Chapter 185 Skin and Wound Care
A multidisciplinary approach to skin care can effectively minimize the unnecessary morbidity and mortality secondary to pressure ulcers (PUs). In addition to contributing to patient morbidity and negatively affecting quality of life, PUs also result in considerable expense. It has been reported that 1.6 million PUs develop in U.S. hospitals every year. The total cost to treat PUs has been estimated to be between $2.2 billion and $3.6 billion annually. In 2006, adult hospital stays noting a diagnosis of PUs totaled $11 billion.1 Approximately $125 to $200 is spent for each stage I and stage II PU that develops, and $14,000 to $23,000 is spent for each stage III and stage IV PU. Seventy-five percent of acute care acquired ulcers occur in patients who have undergone a surgical procedure that lasted 3 hours or longer. This same group accounts for 30% to 40% of the total cost associated with PUs.2 Hospitalizations involving patients with PUs developed either before or after admission increased by nearly 80% between 1993 and 2006. 1
It has been estimated that 25% of the medical costs associated with spinal cord injuries (SCIs) are incurred as a result of PUs. Overall, the average cost of treating a single PU can range from $5000 to $50,0003,4; 1 to 6 months of additional hospital stay is often required. Infectious complications of PUs, such as cellulitis, osteomyelitis, sepsis, and endocarditis, account for more than 60,000 deaths annually.5–7
A PU (also known as a pressure sore, decubitus ulcer, or bedsore) is an area of damaged skin and underlying soft tissues resulting from prolonged unrelieved pressure between a bony prominence and an external surface. In a patient, pressure ulcer injury can occur over the scapula, occiput, sacrum, and heels when placed in the supine position; the ear, shoulder, greater trochanter, medial knee, malleolus, and foot edge when laterally positioned; and the nose, forehead, chest, iliac crests, foot edge, and toes when placed in the prone position.8
Incidence and Prevalence
The incidence of PUs occurring in postoperative patients varies from 12% to 45%9; others report an incidence of 12% to 66%.9,10,11 In one study the prevalence of ulcer development within 4 days of surgery, by stage, ranged from 0.65% (unstageable) to 6.44% (stage I). The total number of intraoperatively acquired PUs is 23% of the total number of ulcers developed in hospitals.2
PUs occur in 28% of SCI patients. According to the National Spinal Cord Injury Statistical Center, the incidence of PUs during the initial hospital stay is 32%.12 Another study reported a PU rate of 30% to 85% during the first month after injury.13–19 In a retrospective study of SCI the PU rate was found to be 60% and 50% in quadriplegic and paraplegic patients, respectively; also, multiple PUs developed in most quadriplegic patients.20–24
Etiology
Historically, PUs have been blamed on poor nursing care and have been used as outcome indicators to quantify good versus poor nursing care.11,25 In fact, PUs are acute injuries that develop rapidly when compression of tissues causes ischemia and necrosis during serious illness and trauma, including surgery.26 The primary factor contributing to PU formation is constant pressure for extended periods. Pressure induces ischemia and causes reactive hyperemia. Because muscles and subcutaneous tissues are more susceptible than epidermis to pressure-induced injury, PUs are usually worse than they initially appear. The visible portion of a PU is not truly indicative of the extent of the problem.27
The mean skin capillary pressure in healthy persons is approximately 25 mm Hg.28 External compression with a pressure of more than 30 mm Hg occludes the blood vessels, so that the surrounding tissue becomes anoxic and cell death occurs. Tissue pressure, however, depends on the patient’s health. In addition, the amount of tissue damage is proportional to the magnitude and length of application of the pressure. PUs can develop within 24 hours of the insult but can take as long as 5 days to manifest themselves.27 Kosiak28 demonstrated that applying a constant pressure of 70 mm Hg to the skin caused irreversible changes in less than 2 hours. He also demonstrated an inverse relationship between time and pressure. Intense pressure for short periods was tolerated by patients as well as low pressure for long periods of time without sustaining tissue injury. Even a brief period of pressure relief can reduce the likelihood of PUs.
Risk Factors and Their Assessments
Most hospitals use a standardized risk assessment tool to predict the likelihood of an individual developing a PU. An individual prevention plan will be created and implemented based on the patient’s risk assessment/score. Several tools for risk assessment of PU prevention are available. The most commonly used validated and reliable tool for predicting patients at risk for pressure ulcer development is the Braden Scale for Predicting Pressure Sore Risk. Full risk assessment includes determining a person’s risk for pressure ulcer development and inspection of skin condition, particularly of pressure points.29 Recommendations for culturally sensitive early assessment for stage I pressure ulcers in patients with darkly pigmented skin include the use of a halogen light to look for skin color changes, which may occur in blue hues, and to compare skin over bony prominences to surrounding skin, which may be boggy or stiff, warm or cooler.30
Intrinsic Risk Factors
Age
Several changes that occur in normal skin with aging may predispose older persons to PU development. These factors include decreased epidermal turnover, flattening of the dermoepidermal junction, and decreased number of dermal blood vessels. Bridel31 reported gradual reduction in collagen formation between ages 20 and 60. A marked drop in collagen synthesis with concurrent loss of its protective mechanism occurs after age 60. In general, the risk of PU development doubles after age 40 and triples after age 70.
