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38. Chan STF, Kapadia CR, Johnson AW, etal. Extracellular uid volume expansion and third space sequestration at the site of small bowel anastomoses. Br J Surg. 1983;70:36–9.
39. Brandstrup B.Restricted intravenous uid therapy in colorectal surgery, results of a clinical randomised multi centre trial; 2003. https://www.researchgate.net/publication/279931470_
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40. Marjanovic G, Villain C, Juettner E, etal. Impact of different crystalloid volume uid regimens on intestinal anastomotic stability. Ann Surg. 2009;249:181–5.
41. Kulemann B, Timme S, Sifert G, etal. Intraoperative crystalloid overload leads to substantial inammatory inltration of intestinal anastomosis—a histomorphological analysis. Surgery. 2013;154:596–603.
42. Jacob M, Chappel D, Rehm M. The third space—fact or ction? Best Pract Res Clin Anaesthesiol. 2009;23:145–57.
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44. Rehm M, Hulde N, Kammerer T, Meidert AS, Hofmann-Kiefer K.State of the art in uid and volume therapy : a user-friendly staged concept. Anaesthesist. 2019;68(Suppl 1):1–14.
45. Burlew CC.The open abdomen: practical implications for the practicing surgeon. Am J Surg. 2012;204(6):826–35.
46. Cumin D, Fogarin J, Mitchell SJ, Windsor JA.Perioperative hypothermia in open and laparo­scopic colorectal surgery. ANZ J Surg. 2022;92(5):1125–31.
47. Biegner AR, Anderson D, Olson RL, etal. Quantication of insensible water loss associ­ated with insufation of nonhumidied CO2in patients undergoing laparoscopic surgery. J Laparoendosc Adv Surg Tec A. 1999;9:325–9.
48. Clark RB, Thompson DS, Thompson CH.Prevention of spinal hypotension associated with cesarean section. Anesthesiology. 1976;45:670–4.
49. Fanelli G, Casati A, Berti M, etal. Incidence of hypotension and bradycardia during integrated epidural/general anaesthesia. An epidemiologic observational study on 1200 consecutive patients. Italian Study Group on Integrated Anaesthesia. Minerva Anesthesiol. 1998;64:313–9.
50. Massoth C, Töpel L, Wenk M.Hypotension after spinal anesthesia for cesarean section: how to approach the iatrogenic sympathectomy. Curr Opin Anaesthesiol. 2020;33(3):291–8.
51. Kinsella SM, Pirlet M, Mills MS, etal. Randomized study of intravenous uid preload before epidural analgesia during labour. Br J Anaesth. 2000;85:311–3.
52. Kubli M, Shennan AH, Seed PT, etal. A randomised controlled trial of uid pre-loading before low dose epidural analgesia for labour. Int J Obstet Anesth. 2003;12:256–60.
53. Nishimura N, Kajimoto Y, Kabe T, etal. The effect of volume loading during epidural analge­sia. Resuscitation. 1985;13:31–9.
54. Jackson R, Reid JA, Thorburn J.Volume preloading is not essential to prevent spinal-induced hypotension at caesarean section. Br J Anaesth. 1995;75:262–5.
55. Park GE, Hauch MA, Curlin F, etal. The effects of varying volumes of crystalloid administra­tion before cesarian delivery on maternal hemodynamics and colloid osmotic pressure. Anesth Analg. 1996;83:299–303.
56. Rout CC, Rocke DA, Levin J, etal. A reevaluation in the role of crystaloid preload in the prevention of hypotension associated with spinal anesthesia for elective cesarean section. Anesthesiology. 1993;79:262–9.
57. Rivers E, Nguyen B, Havstad S, etal. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368–77.
58. Shoemaker WC, Appel PL, Kram HB, etal. Prospective trial of supranormal values of survi­vors as therapeutic goals in high risk surgical patients. Chest. 1987;94:1176–86.
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19 Perioperative Fluid Administration and Complications in Emergency…
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59. Navarro LH, Bloomstone JA, Auler JO Jr, etal. Perioperative uid therapy: a statement from the international Fluid Optimization Group. Perioper Med. 2015;4:1–20.
60. Jones AE, Shapiro NI, Trzeciak S, et al. Emergency Medicine Shock Research Network (EMShockNet) Investigators. Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. JAMA. 2010;303:739–46.
