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Part V
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Fluids, Electrolytes and Shock
Chapter 17
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Damage Control Resuscitation: Massive
Transfusion Protocols andPharmacologic
Adjuncts
DavidRayVelez
Abbreviations
EAST Eastern Association for the Surgery of Trauma
FAST Focused Assessment with Sonography in Trauma
MTP Massive transfusion protocol
pRBC Packed red blood cells
TEG Thrombelastography
TXA Tranexamic acid
Introduction
In the United States, hemorrhagic shock is responsible for 1.5million deaths annually [1]. In this disproportionately young population, it results in nearly 75million
years of life lost. Over the last 400years, management has signicantly evolved.
Caring for injured gladiators, Galen (129–210) was closely familiar with hemorrhage and accepted the Hippocratic theory of the four bodily humors. From this
theory he advocated bloodletting in the management of hemorrhage and the rst
1600years of the modern era were heavily inuenced by his work [1]. With the
discovery of blood circulation in the 1600s, the rst transfusions were seen—rst
from dog-to-dog, then lamb-to-human, and eventually human-to-human in 1795 [1].
Through the 1800s, there were multiple attempts at intravenous uid administration using various products. These including formulations such as water with ascetic
acid, alkali-containing uids, and even milk. Saline was rst pioneered during the
D. R. Velez (*)
Department of Surgery, University of Nevada, Las Vegas, Las Vegas, NV, USA
e-mail: david.velez@unlv.edu
Switzerland AG 2024
J. Faintuch, S. Faintuch (eds.), Recent Strategies in High Risk Surgery,
https://doi.org/10.1007/978-3-031-56270-9_17
271© The Author(s), under exclusive license to Springer Nature
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cholera epidemic and became more widely available during World War I [1]. The
introduction of crystalloid resuscitation resulted in improved outcomes and
decreased mortality although later was found to cause damage at the cellular level
by inciting a systemic inammatory response with reperfusion injury [2, 3].
Transition to resuscitation with blood and blood products is now emphasized while
limiting this crystalloid infusion. More recently, a signicant coagulopathy has been
noted, especially by the military during Operation Iraqi Freedom and Operation
Enduring Freedom [4, 5]. An acute traumatic coagulopathy (ATC) was present in
24.4% of the patients and was associated with high mortality [4, 5]. ATC has also
been referred to as trauma-induced coagulopathy (TIC).
The term “damage control” was rst used in 1993 to describe abbreviated surgical procedures that were aborted early after control of life-threatening injuries and
contamination to allow for physiologic resuscitation prior to denitive managements. The term was based on a United States Navy principle to describe the emergency management of sinking watercraft. “Damage Control Resuscitation” was a
concept codied as a United States Department of Defense clinical practice guideline in 2004, during the military conicts in the Middle East [6, 7].
Today there are numerous approaches in the management of hemorrhagic shock
and multiple adjuncts have been proposed. The surrounding literature is extensive
and complex. This review seeks to condense and summarize the plethora of concepts to make it more accessible to the practicing surgeon. It will explain modern
damage control resuscitation, the various approaches to massive transfusion, and
the numerous pharmacologic adjuncts.
D. R. Velez
Pathophysiology ofHemorrhagic Shock
The word “shock” stems from the French “choc”, meaning a violent act, such as the
impact of jousting lance. Today, hemorrhagic shock is generally described as inadequate tissue prefusion due to blood loss. However, despite the signicant advancements in its understanding, the exact denition still remains murky. In fact, the more
poetic denitions of the past may be better at capturing the true sense of “shock”
than are phrases that deconstruct ideas of tissue perfusion [8].
Hemorrhage results in many physiologic and compensatory changes that are
directly related to the degree of blood loss [9]. These changes are described by the
classes of shock and are summarized in Table 17.1. Class I hemorrhagic shock
occurs with loss of less than 15% total blood volume and shows minimal change in
vital signs. Class II occurs when 15–30% of total blood volume is lost and we begin
to see low-level tachycardia and decreased pulse pressure although blood pressure
remains normal. Class III occurs once over 30% of total blood volume is lost and it
is at this point that hypotension, tachypnea, and oliguria are seen. Class IV shock
occurs when over 40% of total blood volume is lost and the patient will show marked
tachycardia, signicant hypotension, negligible urine output, and lethargy.
