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Nutrition

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Overview
Effects Of The Tumor
Effect Of Cancer Therapies
Psychosocial Effects
Nutritional Assessment
General Management Guidelines
Enteral / Parenteral Support


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Information from PDQ -- for Health Professionals


OVERVIEW

Inability to maintain nutritional status is a particularly common problem for persons with cancer. The disease process and its treatment can lead to severe protein-calorie malnutrition, which is the single most common paraneoplastic syndrome or secondary diagnosis in the cancer patient. It is a major cause of morbidity and mortality. Protein-calorie malnutrition exists when the intake of macronutrients is inadequate to meet metabolic requirements. Progressive wasting, weakness, debilitation, compromised immune function, potential therapy intolerance, and ultimately death may result.

Anorexia, the loss of appetite or desire to eat, is the most common symptom in people with cancer that may occur early in the disease process or later as the tumor grows and metastasizes.[1] Anorexia is present in 15% to 25% of all cancer patients at the time of diagnosis and is almost universal in patients with widely metastatic disease.[2,3] Anorexia is the most common cause of decreased nutrient intake triggering malnutrition and progressive inanition (progressive deterioration with muscle wasting and body compositional change) in malignancy.

Cachexia is a clinical wasting syndrome evidenced by weakness and a marked and progressive loss of body weight, fat, and muscle.[4] Anorexia and cachexia frequently occur together, but cachexia may occur in individuals who are ingesting adequate calories and protein but experience malabsorption of nutrients. It has been estimated that one half of all people with cancer experience cachexia, two thirds while in a terminal phase of the disease.[5] In addition, investigators have found no association between cachexia and tumor size, type, or extent.[6] It has been observed that cancer cachexia differs from simple starvation.[7] Individuals adapt to starvation by decreasing their basal metabolic rate, whereas in cancer patients, the basal metabolic rate is not adaptive and may be increased, decreased, or normal.[8] Although the exact mechanisms causing cancer cachexia are unknown, several theories regarding its pathogenesis point to a complex mix of tumor, host, and treatment variables, which make this syndrome difficult to study.

The prognostic impact of weight loss and malnutrition has been documented since the 1930s [9] in benign disease and later in malignant disease.[10-13] It has been estimated that up to 20% of people with cancer may die of the effects of cancer-included or treatment-related inanition. Additionally, the impact of malnutrition on health care costs is substantial.[14,15]

References:

  1. Donoghue M, Nunnally C, Yasko JM: Nutritional Aspects of Cancer Care. Reston, VA: Reston Publishing Company, Inc., 1982.
  2. Langstein HN, Norton JA: Mechanisms of cancer cachexia. Hematology/Oncology Clinics of North America 5(1): 103-123, 1991.
  3. Tisdale MJ: Cancer cachexia. Anti-Cancer Drugs 4: 115-125, 1993.
  4. Theologides A: Cancer cachexia. Current Concepts in Nutrition 6: 75-94, 1977.
  5. Lindsey AM, Piper BF, Stotts NA: The phenomenon of cancer cachexia: a review. Oncology Nursing Forum 9(2): 38-42, 1982.
  6. Smith SA: Theories and intervention of nutritional deficit in neoplastic disease. Oncology Nursing Forum 9(2): 43-46, 1982.
  7. Lindsey AM: Cancer cachexia: effects of the disease and its treatment. Seminars in Oncology Nursing 2(1): 19-29, 1986.
  8. Ottery FD: Cancer cachexia: prevention, early diagnosis, and management. Cancer Practice 2(2): 123-131, 1994.
  9. Studley HO: Percentage of weight loss: a basic indicator of surgical risk in patients with chronic peptic ulcer. JAMA: Journal of the American Medical Association 106(6): 458-460, 1936.
  10. Blackburn GL, Bistrian BR, Maini BS, et al.: Nutritional and metabolic assessment of the hospitalized patient. Journal of Parenteral and Enteral Nutrition 1(1): 11-22, 1977.
  11. Tubiana M, Attie E, Flamant R, et al.: Prognostic factors in 454 cases of Hodgkin's disease. Cancer Research 31: 1801-1810, 1971.
  12. Dewys WD, Begg C, Lavin PT, et al.: Prognostic effect of weight loss prior to chemotherapy in cancer patients. American Journal of Medicine 69(4): 491-497, 1980.
  13. DeWys WD, Begg C, Band P, et al.: The impact of malnutrition on treatment results in breast cancer. Cancer Treatment Reports 65(Suppl 5): 87-91, 1981.
  14. Robinson G, Goldstein M, Levine GM: Impact of nutritional status on DRG length of stay. Journal of Parenteral and Enteral Nutrition 11(1): 49-51, 1987.
  15. Reilly JJ, Hull SF, Albert N, et al.: Economic impact of malnutrition: a model system for hospitalized patients. Journal of Parenteral and Enteral Nutrition 12(4): 371-376, 1988.

