AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Background

The terms decubitus ulcer and pressure sore often are used interchangeably in the medical community. Decubitus, from the Latin decumbere, means "to lie down." Therefore, decubitus ulcer does not adequately describe ulceration that occurs from other positioning such as prolonged sitting, which causes the commonly encountered ischial tuberosity ulcer. Because the term decubitus ulcer is not all inclusive and the common denominator of all such ulcerations is pressure, the term that best describes this condition is pressure sore.

Pressure sores probably have existed since the dawn of our infirm species. They have been noted in unearthed Egyptian mummies, and scientific writings have addressed them since the early 1800s. Presently, treatment of pressure sores in the US is estimated to cost in excess of 1 billion dollars annually.

Pathophysiology

Many factors contribute to the development of pressure sores, but pressure leading to ischemia and necrosis is the final common pathway. Pressure is exerted on the skin, soft tissue, muscle, and bone by the weight of an individual against the surface beneath. These pressures often are in excess of capillary filling pressure, approximately 32 mm Hg. Tissues are capable of withstanding enormous pressures when brief in duration, but prolonged exposure to pressures just slightly above capillary filling pressure initiates a series of events potentially leading to tissue necrosis and ulceration. The inciting event is compression of the tissues against an external object such as a mattress, wheelchair pad, bed rail, or other surface.

Shear forces and friction aggravate the effects of pressure and are important components of the mechanism of injury. Maceration may occur in the incontinent patient, predisposing the skin to injury. Pressure, shear, and friction cause microcirculatory occlusion resulting in ischemia, which leads to inflammation and tissue anoxia. Tissue anoxia leads to cell death, necrosis, and ulceration. Irreversible changes may occur during as little as 2 hours of uninterrupted pressure.

In patients with normal sensitivity, mobility, and mental faculty, pressure sores do not occur. Feedback, both conscious and unconscious, from the areas of compression leads us to change our position. This shifts the pressure from one area to another prior to any irreversible ischemic damage to the tissues.

Individuals unable to avoid long periods of uninterrupted pressure are at increased risk for developing necrosis and ulceration. This group of patients typically includes the elderly, the neurologically impaired, and patients hospitalized with acute illness. These individuals cannot protect themselves from the pressure exerted on their bodies unless they consciously change position or have assistance in doing so. Even the most conscientious patient with an extensive support group and financial resources may suffer from ulceration as the result of a brief lapse in avoidance of the detrimental effects of pressure.

Frequency

United States

Prevalence in nursing homes is an estimated 17-28%. Among the neurologically impaired, pressure sores occur with an incidence of 5-8% annually, with a lifetime risk estimated to be 25-85%. Patients hospitalized with acute illness have a pressure sore rate of 3-11%.

Anatomically, the hip and buttock region account for approximately 67% of all pressure sores, with ischial tuberosity, trochanteric, and sacral locations being most common. The lower extremities account for an additional 25% of all pressure sores, with malleolar, heel, patellar, and pretibial locations being most common. The remaining approximately 10% of pressure sores may occur in any location that experiences long periods of uninterrupted pressure. Nose, chin, forehead, occiput, chest, back, and elbow are among the infrequent sites for pressure ulceration. There is no surface of the body that may be considered immune to the ischemic effects of unrelieved pressure, but ulcers most often occur over a bony prominence.

Mortality/Morbidity

Pressure sores are listed as the direct cause of death in 7-8% of all patients with paraplegia. Evaluation of large groups of patients has revealed that one third of hospitalized patients with pressure sores die during their hospitalization. Among those developing a pressure sore in the hospital, more than half will die within the next 12 months. In general, these patients die of their primary disease process, but the pressure sore may be a contributing factor in some instances.

Sex

Most younger individuals suffering from pressure ulceration are males. This reflects the greater number of men suffering traumatic spinal cord injuries. In the older population, most patients are women because of their survival advantage over men.

