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16 Complications Associated with Parenteral Nutrition 179
9. Llop JM, Leiva E, Mateu-de Antonio J, Berlana D, Badia M, Casasín T, Miana M, Pons M,
Maroto M, Chicharro L, López-Suñé E, Díaz-Munio E, Sevilla D, Martínez I, Vitales M,
Casajuana MT, Bobis MA. Study of hyperglycemia in non critically-ill patients receiving
parenteral nutrition: incidence and risk
org/10.3305/nh.2012.27.5.5880. PMID: 23478700.
10. van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D,
Ferdinande P, Lauwers P, Bouillon R. Intensive insulin therapy in critically ill patients. N Engl J
Med. 2001;345(19):1359–67. https://doi.org/10.1056/NEJMoa011300. PMID: 11794168.
11. Van den Berghe G, Wilmer A, Hermans G, Meersseman W, Wouters PJ, Milants I, Van
Wijngaerden E, Bobbaers H, Bouillon R. Intensive insulin therapy in the medical ICU. N
Engl J Med. 2006;354(5):449–61. https://doi.org/10.1056/NEJMoa052521. PMID: 16452557.
12. NICE-SUGAR Study Investigators, Finfer S, Chittock DR, Su SY, Blair D, Foster D,
Dhingra V, Bellomo R, Cook D, Dodek P, Henderson WR, Hébert PC, Heritier S, Heyland
DK, McArthur C, McDonald E, Mitchell I, Myburgh JA, Norton R, Potter J, Robinson BG,
Ronco JJ. Intensive versus conventional glucose control in critically ill patients. N Engl J Med.
2009;360(13):1283–97. https://doi.org/10.1056/NEJMoa0810625. Epub 2009 Mar 24. PMID:
19318384.
13. Berger MM, Reintam-Blaser A, Calder PC, Casaer M, Hiesmayr MJ, Mayer K, Montejo JC,
Pichard C, Preiser JC, van Zanten ARH, Bischoff SC, Singer P. Monitoring nutrition in the
ICU. Clin Nutr. 2019;38(2):584–93. https://doi.org/10.1016/j.clnu.2018.07.009. Epub 2018 Jul
20. PMID: 30077342.
14. Zaloga GP. Phytosterols, lipid administration, and liver disease during parenteral nutrition.
JPEN J Parenter Enteral Nutr. 2015;39(1 Suppl):39S–60S. https://d oi.org/10.1177/
0148607115595978. Epub 2015 Jul 15. PMID: 26177665.
15. Da Silva JS, Seres DS, Sabino K, Adams SC, Berdahl GJ, Citty SW, Cober MP, Evans DC,
Greaves JR, Gura KM, Michalski A, Plogsted S, Sacks GS, Tucker AM, Worthington P, Walker
RN, Ayers P, Parenteral Nutrition Safety and Clinical Practice Committees, American Society
for Parenteral and Enteral Nutrition. ASPEN consensus recommendations for refeeding syndrome. Nutr Clin Pract. 2020;35(2):178–95. https://doi.org/10.1002/ncp.10474.
16. Solomon SM, Kirby DF. The refeeding syndrome: a review. JPEN J Parenter Enteral Nutr.
1990;14:90–7.
17. Stanga Z, Brunner A, Leuenberger M, et al. Nutrition in clinical practice-the refeeding syndrome: illustrative cases and guidelines for prevention and treatment. Eur J Clin Nutr. 2008;62
(6):687–94.
18. Friedli N, Stanga Z, Sobotka L, et al. Revisiting the refeeding syndrome: results of a systematic
review. Nutrition. 2017;35:151–60.
19. Burger GCEDJ, Sandstead HR. Malnutrition and starvation in Western Netherlands September
1944–July 1945. Part I. Part II: appendices. JAMA. 1950;142(11):857–8.
20. Schnitker MA, Mattman PE, Bliss TL. A clinical study of malnutrition in Japanese prisoners of
war. Ann Intern Med. 1951;35(1):69–96.