EFFECTS OF THE TUMOR

Many nutritional problems in the person with cancer stem from a local tumor effect.[1] Enlarging tumors in the gastrointestinal tract, for example, can cause obstruction, nausea and vomiting, impaired digestion, delayed transit, and malabsorption. Ovarian and genitourinary cancers may be associated with ascites leading to early satiety, progressive protein malnutrition (especially with fluid loss at surgery or paracentesis), and fluid and electrolyte imbalances. Pain related to tumor bulk or location may be associated with severe anorexia and decreased oral intake. Central nervous system tumors that cause confusion or somnolence may affect nutritional status because lack of attention may lead to decreased intake.

In addition to local tumor effects (from either the tumor itself or the patient's response to the tumor), nutritional problems can also stem from metabolic alterations.[2] Marked alteration in normal metabolism of carbohydrate, protein, and lipid can occur. Tumor cells may derive significant energy from metabolism of glucose to lactate (Cori cycle) rather than from more complete oxidation of carbon dioxide and water (Krebs cycle).[3] Additionally, conversion of lactate to glucose for gluconeogenesis by the liver consumes six ATP molecules per lactate-glucose cycle, producing energy-inefficient cycling. Tumor cells have an increased requirement for glucose as an energy source, either through altered enzymatic activity or due to relative hypoxia induced by poor tumor vascularization. Differences in the contribution of Cori cycle activity have been seen in patients who lose weight and in those with stable weight.[2] Inhibition of phosphoenolpyruvate carboxykinase by hydrazine sulfate may decrease excess Cori cycle activity and improve glucose tolerance in cancer patients, but weight loss may not be reversed.[2] Altered protein metabolism in patients with cancer may stem from increased uptake of amino acids by the tumor cells compared with that of normal cells, decreased protein synthesis, increased protein degradation, and protein loss through fistulas or by gastrointestinal losses. In addition, decreased intake secondary to anorexia, when need is increased or normal, is often the basis of negative nitrogen balance. Altered lipid metabolism can occur as a result of mobilization and the use of fatty acids as an additional energy source when the glucose supply of the body is exhausted by the tumor.[4] A decrease in fat mobilization has also been observed.[5,6]

Mediators of primary cachexia (i.e., cachexia without a mechanical or function etiology) can include substances with hormone-like characteristics or products of host tissues that influence metabolism indirectly. The latter include a number of cytokines such as tumor necrosis factor (TNF-alpha), interleukin-6, and gamma-interferon. Additionally, lipid mobilizing factors have also been implicated.[2] Lack of enteral stimulation may increase levels of circulating cytokines.

In addition to alterations in carbohydrate, protein, and lipid metabolism, cancer cells produce peptides, oligonucleotides, and other metabolites that may be responsible for the genesis of anorexia and cachexia.[2] For example, tumor-produced substances may alter a person's sense of taste, leading to an aversion to meat and a decreased taste sensation. Tumors may cause anorexia through a peripheral effect on neuroendocrine cells or neuroreceptors and through a direct effect on hypothalamic and other central nervous system peptidergic and responder cells. Early satiety or a sense of fullness is a frequent symptom in anorectic cancer patients, suggesting the importance of inhibitory signals from the gastrointestinal tract in limiting their food intake. Tumors can also produce hormone substances, similar to those seen in paraneoplastic syndromes, which can alter nutrient intake, absorption, and metabolism.[7]

References:

  1. Szeluga DJ, Groenwald SL, Sullivan DK: Nutritional disturbances. In: Groenwald SL, Frogge MH, Goodman M, et al.: Cancer Nursing: Principles and Practice. Boston: Jones and Bartlett Publishers, 2nd Edition, 1990, pp 495-519.
  2. Tisdale MJ: Cancer cachexia. Anti-Cancer Drugs 4: 115-125, 1993.
  3. DeWys WD: Nutritional care of the cancer patient. JAMA: Journal of the American Medical Association 244(4): 374-376, 1980.
  4. Goodlad GA, Clark CM: Protein metabolism in the tumour-bearing host. Acta Chirurgica Scandinavica. Supplementum (498): 137-140, 1980.
  5. Axelrod L, Costa G: The contribution of fat loss to weight loss in cancer. Nutrition and Cancer 2(1): 81-83, 1980.
  6. Waterhouse C: Oxidation and metabolic interconversion in malignant cachexia. Cancer Treatment Reports 65(Suppl 5): 61-66, 1981.
  7. Smith SA: Theories and intervention of nutritional deficit in neoplastic disease. Oncology Nursing Forum 9(2): 43-46, 1982.

