Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5224_Библиотеки_им_академика_М_И_Перельмана.pdf
240 C. Iacovazzo et al.
Macronutrients
The metabolic response to trauma is characterized by hypersecretion of the hormonal
triad of stress injury, i.e., glucocorticoids, catecholamines, and glucagon. The ideal
target of glucose control remains controversial in patients with trauma. Although
most authors agree that hypo- and hyperglycemia should be avoided, the exact
thresholds are still undefined [40, 80].
Besides that, the type of lipid to be administered in trauma patients is important
since ω3 fatty acids can counterbalance the inflammatory effects of ω 6 fatty acids
and favorably modulate the innate immunity involved in inflammation [89 ]. Thus,
the current recommendations for lipids in the event of trauma, including TBI,
suggest 25–40% of the total calories, with a ratio of ω3/ω6 ranging from 2:1 to 8:1
and a concentration from 2 to 6 g/day of ω3[90, 91].
Several authors have shown that trauma patients lose increased amounts of
nitrogen independently of the corresponding administered quantity and that nitrogen
excretion increases concomitantly and steadily for up to 4 weeks from the primary
injury, making it very difficult to equalize the nitrogen balance. Thus, clinical
guidelines recommend an early provision of 1.5–2.0 g/kg/day of protein, accompanied by at least 50% of energy needs up to 25–30 kcal/kg/day. A corollary of this
concept of programmed short permissive underfeeding is the interrelationship of
energy and protein intake. When energy intakes are limited, supplying greater levels
of protein, up to 1.5 g/kg/day, will improve the preservation of fat-free mass and
improve protein synthetic rates [40, 52].
Conclusions
In this chapter, we have shown how nutritional support in the severe burn or trauma
patient shares common aspects with the management of other categories of critically
ill patients but how it also has some specific peculiarities, chief among them a focus
on a hypermetabolic reaction and a more prominent catabolism, and a more significant role for immunonutrition.
References
1. Porter C, Tompkins RG, Finnerty CC, Sidossis LS, Sunan OE, Herndon DN. The metabolic
stress response to burn trauma: current understanding and therapies. Lancet. 2016;388(10052):
1417–26.
2. Jacobs DG, Jacobs DO, Kudsk KA, Moore FA, Oswanski MF, Poole GV, et al. Practice
management guidelines for nutritional support of the trauma patient. J Trauma. 2004;57(3):
660–78.
21 Nutrition in Trauma and Burns 241
3. Clark A, Imran J, Madni T, Wolf SE. Nutrition and metabolism in burn patients. Burns Trauma.
2017;5:11.
4. Rousseau AF, Losser MR, Ichai C, Berger MM. ESPEN endorsed recommendations: nutritional
therapy in major burns. Clin Nutr. 2013;32:497–502.
5. Porter C, Tompkins RG, Finnerty CC, Sidossis LS, Suman OE, Herndon DN. The metabolic
stress response to burn trauma:
1417–26.
6. Hart DW, Wolf SE, Mlcak R, Chinkes DL, Ramzy PI, Obeng MK, et al. Persistence of muscle
catabolism after severe burn. Surgery. 2000;128(2):312–9.
7. Porter C, Herndon DN, Børsheim E, Bhattarai N, Chao T, Reidy PT, et al. Long-term skeletal
muscle mitochondrial dysfunction is associated with hypermetabolism in severely burned
children. J Burn Care Res. 2016;37(1):53–63.
8. Yu YM, Tompkins RG, Ryan CM, Young VR. The metabolic basis of the increase in energy
expenditure in severely burned patients. J Parenter Enter Nutr. 1999;23(3):160–8.
9. Suri MP, Dhingra VJS, Raibagkar SC, Mehta DR. Nutrition in burns: need for an aggressive
dynamic approach. Burns. 2006;32(7):880–4.