61. Wilms H, Mittal A, Haydock MD, et al. A systematic review of goal directed uid therapy: rating of evidence for goals and monitoring methods. J Crit Care. 2014;29:204–9.
62. Forget P, Lois F, de Kock M.Goal-directed uid management based on the pulse oximeter­derived pleth variability index reduces lactate levels and improves uid management. Anesth Analg. 2010;111:910–4.
63. Lobo SM, Lobo FR, Polachini CA, et al. Prospective, randomized trial comparing uids and Doputamine optimization of oxygen delivery in high-risk surgical patients. Crit Care. 2006;10:R72.
64. Lobo SMA, Salgado PF, Castillo VGT, etal. Effects of maximizing oxygen delivery on mor­bidity and mortality in high-risk surgical patients. Crit Care Med. 2000;28:3396–404.
65. Benes J, Chytra I, Altmann P, et al. Intraoperative uid optimization using stroke volume variation in high risk surgical patients: results of prospective randomized study. Crit Care. 2010;14:1–15.
66. Gan TJ, Soppitt A, Maroof M, etal. Goal-directed intraoperative uid administration reduces length of hospital stay after major surgery. Anesthesiology. 2002;97:820–6.
67. Lopes MR, Olivera MA, Pereira VOS, etal. Goal-directed uid management based on pulse pressure variation monitoring during high-risk surgery: a pilot randomized controlled trial. Crit Care. 2007;11:R100.
68. Mayer J, Boldt J, Mengistu AM, etal. Goal-directed intraoperative therapy based on autocali­brated arterial pressure waveform analysis reduces hospital stay in high-risk surgical patients: a randomized, controlled trial. Crit Care. 2010;14:1–9.
69. Salzwedel C, Puig J, Carstens A, et al. Perioperative goal-directed hemodynamic therapy based on radial arterial pulse pressure variation and continuous cardiac index trending reduces postoperative complications: a multi-center, prospective, randomized study. Crit Care. 2013;17:1–11.
70. Wakeling HG, McFall MR, Jenkins CS, etal. Intraoperative oesophageal Doppler guided uid management shortens postoperative hospital stay after major bowel surgery. Br J Anaesth. 2005;95:634–42.
71. Buettner M, Schummer W, Huetttemann E, et al. Inuence of systolic-pressure-variation­guided intraoperative uid management on organ function and oxygen transport. Br J Anaesth. 2008;101:194–9.
72. Challand C, Struthers R, Sneyd JR, etal. Randomized controlled trial of intraoperative goal­directed uid therapy in aerobically t and unt patients having major colorectal surgery. Br J Anaesth. 2012;108:53–62.
73. Conway DH, Mayall R, Abdul-Latif MS, etal. Randomised controlled trial investigating the inuence of intravenous uid titration using oesophageal Doppler monitoring during bowel surgery. Anaesthesia. 2002;57:845–9.
74. Perner A, Haase N, Guttormsen AB, etal. Hydroxyethyl starch 130/0.42 versus Ringer’s ace­tate in severe sepsis. N Engl J Med. 2012;367:124–34.
75. Zheng H, Guo H, Ye J, etal. Goal-directed uid therapy in gastrointestinal surgery in older coronary heart disease patients: randomized trial. World J Surg. 2013;37:2820–9.
76. Srinivasa S, Taylor MH, Singh PP, et al. Randomized clinical trial of goal-directed uid therapy within an enhanced recovery protocol for elective colectomy. Br J Anaesth. 2013;100:66–74.
77. Phan TD, D'Sousa B, Rattray MJ, etal. A randomised controlled trial of uid restriction com­pared to oesophageal Doppler-guided goal-directed uid therapy in elective major colorec­tal surgery within an Enhanced Recovery After Surgery program. Anaesth Intensive Care. 2014;42:752–60.
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78. Brandstrup B, Svendsen PE, Rasmussen M, etal. Which goal for uid therapy during colorec­tal surgery is followed by the best outcome: near maximal stroke volume or zero uid balance? A clinical randomized double blinded multi centre trial. Eur J Anaesth. 2010;27:4.
79. Wrzosek A, Jakowicka-Wordliczek J, Zajaczkowska R, etal. Perioperative restrictive ver­sus goal-directed uid therapy for adults undergoing major non-cardiac surgery. Cochrane Database Syst Rev. 2019;12:CD012767.
80. Colantonio L, Claroni C, Fabrizi L, etal. A randomized trial of goal directed vs. standard uid therapy in cytoreductive surgery with hyperthermic intraperitoneal chemotherapy. J Gastrointest Surg. 2015;19:722–9.
