Pressure Ulcer Management

Author(s): Sarah Wagers, MD, Preeti Panchang, MD

Originally published:11/15/2011

Last updated:05/05/2016

1. DISEASE/DISORDER:

Definition

A pressure ulcer (PrU), also known as a bedsore or decubitus ulcer, is a localized injury to the skin and/or underlying tissue usually over a bony prominence as a result of unrelieved pressure. Most commonly seen over the sacrum, heels, ischial tuberosities, heels, and lateral malleoli.

Etiology

Pressure ulcers occur due to prolonged external pressure on tissue overlying a bony prominence, which impedes blood flow resulting in local ischemia and tissue deformation.  Tissue response to such stresses depends on its viscoelastic and microvascular properties.

Epidemiology including risk factors and primary prevention

Pressure sores are associated with increased morbidity and mortality. About 70% die within six months (17). A large cohort study of PrUs prevalence in 2008-2009, showed prevalence and incidence rate of facility-acquired PrUs was 12%-13% and 5%-6%, respectively. Facility-acquired PrUs occurred most frequently in adult intensive care units (rates range from 9%-12%, with ~3% of ICU patients with severe PrUs). Overall prevalence rates were highest in long-term acute care (22%). Lifetime rates of PrUs development in people with spinal cord injury are estimated at 25%-85%. Pressure ulcer incidence is now a quality-of-care indicator for long-term care facilities with Center of Medicare and Medicaid Services regulating compliance.

Risk factors for development of pressure sores:

  • Impaired mobility: One of the more common reasons of exposure to prolonged, uninterrupted pressure. Seen in patients who are unable to independently alter their position in bed or on hard surfaces such as wheelchairs and stretchers (neurologic abnormalities, sedation, paralysis, spasticity, contractures). Lack of activity also causes loss of subcutaneous tissue and muscle atrophy, thereby decreasing the cushioning over the bony prominences.
  • Incontinence of bowel or bladder: Moist environment from urinary incontinence leads to maceration and development of a pressure sore. Bowel incontinence would result in an infection.
  • Excessive moisture and perspiration: Creates warm, moist reservoirs for bacterial contamination, which increases the risk of ulceration and infection.
  • Pressure from hard surfaces – wheelchair, stretchers.

Conditions affecting healing:

  • Co-morbidities :DM, cardiovascular disease vasculitis or collagen vascular disorders, PVD, immunodeficiency, steroid use, dementia. These have been identified as risk factors and also impair healing. Most of these conditions result in impaired circulation and sensation
  • Aging: Not a risk factor in itself for the development of pressure sores but advanced age cause skin atrophy and loss of elasticity, predisposing it to breakdown and increasing the duration for healing. Epidermal turnover and vascularity are affected as well.

Patho-anatomy/physiology

Main external factors contributing to pressure sores are prolonged pressure, shearing forces, friction and moisture. Shearing forces result when the superficial and deep layers of the skin move in different directions, such as when the patient slides down or is moved from the bed or wheelchair. Friction occurs due to interaction between two surfaces, such as bed linen or clothing and skin. Shear forces are not visible and occur beneath the skin while friction forces may be seen on the surface of the skin. Interaction of these elements with specific factors such as immobility, incontinence, and poor nutritional status eventually culminates in tissue damage.  Impaired skin perfusion, hypotension, shock and peripheral artery disease are increasingly recognized as playing an important role in the development of pressure sores. These factors lead to occlusion of microvessels causing ischemia and in turn inflammation and tissue anoxia. Tissue anoxia eventually leads to cell death, necrosis and ulceration.  Moist skin from perspiration or incontinence would cause maceration and may initiate or worsen trauma to the skin.  A pressure sore may start developing within 2-4 hours of unrelieved pressure. Reperfusion injury is suggested as an etiology of ongoing damage to an ulcerated area. Formation of inflammatory mediators (i.e bradykininin) and reactive oxygen species during tissue ischemia-reperfusion is believed to contribute to the chronicity of pressure sores. (r)

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

The National Pressure Ulcer Advisory Panel (NPUAP) PrU Classification System was last updated in 2014.

