Decubitus Ulcers and Wound Care

Decubitus ulcers (DU) are pressure ulcers. 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. Despite current interest and advances in medicine, surgery, nursing care, and self- care education, pressure ulcers remain a major cause of morbidity and mortality. This is particularly true for persons with impaired sensation, prolonged immobility, or advanced age.

Research in the area of pressure ulcers, specifically in characterization, prevention, and treatment of pressure ulcers, is important in preventing secondary complications in persons with disabilities. As the standards of acute care, posttraumatic care and rehabilitation care improve, the population of persons with lifelong functional impairments continues to grow and preventing secondary complications including pressure ulcers becomes an increasingly prominent concern.

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The most important factor in the development of pressure ulcers is unrelieved pressure. Pressure ulcers arise from prolonged tissue ischemia caused by pressure that exceeds the tissue capillary pressure. Prolonged pressure deprives tissues of oxygen and essential nutrients, owing to ischemia and hypoxia, which then causes the ulcers. Several critical questions at the heart of pressure ulcer research still remain unanswered: How much pressure is required to produce predictable ulceration? How long must pressure be sustained to produce predictable ulceration? Which tissues are at greatest risk of ulceration?

Immobility is a major extrinsic factor associated with the risk and formation of pressure ulcers. Immobility in bed tends to cause pressure ulcers on the occiput, sacrum, heels, malleoli, and trochanteric regions, whereas patients who use wheelchairs for mobility tend to develop pressure ulcers over the ischial tuberosity. In persons who are paralyzed or who are neurologically compromised, the afferent nerves are unable to engage the sensorimotor feedback system. As a result, early warnings of prolonged ischemia, such as discomfort, do not produce the normal adjustments in body position that intermittently relieve pressure on areas at risk.

Pathophysiologic factors underlying pressure ulcers include fever, anemia, infection, ischemia, hypoxemia, hypotension, malnutrition, SCI, neurologic disease, decreased lean body mass, and increased metabolic demands. Nutrition and anemia are important factors in the healing and prevention of pressure ulcers. Individuals with pressure ulcers should have adequate nutrition, especially good protein intake and stores.

Pressure sores can be staged according to the degree of destruction of healthy tissue. Grades I to V describe increasing degrees of tissue degradation. Grade I is characterized by erythema, but intact skin. Grade V is characterized by soft tissue destruction and bony involvement.


Common Sites:

The most common sites include the ischium (28%), the sacrum (17-27%), the trochanter (12-19%), and the heel (9-18%). Pressure ulcers commonly develop on the occiput of geriatric and pediatric patients who spend extended amounts of time lying supine. Patients with the secondary manifestations of osteoporosis and associated thoracic kyphosis can develop pressure ulcers over the spinous processes. Elderly patients and patients with diabetes often have pressure ulcers on the heel.


Approximately 1 million pressure ulcers occur in the United States. The incidence in hospitalized patients ranges from 2.7% to 29%, and the prevalence in hospitalized patients is 3.5%. Patients in critical care units have an increased risk of pressure ulcers, as evidenced by a 33% incidence. Elderly patients admitted to acute care hospitals for nonelective orthopedic procedures, such as hip replacement and treatment of long bone fractures, are at even greater risk, with a 66% incidence. In the nursing home environment, the prevalence of pressure ulcers is in the range of 2.6-24%. Patients with preexisting pressure ulcers demonstrate a 26% incidence of additional pressure ulcer formation over a 6- month period. Persons with spinal cord injury (SCI) and associated comorbidity are also at increased risk. The incidence of pressure ulcers in this population is in the range of 25-66%.

Morbidity and Mortality:

Patients predisposed to pressure ulcers are at higher risk of morbidity and mortality. Infection is the most common major complication of pressure ulcers. The offending pathologic organisms in pressure ulcers can be anaerobic or aerobic. Aerobic pathogens commonly are present in all pressure ulcers, whereas anaerobes tend to be present more often in larger wounds (65% in grade III and above). The most common organisms isolated from pressure ulcers are Proteus mirabilis, group D streptococci, Escherichia coli, Staphylococcus species,Pseudomonas species, and Corynebacterium organisms. Patients with bacteremia are more likely to have Bacteroides species in their pressure ulcers.

Clinical alertness is needed because the signs commonly associated with impeding or fulminating infection are frequently absent in elderly patients or in patients who are immunocompromised. In geriatric patients with pressure ulcers, bacteremia is reported to occur at the rate of 3.5 per 10,000 hospital discharges. Because the mortality rate in this population approaches 50%, antibiotic treatment for wound infection or secondary bacteremia provides the appropriate spectrum of coverage specific to the offending organisms. Sepsis also can occur secondary to osteomyelitis, which has been reported to occur in 26% of nonhealing ulcers. Osteomyelitis should be considered whenever an ulcer does not heal, especially if the ulcer is over a bony prominence.

