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- •Contents
- •Outcome Evaluation
- •Introduction
- •Clinical Presentation of Muscular Weakness in the Critical Patients
- •Critical Illness Polyneuropathy (CIP) and Critical Illness Myopathy (CIM)
- •Ventilator-Induced Diaphragmatic Dysfunction (VIDD)
- •Dysphagia, Swallowing, and Effective Cough
- •The Pathophysiology of Acute Skeletal Muscle Wasting
- •Risk Factors
- •Short-Term and Long-Term Outcome
- •Conclusions
- •References
- •Introduction
- •The Neuroendocrine Response
- •Pathophysiology of Stress Response
- •The Hypothalamus-Pituitary-Adrenal (HPA) Axis
- •GH Axis
- •Pituitary-Thyroid Axis
- •Pituitary-Adrenal Axis
- •Mitochondrial Dysfunction
- •Metabolic Aspects of Stress Response
- •Conclusion
- •References
- •Introduction
- •Disorders of Fluid Balance
- •Dysionemias
- •Dysnatremias
- •Dyskalemias
- •Other Electrolyte Derangements (Calcium, Magnesium, Phosphorus)
- •Alterations of Acid Base Balance
- •Acid-Base Disturbances
- •Metabolic Acidosis
- •Respiratory Acidosis
- •Metabolic Alkalosis
- •Respiratory Alkalosis
- •Conclusion
- •References
- •Introduction
- •Epidemiology and Risk Factors
- •Diagnosis
- •Differential Diagnosis
- •Treatment
- •Prognosis
- •Future Perspectives
- •References
- •Introduction
- •Gut Microbiome
- •Gut-Organ Axis
- •Gut-Lung Axis
- •ICU Dysbiosis
- •Gut Changes
- •Microbial Therapy in ICU
- •Antimicrobial Stewardship
- •Nutrition as a Key Factor for Gut Microbiome Homeostasis
- •Probiotics, Prebiotics, and Synbiotics
- •Fecal Microbiota Transplantation
- •Conclusion
- •References
- •Introduction
- •Validation Process
- •Screening Tools Overview
- •Discussion
- •Conclusion
- •References
- •Introduction
- •Fight-and-Flight Reaction
- •Calorimetry and Total Energy Expenditure
- •Role of Mitochondria in the Various Stages of Intensive Care Recovery
- •REE in Different Clinical Scenarios
- •Conclusions
- •References
- •Introduction
- •Nutrition in ICU: Evidence from RCTs
- •Inclusion of Too Many Patients Considered at Low Nutritional Risk
- •Unfavorable Energy to Protein Doses
- •Absence of Indirect Calorimetry-Guided Energy Dosing
- •Anabolic Resistance
- •Suppression of Fasting-Induced Recovery Pathways
- •Future Perspectives
- •Development and Validation of Tools to Guide Individualized Nutritional Support
- •Implications for Clinical Practice
- •Conclusion
- •References
- •Introduction
- •Protein Metabolism in Critical Illness
- •Protein Requirements and Current Evidence
- •Timing of Introduction
- •Early mobilization, Exercise, and Adjuvant Therapies
- •Conclusion
- •References
- •Introduction
- •Computed Tomography Scan
- •Bioelectrical Impedance Analysis
- •Musculoskeletal Ultrasound
- •Respiratory Muscle Ultrasound
- •Limb Muscles
- •Conclusions
- •References
- •Functional Principles
- •Hydration Status Evaluations in Critically Ill Patients
- •Body Composition and Nutrition in ICU
- •Limits of BIVA in Critically Ill Patients
- •Conclusions
- •References
- •Introduction
- •Introduction
- •Historical Perspective
- •Enteral Versus Parenteral Nutrition Nowadays
- •Conclusions
- •References
- •Enteral Nutrition
- •Components of Enteral Mixtures
- •Choice of the Enteral Mixture
- •Special Composition Formulas
- •Conclusions
- •References
- •Introduction
- •Complications Related to Enteral Feeding Tubes
- •Aspiration
- •Gastrointestinal Intolerance
- •Diarrhea
- •New Horizons
- •New Technologies to Prevent Enteral Nutrition Complications
- •Advanced Tube Feedings
- •smART Platform
- •Conclusions
- •References
- •Introduction
- •Composition of PN Admixtures
- •Energetic Substrates
- •Carbohydrates
- •Lipid Emulsions
- •Proteins
- •Micronutrients: Electrolytes, Vitamins, and Trace Elements
- •Types of Parenteral Nutrition
- •Compatibility and Stability of the Parenteral Nutrition
- •References
- •Introduction
- •Metabolic Complications
- •Hyperglycemia
- •Hypertriglyceridemia
- •Liver Disease: Steatosis, Cholestatic Disease, and Gallbladder Stones
- •Refeeding Syndrome
- •Mechanical Complications
- •Infectious Complications
- •Conclusions
- •References
- •Introduction
- •Macronutrients
- •Glutamine
- •Arginine
- •Leucine
- •ω-3 Fatty Acids
- •Micronutrients
- •Antioxidant Vitamins
- •Antioxidant Trace Elements
- •Probiotics, Prebiotics or Symbiotics
- •Use of Probiotics in Clinical Practice?
