eMedicine Specialties > General Surgery > Abdomen

Decubitus Ulcers

Don R Revis Jr, MD, Consulting Staff, Department of Surgery, Division of Plastic and Reconstructive Surgery, University of Florida College of Medicine

Updated: Aug 27, 2009

Introduction

The terms decubitus ulcer and pressure sore often are used interchangeably in the medical community. Decubitus, from the Latin decumbere, means "to lie down." Decubitus ulcer, therefore, does not adequately describe ulceration that occurs in other positions, such as prolonged sitting (eg, the commonly encountered ischial tuberosity ulcer). Because the common denominator of all such ulcerations is pressure, pressure sore is the better term to describe this condition. (See images below and Images 1-2.)

Advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture.

Heel pressure ulcer.

History of the Procedure

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

Problem

Pressure is exerted on the skin, soft tissue, muscle, and bone by the weight of an individual against a surface beneath. These pressures are often in excess of capillary filling pressure, approximately 32 mm Hg. In patients with normal sensitivity, mobility, and mental faculty, pressure sores do not occur. Feedback, conscious and unconscious, from the areas of compression leads individuals to change body position. These changes shift the pressure prior to any irreversible tissue damage.

Individuals who are unable to avoid long periods of uninterrupted pressure over bony prominences—a group of patients that typically includes elderly individuals, persons who are neurologically impaired, and patients who are acutely hospitalized—are at increased risk for the development of necrosis and ulceration. These individuals cannot protect themselves from the pressure exerted on their body unless they consciously change position or have assistance in doing so. Even the most conscientious patient with an extensive support group and unlimited financial resources may develop ulceration resulting from a brief lapse in avoidance of the ill effects of pressure.

Frequency

Two thirds of pressure sores occur in patients older than 70 years. The prevalence rate in nursing homes is estimated to be 17-28%.

Among patients who are neurologically impaired, pressure sores occur with an annual incidence of 5-8%, with lifetime risk estimated to be 25-85%. Moreover, pressure sores are listed as the direct cause of death in 7-8% of all paraplegics.

Etiology

Many factors contribute to the development of pressure sores, but pressure leading to ischemia is the final common pathway. Tissues are capable of withstanding enormous pressures when brief in duration, but prolonged exposure to pressures slightly above capillary filling pressure initiates a downward spiral towards ulceration.^3,4

Impaired mobility is an important contributing factor. Patients who are neurologically impaired, heavily sedated, restrained, or demented are incapable of assuming the responsibility of altering their position to relieve pressure. Moreover, this paralysis leads to muscle and soft-tissue atrophy, decreasing the bulk over which these bony prominences are supported.

Contractures and spasticity often contribute by repeatedly exposing tissues to pressure through flexion of a joint. Contractures rigidly hold a joint in flexion, while spasticity subjects tissues to considerable repeated friction and shear forces.

Sensory loss also contributes to ulceration, by removing one of the most important warning signals, pain.

Paralysis and insensibility also lead to atrophy of the skin with thinning of this protective barrier. The skin becomes more susceptible to minor traumatic forces, such as friction and shear forces, exerted during the moving of a patient. Trauma causing deepithelialization leads to transdermal water loss, creating maceration and adherence of the skin to clothing and bedding, which raises the coefficient of friction for further insult.

Malnutrition, hypoproteinemia, and anemia reflect the overall status of the patient and can contribute to vulnerability of tissue and delays in wound healing. Poor nutritional status certainly contributes to the chronicity often observed with these lesions. Anemia indicates poor oxygen-carrying capacity of the blood. Vascular disease also may impair blood flow to the region of ulceration.

Bacterial contamination from improper skin care or urinary or fecal incontinence, while not truly an etiological factor, is an important factor to consider in the treatment of pressure sores and can delay wound healing.

Pathophysiology

The inciting event for a pressure sore is compression of the tissues by an external force, such as a mattress, wheelchair pad, or bed rail. Other traumatic forces that may be present include shear forces and friction. These forces cause microcirculatory occlusion as pressures rise above capillary filling pressure, resulting in ischemia. Ischemia leads to inflammation and tissue anoxia. Tissue anoxia leads to cell death, necrosis, and ulceration.

Irreversible changes may occur after as little as 2 hours of uninterrupted pressure.

Presentation

Clinical presentation of pressure sores can be quite deceiving to the inexperienced observer. Soft tissues, muscle, and skin have a differential resistance to the effects of pressure. Generally, muscle is the least resistant and will necrose prior to skin breakdown. Also, pressure is not equally distributed from the bony surface to the overlying skin. Pressure is greatest at the bony prominence, decreasing gradually towards the periphery. Once a small area of skin breakdown has occurred, one may be viewing only the tip of the iceberg, with a large cavity and extensive undermining of the skin edges.

