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
X
- •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

486 M. Hiesmayr and A. Fischer
Table 41.1 Electrolyte content of selected solutions used in CRRT
Na
+ K+
Ca
++
++
Mg
-
Cl
HCO
-
PO
3
4
Fresenius mmol/L
+
Ci-Ca Dialysate K
Ci-Ca Dialysate K
Ci-Ca Dialysate K
Ci-Ca Dialysate K
HF multiBic 0 K
HF multiBic 4 K
HF multiBic 3 K
HF multiBic 2 K
4, 5 L 133 4 0.0 0.75 118.5 20 0
+
2, 5 L 133 2 0.0 0.75 116.5 20 0
+
4 Plus, 5 L 133 4 0.0 1.00 117.75 20 1.25
+
2 Plus, 5 L 133 2 0.0 1.00 115.75 20 1.25
+
+
, 5 L 140 4 1.5 0.5 113 35 0
+
, 5 L 140 3 1.5 0.5 112 35 0
+
, 5 L 140 2 1.5 0.5 111 35 0
140 0 1.5 0.5 109 35 0
Multi Plus 140 2 1.5 0.75 109.7 35 1
Multi LAC 0 K
Multi LAC 4 K
Multi LAC 3 K
Multi LAC 3 K
+
+
+
+
140 0 1.5 0.5 106 0 0
140 4 1.5 0.5 110 0 0
140 3 1.5 0.5 109 0 0
140 2 1.5 0.5 108 0 0
Sodium citrate 4%, 1500 ml 408 0 0 0 0 0 0
Baxter/Gambro
Phoxilium 1.2 MMOL/L, 5 L 140 4 1.25 0.6 115.9 30 1.20
Prismasol 2 MMOL/L, 5 L 140
2 1.75 0.5 111.50 32 0
Prismasol 4 MMOL/L, 5 L 140 4 1.75 0.5 113.50 32 0
Prism0CAL B22 140 4 0 0.75 120.5 22 0
HF Hemosol-Bicarb, 5 L 140 0 1.75 0.5 109.50 32 0
PrismoCit 4 K, 5 L 140 4 0 0 114 0 0
HF Prismocitrate 10/2, 5 L 136 0 0 0 106 0 0
HF Prismocitrate 18/0, 5 L 140 0 0.0 0.0 86 0 0
B. Braun
Duosol 0 K
Duosol 2 K
Duosol 4 K
+
+
+
B. Braun Bicarbonate 2 K
B. Braun Bicarbonate 4 K
+
+
0Ca
0Ca
140 0 1.5 0.5 109 35 0
140 2 1.5 0.5 111 35 0
140 4 1.5 0.5 113 35 0
2+
136 2 0 0.75 116.5 25 0
2+
136 4 0 0.75 114.5 25 0
Citrasol 4% 404 0 0 0 0 0 0
-
Box 1 Calculation of Mass Transfer by CRRT in General Terms
and for PO
Patient: hematocrit 33%, (PO
3-
Loss
4
4 3-blood
), 1.3 mmol/L
CRRT setting: blood flow, 150 ml/min (=9000 ml/h); citrate flow, 200 ml/h;
predilution flow, 1000 ml/h; no postdilution, dialysate flow, 1500 ml/h; fluid
removal (ultrafiltrate), 250 ml/h; and CaCl
Step 1: Plasma flow (F
plasma
)
, 20 ml/h.
