Skin and Wound Care

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Chapter 185 Skin and Wound Care

Ann M. Henwood, Sait Naderi, Edward C. Benzel

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 $50,000 ^3,⁴; 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

The skin is the largest organ of the body and is composed of a sequence of layers (epidermis, dermis, and subcutaneous fat) that together provide its varied features. The outermost layers provide protection from the elements. These layers permit secretion, excretion, insulation, sensation, and thermoregulation.

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

Although various factors are involved in determining the incidence of PUs, it is clear that the main cause of PUs is pressure over a bony prominence.

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

Numerous factors that influence PU formation have been documented. Both intrinsic and extrinsic factors contribute to the risk of the development of a PU.

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. Bridel ³¹ 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

The patient’s nutritional status has an important effect on the maintenance of tissue vitality. Wound healing can be affected by several variables, such as a negative nitrogen balance, anorexia, obesity, and repeated infections. Negative nitrogen balance and anorexia after SCI frequently contribute to weight loss and tissue wasting. Thus, bony areas become more prominent, resulting in an increase in the applied force per unit area. Obesity can also contribute to the formation of PUs by decreasing mobility.

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

Extrinsic risk factors are those elements that may be manipulated through interventions and help to prevent PUs.

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

FIGURE 185-2 Normal gross anatomy of the skin and its changes in the different stages of the pressure ulcer. A, Normal anatomy. B, Stage I: An observable pressure-related alteration of intact skin compared with adjacent skin. Observable changes may include skin temperature, tissue consistency, and skin sensation. C, Stage II: Superficial, partial-thickness skin loss that presents clinically as a blister or abrasion. D, Stage III: Full-thickness skin loss extending down to the fascia that presents as a deep crater. E, Stage IV: Full-thickness skin loss with extensive destruction or damage to muscle, bone, or supporting structures.

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

The primary goal of this program is to relieve pressure, which is achieved by regular turning. The patient should be placed in the full lateral decubitus position when it is safe. A patient with a very unstable spine perhaps should not be aggressively turned until the spine is surgically fixated. This restriction is uncommon.

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.

FIGURE 185-3 Potential sites for pressure in the sitting position.

Uninterrupted sitting in a chair or wheelchair is a common cause of PU. When in a wheelchair, SCI patients should reposition themselves at least once every hour and shift their weight every 15 minutes. If the patient needs assistance, simply standing the patient and reseating in the chair may minimize the risk of tissue injury. Small shifts in weight such as elevating the legs can help to reduce the risk of tissue injury.²⁷

General Hygiene

Proper patient hygiene can help to prevent or at least minimize the likelihood of PUs. Bathing programs should include washing with mild soap and water to avoid excessive skin drying and cracking. The skin should be kept clean and free of moisture from urinary and fecal incontinence, perspiration, and wound drainage. However, it is important to keep the skin well lubricated with a simple standard hospital skin moisturizer. Studies have shown that petrolatum is more effective than lanolin on dry skin.⁵⁰

The type of material next to the skin may either diminish or increase moisture retention. Cotton disperses moisture, whereas nylon and plastic materials cause moisture to be retained. Clothes should fit properly without causing excessive focal pressure or friction. Tight clothes make dressing difficult and may also cause localized pressure and vasomotor changes. Similarly, the patient’s shoes should be one half or one full size larger than normal.

Nutrition

Proper nutrition is an important factor in maintaining the vitality of intact tissues. Nutritional needs are based on the patient’s age, gender, body mass index, anorexia or obesity, current disease state, severity of illness, and presence and severity of wounds. A through nutritional assessment is an important component of the initial evaluation of a patient with a PU.⁵¹

A high-protein diet, with an increased caloric intake, is initially needed to replace weight loss and to prevent protein deficiency and anemia. If necessary consult a dietitian and correct nutritional deficiencies. Monitor and order vitamins A, C, and E supplementation as needed.³⁰ Normal albumin is 3.5 to 5.5 g/dL and prealbumin is 15 to 25 mg/dL.⁵¹