Category/Stage I: Non blanchable erythema.  Skin intact, non blanchable area of redness over a bony prominence.  Visible blanching may not be seen in dark skinned people.

Category/Stage II: Partial thickness skin loss. Shallow open ulcer with pink wound bed without slough.

Category/Stage III: Full thickness skin loss. Subcutaneous tissue may be visible but bone, tendon and muscle is not exposed.  Slough could be present. Tunneling may be detected as well.

Category/Stage IV: Full thickness tissue loss with exposed bone, tendon or muscle. Slough and eschar may be present in certain areas. Tunneling and undermining often noted.

Unstageable: Full thickness tissue loss with visible slough and/or eschar at the base. Thus depth of the wound is difficult to determine.

Suspected deep tissue injury: Depth unknown. Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear.

http://www.npuap.org/wp-content/uploads/2014/08/Quick-Reference-Guide-DIGITAL-NPUAP-EPUAP-PPPIA-Jan2016.pdf

Specific secondary or associated conditions and complications

Bacterial invasion through non intact skin may spread, resulting in serious systemic infections.

Bed rest utilized for PrU healing is not only a risk for development and worsening of sores but also leads to deconditioning and loss of function, respiratory compromise, and social isolation.  Prevention and treatment involves frequent pressure relief to affected area while in bed.

2. ESSENTIALS OF ASSESSMENT

History

  1. Detailed medical/social history including PrU history: cause of injury and necessary modifications to prevent worsening or recurrence in the future.
    1. Integrity of seating and bed surfaces: wear and tear. Assess condition of the cushion in wheelchairs.
    2. Functional capacity: positioning, posture, and assistive equipment.
    3. Use of and adherence to pressure-relieving maneuvers.
    4. Surgical/procedural history
    5. Neurologic history
    6. Chronic illnesses that may affect wound healing- DM, PVD, neuropathy, SCI
    7. Social and financial support systems.
    8. Nutritional assessment: weight history, ability to eat, calorie counts.
    9. Psychological health, behavior, and cognition.
  2. The individual’s and family’s knowledge of developing and healing a PrU and their goals of care.
  3. PrU-related pain.

Physical examination

  1. Evaluate skin for temperature, edema and consistency in relation to surrounding tissue. PrU assessment should include anatomical location, general appearance of the wound base, size (length, width, depth, and wound area), NPUAP stage, and condition of wound margins/surrounding tissue. Document the presence of exudate/odor, necrosis, undermining, sinus tracts/tunneling, infection, and healing (granulation and epithelialization). Obtain serial photographs, if possible.
  2. Assess for neurovascular integrity (pulses, sensation), signs of local or systemic infection, spasticity, and contractures.

Functional assessment

Assessment of functional mobility level, independence with self-care, cognitive function, and psychosocial condition is important in determining each patient’s ability to actively participate in the healing of PrUs (eg, performing pressure relief regularly, ensuring adequate nutritional intake).

Laboratory studies

Commonly performed laboratory studies include:

  1. Total lymphocytes, C-reactive peptide, and erythrocyte sedimentation rate as markers of inflammation or systemic infection.
  2. Hemoglobin, hematocrit, and associated studies.
  3. Prealbumin, total protein, and albumin.
  4. Zinc level

Imaging

  1. Imaging studies are unable to diagnose a stage I/II PrU.
  2. Serial wound photography is useful for management of an uncomplicated PrU.
  3. Inpatients with stage III or IV PrU and signs of systemic infection, plain radiographs, magnetic resonance imaging with and without contrast, triple-phase bone scan, and indium-tagged WBC scans may aid in diagnosis of osteomyelitis or associated abscess

Supplemental assessment tools

Nutritional Assessment should be done on admission, if there is a change in clinical status or if there is delayed/prolonged healing of the pressure sore. Assess weight, skin turgor and nutritional status.  Ensure adequate protein intake to maintain a positive nitrogen balance in patients at risk for developing pressure sores. Although studies supporting the effectiveness in accelerating healing are inconsistent, consider adding vitamin supplementation such as zinc, Vitamin B and C to promote wound healing and improve skin health.  Evaluate for any underlying vitamin deficiencies. Address dysphagia or poor dentition if present.

