Pressure Ulcers

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DEFINITION

The National Pressure Ulcer Advisory Panel,U.S (NPUAP) defines a pressure ulcer as an area of unrelieved pressure over a defined area, usually over a bony prominence, resulting in ischemia, cell death, and tissue necrosis.

The terms decubitus ulcer (from Latin decumbere, “to lie down”), pressure sore, and pressure ulcer often are used interchangeably

PATHOPHYSIOLOGY

In 1873, Sir James Paget described the production of pressure ulcers remarkably well, and his description is still quite accurate today.

Many factors contribute to the development of pressure ulcers, but pressure leading to ischemia and necrosis is the final common pathway.

Pressure ulcers result from constant pressure sufficient to impair local blood flow to soft tissue for an extended period. This external pressure must be greater than the arterial capillary pressure (32 mm Hg) to impair inflow and greater than the venous capillary closing pressure (8-12 mm Hg) to impede the return of flow for an extended time.Tissues are capable withstanding enormous pressures for brief periods, but prolonged exposure to pressures just slightly above capillary filling pressure initiates a downward spiral toward tissue necrosis and ulceration. The superficial dermis can tolerate ischemia for 2 to 8 hours before breakdown occurs. Deeper muscle, connective, and fat tissues tolerate pressures for 2 hours or less(probably because of its increased need for oxygen and higher metabolic requirements). Thus, there may be significant damage to underlying tissues while the epidermis and dermis remain intact.By the time ulceration is present through the skin level, significant damage of underlying muscle may already have occurred, making the overall shape of the ulcer an inverted cone.

Other factors contributing to pressure ulcers include-

• Friction

Friction is the resistance to motion. It may occur when the skin is dragged across a surface, such as when you change position or a care provider moves you. The friction may be even greater if the skin is moist. Friction may make fragile skin more vulnerable to injury.

• Shear

Shear occurs when two surfaces move in the opposite direction. For example, when a hospital bed is elevated at the head, you can slide down in bed. As the tailbone moves down, the skin over the bone may stay in place — essentially pulling in the opposite direction. This motion may injure tissue and blood vessels, making the site more vulnerable to damage from sustained pressure.

 SITES

The areas most susceptiblle to pressure in recumbent position include:

• SUPINE : 

1. Occiput
2. Scapulae
3. Vertebrae
4. Elbows
5. Sacrum
6. Coccyx
7. Heels

• PRONE :

1. Ears (head rotated)
2. Shoulders (anterior aspect)
3. Illiac crest
4. Male genital region
5. Patella
6. Dorsum of feet  

• SIDE-LYING -   

1. Scapulae
2. Vertebrae
3. Elbows
4. Sacrum
5. Coccyx
6. Heels
7. Ears
8. Shoulders (lateral aspect)
9. Greater trochanter
10. Head of fibula
11. Knees (medial aspect from contact between knees)
12. Lateral malleolus
13. Medial malleolus (contact between malleoli)

RISK FACTORS

People are at risk of developing pressure sores if they have difficulty moving and are unable to easily change position while seated or in bed. Immobility may be due to:

• Generally poor health or weakness
• Paralysis
• Injury or illness that requires bed rest or wheelchair use
• Recovery after surgery
• Sedation
• Coma

Other factors that increase the risk of pressure sores include:

