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64 G. Fullin
Table 6.2 Mini Nutritional Assessment
Has food intake declined over the past 3 months due to loss
of appetite, digestive problems, chewing or swallowing
difficulties?
Weight loss during the last months? 0 = weight loss greater than 3 kg
Mobility? 0 = bed or chair bound
Has suffered physical stress or acute disease in the past
months?
3
Neuropsychological problems? 0 = severe dementia or
BMI 0 = BMI 19 to less than 21
12 points or greater: normal/not at risk → no need to complement assessment
11 points or below: possible malnutrition → continue assessment
0 = severe loss of appetite
1 = moderate loss of appetite
2 = no loss of appetite
1 = does not know
2 = weight loss between 1 and
3k
g
3 = no weight loss
1 = able to get out of bed/chair
does not go out
but
2 = goes out
0 = yes
2 = no
depression
1 = mild dementia
2 = no psychological problems
2 = BMI 21 to less than 23
3 = BMI 21 or greater
Table 6.3 Malnutrition Universal Screening Tool
BMI >20 0
18.5–20 1
<18.5 2
Unplanned weight loss in past 3–6 months % <
If patient is acutely ill and there has been or is likely to be no nutritional intake for
>5 days
Table 6.4 Malnutrition Universal Screening Tool scoring system
Sum of
points Category Explanation
0 Low risk Patient at low risk, routine
1 Medium
risk
2 or more High risk Patient a
week
Patient at medium risk must
intake for 3 days
t high risk required specific dietarian support and have to be
treated properly
clinical care and repeat screening every
be observed, document dietary and fluid
50
5–10 2
>10 2
2
6 Nutrition Risk Screening Tools 65
Table 6.5 NRS 2002—initial screening
Body mass index (BMI) [weight in kg]/[height in m]2 < 20.5 Yes No
Has the patient lost weight within the last 3 months? Yes No
Has the patient had a reduced dietary intake in the last week? Yes No
Is the patient severely ill?
If the answer is “Yes” to any question, the final screening is performed.
If the answer is “No” to all questions, the patient is re-screened at weekly intervals. If the patient,
e.g., is scheduled for a major operation, a preventive nutritional care plan is considered to avoid
the associated risk status.
Table 6.6 NRS 2002—final screening
Impaired nutritional status
Absent
score 0
Mild
score 1
Moderate
score 2
Severe
score 3
Score: + score: = total score
Age: if ≥70 years: add 1 to total score above = age-adjusted total score
Score ≥ 3: the patient is nutritional at-risk and nutritional care plan is initiated
Score < 3: weekly rescreening of the patient.
Normal nutritional status Absent
Wt loss >5% in 3 months or food
intake
requirement in preceding week
Wt
loss >5% in 2 months or BMI
18.5–20.5 + impaired general
condition or food intake 25–60%
of normal requirement in preceding week
Wt loss >5% in 1 month (>15% in
3 months) or BMI
o18.5 + impaired general condition or food intake 0–25% of normal requirement in preceding
week in preceding week.
(e.g., in intensive therapy) Yes No
Severity of disease (≈ increase in
requirements)
Normal nutritional requirements
Hip fracture, chronic patients, in
particular with acute complications: cirrhosis, COPD. Chronic
hemodialysis, diabetes,
oncology
Major abdominal surgery, stroke,
severe pneumonia, hematologic
malignancy.
Head injury, bone marrow transplantation, intensive care patients
(APACHE II ≥ 10).
.
below 50–75% of normal
score 0
Mild
score 1
Moderate
score 2
Severe
score 3
ICU. The score considers body mass index, weight loss in the past 3–6 months,
and the effect of acute disease on nutritional status. A score of >2 indicates a high
risk of malnutrition.
Nutritional Risk
•
Screening 2002 (NRS 2002—Tables
6.5 and 6.6): Developed
by Kondrup et al. [8], this simple tool has been validated for use in ICU patients.
It considers recent weight loss, changes in dietary intake, and disease severity to
determine if a patient is at nutritional risk [9]. Guidelines propose classifying
critical patients as “at nutrition risk” if NRS 2002 >3 and “at high nutritional
risk” if the score is >5, as an expert-based recommendation. The NRS 2002 has
been shown to effectively predict mortality, complications, and length of stay in
critical care patients. One of the main limitations of the NRS 2002 score is that
66 G. Fullin
Table 6.7 Nutrition Risk in
Critically Ill
Table 6.8 Nutrition Risk in Critically Ill scoring system
Sum of
points Category Explanation
If IL-6 available
6–10 High
score
0–5 Low
score
If no IL-6 available
5–9 High
score
0–4 Low
score
Age <50 0
APACHE II <15 0
SOFA <
Number of comorbidities 0–
Days from hospital to ICU admission 0– <
IL-6 0– <400 0
Associated with worse clinical outcomes (mortality, ventilation). These
patients are the most likely to benefit from aggressive nutrition therapy.
