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5 • Prehospital Management of Vascular Injury 65
35
*
Prothrombin ratio
Mortality (%)
1.9–2.0
https://t.me/medicina_free
immediately apparent that the ideal is a high-ow but lowpressure system. This is very difcult to achieve in the early
stages of resuscitation, especially in the prehospital environment. The normal physiological response to blood loss will
ensure a high systemic vascular resistance, and thus a relatively high-pressure but low-ow system will predominate.
PERMISSIVE HYPOTENSION
Some early suggestion of the value of permissive hypotension comes from the First World War.77 Cannon suggested
that:
Injection of a Fluid that will increase blood pressure carries
danger in itself. Haemorrhage in the case of shock may not have
occurred to a large degree because the blood pressure is too low,
and the ow too scant to overcome the obstacle offered by a clot.
If the pressure is raised before the surgeon is ready to check any
bleeding that may take place, blood that is sorely needed may
be lost.
A very similar theory was espoused 80 years later.78
Worse survival for patients with penetrating torso injury
who received aggressive, preoperative, crystalloid resuscitation was demonstrated in a large randomized controlled
trial.78 This formed the bedrock of the arguments for permissive hypotension in the subsequent decades. Although
methodologically rigorous, several things should be considered about this study that limits its external validity and
must be interpreted with caution when applied to how we
should resuscitate patients today. First is the patient demographic. On the whole they were young men with, presumably, few comorbidities.78 Second is the mechanism of injury;
by denition all these patients sustained penetrating injury,
with approximately 30% stabbed and the remainder receiving relatively low-velocity gunshot wounds – given that the
injuries occurred outside of military conict, it is likely that
the weapons involved were, on the whole, low velocity rather
than high-velocity military-style weapons.78 These mechanisms mean that the amount of overall tissue damage was
likely to be low, certainly in comparison to patients with
signicant blunt injury. Finally, the fact that patients in the
early resuscitation group received large volumes of crystalloid may have caused harm due to the type of uid they were
receiving, rather than the timing or, indeed, the amount.
If examined in isolation there is excellent evidence supporting the ndings, suggesting that permissive hypotension is the appropriate strategy for resuscitation in trauma.
However, there is also evidence that this is not the case,
especially in injury caused by blast.
ALTERNATIVE RESUSCITATION STRATEGIES
82
Much of the literature supporting permissive hypotension
is based on models of uncontrolled hemorrhage of arterial
lesions; these are the most likely to re-bleed if blood pressure
is raised, and are likely to be the type of injury that benets
most from a permissive hypotension approach.82 The fundamental problem with permissive hypotension is reduced
oxygen delivery to the tissues.82 The equation:
DO2 = CaO2 × CO
79–81
denes the relationship between oxygen delivery (DO2),
arterial oxygen carriage (CaO2), and cardiac output (CO).82
As well as demonstrating how reduced cardiac output due
to permissive hypotension leads to reduced DO2, it also helps
to explain why replacing lost blood volume with crystalloid
simply does not work. Aside from the deleterious effect of
being a nonphysiological uid, which is acidotic and often
cold, it does not carry oxygen. This leads to a reduction in
CaO2 and therefore DO2. Crystalloid-based resuscitation also
leads to a dilutional coagulopathy. This has been termed
“resuscitation coagulopathy.” This is one component of
trauma induced coagulopathy (TIC), the other being ATC.
This equation also demonstrates the fundamental concern with a prolonged period of permissive hypotension;
CO is signicantly diminished and, as a result, tissue oxygen
delivery is reduced.
Acute Traumatic Coagulopathy
The harms of coagulopathy in trauma patients have been
well demonstrated (Fig. 5.7).83 This graph shows that a
trauma patient with a prothrombin ratio of 1.3 to 1.4 has
a mortality approximately twice that of a trauma patient
with a prothrombin ratio less than 1.3. Mortality continues to increase with prothrombin ratio greater than 1.4 in
a nonlinear manner.
83
There are two key drivers to the development of ATC,
as demonstrated in Fig. 5.8. Signicant tissue disruption,
represented by the injury severity score (ISS) on the X-axis,
and marked hypoperfusion, represented by base decit on
the Z-axis, are associated with a raised prothrombin ratio
(Y-axis). There is little that can be done after injury to limit
tissue damage. However, ensuring adequate perfusion is
possible, but this conicts with the concept of permissive
hypotension.
The harm of prolonged permissive hypotension has
been demonstrated in animal models.82 In pigs exposed to
a model of either hemorrhage and blast or hemorrhage
and sham blast, those resuscitated to normotension had
improved survival compared to those resuscitated following
a regimen of permissive hypotension.82 Although the effect
30
25
20
15
10
5
0
0.8–0.9
Fig. 5.7 The effect of coagulopathy on mortality in trauma. Prothrombin ratio is a measure of coagulopathy. The higher the ratio, the worse
the coagulopathy. (With permission from Frith D, et al. Definition and
drivers of acute traumatic coagulopathy: clinical and experimental
investigations. J Thromb Haemost. 2010;8(9):1919–1925.)
1 1.1–1.2 1.3–1.4 1.5–1.6 1.7–1.8
*
*
*
66 SECTION 2 • Immediate Management and Diagnostic Approaches
ISS
Prothrombin ratio
Base deficit
1.00
Time after onset of resuscitation (min)
Survival
500
https://t.me/medicina_free
was most marked in pigs exposed to blast (and thus with the
greatest degree of tissue injury), the effect was also seen in
those pigs with sham blast.82 This was despite the fact that
the only resuscitative uid used was 0.9% normal saline.82
Interestingly, there was no difference in survival at 1 hour
(Fig. 5.9). These ndings led to the suggestion that a combi-
nation approach may be most appropriate.
