythematous base. Subcutaneous tissue is not exposed. Note surrounding areas of stage 1 pressure injury (for an example, see arrowhead) with nonblanching erythema over intact epidermis.

This patient has a stage 2 pressure injury on the upper right buttock (arrow). There is loss of epidermis and an erythe

... read more

BOILERSHOT PHOTO/SCIENCE PHOTO LIBRARY

Stage 3 Pressure Injury (Foot)

This photo of a stage 3 pressure injury shows full thickness skin loss but no exposure of muscle or bone.

This photo of a stage 3 pressure injury shows full thickness skin loss but no exposure of muscle or bone.

Roberto A. Penne-Casanova/SCIENCE PHOTO LIBRARY

Stage 3 Pressure Injury (Base of Spine)

This photo of a stage 3 pressure injury shows subcutaneous tissue but no muscle or bone.

This photo of a stage 3 pressure injury shows subcutaneous tissue but no muscle or bone.

DR BARRY SLAVEN/SCIENCE PHOTO LIBRARY

Stage 4 Pressure Injury (Knee)

This photo of a stage 4 pressure injury shows visible deep structures, such as tendon and joint.

This photo of a stage 4 pressure injury shows visible deep structures, such as tendon and joint.

Photo from Gordian Medical, Inc. dba American Medical Technologies; used with permission.

Staging definition reference

1. 1. Editors of Nursing: Pressure ulcers get new terminology and staging definitions. Nursing 47(3):68–69, 2017. doi: 10.1097/01.NURSE.0000512498.50808.2b

Diagnosis references

1. 1. National Pressure Injury Advisory Panel. Pressure Ulcer Scale for Healing. Accessed July 30, 2025.

2. 2. Bharadwaj S, Ginoya S, Tandon P, et al. Malnutrition: Laboratory markers vs nutritional assessment. Gastroenterol Rep (Oxf) 4(4):272–280, 2016. doi: 10.1093/gastro/gow013

Pressure reduction

Reducing tissue pressure is accomplished through careful positioning of the patient, protective devices, and use of support surfaces (2, 3).

Frequent repositioning (and selection of the proper position) is the most important factor in maintaining pressure reduction. A written schedule should be used to direct and document repositioning of the patient. Patients confined to a bed should be turned a minimum of every 2 hours and should be placed at a 30° angle to the mattress when on their side (lateral decubitus) to avoid direct trochanteric pressure (4). Elevation of the head of the bed should be minimal to avoid the effects of shearing forces (ie, the forces the patient may experience in needing to change position). When repositioning patients, lifting devices (eg, a Stryker frame) or bed linen should be used instead of dragging patients to avoid unnecessary friction. Patients placed in chairs should be repositioned every hour and encouraged to change position on their own every 15 minutes.

Protective padding such as pillows, foam wedges, and heel protectors can be placed between and/or under the knees, ankles, and heels when patients are supine or on their side. Windows should be cut out of plaster casts at pressure sites in patients immobilized by fractures. Soft seat cushions should be provided for patients able to sit in a chair.

Support surfaces under patients confined to a bed can be changed to reduce pressure. They may be static or dynamic. They are often combined with other measures when treating pressure injuries. Support surfaces are classified based on whether they require electricity to operate. Static surfaces do not require electricity, whereas dynamic surfaces do.

Static surfaces include air, foam, gel, and water overlays and mattresses. Egg-crate mattresses offer no advantage. In general, static surfaces increase surface support area and decrease pressure and shearing forces. Static surfaces have traditionally been used for pressure injury prevention or stage 1 pressure injuries.

Dynamic surfaces include alternating-air mattresses, low-air-loss mattresses, and air-fluidized mattresses. In addition to reducing pressure, some dynamic mattresses increase the area of support, reduce heat and promote cooling, and decrease shear. Alternating-air mattresses have air cells that are alternately inflated and deflated by a pump, thus shifting supportive pressure from site to site. Low-air-loss mattresses are giant air-permeable pillows that are continuously inflated with air; the air flow has a drying effect on tissues. These specialized mattresses are indicated for patients with stage 1 pressure injuries who develop hyperemia on static surfaces and for patients with stage 3 or 4 pressure injuries. Air-fluidized (high-air-loss) mattresses contain silicone-coated beads that liquefy when air is pumped through the bed. The advantages of dynamic support surfaces include reduction of moisture and cooling. These mattresses are indicated for patients with nonhealing stages 3 and 4 pressure injuries or numerous truncal injuries (see table Options for Support Surfaces).