Many classification systems for staging pressure ulcers have been presented in the literature.⁵ The most widely accepted system is that of Shea, which has been modified to represent the present National Pressure Ulcer Advisory Panel classification system. 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 healed wound. Rather, it is a system designed to describe the depth of a pressure sore at the specific time of examination, in order to facilitate communication among the various disciplines involved in the study and care of such patients.

Stage I represents intact skin with signs of impending ulceration. Initially this would consist of blanchable erythema from reactive hyperemia that 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. This may be 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 a crater with or without undermining of adjacent tissue.

Stage IV represents full-thickness loss of skin and subcutaneous tissue and extension into muscle, bone, tendon, or joint capsule. Osteomyelitis with bone destruction, dislocations, or pathologic fractures may be present. Sinus tracts and severe undermining commonly are present.

Other important characteristics of the wound should be noted in addition to depth. One should note the presence or absence of foul odors, wound drainage, eschar, necrotic material, and soilage from urinary or fecal incontinence. This provides information regarding the level of bacterial contamination and the need for débridement or diversionary procedures.

The overall state of health, comorbidities, nutritional status, mental status, and smoking history also should be noted. Presence or absence of contractures and spasticity also are important in the formulation of a treatment plan. One should note where the patient normally resides and the extent of his or her support structure. Examining the support surfaces present on the patient's bed or wheelchair also is important.

Relevant Anatomy

The hip and buttock regions account for 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 10% or so 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 more common of the infrequent sites for pressure ulceration. No surface of the body can be considered immune to the effects of pressure.

Contraindications

See "Ethical Considerations," under Future and Controversies.

Workup

Diagnostic Procedures

• Differentiation of bacterial infection from simple contamination is best made with a tissue biopsy, which allows quantitative wound culture techniques. This will indicate whether antibiotics should be administered.

Treatment

Medical Therapy

The first step in resolution is to reduce or eliminate the cause, that is, pressure. Specialized support surfaces are available for bedding and wheelchairs, which can maintain tissues at pressures below 30 mm Hg. These specialized surfaces include foam devices, air-filled devices, low–air loss beds (eg, Flexicair, KinAir), and air-fluidized beds (eg, Clinitron, FluidAir). Low–air loss beds support the patient on multiple inflatable air-permeable pillows. Air-fluidized beds suspend the patient as air is pumped into an air-permeable mattress containing millions of microspheric, uniformly sized, silicone-coated beads. No one device has been shown to be clearly superior over the others, but they all have been shown to reduce tissue pressure over conventional hospital mattresses and wheelchair cushions. Over 75 companies sell pressure-reduction devices, withannual industry revenues in excess of $8 billion.

Regardless of the choice of support surface, turning and repositioning the patient remain the cornerstones of prevention and treatment. This should be performed every 2 hours, even in the presence of a specialty surface or bed.

The wound and surrounding skin must be kept clean and free of urine and feces. This should be done through frequent cleansing and the establishment of a bowel and bladder regimen. Constipating agents may be helpful. Bacterial contamination must be assessed and treated appropriately. Differentiation of bacterial infection from simple contamination is best made with a tissue biopsy, which allows quantitative wound culture techniques. This will indicate whether antibiotics should be administered.

Wound dressings vary with the state of the wound. A stage I lesion with signs of impending breakdown may require no dressing. Stage II ulcers confined to the epidermis or dermis may be treated with a hydrocolloid occlusive dressing (DuoDerm), which maintains a moist environment to facilitate reepithelialization. For more advanced ulcers, a large variety of treatment options is available. These include wet-to-dry dressings, incorporating isotonic sodium chloride solution or dilute Dakins solution (sodium hypochlorite), Silvadene, Sulfamylon, hydrogels (Carrington gel), xerogels (Sorbsan), and vacuum-assisted closure (VAC) sponges. Daily whirlpool use also may serve to irrigate and mechanically débride the wound.

The choice of treatment and dressings is not as important as their appropriate application. These dressings are not a substitute for sharp débridement in severely contaminated wounds with necrotic material. Although uncommon, grossly infected pressure sores can lead to sepsis, myonecrosis, necrotizing fasciitis, and gangrene if not adequately débrided.

Spasticity should be relieved with diazepam, baclofen, dantrolene sodium, mephenesin carbonate, dimethothiazine, or orciprenaline. Flexion contractures may be relieved surgically.