10. Barret JP, Jeschke MG, Herndon DN. Fatty infiltration of the liver in severely burned pediatric
patients: autopsy findings and clinical implications. J Trauma. 2001;51(4):736–9.
11. Bower RH, Cerra FB, Bershadsky B, Licari JJ, Hoyt DB, Jensen GL, et al. Early enteral
administration of a formula (impact) supplemented with arginine, nucleotides, and fish oil in
intensive care unit patients: results of a multicenter, prospective, randomized, clinical trial. Crit
Care Med. 1995;23(3):436–49.
12. Tihista S, Echavarria E. Effect of omega 3 polyunsaturated fatty acids derived from fish oil in
major burn patients: a prospective randomized controlled trial. Clin Nutr. 2018;37(1):107–12.
13. Boldeanu L, Boldeanu MV, Bogdan M, Meca AD, Coman CG, Buca BR, et al. Immunological
approaches and therapy in burns (Review). Exp Ther Med. 2020;20(3):2361–7.
14. Arabi YM, Aldawood AS, Haddad SH, Al-Dorzi HM, Tamim HM, Jones G, et al. Permissive
underfeeding or standard enteral feeding in critically ill adults. N Engl J Med. 2015;372(25):
2398–408.
15. Herndon DN, Barrow RE, Stein M, Linares H, Rutan TC, Rutan R, et al. Increased mortality
with intravenous supplemental feeding in severely burned patients. J Burn Care Rehabil.
1989;10(4):309–13.
16. Hamblin MR. Novel pharmacotherapy for burn wounds: what are the advancements. Expert
Opin Pharmacother. 2019;20(3):305–21.
17. Moreira E, Burghi G, Manzanares W. Update on metabolism and nutrition therapy in critically
ill burned patients. Med Intensiva. 2018;42:306–16.
18. da Silva JSV, Seres DS, Sabino K, Adams SC, Berdahl GJ, Citty SW, et al. ASPEN consensus
recommendations for refeeding syndrome. Nutr Clin Pract. 2020;35(2):178–95.
19. Boirie Y, Dangin M, Gachon P, Vasson MP, Maubois JL, Beaufrère B. Slow and fast dietary
proteins differently modulate postprandial protein accretion. Proc Natl Acad Sci USA. 1997;94
(26):14930–5.
20. Dangin M, Boirie Y, Guillet C, Beaufrere B. Influence of the protein digestion rate on protein
turnover in young and elderly subjects. J Nutr. 2002;132:3228S–33S.
21. Teixeira FJ, Santos HO, Howell SL, Pimentel GD. Whey protein in cancer therapy: a narrative
review. Pharmacol Res. 2019;144:245–56.
22. Bumrungpert A,
protein supplementation improves nutritional status, glutathione levels, and immune function in
cancer patients: a randomized, double-blind controlled trial. J Med Food. 2018;21(6):612–6.
23.
Masters B,
low-carbohydrate, high-protein, high-fat enteral feeds for burns. Cochrane Database Syst
Rev. 2012;1:CD006122.
Pavadhgul
Aarabi S, Sidhwa F, Wood F. High-carbohydrate, high-protein, low-fat versus
current understanding and therapies. Lancet. 2016;388(10052):
P, Nunthanawanich P, Sirikanchanarod A, Adulbhan A. Whey
242 C. Iacovazzo et al.
24. Zhou LM, Xu JY, Rao CP, Han VS, Wan Z, Qin LQ. Effect of whey supplementation on
circulating C-reactive protein: a meta-analysis of randomized controlled trials. Nutrients.
2015;7:1131–43.
25. Mosier MJ, Pham TN, Klein MB, Gibran NS, Arnoldo BD, Gamelli RL, et al. Early enteral
nutrition
Burn Care Res. 2011;32(1):104–9.
26. Grammatikopoulou MG, Theodoridis
Dardavessis T, et al. AGREEing on guidelines for nutrition management of adult severe burn
patients. JPEN J Parenter Enteral Nutr. 2019;43(4):490–6.
