# 16 - 345 Malnutrition and Nutritional Assessment

### 345 Malnutrition and Nutritional Assessment

copper plays a role in iron metabolism, melanin synthesis, energy 
production, neurotransmitter synthesis, and CNS function; the syn­
thesis and cross-linking of elastin and collagen; and the scavenging of 
superoxide radicals. Dietary sources of copper include shellfish, liver, 
nuts, legumes, bran, and organ meats.
Deficiency 
Dietary copper deficiency is relatively rare, although 
it has been described in premature infants who are fed milk diets 
and in infants with malabsorption (Table 344-2). Copper-deficiency 
anemia (refractory to therapeutic iron) has been reported in patients 
with malabsorptive diseases and nephrotic syndrome and in patients 
treated for Wilson’s disease with chronic high doses of oral zinc, which 
can interfere with copper absorption. Menkes kinky hair syndrome is 
an X-linked metabolic disturbance of copper metabolism character­
ized by intellectual disability, hypocupremia, and decreased circulating 
ceruloplasmin (Chap. 425). This syndrome is caused by mutations in 
the copper-transporting ATP7A gene. Children with this disease often 
die within 5 years because of dissecting aneurysms or cardiac rupture. 
Aceruloplasminemia is a rare autosomal recessive disease character­
ized by tissue iron overload, mental deterioration, microcytic anemia, 
and low serum iron and copper concentrations.
The diagnosis of copper deficiency is usually based on low serum 
levels of copper (<65 μg/dL) and low ceruloplasmin levels (<20 mg/
dL). Serum levels of copper may be elevated in pregnancy or stress con­
ditions since ceruloplasmin is an acute-phase reactant and 90% of cir­
culating copper is bound to ceruloplasmin. It has been suggested that 
mild or subclinical copper deficiency is more common than expected; 
at-risk individuals include patients with cholestasis or chronic diar­
rheal diseases, dialysis patients, and people on long-term zinc supple­
ments. The role of copper in cardiovascular disease, immune function, 
bone health, or neurodegenerative diseases is still unclear.
Toxicity 
Copper toxicity is usually accidental (Table 344-2). In 
severe cases, kidney failure, liver failure, and coma may ensue. In Wil­
son’s disease, mutations in the copper-transporting ATP7B gene lead 
to accumulation of copper in the liver and brain, with low blood levels 
due to decreased ceruloplasmin (Chap. 427). A potential negative role 
of copper in the pathogenesis of Alzheimer’s disease has been reported.
■
■SELENIUM
Selenium, in the form of selenocysteine, is a component of the enzyme 
glutathione peroxidase, which serves to protect proteins, cell mem­
branes, lipids, and nucleic acids from oxidant molecules. As such, 
selenium is being actively studied as a chemopreventive agent against 
certain cancers, such as prostate cancer. However, it remains unclear 
whether selenium is effective as a chemopreventive agent or whether 
it increases cancer risk (e.g., prostate cancer). Convincing evidence for 
a protective effect of selenium on cognitive decline or cardiovascular 
disease risk is presently lacking. Selenocysteine is also found in the 
deiodinase enzymes, which mediate the deiodination of thyroxine to 
triiodothyronine (Chap. 394). Rich dietary sources of selenium include 
seafood, muscle meat, and cereals, although the selenium content of 
cereal is determined by the soil concentration. Countries with low soil 
concentrations include parts of Scandinavia, China, and New Zealand. 
Keshan disease is an endemic cardiomyopathy found in children and 
young women residing in regions of China where dietary intake of 
selenium is low (<20 μg/d). Concomitant deficiencies of iodine and 
selenium may worsen the clinical manifestations of cretinism. Chronic 
ingestion of large amounts of selenium leads to selenosis, character­
ized by hair and nail brittleness and loss, garlic breath odor, skin rash, 
myopathy, irritability, and other abnormalities of the nervous system.
■
■CHROMIUM
Chromium potentiates the action of insulin in patients with impaired 
glucose tolerance, presumably by increasing insulin receptor–medi­
ated signaling, although its usefulness in treating type 2 diabetes is 
uncertain. In addition, improvement in blood lipid profiles has been 
reported in some patients. The usefulness of chromium supplements 
in muscle building has not been substantiated. Rich food sources of 
chromium include yeast, meat, and grain products. Chromium in the 

trivalent state is found in supplements and is largely nontoxic; however, 
chromium-6 is a product of stainless steel welding and is a known pul­
monary carcinogen as well as a cause of liver, kidney, and CNS damage.

