Nutritional assessment is an integral part of the clinical care of children with gastrointestinal disorders, as nutritional status can affect response to illness and outcome. Given the complex processes of growth and development in children, nutrition is of paramount importance. Understanding growth patterns and body composition changes in childhood, along with identifying the components of a nutritional assessment, is part of a comprehensive medical evaluation of children with gastrointestinal disease.
Normal Growth and Body Composition in Children
Age-appropriate growth is the hallmark of adequate nutrition; children with abnormal growth patterns should be evaluated for diet adequacy, organic disease, and access to food. Universally, growth can be measured objectively, but growth characterization must be interpreted in the context of a clinical assessment. Length in infants increases about 2.5 cm per month for the first 6 months and by 1.3 cm per month from 7 months to 1 year of age. Growth subsequently slows to 7.6 cm per year until age 10 and stays constant until puberty, with no difference for boys or girls. Growth spurts occur between the ages of 12 and 17 year for boys, with expected gain of more than 10 cm in the year of peak velocity; and for girls between the ages of and , with expected gain of 9 cm in the year of peak velocity.
Adequate weight gain in full-term infants from birth to 3 months is 25 to 35 g per day, then 15 to 21 g per day at 3 to 6 months, and 10 to 13 g per day until 12 months of age. The infant will triple his birth weight by the first birthday and quadruple it by 2 years of age. From 2 years through adolescence, weight increases approximately 2 kg per year, and peak weight velocity in adolescents can average 3 kg in 6 months.
Head circumference is routinely measured until 2 years of age and is reflective of brain growth; head circumference will average 35 cm at birth, which is 25% of adult size. During the first year of life, increases of 1 cm per month occur and the brain becomes approximately 75% of its adult size.
Body composition is complex and can be approached using different measurement techniques. In the two compartment model, the body is divided into fat and fat free mass, or lean body mass (LBM). This model allows the trained clinician to differentiate tissue, estimate measurements of stored adiposity, and compare measurements to available published standards. Anthropometric measurements, such as the fat-fold measurements of stored adiposity, can be used serially to monitor health and overall impact of disease. Direct measures of body composition include, but are not limited to, bioelectrical impedance analysis, total body potassium, isotope dilution, hydrodensitometry, dual-energy X-ray absorptiometry, and hand dynamometry as a surrogate gauge of muscle function. These methods vary in cost, accuracy, and utility for estimating body composition relevant to nutritional status.
Prevalence and Classification of Malnutrition in Pediatric Patients
Although lack of a uniform definition currently exists, malnutrition is generally described as a state of nutrition in which deficiency or excess of energy, protein, and other nutrients leads to measurable adverse effects on body mass and function. The exact prevalence of malnutrition in the pediatric population is unknown . Children with gastrointestinal disorders are among those most susceptible to chronic malnutrition. For example, it has been reported that 22% to 31% of children with Crohn’s disease encounter linear growth impairment preceding disease diagnosis. In assessing the nutritional status of children, dietitians are attempting to recognize malnourished people in whom nutrition-associated morbidities are likely to occur, and for whom applied nutrition therapy can improve outcomes.
Historically, the classification of malnutrition has been based on assessment of anthropometric variables. In 1956, Gomez et al. introduced a classification of malnutrition based on weight below a specified percentage of median weight for age. This method also introduced the calculation of height for age to distinguish stunting (chronic malnutrition) from wasting (acute malnutrition). In 1977, Waterlow et al. recommended the use of percentiles and standard deviations (SDs) below the median to define underweight, wasting, and stunting. More recently, the World Health Organization (WHO) recommended the use of Z-score cut-off points for weight-for-age (WFA) or height-for-age (HFA) to classify degree of wasting or stunting, respectively. Although the focus of this chapter is undernutrition, obesity is also a form of abnormal, where cut-off points of 2 or more SDs classify high weight for height as overweight in children. Table 86-1 summarizes the most commonly used classification schemes for pediatric malnutrition.
