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| A) | epidermis and the dermis. | ||
| B) | epidermis and the basement membrane. | ||
| C) | stratum corneum and stratum lucidum. | ||
| D) | stratum granulosum and the stratum spinosum. |
Human skin has two primary layers: the epidermis (outer layer) and the dermis (inner layer). The basement membrane separates the two layers. Beneath the dermis is the hypodermis, which is a layer of connective tissue also referred to as the subcutaneous tissue.
| A) | "true skin." | ||
| B) | subcutaneous tissue. | ||
| C) | thinnest layer of the skin. | ||
| D) | All of the above |
The dermis is the most important part of the skin and is often referred to as the "true skin" [3]. It is the thickest layer of the skin, varying in thickness from 0.2 mm to 4 mm. The reticular dermis anchors the skin to the subcutaneous tissue and contains sweat glands, hair follicles, nerves, and blood vessels [1]. The dermis also contains the sebaceous glands, which secrete sebum, a substance rich in oil that lubricates the skin.
| A) | 10 days. | ||
| B) | 2 weeks. | ||
| C) | 21 days. | ||
| D) | 3 months. |
Adult skin shows a gradual increase in epidermal turnover time and decreasing dermal thickness. In young adults, epidermal turnover is around 21 days; by 35 years of age, this time doubles [2]. In addition, melanocytes decrease 6% to 8% each decade after 30 years of age. This loss of skin melanocytes is thought to increase the risk of skin cancer [1].
| A) | dermal thickness. | ||
| B) | absorption via the skin. | ||
| C) | number of Langerhans cells. | ||
| D) | All of the above |
In elderly individuals, there is a 50% reduction in the cell turnover rate in the stratum corneum (outer most layer) and a 20% reduction in dermal thickness. Elderly patients experience an overall reduction in dermal vascularization and associated drop in blood flow to the skin. The collagen bundles in the dermis shrink, causing permanent wrinkles to develop [2].
Rete ridges and pegs flatten, resulting in decreased adhesion between the skin layers. The area of contact between the epidermis and the dermis is reduced by 50% [4]. There is increased capillary fragility; slight pressure can cause bruising. A decrease in subcutaneous tissue causes a reduction in thermal insulation and increases the risk of shear/pressure injury. Reduced activity of sweat glands and sebaceous glands can lead to dry skin.
Elderly individuals experience a drop in the number of Langerhans cells, a 50% decrease in the number of mast cells, and up to a 50% decrease in the function of the remaining cells. As a result, there is an increased risk of skin cancer and fungal and other infections [1].
Other age-related changes include decreased absorption, reduction in the skin's ability to synthesize vitamin D, and significantly marked reduction in the ability of the skin to sense pressure, heat, and cold. Decreased cellular competence and activity leads to a reduction in cell repair and the increased possibility of nonhealing wounds [2].
| A) | adipose tissue. | ||
| B) | casts and splints. | ||
| C) | bony prominences. | ||
| D) | exposed skin surface. |
Pressure injuries usually occur over a bony prominence such as the sacrum, the ischial tuberosity, the trochanter, and the heels, but they can occur anywhere on the body. In some cases, pressure injuries will develop around a tracheostomy tube or under a cast, splint, or cervical collar [1]. The most common locations for pressure injuries are the sacrum and the heels because there is less soft tissue present between the bone and the skin in these areas. An estimated 95% of pressure injuries occur on the lower body; of these, about 65% develop in the pelvic area and 30% in the lower extremities [7]. There is a two to six times greater mortality risk with pressure injury development. Many factors impact the level and extent of tissue trauma (Table 1) [8].
