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276 BASIC SKILLS IN INTERPRETING LABORATORY DATA
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TABLE 12-1. Prevalence of Sarcopenia Among
Patient Populations Based on Recent Clinical
Studies
PATIENT POPULATION PREVALENCE (%)
Older adults
60–70 years old 5–13
≥ 80 years old 11–50
Adult patients admitted to medical
5–25
and surgical oors
Adult patients admitted to the ICU 60–70
Patients with cancer 15–60
TABLE 12-2. ICD-10 codes for Malnutrition
CODES DESCRIPTION
E40 Kwashiorkor
E41 Nutritional marasmus
E42 Marasmic kwashoikor
E43 Unspecied severe protein- calorie malnutrition
E44 Protein-
mild degree
E45 Retarded development following protein-
malnutrition
E46 Unspecied protein-
e current etiology- based disease denition accepted in the
eld of nutrition is that malnutrition is a syndrome that includes
chronic starvation without inammation (eg, anorexia nervosa
or major depression with lack of interest in eating); chronic
disease- associated malnutrition, when inammation is chronic
and of mild to moderate degree (eg, organ failure, pancreatic
cancer, rheumatoid arthritis, or sarcopenic obesity); and acute
disease or injury- associated malnutrition, when inammation is
acute and of severe degree (eg, major infection, burns, trauma,
or closed head injury).11 Since 2016, a group of international
researchers have come together and started a workgroup called
Global Leadership Initiative on Malnutrition (GLIM). is
group aims to develop a consensus- based framework to dene,
describe, and record the occurrence of malnutrition that would
be applicable worldwide.
Inammation is an important component in the current/
modern denition of malnutrition. Inammation alters food
intake, nutrition absorption, and/or assimilation and leads to
altered body composition and impairs certain biological functions.14 Inammation is a critical pathophysiological process
that leads to or accelerates the loss of lean body mass and muscle size (ie, sarcopenia) and cellularity. Chronic inammation
may progress to severe functional loss, and increases morbidity
and mortality. erefore, identifying the presence and severity
of inammation is crucial to the screening, characterization,
calorie malnutrition of moderate and
calorie
calorie malnutrition
13
and assessment of malnutrition as well as developing a patientspecic therapeutic plan to reverse malnutrition and functional
loss. It also aects what monitoring parameters, including laboratory surrogate markers, are more accurate and specic for
monitoring progress and response toward nutritional interventions. Laboratory tests that are signicantly impacted by inammation may not accurately reect a person’s nutritional status
and, therefore, are unreliable nutritional markers.
Serum visceral protein concentrations, such as albumin,
prealbumin, transferrin, and retinol binding protein, have been
extensively used as laboratory markers for malnutrition since the
15,16
1970s.
Each of these serum proteins has dierent physiologic
characteristics (Table12-3). However, the regulation, synthesis,
and degradation of these serum proteins are all aected by other
factors in addition to decreased nutrient intake. End organ dysfunction, specic nutrient deciency, and inammation all have
a direct impact on the homeostasis of these compounds. With
the current knowledge that malnutrition is associated with an
inammatory state, none of these visceral proteins is a sensitive or specic marker in the clinical assessment of a patient’s
nutritional status and response to nutrition therapy. ey should
not be used for nutritional assessment. e history of each of
the visceral proteins as a nutrition marker and their respective
limitations are discussed next.
SERUM ALBUMIN
Albumin is a major serum protein that is exclusively synthesized in the liver. Its primary functions include maintaining colloidal osmotic pressure for plasma, serving as the carrier and
binding protein for many physiologic compounds (eg, bilirubin;
long- chain fatty acids; divalent cations such as calcium, magnesium and zinc; bile acids; vitamin D; sex hormones; cortisol;
thyroxine; and catecholamines) and drugs, maintaining acid–
base balance for plasma, and providing important extracellular antioxidant function of the plasma to scavenge free radicals
generated under normal physiology.
albumin is ~280g for an average adult, as determined by tracer
method. Of the total albumin pool, ~40% is found in the intravascular space and the rest is distributed in the interstitial space
of dierent vital organs, such as muscle, connective tissues, and
skin. e average hepatic synthetic rate of albumin for a healthy
adult is ~150 mg/kg/day (~10 to 15 g/day). e average total
body turnover time is ~25 days.
renal and gastrointestinal (GI) loss of albumin should be less
than 6% and 10% of the total body albumin pool, respectively.
e rest of the turnover mechanism is not fully understood.
Some studies have suggested that albumin undergoes degradation in the extravascular compartment.20 When the synthetic
and removal rate of albumin is at steady state, the serum albumin concentration is maintained between 3.5 and 4 g/dL.
With its hepatic origin and the early studies linking its serum
changes with kwashiorkor, it has been assumed historically that
serum albumin concentration reects a person’s nutritional
status given the liver is the primary organ for plasma protein
synthesis.