• Age. The skin of older adults is generally more fragile, thinner, less elastic and drier than the skin of younger adults. Also, older adults usually produce new skin cells more slowly. These factors make skin vulnerable to damage.
• Lack of sensory perception. Spinal cord injuries, neurological disorders and other conditions can result in a loss of sensation. An inability to feel pain or discomfort can result in not being aware of bedsores or the need to change position.
• Weight loss. Weight loss is common during prolonged illnesses, and muscle atrophy and wasting are common in people with paralysis. The loss of fat and muscle results in less cushioning between bones and a bed or a wheelchair.
• Poor nutrition and hydration. People need enough fluids, calories, protein, vitamins and minerals in their daily diet to maintain healthy skin and prevent the breakdown of tissues.
• Excess moisture or dryness. Skin that is moist from sweat or lack of bladder control is more likely to be injured and increases the friction between the skin and clothing or bedding. Very dry skin increases friction as well.
• Bowel incontinence. Bacteria from fecal matter can cause serious local infections and lead to life-threatening infections affecting the whole body.
• Medical conditions affecting blood flow. Health problems that can affect blood flow, such as diabetes and vascular disease, increase the risk of tissue damage.
• Smoking. Smoking reduces blood flow and limits the amount of oxygen in the blood. Smokers tend to develop more-severe wounds, and their wounds heal more slowly.
• Limited alertness. People whose mental awareness is lessened by disease, trauma or medications may be unable to take the actions needed to prevent or care for pressure sores.
• Muscle spasms. People who have frequent muscle spasms or other involuntary muscle movement may be at increased risk of pressure sores from frequent friction and shearing.
  

PRESSURE SORE GRADING

The definitions of the four pressure ulcer stages are revised periodically by the National Pressure Ulcer Advisor Panel (NPUAP) in the United States and the European Pressure Ulcer Advisor Panel (EPUAP) in Europe. 

The updated staging system includes the following definitions:

Pressure Injury:
A pressure injury is localized damage to the skin and/or underlying soft tissue usually over a bony prominence or related to a medical or other device. The injury can present as intact skin or an open ulcer and may be painful. The injury occurs as a result of intense and/or prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear may also be affected by microclimate, nutrition, perfusion, co-morbidities and condition of the soft tissue.

• Stage 1 Pressure Injury: Non-blanchable erythema of intact skin

Intact skin with a localized area of non-blanchable erythema, which may appear differently in darkly pigmented skin. Presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes. Color changes do not include purple or maroon discoloration; these may indicate deep tissue pressure injury.

• Stage 2 Pressure Injury: Partial-thickness skin loss with exposed dermis

Partial-thickness loss of skin with exposed dermis. The wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister. Adipose (fat) is not visible and deeper tissues are not visible. Granulation tissue, slough and eschar are not present. These injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel. This stage should not be used to describe moisture associated skin damage (MASD) including incontinence associated dermatitis (IAD), intertriginous dermatitis (ITD), medical adhesive related skin injury (MARSI), or traumatic wounds (skin tears, burns, abrasions).

• Stage 3 Pressure Injury: Full-thickness skin loss

Full-thickness loss of skin, in which adipose (fat) is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present. Slough and/or eschar may be visible. The depth of tissue damage varies by anatomical location; areas of significant adiposity can develop deep wounds. Undermining and tunneling may occur. Fascia, muscle, tendon, ligament, cartilage and/or bone are not exposed. If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury.

• Stage 4 Pressure Injury: Full-thickness skin and tissue loss

Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone in the ulcer. Slough and/or eschar may be visible. Epibole (rolled edges), undermining and/or tunneling often occur. Depth varies by anatomical location. If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury.

• Unstageable Pressure Injury: Obscured full-thickness skin and tissue loss

Full-thickness skin and tissue loss in which the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar. If slough or eschar is removed, a Stage 3 or Stage 4 pressure injury will be revealed. Stable eschar (i.e. dry, adherent, intact without erythema or fluctuance) on the heel or ischemic limb should not be softened or removed.

CLINICAL PRESENTATION

The severity of pressure ulceration can be estimated by observing clinical signs. A progression from least tissue damage to most severe damage is presented here.

• The first clinical sign of pressure ulceration is blanchable erythemaalong with increased skin temperature. If pressure is relieved, tissues may recover in 24 hours. If pressure is unrelieved, nonblanchable erythema occurs.

• Progression to a superficial abrasion, blister, or shallow crater indicates involvement of the dermis.

• When full-thickness skin loss is apparent, the ulcer appears as a deep crater. Bleeding is minimal, and tissues are indurated and warm. Eschar formation marks full-thickness skin loss. Tunneling or undermining is often present.

• The majority of all pressure ulcers develop over six primary bony areas sacrum, coccyx, greater trochanter, ischial tuberosity, calcaneus (heel), and lateral malleolus.

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