| A) | over elbows. | ||
| B) | on the lower body. | ||
| C) | under breast tissue. | ||
| D) | over the occipital area. |
Pressure injuries usually occur over a bony prominence such as the sacrum, the ischial tuberosity, the trochanter, and the heels, but they can occur anywhere on the body. In some cases, pressure injuries will develop around a tracheostomy tube or under a cast, splint, or cervical collar [1]. The most common locations for pressure injuries are the sacrum and the heels because there is less soft tissue present between the bone and the skin in these areas. An estimated 95% of pressure injuries occur on the lower body; of these, about 65% develop in the pelvic area and 30% in the lower extremities [7]. There is a two to six times greater mortality risk with pressure injury development. Many factors impact the level and extent of tissue trauma (Table 1) [8].
| A) | friction and gravity. | ||
| B) | gravity and pressure. | ||
| C) | friction and pressure. | ||
| D) | moisture and pressure. |
Shear is the result of gravity pushing down on the body and resistance (friction) between the patient and a surface, such as the bed or the chair, holding the skin in place [2]. For example, when the head of the bed is raised (e.g., high Fowler position), gravity facilitates forward slide, pulling the body down toward the foot of the bed. The skin on the patient's lower back and gluteal area resists the motion and is held in place by the bed's surface while the bones and tissues beneath the area begin to slide. This causes puckering of the skin, stretching and angulation of small vessels, impedance of blood flow, and traction on subcutaneous tissue and muscle. Left unchecked, the net effect may result in ischemic injury to tissues at the fascia layer. When the head of the bed is elevated more than 30 degrees, shear force occurs over the sacrum and coccyx. Shear injury is not usually visible at the skin level, but shear is responsible for much of the damage associated with initiation of pressure injuries [4]. The areas of the body most vulnerable to shearing forces are shoulder blades, elbows, sacrum, ischial tuberosities, and heels. Signs of shear injury include irregular deep lesions, undermining, and tunneling.
| A) | sweating. | ||
| B) | incontinence. | ||
| C) | wound drainage. | ||
| D) | All of the above |
Major sources of moisture are incontinence, wound drainage, tube leakage, and sweating. Urinary and fecal incontinence expose the skin to excessive amounts of moisture and chemical irritation. There is a higher risk for skin breakdown with fecal incontinence than urinary incontinence because of the pathogens in stool.
| A) | There is increased granulation tissue. | ||
| B) | There is less bleeding from the wound bed. | ||
| C) | The injury goes from a stage 4 to a stage 3. | ||
| D) | A pressure injury should never be down staged. |
Staging of a pressure injury can only occur after all necrotic tissue has been removed and it is possible to see the injury bed [1]. If this is not possible, the injury will be classified as unstageable. Pressure injury staging is not used to indicate pressure injury healing; a pressure injury should never be "down staged" or reverse staged (e.g., a pressure injury that is healing does not go from a stage 4 to a stage 3).
| A) | a chronic wound. | ||
| B) | bruising under intact or non-intact skin. | ||
| C) | a difficult-to-heal stage 1 pressure injury. | ||
| D) | hypergranulation tissue in the wound bed. |
Deep tissue pressure injury, previously suspected deep tissue injury, is a pressure-related injury, much like a bruise, that is characterized by persistent non-blanchable, deep red, maroon, purple discoloration or epidermal separation revealing a dark wound bed or blood-filled blister. Deep tissue pressure injuries can present on either intact or non-intact skin. This type of injury is caused by intense and/or prolonged pressure and/or shear. Deep tissue pressure injury may resolve without tissue loss or may rapidly change to reveal the extent of the tissue injury. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle, or other underlying structures are visible, this indicates a full thickness pressure injury (Unstageable, stage 3, or stage 4). The NPIAP does not recommend using deep pressure tissue injury to describe vascular, traumatic, neuropathic, or dermatologic conditions [6].
| A) | immobility. | ||
| B) | hypotension. | ||
| C) | contractures. | ||
| D) | decreased sensation. |
Immobility is possibly the greatest risk factor for pressure injury development [4]. According to the United Spinal Association, up to 80% of patients with spinal-cord injuries will develop pressure injuries during their lifetime and 30% will have more than one pressure injury [15]. Patients who have lost the ability to ambulate, either for physical or cognitive reasons, will commonly develop pressure injuries while chair- or bedridden. The prevention of injuries in these patients is a vital aspect of ensuring an optimal quality of life.