■
■MAGNESIUM
See Chap. 421.
■
■FLUORIDE, MANGANESE, AND ULTRATRACE 
ELEMENTS
An essential function for fluoride in humans has not been described, 
although it is useful for the maintenance of structure in teeth and 
bones. Adult fluorosis results in mottled and pitted defects in tooth 
enamel as well as brittle bone (skeletal fluorosis).
Manganese and molybdenum deficiencies have been reported in 
patients with rare genetic abnormalities and in a few patients receiv­
ing prolonged total parenteral nutrition. Several manganese-specific 
enzymes have been identified (e.g., manganese superoxide dismutase). 
Deficiencies of manganese have been reported to result in bone demin­
eralization, poor growth, ataxia, disturbances in carbohydrate and lipid 
metabolism, and convulsions.
Ultratrace elements are defined as those needed in amounts <1 mg/d. 
Essentiality has not been established for most ultratrace elements, 
although selenium, chromium, and iodine are clearly essential 
(Chap. 394). Molybdenum is necessary for the activity of sulfite and 
xanthine oxidase, and molybdenum deficiency may result in skeletal 
and brain lesions.
■
■FURTHER READING
Combs GF Jr, Mcclung JP: The Vitamins: Fundamental Aspects in 
CHAPTER 345
Nutrition and Health, 6th ed. London, Academic Press, 2022.
DeAngelo SL et al: Selenoproteins and tRNA-Sec: Regulators of can­
cer redox homeostasis. Trends Cancer 9:1006, 2023.
Fan D et al: Cell signaling pathways based on vitamin C and their appli­
cation in cancer therapy. Biomed Pharmacother 162:114695, 2023.
Imdad A et al: Vitamin A supplementation for preventing morbid­
Malnutrition and Nutritional Assessment 
ity and mortality in children from six months to five years of age. 
Cochrane Database Syst Rev 3:CD008524, 2022.
Lassi ZS et al: Zinc supplementation for the promotion of growth 
and prevention of infections in infants less than six months of age. 
Cochrane Database Syst Rev 4:CD010205, 2020.
Mechanick JI et al: Clinical practice guidelines for the perioperative 
nutrition, metabolic, and nonsurgical support of patients undergoing 
bariatric procedures–2019 update. Surg Obes Relat Dis 16:175, 2020.
Ota Y et al: Comprehensive review of Wernicke encephalopathy: 
Pathophysiology, clinical symptoms and imaging findings. Jpn J 
Radiol 38:809, 2020.
Staub E et al: Enteral zinc supplementation for prevention of morbid­
ity and mortality in preterm neonates. Cochrane Database Syst Rev 
3:CD012797, 2021.
Charles Chin Han Lew, Charlene W. Compher

Malnutrition and 

Nutritional Assessment
Malnutrition occurs in 30–50% of hospitalized patients depending 
on the setting, the patient’s diagnosis, and the criteria that are used to 
diagnose malnutrition. Notable adverse outcomes associated with mal­
nutrition include poor wound healing, compromised immune status, 
and impaired organ function. These can lead to increased length of 
hospital stay, readmissions, higher mortality, and increased health care 
costs. It is now widely appreciated that acute or chronic inflammation

At risk for malnutrition
 
Use validated screening tools
Risk screening
Diagnostic
Assessment
Assessment criteria
 
Phenotypic
 
 
Non-volitional weight loss
 
 
Low body mass index
 
 
Reduced muscle mass
 
Etiologic
 
 
Reduced food intake or assimilationa
 
 
Disease burden/inflammatory conditionb
Diagnosis
Meets criteria for malnutrition diagnosis
 
