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Pressure injury (PI) is defined as localized damage to the skin and/or underlying soft tissue usually over a bony prominence or related to a medical or other device.1 The following pressure injury stages and categories are described.

  • Stage 1 describes non-blanching erythema of intact skin.
  • Stage 2 is a partial-thickness skin loss exposing the dermis.
  • Stage 3 is a full-thickness skin loss.
  • Stage 4 is a full-thickness skin loss with exposed or palpable fascia, muscle, tendon, ligament, cartilage, or bone.
  • An unstageable pressure injury is characterized by full-thickness skin and tissue loss whereby the extent of damage cannot be confirmed because the base is obscured by slough or eschar.
  • A deep tissue injury (DTI) is intact or non-intact skin with persistent non-blanchable deep red or purple discoloration or bruising.

In 2016, the terminology of pressure ulcer was changed to pressure injury and specific pressure injury definitions were added. Medical device related pressure injury describes the etiology of the injury and should follow the above classification system for staging. Mucosal membrane pressure injury describes injury due to use of medical device at the location of mucous membranes and cannot be staged according to the above classification system.1


Pressure injuries occur from intense and/or prolonged pressure, or from pressure in combination with shear. An external mechanical load causes axial pressure and shear (i.e., force or stress tangential to the skin), leading to the body’s internal response and formation of the pressure injury. Pressure injuries can form within 1-2 hours of sustained external load and can manifest immediately from time of external load up to several days after insult. Shear stress has two deleterious effects: first, it can cause deep tissue deformation and necrosis; second, it can lead to superficial friction to the stratum corneum, damaging the barrier function. Pressure injuries can form on buttocks, coccyx, sacrum, ischia, trochanters, occiput, heels and other bony prominences.

Epidemiology including risk factors and primary prevention

Pressure injuries affect millions of individuals in the US each year, in various settings including acute care, long-term care, and the home. Complications can be very serious, including localized infection, sepsis, and even death. Pressure injuries have a large impact on the health care system, with total annual costs in the billions.2

Risk factors for pressure injuries include pressure, shear, impaired mobility, skin moisture, malnutrition, diminished capillary perfusion, and aging.3 Pressure injuries are also associated with dementia, critical illness, pain, immobility, diabetes, atherosclerosis, end-stage renal disease, medications (steroids, immune-suppressants), smoking, upper or lower motor neuron disease, contractures, and non-adherence to treatments.4

Two groups at high risk include the spinal cord injured and the elderly. For community-dwelling elderly, the incidence increases significantly with advancing patient age.5 The absence of protective sensation increases risk of pressure injury, such as from spinal cord injury (SCI) or other neurologic conditions. From SCI model systems data, the prevalence of pressure injury increases in time post-injury, from 25.2% during the first-year post-injury, to 27.1% fifteen years post-injury.6

Other risk factors may include improper seating and sleeping surfaces, cushion or mattress malfunction, incomplete skin clearance during transfers, prolonged travel limiting pressure releases, and any other equipment malfunction.


The skin is the largest organ in the body, composed of three layers: (1) epidermis, the outermost layer of the skin; (2) dermis, the layer beneath the epidermis, composed of connective tissue, glands, and follicles; and (3) the subcutaneous deeper layer (hypodermis), made up of fat and connective tissue.

One can think of pressure injury formation in two ways: forming “top-down” and “bottom-up.” Top-down formation involves pressure and shear damaging surface skin and the upper few millimeters of the sub-cutaneous layer. Bottom-up formation usually occurs with DTI. Sustained strain of muscle between the external load and a bony prominence forms the injury beneath the skin surface, damaging the deep tissues.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

From the “top-down”, pressure injuries can form when an external mechanical load or pressure is applied on or against the skin, so that blood flow is compromised to that area. Initially, after short periods of pressure there is reversible damage to the skin which is manifested as blanching erythema. However, once the erythema is non-blanching, localized tissue damage has occurred, leading to the formation of a Stage 1 pressure injury. Depending on the depth and severity of the tissue damage, a pressure injury can present as a Stage 2, Stage 3, or Stage 4 injury. Another presentation is a DTI, described below.

