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PARTV Nutrition and Hydration in Children with Cancer

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Contents

26.1 Introduction . . . 387

26.2 Principles of Treatment . . . 388

26.2.1 Nutritional Assessment . . . 388

26.3 Method of Delivery . . . 389

26.3.1 Oral and Enteral Replacement Strategies 389 26.3.2 Selection of Supplemental Enteral Nutritional Solutions . . . 389

26.4 Special Considerations . . . 390

26.4.1 Common Complications of Oral/ Enteral Nutritional Supplementation . . . 390

26.4.2 Total Parental Nutrition (TPN)/Hyperalimentation . . . 391

26.4.3 Complications of TPN/Hyperalimentation . . . 393

26.4.4 Glutamine . . . 393

26.4.5 Intravenous Fluid and Electrolyte Requirements . . . 393

26.4.6 Specific Nutritional Concerns During Palliative Care . . . 394

References . . . 396

Bibliography . . . 396

26.1 Introduction

Cachexia is a well-known form of malnutrition that results from malignant tumors, therapy, and associat- ed side effects. Children are at a higher risk of devel- oping cachexia due to limited nutritional reserves and increased demands already required for normal growth and development. Weight loss in children with cancer is attributed to a phenomenon called anorexia-cachexia syndrome and differs greatly from the weight loss seen with starvation (Inui, 2002).

Factors contributing to the development of cachexia in children with cancer include tumor ef- fects, therapy-related effects, and host response. Tu- mor site, histology, and rate of growth affect normal nutrient metabolism and homeostasis. Tumor pro- duction of cytokines (tumor necrosis factor alpha [TNF-a], IL-6, IL-1 and interferon-gamma) is pro- posed to promote cachexia by altering the leptin feedback signal, mimicking a hypothalamic effect.

Altered protein, carbohydrate, and lipid metabolism contributes to cancer cachexia. Protein stores are de- pleted during cachexia in place of fat typically used during starvation. The demand for amino acids is met in the form of nitrogen depletion, leading to skeletal muscle breakdown and eventual lactic acido- sis. Additionally, cytokine release by tumors affects the muscle repair process. Carbohydrate metabolism is altered, promoting glucose intolerance and mim- icking insulin resistance. Abnormal lipid metabolism includes depletion of lipid stores; increased oxidation of fatty acids, causing hyperlipidemia; and decreased activity of lipoprotein lipase. Lipoprotein lipase pro- duction is also inhibited by cytokines. Tumors may block areas of the gastrointestinal (GI) tract, causing altered absorption.

Nutrition and Hydration in Children with Cancer

Elizabeth Kassner

PART V

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Common side effects of cancer therapy may inter- fere with the child’s ability to ingest, digest, and ab- sorb food. Nausea, vomiting, anorexia, diarrhea, ear- ly satiety, altered taste perception, disruption of mu- cous membranes, xerostomia, colitis, and enteritis contribute to decreased intake or absorption.Admin- istration of high-dose steroids for some treatment protocols may cause steroid-induced diabetes, fur- ther affecting carbohydrate metabolism. Children can experience anticipatory vomiting, depression, anxiety, and learned food aversion behaviors, con- tributing to decreased caloric intake.

Symptoms of cachexia vary depending on tumor location, size, and rate of growth; treatment plan; and developmental stage. Common symptoms include wasting, weakness, anorexia, anemia, hypoglycemia, lactic acidosis, hypoalbuminemia, hyperlipidemia, glucose intolerance, skeletal muscle atrophy, anergy, impaired liver function, and tissue depletion.

