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47]. Despite this, many advocate whole blood as the best resuscitation product.
Although availability is currently limited, it is being used with increasing frequency
and rapidly spreading among major trauma centers.
D. R. Velez
Pharmacologic Adjuncts
Recombinant Activated Factor VIIa (rVIIa)
Recombinant activated factor VIIa (rVIIa) binds to the surface of activated platelets
and promotes the activation of factor X with thrombin generation. It was rst used
in 1999 for the management of uncontrolled hemorrhage but today trauma remains
an off-label use in the United States [48]. Dosing has varied although both past
randomized control trials have used 200μg/kg initially followed by 100μg/kg at 1
and 3h [49, 50]. Although early retrospective analysis was promising, further studies have failed to consistently show benet. Both past randomized control trials,
including the CONTROL trial, indicated reduced blood product use, signicantly so
after blunt trauma, however no difference in mortality was seen [49, 50].
Although there was initially great hope with its introduction and some retrospective cohort studies saw reduced mortality, when taken together current literature has
failed to show any high-grade evidence of decreased transfusion requirements or
improved mortality [28]. To date no change in the rate of venous thromboembolism
formation has been seen [28]. 2017 Eastern Association for the Surgery of Trauma
(EAST) guidelines were unable to recommend for or against its use [28]. At this
time, with no clear benet, the use of recombinant activated factor VIIa has mostly
fallen out of favor.
Tranexamic Acid (TXA)
TXA inhibits plasminogen conversion to the active protease plasmin, thereby inhibiting brinolysis and clot breakdown. Similar to recombinant activated factor VIIa,
its use in trauma remains off-label in the United States. TXA is typically given as a
1g bolus followed by a second 1g infused over 8h.
CRASH-2, the largest study to date, was an international randomized control
trial throughout 40 countries with over 20,000 patients [51]. It saw signicantly
decreased risk of death due to bleeding and decreased risk of all-cause mortality
[51]. Subgroup analysis saw signicantly decreased risk of mortality if given within
3h of injury but increased risk if given after 3h [52]. CRASH-2 was an excellent
trial however there were potential weaknesses that should be recognized. There was
selection bias as physicians could exclude patients if the felt TXA was either indicated or contraindicated and there was no report in how many were excluded in this
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way. There is also a signicant question of external validity due to wide variation in
trauma systems with the majority of patients being treated in countries that do not
routinely provide rapid access to blood products, damage control surgery, or
advanced critical care [53].
Other retrospective observational studies such as the military MATTERs and
MATTERs II have also evaluated TXA use [51, 54–56]. Although some studies
have shown improved mortality, when results are combined there is no clear mortality benet or difference in transfusion requirements [28]. Risk for venous thromboembolism is unknown at this time due to lack of standardization in its reporting
[28]. Based largely on the CRASH-2 ndings, 2017 EAST guidelines did give a
conditional recommendation for its use [28]. TXA is recommended in the early
management of signicant traumatic hemorrhage but only if given within 3h of
injury and potential limitations should be noted.
279
Cryoprecipitate (Cryo)
Fibrinogen is the rst coagulation factor to reach critically low concentrations in
major blood loss and low levels in the trauma patient have been associated with
worse outcomes [57, 58]. Cryoprecipitate serves as the standard source for brinogen administration. High-grade research has been limited. CRYOSTAT-1 was a
United Kingdom feasibility randomized control trial evaluating the use of early
cryoprecipitate in trauma by giving two early pools of cryoprecipitate within a goal
of less than 90min [59]. Results suggested reduced mortality, although the difference was not signicant (P=0.14) [59]. CRYOSTAT-2 will follow up with a larger
multicenter randomized control trial throughout the United Kingdom. By retrospective observation in the United States, MATTERs II found a mortality benet of
cryoprecipitate similar to TXA and proposed that cryoprecipitate may independently add to the survival benet of TXA if given together [56]. MATTERs II however is limited due to the potential bias in the retrospective observational nature and
venous thromboembolism rates were not reported. Current evidence to guide the
use of cryoprecipitate is insufcient with no clear guidelines and further evaluation
is needed.
Vasopressors
Vasopressors have previously been considered heresy in the treatment of hemorrhagic shock. Research has demonstrated increased mortality with most vasopressors and their use had mostly been abandoned [60]. However, the potential is
again being questioned. A recent systematic review evaluating vasopressor use
found that the only randomized control trial was “too imprecise to yield meaningful results” and that although all the observational studies found increased
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short-term mortalities, with relative risk 2.31–7.39, there was high risk of bias as
patients receiving vasopressors were signicantly more ill [61]. The review concluded that the existing data were of low quality [61]. When Sperry etal. evaluated the use of early vasopressors they found signicantly increased mortality,
however on logistic regression arginine vasopressin (AVP) was the only vasopressor not associated with signicantly increased mortality [60]. Collier etal. then
found increased risk of mortality with the use of arginine vasopressin, however
84% received it in combination with other vasopressors making it difcult to draw
strong conclusions [62].