81. Warrillow SJ, Weinberg L, Parker F, et al. Perioperative uid prescription, complica­tions and outcomes in major elective open gastrointestinal surgery. Anaesth Intensive Care. 2010;38:259–65.
82. Wuethrich PY, Burchard FC, Thalmann GN, et al. Restrictive deferred hydration com­bined with preemptive norepinephrine infusion during radical cystectomy reduces postop­erative complications and hospitalization time: a randomized clinical trial. Anesthesiology. 2014;120:365–77.
83. National Heart and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Comparison of two uid management strategies in acute lung injury. N Engl J Med. 2006;354:2564–75.
84. Bhaskaran K, Arumugam G, Kumar PV.A prospective randomized comparison study on effect of perioperative use of chloride liberal intravenous uids versus chloride restricted intravenous uids on postoperative acute kidney injury in patients undergoing off-pump coronary artery bypass grafting surgeries. Ann Card Anaesth. 2018;21:413–8.
85. McArdle GT, McAuley DF, McKinley A, etal. Preliminary results of a prospective random­ized trial of restrictive versus standard uid regime in elective open abdominal aortic aneuri­ysm repair. Ann Surg. 2009;250:28–34.
86. Stewart RM, Park PK, Hunt JP, etal. Less is more: improved outcomes in surgical patients with conservative uid administration and central venous catheter monitoring. J Am Coll Surg. 2009;208:725–37.
87. Myles PS, Bellomo R, Corcoran T, et al. Restrictive versus liberal uid therapy for major abdominal surgery. N Engl J Med. 2018;378:2263–74.
88. Brandstrup B.Finding the right balance. N Engl J Med. 2018;378:2335–6.
89. Tengberg LT, Bay-Nielsen M, etal. Multidisciplinary perioperative protocol in patients under­going acute high-risk abdominal surgery. Br J Surg. 2017;104:463–71.
90. Voldby AW, Aaen AA, Loprete R, etal. Perioperative uid administration and complications in emergency gastrointestinal surgery—an observational study. Perioper Med. 2022;11:9.
91. Brandstrup B, Møller AM.The challenge of perioperative uid management in elderly patients. Curr Anesthesiol Report. 2019;9:406–13.
92. ERAS Society. ERAS programs; 2019. https://www.erassociety.org/guidelines/list- of-
guidelines/. Accessed 28 Aug 2023.
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Chapter 20
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The Surgical Critically Ill Patients: AFocus onDeresuscitation Strategy
MartinRuste , Jean-LucFellahi, andMatthiasJacquet-Lagrèze
Preliminary Concepts
Fluid Overload
The denition of uid overload is heterogeneous in the literature and originates in the association of a daily positive cumulative uid balance (the difference between total uid intake and total uid outputs, usually adjusted in percentage of body weight) with a worse prognosis. From a statistical approach, it is usually described as an all-or-nothing phenomenon, ranging from 5% to 10% of the patient’s body weight, without discriminating intravascular and extravascular compartments nor characterizing the related damaged end-organ [13]. Such an approach is ques­tionable as:
– there is no identied threshold effect between cumulative uid balance and prog-
nosis and each 1% of body weight or positive Liter in cumulative uid balance is associated with an increase in morbimortality [4, 5];
– the various measurement methods of the cumulative uid balance are not accu-
rate nor interchangeable with body weight variation [68];
– peripheral edema may coexist with intravascular hypo or hypervolemia [9];
M. Ruste (*) · J.-L. Fellahi · M. Jacquet-Lagrèze Service d’anesthésie-réanimation, Hôpital Louis Pradel, Hospices Civils de Lyon, Bron Cedex, France
Faculté de Médecine Lyon Est, Université Claude Bernard Lyon 1, Lyon Cedex 08, France
Laboratoire CarMeN, Inserm UMR 1060, Université Claude Bernard Lyon 1, Lyon, France e-mail: martin.ruste@chu-lyon.fr; jean-luc.fellahi@chu-lyon.fr;
matthias.jacquet-lagreze@chu-lyon.fr
Switzerland AG 2024 J. Faintuch, S. Faintuch (eds.), Recent Strategies in High Risk Surgery,
https://doi.org/10.1007/978-3-031-56270-9_20
323© The Author(s), under exclusive license to Springer Nature
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– the evaluation of the uid overload impact on end-organ function may serve as a
therapeutic trigger and/or target [10].
