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The European Trauma Course Manual

Edition 4.0
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5.
Shock
Learning outcomes
Following this part of the course you will be able to demonstrate competence in:
QDefining shock and knowing its causes in trauma patients

QAssessing, managing and monitoring trauma victims with shock

QAssessing medical factors complicating shock management

QImplementing haemorrhage control

QHaemostatic resuscitation and applying a major haemorrhage protocol

QAssessing, monitoring and managing burned victims

QVascular access and the use of intraosseous needles

Introduction hypovolaemia. Later, as shock progresses, there is an

Shock is best defined as a generalized, life-threatening,
inadequate oxygen delivery to organs and tissues.
It occurs when there is an imbalance between the
processes determining oxygen delivery and oxygen
consumption (figure 5.1). Initially the mismatch is
primarily a result of impaired delivery (hypoperfusion),
which in the trauma patient is usually due to
increase in oxygen uptake as a result of a response to
stress, inflammation or sepsis, each of which increase
oxygen requirements beyond levels seen in health.
The causes of shock
Although hypovolaemia is by far the commonest cause
of shock in the trauma patient, there can be other
co-existing pathophysiological disorders affecting

ate
Adequ

uate
Inadeq

Reduced Increased oxygen Reduced oxygen Increased oxygen

oxygen delivery consumption consumption delivery

arterial oxygen cardiac output

­ ­ ­
­

saturation haemoglobin
haemoglobin
­ ­

Adequacy of arterial oxygen

cardiac output saturation
oxygen delivery

Figure 5.1 Factors affecting the adequacy of oxygen delivery

CHAPTER 5 SHOCK | 67
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TABLE 5.1

Classification of shock
Type of shock Examples of causes Effect on cardiac output
Hypovolaemic Haemorrhage, interstitial (third space) losses, burns, dehydration Decreased
Obstructive Tension pneumothorax, cardiac tamponade, massive pulmonary embolus Decreased
Cardiogenic Myocardial injury or ischaemia Decreased
Distributive:
Q Neurogenic Spinal cord injury (usually above T6) Decreased
Q Septic Pneumonia, bowel perforation, infection (late complication of trauma), Decreased, normal or
delayed resuscitation increased
Q Anaphylactic Acute allergic reaction (type I hypersensitivity) Normal or decreased

oxygen delivery. These are classified in table 5.1. All can
eventually lead to cellular hypoxia, microcirculatory
or mitochondrial dysfunction and cell death. If left
untreated, this causes the release of various mediators
initiating a systemic inflammatory response syndrome.
When the patient has multisystem trauma, these
changes are cumulative. For example, consider a case
of blunt trauma with pulmonary contusions and intra-
abdominal haemorrhage. Oxygen delivery will be
impaired by reductions in arterial oxygen saturation
(SaO2), cardiac output (hypovolaemia reducing
preload) and haemoglobin concentration if replaced
with cristalloids. This will be exacerbated by the
increase in oxygen consumption from pain, shivering
and, if inadequately treated, the development of an
inflammatory response syndrome.
Recognition of shock
The lack of sensitivity with tests used to identify shock in
the resuscitation room means its early development can
be difficult to detect. A common mistake is to overlook
patients with established tissue hypoperfusion because
their blood pressure is within the normal range for their
age group. Early recognition therefore relies on:
Clinical examination
Qsigns of external or internal haemorrhage.
Estimating the volume of blood lost
Qheart rate;
On their own, these changes are not accurate enough
to estimate the reduction in blood volume because of
the presence of confounding factors which affect the
trauma victim’s response to hypovolaemia.
Factors affecting estimation of blood loss
The classic presentation of the shock response
following trauma is most likely to be seen in the
young, fit adult with an isolated penetrating injury
with little tissue damage (e.g. a stab wound to a major
artery). More frequently, the patient has significant
tissue damage following blunt trauma and is anxious,
frightened and in pain. All of these variables will
modify the physiological response. The situation may
be further complicated by the presence of drugs, or
pre-existing comorbidities that modify the patient’s
ability to respond to haemorrhage. These factors may
lead to a serious risk of over- or underestimation of
blood loss (table 5.2).
TABLE 5.2
Patients with a risk of over or under estimation of
blood loss
Blood loss over-estimation Blood loss under-estimation
Pre-existing medical conditions Young children (chapter 11)
Drugs/pacemakers Pregnancy (chapter 6b)
Hypothermia Athlete
Penetrating trauma Blunt trauma

Qblood pressure; Pre-existing medical conditions

Qrespiratory rate; The response to trauma in these patients can vary.
Qcapillary refill time; Those with a reduced cardiorespiratory reserve due to
Qskin colour and temperature; myocardial ischaemia, valvular disease or sympathetic
Qurine output; neuropathy (e.g. diabetics) have a restricted ability to
Qconscious level. compensate for acute hypovolaemia. As a result, blood
pressure can fall when relatively smaller volumes
Metabolic disturbances (blood gases) of blood are lost, leading to an overestimation of
QpH; blood loss. Alternatively, if the patient is normally
Qlactate; hypertensive, haemorrhage may only lower the BP
Qbase deficit. into the normal range for that age group, leading to
an underestimation of blood loss.