Compared with some static surfaces (eg, foam) reactive air surfaces (eg, alternating-air mattresses) may reduce pressure ulcer risk and may increase complete ulcer healing, however the certainty of available evidence is low (5). 

Friction reduction using barrier protectants such as petroleum jelly has been shown to reduce the friction caused by personal protective equipment immediately after application. However, frequent reapplication (every hour) is necessary to maintain the protective effect, limiting their potential usefulness.

Moisture reduction strategies, such as promptly addressing incontinence and keeping the skin clean, dry, and protected from excessive dampness by the use of appropriate barrier creams or dressings, may additionally help in preventing the development of moisture-associated skin damage and pressure injury.

Direct wound care

Appropriate wound care involves cleaning, debridement, and dressings.

Cleaning should be performed initially and also with each dressing change. Normal saline is usually the best choice of a cleansing agent. Cleaning often involves irrigation at pressures sufficient to remove bacteria without traumatizing tissue; commercial syringes, squeeze bottles, or electrically pressurized systems can be used. Irrigation may also help remove necrotic tissue (debridement). Alternatively, a 35-mL syringe and an 18-gauge IV catheter can be used. Irrigation should continue until no further debris can be loosened. Antiseptics and antiseptic washes (eg, iodine, hydrogen peroxide, sodium hypochlorite) can destroy healthy granulation tissue and keratinocytes and thus should generally be avoided. However, hypochlorous acid–based wound cleansers have been developed that reduce microbial burden without impairing normal cell function and, thus, may be used in many treatment settings (should be performed initially and also with each dressing change. Normal saline is usually the best choice of a cleansing agent. Cleaning often involves irrigation at pressures sufficient to remove bacteria without traumatizing tissue; commercial syringes, squeeze bottles, or electrically pressurized systems can be used. Irrigation may also help remove necrotic tissue (debridement). Alternatively, a 35-mL syringe and an 18-gauge IV catheter can be used. Irrigation should continue until no further debris can be loosened. Antiseptics and antiseptic washes (eg, iodine, hydrogen peroxide, sodium hypochlorite) can destroy healthy granulation tissue and keratinocytes and thus should generally be avoided. However, hypochlorous acid–based wound cleansers have been developed that reduce microbial burden without impairing normal cell function and, thus, may be used in many treatment settings (6).

Debridement is necessary to remove necrotic tissue. Necrotic tissue serves as a medium for bacterial growth and blocks normal wound healing. Methods include:

• Mechanical debridement: This method includes hydrotherapy (eg, whirlpool baths, pulsatile lavage) and most commonly wet-to-dry dressings. Cleaning wounds by irrigation at sufficient pressures can also accomplish mechanical debridement. Mechanical debridement removes necrotic debris on the wound’s surface and should only be performed on wounds with very loose exudate. In wet-to-dry dressings, exudate and necrotic tissue adhere to a gauze dressing as it dries so that removal of the gauze thus debrides the wound; this method must be used cautiously because dressing changes are painful and may remove underlying healthy granulation tissue (ie, tissue necessary for proper healing).

• Sharp (surgical) debridement: This method involves using a sterile scalpel or scissors to remove eschar and thick necrosis. Modest amounts of eschar or tissue can be debrided at the patient’s bedside, but extensive or deep areas (eg, if underlying bone, tendon, or joints are exposed) should be debrided in the operating room.

• Autolytic debridement: Synthetic occlusive (hydrocolloids/hydrogels) dressings or semi-occlusive (transparent film) dressings are used to facilitate the digestion of dead tissues by the enzymes already normally present in the wound. Autolytic debridement may be used for smaller wounds with little exudate. This method should not be used if a wound infection is suspected.

• Enzymatic debridement: This technique (using collagenase, papain, fibrinolysin, deoxyribonuclease, or streptokinase/streptodornase) can be used for patients with mild fibrotic or necrotic tissue within the ulcer. It can also be used for patients whose caretakers are not trained to perform mechanical debridement or for patients unable to tolerate surgery. It is most effective after careful and judicious cross-hatching of the wound with a scalpel to improve penetration. This technique (using collagenase, papain, fibrinolysin, deoxyribonuclease, or streptokinase/streptodornase) can be used for patients with mild fibrotic or necrotic tissue within the ulcer. It can also be used for patients whose caretakers are not trained to perform mechanical debridement or for patients unable to tolerate surgery. It is most effective after careful and judicious cross-hatching of the wound with a scalpel to improve penetration.

