Добавил:
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
Скачиваний:
0
Добавлен:
02.09.2026
Размер:
21 Мб
Скачать
23 Nutrition in Acute Liver Failure and Severe Acute Pancreatitis 271
Nevertheless, semi-elemental nutrition is more expensive and has increased osmo­lality compared to polymeric nutrition formulas [47]. Semi-elemental formulas contain peptides of various chain lengths, simple sugars, glucose polymers or starch, and medium-chain triglycerides (MCTs). Polymeric formulas contain intact pro­teins, complex carbohydrates, and long-chain triglycerides (LCTs). Elemental and semi-elemental formulas have been preferred in many trials on AP because they have a better absorption prole than polymeric ones. However, several works demon­strated that standard formu nasojejunal tube. All international guidelines recommend a small peptide and medium-chain triglyceride (MCT) oil-based formulation (grade B recommendation). ESPEN guidelines recommend peptide-based formulas with a grade A recommen­dation, even if they acknowledge that a standard formula can be tried and kept if tolerated [
36].
lations are also safe and effective if administered via

IAP Management

Sixty to eighty percent of patients with severe AP may develo p an elevation in intra­abdominal pressure (IAP) [48], due to retroperitoneal edema, uid collection, ascites, and paralytic ileus [48]. Intra-abdominal hypertension is a sustained increase in IAP >12 mmHg, instead of the normal range of 0–5 mmHg, varying with respiratory cycles. IAP increments above 20 mmHg can lead to abdominal compart­ment syndrome [48]. IAP elevation is correlated with increased mortality risk (25–66%) [ loss (20–40 g/day), and proteolysis increase (up to 80%). Energy expenditure may be increased by decreased splanchnic blood ow, acidosis, and bacterial transloca­tion. EN reduces mortality and infectious complications and decreases organ failure and hospital stay; nevertheless, it may increase intraluminal pressure with IAP elevation and subsequent complications. Therefore, in patients with severe AP and IAP <15 mmHg, early EN could be started via both nasogastric and nasojejunal routes; IAP and clinical condition should be continuously monitored, evaluating gastrointestinal symptoms and signs like absence of bowel movements, abdominal distension, and high gastric residual volume. If IAP rises over 15 mmHg, EN should be initiated via the nasojejunal route starting at 20 ml/h, increasing the rate according to tolerance, eventually reducing or discontinuing EN if IAP further increases. In patients with severe AP and IAP >20 mmHg, EN should be temporarily halted, and parenteral nutrition should be started [ likely to be benecial in moderately severe and severe AP with oral/enteral feeding until fecal elastase-1 testing is repeatedly normal (200 μg/g); this therapy is routinely recommended for such patients and for a longer time for patients with >50% necrosis. The presence of exocrine pancreatic insufciency suggested by steatorrhea warrants pancreatic enzyme replacement therapy until fecal elastase-1 remains <100 μg/g (this therapy does not have to be stopped for fecal elastase-1 testing) [
42],
rising in resting energy expenditure (up to 1.49) [42
42].
Pancreatic enzyme replacement therapy is
34].