Pattern of Spinal Cord Injury
Each year 25% of SCI patients will develop a PU. Regardless of the type of treatment of these PUs, they will recur in 5% to 91% of SCI patients.27 The pattern of SCI (completeness of neurologic deficit, level of injury [quadriplegia vs. paraplegia], and muscle tone [spastic vs. flaccid]) can affect skin care and PU formation. Richardson and Meyer18 examined variables related to PU formation in acutely injured SCI patients and found that quadriplegic patients with complete injuries were more likely to develop PUs than were those with lower level or incomplete injuries. However, Curry and Casady14 reported that cervical injuries were not associated with an increased rate of PU formation. They reported PUs in 22.2% and 28.5% of patients with cervical and thoracolumbar injuries, respectively. Spasticity can contribute to PU development. Shearing forces in SCI are increased threefold, partly as a result of lower limb spasticity.
Immobility
Immobility has been found to be the most significant risk factor for PU development.32 Immobility may be caused by mental status changes, physical deficit, or neurologic deficit, or may occur during surgery.
Malnutrition
Increased PU risk occurs in malnourished patients by the reduction of tissue tolerance.33 Integrity of the skin and support structures is influenced by nutritional status. Low serum albumin levels have been shown to predict injury from pressure.12 Collagen and elastin can diminish the ability of soft tissue to absorb pressure. Lack of vitamins and trace elements necessary for collagen formation and cell metabolism can predispose the patient to increased risk of pressure damage.34
Decreased fluid intake in the malnourished patient can lead to increased risk for dehydration. Dehydration can affect tissue perfusion, resulting in reduced pliability and dry, flaky, or scaling skin associated with fissuring and cracking of the stratum corneum. This ultimately places the patient at an increased risk for PU formation.27
Body Weight
The emaciated patient has little padding over bony prominences and is vulnerable to pressure injury. The obese patient may be malnourished with poor tissue perfusion and may be difficult to move while avoiding shearing and frictional forces. Patients are at risk of pressure damage if they are less than 90%, or more than 120%, of their ideal body weight.9
Cardiovascular Changes
Some cardiovascular changes secondary to SCI can diminish tolerance to pressure and pressure-induced ischemia. The loss of sympathetic innervation and unopposed parasympathetic activity contribute to vascular stasis and tissue hypoxia in SCI patients. The loss of vasomotor tone produces vasodilation, bradycardia, and an increased cardiac index. This results in an increased stroke volume and a decreased venous return. The reduction in venous return is further accentuated by decreased muscle tone and the absence of the muscle pump. Gravity, acting mainly when the patient is in the sitting position, and a decreased negative inspiratory force, resulting from pulmonary insufficiency, may also diminish venous return. In the SCI patient, soft tissue blood flow below the level of injury is reduced to 33% of its normal value. A decrease in transcutaneous oxygen tension is observed in the SCI patient, even in the absence of pressure.17 All of these factors contribute to the formation of PUs. In summary, poor tissue oxygenation, poor cell nutrition, and a decrease in venous return may accentuate the process of PU formation.
Extrinsic Risk Factors
Shearing
Shear forces are the second key factor in the development of PUs. Shear forces are defined as forces created by sliding adjacent structures, which cause a relative displacement of tissue and, in turn, occlusion of capillaries. Shear forces can be more significant than pressure itself in the dermis (where capillaries run perpendicular to the skin) and near the bone (where nutrient vessels pierce the fascia, also in a perpendicular manner) (Fig. 185-1). Shear forces, alone or in combination with pressure, significantly compromise circulation in tissues, whereas the skin may remain stationary. The elevation of the head of the bed by more than 30 degrees may increase shear forces.
Moisture
Contact of skin with moisture, resulting from urinary or fecal incontinence, leads to skin maceration and edema. This makes the epidermis more susceptible to abrasion. The likelihood of further tissue breakdown thus increases. The effect of moisture on PU formation is well known. One study demonstrated that incontinence caused a 5.5-fold increase in the incidence of PUs.35 Fecal incontinence is a greater risk factor for PU development than urinary incontinence, because stool contains bacteria and enzymes that are caustic to the skin.11,27
Surgery
Preoperative factors that place patients at risk for PUs include the following comorbidities: diabetes, underlying respiratory disease, hypertension, and vascular disease. Low preoperative hemoglobin and hematocrit, as well as a preoperative serum albumin level lower than 3 g/dL, also have been shown to place patients at greater risk for PU.12,36,37
Surgical patients are at an increased risk because of forced immobility during surgery.12 The amount of time on the operating room (OR) table is the most statistically significant risk factor associated with PU injury in perisurgical patients.9 Studies have shown variable amounts of time before PU injury occurs. Hoshowsky and Schramm38 found that PU injury can occur in as little as 2.5 hours on the OR table. Surgery lasting more than 4 hours can triple the risk of skin changes and quadruple the risk of PU formation. Hicks39 found that PU injury was twice as likely to occur if time on the OR table was more than 4 hours.