• Biological debridement: Medical maggot therapy is useful for selectively removing dead necrotic tissue; maggots (fly larvae) eat only dead tissue. This method is most helpful in patients who have exposed bone, tendons, and joints in the wound where sharp debridement is contraindicated.

Dressings are helpful for protecting the wound and facilitating the healing process. They should be used for stage 1 pressure injuries that are subject to friction or incontinence and for all other pressure injuries (see table Options for Pressure Injury Dressings).

In stage 1 pressure injuries subject to increased friction, transparent films are sufficient. For injuries with minimal exudate, transparent films or hydrogels, which are cross-linked polymer dressings that come in sheets or gels, are used to protect the wound from infection and create a moist environment that optimizes physiologic healing processes. Transparent films or hydrogels should be changed every 3 to 7 days.

Hydrocolloids, which combine gelatin, pectin, and carboxymethylcellulose in the form of wafers and powders, are indicated for pressure injuries with light exudate and can be left in place for up to 1 week depending on the amount of drainage.

Alginates (polysaccharide seaweed derivatives containing alginic acid), which come as pads, ropes, ribbons, and gelling fiber dressings are indicated for absorbing extensive exudate. Alginates also have hemostatic properties useful for controlling bleeding after surgical debridement. Both of these dressings can be placed for up to 7 days but must be changed earlier if they become saturated.

Foam dressings can be used in wounds with various levels of exudate and provide a moist protective environment for wound healing. Foam dressings can often stay in place for up to 7 days but must be changed once saturated. Waterproof versions protect the skin from incontinence.

Management of pain

Pressure injuries can cause significant pain. Pain should be monitored regularly using a pain scale.

Primary treatment of pain is treatment of the injury itself, but a nonsteroidal anti-inflammatory drug (NSAID) or acetaminophen is useful for mild-to-moderate pain. Opioids should be avoided if possible because sedation promotes immobility. However, opioids or topical nonopioid preparations such as mixtures of local anesthetics may be necessary during dressing changes and debridement. Primary treatment of pain is treatment of the injury itself, but a nonsteroidal anti-inflammatory drug (NSAID) or acetaminophen is useful for mild-to-moderate pain. Opioids should be avoided if possible because sedation promotes immobility. However, opioids or topical nonopioid preparations such as mixtures of local anesthetics may be necessary during dressing changes and debridement.

In cognitively impaired patients, changes in vital signs can be used as indicators of pain (eg, tachycardia, tachypnea).

Control of infection

Pressure injuries should be continually assessed for signs of bacterial infection such as increased erythema, foul odor, warmth, drainage, fever, and elevated white blood cell count. Impaired wound healing should also raise concern of infection. These abnormal findings indicate a wound culture should be performed. However, because all pressure ulcers are colonized, results should be interpreted with caution; bacterial count rather than bacterial presence should guide treatment.

Superficial skin infection or critical colonization can be treated topically with agents such as silver sulfadiazine, mupirocin, polymyxin B, and metronidazole. Superficial skin infection or critical colonization can be treated topically with agents such as silver sulfadiazine, mupirocin, polymyxin B, and metronidazole.Silver sulfadiazine and similar opaque topical agents should be used cautiously because they can impair visualization of the underlying wound and can be difficult to remove.

Systemic antibiotics should be given for cellulitis, bacteremia, or osteomyelitis. Tissue culture and/or blood cultures should be obtained, followed by initiation of empiric antibiotics until culture growth and sensitivity results can be obtained. Treatment should then be narrowed as appropriate based on tissue culture growth and sensitivity results. Tissue culture is always preferred to surface swab culture when possible. Limiting the use of broad-spectrum antibiotics is important to help prevent adverse effects, minimize bacterial resistance, and limit disruption of the skin and gut microbiome.