- •References
- •Introduction
- •Pathophysiological Mechanisms, Risk Factors, and Clinical Implications
- •Pathophysiological Mechanisms of ICUAW
- •Risk Factors Associated with Physical and Functional Recovery in Critically Ill Patients
- •Clinical Impact of Poor Physical and Functional Recovery in Critical Illnesses
- •How to Assess Physical and Functional Recovery in Critical Illnesses
- •Management and Therapies
- •Nutritional Therapy
- •Other Supportive Therapies
- •Patient- and Family-centered ICU Environment
- •Conclusions
- •References
- •Bioethics in Clinical Practices
- •Ethical Consideration on Nutrition
- •Conclusion
- •References
- •Introduction
- •Nutrition in ARDS
- •Caloric Goals
- •Diet Composition
- •Immunonutrition
- •Oral Versus Enteral Versus Parenteral Nutrition
- •Nutrition in COVID-19 Respiratory Failure
- •Nutrition in ECMO Support
- •Enteral Nutrition
- •Parenteral Nutrition
- •Nutritional Goals
- •Conclusions
- •References
- •Introduction
- •Timing and Route of Nutritional Support
- •Initial Assessment of the Burn Patient
- •Estimation of Energy Expenditure
- •Macronutrients and Micronutrients
- •Proteins
- •Carbohydrates
- •Immunonutrients
- •Arginine
- •Nucleotides
- •ω3 Fatty Acids
- •Glutamine
- •Monitoring of Nutritional Support
- •Nutritional Support for Trauma Patients
- •Route of Feeding: Digestive Tract (Enteral Nutrition) Versus Intravenous (Parenteral Nutrition)
- •Standard or Immune-Enhancing Enteral Nutrition
- •Estimation or Measurement of Energy Requirements
- •Macronutrients
- •Conclusions
- •References
- •Introduction
- •General Considerations
- •Assessment of Nutritional Needs
- •Metabolic Changes Induced by Sepsis, AKI, and CRRT
- •Protein Metabolism
- •Lipid Metabolism
- •Vitamins and Trace Elements
- •Phosphates
- •Approaches to Nutrition
- •Enteral
- •Parenteral
- •Timing
- •Recommendations
- •Conclusion
- •References
- •Introduction
- •Acute Liver Failure
- •Nutrition in ALF
- •Acute Pancreatitis
- •IAP Management
- •Conclusions
- •References
- •Introduction
- •Nutritional Considerations in Major Surgery
- •Nutritional Requirements During and After Major Surgery
- •Challenges in Meeting Nutritional Needs Post-Surgery
- •Strategies for Enhancing Nutritional Intake and Absorption
- •Intestinal Failure: Nutritional Challenges and Management
- •Impact of Intestinal Failure on Nutritional Status
- •Nutritional Management Strategies for Patients with Intestinal Failure
- •Role of Parenteral Nutrition and Enteral Nutrition in Intestinal Failure Cases
- •Open Abdomen: Nutritional Support and Wound Healing
- •Nutritional Requirements for Patients with Open Abdomen Wounds
- •Challenges in Providing Nutritional Support to Patients with Open Abdomen
- •Clinical Protocols and Guidelines for Nutritional Support
- •Conclusions
- •References
- •Introduction
- •Nutrition Therapy
- •Determination of Energy Expenditure
- •Route and Timing of Enteral Nutrition
- •Intolerance to Enteral Nutrition
- •Brain Energy Metabolism and Energy Dysfunction Following Acute Brain Injury
- •In Vivo Brain Energy and Glucose Monitoring
- •Alternative Energy Substrates
- •Lactate
- •Ketone Bodies
- •Immunonutrition and Micronutrients
- •Conclusions and Future Directions
- •References
- •Introduction
- •AKI and Cardiac Surgery
- •AKI and Vascular Surgery
- •AKI and Sepsis
- •AKI and Surgery
- •Trauma
- •Burn
- •AKI and COVID-19
- •Conclusion
- •References
- •Introduction
- •AKI Etiology
- •Subclinical AKI and AKI Biomarkers
- •Subphenotyping AKI
- •Conclusions
- •References
- •Introduction
- •What Are Biomarkers?