82
Novel Hybrid Resuscitation
This strategy consists of an initial period of an hour with
a hypotensive resuscitation target followed by a period of
resuscitation to normotension, even if denitive control of
bleeding has not been achieved. The physiological rationale
for this is sound and its efcacy is supported by the available literature, albeit in a porcine model.82 The initial hour
allows time for any clot to form and stabilize prior to challenging it with increased pressures. The return to normo-
2
1.9
1.8
1.7
1.6
1.5
1.4
1.3
1.2
1.1
1
< 16
16–24
*
25–35
*
**
*
*
> 35
*
> 12
6.1–12
0.1–6
0
(mmol L–1)
tension ensures improved perfusion and hopefully improved
oxygen delivery, leading to, at best, a reversal of the negative effects of permissive hypotension. In further work, in
a mixed arteriovenous porcine model of hemorrhage, this
strategy showed a signicant improvement in survival compared to prolonged hypotensive resuscitation in the blast
injured group, but no signicant difference in the sham
blast group.82 There was no evidence of increased re-bleeding in novel hybrid resuscitation compared to prolonged
permissive hypotension.
82
Practical Application
In terms of resuscitation strategy, current evidence suggests that novel hybrid resuscitation is likely to be the best
option.84 There are greater risks of resuscitation to normotension in penetrating injury, and the reduction in burden
of tissue damage means that there is less chance of developing ATC, certainly in low-velocity penetrating injury. Even
so, prolonged hypoperfusion is still likely to be detrimental.
As such an initial period of hypotension to avoid “popping
the clot”, followed by resuscitation to normotension or near
normotension, is advisable. Exact durations and blood pressure values are more uncertain. However, best available evidence would point toward a BP target of 100 mm Hg, and
never lower than 90 mm Hg, for the period of permissive
hypotension, with resuscitation to 110 mm Hg subsequent
to this period.
84
Even this guidance may need to be adjusted when dealing
with an individual patient. Given that the primary driver in
resuscitation is to ensure good oxygen delivery to tissues,
some account must be taken of a patient’s normal physiological state. For example, in a usually hypertensive arteriopath, the blood pressure target for both the hypotensive
and normotensive period may be higher still.
Fig. 5.8 Causes of the acute coagulopathy of trauma. This demonstrates that both tissue damage, represented by injury severity score
(ISS), and tissue hypoperfusion, represented by base deficit, are
required for coagulopathy to occur. (With permission from Frith D, et al.
Definition and drivers of acute traumatic coagulopathy: clinical and experimental investigations. J Thromb Haemost. 2010;8(9):1919–1925.)
0.75
0.50
0.25
0.00
Fig. 5.9 Survival following different resuscitation strategies in pigs
exposed to a combined hemorrhage and blast or hemorrhage and
sham blast. (From Kirkman E, et al. Blast injury research models. Philos
Trans R Soc Lond B Biol Sci. 2011;366(1562):144–159.)
WHAT TO USE DURING RESUSCITATION
Choice of Fluid
The concept that patients who are bleeding should receive
blood as replacement uid during resuscitation is now well
established. However, although a large systematic review
on the use of prehospital blood product resuscitation demonstrated that prehospital blood transfusion was safe and
feasible, it failed to nd any short- or long-term mortality
benet, improvement in biochemical markers, or reduction
in in-hospital blood transfusion in those getting prehospital
blood.85 This review was signicantly handicapped by both
S Normot
B Normot
S Hypot
B Hypot
the paucity of evidence available at that time and the poor
quality of the evidence that was available.
Transfusion of blood products to bleeding trauma
patients is the standard of care in-hospital. Given the lack of
available evidence specically looking at prehospital blood
product administration, it seems reasonable to extrapolate
85
that prehospital blood transfusion is appropriate. Further
0
100 200
300 400
evidence from clinical trials focusing on prehospital blood
product administration is emerging on this subject.
There are potential difculties with prehospital blood
transfusion. As has been described in the section on “stopping the bleeding,” the rst priority in managing the
bleeding patient must be to stop the bleeding; it is almost
impossible to denitively control hemorrhage prehospital,
5 • Prehospital Management of Vascular Injury 67
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and delaying denitive treatment is deleterious. Therefore,
the administration of blood products must not be allowed to
prolong on-scene times.
Both packed red blood cells (pRBC) and plasma have been
carried prehospital. The logistics of carrying prehospital
platelets are such that it is not currently feasible. Given that
pRBCs do not contain clotting factors, transfusion of them
alone may contribute to coagulopathy. The gold standard
in theory would be replacement of whole blood. However,
reduced mortality from exsanguination in patients receiving a balanced transfusion of pRBCs, plasma, and platelets
in a 1:1:1 ratio compared with patients receiving twice
as many units of pRBCs compared with plasma has been
shown in-hospital.86 Therefore, a 1:1 transfusion of plasma
to pRBC is currently seen as a reasonable compromise
when replacing lost intravascular volume. Due to the logistical burden of carrying plasma, many services are choosing to carry lyophilized plasma rather than frozen plasma.
The lyophilization process seems to have minimal effect on
the biological function of the plasma, with no difference
in thrombin generation assays and extensive clinical use
suggesting equivalence.87 Work is ongoing to determine
whether the early addition of cryoprecipitate to pRBCs and
plasma would be benecial.
