TRAUMA
Management of shock in
trauma
Matthew Boyd
Damian D Keene
Abstract
Shock is defined as the failure of the circulatory system to provide the
organ perfusion and tissue oxygenation required to meet cellular
metabolic demands. Traumatic shock is most commonly associated
with haemorrhage, although non-haemorrhagic shock can be found
in trauma in the form of cardiogenic or neurogenic shock. Over the
last decade evidence has demonstrated that trauma patients have
an acute traumatic coagulopathy (ATC) caused by the injury process
itself. This has been fundamental to the development of the current
approach to management of traumatic shock, known as damage con-
trol resuscitation (DCR). DCR encompasses three key resuscitative
strategies, permissive hypotension, haemostatic resuscitation (the
use of blood products as primary resuscitative fluids) and damage
control surgery. The implementation of DCR alongside the creation
of trauma networks has been revolutionary in the management of
the shocked trauma patient. Current focus is on evolving and refining
these strategies including identifying the subsets of patients at great-
est risk as early as practicable following injury.
Keywords Coagulopathy; haemorrhage; hypovolaemia; lethal triad;
massive transfusion; shock; trauma; trauma team
Royal College of Anaesthetists CPD Matrix: 1A01; 1B04; 1H02; 2A02;
2A05; 3A10; 3A14
Shock
Shock is defined as a failure of the circulatory system to provide
adequate organ perfusion to meet the oxygen demand of cellular
metabolism. Shock in trauma is most commonly due to hae-
morrhage accounting for up to 40% of deaths following trauma.
It remains the leading preventable cause of trauma-related death.
It is vital to remember that not all shock results from blood loss.
Cardiogenic shock can result from blunt force trauma, obstruc-
tive shock from cardiac tamponade and tension pneumothorax,
neurogenic shock may be associated with acute spinal cord
injury. This article will focus on haemorrhagic shock in trauma.
Physiological response to haemorrhage
Significant haemorrhage will lead to a transient fall in blood
pressure that triggers sympathetic stimulation. This results in an
Matthew Boyd MBChB RAMC is an Anaesthetic Registrar at Derriford
Hospital, Plymouth, Devon, UK. Conflicts of interest: none declared.
Damian D Keene MBChB BMedSc(Hons) FRCA DipIMC RAMC is a
Consultant in Anaesthesia and Pre-Hospital Emergency Medicine at
Queen Elizabeth Hospital, Birmingham, UK; and Clinical Lecturer,
Department of Military Anaesthesia and Critical Care. Conflicts of
interest: none declared.
ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
Please cite this article in press as: Boyd M, Keene DD, Management of shock in trauma, Anaesthesia and intensive care medicine (2017), http://
dx.doi.org/10.1016/j.mpaic.2017.05.002
Learning objectives
After reading this article, you should be able to:
C Describe the physiological response to haemorrhage
C Describe the lethal triad of trauma
C Describe the clinical management of traumatic shock
C Explain the role and benefits of the trauma team
increased cardiac output (through a rise in heart rate and
contractility) as well as arterial and venous constriction with the
overall aim being to maintain blood flow to the vital organs. This
cannot occur indefinitely, severe blood loss reduces oxygen de-
livery to the tissues resulting in anaerobic cell respiration
generating a lactic acidosis.
The lethal triad
Prolonged acidosis (pH < 7.2/[Hþ] > 63 nM/L) inhibits platelet
and clotting factor function as well as impairing ventricular
function. The reduced platelet and clotting factor activity sec-
ondary to the metabolic acidosis results in a coagulopathy. In
turn this leads to further bloodloss worsening the metabolic
acidosis. Poor tissue perfusion coupled with removal of clothing,
environmental exposure and administration of cold fluids results
in hypothermia again worsening enzyme function. This results in
a vicious cycle where physiological derangement reduces the
ability of the body to maintain homeostasis. The interplay of
these three factors is known as the ‘lethal triad’ consisting of
acidosis, coagulopathy and hypothermia that if allowed to
continue results in death.
Acute traumatic coagulopathy
In 2003 Brohi et al. demonstrated that coagulopathy was present
in up to one-third of trauma patients (Injury Severity Score >15)
presenting to the emergency department even before the
administration of fluids. This has led to the concept of acute
traumatic coagulopathy (ATC). Patients with ATC have a
significantly higher mortality and are at greater risk of multi-
organ failure. ATC occurs as part of the body’s response to injury
and is directly related to the degree of tissue damage and dura-
tion of shock.