Requires at least 1 Phenotypic criterion and
 
1 Etiologic criterion
Severity
Grading
Determine severity of malnutrition
 
Severity determined based on Phenotypic
 
criterion
FIGURE 345-1  Global Leadership Initiative on Malnutrition (GLIM) diagnostic 
scheme for screening, assessment, diagnosis, and grading of malnutrition. a≤50% 
of energy requirement >1 week, or any reduction for >2 weeks, or any chronic 
gastrointestinal condition that adversely impacts food assimilation or absorption. 
bAcute disease/injury (e.g., major infection, burns, trauma or closed head injury) or 
chronic disease (e.g., malignant disease, chronic obstructive pulmonary disease, 
congestive heart failure, chronic renal disease or any disease with chronic or 
recurrent inflammation) or C-reactive protein may be used as a supportive laboratory 
measure (mild inflammation: 3.0-9.9 mg/L, moderate inflammation: 10-50 mg/L, severe 
inflammation: >50 mg/L). (Reproduced with permission from Jensen GL et al: GLIM 
criteria for the diagnosis of malnutrition: A consensus report from the global clinical 
nutrition community. JPEN J Parenter Enteral Nutr 43:32, 2019, Figure 1.)
PART 10
Disorders of the Gastrointestinal System
contributes to the pathophysiology of malnutrition. The presence 
of inflammation can also render historic nutrition parameters, like 
albumin and prealbumin, unreliable. In patients with high levels of 
inflammation, nutrition care is supportive. At moderate or low levels 
of inflammation, nutrition care may be therapeutic in reducing the 
nutritional deficits and improving clinical outcomes.
■
■MALNUTRITION DIAGNOSIS IN CLINICAL 
SETTINGS
Several tools have been used to diagnose malnutrition, such as the Sub­
jective Global Assessment, Mini Nutrition Assessment, and the Acad­
emy of Nutrition and Dietetics and American Society for Parenteral 
and Enteral Nutrition Indicators of Malnutrition. These tools use com­
mon parameters such as dietary intake and weight history, muscle and 
fat loss, body mass index (BMI), and/or physical function to diagnose 
malnutrition. However, nuances between them lead to incomparable 
malnutrition prevalence rates in the literature.
TABLE 345-1  Thresholds for Severity Grading of Malnutrition Into Stage 1 (Moderate) and Stage 2 (Severe) Malnutrition
WEIGHT LOSS (%)
LOW BODY MASS INDEX (kg/m2)b
REDUCED MUSCLE MASSc
Stage 1/moderate malnutrition (requires 1 
phenotypic criterion that meets this grade)
5%–10% within the past 6 months, or 
10%–20% beyond 6 months
Stage 2/severe malnutrition (requires 1 
phenotypic criterion that meets this grade)
>10% within the past 6 months, or 
>20% beyond 6 months
aSeverity grading is based on the noted phenotypic criteria, whereas the etiologic criteria described in the text and Figure 345-1 are used to provide the context to guide 
intervention and anticipated outcomes. bFurther research is needed to secure consensus reference body mass index for Asian populations in clinical settings. cFor example, 
appendicular lean mass index (kg/m2) by dual-energy absorptiometry or corresponding standards using other body composition methods such as bioelectrical impedance 
analysis, computed tomography, or magnetic resonance imaging. When not available or by regional preference, physical examination or standard anthropometric measures 
such as mid-arm muscle or calf circumferences may be used. Functional assessments such as hand-grip strength may be used as a supportive measure.
Source: Reproduced with permission from Jensen GL et al: GLIM criteria for the diagnosis of malnutrition: A consensus report from the global clinical nutrition community 
JPEN J Parenter Enteral Nutr 43:32, 2019, Table 4.