Arginine vasopressin, specically, has recently been reevaluated. In hemorrhagic
shock, the baroreceptor-mediated secretion of this pituitary hormone is impaired
and the circulating levels are rapidly depleted [63]. The AVERT-Shock trial evaluated the use of low-dose arginine vasopressin on the early resuscitation of adult
trauma patients who received at least 6units of blood product within 12h of injury
[64]. It was randomized, double-blind, and placebo-controlled. Patients were given
a 4-unit bolus of arginine vasopressin, started on a 0.04-unit/min infusion, and then
titrated following denitive hemorrhage control. They saw decreased transfusion
requirements but no change in mortality [64]. There was no increased risk of complications however, unexpectedly, venous thromboembolism risk was signicantly
reduced by the use of arginine vasopressin [64]. At this time, with no improvement
in mortality seen the denitive use of arginine vasopressin in trauma remains
questioned.
D. R. Velez
Conclusion
The understanding of damage control resuscitation is essential to the management
of the critically injured patient. It generally begins with 1–2L of a warmed lactated
Ringer’s uid bolus. For patients that fail to mount an appropriate response rapidly,
additional crystalloid infusion should be forgone, and the patient should be transitioned to blood and blood products. Hemodynamically unstable patients in class
III–IV hemorrhagic shock should immediately be transfused with blood products
and the initial crystalloid bolus should be bypassed. Massive Transfusion Protocols
should be activated in more critical conditions, encompassing a 1:1:1 approach
although the use of whole blood is reemerging and considered by many to be superior, if available. TEG-guided resuscitation should be considered as a potentially
valuable resource.
Among the various pharmacologic adjuncts available, TXA can be administered
within 3h of injury if large volumes are likely to be required. Cryoprecipitate or
arginine vasopressin are other options, used it at the surgeon’s discretion.
Recombinant factor VIIa, although once showed signicant promise, has now
mostly fallen out of favor. “Permissive hypotension” is contraindicated in the presence of traumatic brain damage or previous hypertension. Denitive control of
bleeding must be the ultimate goal.
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281
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Chapter 18
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Perioperative Fluid Management
andVolume Assessment
RakshaBangalore, KathrynJan, JenniferElia, andKunalKaramchandani
Introduction
While optimal uid therapy serves to ensure adequate end-organ perfusion by maintaining cardiac preload and stroke volume, both insufcient and excessive uid
administration have serious implications during the perioperative period [1–5].
Hypovolemia leads to a decrease in organ perfusion which may result in myocardial
demand ischemia, acute kidney injury, multiorgan failure, and even death.
Alternatively, hypervolemia can lead to pulmonary congestion, postoperative ileus,
nausea/vomiting, dilutional coagulopathy, and death in predisposed patients.
Fluid Physiology During thePerioperative Period
In a homeostatic adult, approximately 60% of the total body weight is composed of
water. In the elderly population it is progressively reduced to 50% [6, 7]. At the cellular level, a third of the total body water content is extracellular while the remainder is intracellular. Within the extracellular volume, a quarter is represented by
blood plasma and the remainder is interstitial [2, 3, 8]. Fluid may shift between
these compartments based on the hydrostatic, oncotic, and osmotic pressure
R. Bangalore · K. Jan · K. Karamchandani (*)
Department of Anesthesiology and Pain Management, University of Texas Southwestern
Medical Center, Dallas, TX, USA
e-mail: Raksha.bangalore@utsouthwestern.edu; Kathryn.Jan@UTSouthwestern.edu;
kunal.karamchandani@utsouthwestern.edu
J. Elia
Department of Anesthesiology & Perioperative Care, University of California,
Irvine, CA, USA
Switzerland AG 2024
J. Faintuch, S. Faintuch (eds.), Recent Strategies in High Risk Surgery,
https://doi.org/10.1007/978-3-031-56270-9_18
285© The Author(s), under exclusive license to Springer Nature
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R. Bangalore et al.
gradients, considering that the vascular endothelium separating the plasma and
interstitial tissue as well as cellular membranes are permeable to water.
Frank-Starling Curve
Intravascular uid serves as preload to the heart which then ejects it as stroke volume to perfuse vital organs. This is called the Frank-Starling relationship and is
based on the relationship between the length of myocardial bers and the force
generated by their contraction. It is depicted by the Frank-Starling curve which
relates preload or the left ventricular end-diastolic pressure to cardiac performance,
measured as ventricular stroke volume (SV), or as cardiac output (CO) which corresponds to SV X heart rate (Fig.18.1). When the myocardial performance is normal, myocardial contractility increases with more massive preload. However, the
contractility reaches a maximum point limited by the cardiac muscle bers, after
which any further increase in preload does not benet CO.