21. McCray S, Walker S, Parrish CR. Much ado about refeeding. Pract Gastroenterol. 2004;XXVIII
(12):26–44.
22. Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and
treat it. BMJ. 2008;336:1495.
23. Anderson E, Long JA. The effect of hyperglycemia on insulin secretion as determined with the
isolated rat pancreas in a perfusion apparatus. Endocrinology. 1947;40(2):92–7.
24. Porte D Jr, Pupo AA. Insulin responses to glucose: evidence for a two pool system in man. J
Clin Invest. 1969;48(12):2309–19.
25. Brownlee M.
2001;414(6865):813–20.
26.
Schenk G,
dependent enzyme transketolase. Int J Biochem Cell Biol. 1998;30(12):1297–318.
Biochemistry
Duggleby RG, Nixon PF. Properties and functions of the thiamin diphosphate
and molecular cell biology of diabetic complications. Nature.
factors. Nutr Hosp. 2012;27(5):1521– 6. https://doi.
180 L. D
27. Hazell AS, Todd KG, Butterworth RF. Mechanisms of neuronal cell death in Wernicke’s
encephalopathy. Metab Brain Dis. 1998;13(2):97–122.
28. Thomson AD. Mechanisms of vitamin deficiency in
opment of the Wernicke-Korsakoff syndrome. Alcohol Alcohol
29. Coelho LS, Hueb JC, Minicucci MF, Azevedo PS, Paiva SA, Zornoff LA. Thiamin deficiency
as a cause of reversible cor pulmonale. Arq Bras Cardiol. 2008;91(1):e7–9.
30. DiNicolantonio JJ, Niazi AK, Lavie CJ, O’Keefe JH, Ventura HO. Thiamine supplementation
for the treatment of heart failure: a review of the literature. Congest Heart Fail. 2013;19(4):
214–22.
31. Braga M, Ljungqvist O, Soeters P, Fearon K, Weimann A, Bozzetti F, ESPEN. ESPEN
guidelines on parenteral nutrition: surgery. Clin Nutr. 2009;28(4):378–86. https://doi.org/10.
1016/j.clnu.2009.04.002. Epub 2009 May 21. PMID: 19464088.
32. Pittiruti M, Hamilton H, Biffi R, MacFie J, Pertkiewicz M, ESPEN. ESPEN guidelines on
parenteral nutrition: central venous catheters (access, care, diagnosis and therapy of complications). Clin Nutr. 2009;28(4):365–77. https://doi.org/10.1016/j.clnu.2009.03.015. Epub
2009 May 21. PMID: 19464090.
33. Timsit JF, Baleine J, Bernard L, Calvino-Gunther S, Darmon M, Dellamonica J, Desruennes E,
Leone M, Lepape A, Leroy O, Lucet JC, Merchaoui Z, Mimoz O, Misset B, Parienti JJ, Quenot
JP, Roch A, Schmidt M, Slama M, Souweine B, Zahar JR, Zingg W, Bodet-Contentin L,
Maxime V. Expert consensus-based clinical practice guidelines management of intravascular
catheters in the intensive care unit. Ann Intensive Care. 2020;10(1):118. https://doi.org/10.
1186/s13613-020-00713-4. PMID: 32894389; PMCID: PMC7477021.
34. Balsorano P, Virgili G, Villa G, Pittiruti M, Romagnoli S, De Gaudio AR, Pinelli F. Peripherally
inserted central catheter-related thrombosis rate in modern vascular access era-when insertion
technique matters: a systematic review and meta-analysis. J Vasc Access. 2020;21(1):45–54.
https://doi.org/10.1177/1129729819852203. Epub 2019 Jun 10. PMID: 31177939.
35. Brescia F, Pittiruti M, Spencer TR, Dawson RB. The SIP protocol update: eight strategies,
incorporating Rapid Peripheral Vein Assessment (RaPeVA), to minimize complications associated with peripherally inserted central catheter insertion. J Vasc Access. 2022;27:
11297298221099838. https://doi.org/10.1177/11297298221099838. Epub ahead of
print. PMID: 35633065.