2
(continued)

41 Nutrition in ICU Patients with Acute Kidney Injury 487
Box 1 (continued)
F
plasma
Step 2:PO
(PO
4 3-filter
= F
= 9000 × (1–0.33) = 6000 ml/h
3-
4
× (1-haematocrit)
blood
concentration at hemofilter entry (PO
) = (PO
4 3-blood
) × (F
plasma
/(F
plasma +Fcitrate +Fpredilution
4 3-filter
)
)
= 1.3 × 6000/ (6000 + 200 + 1000) = 1.08 mmol/L
Step 3:Effluent flow (F
effluent
= F
dialysate
F
effluent
+F
)
predilution
+F
postdilution
+F
citrate
+F
CaCl2
+ fluid
removal
= 1500 + 1000 + 0 + 200 + 20 + 250 = 2970 ml/h
3-
Step 4:PO
3-
PO
4
loss per day
4
loss = F
effluent
× (PO
4 3-filter
) × 24 h
= 2.97 × 24 × 1.08 = 77 mmol PO
3-
4
per 24 h
Macronutrient Loss in CRRT
Macronutrients can be lost or gained via CRRT. Glucose is typically lost because
either the replacement fluid does not contain any glucose (Table 41.2) or the
replacement concentration is below the blood concentration. Most replacement
fluid contains 1 g/L (100 mg/dL) glucose. If blood glucose is 150 mg/dL, 0.5 g
glucose will be lost for each liter of ef fluent, but it will be three times higher if
glucose-free replacement solutions are used (see Table 41.2). The loss of amino
acids can only be estimated because only a few institutions can determine a complete
aminogram. Amino acids freely pass the filter due to their small molecular size.
Therefore, amino acid concentrations in the blood and effluent should be similar
[20, 21].
fact that most amino acids have a sieving coefficient of 1 [22], it can be approximated that at an effluent volume of 50 L per day, about 20 g of AA are lost, and at a
higher effluent volume of 70 L, nearly 30 g of AA. In intermittent dialysis that uses a
much higher dialysate flow over a few hours, the effluent AA concentration (85 mg/
L) has been found to be only 25% of plasma concentration at a dialysate flow of
30 L/h. This example shows that differences in apparent sieving coefficient, as has
been found for middle-sized molecules such as cytokines, also apply for smaller
molecules if the dialysate flow through the filter is increased.
a typical total amino acid concentration of 400–500 mg/L and the
Using
Macronutrient Gain in CRRT
Lactate is the largest contributor to macronutrients if present in replacement fluid
with as much as 70 mmol/h entering the circulation, and citrate, with 24–36 mmol/h,
is the second largest one. In terms of macronutrients, gains from lactate have been
calculated to be as high as 500 Kcal per day and up to 180–360 Kcal from citrate

488 M. Hiesmayr and A. Fischer
Table 41.2 Nutrient content of selected solutions used in CRRT
Glucose Lactate Citrate
Fresenius g/L mmol/L mmol/L
+
Ci-Ca Dialysate K
Ci-Ca Dialysate K
Ci-Ca Dialysate K
Ci-Ca Dialysate K
HF multiBic 0 K
HF multiBic 4 K
HF multiBic 3 K
HF multiBic 2 K
4, 5 L 1 0 0
+
2, 5 L 1 0 0
+
4 Plus, 5 L 1 0 0
+
2 Plus, 5 L 1 0 0
+
+
,5L 1 0 0
+
,5L 1 0 0
+
,5L 1 0 0
10
0
Multi Plus 1 0 0
Multi LAC 0 K
Multi LAC 4 K
Multi
LAC 3 K
Multi LAC 3 K
+
+
+
+
138
138
138
138
0
0
0
0
Sodium citrate 4%, 1500 ml 0 0 136 (=39.8 g/l)
Baxter/Gambro
Phoxilium 1.2 MMOL/L, 5 L 0 0 0
Prismasol 2 MMOL/L, 5 L 1.1 3 0
Prismasol 4 MMOL/L, 5 L 1.1 3 0
Prism0CAL B22 1.1 3 0
HF Hemosol-Bicarb, 5 L 0.0 3 0
PrismoCit 4 K, 5 L 0 0 10 citrate/2 citric acid
HF Prismocitrate 10/2, 5 L 0 0 10 citrate/2 citric acid
HF Prismocitrate 18/0, 5 L 0.0 0 18 (=5.3 g/l)
B. Braun
Duosol 0 K
Duosol 2 K
Duosol 4 K
+
+
+
B. Braun Bicarbonate 2 K
B. Braun Bicarbonate 4 K
+
+
0Ca
0Ca
2+
2+
1
1
1
0
0
Citrasol 4% 0 136.4 (=39.8 g/l)
depending on the CRRT dose and dilution type [23]. There is no clear recommendation on how to modify nutrition, but reducing the energy from glucose and fat
while maintaining the amino acid/protein supply may be an option.
