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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 ow, 150 ml/min (=9000 ml/h); citrate ow, 200 ml/h; predilution ow, 1000 ml/h; no postdilution, dialysate ow, 1500 ml/h; uid removal (ultraltrate), 250 ml/h; and CaCl Step 1: Plasma ow (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 hemolter 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 ow (F
efuent
= F
dialysate
F
efuent
+F
)
predilution
+F
postdilution
+F
citrate
+F
CaCl2
+ uid
removal
= 1500 + 1000 + 0 + 200 + 20 + 250 = 2970 ml/h
3-
Step 4:PO
3-
PO
4
loss per day
4
loss = F
efuent
× (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 uid does not contain any glucose (Table 41.2) or the replacement concentration is below the blood concentration. Most replacement uid 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 uent, 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 lter due to their small molecular size. Therefore, amino acid concentrations in the blood and efuent should be similar [20, 21]. fact that most amino acids have a sieving coefcient of 1 [22], it can be approxi­mated that at an efuent volume of 50 L per day, about 20 g of AA are lost, and at a higher efuent volume of 70 L, nearly 30 g of AA. In intermittent dialysis that uses a much higher dialysate ow over a few hours, the efuent AA concentration (85 mg/ L) has been found to be only 25% of plasma concentration at a dialysate ow of 30 L/h. This example shows that differences in apparent sieving coefcient, as has been found for middle-sized molecules such as cytokines, also apply for smaller molecules if the dialysate ow through the lter 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 uid 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 lter. 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 uid (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 sufcient 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 sufcient 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, Ingelnger 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 hemodialtration 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: inuence of lter 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 hemoltration and hemoltration 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 hemoltration 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. Modication 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 hemoltration 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 DAscoli

Introduction

Acute kidney injury (AKI) represents a condition associated with signicant 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 classication) 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 purication 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. DAscoli
493
Cotoia et al. (eds.), Nutrition, Metabolism and Kidney Support,
494 F. Nalesso et al.
DIFFUSION HEMODIAFILTRATION
ULTRAFILTRATION
Fig. 42.1 Mechanism of blood purication
Extracorporeal renal replacement techniques achieve solute clearance and water removal through different physical mechanisms (Fig. 42.1, Mechanism of blood purication):
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 ows countercurrent with respect to
the blood to enhance and maintain the diffusion process along the lter bers. The
diffusive process depends mainly on the concentration gradient, the temperature,
the surface of the membrane, the thickness of the membrane, and the diffusivity
coefcient for the single molecule. The higher the molecular weight, the lower the
diffusivity coefcient. Through this process, low molecular weight molecules
(e.g., urea and potassium) pass through the membrane from the patients blood to
the dialysate compartment. Diffusion is the physical principle of hemodialysis
(HD).
2. Ultraltration (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). Ultraltration depends on
TMP and the coefcient of ultraltration (Kf), which is based on the intrinsic
characteristic of the membrane. Based on Kf, membranes are classied into:
Low-ux membrane: Kf < 10 ml/h/mmHg × m
Middle-ux membrane: 10 ml/h/mmHg × m2 < Kf < 25 ml/h/mmHg × m
High-ux membrane: >25 ml/h/mmHg × m
2
2
2
42 Overview, Technical Aspects, and Safety of RRT Modalities in Critical Care 495
Net ultraltration (UF
) is the difference between the UF and the volume
net
replaced in the circuit and represents the amount of uid removed from the patient
(weight loss). The clearance of solutes in convective processes depends on the
ultraltration rate and the sieving coefcient (S) of the solute (the ratio between
the solute concentration in the ultraltrate 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 hemoltration (HF), where the amount of plasmatic water
removed through the membrane can be reinfused in predilution (prelter),
postdilution (postlter), or pre- and postdilution. The processes of diffusion and
convection can be combined in the same space to obtain hemodialt
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 lter (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 classication, renal replacement therapies are categorized into intermittent therapies, continuous thera­pies, and hybrid therapies:
Continuous therapies (CRRTs): continuous therapies provide continuous blood purication, 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 (hemoltration (HF)), or a combination of both (hemodialtration (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 hemodialtration (HDF) in postdilution.
496 F. Nalesso et al.
Continuous Therapies
SCUF: slow continuous ultraltration is based on the ultraltration of plasmatic water through the membrane. This technique allows the removal of plasmatic water from the patient, determining weight loss without blood purication. 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 uid than diuretics and can decrease rehospitalization for heart failure [5].
CVVH: continuous veno-venous hemoltration is a technique based on convec- tion that provides solute clearance and uid overload correction. The replacement of the uid removed by convection can be infused before the hemolter (predilution) or after the hemolter (postdil ution) or in both pre- and postdilution. Postdilution is more efcient in terms of solute balancing but can determine a higher ltration fraction with a higher risk of circuit and lter clotting.
CVVHD: continuous veno-venous hemodialysis is a form of RRT based exclu- sively on diffusion. The dialysate ows countercurrent with respect to the blood and removes small solutes according to their gradient of concentration. The higher the dialysate ow rate and/or the blood ow rate, the more effective the clearance of solutes.
CVVHDF: continuous veno-venous hemodialtration is the modality bines
diffusion and convection in the same technique, allowing either an effective solute clearance for small and middle molecules or uid overload control through the ultraltration 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 classicazione precedente, possiamo denire quanto segue:
HD: Emodialisi
HF: Emoltrazione
HDF: Emodia
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 ultraltrazione per ora compatibile con lemodinamica 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