Pressure ulcer
Pressure ulcers, also known as pressure sores, bed sores or pressure injuries, are localised damage to the skin and/or underlying tissue that usually occur over a bony prominence as a result of usually long-term pressure, or pressure in combination with shear or friction. The most common sites are the skin overlying the sacrum, coccyx, heels, and hips, though other sites can be affected, such as the elbows, knees, ankles, back of shoulders, or the back of the cranium.
Pressure ulcers occur due to pressure applied to soft tissue resulting in completely or partially obstructed blood flow to the soft tissue. Shear is also a cause, as it can pull on blood vessels that feed the skin. Pressure ulcers most commonly develop in individuals who are not moving about, such as those who are on chronic bedrest or consistently use a wheelchair. It is widely believed that other factors can influence the tolerance of skin for pressure and shear, thereby increasing the risk of pressure ulcer development. These factors are protein-calorie malnutrition, microclimate, diseases that reduce blood flow to the skin, such as arteriosclerosis, or diseases that reduce the sensation in the skin, such as paralysis or neuropathy. The healing of pressure ulcers may be slowed by the age of the person, medical conditions, smoking or medications such as anti-inflammatory drugs.
Although often prevented and treatable if detected early, pressure ulcers can be very difficult to prevent in critically ill people, frail elders, and individuals with impaired mobility such as wheelchair users. Primary prevention is to redistribute pressure by regularly turning the person. The benefit of turning to avoid further sores is well documented since at least the 19th century. In addition to turning and re-positioning the person in the bed or wheelchair, eating a balanced diet with adequate protein and keeping the skin free from exposure to urine and stool is important.
The rate of pressure ulcers in hospital settings is high; the prevalence in European hospitals ranges from 8.3% to 23%, and the prevalence was 26% in Canadian healthcare settings from 1990 to 2003. In 2013, there were 29,000 documented deaths from pressure ulcers globally, up from 14,000 deaths in 1990.
The United States has tracked rates of pressure injury since the early 2000s. Whittington and Briones reported nationwide rates of pressure injuries in hospitals of 6% to 8%. By the early 2010s, one study showed the rate of pressure injury had dropped to about 4.5% across the Medicare population following the introduction of the International Guideline for pressure injury prevention. Padula and colleagues have witnessed a +29% uptick in pressure injury rates in recent years associated with the rollout of penalizing Medicare policies.
Presentation
Complications
Pressure ulcers can trigger other ailments, cause considerable suffering, and can be expensive to treat. Some complications include autonomic dysreflexia, bladder distension, bone infection, pyarthrosis, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation. Sores may recur if those with pressure ulcers do not follow recommended treatment or may instead develop seromas, hematomas, infections, or wound dehiscence. Paralyzed individuals are the most likely to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from kidney failure and amyloidosis.Pressure ulcers are also painful, with individuals of all ages and all stages of pressure ulcers reporting pain.
Cause
There are four mechanisms that contribute to pressure ulcer development:- External pressure applied over an area of the body, especially over the bony prominences can result in obstruction of the blood capillaries, which deprives tissues of oxygen and nutrients, causing ischemia, hypoxia, edema, inflammation, and, finally, necrosis and ulcer formation. Ulcers due to external pressure occur over the sacrum and coccyx, followed by the trochanter and the calcaneus. In healthy individuals, ulcers caused by external pressure do not occur when the body is stationary, such as during sleep, as involuntary movements of the body frequently occur, allowing for repositioning and the relief of pressure.
- Friction is damaging to the superficial blood vessels directly under the skin. It occurs when two surfaces rub against each other. The skin over the elbows can be injured due to friction. The back can also be injured when patients are pulled or slid over bed sheets while being moved up in bed or transferred onto a stretcher.
- Shearing is a separation of the skin from underlying tissues. When a patient is partially sitting up in bed, skin may stick to the sheet, making the skin susceptible to shearing in case underlying tissues move downward with the body toward the foot of the bed. This may also be possible on a patient who slides down while sitting in a chair.
- Moisture is also a common pressure ulcer culprit. Sweat, urine, feces, or excessive wound drainage can further exacerbate the damage done by pressure, friction, and shear. It can contribute to maceration of surrounding skin thus potentially expanding the deleterious effects of pressure ulcers.
