Critical illness or chronic conditions like trauma, injury, burns, wounds, pressure ulcers, major surgery, or sepsis cause a stress response that can result in hypermetabolism, increased catabolism, and loss of lean body mass (LBM). As a result, patients under stress may experience unintended weight loss and protein energy malnutrition (PEM), which contribute to immune impairment, weakness, and increased risk of pressure ulcers. Understanding the reasons why this happens can help practitioners understand how to treat patients under stress.
Metabolic responses during stress or trauma have a dramatic impact on the body. Reactions include increases in resting energy expenditure (REE), breakdown of protein and branched chain amino acids, nitrogen loss through the urine, and conversion of protein to glucose for energy use (1,2).
Proinflammatory proteins called cytokines are released in response to inflammation resulting from stress, tissue damage, or infection. Cytokines stimulate cell growth, cause signs of infection such as fever, contribute to metabolic changes and changes in the gastrointestinal system that can create anorexia and malaise (2). The release of cytokines stimulates an increase in the catabolism of lean body mass. At the same time, counter-regulatory hormones (such as glucagons, cortisol and catecholamines) are released. These hormones mobilize fatty acids, promote breakdown of glucose, and the conversion of dietary protein to glucose for energy. As a result, energy production becomes increasingly dependent on dietary protein, and branched-chain amino acids fuel the muscles (1).
Metabolic stress causes poor utilization of carbohydrate, protein and fat and results in rapid breakdown of lean body mass (LBM). Fat metabolism increases to create energy. This series of events results in an acute PEM in which albumin, transferrin, prealbumin and retinol-binding protein decrease because of inflammation. C-reactive protein may increase during the inflammatory response. A negative nitrogen balance occurs due to rapid loss of LBM, resulting in muscle wasting. Hyperglycemia is also common during stress as the body rushes to produce energy, but simultaneously reduces the production of insulin. At the same time these catabolic activities are taking place, anabolic hormones such as testosterone and growth hormone decrease, resulting in a decrease in tissue synthesis (1).
In a trauma or acute situation, the stress response typically peaks at 3 to 4 days, and subsides in 7 to 10 days. However, in situations of a chronic nature (i.e. severe wounds, pressure ulcers, and chronic diseases like cancer or COPD), hypermetabolism and the catabolic response may last weeks or even months. Changes in metabolism begin at the time of the injury or acute illness and continue until recovery/healing is complete. Unfortunately, the rate of recovery of LBM is much slower during the recovery stage than the rate of loss during the inflammatory stage.
Lean body mass makes up 75% of body weight mostly in the form of muscle, bone and tendon, and provides the majority of the body’s protein including visceral protein, collagen, enzymes, antibodies and growth factors. Protein is critical for growth and maintenance, fluid and electrolyte balance, acid-base regulation, blood clotting, enzymatic functions, metabolism, and immune function (3,4). To reverse the catabolic state and promote anabolism, adequate nutrition along with resistance exercise is needed (5).
Nutrition interventions including provision of adequate protein, calories, and fluids can help manage the metabolic effects of prolonged stress by meeting increased needs due to the stress response.
- Dorner B, Posthauer ME, Thomas D. The Role of Nutrition in Pressure Ulcer Prevention and Treatment: National Pressure Ulcer Advisory Panel White Paper. National Pressure Ulcer Advisory Panel, 2009.
- Mahan K and Escott-Stump S, Krause’s Food and Nutrition Therapy, 12th ed, 2008. Saunders, Philadelphia, PA.
- Demling R, Involuntary Weight Loss, Protein-Energy Malnutrition, and the Impairment of Cutaneous Wound Healing, Wounds: A Compendium of Clinical Research and Practice; Supplement D. Vol 13, No. 4, July/August 2001.
- Demling R, DeSanti L, Protein-Energy Malnutrition, and the Nonhealing Cutaneous Wound, 2003.
- Dimant J, Gruber, et al. Pressure Ulcer Therapy Companion Clinical Practice Guideline, American Medical Directors Association, Columbia, MD, 1999.
©2012 Becky Dorner & Associates, Inc.
This article was adapted from materials found in The Complete Guide to Nutrition Care for Pressure Ulcers: Prevention and Treatment, Becky Dorner & Associates, Inc. 2012.
Becky Dorner, RD, LD is widely-known as one of the nation's leading experts on nutrition and long-term health care. Her company, Becky Dorner & Associates, Inc. (BDA) is a trusted source of valuable resources dedicated to improving quality of life for older adults. For valuable resources for healthcare professionals, sign up for our free membership at www.BeckyDorner.com
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Becky Dorner, RD, LD