During states of increased left ventricular contractility, for example due to infusion of inotropic drugs, there is a greater cardiac performance for a given preload,
represented graphically as an upward shift of the normal curve. Conversely, during
states of decreased left ventricular contractility, such as systolic heart failure, the
opposite occurs representing a downward shift of the normal curve. This relationship can be used to identify patients that are uid responsive during the perioperative period (Fig.18.1).
Fig. 18.1 Frank-starling curve
18 Perioperative Fluid Management andVolume Assessment
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Fluid Responsiveness (FL)
An augmentation in SV or CO by 10–15% with moderate volume administration is
dened as FL [9]. Likewise, when SV or CO is unchanged with a uid bolus, the
patient is considered volume non-responsive.
287
Factors Impacting Fluid Status During
thePerioperative Period
Preoperative Fasting
Dehydration before elective surgery is common and is compounded by longer preoperative fasting times [10]. Historically, the increased risk of aspiration, as
described by Mendelson, led to recommendations of ‘nil by mouth after midnight’
prior to surgery requiring general anesthesia [11, 12]. Currently both European and
American guidelines promote the intake of clear uids up to 2h before elective
surgery [13, 14]. Additionally, the advent of enhanced recovery after surgery
(ERAS) protocols, has led to promoting the intake of carbohydrate-containing clear
liquids up to 2h prior to surgery to improve patient comfort (thirst, hunger) and
glycemic control, usually without increasing the risk of aspiration [15–20].
However, especially for patients with lower health literacy, nil by mouth after
midnight is still commonly instructed instead of established guidelines [20].
Mechanical bowel preparation can also be a mechanism of uid loss [7]. Pediatric
patients are instructed to drink clear uids up until an hour before induction of anesthesia, and there is a renewed interest in adopting the same guideline for all age
groups [21, 22]. Similarly, mechanical bowel preparation before colorectal surgery
is less practiced in recent years [21].
Intraoperative Fluid Losses
Insensible losses (breathing, evaporation, sweating) are related to induction of anesthesia and surgical exposure and should be added to measured or estimated blood
and other bodily uid losses, all of which lead to a decrease in effective circulatory
blood volume [23, 24]. Larger wounds with more exposed viscera tend to have
higher uid losses; these are less in laparoscopic surgery as compared to open procedures. However, evaporative losses still exist due to insufation. Minor wounds
with slightly exposed viscera lose approximately 2mL/h of uid, whereas for major
wounds with a completely exposed abdomen up to 32mL/h should be expected
[24]. Insensible losses due to anesthesia-induced vasodilation potentially contribute
to hypovolemia. Intraoperative insensible losses from a patient’s skin and airway
alone are estimated to be 0.3mL/kg/h [23, 24].
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Postoperative Factors
Although hypovolemia may persist postoperatively through continued bleeding as
well as drainage from the surgical site or high ostomy output, other factors lead to
generalized uid retention, with possible edema as well as hypervolemia.
Antidiuretic hormone, aldosterone, cortisol, and atrial natriuretic peptide are
secreted after surgical interventions and lead to increased sodium and water retention as well as decreased diuresis [4].
Surgical stress and trauma can additionally promote capillary permeability via
release of cytokines such as interleukin-6, tumor necrosis factor, substance-P, and
bradykinin. Due to such inammatory mediators, patients frequently become intravascularly depleted while showing signs of extravascular uid overload, edema
occurring mostly in the lungs, gut, and subcutaneous tissues. This combination of
systemic and regional phenomena contributes to classic “third-spacing” in directly
manipulated or damaged tissues (anastomoses, dissected peritoneal surfaces, zones
of accidental or surgical trauma). When signicant amounts of uid remain in the
local interstitial tissue (third space) rather than the cardiocirculatory system, such
will lead to intravascular volume contraction [2, 5].
R. Bangalore et al.
Perioperative Volume Assessment andFluid Responsiveness
Physical exam signs such as skin turgor, capillary rell, and neck vein assessments
can preliminarily suggest overall volume status, however monitoring of static and
dynamic parameters as well as of uid responsiveness are essential for improvement in clinical outcomes.
Static Parameters
They include blood pressure, heart rate, central venous pressure (CVP), pulmonary
artery occlusion pressure (PAOP), inferior vena cava (IVC) diameter, and left ventricular end-diastolic volume, which provide a single time point evaluation of the
patient’s volume status. Historically, CVP and PAOP have also been used to determine uid responsiveness, but they are unreliable predictors of improvement in cardiac output due to volume administration [25, 26]. This is likely due to a combination
of the inability to accurately measure preload by these variables, the complex relationship between SV and ventricular preload, and the critical effect of ventricular
contractility on cardiac output [25, 27].
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