AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

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

INTRODUCTION

Section 2 of 10  

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

Background

Although they are technically separate entities, the terms decubitus ulcer, bedsore, and pressure sore are often used interchangeably in the medical community. Decubitus, from the Latin decumbere, means "to lie down." Decubitus ulcers, therefore, occur at sites overlying bony structures that are prominent when the person is lying in a recumbent position. Decubitus ulcers may occur on the scalp, back, tailbone, hip, heel, or any other area to which pressure is applied while a person is lying down. Therefore, decubitus ulcer does not adequately describe ulceration that occurs while in other positions such as prolonged sitting. The pressure from prolonged sitting may cause an ischial tuberosity ulcer, which is commonly seen in persons confined to the sitting position. Because the common denominator of all such ulcerations is pressure, the term that best describes this condition is pressure sore.

Pressure sores have likely existed since the dawn of our infirm species. J. Thompson Rowling described pressure sores in unearthed Egyptian mummies in 1961, and scientific writings have addressed them since the early 1800s. Pressure sores continue to be an ever-present problem within our society. The prevalence of pressure sores in hospitalized patients has been reported to be from 14-21% over the last decade. The cost to heal a single full-thickness pressure sore may be as high as 70,000 dollars.¹ The overall annual cost has recently been estimated to be between 5 billion and 8.5 billion dollars,² with the cost of hospital-acquired pressure ulcers between 2.2 and 3.6 billion dollars.³

Click here to complete a Medscape CE activity on the treatment of pressure ulcers.

Pathophysiology

In 1873, Sir James Paget described remarkably well the production of the pressure sore, and his description is still quite accurate today.⁴ 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 are often in excess of capillary filling pressure (approximately 32 mm Hg). Tissues are capable of briefly withstanding enormous pressures, but prolonged exposure to pressures just slightly above capillary filling pressure initiates a series of events that potentially leads 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.⁵ Maceration may occur in a patient who has incontinence, predisposing the skin to injury. Pressure, shear forces, and friction cause microcirculatory occlusion resulting in ischemia, which leads to inflammation and tissue anoxia. Tissue anoxia leads to cell death, necrosis, and ulceration.

Of the various tissues that are at risk of death due to pressure, muscle tissue is damaged first, likely because of its increased need for oxygen and higher metabolic requirements. Irreversible changes may occur during as little as 2 hours of uninterrupted pressure. Skin is able to withstand ischemia from direct pressure for up to 12 hours. By the time ulceration is present through the skin level, significant damage of underlying muscle may already have occurred, making the overall shape of the ulcer an inverted cone.

Restoration of blood flow to an ischemic area of tissue, or reperfusion, has recently been suggested as a cause of more damage to that area, causing a pressure sore to enlarge or become more chronic. This occurs, for example, when a paraplegic or quadriplegic patient is turned from one side to the other, in a well-intentioned attempt to combat prolonged pressure on a given side. The exact mechanism of the ischemia-reperfusion cycle of injury has yet to be fully understood. Continued production of inflammatory mediators and reactive oxygen species during ischemia reperfusion may contribute to the chronicity of pressure sores. 

In patients with normal sensitivity, mobility, and mental faculty, pressure sores are unlikely to occur. Feedback, both conscious and unconscious, from the areas of compression leads one to change position. This shifts the pressure from one area to another long before any irreversible ischemic damage to the tissues occurs.

Individuals who are unable to avoid long periods of uninterrupted pressure are at increased risk for developing necrosis and ulceration. This group of patients typically includes people who are elderly, neurologically impaired, or 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

The fifth National Pressure Ulcer Prevalence Survey, conducted in 1999 among patients in acute care hospitals, showed an overall prevalence rate of 14.8%, with 7.1% having occurred during that hospital visit.⁶ Intensive care units had the highest prevalence rates among different hospital settings, at 21.5%.⁶ The predominant age group of patients with pressure ulcers was the patients aged 71-80 years (29%).⁶

Pressure ulcer prevalence in long-term care facilities is an estimated from 11-30%. Among patients with neurological impairments, pressure sores occur with an incidence of 7-8% annually,⁷ with a lifetime risk estimated to be 25-85%.⁸

Anatomically, the buttock region is by far the most common area for pressure sores to develop. These account for over 70% of all occurrences, with sacral (46%) and ischial (26%) locations being most common.⁹ The lower extremities account for an additional 15% of all pressure sores, with malleolar, patellar, pretibial, and especially heel locations being most common.⁹ The remaining approximately 15% of pressure sores may occur in any location that experiences long periods of uninterrupted pressure.⁹ Nose, chin, forehead, occiput, chest, back, and elbow are among the infrequent sites for pressure ulceration. No surface of the body is 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.^{10, 7} Evaluation of large groups of patients has revealed that one third of hospitalized patients with pressure sores die during their hospitalization. More than half of patients who develop a pressure sore in the hospital 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. As patients move from the age category of 40–58 years to the age category of 75 years or older, a larger increase in the incidence of pressure ulcers occurs.² Two thirds of pressure sores occur in patients older than 70 years.¹¹