Zinc and Vitamin C supplements should be considered if deficiency is present, although studies supporting their effectiveness in accelerating healing are inconsistent. According to a retrospective cohort study that looked at 95 long-term care facilities, total caloric intake of at least 30 kcal/kg is required to promote healing and decreasing the size of stage 3 and 4 pressure ulcers. (20). Increased dietary protein intake fosters the healing of pressure ulcers. Per present NUPAP guidelines, 1.25 – 1.5 g/kg/day should be offered to those at risk of developing or those with existing pressure sores.

Visual skin assessment for erythematous areas (blanchable or unblanchable) or overt skin breakdown can be performed daily by the individual or caregivers, and can be helpful in early detection. This is particularly true in light-skinned individuals, but may be difficult in individuals with dark skin pigments, which may mask the earliest signs of deep tissue injury and stage I PrU. Norton and Braden Scales can be used to assess PrU risk.

Bone biopsy is recommended for definitive diagnosis of PrU-related osteomyelitis and identification of bacterial antibiotic sensitivities.

Early predictions of outcomes

Evidence of healing of the PrU include presence of granulation tissue in the ulcer base and epithelialization across the surface of the ulcer. Chronic wounds are defined as those which fail to heal within 30 days of occurrence.

Environmental

When a PrU develops, deteriorates or does not heal, support surfaces (eg, wheelchair cushions and specialized mattresses), positioning practices (turning frequency, use of wedges pillows, and pressure relief footwear), shear reduction, and microclimate control (heat and moisture) should be re-evaluated.

Social role and social support system

It is important to assess the individual’s social situation when determining PrU risk and making clinical decisions.

Adequate social support to assist the individual with a PrU in obtaining services.

Professional Issues

Noncompliance with prevention and treatment recommendations for PrU issues. Hospital-acquired PrUs are commonly used as a measure of quality of inpatient or nursing home care. However, the NPUAP Consensus Panel deemed (2010) that certain situations will make PrU development unavoidable, particularly in the intensive care or hospice settings. Inappropriate or lack of management of pressure ulcers can result in major lawsuits for institutions.

3. REHABILITATION MANAGEMENT AND TREATMENTS

Prevention of pressure ulcers

  • Skin care: avoid positioning patient on an area with erythema/irritation. Skin should be kept clean and dry. Try to conform to an individualized continence management schedule. Monitor skin integrity regularly. Avoid massaging/rubbing on bony prominences or on areas at risk for pressure sores.
  • Positioning: Frequent repositioning ensuring pressure relief or redistribution. Educating patients on performing “pressure relief lifts” or other maneuvers when indicated. Avoid positioning patients on prominent bony prominences when possible. Caution while repositioning patients so as to avoid any shearing or friction forces with the surface –“lift, don’t drag.” A two-hour interval is recommended for repositioning. Encourage individuals to sleep in in 30 – 40 degree side lying position or flat in bed if possible. 90-degree side lying position or semi-recumbent positions increase positions. Limit head-of-bed elevation to 30 degrees (if not contraindicated) to prevent friction and sliding. Keep heels elevated (pillows, foam) to distribute pressure along the calf instead of the Achilles tendon to prevent skin breakdown on the heels.
  • Nutrition: Maintain positive nitrogen balance with sufficient protein intake. Ensure adequate hydration and balanced diet. Monitor and control blood sugars in diabetics.
  • Provide proper mattresses and wheelchair cushions.
  • Staff, patient, and family education on the importance of preventing pressure ulcers.

At different disease stages

Basic elements of a treatment plan include cleansing and debridement, dressings, surgery (if indicated), nutrition, and management of tissue pressure loads. If no healing is noted within two weeks, the treatment plan should be modified. Assess for signs of local or systemic infection.

Overview of wound dressings: choice should be made on the ability to keep the wound base moist, ulcer size, depth and location and need to address bacterial burden.