Age

The prevalence of pressure sores appears to have a bimodal age distribution. A small peak occurs during the third decade of life, reflecting ulceration in those with traumatic neurologic injury, and a much larger peak occurs during the eighth decade of life. Two thirds of pressure sores occur in patients older than 70 years.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

History

When initially evaluating a patient with pressure ulceration, it is important to note the following information from the history:

• Overall physical and mental health including life expectancy
• Prior hospitalizations, operations, or ulcerations
• Diet and recent weight changes
• Bowel habits and continence status
• Presence of spasticity or flexion contractures
• Medications and allergies to medications
• Tobacco, alcohol, and recreational drug use
• Place of residence and the support surface used in bed or while sitting
• Level of independence, mobility, and ability to comprehend and cooperate with care
• Underlying social and financial support structure
• Presence of specific cultural, religious, or ethnic issues
• Presence of advanced directives, power of attorney, or specific preferences regarding care
• Presence of signs or symptoms related to the current ulceration
• • Pain
  • Fever
  • Discharge
  • Odor
• Natural history of the present ulcer
• • Length of time the ulcer has been present
  • Local treatments employed

Physical

A thorough physical examination is necessary to evaluate the overall state of health, comorbidities, nutritional status, and mental status of the patient. The level of comprehension and cooperation indicate the intensity of nursing care that will be required. The presence of contractures or spasticity is important to note and may help identify additional areas at risk for pressure ulceration. Following the general physical examination, turn attention to the wound. Adequate examination of the wound may require the administration of intravenous or oral pain medications to ensure patient comfort. Chronic pain is common among these patients and may be exacerbated by ulcer examination.

• Clinical assessment and description of pressure sores can be quite difficult for the inexperienced observer. Many classification systems for the staging of pressure ulcers have been presented in the literature. Shea, the most widely accepted system, has been modified to represent the present system endorsed by the National Pressure Ulcer Advisory Panel. This system consists of 4 stages of ulceration but is not intended to imply that all pressure sores follow a standard progression from stage I to stage IV. Nor does it imply that healing pressure sores follow a standard regression from stage IV to stage I to a healed wound. Rather, the system is designed to describe the degree of tissue damage observed at the specific time of examination and is meant to facilitate communication among the various disciplines involved in the study and care of these patients.
• • Stage I represents intact skin with signs of impending ulceration. Initially, this presents as blanchable erythema indicating reactive hyperemia. When tissue becomes temporarily ischemic, relief of pressure causes hyperemia, probably a protective mechanism of increased blood flow designed to oxygenate the tissues and remove potentially harmful products of metabolism. Reactive hyperemia should resolve within 24 hours of the relief of pressure. Warmth and induration also may be present. Continued pressure creates erythema that does not blanch with pressure and may well represent the first outward sign of tissue destruction. Finally, the skin may appear white from ischemia.
  • Stage II represents a partial thickness loss of skin involving epidermis and possibly dermis. This lesion may present as an abrasion, blister, or superficial ulceration.
  • Stage III represents a full thickness loss of skin with extension into subcutaneous tissue but not through the underlying fascia. This lesion presents as an ulcer with or without undermining of adjacent tissue.
  • Stage IV represents extension into muscle, bone, tendon, or joint capsule. Osteomyelitis with bone destruction and dislocations or pathologic fractures may be present. Sinus tracts and severe undermining commonly are present.
• Consider several additional points when applying this staging system to clinical situations. The presence of an eschar or necrotic material does not allow adequate assessment of wound depth until the eschar or necrotic material is removed. In addition, soft tissues, muscle, and skin may have a differential resistance to the effects of pressure. Pressure may actually be greatest at the bony prominence, decreasing gradually towards the periphery. Necrosis may begin deep within the tissues in the absence of an outward sign. By the time necrosis reaches the skin and ulceration occurs, one may be looking at the tip of the iceberg with the base of the wound being much larger than the skin opening.
• Staging of wound depth is only a small part of the initial assessment. Record the location of the ulcer, size of the skin opening, and presence of any surrounding maceration or induration. The presence of multiple pressure ulcers prompts the search for interconnecting fistula tracts that may not be readily apparent. Also note the presence or absence of foul odors, wound drainage, and soilage from urinary or fecal incontinence. This provides information regarding the level of bacterial contamination and need for debridement or diversionary procedures.

Causes

Although prolonged, uninterrupted pressure is the cause, impaired mobility is probably the most common reason patients are exposed to uninterrupted pressure. This situation may be present in patients who are neurologically impaired, heavily sedated or anesthetized, restrained, demented, or those suffering traumatic injury such as a pelvic or femur fracture. These patients are incapable of assuming the responsibility of altering their position to relieve pressure. Moreover, this immobility, if prolonged, leads to muscle and soft tissue atrophy, decreasing the bulk over which bony prominences are supported.

