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
22 Nutrition in Sepsis, AKI,
and CRRT 251
hypervolemic, and appropriate assessment is cumbersome. Current guidelines recommend meeting 70% of estimated energy expenditure in the first 24–48 h, which
increases to 80–100% on the third day. ASPEN and ESPEN guidelines recommend
20–30 kcal/kg of total daily caloric intake.
Protein Metabolism
The catabolic state of critical illness initially utilizes stored carbohydrates by breaking down the glycogen stored in the liver and skeletal muscle. After this resource is
exhausted, protein is degraded, and the amino acids are used for gluconeogenesis,
resulting in a net loss of 1.3 to 1.8 g/kg IBW-1 day-1, or 1% of muscle mass per day
[15]. The process cannot be reversed solely by increasing the availability of amino
acids; however, interventions may help enhance the overall nitrogen balance. Furthermore, there is a reduction in the uptake of amino acids in skeletal muscles,
disruption in the pool of intra and extracellular amino acids, and decreased synthesis
of new protein, leading to overall protein catabolism and a negative nitrogen balance
(Fig. 22.1)[16].
RRT invariably leads to an increased loss of free amino acids, and in patients with
AKI, the daily amino acid loss can rise up to 15 g/day [17, 18]. The combination of
RRT-induced amino acid losses and disturbances in the amino acid pool leads to a
conditional transformation of several nonessential amino acids into essential ones
Acute
kidney
injury
Hypoproteinemia
Continuous
renal
replacement
therapy
Fig. 22.1 Effects of AKI, sepsis, and CRRT on protein metabolism
•Uremia and acidosis
• Catabolic hormone
release
• Proteinuria
Sepsis
• Free amino acid clearance
• Protein clearance
• Negative nitrogen balance
• Stored protein catabolism
• Decreased synthesis de
novo
• Shunting of free amino
acids to the liver
252 V. Premuzic and A. Atic
(e.g., tyrosine, arginine) [19]. Glutamine is postulated to provide additional benefits
owing to its diverse metabolic and immunomodulatory roles. It can act as a substrate
in gluconeogenesis, serve as a precursor for endogenous antioxidants, and exhibit
positive effects on insulin resistance that often develops during stress. Furthermore,
animal studies have indicated that glutamine may p revent acute kidney injury (AKI)
by reducing oxidative stress [
day [20]. Potential harm from separate glutamine infusion was demonstrated in a
study by Heyland et al., which is a post-hoc analysis of patients with multi-organ
failure. However, they included critically ill patients of different etiologies and did
not include a separate analysis for AKI or CRRT patients [21]. The study found
negative effects of combined selenium, zinc, vitamins E and C, and beta-carotene
substitution. Nevertheless, despite these findings, some guidelines, including
ESPEN, recommend their supplementation during CRRT as well as in burn patients.
Despite the lack of clear evidence of harm, the Surviving Sepsis Guidelines recommend against the use of glutamine in sepsis [
]. CRRT causes losses of up to 1.2 g of glutamine per
3
22].
Lipid Metabolism
Primary disturbances of lipid metabolism in AKI stem from the reduced activity of
hepatic and lipoprotein lipases, leading to increased lipolysis, elevated serum triglyceride levels, and reduced HDL cholesterol. Sepsis induces similar metabolic
changes, while in AKI, the degree of lipid oxidation to carbohydrates appears to be
higher than in other conditions, persisting despite a high carbohydrate intake in AKI
patients [23
not necessitate additional changes in nutrition prescription. Lipid formulations
enable higher caloric intake while avoiding excessive carbohydrate intake and
serve as a source of essential fatty acids and lipid-soluble vitamins.
Hypertriglyceridemia, typical in AKI patients, requires regular monitoring of triglyceride concentration. Another potential benefit of lipid formulations is the delivery of polyunsaturated fatty acids, which may confer an immunological advantage.