The exact pathophysiology remains unclear as there are a
number of conflicting processes at work, some resulting in con-
sumption of factors due to procoagulation and others favouring
an anticoagulant process.
Tissue damage exposes tissue factor (TF). This drives local
thrombin and fibrin production. Platelets are activated by
thrombin and adhere to the damaged tissue in turn amplifying
thrombin generation. Recent studies have shown that despite this
there are still adequate amounts of clotting factors and preserved
thrombin generation in patients with ATC.
Conversely hypoperfusion (through hypoxia, and epinephrine
and vasopressin release) activates tissue plasminogen activator (t-
PA) and inhibits plasminogen activator inhibitor (PAI), thus pro-
moting hyperfibrinolysis. This may explain the survival benefit
from tranexamic acid administration. Additionally, there is
1 Ó 2017 Published by Elsevier Ltd.
 TRAUMA
evidence that activated Protein C (aPC) levels are increased adding
to the anticoagulant element of ATC by cleaving factors Va and
VIIIa as well as binding PAI and further encouraging fibrinolysis.
Platelet function is reduced early in the period following
trauma, often despite normal platelet counts, possibly due to a
blunted thrombin activation effect.
Haemodilution of coagulation factors occurs through the
administration of crystalloids, colloids or packed red cells, whilst
hypothermia has a negative effect on platelet function and the
enzymes of the clotting cascade. This all exacerbates the coa-
gulopathy of ATC.
Clinical management of traumatic shock
Damage control resuscitation (DCR)
Over the past decade the multiple interventions and stages of
trauma resuscitation have been unified under one concept,
damage control resuscitation (DCR). The UK military definition
of DCR encompasses all care from point of injury through to post
surgical care on the Intensive Care Unit. The overall aim being ‘to
minimize blood loss, maximize tissue oxygenation and optimize
outcome’. This entails haemorrhage control with the early use of
tourniquets and haemostatic dressings at the point of wounding,
alongside the use of permissive hypotension. The use of
advanced pre-hospital teams allows the early commencement of
haemostatic resuscitation and rapid sequence induction. These
techniques are continued and expanded upon in the Emergency
Department with prompt access to diagnostic and interventional
imaging. In combination, these strategies aim to reverse the le-
thal triad and return the patient to homeostasis. In shocked pa-
tients whose organ perfusion cannot be maintained with ongoing
resuscitation, rapid surgical intervention is required.
Permissive hypotension (PH)
The aim of PH is to minimize blood loss prior to control of
bleeding. This can be temporary control with tourniquets, pelvic
binder or permanent surgical control. 250 ml fluid boluses are
given to achieve the target systolic blood pressure of 80e90
mmHg. A radial pulse can be used as a surrogate until a blood
pressure is available. However, whilst absence of a radial pulse
signifies significant shock, its presence does not guarantee a
blood pressure of 80 mmHg. If there is no head injury fluid can
be titrated to maintain consciousness.
The concept is based on the principle that the first clot is the best
clot. By allowing a state of ‘controlled shock’ perfusion to vital or-
gans can be maintained, whilst the risk of clot disruption by
increasing blood pressure is reduced. Evidence for improved mor-
tality from PH is still lacking particularly in blunt trauma. Evidence
in animal studies using pigs suggests hypotension can be main-
tained for up to 60 minutes, but past this point the oxygen debt of the
tissues may be impossible to overcome even with aggressive DCR.
PH is contraindicated in patients with head injuries or preg-
nancy both of which require higher blood pressures. There is
little guidance in the paediatric population where its use is still
debated.
Haemostatic resuscitation (HR)
The aim of haemostatic resuscitation is to restore tissue perfusion by
replacement of blood volume, ensure optimal oxygen delivery by
ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
Please cite this article in press as: Boyd M, Keene DD, Management of shock in trauma, Anaesthesia and intensive care medicine (2017), http://
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the replacement of red blood cells and reverse coagulopathy by the
replacement of clotting factors and platelets. It may only be possible
to stop or slow the coagulopathy prior to control of bleeding. The use
of crystalloid fluid replacement in trauma can have a detrimental
effect on coagulation. The early use of blood products is advocated.
Haemostatic resuscitation consists of two phases: fluid
administration before and after control of bleeding. Whilst
bleeding is ongoing blood products are administered at fixed ratios
targeted to maintain a systolic blood pressure of 80e90 mmHg.
