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ndings highlighted the advantages of delayed renal replacement therapy in critically ill patients [60], which does not promote early initiation of renal replacement therapy for uid removal. In continuous renal replacement therapy, a net
ultraltration between 1 and 1.75mL/kg/h is associated with a better prognosis
[33]. Targeting a net ultraltration of 2mL/kg/h provides a signicant decrease in
uid balance (if uid intake is restrictive) and seems safe, provided a strict hemodynamic monitoring [38]. In chronic intermittent hemodialysis, a net ultraltration over 10mL/kg/h is associated with increased mortality [61]; hence, it seems
reasonable to use lower net ultraltration rate in critically ill patients. To this
purpose, prolonged, more frequent sessions or isolated ultraltration may be carried out to induce a negative uid balance [62]. Regarding the control of uid
balance, experts have suggested to not wean renal replacement if the diuresis is
lower than 2L/day with diuretics [63]. To nish, recent data indicates to avoid
transition from continuous renal replacement therapy to intermittent hemodialysis if uid accumulation persists, as it has shown as a marker of poor hemodynamic tolerance of intermittent hemodialysis [64].
M. Ruste et al.
Deresuscitation: Do Not Forget Fluid Intake
If restrictive strategies to initial resuscitation is beyond the scope of this focus, a
tight control of uid intake remains an integral part of deresuscitation strategy. A
recent cohort emphasized that, in real-life, resuscitation uids only count for 6.6%
of the uid intake during the ICU stay, whereas maintenance uids count for 25%,
nutrition for 33% and uid creep (uids administrated as a vehicle for medication
or electrolytes) for 33%. Besides, resuscitation uids’ contribution to uid balance
decreases throughout the ICU stay, and the major determinants of the positive
cumulative uid balance, sodium and chloride burden are uids of maintenance and
uid creep [20]. In this regard, the prescription of maintenance uids and dilution
for medication needs special attention as they largely participate to sodium and
chloride load. As sodium-induced uid retention and chloride-related renal vasoconstriction could be responsible for uid accumulation themselves, maintenance
uids should preferably be orally administrated, hypotonic and for a total amount of
intake without exceeding 25–30mL/kg/day and 1mmol/kg/day of sodium [65]. To
20 The Surgical Critically Ill Patients: AFocus onDeresuscitation Strategy
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331
this purpose, dissolving as many medications as possible in glucose 5% is efcient
and probably safe [66].
Suggestions for daily clinical practice concerning deresuscitation are provided in
Figs.20.2 and 20.3.
Fig. 20.2 Deresuscitation and monitoring
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M. Ruste et al.
Fig. 20.3 Deresuscitation: suggestions for clinical practice. RRT Renal replacement therapy
20 The Surgical Critically Ill Patients: AFocus onDeresuscitation Strategy
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333
Deresuscitation: Evidence-Based Patient-Centered Impact
If uid overload was constantly associated with a worse prognosis, the causality
link is not well-established. Thus, as a patient–physician interaction, uid accumulation is probably in part inherent to pathological patient-related factors as capillary
leakage and organ failure, which obviously participate in this worse prognosis. In
this regard, interventional studies aiming to decrease uid overload have shown
relatively disappointing results. If restrictive strategies may help the mechanical
ventilation weaning without improving mortality [67, 68], high-quality trials are
scarce on deresuscitation strategy itself. They have shown difculties to elaborate
allowing a signicant decrease in cumulative uid balance and did not show any
signicant improvement in patients with sepsis outcomes [69]. A recent large randomized trial illustrates those difculties: a protocol targeting a progressive weight
decrease after day 2, using albumin, diuretics or ultraltration failed to decrease
cumulative uid balance compared to usual care [70]. Despite a complex dedicated
design, the trial suffered from contamination between groups. Suboptimal protocol
adherence was also reported and the strict safety criteria (suspension of the deresuscitation strategy if arterial hypotension, vasopressor requirement, renal function
deterioration) may have induced undertreatment in the interventional group.
However, to decrease cumulative uid balance with deresuscitation strategy is not a
quixotic goal as shown by two recent interventional or quasi-experimental studies
[38, 71]. It must be noted that besides acute kidney injury and restrictive strategies
in the peri-operative setting [72, 73] or cognitive dysfunction and restrictive strategy
in acute respiratory distress syndrome [74], no sign of harm were suggested by studies on deresuscitation. It has to be modulated by the fact that data are scarce and
originate from deresuscitation protocols with restrictive safety criteria applied to
stabilized patients.