These patients have a low malnutrition risk.
Associated with worse clinical outcomes (mortality, ventilation).
patients are the most likely to benefit from aggressive nutrition therapy.
These patients have a low malnutrition risk.
50– <75 1
≥75 2
15– <20 1
20–28 2
≥28 3
60
6– <10 1
≥10 2
10
≥
21
10
≥
11
≥400 1
These
any critically ill patient with an APACHE II score above 10 will fall into the highrisk category.
• Nutrition Risk i
n Critically Ill (NUTRIC— Tables
6.7 and 6.8): [10] This is the
first nutritional risk assessment tool developed specifically for the ICU population
that could identify patients requiring more aggressive nutritional support, based
on their nutritional risk [
11]. The
NUTRIC score combines pre-hospitalization
parameters like chronic (BMI) and acute starvation (prehospital admission duration) with acute (Interleukin-6—IL-6) and chronic inflammatory parameters
(number of comorbidities) and the severity of illness (APACHE-II and SOFAscores) on ICU admissi on, to assess nutritional risk and associated outcomes
(mortality and ventilation durat ion). A high score is associated with higher 28-day
mortality and a longer duration of mechanical ventilation. IL-6 levels are not
commonly measured in ICUs; nevertheless, the performance of the NUTRIC
6 Nutrition Risk Screening Tools 67
score varies only slightly when excluding IL-6 levels from the score (only
decreasing the c-index by 0.007, being neither clinically nor statistically different). The modi fied NUTRIC score (without IL-6) has been validated. The
NUTRIC Score has been shown to effectively identify nutritional risk and predict
adverse clinical outcomes in critical care patients. However, there are some
limitations to using this score. For instance, APACHE II is seldom used in Europe
and may be complex to calculate at the bedside, making it more time-consuming
compared to tools like the NRS 2002 and MUST. Another limitation of this score
is that no nutritional parameters or micronutrient deficiencies are included.
Discussion
Among all the screening tools, only the NRS 2002 and the NUTRIC have been
extensively studied. The NRS 2002 has been proposed for use in the hospitalized
population in general, whereas the NUTRIC score was developed and validated
specifically for patients hospitalized in the ICU. Comparative studies between
NUTRIC and NRS 2002 scores showed inconsistent results; only fair agreement
between the two scores was identified [
literature, NUTRIC and NRS 2002 were expected to show more highly concordant
results [14]. Both NRS 2002 and NUTRIC were recommended in the guidelines for
the provision and assessment of nutrition support therapy in the adult critically ill
patient by ASPEN [15]. From 2019 onward, guidelines by ESPEN [16, 17] recommend, in disagreement with the ASPEN guidelines, that there is no gold standard to
define nutrition risk in the intensive care setting, and patients should not be categorized according to NRS 2002 or NUTRIC. In addition, it is suggested that mortality
is not the best outcome to assess the effectiveness of a nutrition intervention, given
the numerous factors influencing the ICU that cannot be used as a parameter for tool
validation. Instead, ESPEN advises that all critically ill patients staying for >48 h in
the ICU shoul d be considered at risk for malnutrition.
In conclu
clinical nutrition societies with the aim to build a global consensus around core
diagnostic criteria for malnutrition in adults in clinical settings. The Global Leadership on Malnutrition criteria (GLIM—Table 6.9) [18] are based on the presence of at
least two of the three phenotypic criteria and at least one of the two etiologic criteria.
While GLIM is not yet validated, both the European and American Society for
Parenteral and Enteral Nutrition (ESPEN—ASPEN) believe it holds promise and has
the potential to become the new gold standard for diagnosing malnutrition.
sion, we would like to highlight an initiative led by several major global
12, 13]. As both were equally indicated in the
68 G. Fullin
Table 6.9 Global Leadership on Malnutrition
Phenotypic
criteria
Etiologic
criteria
Weight loss % > 5% within past 6 months or > 10% beyond
Low BMI < 20 it <70 years or < 22 if >70 years
Reduced muscle mass By validated body composition measuring techniques
Decreased food intake or
malabsorption
Inflammation Acute disease/injury or chronic disease related
6 months
<50% of ER >1 week, or any reduction for > 2 weeks,
or any chronic gastrointestinal malabsorption
inflammation
Conclusion
Timely nutritional intervention proves imperative for most critical care patients.