26.2 Principles of Treatment 26.2.1 Nutritional Assessment

A registered dietician should be consulted once a di- agnosis of cancer has been determined and a therapy regimen selected. The dietician can assist the treat- ment team to determine nutritional requirements for the child related to diagnosis and GI function. They may also discuss and provide written materials for managing treatment toxicities (e.g., nausea, vomit- ing, diarrhea, anorexia, stomatitis, mucositis, mouth dryness, dysphagia, constipation, and altered taste and sense of smell) with the family and patient. A complete nutritional assessment should include as- sessment of the family’s and patient’s capabilities and compliance, available resources (e.g., insurance, home health), financial issues, and potential cultural or ethical issues relative to nutritional support. Nu- tritional assessment begins by determining the exis- tence and extent of cachexia (Table 26.1).

A complete biochemical assessment would include evaluation of sodium, potassium, chloride, bicarbon- ate, glucose, creatinine, blood urea nitrogen (BUN), calcium, phosphorus, magnesium, total protein, albu- min, triglycerides, cholesterol, alkaline phosphatase,

alkaline aminotransferase, y-glutamyltransferase, to- tal bilirubin, serum albumin (<3.2 mg/dl indicates decreased protein stores), serum prealbumin (in- creases with impaired renal function and decreases with altered hepatic function), and transferase. Clin- ical findings during physical exam may include ab- normal core temperature (normothermic, febrile, or hypothermic); cheilosis; glossitis; sunken cheeks;

prominent zygomatic arches; bulging appearance of eyeballs; dry, scaly, shiny, flaky, atrophic skin; muscle wasting or atrophy; and peripheral edema.

Measurements of nutritional status and energy re- quirements should be ongoing during therapy. Serial anthropometric studies (e.g., weight, weight/height ratio, calf circumference, midarm circumference) provide easy and quick monitoring of weight loss or body mass changes. The degree of malnutrition may be determined by dividing the patient’s actual weight by the ideal body weight for height. Body mass index (BMI) is a measurement used to assess nutritional changes based on the child’s weight in relation to height (Table 26.2). Basal metabolic rate (BMR) is used to calculate energy needs for acute or chronical- ly ill individuals and expresses BMR in kcal/24 hours.

Resting energy expenditure (REE) represents the number of calories the body requires in a 24-hour nonactive period (Table 26.2). Estimated REE in- creases during normal activity and with psychologi- cal and physiological stressors. The human body at-

Table 26.1. Measurements of developing cachexia

Intake <80 % estimated needs

Growth charts demonstrate decrease of 2 percentile channels

>5 % weight loss from prediagnosis

>5 % weight loss over 1 month

Weight loss percentage should be calculated based on the previous highest weight; not allowing for weight gains related to large tumors, edema, pulmonary congestion, or the administration of large volumes of fluids

<5th percentile for height and or weight

<5 % percentile weight for age

<90 % ideal body weight for height

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tempts to maintain homeostasis by regulating REE in accordance with calorie consumption. Children often experience imbalance because of continued growth and development requirements. One of the more fre- quently used formulas to predict energy expenditure is the Harris-Benedict equation, which takes into ac- count gender, age, height, and weight.

Goals for optimal nutrition include preventing or correcting malnutrition, muscle, and organ wasting;

maintaining or promoting strength, energy, and im- mune functioning; and promoting the tolerance of cancer treatment and its associated side effects. Nu- tritional therapy options include medications to stimulate appetite, supplemental high-caloric solu- tions, enteral feedings, and total parenteral nutrition (intravenous hyperalimentation). Commonly admin- istered appetite stimulants include the following:

Megestrol acetate (Megace) Progestational agent

10 mg/kg PO given in one or two doses (maximum dose 800 mg/day)

Dronabinol (Marinol TCH) 15 mg/m2/day

Metoclopramide hydrochloride or cisapride Prokinetic agent with additional dyspeptic symp- tom relief benefit

Metoclopramide: 1–2 mg/kg/dose Cisapride: 0.15–0.3 mg/kg/dose (maximum dose 10 mg)

26.3 Method of Delivery

26.3.1 Oral and Enteral Replacement Strategies

Oral replacement is the nutritional treatment of choice, if tolerated. Some children may require enter- al tube feedings, which allow for the maintenance of GI flora immune status and prevention of mucosal at- rophy. Assessment to determine physical safety for tube placement includes oral mucosa status; function of the GI tract; tolerance of feedings without acute side effects; presence of nausea, vomiting, or diar- rhea; and an adequate platelet count. Nasogastric (NG) tube placement is warranted when short-term requirement is anticipated. In general, a small bore (i.e., 6–12 French) silicone tube is placed and re- quires replacement every 4–6 weeks.