Recently, experts proposed new denitions for the “uid accumulation,” related to a pathologic state of overhydration whatever intravascular status and the “uid accumulation syndrome” as the association between the uid accumula­tion and impact on end-organ function [10].
M. Ruste et al.
Deresuscitation or De-escalation
A four-phase strategy of uid management was rst described 10years ago in septic shock [11]. The rst “salvage” or “rescue” phase consists of an aggressive therapy to restore organ perfusion at the very early management of shock state, which is then tightly promoted during the rst hours (optimization phase). The following stabilization phase aims to maintain homeostasis by the way of organ support, titra­tion of uids and vasoactive medications and to initiate a late conservative uid management inducing a slight negative uid balance. Initially described as de-esca­lation, the fourth phase consists of achieving a net negative uid balance after circu­latory shock resolution to counteract the side effects of uid accumulation. The term “deresuscitation” is suggested by other authors as a more “active” strategy of uid removal [10]. This strategy involves uid intake restriction with a forced diuresis or the application of net ultraltration to remove a large amount of uid over several days (Fig.20.1). There are no widely admitted nor accurate denitions of the begin­ning and end of each phase.
If this four-phase approach of uid therapy ts well to the global intensive care trajectory for a large part of critically ill patients, a myriad of situations is encoun­tered in clinical practice. For example, uid overload may exist without or precede any circulatory shock (congestive cardiopathy, liver or renal failure, iatrogenia…) or may develop after initial resuscitation.
20 The Surgical Critically Ill Patients: AFocus onDeresuscitation Strategy
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Fig. 20.1 Four-phase uid management strategy of shock state 1. Salvage or Rescue Phase (Minutes to Hours) Lifesaving measures to restore a minimal arterial pressure and organ per­fusion (aggressive uid therapy, early introduction of Norepinephrine, blood transfu­sion) 2. Optimization Phase (Hours to Days) Personalized uid therapy (uid responsiveness assessment), catecholamine administration (echocardiography) and perfusion maximization (clinical and biological assessment) 3. Stabilization Phase (Days) Providing organ support and initiate their progressive weaning: decrease in catecholamine support, slight decrease in uid balance to promote weaning from mechanical ventilation, venous congestion evaluation and treatment. Minimizing complications 4. De-escalation or deresuscitation phase (days to weeks) Correction of uid accumulation: uid intake restriction associated with uid removal by the way of diuretics or ultraltration
325
Pathophysiology ofFluid Overload
Physiologically, uid overload may be dened as a “pathologic accumulation of water and electrolytes in the body beyond that seen in healthy individuals” [12]. This accumulation originates in an inadequacy between the uid intake and the outputs, largely mediated by a patient-physician interaction [12]. For example, if a crystalloid administration is temporarily efcient to increase plasma volume, only 20% of the initially administrated volume persists in intravascular compartment 30min after the administration, with a re-distribution to the extravascular space fol­lowed by an elimination phase. Such transfers are moreover highly dependent on hemodynamic parameters and patient’s related factors (i.e. context sensitive) [13,
14]. The extravasation is reinforced in systemic inammatory state, where the endo-
thelial glycocalyx and tight junction deterioration impaired the regulation of uid
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M. Ruste et al.
and electrolytes movements across the capillary membrane [15, 16], promoting a high capillary permeability clinically traducing by the so-called capillary leak syn­drome. There are reasons to believe that it is associated with a quasi-ubiquitarian impact on end-organ function [17, 18].
Following the four-phase concept of uid management and clinicians’ beliefs [19], uid overload is inherent to the initial salvage phase responsible for a large amount of intravenous uid and sodium intake. However, recent ndings challenge this assumption as volume and sodium overload during the ICU stay are mainly driven by uid creep (unintentional administration for vehiculate intravenous, oral or enteral medication) and maintenance uids, much more than resuscitation uids [20]. It may explain the progressive development of uid overload in the case of inadequate diuresis as shown in patients with acute kidney injury [5].