Nutritional status should be evaluated and optimized. This is one of the only contributing factors that may be considered reversible. This may require dietary supplements, enteral feedings, or even parenteral feedings. Restoring a positive nitrogen balance and a serum protein level of 6 mg per 100 mL or higher has been shown to facilitate wound healing.

A multidisciplinary approach can lead to maximum benefit for the patient. Consultations with a neurosurgeon, urologist, plastic surgeon, orthopedic surgeon, and general surgeon all may be indicated in a particular patient. A rehabilitation medicine specialist, social worker, and psychologist or psychiatrist may work together with geriatricians or internists to improve the patient's health, attitude, support structure, and living environment.

When medical management has been optimized, many stage I and stage II pressure sores heal spontaneously. However, stage III and stage IV ulcers almost always require a surgical approach. Plastic surgeons perform most pressure sore reconstructions, and consulting a plastic surgeon with any complex or chronic wound is appropriate.

Surgical Therapy

Even with optimal medical management, many patients require a trip to the operating room for débridement, diversion of the urinary or fecal stream, release of flexion contractures, wound closure, or amputation.

Débridement is aimed at removing all devitalized tissue that serves as a reservoir for ongoing bacterial contamination and possible infection. Extensive débridement should be done in the operating room, but minor débridement is commonly performed at the bedside. Although many of these patients are insensate, others are unable to communicate pain sensation due to underlying disease processes. Pain medication should be administered liberally, and vital signs often are a good indicator of pain perception. Care also should be taken when débriding at the bedside because wounds may bleed significantly.

Urinary or fecal diversion may be necessary to optimize wound healing. Many of these patients are incontinent and their wounds are contaminated with urine and feces daily. Patients with loose stools benefit from constipating agents and a low-residue diet.

Release of flexion contractures resulting from spasticity may assist with positioning problems, and amputation may be necessary for a nonhealing wound in a patient who is not a candidate for reconstructive surgery.

Reconstruction of a pressure ulcer is aimed at improvement of patient hygiene and appearance, prevention or resolution of osteomyelitis and sepsis, reduction of fluid and protein loss through the wound, and prevention of future malignancy (Marjolin ulcer).

Preoperative Details

The concept that medical management must be optimized prior to surgical reconstruction of a pressure sore cannot be overemphasized; otherwise, reconstruction is doomed to failure. This means that spasticity must be controlled, nutritional status must be optimized, and the wound must be clean and free of infection.

Two units of type-specific packed red blood cells should be available during the operation, because blood loss may be significant.

Intraoperative Details

Patient positioning is dictated by the location of the ulcer and the planned reconstruction. Many pressure sores occur in the gluteal region and require prone positioning. Most anesthesiologists choose to use general endotracheal anesthesia, particularly if the patient is prone, but ulcer closure may be performed under regional or local anesthesia if necessary.

The first step is to adequately excise the ulcer. This includes the bursa or lining of the ulcer, surrounding scar, and any heterotopic calcification found. Underlying bone must be adequately débrided to avoid a retained nidus of osteomyelitis. Some evidence in the literature indicates that pulsed lavage can be beneficial in reducing bacterial counts in wounds, and some surgeons routinely use this method following débridement.

Once appropriately débrided, the wound may be closed in a variety of ways depending on the location of the pressure sore, previous scars or surgeries, and surgeon preference. However, the tenets of reconstruction remain the same in all pressure sore reconstructions.

Very few pressure sores can or should be closed primarily following débridement because of unacceptably high complication rates. A well-vascularized pad of tissue should be placed in the wound. This tissue usually is a musculocutaneous flap transposed or rotated on a pedicle containing its own blood supply. This also may involve the use of tissue expansion or a free flap with microvascular anastomosis. The purpose of this tissue is to eliminate dead space within the wound, enhance perfusion, decrease tension on the wound closure, and provide a new source of padding over the bony prominence. (See images below and Images 3-4.)

Small sacral pressure sores can be reconstructed with the inferior-based skin rotation flap, with or without the superior gluteus maximus myocutaneous flap.

Sacral pressure ulcer before and after flap closure.

Postoperative Details

The ultimate success or failure of pressure sore reconstruction only begins in the operating room. Wound healing and prevention of recurrence become the goals following successful closure of a pressure sore.

Postoperatively, the patient should be maintained on a specialized support surface for no fewer than 6 weeks. This may be in the hospital, at a rehabilitation facility, or at home.

After approximately 6 weeks, at the discretion of the surgeon, patients may gradually reintroduce temporary pressure to the surgical site by sitting. The patient must accept the responsibility that he or she never again sits for more than 2 hours in one position.