To conclude, if several experts support the concept of deresuscitation or deescalation [40, 75], the lack of solid evidence-based demonstration of its clinical
interest highlights the gap between physician practices and scientic knowledge. It
may explain the heterogeneity in diagnosis and therapeutic interventions observed
worldwide in several surveys on uid overload and uid removal [19, 76–78]. In
this context, trials are urgently needed to determine the eligible population, the
safety criteria, the targets and the means to “deresuscitate.”
Acknowledgment Authors thank Lucie Bernigaud for help in manuscript preparation.
Conict of Interest Statement The authors have no conicts of interest related to the manuscript
to declare.
Funding Sources
Author Contributions Drafting of manuscript: MR.
Critical revision of the manuscript for important intellectual content: MR, MJL, JLF.
No funding source.
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M. Ruste et al.
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Chapter 21
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Extracorporeal Membrane Oxygenation
SasaRajsic, BenediktTreml, andRobertBreitkopf
Introduction
Extracorporeal membrane oxygenation (ECMO, extracorporeal life support
[ECLS]) presents a temporary life-saving technology used in patients with refractory cardiogenic shock or severe pulmonary failure. The main aim of ECMO is
providing cardiac or respiratory support until the patient’s heart or lungs recover.
Moreover, it can bridge the time to organ transplantation or permanent organ assistance, such as mechanical circulatory support devices, ventricular assist devices, or
total articial heart.
The rst reports on the use of a prolonged extracorporeal circuit and the beginning of ECMO support date from 1972 (Bramson-membrane heart-lung machine)
[1]. Over the last two decades, the use of ECMO has expanded beyond severe cardiorespiratory failure, comprising an assortment of clinical presentations. Refractory
cardiac arrest requiring prolonged resuscitation (i.e., refractory ventricular arrhythmias, local anesthetics intoxication, etc.) is an evolving indication for extracorporeal cardiopulmonary reanimation (eCPR). The successful use of ECMO support
for out-of-hospital cardiac arrest is gaining popularity [2–5]. Moreover, ECMO support is increasingly used as bridge to heart and/or lung transplantation, rewarming
of patients with deep hypothermia, or treating hypoxic respiratory failure triggered
by trauma [6–10] or COVID-19 [11].
However, the overall survival after ECMO depends on many intrinsic variables
of the patient, besides the interactions between extracorporeal circulation, circuit
S. Rajsic (*) · B. Treml · R. Breitkopf
Medical University Innsbruck, Innsbruck, Austria
e-mail: sasa.rajsic@i-med.ac.at; benedikt.treml@i-med.ac.at;
robert.breitkopf@tirol-kliniken.at
Switzerland AG 2024
J. Faintuch, S. Faintuch (eds.), Recent Strategies in High Risk Surgery,
https://doi.org/10.1007/978-3-031-56270-9_21
339© The Author(s), under exclusive license to Springer Nature
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S. Rajsic et al.
surface, hemostatic factors and blood components; generating complex coagulation
and inammatory reactions; and making the management of the critically ill more
complex [12].
ECMO Physiology andCircuit
Homeostasis in critically ill patients, particularly those receiving ECMO support, is
multifactorially compromised. Cardiac surgery or ECMO implantation (surgical
trauma) and exposure of the patient’s blood to the large surface of the circuit initiate
and propagate an immediate inammatory reaction and activation of the coagulation cascade [13]. Numerous cellular and humoral systems are involved in these
complex inammatory responses during ECMO support, resulting in a procoagulant state of the organism and the need for systemic anticoagulation. The balance
between procoagulant factors and the iatrogenic coagulopathy is crucial to avoid
severe adverse events (both hemorrhagic and/or thromboembolic), and for the
patency of the circuit and its components [13].
The ECMO circuit is a closed system with a membrane-type gas-exchange technology. The main distinction between ECMO and a cardiopulmonary bypass is in the
air–blood interface and the duration of support. In contrast to ECMO, venous reservoirs are integrated into cardiopulmonary bypass circuits for cardiotomy suction and
venting of blood. Moreover, while cardiopulmonary bypass is usually used only for
the surgery duration, ECMO support may be employed for weeks or even months [14].
The ECMO circuit comprises of inow and outow cannulas, a pump, an oxygenator, and heat exchanger (Fig.21.1). The system components are connected by
Fig. 21.1 Venovenous-ECMO circuit: cannulation of the internal jugular and femoral vein
(Courtesy Getinge AB, Rastatt, Germany)
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