36. Spencer TR, Pittiruti M. Rapid central vein assessment (RaCeVA): a systematic, standardized
approach for ultrasound assessment before central venous catheterization. J Vasc Access.
2019;20(3):239–49. https://doi.org/10.1177/1129729818804718. Epub 2018 Oct 4. PMID:
30286688.
37. Brescia F, Pittiruti M, Ostroff M, Biasucci DG. Rapid Femoral Vein Assessment (RaFeVA): a
systematic protocol for ultrasound evaluation of the veins of the lower limb, so to optimize the
insertion of femorally inserted central catheters. J Vasc Access. 2021;22(6):863–72. https://doi.
org/10.1177/1129729820965063. Epub 2020 Oct 16. PMID: 33063616.
38. Bell T, O’Grady NP. Prevention of central line-associated bloodstream infections. Infect Dis
Clin North Am. 2017;31(3):551–9. https://doi.org/10.1016/j.idc.2017.05.007. Epub 2017 Jul
5. PMID: 28687213; PMCID: PMC5666696.
39. Moureau NL, Marsh N, Zhang L, Bauer MJ, Larsen E, Mihala G, Corley A, Lye I, Cooke M,
Rickard CM. Evaluation of skin colonisation and placement of vascular access device exit sites
(ESCAPE study). J Infect Prev. 2019;20(1):51–9. https://doi.org/10.1177/1757177418805836.
Epub 2018 Nov 9. PMID: 30719089; PMCID: PMC6346323.
Ostroff MD,
40.
options (RAVESTO): a new decision tool in the management of the complex vascular access
patients. J Vasc Access. 2023;24(2):311–7. https://doi.org/10.1177/11297298211034306. Epub
2021 Jul 21. PMID: 34289721.
Moureau N, Pittiruti M. Rapid assessment of vascular exit site and tunneling
chronic alcohol misusers and the devel-
’Alessandro
Suppl. 2000;35(1):2–7.
and F. Barbani
Chapter 17
Pharmaconutrition in Critical Care
Antonella Cotoia, Paola Sara Mariotti, Andreas Edel, and Stefan J. Schaller
Introduction
Definition
The concept of “pharmaconutrition” refers to specific nutrients admi nistered at
pharmacological levels, while “immunonutrition” is the use of specific nutritional
substrates having the ability of modulating specific mechanisms involved in several
immune and inflammatory pathways. To achieve these goals, these substrates must
be administered with an over physiologic dose [1].
Pharmaconutritional supplementation is quite different from classical nutrient
cement to replenish losses [
repla
relate
to immune response alteration and prolonged inflammatory status observed in
critically ill patients. For this reason, support formulas were designated as
immunonutrition. In 2008, Jones and Heyland suggested shifting the terminology
to pharmaconutrition, to indicate all specific nutrients administered at pharmacological levels [3]. Currently, the concept of pharmaconutrition is quite distinct from
immunonutrition, whereby immune-modulating macronutrients such as arginine,
glutamine, and ω-3 fatty acids are combined with micronutrients, such as
2]. Initially, pharmaconutrients were introduced to
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_17.
A. Cotoia (
Department of Anesthesia and Intensive Care, University of Foggia, Azienda OspedalieroUniversitaria Ospedali Riuniti, Foggia, Italy
e-mail: antonella.cotoia@unifg.it; paola.mariotti@unifg.it
A. Edel · S. J. Schaller
Department of Anesthesiology and Operative Intensive Care Medicine (CVK/CCM), Charité