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Drugs and pacemakers
Various medications alter the physiological response
to blood loss, (e.g. β-blockers). Illicit drugs (e.g. cocaine)
can also affect the normal physiological response. The
effect of a pacemaker will depend upon its complexity;
they may pace at a fixed rate (approximately 70-100/
min) irrespective of volume loss or arterial blood
pressure, giving rise to errors in estimation of acute
blood loss. A history of therapeutic anticoagulation
should also be considered, being either sought from
the history, medic alert bracelet or early assessment of
clotting function. Abnormalities should be corrected
when discovered, especially in the actively bleeding or
brain injured patient.
The athlete
The resting heart rate in an athlete may be less than
50 beats/min and accompanied by an increase in
blood volume of 15-20%. Therefore a compensatory
tachycardia indicative of significant acute blood loss
can be less than 100 beats/min.
The patient with hypothermia
A core temperature below 350C will reduce arterial
blood pressure, heart and respiratory rate in its own
right, irrespective of any blood loss. If this is ignored,
hypovolaemia may be overestimated. Hypothermic
patients who are also hypovolaemic are often ‘resistant’
to appropriate fluid replacement. Estimation of the
fluid requirements of these patients may therefore be
very difficult and invasive haemodynamic monitoring
is often required.
Penetrating or blunt trauma
Minimal tissue damage, typically associated with a
penetrating wound (e.g. stab wound) will result in
tachycardia, and vasoconstriction. Initially, this may
be sufficient to maintain a relatively normal blood
pressure. However continued blood loss will eventually
result in a reduction in heart rate, loss of sympathetic
tone (particularly in skeletal muscle and kidneys) and a
profound fall in blood pressure. In contrast, significant
tissue damage (e.g. blunt trauma with long bone
fractures) results in prolonged progressive sympathetic
stimulation with an increasing tachycardia and marked
vasoconstriction in non-essential organs e.g. the gut,
skin and kidneys. These patients will continue to
compensate, despite ongoing blood loss. Eventually
as blood loss continues, no further compensation is
possible and hypotension ensues. It is therefore a late
sign of impending cardiovascular collapse.
Patients with penetrating or blunt trauma can
appear to have similar signs and symptoms of
shock having lost very different volumes of
blood.
In trauma patients, two other factors complicate the
situation further; coagulopathy and acidosis. These
combine with hypothermia to produce an interlinked
‘lethal triad’ (figure 5.2). Inadequate tissue oxygenation
leads to lactic acidosis, whilst environmental exposure
and the use of cold fluids lead to hypothermia. Trauma
is associated with the development of coagulopathy
which is exacerbated by acidosis, hypothermia, the
depletion of clotting factors by clot formation, ongoing
haemorrhage and the use of fluids devoid of clotting
factors. As a result the cycle of coagulopathy, acidosis
and hypothermia is established.
Injury
Haemorrhage Exposure
Coagulopathy
Acidosis Hypothermia
Figure 5.2 The lethal triad: hypothermia, acidosis and coagulopathy
Primary survey and resuscitation
The initial management of the shocked patient focuses
on eliminating the lethal triad, by:
Qpreventing further haemorrhage;
Qrestoring adequate oxygen delivery;
Qminimizing further heat loss and rewarming;
Qrecognizing and correcting any coagulopathy.
The real challenge of trauma care is to achieve all of
this as rapidly as possible and certainly within the
first hour. Consequently these measures need to be
implemented while the patient is being transferred
from the pre-hospital arena to the resuscitation room
and subsequently to either the CT scanner, operating
theatre, radiology suite or the intensive care unit.
Before the patient arrives
Good preparation based on pre-hospital information
is essential, this includes ensuring that:
Qthe resuscitation room is warm;
QIV fluids are warm;
Qthe blood warmer is prepared;
Qwarming blankets are available;
Qtranexamic acid is available;
Qthe major haemorrhage protocol is activated
appropriately;
Qa team briefing has occurred.
On arrival
The same plan described in chapter 2 is used with
members of the team carrying out their tasks
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Management of shock
Recognise the Vascular access
presence of shock (or IO) Coagulation Consider
Control
assay need for
external
Send trauma (including tranexamic
haemorrhage Identify Identify bloods &
calcium & acid
non-haemorrhagic source(s) of blood gas
causes of shock haemorrhage fibrinogen)
Fluid
resuscitation
Plan and prioritise
Give
Haemostatic/
Control Treat tranexamic
Consider balanced
haemorrhage coagulopathy acid
applying Treat as transfusion
pelvic appropriate appropriately
binder Monitor response to
guide further use of
blood/blood products

Reassess

Plan and prioritise

further management

Figure 5.3 Overview of approach to shock management

simultaneously. Specific features that the circulation
personnel will have to address are summarised in
figure 5.3. Each of these will be considered in turn.
Haemorrhage control in the resuscitation room
The techniques available to control haemorrhage in
the resuscitation room include:
Qdirect pressure and elevation at the point of
haemorrhage;
Qtopical haemostatic dressing;
Qtourniquets for limb haemorrhage;
Qsplints to minimize further blood loss from long
bone fractures;
Qapplication of a pelvic binder in a
haemodynamically unstable patient with a
suspected pelvic fracture (chapter 7).
Having identified any external haemorrhage, one of the
circulation personnel should apply direct pressure over
the wound with an antiseptic dressing supplemented
with elevation if practical. When the bleeding stops
or is significantly reduced, a compression bandage
can be applied. If this fails to control the bleeding,
as demonstrated by bleeding through the dressing,
a further one should be applied. The next step is to
consider using a haemostatic dressing and tourniquet.
Once in place these should be left until there is time to
gain definitive control of the bleeding source.
Tourniquets are becoming increasingly used in the
pre-hospital environment, particularly in areas where
there is significant lower limb trauma. The aim should
be that a tourniquet is left on for the shortest time
possible, (certainly not for more than two hours), until
the source of bleeding has been controlled surgically
or by interventional radiology.
Splinting a limb is an effective way of limiting further
blood loss. A pelvic binder can also be life-saving
when applied to severe pelvic fractures as it stabilises
the bone fragments, and decreases the pelvic volume
thereby reducing the risk of major hemorrhage. A
number of devices are available to temporarily bind
a fractured pelvis in a haemodynamically unstable
patient until surgical stabilization can be achieved (see
chapter 7).
Vascular access
Peripheral venous access
With overt bleeding controlled, vascular access should
be obtained by inserting two large bore peripheral
IV lines (14 or 16g). If peripheral venous access is
unavailable or fails, the alternatives are cannulation of
a central vein (subclavian, internal jugular or femoral)
or intraosseous (IO) access.
Intraosseous access
This technique can be used in patients of all ages
when it is not possible to cannulate a peripheral vein
and as an alternative when time or expertise limit the
use of central access. It is simple to learn and has a low
incidence of complications.