For DTIs, disease progression generally manifests when pressure is applied over a bony prominence, causing compression in the deep or underlying tissues. Initially or within a few days there is non-blanching erythema seen as red-purple or dark-maroon rather than pink-red. Following this, there is often sloughing and blistering of the surface, with a darker base often seen. One can see demarcation of black or yellow eschar at the site base. DTI can be a marker of pre-terminal status. “Skin failure” is a phenomenon where DTI forms with greater frequency and severity near death.7

For medical device related, the resultant pressure injury usually follows the pressure pattern from the device in question. As mentioned above, mucosal membrane pressure injuries cannot be staged due to the anatomy of mucosal membrane tissues.1

Specific secondary or associated conditions and complications

Secondary conditions and associated complications of pressure injuries are varied. Commonly, one sees associated infection, osteomyelitis, cellulitis and possibly sepsis. Pressure injuries can erode into joint capsules causing septic arthritis. Ischial pressure injuries can form fistulae to the rectum or bladder. Pressure injuries of the heel, if Stage 4, may lead to ischemia, infection and/or ultimately limb loss.

Essentials of Assessment


The clinical interview and history are key in the assessment of pressure injury.

  • When did the patient notice the skin changes and pressure injury?
  • Did it occur after a specific inciting event, trauma, or fall?
  • Has the individual experienced a change in their mobility and/or functional status?
  • Has the individual been limited to bedrest for some reason?
  • Which dressings, topical ointments or antibiotics have been used?
  • Does the patient have sensation and complain of any discomfort in the area?
  • Has the patient experienced any weight changes or weight loss?
  • Has there been any equipment (i.e., bed, mattress, wheelchair cushion) malfunction noted?
  • Is the patient unable to communicate the problem due to speech or memory deficit?

Physical examination

For the general physical exam: evaluate body habitus and nutritional status. Note if the individual appears thin, pallid, frail, or chronically ill. Assess for weight loss, Body Mass Index (BMI), contractures, muscle strength, range of motion, memory and cognitive deficits, pedal pulses, and sensory impairments.

For the pressure injury: examine skin with patient in side-lying or lateral decubitus position. Note exact location and side (right vs. left) if indicated. Wound length, width and depth are measured in centimeters. Measure depth at the deepest point in the wound bed. Evaluate for any tunneling or undermining “by the clock” (e.g., 4 centimeters of tunneling at 6 o’clock; with noon toward the head). Note color of the wound bed (i.e., beefy red, dusky pink, yellow or black necrotic). Assess the wound base itself for percentage of slough or necrotic tissue (i.e., scab or eschar).  Note any odor, drainage (quality and amount), palpable bone, rolled or thickened edges, and peri-wound skin status as well. Wounds typically appear as follows. The National Pressure Ulcer Advisory Panel provides the following illustrations of each pressure injury Stage.1 Please refer to definitions of each Stage described above in the definition section.

Functional assessment

Watch for impaired bed mobility, weight shifts, transfers and ambulation. Assess for cognitive or communication deficits and be mindful of non-verbal signs of discomfort. Consider the location of the pressure injury as clues to formation:

  • Sacral injuries: Supine positioning
  • Coccygeal injuries: Supine positing or “sacral sitting” (i.e., slouching)
  • Trochanteric injuries: Lateral decubitus position
  • Ischial injuries: Sitting
  • Heel or lateral ankle injuries: External rotation with lateral compression.
  • Malleoli, fibular head, lateral forefoot injuries: Wheelchair leg rests, shoes, orthotics.
  • Elbow injuries: Wheelchair armrests.
  • Scapular injuries: Wheelchair backrests.
  • Occipital injuries: Cervical collars, bed/pillow positioning.
  • Medical device and mucosal membrane injuries: Examine trajectory or pressure pathway related to device or mucous membrane irritant (i.e., urinary catheter).

The location of a pressure injury is often multifactorial. However, the etiology of CNS disorder can provide insight on which locations are most likely to be impacted. Patients with spinal cord injuries typically experience pressure injuries at the sacrum (most common), heels, and ischium.8 A study in patients with traumatic brain injury noted the sacrum to be the most common area for pressure injury within the first 30 days of injury.9 Additionally, pressure injuries noted in patients after ischemic or hemorrhagic strokes were most commonly seen in the sacral region.10

Laboratory studies

White blood count (WBC) can evaluate systemic infection or inflammation. C-reactive protein and erythrocyte sedimentation rate are non-specific inflammatory markers of osteomyelitis which can be used to guide response to treatment only. Other lab markers for underlying diseases may be helpful to assess secondary disease control (i.e., A1C for Diabetes).