Elevated blood glucose is indicative of more severe AP. Development
],
net nitrogen
272 K. Donadello et al.
of impaired glucose tolerance can be as high as 60% during the 5 years following a rst attack of acute pancreatitis; unsurprisingly, the greatest risk is in those who develop pancreatic necrosis. Those requiring necrosectomy are among those who lose the most pancreatic parenchyma and, therefore, the major quantity of islets. The development of clinical diabetes has been estimated around 15–40% following mild or severe acute pancreatitis, respectively [
34]. Due to the loss of pancreatic paren-
chyma, insulin production is reduced, when multiple daily insulin injections may be appropriate. Various supplements, such as probiotics, glutamine, omega-3-fatty acids, and different formulations of enteral and parenteral nutrition, have been suggested to reduce inammation and improve outcome in acute pancreatitis, although different studies have given different results and the evidence is still lacking [
36, 4
2, 47]. P
robiotics are considered healthy bacteriaas they may play an important role in preventing intestinal colonization. There are no robust random­ized controlled trials (RCTs) that clearly demonstrate the effectiveness of probiotics; therefore, current guidelines do not recommend the administration of probiotics for the treatment of acute pancreatitis [13, 42, 47]. Glutamine accounts for 30– 35% of all amino-acidic nitrogen transported in plasma and is recognized to have a protec­tive role against toxic effects of circulating ammonia; in addition, it is important for nitrogen transfer between tissues (liver, lymphocytes, gut, kidney) and is the pre-
47]
astly, it has antioxidant prop-
cursor for many biologically active molecules [
; l erties and enhances intestinal health and prevents bacterial translocation [44]. While some RCTs demonstrate glutamine supplementation benet during total PN, there is still no clear evidence about its benecial effect during EN [42, 44, 47]. Arginine is a nonessential amino acid that plays a role in ureagenesis, immune function, wound healing, vasodilation, cell growth, and differentiation [44]. The supplementation of arginine is thought to increase nitric oxide levels and, therefore, to improve blood ow and tissue perfusion. Both ESPEN and ASPEN guidelines do not recommend
44]
ong-chain
its routine use, but some studies are investigating its safety [
. L polyunsaturated fatty acid derivatives may have a benecial effect on inammatory processes. At present, there are not adequately powered randomized trials that support omega-3 routine use in AP; therefore, guidelines do not suggest them
]. During acute inammation, various micronutrients are in demand, includ-
[44, 47 ing vitamins A, C, E, B6, folate, B12, and pantothenic acid. They have various roles in cell-mediated immunity, and when their levels are low, these can contribute to the poor/delayed immune response seen in AP. Deciencies of these nutrients are more common in chronic pancreatitis, but nutrition-focused physical examination can assist in identifying micronutrient deciencies in patients w
ith moderate to severe malnutrition. If micronutrient deciency is suspected, serum levels can be evaluated once inammation has been resolved, although the accuracy of these parameters as a reection of total body stores is still questionable [
41, 4
4, 47]. Z
inc levels can inuence tissue development, renewal, and repair, including proliferation and apo­ptosis. Such responses have been shown in epithelial differentiation and prolifera­tion, neuronal differentiation, and immunity. Its de
i
ble immunological disorder with both immune-decient and
revers
ciency leads to a persistent but
hyperinammatory responses. Robust studies on the efcacy of zinc
23 Nutrition in Acute Liver Failure and Severe Acute Pancreatitis 273
ACUTE PANCREATITIS
Diagnostic criteria (2 of 3):
. Upper abdominal pain
. Serum amilase or lipase (or both) > 3 x upper limit
. Imaging findings consistent with pancreatitis
all patients mild to moderate risk should be
all severe patients shoul be considered
Energy supply: 25-35 kcol/kg/dieProtein/day: 1.2-1.2 g/kg/dieCarbohydrates: 3-6g/kg/dieLipid: 2g/kg/die
. ORAL: as soon as tolerated (indipendent of serum lipase). Only exception:
. ENTERAL: within 24–48 h of admission, preferred route, semielemental
. PA REN TE RA L: only if EN route is absolutely contraindicated (bowel obstruction,
NUTRITION
nutritionally screened
malnourished
ESPEN GL
ROUTE AND TIMING
hypertriglyceridemia etiology.
formula with MCT recommended
standard
abdominal compartment syndrome, prolonged paralitic ileus, mesenteric ischemia)
SEVERITY SCORING:
Pancreatitis Activity Scoring
System
or
IAP MANAGEMENT
(Increased Abdominal Pressure: >12mmHg)
Severe AP + IAP <15mmHg
EN via nasoenteral or nasogastric
tube + monitor IAP continuously
IAP 15-20mmHg
EN only via nasojejunal tube
starting at 20ml/h + monitor IAP
continuously
IAP > 20mmHg
STOP EN +
START PN
Fig. 23.3 Acute pancreatitis: Diagnostic criteria, scoring, nutrition guidelines, feeding route and timing, IAP management
supplementation are lacking; thus, its supplementation is not recommended by guidelines [49] (Fig. 23.3).