CLINICAL

Section 3 of 10  

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

History

When initially evaluating a patient with pressure ulceration, note the following important 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 may be present at the ulcer site. However, it is more commonly absent because of paraplegia or the patient being in critical condition and unable to acknowledge pain.
  • A foul odor or discharge could be a sign of a more serious infection at the ulcer site.
• Natural history of the present ulcer  
• • Length of time the ulcer has been present
  • Circumstances under which the ulcer has developed
  • Local treatments currently and previously 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 of the patient dictates the intensity of nursing care that is 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, attention should be turned to the wound. Adequate examination of the wound may require the administration of intravenous or oral pain medications to ensure patient comfort. Chronic pain may be present 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; therefore, many classification schemes have been developed to define the severity of pressure ulcers. The National Pressure Ulcer Advisory Panel has recently updated its classification scheme for pressure ulcers.¹² The goal of the revision was to clarify each stage and reduce the number of incorrectly staged ulcers or other types of wounds and skin lesions. 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 or 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.

• (Suspected) Deep Tissue Injury: This is the most recent addition to the staging system. This stage is described as a “purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear.”¹² This stage may be difficult to detect in individuals with dark skin.
• Stage I: This classification 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, which is 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: This classification represents a partial-thickness loss of skin involving epidermis and dermis that appears as an open shallow ulcer with a pink wound bed.
• Stage III: This classification represents a full-thickness loss of skin with extension into subcutaneous tissue but not through the underlying fascia. This lesion presents as an ulcer that may include undermining and tunneling of adjacent tissue. Bone, tendon, and fascia are not exposed.
• Stage IV: This classification represents full-thickness tissue loss with extension into muscle, bone, tendon, or joint capsule. Slough or eschar may be present in the wound. Osteomyelitis with bone destruction and dislocations or pathologic fractures may be present. Sinus tracts and severe undermining are commonly present.
• Unstageable: An unstageable ulcer is defined as full-thickness tissue loss in which the base of the ulcer is covered by slough or eschar such that the full depth of the wound cannot be appreciated. Only when the slough or eschar is removed can the depth of the ulcer be evaluated and correctly staged.

Staging of wound depth is only a small part of the initial assessment. Ulcer location, size of the skin opening, and presence of any surrounding maceration or induration must be accurately recorded. The presence of multiple pressure ulcers prompts the search for interconnecting tracts with overlying skin bridging 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 the need for debridement or diversionary procedures. Click here to complete a Medscape CME activity on fecal and urinary incontinence in adults.

Causes

Although prolonged uninterrupted pressure is the cause of pressure sores, 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 recovering from a traumatic injury such as a pelvic or femur fracture. These patients cannot adequately alter their position with enough frequency to relieve pressure. Moreover, this immobility, if prolonged, may lead to muscle and soft tissue atrophy, decreasing the bulk over which bony prominences are supported.

• Contractures and spasticity often contribute to ulcer formation 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. Skin breakdown and pressure ulcers may frequently be found under and between toes and on the palm of the hand.
• 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 or unable 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 with advanced age. The skin becomes more susceptible to minor traumatic forces, such as friction and shear forces typically exerted during the moving of a patient. Trauma that causes de-epithelialization or skin tears 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 an open 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 or prevent wound healing. These wounds serve as warm, moist reservoirs for bacterial overgrowth where antibiotic resistance may develop over time. Pressure sores may progress from being simply contaminated, as all open wounds are, to being grossly infected, which indicates tissue invasion by bacteria. This may lead to uncommon but life-threatening complications such as bacteremia, 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. (Click here to complete a Medscape CME activity about a recently FDA-approved treatment for hypovolemia and other conditions.)

WORKUP

Section 4 of 10  

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

Lab Studies

• CBC with differential may show an elevated white blood cell count indicative of inflammation or invasive infection, such as osteomyelitis.
• Erythrocyte sedimentation rate should be obtained to evaluate for inflammation and infection.
• Nutritional parameters should be evaluated to assess adequate nutritional stores needed for adequate wound healing. Lab studies include the following:
• • Albumin level
  • Prealbumin level
  • Transferrin level
  • Serum protein level
• When indicated by the specific clinical situation, the following laboratory studies should be obtained:
• • 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

• A tissue biopsy should be performed of wounds that do not demonstrate clinical improvement despite adequate care and wounds in which 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.
• A bone biopsy should be performed for a stage IV pressure ulcer with exposed bone. If osteomyelitis is confirmed, treatment with a prolonged course of antibiotic therapy may be indicated.
• A tissue biopsy of chronic wounds should be performed to rule out the presence of an underlying malignancy, called a Marjolin ulcer, 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, a biopsy should be performed. Scar carcinoma is uncommon and typically occurs in wounds that have been open for many years.

TREATMENT

Section 5 of 10  

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

Medical Care

With thorough and comprehensive medical management, many pressure ulcers may heal completely without the need for surgical intervention. Successful medical management of pressure ulcers relies on key principles, including pressure reduction, adequate debridement of necrotic and devitalized tissue, control of infection, and meticulous wound care.