There is no lab test that is both sensitive to and specific for malnutrition.11 In the past, clinicians have used prealbumin and albumin as a reflection of nutritional status. Current practice is to perform a nutrition-focused physical examination (NFPE) to diagnose malnutrition. The subjective global assessment (SGA) is a well-validated tool for recognizing malnutrition, assessing nutritional status based on history and physical findings. The clinician’s history should assess weight loss in the last six months, dietary intake changes, comorbid disease states and related nutritional demands, functional capacity, and gastrointestinal symptoms. The exam should evaluate for edema, muscle wasting, subcutaneous fat, and ascites.12


  • X-ray can help make the diagnosis of osteomyelitis if positive for bony erosion.
  • MRI for osteomyelitis can localize the lesion anatomically and give information about acute vs. chronic infection.
  • Consider bone scan when MRI is contraindicated.
  • Consider vascular studies to assess peripheral arterial disease (PAD) and distal limb blood supply for heel ulcers.

Supplemental assessment tools

The Braden scale is a valid, reproducible measure, which quantifies pressure injury risk. The classical Braden scale involves six sub-scales, each with four levels. The sub-scales are: 1) Insensitivity; 2) Mobility; 3) Activity; 4) Nutrition; 5) Moisture; 6) Friction and shear. The overall scale ranges from 6 to 24, with the highest score indicating lowest risk.13 The Norton risk assessment tool has five sub-scales and is also valid.

Early predictions of outcomes

Predictors of good outcomes for pressure injury are maintaining good nutrition, diligence with wound treatment regimen and pressure off-loading, utilizing optimal seating and mattress surfaces for skin protection, control of secondary medical conditions, and compliance from both the patient and caregiver with pressure injury prescription and treatment program.

  • Stage 1 pressure injuries often resolve within days to weeks.
  • Stage 2 pressure injuries generally heal within weeks.
  • Stage 3 pressure injuries may take weeks to months
  • Stage 4 injuries may require 6-12 months to conservatively close.


Assess pressure support surfaces: bed, wheelchair, cushion, and lift/sling mechanisms used for transfers.

Ask about recliner use: recliners are associated with pressure injury formation of the sacrum, as turning and positioning are difficult, and positioning often enables sacral sitting.

Evaluate caregiver support and assistance available for skin prevention and prevention off-loading techniques.

Professional issues

All members of the rehabilitation team play a key role in the management of pressure injuries: nursing (health promotion and teaching, bowel and bladder management, wound care), physical therapy (mobility and equipment review), occupational therapy (self-care, equipment review), speech-language pathology (cognition, carryover, mental status), clinical dietician or nutritionist (calorie and protein assessment, monitor nutritional status), and psychologist (emotional adjustment). As function improves, healing occurs.

Outpatient team staffing may be more limited to outpatient or home health nursing (dressing changes and teaching), and physical therapy for bed mobility and functional transfers.

Consultants: For specialty wound care treatment and recommendations, consult a wound care specialist if available. For osteomyelitis, consider infectious disease; for debridement or flap surgery consider plastic, general, or orthopedic surgery; for a heel pressure injury, consider podiatry and/or vascular surgery.

Rehabilitation Management and Treatments

Available or current treatment guidelines

Pressure injury care has the benefit of several excellent guidelines over the years for prevention and management. Two current guidelines are highly recommended

  • National Pressure Ulcer Advisory Panel (NPUAP) guidelines, 20161
  • Consortium for Spinal Cord Medicine Clinical Practice Guidelines, 20143