21,22
In 1977, it was rst suggested by Blackburn et al
that serum proteins, including albumin and transferrin, could
17,18
e estimated total body
18,19
Under normal physiology,
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TABLE 12-3. Summary of General Physiologic Functions and Serum Half-Lives of Visceral Proteins Used
Historically as Nutrition Markers
VISCERAL PROTEIN
AND NORMAL RANGE
Albumin
(3.5–4.5 g/dL)
Transferrin
(200–350 mg/dL)
Prealbumin
(15–36 mg/dL)
Retinol-binding protein
(40–60 mcg/mL)
SERUM HALF- LIFE (UNDER
NORMAL PHYSIOLOGY) PRIMARY FUNCTIONS
14–20 days Maintaining oncotic pressure of
plasma
Transporting a number of divalent
FACTORS THAT AFFECT
PLASMA CONCENTRATION
Inammation
Liver disease
Pregnancy
cations (eg, calcium)
Transporting a number of
peptide hormones and biological
compounds
Serving as an antioxidant molecule
10 days Transporting iron Inammation
Iron deciency
Kidney disease
Pregnancy
Dehydration
2–3 days Transporting thyroxine in the
plasma and across the blood–brain
barrier
Inammation
Liver disease
Kidney disease
Serving as a carrier protein for
retinol-
12 hr Transporting vitamin A,
specically retinol
binding protein
Inammation
Vitamin A status
Prealbumin
Kidney disease
be used as a marker of nutritional assessment for hospitalized
patients.23 With a number of studies published shortly aer that
also demonstrating a correlation between serum albumin concentration and prognosis of hospitalized patients, serum albumin was widely suggested as a clinical marker of malnutrition.
In their retrospective study involving 500 consecutively admitted patients, Seltzer and colleagues showed that patients with
a serum albumin concentration <3.5 g/dL on admission had
statistically signicant higher complication rates (33% versus
7.3%) and mortality rates (0.8% versus 0%) for that hospital stay.
Compared with patients with serum albumin >3.5 g/dL, those
with hypoalbuminemia were associated with a 4- fold increase
in complications and a 6- fold increase in deaths. When the
data were further compared between surgical versus nonsurgical
patients, hypoalbuminemia was associated with a 9.7times higher
mortality rate for nonsurgical patients. Based on their ndings,
the authors called for using serum albumin as an “instant nutritional assessment information” that should be used for every
hospital admission.
24
In the following year, a pivotal trial by
Rheinhart et al showed a negative linear correlation between
serum albumin concentration and 30- day mortality in 509 adult
patients with hypoalbuminemia.25 e hospital mortality rate for
those with albumin <2.1 g/dL was more than 10 times higher
than for patients with albumin <3.4 g/dL. ese ndings paved
the way in making serum albumin a routine laboratory test in
assessing nutritional status of patients.
Contemporary research in clinical nutrition and metabolism
has signicantly increased our understanding of the pathophysiology of malnutrition and the physiological response to feeding.
It is now clear that although serum albumin concentration may
have a prognostic value in predicting survival, it is not a valid
surrogate marker of total muscle mass or clinical response to
feeding. Increased vascular permeability, changes in interstitial
volume, and systemic inammation can alter serum albumin
concentration independent of liver function, nutrient intake,
and nutrient utilization. us, it should not be used as a clinical
marker for a patient’s nutritional status.
15
Hypoalbuminemia is a common presentation in hospitalized
patients, especially among individuals who are critically ill. Multiple factors may contribute to decreased serum albumin concentration. e most important driving factor is inammation
associated with an acute phase response. Acute phase response
may occur in acute illnesses (eg, trauma, sepsis, pancreatitis)
and ongoing, uncontrolled chronic diseases (eg, gout, heart failure, inammatory bowel disease, autoimmune diseases). In both
situations, it is associated with increased plasma and cellular
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concentrations of proinammatory cytokines (eg, tumor necrosis factor, interleukin-6). e inammatory process can also be
conrmed by the presence of nonspecic surrogate markers of
inammation, such as an elevated C- reactive protein concentration in the plasma.
It is proposed that inammation aects serum albumin
in at least three dierent mechanisms: (1) increased capillary
permeability and leak resulting in serum albumin leaving the
intravascular compartment to the interstitium; (2) hepatic repri
oritization of protein synthesis— a process in which the liver
increases the synthesis of other proteins and compounds essential for host defense and survival over visceral proteins such as
albumin and transferrin; (3) increased degradation to immediately increase the free concentrations of hormones, cytokines,
and other vital peptides available in the plasma to promote healing and recovery of the body as well as be recycled aer serving
specic physiologic functions, such as oxidation, glycation, or
binding of other highly reactive substances that may be harmful to cells and tissues.