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Insertion of IO needle (see skills section)
KEY POINTS
Indications: inability to cannulate a peripheral vein,
lack of time or expertise to insert a
central venous catheter
Procedure: insertion of intraosseous needle
Complications: failure to enter marrow cavity, infection,
compartment syndrome
Common delay in use, inserted distally to fracture
pitfalls:
Fluids and blood products for resuscitation
Crystalloids
The most commonly used crystalloid solutions
are Hartmann’s, Ringer’s acetate and 0.9% saline.
Hypotonic solutions (e.g. 5% glucose, 4% glucose
and 0.18% saline) diffuse into both the extracellular
and intracellular spaces with little remaining in the
intravascular space. Consequently they have no role in
the resuscitation of trauma patients.
Hypertonic crystalloid solutions have been advocated
for initial resuscitation of hypovolaemia. The most
widely used is hypertonic saline, consisting of
between 1.8% and 7.5% saline. The main advantage
appears to be in patients with traumatic brain injury
where it may reduce cerebral oedema and intracranial
pressure (ICP), thereby restoring cerebral perfusion
and reducing neuronal injury (chapter 8).
Blood and blood products
Warmed blood products are the fluids of choice
for the resuscitation of the unstable hypovolaemic
trauma patient (Fig. 5.5). Stored blood has usually been
processed into a number of products to allow the
most appropriate to be given. Knowledge of the local
provision of blood products is important as different
countries may carry this out in different ways. For
example, fibrinogen concentrate is available in some
European countries and clotting factor concentrates
are becoming more widely used in trauma.
Initially, red cell replacement to restore haemoglobin
concentration is typically given in the form of packed
red blood cells (PRBCs). This is devoid of clotting factors
and platelets. Ideally all blood transfusions should have
undergone a full crossmatch to ensure compatibility,
however, this can take up to an hour. In the urgent
situation the use of uncrossmatched O-negative
blood may be necessary. Subsequently type-specific
blood should be used as soon as it is available, as the
recipient and donor blood are checked for ABO and
Rhesus compatibility. When bleeding is ongoing, or
when large volumes of blood have been lost, red cells
need to be supplemented with fresh frozen plasma
(FFP), clotting factor concentrate, cryoprecipitate and
platelets. This is best achieved by following a major
haemorrhage protocol (MHP). The use of the MHP
has become the cornerstone of fluids resuscitation
in patients who are physiologically compromised by
their blood loss or have ongoing bleeding. In some
areas, blood is also available for use in the pre hospital
setting.
All fluids should be warmed before being given to
prevent iatrogenic hypothermia. This is best achieved
by storing crystalloids in a warming cupboard and
delivering them through a warming device to minimize
heat loss as the fluid passes through the giving set. The
use of rapid infusion devices which can deliver large
volumes of warmed blood products or fluid should be
available for the resuscitation of profoundly shocked
patients.
Identifying the causes of shock
The initial assessment aims not only to identify the
presence of shock but also the causes.
Sonography (eFAST) can quickly reveal the cause of
shock in the haemodynamically unstable patient.
eFAST helps to target the resuscitation of the critical
patient towards the affected cavity (see chapter
2,4 and 6). This allows an early decision regarding
damage control surgery. In abdominal trauma, free
fluid indicates intrabdominal haemorrhage. Common
sources of haemorrhage are a splenic rupture or a
hepatic rupture. Early CT scanning is the investigation
of choice and Whole Body scanning has become part
of the primary survey in many advanced trauma care
systems. There seems to be a survival benefit if carried
out immediately on admission.
Damage control resuscitation
In cases of ongoing, uncontrollable bleeding, the
team leader will also have to assess the need for
damage control resuscitation; a combined process of
controlled hypotension, haemostatic resuscitation,
damage control surgery and interventional radiology
(figure 5.4). There are three main types of patients who
may require this approach.
Damage Control Resuscitation
Hypotensive Haemostatic Damage Damage
Resuscitation Resuscitation Control Control
Surgery Radiology
Figure 5.4 Damage control resuscitation
CHAPTER 5 SHOCK | 71
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1. Penetrating trauma
Patients with penetrating trauma and minimal tissue
damage may have ongoing haemorrhage into a body
cavity that cannot be controlled externally. Although
aggressive resuscitation with rapid infusion of a large
volume of fluid tends to raise arterial blood pressure,
there may be adverse effects, such as dislodgement of
an effective thrombus and a dilutional coagulopathy,
leading to further haemorrhage. The priority in
these patients is emergency haemostasis either
surgically (damage control surgery) or radiologically,
depending on the site of haemorrhage and local
facilities. Only essential investigations should be
performed in order to minimize any delay in starting
surgery/interventional radiology, thereby reducing
the period of shock. Providing there is no head injury,
fluid resuscitation prior to any intervention should
be limited to achieving a blood pressure sufficient to
maintain organ viability in the short term; a systolic
blood pressure (SBP) of 80-90mmHg is an appropriate
target. Hypotensive Resuscitation is only a short term
measure whilst haemorrhage is controlled. As soon
as it is, the patient should be further resuscitated,
aiming to restore normal oxygen delivery and
haemodynamics.
2. Blunt trauma
This typically gives rise to soft tissue and/or bony
injuries which requires investigations (x-rays,
sonography, CT scan). As described previously, the
presence of a low BP in this group of patients is an
indication of the need for more active treatment in
order to limit cellular damage and prevent the later
development of an inflammatory response syndrome
and multi-organ failure. In the absence of a head
injury, these patients may benefit from hypotensive
resuscitation using a target SBP of 80-90mmHg.
3. The complex patient - Traumatic Brain and Spinal
Cord Injuries
When a patient has both traumatic brain injury
and significant, uncontrollable haemorrhage, it is
reasonable to aim for a MAP > 80mmHg (or SBP around
100mmHg) in the short term, as mortality is significantly
increased in patients with traumatic brain injury
who have even brief periods with a SBP < 90mmHg.
Surgical/radiological control of the bleeding should
then be achieved in the shortest time possible. The
resuscitation of the head injury then takes precedence
and most authorities agree that the aim is for a MAP
> 90mmHg. When monitoring of intracranial pressure
is in place, blood pressure should be titrated to achieve
an adequate cerebral perfusion pressure.
Patients with isolated traumatic brain or spinal cord
injury represent another group where different
specific goals are now used to guide resuscitation