27. Klein GL, Herndon DN, Chen TC, Kulp G, Holick MF. Standard multivitamin supplementation
does not improve vitamin D insufficiency after burns. J Bone Miner Metab. 2009;27(4):502–6.
28. Berger MM. Antioxidant micronutrients in major trauma and burns: evidence and practice. Nutr
Clin Pract. 2006;21(5):438–49.
29. Rock CL, Dechert RE, Khilnani R, Parker RS, Rodriguez JL. Carotenoids and antioxidant
vitamins in patients after burn injury. J Burn Care Rehabil. 1997;18(3):269–78.
30. Berger MM, Shenkin A. Trace element requirements in critically ill burned patients. J Trace
Elem Med Biol. 2007;21(Suppl 1):44–8.
31. Alexander JW, Supp DM. Role of arginine and omega-3 fatty acids in wound healing and
infection. Adv Wound Care (New Rochelle). 2014;3(11):682–90.
32. Kurmis R, Parker A, Greenwood J. The use of immunonutrition in burn injury care: where
are we? J Burn Care Res. 2010;31:677–91.
33. Zhu X, Pribis JP, Rodriguez PC, Morris SM Jr, Vodovotz Y, Billiar TR, et al. The central role of
arginine catabolism in T-cell dysfunction and increased susceptibility to infection after physical
injury. Ann Surg. 2014;259(1):171–8.
34. Horiguchi H, Loftus TJ, Hawkins RB, Raymond SL, Stortz JA, Hollen MK, et al. Innate
immunity in the persistent inflammation, immunosuppression, and catabolism syndrome and
its implications for therapy. Front Immunol. 2018;9:595.
35. Wibbenmeyer LA, Mitchell MA, Newel IM, Faucher LD, Amelon MJ, Ruffin TO, et al. Effect
of a fish oil and arginine-fortified diet in thermally injured patients. J Burn Care Res. 2006;27
(5):694–702.
36. Hess JR, Greenberg NA. The role of nucleotides in the immune and gastrointestinal systems:
potential clinical applications. Nutr Clin Pract. 2012;27(2):281–94.
37. Vicic VK, Radman M, Kovacic V. Early initiation of enteral nutrition improves outcomes in
burn disease. Asia Pac J Clin Nutr. 2013;22(4):543–7.
38. ISBI Practice Guidelines Committee. ISBI practice guidelines for burn care. Burns. 2016;42(5):
953–1021.
39. Santora R, Kozar RA. Molecular mechanisms of pharmaconutrients. J Surg Res. 2010;161(2):
288–94.
40. Singer P, Blaser AR, Berger MM, Alhazzani W, Calder PC, Casaer MP, et al. ESPEN guideline
on clinical nutrition in the intensive care unit. Clin Nutr. 2019;38(1):48–79.
41. Huber S, Biberthaler P, Delhey P, Trentzsch H, Winter H, van Griensven M, et al. Predictors of
poor outcomes after significant chest trauma in multiply injured patients: a retrospective
analysis from the German Trauma Registry (Trauma Register DGU®). Scand J Trauma Resusc
Emerg Med. 2014;22:52.
42. Bar-Or D, Bar-Or R, Rael LT, Brody EN. Oxidative stress in severe acute illness. Redox Biol.
2015;4:340–5.
43. Vincent J. Nosocomial infections in adult intensive-care units. Lancet. 2003;361:2068–77.
44. Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013;369(9):840–51.
45. Papurica M, Rogobete AF, Sandesc D, Dumache R, Cradigati CA, Sarandan M, et al. Advances
in biomarkers in critical ill polytrauma patients. Clin Lab. 2016;62(6):977
46.
Rogobete AF, Sandesc D, Papurica M, Stoicescu ER, Popovici SE, Bratu LM, et al. The
influence of metabolic imbalances and oxidative stress on the outcome of critically ill
polytrauma patients: a review. Burns Trauma. 2017;5:8.
in burns: compliance with guidelines and associated outcomes in a multicenter study. J
X, Gkiouras K, Stamouli EM, Mavrantoni ME,
–86.