| A) | increased moisture. | ||
| B) | decreased vascularization. | ||
| C) | decreased vascular fragility. | ||
| D) | increased sensory perception. |
Patients older than 65 years of age experience pressure injuries most frequently [1]. With aging, the skin becomes more fragile. The skin layers adhere less securely to each other and often appear paper thin and almost transparent. There is also evidence of increased dryness, decreased vascularization, and increased vascular fragility.
In elderly individuals, there is a decrease in surface barrier function. The ability of the soft tissue to evenly distribute the mechanical load without compromising blood flow is impaired. There is less subcutaneous tissue to cushion boney prominences. This, in addition to decreased sensory perception, makes elderly skin more vulnerable to pressure, shear, and friction [2]. Research has shown that, in the geriatric population, blood flow in the area of the ischial tuberosity while sitting on an unpadded surface is lower than in younger adults [4].
| A) | Obese patients | ||
| B) | Female patients | ||
| C) | Pediatric patients | ||
| D) | Geriatric patients |
Factors that contribute to pressure injury development in obese individuals include decreased blood supply in adipose tissue, difficulty in turning and repositioning, moisture within skin folds, incontinence, skin-to-skin friction, immobility, and poor nutrition. Obese patients are particularly at risk for "unusual" pressure injuries resulting from pressure within skin folds. Obese patients may have large panniculi ("aprons"), weighing up to 50 pounds. The abdominal panniculus must be regularly repositioned in order to prevent pressure injury. This may be accomplished by placing the patient in the side-lying position and lifting the panniculus away from the underlying skin surface, which allows air to the area and simultaneously relieves pressure.
| A) | A BMI of 25 | ||
| B) | Increased caffeine intake | ||
| C) | Vitamin D and K deficiency | ||
| D) | Weight less than 119 pounds |
Low body weight and impaired nutrition are also concerns. Weight less than 119 pounds or a BMI less than 20 are indicators of increased risk for pressure injury development [19].
Recent weight loss, decreased nutritional intake, inadequate dietary protein, and impaired ability to feed oneself have been identified as risk factors for pressure injury development. An estimated 50% of elderly patients admitted to the hospital have suboptimal protein nutrition [19]. When there is a sustained deficit of protein as an energy source, skin and soft tissues become more vulnerable to injury. Low protein levels also result in decreased resistance to infection. Older adults also have increased incidence of low calorie intake and low levels of zinc and vitamin B12.
Vitamin A, C, and E deficiencies have been associated with pressure injury formation. Vitamin A works in the body to maintain epithelial integrity and is involved in collagen synthesis. It also plays a role in protection against infection. A deficiency of vitamin A can inhibit collagen synthesis, delay re-epithelialization, and decrease cellular cohesion. Vitamin C is also involved in collagen synthesis, immune function, and wound repair. A deficiency of vitamin C can result in capillary fragility. Vitamin E deficiency often decreases the immune function of the skin.
| A) | slower wound healing. | ||
| B) | increased phagocytic activity. | ||
| C) | increased response to pressure. | ||
| D) | increased blood flow to the skin. |
Elevated blood sugar levels characteristic of diabetes result in decreased phagocytic ability of neutrophils and diminished wound strength. Patients with diabetes are more prone to infection, and wound healing is slower in this population than in patients without diabetes. Hyperglycemia can also result in protein-energy malnutrition, dehydration, and alteration in microcirculation [1]. Peripheral neuropathy, a common complication associated with diabetes, results in decreased sensation, an established risk factor for pressure injuries.