Once bleeding is controlled a more targeted approach can be un-
dertaken with the use of viscoelastic tests such as thromboelas-
tography (TEG) or rotational thromboelastometry (ROTEM).
Attention must be given to biochemical correction of the pa-
tient. The use of large volumes of stored blood products will lead
to hypocalcaemia and hyperkalaemia, both of which need to be
managed, preferably in a pre-emptive manner.
Massive haemorrhage protocol
The logistical challenges in undertaking massive transfusions are
significant. To allow teams to concentrate on other pressing
clinical issues and release ‘cognitive bandwidth’, the use of
massive transfusion protocols is advised. Each institution will
have their own protocol with subtle variations due to the set up
of the blood bank service but a common theme runs through
them all. Once the recognition or expectation of a massive
transfusion is present, one call to a dedicated phone line can be
made to trigger the protocol. Blood boxes containing pre defined
blood products are released until the protocol is terminated by
the treating clinicians. This allows rapid administration of fixed
ratios of Fresh Frozen Plasma (FFP), Packed Red Blood Cells
(PRBC) and platelets. While there is significant ongoing hae-
morrhage, reliance on blood test results to guide resuscitation
may not be helpful, even tests with a fast turnaround time are
likely to provide ‘historical’ results. During this phase a fixed
ratio transfusion is recommended.
The exact ratio is debated with the PROPPR Trial comparing
1:1:1 or 1:2:1 (FFP:PRC:PLTs).1 There was no difference in the 24
hour or 30 day mortality with each ratio but haemostasis was
achieved in more patients in the 1:1:1 group. Findings in the
observational ACIT trial however found increased survival in the
arm with a higher ratio of platelets and plasma to blood.2
Hypocalcaemia complicates massive transfusion due to citrate
in stored blood products binding calcium. In hypocalcaemia
fibrin will not polymerize and platelet function is reduced as well
as myocardial contractility and systemic vascular resistance.
During the phase of rapid administration Calcium (10 ml 10%
calcium chloride) should be given with every four units of FFP
and four units of PRBC as a minimum.
Part of the coagulopathy in trauma is caused by fibrinolysis.
To prevent this 1 gram of intravenous tranexamic acid should be
given as early as possible, preferably in the pre hospital phase.
The strongest evidence for use in the CRASH 2 trial came in those
given it within the hour. There was some benefit if given be-
tween 1 and 3 hours of injury, after this period it is associated
with an increase in mortality.
Targeted resuscitation
Once bleeding is controlled a more tailored approach is employed
with both the volume and the type of blood products
2 Ó 2017 Published by Elsevier Ltd.
 TRAUMA
administered. Efforts are deliberately made to blunt the sympa-
thetic drive of the casualty using opiates. Any resulting drop in
blood pressure is then corrected with PRBC and FFP (1:1) with
the aim of restoring the patients normal blood volume. The de-
gree of metabolic acidosis is used as a marker of adequate
resuscitation, the target being normalization of the base excess
and lactate. This is tested at least every 30 minutes, more
frequently if the casualty is unstable.
The aim of this process is to restore the patients’ homeostasis
allowing them to tolerate further blood loss that may occur.
Standard vital signs are poor markers of adequate resuscitation.
Often, once initial surgical control is gained, the patient will may
be normo/hypertensive due to a high sympathetic tone. They
will still be significantly acidotic and hypovolemic. If control
were to be lost prior to volume resuscitation, rapid deterioration
or death will result. At this point a pause in surgery allowing time
to ‘catch up’ maybe necessary with surgery continuing once
physiological stability is improved.
Use of prothrombin time (PT) or international normalized
ratio (INR) and activated partial thromboplastin time (aPTT) to
guide product replacement has significant limitations. An INR
> 1.5 represents an established coagulopathy but significant
degrees of coagulopathy can still be present even with an INR
< 1.5. These tests take no account of platelet function or the
whole blood clotting. Point-of-care coagulation monitoring using
TEG/ROTEM to target product replacement has been demon-
strated to reduce blood product administration.3,4 If only labo-
ratory test results are available the following minimal targets
should be aimed for (Table 1).5
Hypothermia mitigation
Reduced body heat production secondary to anaerobic meta-
bolism occurs with hypo-perfusion. Once heat is lost rewarming
can take significant periods of time to achieve. The best strategy
here is prevention. Limiting casualty exposure, warmed intra-
venous fluids, warming devices and methods to reduce evapo-
rative losses.
Electrolyte control
As previously mentioned hypocalcaemia will occur due to the
citrate the blood products are stored in if not supplemented.