15,18,26-28
ese mechanistic explanations
are consistent with clinical observations. In fact, serum albumin concentration falls quickly shortly aer injuries and acute
illnesses. For example, in the pivotal study published by Rheinhart et al, the lowest serum albumin concentration was recorded
in 48.9% of the patients within 1 week of hospital admission.25
In an ICU study with nine mild- to- moderate critically ill adults
(mean APACHE II score 7.5) with hypoalbuminemia, feeding
patients with parenteral nutrition at 35 to 40 kcal/kg/day with 1.2
to 1.6g/kg/day of protein did not change the mean serum albumin concentration (2.0 g/dL to 2.1 g/dL) or extend the shortened
serum half- life of albumin (9.1 days).29 Serum albumin concentration is inversely correlated with C- reactive protein concentration and remains low as long as plasma C- reactive protein
concentration is elevated (Figure12-1).30 ese results indicate
that although albumin consistently shows a positive correlation
with survival, hypoalbuminemia is a more accurate reection of
the magnitude of systemic inammation (and possibly severity
of acute illnesses) experienced by a patient rather than a true,
reliable surrogate marker of a patient’s nutritional status.
A related topic is whether serial serum albumin concentrations can be used to reliably assess a patient’s response to
nutritional interventions and guide therapeutic changes to the
nutrition support regimen. Despite the relatively small num-
-
ber of clinical studies, the results have failed to conrm a positive relationship. For example, Li et al showed that among older
adults undergoing gastric cancer surgery, continuous feeding
by either enteral or parenteral route at 30 kcal/kg/day for up to
7days did not improve serum albumin concentration (3.4 versus
3.1 g/dL on days1 and 7, respectively). e lack of improvement
was likely due to the ongoing, uncontrolled systemic inammation, as reected by the continued increase in serum C- reactive
protein concentration (2.9 to 11.6 mg/L on days1 and 7, respectively).31 Yeh et al also showed that changes in serum albumin
concentration did not correlate with the adequacy of nutrient
delivery and clinical response to feeding in patients in the surgical ICU.32 Overall, serum albumin concentration has not been
shown to be a sensitive marker of energy and protein intake
adequacy, especially in hospitalized patients. Normalization of
serum albumin concentration during the hospital stay or course
of care may merely be a reection of the resolution of inammation (ie, optimal and positive response to the treatment of
the current illness) and does not suggest an improvement of
nutritional status or decreased need for nutrition intervention.
In summary, based on current knowledge and evidence,
serum albumin concentration is signicantly aected by inammation. Hypoalbuminemia in patients is likely a reection of
ongoing and uncontrolled illness involving a heightened inammatory state. Serum albumin concentration does not serve as a
proxy measure of total body protein or total muscle mass and
should not be used to assess nutritional status or guide nutritional intervention.
FIGURE 12-1. Serum albumin concentration is negatively
correlated with C- reactive protein concentration, a
marker of systemic inammation. Data are based on
adult patients admitted to the medical ICU.
30
SERUM PREALBUMIN
Prealbumin, also known as transthyretin, is another visceral
serum protein that has been proposed as a useful laboratory
marker for nutritional assessment. Prealbumin is also a hepatic
plasma protein and is partly catabolized by the kidneys. Its primary functions include transport of thyroid hormones and
retinol- binding protein both in the plasma and across the
blood–brain barrier. It may also play a role in regulating epinephrine availability because it has binding anity for this
neuropeptide.33 Recently, it has also been found to be a major
binding protein for β- amyloid (Aβ) peptide in the brain, suggesting its neuroprotective eect or as a potential treatment target for Alzheimer disease.
e interest of using prealbumin as a nutrition marker can
be traced back to the early 1970s. In 40 hospitalized children
with protein- calorie malnutrition, serum prealbumin concentration was found to be depleted but quickly reversible upon
dietary protein replenishment and with a much faster response
rate than albumin.35 e higher degree of responsiveness in the
34
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normalization of serum concentration can be attributed to its
shorter biological half- life of 2 days, compared with 20 days
for albumin.36 In the following 30 years, numerous studies and
conference proceedings have suggested and even emphasized
the use of prealbumin as the preferred laboratory test to assess
patient nutritional status and guide nutritional interventions.
37,38
One of the major limitations of using prealbumin as a nutrition marker is that it is a negative acute phase reactant. It can
be useful for estimating nutrition risk by identifying patients
whose inammatory state is heightened and can help determine
whether these patients are at an increased risk of poor outcomes
if nutritional intervention is not initiated. Because it is a visceral
transport protein synthesized by the liver, however, it shares
the same characteristics with albumin in response to stress and
inammatory response and thus is subject to the same limitations
as a marker for nutritional status. Under acute stress conditions,
the synthesis of prealbumin is abruptly depressed by a cytokinedirected hepatic reprioritization of metabolic and synthetic processes for plasma proteins as well as a redistribution of organ and
tissue protein pools.