Various tests can be used to diagnose osteomyelitis in patients with pressure ulcers. Plain radiographs have a sensitivity of 78% and a specificity of 50%, but radiographic findings often are not present in the early stages of infection. Bone scans are more sensitive, but they have low specificity (50%). Bone biopsy has the highest specificity (96%) and sensitivity (73%). A combination of diagnostic tests, such as a determination of the leukocyte count and erythrocyte sedimentation rate (ESR) with plain radiography provides a sensitivity of 89% and a specificity of 88%. If all 3 test results are positive, the positive predictive value of this combination is 69%. If all 3 test results are negative, the negative predictive value is 96%.

Approximately 60,000 people die each year from complications of pressure ulcers. Development of pressure ulcers has been associated with a 4.5-times greater risk of death than that for persons with the risk factors but without pressure ulcers. A secondary complication, wound-related bacteremia, can increase the risk of mortality to 55%.



Once a pressure ulcer has developed, immediate treatment is required. Commonly used treatments over the years have included innovative mattresses, ointments, creams, solutions, dressings, ultrasound, ultraviolet heat lamps, sugar, and surgery. In choosing a treatment strategy, consideration should be given to the stage of the wound and the purpose of the treatment (e.g., protection, moisture, removing necrotic tissue).

Debridement is an important intervention in the management of pressure ulcers. The purpose of wound debridement is to remove all materials that promote infection, delay granulation, and impede healing, including necrotic tissue, eschar, and slough (ie, the stringy yellow, green, or gray nonviable debris in an ulcer). Accurate ulcer staging cannot be made until necrotic tissue is removed. Three debridement procedures are commonly used: enzymatic debridement, mechanical nonselective debridement, and sharp debridement.

Wound dressings must be addressed. Transparent adhesive dressings are semipermeable and occlusive. They allow gaseous exchange and transfer of water vapor from the skin, and they prevent maceration of the healthy skin around the wound. In addition, these dressings are not absorptive, they reduce the incidence of secondary infection, and they eliminate the risk of traumatic removal. Hydrocolloid wafer dressings contain hydroactive particles that interact with wound exudate to form a gel. These dressings provide absorption of minimal to moderate amounts of exudate and keep the wound surface moist. This gel can have fibrillolytic properties that enhance wound healing, protect against secondary infection, and insulate the wound from contaminants. Calcium alginate dressings are semiocclusive, highly absorbent, and easy to use. Calcium alginate dressings are extremely effective in treating wet (exudative) wounds and can be used on wounds that are contaminated or infected.

With antibiotics and antisepsis, an algorithmic approach is important when one evaluates a patient with an infected wound. First, the practitioner must decide whether the patient has a local or a systemic infection. Local signs of infection in a wound include rubor, dolor, and calor; systemic signs of infection include fever, tachycardia, hypotension, delirium, and alterations in mental status in older patients. Then, the practitioner must decide which antibiotic is most appropriate for the patient. Systemic antibiotics administered to combat wound infection can be divided into 5 main groups: penicillins, cephalosporins, aminoglycosides, fluoroquinolones, and sulfonamides. Other antibiotics include clindamycin, metronidazole, and trimethoprim. The most frequently used antibiotic cream is Silver sulfadiazine which has an excellent antimicrobial spectrum of activity, low toxicity, ease of application, and minimal pain.


Ulcer Healing:

These ulcers heal by both primary and secondary mechanisms. Primary union only requires reepithelialization. Secondary union, or "secondary intention" involves the formation of granulation tissue, essentially filling in the ulcer crater from the bottom up. This occurs for ulcers that are stage III and beyond. Reepithelialization then follows.

Many factors influence the development and healing of pressure ulcers. Nursing plays a pivotal role in this challenging and complex process, using a multifaceted approach involving skin care, pressure relief, and nutritional support. Prevention is the key to managing pressure ulcers, and it begins with a complete medical and nursing history, a risk assessment, and skin examination when the patient is admitted.


Advanced Surgical Techniques:

Several options are available for surgical management of pressure ulcers, including direct closure, skin grafting, skin flaps, and musculocutaneous flaps. Surgical management of pressure ulcers can provide skin coverage as well as soft tissue coverage. Flaps containing muscle provide a physiologic barrier to infection, eliminate dead space in the wound, and improve vascularity. Improved vascularity enhances local oxygen tension, provides extended soft tissue penetration for antibiotics, and improves total lymphocyte function.

Factors associated with impaired healing should be corrected preoperatively. The nutritional status of the patient must be considered because good nutritional parameters are required for good wound healing and immune function. Also, tobacco use is associated with intrinsic factors that compromise wound healing. Nicotine is a potent vasoconstrictor that increases blood viscosity and predisposes tissue to excessive oxidase activity and free radical injury.


Medical/Legal Concerns:

Pressure ulcers can be prevented from progressing by providing good care, good nutrition, and by instituting a comprehensive team approach to the developing problem. Delays in recognition and management often lead to litigation. Damages range from severe morbidity to death, and always involve increased costs to the patient. In fact, the treatment costs and the costs of hospitals stays for patients who developed ulcers during hospitalization were estimated to be as much as $6 billion a year.

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