Cachexia, a complex syndrome associated with metabolic changes, fat and muscle wasting, loss of appetite, and involuntary weight loss, is common with many progressive diseases. The true incidence of cachexia is difficult to determine because studies use inconsistent criteria for defining cachexia and because some studies report the incidence based on all patients with a particular disease while others include only patients with an advanced stage of the disease. It is estimated that cachexia occurs in about 80% of patients with advanced cancer, 33% of patients with acquired immunodeficiency syndrome, 20% of those with congestive heart failure, and up to 50% of patients with chronic hypoxemia associated with chronic lung disease (Anker, Ponikowski, Varney et al., 1997; Castillo-Martinez, Orea-Tejeda, Rosales et al., 2005; Davis & Dickerson, 2000; Schols, Soeters, Dingemans et al., 1993; Wanke, 2000). The complex metabolic changes associated with cachexia are characterized by increased energy expenditures that are unaffected by caloric intake. In comparison, starvation leads to energy conservation and is reversed by caloric intake. Thus, cachexia is not synonymous with starvation. Cachexia is correlated with decreased quality of life and decreased survival in all disease populations. An estimated 30% of oncology patients die due to the effects of cachexia (Illman, Corringham, Robinson et al., 2005; Strasser & Bruera, 2002).

Although the syndrome of weight loss, loss of appetite, and profound weakness has long been recognized in patients with advanced diseases, there is not yet a complete understanding of or agreement on the factors that contribute to its cause. Cancer cachexia was previously thought to be the result of excessive use of nutrients by tumors and decreased energy intake on the part of the individual. Research involving a number of wasting syndromes has now identified several overlapping mechanisms that mediate cachexia, including metabolic alterations, neurohormonal alterations, and changes in anabolic processes (Andreas, 2005; Anker, Steinborn, & Strassberg, 2004; Esper & Harb, 2005; Strasser, 2003; Wouters, Creutzbergt, & Schols, 2002).

Proinflammatory cytokines such as interleukin 1, interleukin 6, interferon γ, and tumor necrosis factor α are likely involved in mediating the cachexia syndrome. These substances may (1) interfere with appetite signals in the hypothalamus, causing anorexia; (2) increase the metabolic rate by inducing thermogenesis and muscle wasting; (3) interfere with lipid storage; and (4) contribute to muscle protein loss and increased energy expenditure (Davis, 2002; Illman et al., 2005; Inui, 2002, McCarthy, 2003; Strasser, 2003; Winter, 2002). Dietary supplementation does not reverse this process. Thus, the cachexia syndrome may be viewed as a chronic inflammatory condition rather than a nutritional aberration (McCarthy, 2003).

In addition to the metabolic syndrome of cachexia, there are other problems that may contribute to a decreased appetite and weight loss (Strasser, 2003; Strasser & Bruera, 2002):

Patients must be assessed for potentially reversible causes of weight loss or lack of appetite before the diagnosis of cachexia-anorexia syndrome can be made. Consider the following factors (Ross & Alexander, 2001):

Weight may be monitored using scales, although the rapidly falling numbers may be a source of distress to some patients. Appetite is a subjective experience that may be measured by using a visual analog or numerical scale. By asking a patient to indicate a number between 0 and 10, where 10 represents an excellent appetite and 0 means no appetite at all, it is possible to monitor the patient’s status and the results of interventions.

A thorough history includes the following information (Montagnini & Moat, 2004):

Cachectic patients will probably show evidence of a low serum albumin level, decreased total protein levels, anemia, and increased serum triglyceride level, glucose levels, and lactic acidosis. However, these laboratory investigations are generally considered to be nonspecific, too variable, and not helpful in diagnosing or monitoring anorexia and cachexia in people with a terminal illness (Nelson & Walsh, 2002).

Depending on the stage of illness and treatment goals, it may be appropriate to monitor easily reversible problems such as electrolyte and metabolic imbalances (sodium, potassium, magnesium, and calcium levels). More elaborate evaluations such as the use of extensive dietary intake monitoring and skinfold thickness measurements should be reserved for clinical trials. Radiologic investigations may be helpful to rule out treatable problems such as bowel obstruction and constipation.

With the palliative care goal of improving quality of life, treatment must be aimed at treating any reversible conditions, minimizing symptoms that affect appetite, implementing measures to improve appetite, and educating patients and families about the potential benefits and limits of treatment interventions (Waller & Caroline, 2000). When patients lose weight and family members are distressed about the failing appetites of their loved ones, clinicians must understand that their responses cannot be simply to find ways to introduce more nutrients into patients. This approach has not been successful and may actually create harm (Strasser, 2003).