Perform skin care daily. This involves a careful inspection of all skin surfaces to identify areas of impending breakdown prior to their occurrence. Skin should be washed with soap and water and completely dried. Moisture should not be allowed to accumulate on the skin or in clothing or bedding, nor should the skin be allowed to become overly dry and scaly. Skin moisturizers are useful to maintain the appropriate level of moisture at the surface of the skin.

Control of spasticity and maintenance of adequate nutrition also must be continued into the outpatient setting to prevent recurrence.

Follow-up

Follow-up should be performed every 3 weeks for the first several months. The interval may then be increased to every 6 months and then yearly. Early issues include suture removal, drain removal, and when to allow the patient to exercise or sit up.

Once healing is complete, long periods of uninterrupted pressure must be avoided. This involves frequent repositioning by the patients themselves or their support group. Seated patients with upper extremity function should lift themselves from their wheelchair for at least 10 seconds every 10-15 minutes. Patients in bed should be repositioned at least every 2 hours.

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. This is an adjunct to the alternating of weight-bearing surfaces and maintains low pressures on the tissues at all times.

Complications

Complications fall into 1 of 2 categories: complications of chronic ulceration and complications of ulcer reconstruction.

The most 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 patients with chronic pressure sores. These malignancies typically are highly aggressive squamous cell carcinomas with a high likelihood of nodal metastasis at the time of diagnosis. Any long-standing, nonhealing wound should alert the examiner to the need for biopsy. (See images below and Images 5-6.)

Heaps of verrucous white tissue around the ulcer suggest malignant transformation, as observed with Marjolin ulcers.

Close-up view of area with heaps of verrucous white tissue around the ulcer, the presence of which suggests malignant transformation (as observed with Marjolin ulcers).

Outcome and Prognosis

Achieving a closed wound is the beginning of a lifelong struggle to prevent recurrent ulceration at the surgery site or at a new site. Recurrence rates in the literature are reported to be as high as 90%.

Future and Controversies

Promising research in the field of growth factors and wound healing has shed light on the complex interactions that ensue 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 US Food and Drug Administration (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 also are being evaluated for use in human clinical settings. This expanding field surely will contribute further applications of basic science to clinical wound healing, with improvement of our understanding and patient care.

Ethical considerations

As a final note, one should consider the ethics of pressure sore treatment. The aggressive treatment of pressure ulceration is outlined in this article. This treatment certainly is indicated for one subset of patients who have pressure ulceration, that is, acutely hospitalized patients with a recoverable illness.

For other persons, such as chronically or terminally ill patients with long-standing or recurrent ulceration, aggressive treatment may not be in their best interests. In these instances, the wishes of the patient or the patient's family should be weighed carefully. In many cases, medical care and the maintenance of patient comfort, rather than the institution of major invasive procedures, should be the goals.

Multimedia

Media file 1: Advanced sacral pressure ulcer shows the effects of pressure, shearing, and moisture.

Media file 2: Heel pressure ulcer.

Media file 3: Small sacral pressure sores can be reconstructed with the inferior-based skin rotation flap, with or without the superior gluteus maximus myocutaneous flap.

Media file 4: Sacral pressure ulcer before and after flap closure.

Media file 5: Heaps of verrucous white tissue around the ulcer suggest malignant transformation, as observed with Marjolin ulcers.

Media file 6: Close-up view of area with heaps of verrucous white tissue around the ulcer, the presence of which suggests malignant transformation (as observed with Marjolin ulcers).

References

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Keywords

decubitus ulcer, decubitus, pressure ulcer, pressure ulcers, bed sores, bed sore, pressure sore, pressure sores, bedsores, diabetic ulcer, decubitus ulcers, pressure ulcer staging, decubitus sore, ischial tuberosity ulcer, bed ridden, bedridden, bed rest injury, bedrest injury, chronic ulceration, pressure ulceration, decubitus ulceration

Contributor Information and Disclosures

Author

Don R Revis Jr, MD, Consulting Staff, Department of Surgery, Division of Plastic and Reconstructive Surgery, University of Florida College of Medicine
Don R Revis Jr, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Society for Aesthetic Plastic Surgery, and American Society of Plastic Surgeons
Disclosure: Nothing to disclose.

Medical Editor

Alex Jacocks, MD, Program Director, Professor, Department of Surgery, University of Oklahoma School of Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Michael A Grosso, MD, Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital
Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons
Disclosure: Nothing to disclose.

CME Editor

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MA, Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital
John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract
Disclosure: AMGEN Royalty Other

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