efforts. Some patients will present with hypertension
and a relative bradycardia. This elevation of the
72 | EUROPEAN TRAUMA COURSE
blood pressure is an indication of raised intracranial
pressure and an attempt by the body to maintain
cerebral perfusion. No action should be taken to
lower it. Isotonic fluids should initially be given
at a normal maintenance rate. Otherwise, the
aim should be for a SBP > 110mmHg, a MAP of
> 90mmHg, or normotension for the patient if known
to be hypertensive. The same targets apply to patients
with isolated spinal cord injury.
Assessing the patient’s response to fluid
resuscitation
Essentially, there are three possible outcomes:
The patient is improving
This suggests that the combined effect of the body’s
compensatory mechanisms and the rate of fluid input
are greater than the rate of blood loss. Such patients
may require PRBCs later but this can wait for a full
crossmatch. Vital signs should be monitored closely and
the team leader informed of any sudden deterioration.
The patient initially improves, then deteriorates
In these cases the rate of bleeding has increased
either because of a new source of bleeding or loss
of haemostasis at the original site. The latter may be
a result of excessive resuscitation and rise in blood
pressure. These patients require urgent surgical
assessment with the majority needing surgery or
interventional radiology. Blood (usually as PRBCs)
is also required, the choice being between group O,
type specific or fully crossmatched. Blood will need
to be transfused in a balanced manner with FFP and
platelets and regular checking of clotting. The ongoing
management decision will depend on the clinical state
of the patient and results of investigations.
The patient does not improve
These patients are either bleeding faster than fluids
and/or blood are being given or they are not suffering
from hypovolaemic shock alone but there is a co-
existing cause e.g. cardiogenic or neurogenic shock.
Aspects of the history, examination and vital signs are
essential to distinguish between these possibilities.
Those suffering massive ongoing haemorrhage
will require urgent intervention with ongoing
resuscitation. This is often referred to as ‘damage
control surgery’. For this group of patients, activation
of the major haemorrhage protocol, with early use of
balanced transfusion, correction of coagulopathy and
prevention or treatment of hypothermia is vital. The
principles are summarised in figure 5.5. If available this
can be informed by the use of thromboelastography
or thromboelastrometry. The aim is to deliver products
in a ratio that approximates whole blood, ensuring
that there are adequate clotting factors and platelets.
Trauma Induced Coagulopathy (TIC) is characterised
by depletion of fibrinogen and early substitution of
fibrinogen improves survival.
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Surgical and radiological management of
haemorrhage –‘damage control surgery
and radiology’
Damage control surgery seeks to control
haemorrhage with minimal intervention whilst there
is ongoing resuscitation, rewarming and correction
of any coagulopathy. It is not in a patient’s immediate
best interest to undergo prolonged, definitive
general or orthopaedic surgery while they are cold,
coagulopathic and acidotic. Surgery concentrates
on debridement and external fixation of fractures,
haemostasis and stapling of perforated bowel,
peritoneal lavage, packing and delayed closure of the
abdomen (laparostomy). The patient is then taken to
the ICU where they are stabilized, following which
further surgical procedures can be planned.
Interventional radiology in the trauma patient
Once appropriate imaging has located the source
of bleeding a decision should be made as to the
best way to proceed; non-operative management,
interventional radiology, damage control surgery, or a
combination (table 5.3). It is essential that the members
of the trauma team (including the interventional
radiologist and surgeon) decide upon the best
management for the patient based on all the available
information, both clinical and logistical.
TABLE 5.3
Comparison of management of the trauma patient
Site of trauma Non-operative
Thoracic aorta No role except in small partial
thickness tears
Abdominal aorta No role
Kidney Subcapsular or retroperitoneal
haematoma without active arterial
bleeding
Spleen Lacerations, haematoma without
active bleeding or evidence of false
aneurysm
Liver Subcapsular or intraperitoneal
haematoma or lacerations without
active arterial bleeding
Pelvis Minor injury with no active bleeding
Intestine Focal contusion with no evidence of
ischaemia,
perforation or haemorrhage
Major haemorrhage protocols
Most current protocols involve giving PRBCs and FFP
at between a 1:1 and 2:1 ratio, along with appropriate
amounts of platelets. Checking of fibrinogen levels
and giving cryoprecipitate or fibrinogen concentrate
is important to provide a substrate for effective clot
strength. This approach ensures that resuscitation with
blood products is haemostatic and contributes as little
as possible to the development of coagulopathy. The
point at which FFP and platelets are given will depend
on local protocol, but most units will have a regime
similar to that outlined in (Table 5.3 and figure 5.5).
Tranexamic acid
Tranexamic acid should be given to any patients, who
have or are at risk of major haemorrhage, as part of
their resuscitation provided this is within three hours
of injury. It can be safely given to patients who also
have a head injury, but is not indicated if this is the only
injury. The adult loading dose of 1g is given over 10
minutes followed by an infusion of 1g over eight hours.
Coagulopathy in trauma
The significance of coagulopathy in trauma is often
underestimated with over one-third of civilian and
military trauma patients having deranged clotting on
admission to the resuscitation room. All trauma patients
Interventional radiology Damage control surgery
Stent graft for suitable lesions Ascending aortic injury or arch
injury involving great vessels
Occlusion balloon, stent graft for Injury requiring visceral revasculari-
suitable lesions sation or untreatable by endovas-
cular aneurysm repair
Active arterial bleeding: Renal injury in association with
embolisation or stent graft multiple other bleeding sites or
other injuries requiring urgent
surgical repair
Active arterial bleeding or false Packing or splenectomy for active
aneurysm: bleeding in association with
• focal embolisation for local multiple other bleeding sites
lesion,
• proximal embolisation for diffuse
injury
Active arterial bleeding: Packing if emergency laparotomy
• focal embolisation if possible, needed with subsequent repeat CT
• non selective embolisation if and embolisation if required
multiple bleeding sites as long as
portal vein is patent
Focal embolisation for arterial External fixation and
injury (bleeding, false aneurysm or subsequent packing if bleeding
cut-off) from veins or bones
Focal bleeding with no evidence Ischaemia or perforation requiring
of ischaemia or perforation. Or, to laparotomy ± bowel resection
stabilise patient, allowing interval
laparotomy pending treatment of
other injuries
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Major Trauma?
Major Haemorrhage? Then...