88
The administration of fresh, warmed, whole blood to
trauma patients is now being explored and, in some circumstances, implemented.89 Administering this prehospital
is a signicant challenge, although it has been achieved in
small groups of elite service personnel. There is an ongoing
trial into the feasibility of doing so in the civilian setting.
However, many prehospital providers do not carry blood
products at all and only have the option of administering
crystalloid solutions. There is no denitive answer as to
when the benets of greater volume outweigh the harms
of administering crystalloid, although, as described previously, improvements in survival were seen in a porcine
model of injury when only crystalloid-based resuscitation
was carried out. When administering any uid in trauma, it
should be warmed. The best available evidence emphasizes
that blood products should be used where possible, but does
not give any different targets for resuscitation end points
where only crystalloid is available.
84
Pharmacological Adjuncts
There are two pharmacological adjuncts that should currently form part of the prehospital management of patients
with vascular injury: TXA and calcium.
The results of the CRASH-2 study, the largest ever trial
related to trauma, suggest that all patients who are within
3 hours of injury and are suspected of having signicant
bleeding should be administered TXA.14 In some groups,
risk of death was reduced by a third in patients administered
TXA,90 which should be administered as early as possible
in the patient’s disease course; for every 15-minute delay,
there is a 10% reduction in improved survival.
91
Calcium has two vital roles related to the management of
trauma patients. It is a key co-factor in the clotting cascade
and it also maintains myocardial contractility. Packed RBCs
are stored in sodium citrate in order to stop the cells aggregating, which causes potent chelation of ionized (biologically
active) calcium. As such, if a patient is administered pRBC,
calcium should be co-administered and is a key component
of major hemorrhage protocols. Recent work demonstrates
that 55% of major trauma patients who have not received
pRBC are hypocalcemic.92 Given the vital role calcium plays
in the clotting cascade we would contend that it should be
routinely administered to bleeding, trauma patients.
TRANSPORT DESTINATION
The nal responsibility of a prehospital team managing
a patient with vascular injury is to ensure they are transported to an appropriate center. Since the introduction of a
trauma system in the UK, survival from major trauma has
signicantly improved.93 Decision-making around a destination for a patient is especially challenging when long distances are involved.
SUMMARY
The optimum resuscitation strategy is likely to vary from
patient to patient depending on their own premorbid state
and their mechanism of injury. If giving volume for resuscitation of a bleeding patient, then balanced transfusion or
ideally fresh whole blood should be used in preference to
crystalloid. TXA should be given to bleeding patients and
calcium should be considered, especially if patients are
receiving citrated blood products.
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invasive external pelvic compression: a systematic review of the
literature. Scand J Trauma Resusc Emerg Med. 2016;24:73–81.
72. Schaller TM, Sims S, Maxian T. Skin breakdown following circum-
ferential pelvic antishock sheeting: a case report. J Orthop Trauma.
2005;19:661–665.
73. Shank JR, Morgan SJ, Smith WR, Meyer FN. Bilateral peroneal nerve
palsy following an emergent stabilization of a pelvic ring injury.
J Orthop Trauma. 2003;17:67–70.
74. Scott I, Porter K, Laird C, Greaves I, Bloch M. The prehospital
management of pelvic fractures: initial consensus statement. Emerg
Med J. 2013;30(12):1070–1072.
75. Devon Air Ambulance Trust. Standard Operating Procedure:
Management of Maxillofacial Haemorrhage. 2017.
76. Kashuk JL, Moore EE, Millikan JS, Moore JB. Major abdominal
vascular trauma—a unied approach. J Trauma. 1982;22(8):
672–679.
77. Cannon EB, Fraser J, Cowell E. The preventative treatment of wound
shock. JAMA. 1918;70:618–621.
78. Bickell WH, Wall MJ, Pepe PE, etal. Immediate versus delayed uid
resuscitation for hypotensive patients with penetrating torso injuries.
N Engl J Med. 1994;331(17):1105–1109.
79. Kutcher ME, Kornblith LZ, Narayan R, etal. A paradigm shift in
trauma resuscitation: evaluation of evolving massive transfusion
practices. JAMA Surg. 2013;148(9):834–840.
80. Kasotakis G, Sideris A, Yang Y, etal. Aggressive early crystalloid resus-
citation adversely affects outcomes in adult blunt trauma patients:
an analysis of the Glue Grant database. J Trauma Acute Care Surg.
2013;74(5):1215–1221.
81. Duchesne JC, Heaney J, Guidry C, etal. Diluting the benets of hemo-
static resuscitation: a multi-institutional analysis. J Trauma Acute Care
Surg. 2013;75:76–82.
82. Kirkman E, Watts S, Cooper G. Blast injury research models. Philos
Trans R Soc Lond B Biol Sci. 2011;366(1562):144–159.
83. Frith D, Goslings JC, Gaarder C, etal. Denition and drivers of acute
traumatic coagulopathy: clinical and experimental investigations. J
Thromb Haemost. 2010;8(9):1919–1925.
84. Woolley T, Thompson P, Kirkman E, et al. Trauma Hemostasis
and Oxygenation Research Network position paper on the role of
hypotensive resuscitation as part of remote damage control
resuscitation. J Trauma Acute Care Surg. 2018;84(6):S3–S13.
85. Smith IM, James RH, Dretzke J, Midwinter MJ. Prehospital blood
product resuscitation for trauma: a systematic review. Shock.
2016;46(1):3–16.
86. Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma,
platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: The PROPPR randomized clinical
trial. JAMA. 2015;313(5):471–482.
87. Acker JP, Marks DC, Shefeld WP. Quality assessment of established
and emerging blood components for transfusion. J Blood Transfus.
2016:1–28.
88. Brohi K, Stanworth S, Davenport R, et al. A multi-centre,
randomized, controlled trial evaluating the effects of early highdose cryoprecipitate in adult patients with major trauma haemorrhage requiring major haemorrhage protocol (MHP) activation.
Br J Anaesth. 2015;115(1):76–83. Accessed from: https://cryostat2.
co.uk/downloads/trial-protocol.pdf. 17 May 2019.
89. Spinella PC, Perkins JG, Grathwohl KW, Beekley AC, Holcomb JB.
Warm fresh whole blood is independently associated with improved
survival for patients with combat-related traumatic injuries. J Trauma.
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90. Roberts I. Tranexamic acid in trauma: how should we use it? J Thromb
Haemost. 2015;13(S1):S195–S199.
91. Gayet-Ageron A, Prieto-Merino D, Kex K, et al. Effect of treatment
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severe haemorrhage: a meta-analysis of individual patient-level data
from 40138 bleeding patients. Lancet. 2018;391:125–132.
92. Webster S, Todd S, Redhead J, Wright C. Ionised calcium levels
in major trauma patients who received blood in the Emergency
Department. Emerg Med J. 2016;33:569–572.
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trauma system on quality of care. Ann Surg. 2016;264(1):188–194.
6
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Damage Control and Immediate
Resuscitation for Vascular
Trauma
TOM WOOLLEY, RAVI CHAUHAN, and ALLAN PANG
Introduction
Hemorrhage occurs when there is disruption of the blood
vessel wall after an injury, i.e., vascular trauma. Hemorrhage remains a leading cause of death in trauma patients,
accounting for 40% of deaths.1 In order to reduce mortality
from hemorrhage there must be early and effective control
of the bleeding, with concurrent replacement of blood volume. There remains debate as to the most effective uid with
which to resuscitate patients, but resuscitation is equally as
important as any operative maneuvers required to expose,
control, and reconstruct an injured blood vessel.
New understanding of the pathophysiology of trauma has
inuenced the military approach to resuscitation, which is
centered around the prevention and mitigation of acidosis,
hypothermia, and coagulopathy while maintaining tissue
oxygenation.2 In particular, novel transfusion protocols have
been developed to counter the lethal triad; these protocols
adopt early blood transfusion, increased red cell to plasma
transfusion ratios, dynamic monitoring of coagulopathy, and
tailoring of transfusion to the individual’s need.
This chapter will focus on the early management of the
physiological insult caused by major vascular trauma, with
a particular emphasis on trauma team response, transfusion therapy, safe anesthetic practice, and circulatory support. Resuscitation end points are discussed, as are other
handrails that provide guidance during complex clinical
scenarios. The ethics of trauma resuscitation are also deliberated, recognizing that these decisions are more pressing
when resources (clinicians, operating-theater capacity, critical care capacity, blood products) are constrained.
DAMAGE CONTROL DEFINITIONS
The term “damage control” originates from maritime terminology, relating to the emergency measures used to manage
during the emergency crisis of the sinking of a ship. This is
the principle that action taken is that which is necessary to
keep the ship “aoat” in times of crisis rather than comprehensively completing the repair. When applied to trauma,
“damage control” incorporates a mosaic of interventions
that collectively provide an effective hematological and
mechanical “plug” to arrest blood loss and keep the patient
“aoat.”
Damage control resuscitation (DCR) is formally dened
as “a systematic approach to major trauma combining the
<C>ABC (catastrophic bleeding, airway, breathing, circulation) paradigm with a series of clinical techniques from
point of wounding to denitive treatment in order to minimize blood loss, maximize tissue oxygenation, and optimize
outcome.”3 DCR reects advances in combat casualty care
made in the recent military campaigns in Afghanistan and
Iraq and spans the spectrum of vascular trauma management. This practice has evolved as an overarching concept that draws together all those interventions. It starts
from immediate rst aid measures delivered at the point of
injury, such as application of tourniquets and optimization
for surgical intervention by effective volume resuscitation,
through to the critical care unit with the management of
coagulopathy, systemic inammatory response, and any
associated organ dysfunction, which is encompassed by the
emerging concept of endotheliopathy.
DCR includes damage control surgery (DCS). DCS is the
operative stage of DCR that sacrices the completeness
of the immediate surgical repair in order to address the
physiological consequences of the injury. DCS has come to
mean a time-limited surgical procedure (i.e., abbreviated
operation) where the imperative is the minimal intervention to save life and limb before the trauma triad of death
of hypothermia, coagulopathy, and metabolic acidosis
becomes established.
Currently there is no universally ag reed time period where
surgical intervention must be complete. Previously this was
thought to be time limited to a maximum of 60 minutes.
As our understanding and delivery of resuscitation has
improved, so this arbitrary 60-minute rule has become less
critical. Patients with signicant injury severity are arriving to theatres with less physiological derangement, and so
increasing the options available to surgeons for their operative repairs. The main determinate of surgical time should
be the physiological state of the patient. The more effective
and coordinated the early resuscitation, the more options
become available to the surgeon.