Micronutrients and Vitamin Loss in CRRT
Micronutrient loss depends on the amount bound to proteins. Thus, measurement in
plasma that takes free and bound micronutrients into account cannot be used to
estimate losses that primarily occur from free micronutrients. The loss of water-

41 Nutrition in ICU Patients with Acute Kidney Injury 489
soluble vitamins has been found inconsistently, but doubling the daily dose has been
recommended [24]. Recent research suggests that the early administration of thiamine improves the prognosis of AKI [8 ].
Management of Losses During CRRT
Current guidelines recommend increasing the AA and/or protein dose during CRRT.
Given the fact that these losses depend on the varying settings of CRRT, it appears
simpler to compensate AA losses with a separate AA infusion, which can easily be
stopped when CRRT is interrupted. Such a compensatory infusion could also
contain an additional dose of micronutrients and water-soluble vitamins. Electrolytes
that need to be replaced in large amounts should not be compounded with nutrition
care to avoid multiple changes in the amount of nutrition given per unit of time.
Monitoring During CRRT
Electrolytes such as K+ ,Mg
++
,Ca
++
, and PO
3-
need to be checked at least twice
4
daily until a stable CRRT and the replacement of losses have been established. Any
interruption in CRRT may also be accompanied by rapid changes in these electrolytes. Urea and creatinine are needed to adjust the dosing of CRRT or to detect any
clotted or dysfunctional CRRT filter. In the case of the worsening of the neurologic
state or level of consciousness, monitoring the ammonia level is mandatory.
Indirect Calorimetry During CRRT
IC can be used during CRRT with a slight overestimation of CO2 production if
bicarbonate is introduced with the replacement fluid (Table 41.2). The error in
energy expenditure has been found to be <5% [
25].
ICU Phase After CRRT
The phase after CRRT is characterized by a limited kidney function since most
patients with AKI necessitating CRRT do not fully recover their previous kidney
function [13]. These patients must be treated like CKD patients. Many patients
remain relatively polyuric for several days. Losses of electrolytes, micronutrients,
and vitamins may still be above normal and necessitate supplementation. The
amount of protein tolerated will depend on the anabolic drive and kidney function.

490 M. Hiesmayr and A. Fischer
The most objective approach is to measure 24-h nitrogen excretion (urea production
rate) in the urine and to use this measurement to estimate the amount of protein
needed. In general, 0.6–0.9 g/kg BW/day may be sufficient but depends on the
degree of renal recovery and the stage of AKD. Moreover, oral bicarbonate to treat
metabolic acidosis and phosphate binding drugs may be necessary. Dietary advice
and nephrologic follow-up are highly recommended [
26].
EN and PN Product Selection
During phase 1 before KRT and phase 2 with KRT, standard EN and PN can be
used. The electrolytes, micronutrients, and vitamins in standard EN are not sufficient
to equilibrate the losses generated by CRRT. During phase 3 after KRT, EN products
with lower protein and electrolyte content may be advisable if kidney function has
not returned to normal. Industrial PN, all in one with lower protein content and
without electrolytes, may be used.
Conclusions
Adequate nutrition care in AKI patients must be adapted to the phase of illness and
especially take into account losses and gains in nutrients via CRRT. Nutrition care
after AKI with partially recovered kidney function needs careful adjustments similar
to CKD patients. An anabolic effect will only be achieved when physical activity is
again possible.