• 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 also 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 caloric intake has been shown to improve healing of pressure sores. Implementation of more invasive methods of nutrient delivery becomes an ethical issue and must be weighed against the complications of such delivery. Goals of nutritional support should include adequate protein intake and the establishment of a positive nitrogen balance, with 1.0-2.0 g/kg/day being recommended for patients with pressure ulcers.
• 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. Initial studies of electrotherapy seem promising, and topical application of the recombinant human growth factor becaplermin (Regranex) has been approved for use in patients with diabetic neuropathic ulcers of the lower extremity. However, not enough evidence is available 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 resolve. Approximately 75% of stage II pressure sores also heal with conservative management. However, stage III and IV ulcers are much less likely to heal spontaneously and often require a surgical approach.¹³

Pressure Reduction

The first step in healing a pressure ulcer is determination of the cause, ie, pressure, friction, or shear. Turning and repositioning the patient remains the cornerstone of prevention and treatment through pressure relief. Repositioning should be performed every 2 hours, even in the presence of a specialty surface or bed. Patients who are bedbound should be positioned at a 30 degree angle when lying on their side to minimize pressure over the ischial tuberosity and greater trochanter. Efforts should be made to avoid sliding the patient over a surface to prevent shear forces and friction. Patients who develop a pressure sore while sitting should be placed on bed rest with frequent repositioning.

These devices are often heavy, expensive, difficult to clean, and require ongoing maintenance to ensure proper function. Pressure reduction beds have been shown to reduce pressure sore incidence and severity when compared to conventional hospital mattresses. 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, these devices must 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. Special consideration should be given 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, which resolves 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. A bladder catheter or condom catheter in males may be used to control urinary incontinence. In the most severe cases involving chronic stool contamination, surgical diversion should be considered.
• 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

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 not require dressing. For more advanced ulcers, various dressing options are available, depending on the state of the wound.

• Hydrocolloid dressings (eg, DuoDerm) form an occlusive barrier over the ulcer while maintaining a moist wound environment and preventing bacterial contamination. A gel is formed when wound exudate comes in contact with the dressing. Hydrocolloids help prevent friction and shear, and may be used in stage I, II, III, and some stage IV ulcers with minimal exudate.
• Transparent adhesive dressings (eg, OpSite, Tegaderm) also provide a moist wound setting and prevent bacterial entry while promoting epithelialization. They minimize friction and shear, and may be used in shallow stage I, II, and III ulcers.
• Alginate dressings (eg, SilvaSorb, Sorbsan) are fibrous products derived from brown seaweed and are available in nonwoven sheets and ropes. Alginate forms a gel when it comes into contact with wound drainage, and may be used in light to heavily draining stage II, III, and IV ulcers. It may be used in both infected and noninfected wounds; however, it should not be applied to dry or minimally draining wounds, as it can cause dehydration and delay wound healing.

Wound Debridement

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. For more information, please see Pressure Ulcers, Surgical Treatment and Principles.

• 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. Adequate pain control should be provided prior to any debridement, and vital signs often are a good indicator of pain perception. Great care should be taken during bedside debridement, as significant bleeding may occur.
• 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. 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 various 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.

For information on specific flap surgery, see the Flaps section of eMedicine’s Plastic Surgery journal. For more information on wound management, visit Medscape’s Wound Management Resource Center.

Surgical Care

For information on the surgical care of pressure sores, please refer to the eMedicine article Pressure Ulcers, Surgical Treatment and Principles.

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 consulting a plastic surgeon is appropriate with any complex or chronic wound.

Activity

Following successful wound closure, ambulatory patients should be out of bed with assistance as soon as possible. More strenuous physical activity should be delayed for approximately 6 weeks. In patients with ischial tuberosity ulceration, sitting may be resumed 6 weeks after a healed wound is achieved. Sitting may be gradually reintroduced over several weeks, and detailed guidelines have been published. Because of the extremely high pressures generated over the ischial tuberosities during sitting, wheelchair patients should 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 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• 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 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• 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

• Spasticity should be alleviated and adequate nutrition maintained 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. Long periods of uninterrupted pressure should still be avoided 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.
• Skin care should be performed 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. Skin should be washed with soap and water and completely dried at regular intervals and immediately upon soiling. Moisture should not accumulate on the skin or in clothing or bedding, nor should one allow the skin to become overly dry and scaly. 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 bacteremia, 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 system must realize that it is their responsibility to avoid recurrent and new ulceration and that this is a lifelong process.¹⁴ Education on the proper avoidance of pressure should begin in the hospital and continue into the home.

MISCELLANEOUS

Section 8 of 10  

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

Medical/Legal Pitfalls

• The ethics of pressure sore treatment should be carefully considered. The aggressive treatment of pressure ulceration is outlined in this article and others. This treatment is certainly indicated for a subset of patients who experience pressure ulceration: the acutely hospitalized patient with a recoverable illness.
• For others, such as patients who are chronically or terminally ill 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 considered. 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 9 of 10  

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

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Don R Revis Jr, MD, to the development and writing of this article.

REFERENCES

Section 10 of 10

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

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Article Last Updated: Jul 8, 2008