Conclusions

Given the close relationship between gastrointestinal, liver and pancreatic function, a multidisciplinary approach is essential in case of acute organ failure. Prompt detec­tion of organ complications is vital. Early enteral nutrition, effective organ support and early complication management are the key aspects of an optimized treatment. While evidence on diagnosis, monitoring and early feeding in ALF and AP have broad expert consensus, evidence on protein, micronutrients and microbiota supple­mentation is still lacking.

References

1. Moonen PJ, Reintam Blaser A, Starkopf J, Oudemans-van Straaten HM, Van der Mullen J, Vermeulen G, Malbrain MLNG. The black box revelation: monitoring gastrointestinal function. Anaesthesiol Intensive Ther. 2018;50(1):72–81. 2017 Nov 20.
2. Grek A, Arasi L. Acute Liver Failure. AACN Adv Crit Care. 2016;27(4):420–9. https://doi.org/
10.4037/aacnacc2016324.
Govil D,
3.
Pal D. Gastrointestinal motility disorders in critically ill. Indian J Crit Care Med. 2020;24(Suppl 4):S179–82. https://doi.org/10.5005/jp-journals-10071-23614. PMID: 33354038; PMCID: PMC7724947.
https://doi.org/10.5603/AIT.a2017.0065. Epub
274 K. Donadello et al.
4. McClave SA, Gualdoni J, Nagengast A, Marsano LS, Bandy K, Martindale RG. Gastrointestinal dysfunction and feeding intolerance in critical illness: do we need an objective scoring system? Curr Gastroenterol Rep. 2020;22(1):1. https://doi.org/10.1007/
s11894-019-0736-z.
5. Atasever AG, Ozcan PE, Kasali K, Abdullah T, Orhun G, Senturk E. The frequency, risk factors, and complications of gastrointestinal dysfunction during enteral nutrition in critically ill patients. Ther Clin Risk Manag. 2018;14:385–91. https://doi.org/10.2147/TCRM.
S158492. PMID: 29503558; PMCID: PMC5827748.
6. Klingensmith NJ, Coopersmith CM. The gut as the motor of multiple organ dysfunction in critical illness. Crit Care Clin. 2016;32(2):203–12. https://doi.org/10.1016/j.ccc.2015.11.004. Epub 2016 Feb 4. PMID: 27016162; PMCID: PMC4808565.
7. Padar M, Starkopf J, Uusvel G, Reintam BA. Gastrointestinal failure affects outcome of intensive care. J Crit Care. 2019;52:103–8. https://doi.org/10.1016/j.jcrc.2019.04.001. Epub 2019 Apr 2.
8. Reintam Blaser A, Jakob SM, Starkopf J. Gastrointestinal failure in the ICU. Curr Opin Crit Care. 2016;22(2):128–41. https://doi.org/10.1097/MCC.0000000000000286.
9. Reintam Blaser A, Preiser JC, Fruhwald S, Wilmer A, Wernerman J, Benstoem C, Casaer MP, Starkopf J, van Zanten A, Rooyackers O, Jakob SM, Loudet CI, Bear DE, Elke G, Kott M, Lautenschläger I, Schäper J, Gunst J, Stoppe C, Nobile L, Fuhrmann V, Berger MM, Oudemans-van Straaten HM, Arabi YM, Deane AM, Working Group on Gastrointestinal Function within the Section of Metabolism, Endocrinology and Nutrition (MEN Section) of ESICM. Gastrointestinal dysfunction in the critically ill: a systematic scoping review and research agenda proposed by the section of metabolism, endocrinology and nutrition of the European Society of Intensive Care Medicine. Crit Care. 2020;24(1):224. https://doi.org/10.
1186/s13054-020-02889-4. PMID: 32414423; PMCID: PMC7226709.
10. Hayashi M, Ikezawa K, Ono A, Okabayashi S, Hayashi Y, Shimizu S, Mizuno T, Maeda K, Akasaka T, Naito M, Michida T, Ueshima D, Nada T, Kawaguchi K, Nakamura T, Katayama K. Evaluation of the effects of combination therapy with branched-chain amino acid and zinc supplements on nitrogen metabolism in liver cirrhosis. Hepatol Res. 2007;37(8):615–9. https://
doi.org/10.1111/j.1872-034X.2007.00095.x. Epub 2007 May 22.