Validated nutritional risk screening scores serve as valuable guides for interventions.
Nevertheless, a consensus on the optimal assessment tool remains elusive. Among
the available scores, NUTRIC has demonstrated the highest predictive power. It
seems reasonable to consider all the most severely ill patients in intensive care at
high risk of malnutrition. The GLIM score emerges as a proficient tool for diagnosing malnutrition.
References
1. McDermid RC, Stelfox HT, Bagshaw SM. Frailty in the critically ill: a novel concept. Crit Care.
2011;15:301.
2. Lew CCH, Yandell R, Fraser RJL, et al. Association between malnutrition and clinical outcomes in the intensive care unit: a systematic review. JPEN J Parenter Enteral Nutr. 2017;41(5):
744–58.
3. Detsky A, McLaughlin JR, Baker J, et al. What is subjective global assessment of nutritional
status? J Parenter Enter Nutr. 1987;11(1):8–13.
4. Rubenstein LZ, Harker JO, Salva A, et al. Screening for undernutrition in geriatric practice:
developing the short-form mini nutritional assessment (MNA-SF). J Geront. 2001;56A:
M366–77.
5. Kaiser MJ, Bauer JM, Ramsch C, et al. Validation of the mini nutritional assessment short-form
(MNA®-SF): a practical tool for identification of nutritional status. J Nutr Health Aging.
2009;13:782–8.
6. Stratton RJ, Hackston A, Longmore D, et al. Malnutrition in hospital outpatients and inpatients:
prevalence, concurrent validity and ease of use of the ‘malnutrition universal screening tool’
(‘MUST’) for adults. Br J Nutr. 2004;92(5):799–808.
7. de Vries MC, Koekkoek WK, Opdam, at al. Nutritional assessment of critically ill patients:
validation of the modified NUTRIC score. Eur J Clin Nutr. 2018;72(3):428–35.
8. Kondrup J, Rasmussen HH, Hamberg O, et al. Ad Hoc ESPEN Working Group. Nutritional risk
screening (NRS 2002): a new method based on an analysis of controlled clinical trials. Clin
Nutr. 2003;22(3):321–36.
9. Compher C,
therapy in the adult critically ill patient: the American Society for Parenteral and Enteral
Nutrition. JPEN J Parenter Enteral Nutr. 2022 Jan;46(1):12–41.
Bingham AL, McCall M, et al. Guidelines for the provision of nutrition support
6 Nutrition Risk Screening Tools 69
10. Heyland DK, Dhaliwal R, Jiang X, et al. Identifying critically ill patients who bene
fit the most
from nutrition therapy: the development and initial validation of a novel risk assessment tool.
Crit Care. 2011;15(6):R268.
11. Rahman A, Hasan RM, Agarwala R, et al. Identifying critically-ill patients who will benefit
most from nutritional therapy: further validation of the “modified NUTRIC” nutritional risk
assessment tool. Clin Nutr. 2016;35(1):158–62.
12. Rattanachaiwong S, Zribi B, Kagan I, et al. Comparison of nutritional screening and diagnostic
tools in diagnosis of severe malnutrition in critically ill patients. Clin Nutr. 2020;20(Suppl):
S0261–5614.
13. Canales C, Elsayes A, Yeh DD, et al. Nutrition risk in critically ill versus the nutritional risk
screening 2002: are they comparable for assessing risk of malnutrition in critically ill patients? J
Parenter Enteral Nutr. 2019;43(1):81–7.
14. Coruja MK, Cobalchini Y, Wentzel C, et al. Nutrition risk screening in intensive care units:
agreement between NUTRIC and NRS 2002 tools. Nutr Clin Pract. 2020 Jun;35(3):567–71.
15. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of
nutrition support therapy in the adult critically ill patient: society of critical care medicine
(SCCM) and American society for parenteral and enteral nutrition (A.S.P.E.N.). J Parenter
Enter Nutr. 2016;40(2):159–211.
16. Singer P, Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition in the intensive
care unit. Clin Nutr. 2019 Feb;38(1):48–79.
17. Singer P, Blaser AR, Berger MM, et al. ESPEN practical and partially revised guideline: clinical
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Jensen GL,
18.