In 2019, four international nutrition societies introduced the Global 
Leadership Initiative on Malnutrition (GLIM) consensus criteria for 
diagnosing malnutrition in adults (Fig. 345-1). GLIM incorporates 
broadly available nutrition parameters that are commonly used in other 
diagnostic tools to enable data from these earlier assessment methods 
to be described in the GLIM framework. To diagnose malnutrition and 
its severity, GLIM requires one etiologic criterion (inflammation/
disease burden or reduced food intake/assimilation) and one phenotypic 
criterion (weight loss, low BMI, or reduced muscle mass) (Table 345-1). 
To facilitate the diagnosis of malnutrition in settings with variable 
availability and expertise of personnel and equipment across clinical 
settings, several options are suggested for the phenotypic criterion. 
The phenotypic criterion is used to define the severity of malnutrition. 
Recent publications highlight GLIM’s widespread adoption in hospitals 
and clinical settings, showing predictive value for adverse outcomes.
■
■NUTRITION ASSESSMENT FOR PROTEINCALORIE MALNUTRITION
The Nutrition Care Process in the hospital setting involves screening 
for malnutrition risk, comprehensive nutrition assessment of patients 
at malnutrition risk, development of a nutrition care plan, and moni­
toring for needed adjustments to the plan. Screening for the risk of 
malnutrition is typically undertaken by the bedside nurse or by a clini­
cal dietitian using validated tools such as the Malnutrition Screening 
Tool, Malnutrition Universal Screening Tool, Nutritional Risk Screen­
ing 2002, or other in-house tools. A comprehensive nutrition assess­
ment includes a review of medical, surgical, and social history; dietary 
intake and weight history; medication profile; available laboratory, 
diagnostic tests, body composition, and anthropometric measures; and 
nutrition-focused physical examination. The clinical dietitian designs 
an individualized intervention and monitoring plan for the patient. 
The nutrition assessment findings and care plan are shared with the 
physician who may make a malnutrition diagnosis and prescribe the 
recommended nutrition care plan. The response to nutrition therapy is 
monitored with adjustments to the care plan as needed. Micronutrient 
deficiencies of clinical relevance may be detected in association with 
malnutrition, but a detailed discussion of their assessment is beyond 
the scope of this chapter (see Chap. 344).
In ambulatory clinic settings, physicians may have less access to 
dietitian support than in inpatient settings. However, the GLIM criteria 
are designed to be feasible even in an outpatient setting. Nurses can 
obtain measures of height and weight (for BMI) and calf or arm cir­
cumference to assess muscle mass. A diagnosis of malnutrition can be 
made in the clinic with referral of the patient to a dietitian for a detailed 
nutrition assessment and development of a care plan.
■
■COMPONENTS OF A DETAILED NUTRITIONAL 
ASSESSMENT
Medical/Surgical History and Clinical Diagnosis 
The risk 
of malnutrition varies widely across medical/surgical diagnoses and 
clinical settings. During the early stages of diseases, malnutrition may 
be less likely than with disease progression. Knowledge of a patient’s 
PHENOTYPIC CRITERIAa
<20 if <70 years, <22 if ≥70 years
Mild-to-moderate deficit (per validated 
assessment methods; see below)
<18.5 if <70 years, <20 if ≥70 years
Severe deficit (per validated 
assessment methods; see below)