Tranexamic Acid Q If not given pre-hospital, administer to the bleeding

trauma patient if within 3 hours of injury, or continued

T hyperfibrinolysis:
Q1 g bolus, followed by

Q1 g infusion over 8 hours

Resuscitation QActivate Major Haemorrhage Protocol

QInitial Transfusion Ratio 1:1:1 and consider:

R QRapid infuser and cell salvage

QTime-Limited hypotensive resuscitation

QPelvic binder / splint fractures / tourniquet

QAvoid crystalloid use

Avoid Hypothermia Q Target temperature > 36°C

A QRemove wet clothing and sheets

QWarm blood products / fluids

QUse warming blanket / mattress

Unstable? QIf unstable, coagulopathic, hypothermic or acidotic,

Damage Control perform damage control surgery of:

U Surgery
QHaemorrhage control, decompression,

decontamination and splintage

QAim surgery time < 90 minutes and conduct regular

‘surgical pauses’
Metabolic QPerform regular blood gas analysis

M QBase excess guides resuscitation

QIf lactate > 5mmol/L or rising, consider stopping surgery,

splint and transfer to ICU

Avoid Q Inappropriate use of vasoconstrictors doubles mortality

A Vasoconstrictors Q However, use may be required in cases of spinal cord or

traumatic brain injury

Test Clotting QCheck clotting regulary and target transfusion:

QL aboratory or point of care (TEG/ROTEM)

T QAim platelets > 100x10 /L

QAim INR & aPTTR ) 1.5

QAim fibrinogen > 2g/L

9

Imaging QConsider:

I QCT: Most severely injured / haemodynamically unstable

patients gain most from CT
QInterventional radiology

Calcium QMaintain ionised Ca2+ > 1.0 mmol/L

C QAdminister 10mls of 10% Calcium Chloride over 10 mins

as required

Figure 5.5 Major haemorrhage protocol

Copyright: L May, A Kelly, M Wyse

must have their PT, aPTT, platelets and fibrinogen The targets to achieve in the bleeding trauma patient
measured, along with an arterial blood gas, serum include:
lactate and ionised calcium. Increasingly, point of care QHb 7 – 9g/dl;

Qplatelets >100 x 10 /l;

9
coagulation monitoring using thromboelastography
(TEG) or rotational thromboelastometry (ROTEM) is Qfibrinogen >1.5-2.0g/l;
proving useful in guiding rapid identification and Qionised calcium >0.9mmol/l.
correction of coagulopathy in the acute phase. The
cause of coagulopathy is multi-factorial (figure 5.6).
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Hypothermia Acidosis Giving fluids
Decreased
calcium
Platelet Impaired Decreased
dysfunction clotting factor platelet
function concentration
Coagulopathy
Figure 5.6 Trauma Induced Coagulopathy. TPA = Tissue Plasminogen Activator
Patients on anticogulants and
Anti-Platelet-Medication (APM)
Therapeutically anticoagulated bleeding trauma
patients, should have their anticoagulation reversed
promptly. The early use of prothrombin complex
concentrate (PCC) is recommended for the emergency
reversal of vitamin K dependent oral anticoagulants.
PCC also mitigates life-threatening post-traumatic
bleeding in patients treated with novel oral
anticoagulants (NOAC).
Idarucizumab (5 g intravenously) is recommended for
the emergency reversal of dabigatran.
Patients on anti-platelet medication are at high risk of
major haemorrhage after trauma. The effect of these
drugs can only be reversed by platelet transfusion.
DDAVP can be used additionally at a dose of 0.4 mcg/
kg. It is important that the use of such medications is
sought when taking an AMPLE history.
Monitoring the shocked patient
The overview above is aimed at maintaining the
function of the vital organs whilst haemostasis is
achieved. However patients are often complex and
may not fit neatly into the categories described. A
further problem is that non-invasive vital signs used
initially become increasingly imprecise and unreliable
as the severity of shock increases. This is particularly
true of non-invasive blood pressure measurement
and heart rate. Consequently invasive arterial pressure
monitoring should be considered at an early stage in
the resuscitation of patients with significant trauma.
This allows more accurate and continuous monitoring
of the patient’s blood pressure and repeated sampling
of blood for markers of cellular hypoxia, including
serum lactate, pH and base excess.
Accurate measurement of urine output will obviously
require the insertion of a urinary catheter with the volume
recorded whenever the other vital signs are measured.
Giving PRBCs Clot formation Tissue injury
Dilution Platelet Clotting factor Release of TPA
consumption consumption
Decreased Increased
clotting factor fibrinolysis
concentration
The patient’s core temperature also needs to be
monitored. Throughout the resuscitation efforts
should be made to avoid heat loss by minimizing the
patient’s exposure and using warmed IV fluids, patient
covers and active warming devices.
Completion of the primary survey
By the end of the primary survey, the team leader must
ensure that the required tasks have been completed
or are being carried out. Analysis of an arterial blood
gas sample should be available at this stage. Metabolic
acidosis is invariably a result of anaerobic metabolism in
poorly perfused tissues. Management consists of oxygen
delivery by early use of blood products and, optimising
PaO2, and achieving normothermia. Patients with a
persistent acidosis may require intubation and controlled
ventilation. Sodium bicarbonate is rarely required
and is generally reserved for cases of immediately
life-threatening acidosis in the presence of adequate
perfusion and ventilation. As described in chapter 2 the
primary survey concludes with the planning round and
the secondary survey if the patient does not require any
further immediate intervention.
Traumatic cardiac arrest
As described in chapter 2, one objective of the
5-second round is to confirm that the patient still has
a cardiac output. If not, this triggers a rapid change in
priorities and team tasks. If the patients presents in
traumatic cardiac arrest (TCA) or periarrest the TCA
algorithm applies as described in chapter 5c.
CHAPTER 5 SHOCK | 75
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the laboratory for routine bloods and used for