EFFECT OF CANCER THERAPIES

Cancer therapies and their side effects can also greatly contribute to progressive nutritional deterioration. The therapy may have a direct effect, such as protein and fat malabsorption after a gastrectomy or pancreatectomy, or indirect effects, such as increases in metabolic demands caused by infection or a neutropenic febrile reaction (there is an increased caloric need of approximately 10% to 13% per degree above 37 degrees Celsius). Nutritional problems can be induced by each general type of antineoplastic therapy.[1,2] The nutritional literature has defined severe malnutrition in two ways:

functionally (increased risk of morbidity and/or mortality) and by degree of weight loss (greater than 2% per week, 5% per month, 7.5% per 3 months, and 10% per 6 months).[3] In the cooperative group format, nutrition toxicity does not generally take into account baseline deficit and includes degrees of weight loss that are much greater than the above criteria. Grading (without consideration of time course) is as follows: grade 0 = less than 5.0% loss, grade 1 = 5.0%-9.9%, grade 2 = 10.0%-19.9%, grade 3 = greater than 20.0%. Grade 4 (life-threatening) is not specifically defined. Attention to weight loss at an earlier time point is required to successfully prevent deterioration of weight, body composition, and performance status.

Surgery

Head and neck surgery may directly cause difficulty in chewing and swallowing or may be associated with substantial psychosocial stresses related to the degree of surgical resection. Esophageal surgery may cause gastric stasis and fat malabsorption secondary to vagal sectioning. Fat and protein malabsorption, dumping syndrome with reactive hypoglycemia, and early satiety may occur following gastric surgery. Pancreatic surgery may also cause protein and fat malabsorption, as well as vitamin and mineral deficiencies, and diabetes mellitus. Small bowel and colon surgery may cause protein and fat malabsorption, vitamin and mineral deficiencies, diarrhea, and excessive fluid and electrolyte losses. Surgery involving the urinary tract can lead to acid-base imbalances and electrolyte abnormalities. Additionally, complications of surgery with nutritional implications may include infection, fistulae (internal or enterocutaneous), and short-bowel syndrome. Patients may actively decrease their oral intake after a diverting or end colostomy to decrease the ostomy output. This should be addressed in any patient with a marked decrease in oral intake after such surgery.

Chemotherapy

Chemotherapy can cause anorexia, nausea and/or vomiting, diarrhea or constipation, stomatitis/mucositis, taste alterations or aversions, and infectious complications. Symptoms that have an impact on nutrition and that last longer than 2 weeks are especially significant. The frequency and severity of these side effects depend on the class of drug, the dose, the drug combination, and whether the chemotherapy is part of a combined modality program. Nutritional status may be strongly affected with prolonged treatment of febrile neutropenia where metabolic needs may increase 25% with a temperature of 39 degrees Celsius.

Radiation therapy

Radiation therapy is associated with both acute and late sequelae that affect nutritional status. Irradiation of the head and neck area can induce or be associated with anorexia, taste alterations or aversions, dry mouth, mucositis, gingivitis, dysphagia, trismus, dental caries, and abscess formation. Thoracic irradiation may be associated with esophagitis (radiation-induced esophageal mucositis, candidiasis, or viral infections), dysphagia, esophageal reflux, and nausea and vomiting. Diarrhea, nausea and vomiting, enteritis, proctitis, or fistula formation are possible side effects caused by abdominal or pelvic irradiation. Use of a pelvic sling, tissue expander in the pelvis, or other methods for removing the small bowel from a pelvic irradiation field may be included as part of surgery to decrease these complications. Radiation therapy may also be associated with fatigue, which may result in decreased appetite and motivation to eat. Late sequelae include strictures, chronic radiation enteritis, malabsorption, or gastrointestinal obstruction.