References
1. Kellum JA, Romagnani P, Ashuntantang G, Ronco C, Zarbock A, Anders HJ. Acute kidney
injury. Nat Rev Dis Primers. 2021;7(1):52.
2. Haines RW, Fowler AJ, Wan YI, Flower L, Heyland DK, Day A, et al. Catabolism in critical
illness: a reanalysis of the REducing Deaths due to OXidative Stress (REDOXS) trial. Crit Care
Med. 2022;50(7):1072–82.
3. Heyland DK, Patel J, Compher C, Rice TW, Bear DE, Lee ZY, et al. The effect of higher protein
dosing in critically ill patients with high nutritional risk (EFFORT Protein): an international,
multicentre, pragmatic, registry-based randomised trial. Lancet. 2023;401(10376):568–76.
4. Susantitaphong P, Cruz DN, Cerda J, Abulfaraj M, Alqahtani F, Koulouridis I, et al. World
incidence of AKI: a meta-analysis. Clin J Am Soc Nephrol. 2013;8(9):1482–93.
5. Hoste EAJ, Kellum JA, Selby NM, Zarbock A, Palevsky PM, Bagshaw SM, et al. Global
epidemiology and outcomes of acute kidney injury. Nat Rev Nephrol. 2018;14(10):607–25.
Evans L,
6.
sepsis campaign: international guidelines for management of sepsis and septic shock 2021.
Intensive Care Med. 2021;47(11):1181–247.
Rhodes A, Alhazzani W, Antonelli M, Coopersmith CM, French C, et al. Surviving

41 Nutrition in ICU Patients with Acute Kidney Injury 491
7. Scholz H, Boivin FJ, Schmidt-Ott KM, Bachmann S, Eckardt KU, Scholl UI, et al. Kidney
physiology and susceptibility to acute kidney injury: implications for renoprotection. Nat Rev
Nephrol. 2021;17(5):335–49.
8. Legouis D, Ricksten SE, Faivre
tubular cell glucose metabolism during acute kidney injury is associated
Metab. 2020;2(8):732–43.
9. Bernardi MH, Ristl R, Neugebauer T, Hiesmayr MJ, Druml W, Lassnigg A. Very early changes
in serum creatinine are associated with 30-day mortality after cardiac surgery: a cohort study.
Eur J Anaesthesiol. 2020;37(10):898–907.
10. Lassnigg A, Schmidlin D, Mouhieddine M, Bachmann LM, Druml W, Bauer P, et al. Minimal
changes of serum creatinine predict prognosis in patients after cardiothoracic surgery: a
prospective cohort study. J Am Soc Nephrol. 2004;15(6):1597–605.
11. Levey AS, Eckardt KU, Dorman NM, Christiansen SL, Hoorn EJ, Ingelfinger JR, et al.
Nomenclature for kidney function and disease: report of a kidney disease: improving global
outcomes (KDIGO) consensus conference. Kidney Int. 2020;97(6):1117–29.
12. Druml W, Kalantar-Zadeh K. The metabolic management and nutrition of acute kidney
injury. In: Koyner J, Topf J, Lerma E, editors. Handbook of critical care nephrology. Philadelphia: Wolters Kluwer; 2021. p. 169–79.
13. Kellum JA, Ronco C, Bellomo R. Conceptual advances and evolving terminology in acute
kidney disease. Nat Rev Nephrol. 2021;17(7):493–502.
14. Heyland D, Muscedere J, Wischmeyer PE, Cook D, Jones G, Albert M, et al. A randomized trial
of glutamine and antioxidants in critically ill patients. N Engl J Med. 2013;368(16):1489–97.
15. Cano NJ, Aparicio M, Brunori G, Carrero JJ, Cianciaruso B, Fiaccadori E, et al. ESPEN
guidelines on parenteral nutrition: adult renal failure. Clin Nutr. 2009;28(4):401–14.
