Decubitus ulcers are a worldwide health care concern affecting tens of thousands of patients and costing over a billion

dollars a year. Susceptibility to pressure ulcers comes from a combination of external factors (pressure, friction, shear force, and moisture), and internal factors (e.g. fever, malnutrition, anaemia, and endothelial dysfunction). Often, enough damage is done to create the basis for a decubitus ulcer after as little as 2 h of immobility, a situation which may be difficult to avoid if the patient must undergo prolonged surgery or remain bedridden. Damage owing to pressure may also occur hours before the patient receives medical attention, especially if the patient falls or becomes immobilized owing to a vascular event. Several classification systems for decubitus ulcers have been described, based on where injury first occurs. The histologic progression of decubitus ulcers is a dynamic process involving several stages, each having characteristic histologic features. A team-focused approach integrating all aspects of care, including pressure relief, infection control, nutrition, and surgery, may improve healing rates. With accurate risk assessment and preventative care, we can hope to minimize complications and mortality owing to decubitus ulcers. Introduction and Pathogenesis Decubitus ulcers, also known as bedsores and pressure sores, are caused by impaired blood supply and tissue malnutrition owing to prolonged pressure over skin, soft tissue, muscle, and/or bone. Decubitus ulcers have probably existed since the dawn of humankind. They have been observed in unearthed human mummies and addressed in scientific writings of the 19th century. Prolonged pressure along with tissue compression can lead to capillary bed occlusion and local ischemia. Without adequate blood flow, toxic metabolites accumulate locally, increasing the rate of cell death. This leads to ulceration and necrosis of skin and underlying tissue. This process can be accelerated if lymphatic ducts are blocked and if reperfusion injury occurs after load removal. Constant pressure can come from lying down (decubitus from the Latin decumbere, to lie down) or from sitting. Pressures greater than capillary filling pressure (32 mmHg) at the heels and sacrum of patients on operating room tables with standard padding are enough to cause necrosis if the duration of pressure exceeds 2 h. The skin overlying the sacrum and hips is most often affected (67%), but decubitus ulcers may also be observed over the occiput, helices, elbows, and lower extremities (25%), including heels and ankles. Decubitus ulcers can develop on any part of the body where sustained pressure and compressive forces are maintained for a sufficient period of time. Other susceptibility factors may also contribute to decubitus ulcer formation. Susceptibility to pressure ulcers comes from a combination of external factors (pressure, friction, shear force, and moisture), and internal factors (e.g. fever, malnutrition, anaemia, and endothelial dysfunction). Often the seeds of a decubitus ulcer are planted long before the patient receives medical attention. Pre-operative serum albumin levels less than 3.0 g/dl have been shown to increase the risk of pressure ulcers.

Other pathological processes can contribute to ulcer formation including contractures, spasticity, diabetes mellitus, peripheral vascular disease, and hypotensive episodes. Dysfunction of autonomic regulatory mechanisms of local blood flow may increase susceptibility to decubitus ulcers. Any agent that creates immobility, such as neuromuscular paralyzing agents, braces, and splints also may contribute to the pathogenesis of decubitus ulcers. Excessive heat from heating pads and blankets may further irritate skin, increasing susceptibility to ulcer formation. In patients with normal sensitivity, mobility, and mental faculty, decubitus ulcers usually do not occur. Conscious and unconscious feedback leads to position shifts before irreversible tissue damage occurs. Thus, decubitus ulcers occur most often in aged, incontinent, debilitated, paralyzed, and unconscious patients. Patients with the following conditions are most susceptible: neurologic disease, cardiovascular disease, prolonged anesthesia, dehydration and malnutrition, hypotension, and surgical patients. Two-thirds of decubitus ulcers occur in patients aged > 70 years. Twenty-five percent of decubitus ulcers start in the operating room during surgery. Eighty-three percent of hospitalized patients with decubitus ulcers developed them in the first 5 days of hospitalization. The largest number occurred on the day of operation. The prevalence rate in nursing homes is estimated to be 1728%. Among neurologically impaired patients decubitus ulcers occur at an annual rate of 5 8%, with lifetime risk estimated to be 2585%. Decubitus ulcers are listed as the direct cause of death in 7 8% of paraplegics. Hospitalized patients have a 317% incidence rate, while hospitalized surgical patients have a 12 66% incidence rate. Immobilized patients in long-term care facilities have a 33% incidence rate. Some estimates suggest that 60,000 people die from decubitus ulcers or their sequelae per year. Recurrence rates for decubitus ulcers maybe as high as 90%. Present treatment costs for decubitus ulcers in the US is estimated in excess of $1 billion per year. Morphology The clinical presentation of decubitus ulcers may not reveal the full extent of damage. Several classification systems for decubitus ulcers have been described: Daniels, Sheas,and the National Pressure Ulcer Advisory Panel (NPUAP), which is a modification of Sheas classification. In Daniels classification, muscle and subcutaneous tissue breakdown occurs before dermal and epidermal changes are observed. Epidermal necrosis occurs late in the course because epidermal cells are better able to withstand prolonged absence of oxygen than deeper cells both in vivo And in vitro. Often this type of decubitus ulcer results from injury to the skin days before