Adequate fluid intake is 30 to 35 mL/kg of body weight. Patients on air-fluidized beds for the prevention of PUs must have their fluid intake increased an additional 10 to 15 mL/kg of body weight to prevent dehydration.⁵²

The nutritional state of the patient is also affected by drugs, alcohol, nicotine, and caffeine. Nicotine and caffeine are vasoconstrictive, leading to a decrease in tissue oxygenation that, in turn, affects tissue healing. Smokers have a higher rate of extensive PUs than do nonsmokers.^44,⁵³^–⁵⁵

Patient Support Surfaces

Patients with an unstable spine, who cannot tolerate frequent turning, may require a pressure support surface that can lower the surface pressure below capillary filling pressure (32 mm Hg). Thick foam mattresses, water mattresses, alternating-pressure air mattresses, and static multilayered air mattresses have been found useful in preventing PUs. Air-fluidized beds and low-air-loss beds, which have elaborate support surfaces, probably provide the most effective surface for functionally dependent patients with large, deep, or multiple PUs.

Beds

A variety of beds can be used to prevent PUs, with some being appropriate for patients with unstable spines. For patients with a stable spine, low-air-loss beds, oscillating low-air-loss beds, or air-fluidized beds can be used alternatively. The patient, the caregiver, and the family may develop a false sense of security with use of these beds. Specialized beds do not prevent PUs but can minimize their likelihood. However, skin care may be difficult when using these beds.

In general, studies comparing several specialized beds show no statistical significance in the prevention or healing of PUs from one bed to another. However, studies do show that PUs heal more quickly on specialized beds when compared to foam overlays or standard hospital mattresses.⁵⁶

Rotating Beds

A patient with an unstable spine can be placed on a rotating bed that rocks side to side in a continuous motion or on an oscillating support surface or kinetic treatment table to prevent PUs. These beds are often used in trauma or intensive care units but are usually not practical for rehabilitation units. A rotating bed must be adjusted properly; otherwise it slides the patient back and forth as it rocks. This sliding, in turn, subjects the skin to shear forces, causing, rather than preventing, skin breakdown.

Air-fluidized Beds

An air-fluidized bed is an oval space with up to 2000 pounds of glass beads covered by a polyester sheet. The beads are fluidized by a flow of warm, pressurized air that floats the polyester cover on which the patient is placed. Feces and body fluids are able to flow through the polyester sheet; thus the skin is kept dry. Most studies have demonstrated a rapid rate of wound healing using these beds, compared with conventional treatment.^5,^43,^57,⁵⁸ These beds have a bactericidal effect because of sequestration and desiccation of micro-organisms by the ceramic beads. Adverse effects include fluid loss, dehydration, dry skin, scaly skin, and epistaxis from the flow of the dry air. Turning and repositioning may be difficult.

Low-Air-Loss Beds

Low-air-loss beds consist of multiple inflatable fabric pillows that are attached to a modified hospital bed frame. An electric fan maintains the buoyancy of the pillows. The head and foot of the bed can be elevated. They are cooler and more portable than air-fluidized beds; however, urine and feces cannot pass through the fabric. Their use has been found to be associated with a threefold increase in tissue healing.⁴³

Cushions

Several different forms of gel- or water-filled mattresses and cushions are used with beds or wheelchairs. These mattresses and cushions may aid or inhibit patient mobility, particularly during transfer. Smooth surface cushions provide less resistance to sliding and aid in board placement during transfer. However, they do not optimally eliminate pressure. Furthermore, the patient cannot perform meticulous skin care and inspection. Cushions and mattresses may increase local tissue temperature, which, in turn, causes an additional rise in tissue metabolism and greater oxygen demand.

Patient Positioning

Perhaps the most important anatomic and soft tissue bony prominences in the bedridden patient are the sacrum and the heels.⁵⁹ The importance of these pressure points is diminished when the patient assumes positions other than the supine position.