Cederholm T, Correia MITD, et al. GLIM criteria for the diagnosis of malnutrition:
a consensus report from the global clinical nutrition community. JPEN J Parenter Enteral Nutr.
2019;43(1):32–40.
Chapter 7
Dynamic Metabolic Changes Measured by
Indirect Calorimetry
Marialaura Scarcella, Emidio Scarpellini, Riccardo Monti,
and Ludovico Abenavoli
Introduction
The energy expenditure (EE) of critically ill individuals may vary based on the
extent of metabolic stress and the progression of the disease [1]. Consequently,
meas
uring the EE of critically ill patients is advisable [1]. The current guidelines
from
the European Society for Clinical Nutrition and Metabolism (ESPEN) recommend the use of indirect calorimetry (IC) to measure EE in mechanically ventilated
patients [2]. Similarly, the guidelines from the American Society for Parenteral and
Enteral
guidelines suggest using either a predictive equation or a simplistic weight-based
eq. (25–30 kcal/kg/day) [3]. However, the agreement between measured and
predi
Nutrition also advocate for IC in determining EE. In the absence of IC, these
cted EE in critically ill patients varies, depending on the formulas used and
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_7.
M. Scarcella (
Anesthesia, Intensive Care Unit and Nutritional Science, Azienda Ospedaliera “Santa Maria”,
Terni, Italy
e-mail: m.scarcella@aospterni.it
E. Scarpellini
Clinical Nutrition Unit and Internal Medicine Unit, “Madonna del Soccorso” General Hospital,
San Benedetto del Tronto, Italy
e-mail: emidio.scarpellini@sanita.marche.it
R. Monti
Cardiologic,
e-mail: r.monti@aospterni.it
L. Abenavoli
Department
e-mail: l.abenavoli@unicz.it
© The
A. Cotoia et al. (eds.), Nutrition, Metabolism and Kidney Support,
https://doi.org/10.1007/978-3-031-66541-7_7
✉)
Obstetric and Neonatal Intensive Care Unit, Terni, Italy
of Health Sciences, University “Magna Graecia”, Catanzaro, Italy
Author(s), under exclusive license to Springer Nature Switzerland AG 2024
71
72 M. Scarcella et al.
the specific critically ill population studied, increasing the risk of over or undernutrition [4]. Recent data continue to highlight the poor correlation between measured
and equation-predicted energy expenditure (EE), underscoring the imperative for IC
to become the standard of care. Different phases during the stay of critically ill
patients have been identified, influencing energy expenditure and, consequently,
caloric delivery. In 1942, Sir Cuthbertson delineated the metabolic response to
5]. I
traumatic stress into an ebb phase and a flow phase [
docrinology, the term “stress” indicates a factor causing an imbalance in the body,
shifting it away from homeostasis. This process involves a series of reactions in the
nervous system, endocrine system, and immune system, closely interdependent with
each other. During stress, the body prioritizes supporting vital functions, deferring
functions of seconda ry importance, such as growth, reproduction, and long-term
immunity [6
trauma, lasting from minutes to hours (24/48 h). It is characterized by a decline in
metabolism, reduced body temperature, oxygen consumption, and enzymatic activities. This shock phase involves hemodynamic instability and hormonal changes,
including a decrease in metabolic response with lowered oxygen consumption,
elevated plasma glucose concentration, peripheral insulin resistance, sodium rete
tion, and tissue edema due to increased vascular permeability.
These alterations aim to
crucial for the immediate survival of the organism, achieved through an increase in
endogenous glucose production and a reduction in energy expenditure. In this
hyperacute phase, central activation occurs at the Locus Ceruleus and the
paraventricular nucleus, leading to increased secretion of norepinephrine,
5-hydroxytryptamine (serotonin), corticotropin-releasing hormone (CRH), and
dopamine.
]. The ebb phase, or “EBB phase,” commences immediately after
sustain the transport of energy substrates to vital organs,
n physiology and neuroen-
n-
Fight-and-Flight Reaction
The activation of the sympathetic-adrenergic nervous system occurs within milliseconds of the acute stressful event and is mediated by the release of catecholamines
from sympathetic nerves and the adrenal medulla, potentiated by the inhibition of
parasympathetic system activity [6]. Immediate activation of the medullary
sympatho-adrenergic system determines the so-called fight-and-flight reaction, characterized by stereotyped pathophysiological alterations (tachycardia, increase in
blood pressure, tachypnea, fear, increased alertness, activation movement with
tremor, piloerection). The effector hormones of these alterations are mainly the
catecholamines released by the adrenal medulla, which act on specific cellular
receptors widely distrib uted throughout the body, inducing glycolysis, activation
of the immune system, and increased blood flow to “noble” organs such as the brain
with simultaneous reduction of blood flow to less essential organs such as the bowel.