medical/surgical history and associated clinical diagnoses is especially 
helpful in discerning the likelihood of malnutrition and inflamma­
tion. Several conditions or diseases are characterized by severe acute 
inflammatory response (e.g., critical illness), whereas others are more 
typically associated with a chronic inflammatory response that is mild 
to moderate in severity (e.g., chronic cardiometabolic, oncologic, or 
gastrointestinal disease, or organ failure) and may be relapsing and 
remitting. It is common for acute inflammatory events to be superim­
posed on patients with chronic conditions; for example, a patient with 
chronic renal disease may be admitted to the hospital with sepsis, such 
that the acute increase in inflammation should be time-limited while 
the chronic inflammation will continue.
The inflammatory milieu, especially when severe, may modify 
nutrient requirements by elevating resting energy expenditure and 
promoting anabolic resistance and catabolism in muscle. Inflamma­
tion also promotes anorexia, decreases food intake, and further com­
promises nutritional status. A deteriorating course may result because 
severe inflammation may reduce the benefit of nutritional interven­
tions to being supportive rather than therapeutic, and the associated 
malnutrition may diminish the effectiveness of medical therapies.
It is also imperative to recognize medical/surgical conditions that 
place patients at increased risk of becoming malnourished because 
they have increased nutritional requirements or compromised intake 
or assimilation. Chronic gastrointestinal disease, even if relapsing and 
remitting, may limit nutrient assimilation. Therefore, patients with 
seemingly adequate oral intake may still be at risk of malnutrition due 
to compromised nutrient assimilation.
Clinical Signs and Physical Examination 
Nonspecific clinical 
indicators of inflammation include fever, hypothermia, and tachy­
cardia. The nutrition-focused physical examination should identify 
edema as well as physical signs of weight gain/loss. Physical findings 
of weight loss associated with decreased muscle and subcutaneous fat 
mass should be noted. If edema is present, an estimation of dry weight 
may be needed to identify actual weight loss.
Anthropometric Data 
Nonvolitional weight loss is a well-val­
idated nutrition parameter associated with underlying disease or 
inflammation. The degree and duration of nonvolitional weight loss 
determine its clinical significance. A 5–10% loss of body weight over 
6 months is clinically relevant, whereas >10% loss over the same dura­
tion is severe.
The trend in body weight may be obtained from patients, their 
family or caregivers, and the medical record. Obtaining body weight 
at each clinic, emergency department, and hospital visit will support 
efforts to detect changes in this important parameter. Training staff 
members to weigh patients consistently without shoes and heavy outer 
garments and maintaining scales and stadiometers in good calibration 
facilitate acquisition of trustworthy weight data. Clinical sites may 
maintain chair or bed scales for patients who cannot stand. Height may 
be estimated by doubling the arm span measurement from the sternal 
notch to the end of the longest finger or by measurement of knee height 
using a caliper.
BMI, defined as weight (kg)/height (m2), is used primarily to screen 
for overweight or obesity. The National Institutes of Health/World 
Health Organization BMI categories for adults are as follows: BMI 
<18.5 kg/m2 = underweight, BMI 18.5–24.9 kg/m2 = desirable, BMI 
25.0–29.9 kg/m2 = overweight, and BMI ≥30 kg/m2 = obese. Note that 
patients of any BMI status can be malnourished. Overweight or obese 
patients can be malnourished due to weight loss or loss of muscle 
mass (e.g., sarcopenic obesity). Similarly, being underweight does not 
equate to malnutrition. BMI <18.5 kg/m2 is infrequent in economically 
developed countries.
Classical anthropometric measurements such as arm and calf cir­
cumference can be helpful. However, measuring the calf circumfer­
ence may be more accessible as it requires less specialized training in 
comparison to measuring the arm circumference. Additionally, calf 
circumference has established cutoff values validated for various BMI 
ranges and ethnicities. Clinically available body composition mea­
sures include bioelectrical impedance analysis (BIA), dual-energy x-ray 

absorptiometry (DXA), and air displacement plethysmography (Table 
345-2). BIA has the advantage of being portable and is used for patients 
in diverse clinical settings. Abdominal computed tomography (CT) 
and magnetic resonance imaging (MRI) taken for disease diagnostic 
purposes can be interpreted to measure muscle mass, though they are 
not routinely used to aid in the diagnosis of malnutrition.