When long-term use is anticipated, or in children prone to dislodging an oral tube, percutaneous place- ment may be indicated. Gastrostomy tubes are placed via a surgical opening through the abdominal wall di- rectly into the stomach. The stomach retains the abil- ity to dilute hyperosmolar solutions. There is less in- cidence of diarrhea with gastrostomy tubes than with jejunostomy tubes. Jejunostomy tubes are surgically placed through the abdominal wall directly into the jejunum. This method is recommended if the child has known upper GI dysfunction, insufficient gastric motility, high aspiration risk, obstruction, or fistulas.

Jejunostomy tubes have fewer problems with stomal leakage and skin erosion, nausea, vomiting, or bloat- ing than gastrostomy tubes do, but have an increased risk of diarrhea.

26.3.2 Selection of Supplemental Enteral Nutritional Solutions

Standard polymeric (full digestion) options contain whole proteins, triglycerides, and long-chain carbo- hydrates, with an average caloric density of 1–2 calo- ries/ml. These supplemental solutions require an in- tact GI tract capable of digestion, absorption, and ex- cretion. Examples include blenderized food, Carna- tion Instant Breakfast, Pediasure, Osmolite, Isocal, Sustacal, and Nutren Junior.

Table 26.2. Calculating body mass index and resting energy expenditure (W weight in kg, H height in cm, A age in years, BMR basal metabolic rate; adapted from Apovian et al., 1998)

BMI = kg m2

Harris-Benedict equation: (expresses BMR in kcal/24 hours)

Male BMR = 66.5 + (13.7W) + (5H) ¥(6.8A)

Female BMR = 65.5 + (9.6W) + (1.8H) ¥(4.7A)

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Chemically defined or specifically formulated (partial digestion) options require little or no diges- tive capability, allowing for easy absorption. These products contain protein in the form of essential and nonessential amino acids and low fat percentages.

Partial digestion solutions are recommended for patients with malabsorption, maldigestion, or rapid GI transit. Examples include high-calorie Nutren, Magnacal, Resource Plus, Ensure Plus, High Nitro- gen-Osmolite HN, Isocal HN, Replete, Ensure HN,Vi- tal High Nitrogen, Predigested- Peptamen, Vivonex, products, and Neocare.

Supplemental solutions may be delivered by a feeding pump or by gravity flow. Feeding schedules can be adjusted to meet the individual child’s re- quirements, activity levels, and family administration requirements. Some children benefit from continu- ous nocturnal feeding that delivers one-half the esti-

mated calorie and energy needs, followed by daytime feedings that provide the other half of the calorie re- quirements. Bolus feeding schedules mimic normal feeding routines and may be divided into two or three boluses. Continuous infusions may be better tolerat- ed in children who have a high incidence of nausea.

The child’s individual tolerance and the duration of time the child has been without oral intake deter- mine initiation and progression of tube feedings (Table 26.3). Monitoring for all children receiving en- teral feedings includes daily weight, fluid intake and output, assessment of GI function, daily confirmation of tube placement, and assessment for residual feed- ing. Monitoring of biochemical laboratory values (i.e., glucose, BUN/urea, electrolytes, calcium, phos- phorus, magnesium) is recommended daily until sta- bilized, and then every 3–7 days.