The sacrum is located superficially at its dorsal aspect, with very little soft tissue separating the bone from the integument. When the supine position is assumed, significant pressure is applied to this point. Although the sacrum is a common site for PU formation related to supine positioning, the scapula and occiput are also potential points of pressure (Fig. 185-4). Both regions have bony prominences with minimal overlying soft tissue. The prevention of sacral, scapular, and occipital PUs is predicated on limiting the time spent in the supine position.

FIGURE 185-4 The supine position can lead to pressure application predominantly on sacrum, scapula, heels, and occiput.

Evidence suggests that when the side-lying position is used, pressure on the greater trochanter should be minimized; the patient should be placed at a 30-degree laterally inclined angle rather than a 90-degree angle to avoid direct pressure on the greater trochanter.¹¹ Placing a patient in a position that is intermediate between the full lateral decubitus and the supine position perhaps applies significant pressure to the downside scapula while lessening pressure on the sacrum. Dorsolateral buttock pressure is also increased. This, however, is usually tolerated well because of the significant soft tissue mass overlying this region. This position, for the reasons listed, is a reasonable alternative intermittent position. No single position should be maintained for any significant length of time, however. The full lateral decubitus position exposes the downside greater trochanteric region to significant focal pressure, if proper technique is not used. The anatomic arrangement of the greater trochanter and surrounding soft tissues is of great importance in this regard. One must keep in mind the dynamic relationship between the overlying soft tissues and the bony prominence (greater trochanter).¹¹

In the hip-flexed position the greater trochanter is more superficial (exposed) relative to the immediately overlying soft tissue surrounding the trochanter itself. The latter is composed of the gluteus maximus and the lateral thigh muscles. When the hip is extended (leg straightened), the greater trochanter retracts relative to the surrounding soft tissue. This extended position results in a distribution of pressure over a significantly wider surface area, thereby minimizing focal trochanteric pressure (Fig. 185-5). It would therefore seem prudent to straighten the downside leg in the full lateral decubitus position. This essentially eliminates the negative effects of the lateral decubitus position (Fig. 185-6).¹¹

FIGURE 185-5 The lateral position can lead to pressure application on the greater trochanter, ribs, shoulder, and lateral aspect of the knee and foot. Note that the perineum and medial aspect of the foot and ankle may also be exposed to increased focal pressure.

FIGURE 185-6 The lateral decubitus position, using pillows, may reduce the pressure applied to the body surface, particularly the greater trochanter.

Heels are at an increased risk of PU development because they have higher tissue interface pressures than other tissues covering bony prominences. Heels must be elevated off the bed surface by some protective mechanism. A common practice is to use pillows under the calves to prevent heels from bearing pressure loads, which prevents them from resting on the surface of the bed.²⁷

Treatment of Pressure Sores

When a PU occurs it can be treated either medically or surgically, depending on the chronicity, position, and size. When developing a plan of care for treatment, the treatment goal must first be determined. The care will be healing, palliative, or maintenance; the treatment goal will help to determine the plan of care.⁵¹

Knowledge of comorbidities and chronic conditions and how they affect the healing process by reducing available oxygen, amino acids, vitamins, and minerals at the wound site determines the appropriate interventions for optimal PU healing.⁵¹ Many of the components used in prevention of PUs are also used in their treatment, but at a more intense level of management. The extrinsic and intrinsic contributing factors of PU formation must be identified. Eliminating the cause of pressure should improve the course of treatment.

The stage of a PU determines its treatment. A stage I PU most often heals spontaneously, simply following relief of pressure. Depending on the source of the trauma to the skin, pressure relief may be easily attained by adjusting an orthosis or, with multiple PUs, by avoiding a certain posture. A special bed may occasionally be necessary to reduce the pressure.

Treatment of an open wound (stages II, III, and IV), however, is more complex. Prevention or elimination of infection facilitates healing. Local treatment combined with systemic antibiotic and supportive therapy often heals a PU. Chronic PUs, however, are more resistant to therapy.