Risk factors
Pathophysiology
Pressure ulcers may be caused by inadequate blood supply and resulting reperfusion injury when blood re-enters tissue. A simple example of a mild pressure sore may be experienced by healthy individuals while sitting in the same position for extended periods of time: the dull ache experienced is indicative of impeded blood flow to affected areas. Within 2 hours, this shortage of blood supply, called ischemia, may lead to tissue damage and cell death. The sore will initially start as a red, painful area. The other process of pressure ulcer development is seen when pressure is high enough to damage the cell membrane of muscle cells. The muscle cells die as a result and skin fed through blood vessels coming through the muscle die. This is the deep tissue injury form of pressure ulcers and begins as purple intact skin.According to Centers for Medicare and Medicaid Services, pressure ulcers are one of the eight preventable iatrogenic illnesses. If a pressure ulcer is acquired in the hospital, the hospital will no longer receive reimbursement for the person's care. Hospitals spend about $27 billion annually for treatment of pressure injuries. Whereas, the cost of pressure injury prevention is cost-effective, if not cost-saving, and would cost less than half the amount of resources to prevent compared to treat in health systems.
Sites
Common pressure sore sites include the skin over the coccyx, the sacrum, the ischia/ischium, the heels of the feet, over the heads of the long bones of the foot, buttocks, over the shoulder, and over the back of the head.Pressure reduction
Pressure must be removed from high risk body areas by frequent changes in position in bed or chair including turning side to side. Chair cushions and air mattresses should be used for immobile patients. Heels should be off of the bed.Adequate diet
Eating by mouth is preferred and intake of food and fluid should meet calorie, protein and fluid needs. Work with a dietician if needed. Supplements may be needed.Biofilm
is one of the most common reasons for delayed healing in pressure ulcers. Biofilm occurs rapidly in wounds and stalls healing by keeping the wound inflamed. Frequent debridement and antimicrobial dressings are needed to control the biofilm. Infection prevents the healing of pressure ulcers. Signs of pressure ulcer infection include slow or delayed healing and pale granulation tissue. Signs and symptoms of systemic infection include fever, pain, redness, swelling, warmth of the area, and purulent discharge. Additionally, infected wounds may have a gangrenous smell, be discolored, and may eventually produce more pus.In order to eliminate this problem, it is imperative to apply antiseptics at once. Hydrogen peroxide is not recommended for this task as it increases inflammation and impedes healing. Cleaning the open wound with hypochlorous acid is helpful. Dressings with cadexomer iodine, silver, or honey have been shown to penetrate bacterial biofilms. Systemic antibiotics are not recommended in treating local infection in a pressure ulcer, as it can lead to bacterial resistance. They are only recommended if there is evidence of advancing cellulitis, bony infection, or bacteria in the blood.
Diagnosis
Classification
The definitions of the pressure ulcer stages are revised periodically by the National Pressure Injury Advisory Panel in the United States and the European Pressure Ulcer Advisory Panel in Europe. Different classification systems are used around the world, depending upon the health system, the health discipline and the purpose for the classifying.- Stage 2: 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 stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation.
- Stage 3: 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 tunneling. The depth of a stage 3 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and stage 3 ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage 3 pressure ulcers. Bone/tendon is not visible or directly palpable.
- Stage 4: 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 tunneling. The depth of a stage 4 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. Stage 4 ulcers can extend into muscle and/or supporting structures making osteomyelitis likely to occur. Exposed bone/tendon is visible or directly palpable. In 2012, the National Pressure Injury Advisory Panel stated that pressure ulcers with exposed cartilage are also classified as a stage 4.
- Unstageable: Full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough and/or eschar in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. Stable eschar on the heels is normally protective and should not be removed.
- Deep Tissue Pressure Injury : Intact or non-intact skin with localized area of persistent non-blanchable deep red, maroon, purple discoloration or epidermal separation revealing a dark wound bed or blood filled blister. Pain and temperature change often precede skin color changes. Discoloration may appear differently in darkly pigmented skin. This injury results from intense and/or prolonged pressure and shear forces at the bone-muscle interface. The wound may evolve rapidly to reveal the actual extent of tissue injury, or may resolve without tissue loss. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle or other underlying structures are visible, this indicates a full thickness pressure injury. Do not use DTPI to describe vascular, traumatic, neuropathic, or dermatologic conditions.