However, the Surviving Sepsis Guidelines recommend against the use of omega-3
fatty acids in septic patients, as one randomized controlled trial found harm in
patients treated with omega-3 FAs, and other studies have reported little to no
benefit while using different compounds in their nutrition, potentially influencing
the results [
relies on their transport by L-carnitine, an amino acid derivative. L-carnitine has
been extensively studied in septic shock patients, yet most randomized controlled
trials (RCTs) and meta-analyses indicate no significant effects of L-carnitine on
survival or the development of multi-organ failure in septic shock patients. Despite
its potential depletion in patients undergoing CRRT, as carnitine is filtered, there is
insufficient data available to make recommendations regarding L-carnitine supplementation in these patients at present.
]. CRRT does not affect lipid metabolism, and its implementation does
The intramitochondrial availability of medium-chain fatty acids
24].
22 Nutrition in Sepsis, AKI, and CRRT 253
Vitamins and Trace Elements
Previously, it was believed that the primary source of vitamin and trace element
losses in patients with AKI was associated with CRRT. This assumption was based
on measured concentrations of these molecules in the effluent, suggesting that CRRT
might be responsible for deficiencies of water-soluble vitamins and trace elements in
AKI. However, a recent study comparing patients with severe AKI treated with or
without CRRT revealed that most of these patients already exhibited altered vitamin
and trace element status before treatment. Furthermore, deficiencies in the measured
compounds among AKI patients showed no significant difference between the
CRRT and non-CRRT groups [25]. Significant differences were noted only for
carnitine and glutamate, whereas all water-soluble vitamins and trace elements
were detectable in the effluent. Despite studies indicating associations between
increased mortality and deficiencies in vitamins and trace minerals, no study has
yet confirmed any survival benefit from supplementation of these deficient compounds. Nevertheless, ESPEN guidelines recommend monitoring for de ficiencies
[12, 26, 27]. The Surviving Sepsis Guidelines advise against selenium supplementation and do not specifically mention other trace elements or vitamins.
Phosphates
Beyond routine electrolyte management in critically ill patients, the utilization of
CRRT is linked to notable rates of hypophosphatemia. This condition is correlated
with prolonged respiratory failure and a slower weaning process from mechanical
ventilation, as well as generalized muscle weakness and myocardial dysfunction
[28]. The occurrence and severity of hypophosphatemia depend on the intensity of
CRRT, necessitating suitable prevention and treatment for all patients undergoing
CRRT. Supplementation can be administered through oral, enteric, and intravenous
routes, or it can be included in the dialysis and replacemen t fluids. The latter method
is gaining popularity, showing effectiveness in clinical studies [28, 29].
Approaches to Nutrition
Enteral
Feeding through the enteral route is both safe and effective for patients with AKI,
sepsis, and those undergoing CRRT, and it may contribute to improved outcomes.
Clinicians are encouraged not to hesitate in choosing the enteric route, even in cases
of severe illness or when sedatives are administered, which may slow gastric
emptying and intestinal function. The Surviving Sepsis Campaign recommends
254 V. Premuzic and A. Atic
enteral nutrition for eligible critically ill patients, favoring it over total parenteral or
combined enteral and parenteral nutrition [24]. This recommendation stems from a
lack of evidence demonstrating improved outcomes with total parenteral nutrition
(TPN), the associated lower costs, and potential physiological benefits of enteral
feeding. Other organizations, such as the European Society for Nutrition and Metabolism (ESPEN), the American Society for Parenteral and Enteral Nutrition
(ASPEN), and the International Symposium on Intensive Care and Emergency
Medicine (ISICEM), also endorse th
ill patients. The initiation of CRRT helps reduce intestinal wall edema, further
supporting the preference for enteral nutrition over parenteral nutrition [30]. In
animal models, CRRT has demonstrated the ability to reduce intestinal permeability,
subsequently lowering the translocation of intestinal bacteria into the bloodstream
[31]. Elevated intestinal permeability is linked to a pro-inflammatory state and is
regarded as a contributing factor to the severe inflammatory response syndrome
observed in critically ill patients, especially those undergoing extracorporeal membrane oxygenation treatment [
e early initiation of enteral feeding in critically
32].
