Spring 2002: Volume 11, Number 1

New Findings in Pressure Ulcer Prevention and Treatment

Pressure ulcers are a common, debilitating, and costly complication of SCI, often requiring long periods of immobility, hospitalization, and/or surgery. Patients with SCI are therefore carefully instructed to perform regular, frequent pressure releases in order to maintain blood flow to the skin and avoid skin breakdown.

Yet many individuals with SCI get pressure ulcers despite diligent pressure release behavior, and others get pressure ulcers that don't heal for years, said Jennifer James, MD, clinical assistant professor at the UW Department of Rehabilitation Medicine. James and her colleagues at the Seattle Veterans Affairs SCI Unit are finding that system-wide abnormalities, including deficiencies in the metabolic, anabolic and endocrine systems, are often present in patients with non-healing wounds. These complex medical conditions can both predispose a patient to pressure ulcers as well as prevent a wound from healing.

A pressure ulcer that has not healed after eight weeks of wound care and adequate nutrition is called a non-healing wound and may be an indication that the patient is in a catabolic state. Catabolism is a destructive metabolic process that converts living tissue to waste, in contrast to healthy anabolic metabolism, in which nutrients are converted to living tissue. The catabolic state creates a vicious cycle of non-healing and multiple coexisting medical problems, James said, and "unless this systemic catabolic state is reversed, the wound cannot heal."

According to James, the most common and least recognized systemic abnormality evident in patients with non-healing wounds is protein-calorie malnutrition (PCM), characterized by protein catabolism and loss of lean body mass (LBM). PCM inhibits the formation of collagen, which is the key protein in wound healing. Signs that PCM is present include low albumin and prealbumin, anemia, low serum zinc, and reduced weight/height ratio.[1] The severity of the pressure ulcer correlates closely with the degree of malnutrition, measured by albumin.[2]Non-healing wounds are also associated with low Vitamin B12, a necessary factor in protein synthesis.

Nutritional supplementation with a high protein content is necessary but not sufficient to reverse the catabolic process. Low testosterone levelsa common deficiency in the SCI population[3]can also hasten the loss of LBM[4] and contribute to a catabolic, non-healing state. The medication oxandrolone, an agent that is structurally similar to testosterone, can help correct this. When used in conjunction with high protein intake, oxandrolone can stimulate or jump-start the patient out of the downward spiral of catabolism, James explained.

A loss of LBM and an increase in body fat is common in the SCI population and increases the risk for diabetes and heart disease. It is not unusual for a person with SCI to be both obese and very malnourished at the same time. LBM loss is also associated with impaired immune function and increased infections, which further compromise the body's healing capabilities. Some medications that are frequently used by patients with SCI can cause malabsorption problems that contribute to malnutrition. Malnutrition can also result in decreased oxygenation to the skin, which undermines the healing of wounds and jeopardizes healthy tissue.

Once a pressure ulcer is present, the patient is already in a catabolic state, James said. But determining which came firstthe pressure ulcer or the systemic declineis a classic "chicken-or-egg" enigma. "We all wonder about that," she said. "Why do we have so many patients who do pressure releases regularly but still get pressure ulcers? And the reverse is also true" (patients who do not do pressure releases do not necessarily get pressure ulcers). Recent evidence collected and analyzed by James and other researchers at the Seattle VA now suggests that "patients who start out with decreased albumin and other metabolic deficiencies are predisposed to getting pressure ulcers because of their catabolic state, regardless of their pressure releases," James said.

Based on their findings, James and her colleagues have developed a new protocol for patients with pressure ulcers that includes testing for low albumin, B12 and testosterone levels. Using this approach, they have been able to diagnose systemic abnormalities and treat non-healing pressure ulcers of many years' duration that previously defied conventional inpatient and outpatient wound care[5]. By identifying and reversing the catabolic state, "we're getting more patients to avoid surgery," James said. "We're beginning to think we should check testosterone and B12 on routine annual checkups."

James insists that it's still important to do regular pressure releases. "But we need to look into other systemic factors that affect patients who get pressure ulcers. We're just discovering them. There is no data yet on the presence of systemic decline and the healing of wounds. This is a new frontier."

References

Allman RM, et al. Pressure ulcer risk factors among hospitalized patients with activity limitation. JAMA. 1995;273-865-870.
Pinchcofshy-Devin GD, et al. Correlation of pressure sores and nutritional status. J Am Geriatr Soc. 1986;34:435-440.
Tsitouras PD, et al. Serum Testosterone, growth hormone, insulin-like growth factor-I in adults with spinal cord injury. Horm Metab Res. 1995;27:287-292.
Bauman WA, et al. Blunted anabolic hormone response to intravenous arginine in subjects with spinal cord injury. Horm Metab Res. 1994:26:152-156.
Spungeon A, et al. Effect of anabolic steroid therapy on healing of long-standing pressure sores: nine case reports in patients with SCI. J Spinal Cord Med. 1999;22:27.