11. Waseem N, Limketkai BN, Kim B, Woreta T, Gurakar A, Chen PH. Risk and prognosis of acute liver injury among hospitalized patients with hemodynamic instability: a Nationwide analysis. Ann Hepatol. 2018;17(1):119–24. https://doi.org/10.5604/01.3001.0010.7543. PMID: 29311395; PMCID: PMC8021458.
12. Sun J, Zhang J, Wang X, Ji F, Ronco C, Tian J, Yin Y. Gut-liver crosstalk in sepsis-induced liver injury. Crit Care. 2020;24(1):614. https://doi.org/10.1186/s13054-020-03327-1. PMID: 33076940; PMCID: PMC7574296.
13. Boxhoorn L, Voermans RP, Bouwense SA, Bruno MJ, Verdonk RC, Boermeester MA, van Santvoort HC, Besselink MG. Acute pancreatitis. Lancet. 2020;396(10252):726–734. doi:
https://doi.org/10.1016/S0140-6736(20)31310-6. Erratum in: Lancet 2021;398(10312):1686..
14. Ding L, Chen HY, Wang JY, Xiong HF, He WH, Xia L, Lu NH, Zhu Y. Severity of acute gastrointestinal injury grade is a good predictor of mortality in critically ill patients with acute pancreatitis. World J Gastroenterol. 2020;26(5):514–23. https://doi.org/10.3748/wjg.v26.i5.
514. PMID: 32089627; PMCID: PMC7015716.
15. Ge P, Luo Y, Okoye CS, Chen H, Liu J, Zhang G, Xu C, Chen H. Intestinal barrier damage, systemic inammatory response syndrome, and acute lung injury: a troublesome trio for acute pancreatitis. Biomed Pharmacother. 2020;132:110770. https://doi.org/10.1016/j.biopha.2020.
110770. Epub 2020 Oct 2.
16. Kappus MR. Acute hepatic failure and nutrition. Nutr Clin Pract. 2020;35(1):30–5. https://doi.
org/10.1002/ncp.10462. Epub 2019 Dec 23.
17.
Dong V, 2020;35(1):24–9. https://doi.org/10.1002/ncp.10459. Epub 2019 Dec 15.
Nanchal R, Karvellas CJ. Pathophysiology of acute liver failure. Nutr Clin Pract.
23 Nutrition in Acute Liver Failure and Severe Acute Pancreatitis 275
18. Weiss E, Paugam-Burtz C, Jaber S. Shock etiologies and uid management in liver failure. Semin Respir Crit Care Med. 2018;39(5):538–45. https://doi.org/10.1055/s-0038-1672139. Epub 2018 Nov 28.
19. Tranah TH, Edwards LA, Schnabl B, Shawcross DL. Targeting the gut-liver-immune axis to treat cirrhosis. Gut. 2021;70(5):982–94. https://doi.org/10.1136/gutjnl-2020-320786. Epub 2020
20. Pavlidis ET, Pavlidis TE. Pathophysiological consequences of obstructive jaundice and peri-
21. Bozeman MC, Benns MV, McClave SA, Miller KR, Jones CM. When can nutritional therapy
22. Bischoff SC, Bernal W, Dasarathy S, Merli M, Plank LD, Schütz T, Plauth M. ESPEN practical
23. Abenavoli L, Maurizi V, Boccuto L, Di Berardino A, Giostra N, Santori P, Scarcella ML,
24. Preiser JC, Arabi YM, Berger MM, Casaer M, McClave S, Montejo-González JC, Peake S,
25. Schütz T, Bechstein WO, Neuhaus P, Lochs H, Plauth M. Clinical practice of nutrition in acute
26. Zhang T, Sun K, Wang Y, Huang L, Lang R, Jiang W. Disruption of the gut-liver axis in the
27. Swaminathan M, Ellul MA, Cross TJ. Hepatic encephalopathy: current challenges and future
28. Tornai D, Szabo G. Emerging medical therapies for severe alcoholic hepatitis. Clin Mol
29. Lisman T, Bakhtiari K, Adelmeijer J, Meijers JC, Porte RJ, Stravitz RT. Intact thrombin
30. Harrison MF. The misunderstood coagulopathy of liver disease: a review for the acute setting.
31. Shimomura Y, Murakami T, Nagasaki M, Honda T, Goto H, Kotake K, Kurokawa T, Nonami
32.