Parenteral
In some critically ill patients, exclusive enteral feeding may not be feasible. However, parenteral and enteral nutrition are not mutually exclusive. In these cases,
clinicians may choose combined enteral/parenteral feeding or total parenteral nutrition (TPN). Parenteral nutrition should be prescribed to meet sufficient energy needs
and provide all individual nutrients. Attention must be paid to the regulation of
hyperglycemia, as its prevention appears to have a renoprotective effect. It is
important to note that the goals of glycemic regulation are not normoglycemia but
rather moderate hyperglycemia (6.1–8.3 mmol/l), as recom mended by the Kidney
Disease Improving Global Outcomes (KDIGO) Clinical Practice Guideline for
Acute Kidney Injury [33].
Timing
Nutritional targets in critically ill patients, especially in the early phase, remain
controversial; however, clinical practice guidelines suggest permissive underfeeding. The use of low-energy, low-protein nutrition in the first 24–48 h in the ICU is
postulated not to cause dysfunction in autophagy. Autophagy in sepsis promotes the
immune processes of immune cells, while its inhibition is associated with a
pro-inflammatory state and immunosuppression in sepsis [
ments (80–100% of estimated energy expenditure) should be met after the initial
48 h in most patients. However, acute kidney injury blurs the clinical picture, as
adequate protein delivery may be necessary to maintain body composition and
34].
Full energy require-
22 Nutrition in Sepsis, AKI, and CRRT 255
immune function [35]. A study involving 111 acute kidney injury (AKI) patients
demonstrated no increased need for renal replacement therapy (RRT) despite high
doses of protein in their nutrition. However, in a study of ICU patients treated with
continuous renal replacement therapy (CRRT), higher doses of protein (2.5 g/kg)
were associated with the need for more intense CRRT [
high-protein prescriptions are available. CRRT itself does not affect the timing of
feeding or its cessation.
17]. Of note, low-caloric
Recommendations
The first step in ensuring adequate nutrition is the appropriate assessment of nutritional status. Despite the drawbacks of individual screening and testing methods,
combining various approaches while taking into account the unique characteristic of
each patient is likely the most effective strategy. Although certain imaging methods
show promise, they remain experimental until further research and validation,
particularly considering body composition changes and fluid imbalances in acute
illnesses. Regular assessments of nutritional status and dietary plans are crucial,
especially for patients with prolonged hospitalization. Ideally, indirect calorimetry
should be conducted before initiating Continuous Renal Replacement Therapy
(CRRT), as it provides the most reliable estimate of energy expenditure. If CRRT
has already started, indirect calorimetry may be performed, but any significant
changes in CRRT delivery or a shift to citrate anticoagulation may require
reassessment with indirect calorimetry.
Whenever possible, enteral feeding is preferred over parenteral nutrition, aligning
with current guidelines. Enteral nutrition can be initiated within the first 24–48 h of
admission. Full nutrition should begin after the period of permissive underfeeding
during the acute phase of illness, typically defined as after the initial 48 h. However,
timing must be assessed for each patient individually, as, currently, there is no
established method for determining the best timing.
Guidelin
and failure to achieve tissue perfusion goals. Enteral nutrition should be postponed
in patients with overt bowel ischemia, abdominal compartment syndrome, highoutput intestinal fistulas without the ability to form a feeding access distal to the
fistula, or if gastric aspirate volume exceeds 500 ml/6 h [27]. If enteral nutrition is
contraindicated, parenteral nutrition can be initiated, provided there are no other
contraindications. During the acute phase of illness, current recommendations advocate providing 70% of estimated energy expenditure [36]
treatment of AKI recommend a total energy intake of 20–30 kcal/kg/day, distributed
as 3–5 (up to 7) g/kg of carbohydrates, and 0.8–1 g/kg of lipids. After the initial 48 h,
total caloric delivery should amount to 80–100% of the estimated energy
expenditure [36].