Immunotherapy

Immunotherapy (e.g., biologic response modifiers) may be associated with fever, fatigue, and weakness, which can lead to decreased appetite and increased need for protein and calories. Again, febrile reactions are associated with an approximate 10% increase in metabolic requirements per degree above 37 degrees Celsius.

References:

  1. Clark J, McGee R, Preston R: Nursing management of responses to the cancer experience: nutrition. In: Clark J, McGee R, eds.: Core Curriculum for Oncology Nursing. Philadelphia: W.B. Saunders, 1992, pp 93-106.
  2. Kokal WA: The impact of antitumor therapy on nutrition. Cancer 55(1, Suppl): 273-278, 1985.
  3. Blackburn GL, Bistrian BR, Maini BS, et al.: Nutritional and metabolic assessment of the hospitalized patient. Journal of Parenteral and Enteral Nutrition 1(1): 11-22, 1977.

PSYCHOSOCIAL EFFECTS

Dining is a major focus of social activity. Anorexia and food aversions contribute to social isolation when people cannot participate in communal activities associated with eating. Multiple psychological and social factors can affect a person's desire and willingness to eat. The stress of coping with the cancer diagnosis and its treatment can have a major role. Depression, anxiety, anger, and fear are common emotions experienced by persons with cancer and can contribute to anorexia. A sense of loss of control or helplessness may also have a role in nutritional intake. Refusing to eat despite strong recommendations or pleading by family members, friends, or health professionals may be one way in which a patient (who may feel no option to refuse antineoplastic therapy) feels able to exercise some control in life. Learned food aversions may also contribute to decreased oral intake, nausea, and/or vomiting.[1] Individuals who have experienced unpleasant symptoms after eating a specific food may begin to avoid this food or food group.

Factors such as living alone, inability to cook or prepare meals, or even to walk to the kitchen as a result of physical limitations can contribute to eating disorders. A thorough evaluation of the home situation by a social worker or visiting nurse may identify easily correctable factors that contribute to poor eating habits.

Establishing the cancer diagnosis and initiating treatment often require the patient to spend large amounts of time away from normal routines, including meals. Cultural food preferences may not be accessible in treatment settings or may not be well tolerated because of treatment side effects. A person who enjoys hot, spicy food and has esophagitis may dislike the taste of bland food and eat very little. Taste alterations can psychologically affect a person's appetite and desire for food.

Unfortunately, lack of adequate nutritional intake leads to progressive nutritional deterioration, representing to the patient and family, progression of the cancer process. The wasting is a constant reminder to the patient, family, and health care team of the cancer diagnosis and expected poor prognosis. This can significantly influence quality of life, social interaction, and outlook. Additionally, with progressive wasting, and its associated fatigue, the person generally decreases social interaction. Because of the role food and eating have in society, this can serve as a significant isolation factor for a person with cancer.

Studies have reported a positive impact of exercise (e.g., walking or mild aerobic) on the sense of well-being, nausea and vomiting, and nutritional intake.[2] Patients forced to rely on artificial feeding methods (including forced oral feeding as well as enteral or parenteral feeding) can experience depression, body image changes, and stress related to problems with feeding tubes and equipment.[3] Problems related to nutrition have been identified by cancer patients as the most important factor in affecting their sense of well-being, more important than sexuality and continued employment.[4]

References:

  1. Bernstein IL: Physiological and psychological mechanisms of cancer anorexia. Cancer Research 42(2, Suppl): 715s-720s, 1982.
  2. Ottery FD: Cancer cachexia: prevention, early diagnosis, and management. Cancer Practice 2(2): 123-131, 1994.
  3. Padilla GV, Grant MM: Psychosocial aspects of artificial feeding. Cancer 55(1, Suppl): 301-304, 1985.
  4. Padilla GV, Presant C, Grant MM, et al.: Quality of life index for patients with cancer. Research in Nursing and Health 6(3): 117-126, 1983.

NUTRITIONAL ASSESSMENT

The history and physical examination are the most important components of assessment of nutritional status. This should include weight history (current, usual, and ideal); assessment of oral intake changes (type and duration); symptoms impacting on nutrition (including anorexia, nausea and vomiting, diarrhea, constipation, stomatitis/mucositis, dry mouth, taste/olfactory abnormalities, and pain); medications that may affect intake or metabolic requirements; other medical conditions that may affect nutritional intake or nutrition intervention options; and performance status evaluation. The person with cancer should be asked about changes in intake compared with what is normal for them and the duration of the change if present. Physical examination entails a general assessment of physical condition, including evidence of weight loss, loss of subcutaneous fat, muscle wasting, presence of sacral or tibial edema, or ascites. Standardized staging criteria for degree of nutritional deficit or risk have been developed and validated.[1,2] Known as the Subjective Global Assessment (SGA) of nutritional status, this evaluation tool has been validated in a number of patient populations including surgical, human immunodeficiency virus (HIV), and acquired immunodeficiency syndrome (AIDS) populations.[2,3] With appropriate training, the method is sensitive, specific, and has little interobserver variability. A modification specifically developed for oncology patients is currently being piloted.