Once the initial surgery is complete, the resuscitation
must continue and this will likely occur in the critical
care unit. Unlike DCS, DCR is not time limited and is complete once a patient’s physiology is returned to normal. It
is often thought that once a patient has arrived in Critical Care that the job is done. This is not the case and DCR
principles, especially the use of blood products, should
continue until the patient is fully resuscitated. Thus, from
the anesthetist’s perspective, DCR occurs from the point of
injury by minimizing the insult, through the initial resuscitation, to optimize the patient for the further insult of
surgery, and on to critical care until the patient’s physiology is returned to normal.
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Pathophysiology of Coagulopathy/
Trauma-Induced Coagulopathy (TIC)
Within the context of major vascular trauma, the pathophysiology of coagulopathy is multifactorial and is still not
fully understood. Traditionally, teaching of the trauma
triad of death of acidosis, hypothermia, and coagulopathy
fed into each other as a vicious cycle. Although acidosis and
hypothermia do play a role in exacerbating coagulopathy,
our understanding of trauma science has shown that there
are more nuanced factors at play that lead to coagulopathy
in the context of trauma.
HYPOTHERMIA
The activation of the coagulation cascade is an enzymatic
process and therefore requires two physiological conditions
to function. Tissue factor (Factor VIIa) activity decreases by
50% at 28°C4 and platelet adhesion to Von Willebrand Factor is essentially absent below 30°C.5 Trauma patients have
often suffered a period of exposure during the prehospital
phase and, when combined with signicant blood loss, are
extremely prone to hypothermia. Combined with interventions such as uid resuscitation with nonwarmed uids or
cold blood products, the vasodilatory effect of general anesthesia, and the exposure of body cavities during surgery, it
becomes easy to see how hypothermia is an ever-present
risk during this initial phase of DCR.
Clinically signicant effects of coagulopathy have been
shown where core temperature is below 34°C
tality from hemorrhage is markedly increased when core
temperature is below 32°C7; however, what is not clear is
whether the hypothermia in itself is an independent factor
or merely a marker of the severity of shock and physiological compromise.
HEMODILUTION
Where there is signicant disruption to the vasculature,
larger clots are required, consuming coagulation products such as platelets, coagulation factors, and brinogen.
Within earlier versions of advanced trauma life support
(ATLS) teaching, liberal uid resuscitation was advocated,
which aimed to improve tissue perfusion, but risked worsening coagulopathy by diluting coagulation factors within an
already depleted blood volume. Dilution has been shown to
have detrimental effects on coagulation and impair hemo-
8
stasis.
For the same reason, the sole use of packed red cells as
a means of volume replacement will also lead to a dilutional coagulopathy as platelets, coagulation factors, and
brinogen are not replaced.9 Mathematical models have
suggested that use of 1:1:1 ratio with red cells, plasma, and
platelets will minimize the dilution and provide a solution
closest to whole blood.
campaigns in Afghanistan and Iraq have shown that this
ratio is possible and does have better outcomes12—ndings
also replicated in a civilian setting in the PAMPER Trial.13
Of note, component therapy itself has a dilutional effect as
each component has its own additive solutions.14 In order
to minimize the dilutional effects of component therapy,
10,11
Experience from recent military
4,6
and mor-
the military, for many years, have used whole blood in the
sickest patients. Whole blood for bleeding trauma patients
has increased in civilian practice in recent years, particularly in the United States, where the American Association
of Blood Banks recently endorsed the use of whole blood.
Whole blood in civilian trauma has less uptake outside of
the United States, but is now used in the United Kingdom,
Israel, and Norway.
ACIDOSIS
Trauma to vasculature leads to signicant blood loss, which
itself will lead to hypovolemia and therefore hypoperfusion,
along with reduced oxygen delivery to peripheral tissues. At
the cellular level, anaerobic respiration becomes the predominant means of energy production, which leads to the
production of lactic acid and therefore a metabolic acidosis.
Within animal studies, acidosis has shown to have multiple
effects on coagulation, such as reducing the activity of clotting factors (50% at pH 7.2, 70% at pH 7.0, and 90% at pH
6.8) and increasing degradation of brinogen, i.e., hyperbrinolysis.
15
TISSUE TRAUMA
Although acidosis does play a signicant part in trauma
coagulopathy, it is not the only factor, as signicant clinical
coagulopathy is detected even with mild degrees of acidosis,16 and coagulopathy can still occur even when acidosis
is corrected.15 It is now apparent that tissue damage and
disruption of the endothelium, which leads to the exposure
of the subendothelial layer and release of tissue factor, also
has implications for coagulation.
The exposure of subendothelial layer leads to activation
of plasma proteases, which leads to the activation of the
coagulation cascade and so the formation of thrombin and
brin. In signicant trauma, where there are multiple sites
of endothelial disruption, there is activation of procoagulation factors such as X, II, V, and VIII. These factors then
subsequently enter the systemic circulation and generate
thrombin, affecting macro and microvascular ow as well as
giving rise to a process where platelets, coagulation factors,
and brinogen are consumed and coagulopathy develops.
Tissue disruption also leads to release of tissue-type plasminogen activator (tPA) and increased tissue expression of
tPA. tPA activates plasmin from plasminogen, which lyses
the clot, i.e., brinolysis. Within the context of hemorrhagic
trauma, hypoperfusion leads to further release of tPA from
the Weibel-Palade bodies within endothelium
17,18
and fur-
ther weakening of the clot.
The combination of excessive activation of coagulation
with hyperbrinolysis has led to trauma-induced/-associated coagulopathy described as the “brolytic phenotype”
of disseminated intravascular coagulation.