With respect to wound care, the goal is to achieve a clean wound with a low level of bacteria that is kept moist with a nonadherent dressing until complete wound healing has occurred.¹¹

Systemic Therapy

In some circumstances, oral antibiotics and vitamin C may be indicated. Vitamin C has been found to help in chronic nonhealing PUs.⁶⁰

With osteomyelitis, cellulitis, and sepsis, and also as prophylaxis for endocarditis, systemic antibiotic therapy may be indicated.⁶¹ Sepsis secondary to PU infections is associated with 50% mortality in the hospital setting (Fig. 185-7). Gentamicin and clindamycin are antibiotics of choice in patients with good renal function. In older patients cefotetan disodium or ticarcillin-clavulanic acid and fleroxacin are reasonable alternatives.^4,⁶² First-generation cephalosporins do not penetrate PU wounds well and should not be used.

FIGURE 185-7 Macroscopic appearance of a stage IV pressure ulcer in a patient who developed osteomyelitis and deep soft tissue infection. He ultimately died of these complications.

Topical Therapies

Topical therapies for PUs include a variety of cleaning and open-air wound care regimens; antibiotics; topical surface materials; biologic, mechanical, and chemical debridement; electrical stimulation; laser therapy; whirlpools; and hyperbaric oxygen strategies.

Wound Dressings

The main goal when using moist PU wound dressings is to keep the wound moist and the surrounding skin intact and dry.⁵¹ Traditional wound dressings are considered to be passive products because they protect the wound from further injury while healing occurs. However, many new wound dressings are interactive in that they act to alter the local wound environment. Regardless of the type of dressing selected, the main purpose is to absorb exudates, provide thermal insulation, allow gaseous exchange, protect the wound from infection, maintain a moist wound environment, and relieve pain. Interactive dressings have a varying number of properties and are currently undergoing research.^27,⁶³

Gauze

Currently most gauze dressings are inexpensive. They must be changed two or three times daily. Maintaining moistness may be difficult with gauze dressings. If they become dry, they may adhere to the wound. Their removal may then be painful and the risk of removing healthy granulation tissue will be increased. Gauze dressings must be fixed with a cover dressing or wrap.

Films

Semipermeable polyurethane films allow gases to pass through but are impermeable to water. They are believed to mimic the function of the skin and may enhance healing by sequestering wound fluids. Because the films are transparent, the wound can be directly visualized with the dressing in place. Such a dressing can remain in place as long as 7 days. This type of dressing, if used, is appropriate for stage I PUs.

Foams

Semipermeable polyurethane foams are transparent and waterproof. They absorb excessive wound exudate. A moist environment is maintained, and excessive autolysis or maceration is avoided. Because these foams do not adhere to the wound, they must be fixed with a cover dressing or tape; hence, direct visualization of the wound is obscured. Foams can be used for stage I and stage II PUs. They should not be used for deep PUs extending into the underlying muscle, sores covered by eschar, infected sores, or heavily exuding PUs.

Hydrocolloid

Hydrocolloids contain an adhesive material that physically interacts with wound fluid. These occlusive or semiocclusive dressings encourage wound cleaning and debridement through the process of autolysis. They promote the development of granulation tissue by stimulating angiogenesis. They may not adhere to highly exudative wounds. They can be used for stage II and stage III PUs.^43,⁶⁴ Currently, hydrocolloids are cost effective and require changing every 3 to 7 days.

Hydrogel

Hydrogels are three-dimensional hydrophilic polymers that interact with aqueous solutions by swelling and maintaining water in their structure. They are nonadhesive and conform to the wound surface. Hydrogels are very absorbent and dehydrate easily. They can be used in stage IV PUs.