Obtaining a quantitative as well as qualitative dietary history can be helpful in dietary assessment, especially as a means of demonstrating to the person with cancer and his or her family or caregiver, that changes can be made to increase calorie, protein, and micronutrient intake. Useful data also include specific likes, dislikes, and intolerances of the person with cancer. The latter may help to determine the need for specific supplemental enzymes (lactase, other disaccharidases, or pancreatic enzymes).

Anthropometric measurements such as skin fold thickness and midarm muscle circumference are not useful in clinical situations. However, clinical palpation of the tricep muscle can often provide an excellent estimate of nutrition, since extensors tend to lose muscle faster than flexors.[4] This method of nutritional assessment is limited by both the technique and interobserver variability. Laboratory evaluations that may contribute to nutritional evaluation or appropriate nutritional intervention include assessment of visceral protein status (serum transferrin or albumin), renal and liver function, pancreatic endocrine function (glucose), serum electrolytes and minerals (calcium, magnesium, and phosphorus), and hematologic evaluation (total lymphocyte count and red cell indices). Although not routinely used, delayed cutaneous hypersensitivity testing (skin test antigens) may be helpful to gauge systemic immune function.

Determination of nitrogen balance by 24-hour urinary urea nitrogen (UUN) is helpful in nutritional intervention regimens, particularly in the use of enteral or parenteral nutrition. The aim of nutritional intervention is to minimize the degree of negative nitrogen balance (i.e., excessive loss of body protein not compensated by adequate nutritional intake). Nitrogen balance is defined as nitrogen intake (in grams) minus nitrogen output (in grams) and can be estimated from (protein intake/6.25) - (UUN+4). If nitrogen intake is less than output, the patient is considered to be in negative nitrogen balance, with a net loss of body protein. This contributes to progressive muscle wasting, fatigue, and immune compromise.

References:

  1. Detsky AS, McLaughlin JR, Baker JP, et al.: What is subjective global assessment of nutritional status? Journal of Parenteral and Enteral Nutrition 11(1): 8-13, 1987.
  2. Hirsch S, de Obaldia N, Petermann M, et al.: Subjective global assessment of nutritional status: further validation. Nutrition 7(1): 35-38, 1991.
  3. Detsky AS, Baker JP, O'Rourke K, et al.: Predicting nutrition-associated complications for patients undergoing gastrointestinal surgery. Journal of Parenteral and Enteral Nutrition 11(5): 440-446, 1987.
  4. Winick M, Ed.: Hunger Disease: Studies by the Jewish Physicians in the Warsaw Ghetto. New York: John Wiley & Sons, 1979.

GENERAL MANAGEMENT GUIDELINES

Options for supportive nutritional care of the person with cancer are determined by one or more of the following:

1. Presence of a functional gastrointestinal tract

2. Type of therapy (independent of palliative or curative intent), i.e., site
and extent of surgical resection, specific type of chemotherapy, site and size of radiation field, use of biologic response modifiers, or multimodality therapy

3. Quality of life, performance status, or prognosis

4. Cost effectiveness and cost-utility determinations

It is believed that maintenance of body composition and adequate nutritional status can help people with cancer feel and look better and can maintain or improve performance status and daily functional status. It may also help them tolerate therapy.[1] The type of nutritional intervention used will depend on the basis of the nutritional risk or deficit. Problems caused by local tumor effects may subside when the tumor responds to therapy. Those nutritional impact symptoms related to side effects of therapy must be proactively addressed to ensure adequate symptom control measures. (Refer to the PDQ summaries on Constipation, Impaction, and Bowel Obstruction; Pain; Nausea and Vomiting; and Oral Complications for more information.)

A major cause of anorexia in patients with cancer is food odor. Patients suffering from anorexia should not be in a room where the odors of food preparation can be detected. Foods with reduced odors are preferable for patients with cancer. This explains why cancer patients will often eat best at breakfast, since many breakfast foods have little odor.