15,33
Additionally, prealbumin concentrations
may be increased in renal dysfunction, corticosteroid therapy,
or dehydration. Studies have also shown that prealbumin concentration does not correlated with anthropometric assessment
ndings in patients with cancer and eating disorders.
39,40
Regarding its role for monitoring nutrition interventions and
guiding nutrient provision, serum prealbumin is also found to be
inconsistent and unreliable as a nutrition marker. Although some
studies have suggested that prealbumin is more sensitive than
transferrin and albumin as an indicator of adequate nutritional
provision, additional studies have showed that prealbumin more
accurately reects systemic inammation rather than adequacy of
calorie and protein provision.
32,41-43
Figure12-2 summarizes the
relationship between plasma concentration of prealbumin and
high- sensitivity C- reactive protein over time for 36 adult patients
in the medical ICU. It shows that while a patient is under a heightened inammatory state on ICU admission, prealbumin concentration is suppressed. As the patient’s clinical status improved and
C-reactive protein concentration dropped to <100 mg/L, prealbumin concentration increased signicantly. However, as these
patients experienced new clinical complications with C- reactive
protein concentration rising once again, their prealbumin con
centration also trended downward despite adequate caloric and
protein provision through nutrition support (Figure12-2).
44
In summary, although prealbumin has been used and continues to be used as a laboratory marker for nutrition assessment
and response to nutritional intervention, more recent knowledge and clinical data show that changes in its serum concentration are more likely related to system inammation. erefore, it
should not be used to assess a patient’s nutritional status. Its role
as a surrogate marker for response to feeding is highly questionable and requires further investigation.
SERUM TRANSFERRIN
Transferrin is another hepatic visceral protein with the primary
function as a carrier protein for iron. Its expression is regulated
by the iron status of the body, with increased expression in
iron deciency. Its use as a nutritional marker dates back in the
1970s. Its serum half- life is approximately 10 days, making it a
more favorable serum marker than album.45 However, it is also
a negative acute phase reactant, and its serum concentration
is increased with renal failure, pregnancy, anemia, and dehydration. Abrupt reduction in serum transferrin concentration
in critically ill patients is common and is caused by inammation and reprioritization of hepatic protein synthesis. Given the
confounders that aect its homeostasis, transferrin is an unreliable marker for nutrition assessment. Studies have also shown
conicting results regarding its change in serum concentration
in response to nutritional interventions.
malnutrition marker or as a marker for nutrition response is
not recommended.
46-49
Its use as a general
-
FIGURE 12-2. Comparison of longitudinal changes
between transthyretin (prealbumin) and C- reactive
protein (n = 36). A negative correlation is found
between serum concentrations of prealbumin and
C- reaction protein. Data based on Chan et al.
OTHER HISTORICAL LABORATORY
MARKERS
Serum Retinol-Binding Protein
e use of retinol- binding protein as a laboratory marker to
assess nutritional status was initially proposed by Ingenbleek
and colleagues in 1975 in a study involving 37 children aged
18 to 30 months. All the patients in the study presented with
protein- calorie malnutrition with clinical presentations including weight loss, growth failure, hair discoloration, skin lesions,
diarrhea, and swollen limbs. Serial serum visceral protein concentrations were measured at baseline and weekly for 3 weeks
aer oral diet treatment was initiated. Serum viscera protein
measured included albumin, transferrin, prealbumin, and
44
retinol- binding protein. Retinol- binding protein was selected
because it binds to prealbumin and has a short biologic half- life
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of approximately 12 hours. It theoretically oers a benet over
prealbumin and transferring by having a faster turnover rate in
detecting responses to feeding. Investigators found that prealbumin and retinol- binding protein had the most pronounced
decline in their plasma concentration at baseline. e serum
recovery rate aer dietary intervention was initiated was comparable between the two proteins. By day22, plasma retinolbinding protein concentration was increased by 3- to 4- fold
from baseline. e authors suggested that retinol- binding protein is a more sensitive marker than albumin and transferrin in
assessing nutritional status.
16
Despite its potential benets over other visceral proteins,
there are an insucient number of high- quality validation
studies to conrm the role of retinol- binding protein in nutritional assessment across dierent patient populations. Additionally, retinol- binding protein is aected by a patient’s
vitamin A status and the presence of inammation.
50,51
Currently, retinol- binding protein concentration should be considered a component of a comprehensive assessment for vitamin
A status rather than a general laboratory marker for nutritional
assessment.