When calculating
calories to mitigate the risk of underfeeding. In septic patients with AKI undergoing
es r
ecommend delaying nutrition in cases of hemodynamic instability
. K
DIGO guidelines for the
energy intake, it is crucial to account for non-nutritional
256 V. Premuzic and A. Atic
CRRT, special attention should be given to total protein and amino acid intake, as
losses are highest in this population, and inadequate intake is linked to poorer
outcomes. High-protein diets can be implemented even in patients on lower-calorie
regimens. Current guidelines recommend up to 1.7 g/kg/day of protein, with additional amino acids, for critically ill patients with AKI treated by CRRT (KDIGO).
However, some studies have reported that doses up to 2.5 g/kg/da
tolerated, and this recommendation is supported by the ASPEN guidelines [
y are well
18, 3
7].
Hypophosphatemia associated with CRRT may be corrected by adding phosphate
supplementation to
the dialysate and replacement solutions at concent rations of
2.0 mmol/L or 3.0 mmol/L [28]. ESPEN guidelines for nutrition in critically ill
patients recommend B complex vitamin supplementation in the following doses: B1
100 mg/day, B7 200 mcg/day, folic acid 1 mg/day, B12 4 mcg/day, vitamin C
250 mg/day, and reduced vitamin A dosing [36]. These guidelines also recommend
supplementing certain trace elements, such as selenium at 100 mcg/day, zinc at
50 mg/day, and copper at 5 mg/day. Notably, trace element supplementation has
shown no mortality benefit in critically ill patients.
Conclusion
This chapter has delved into the profound impact of sepsis, AKI, and CRRT on the
metabolic dynamics of critically ill individuals, unraveling the intricate interplay
between nutritional requirements, energy expenditure, and the unique challenges
posed by CRRT. The metabolic shifts induced by sepsis, AKI, and CRRT have been
dissected, shedding light on the complexities of energy requirements, protein metabolism, lipid dynamics, and the intricate balance of vitamins, trace elements, and
phosphates.
References
1. Casaer MP, Mesotten D, Schetz MRC. Bench-to-bedside review: metabolism and nutrition. Crit
Care. 2008;12:222.
2. Fiaccadori E, Cremaschi E, Regolisti G. Nutritional assessment and delivery in renal replacement therapy patients. Semin Dial. 2011;24:169–75.
3. Fiaccadori E, Regolisti G, Maggiore U. Specialized nutritional support interventions in critically ill patients on renal replacement therapy. Curr Opin Clin Nutr Metab Care. 2013;16:217.
4. Bousie E, van Blokland D, Lammers HJW, van Zanten ARH. Relevance of non-nutritional
calories in mechanically ventilated critically ill patients. Eur J Clin Nutr. 2016;70:1443–50.
5. Li P, Huang Y, Wong A. An analysis of nonnutritive calories from propofol, dextrose, and
citrate among patients who are critically ill that are receiving continuous renal replacemen t
therapy. JPEN J Parenter Enteral Nutr. 2022;46:1883–91.
6. Nystrom EM, Nei AM. Metabolic support of the patient on continuous renal replacement
therapy. Nutr Clin Pract. 2018;33:754–66.
22 Nutrition in Sepsis, AKI, and CRRT 257
7. Cruz-Jentoft AJ, Bahat G, Bauer J, et al. Sarcopenia: revised European consensus on definition
and diagnosis. Age Ageing. 2019;48:16–31.
8. Sabatino A, Regolisti G, Bozzoli L, Fani F, Antoniotti R, Maggiore U, Fiaccadori E. Reliability
of bedside ultrasound for measurement of quadriceps muscle thickness in critically ill patients
with acute kidney injury. Clin Nutr. 2017;36:1710–5.
9. Duan J-Y, Zheng W-H, Zhou H, Xu Y, Huang H-B. Energy delivery guided by indirect
calorimetry in critically ill patients: a systematic review and meta-analysis. Crit Care.
2021;25:88.