• Contractures and spasticity often contribute by repeatedly exposing tissues to trauma through flexion of a joint. Contractures rigidly hold a joint in flexion, while spasticity subjects tissues to repeated friction and shear forces.
• The inability to perceive pain, from neurologic impairment or medication, contributes to pressure ulceration by removing one of the most important stimuli for repositioning and pressure relief. Conversely, pain from surgical incisions, fracture sites, or other sources may make the patient unwilling to change position.
• Skin quality also affects whether pressure leads to ulceration. Paralysis, insensibility and aging lead to atrophy of the skin with thinning of this protective barrier. A decrease in epidermal turnover, flattening of the dermal-epidermal junction, and loss of vascularity occur. The skin becomes more susceptible to minor traumatic forces, such as friction and shear forces typically exerted during the moving of a patient. Trauma causing de-epithelialization removes the barrier to bacterial contamination and leads to transdermal water loss, creating maceration and adherence of the skin to clothing and bedding.
• Incontinence or presence of a fistula contributes to ulceration in several ways. These conditions cause the skin to be continually moist, leading to maceration. In addition, frequent soiling has the effect of regularly introducing bacteria to the wound.
• Bacterial contamination from improper skin care or urinary or fecal incontinence, while not truly an etiologic factor, is an important element to consider in the treatment of pressure sores and can delay wound healing. These wounds serve as warm, moist reservoirs for bacterial overgrowth where antibiotic resistance may develop as a result of the injudicious use of antibiotics. Pressure sores may progress from being simply contaminated, as all open wounds are, to being seriously infected, which indicates tissue invasion by bacteria. This may lead to uncommon but life-threatening complications such as sepsis, myonecrosis, gangrene, or necrotizing fasciitis.
• Malnutrition, hypoproteinemia, and anemia reflect the overall status of the patient and can contribute to tissue vulnerability to trauma as well as cause delayed wound healing. Poor nutritional status certainly contributes to the chronicity often seen in these lesions and inhibits the ability of the immune system to prevent infections. Anemia indicates poor oxygen carrying capacity of the blood. Vascular disease and hypovolemia also may impair blood flow to the region of ulceration.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

Pressure Sore, Heel

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab Studies

• CBC with differential
• Electrolyte determination
• Evaluation of nutritional parameters
• • Albumin
  • Prealbumin
  • Transferrin
  • Serum protein level
• When indicated by the specific clinical situation, obtain the following:
• Urinalysis and culture in the presence of urinary incontinence
• Stool examination for fecal white blood cells and Clostridium difficile toxin when pseudomembranous colitis may be the cause of fecal incontinence
• Blood cultures if bacteremia or sepsis is suggested

Procedures

• Perform a biopsy of those wounds not demonstrating clinical improvement despite adequate care and wounds where tissue invasion by bacteria is suggested. This allows quantification and identification of bacterial species and their antibiotic susceptibilities. Biopsy also allows distinction between simple contamination and the more serious tissue invasion that is not revealed by the common practice of swabbing the wound surface for culture.
• Perform a biopsy of chronic wounds to rule out the presence of an underlying malignancy, which has been reported in chronic pressure sores as in other chronic wounds. If a chronic pressure sore has been stable for months or years but has recently deteriorated, perform a biopsy. Scar carcinoma is uncommon and typically occurs in wounds that have been open for many years.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical Care

The first step in healing is to reduce or eliminate the cause, ie, pressure. Turning and repositioning the patient remains the cornerstone of prevention and treatment through pressure relief. Perform this every 2 hours, even in the presence of a specialty surface or bed. During transfer and repositioning, make efforts to avoid sliding the patient over a surface to prevent shear forces and friction. Patients suffering a pressure sore while sitting should be placed on bed rest.

• Pressure reduction may be achieved through the use of specialized support surfaces for bedding and wheelchairs that can maintain tissue pressures less than 30 mm Hg. In theory, reduction of tissue pressures below capillary filling pressures should allow for adequate tissue perfusion. These specialized surfaces include foam devices, air-filled devices, water-filled devices, gel-filled devices, low-air-loss beds (Flexicair, KinAir), and air-fluidized beds (Clinitron, FluidAir). Low-air-loss beds support the patient on multiple inflatable air-permeable pillows. Air-fluidized beds suspend the patient on an air-permeable mattress containing millions of uniformly sized silicone-coated beads.