33. Nanchal R, Subramanian R, Karvellas CJ, Hollenberg SM, Peppard WJ, Singbartl K, Truwit J,
Oct 15.
operative management. Hepatobiliary Pancreat Dis Int. 2018;17(1):17–21. https://doi.org/10.
1016/j.hbpd.2018.01.008. Epub 2018 Jan 31.
impact liver disease? Curr Gastroenterol Rep. 2014;16(10):411. https://doi.org/10.1007/
s11894-014-0411-3.
guideline: clinical nutrition in liver disease. Clin Nutr. 2020;39(12):3533–62. https://doi.org/10.
1016/j.clnu.2020.09.001. Epub 2020 Oct 27.
Procopio AC, Rasetti C, Scarpellini E. Nutritional support in acute liver failure. Diseases. 2022;10(4):108. https://doi.org/10.3390/diseases10040108. PMID: 36412602; PMCID: PMC9680263.
Reintam Blaser A, Van den Berghe G, van Zanten A, Wernerman J, Wischmeyer P. A guide to enteral nutrition in intensive care units: 10 expert tips for the daily practice. Crit Care. 2021;25 (1):424. PMC8669237.
liver failure – a European survey. Clin Nutr. 2004;23(5):975–82. https://doi.org/10.1016/j.clnu.
2004.03.005.
pathogenesis of acute-on-chronic liver failure. Eur J Gastroenterol Hepatol. 2018;30(2):130–5.
https://doi.org/10.1097/MEG.0000000000001026. PMID: 29200007; PMCID: PMC5738259.
prospects. Hepat Med. 2018;10:1–11. https://doi.org/10.2147/HMER.S118964. PMID: 29606895; PMCID: PMC5868572.
Hepatol. 2020;26(4):686–96. https://doi.org/10.3350/cmh.202 0.0145. Epub 2020 Sep
28. PMID: 32981291; PMCID: PMC7641578.
generation and decreased brinolytic capacity in patients with acute liver injury or acute liver failure. J Thromb Haemost. 2012;10(7):1312–9. https://doi.org/10.1111/j.1538-7836.2012.
04770.x.
West. J Emerg Med. 2018;19(5):863–71. https://doi.org/10.5811/westjem.2018.7.37893. Epub 2018 Aug 8. PMID: 30202500; PMCID: PMC6123093.
T. Regulation of branched-chain amino acid metabolism and pharmacological effects of branched-chain amino acids. Hepatol Res. 2004;30S:3–8. https://doi.org/10.1016/j.hepres.
2004.09.001
Honda T, Fukuda Y, Nakano I, Katano Y, Goto H, Nagasaki M, Sato Y, Murakami T, Shimomura Y. Effects of liver failure on branched-chain alpha-keto acid dehydrogenase complex in rat liver and 2004;40(3):439–45. https://doi.org/10.1016/j.jhep.2003.11.003.
Al-Khafaji AH, Killian AJ, Alquraini M, Alshammari K, Alshamsi F, Belley-Cote E, Cartin-
https://doi.org/10.1186/s13054-021-03847-4. PMID: 34906215; PMCID:
.
muscle: comparison between acute and chronic liver failure. J Hepatol.
276 K. Donadello et al.
Ceba R, Dionne JC, Galusca DM, Huang DT, Hyzy RC, Junek M, Kandiah P, Kumar G, Morgan RL, Morris PE, Olson JC, Sieracki R, Steadman R, Taylor B, Alhazzani W. Guidelines for the management of adult acute and acute-on-chronic liver failure in the ICU: endocrine, hematologic, pulmonary, and renal considerations. Crit Care Med. 2020;48(3): e173–91. https://doi.org/10.1097/CCM.0000000000004192.