| A) | Foley Scale. | ||
| B) | Homer Scale. | ||
| C) | Braden Scale. | ||
| D) | Bergström Scale. |
The Braden Scale was developed in 1987 by Barbara Braden and Nancy Bergstrom [23]. Since then, it has undergone testing in several clinical settings, and its validity has been established by expert opinion. It is considered one of the most reliable tools for identifying patients at risk for pressure injury development, and it is the most widely used. The Braden Scale scores factors that contribute to prolonged pressure and factors that result in diminished tissue tolerance for pressure [23]. There are six items scored in the assessment [23]:
Sensory perception
Moisture
Activity
Mobility
Nutrition
Friction and shear
| A) | wound size. | ||
| B) | location of wound. | ||
| C) | amount of wound drainage. | ||
| D) | All of the above |
Documentation of a pressure injury should include location, stage (per NPIAP definitions), wound description (e.g., size, color, drainage), and pain level. Wound size should always be recorded in centimeters. The length is the longest head-to-toe measurement, while the width is the longest hip-to-hip measurement. The best practice recommendation is to measure the wound at the point of greatest length and the point of greatest width. Wound depth is measured by gently inserting a pre-moistened, sterile cotton swab into the deepest part of the wound. The measurement from the tip of the applicator to the level of the skin surface is recorded as the depth [4].
| A) | coccyx. | ||
| B) | sacrum. | ||
| C) | right trochanter. | ||
| D) | ischial tuberosities. |
Pressure injuries are a particular concern for patients who spend a significant amount of time in chairs. A patient is more likely to develop pressure injuries from sitting than from reclining, as sitting puts the patient's weight on the relatively small surface areas of the buttocks, thighs, and soles of the feet. Much of this weight is focused over the small area of tissue covering the ischial tuberosities. It is important for patients who sit in a chair to regularly change position. A dependent patient must have his/her position changed in a chair at least every hour. Patients who are able to move themselves should shift their weight (even slightly) every 15 minutes.
| A) | dissolves lipids. | ||
| B) | is mild scented. | ||
| C) | is pH balanced. | ||
| D) | contains alkaline products. |
Maintaining skin cleanliness and moisturizing frequently can protect skin integrity. The skin should be cleaned with water and a gentle soap, preferably a pH-balanced cleanser. Alkaline products remove skin lipids, which increases water loss and weakens the barrier function of the skin [14]. Avoid hot water for bathing and scrubbing or using harsh cleaning agents. A soft cloth should be used to pat rather than rub the skin dry. Thromboembolic deterrent (TED) stockings should be removed when bathing, and the nurse or physician should be notified of any redness, discoloration, or skin breakdown.
| A) | explain the plan of care to cognitively aware patients. | ||
| B) | teach the patient/family what they can do to facilitate pressure relief. | ||
| C) | ensure that the patient and/or family understand what a pressure injury is. | ||
| D) | All of the above |
A vital component of a pressure injury prevention program is education. If possible, pressure injury prevention should not be a passive process for the patient and his/her family members. Rather, it should be a dialogue in which the patient or family feels comfortable asking questions and discussing problems. Patients should have as much control as possible in the plan of care. Empowerment is very important in maintaining the patient's physical and emotional well-being. The plan of care should be explained thoroughly to cognitively aware patients and their family.
At the same time, it is vital to evaluate the patient's/family's existing knowledge regarding pressure and pressure injuries. Healthcare professionals should show patients what they can do to facilitate pressure relief (e.g., how to make small position changes while in the chair). If possible, it is often beneficial to teach patients how to do simple range-of-motion exercises. Take time to train the patient as often as is appropriate; not everyone will absorb the information the first time it is heard [4]. It is important not to let noncompliance or a bad attitude from the patient or family discourage the teaching process. The subject should be approached as often as is reasonable. Include the family members and caregivers in the instructions. As well as assisting with care, they can encourage compliance. All efforts at patient and family/caregiver education should be documented, along with the patient's response (both verbal and behavioral).