16. Fiaccadori E, Sabatino A, Barazzoni R, Carrero JJ, Cupisti A, De Waele E, et al. ESPEN
guideline on clinical nutrition in hospitalized patients with acute or chronic kidney disease. Clin
Nutr. 2021;40(4):1644–68.
17. 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.
18. Bollmann MD, Revelly JP, Tappy L, Berger MM, Schaller MD, Cayeux MC, et al. Effect of
bicarbonate and lactate buffer on glucose and lactate metabolism during hemodiafiltration in
patients with multiple organ failure. Intensive Care Med. 2004;30(6):1103–10.
19. Datzmann T, Trager K, Reinelt H, von Freyberg P. Elimination rates of electrolytes, vitamins,
and trace elements during continuous renal replacement therapy with citrate continuous venovenous hemodialysis: influence of filter lifetime. Blood Purif. 2017;44(3):210–6.
20. Kihara M, Ikeda Y, Fujita H, Miura M, Masumori S, Tamura K, et al. Amino acid losses and
nitrogen balance during slow diurnal hemodialysis in critically ill patients with renal failure.
Intensive Care Med. 1997;23(1):110–3.
21. Maxvold NJ, Smoyer WE, Custer JR, Bunchman TE. Amino acid loss and nitrogen balance in
critically ill children with acute renal failure: a prospective comparison between classic
hemofiltration and hemofiltration with dialysis. Crit Care Med. 2000;28(4):1161–5.
22. Stapel SN, de Boer RJ, Thoral PJ, Vervloet MG, Girbes ARJ, Oudemans-van Straaten
HM. Amino acid loss during continuous venovenous hemofiltration in critically ill patients.
Blood Purif. 2019;48(4):321–9.
23. Oudemans-van Straaten HM, Ostermann M. Bench-to-bedside review: citrate for continuous
renal replacement therapy, from science to practice. Crit Care. 2012;16(6):249.
24. Jonckheer J, Vergaelen K, Spapen H, Malbrain M, De Waele E. Modification of nutrition
therapy during continuous renal replacement therapy in critically ill pediatric patients: a
narrative review and recommendations. Nutr Clin Pract. 2019;34(1):37–47.
25. Jonckheer J, Demol J, Lanckmans K, Malbrain M, Spapen H, De Waele E. MECCIAS trial:
metabolic consequences of continuous veno-venous hemofiltration on indirect calorimetry. Clin
Nutr. 2020;39(12):3797–
26.
MacLaughlin HL, Friedman
Am J Kidney Dis. 2022;79(3):437–49.
A, Verissimo T, Gariani K, Verney C, et al. Altered proximal
with mortality. Nat
803.
AN, Ikizler TA. Nutrition in kidney disease: core curriculum 2022.

Chapter 42
Overview, Technical Aspects, and Safety
of RRT Modalities in Critical Care
Federico Nalesso, Martina Cacciapuoti, Marco Bogo, and Marco D’Ascoli
Introduction
Acute kidney injury (AKI) represents a condition associated with significant morbidity and mortality. Approximately 57% of patients admitted to critical care units
develop AKI of any stage within 1 week, with severe AKI (stage 2 and stage 3 of
KDIGO AKI classification) affecting up to 39% of patients, among whom 13.5%
require renal replacement therapy (RRT) [1]. Research indicates that sepsis-
ated AKI is a critical risk factor determining the necessity for RRT [2]. The
associ
mortali
ty rates for AKI requiring RRT range from 40% to 55%, surpassing those
reported for other severe conditions, such as myocardial infarction in intensive care
units, sepsis without AKI, and acute respiratory distress syndrome (ARDS) requiring
mechanical ventilation. Patients who survive AKI in intensive care units are at risk of
developing chronic kidney disease (CKD), end-stage kidney disease (ESKD), and
functional impairment with extended recovery periods [1].