Total Lymphocyte Count
Total lymphocyte count has been used historically as a laboratory marker for nutritional assessment. Seltzer et al showed
that an abnormal total lymphocyte count, dened as <1,500
cell/mm3 of absolute lymphocyte, was associated with 1.8- fold
increase in complications and a 4- fold increase in mortality
among 500 hospitalized patients.24 It is thought that malnutrition, especially protein- calorie malnutrition, may lead to
decreased lymphocyte production by the body; however, this
change is neither sensitive nor specic to malnutrition. Concomitant diseases and a severe stress reaction may also aect
lymphocyte count and bone marrow response. Chronic deciency in specic nutrients, such as hypocupremia from intestinal malabsorption, can also lead to lymphopenia. Although it
continues to be used by some investigators as a marker of nutritional status, a consistent relationship between total lymphocyte
count and malnutrition based on anthropometric assessment or
validated nutrition screening tools is lacking.
52,53
Total lymphocyte count responds slowly to the correction of the nutritional
status, even in the absence of other factors. erefore, it is neither an accurate nor a clinically reliable laboratory marker as a
diagnostic tool for malnutrition for assessment of response to
nutritional support.
Additional Laboratory Tests Used in Clinical
Nutrition
Nitrogen Balance Study
Nitrogen balance study is intended to assess the adequacy of
protein intake and is the most established and accepted clinical
procedure and laboratory assessment for this purpose in current
practice and clinical research. Amino acids are important building blocks for tissues and other vital cellular components, such
as transport proteins and peptide hormones. Protein synthesis
involves the incorporation of an amine group into carbon molecules. By measuring the rate of dietary nitrogen entering and
leaving the body and calculating the dierence in a dened
period, it can help optimize nutritional provision, especially
for daily protein, which can, in turn, help prevent malnutrition
by preserving or increasing body cell mass. Nitrogen balance
study is the technique used to optimize dietary nitrogen (thus
protein) intake.
Nitrogen is primarily eliminated from the body in the urine
and feces. Other minor sources of nitrogen loss include dermal
loss and daily tissue turnover such as from hair, nails, and secretions.54 e nonurinary and fecal loss is generally considered
negligible and clinically insignicant. Because most nitrogen
loss is through the urine in the form of mostly urea but also
as ammonium and creatinine, nitrogen balance study typically
involves collecting 24- hour urine to quantify the urinary urea
nitrogen (UUN). e following is the general equation to deter
mine nitrogen balance:
Nitrogen balance = (Total protein intake in grams/6.25) −
(UUN in grams + 4)
In this equation, UUN is the directly measured value from a
24- hour urine collection. e +4 is added to account for fecal
and other minor sources of nitrogen loss based on historical
data. Daily dietary protein intake in grams per day is divided
by 6.25 because the metabolically active proteins in the human
body, as well as in most dietary proteins, generally contain 16%
nitrogen by weight.
55
Based on the setup of this equation, ideal candidates for accurate nitrogen balance study include patients whose total protein
intake can be fully and accurately quantied, who are preferably
receiving full enteral or parenteral feeding, who have normal
renal function, and who are not experiencing excessive nonurinary nitrogen loss, such as through diarrhea, open wounds, or
GI drainage. In patients with renal insuciency, nitrogen kinetics can be evaluated by analyzing nitrogen content in the dialyzed uid and the rate of change in serum blood urea nitrogen
concentration.
56-59
e details of determining nitrogen kinetics
are beyond the scope of this chapter. In catabolic patients, the
goal is the achieve a nitrogen balance of +2 or higher to facilitate anabolism.
Nitrogen balance studies are more commonly performed in
the critical care setting, in which patients are likely receiving
continuous nutritional support and an accurate timed urine
sample collection is more feasible. Critically ill patients are in
a severe inammatory and catabolic state. erefore, it is also
important to meet their protein requirement to promote healing and recovery.
C-Reactive Protein
C- reactive protein is a pentameric protein synthesized by the
liver. It is released in response to inammation; thus, it is a nonspecic positive acute phase reactant. Plasma C- reactive protein
concentration is elevated in both acute and chronic inammatory responses. It has a serum half- life of 19 hours.60 erefore, it
can uctuate throughout the course of a patient’s treatment and
-
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oer some information on whether the patient’s inammatory
state is worsening or improving. However, it must be interpreted
according to patient- specic clinical context and presentation.
No single value can be used to rule in or rule out a specic diagnosis or disease.
C- reactive protein is not a direct marker to reect a patient’s
nutritional status. However, because the current consensus is
that the etiology of malnutrition includes inammation, deter-
nicians determine if a patient is at risk for malnutrition and
prioritize the need for nutritional intervention.
11,13
WHAT ARE THE BEST APPROACHES
TO ASSESS NUTRITION STATUS,
DIAGNOSE MALNUTRITION, AND
MONITOR NUTRITIONAL RESPONSE?
Based on the contemporary understanding and clinical denition of malnutrition, it appears that none of the laboratory tests
historically or currently in use are sensitive markers for nutritional assessment and monitoring. Instead, changes in the serum
concentrations of these visceral proteins reect the magnitude
of ongoing inammation experienced by the patients. So, what
are the optimal approaches in assessing nutritional status and
response to nutritional interventions?