Inadequate elimination of uids administrated to critically ill patients is proba­bly multifactorial. The end-organ implied in hydro-electrolytic balance may be impaired because of tissue injury, hemodynamic impairment or hormonal perturba­tions. At the ICU admission, 25% of patients were reported to present oliguria in the rst 24h, and this oliguria persists during the whole ICU stay in almost two out of three of them [21]. Among patients admitted for sepsis, almost one out of two have diastolic dysfunction [22] and one out of six a reduced left ventricular ejection frac­tion (<40%) [23]. Secondary acquired liver injury could concern as many as one out of three patients in the ICU [24]. Furthermore, several local factors promote the persistence of interstitial edema. The glycocalyx degradation is not rapidly revers­ible after the aggression. The extracellular matrix distortion decreases the intersti­tial pressure. The lymphatic dysfunction reduces the capacity for vascular relling, which is the main determinant of edema resolution in the low ltration-low resorp­tion revised Starling principle of microvascular uid exchange [25]. All these phe­nomena are responsible for a vicious circle [26], making the spontaneous resolution of uid accumulation unlikely or tardy. In this context, “active” uid removal may decrease the intensity and the exposure duration to uid overload and thus be con­sidered as a full therapeutic tool to enhance organ recovery and prevent complica­tions’ occurrence.
In the particular context of the surgical critically ill patient, various factors pre­disposing for uid overload may be encountered in the operating room: goaled­directed therapy improves prognosis but requires intravenous uid therapy, hemorrhage may require blood product administration, surgical trauma or ischemia­reperfusion induce systemic inammatory response, uid creep may be related to medications or the priming of cardiopulmonary bypass. After the surgery, postop­erative organ dysfunction (renal, cardiac or liver failures) may be responsible for inadequate outputs, and postoperative complications may require uid creep, main­tenance or resuscitation uids. Data are scarce concerning this population speci­cally, but uid overload >5% could concern more than 10% of the patients admitted in ICU after surgery [27] and capillary leak syndrome was recently reported in 50% of a cohort of surgical critically ill patients [28]. A positive cumulative uid balance is associated with a worse prognosis after cardiac [29, 30] and non-cardiac surgery [27, 31, 32].
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Fluid Removal: Tolerance andTargets
In deresuscitation strategy, uid removal consists of an intravascular volume with­drawal by the way of diuretics or net ultraltration. Thus, whether the intravascular volume will keep constant or decrease depends on the vascular relling rate, which in critically ill patients, as previously discussed, is probably low. Such an assump­tion is reinforced by the J-shaped association between net ultraltration intensity and prognosis in patients with continuous renal replacement therapy reported by several cohort studies [33]. On the one hand, in patients with intravascular hyper­volemia, targeting a decrease in circulating blood volume makes sense. Indeed, it may participate in reducing venous congestion and thus improve end-organ func­tion as the kidney or the liver [34]. But, on the other hand, in patients without intravascular hypervolemia, decreasing intravascular volume exposes to iatrogenic hypovolemia and hypoperfusion [33]. In this situation, the adequacy between the vascular relling rate and the uid removal rate is probably the cornerstone of hemodynamic tolerance during deresuscitation. However, such an approach remains simplistic regarding the complexity of the interaction between intravascu­lar volume status and hemodynamic. Various strategies have been proposed to safely guide the uid removal: passive leg raising predicts arterial hypotension dur­ing intermittent hemodialysis with high rate ultraltration [35] and peripheral per­fusion index during continuous renal replacement therapy [36]; central venous pressure and cardiac output may be associated to estimate both efciency and toler­ance [37]; clinical and biological peripheral perfusion monitoring allows a more efcient uid removal without sign of harm [38]. In any event, an individualization of the uid removal rate associated with a frequent re-assessment of its tolerance reaches consensus [39, 40].
If applying uid withdrawal to decrease the side effect of uid accumulation raises the question of how to do it safely, the targets also remain unclear. The dry weight, an already challenging concept in patients with chronic hemodialysis, may look like a pipe dream in critically ill patients. Non-accurate or unavailable baseline weight measures, multifactorial and quick loss of muscle mass and imprecision of the measure during the ICU stay do not encourage to use it alone. A rigorous cumu­lative uid balance estimation may help to quantitatively estimate the efciency of the uid removal strategy. Bio-electrical impedance analysis is a promising non­invasive and easy-to-use method to determine body composition at the bedside. Several of its derived parameters oriented to estimate uid accumulation are associ­ated with prognosis [4144]. However, its sensibility seems to be low, the multi­compartmental models available are heterogenous, the estimation of the uid status is not well validated in critically ill patients, a lot of research angles persist and no interventional study has demonstrated its impact on outcome [43, 45]. An end-organ approach may be used as a trigger and/or a target to guide uid removal. Fluid removal decreases intraabdominal pressure and extravascular lung water [46], helps to decrease left and right ventricular lling pressure accelerating the mechanical ventilation weaning [47, 48], could improve renal venous congestion and decrease
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worsening kidney failure in acute heart failure [49, 50] and may participate to post­operative microcirculation improvement [51]. These factors may be estimated rou­tinely with more or less invasive monitoring as pulmonary artery catheter, transpulmonary thermodilution, point of care ultrasound evaluation [52, 53] or non- invasive sublingual device.