Suggestions for helping people with cancer manage anorexia include the following:[2-4]

1. Eat small frequent meals (every 1-2 hours by the clock).

2. Eat food (including snacks) that is caloric- and protein-dense.

3. Avoid foods low in calories and protein and avoid empty calories (i.e.,
food without protein and micronutrients, such as soda).

4. Avoid liquids with meals (unless used sparingly to improve dry mouth or
dysphagia) to decrease problem of early satiety.

5. Time meals to coincide with periods during the day when the patient is
feeling best; use nutritional supplements at times of decreased appetite or desire to eat. (Generally, patients tend to feel better and have improved appetites early in the day with a progressive decrease in appetite as the day progresses.)

6. Taste-test several different commercially available nutritional supplements
or different high-calorie, high-protein drink or pudding recipes. Adding the juice from half of a freshly-squeezed lemon can help lessen the excessive sweetness and bitter aftertaste that sometimes distresses patients with cancer, but which may not be detectable to individuals who do not have cancer.

7. Stimulate appetite with light exercise (e.g., walking), glass of wine or
beer if not contraindicated, and use of orexigenic agents (appetite stimulants).

8. Add extra calories and protein to food (e.g., butter, skim milk powder,
honey, brown sugar).

9. Take medications with high-calorie fluids (e.g., commercial nutritional
supplement) unless the medication must be taken on an empty stomach.

10. Make surroundings pleasant and varied; food presentation should be
attractive (e.g., try new recipes, eat with friends, prepare food with color and texture variation).

11. Experiment with recipes, flavorings, spices, types and consistencies of
food. This is important since food preferences may change from day to day.

12. Avoid strong aromas if they are bothersome. Strategies include the use of
boiling bags, cooking outdoors on a grill, the use of kitchen fan when cooking, serving cold plates rather than hot foods (since odors come from the rising steam), and removal of hospital food tray covers in the hallway rather than at the patient's bedside to dissipate some of the odors. A portable fan can be used to blow away the aroma of hot foods. Food ordered from outside so that preparation odors are not detected will often be tolerated if consumed immediately after arrival (e.g. pizza).

Suggestions for helping people with cancer manage taste changes include the following:

1. Use plastic utensils if patient experiences metallic taste while eating.

2. Substitute poultry, fish, eggs, and cheese for red meat.

3. Marinate meats with sweet marinades or sauces.

4. Serve meats chilled rather than hot.

5. Use extra seasonings, spices, and flavorings, but avoid flavorings that
are very sweet or very bitter. An elevated threshold for taste may make food taste bland or boring.

6. Substitute milk shakes, puddings, ice cream, cheese, and other high-protein
foods for meats if patient experiences an aversion to meat.

7. Rinse mouth before eating.

8. Use lemon-flavored drinks to stimulate saliva and taste, but avoid
artificial lemon and use sweeteners sparingly.

Suggestions for prevention of conditioned taste aversions include the following:

1. Try new foods and supplements when feeling best/well, e.g., on Sundays for
patients undergoing daily radiation therapy or after the patient leaves the hospital rather than during chemotherapy infusion.

2. Eat lightly on the morning of or several hours prior to receiving
chemotherapy.

3. Separate novel taste introductions from noxious stimuli.

Suggestions for lessening or alleviating either dry mouth or dysphagia include the following:

1. Eat soft or moist foods.

2. Process foods in blender.

3. Lubricate foods with creams, gravies, or oils.

4. Avoid rough, irritating foods.

5. Avoid hot or cold foods.

6. Avoid foods that adhere to the roof of the mouth.[5]

7. Take small bites and chew thoroughly.[5]

Suggestions for stomatitis: (Refer to the PDQ summary on Oral Complications for more information.)

No matter what the nutritional deficit, the person with cancer should be encouraged to maintain a positive attitude toward treating the cause and assuring adequate intake of protein and calories. Calculating individualized calorie and protein requirements and explaining to the person with cancer (and/or family or caregiver) will allow specific and realistic goals. The actual amount of protein and calories needed by each cancer patient will vary depending on the person's baseline and current nutritional status, particular nutritional deficits, and individual factors.