21 Nutrition in Trauma and Burns 243
47. Meagher AD, Zar BL. Epidemiology. In: Feliciano DV, Mattox KL, Moore EE, editors.
Trauma. 9th ed. New York: McGraw Hill; 2020.
48. Centers for Disease Control and Prevention. Key injury and violence data. https://www.cdc.
gov/injury/wisqars/overview/key_data.html. Accessed Aug 2021.
49. Demetriades D, Kimbrell B, Salim
mature urban trauma system: is “trimodal” distribution a valid concept? J Am Coll Surg.
2005;201(3):343–8.
50. Casaer MP, Mesotten D, Hermans G, Wouters PJ, Schetz M, Meyfroidt G, et al. Early versus
late parenteral nutrition in critically ill adults. N Engl J Med. 2011;365(6):506–17.
51. Cahill NE, Dhaliwal R, Day AG, Jiang X, Heyland DK. Nutrition therapy in the critical care
setting: what is “best achievable” practice? An international multicenter observational study.
Crit Care Med. 2010;38(2):395–401.
52. McClave SA, Taylor BE, Martindale RG, Warren MM, Johnson DR, Braunschweig C, 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 (ASPEN). JPEN J Parenter Enteral Nutr. 2016;40(2):159–211.
53. De Waele E, Jakubowski JR, Stocker R, Wischmeyer PE. Review of evolution and current
status of protein requirements and provision in acute illness and critical care. Clin Nutr. 2021;40
(5):2958–73.
54. Hoffer LJ, Bistrian BR. Appropriate protein provision in critical illness: a systematic and
narrative review. Am J Clin Nutr. 2012;96(3):591–600.
55. Hoffer LJ. Protein and energy provision in critical illness. Am J Clin Nutr. 2003;78(5):906–11.
56. Hoffer LJ, Bistrian BR. Why critically ill patients are protein deprived. JPEN J Parenter Enteral
Nutr. 2013;37(4):441.
57. Hoffer LJ, Bistrian BR. Nutrition in critical illness: a current conundrum. F1000Res. 2016;5:
2531.
58. Zusman O, Theilla M, Cohen J, Kagan I, Bendavid I, Singer P. Resting energy expenditure,
calorie and protein consumption in critically ill patients: a retrospective cohort study. Crit Care.
2016;20:367.
59. Van der Kuip M, de Meer K, Oosterveld MJS, Lafeber HN, Gemke RJBJ. Simple and accurate
assessment of energy expenditure in ventilated paediatric intensive care patients. Clin Nutr.
2004;23:657–63.
60. Tobin MJ. Respiratory monitoring during mechanical ventilation. Mech Vent. 1990;6:679–709.
61. Rostami E. Glucose and the injured brain-monitored in the neurointensive care unit. Front
Neurol. 2014;5:91.
62. Hartl WH, Jauch KW. Metabolic self-destruction in critically ill patients: origins, mechanisms
and therapeutic principles. Nutrition. 2014;30:261–7.
63. Collier BR, Giladi A, Dossett LA, Dyer L, Fleming SB, Cotton BA. Impact of high-dose
antioxidants on outcomes in acutely injured patients. JPEN J Parenter Enter Nutr. 2008;32:384–
8.
64. Krishnan JA, Parce PB, Martinez A, Diette GB, Brower RG. Caloric intake in medical ICU
patients: consistency of care with guidelines and relationship to clinical outcomes. Chest.
2003;124(1):297–305.
65. Luca L, Rogobete AF, Bedreag OH, Sarandan M, Cradigati CA, Papurica M, et al. Intracranial
pressure monitoring as a part of multimodal monitoring management of patients with critical
polytrauma: correlation between optimised intensive therapy according to intracranial pressure
parameters and clinical picture. Turk J Anaesthesiol Reanim. 2015;43:412–7.