34. Szatmary P, Grammatikopoulos T, Cai W, Huang W, Mukherjee R, Halloran C, Beyer G, Sutton R. Acute pancreatitis: diagnosis and treatment. Drugs. 2022;82(12):1251–76. https://doi.
org/10.1007/s40265-022-01766-4. Epub 2022 Sep 8. PMID: 36074322; PMCID:
PMC9454414.
35. Zhang R, Deng L, Jin T, Zhu P, Shi N, Jiang K, Li L, Yang X, Guo J, Yang X, Liu T, Mukherjee R, Singh VK, Windsor JA, Sutton R, Huang W, Xia Q. Hypertriglyceridaemia­associated acute pancreatitis: diagnosis and impact on severity. HPB (Oxford). 2019;21(9): 1240–9. https://doi.org/10.1016/j.hpb.2019.01.015. Epub 2019 Mar 15.
36. Rinninella E, Annetta MG, Serricchio ML, Dal Lago AA, Miggiano GA, Mele MC. Nutritional support in acute pancreatitis: from physiopathology to practice. An evidence-based approach. Eur Rev Med Pharmacol Sci. 2017;21(2):421–32.
37. James TW, Crockett SD. Management of acute pancreatitis in the rst 72 hours. Curr Opin Gastroenterol. 2018;34(5):330–5. https://doi.org/10.1097/MOG.0000000000000456. PMID: 29957661; PMCID: PMC6245573.
38. Buxbaum J, Quezada M, Chong B, Gupta N, Yu CY, Lane C, Da B, Leung K, Shulman I, Pandol S, Wu B. The pancreatitis activity scoring system predicts clinical outcomes in acute pancreatitis: ndings from a prospective cohort study. Am J Gastroenterol. 2018;113(5): 755–64. PMCID: PMC6123248.
39. Wu BU, Batech M, Quezada M, Lew D, Fujikawa K, Kung J, Jamil LH, Chen W, Afghani E, Reicher S, Buxbaum J, Pandol SJ. Dynamic measurement of disease activity in acute pancre­atitis: the pancreatitis activity scoring system. Am J Gastroenterol. 2017;112(7):1144–52.
https://doi.org/10.1038/ajg.2017.114. Epub 2017 May 2. PMID: 28462914; PMCID:
PMC5519418.
40. Ye S, Si C, Deng J, Chen X, Kong L, Zhou X, Wang W. Understanding the effects of metabolites on the gut microbiome and severe acute pancreatitis. Biomed Res Int. 2021;2021:
1516855. https://doi.org/10.1155/2021/1516855. PMID: 34712726; PMCID: PMC8548099.
41. Petrov MS, Windsor JA. Nutritional management of acute pancreatitis: the concept of gut rousing. Curr Opin Clin Nutr Metab Care. 2013;16(5):557–63. https://doi.org/10.1097/MCO.
0b013e3283638ed1.
42. Arvanitakis M, Ockenga J, Bezmarevic M, Gianotti L, KrznarićŽ, Lobo DN, Löser C, Madl C, Meier R, Phillips M, Rasmussen HH, Van Hooft JE, Bischoff SC. ESPEN guideline on clinical nutrition in acute and chronic pancreatitis. Clin Nutr. 2020;39(3):612–31. https://doi.org/10.
1016/j.clnu.2020.01.004. Epub 2020 Jan 22.
43. Hackert T, Schütte K, Malfertheiner P. The pancreas: causes for malabsorption. Viszeralmedizin. 2014;30(3):190–7. https://doi.org/10.1159/000363778. PMID: 26288593; PMCID: PMC4513827.
44. Roberts KM, Nahikian-Nelms M, Ukleja A, Lara LF. Nutritional aspects of acute pancreatitis. Gastroenterol Clin N Am. 2018;47(1):77–94. https://doi.org/10.1016/j.gtc.2017.10.002. Epub 2017 Dec 6.
45. Mandaliya DK, Seshadri S. Short chain fatty acids, pancreatic dysfunction and type 2 diabetes. Pancreatology. 2019;19(2):280–4. https://doi.org/10.1016/j.pan.2019.01.021. Epub 2019 Jan 28.