  These devices often are heavy, expensive, difficult to clean, and require ongoing maintenance to ensure proper function. No one device has been shown to be clearly superior, but all reduce pressure sore incidence and severity when compared to conventional hospital mattresses and wheelchair cushions. However, pressure sores may develop in patients using these devices, and the importance of turning and repositioning cannot be overemphasized. More than 75 companies sell pressure-reduction devices with annual industry revenues in excess of 8 billion dollars.

  When employing a pressure relief surface, it is important that these devices be used properly. The patient's head and shoulders should be only minimally elevated on one pillow or foam wedge to reduce shear forces and prevent the patient from "bottoming out" or having the sacrum or ischial tuberosities resting on the bed frame. In addition, air-permeable devices may warm the patient considerably and lead to significant insensitive fluid losses. Give special consideration to temperature and hydration in these patients.

• The wound must be kept clean and free of urine and feces. The surrounding intact skin must be kept clean and dry. This should be done through frequent inspection and cleansing. The appropriate evaluation of urinary or fecal incontinence is complex but must be performed thoroughly. Potentially reversible causes should be identified and treated. Urinary incontinence secondary to urinary tract infection should be treated with antibiotics. Fecal incontinence secondary to diarrhea may be related to an infectious cause such as C difficile pseudomembranous colitis that will resolve with appropriate antibiotics.

  Manual disimpaction and the addition of stool bulking agents to the diet may relieve overflow fecal incontinence. Urinary or fecal incontinence with no treatable cause may be minimized through the establishment of a bowel and bladder regimen. Constipating agents and a low residue diet also may be helpful. Diapers and incontinence pads may be helpful by absorbing moisture away from the surface of the skin if they are checked regularly and changed when soiled. If used inappropriately, these products may actually aggravate maceration and result in dermatitis. As a final resort in difficult cases, consider operative diversion.

• Bacterial contamination must be assessed and treated appropriately. Differentiation of infection from simple contamination through tissue biopsy guides the judicious use of antibiotics only in the former situation and hopefully avoids the development of resistant species. Antibiotics also are indicated when accompanying osteomyelitis, cellulitis, bacteremia, or sepsis is present.
• Wound dressings vary with the state of the wound, and the goal is to achieve a clean, healing wound with granulation tissue. A stage I lesion may require no dressing. Stage II ulcers confined to the epidermis or dermis may be treated with a hydrocolloid (DuoDerm) occlusive dressing or a transparent adhesive dressing (OpSite), both of which maintain a moist environment to facilitate reepithelialization. For more advanced ulcers, a variety of dressing options are available, depending on the state of the wound.

  Wounds with surface debris or fibrinous exudate may be mechanically debrided with wet-to-dry dressings incorporating normal saline or enzymatically debrided with collagenase (Santyl). Wounds with a high level of bacterial contamination may benefit from an antibiotic cream such as silver sulfadiazine (Silvadene), which is bactericidal to many gram-positive and gram-negative organisms as well as being effective against yeast.

  Sulfamylon, bacteriostatic to many gram-positive and gram-negative organisms including Pseudomonas aeruginosa, can penetrate an eschar and promote autolytic softening of the eschar prior to debridement. For exudative wounds, hydrogels (Carrington gel) and xerogels (Sorbsan) absorb a large volume of exudate and facilitate moist wound healing. Vacuum-assisted closure (VAC) sponges conform to the wound surface by suction and stimulate wound contracture while removing exudate and edema. Daily whirlpool therapy also may irrigate and mechanically debride the wound.

  The choice of dressings is not as important as their appropriate application. These dressings are not a substitute for sharp debridement in the presence of eschar or other necrotic material. Trained individuals should apply dressings. Take care to keep the wound dressing within the boundaries of the wound to prevent maceration of the surrounding skin. Avoid tape if at all possible. A hydrocolloid pad or skin sealant can be used to protect the surrounding skin and serve as a surface to which tape may be applied to hold dressings in place. Tubular mesh gauze, often used in burn patients, is another alternative to hold dressings in place in patients with extremely fragile skin.