clinical findings are evident. Eventually the skin ruptures revealing a deep, draining wound. Once skin damage is visible, irreversible internal damage may have already occurred. These deep ulcers are often observed in surgical or bedridden patients. Sheas classification system describes ulcers that originate superfically and progress deeper into muscle and occasionally to bone. Patients incontinent of urine and feces often have weakened skin that is less able to withstand pressure, thus epidermis and dermis show visible damage early on. The most widely accepted classification system for decubitus ulcers is the NPUAP. This four-stage classification is designed only to describe the depth of a visible ulcer at the time of examination. It is not designed to follow progression/regression of the wound or document healing. The NPUAP classification is also of no use with eschar or deep tissue injury because it relies on visible findings. In the eschar stage, the epidermis and dermis have necrosed, and in deep tissue injury the visible findings do not appear until much later in the progression of the lesion. It is important to note that staging conveys a somewhat misleading suggestion that there is an orderly progression of damage from the epidermis to the dermis and subcutis. Stage I of the NPUAP classification represents intact skin with signs of impending ulceration: blanching and/or nonblanching erythema, warmth, and induration. It is especially important to recognize and effectively treat Stage I ulcers because they can resolve, with proper care, in 510 days. Stage I is often difficult to directly determine in patients with pigmented skin, unless one specifically feels for warmth, erythema, and induration. Stage II ulcers present clinically as a shallow ulcer (including epidermis and possibly dermis) with pigmentation changes. The lesion may present as an abrasion, blister, or superficial ulcer. Stage II ulcers, like Stage I, can be reversible. Stage III ulcer, or a typical decubitus, represents a full-thickness loss of skin with extension through subcutaneous tissue, but not underlying fascia. The lesion presents as a necrotic, foul-smelling crater with altered light and dark pigmentation. Stage IV represents full-thickness skin and subcutaneous tissue loss, with ulcer penetration Histopathology Decubitus ulcers have many histologic stages. Clinically, the decubitus ulcer spectrum includes blanching erythema, nonblanching erythema, decubitus dermatitis, early ulcer, healing ulcer, chronic ulcer, and black eschar/gangrene. The progression is dynamic and multiple stages are often observed in one decubitus ulcer. The salient histopathologic feature of blanching erythema is dilated capillaries and venules with large endothelial cells in the papillary dermis.

There is a mild lymphocytic perivascular infiltrate. Epidermis and reticular dermis are normal at this stage. Because blanching erythema occurs before nonblanching erythema, it is often ignored, even though there is histologic change. Nonblanching erythema shows red blood cell engorgement of already dilated capillaries and venules. Platelet aggregates and hemorrhage are observed. In decubitus dermatitis, four types of epidermal responses are observed: diffuse eosinophilia, focal eosinophilia, epidermal atrophy with subepidermal blister, and normal-appearing epidermis with subepidermal blister. Friction may play a secondary role in the pathogenesis of decubitus dermatitis by removing already devitalized epidermis. The early ulcer stage is similar in morphology to the decubitus dermatitis stage, but lacks a prominent epidermis. This stage includes blanching erythema, nonblanching erythema, bullae, and scarring changes. There is a perivascular infiltrate of mononuclear inflammatory cells and acute inflammatory cells in the papillary and reticular dermis. Healing ulcers contain granulation tissue, new blood vessels, and growth. Fibroblast proliferation may also be present. Chronic ulcers are encrusted with red blood cells and acute inflammatory cells. The remaining dermis is fibrotic and contains many capillaries. The black eschar phase represents full-thickness skin destruction (epidermis, dermis, and subcutis). Perilesional surrounding tissue is crusted and epidermis is absent. Often there is necrosis of inflammatory cells and red blood cells. Treatment Few diseases have had so many attempted treatments as decubitus ulcers. Historically, various chemical treatments have been tried, including poultices of vegetables, enzymes, vitamins, cod liver oil, dried blood plasma, various precious and nonprecious metals, chlorophyll, sugar, and salt. Mechanical treatments included electric lamps, ultraviolet light, hyperbaric oxygen, rubber rings, sawdust beds, and a variety of pressure beds and padding. Today, the treatment of decubitus ulcers is based on four primary modalities: (1) pressure reduction and prevention of additional ulcers, (2) wound management, (3) surgical intervention, and (4) nutrition. Table 1 summarizes some of the key Dos and Donts for decubitus ulcer management. The cornerstone of decubitus ulcer therapy is to reduce or eliminate pressure. This is carried out through the use of support surfaces, turning, padding, positioning, and, if possible, mobilization of the patient. Two major types of support surfaces exist: static and dynamic. Static surfaces include air, foam, and water mattress overlays. Candidates for static surfaces are patients who have Stage I or II ulcers who can lay comfortably without putting pressure on their ulcers but who may be at risk of developing additional ulcers. Dynamic surfaces for pressure reduction include alternating air overlay, low air loss bed and air-fluidized beds. These are for patients with deep and/or