26.4 Special Considerations 26.4.1 Common Complications

of Oral/Enteral Nutritional Supplementation

Refeeding syndrome develops within 1–2 weeks after initiation of nutritional supplementation in children with chronic nutritional deficits. Symp- toms include metabolic complications, severe fluid shifts, hypophosphatemia, and hypokalemia.

Treatment is achieved through slow replacement of nutrients during initiation of refeeding. Strict monitoring of sodium, magnesium, potassium, chloride, bicarbonate, BUN/urea, creatinine, calci- um, and phosphorus is required.

High gastric residual volume is caused by delayed gastric emptying, and confirmation of correct tube placement is needed. Treatment options in- clude holding the feedings if the residual volume is determined less than 2 hours of the feeding and reassessing for residual volume every hour until the volume is absorbed. Administration of proki- netic medications (cisapride or metoclopramide) and elevating the head of the bed at least 30° dur- ing and after feeding may decrease the incidence of recurrent gastric residual.

Aspiration pneumonia may occur from incorrect placement or movement of an NG tube. Symptoms

Table 26.3. Initiation and progression of feedings

NPO <3 days

Continuous

Start with full-strength formula at 0.5–2 ml/kg/hr Increase 1–2 ml/kg/hr q8–24h as tolerated Bolus

Start with full-strength formula at 1–5 ml/kg/hr Advance as tolerated

<12 months 10–30 ml/feeding 1–6 years 30–45 ml/feeding

>7 years 60–90 ml/feeding

NPO >3 days or with GI problems

Continuous

Start with half-strength formula at 0.5–2 ml/kg/hr Increase to full-strength formula in 12–24 hours Increase 1–2 ml/kg/hr q8–24h as tolerated Bolus

Start with half-strength formula at 1–5 ml/kg/hr Increase to full-strength formula in 24 hours Advance as tolerated

<12 months 10–30 ml/feeding 1–6 years 30–45 ml/feeding

>7 years 60–90 ml/feeding

May require water in addition to supplemental feedings

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include cough, congestion, rales, rhonchi, wheez- ing, and respiratory distress. Appropriate place- ment of the NG tube should be assessed before any bolus feeding and when placement is in question.

Elevating the head of the bed at least 30° during feedings decreases the risk of aspiration.

Skin irritation and excoriation may occur at the site of NG, gastrostomy, or jejunostomy tubes. Lo- cal infection and cellulitis can be treated with strict skin care and antibiotics as needed.

Tube obstruction can occur when the tube is not flushed adequately between fluid boluses or medication administration. All tubes should be flushed with water at least every 4 hours during continuous feedings and after all boluses and medication administration. The use of medication in liquid elixir formulations is recommended.

Many institutions recommend once-daily mainte- nance flushes using one of the following: water and 1 tablespoon meat tenderizer or water and 1 tablespoon seltzer mixed with 1/8 teaspoon bak- ing soda or cola beverage.

Vomiting, bloating, or diarrhea may occur if the rate is too fast for the child’s absorption capabili- ties or if the child has lactose intolerance. Treat- ment options include slowing the infusion rate and doing frequent residual assessments. Addi- tionally, administering lactose-free supplements, formulas with a lower fat content, and room-tem- perature formulas may decrease GI side effects.

Hyperglycemia is treated by reducing the infusion rate, using formula with less carbohydrate and sugar, or administering insulin as needed.

26.4.2 Total Parental Nutrition (TPN)/

Hyperalimentation

Total parental nutrition (TPN) is required when oral and enteral feedings are unable to provide adequate calories and nutrients; components of TPN are listed in Table 26.4. There is no clear evidence that initia- tion of TPN is helpful or detrimental to treatment tol- erance, response rates, or survival. Therapeutic goals of TPN include restoring the child’s normal body weight, reversing malnutrition, promoting growth, improving immunologic status, potentially accelerat-

ing marrow recovery, and generally supporting activ- ity and energy expenditure.