• Spasticity should be controlled pharmacologically with such medications as diazepam, baclofen, or dantrolene sodium. Patients with spasticity refractory to medication may be candidates for neurosurgical ablation. Flexion contractures may be relieved surgically.
• Nutritional status should be evaluated and optimized to ensure adequate intake of calories, proteins, and vitamins. Malnutrition is one of the few reversible contributing factors, and establishing adequate nutrition has been shown to improve healing of pressure sores. This may require dietary supplements, enteral feedings, or even parenteral feedings. Implementation of more invasive methods of nutrient delivery become an ethical issue and must be weighed against the complications of such delivery. Goals of nutritional support should include the establishment of a positive nitrogen balance and a serum protein level greater than 6 mg/100 mL.
• Other important considerations include the cessation of smoking, adequate pain control, maintenance of adequate blood volume, and correction of anemia. These issues are directed at preventing vasoconstriction in the wound and optimizing the oxygen carrying capacity of the blood.

  A system of assessing wound healing must be in place to facilitate continuity of care among the various health care providers involved in the care of the patient. This often includes serial photography, detailed descriptions of the wound, and measurement of wound dimensions.

  Other treatment options of unproven efficacy are presently being studied. These include the use of hyperbaric oxygen, electrotherapy, and growth factors. While initial studies of electrotherapy seem promising and topical application of growth factors has been approved for use in patients with diabetic neuropathic ulcers of the lower extremity, at this time there is not enough evidence to support their recommendation for use in treating pressure sores.

  When medical management has been optimized, most of the signs of impending ulceration of stage I pressure sores will resolve. Approximately 75% of stage II pressure sores also will heal with conservative management. However, stage III and IV ulcers are much less likely to heal spontaneously and often require a surgical approach.

Surgical Care

Even with optimal medical management, many patients require operative debridement, diversion of urinary or fecal stream, release of flexion contractures, neurosurgical ablation of spasticity, amputation, or reconstruction.

• Debridement is aimed at removing all devitalized tissue that serves as a reservoir for ongoing bacterial contamination and possible infection. Extensive debridement should be performed in the operating room, but minor debridement is commonly performed at the bedside. Although many of these patients are insensate, others are unable to communicate pain sensation because of cognitive dysfunction. Administer pain medication liberally, and vital signs often are a good indicator of pain perception. Take care when debriding at the bedside, because these wounds may bleed significantly.
• Urinary or fecal diversion to prevent frequent bathing of the wound with urine or feces may be necessary in difficult instances where incontinence or fistulas do not resolve with medical therapy.
• Release of flexion contractures or neurosurgical ablation of spasticity may assist with positioning problems and make tissues over the involved joint less susceptible to further injury.
• Amputation may be necessary for a nonhealing extremity wound in a patient who is not a candidate for reconstructive surgery.
• The goals of pressure sore reconstruction are improvement of patient hygiene and appearance, prevention or resolution of osteomyelitis or infection, reduction of fluid and protein loss through the wound, and prevention of future malignancy (Marjolin ulcer). Reconstructive options vary with the anatomic site of the ulcer, previous scars or surgeries, and surgeon preference. Although they will be discussed in succeeding articles, the basic tenets of pressure sore reconstruction bear mentioning. All reconstructions initially must begin with adequate debridement, including the removal of the entire bursal sac and any involved bone or heterotopic calcifications.

  Wound closure then may be achieved in a variety of ways. Few pressure sores can or should be closed primarily because of unacceptably high complication rates, primarily wound dehiscence resulting from excess tension on suture lines. A well-vascularized pad of tissue should be placed in the wound to eliminate dead space, enhance perfusion, decrease tension on the wound closure, and provide a new source of padding over the bony prominence. This tissue is typically a musculocutaneous or fasciocutaneous flap transposed or rotated on a pedicle containing its own blood supply, although more complex or recurrent wounds may require the use of a free flap with microvascular anastomosis. Prior to wound closure, drains should be placed in the bed of the wound. This allows external drainage of any fluid that may accumulate beneath the flap and hopefully avoids wound complications such as hematoma or seroma.

Consultations

A multidisciplinary approach can lead to maximum benefit for the patient. Neurosurgery, urology, plastic surgery, orthopaedic surgery, and general surgery consultations all may be indicated in a particular patient. Rehabilitation medicine specialists, social workers, and psychologists or psychiatrists may work together with geriatricians and internists to improve the patient's health, attitude, support structure, and living environment. Plastic surgeons perform most pressure sore reconstructions, and it is appropriate to consult a plastic surgeon with any complex or chronic wound.