10. Menegueti MG, de Araújo TR, Laus AM, Martins-Filho OA, Basile-Filho A, AuxiliadoraMartins M. Resting energy expenditure and oxygen consumption in critically ill patients with vs
without sepsis. Am J Crit Care. 2019;28(2):136–41.
11. Jonckheer J, Spapen H, Malbrain MLNG, Oschima T, De Waele E. Energy expenditure and
caloric targets during continuous renal replacement therapy under regional citrate
anticoagulation. A viewpoint. Clin Nutr. 2020;39:353–7.
12. Jonckheer J, Demol J, Lanckmans K, Malbrain MLNG, Spapen H, De Waele E. MECCIAS
trial: metabolic consequences of continuous veno-venous hemofiltration on indirect calorimetry. Clin Nutr. 2020;39(12):3797–803. https://doi.org/10.1016/j.clnu.2020.04.017.
13. Ostermann M, Lumlertgul N, Mehta R. Nutritional assessment and support during continuous
renal replacement therapy. Semin Dial. 2021;34:449–56.
14. Bellomo R, Cass A, Cole L, et al. Calorie intake and patient outcomes in severe acute kidney
injury: findings from the randomized evaluation of Normal vs. augmented level of replacement
therapy (RENAL) study trial. Crit Care. 2014;18:R45.
15. Onichimowski D, Goraj R, Jalali R, Grabala J, Mayzner-Zawadzka E, Czuczwar M. Practical
issues of nutrition during continuous renal replacement therapy. Anaesthesiol Intensive Ther.
2017;49:309–16.
16. Fiaccadori E, Regolisti G, Cabassi A. Specific nutritional problems in acute kidney injury,
treated with non-dialysis and dialytic modalities. NDT Plus. 2010;3:1–7.
17. Bellomo R, Tan HK, Bhonagiri S, Gopal I, Seacombe J, Daskalakis M, Boyce N. High protein
intake during continuous hemodiafiltration: impact on amino acids and nitrogen balance. Int J
Artif Organs. 2002;25:261–8.
18. Fishman G, Singer P. Metabolic and nutritional aspects in continuous renal replacement
therapy. J Intensive Med. 2023;3:228–38. https://doi.org/10.1016/j.jointm.2022.11.001.
19. Englert JA, Rogers AJ. Metabolism, metabolomics, and nutritional support of patients with
sepsis. Clin Chest Med. 2016;37:321–31.
20. Chua HR, Baldwin I, Fealy N, Naka T, Bellomo R. Amino acid balance with extended daily
diafiltration in acute kidney injury. Blood Purif. 2012;33:292–9.
21. Heyland DK, Elke G, Cook D, Berger MM, Wischmeyer PE, Albert M, Muscedere J, Jones G,
Day AG. Glutamine and antioxidants in the critically ill patient: a post hoc analysis of a largescale randomized trial. JPEN J Parenter Enteral Nutr. 2015;39:401–9.
22. Druml W, Joannidis M, John S, et al. Metabolic management and nutrition in critically ill
patients with renal dysfunction: recommendations from the renal section of the DGIIN,
ÖGIAIN, and DIVI. Med Klin Intensivmed Notfmed. 2018;113:393–400.
23. Hellerman M, Sabatino A, Theilla M, Kagan I, Fiaccadori E, Singer P. Carbohydrate and lipid
prescription, administration, and oxidation in critically ill patients with acute kidney injury: a
post hoc analysis. J Ren Nutr Off J Counc Ren Nutr Natl Kidney Found. 2019;29:289–94.
24. Rhodes A, Evans LE, Alhazzani W, et al. Surviving sepsis campaign: international guidelines
for management of sepsis and septic shock: 2016. Intensive Care Med. 2017;43:304–77.
25. Ostermann M,
Peacock J, Bear DE. Micronutrients in critically ill patients with severe acute kidney injury – a
prospective study. Sci Rep. 2020;10:1505.
26.
Wiesen P,
acute renal failure and renal replacement therapy. JPEN J Parenter Enteral Nutr. 2011;35:217–
22.