During hemorrhagic shock oxygen delivery is unable to meet oxygen demand at
the cellular level. Aerobic metabolism is converted to anaerobic metabolism with
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273
Table 17.1
Class
I <750cc (<15%) <100 Normal Normal 14–20 Normal Slightly
II 750–1500cc
III 1500–2000cc
IV >2000cc (>40%) >140 Decreased Narrow > 40 Negligible Confused,
Classication of hemorrhagic shock
Heart
Blood loss
(percentage total
blood volume)
(15–30%)
(30–40%)
rate
(beats/
min)
100–
120
120–
140
Blood
pressure
Normal Narrow 20–30 Normal Mildly
Decreased Narrow 30–40 Decreased Confused,
Pulse
pressure
Respiratory
rate
(breaths/
min)
Urine
output
Mental
status
anxious
anxious
anxious
lethargic
the resultant oxygen debt [10]. This results in a buildup of oxygen free radicals [10].
Additionally, lactic acid and inorganic phosphates accumulate [10]. A systemic
inammatory response is ignited by the release of damage-associated molecular
patterns (DAMPs) [11]. Hypovolemia additionally causes vasoconstriction, causing
end-organ hypoperfusion and damage. Major blood ow impairment to the heart
and brain can be immediately followed by serious arrhythmias and cerebral
anoxia [12].
It has been shown that hemorrhagic shock results in a diffuse coagulopathy due
to multiple complex mechanisms [13]. Activated protein C (APC) inactivates factors Va and VIIIa, thereby inhibiting coagulation. Increased activity of activated
protein C has been noted after trauma, which is believed to be due to increased
activity of thrombomodulin [14, 15]. Thrombomodulin promotes activated protein
C activation and is activated in the setting of hypoperfusion. The endothelial glycocalyx layer has anticoagulant components such as chondroitin sulfate and heparan
sulfate [13]. The endothelial glycocalyx layer can “shed” after injury due to yet
undetermined mechanisms [13]. Although the clotting cascade is activated locally
to physiologically stop the bleed, distant sites see an increase in brinolytic activity,
likely to prevent microvascular thrombosis [13, 16]. In addition, platelet numbers
are depleted, migration is decreased, and their function is impaired [10]. With hemorrhagic shock the lethal triad of hypothermia, acidosis, and coagulopathy results in
signicant morbidity and devastating outcomes [17].
Damage Control Resuscitation
Damage control resuscitation encompasses stopping the bleeding, reducing excessive crystalloid replenishment, prompt however carefully managed blood transfusion, permissive hypotension, and attention to coagulopathy, acidosis, and
hypothermia.
As with any trauma, resuscitation begins with an efcient primary and secondary
survey following Advanced Trauma Life Support (ATLS) algorithms. Physiologic
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D. R. Velez
compensation occurs early in hemorrhagic shock and it often takes a loss of 30%
total blood volume before hypotension is seen. Some of the earliest signs to beware
include tachycardia and cutaneous vasoconstriction. A cold-pale patient with tachycardia should be presumed to be in shock until proven otherwise. Hemorrhagic
shock in injured patients is most common although any form of shock can be present and once identied, the cause should be sought. Diagnosis, however, should not
delay appropriate resuscitation.
Prompt actions to stop the bleed are critical. Temporary control of extremity
wounds should be obtained with direct pressure, suture closure, hemostatic dressings, or proximal tourniquet. Thoracic and abdominal bleeding, however, are noncompressible. Patients in hemorrhagic shock do not afford the luxury of CT
evaluation and require immediate intervention. Surgeons may consider resuscitative
endovascular balloon occlusion of the aorta (REBOA) for patients in hemorrhagic
shock due to abdominopelvic hemorrhage although there are strict contraindications and to date there is no high-grade evidence demonstrating improved survival
or outcomes.
Initial uid therapy starts with 1–2L of a warmed lactated Ringer’s solution. In
the pediatric patient, bolus should be limited to 20cc/kg if weight is under 40kg.
Balanced crystalloids such as lactated Ringer are preferred over normal-saline as it
has been shown to cause hyperchloremic metabolic acidosis with increased risk for
renal dysfunction and increased mortality [18, 19]. There was previously a concern
with giving lactated Ringer in the setting of blood transfusion due to an increased
risk of clot formation and tubing dysfunction. However, at the high transfusion rates
used in standard trauma resuscitation this is not an issue [20].