- •Novel Biomarkers: How Can They be Implemented?
- •Biomarkers for the Prediction of AKI and Detection of Subclinical Stages
- •Postoperative Biomarker-Guided Prevention of AKI in Patients at High Risk
- •Biomarkers for Other Indications
- •Conclusion
- •References
- •Introduction
- •The Machine Learning Arena
- •The Challenges of Timely Prediction of Acute Kidney Injury
- •Early Machine Learning Models for AKI Prediction
- •New Techniques for AKI Prediction Using Deep Learning ML Models
- •Clinical Decision Support Systems
- •The Translational Research Gap and the Value of Data Sharing: A Plea for Data Sharing
- •Limitations of Machine Learning Models
- •Conclusions
- •References
- •Introduction
- •Doppler Assesses Vascular Congestion
- •Arterial Renal Doppler Ultrasound in AKI
- •Integration of Renal Resistive Index and Intrarenal Venous Flow
- •Contrast-Enhanced Ultrasound for Assessing Renal Perfusion
- •Conclusions
- •References
- •Introduction
- •Renal Perfusion and Goals of Fluids in AKI
- •Clinical Evaluation of a Patient with AKI in ICU
- •Studies Which Investigated the Association of Fluid Therapy and AKI
- •Volume of Fluid
- •Type of Fluid
- •Crystalloids
- •Colloids
- •Starches
- •Gelatins
- •Conclusion
- •References
- •Introduction
- •Pathophysiology of Renal Perfusion
- •Acute Kidney Injury
- •Norepinephrine
- •Epinephrine
- •Dopamine
- •Vasopressin
- •Terlipressin
- •Angiotensin II
- •Conclusions
- •References
- •Introduction
- •Pharmacology of Diuretics
- •Loop Diuretics
- •Other Classes of Diuretics
- •Indications for Diuretics in AKI
- •Control of Fluid Overload
- •AKI Prognostication
- •Situations in Which Diuretics Are Not Indicated
- •AKI Recovery
- •How to Use Diuretics in the ICU
- •Class and Dose Selection
- •Modality of Loop Diuretic Administration
- •Conclusions
- •References
- •Introduction
- •What Is Acute Kidney Disease?