Classification | Variable | Grade | Definition |
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Gomez et al. | Weight below % median WFA | Mild (Grade 1) | 75% to 90% WFA |
Moderate (Grade 2) | 60% to 74% WFA | ||
Severe (Grade 3) | <60% WFA | ||
Waterlow (wasting) | Weight below % median WFA | Mild | 80% to 89% WFA |
Moderate | 70% to 79% WFA | ||
Severe | <70% WFA | ||
Waterlow (stunting) | Height below % median HFA | Mild | 90% to 94% HFA |
Moderate | 85% to 90% HFA | ||
Severe | <85% HFA | ||
WHO (wasting) | Z-scores (SD) below median WFH | Moderate | Z-score between −2 and −3 |
Severe | Z-score ≤3 | ||
WHO (stunting) | Z-scores (SD) below median HFA | Moderate | Z-score between −2 and −3 |
Severe | Z-score ≤3 |
The two main clinical syndromes of the extreme forms of undernutrition are marasmus and kwashiorkor. These are differentiated on the basis of clinical findings, with the primary distinction being the presence of edema in kwashiorkor. A mix of the two syndromes, known as marasmic kwashiorkor can also be seen. A more detailed comparison of the etiologies and clinical distinctions among these three syndromes can be found in Table 86-2 .
Marasmus | Kwashiorkor | Marasmic-Kwashiorkor |
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Extremely emaciated (without edema) | Bilateral pitting edema, which can become more generalized | Concurrent gross wasting and edema |
Distended abdomen | ||
Depletion of subcutaneous fat stores and muscle wasting | Reduced fat and muscle tissue (may be masked by edema) | Frequently stunted |
Almost normal weight for age | ||
Hepatosplenomegaly | Enlarged palpable fatty liver | |
Normal hair | Hypopigmented hair | |
Xerotic, wrinkled, and loose skin | Dermatosis | Mild hair and skin changes |
Frequent infections with minimal external signs (not often showing fever) | Frequent infections due to skin lesions | |
Usually active and alert | Apathetic and lethargic; irritable when handled |
Once severity has been determined, malnutrition should be categorized as primary, secondary, or a combination of both. Primary malnutrition is caused by environmental or behavioral factors, such as extreme social neglect or poor nutritional intake arising from ignorance of proper feeding practices. In contrast, secondary or “illness-related” malnutrition is associated with an underlying disease process or disorder that predisposes the child to undernourishment ( Table 86-3 ). This form of malnutrition may be attributed to abnormal nutrient loss, increased energy expenditure, or decreased food intake. In developed nations, secondary malnutrition is the more common form.
Disease | Etiology of Malnutrition | Special Considerations |
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Inflammatory bowel disease | Increased energy expenditure from chronic inflammation | Medical control of underlying pathology essential to improving nutritional status |
Nutrient loss from malabsorption | Undernutrition more significant in Crohn’s disease compared with ulcerative colitis | |
Decreased oral intake due to abdominal pain, diarrhea, and cachexia | Long-term growth may be significantly affected | |
Chronic liver disease | Nutrient loss from malabsorption | Specific vitamin/mineral supplementation often required, i.e., vitamins A, D, E, and K |
Inappropriate substrate use | May need to modify fat content in formula/diet (increase MCT/decrease LCT) | |
Increased metabolic needs | Calorie intake is often as high as 130% to 150% estimated requirement | |
Decreased oral intake as a result of abdominal pain, altered taste, cachexia (if prominent inflammatory component) | Monitor arm anthropometrics in addition to standard growth parameters (especially in ESLD) to account for fluid shifts | |
Short bowel syndrome | Nutrient loss from malabsorption | Micronutrient deficiencies will vary depending on what region of the intestine is affected |
Recently, an interdisciplinary work group from the American Society of Parenteral and Enteral Nutrition (ASPEN) proposed a new definition and classification scheme for pediatric malnutrition. This definition, which was based on available evidence and multidisciplinary consensus, incorporates chronicity, etiology, mechanisms of nutrient imbalance, severity of malnutrition, and its impact on outcomes. According to the authors, current terminologies such as marasmus and kwashiorkor describe the effects of malnutrition but do not account for the “variety of etiologies and dynamic interactions” that also play a significant role in nutritional depletion.