Further management is then based on the patient’s response to this initial bolus
which is indictive of shock class. “Rapid responders” likely have class I hemorrhagic shock. “Transient responders” will initially respond but then begin to show
signs of deterioration, indicating class II–III hemorrhagic shock. Patients with minimal- no response are highly concerning for exsanguination with class IV hemorrhagic shock. Rapid responders require no further immediate uid boluses. Both
transient responders and non-responders should be further resuscitated with blood
or blood products. For hypotensive patients with immediate concern for class III–IV
hemorrhagic shock this initial crystalloid bolus should be bypassed and transfusion
with blood and blood products should begin immediately. When signicant volumes of blood transfusion are anticipated massive transfusion protocols should be
activated and consideration for pharmacologic adjuncts should be given.
Maintaining a “normal” blood pressure was historically highlighted by the early
resuscitation strategies [21]. Rapid resuscitation in a bleeding patient, however, is
now thought to worsen bleeding. This rapid uid resuscitation decreases the viscosity of blood, disrupts fragile new clots, and worsens elements of the lethal triad.
Although originally proposed by Walter Cannon during World War I, the
1990s–2000s saw a reinvigorated interest in the idea of “hypotensive resuscitation”
[22]. This was also referred to as “permissive hypotension” or “controlled resuscitation”. A lower blood pressure goal, often a systolic blood pressure of ≥70mmHg,
is initially targeted until the physician is able to achieve denitive hemostasis, [23].
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aiming to lower blood loss, use of blood products, and higher survival [23]. A signicant contraindication would be the suspicion of traumatic brain injury (TBI) in
which maintenance of cerebral perfusion pressure is essential to limit secondary
brain injury. In the presence of traumatic brain injury initial goal systolic blood
pressures should be ≥110mmHg for ages 15–49, ≥100mmHg for ages 50–69 or
≥110mmHg for ages ≥70 [24]. However, uid resuscitation will allow recovery
only once the bleeding has been stopped. The ultimate goal for all patients must be
denitive hemorrhage control.
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Massive Transfusion Protocol (MTP)
Only in the 1960s we began to separate blood into its components: red cells, platelets, and plasma [25]. Over the next 10–20years, this “component therapy” began
to replace the traditional use of whole blood [26]. Trauma only represents a small
proportion of blood transfusions (10–15%) and individualized therapies with specic components are frequently preferred [26, 27]. “Component therapy”, as
opposed to whole blood, lengthened storage times and reduced blood product waste
[26], becoming the preferred transfusion approach to trauma by the 1990s.
With the recognition of acute traumatic coagulopathy, the understanding has
evolved that severely injured patients require not just pRBC transfusions but also
plasma and platelets. Massive transfusion protocol (MTP) is typically dened as
≥10units pRBC in 24h or ≥4units pRBC in 1h. MTP activation has historically
proceeded with hemostatic resuscitation although the use of thrombelastography
and whole blood are evolving.
MTP Activation Indications
MTP improves patient survival, decreases the use of blood products, and decreases
costs [28]. MTP should be activated as soon as large-volume transfusions are anticipated although the exact determination is debated. Over a dozen scoring systems
have been developed to predict the need for MTP activation. They differ in their
criteria and the signicance applied to each value. Some of the most common criteria include a positive Focused Assessment with Sonography in Trauma (FAST)
exam, hypotension with systolic blood pressure ≤90mmHg, tachycardia with heart
rate ≥120 beats/min, unstable pelvic fracture, and decreased hemoglobin.
A recent systematic review compared 15 of the most commonly described scores
[29]. They found that when using a combination of clinical assessment, laboratory
values, and FAST the Trauma-Associated Severe Hemorrhage (TASH) score was
the most well validated. When laboratory results are unavailable the Assessment of
Blood Consumption (ABC) score “balances accuracy with ease of use”. When
FAST is not available the Vandromme score is most accurate but the Schreiber score
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is most sensitive. If all that is available to the surgeon is clinical assessment, the
Shock Index has fair performance. Ultimately, a universal set of indications is
doubtful. Scoring systems should be individualized and each hospital system should
implement what is feasible based on their own available resources.
D. R. Velez
Hemostatic Resuscitation
“Damage Control Resuscitation” was an approach codied by the United States
Department of Defense (DOD) as a clinic practice guideline during the military
operations in the Middle East in 2004 [6, 7]. The most critically ill trauma patients
were transfused at a ratio of 1:1 pRBC and plasma [6, 30]. With the addition of
platelets this converted into the “1:1:1” ratio [31].