Renal replacement therapy (RRT) serves to support some of the physiological
processes normally carried out by the kidneys, including electrolyte and acid-base
control, volume balance, and toxin removal. This therapeutic intervention involves
the use of a semipermeable membrane capable of facilitating diffusive, convective,
or both diffusive and convective processes of purification simultaneously. However,
it is important to note that none of these techniques can fully replicate the synthetic
functions of the kidney, such as the production of vitamin D and erythropoietin or
the reabsorptive activities of the renal tubules.
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/978-3-031-66541-7_42.
F. Nalesso (
Department of Medicine, Nephrology, Dialysis and Transplant, University of Padua, Padua,
Italy
e-mail: federico.nalesso@unipd.it
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
A.
https://doi.org/10.1007/978-3-031-66541-7_42
✉) · M. Cacciapuoti · M. Bogo · M. D’Ascoli
493
Cotoia et al. (eds.), Nutrition, Metabolism and Kidney Support,

494 F. Nalesso et al.
DIFFUSION HEMODIAFILTRATION
ULTRAFILTRATION
Fig. 42.1 Mechanism of blood purification
Extracorporeal renal replacement techniques achieve solute clearance and water
removal through different physical mechanisms (Fig. 42.1, Mechanism of blood
purification):
1. Diffusion: it consists in the movement of solutes through a semipermeable
membrane from the compartment at a higher concentration to the one at a
lower concentration. Usually, the dialysate flows countercurrent with respect to
the blood to enhance and maintain the diffusion process along the filter fibers. The
diffusive process depends mainly on the concentration gradient, the temperature,
the surface of the membrane, the thickness of the membrane, and the diffusivity
coefficient for the single molecule. The higher the molecular weight, the lower the
diffusivity coefficient. Through this process, low molecular weight molecules
(e.g., urea and potassium) pass through the membrane from the patient’s blood to
the dialysate compartment. Diffusion is the physical principle of hemodialysis
(HD).
2. Ultrafiltration (convection): it is a process whereby a solvent is dragged through
a semipermeable membrane by the hydrostatic pressure gradient across the
membrane, the so-called transmembrane pressure (TMP = pressure in blood
compartment - pressure in dialysate compartment). Ultrafiltration depends on
TMP and the coefficient of ultrafiltration (Kf), which is based on the intrinsic
characteristic of the membrane. Based on Kf, membranes are classified into:
• Low-flux membrane: Kf < 10 ml/h/mmHg × m
• Middle-flux membrane: 10 ml/h/mmHg × m2 < Kf < 25 ml/h/mmHg × m
• High-flux membrane: >25 ml/h/mmHg × m
2
2
2

42 Overview, Technical Aspects, and Safety of RRT Modalities in Critical Care 495
Net ultrafiltration (UF
) is the difference between the UF and the volume
net
replaced in the circuit and represents the amount of fluid removed from the patient
(weight loss). The clearance of solutes in convective processes depends on the
ultrafiltration rate and the sieving coefficient (S) of the solute (the ratio between
the solute concentration in the ultrafiltrate and the solute concentration in the
plasmatic water: S = [Uf]/[Pw]). This process allows the clearance of th
of middle-molecular weight molecules (e.g., beta
- microglobulin), which are less
2
e solutes
removed by diffusion due to their higher molecular weight. Convection is the
physical process of hemofiltration (HF), where the amount of plasmatic water
removed through the membrane can be reinfused in predilution (prefilter),
postdilution (postfilter), or pre- and postdilution. The processes of diffusion and
convection can be combined in the same space to obtain hemodiafilt
ration (HDF).
In these techniques, molecules can be removed by diffusion and convection,
allowing the increase of the spectrum of removable molecules.
3. Adsorption: it is a process whereby solute removal occurs by binding to the
membrane surface of the filter (hemoperfusion) to remove very high molecular
weight molecules such as cytokines [
3].