  • Hydrocolloid dressing: for Category/Stage II or shallow, non-infected Category/Stage III.
  • Hydrogel dressing: Shallow, with minimal exudate. Soothing & alleviates pain. Amorphous gel used to pack deep wounds and in clinically non-infected wounds.
  • Alginate: in moderate-heavy exuding pressure sores and in clinically infected sores (used in conjunction with treatment). Facilitates autolytic debridement.
  • Transparent film dressing: May be used as secondary dressing for sores treated with fillers that will remain in the wound for extended periods of time (3-5 days).
  • Foam: provides moist environment and insulation. Consider in exuding Category/Stage II and shallow Category/Stage III pressure sores.
  • Silver impregnated: for heavily infected wounds.
  • Honey-impregnated: treatment of Category/Stage II and Category/Stage III sores.
  • Cadexomer Iodine dressing: in moderately- highly exudating sores.
  • Moist gauze: when other moisture-retentive dressings are not accessible, used for packing deep wounds.
  • Collagen matrix: non-healing Category / Stage III / Category / Stage IV sores.

Biophysical agents in pressure ulcer treatment include electrical stimulation, pulsed electromagnetic field, and pulsed radiofrequency energy. Presently there is insufficient data to support or refute the use of phototherapy, hyperbaric oxygen therapy and ultrasound in promoting wound healing. Negative pressure wound therapy may be considered as an adjuvant therapy for deep Category III/IV ulcers.  Whirlpool therapy should not be considered as routine management due to risk of contamination.

Surgical: Flap procedures or primary closures are indicated for a complex stage III/IV PrU and treatment of osteomyelitis.

Attempt preoperative smoking cessation and optimization of nutrition, bowel regulation, management of spasticity and contractures, comorbid conditions, and heterotopic ossification. Postoperative positioning and support surface management is critical (avoid pressure to operative site). Mobilization begins after 3-6 weeks of satisfactory healing.

Coordination of care

Optimal management of a PrU, particularly those stage III or worse, is best achieved using an interdisciplinary team approach including physicians (physiatrists, infectious disease specialists, and surgeons), wound care specialists, nursing, nutritionists, physical therapy, and family/caregivers.

For individuals with SCI, social work assistance may be necessary to arrange supplemental supports during the healing period.

Patient & family education

A consumer guideline titled “Pressure Ulcers: What You Should Know. A guide for people with spinal cord injury” is available from the Consortium for Spinal Cord Medicine

Emerging/unique Interventions

Weekly assessment of healing progress by a wound care professional is recommended:

  1. Validated tools: Pressure Ulcer Scale for Healing Tool or the Bates-Jensen Wound Assessment Tool.
  2. Clinical judgment of signs of healing: decreasing exudate, decreasing wound size, and improvement in wound bed tissue.
  3. Consider baseline and serial photographs.
  4. Re-evaluate the PrU, plan of care if the PrU does not progress toward healing within 2 weeks.

Signs of deterioration should be addressed immediately if the goal of intervention is complete healing.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

Microclimate control: Using specialized surfaces that have the ability to alter temperature and moisture after coming in contact with skin surface.

Prophylactic dressings and fabrics: utilizing polyurethane dressing over bony prominences. Silk fabric over cotton may assist with reduction in shearing forces/friction.

Electrical stimulation of muscles: emerging evidence showing that intermittent tetanic muscle contractions of the muscles through e-stim may be effective in preventing pressure ulcers, especially in SCI patients.

Advanced imaging techniques (subepidermal moisture measurement, multispectral imaging, diagnostic ultrasound, 3-dimensional elastography, and tissue viscoelasticity measurements) are being investigated for their ability to identify and predict the progression of deep tissue injury to overtPrU, but currently are neither available nor validated for routine use.

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

Critical gaps exist in PrU knowledge. One of the most significant is the inability to predict when individuals are developing occult PrU. Best practices for management, educational methods for caregivers, and standardized seating and support-surfaces assessments remain poorly defined.

REFERENCES

European Pressure Ulcer Advisory Panel and National Pressure Ulcer Advisory Panel. Prevention and Treatment of Pressure Ulcers: Quick Reference Guide. Washington DC: National Pressure Ulcer Advisory Panel; 2009.