ENDOTHELIAL DYSFUNCTION
The formation of lactic acid and other metabolites can be seen
as a surrogate for oxygen debt, which needs to be addressed
and “repaid” in a timely manner, or else excessive morbidity and mortality due to multiorgan failure
Multiorgan failure is traditionally viewed as dysfunction
19–21
is risked.
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of one or more of the respiratory, cardiac, renal, and
hepatic systems. The blood and endothelium unit should
also be considered an organ, which may also suffer from the
effects of prolonged hypoxia and acidemia and thus oxygen
debt. This concept has been described as “blood failure” by
the Trauma Hemostasis and Oxygenation Research (THOR)
Network.
22
In health, the endothelium undertakes a range of physiological functions including control of vasomotor tone,
maintenance of blood uidity, and regulated transfer of
water, nutrients, and leukocytes across the vascular wall,
as well as regulation of immunological cell migration.23
The inner endothelial wall has anticoagulative properties
via various systems such as the thrombomodulin/protein C
system, heparinoid-lined glycocalyx, and potential release
of tPA and urokinase plasminogen activator.
24,25
Although
not fully understood, it has been proposed that damage to
the endothelium, either by direct damage by trauma or by
hypoperfusion, leads to the release of these anticoagulative
factors and the glycocalyx into the systemic circulation,
leading to global hypocoagulability should the insult be of
signicant magnitude.
26
Other factors may lead to further endothelial dysfunction. The initial procoagulative state leads to microemboli
and therefore microvascular occlusion, compromising ow
and oxygen delivery. There is also increased paracellular
permeability due to loss of endothelial integrity and tissue
edema—compounding the impairment of oxygen delivery
and increasing oxygen decit. In the face of global hypoperfusion, there will be hyperstimulation of the sympathetic-adrenal system leading to high circulating levels of
catecholamines. High levels of catecholamines have been
implicated as a proposed mechanism of endothelial damage known as shock-induced endotheliopathy,27 which may
be common to other acute critical illness syndromes such
as postcardiac arrest syndrome, sepsis, and myocardial
infarction.
As a better understanding of the mechanisms of traumarelated coagulopathy is developed, we will nd better tools
to quantify the contributory factors described previously.
Although the extent of tissue damage and therefore the
extent of endothelial damage is not a reversible factor, trying to limit endothelial dysfunction and further damage
by ensuring adequate oxygen delivery and limiting oxygen
debt is desirable. Currently, there is no way of measuring
or quantifying oxygen debt and, although lactate clearance has been quoted as a useful marker for resuscitation
end point in the critically ill28 (and probably our best widely
measurable marker), it does not signal whether oxygen debt
has been repaid.
Emergency Department Reception
Patient evaluation in the Emergency Department (ED)
allows assessment from both a surgical and a physiological point of view. There is a balance that needs to be struck
between early surgical intervention and the need to optimize
the patient physiologically, which is situation dependent.
The role of the trauma team is to enforce a systematic
approach to patient assessment and action, but the nature
of medical rotas means that the team will consist of indi-
viduals who may not have worked with each other before
and have their own competing priorities for the patient.
The team leader will need to manage multiple information
streams about the patient and clinical trajectory while also
weighing up options for the next place and phase of care.
Preparation prior to patient arrival is important. The use of
pre-alerts based from the prehospital team can in turn activate members of the trauma team to the ED prior to patient
arrival, to assign roles, pre-rehearse likely scenarios, and
prepare equipment/drugs.
This may include drawing up induction and maintenance
anesthetic drugs, anticipating necessary procedures, priming universal donor red cells (O negative) and plasma (AB
positive) for administration using a rapid transfusion device
with or without a warming mechanism, and informing the
CT radiographer/radiologist and the theatre coordinator.
Performing these actions can not only smooth out transitions of care and enhance the patient ow, but also allow for
more mental bandwidth such that task-critical operators
can rehearse and concentrate on relevant procedures, i.e.,
the anesthetist performing rapid sequence induction (RSI).
Traditional resuscitation protocols emphasized a linear/
2-D approach, where the patient arrives in ED, undergoes
initial assessment and resuscitation, is transferred to CT
Scan for imaging, and then undergoes surgical correction or
intervention in the theatre or interventional suite. Another
approach, however, is to bypass ED and transfer directly
to theatre in order to save time in a severely compromised
patient.
So-called 3-D resuscitation is a concept that has been
developed in the deployed military hospital and in select
civilian trauma centers. In this scenario, advanced notication from the eld or en-route care platform allows the
team leader to identify the small number of patients who
will benet from direct transfer from the ambulance or helicopter to the operating theatre or Hybrid Suite. In the wartime setting, these patients are often injured from explosive
events, have single or multiple amputations, or have torso
injuries and are in pending cardiovascular collapses from
hypovolemia.
INITIAL PRIORITIES IN MANAGEMENT
The use of a C-ABC framework allows identication and prioritization of the immediate steps in stabilization and management.
C—Catastrophic Hemorrhage Control
Catastrophic hemorrhage is signicant bleeding which
requires immediate management to stop exsanguination.
For the patient suffering catastrophic hemorrhage to arrive
into the ED alive, there will be some form of catastrophic
hemorrhage control, which may or may not be complete, or may have become ineffective between application
and arrival. Verbal handover and visual checks should be
made of:
n Tour niquet—Check positioning and adequacy (i.e., needs
tightening/requires second). Consider judicious release
(after primary survey, and assuming physiology is stable)
if wound pattern suggests it is not required (controlled
release).