The mecha
response occur with the release of cytokines such as tumor necrosis factor (TNF),
nisms involved in the activation of the hormones of the “flight or fight”
7 Dynamic Metabolic Changes Measured by Indirect Calorimetry 73
interleukin-1, and interleukin-6, which characterize the inflammatory state and lead
to activated gluconeogenesis, glycogenolysis, the mobilization of free fatty acids,
and proteolysis to quickly cope with the increased metabolic demand. Following this
phase of hypometabolism, a phase of post-shock hypermetabolism, or “Flow Phase,”
takes place. This begins after 48 h and lasts about 3–10 days, consisting of a
traumatic inflammation condition characterized by an
tion, cata with muscle proteolysis, activation of gluconeogenesis from amino acids
and free fatty acids (to provide the energy substrates necessary for the fight or flight
response), increased synthesis of acute-phase proteins, and substrates needed for
wound healing, reducing the risk of bleeding and infection, and an elevation of REE.
This high rate of catabo lism causes a negative nitrogen balance. This phase ends
with the beginning of the
metabolism towards an anabolic phase with the resynthesis of lost muscle tissue.
This phase has much greater clinical relevance than the EBB phase, as it can cause
long-term hyperglycemia and insulin resistance. The crucial importance of this
metabolic moment makes it necessary to accurately determine energy intake, administered with the aim of inhibiting gluconeogenesis and the depletion of lean body
7]
mass [
.
healing process and tissue stock restoration, moving
increase in oxygen consump-
Calorimetry and Total Energy Expenditure
Currently, three phases have been described, characterized by significant variations
in the critically ill patient’s basal metabolism: the early acute phase (first 24–48 h
after the acute event), late acute phase (from 3 to 7 days), and the anabolic recovery
phase (after the 7th day of admission to intensive care). Indeed, it is currently not
possible to identify biochemical or physiological indicators that can precisely pinpoint the transition between one phase and another. However, the use of Indirect
Calorimetry can aid in recognizing the various phases: from the early acute phase to
the late acute catabolic phase and the anabolic recovery phase (Fig.
less, calculating energy expenditure remains challenging, considering the influence
of the normal course of the disease, individual inflammatory and immunological
responses, and the pharmacological response of the organism on the basal metabolic
rate itself. Energy expenditure is influenced by numerous individual and iatrogenic
factors and by the different metabolic phases of critical illness and convalescence. It
is subject to considerable individual variations due to various conditions that influence metabolism by modifying energy consumption. Total energy expenditure
(TEE) represents the energy necessary to support various biological functions of
the organism. TEE is composed of about 2/3 Resting Energy Expenditure (REE) and
the remaining 1/3 Activity-related Energy Expenditure (AEE). REE includes Basal
Energy Expenditure (BEE) and Diet-Induced Thermogenesis (DIT). REE represents
the energy expended by the body during 24 h of inactivity to maintain involuntary
biological functions necessary for survival, such as cell turnover, respiration, heart
rate and output, and body temperature regulation, as well as digesting and storing
7.1). Neverthe-
74 M. Scarcella et al.
Fig. 7.1 Metabolic dynamics in intensive care: unpredictable rise in Resting Energy Expenditure
(REE) and the crucial role of indirect calorimetry (IC)
macronutrients [6, 7]. Several equations have been developed to predict REE in the
absence of a direc t measurement with IC, which are relatively accurate and precise in
healthy subjects. However, in the case of illnesses or trauma, REE is influenced by
various factors that can have a synergistic or antagonistic impact. For these reasons,
indirect calorimetry remains the only available tool to calculate the exact caloric
, 9]
needs in critically ill patients [8
.
Role of Mitochondria in the Various Stages of Intensive Care Recovery
Mitochondria are renowned as the powerhouse of the cell due to their crucial role in
generating energy in the form of adenosine triphosphate (ATP). During critical
illness, especially in the acute phase, mitochondrial function is severely
compromised, leading to a reduction in the capacity to utilize macronutrients for
energy production. Con sequently, there is a decrease in ATP synthesis and an
increase in the generation of reactive oxygen species (ROS). Mitochondrial dysfunction has been linked to disease severity, particularly associated with long-term
adverse clinical outcomes such as prolonged mechanical ventilation and extended
stays in the ICU and hospital.