Cath Lab Digest

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     As a population, we are extremely concerned about weight. Whether it is the epidemic of overweight children developing very adult problems due to obesity or the rail thin models splashed across the pages of the latest fashion magazines, weight is a hot topic of conversation. As wound care clinicians, we, too, should be very concerned with weight. Instinctively, we understand that patients who are losing body weight may heal slowly or develop chronic wounds. Scientifically, we know when the amount of nutritional substrate is inadequate to meet all the body’s physiologic needs, a competition for the limited available nutrients ensues. Often the wound loses this competition because the body, by necessity, must keep the vital organs functioning; this is a higher priority than wound healing.

     Ideally, each patient should meet 100% of his nutritional needs daily but realistically, this often does not happen. As practitioners, we see the end result manifest itself as weight loss. Even more frustrating is seeing weight loss occur despite a seemingly optimal diet. Until recently, all weight loss has been lumped into a single category but this is not the complete picture. Declines in body weight may be the result of loss of lean body mass, loss of fat mass, loss of bone, and/or a change in fluid volume. This article discusses three causes of weight loss — sarcopenia, cachexia, and starvation.

Sarcopenia

     Sarcopenia often is defined as an age-related shift in body composition, specifically the loss of muscle mass. The word sarcopenia has Greek origins and literally means “poverty of flesh.” As we age, we naturally lose muscle mass and replace it with fat — anyone over the age of 45 can tell you how the body changes. Nearly 3.6 million people in the United States have sarcopenia, putting them at increased risk for physical disability and frailty.¹ People who are obese also can suffer this loss of muscle loss. In this case, we term it sarcopenic obesity. Although sarcopenia is seen mostly in physically inactive individuals, it is also evident in individuals who remain physically active throughout their lives. This finding suggests that physical inactivity is not the only contributing factor to sarcopenia. Current research is finding that the development of sarcopenia is a multifactorial process² generally attributed to three factors: motor unit restructuring, protein deficiency, and changes in hormone concentrations.

     Motor unit restructuring. Motor units are the motor neurons and the muscle fibers they control. There are two types of motor neurons: fast twitch (FT) and slow twitch (ST). FT motor neurons die sooner than ST. When this occurs, the muscle fibers commanded by the FT neuron can deteriorate and die as well, a process we commonly call atrophy. To prevent atrophy, when a FT neuron dies, a ST neuron situated nearby will attach itself to the muscle fibers the dead neuron commanded in order to innervate it and keep it alive. This change in command is known as motor unit restructuring.³ This process is imperfect because ST neurons act with much less precision than FT neurons. We can easily see this process with the naked eye when we look at our aging faces in the mirror. An entire cosmeceutical industry is devoted to minimizing the sagging (atrophy) of our faces. Skin sags and droops because it has lost the muscle fiber underneath due to natural aging.

     Protein deficiency. Protein deficiency also is thought to play a role in sarcopenia. The recommended dietary allowance (RDA) for protein, set by the Food and Nutrition Board of the United States National Academy of Science, is 0.8 g protein/kg body weight/day for adults regardless of age. The issue of the adequacy of the protein RDA, especially for elderly, is currently being debated in order to set future RDAs.