Consortium for Spinal Cord Medicine Clinical Practice Guidelines. Pressure ulcer prevention and treatment following spinal cord injury: a clinical practice guideline for health-care professionals. J Spinal Cord Med.2001;24 Suppl 1:S40-101.

Landis EM. Microinjection studies of capillary blood pressure in human skin. 1930;15:209-228.

Nola GT, Vistnes LM. Differential response of skin and muscle in the experimental production of pressure sores. Plast Reconstr Surg. 1980;66:728-733.

Gefen A. How much time does it take to get a pressure ulcer? Integrated evidence from human, animal, and in vitro studies.Ostomy Wound Manage.2008;54:26-28, 30-35.

Berlowitz DR, Brienza DM.Are all pressure ulcers the result of deep tissue injury? A review of the literature. Ostomy Wound Management.2007;53:34-38.

VanGilder C, Amlung S, Harrison P, Meyer S. Results of the 2008-2009 International Pressure Ulcer Prevalence Survey and a 3-year, acute care, unit-specific analysis. Ostomy Wound Manage.2009;55:39-45. http://www.cms.gov/manuals/downloads/ncd103c1_Part4.pdf. Accessed July 19, 2011.

Black JM, Edsberg LE, Baharestani MM, et al. Avoidable or unavoidable? Results of the National Pressure Ulcer Advisory Panel Consensus Conference. Ostomy Wound Management.2011;57:24-37.

Consortium for Spinal Cord Medicine’s Consumer Guideline. Pressure Ulcers: What You Should Know. A Guide for People with Spinal Cord Injury. XX: Paralyzed Veterans of America; 2002.

Sprigle S, Linden M, Riordan B. Analysis of localized erythema using clinical indicators and spectroscopy. Ostomy Wound Manage.2003;49:42-52.

Bates-Jensen BM, McCreath HE, Pongquan V. Subepidermal moisture is associated with early pressure ulcer damage in nursing home residents with dark skin tones: pilot findings. J Wound Ostomy Continence Nurs.2009;36:277-284.

Sprigle S, Zhang L, Duckworth M. Detection of skin erythema in darkly pigmented skin using multispectral images. Adv Skin Wound Care.2009;22:172-179.

Aoi N, Yoshimura K, Kadono T, Nakagami G, et al. Ultrasound assessment of deep tissue injury in pressure ulcers: possible prediction of pressure ulcer progression.Plast Reconstr Surg.2009;124:540-550.

Makhsous M, Venkatasubramanian G, Chawla A, Pathak Y et al. Investigation of soft-tissue stiffness alteration in denervated human tissue using an ultrasound indentation system. J Spinal Cord Med. 2008;31:88-96.

Quintavalle PR, Lyder CH, Mertz PJ, Phillips-Jones C, Dyson M. Use of high-resolution, high-frequency diagnostic ultrasound to investigate the pathogenesis of pressure ulcer development.Adv Skin Wound Care.2006;19:498-505.

Henzel MK, Bogie KM, Guihan M, Ho CH. Pressure ulcer management and research priorities for patients with spinal cord injury: Consensus opinion from SCI QUERI Expert Panel on Pressure Ulcer Research Implementation. J Rehabil Res Dev.2011;48:xi-xxxii.

Sharon DM. Wound and Pressure Ulcer Management. DeMarco S. Wound and Pressure Ulcer Management. org. Accessed 2015.

Epidemiology, pathogenesis and risk assessment of pressure ulcers. Epidemiology, pathogenesis and risk assessment of pressure ulcers. http://www.uptodate.com/contents/epidemiology-pathogenesis-and-risk-assessment-of-pressure-ulcers#h2. Accessed 2015.

http://www.npuap.org/wp-content/uploads/2014/08/updated-10-16-14-quick-reference-guide-digital-npuap-epuap-pppia-16oct2014.pdf. Accessed 2015.

Bergstrom N, Horn SD, Smout RJ, et al. The National Pressure Ulcer Long-Term Care Study: outcomes of pressure ulcer treatments in long-term care. J Am Geriatr Soc 2005; 53:1721.

Original Version of the Topic:

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

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Sarah Wagers, MD
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Preeti Panchang, MD
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