66. Doley J, Phillips W. Coding for malnutrition in the hospital: does it change reimbursement. Nutr
Clin Pract. 2019;34(6):823–31.
67. Perel P, Yanagawa T, Bunn F, Roberts I, Wentz R, Pierro A. Nutritional support for headinjured patients. Cochrane Database Syst Rev. 2006;18:CD001530.
68. Bistrian BR, Askew W, Erdman JW, Oria MP. Nutrition and traumatic brain injury: a perspective from the Institute of Medicine report. JPEN J Parenter Enteral Nutr. 2011;35:556–9.
A, Velmahos G, Rhee P, Preston C, et al. Trauma deaths in a
244 C. Iacovazzo et al.
69. Hartl R, Gerber LM, Ni Q, Ghajar J. Effect of early nutrition on deaths due to severe traumatic
brain injury. J Neurosurg. 2008;109:50–6.
70. Wang X, Dong Y, Han X, Qi XQ, Huang CG, Hou LJ. Nutritional support for patients
sustaining traumatic brain injury: a systematic review and meta-analysis of prospective studies.
PLoS One. 2013;8:e58838.
71. Reintam Blaser A, Starkopf
enteral nutrition in critically ill patients: ESICM clinical practice guidelines. Intensive Care
Med. 2017;43(3):380–98.
72. Pettersson L, Ryden S, Smedberg M, Tjader I, Rooyackers O, Wernerman J. Validation of a
point-of-care instrument for bedside glutamine screening in the intensive care unit. Clin Nutr.
2017;36:186–90.
73. Chapple LS, Deane AM, Williams LT, Strickland R, Schultz C, Lange K, et al. Longitudinal
changes in anthropometrics and impact on self-reported physical function after traumatic brain
injury. Crit Care Resusc. 2017;19:29–36.
74. Kompan L, Vidmar G, Spindler-Vesel A, Pecar J. Is early enteral nutrition a risk factor for
gastric intolerance and pneumonia. Clin Nutr. 2004;23:527–32.
75. Justo Meirelles CM, de Aguilar-Nascimento JE. Enteral or parenteral nutrition in traumatic
brain injury: a prospective randomized trial. Nutr Hosp. 2011;26:1120–6.
76. Fan M, Wang Q, Fang W, Jiang Y, Li L, Sun P, et al. Early enteral combined with parenteral
nutrition treatment for severe traumatic brain injury: effects on immune function, nutritional
status and outcomes. Chin Med Sci J. 2016;31:213–20.
77. Genton L, Pichard C. Massive N2 loss protein catabolism and requirements in severe illness. Int
J Vitam Nutr Res. 2011;81:143–52.
78. Pan J, Shaffer R, Sinno Z, Tyler M, Ghosh J. The obesity paradox in ICU patients. Conf Proc
IEEE Eng Med Biol Soc. 2017;2017:3360–4.
79. Dickerson RN, Patel JJ, McClain CJ. Protein and calorie requirements associated with the
presence of obesity. Nutr Clin Pract. 2017;32:86S–93S.
80. Carney N, Totten AM, O’Reilly C, Ullman JS, Hawryluk GW, Bell MJ, et al. Guidelines for the
management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017;80:6–15.
81. Cook AM, Peppard A, Magnuson B. Nutrition considerations in traumatic brain injury. Nutr
Clin Pract. 2008;23:608–20.
82. Painter TJ, Rickerds J, Alban RF. Immune enhancing nutrition in traumatic brain injury – a
preliminary study. Int J Surg. 2015;21:70–4.
83. Cotoia A, Paradiso R, Ferrara G, Borriello G, Santoro F, Spina I, et al. Modifications of lung
microbiota structure in traumatic brain injury ventilated patients according to time and enteral
feeding formulas: a prospective randomized study. Crit Care. 2023;27(1):244.