Activity

Following successful wound closure, ambulatory patients should be out of bed with assistance as soon as possible. Delay resumption of more strenuous physical activity for approximately 6 weeks. In patients with ischial tuberosity ulceration, sitting may be resumed 6 weeks after a healed wound is achieved. Reintroduce sitting gradually over several weeks. Because of the extremely high pressures generated over the ischial tuberosities during sitting, instruct wheelchair patients to lift themselves out of their seat or rock back in the chair every 15 minutes. These recommendations regarding the resumption of activity vary according to the clinical situation and are at the discretion of the treating physician.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The relief of spasticity when present is essential in the treatment and prevention of pressure ulceration. The most commonly employed medications are presented here.

Drug Category: Skeletal muscle relaxants (centrally acting)

Centrally acting skeletal muscle relaxants inhibit reflexes at the spinal level.

Drug Category: Skeletal muscle relaxants (direct acting)

Direct-acting skeletal muscle relaxants inhibit muscle contraction by decreasing calcium release from the sarcoplasmic reticulum in muscle cells.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Further Inpatient Care

• Patients may benefit from transfer to a subacute or rehabilitation facility following wound closure. This allows for ongoing education, observation, and rehabilitative therapies prior to returning to their usual place of residence.

Further Outpatient Care

• Patients also may benefit from visits from a home health care organization once they return home. This may ease the transition and ensure that pressure avoidance strategies are adapted to the home and continued over the long term.

In/Out Patient Meds

• Also consider control of spasticity and maintenance of adequate nutrition in the outpatient setting to prevent recurrence or new ulceration.

Deterrence/Prevention

• The ultimate success or failure of pressure sore healing only begins with wound closure. Prevention of recurrence and new ulceration then becomes the goal. Avoid long periods of uninterrupted pressure through frequent repositioning. Pressure dispersion through the application of specialized support surfaces on beds and wheelchairs should be extended through the wound healing period and into the outpatient setting if available and tolerated by the patient. These products are an adjunct to and not a replacement for alternating weight-bearing surfaces.
• Perform skin care daily. This involves a careful inspection of all skin surfaces to identify areas of impending breakdown prior to their occurrence. An often overlooked but necessary detail is to remove compression stockings and inspect the heels. Wash skin with soap and water and completely dry it at regular intervals and immediately upon soiling. Do not allow moisture to accumulate on the skin or in clothing or bedding, nor should one allow the skin to become overly dry and scaling. Skin moisturizers are useful to maintain the appropriate level of moisture at the skin surface.

Complications

• Complications fall into 1 of 2 categories, complications of chronic ulceration and complications of ulcer reconstruction.
• Although uncommon, grossly infected pressure sores leading to sepsis, myonecrosis, necrotizing fasciitis, or gangrene represent the most serious complication. Another serious complication of chronic ulceration is malignant degeneration, or Marjolin ulceration. Initially described by Marjolin in 1828 as a cancer arising in burn scars, malignant degeneration has been reported in chronic pressure sores. These malignancies are typically aggressive squamous cell carcinomas with a high likelihood of nodal metastasis at the time of diagnosis. Any longstanding nonhealing wound should alert the examiner to the need to perform a biopsy.
• Complications as a result of reconstructive surgery are, unfortunately, considerable. These include hematoma, seroma, wound dehiscence, wound infection, flap necrosis, and recurrence.

Prognosis

• Even with the development and implementation of new pressure-relieving surfaces and an increase in awareness among health care providers, no studies have demonstrated a decrease in incidence or prevalence of pressure ulceration during the last 3 decades. More distressing, recurrence rates as high as 90% are reported in the literature.

Patient Education

• Patients and their support group must realize that it is their responsibility to avoid recurrent and new ulceration and that this is a lifelong process. Education on the proper avoidance of pressure should begin in the hospital and continue into the home.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical/Legal Pitfalls

• Consider the ethics of pressure sore treatment. The aggressive treatment of pressure ulceration is outlined in this chapter and those that follow. This treatment is certainly indicated for a subset of patients who suffer from pressure ulceration, the acutely hospitalized patient with a recoverable illness.
• For others, such as chronically or terminally ill patients with longstanding or recurrent ulceration, aggressive treatment may not be in the best interest of the patient. In these instances, the wishes of the patient or the patient's family should be weighed carefully. The presence of advanced directives, a living will, or a person recognized as having power of attorney should be consulted. In many instances, conservative medical care and maintaining patient comfort should be the goals rather than the institution of major invasive procedures.