Initially, calcium should be replaced at set intervals, more if the
ionized calcium is still reduced. Once bleeding is controlled,
regular arterial blood gases should guide calcium replacement.
Coagulation targets
Factor Target Response
INR and aPTT <1.5 of normal If high give
FFP 30 ml/kg
Fibrinogen 1.5e2 g/L Replace with
cryoprecipitate
Platelet count 75  109/L Replace with 1 ATD
(100 if ongoing bleeding
OR head injury)
Table 1
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Please cite this article in press as: Boyd M, Keene DD, Management of shock in trauma, Anaesthesia and intensive care medicine (2017), http://
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Potassium concentrations in PRBCs can range from 7 to 77
mmol/L depending on the age of stored blood. Development of
hyperkalaemia will depend on the underlying renal function,
severity of tissue injury and rate of transfusion. Potassium levels
must be closely monitored and hyperkalaemia treated with a
glucose and insulin infusion.
Anticoagulants
In developed countries many victims of trauma are increasingly
elderly with significant comorbidities requiring anticoagulation.
Many of these patients are now taking novel oral anticoagulants
(NOAC), which are less detectable with standard laboratory tests
or TEG/ROTEM. If, despite normal testing, the patient is clini-
cally coagulopathic these must be considered. The drugs are
currently difficult or impossible to reverse but agents are un-
dergoing approval for clinical use for this purpose. Expert advice
from a Haematologist should be sought.
Damage control surgery (DCS)
DCS comprises of a range of surgical interventions targeted at
halting deterioration of the patient’s physiological condition
rather than attempting definitive restoration of function.
The concept of DCS was developed following recognition that
severely injured trauma patients are more likely to die from the
metabolic consequences of their injuries than incomplete surgical
repair. Previously surgery and resuscitation were considered in
series rather than the current parallel system that recognizes that
neither could occur without the other in the patient with un-
controllable haemorrhage.
In this instance, haemostatic resuscitation provides time for
the surgeon to rapidly control bleeding. This allows further
haemostatic resuscitation and optimization; and, when physio-
logical catch-up has been achieved, secondary surgery to com-
plete definitive procedures can take place.
In the majority of blunt trauma patients there will be time to
undertake computed tomography (CT) to help guide surgical
intervention. A small subset will require rapid surgical inter-
vention. Senior clinicians are key to identifying and managing
this group.
The trauma team
The ATLS approach was developed so that a lone doctor can
safely manage a multiple injured patient by following a system-
atic ABCDE approach. The aim is to remove the likelihood of
missing severe injuries in hospitals with infrequent exposure to
trauma and improve mortality and morbidity. Both military and
civilian experience over the last decade has led to significant
changes in this approach. The first is a shift in recognition that
uncontrolled haemorrhage is the commonest preventable cause
of death from injury. This has led to a shift from the classical
ABC approach to <C>ABC approach, with catastrophic hae-
morrhage being addressed first.
The second key change is a ‘horizontal’ approach to man-
agement of the injured patient. The same key assessments are
still made but, concurrently rather than sequentially. Vital to this
is having a clear allocation of roles including a team leader who
can maintain overall situational awareness and coordinate clin-
ical efforts. The ultimate aim of horizontal resuscitation is to
3 Ó 2017 Published by Elsevier Ltd.
 TRAUMA
reduce the time in the resuscitation room before clinical in-
terventions to stop bleeding are carried out.
With the establishment of major trauma centres in the UK and
their associated concentration of expertise, trauma team training
is becoming increasingly commonplace. The European Trauma
Course (ETC) has been established; this not only focuses on
current management protocols but also on non-technical skills
such as communication, team working, situational awareness
and decision-making.
Summary
By greater understanding of the physiology of shock in trauma,
including the lethal triad of coagulopathy, metabolic acidosis and
hypothermia, we can deliver evidence-based treatment strategies
designed to reverse the physiological insult and achieve
improved patient outcomes. Targeted strategies based on the
principles of damage control resuscitation are influencing
morbidity and mortality but to deliver to their best effect requires
a well-rehearsed and experienced trauma team. A 605e12.
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ANAESTHESIA AND INTENSIVE CARE MEDICINE --:-
Please cite this article in press as: Boyd M, Keene DD, Management of shock in trauma, Anaesthesia and intensive care medicine (2017), http://
dx.doi.org/10.1016/j.mpaic.2017.05.002
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FURTHER READING
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4 Ó 2017 Published by Elsevier Ltd.