84. Cotoia A, Cantatore LP, Beck R, Tullo L, Fortarezza D, Marchese F, et al. Immunological
effects of glutamine supplementation in polytrauma patients in intensive care unit. J Anesth
Analg Crit Care. 2022;2(1):41.
85. Clifton GL, Robertson CS, Choi SC. Assessment of nutritional requirements of head-injured
patients. J Neurosurg. 1986;64:895–901.
86. Osuka A, Uno T, Nakanishi J, Hinokiyama H, Takahashi Y, Matsuoka T. Energy expenditure in
patients with severe head injury: controlled normothermia with sedation and neuromuscular
blockade. J Crit Care. 2013;28(218):e9–13.
87. Mtaweh H, Smith R, Kochanek PM, Wisniewski SR, Fabio A, Vavilala MS, et al. Energy
expenditure in children after severe traumatic brain injury. Pediatr Crit Care Med. 2014;15:
242–9.
88. Badjatia N, Vespa P. Monitoring nutrition and glucose in acute brain injury. Neurocrit Care.
2014;21(Suppl 2):S159–67.
Wali
89.
ke JW. Tube feeding syndrome in head and neck surgery. Arch Otolaryngol.1969;89:533–6.
J, Alhazzani W, Berger MM, Casaer MP, Deane AM, et al. Early
21 Nutrition in Trauma and Burns 245
90. van der Meij BS, van Bokhorst-de van der Schueren MA, Langius JA, Brouwer IA, van
Leeuwen PA. n-3 PUFAs in cancer, surgery, and critical care: a systematic review on clinical
effects, incorporation, and washout of oral or enteral compared with parenteral supplementation. Am J Clin Nutr. 2011;94(5):1248–65.
Scrimgeour AG,
91.
Condlin ML. Nutritional treatment for traumatic brain injury. J Neurotrauma.
2014;31:989–99.
Chapter 22
Nutrition in Sepsis, AKI, and CRRT
Vedran Premuzic and Armin Atic
Introduction
Nutrition in critically ill patients is a challenging issue with the potential for both
benefit and harm, dependent on adequate patient evaluation, nutrition type, timing,
follow-up, and frequent reassessments. Sepsis represents a metabolically active state
in which the response relies on the patient’s existing nutritional resources and
nutritional intake and generates large amounts of waste products and toxins. Significant cofactors include malnutrition and prior comorbidities, both increasing the risk
of acute kidney injury (AKI) and further complicating nutritional assessment and
prescription. Continuous renal replacement therapy (CRRT) adds complexity to the
metabolic mosaic of critically ill septic patients with AKI, affecting the baseline
metabolic state, clearance of compounds, and removal of proteins, free amino acids,
vitamins, and trace elements. One hallmark of AKI is the loss of kidney homeostatic
function, leading to a pro-inflammatory state and dysfunction in other organs,
contributing to the high mortality of AKI, prevalent in sepsis. Derangements in
homeostatic balance result in catabolism, protein-energy wasting (PEW), and fat
mass depletion, further enhanced by insulin resistance and the release of inflammatory cytokines. This triggers protein catabolism, increased amino-acid turnover,
negative nitrogen balance, hyperglycemia, altered lipid metabolism, and water,
electrolyte, and acid–base imbalances [
also affected by other particularities of their treatment during the intensive care unit
stay, including mechanical ventilation and the effects of intravenous drugs and
fluids. Each element of this topic presents pitfalls that may lead to errors in the
1, 2]. Additionally, critically ill patients are
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_22.
V. Premuzic (
Nephrology, Hypertension, Dialysis and Transplantation, University Hospital Center Zagreb,
Zagreb, Croatia
© 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_22
✉) · A. Atic
247
248 V. Premuzic and A. Atic
assessment of the patient, nutrition prescription, micronutrient and vitamin prescription, and the timing or route of nutrition administration.
