Nutritional Assessment

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.

TABLE 86-1


Adapted from: Mehta NM, Corkins MR, Lyman B, et al. Defining pediatric malnutrition: a paradigm shift toward etiology-related definitions. JPEN J Parenter Enteral Nutr 2013; 37 (4):460–81.

Classification Variable Grade Definition
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

WFA, Weight for age; HFA, height for age; WFH, weight for height; SD, standard deviation.

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 .

TABLE 86-2


Adapted from: Grover Z, Ee L. Protein Energy Malnutrition. Pediatr Clin N Am 2009; 56 :1055–68 and UNICEF.

Marasmus Kwashiorkor Marasmic-Kwashiorkor
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.

TABLE 86-3


Adapted from Gibbons T, Fuchs G. Malnutrition: A hidden problem in hospitalized children. Clin Pediatr 2009; 48 :356–61.

Disease Etiology of Malnutrition Special Considerations
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:

  • Height less than 10th percentile for age

  • Weight-for-age plotting less than the 3rd or 5th percentile on Centers for Disease Control and Prevention (CDC)/WHO growth curves

  • Weight-for-height/length plotting less than 3rd or 5th t percentile on the CDC/WHO growth curves

  • Change in more than two standard deviations on the growth curve over a 3- to 6-month period

  • Decreased growth velocity where weight falls more than two major percentile curves over 3 to 6 months

  • >= 5% weight loss 5% or greater weight loss from usual body weight

  • 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 ).

TABLE 86-4


References: Traub S, Basic Skills in Interpreting Laboratory Data, second edition. Bethesda, Maryland: American Society of Health-systems Pharmacists, 1996. Bakerman S, Bakerman P, Strausbauch P. ABC’s of Interpreting Lab data. fourth edition; Phoenix, Arizona: Century Graphics; 2002. Institute of Medicine, Food and Nutrition Board. Editors Otten J, Hellwig J. Meyers L. Dietary reference Intakes, 10th edition. Washington DC: The National Academies Press; 2006 .

Vitamin/Mineral Mechanisms Symptoms of Deficiency Excess Diagnosis Food Sources
B vitamins (water soluble) B1
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

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Jul 24, 2019 | Posted by in GASTROENTEROLOGY | Comments Off on Nutritional Assessment

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