AHRQ guidelines recommend cleaning PUs at each dressing change. Techniques should be chosen that use the least amount of chemical and mechanical trauma necessary to clean the wound adequately. Traumatized wounds have a higher rate of infection and slower healing time.⁵¹ For some wounds isotonic saline irrigation is a sufficient cleanser. Extremely dirty wounds may need a stronger cleanser and more mechanical force. As the wound heals and becomes cleaner, less mechanical force and a gentler cleanser should be used.^11,⁶⁶

It has been shown that whirlpool therapy results in faster wound healing than standard treatment. Pulsatile irrigation and lavage of PUs has been shown to be more effective than whirlpool therapy, especially in the presence of slough and necrotic tissue.^11,⁵¹

Normal saline solution is a safe and effective cleanser for all wounds because it is physiologic and will not harm tissue. New guidelines recommend against the use povidone-iodine, acetic acid, hydrogen peroxide, and sodium hypochlorite because they are cytotoxic and may impair wound healing by damaging granulation tissue.⁵¹ Some antimicrobial agents, such as mupirocin ointment and silver sulfadiazine, may decrease the bacterial count. In general, topically applied antibiotics do not penetrate deeply into the ulcer, and their use is not recommended. They can lead to a resistance to antibiotics, as well as cause hypersensitivity reactions, contact dermatitis, and drug toxicity from drug absorption.⁶⁷ A 2007 Cochrane Review of wound cleaning for pressure ulcers determined that there is no good evidence that cleaning PUs or cleaning with a particular solution helps healing. Very little research has studied the cleaning of PUs; therefore, conclusions cannot be drawn.⁶⁸

Negative Pressure Wound Therapy

Negative pressure wound therapy creates a controlled negative pressure in an attempt to provide evacuation of wound fluid, stimulate granulation tissue, decrease bacterial colonization, and enhance the body’s natural capacity to heal.⁵¹

Vacuum-assisted closure uses an open-celled foam that can be cut to the size of the PU and placed on top of or inside the PU. It is then secured with a transparent film. Negative pressure is applied to the wound by means of flexible tubing that is embedded in the foam and attached to a vacuum pump. Constant tension approximation uses a device to place tension traction on the wound margins.⁶⁶ Although this is a new PU wound treatment, the literature is equivocal. Studies do not show that it is inferior to other treatments, and it may increase patient comfort and decrease nurse staff hours for fewer dressing changes.⁵¹ A patient must have an overall physiologic capacity of heal to be an appropriate candidate for negative pressure wound therapy.⁵¹ Currently, negative pressure therapy is recommended for patients with stage III or IV nonhealing PUs in whom other conventional treatments have failed. Contraindications for negative pressure dressings include necrotic tissue with eschar, untreated osteomyelitis, or malignancy in the wound. Precautions to consider include active bleeding, anticoagulation use, and difficult wound hemostasis.⁵¹

Adjunctive Therapies

The role of several adjunctive therapies in PUs has been investigated. These therapies include electrotherapy, infrared therapy, ultraviolet therapy, low-energy laser irradiation therapy, ultrasound therapy, hyperbaric oxygen therapy, vacuum-assisted closure, constant tension approximation, normothermia, use of miscellaneous topical agents (e.g., sugar, vitamins, hormones, cytokine growth factors, skin equivalents), and systemic drugs other than antibiotics, such as vasodilators, hemorheologics, serotonin inhibitors, and fibrinolytic agents.

Electrical Stimulation

Low-voltage direct current and high-voltage pulsed galvanic stimulation has been used successfully in treating PUs. During treatment, the negative electrode is placed directly on the wound and the positive electrode is placed at some point distally. In a randomized, double-blind, multicenter study, electrical stimulation has been shown to increase the rate of healing of PUs. The Pressure Ulcer Guideline Panel recommended the use of electrotherapy in stage III and stage IV PUs that have proven to be unresponsive to conventional therapy. Electrical stimulation may also be useful for recalcitrant stage II PUs.^43,^66,⁶⁹