Nomenclature
A Consensus Conference held in 2016 established the nomenclature of renal
replacement therapy (RRT) currently in use. According to this classification, renal
replacement therapies are categorized into intermittent therapies, continuous therapies, and hybrid therapies:
• Continuous therapies (CRRTs): continuous therapies provide continuous blood
purification, operating 24 h a day. The KDIGO 2012 Guidelines on Acute Kidney
Injury (AKI) recommend the use of CRRT over standard intermittent RRT for
hemodynamically unstable patients (grade 2B). It also suggests CRRT over
intermittent RRT for AKI patients with acute brain injury or other causes of
increased intracranial pressure or generalized brain edema (grade 2B).
• Intermittent therapies: intermittent therapies are administered in sessions lasting
for 3–5 h per day, necessitating a higher depuration rate compared to CRRTs.
These techniques rely on diffusion (hemodialysis (HD)), convection
(hemofiltration (HF)), or a combination of both (hemodiafiltration (HDF)).
•
Hybrid therapies:
hybrid therapies exhibit characteristics common to both intermittent and continuous modalities. They are typically administered using standard intermittent hemodialysis equipment, providing treatments lasting for
8–12 h per day. The primary physical mechanism employed is diffusion, although
some treatments may incorporate a small amount of convection in postdilution to
achieve hemodiafiltration (HDF) in postdilution.

496 F. Nalesso et al.
Continuous Therapies
• SCUF: slow continuous ultrafiltration is based on the ultrafiltration of plasmatic
water through the membrane. This technique allows the removal of plasmatic
water from the patient, determining weight loss without blood purification. For
this reason, this modality is not adequate in patients with severe electrolyte or
acid-base disorders [4]. A meta-analysis revealed that in patients with ADHF
(acute decompensated heart failure), UF is more effective in removing fluid than
diuretics and can decrease rehospitalization for heart failure [5].
• CVVH: continuous veno-venous hemofiltration is a technique based on convec-
tion that provides solute clearance and fluid overload correction. The replacement
of the fluid removed by convection can be infused before the hemofilter
(predilution) or after the hemofilter (postdil ution) or in both pre- and postdilution.
Postdilution is more efficient in terms of solute balancing but can determine a
higher filtration fraction with a higher risk of circuit and filter clotting.
• CVVHD: continuous veno-venous hemodialysis is a form of RRT based exclu-
sively on diffusion. The dialysate flows countercurrent with respect to the blood
and removes small solutes according to their gradient of concentration. The
higher the dialysate flow rate and/or the blood flow rate, the more effective the
clearance of solutes.
• CVVHDF: continuous veno-venous hemodiafiltration is the modality
bines
diffusion and convection in the same technique, allowing either an effective
solute clearance for small and middle molecules or fluid overload control through
the ultrafiltration process [4] (Fig. 42.2).
that com-
Intermittent Renal Replacement Therapies (IRRTs)
Le terapie intermittenti nel Trattamento di Sostituzione Renale (TSR) si basano sulla
diffusione, convezione o una combinazione di entrambi i meccanismi. La durata del
trattamento √® tipicamente intermittente, della durata di 4–6 ore per sessione.
In base alla classificazione precedente, possiamo definire quanto segue:
• HD: Emodialisi
• HF: Emofiltrazione
• HDF: Emodiafi
erapie i
Le t
emodinamicamente stabili. Possono essere somministrate in unit√{ di terapia
intensiva (UTI) solo per i pazienti stabili, con un bilancio idrico ottenibile attraverso
la rimozione di 2–3 litri al giorno, con un tasso di ultrafiltrazione per ora compatibile
con l’emodinamica del paziente [4].
A seconda
TSR, i singoli centri possono utilizzare la Terapia Continua di Sostituzione Renale
ltrazione
ntermittenti sono le modalit√{ di TSR preferite per i pazienti
delle politiche locali, della disponibilit√{ di personale e monitoraggi
Соседние файлы в папке Библиотека им академика М.И. Перельмана