recalcitrant ulcers, such as stages III and IV. No one dynamic pressure reduction device has been found to be superior to the others. An additional way to reduce pressure involves turning and repositioning the patient every 2 h to reduce pressure on vulnerable areas. This number came about through historical nursing shortages: the time it took for the nurses to rotate all patients on the wards was 2 h. However, current research indicates that the 2-h interval may not be adequate in some cases and may be too much in others. Once an ulcer develops, wound management is critical. The key aspects of wound management to ensure effective healing are cleaning and effective drainage and absorption while protecting the skin adjacent to the wound. The goal of wound cleaning is to remove the dead tissue and debris, which impede healing. Products such as Sterile Saline, Comfeel Sea-Clens (Coloplast AIS, Humlebaek, Denmark) are effective cleaning agents. Non-FDA approved cleansers and antiseptics are not appropriate for open wounds. The pressure needed to clean wounds with no necrotic tissue should be about 25 pounds per square inch (PSI). Wounds with necrotic tissue may require up to 23 times more pressure. Finally, debris removal may occasionally require chemical or surgical debridement. Drainage and absorption management are critical to healing. The need for drainage and absorption can vary from wound to wound and over the healing cycle. With a heavy draining wound, a dressing such as Alginate or Foam is appropriate. For medium and light draining wounds, products such as Hydrocolloid (Coloplast AIS, Humlebaek, Denmark)work well. Finally, for wounds with no drainage, Hydrogellamorphous (Gentell, Inc., Trevose, PA, USA) or simple gauze is appropriate. Skin adjacent to the wound may be lubricated to decrease friction and be kept relatively dry. Additionally, the dressing should have adequate padding to protect from outside mechanical forces. The dressing should be changed according to the agreed protocol. Surgical intervention for decubitus ulcers involves debridement or flap creation for some Stage III and Stage IV ulcers. Debridement is the process of removing devitalized tissue. It can be performed via surgical, autolytic, mechanical, or enzymatic means. The type of debridement performed depends on many factors, including perfusion status, wound location, pain tolerance, timing, staff, and equipment needed. Surgical flaps to replace unstable scars in Stage III or IV ulcers were first suggested in 1938. Various types of flaps are used today, including perforant, musculocutaneous, and fasciocutaneous flaps, most often for large sacral or greater trochanteric pressure sores. Current regrafting with flaps has been successful, but larger studies are needed to fully determine risks and benefits. Schoeller et al. found that flaps provided stable coverage in four of five patients at 12 months follow up.