- •Clinical Course of AKD Within the ICU
- •Management of AKD in Critical Care and Beyond
- •Conclusions and Future Directions
- •References
- •Introduction
- •Renal Functional Reserve
- •Renal Functional Reserve and Renal Recovery After Acute Kidney Injury
- •Conclusion
- •References
- •Background
- •Membrane and Filter Characteristics
- •Geometric Characteristics
- •Performance Characteristics
- •Mechanisms of Fluid and Solute Transport
- •Treatment Modalities
- •Treatment Dose
- •Nomenclature of Renal Replacement Therapies
- •Continuous Therapies
- •Intermittent Therapies
- •Hybrid Therapies
- •Conclusion
- •References
- •Introduction
- •Dialysis Catheters: Technical Aspects
- •Selection of the Site for Dialysis
- •Catheter Insertion Technique
- •Dialysis Catheter Complications
- •Dialysis Catheter Maintenance
- •Conclusions
- •References
- •Introduction
- •Non-pharmacological Strategies to Reduce Membrane Fouling
- •Pharmacological Strategies to Reduce Membrane Clotting
- •Unfractionated Heparin (UFH) Systemic Anticoagulation
- •Systemic Anticoagulation with Low Molecular Weight Heparin (LMWH)
- •Regional Citrate Anticoagulation (RCA)
- •Systemic Anticoagulation with Direct Thrombin Antagonists
- •Nafamostat
- •Conclusions
- •References
- •Introduction
- •CRRT Dose/Outcome Studies: Consideration of Solute Kinetics
- •CRRT Dose as a Quality Criterion
- •CRRT Dose in the Context of Therapy Quality
- •Conclusions
- •References
- •Introduction
- •Patient Selection and Indications for Starting RRT
- •Strategies to Identify Need for RRT
- •Rationale for an Early Strategy to Starting RRT
- •Rationale for a Conservative Strategy to Starting RRT
- •RRT Replacement Therapy and Clinical Outcomes
- •Current Clinical Practice Guideline Recommendations
- •Clinical Trial Evidence on Timing of Starting RRT
- •Implications for Practice
- •Existing Knowledge Gaps and Future Research
- •Conclusions
- •References
- •Introduction
- •Early ICU Phase before KRT
- •Nutrition Care
- •Monitoring
- •ICU Phase with KRT
- •Gains and Losses During CRRT
- •Electrolyte Loss in CRRT
- •Macronutrient Loss in CRRT
- •Macronutrient Gain in CRRT
- •Micronutrients and Vitamin Loss in CRRT
- •Management of Losses During CRRT
- •Monitoring During CRRT
- •Indirect Calorimetry During CRRT
- •ICU Phase After CRRT
- •EN and PN Product Selection
- •Conclusions
- •References
- •Introduction
- •Nomenclature
- •Continuous Therapies
- •Intermittent Renal Replacement Therapies (IRRTs)
- •Hybrid Therapies
- •Technical Aspects of RRT Techniques
- •Hemodynamic Stability
- •Solute Clearance
- •Fluid Balance
- •Vascular Access
- •Anticoagulation
- •Drug Dosing
- •Patient Mobilization
- •The Process of RRT Prescription and Administration
- •Indications of RRT
- •Timing
- •Prescription Parameters
- •Dosing
- •Membrane Choice
- •Dialysate and Reinfusion Solutions
- •Limitations of RRT in Critical Care
- •Patient Safety During RRT in Critical Care
- •Introduction
- •Steps in RRT Management and Protocol Application

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 profile 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, fluid 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 flow, 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 beneficial 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 insufficiency 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
first 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 inflammation 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 bacteria” as 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 benefit during total PN, there is
still no clear evidence about its beneficial 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
flow 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 beneficial effect on inflammatory
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 inflammation, 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. Deficiencies of these nutrients are more
common in chronic pancreatitis, but nutrition-focused physical examination can
assist in identifying micronutrient deficiencies in patients w
ith moderate to severe
malnutrition. If micronutrient deficiency is suspected, serum levels can be evaluated
once inflammation has been resolved, although the accuracy of these parameters as a
reflection of total body stores is still questionable [
41, 4
4, 47]. Z
inc levels can
influence tissue development, renewal, and repair, including proliferation and apoptosis. Such responses have been shown in epithelial differentiation and proliferation, neuronal differentiation, and immunity. Its defi
i
ble immunological disorder with both immune-deficient and
revers
ciency leads to a persistent but
hyperinflammatory responses. Robust studies on the efficacy 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/die
➤ Protein/day: 1.2-1.2 g/kg/die
➤ Carbohydrates: 3-6g/kg/die
➤ Lipid: 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.
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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 body’s
healin
g mechanisms, enhancing immune function, and facilitating tissue repair,
thereby significantly 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 body’s
increased metabolic demands and promote efficient recovery [4]. Intestinal failure
presents a unique challenge wherein the gastrointestinal tract is unable to absorb
nutrients and fluids 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 patient’s 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
patient’s needs and clinical circumstances. By addressing specific 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 benefit from perioperative interventions aimed at reducing the hypermetabolic
and inflammatory 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 significant 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 significantly shorter in those who received treatment [10]. Similarly, preoperative enteral or parenteral support reduces the risk of postoperative complications
significantly 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 significant 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 influenced by underlying inflammatory states, which in turn
induce a catabolic state. Serum concentration is also primarily linked to redistribution and dilution secondary to fluid 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 sufficient 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].
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