Summary bedside glucose estimation.
QInject a small volume of local anaesthetic to ease

All members of the trauma team must recognize the pain caused by injection.
and initiate treatment in shocked patients as early QFlush the system with 20ml saline to clear any

as possible. In trauma, the cause of the shock is debris or clot.

frequently multifactorial but will invariably have QFluids need to be given in boluses. This is easiest

a hypovolaemic component. Tissue hypoxia
is minimized by early assessment, constant
monitoring and appropriate interventions.
Regular reassessment is essential as any
subsequent deterioration needs to be detected
to achieve using a syringe and three-way tap.
The flow rates under gravity alone are not high enough
for resuscitation.
QIntraosseous lines need to be replaced by venous

quickly and treated. In addition as the patient cannulation as soon as possible.

improves, other problems may become apparent.
Complications:
These cognitive abilities will be integrated with Qextravasation;

the practical skills during the course workshops. Qsubperiosteal infusion;

Qfat and bone marrow embolism;

Qosteomyelitis;

Further information Qdamage to the growth plate and cortex;

Qpain and subcutaneous oedema;

Q Rossaint R, Bouillon B, Cerny V et al. The European

guideline on management of major bleeding and
coagulopathy following trauma: fourth edition. Crit
Care 2016;20:100
Q The Royal College of Radiologists. Standards of practice

and guidance for trauma radiology in severely injured

patients, Second edition. London: The Royal College of
Radiologists, 2015.
Q Gruen RL, Reade MC. Administer tranexamic acid early

to injured patients at risk of substantial bleeding. BMJ

2012 Nov 19;345:e7133 doi: 10.1136/bmj.e7133

Skills Figure 5.7 Insertion of an IO needle into the proximal humerus

Insertion of an intraosseous needle Application of a pelvic binder

The greater tubercle of the humerus is the primary This skill is described in detail in chapter 7.
intrasseous access site in adults and older children.
This site allows for the highest flow rates and avoids
the risk of compartment syndrome. Fractured bones
should be avoided

Technique:
QThe patient’s hand should rest palm down on the

their abdomen with the elbow adducted

QSlide thumb up the anterior shaft of the humerus

until you feel the greater tubercle, this is the

surgical neck
Q~ 1 cm above the surgical neck is the insertion site.

QThe needle is inserted 90° to the skin and

advanced until the bone is reached.

QThe drill is then activated and gentle pressure

applied until a ‘give’ is felt as the cortex is

penetrated.
QRemove the trocar and attach a syringe via a short

extension. Correct placement is confirmed by

aspiration of marrow content and easy infusion
of fluid. The aspirated sample can be sent to

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5b.
Injuries due to burns
Learning outcomes
Following this part of the course you will be able to demonstrate competence in:
QCarrying out a primary survey and initial resuscitation of a burned patient

QCalculation of percentage of body surface area burned

QCalculation of fluid resuscitation requirements for patients with burns

QUnderstanding which patients need referral to a specialist burns centre

QBasic principles of transferring burns patients

Introduction Airway, cervical spine control and breathing

Significant burns typically result from exposure to
flames, with scalds being the next most common
cause; electrocution and chemical injuries occur rarely.
In the UK, Emergency Departments see an estimated
Assessment of the airway may reveal early signs of
inhalational injury.
History:
Qexposure to fire and/or smoke in an enclosed space;

175,000 burn patients per year, around 10% require Qexposure to a blast;

admission, and approximately 300 die. The incidence Qcollapse, confusion or restlessness at any time.

is similar in many European countries, are higher in

the United States, with developing countries having Signs and symptoms:
the highest mortality rate. The definitive care of burns Qhoarseness or other voice changes;

is complex and requires a multidisciplinary team Qharsh cough;

approach with specialised involvement. Although Qstridor;

all large burns should be cared for in burns centres, Qfacial burns;

the management of the patient must start from the Qsinged nasal hair;

initial contact because early treatment can have a Qsoot in saliva or sputum;

major effect on outcome. It is important to remember Qan inflamed or swollen oropharynx.

that patients may also have other injuries and need

accurate assessment, careful initial resuscitation and Investigations:
rapid transfer to specialist care. Although the latter Qraised carboxyhaemoglobin levels;

is important, adequate resuscitation and careful Qrespiratory failure.

preparations take precedence.