Universitätsmedizin Berlin, Berlin, Germany
e-mail: andreas.edel@charite.de; tefan.schaller@charite.de
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
A. Cotoia et al. (eds.), Nutrition, Metabolism and Kidney Support,
https://doi.org/10.1007/978-3-031-66541-7_17
✉) · P. S. Mariotti
181
182 A. Cotoia et al.
antioxidants, and are provided in so-called immune-enhancing diets by the enteral
route [3, 4]. These immune-enhanci ng formulas have been considered as logical and
attractive options in critically ill patients [5, 6]. Several publications [7–9] showed a
reduction in infection rate and length of stay in the ICU for patients receiving
pharmaconutrition. However, other studies conducted on critically ill and surgical
patients reported disparate results [
10]. The definition of the optimal dose of single
and combined nutrients as well as the best route of their administration remains
debated. According to Jones et al. [11], key nutrients should be administered
separately from classical parenteral nutrition (PN) or enteral nutri tion (EN) so that
their full dose can be delivered and their therapeutic effects evaluated appropriately.
Macronutrients
Glutamine
Glutamine (GLN) is the most abundant nonessential amino acid in circulation under
physiological circumstances, 60% of which is stored in skeletal muscle in the form
of free amino acid [12, 13]. GLN is also synthesised in nearly every tissue by
glutamine-synthetase and hydrolysed via a glutaminase in mitochondria. This
amino acid has many essential metabolic functions, indicated in Table 17.1.I
addition to metabolic contributions, GLN promotes heat shock protein (HSP)
responses and modulates gene regulation linked to apoptosis and signal transduction.
n
Table 17.1 Glutamine functions and effects
Functions Effects
Nitrogen/carbon metabolism
and transport
Fuel source for enterocytes Maintenance of gut barrier strength
Chief precursor to
γ-aminobutyric acid synthesis
Improved insulin sensitivity and
gluconeogenesis
Substrate involved in renal
ammonia genesis
Precursor to the antioxidant
glutathione
Expression o
f H
SP
Cellular energy for rapidly dividing cells (particularly lymphocytes, enterocytes, colonocytes)
Purine and pyrimidine synthesis
during immune cell proliferation
Carbon backbones required for glucose production
Maintenance immune cells within the gut-associated lymphoid
tissue
Inhibitory cerebral neurotransmitter
Regulation of glucose metabolism
Renal acid base regulation
Promotes HSP responses and modulates gene regulation
linked to apoptosis and signal transduction
Enhance stress
and attenuate the inflammatory response in oxidative stress
tolerance, improve tissue metabolic function,
of DNA and
messenger RNA
17 Pharmaconutrition in Critical Care 183
The expression of HSP, in particular, is protective during cellular stress, specifically
HSP-70, which can enhance stress tolerance, improve tissue metabolic function, and
attenuate the in flammatory response in oxidative stress [3, 12, 13].
During severe metabolic stress (i.e., trauma,
transplant, chemotherapy, and radiotherapy), GLN may even become a “conditionally essential” amino acid because its requirement exceeds the synthesis and supply
from proteolysis, resulting in depletion of GLN stores [13].
An updated metanalysis [14] showed a significant reduction in infectious complications, length of stay, and mortality when GLN was supplemented in critically ill
patients. In severely burned patients, enterally administered GLN decreased the rate
of infections, improved gut function and survival, but did not reduce the time to
discharge from the hospital [
improvement in humoral and cell-mediated immunity with GLN supplementation in
poly-traumatised patients using recommended doses [13]. Current guidelines rec-
ommend its use only in burn and trauma patients via EN [
Independently from the route of administration, GLN daily administration may
vary from a fixed dose of 20–35 g/24 h to an adjusted dose of 0.3 g–0.5 g per kg of
body weight [18]. Chronic consumption of GLN can lead to a number of negative
biochemical pathways and cellular functions such as (1) alterations in amino acid
transport impairing their distribution and absorption; (2) alte rations in GLN metabolism that enhance glutamate and ammonia production; (3) alterations in ammonia
transport among tissues; (4) abnormalities in aminoacidemia; (5) alterations in
immune system; (6) effect on tumour growth; (7) and effect of the withdrawal of
GLN supplementation due to the adaptive response of the organism to enhanced
GLN consumption [19].
According to international guidelines, intravenous GLN supplementation is
recommended in patients receiving exclusive PN, but no longer in other
situations [9].