At different disease stages

  • As a pressure injury heals, it continues to be referred to by the stage at which it initially presented.
  • Consider infectious disease consultation for systemic signs or symptoms of acute infection. Sterile or intra-operative cultures are best to drive antibiotic treatment. Wound swab cultures are usually polymicrobial. Antibiotics are generally not recommended unless there is acute infection or active osteomyelitis. Where there are signs or symptoms of acute infection or systemic illness, consider inpatient admission.
  • If wound debridement is needed, may use chemical or enzymatic debridement with collagenase. Sharp debridement can also be performed with pickups, scissors, curette, or scalpel. For sensate patients and/or to reduce discomfort, pre-medicate, using topical anesthesia and offer “time out” and redirection during the procedure.
  • Consider podiatry consult for unstageable or Stage 4 of the heel. If heel eschar is present, leave in place until appropriate surgical debridement can take place. Steps to preserve the limb include 1) revascularization; 2) appropriate surgical debridement; 3) antibiotics for osteomyelitis; 4) consideration of hyperbaric oxygen for osteomyelitis.14
  • Negative pressure wound therapy (NPWT or wound vacuum therapy) for Stage 3 or 4 injuries. Indication: when the pressure injury is debrided to about an 80% red base, wound bed is clean and free of acute infection. Purpose: promote granulation tissue formation.15 Endpoint: Granulation tissue fills most of the “dead space.” Contraindications: Untreated cellulitis, osteomyelitis, or exposed artery.
  • For Stage 3-4 pressure injuries in persons with spinal cord injury, reconstructive surgery might be the best option and should be considered.
  • Nutritional requirements can vary for each individual patient. Consultation with clinical dietician or nutritionist is key to assess average caloric needs and optimize nutrition for wound healing. Consider vitamin and mineral supplementation including Vitamin C and Zinc.
  • Wound dressings can vary by pressure injury Stage.
  • For Stage 1 injuries, protective dressings can provide adequate cushioning.
  • For Stage 2 or shallow Stage 3 with scant to minimal drainage foams or films, zinc oxide paste (which is relatively imperious to moisture and shear) or barrier creams are often sufficient.
  • For Stage 3-4 with moderate or significant drainage consider alginate or absorptive dressings.

At all disease stages

Pressure injuries are assessed at least weekly. Key assessments include length, width, depth, undermining, tunneling, drainage, odor, peri-wound skin status. Evaluation with serial photographs is best if available and practice complies with patient privacy regulations. Assessments are graphed versus time to illustrate healing rate and progression. If pressure injury does not show improvement in 2-3 weeks with the current treatment regimen, consider therapeutic change.

Wheelchair and cushions: Patients with stage 3 or 4 ischial pressure injuries, especially if insensate, should limit sitting as much as possible (if not completely) while pressure injuries are healing. Of course, the benefits of pressure off-loading must be balanced against potential risks (i.e., depression, social isolation, quality of life). One should consider a tilt-in-space wheelchair with a custom seating cushion system and appropriate leg rests for patients with a greater than Stage 2-4 pressure injuries who require assistance with pressure off-loading. Consider pressure mapping.

Specialty bed: For stage 1 and 2 pressure injuries, a foam or air overlay is often enough. For the patient with a stage 3 or 4 sacral pressure injury, a low air loss or dynamic pressure relief mattress is appropriate. Turn and reposition every two hours.1

Cutting Edge/ Emerging and Unique Concepts and Practice

There are many emerging treatment practices in the field of pressure injury management, including but not limited to the following:

  • Electrical Stimulation (ES) has been shown to be beneficial in the healing of PIs. Electrodes are placed on the skin, which provide electrical current to the treatment area, either in direct or pulsed current. There are many theories of how ES affects the inflammatory, proliferative, epithelialization, and remodeling phases of healing of PIs. It thought to increase blood flow to the area and increases tissue oxygenation. There is some thought that ES can also provide a bacteriostatic effect.16
  • Hyperbaric Oxygen (HBO) has been used for various skin conditions, including diabetic ulcers, vascular ulcers, and PIs. Patients are placed in a chamber using pure oxygen at pre-set flow rates. It is thought to increase oxygen transport to the wound bed and speed of wound healing by reducing inflammation and edema, improving circulation, and possibly reducing infection by stimulating the immune system and eliminating toxins in the blood.17
  • Bone marrow/autologous stem cells uses live cells to try to repair or restore the damaged tissue area of the wound bed. The bone marrow or stem cells are thought to recruit macrophages and endothelial cells to the wound bed, enhancing wound healing by preventing apoptosis, promoting angiogenesis, and assisting in wound matrix reorganization. It is a newer therapy but has demonstrated efficacy in healing skin wounds and sores.17
  • Bio-engineered skin, or skin substitutes, had been used for treatment of wounds, particularly in partial or full-thickness wounds as biological wound dressings. It is thought that this modality induces angiogenesis. Limitations of this therapy include difficulties in application due to amounts of exudate in the wound bed and/or external forces that prevent graft adherence.17
  • Cytokines and growth factors are thought to affect the inflammation, collagen matrix structure, apoptosis, and rate of healing of wounds. Some examples include fibroblast growth factor, granulocyte-macrophage colony-stimulating factor, interleukins, tumor necrosis factor, and endothelial growth factor. These substances may have an integral role in the treatment of PIs in the future.

Gaps in the Evidence-Based Knowledge

The knowledge and science of PI assessment, treatment, and prevention is constantly evolving. Current gaps in the clinical care of individuals with PIs are varied.