Primary survey and resuscitation
A full primary survey using the sequence described
in chapter 2 needs to be carried out on arrival. This
will identify any immediately life-threatening injuries.
A more thorough assessment of the burns can be
undertaken later.
The signs and symptoms from airway oedema and
pulmonary injury may take from minutes to hours to
develop. Therefore the key to diagnosis is having a high
index of suspicion with the frequent re-evaluation of
those considered to be at risk.
All patients should be given high flow oxygen, preferably
humidified. Signs of upper airway obstruction,
particularly stridor, indicate the need for early assessment

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by an experienced anaesthetist. The safest option is
usually early tracheal intubation as swelling will increase
over the first few hours, making this task progressively
more difficult. In severe cases a surgical airway may be
required. Tracheal intubation may also be required in
those patients with significant lung injury to optimise
ventilation and, on the rare occasion of circumferential
chest burns restricting inspiration.
The cervical spine must not be overlooked, particularly
when the mechanism of injury suggests that it may
be injured. The classic case would be where the burn
victim in a house fire jumps from an upper floor and
has spinal injuries from the impact of the fall.
Circulation and haemorrhage control
Hypovolaemic shock due to burns takes time
to develop. Therefore signs of shock in the
resuscitation room will not be due to the burn. The
team must look for another cause. The mechanism
of injury may give clues as to the possibility of other
trauma (e.g. a fall whilst escaping a fire) and the patient
managed as described in chapter 5, irrespective of the
burns. Intravenous access is achieved using two large
bore cannulas. Although it is acceptable to insert a
cannula through burnt skin, this should be avoided
if possible. A preferred option in these circumstances
would be using the central veins or the intraosseous
route. When blood is sent for laboratory baseline
investigations carboxyhaemoglobin levels should be
included where an inhalation injury is suspected.
blood gas analysis and a chest x-ray are also essential.
These provide an important baseline as the patient
may deteriorate from an initially normal state. There is
no evidence that giving steroids is beneficial.
The cutaneous burn
Regardless of the cause of the burn, the severity of the
injury is proportional to the volume of tissue damaged.
Mortality is predicted by the percentage of total body
surface area (% TBSA) burned. Functional outcome is
more often dependent on the depth and site of the burn.
Calculating the percentage of total body surface
area burned
There are several techniques for calculating the %
TBSA. Initial assessment can be made with the ‘rule of
nines’ or a serial halving technique. The former divides
the body into multiples of nine (figure 5b.1). Serial
halving assesses burn size on the basis of asking the
question ‘is half of the body burned?’ If not, ‘is it half of
that?’ and so on until an estimate is achieved.

Disability
Reduced level of consciousness, confusion and
restlessness may occur with hypoxia secondary to an
inhalation injury. However, the possibility of alcohol or
drug ingestion and the presence of other injuries must
also be considered.

Exposure and environmental control

Clothing and any restricting items need to be removed.
However this action and the use of cold water at
the scene, during transfer and in the Emergency
Department often leads to hypothermia. This can be
minimized by covering uninvolved areas and raising Figure 5b.1 The ‘rule of nines’; the body surface is divided into
the ambient temperature to ideally 30°C. regions each equating to approximately 9% of the total surface
area.

Management of thermal burns

Inhalation injury
As described already intubation and ventilation are the
mainstay of early management because the burned
airway can become compromised at a rate that is
difficult to predict. Patients with suspected inhalation
injuries require close observation in an area equipped
for immediate intubation and should be accompanied
by an experienced anaesthetist until arrival at the
receiving burns centre. Pulse oximetry readings
should be interpreted with caution, especially in the
presence of carboxyhaemoglobinaemia. Arterial
A more accurate method is by using the Lund and
Browder chart (figure 5b.2). The burnt areas, ignoring
erythema, are drawn onto the chart and then the %
TBSA burnt is calculated. In very large burns it can
be easier to calculate the size of area not affected.
At this stage differentiating between full and partial
thickness burns is not essential. The palmar surface of
the patient’s hand including the fingers equates to 1%
TBSA and can be used to estimate small areas of burn.

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When the patient has additional significant injuries, or

LUND AND BROWDER CHART
The numbers represent % TBSA.
Letters are age dependent: see chart.
the % TBSA is greater than 15%, blood in addition to
the calculated volume of crystalloid may be required.
Management of the thermal burn wound
Effective burn care aims to achieve maximum
functional and cosmetic outcome. Apart from small
superficial burns, wound management should be
performed in a burns centre. After the affected area is
cooled and dressed there are rarely any indications for
further interventions before transfer.

Initial treatment
Dressing the wound can be achieved by loosely covering
the burn with plastic film. Hands can be placed in plastic
bags. The patient should then be kept warm with dry
blankets. Further accurate assessment of the wound
can take place at the burns centre after transfer. Topical
antiseptic solution and creams should not be applied.

Escharotomy
A circumferential full thickness burn can act like a
tourniquet and compromise the distal circulation.
Surgical division of the constriction is known as
Area Age 0 yr 1 yr 5 yr 10 yr 15 yr Adult escharotomy. There is rarely a need to perform this
A=½ head 9 ½ 8½ 6½ 5½ 4½ 3½
procedure within the first few hours, the exception
being a full thickness burn of the entire trunk that is
B=½ thigh 2 ¾ 3¼ 4 4½ 4½ 4¾
compromising ventilation. If this is carried out, note
C=½ leg 2½ 2½ 2¾ 3 3¼ 3½ that the wounds can bleed excessively as the incision
is down to areas of vascularity. Crossmatching blood
Figure 5b.2 Lund and Browder chart allows accurate calculation of for the patient, if not already done, is essential.
the % TBSA burned adjusted for age
Other initial interventions
Fluid resuscitation Ensure immunity against tetanus. In the absence of any
Any burn greater than 10% TBSA in a child, or 15% TBSA specific indications such as associated contaminated
in an adult, will require intravenous fluids to prevent wounds, there is no requirement for antibiotic
the development of burn shock. There are various prophylaxis at this stage. In contrast a nasogastric
formulae available to calculate fluid requirements, the tube and urinary catheterisation will be needed
Parkland formula is commonly used: in all patients with complex burns. As superficial
and deep dermal burns are painful, adequate pain
2-4ml Hartmann’s solution x % TBSA burned relief is a priority from an early stage. In addition to
x humanitarian reasons, pain leads to catecholamine
body weight (kg) release and may increase peripheral ischaemia and,
potentially, burn depth. Intravenous opiates should be
Use the higher value of 4ml initially. Weigh the patient given until the patient is comfortable.
or ask his/her weight as estimates are often inaccurate.
A child’s weight can be obtained by using a recognized Transfer to definitive care
formula (see chapter 11) or a Broselow tape. Half this In all cases, early contact should be made with a burns
calculated volume is given in the first eight hours from centre so that advice on initial management and
the time of injury and the second half over the next transfer can be given. The team leader needs to be
sixteen hours. Consequently many patients will already aware of the guidelines for referral taking into account
be behind with requirements by the time they arrive in the size of the burn, other indicators of complexity and
the resuscitation area. In addition, allowance has to be local policies. In most countries, all complex burns are
made for deficit due to other injuries and the patient’s managed in specialised burns centres. The following
normal maintenance fluids. A guide to the adequacy of is a guide to the types of complex burns that should
fluid resuscitation is the patient’s urine output (usually receive specialist attention.
requiring urinary catheterisation) which should be:
Q1ml/kg/h in adults