Not only does the amount of time on the OR table contribute to PU formation, but anesthetic agents lower blood pressure and alter tissue perfusion, which also contributes to tissue damage.40 Surgical patients’ skin may be made more susceptible to PUs because of pooled prep solution, causing skin maceration, change in skin pH, and the removal of protective oils.9,11 In addition, one study showed that 75% of patients placed on a hyperthermia blanket during surgery went on to develop PUs.9,10,41
Firm positioning devices in the OR are used to hold patients in place by exerting pressure on bony prominences, retractors increase pressure on internal tissues, and OR personnel increase pressure on external tissues by leaning on the patient.11 All of these events can cause pressure over bony prominences, eventually leading to PU injury.
Assessment and Staging of Pressure Sores
Routine skin inspection is customarily included in any skin care program because it provides important information regarding the formulation and evaluation of skin care plans. At least once daily the skin should be examined from head to toe, and high-risk areas should be assessed more frequently, with special attention paid to bony prominences. Assessment involves the entire integument, not just the ulcer, and is the basis for a treatment plan and its evaluation. PU assessment should include location, size (length, width, and depth), the extent of sinus tract undermining or tunneling, exudate, color of wound bed, epithelialization, and staging.11 Photographs can document PU status better than hand-drawn diagrams.
Although several different staging and classification systems have been developed for PU classification, the Agency for Healthcare Research and Quality (AHRQ) (formerly the Agency for Healthcare Policy and Research) has adopted the National Pressure Ulcer Advisory Panel’s PU classification system as part of the PU clinical practice guidelines. PUs are staged to classify the degree of observed tissue damage. The use of this classification tool permits universal assessment and consistent communication of the severity of tissue damage among health care personnel (Fig. 185-2).19,36
Skin inspection should be followed by laboratory investigations, such as culture and assessment for infection markers. In the case of a chronic nonhealing PU and underlying osteomyelitis, a triad of a white blood cell count higher than 15,000/μL, plain radiographic signs, and a high sedimentation rate (>100 mm/hr) provides a sensitivity and specificity of 90% for diagnostic screening of this complication.4
Prevention
The foundation for the prevention of PUs is based on the elimination of risk factors. The first step in PU prevention is to be knowledgeable of risk factors, specifically which ones place the patient at high risk for PU development. The second step in prevention is to be aware of the interventions that reduce the risk of pressure injury. The third step is to evaluate the effectiveness of the intervention.27 Proper measures can minimize the PU rate by as much as 59%.4,23,42–44 Prevention is a 24-hour, ongoing process. Management of PU risk includes an understanding of body positioning, turning, and mobilization of the patient in the bed and wheelchair. It also includes paying attention to hygiene and the use of pressure reduction devices and strategies, as well as the appropriate monitoring of nutritional and hydration status.
Mobilization and Turning Program
At-risk patients should be turned every 2 hours to minimize pressure on bony prominences.15,45,46 A written schedule for systematically turning and repositioning the patient should be used. Norton et al. reported a lower incidence of PUs in at-risk patients who were turned every 2 to 3 hours.47
The goal of repositioning is to facilitate tissue reperfusion before the tissue becomes ischemic. Repositioning should involve a sustained relief of pressure. As skin tolerance improves, the amount of time spent in one position may be increased gradually.
After the acute phase of care, when the SCI patient is able to tolerate wheelchair activities, continuation of pressure relief techniques in the wheelchair is equally important. These activities serve to relieve pressure and maintain (and increase) the strength in the upper extremities. Wheelchair pushups, lateral weight shifts to each side, and forward over-the-knees positioning are some of the effective pressure relief techniques used.48
Improper transport of the patient increases the incidence of PUs. When transferring patients, care should be taken to not slide or drag the skin across the bed surface.49 The patient may also help prevent friction injuries by taking an active role and using the trapeze during turning and repositioning (if the spine is stable).
Ischial PUs are a manifestation of prolonged sitting without focal pressure reduction. Appropriate care, patient education, and patient diligence should minimize incidence of this complication (Fig. 185-3). Sacral PUs also may be caused by sitting, particularly if an inappropriate or worn-out chair is used or if the patient sits with the pelvis excessively flexed.