Peripheral venous catheter administration of TPN is appropriate for short-term therapy. Central venous catheter administration is indicated if TPN is antici- pated to be required for several weeks or months. The initiation of TPN should be coordinated with a phar- macist, dietician, and physician or nurse practitioner.

Guidelines for formulation are frequently institu- tion-specific. Patient-specific energy needs should be calculated based on the degree of malnutrition, diag- nosis, and individual treatment plan. A basic ap- proach for initiating TPN includes the following steps:

1. Assess protein and energy requirements of child 2. Protein g/day = (g/kg/day) ¥ weight (kg) 3. Energy/day = (kcal/kg/day) ¥ weight (kg) 4. Calculate maintenance fluid requirements

– 1,500 ml for the first 20 kg, then 20–30 ml/kg for each additional kg of body weight

5. Determine fat, dextrose, and amino acid energy requirements

– (30% fat, 70% dextrose) 6. Determine lipid requirements

7. Select amino acid, electrolyte, mineral, and vita- min concentration

– Typically institution-dependent 8. Determine volume based on calculations

9. Compare maintenance fluids, calculate with total fluids, and adjust as needed

Table 26.4. Components of total parenteral nutrition

Component Contents

Protein Amino acids

Fat Lipids

Carbohydrate Glucose

Electrolytes Sodium, potassium, chloride, calcium, phosphate, magnesium

Trace elements Copper, zinc, manganese, chromium, selenium

Vitamins A, C, D, E, K, thiamine, riboflavin, niacin, pantothenic acid, pyridoxine, B12, choline, biotin, folic acid

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Electrolyte needs and protein and energy require- ments are listed in Tables 26.5 and 26.6, respectively.

Peripheral and central TPN concentrations will differ in composition, primary calorie source, rate of administration, and associated risks. Peripheral ad- ministration of TPN limits dextrose concentrations to 10%, protein (amino acids) concentrations to 1.5–2%, and lipid solutions to either 20%, providing 2 kcal/ml, or 10%, providing 1.1 kcal/ml. Administra- tion of TPN via central venous access allows delivery of greater volumes and greater caloric replacement.

Dextrose concentrations may range from 10–12.5%, providing 3.4 kcal/g, with rates of administration ranging from 3–4 mg/kg/hour. Dextrose may be ad- vanced by 2.5–5% every 24 hours as tolerated until the preferred caloric level of 20–25% dextrose con- centration is attained. Infusion rates should not ex-

ceed 5 mg/kg/min. Protein (standard amino acids) concentrations of 10% will deliver 4 kcal/g and may be administered at 1 g/kg/day. Protein levels may be advanced by 0.5–1 g/kg/day until the maximum goal of 1.5–3 g/kg/day is achieved. Lipid concentrations of 20%, administered at 1–2 g/kg/day, are advanced by 0.5–1 g/kg/day until a total of 1–3 g/kg/day are at- tained as tolerated. Lipid concentrations should not exceed 4 g/kg/day or 60% of the total calories in or- der to prevent essential fatty acid deficiency.

Recommended monitoring during TPN adminis- tration includes daily weights and intake and output measurements. Urine glucose should be monitored initially with each void and may be decreased to dai- ly monitoring if normal. Electrolyte and BUN evalu- ation is recommended two to three times a week un- til the TPN dose is stabilized, and then monitoring

Table 26.5. Electrolyte requirements by patient weight

Electrolyte 25 kg (mEq/kg) 25–45 kg (mEq/kg) >45 kg

Sodium 2–6 2–6 60–150 mEq

Potassium 2–5 2–5 60–150 mEq

Calcium 1–2 1 0.2–0.3 mEq

Magnesium 0.5 0.5 0.35–0.45 mEq

Phosphate 0.5–1 mmol 0.5–1 mmol 7–10 mmol/1,000 cal

Chloride 2–3 mEq/kg/day 2–3 mEq/kg/day

Table 26.6. Energy and protein requirement recommendations

Age in years Resting energy expenditure Total energy Protein requirement

kcal/kg/day kcal/kg/day g/kg/day (total g/day)

