Nonsurgical Treatment of Pressure Ulcers 

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]

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.

International

A recent study from Germany reviewed the pressure ulcer prevalence in the patient population residing in long-term care facilities. In the review of over 18,000 patients, the prevalence rate decreased from 12.5% in 2002 to 5% in 2008. The decrease in pressure ulcer prevalence in Germany is thought to be due to more effective strategies and better prevention.^[10]

Mortality/Morbidity

Pressure sores are listed as the direct cause of death in 7-8% of all patients with paraplegia.^{[11, 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.^[12]