Assessment of nutritional needs

Evidence from various studies (including clinical trials) underscores the importance of personalized nutritional interventions in managing pressure injury (7). Undernutrition is common among patients with pressure injuries and is a risk factor for delayed healing. Markers of undernutrition include albumin < 3.5 g/dL (< 35 g/L) or weight < 80% of ideal. Protein intake of 1.25 to 1.5 g/kg/day, sometimes requiring oral, nasogastric, or parenteral supplementation, is desirable for optimal healing.

Adjunctive therapy

Multiple adjunctive therapies to promote healing are being evaluated, and their benefit remains uncertain (3). These therapies include the following:

• Negative-pressure wound therapy (vacuum-assisted closure, or VAC): This therapy is used to apply suction to the wound. It can be applied to clean wounds. High-quality evidence of efficacy does not yet exist, but negative-pressure wound therapy has shown some promise in small studies.

• Topical recombinant growth factors: Some evidence suggests that topical recombinant growth factors (eg, nerve growth factor, platelet-derived growth factor) facilitate wound healing.

• Cellular and tissue-based products: Cellular and acellular matrices (ie, skin substitutes) have been used to treat a variety of chronic wounds and have been reported to show benefit in advanced pressure injuries, but evidence is preliminary and randomized trials are lacking.

• Electrical stimulation therapy: Electrical stimulation therapy combined with standard wound therapy can increase wound healing.

• Hyperbaric oxygen therapy:This therapy not established as a standard treatment and its role remains investigational. It may be considered as an adjunct in select refractory cases of chronic nonhealing wounds.

• Therapeutic ultrasound: Ultrasound is sometimes used, but there is no good evidence of benefit or harm.

• Electromagnetic, phototherapy (laser) heat, massage: No evidence supports efficacy of these treatments.

Surgery

Large defects require surgical closure, especially when there is associated exposure of underlying musculoskeletal structures.

Skin grafts are useful for large, shallow defects. However, because grafts do not add to blood supply, measures must be taken to prevent pressure from developing to the point of ischemia and further breakdown.

Skin flaps, including myocutaneous, fasciocutaneous, and perforator-based flaps, are preferred and are the closures of choice over large bony prominences (usually the sacrum, ischia, and trochanters) (8).

Surgery may rapidly improve the quality of life in patients with pressure injuries. Surgical outcomes are best if preceded by optimal treatment of underlying risk factors such as undernutrition and comorbid disorders.

Treatment references

1. 1. Mervis JS, Phillips TJ. Pressure ulcers: Prevention and management. J Am Acad Dermatol. 2019;81(4):893-902. doi:10.1016/j.jaad.2018.12.068

2. 2. Reddy M, Gill SS, Kalkar SR, et al. Treatment of pressure ulcers: a systematic review. JAMA. 2008;300(22):2647-2662. doi:10.1001/jama.2008.778

3. 3. Qaseem A, Humphrey LL, Forciea MA, et al; Clinical Guidelines Committee of the American College of Physicians. Treatment of pressure ulcers: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2015;162(5):370-379. doi:10.7326/M14-1568

4. 4. National Clinical Guideline Centre (UK). The Prevention and Management of Pressure Ulcers in Primary and Secondary Care: NICE Clinical Guidelines, No. 179. London: National Institute for Health and Care Excellence (NICE); 2014. Accessed July 30, 2025.

5. 5. Shi C, Dumville JC, Cullum N, et al. Beds, overlays and mattresses for preventing and treating pressure ulcers: an overview of Cochrane Reviews and network meta-analysis. Cochrane Database Syst Rev. 2021;8(8):CD013761. Published 2021 Aug 16. doi:10.1002/14651858.CD013761.pub2

6. 6. Mallow PJ, Black J, Chaffin AE, et al. The economic and quality effects of wound cleansing with pure hypochlorous acid: evidence-based evaluation and clinical experience. Wounds. 2024;36(10):S1-S13. doi:10.25270/wnds/24101

7. 7. Kassym L, Zhetmekova Z, Kussainova A, et al. Pressure Ulcers and Nutrients: From Established Evidence to Gaps in Knowledge. Curr Med Chem. Published online November 4, 2024. doi:10.2174/0109298673322825241018174928

8. 8. Sameem M, Au M, Wood T, et al: A systematic review of complication and recurrence rates of musculocutaneous, fasciocutaneous, and perforator-based flaps for treatment of pressure sores. Plast Reconstr Surg 130(1):67e–77e, 2012. doi: 10.1097/PRS.0b013e318254b19f