Pressure sores develop secondary to unrelieved pressure exerted on soft tissue overlying bony prominences. The National Pressure Ulcer Advisory Panel defines pressure ulcers as localized areas of tissue necrosis that develop when soft tissue is compressed between a bony prominence and an external surface for a prolonged period of time [1]. Clinicians frequently use the terms decubitus ulcer and pressure sore interchangeably. The word decubitus has its origin from the Latin word decumbre, which means to lie down [2]. The term decubitus ulcer therefore only applies to ulcers that occur in a lying position; it fails to describe ulcers that may occur in seated or other positions. Pressure sore is the preferred term because it describes all ulcers that result from pressure over weight-bearing areas regardless of position.

Landis [3] in 1930 suggested that constant pressure greater than the normal arterial capillary pressure, 32 mm Hg, can impair local perfusion. This is the most important determinant
in the development of pressure sores. The distribution of pressure in healthy patients in supine, prone, and various sitting positions has been extensively documented by various authors [4,5]. It is well accepted that the sacrum, buttocks, heels, and occiput are subject to the highest pressures in the supine position, with a range of 40 to 60 mm Hg. In the sitting position, pressures in excess of 75 mm Hg have been recorded over the ischial tuberosities [6]. The majority of pressure sores occur below the umbilicus, two-thirds in the hip and buttock region, and one-fourth to one-third in the lower extremities.

Studies of pressure tolerance in various tissue types by Husain [7] have demonstrated that muscle has a lower pressure tolerance when compared with skin and subcutaneous tissue. Le et al. [8] demonstrated that pressure applied to the soft tissue over bony prominences can cause infarction of muscle and subcutaneous tissue without skin necrosis. This explains the “tip of the iceberg” phenomenon not infrequently seen in clinical pressure sores. One of the most important studies regarding pressure tolerance was performed by Kosiak [9]. He demonstrated irreversible changes in dog muscle and skin when subjected to a pressure of 70 mm Hg applied continuously for 2 hours. More importantly, he showed that no changes occurred if pressure was relieved every 5 minutes. These findings illustrate the mechanism of pressure sore formation as well as reveal the major key to prevention.

There are multiple additional factors that contribute to the formation of pressure sores outside the local effects of unrelieved pressure. As suggested by the multifactorial hypothesis of Enis and Sarmiento [10], the intrinsic factors of malnutrition, advanced age, hypotension, impaired mobility, impaired sensation, and sepsis predispose critically ill patients to the development of pressure sores. Skin contamination with stool, excess moisture, and shear forces are extrinsic factors that further increase the risk of pressure sore formation.

In the early twentieth century, pressure sores were most commonly observed in young patients with chronic diseases such as tuberculosis, osteomyelitis, and chronic renal disease. This changed in the mid-1940s with improved early and late mortality rates after spinal cord injury. Spinal cord injury patients became the largest high-risk group for the development of pressure sores. Today, the elderly citizens have become the fastest growing segment in the American population. Residents in nursing homes and chronic care facilities are now recognized as the largest high-risk group for the development of pressure sores.

In an acute care hospital, the prevalence of pressure sores ranges from 3% to 11% of all admissions. It increases to 28% when subpopulations of high-risk patients are studied. The average cost of treating an established pressure ulcer ranges from $4,000 to $40,000. This does not include medicolegal liability costs, which are an increasing concern and focus.

Patients in the intensive care unit (ICU) often have multiple risk factors for the development of pressure sores: restricted mobility, impaired sensation and/or mental status, impaired perfusion, fecal and urinary incontinence, poor nutrition, advanced age, shear forces, and friction. In addition, ICU patients have various other physiologic impairments. A study by Eachempati et al. [11] has revealed emergent admission, age, days in bed, and days without nutrition as independent predictors of pressure sore formation. Even more recently, Feuchtinger et al. [12] have found in the cardiac surgery population temperature manipulation, vasoactive agents, hypotensive periods, anemia, operating room time, steroids, and low albumin levels to be significant risk factors for the development of pressure sores. Diabetes mellitus and high acute physiology and chronic health evaluation (APACHE II) scores also identify high-risk patients [13]. Spinal cord injury patients continue to be a challenging subgroup. Improved awareness of the risk factors as well as knowledge of the options for prevention and treatment of pressure sores will improve patient care and allow for more efficient use of healthcare resources. Once pressure sores develop. There are few patients who will be candidates for definitive surgical closure because of their concurrent medical disabilities. The pressure sore then becomes a costly chronic medical problem. In any debilitated patient population, pressure sores are extremely difficult to heal.

Prevention of pressure sores in the ICU begins with education of the entire hospital staff. Identification of patients at high risk is the initial step. All patients should be routinely screened on admission for risk factors that may predispose them to the development of pressure sores. The basic tenets of prevention include pressure reduction over bony prominences, alternation of weight-bearing surfaces, good skin hygiene, and the maintenance or restoration of adequate nutrition. At this time, there is no universally accepted screening tool for quantifying risk for pressure sore development, but the risk factors are well known. Considering the cost of managing an established pressure sore, it is likely that excess prevention is less costly than nonaction. The Braden scale is one of the most widely used risk assessment tools. It has six subscales: sensory perception, skin moisture, activity, mobility, friction and shear, and nutritional status. Regardless of the screening tool, the most important factor is starting preventive measures as soon as patients at risk are identified [14]. Inattention to previously noted risk factors or early signs of skin breakdown can result in a clinically significant pressure sore in less time than the standard 8-hour nursing shift.