0–1 55 90–120 1.6–3.2 (16–18)

1–3 50 70–100 1.2–3 (19–22)

4–10 40–45 50–70 1–3 (25–39)

11–14 30 1–2.5 (51–74)

Males 60–70

Females 50–60

>15 25 0.9–2.5 (66–80)

Males 45–55

Females 35–45

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may be decreased to weekly. Calcium, phosphorus, and magnesium serum levels should be obtained weekly until the TPN rate is stable, and then moni- toring may be decreased to every other week. A base- line albumin should be obtained and then repeated every 3 weeks. Prealbumin levels are recommended weekly, and triglyceride levels should be obtained 4 hours after the initiation of TPN and 4 hours after each rate increase.

26.4.3 Complications of TPN/Hyperalimentation

Hypoglycemia is a common side effect and is eas- ily prevented by avoiding rapid discontinuation of TPN and by tapering the administration rate when an infusion is being discontinued.

Hyperglycemia can be managed by decreasing dextrose concentrations or by adding insulin.

Hepatic dysfunction may include fatty liver symp- toms or cholestatic jaundice. Treatment strategies include avoiding excessive infusion of carbohy- drates; maintaining a balance of dextrose, protein and lipids; and converting to enteral feeding as soon as therapeutically possible.

Hyponatremia, fluid overload, and infection are all possible complications of TPN; they can be pre- vented or treated with strict monitoring and early interventions.

Mechanical difficulty may include catheter tip mi- gration, obstruction, or thrombosis. Evaluation of proper line functioning is essential and is deter- mined by adequate blood return. Radiologic eval- uation is warranted if displacement or obstruction is suspected.

26.4.4 Glutamine

Glutamine is a nonessential amino acid that is an important fuel source for proliferating cells. During periods of physiological stress (i.e., injury, illness), the body’s demand for plasma glutamine increases.

Preliminary investigational use of supplemental glutamine suggests that it may promote improved muscle protein and facilitate muscle repair and ex- cessive catabolism. Additional studies have shown

that glutamine supplements may improve a sup- pressed immune system by supporting lymphocytes and macrophages. Research is still indicated to deter- mine safety data, appropriate replacement dose lev- els, and long-term effects. Large doses of glutamine have been associated with abdominal pain and diar- rhea (Bechard et al., 2002).

26.4.5 Intravenous Fluid and Electrolyte Requirements

The hydration status of a child receiving treatment for cancer is another important area to continually assess. Early intervention may prevent severe elec- trolyte imbalance and even prevent hospitalizations.

Most hydration imbalances result from therapy and its associated side effects. Children receiving chemotherapy and blood products are at increased risk of fluid overload, and side effects of chemother- apy and radiotherapy that affect gastric functioning and the perception of taste and smell predispose the child to dehydration.

Weight is the single most accurate variable for as- sessing hydration status.Additional measurements of hydration include vital sign monitoring to assess vas- cular volume and 24-hour input and output monitor- ing to provide data regarding hydration imbalances.

Serum electrolytes, serum osmolality, blood sugar, BUN, creatinine, and urine electrolytes and osmolal- ity can provide additional information regarding the child’s hydration status. Common findings observed on physical exam are listed in Table 26.7.

Fluid requirements for a healthy child with a routine activity level may be based on body surface area (1500 ml/m2/day) or more often by weight (Table 26.8). Intravenous replacement options in- clude isotonic or hypotonic fluids or colloids. The most common form of dehydration is isotonic dehy- dration, which is corrected using isotonic fluids. Ex- amples of isotonic fluids include normal saline (NS), lactated Ringer’s (LR), and D51/2NS. Hypotonic fluids such as 1/2NS or D5W have a lower degree of osmot- ic pressure than individual cells. The administration of hypotonic fluids causes migration of fluid into the cells and could cause cellular rupture. Hypertonic so- lutions such as D5NS or D5LR cause the flow of intra-

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cellular fluids into extracellular space, causing blood volume to expand and blood pressure to increase.