M. Ruste et al.
Fluid Removal: with what tools?
Diuretics
A diuretic is a substance that increases the ow of urine, mainly by the way of a kidney action, allowing the removal of water and electrolytes. A recent large database cohort study reported an exposition to diuretics in nearly one out of two critically ill patient. The use was particularly important in patients with a history of heart failure, under mechanical ventilation or in postoperative care after car­diac surgery. Loop diuretic was by far the most frequently administrated class and diuretic combinations that concern less than one out of four patients receiv­ing diuretics [54]. The continuous infusion of loop diuretics rather than an inter­mittent administration and their association with carbonic anhydrase inhibitors or thiazides could be more efcient to decrease cumulative uid balance but are associated with more metabolic complications. However, the combination of loop diuretics with a thiazide decreases the risk for hypernatremia, and the administration of potassium sparing diuretics may help to avoid hypokalemia at the cost of decreasing diuresis [55]. These four pharmacological classes of diuretics are detailed in Table 20.1. Acute kidney injury and norepinephrine administration should probably not be impediments to diuretic prescription as it did not alter the outcome for the former [56] and worsen the prognosis for the latter [57].
Ultraltration
Extracorporeal ultraltration consists of the removal of water, electrolytes and molecules from the plasma below a certain weight mediated by hydrostatic pres­sure applied across a dedicated semi-permeable membrane. It is carried out with a double lumen central venous catheter, continuously or intermittently, and most of the time in association with renal replacement therapy (rather than isolated). Isolated ultraltration has no signicant impact on plasma electrolytes, small sol­utes and proteins, whereas during renal replacement therapy, it contributes to the exchanges required to maintain homeostasis. In this case, the ultraltrate is totally
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Table 20.1
Site of action NKCC-2
Main effects Loss of water
Molecules Furosemide
Main adverse events
Cautions for usage
Main interests for combination with loop diuretics
Diuretics for deresuscitation
Loop diuretics Thiazides
(Loop of Henle)
+++ Natriuretic + Kaliuretic ++ Calciuretic
Bumetanide Torsemide
Metabolic alkalosis Hypo/ hypernatremia Hypokaliemia Ototoxicity
Resistance Dysnatremia Alkalosis Hypokaliemia Prefer continuous infusion
NCC (Distal convoluted tubule)
Loss of water + Natriuretic ++ Kaliuretic +
2+
Ca
reabsorption
Hydrochlorothizide Indapamide Metolazone
Metabolic alkalosis Hyponatremia Hypokaliema
Hyponatremia Hypokaliemia
Efciency to decrease cumulative uid balance Avoiding hypernatremia
Carbonic Anhydrase inhibitors
Carbonic anhydrase (Proximal convoluted tubule)
Loss of water + Natriuretic ++ Kaliuretic +
Acetazolamide Amiloride
Metabolic acidosis Hypokaliemia
Tolerance after 48h Respiratory acidosis Advance liver disease Hyponatremia Hypokaliemia
Efciency to decrease cumulative uid balance
Potassium sparing diuretics
ENaC or mineralocorticoid receptor (Distal convoluted tubule, connecting tubule, collecting tubule)
Loss of water + Natriuretic +
+
K
reabsorption +
Spironolactone Aldactone
Metabolic acidosis Hyperkaliemia
Shock state Hyperkaliemia (particularly if renal failure)
Avoiding hypokaliemia
or not compensated by uid replacement, and the volume subtracted during renal replacement therapy is called the “net ultraltration” [33]. One of the theoretical advantages of ultraltration over diuretics is the lack of induced metabolic disor­ders as frequently observed with the former, and the easy-to-use and precise char­acteristics of the method. However, independently from the hemodynamic impact of uid removal per se, renal replacement therapy is not devoid of side effects [58, 59], and some of them, such as complications related to catheter or blood- membrane interactions, probably exist in isolated ultraltration. Moreover, recent