Indications for Nutrition Assessment
Nutrition assessment in the pediatric patient is warranted if a child meets recognized screening standards for increased risk of developing growth failure, protein-energy malnutrition, or obesity. Criteria may include children with restrictive diets, multiple food allergies, anemia, feeding difficulties, nutrition support, developmental disabilities, and patients taking long-term medications that alter metabolism/nutrient utilization. Evidence urges the clinician to include the patient’s current inflammatory state when considering nutritional assessment.
Clinical determinants for initiating nutrition assessment:
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Height less than 10th percentile for age
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Weight-for-age plotting less than the 3rd or 5th percentile on Centers for Disease Control and Prevention (CDC)/WHO growth curves
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Weight-for-height/length plotting less than 3rd or 5th t percentile on the CDC/WHO growth curves
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Change in more than two standard deviations on the growth curve over a 3- to 6-month period
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Decreased growth velocity where weight falls more than two major percentile curves over 3 to 6 months
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>= 5% weight loss 5% or greater weight loss from usual body weight
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BMI (body mass index) >85th percentile, with at least one parent who is overweight or obese
Components of a Nutritional Assessment
A comprehensive nutritional assessment should include four key components: (1) clinical history combined with physical assessment; (2) detailed diet history; (3) anthropometric measurements of growth; and (4) biochemical analyses. The individual components of a nutritional assessment when considered alone have weaknesses. Ideally, a combination of the measures listed earlier will provide the most thorough approach to a complete nutritional assessment.
Clinical History and Physical Assessment
A clinical history incorporates the patient’s diagnosis, birth, medical, and surgical history, medications, and/or treatments, as well as neurologic function, with attention paid to the ability to safely chew and swallow. This information considered in conjunction with a physical assessment directs the care of the patient. A nutrition-focused physical examination must evaluate the patient from head to toe. An overall review of height and weight; assessment of muscle and fat mass; the appearance of skin, hair, eyes, and fingernails; as well as the presence or absence of edema should be included. The patient’s oral health, including teeth, lips, tongue, and gums is a key piece of the physical assessment. Signs of bone disease, such as rachitic rosary and bowed legs, may be observed during the examination. Although many physical findings of the clinical assessment are most likely multifactorial, some are diagnostic of nutrient deficiencies ( Table 86-4 ).