3, 15, 16]. Another study showed that there was an
sepsis, major surgery, bone marrow
17].
Arginine
Arginine (ARG) is a conditionally essential amino acid in humans, which is
synthesised from citrulline by the kidneys, and it is implicated in numerous functions, with a pleiotropic effect according to the clinical situations. Depending on the
underlying pathophysiology, there is an upregulation of different enzymes and,
therefore, a different metabolism of ARG [11]. Important physiological roles of
ARG include the function of arginase, regulation of gene expression, cellular
proliferation, immune response, intestinal cell homeostasis, and wound healing [
(Fig. 17.1).
recent studies suggest that ARG supplementation may be harmful in infected or
septic critically ill patients. This potential toxicity may be due to its role as a
substrate for inducible nitric oxide synthase (iNOS). iNOS is upregulated during
The underl ying pathophysiology of critical illness varies widely, and
9]
184 A. Cotoia et al.
Viral binding and invasion
Cytokine storm. Release
of pro-inflammatory
factors like IL-1β, IL-6
and TNF
–
Immune cells. Phagocytosis by
macrophages and neutrophils
+
ω-3FA
–
vessels
Epithelial
damage
fluid
Ma
lungs
alveolus
Ma
Ne
Ne
Ne
Ma release: TNFalpha,
IL-1β, IL-6, IL-8.
Ne release: ROS,
cytokines
Viral replication
respiratory epithelium
Fig. 17.1 Arginine functions in the human body. NO nitric oxide
inflammatory states resulting in an increased production of nitric oxide (NO),
contributing to impaired microcirculation and organ dysfunction [
The normal plasma concentration of
ARG is 75–100 μmol/L. During stressful
11, 20, 21].
states, if dietary intake and endogenous production of ARG are insufficient, ARG
supplementation may be indicated for adequate muscle and connective tissue growth
22]. Doses of 3–8 g/die appear to be safe and not to cause acute pharmacologic
[
effects in humans. An acute vasodilator effect has been shown only in studies in
which L-arginine was administered via PN, either intravenously or intra-arterially.
Association between L-arginine plasma concentration range and vascular effects can
be related to endocrine secretagogue and unspecific vasodilator actions, which have
been shown to be absent in the low dose range [
21].
Leucine
Leucine (LEU) is an essential branched-chain amino acid that promotes cell growth
by stimulating protein synthesis in skeletal, cardiac, and intestinal musc le, as well as
other tissue and cell types, through stimulation of the mammalian target of
rapamycin (mTOR) pathway. Since critical illness is characterised by muscle catabolism and a loss of lean muscle, the addition of LEU to nutrition support formulas
has the potent ial to slow muscle prote olysis in the critically ill [3]
Administration
of LEU (1.2–6 g leucine/day) significantly improves sarcopenia
in obese and elderly frail individuals, mainly by improving lean muscle mass
23]. Literature reported that administration of β-hydroxy-β-methyl butyrate, a
[
.
17 Pharmaconutrition in Critical Care 185
metabolite of LEU, improved muscle mass and strength, albeit all studies had high
risk of bias and effect size was modest [24]. Larger controlled studies are necessary
to determine the effects and the dose of administration of LEU in specific critically ill
patient subgroups.
ω-3 Fatty Acids
Omega-3 fatty acids (ω-3FA) are polyunsaturated fatty acids widely distributed in
nature, highly contained in fish, which play an important role in the human diet and
in human physiology. The three types of ω-3 FA involved in human physiology are
α-linolenic acid, eicosapentaenoic acid, and docosahexaenoic acid. The theoretical
benefitof ω-3FA supplementation is the modulation of inflammation and immunity.