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n External Dressings—appropriate packing, consider use
of hemostatic agent impregnated dressings.
n REBOA—Time to balloon deation is critical, particu-
larly in zone 1 deployment. Consider timing, extent, and
place of deation as per Chapter 11.
A—Airway (and C-Spine Protection)
Most anesthetists would consider airway management the
most important early priority in the treatment of the critically unwell patient—as without adequate oxygenation
the patient will quickly deteriorate. Ultimately, the patient
with major vascular trauma will require a denitive airway
as part of general anesthesia and operative intervention,
although the timing and place of RSI will be dictated by
case specics. It has become common practice to secure the
airway to facilitate transfer either to CT or theatre. Other
indications include:
n Signicant hypoxia/respiratory failure
n Loss of protective airway reex due to reduced Glasgow
Coma Score (GCS) ≤8
n Signicant chest trauma
n Airway soiling
n Dropping GCS
n Requirement for sedation/analgesia for humanitarian
reasons
From the team leader’s perspective, securing the airway
has to be balanced with other pressing priorities in the
patient’s care (i.e., hemorrhage control and volume resuscitation). The airway can be interim managed using less
invasive measures such as airway maneuvers and adjuncts
(ora-/nasopharyngeal airways), providing these enable successful ventilation.
Securing the airway itself is not a risk-free intervention.
Induction of anesthesia and the introduction of positive
pressure ventilation (PPV) are fraught with risk, especially in
the context of hemorrhagic shock. Securing the airway may
be technically challenging and may need multiple attempts
at laryngoscopy and/or specialist airway equipment. The
“can’t intubate, can’t oxygenate” scenario, which can rapidly lead to life-threatening hypoxia, is an ever-present concern. Securing the airway in a more controlled manner in
a patient who has progressed to a safer physiological state
after a short period of resuscitation, where RSI can be conducted in a dedicated environment, is preferable to an overhasty or under-prepared attempt at intubation.
RSI comprises rapid induction and swift intubation with
the use of cricoid pressure, without the use of bag-mask
ventilation. Although these components make sense in an
unfasted patient to prevent aspiration, there are associated
drawbacks in the critically unstable patient. These include
impaired view at laryngoscopy, reducing the ability to bagmask ventilate in a failed laryngoscopy, and increasing
the risk of hypoxia and risk of cardiovascular collapse. A
concept known as controlled sequence induction offers the
operator a gentler approach. This technique allows rapid
intubation and gentle bag-mask value ventilation during
the apneic phase of induction, reducing the risk of hypoxia.
The concept is well-established within pediatric practice,29
and is gaining traction amongst critical care practitioners.
30
When considering the need for C-Spine immobilization,
the mechanism of injury and pros and cons of immobilization must be weighed up and considered. Immobilization
increases the difculty of managing the airway, raises the
risk of aspiration in the event of vomiting, and increases
intracranial pressure. Blanket immobilization has been deemphasized in favor of a risk-stratied approach in both
military31 and civilian32 practice.
B—Breathing: Optimizing Gas Exchange
As part of the primary survey, the emphasis of detection
and immediate treatment of life-threatening thoracic injuries can be summarized with the mnemonic ATOM FC (Airway obstruction/disruption, Tension pneumothorax, Open
pneumothorax, Massive hemothorax, Flail Chest).
The place of supplemental oxygen in critically unwell
patients is changing. The unmitigated use of supplemental oxygen for every patient is not necessary and, in some
cases, is potentially harmful due to hyperoxia.33 National
guidelines in the United Kingdom, Australia, and New Zealand now dictate careful titration of supplemental oxygen
to target pulse oximetry (SpO2) between 92% and 96%.
34,35
A recent systematic review36 concerning supplemental oxygen in the military trauma population made a number of
recommendations on indications (Table 6.1).
Mechanical ventilation has physiological implications
that are counterproductive to the shocked patient’s resuscitation goals. By introducing positive pressure within the
intrathoracic cavity, venous return to the heart is impeded
and cardiac lling reduced, diminishing cardiac contractility and cardiac output. PPV also negatively affects the lungs
by reducing alveolar perfusion, reducing O2 transfer/CO2
clearance and inducing atelectasis by contributing to V/Q
mismatching. Inadvertent attempts to compensate for this
by increasing positive end expiratory pressure (PEEP) and
raising ventilatory pressures to achieve a higher minute
volume will worsen the cardiovascular insult and may precipitate a cardiac arrest.
The vascular trauma patient will undergo signicant
uid shift during volume resuscitation, increasing the risk
of lung injury in the form of acute respiratory distress
Table 6.1 Use of Supplementary Oxygen in Emergency
Patients
Supplemental O2 Required
Chest injuries Evidence of hypotension without
Injuries at altitude Truncal injuries
Decompression injuries GCS <15
Smoke inhalation and carbon
monoxide poisoning
Cardiopulmonary resuscitation
Preoxygenation prior to RSI
Ventilated patients
GCS, Glasgow Coma Score; RSI, rapid sequence induction.
Adapted from Cottey L, Jefferys S, Woolley T, Smith JE. Use of supplementary oxygen in emergency patients: a systematic review and recommendations in military clinical practice. J R Army Med Corps. 2019;165(6):416–420.
36
Regardless of SpO
Supplemental O2 May Be
2
Required Based on SpO
hypovolemia
Return of spontaneous circulation
following cardiac arrest
2
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syndrome (ARDS) or transfusion-related acute lung injury
(TRALI), impairing gas exchange. These syndromes tend
to occur 24 to 48 hours following the initial trauma insult
and, although there are various ventilatory strategies aiming to prevent/minimize the effect of these syndromes, they
lie outside the scope of this chapter.