Summers
Van Overmeire L, Delanaye P, Dubois B, Preiser J-C. Nutrition disorders during
J, Lei K, Card D, Harrington DJ, Sherwood R, Turner C, Dalton N,
258 V. Premuzic and A. Atic
27. Fiaccadori E, Sabatino A, Barazzoni R, Carrero JJ, Cupisti A, De Waele E, Jonckheer J,
Singer P, Cuerda C. ESPEN guideline on clinical nutrition in hospitalized patients with acute
or chronic kidney disease. Clin Nutr. 2021;40:1644–68.
28. Lim C, Tan HK, Kaushik M. Hypophosphatemia in critically ill patients with acute kidney
injury treated with hemodialysis is associated with adverse events. Clin Kidney J. 2017;10:341 –
7.
29. Troyanov S, Geadah D, Ghannoum M, Cardinal J, Leblanc M. Phosphate addition to
hemodiafiltration solutions during continuous renal replacement therapy. Intensive Care Med.
2004;30:1662–5.
30. Zhang J, Tian J, Sun H, Digvijay K, Neri M, Bhargava V, Yin Y, Ronco C. How does
continuous renal replacement therapy affect septic acute kidney injury? Blood Purif. 2018;46:
326–31.
31. He C, Yang S, Yu W, Chen Q, Shen J, Hu Y, Shi J, Wu X, Li J, Li N. Effects of continuous renal
replacement therapy on intestinal mucosal barrier function during extracorporeal membrane
oxygenation in a porcine model. J Cardiothorac Surg. 2014;9:72.
32. McILwain RB, Timpa JG, Kurundkar AR, et al. Plasma concentrations of inflammatory
cytokines rise rapidly during ECMO-related SIRS due to the release of preformed stores in
the intestine. Lab Investig. 2010;90:128–39.
33. Khwaja A. KDIGO clinical practice guidelines for acute kidney injury. Nephron Clin Pract.
2012;120:c179–84.
34. Yin X, Xin H, Mao S, Wu G, Guo L. The role of autophagy in sepsis: protection and injury to
organs. Front Physiol. 2019;10:1071.
35. Mochizuki M, Nakano H, Ikechi D, Takahashi Y, Hashimoto H, Nakamura K. The nitrogen
load is affected by high protein provision according to kidney function in critically ill patients. J
Clin Biochem Nutr. 2023;72:289–94.
36. Singer P, Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition in the intensive
care unit. Clin Nutr. 2019;38:48–79.
37. Scheinkestel CD, Kar L, Marshall K, Bailey M, Davies A, Nyulasi I, Tuxen DV. Prospective
randomized trial to assess caloric and protein needs of critically ill, anuric, ventilated patients
requiring continuous renal replacement therapy. Nutrition. 2003;19:909–16.
Chapter 23
Nutrition in Acute Liver Failure and Severe
Acute Pancreatitis
Katia Donadello, Beatrice Milan, Giulia D’Agostini, and Enrico Polati
Introduction
Gastrointestinal (GI) function is essential not only for nutrient absorption and barrier
control but also for modulating end ocrine and immune functions. Perfusion, secretion, motility, and coordinated microbiome interactions are essential to maintain
adequate GI activity [1]. The small intestine facilitates nutrient breakdown and
tion, with an average length of 3–5 m and divided into the duodenum,
absorp
jejunum, and ileum. The duodenum, the shortest section, measures 20–25 cm in
length, surrounds the pancreas in a “C” shape, and contains Brunner’s glands. The
jejunum, 2.5 m in length, contains villi for absorbing digestion products, while the
ileum, the final portion, measures 3 m and absorbs residual nutrients. The duodenum
initiates absorption receives pancreatic enzymes via the hepatopancreatic ampulla
and neutralizes stomach acid before reaching the jejunum. Bile produced by the liver
aids in lipid breakdown and absorption. The jejunum absorbs sugars, amino acids,
and fatty acids, while the ileum absorbs remaining nutrients, particularly vitamin
B12 and bile acids. Lymphatic drainage transports absorbed lipids and immune
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_23.