Laboratory Indicators 
There is, unfortunately, no biomarker 
descriptive of comprehensive nutritional status. Laboratory findings 
(Table 345-2) should be evaluated in combination with other assess­
ment parameters to appropriately diagnose malnutrition. Albumin and 
prealbumin are often available in patients with suspected malnutrition; 
however, these measures have poor sensitivity and specificity as indi­
cators of malnutrition. Albumin and prealbumin are negative acutephase reactants with levels that are reduced by the systemic response 
to injury, disease, or inflammation. C-reactive protein, a positive acutephase reactant, may be useful to identify the presence of inflammation, 
particularly if the clinical context is unclear about the extent of inflam­
mation. Trends in repeated levels of C-reactive protein over time may 
help to clarify the extent and trajectory of the inflammatory challenge. 
Research suggests that interleukin 6, and perhaps other cytokines, may 
offer promise as indicators of inflammatory status. Nonspecific labora­
tory indicators that are often associated with inflammatory response 
include leukocytosis and hyperglycemia. Additional tests that may 
be obtained to help confirm the presence of inflammatory response 
include 24-h urine urea nitrogen and indirect calorimetry to measure 
energy expenditure. In the setting of a severe acute systemic inflamma­
tory response, negative nitrogen balance and elevated resting energy 
expenditure are anticipated.
CHAPTER 345
Diet History 
Brief diet surveys are available to target specific 
aspects of the diet, such as food patterns, to prevent disease or track 
intake of nutrients of key importance such as calcium, vitamin D, and 
phosphorus for bone disease management. However, more specific 
information about the adequacy of intake of key nutrients or food 
patterns relative to estimated requirements is most often obtained 
by consultation with a clinical dietitian. Since patients often present 
to health care practitioners with acute medical events superimposed 
upon chronic health conditions, it is common for patients to have had 
decreased food intake and progressive malnutrition for extended peri­
ods prior to assessment. Therefore, compromised dietary intake must 
not be overlooked so that appropriate intervention may be undertaken.
Malnutrition and Nutritional Assessment 
Assessment of the adequacy of nutritional intake must include oral 
nutrition supplements, enteral tube feedings, and parenteral nutrition 
both during hospitalization and as a component of home nutrition 
support. Ongoing reassessment of actual intake received by the patient 
is undertaken in hospital settings, most commonly by the clinical 
dietitian, the bedside nurse, and the nutrition support team if available. 
Changes in the adequacy of oral intake, body weight, or tolerance to 
enteral or parenteral feedings would all require adjustment of the feed­
ings to optimize patient care.
A comprehensive assessment should also include a review of medi­
cations, vitamin/mineral supplements, or herbal remedies with atten­
tion to undesirable nutrition-sensitive side effects such as anorexia, 
dysgeusia, oral mucositis, nausea, vomiting, diarrhea, and constipation. 
Potential drug–nutrient interactions should also be identified to enable 
alternative therapeutic options.
Functional Outcomes 
Advanced malnutrition is accompanied 
by declines in muscle mass and function that can be detected by 
various functional test outlined in Table 345-2. Among them, hand­
grip strength may have better clinical utility since it is easily assessed 
and helps to identify which patients benefit most from individualized 
nutritional support.
In summary, malnutrition puts patients at risk of adverse outcomes. 
Therefore, timely diagnosis and treatment of malnutrition should be 
provided to improve patient outcome. Robust evidence exists dem­
onstrating that a multipronged approach to malnutrition intervention 
reduces mortality and holds promise to improve the quality of life of 
patients.