46.
Verkijk M, Gielkens HA, Lamers CB, Masclee AA. Effect of gastrin on antroduodenal motility: role of intraluminal acidity. Am J Phys. 1998;275(5):G1209–16. https://doi.org/10.1152/ajpgi.
1998.275.5.G1209.
Lodewijkx PJ,
47. Bakker OJ, Dutch Pancreatitis Study Group. Nutrition in acute pancreatitis: a critical review.
https://doi.org/10.1038/s41395-018-0048-1. Epub 2018 Mar 15. PMID: 29545634;
Besselink MG, Witteman BJ, Schepers
NJ, Gooszen HG, van Santvoort HC,
cardiovascular,
23 Nutrition in Acute Liver Failure and Severe Acute Pancreatitis 277
Expert rev. Gastroenterol Hepatol. 2016;10(5):571–80. https://doi.org/10.1586/17474124.
2016.1141048. Epub 2016 Mar 15.
48. Aggarwal A, Manrai M, Kochhar R. Fluid resuscitation in acute pancreatitis. World J Gastroenterol. 2014;20(48):18092–103. https://doi.org/10.3748/wjg.v20.i48.18092. PMID: 25561779; PMCID: PMC4277949.
49. Wang M, Phadke M, Packard D, Yadav D, Gorelick F. Zinc: Roles in pancreatic physiology and disease. Pancreatology. 2020;20(7):1413–20. https://doi.org/10.1016/j.pan.2020.08.016. Epub 2020 Sep 3. PMID: 32917512; PMCID: PMC7572834.
Chapter 24
Nutrition in Major Surgery, Intestinal Failure, and Open Abdomen
Lucia Cattin, Francesco Cundari, Silvia De Rosa, and Francesco Corradi

Introduction

The role of nutrition in the recovery process of patients undergoing major surgery, coping with intestinal failure, or managing an open abdomen condition cannot be overstated [1]. Adequate nutrition serves as a cornerstone in supporting the bodys healin
g mechanisms, enhancing immune function, and facilitating tissue repair,
thereby signicantly improving overall surgical outcomes [2, 3].
Major surgery encompasses a broad spectrum of invasive procedures that involve
us organ systems and often pose substantial physiological stress on the body. In
vario such cases, ensuring optimal nutrition becomes paramount to support the bodys increased metabolic demands and promote efcient recovery [4]. Intestinal failure presents a unique challenge wherein the gastrointestinal tract is unable to absorb nutrients and uids adequately [5]. This necessitates the implementation of
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_24.
L. Cattin Department of Anesthesiology and Intensive Care Medicine, San Bortolo Hospital of Vicenza, Veneto, Italy e-mail: lucia.cattin@aulss8.veneto.it
F. Cundari · F. Corradi Department of Pisa, Pisa, Italy e-mail: francesco.corradi@unipi.it; f.cundari@studenti.unipi.it; francesco.corradi@unipi.it
S. De Rosa ( Centre for Medical Sciences – CISMed, University of Trento, Trento, Italy
Anesthesia and Intensive Care, Santa Chiara Regional Hospital, APSS Trento, Trento, Italy e-mail: silvia.derosa@unitn.it
© The A. Cotoia et al. (eds.), Nutrition, Metabolism and Kidney Support,
https://doi.org/10.1007/978-3-031-66541-7_24
of Surgical, Medical, Molecular Pathology and Critical Care Medicine, University
✉)
Author(s), under exclusive license to Springer Nature Switzerland AG 2024
279
280 L. Cattin et al.
alternative forms of nutrition support, such as enteral or parenteral nutrition, to sustain the patients nutritional status and prevent complications associated with malnutrition.
Open abdomen conditions, freque gical interventions, pose additional complexit ies in wound management and abdom­inal wall integrity [ promoting tissue healing, preventing infection, and facilitating the closure of the abdominal cavity. Tailored nutritional interventions, including the administration of enteral or parenteral nutrition, must be carefully calibrated to meet the individual patients needs and clinical circumstances. By addressing specic nutritional requirements and adapting strategies accordingly, healthcare providers can mitigate the risk of complications, expedite wound healing, and ultimately reduce hospital­ization duration. Understanding the nuanced nutritional requirements inherent to major surgery, intestinal failure, and open abdomen management is imperative for healthcare providers. By integrating nutritional considerations into treatment plans, clinicians can optimize patient outcomes, enhance recovery trajectories, and promote overall well-being. The objective of this chapter is to underscore the importance of tailored nutritional interventions in optimizing patient outcomes and facilitating the healing process.