C—Circulation: Volume Resuscitation
This concerns the processes of achieving hemostasis and
volume resuscitation, which should occur simultaneously.
Peripheral large bore lines (14–16 G) offer the greatest
ow rates (even compared to most conventional central
venous catheters) and are the preferred means of immediate IV access. Gaining access can be challenging in the
shocked patient, especially if there is associated major
extremity trauma. The subclavian and axillary veins offer
an alternative route and resist collapse even in signicant
hypovolemia. Intraosseous (IO) routes can be quickly and
easily accessed; rapid infusion of uid requires pressure
(i.e., the manual use of a syringe) but good ow rates can
be achieved. Drugs administered via the IO route reach the
central circulation just as quickly as the IV route.
37
A higher pressure to drive IV infusions can be obtained
by simply raising the infusion bag or directly applying pressure to the bag. The use of a pressure bag allows continuous
pressure and is a readily available low-tech option; other
infusion systems such as the Level One and Belmont systems
have the advantage of allowing a second bag of uid to be
primed while an infusion is ongoing, preventing interruption of volume resuscitation and allowing for in-line warming of the uid to reduce the risk of iatrogenic hypothermia.
The benets of using early blood products versus crystalloids as a volume replacement in traumatic hypovolemic shock have now been widely described in the military
population. Two recent randomized controlled trials (RCTs),
PAMPER and COMBAT, studied the outcome of shocked
patients following early, en-route resuscitation with plasma
versus standard uid resuscitation. COMBAT was conducted
in an urban setting, with short prehospital times (less than
20 minutes)—and no mortality difference was observed.
There was a high proportion of penetrating trauma and
most patients did not get their plasma treatment prehospital
due to the rapidity of transfer to the ED.
38
PAMPER,14 on the other hand, was a multisite study
with longer prehospital times (median 40 to 42 minutes in
each study arm) where the control arm protocol defaulted
to local resuscitation standard operating procedures (SOPs)
(including some services where administration of red cells
and crystalloid was the standard of care). In this study
there was a signicant reduction in mortality for the plasma
group, with most benet in those patients who received
both plasma and red cells. The PAMPER and COMBAT data
sets were designed to be combinable, and aggregate analyses revealed that where prehospital times were greater than
20 minutes, there was a mortality benet in the plasma
group, and this was more signicant in blunt, rather than
penetrating, trauma.
“Shock packs” or major hemorrhage packs are a system
improvement that makes balanced trauma resuscitation of
blood products easier to conduct from a logistical perspective. The components of shock packs vary but typically will
include 4 units of O negative packed red cells, 4 units of
fresh frozen plasma, and 1 unit of pooled platelets, giving
a near 1:1:1 ratio.
This ratio is a useful starting point but only an approximation of what the individual patient requires—tailoring
of the mix requires trend analysis of physiological, hematological (and thromboelastogram) data. Close liaison with
the lab-support is essential in the effective delivery of major
hemorrhage protocols (MHP), as well giving them context
to anticipate further blood product requirements. In the
author’s experience, allowing approximately 30 minutes
of lead time of likely requirements will give the laboratory
team enough time to prepare blood products for the following shock pack. Transfusion services vary in their ability to
surge blood products to the ED or Theatre in this manner,
with less mature services, or those situated in the developing world, less able to support the shock pack or MHP
approach.
Other adjuncts to MHP have included off-license use of
recombinant factor VIIa,
to demonstrate any mortality benefit
39,40
although RCT data has failed
41,42
with increasedrisk thromboembolic events.43 Conversely, there is good
evidence around early administration of tranexamic
acid. This antifibrinolytic agent has been shown to reduce
mortality in both the civilian (CRASH-2)44 and military
(MATTERs)45 setting. There appears to be an enhanced
effect when given early in the treatment pathway (less
than 3 hours from injury, ideally less than 1 hour).46
This is now reflected in clinical practice as the initial
loading dose is routinely delivered within the prehospital
setting.
D—Disability and “Cardio-Stable” Induction
Strategies
Assessment of disability involves being aware that by
inducing general anesthesia, the team will be unable to
assess neurological status, which is often the rst and most
sensitive sign of a neurological injury. Prior to induction,
attempts should be made to gauge the best GCS and neurological status, with a rapid assessment for signs suggestive
of gross upper or lower motor neuron injury.
Inducing anesthesia in a hypovolemic patient is fraught
with risk—and careful thought and team discussion/
brieng should precede expedited intubation to check
optimal timing and location. These patients rely on their
increased sympathetic drive to maintain adequate cardiac
output in a relatively underlled state. Conversely, induction agents are generally negatively inotropic and inhibit
the sympathetic nervous system, which will compromise
any compensation the patient is trying to mount. This will
invariably lead to a low cardiac output state or cardiac
arrest if the induction technique is not modied by altering the ratios of medications or by changing the medications used. These techniques are known as “cardio-stable”
induction strategies.
One such technique is to employ high-dose opiate (i.e.,
10 mcg/kg fentanyl), which allows a reduced dose of propofol for induction. This strategy is used routinely in elective
patients with compromised cardiac function where minimizing suppression of cardiac drive is vital. This approach
will be familiar to the general (non-trauma) anesthetist but
takes more time to achieve conditions suitable for intubation, and so carries a higher risk for aspiration.
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