Small volume replacement over a short time period is recommended. Colloids exert an oncotic pressure, pulling fluid from other spaces into vascular com- partments. Examples are 5% albumin, fresh frozen plasma, and dextran 4% and 6%.

Oral replacement of fluids for children with mild and moderate levels of dehydration is preferred. Pa- tients requiring rehydration and electrolyte replace- ment may benefit from products such as Ricelyte, Pe- dialyte, and Rehydrate. Children exhibiting signs and symptoms of hypovolemic shock require rapid intra- venous replacement (Table 26.9).

Children with malignancy can develop electrolyte imbalances due to the disease process itself or to the associated treatment. Routine laboratory evaluations

are necessary at the time of diagnosis and before and during therapy (Table 26.10).

26.4.6 Specific Nutritional Concerns During Palliative Care

Children receiving palliative care for unresponsive or progressive oncologic diseases have different nutri- tional concerns than children receiving aggressive therapy. The primary focus of all interventions dur- ing this time is on the child’s quality of life. Families frequently need education and support to under- stand that reduced nutrient intake will not alter the occurring pathologic process or shorten the child’s life. The child’s loss of interest in food and a de- creased appetite are normal near death and indicate that the body can no longer manage caloric intake.As adequate metabolization is declining, forcing the child to consume foods will only tire the child and cause discomfort in the form of diarrhea, nausea, vomiting, choking, or pneumonia. Family members should be encouraged to give permission for child to refuse intake. Children who remain interested in eat- ing may benefit from smaller, more frequent meals of soft, easily digested foods and by avoiding strong smells.

Fluid requirements during palliative care are also decreased. Thirst is rare during the final days of life.

Again, there are no data to suggest that withholding fluids, orally or intravenously, in the final stages of life is detrimental. Children may be supported with min- imal intravenous fluid (IVF) administration if intra- venous access is not a problem and it is the wish of the child or family. Advantages of IVF administration

Table 26.7. Physical exam findings associated with dehydra- tion

Sign Symptom

Weight loss 5–15 % of body weight Behavior irritable to lethargic

Thirst slight to intense

Mucous membranes dry

Tears absent

Anterior fontanel flat or sunken Skin turgor decreased, dry, warm Urine output decreased, concentrated,

increased urine specific gravity Cardiac Pulse increased, weak

Laboratory increased hematocrit, BUN/urea

Table 26.8. Weight-based fluid requirements

Weight Volume

<10 kg 100 ml/kg/day

11–20 kg 1,000 ml + (50 ml for each kg >10)kg/day 20–30 kg 1,500 ml + (20 ml for each kg >20)kg/day

>30 kg 35 ml/kg/day

Table 26.9. Volume replacement guide for dehydration

Degree of dehydration Volume

Mild 50 ml/kg within 4 hours

Moderate 100 ml/kg within 4 hours

Severe IVF for stabilization,

then 100 ml/kg Hypovolemic shock 20 ml/kg in two aliquots

of 10 ml/kg

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Table 26.10. Common electrolyte imbalances in pediatric cancer patients