Malnutrition should be determined based on the presence
of phenotypic or etiologic criteria. Phenotypic criteria include
changes such as unintended weight loss of ≥5% within the past
6months, lower body mass index (exact cuto is being addressed
by the GLIM workgroup and is likely to be region/demographicspecic), or reduced muscle mass as measured by validated
body composition–measuring techniques, such as dual- energy
absorptiometry, computed tomography, bioelectrical impedance
analysis, magnetic resonance imaging, and ultrasound. Etiologic
criteria include reduced food intake and the presence of systemic
inammation.
inammation should be routinely evaluated because they help
determine a patient’s malnutrition risk and prioritize the needs
for nutritional intervention.
Ultimately, laboratory tests alone should not be used to
replace a detailed nutritional assessment in determining a
patient’s malnutrition risk. e purpose of a nutritional assessment is to gather relevant information to provide evidence for
the nutrition diagnosis and aid in the development of a patientspecic nutrition intervention plan. Assessing nutritional
status and monitoring for clinical response to nutritional intervention require the application of basic clinical skills, which
include collecting a detailed patient’s history, performing
physical examinations whenever possible, and using validated
screening tools where applicable.
a critical component of nutritional screening, assessment, and
ongoing monitoring. It is important to identify risk factors that
would increase a patient’s malnutrition risk, such as inammation, the use of certain medications (eg, corticosteroids,
chemotherapeutics agents), and the presence of underlying
8,61
Importantly, the presence and the severity of
62,63
Detailed history- taking is
TABLE 12-4. Factors Contributing to Increased Risk
for Malnutrition in Patients
Changes in Body Composition
Unintentional weight loss
Moderate malnutrition: 5%–10% within 6 mo or
10%–20% beyond 6 mo
Severe malnutrition: >10% within 6 mo or >20% beyond
6 mo
High or low body mass index
Moderate malnutrition: <20 kg/m
if ≥70 yr
Severe malnutrition: <18.5 kg/m2 if <70 yr; <20 kg/m2
if ≥70 yr
Changes in intake
Decreased or loss of appetite
Swallowing difculty
Loss of smell or taste
Dental problems
Decreased food intake
Severe dry mouth
Disease-
related
Inammation (acute and/or chronic)
Chronic diseases not being controlled
Acute injuries and changes to the state of health
Surgeries
Signicant decline or loss of visual acuity
GI complications
Social and psychological factors
Traumatic experience
Depression
Social isolation
Neglect
Grief
Loss of companionship (eg, partners, pet)
Recent hospitalization
Economic hardship
Drug- induced changes in intake or GI tract functions
medical, health, or social conditions (eg, loss of dentition,
depression, chronic nausea, dry mouth, lack of access to food)
that could impair food intake or nutrient use (Table 12-4). Performing simple and basic physical examination, such as deter
mining uid status, adiposity, weight changes, and symptoms
associated with specic nutrient deciencies can help identify
at- risk patients and expedite nutritional intervention. Finally,
the use of validated nutritional assessment tools, such as Mini
Nutritional Assessment or Subjective Global Assessment, can
provide a comprehensive evaluation of a patient’s malnutrition risk.
2
if <70 yr; <22 kg/m2
-
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SUMMARY
Inammation is an important component of malnutrition that
can lead to loss of muscle mass, impair physiologic and body
function, and negatively impact clinical outcomes. Although
a number of laboratory tests, such as albumin, prealbumin,
and transferrin, are routinely used as surrogate markers of
MINICASE 1
Nancy M. is a 68-year-old woman admitted to the hospital for an
aortic valve replacement and coronary artery bypass graft surgery.
Her past medical history includes hypertension, type 2 diabetes
mellitus, hypercholesterolemia, and chronic constipation. Her
current medications include metformin, sitagliptin, simvastatin,
fosinopril, and polyethylene glycol 3350.
Her height is 165cm and weight is 89.4kg. She has gained 2.5kg
in the last 2 weeks. Her vital signs on admission include blood
pressure 110/85mm Hg, heart rate 68 beats/min at regular rhythm,
and a respiratory rate 12 breaths/min. Physical examination findings
include +2 edema on both ankles and bilateral numbness in her
thumb and first finger.
Her laboratory test results before surgery include a serum albumin
concentration of 3.8 g/dL and a hemoglobin A1c concentration of
6.3%. All other laboratory values on the chemistry panel are within
normal limits.
nutritional status, they mostly reect the state of inammation
the body is experiencing and are neither accurate nor specic for
nutritional assessment. Nutritional assessment should be performed by using a multicomponent comprehensive evaluation
that includes history- taking, physical examination, and the use
of a validated nutrition assessment tool rather than relying on a
laboratory test or tests in isolation.
a high-
stress procedure. Underlying malnutrition is associated
with increased postoperative mortality, especially in older adults.