General Considerations
One of the key elements of adequate nutrition in critically ill patients is the correct
assessment and frequent reassessment of nutritional requirements. In septic patients
with AKI treated with CRRT, this can be a cumbersome task due to the limitations of
currently available methods validated in other groups of patients. Despite these
limitations, adequate assessment and individualization of nutrition are necessary to
avoid the risks of under or overfeeding. Overfeeding in critically ill patients can
occur due to inappropriate nutrition or poor (re)assessment of the nutrition status,
leading to hyperglycemia, liver steatosis, and an increased risk of infections. A
potential pitfall in nutritional assessment is the failure to account for
non-nutritional calories from medications and volume repletion. The most common
sources of iatrogenic intake of non-nutritional calories are glucose solutions,
propofol, and citrate anticoagulation. All these agents are commonly used in critically ill patients, with citrate frequently used for anticoagulation in CRRT. The
caloric intake of citrate depends on the concentration used for anticoagulation, the
sieving coefficient, filter blood flow, and the infusion rate. In general, citrate
anticoagulation may add 100–200 kcal/day [3]. The most used glucose solutions
are 5% glucose, which add 200 kcal/L of infusion. Propofol contains an emulsifier
(egg phospholipid) and 10% soybean oil, which amount to 1.1 kcal/mL. The caloric
intake depends on the infusion rate, but at an average infusion rate of 20 mL/h,
propofol adds 528 kcal/day [4]. During the initial stages of critical illness, when
patients are typically on low-caloric feeds, non-nutritional calories represent a third
of the total caloric intake [4]. Studies have reported that citrate anticoagulation and
high-dose propofol sedation warrant close monitoring for the risk of overfeeding
[4, 5]. Although a major benefit of CRRT is its ability for volume clearance, attention
must be given to the total volume of nutrition given. Due to the high efficiency of
CRRT for volume clearance, the use of concentrated enteral feeds is rarely
required [6].
Assessment of Nutritional Needs
Nutritional assessment in critically ill patients on CRRT is particularly challenging,
as no available tool has adequate sensitivity for standard use (Table 22.1). Available
methods for nutritional assessment include screening scores, anthropometric measurements, biochemical parameters, and radiological methods. However, all are
burdened by a lack of validation or large variability in critically ill patients. In
critically ill patients, ASPEN recommends the use of nutritional risk screening
22 Nutrition in Sepsis, AKI, and CRRT 249
Table 22.1 Nutritional assessment in patients with AKI and sepsis treated with CRRT
Assessment type Comments
Screening scores SGA
NRS 2002 Part of GLIM criteria
NUTRIC Not validated in AKI
Anthropometry BMI Assessing baseline weight may be difficult
Skin fold thickness May be affected by edema
Grip strength Only possible in conscious patients
Indirect/imaging
methods
Laboratory
parameters
ubjective global a
SGA s
the critically ill, GLIM global leadership initiative on malnutrition, BMI body mass index, BIA
bioimpedance analysis, CT computed tomography, IGF-1 insulin like growth factor, CRRT continuous renal replacement therapy, AKI acute kidney injury
BIA Affected by fluid shifts; Not reliable in criti-
Indirect calorimetry Gold standard for critically ill patients
Ultrasound Lack of defined cut-off values; Experimental
CT Experimental
Stable isotope
measurement
Albumin Negative acute phase
Prealbumin Negative acute phase reactant; Not reliable in
IGF-1 Limited data
Lipids Do
ssessment, NRS 2002 nutritional risk screening, NUTRIC nutrition risk in
cally ill
Difficult to obtain; Rarely used
reactant; Not
acutely ill
acutely ill
in AKI
not reflect nutrition status
reliable in
(NRS 2002) or nutrition risk in the critically ill (NUTRIC) scores; however, only
NRS 2002 is validated in AKI. Additionally, subjective global assessment (SGA) is
also validated in AKI, and most scores are developed and compared to SGA. The
Global Leadership Initiative on Malnutrition (GLIM) has developed an approach for
defining malnutrition independent of the etiology. The approach includes two
steps—the use of a screening tool (such as NRS 2002) and diagnostic asse
ssment,
which must include one etiological and one phenotypical criterion. Phenotypic
criteria are non-volitional weight loss, low BMI, and reduced muscle mass. Etiological criteria are reduced food intake or assimilation and disease burden/inflammation
7]. These criteria have not been validated in ICU patients; however, they reflect the
[
need for a multimodal approach to critically ill patients.