The protein requirement for non-weight losing individuals is approximately 0.5 grams per pound of ideal body weight. For the person who has lost weight, is febrile, or is on medications that increase protein requirements, such as corticosteroids, it is important to aim for approximately 0.7 grams per pound. Ideal body weight (IBW) is calculated as follows:

In terms of caloric needs, the following formulas can be used:

------------------------------------------------------------------------------
     General guidelines of calories required (assuming light activity):

     Underweight adults   - multiply weight in pounds by 18
     Normal weight adults - multiply weight in pounds by 16
     Overweight adults    - multiply weight in pounds by 13
------------------------------------------------------------------------------

Additional calories and increased protein intake may be required for specific people and situations. An oncology nutritionist (dietitian, diet technician, nurse, or physician with specialized education or training in nutrition) can offer guidance in determining the appropriate macronutrient (calories and protein) and micronutrient (vitamins, electrolytes, minerals) needs and options for nutritional intervention.

References:

  1. Irwin MM: Enteral and parenteral nutrition support. Seminars in Oncology Nursing 2(1): 44-54, 1986.
  2. Szeluga DJ, Groenwald SL, Sullivan DK: Nutritional disturbances. In: Groenwald SL, Frogge MH, Goodman M, et al.: Cancer Nursing: Principles and Practice. Boston: Jones and Bartlett Publishers, 2nd Edition, 1990, pp 495-519.
  3. National Cancer Institute: Eating Hints: Recipes and Tips for Better Nutrition During Cancer Treatment. Bethesda: NIH Publication, No. 91-2079, 1990.
  4. Ottery FD: Cancer cachexia: prevention, early diagnosis, and management. Cancer Practice 2(2): 123-131, 1994.
  5. Bloch AS: Nutritional management of patients with dysphagia. Oncology (Huntington NY) 7(11, Suppl): 127-137, 1993.

ENTERAL/PARENTERAL SUPPORT

An algorithm of nutritional options is available [1] to address nutrition proactively and to prevent or treat malnutrition and its complications.

General indications for enteral nutrition (gastric and duodenal/jejunal, with site dependent on the intake gastrointestinal impediment) include the following:

1. Upper gastrointestinal impediment to adequate oral intake (dysphagia,
esophageal stricture, tumor, gastroparesis, gastric outlet obstruction, etc.).

2. Combined modality therapy with chemotherapy and radiation therapy
(especially with radiation therapy to the upper aerodigestive tract) with known esophageal or gastrointestinal tract toxicity that will limit adequate oral intake.

3. Anorexia and/or psychologic inability (e.g., severe depression,
confusion/disorientation) to maintain adequate oral intake.

4. Contraindications/inability to take large volumes of oral nutrition,(e.g.,
pain with bolus eating).

General contraindications to enteral nutrition include the following:

1. Bowel obstruction.

2. Intractable nausea and vomiting unresponsive to optimal antiemetic regimen
(Refer to the PDQ summary on Nausea and Vomiting for more information.)

3. Severe short gut with intractable gastrointestinal output despite attempts
with appropriate enteral formulations and pharmacologic intervention (e.g., somatostatin).

4. Upper gastrointestinal tract or high-output fistula (tumor-related or
iatrogenic).

General indications for parenteral nutrition (complete or supplemental) include the following:

1. Nonfunctioning gastrointestinal tract in the following contexts:

a. Temporary problems impeding oral or enteral intake for longer than 10 days, especially with baseline nutritional deficit.

b. Obstruction or other mechanical problems expected to respond to antineoplastic therapy or surgical intervention.

c. Multiple and/or noncorrectable obstructive/mechanical problems associated with an indolent cancer.

2. Severe short gut secondary to surgical resection, radiation enteritis, high gastrointestinal fistula and inability to maintain weight and body composition with appropriate enteral regimen.

3. Severe and/or continuing nutritional deterioration in a person with indolent cancer or any malignancy in which malnutrition, rather than cancer is the primary problem.

General contraindications to parenteral nutrition include the following:

1. Functional gut.

2. Limited life expectancy (< 40 days).

3. Lack of adequate vascular access.

4. Lack of severe nutritional deficit such as temporary inability to eat
(e.g., post surgery).

Although there remains continued controversy concerning the ultimate benefit of nutritional support,[2] it is believed that a properly nourished cancer patient is better able to tolerate both the cancer therapy and its complications.[3,4] The delivery method chosen for nutritional support should be based on the individual's physiologic requirements, degree of nutritional debilitation, disease process, estimated duration for the need of support, and the resources available. If the gastrointestinal tract is functioning and not adversely affected by the cancer treatment, enteral support is the route of choice, especially when dealing with issues of system immune function. Options for placement of enteral feeding tubes include non-surgical (via nasal route) as well as endoscopic, radiologic, laparoscopic, and open surgical placement. Practical issues of tube options and formulations have been reviewed.[5,6]