Although surgical flaps as therapy for decubitus ulcers may be successful, they are not without risk. If the decubitus ulcer is partially healed and a flap is created, the risk of a Marjolins ulcer (squamous cell carcinoma) may be increased. Malnutrition and infection must be avoided if reconstructive surgery is to be performed. Surgery may also need to be performed if deep tissue is involved, such as bone and muscle. Bone involvement, while important to determine, is often difficult to assess owing to the shape, depth, and location of the ulcer. Macroscopic assessment of Stage IV decubitus ulcers may lead to overestimation of bone involvement. Allman et al. found bone biopsy unnecessary in many cases without concomitant sepsis; however, in 1947, bone excision was suggested for chronic deep ulcers. Currently, bone debridement is recommended to prevent against recurrence of deep ulcers. Often, insufficient excision of soft tissue and bone is a source of flap failure, even if the perfusion and construction are adequate. Infection control is important to keep the ulcer and adjacent skin free of pathogenic bacteria. Dressings are important to maintain wound cleanliness, to protect the wound from outside mechanical forces and contaminants and maintain a moist wound environment conducive to healing. The type of dressing selected should be matched to the status of the wound. Malnutrition should be addressed because the malnourished patient has a higher susceptibility for ulcer formation, and also cannot heal or prevent infection as well as a wellnourished patient. Malnourished patients may require supplements, enteral, or parenteral feedings. Acutely ill patients with low serum albumin and/or multiple illnesses may be candidates for nutritional support therapy. Restoring a positive nitrogen balance has been shown to speed decubitus ulcer healing. Other treatment modalities that can be employed as needed include: blood transfusion to treat anaemia, nutrition for protein depletion, intravenous fluids to treat dehydration, electrolyte imbalance, and antibiotics to treat infection. One of the most difficult tasks in the treatment of decubitus ulcers is identifying patients who may be at risk for additional ulcers. There are several risk assessment scales: Norton,Cubbin and Jackson, Braden, Douglas, and Waterlow. Each of these scales attempt to evaluate the current health of the patient and the presence of factors that contribute to pressure ulcer formation. Potential bias has been inherent in the design of all.Current studies show these risk assessment scales may not as effective as nurses judgement as to which patients are at risk. Outcomes Studies documenting treatment of decubitus ulcers have led to various conclusions. Ferrellet al. found that no pressure ulcerhealed completely or reduced in surface area greater than 50% within 30 days and only 14% of pressure ulcers completely healed within 79 days. This indicates that long-term therapy may be necessary. Yao-Chinet al. found 53% of pressure ulcers healed within 42 days.

Differences in these studies may be attributed to patient characteristics (including stages of ulcers studied), hospital setting, and length of follow up. In general, it is difficult to draw conclusions owing to the great problem inherent in studying such a multifactorial problem with the many accepted treatments. Multivariate analysis has pointed to a constellation of factors that come together to create a decubitus ulcer. No one treatment works completely on its own; rather, a host of complimentary treatments that span the entire spectrum of patient care must be employed for the most favorable outcome. Treatment must continue for the life of the patient as recurrence rates can be as high as 90%. Complications Severe fluid and protein loss from a decubitus ulcer may lead to hypoprotenemia or worsened malnutrition owing to the catabolic nature of these wounds. Osteomyelitis, myonecrosis, necrotizing fasciitis, amyloidosis, sepsis, gangrene, and death may also result in the most severe cases. Firooznia et al . found four of 12 patients with pressure ulcers developed osteomyelitis, and Turk et al . found 13 out of 28 specimens had osteomyelitis. Bone reabsorption can lead to hypercalcemia, hypercalciuria, ectopic calcification, calcium urinary stones,and bladder stasis. Low-grade bacterial infection may occur as a complication; however, full-blown sepsis is rare in patients with decubitus ulcers. Marjolin ulcers (malignancies) may occur in previously healed ulcers that recur. Postsurgical complications include hematoma and seroma (which can be prevented by meticulous surgical drainage of the ulcer bed), wound dehiscence and postoperative wound sepsis, and possible abscess formation. Future Research With proper care and adequate prevention both in and out of the hospital, the risk of developing decubitus ulcers may be decreased. However, there are limits to prevention, even with excellent care. Because skin integrity is dependent upon the function of all the other organ systems for nutrition and immune function, when those organs fail the skin is at a greatly increased risk for ulceration. Growth factors and hyaluronic acid have also been implicated in the process of wound healing. Current research into wound healing has led to the development of Becaplermin (Regranex; OMJ Pharmaceuticals, Inc., Puerto Rico), a recombinant human plateletderived growth factor. Becaplermin has been given FDA approval for treatment of lower extremity diabetic neuropathic ulcers. It may also have a place in the treatment of decubitus ulcers. Superoxide dismutase, a superoxide anion scavenger, was found to promote the survival rate of transplanted skin flaps. Polyphenols such as catechin and black catechu have been found to have scavenger effects on oxygen radicals. Topical vitamin E has been found to accelerate the healing of skin wounds and ulcers.

Summary Decubitus ulcers are a major health care concern affecting tens of thousands of patients and costing over a billion dollars a year. The pathogenesis of decubitus ulcers is dependent upon both external and internal factors as discussed earlier. Many studies show that decubitus ulcers can begin after as little as 2 h of immobility, a situation that may be difficult to avoid if the patient must undergo prolonged surgery or remain bedridden. Often damage owing to pressure occurs hours before the patient receives medical attention, especially if the patient falls or becomes immobilized owing to a vascular event. A team-focused approach integrating all aspects of care, including pressure relief, infection control, nutrition, and surgery may improve healing rates. With accurate risk assessment and preventative care, we can hope to minimize morbidity and mortality associated with decubitus ulcers.