  • Guidelines need to be based on thorough and comprehensive review of available literature and rigorous research methods.
  • Unique characteristics of individuals with CNS disorders must be considered.
  • Clinicians need to stay updated with new terminology and definitions, Staging, and prevention strategies as they are identified in the literature and by professional organizations.
  • Evidence based research must continue forward in the emerging concepts and practices described above, as well as with any new therapies discovered, in order to identify beneficial treatments and interventions for PIs.
  • Research and patient care must be created and carried out in an interdisciplinary framework in order to achieve the greatest success in skin prevention and treatment.


  1. National Pressure Ulcer Advisory Panel (NPUAP). Clinical Practice Guidelines for Prevention and Treatment, www.npuap.org; 2016.
  2. Kruger E, Pires M, et al. Comprehensive management of pressure ulcers in spinal cord injury: Current concepts and future trends. The Journal of Spinal Cord Medicine. 2013;36(6): 572-585.
  3. Garber S, Bryce T, et al. Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury: A Clinical Practice Guideline for Health-Care Professionals. Paralyzed Veterans of America. Second Edition. 2014.
  4. Goldman RJ, Popescu A, et al. Prevention and management of chronic wounds. In: Braddom R, ed. Physical Medicine & Rehabilitation. Philadelphia, PA, Saunders Elsevier; 2007:685-708.
  5. Margolis DJ, Bilker W, et al. The incidence and prevalence of pressure ulcers among elderly patients in general medical practice. Annals of Epidemiology. 2002;12(5): 321-325.
  6. National Spinal Cord Injury Statistical Center. 2019 Annual Statistical Report for the Spinal Cord Injury Model Systems, www.nscisc.uab.edu;2019.
  7. Langemo DK, Brown G. Skin fails too: acute, chronic, and end-stage skin failure. Advances in Skin & Wound Care. 2006;19(4): 206-211.
  8. Verschueren, JM, Post, MM, et al. Occurrence and predictors of pressure ulcers during primary in-patient spinal cord injury rehabilitation. Spinal Cord. 2010; 49(1), 106–112.
  9. Osis, SL, & Diccini, S. Incidence and risk factors associated with pressure injury in patients with traumatic brain injury. International Journal of Nursing Practice. 2020; 26(3).
  10. Farid, J, Amin, R, Sheikh, MA, et al. Prevalence and prediction of pressure ulcers in admitted stroke patients in a tertiary care hospital. Journal of Tissue Viability. 2022; 31(3).
  11. Academy of Nutrition and Dietetics. Pocket Guide to Nutrition Assessment. 3rd ed. Chicago, IL: Academy of Nutrition and Dietetics; 2016:104-106.
  12. Bharadwaj S, Ginoya S, et al. Malnutrition: laboratory markers vs nutritional assessment. Gastroenterology Report. 2016 Nov; 4(4):272-280.
  13. Bergstrom N, Braden B, et al. The Braden Scale for predicting pressure sore risk. Nurs Res. 1987:36:205-210.
  14. Goldman RJ. Hyperbaric oxygen therapy for wound healing and limb salvage: a systematic review. PM&R. 2009;1(5): 471-489.
  15. de Leon JM, Barnes S, et al. Cost-effectiveness of negative pressure wound therapy for postsurgical patients in long-term acute care. Adv Skin Wound Care. 2009;22(3):122-127.
  16. Arora M, Harvey LA, Glinsky JV, Nier L, Lavrencic L, Kifley A, Cameron ID. Electrical stimulation for treating pressure ulcers. Cochrane Database of Systematic Reviews 2016, Issue 5. Art. No.: CD012196. DOI: 10.1002/14651858.CD012196.
  17. Bhattacharya S, Mishra RK. Pressure ulcers: Current understanding and newer modalities of treatment. Indian J Plast Surg. 2015;48(1):4–16. doi:10.4103/0970-0358.155260

Original Version of the Topic:

Scott Campea, MD. Pressure Ulcer Management. 11/15/2011

Previous Revision(s) of the Topic:

Robert J. Goldman, MD. Pressure Ulcer Management. 9/20/2013

Sarah Wagers, MD, Preeti Panchang, MD. Pressure Ulcer Management. 5/05/2016

Juan L Asanza, MD. Pressure Injury Management in CNS Disorders. 10/29/2019

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Juan L Asanza, MD
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Hetal Patel, MD
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