Nutritional support: pharmacological approaches [7]

Pharmacologic intervention to increase oral nutritional intake can range from pain management to treatment of constipation or diarrhea, the use of gastric prokinetic agents, and the use of specific orexigenic agents (appetite stimulants).[8] Megestrol acetate (at a recommended dose of 800 mg/day) has shown success.[9,10] Corticosteroid use in situations other than terminal care is generally not indicated because of exacerbation of progressive muscle wasting. Dronabinol as an appetite stimulant has been used primarily in AIDS cachexia, but has been suggested for cancer patients, with a dose of 2.5 mg/day to 5 mg/day.

Hydrazine sulfate has been studied in three multicenter, randomized, phase III trials sponsored by the National Cancer Institute, however no clinical benefits were found. These trials included 600 patients diagnosed with advanced lung cancer and advanced colon cancer.[11-13] The end points in these studies included survival, weight gain, nutritional parameters and quality of life. The results of these three studies were negative, with no benefit seen. In the two studies of advanced lung cancer patients, the addition of hydrazine sulfate to a standard chemotherapy regimen resulted in somewhat worse quality of life, with no effect on weight gain or loss and a suggestion of decreased time to disease progression and survival when compared with placebo.[11,12] In the trial evaluating hydrazine sulfate in metastatic colon cancer, the survival time for patients receiving the hydrazine was decreased compared with patients receiving placebo.[13] Compared with patients receiving placebo, patients receiving hydrazine sulfate demonstrated a more rapid deterioration of performance scores and quality of life indices, and also experienced more rapid weight loss. The incidence of severe and life threatening treatment-related adverse effects, particularly sensory and motor neuropathies were significantly greater among patients who received hydrazine sulfate.

References:

  1. Ottery FD: Cancer cachexia: prevention, early diagnosis, and management. Cancer Practice 2(2): 123-131, 1994.
  2. Chlebowski RT: Critical evaluation of the role of nutritional support with chemotherapy. Cancer 55(1, Suppl): 268-272, 1985.
  3. Hays DM, Merritt RJ, White L, et al.: Effect of total parenteral nutrition on marrow recovery during induction therapy for acute nonlymphocytic leukemia in childhood. Medical and Pediatric Oncology 11(2): 134-140, 1983.
  4. Copeland EM, Daly JM, Dudrick SJ: Nutrition as an adjunct to cancer treatment in the adult. Cancer Research 37(7, Part 2): 2451-2456, 1977.
  5. Bloch AS: Nutrition Management of the Cancer Patient. Rockville, Maryland: Aspen Publishers, 1990.
  6. Rombeau JL, Caldwell MD, Eds.: Clinical Nutrition: Parenteral Nutrition. Philadelphia: Saunders, 2nd ed., 1993.
  7. Nelson KA, Walsh D, Sheehan FA: The cancer anorexia-cachexia syndrome. Journal of Clinical Oncology 12(1): 213-225, 1994.
  8. Bruera E: Current pharmacological management of anorexia in cancer patients. Oncology (Huntington NY) 6(1): 125-130, 1992.
  9. Parnes H, Tait N, Aisner J: The potential of megestrol acetate in the treatment of cancer cachexia. Nutrition 5(3): 206-209, 1989.
  10. Tchekmedyian NS, Hickman M, Siau J, et al.: Treatment of cancer anorexia with megestrol acetate: impact on quality of life. Oncology (Huntington NY) 4(5): 185-192, 1990.
  11. Loprinzi CL, Goldberg RM, Su JQ, et al.: Placebo-controlled trial of hydrazine sulfate in patients with newly diagnosed non-small-cell lung cancer. Journal of Clinical Oncology 12(6): 1126-1129, 1994.
  12. Kosty MP, Fleishman SB, Herndon JE, et al.: Cisplatin, vinblastine, and hydrazine sulfate in advanced, non-small-cell lung cancer: a randomized placebo-controlled, double-blind phase III study of the Cancer and Leukemia Group B. Journal of Clinical Oncology 12(6): 1113-1120, 1994.
  13. Loprinzi CL, Kuross SA, O'Fallon JR, et al.: Randomized placebo-controlled evaluation of hydrazine sulfate in patients with advanced colorectal cancer. Journal of Clinical Oncology 12(6): 1121-1125, 1994.
Date Last Modified: 10/2002


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