PART 10
Disorders of the Gastrointestinal System
TABLE 345-2  Common Body Composition Studies, Laboratories, and Other Studies Used in Nutrition Assessment
TEST
NOTES
Body Composition Studies (Recommended)
Air plethysmography
May be used to assess body composition. It comprises a dual-chamber, sealed compartment containing an oscillating 
diaphragm, which allows it to measure body volume using Poisson’s law, and compute fat mass and fat-free mass. However, 
its validity in a racially diverse population needs further studies, and it is not readily available in most hospitals.
Bioelectrical impedance analysis (BIA)
A promising method to assess body composition as the equipment is easily portable. It uses the opposition of an electrical 
current through body tissues (i.e., impedance) and population-specific equations to estimate total body water and body 
composition. BIA equations are highly device and population specific. Fever, some medications, and fluid/electrolyte 
disturbances can influence its precision and accuracy.
Calf circumference
A practical and valid clinical estimate of skeletal muscle mass, in which low calf circumference indicates muscle loss. 
Ethnic specific reference ranges are available, and measurements should be adjusted in persons with body mass index 
different from the normal range (underweight, overweight, or obese). The technique requires less training than mid-upper arm 
circumference.
Dual energy x-ray absorptiometry 
(DXA)
May be used to assess regional and total fat mass in a diverse group of adult clinical patients. However, its validity in 
assessing muscle mass is unclear.
Imaging with computed tomography 
(CT) or magnetic resonance imaging 
(MRI)
May be used to quantify fat and fat-free mass when scans are taken for other diagnostic purposes. Both are costly, and CT 
entails x-ray exposure.
Mid-upper arm circumference
Mid-upper arm circumference is the circumference of the upper arm measured at the midpoint between the olecranon 
process and the acromion process. It estimates both muscle and subcutaneous fat stores, but references are population 
specific. Take note that this measurement technique requires reliability training.
Ultrasound
A promising method to assess body composition as the equipment is easily portable. It uses high-frequency sound waves to 
capture live images of muscle tissues. Since most studies examined a single muscle, it is unclear if results can be extrapolated 
to reflect overall nutritional status. More research is needed to establish standardization of measurement protocol.
Laboratory Tests and Other Studies (Recommended)
Complete blood count with differential
May be used to screen for nutritional anemias (iron, B12, and folate deficiencies) and thrombocytopenia (vitamin C and folate 
deficiencies).
C-reactive protein (CRP)
May be used to confirm systemic inflammation. While inflammation may be associated with malnutrition, CRP lacks specificity 
as a biomarker for diagnosing malnutrition. Nevertheless, when combined with other nutrition assessment methods, CRP can 
complement the diagnostic process for malnutrition. In addition, elevated levels may be associated with reduced food intake 
and a lack of response to nutritional interventions.
Indirect calorimetry
May be used to determine resting energy expenditure (REE) to aid in determining caloric intake goal. Predictive equations that 
were based on REE measures in specific populations are also used to estimate REE, especially when indirect calorimetry is 
not available.
Nitrogen balance (NB)
May be used to reflect the degree of catabolism and adequacy of protein replacement delivery in patients with normal renal 
and liver function. Method requires collection of 24-h urine. Nitrogen balance = (protein delivery [g]/6.25) − (urinary urea 
nitrogen + 4 insensible losses).
Specific micronutrients
May be used to validate clinical symptoms of micronutrient deficiencies. Exercise caution with interpretation since levels can 
be influenced by acute illness.
Laboratory Tests and Other Studies (Not Recommended)
Blood urea nitrogen (BUN), serum 
creatinine
Not recommended as malnutrition indicators. Although low BUN and serum creatinine may reflect reduced muscle mass, their 
levels are influenced by factors unrelated to malnutrition (e.g., renal and hepatic insufficiency).
Cholesterol
Not recommended as a malnutrition indicator. While becoming hypocholesterolemic (<120 mg/dL) during hospitalization 
may be linked to poorer clinical outcomes, insufficient evidence supports its use for diagnosing malnutrition and evaluating 
nutritional interventions.
Creatinine height index (CHI)
Not recommended as a malnutrition indicator. CHI = (24-h urinary creatinine excretion/ideal urinary creatinine for gender and 
height) × 100. Although urinary creatinine excretion reflects muscle mass, it can be influenced by renal insufficiency, meat 
consumption, physical activity, and trauma. Requires accurate 24-h urine collection.
Cytokines
Not recommended as malnutrition indicators. Their cutoff values and role as an indicator of inflammatory status are still being 
studied.
Electrocardiogram
Not recommended as a malnutrition indicator. Although prolonged QT interval may be present in severely malnourished 
patients, the former can be influenced by factors unrelated to malnutrition.
Fecal fat test
May be used to validate clinical symptoms of fat malabsorption. It reflects the percentage of dietary fat that the body does not 
absorb. Requires stool samples collected over 72 h during ingestion of high-fat diet.
Serum proteins (albumin, prealbumin, 
transferrin, and retinol-binding protein)
Not recommended as a malnutrition indicator. Their levels are influenced by factors other than malnutrition (e.g., systemic 
inflammation, hepatic and renal insufficiency, protein-losing enteropathies, corticosteroids, hydration, and iron status), 
reducing their specificity in diagnosing malnutrition and evaluating nutritional interventions. However, they remain valuable for 
predicting clinical outcomes.
Skin testing—recall antigens
Not recommended as a malnutrition indicator. Although delayed hypersensitivity is associated with malnutrition, the former 
can be influenced by factors unrelated to malnutrition.
Total lymphocyte count
Not recommended as malnutrition indicator. Low levels are influenced by factors unrelated to malnutrition.
Urine 3-methylhistidine
Not recommended as a malnutrition indicator. Although it reflects muscle mass, its level is influenced by meat intake and 
poorly reflects changes in body protein stores. Requires accurate 24-h urine collection
(Continued)