6]. In these cases, nutritional support plays a crucial role in
ntly stemming from traumatic injuries or sur-

Nutritional Considerations in Major Surgery

Preoperative Nutritional
The preoperative nutritional assessment aims to identify malnourished patients who may benet from perioperative interventions aimed at reducing the hypermetabolic and inammatory status associated with surgical stress on the body, thus enabling quicker recover y [ due to the frequent advanced age of patients, which affects body composition, preoperative oncological therapy, cachexia that may accompany the disease, and socioeconomic factors [1, 8] prior to surgery to allow for the implementation of necessary therapeutic strategies. Various scores for identifying nutritional risk exist, and they utilize BMI, weight loss, current food intake, and the severity of the condition. Among these, the Nutritional Risk Screening 2002 (NRS 2002) is best suited for hospitalized patients.
About the abdominal surgical population, preoperative NRS can identify indi­viduals with a signicant risk of developing complications, length of stay (LOS), and mortality [ individuals with NRS 5 and preoperative nutritional support developed complica­tions, compared to half of the patients without nutritional support. Additionally, LOS was signicantly shorter in those who received treatment [10]. Similarly, preopera­tive enteral or parenteral support reduces the risk of postoperative complications signicantly in patients with nutritional risk Subjective Global Assessment (SGA)
7]. In particular, oncology patients are at high risk of malnutrition
9]. A 2012 study conducted by Jie observed that only a quarter of
Assessment
. N
utritional screening should be performed 2–3 weeks
and Optimization
4
24 Nutrition in Major Surgery, Intestinal Failure, and Open Abdomen 281
class B or C, with a signicant impact on mortality (from 6% in the control group to
2.1% in the treatment group) [11].
To identify surgical patients at high nutritional risk, ESPEN consi ence of at least one of the following criteria [
12]:
ders the pres-
Weight loss >10% of body weight in less than 6 months or 5% in 1 month
BMI <18.5 kg/m
2
SGA score C
Albumin <30 g/l,
NRS > 5
It is important to remember that albumin is not a marker of nutritional status, whose production is inuenced by underlying inammatory states, which in turn induce a catabolic state. Serum concentration is also primarily linked to redistribu­tion and dilution secondary to uid infusion. This makes albumin an important tool for assessing the overall condition of the patient rather than their nutritional status [13]. Therefore, malnourished patients should be considered for specialized nutri­tional assessment and enteral or parenteral support if the oral or enteral route cannot ensure at least 50% of caloric and protein requirements. This support should be initiated 10–14 days before surgery [1].
Nutritional Requirements During and After Major Surgery
Preoperative conditioning involves a series of interventions aimed at fortifying the body through exercise and sufcient nutrition to withstand the stress associated with major surgery and to bolster muscle mass, which is often depleted in the postoper­ative period due to increased synthesis of acute-phase proteins [ requirements, current recommendations advocate for ensuring a protein intake ranging from 1.2 to 2 g per kilogram of body weight per day, along with a daily calorie intake of 25 kilocalories per kilogram [
15, 16].
nutritional intake proves challenging through oral feeding alone, supplementation with balanced standard formulas via enteral route is advised, reserving parenteral formulations solely for patients for whom enteral feeding is not feasible due to underlying medical conditions [
15]. Irrespective of nutritional risk, it is
recommended that all patients undergoing major surgery, except those with severe diabetes, receive a carbohydrate drink. This regimen typically consists of 800 ml the evening before surgery and an additional 400 ml 2 h before surgery, with the formulation containing 12.6% carbohydrates. This approach serves to reduce insulin resistance and mitigate patient anxiety prior to surgery [
14]. To address these
If achieving adequate
17, 18].