Vitamin/Mineral | Mechanisms | Symptoms of Deficiency | Excess | Diagnosis | Food Sources | |
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B vitamins (water soluble) | B1 Thiamine | Inadequate intake | Fatigue, peripheral neuropathy, cardiomyopathy beriberi (severe deficiency) | None | Response to thiamine supplement; serum B 1 if symptoms severe | Liver, pork, milk, grains, beans, seeds, nuts |
B 2 Riboflavin | Inadequate intake | Blurring vision, cheilosis, nasolabial seborrhea, red painful tongue | None | Urinary riboflavin <30 µg/day | Milk, cheese, liver | |
B 6 Pyridoxine | Inadequate intake | Seizure, irritability, sensory ataxia | Neuropathy, photosensitivity | Whole blood concentration plasma pyridoxal phosphate | Meat, poultry, liver, kidney, some nuts and seeds, whole grains, beans | |
Folate | Inadequate intake, malabsorption, medications (methotrexate, sulfasalazine) | Megaloblastic anemia, hyperhomocysteinemia, glossitis, angular stomatitis, depression | Can obscure anemia due to B 12 deficiency | Low serum folate (normal ≥3.0 ng/mL), low red blood cell folate levels, elevated homocysteine levels with normal methylmalonic acids levels | Liver, fortified cereals, dried beans, orange juice, leafy green vegetables, yeast, kidney | |
B 12 Cyanocobalamin | Inadequate intake (vegetarian diet), malabsorption, active ileitis, defective/deficient intrinsic factor, history of ileal or ileocolonic resection | Megaloblastic anemia, pancytopenia, peripheral neuropathy (abnormalities of taste and smell), dementia, loss of appetite, smooth and/or sore tongue, failure to thrive, developmental delays | None | Low serum B 12 , if <400 pg/mL, consider checking methylmalonic acid and homocysteine levels | Liver, meats, fish, shellfish, poultry, eggs, cheese | |
Niacin | Inadequate intake of niacin and/or tryptophan-containing foods | Vomiting, constipation, rash, glossitis, depression, headache, fatigue, memory loss, dementia, pellagra (severe deficiency) | Flushing, nausea, vomiting, liver toxicity, impaired glucose tolerance | Low urinary excretion levels of niacin and metabolites (in 24 hour urine) | Meat, liver, beans, fortified or enriched foods | |
Biotin | Inadequate intake | Pallor, muscle pain, loss of appetite, scaly dermatitis | None | Decreased urinary biotin (in 24 hours) | Liver, lentils, peanuts, mushrooms, chicken, whole wheat, eggs | |
Pantothenic acid | Inadequate intake (usually with other B vitamins) | Fatigue, abdominal pain, vomiting, numbness in feet and hands | Possible diarrhea, water retention | Whole blood pantothenic acid, 24 hour urinary excretion | Liver, whole grains, nuts, dried beans, brewer’s yeast | |
Choline | Restricted diet, inadequate provision in formula/TPN | Fatty liver infiltrate, liver damage | Hypotension, fishy body odor, sweating | Fasting plasma concentration | Milk, liver, eggs, peanuts | |
C | Inadequate intake, increased need with infection, stress of surgery | Poor wound healing, gingivitis, scaly skin, arthralgia, perifolliculitis, corkscrew hairs, scurvy (severe deficiency) | Oxaluria | Mainly based on clinical symptoms; plasma vitamin C | Broccoli, cantaloupe, peppers, collards, citrus fruit, tomato, strawberries, liver | |
Fat Soluble Vitamins | A | Inadequate intake, fat malabsorption/steatorrhea, inadequate bile salts, medications (e.g., cholestyramine) | Poor wound healing, night blindness, xerophthalmia, Bitot’s spots, follicular hyperkeratosis | Nausea, vomiting, headache, vertigo, blurred vision, loss of muscle coordination, bulging fontanel (infants) | Serum retinol, retinol-binding protein, beta carotene | Liver, sweet potato, cantaloupe, carrots, spinach, peas, broccoli, fortified milk |
D | Inadequate intake, fat malabsorption/steatorrhea, lack of sunlight exposure/latitude | Abnormal bone metabolism, rickets, epiphyseal enlargement, bow legs, poor growth, tetany; possible role in increased inflammation | Diarrhea, weight loss, calcification of soft tissues | 25, OH vitamin D | Fatty fish, fortified dairy products | |
