Involuntary Weight Loss and its Effects on the Body’s Ability to Heal—Optimal Wound Healing: A Comprehensive Approach Through M

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Author(s): 
Jennifer J. James, MD

Introduction

Wound healing is a multifactorial process. The presence of an open wound can create a complex catabolic state that can both cause and propagate systemic deficiencies.1 This catabolic state can result in nutritional compromise and the loss of lean body mass (LBM). Conversely, a common complication of involuntary loss of LBM is the development of pressure ulcers—a frequent and serious complication of any disorder characterized by immobility. Involuntary weight loss (IWL) increases the risk of pressure ulcer development by 74 percent, according to the National Pressure Ulcer Long-Term Care Study. 2 Individuals at greatest risk for IWL include those with major burns and trauma (80% prevalence), spinal injury rehabilitation (50%), outpatient rehabilitation (20% to 40%), and nursing home residents (up to 85% prevalence).3 Approximately 10 percent of all hospitalized patients, 20 percent of nursing home residents, and up to 50 percent of individuals with spinal-cord injury (SCI) develop pressure ulcers.4-6 Catabolic breakdown of LBM is significantly associated with pressure ulcer development in hospitalized patients with SCI. In a study by Rochon, et al., those with serum albumin <3.5g/dL had a 45.2-percent incidence of pressure ulcers, compared to only 14.5 percent of patients with normal albumin.7 In the development of a pressure-ulcer risk assessment scale specifically for SCI, Salzberg, et al., cited low albumin as well as the presence of other comorbid conditions as significant factors.8 Loss of LBM significantly compromises immune system function, resulting in an increased incidence of infections.9 This adds to the vicious cycle of nonhealing wounds and perpetuation of the catabolic state, nutritional compromise, and multiple comorbid medical conditions.

Mutually interdependent systemic factors that adversely affect wound healing and predispose a patient to develop pressure ulcers can be placed in four broad categories:
1. Endocrine system: diabetes, testosterone deficiency
2. Immune system function
3. Wound bed perfusion: cardiovascular status, anemia, and oncotic anasarca
4. Nutritional status: malnutrition and vitamin deficiencies.
Identifying and correcting systemic factors that deter wound healing, as well as implementing metabolic and anabolic interventions, have enabled clinicians to heal pressure ulcers of several months’ (or years’) duration.10

Systemic Factors that Contribute to Catabolism

The catabolic state is the response to a variety of stressors, such as trauma, infection, wounds, and malnutrition. The stress response is governed by the endocrine system, central nervous system, inflammatory mediators, and an increase in the production of stress hormones. Catabolism triggers a biochemical cascade that results in IWL, reduced LBM, and systematic devastation, making it almost impossible to heal the wound.

Comorbid Conditions that Contribute to the Catabolic State and
Nonhealing Status

Endocrine system: Diabetes and testosterone deficiency. Diabetes. Spinal-cord injury predisposes individuals to develop metabolic abnormalities in comparison to the normal population. These abnormalities include altered carbohydrate and lipid metabolism, largely as a consequence of reduced activity associated with loss of innervated musculature. This not only results in younger onset of cardiovascular disease but also in an increased incidence of type 2 diabetes mellitus.11 The presence of an open wound can deplete LBM, which further increases insulin resistance. Diabetes and its associated complications also can impede wound healing; thus, wound healing and diabetes are mutually interdependent.

Testosterone. Testosterone is an endogenous anabolic stimulus for protein synthesis.

References: 

References

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