Estimating lean body mass can be achieved by imaging methods, such as
ultrasound, multi-slice computed tomography (MSCT), or stable isotope measurement, which may be particularly useful for diagnosing sarcopenia. However, these
methods are not widely used, and the direct benefits in treatmen
t guidance are not yet
established. The lack of cut-off values for muscle thickness limits the use of
ultrasound for the diagnosis of muscle wasting; nevertheless, it may play a role in
monitoring patients and assessing the effects of nutritional interventions. Ultrasound
is advantageous as it is not affected by fluid shifts frequently present in critically ill
250 V. Premuzic and A. Atic
patients [8]. Indirect calorimetry offers great value for mechanically ventilated
patients, allowing the measurement of VO
and VCO2 through the ventilator. Its
2
use for guiding energy delivery is associated with decreased short-term mortality in
ICU patients [
9]. Interestingly, in critically ill patients, sepsis does not seem to alter
resting energy expenditure [10]. For these reasons, it is considered the gold standard
in critically ill patients and is recommended in both the ASPEN and ESPEN
guidelines. However, the use of CRRT may affect the use of indirect calorimetry
due to unpredictable net CO
removal due to CO2 exchange during blood purifica-
2
tion, citrate anticoagulation, loss of heat during extracorporeal circulation, as well as
an increase in CO
study directly evaluating the effects of CRRT on VCO
when a bicarbonate-based dialysate is used [11]. However, in a
2
,VO2, and resting energy
2
expenditure, no clinically valid relevant alterations were noted [12]. However, highdose continuous venovenous hemofiltration induced a lower metabolism and
increased CO
removal, again emphasizing the need for frequent metabolic need
2
reassessments based on the clinical course as well as important changes in treatment.
In the same study, the only CRRT-related factor of significance to the measured
values was the use of citrate anticoagulation. Bioimpedance analysis (BIA) is a
simple tool using alternating electrical currents to es
timate the fat and fat-free mass,
total body water, and intra- and extravascular water. It has an established role in
chronic kidney disease (CKD) and dialysis patients; however, the equations used for
the estimates are derived from the general population, and the method works from
the assumpti on of equal distribution of fluids in the body, which is infrequent in
critically ill patients, making BIA non-reliable in this patient populatio n
13]. Anthropometric measures, including triceps skin fold thickness, body mass
[
index, or arm circumference, are not validated in critically ill patients, particularly
considering frequent changes in body weight and fluid shifts. Standardly used
laboratory parameters for nutritional status assessment include albumin, prealbumin,
lipid levels, and some other parameters such as insulin-like growth factor 1 (IGF-1).
Albumin, prealbumin, and lipids offer no benefit i
n assessing the nutritional status as
albumin and prealbumin levels are decreased as part of the inflammatory response,
while lipid levels do not correlate with the nutritional status. These parameters can be
used for assessment of disease severity and poorer outcomes.
Metabolic Changes Induced by Sepsis, AKI, and CRRT
Energy R
Adequate energy requirements in critically ill patients have not yet been defined, as
optimal data are lacking. Recommendations for high caloric intakes exist; however,
studies have shown that in patients with AKI treated with CRRT, these were not
associated with RRT-free, ICU-free, or hospital-free days [6, 14]. Determining
adequate estimated energy expenditure (EE) depends on the patient’s normal state
(dry weight) and comorbidities. Patients requiring CRRT are frequently
equirements