E | Inadequate intake, bile salt deficiency, malabsorption/steatorrhea | Peripheral neuropathy, ataxia, retinopathy, anemia | With excessive supplementation: potential for hemorrhagic toxicity and diminished blood coagulation with vitamin K deficiency | Serum (alpha) tocopherol | Vegetable oils, dried beans, sunflower seeds, wheat germ, dark leafy greens | |
K | Inadequate intake, fat malabsorption/steatorrhea, bile salt deficiency, medication (e.g., cholestyramine) | Rare, but can occur from antibiotic use (suppressing menaquinone-synthesizing organisms); symptoms include bleeding and abnormal bone metabolism | No reported effects | Serum phylloquinone, prothrombin time, international normalized ratio, PIVKA II, uncarboxylated osteocalcin (bone levels) | Collards, spinach, salad greens | |
Minerals | Calcium | Inadequate intake, decreased absorption/losses, vitamin D deficiency or insufficiency, hypomagnesemia (e.g., due to excessive diarrhea) | Low bone density, fatigue, depression, memory loss, seizures, tetany | Kidney stones, decreased absorption of other minerals, vascular and soft tissue calcification | Bone density, serum or ionized calcium | Dairy products, calcium-set tofu, calcium-fortified beverages, kale |
Phosphorus | Inadequate intake, decreased absorption, increased losses, large intake of calcium (e.g., antacids) | Anorexia, muscle weakness, bone pain, rickets (children), osteomalacia (adults), anemia | Reduced calcium absorption, calcification of nonskeletal tissues (kidneys) | Serum phosphorus | Dairy products, soda containing phosphoric acid | |
Magnesium | Inadequate intake, losses due to diarrhea, malabsorptive syndromes, excessive laxative use, pancreatitis | Symptomatic hypocalcemia, muscle cramps, interference with vitamin D metabolism, neuromuscular hyperexcitability, latent tetany, spontaneous carpal-pedal spasm, seizures | Diarrhea, nausea, abdominal cramps, hypokalemia, paralytic ileus, metabolic alkalosis (with very large dose) | Serum magnesium, 24-hour urine magnesium (most accurate) | Leafy green vegetables, whole grains, nuts | |
Iron | Inadequate intake, poor bioavailability, blood loss, achlorhydria | Fatigue, pallor, tachypnea, tachycardia, koilonychia (spoon nails) | Vomiting, diarrhea, CNS, kidney, liver, hematologic effects | Ferritin, TIBC transferrin saturation, HgB/HCT, zinc protoporphyrin | Meats, fish, poultry | |
Zinc | Inadequate intake, zinc-deficient TPN, diarrheal losses, high pytic acids in diet, calcium supplements | Growth retardation, alopecia, diarrhea, delayed sexual maturation, impaired appetite, delayed wound healing | Acute epigastric pain, diarrhea, headache, nausea, vomiting, decreased appetite | Serum/plasma zinc; response to zinc supplement | Red meat, seafood, whole grains, fortified cereal | |
Selenium | Inadequate intake, selenium-deficient TPN | Keshan disease, cardiomyopathy, hypothyroidism, cartilage degeneration | Hair and nail brittleness/loss, skin rash, garlic breath | Plasma or serum selenium | Meat, seafood, cereals, grains, dairy | |
Copper | Copper-deficient TPN or formula, chronic diarrhea, losses w/ hemodialysis | Normocytic, hypochromic microcytic anemia, leukopenia, neutropenia, osteoporosis (in growing children) | Observed in Wilson’s disease, idiopathic copper toxicosis, liver damage | Serum copper, ceruloplasmin | Organ meats, seafood, nuts, seeds and cocoa products, whole grains | |
Chromium | Chromium-deficient TPN | Unexplained weight loss, peripheral neuropathy, impaired glucose utilization | Rhabdomyolysis, liver dysfunction, renal failure | Serum, erythrocyte and urine chromium levels | All bran and whole grain cereals | |
Carnitine | Carnitine-deficient TPN | Defective fatty acid oxidation, cardiomyopathy, depressed liver function, hypoglycemia, neurologic dysfunction | Nausea, vomiting, abdominal cramps, fishy body odor | Total and free carnitine levels | Red meats, dairy, nuts, seed, legumes | |
Fat | Inadequate intake, malabsorption, diarrhea | Impaired growth, impaired absorption of fat soluble vitamins A, D, E, and K | Obesity | Triene-to-tetraene ratio | Nuts, seeds, vegetable oils (corn, soybean, flax, canola) fatty fish, animal products |