Special Concerns

• Promising research in the field of growth factors and wound healing has shed light on the complex interactions that take place at the wound surface and in the affected organism as a whole. This has led to the introduction of becaplermin (Regranex), recombinant human platelet-derived growth factor. This topical agent has been approved by the FDA for the treatment of lower extremity diabetic neuropathic ulcers that extend into the subcutaneous tissue or beyond. Studies are underway to possibly expand the approved indications for this drug to include other wounds. Other growth factors are being evaluated for use in clinical settings as well. This expanding field surely will contribute further application of basic science to clinical wound healing with improvement of our understanding and patient care.

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author H Hollis Caffee, MD to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

• Barbenel JC, Jordan MM, Nicol SM, Clark MO. Incidence of pressure-sores in the Greater Glasgow Health Board area. Lancet. Sep 10 1977;2(8037):548-50. [Medline].
• Clark M, Hiskett G, Russell L. Evidence-based practice and support surfaces: are we throwing the baby out with the bath water?. J Wound Care. Nov 2005;14(10):455-8. [Medline].
• Conway H, Griffith BH. Plastic surgery for closure of decubitus ulcers in patients with paraplegia; based on experience with 1,000 cases. Am J Surg. Jun 1956;91(6):946-75. [Medline].
• Crenshaw RP, Vistnes LM. A decade of pressure sore research:1977-1987. J Rehabil Res Dev. 1989;26:63-74. [Medline].
• Dansereau JG, Conway H. Closure of decubiti in paraplegics. Report of 2000 cases. Plast Reconstr Surg. May 1964;33:474-80. [Medline].
• De Laat EH, Schoonhoven L, Pickkers P, et al. Implementation of a new policy results in a decrease of pressure ulcer frequency. Int J Qual Health Care. Nov 10 2005;[Medline].
• Dinsdale SM. Decubitus ulcers: role of pressure and friction in causation. Arch Phys Med Rehabil. Apr 1974;55(4):147-52. [Medline].
• El-Toraei I, Chung B. The management of pressure sores. J Dermatol Surg Oncol. 1977;3:507-511. [Medline].
• Klitzman B, Kalinowski C, Glasofer SL, Rugani L. Pressure ulcers and pressure relief surfaces. Clin Plast Surg. Jul 1998;25(3):443-50. [Medline].
• Ladin DA. Understanding dressings. Clin Plast Surg. 1998;25(3):433-441. [Medline].
• Maklebust J. An update on horizontal patient support surfaces. Ostomy Wound Manage. Jan 1999;45(1A Suppl):70S-77S; quiz 78S-79S. [Medline].
• Mustoe T, Upton J, Marcellino V, et al. Carcinoma in chronic pressure sores: a fulminant disease process. Plast Reconstr Surg. Jan 1986;77(1):116-21. [Medline].
• Piascik P. Use of regranex gel for diabetic foot ulcers. J Am Pharm Assoc (Wash). 1998;38(5):628-630. [Medline].
• Redfern SJ, Jeneid PA, Gillingham ME, Lunn HF. Local pressures with ten types of patient-support system. Lancet. Aug 11 1973;2(7824):277-80. [Medline].
• Relander M, Palmer B. Recurrence of surgically treated pressure sores. Scand J Plast Reconstr Surg Hand Surg. 1988;22(1):89-92. [Medline].
• Reuler JB, Cooney TG. The pressure sore: pathophysiology and principles of management. Ann Intern Med. 1981;94:661-666. [Medline].
• Rogers J, Wilson LF. Preventing recurrent tissue breakdowns after "pressure sore" closures. Plast Reconstr Surg. 1975;56:419-422. [Medline].
• Siegler EL, Lavizzo-Mourey R. Management of stage III pressure ulcers in moderately demented nursing home residents. J Gen Intern Med. 1991;6:507-513. [Medline].
• Staas WE Jr, LaMantia JG. Decubitus ulcers and rehabilitation medicine. Int J Dermatol. 1982;21:437-444. [Medline].
• Stal S, Serure A, Donovan W, Spira M. The perioperative management of the patient with pressure sores. Ann Plast Surg. Oct 1983;11(4):347-56. [Medline].
• Thompson RJ. Pathological changes in mummies. Proc R Soc Med. 1961;54:409. [Medline].

Article Last Updated: Feb 14, 2006