Fortunately, her chronic illnesses appear to be well controlled at this
point. Additional history regarding her dietary habit, appetite, and
approximate daily food intake should be obtained. Each of these
independent factors affects her malnutrition risk.
Studies show that immediately after surgery, patients lose a
substantial amount of muscle mass due to acute inflammation.
The inflammation response will likely be reflected by an elevated
C- reactive protein concentration and a decline in serum albumin
concentration. Her nutritional status should be continually assessed
by following daily intake, weight changes, and presence of any
surgeryconcentrations will not provide any patientregarding her ongoing nutritional status.
related complications. Serum albumin or prealbumin
specific information
QUESTION: What is her malnutrition risk?
DISCUSSION: The fact that this patient is undergoing major cardiac
surgery puts her at high risk for malnutrition. Cardiac surgery is
MINICASE 2
Carrie M., a 32-year-old woman, presents to the emergency
department with 1dizziness, and fever. She rates the pain as 8 out of 10. She reports
three episodes of vomiting within the past 12 hours. Before presenting
to the hospital, she was in her usual state of health. Laboratory values
obtained from her routine health maintenance visit from 6 months
ago show normal findings for her liver function tests, including serum
albumin, serum chemistry, and complete blood count.
Her past medical history includes Crohn disease since age 17years,
resulting in an extensive history of small bowel resection. Her current
GI anatomy includes approximately 300cm of functional small
intestine and an intact colon. She tolerates an oral diet and takes
four small meals daily with an oral protein supplementation. She has
mild chronic diarrhea, which is usually well- controlled by diet at two
day history of severe epigastric pain, nausea,
to three soft bowel movements per day, and she takes loperamide
three times a day and clonidine twice a day.
On admission, her weight is 65.7 kg, which has decreased by 1.1kg
from baseline measured 6 months ago. Her body mass index is
20.7 kg/m2. Physical examination shows she has mild dehydration
with no peripheral edema.
Pertinent laboratory findings are as follows:
• Albumin, 2.8 g/dL
• Prealbumin, 15 mg/dL
• Amylase, 880 units/L
• Lipase, 930 units/L
• C- reactive protein, 49 mg/dL
CHAPTER 12 • InTERPRETATIon of LAboRAToRy TEsTs AssoCIATEd wITH THE AssEssmEnT of nuTRITIonAL sTATus 283
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MINICASE 2 ( cont’d)
The patient is diagnosed with acute pancreatitis and admitted to
the hospital for further management. Intravenous (IV) fluids and pain
medication are started immediately.
QUESTION: Based on her underlying medical condition, clinical
presentation, and laboratory findings, including serum albumin and
prealbumin concentrations upon admission, does the patient have
severe malnutrition necessitating immediate initiation of parenteral
nutrition?
DISCUSSION: Acute pancreatitis is a disease associated with acute
inflammation and catabolism. This is reflected by the elevated
C- reactive protein concentration, which is common among patients
with acute pancreatitis. The inflammation causes an acute decline
in serum albumin and prealbumin concentrations because they are
negative acute phase reactants. Therefore, the current albumin and
prealbumin concentrations do not reflect this patient’s nutritional
status. Rather, these are additional markers besides C- reactive
protein confirming the presence of acute inflammation.
The change of body weight from baseline is likely the result of
dehydration. Along with acute pancreatitis, dehydration, vomiting,
and fever are all independent factors associated with increased
malnutrition risk. Therefore, this patient’s nutritional status and
intake should be carefully monitored in the next 24 to 48 hours.
Nutritional interventions with protein provision should be initiated
as tolerated. However, because she was in her usual state of health
before admission and tolerated an oral diet at baseline, parenteral
nutrition is not indicated at this point. Enteral nutrition should be first
attempted after controlling vomiting and abdominal pain. Postpyloric
feeding tube placement is more likely to increase enteral feeding
tolerance without aggravating pain. This should be attempted
along with IV fluid rehydration and electrolyte replacement, which
are consistent approaches with the current practice standards for
acute pancreatitis. Consistent with the current practice standards,
if she is unable to tolerate enteral feeding in the next 3 to 5 days,
parenteral nutrition would be considered.
Serum albumin and prealbumin will remain suppressed as long as
C- reactive protein concentration is elevated. Therefore, albumin
and prealbumin should not be used during this time as a marker of
nutritional response. Instead, her response to enteral feeding should
be based on daily caloric and protein intake, GI symptoms, pain
control, and general well- being. Additional protein supplementation
is likely necessary upon hospital discharge as she continues to
regain her appetite and reestablish an oral diet that is tolerated by
her underlying medical condition.