Condition Serum levels Causes Symptoms Treatment

Hypercalcemia >10.5 mg/dl Bone malignancies and Weakness, irritability, Hydration, metastases, excessive lethargy, seizures, coma, hemodialysis, concentrations in TPN, abdominal cramping, steroids poor dietary intake of anorexia, nausea, vomiting,

phosphorus, renal absorp- ECG changes tion or excretion, diuretics

Hypocalcemia <8 mg/dl Decreased intake; Neuromuscular irritability, IV or oral replace- vitamin D deficiency, weakness, cramping, fatigue, ment, correct intake, or malabsorption; change in level of con- underlying cause hypoparathyroidism, sciousness, seizures,

pancreatitis ECG changes

Hyperkalemia 6–7 mEq/l Renal failure, cellular ECG changes Kayexalate,

breakdown, leukocytosis, insulin, NaHCO3,

metabolic acidosis calcium gluconate

Hypokalemia <3.5 mEq/l Decreased intake, Skeletal muscle weakness, Replace with increased renal excretion, dysrhythmias: prolonged potassium acetate therapy-induced renal Q-T interval, flattened or gluconate tubular defects, diarrhea, T-waves

vomiting

Hyponatremia <130 mEq/l Syndrome of inappropriate Convulsions, shock, Fluid restriction, secretion of antidiuretic lethargy replace losses,

hormone (SIADH); ectopic treat underlying

secretion of antidiuretic cause

hormone; renal, adrenal cortical, or cardiac insuffi- ciency; excessive loss secondary to vomiting, diarrhea, or salt-losing nephropathy; neurotoxic effect of cyclophosphamide and vinca alkaloids

Hypomagnesemia <1 mEq/l Nephrotoxic agents, Tetany, seizures, tremors, IV or oral magne- decreased intake, diarrhea, anorexia, nausea, cardiac sium sulfate, vomiting, urinary loss abnormalities, weakness, oxide,

clonus or gluconate

Hypermagnesemia >5 mg/dl Renal dysfunction Hyporeflexia, respiratory IV administration depression, confusion, of calcium,

coma diuresis

Hypophosphatemia <3 mg/dl Poor dietary intake, Usually not until severe IV or oral potas- malabsorption, excessive (<1 mg/dl); irritability, sium-phosphate renal excretion, vitamin D paresthesias or sodium-phos-

deficiency phate

Hyperphosphatemia >6 mg/dl Chemotherapeutic agents, Symptoms relative to Restrict intake, renal insufficiency: resulting from hypo- phosphorus glomerular filtration rate calcemia binders: calcium

<25 % normal carbonate, alu-

minum hydroxide

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include possible improved oral comfort and bowel function, less delirium, and a more productive cough due to thinning of secretions. Administration of min- imal IVF allows family members to feel as if they are doing “everything possible.” Disadvantages include increased oral, respiratory, and GI secretions and urine output, which predisposes the child to an in- creased chance of choking, cough, pulmonary con- gestion, edema (peripheral and pulmonary), vomit- ing, and urinary incontinence.

References

Apovian CM, Still CD, Blackburn GL (1998). Nutrition support.

In Berger, Portenoy & Weissman’s Principles and Practice of Supportive Oncology, pp 571–588. Lippincott-Raven, Philadelphia

Bechard LJ, Adiv OE, Jaksic T, Duggan C (2002). Nutritional supportive care. In Poplack & Pizzo’s Principles and Prac- tice of Pediatric Oncology, 4th edn, pp1285–1300. Lippincott Williams & Wilkins, Philadelphia.

Inui A (2002) Cancer anorexia-cachexia syndrome: current is- sues in research and management. CA: A Cancer Journal for Clinicians 52(2):72-91

Bibliography

Sacks N, Meek RS (1997). Nutritional support. In Ablin’s Sup- portive Care of Children with Cancer: Current Therapy and Guidelines from the Children’s Cancer Group, pp 193–209.

The Johns Hopkins University Press, Baltimore

Sacks N, Meek RS (1998). Nutritional support of the child with cancer. In Hockenberry-Eaton’s Essentials of Pediatric On- cology Nursing: A Core Curriculum, pp 164–168. Associa- tion of Oncology Nursing, Glenview, IL

Waller A, Caroline NL (2000). Nutrition and hydration. In Waller & Caroline’s Handbook of Palliative Care in Cancer:

2nd edn, pp 61 – 74. Butterworth-Heinemann: Woburn, MA

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