Hyperbaric Oxygen Therapy

Hyperbaric oxygen therapy is defined here as the use of high-pressure, pure, humidified oxygen applied by a portable chamber to either the entire body or to an extremity. The chamber forces 100% oxygen into superficial tissue and assists with wound healing. This modality has been found helpful in SCI patients, because they have an underlying intact arterial supply.^44,⁷⁰ However, the AHRQ does not recommend this therapy, because its effectiveness has not been established.⁶⁶

Ultrasound

The use of ultrasound for healing of PUs has produced equivocal results, with some studies demonstrating efficacy but more series finding it ineffective.^27,⁷¹

Laser

Laser therapy has been used effectively in animal models for the treatment of PUs. Studies have demonstrated healing of PUs using the helium-neon laser in one third of cases, compared with nonlaser-treated wounds.⁴⁴ Research on the use of lasers for human PUs is still in the early stages.

Growth Factors

Growth factors are naturally occurring proteins secreted from platelets and macrophages that direct the migration of cells into wounds and lead to the process of repair. In current experimental studies topically applied, platelet-derived growth factors and fibroblast growth factors have been used to promote healing of chronic PUs. Preliminary data suggest improved wound healing.^24,⁷² Other growth factors, such as TGF-beta and epidermal growth factor, have been identified as potential therapies.⁷³ Although these modalities hold promise, they are still investigational and consequently are not yet recommended for routine use.

Normothermia

Normothermia therapy is used to encourage local blood flow and oxygen to the wound. A foam collar is placed around the wound, and a transparent film is attached to the collar and placed over the wound. A warming device controlled by a temperature control unit is placed into a pocket on the transparent film, and the environment underneath the film cover is kept at 38°C. Initial studies are showing positive results.⁶⁶

Debridement

Debridement, the removal of necrotic tissue, is fundamental to the healing of a PU. Wounds must be clean for healing to take place. The goal of PU wound debridement is to accelerate wound healing, decrease the risk of infection, and prevent further complications by reducing tissue destruction.⁵¹ The removal of inflammatory stimuli, such as devitalized tissue, reactive chemicals, and bacteria, requires debridement and cleaning.¹¹ Large numbers of bacteria normally reside in necrotic tissue. The presence of necrotic material dictates local debridement to decrease the bacterial cell count to 100,000 per gram of tissue. Eschar is the collection of dead tissue within the wound; slough is the stringy, devitalized tissue that adheres to the wound bed.⁵¹ The different methods of debridement may be combined to achieve the best result.

Mechanical Debridement

Mechanical debridement is accomplished by local cleaning and dressing techniques. Soap and water or hydrogen peroxide and saline solutions, used in a ratio of 1:3 or 1:2, are some of the more common agents used to clean the wound.

The most commonly used method of mechanical debridement is the wet-to-dry dressing technique. It has been shown that woven gauze with larger pores and coarser weave, compared to nonwoven cotton sponges, is more effective for debridement.⁷⁴ This is most effective when used on PUs with necrotic tissue in stages II, III, and IV. The wet-to-dry technique is painful and should be discontinued when the wound bed looks pink.²⁷

Sharp Debridement

Sharp debridement is performed by scissors, forceps, or scalpel. This is indicated in stage II, III, and IV PUs. Eschars underlying necrotic tissue are best removed by sharp debridement. Sharp debridement can be facilitated by chemical debridement.

Chemical Debridement

Autolytic debridement is less painful. When the wound is kept moist with an occlusive dressing, the wound uses its own enzymes to digest the nonviable tissue and viscous exudates.²⁷ To enhance autolysis, exogenous enzymes may be applied to the wound. Enzymatic preparations may be fibrinolytic or collagenolytic and can cause the liquefaction of necrotic tissue and facilitate its removal by sharp or mechanical debridement. As far as possible, eschars should be removed from the wound; the remaining devitalized tissue should be scored with a scalpel before enzymatic debridement.¹¹ Enzymatic preparations are used in the treatment of stages II, III, and IV PUs. Although they are not able to debride hard eschars, these preparations can loosen them.