In the large PROPPR trial death due to exsanguination diminished at 24hours,
however not all-cause mortality [31]. In another analysis hemostatic resuscitation
did benet outcomes and mortality [28], and many have adopted it as the historical
“Gold Standard” during blood transfusion in trauma.
Thrombelastography (TEG)
TEG measures the viscoelastic properties of clot formation in real-time to guide
transfusion efforts. TEG was created in 1940s Germany although the rst clinical
use was during the Vietnam War (1955–1975) [32, 33]. In the late twentieth century
it was adopted by cardiac and liver surgeons although with newer more reliable and
rapid machines it has seen renewed interest in trauma [33]. Conventional coagulation testing performed in the laboratory takes longer than the point-of-care TEG. In
trauma, conventional results are often inaccurate by the time they result due to transfusion and rapid physiologic changes. From time of admission in the resuscitation
bay until results are available RapidTEG takes 30.8 min, standard TEG takes
41.5min, and conventional tests take 64.9min [34]. This is further amplied when
considering that TEG can be viewed in real-time with some useful data available
much sooner.
There has been one past randomized control trial evaluating the use of TEG in
trauma [35]. It evaluated 111 trauma patients after MTP activation. Patients were
given an initial 4U pRBC and then further transfusion was guided by either TEG or
conventional coagulation assays. The study found decreased 28-day mortality with
the largest impact in the rst 6h after injury. There were however potential weaknesses to the study as physicians could request unblinding if the felt TEG was either
indicated or contraindicated, eight of which did so. They were not truly evaluating
a 1:1:1 resuscitation as the median transfusion at 6h for the conventional coagulation assay group had only 8U pRBC, 5U plasma, and 1U platelets. There is also
consideration that the results may be too good as patients treated by TEG had nearly
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one-quarter the mortality at 6 h and one-half at 28 days, questioning risk of
other bias.
To date studies have mostly been retrospective and observational. TEG has
allowed for a more rapid goal-directed resuscitation although denitive high-grade
evidence that it decreases transfusion requirements or improves mortality is lacking
[36, 37]. The use of TEG does involve some complexity requiring understanding of
the results and how to respond although simple algorithms can be followed.
Increased R-Time indicates insufcient factors and should be treated with
FFP. Increased K-time or decreased alpha-angle indicates insufcient brinogen
and requires cryoprecipitate. Decreased maximum amplitude (MA) indicates insufcient or inhibited platelets and should be treated with either platelet transfusion or
DDAVP depending on the situation. An elevated lysis at 30min (LY-30) indicates
rapid clot breakdown and should be treated with TXA.
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Whole Blood
Military conicts in Iraq and Afghanistan have renewed interest in the use of whole
blood transfusion, partially due to the need in austere far-forward environments
where access to conventional blood bank supplies are limited [38, 39]. Although it
has primarily been used in the military setting with “fresh” whole blood from an
available “walking blood bank” of prescreened soldiers, it is now being utilized in
some civilian trauma centers [40]. Multiple factors have limited its use such as the
misconceptions that whole blood must be type ABO specic, whole blood cannot be
leukoreduced, whole blood cannot maintain platelets, or that cold storage of whole
blood causes loss of platelet function. These, however, have all been overcome [41].
After storage and dilution, blood products being given during a balanced resuscitation with a 1:1:1 ratio have a hematocrit 29%, coagulation factor concentration
65% of normal, and platelet count 88,000 [42, 43
period 5–10% of red blood cells are lost and only two-thirds of the administered
platelets will be viable [44, 45]. Effective concentration of transfusion in a 1:1:1
ratio is therefore only hematocrit 26%, coagulation factor concentration 65% of
normal, and platelet count 59,000. At these levels, transfusion with blood products
alone barely keep levels above traditional transfusion indications. Adding more of
one component further dilutes the other two and the addition of uids will dilute all
three. Whole blood however has a hematocrit 35–38%, coagulation factor concentration 85% of normal, and platelet count 150,000–200,000 [43].
Studies evaluating the use of whole blood compared to component therapy are
mostly observational or retrospective with signicant heterogeneity. The only randomized control trial to date was a single center pilot feasibility trial with insufcient power to detect mortality differences. A 2020 systematic review found an
overall poor quality of evidence [46]. There have been some retrospective studies to
suggest decreased transfusion requirements and mortality although sufcient highquality evidence is currently lacking with no major randomized control trial [40,
]. In the immediate post- transfusion
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