Dispersion of pressure is a vital component of preventive measures and management. Before the 1960s, frequent patient body positioning for avoidance of skin maceration was the mainstay of pressure sore prevention. This is still considered the basic tenet in preventive measure. Patients confined to bed should be turned every 2 hours. Alternating 30-degree oblique supine positions are best [15]. The 90-degree lateral position should be avoided. More importantly, patients in a sitting position should have their weight shifted several times every hour [6].

In the 1960s, pressure-reduction technology using the principle of dispersion became available to improve local blood flow and minimize tissue ischemia. These devices are based on the concept of suspension or buoyancy [16]. The greater the body surface area supported by the surface, the greater the distribution of the patient’s weight against the mattress and the lower the effective contact pressure on the skin. The available devices achieve buoyancy through the use of water, air, gel, foam, or circulating ceramic beads. The cost of these various systems ranges from $35 to $140 per day of use.

It has been well demonstrated in the literature that transcutaneous oxygen tension can be maintained in an acceptable range in the supine position with the use of air-fluidized and low-air–loss beds in comparison to standard hospital mattresses [17]. Only with the use of air-fluidized systems is this maintained in the lateral decubitus position. Inman et al. [18] studied 100 consecutive patients who were at risk for pressure ulcer development and randomly assigned half to receive care on a standard ICU bed and half to a low-air–loss surface.
The patient groups were comparable, and all other treatment measures were standardized. The low-air–loss patient group developed fewer and less severe pressure ulcers than those who were treated on the standard surface. Taking into account the cost of the low-air–loss surface and the treatment of an established pressure sore, low-air–loss therapy is not only effective in preventing pressure sores from occurring, but it is also cost-effective. The low-air–loss mattress is a highly valuable preventive measure for the critically ill patient while not interfering with the patient’s care.

Good skin care is another important adjunctive component of pressure sore prevention. This involves keeping the bed free of particulate matter and solid objects that may cause abrasions or lacerations. Daily skin assessments should be a part of routine nursing care to screen for the development of pressure sores, especially heel ulcers. Daily application of creams and lotions to the feet is inexpensive and can be vital to heel ulcer prevention. Control of both urinary and fecal incontinence and diarrhea are also important. As discussed previously, excess moisture may increase the possibility of pressure sore formation. Bacterial contamination can delay wound healing and extend the zone of tissue necrosis. Enterostomal therapists or wound care nurses can be invaluable resources in the management of these wounds. Colostomies are occasionally necessary to obtain control of the fecal stream with complex sacral or perineal wounds and open pelvic fractures. This decision should be made in conjunction with plastic and general surgical consultation.

Heel ulcers are a clinical problem that warrants special attention. A national pressure ulcer prevalence study by Meehan [19] identified the heel as the second most common site for the development of pressure ulcers. With the introduction of pressure-reduction surfaces, the incidence of sacral ulcers decreased, but there was a concomitant increase in heel ulcers. A study by Blaszczyk et al. [20] developed a useful heel pressure ulcer risk assessment tool to identify patients at risk for the development of heel ulcers.

The patient specific variables include; age over 70 years, diabetes mellitus, mental status changes (agitation, confusion, stupor, unresponsiveness), and immobility of the lower extremity. These specific risk factors are added up and the activity level is then assessed; this determines the risk factor level. Ambulatory patients should get universal heel precautions only. Patients who walk with assistance with one or no risk factors receive universal precautions only, two risk factors yield preventive precautions, and three or more risk factors yield strict precautions. Nonambulatory patients without any risk factors receive universal precautions, one risk factor yields preventive precautions, and patients with two or more risk factors receive strict precautions [20].

Universal heel precautions include daily assessment of feet, daily skin care (creams or lotions), turning every 2 hours, standard hospital pressure-reduction mattress, mobilization out of bed three times a day, and active range of motion. Preventive heel precautions additionally include assessment of feet two times a day, friction reduction (creams or lotions twice daily, socks or support hose, transparent films, or hydrocolloid to heels every week), and pressure reduction (pillow support keeping heels off bed, heel roll or heel cushion, passive range of motion exercises). Strict heel precautions additionally include foot assessment three times a day, creams or lotions three times a day, and heel protection (heel lift, heel cushion). This protocol resulted in a decrease of heel pressure ulcers in the medical ICU patient population [20].

Prior to surgical intervention for heel ulcers, including debridement, patients should be evaluated for vascular insufficiency by obtaining an ankle–brachial pressure index. If this is abnormal, a formal vascular surgery consultation should be obtained.

An effort should be made to remove trauma patients from spine boards and also remove rigid cervical collars as quickly as possible. Patients who require a cervical collar for an extended period should be assessed so that the collar fits properly. Blaylock [21] reported a successful routine for care that significantly reduced pressure ulceration from cervical collars. In patients with an unstable cervical spine, an oscillating support surface may reduce the risk of developing pressure sores. These low-air-loss mattresses also oscillate continuously from side-to-side up to 62 degrees to redistribute pressure on the skin. Selection of this surface should be made after consultation with a spine surgeon.

Nutritional assessment and support are obvious integral components in the care of every critically ill patient. It is well known that malnutrition impairs wound healing. A serum albumin less than 2.5 g per dL has been correlated with the development of pressure sores. It is important that a patient’s nutritional status is optimized prior to any reconstructive surgical intervention needed to close a chronic pressure sore. Weekly monitoring of the visceral protein prealbumin can be used to assess the adequacy of the patient’s nutritional status and response to dietary supplementation. A more detailed discussion of nutritional assessment and management is beyond the scope of this chapter.