During illness they are readily incorporated into inflammatory cell membrane
phospholipids, antagonise the production of pro-inflammatory eicosanoids from
ω-6 arachidonic acid (e.g., leukotriene B4, thromboxane A2, prostaglandin E2),
and are precursors for inflammatory eicosanoids (e.g., thromboxane A3, prostaglandin E3, leukotriene B5). Furthermore, ω-3FA decrease the release of
pro-inflammatory cytokines such as IL-1β, IL-6, and TNF in peripheral blood
mononuclear cells and reduce iNOS expression in macrophages. Considering the
ω-3FA potential to reduce NO overproduction by limiting iNOS, their addition to
enteral formulas may advantage septic patients who are expressing Th1/M-1 inflammatory responses [3, 11, 25] (Fig. 17.2).
ω-3FA administration in the perioperative period can be considered a valuable
choice for patients undergoing major abdominal surgery. Preoperative conditioning
by supplementation with fish oils for 2–3 days in abdominal surgery significantly
reduced mortality, the need for mechanical ventilation, and length of hospital stay
[9]. According to Wichmann et al., the parenteral administration of a lipid emulsion
enriched with ω-3FA from fish oil in the postoperative period after major abdominal
surgery resulted in a significantly shorter length of hospital stay
Fig. 17.2 ω-3FA and respiratory alveolus interaction (Ma macrophages, Ne neutrophils)
186 A. Cotoia et al.
[11, 26]. ω-3FA-enriched PN significantly reduces the risk of infections and length
of both ICU and hospital stays compared with standard PN. Furthermore, ω-3FAenriched PN had potentially beneficial effects on liver chemistry, antioxidant status,
markers of inflammation, coagulation, and fatty-acid profile [
plementation of fish oil in patients with acute respiratory distress syndrome significantly improved pulmonary funct ion and reduced lung oedema, mortality, ventilator
3, 9, 1
days, and ICU length of stay [
These findings led to the recommendation
and Enteral Nutrition, the Canadian Critical Care Clinical Practice Guidelines
Committee, and the European Society for Clinical Nutrition and Metabolism to
administer ω-3FA in patients with acute lung injury and acute respirato ry distress
syndrome (ARDS) [
remain controversial.
3, 25, 29–32]. However, formulation, dosage, and duration
1, 25, 29].
by the American Society for Parenteral
27, 28]. Enteral sup-
Micronutrients
Micronutrients include vitamins and trace elements, which have central role in antiinflammatory, antioxidant and immune defence mechanisms and metabolic pathways. Oxidative stress is typically increased in critically ill patients, and reactive
oxygen species (ROS) can activate the nuclear transcription factor kappa B, which is
involved in amplifying the systemic inflammatory response syndrome [
subsequent cell injury, organ failure, and even higher mortality [11]. Clinical trials
testing the effects of antioxidants are heterogeneous on the type of antioxidant used,
antioxidant supplement ation amount given to patients [9], and timing of supplementation. Recent systematic reviews and meta-analysis [6, 11, 33] showed that overall
antioxidants were associated with a significant reduction in duration of mechanical
ventilation, a trend towards a reduction in infections, and a significant reduction in
overall mortality among patients with higher risk of death. These patients may
therefore exhibit a greater clinical improvement with antioxidant supplementation.
However, it was not possible to demonstrate any significant overall effect on ICU or
hospital length of stay.
A research strategy that combines basic investigations into the pharmacokinetic
and pharmacodynamic profiles of pharmaconutrients, with well-powered prospective clinical trials for safety and efficacy, will clarify the future of pharmaconutrition
in critical care medicine and clinical nutrition. The best antioxidant cocktail
approach has not yet been determined.
6] with
Antioxidant Vitamins
A satisfactory absorption of vitamins A, C, and E administered by the enteral route in
critically ill patients and trauma patients showed a reduction in the incidence of
17 Pharmaconutrition in Critical Care 187
organ failure and death [34, 35]. Similarly, patients with acute hypoxic respiratory
failure [9] have shown favourable results in patients receiving enteral nutrition
formula enriched with antioxidant vitamins. Furthermore, several studies have
been conducted on vitamin C that is an important antioxidant compound. Its
administration in ARDS patients and SIRS showed positive effects attributed to
free radical scavenging activity, modulation of TNF-α pathway, protection against
levels
vascular leakage, epithelial barrier disruption, and increased alveolar flu
during sepsis [3]
. Also, in severely burned patients, vitamin C demonstrated to
id
reduce wound oedema, resuscitation fluid volume requirements, and respiratory
failure [35–37].