K. Donadello (
Department of Surgery, Dentistry, Gynaecology and Paediatrics, University of Verona, Verona,
Italy
Anaesthesia and Intensive Care Unit B, Policlinico G.B. Rossi, University Hospital Integrated
Trust of Verona, Verona, Italy
e-mail: katia.donadello@univr.it; enrico.polati@univr.it
B. Milan · G. D’Agostini
Anaesthesia
Trust of Verona, Verona, Italy
e-mail: beatrice.milan@aovr.veneto.it; giulia.dagostini@aovr.veneto.it
© 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_23
✉) · E. Polati
and Intensive Care Unit B, Policlinico G.B. Rossi, University Hospital Integrated
259
260 K. Donadello et al.
defense elements, starting from the small intestine mucosa, through nodes in the
mesentery and arterial arcades, eventually emptying into the venous system via the
thoracic duct [2
]. GI dysfunction, frequently observed in critically ill patients,
encompasses mobility and absorption disturbances, mucosal barrier gaps,
microbiome changes, increased intra-abdominal pressure, impaired mesenteric perfusion, and GI tract infections. Approximately 60% of ICU patients experience GI
dysfunction, significantly prolonging ICU length of stay and worsening clinical
outcomes. GI dysfunction can be both the cause and consequence of critical illn
ess,
exacerbated by shock, multiple organ dysfunction, sepsis, electrolyte disturbances,
hyperglycemia, and hypoxemia. Conversely, GI disease can lead to small intestinal
bacterial overgrowth, increased inflammatory mediator transport through mesenteric
lymphatics to the lungs, and bacterial translocation through portal circulation,
contributing to subsequent sepsis and multiple organ failure [
1, 3, 4]. GI dysfunction
leads to various complications due to different involved pathophysiological pathways: GI motility is crucial for GI absorption, regulating nutrient mix and propulsion. Gastroparesis affects stomach movements, reducing gastric emptying due to
motor dysfunction and lack of coordination between the fundic and pyloric regions.
Critically ill patients often present ileus with multifactorial etiology [3, 5].
The single-layered epitheli
um contains four different cell types responsible for
various functions, including enterocytes, mucus-producing goblet cells, hormoneproducing enteroendocrine cells, and defense-producing Paneth cells. Epithelial
gaps can lead to bacterial translocation and inflammatory mediator transport within
the systemic circulation [6]. The gut microbiome plays a fundamental role in
intestinal absorption and immune response. Dysbiosis and alterations in microbiome
composition can contribute to multiple organ failure through bacterial translocation
and inflammatory mediator travel [4, 6].
Increased intra-abdominal pressure occurs in approximately 22% of ICU patients,
leading to gut edema, altered cytoskeleton, bowel dysmotility, and endotoxemia
[4, 7]. Impaired mesenteric perfusion may cause ischemia-reperfusion injury, altering mucosal barrier and immunoinflammatory reactions [8].
Diagnosing
GI dysfunction is complex due to the lack of a definitive disease
definition, often relying on expert consensus. Acute GI injury (AGI) has been
proposed as a new term to describe changes in severity from mild to severe,
diagnosed based on clinical symptoms and signs. The European Society of Intensive
Care Medicine (ESICM) has proposed four grades of severity for AGI, but a
validated scoring system for severity grading is still unavailable [
8, 9]. The anatom-
ical and physiological connections between the gut and adjoining organs, such as the
liver and pancreas, lead to significant pathophysiological interconnections
10].
Liver failure causes mucosal layer alterations, tight junction disruption,
[
microbiome changes, portal hypertension, mucosal edema, and microvilli congestion. GI dysfunction exacerbates inflammation and hepatic failure, increasing bacterial translocation and endotoxin absorption by the liver [
11, 12]. Similarly, acute
pancreatitis patients may experience worsened outcomes due to concomitant GI
symptoms, including abdominal compartment syndrome, intestinal ischemia, and
gastric outlet dysfunction [
Severe acute pancreatitis is associated with excessive
13].