64
MINICASE 3
Frank K. is a 52-year-man who has systemic lupus erythematosus
(SLE), hypertension, type 2 diabetes, chronic proteinuria, and
chronic kidney disease (CKD) stage 5 and is currently receiving
hemodialysis. The following laboratory results have been obtained
as his dialysis care process:
• Hemoglobin, 10.5 g/dL
• Mean corpuscular volume, 77 fL
• Red cell distribution width, 19.9%
• Serum ferritin, 34 ng/mL
• Transferrin, 382 mg/dL
• Transferrin saturation, 28%
QUESTION: Based on this patient’s medical history and laboratory
results, what are his risk factors for malnutrition?
DISCUSSION: This patient has anemia based on his hemoglobin
concentration, an unsurprising finding due to CKD. The results
of the iron study suggest that he has iron deficiency, which can
increase serum transferrin concentration. This finding makes serum
transferrin an unreliable marker for nutritional status in this patient.
Nutritional status cannot be reliably assessed using retinol- binding
protein because it is increased in CKD. Additionally, it is not
uncommon that chronic inflammation is present in patient’s CKD.
Therefore, if his serum albumin concentration is below the normal
range, it may be a reflection of uncontrolled systemic inflammation.
This also makes hypoalbuminemia and hypo- prealbuminemia
unreliable markers for malnutrition in CKD. Nutrition assessment for
this patient should be based on a comprehensive clinical assessment
using history, clinical findings, and a validated assessment tool.
This patient does have multiple risk factors for malnutrition,
including SLE, hypertension, iron deficiency anemia, and CKD.
SLE is associated with a chronic inflammatory state, which may
have suppressive effect on appetite and oral intake. Along with
proteinuria, this patient is at high risk for developing protein- calorie
malnutrition. Therefore, his treatment plan must include suppressing
chronic inflammation, reducing urinary protein loss, and optimizing
calorie and protein intake. Ideally, in addition to body weight and
oral intake monitoring, routine body composition assessment to
prevent sarcopenia should be considered.
284 BASIC SKILLS IN INTERPRETING LABORATORY DATA
https://t.me/med1917
MINICASE 4
Josha T. is a 39-year-old man has been admitted to the hospital
after being hit by a bus while riding his bicycle to work. His injuries
include multiple fractured ribs and blunt abdominal injury. He
undergoes surgery upon admission to the hospital and is found to
have a small intestinal perforation. Postoperatively, he is transferred
to the trauma/surgical ICU for recovery and supportive care.
Because of abdominal trauma, parenteral nutrition is started on
postoperation day2. The parenteral nutrition prescription provides
2,350 kcal (35 kcal/kg) with 120g (1.8 g/kg) of protein per day.
His serum albumin concentration on admission is 3.5 g/dL. On
the day parenteral nutrition is initiated, his serum albumin level
is 3.1 g/dL. Five days after parenteral nutrition therapy, his serum
albumin concentration is still 3.1 g/L and prealbumin is 18 mg/dL.
The surgical team consults with the clinical nutrition team to optimize
nutrient provision and delivery. At this point, there is still substantial
drainage from his small intestine; therefore, enteral feeding is not
a feasible option.
QUESTION: How should the clinical nutrition team optimize nutrient
provision and delivery for this patient?
DISCUSSION: Traumatic injury is associated with a profound
systemic inflammation. Therefore, continued hypoalbuminemia
in this patient, despite receiving 120g of protein per day, is due
to continued, unsuppressed inflammation. It does not reflect the
patient’s response to nutritional therapy. Neither serum albumin nor
prealbumin should be used to determine the adequacy of nutritional
intervention in this patient.
Because his renal function remains stable with an estimated
glomerular filtration rate of 108 mL/min, the clinical nutrition team
orders 24- hour urine collection for a nitrogen balance study. The
next day, the clinical nutrition team assesses the result, which
shows urine urea nitrogen output of 17.5g in 24 hours. His blood
urea nitrogen and serum creatinine concentrations remain stable at
19 mg/dL and 1.12 mg/dL, respectively. Under normal physiology
with an assumed nonrenal nitrogen loss of 4 g/day, the total daily
nitrogen output for this patient is approximately 21.5g (17.5g + 4 g).
However, because he has continued fluid drainage from this small
intestine, his actual nitrogen output is likely higher than 21.5 g/day.
Based on his current parenteral nutrition prescription, his total
nitrogen input is 120 g/6.25 g = 19.2g. Therefore, he is currently in
a negative nitrogen balance (at least −3 but probably higher).
In response to the nitrogen balance study, the clinical nutrition team
suggests increasing the amino acid content from 120 to 150 g/day
(equivalent to 24g of nitrogen intake per day). In addition, indirect
calorimetry is ordered to ensure that the patient is not overfed in
total calories. The patient will continue to be monitored for vital
signs, daily fluid and electrolyte balance, weight changes, ongoing
inflammatory state, and clinical improvement. Repeat nitrogen
balance study may be considered in a week if his clinical condition
does not improve.
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