Antioxidant Trace Elements
Trace elements, such as selenium, zinc, copper and iron, serve as cofactors to
antioxidant enzymes leading to an efficient detoxifying effect from free radicals
9, 38]. Functions and dosages of trace elements are indicated in Tables 17.2, 17.3,
[
and 17.4.
Probiotics, Prebiotics or Symbiotics
Probiotics are living microorganisms, including various types of bacteria that have
positive effects on the host health. Prebiotics, on the other hand, are indigestible
nutrients promoting the growth of these beneficial microorganisms. A combination
Table 17.2 Selenium description, functions and dosage recommended
Description Functions Dosage
The d
Essential trace mineral most
readily bioavailable in the form
of inorganic salts, such as selenate and selenite
The beneficial effects of the
addition of selenium were confirmed in the burned and
traumatised patient, but not in
septic patients
EN enteral nutrition, PN parenteral
Works as a cofactor in selenium
proteins including immune,
endocrine, and antioxidant
enzymes
Correlates with glutathione
peroxidase GP activity
Inversely correlate with
C-reactive protein,
procalcitonin, and the SOFA
score
Regulates thyroid hormones
through iodothyronine
deiodinase proteins. Selenium
level correlates with thyroid
hormone
nutrition
ietary-recommended
f 55 (20–90) μg/day
intake o
Se is required during ICU
stay
188 A. Cotoia et al.
Table 17.3 Zinc description, functions, and dosage recommended
Description Functions Dosage
Trace
mineral
Table 17.4 Iron description and functions
Description Functions Dosage
Iron is the
abundant micronutrient
Works as a cofactor with catalytic,
structural, and
involved in
healing, with DNA and RNA polymerase involved in cell growth cycle and
with enzymes involved in Paneth cells
activation
and intestinal tight junction proteins
Correlates with level of serum cytokines
IL-6 and IL-8, indicative of inflammatory stress
most
in humans
regulatory proteins
immune function
Its r
s linked to haemoproteins,
ole i
redox equilibrium, inflammatory
processes, and innate immune reactions against infections and cancer
and wound
The existing evidence does not support
the use of zinc supplementation for
patients admitted to the ICU without
risk factors for zinc deficiency and who
are tolerating enteral nutrition
In critically
<100 g/l who have passed the
hyperacute phase of their disease,
1 g ev ferric carboxymaltose can be
administered
ill patients with Hb
of the two is called symbiotics [39]. The efficacy of a probi otic product is highly
dependent on the specific strains it contains. Different strains of bacteria may have
distinct characteristics, functions, and health benefits. Some beneficial effects
include the host immunological response, the gut epithelial barrier, and the supply
of essential micronutrients and vitamins. With regard to immunological properties,
balanced T-helper cell response with upregulation of Toll-like receptors, self-lim
ited
inflammatory response, and increased IgA and IgG secretion are just few key points
of probiotics. This bacterial-epithelial cross talk helps maintain the integrity of the
gastrointestinal barrier [40–45]. In addition, a healthy microbiome is associated with
increased production of vitamins, such as vitamin K or B, as well as short-chain fatty
acids (SCFA) [42]. These SCFAs play a major role in several metabolism pathways,
such as glucose homeo stasis, lipid metabolism, and gut integrity. Unfortunately, in
the ICU, the host microbiome can transform into a so-called pathobiome [46], and
gut and lung microbiota composition can change in terms of richness and evenness
47, 48]. Among several outcome parameters, two important indications emerge
[
from the current study situation: (1) the impact on nosocomial infections, especially
ventilator-associated pneumonia, and (2) the positive effect of probiotic use on
gastrointestinal complications, particularly diarrhoea.