Q2ml/kg/h in children

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Complex burn injuries Qensure the patient is being kept warm;

A burn is defined as complex if one or more of the Qadequate analgesia;
following criteria are met: Qa urinary catheter in place;

Qage: Qa free draining nasogastric tube;

O u nder 5 or over 60 years. Qall findings and interventions, including fluid

Qarea: balance, are clearly and accurately documented.

O o ver 10% TBSA burnt in adults;

O o ver 5% TBSA burnt in children.
Qsite:
O f ace, hands, perineum or feet;
O a ny flexure, particularly the neck or axilla;
O a ny circumferential dermal or full thickness
If it is likely that a delay in transfer will exceed six
hours then the situation needs to be discussed further
with the burns centre. In this circumstance it may be
deemed necessary for:
Qescharotomies to be performed;

burn of the limbs, torso or neck. Qthe burn wound to be cleaned and a specific

Qinhalation injury: dressing applied;

O a ny significant inhalation injury, excluding pure Qthe commencement of maintenance intravenous

carbon monoxide poisoning. fluids and/or nasogastric feeding.

Qmechanism of injury:

O high pressure steam injury;

O h igh voltage electrical injury; Summary

O c hemical injury >5% TBSA burnt;
O h ydrofluoric acid injury (>1% TBSA burnt);
O suspicion of non-accidental injury, adult or
paediatric.
Qpre-existing medical conditions:
O c ardiac disease;
O respiratory disease;
O d iabetes mellitus;
O p regnancy;
O i mmunosuppression of any cause;
O h epatic impairment, cirrhosis.
Qassociated injuries:
Although burns patients comprise a small
proportion of trauma patients, they can be
distressing to the inexperienced and distract
from other serious underlying injuries. For this
reason, management begins with a full primary
survey to identify and treat life-threatening
injuries, whether or not caused by the burns.
Subsequently a more detailed assessment of
the burns can be made along with discussion
with burns experts. Appropriate management of
those requiring transfer can then be organised.

O c rush injuries;

O m ajor long bone fractures;

O h ead injury;

O p enetrating injuries.

Associated injuries may sometimes delay referral of

the patient; in these circumstances advice about burns
management should be sought.

Preparations for transfer

Once the decision to transfer a patient to a burns centre
is made, preparations for safe transport should begin.
Distance to the nearest burns bed and method of
transfer will vary both within and between countries.
With some longer distance transfers, rotary or even
fixed wing aircraft may be required. The principles of
safe transfer are covered in chapter 12. Features specific
to the safe transfer of the burned patient include:
Qa thorough secondary survey to identify and

manage any other injuries;

Qensure adequate oxygenation and ventilation;

if there is any suspicion of an inhalation injury,

the patient should have been assessed by an
experienced anaesthetist and, if necessary,
intubated;
Qensure adequate, secure IV access and appropriate

fluid resuscitation;
Qcover burns;

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5c.
Traumatic cardiac arrest
Learning outcomes
Following this part of the course you will be able to:
QRecognise Traumatic Cardiac Arrest
QRecognise Traumatic peri-Arrest states
QDemonstrate an understanding of the treatment options
QDemonstrate an understanding of the indications for Resuscitative Thoracotomy (RT)
Introduction
Traumatic cardiac arrest (TCA) carries a very high
mortality, but in those where Return of Spontaneous
Ciruclation (ROSC) can be achieved, neurological
outcome in survivors appears to be much better
than in other causes of cardiac arrest. The response
to TCA is time critical and success depends on a well-
established chain of survival, including advanced pre-
hospital and specialised trauma centre care.
Immediate resuscitative efforts in TCA focus on
simultaneous treatment of reversible causes, which
take priority over chest compressions.
Diagnosis
The diagnosis of traumatic cardiac arrest is made
clinically; the patient presents with agonal or absent
spontaneous respiration and absence of a central pulse.
A peri-arrest state is characterised by cardiovascular
instability, hypotension, loss of peripheral pulses in
uninjured regions and a deteriorating conscious level
without obvious CNS cause. If untreated, this state is
likely to progress to cardiac arrest. e-FAST should be
used in the evaluation of the compromised trauma
patient to help establishing the course of shock and
to target life saving interventions. Haemoperitoneum,
haemo- or pneumothorax and cardiac tamponade
can be diagnosed reliably in minutes, even in the pre-
hospital phase. e-FAST is helpful in the immediate
diagnosis and management, but must not delay
resuscitative interventions.
It is vital that a medical cardiac arrest is not
misdiagnosed as a traumatic cardiac arrest and must
be treated with the universal advanced life support
(ALS) algorithm. Cardiac arrest or other causes of
sudden loss of consciousness (e.g. hypoglycaemia,
stroke, seizures) may cause a secondary traumatic
event. Some observational studies have reported
that ~2.5% of non-traumatic out-of-hospital cardiac
arrests (OHCAs) occur in cars. For a cardiac arrest to be
traumatic, an adequate mechanism has to be present
and the secondary trauma usually is not adequate.
Shockable rhythms (VF/pVT) are more common in
non-traumatic cardiac arrest, whereas PEA or asystole
are more common in traumatic cardiac arrest. The
primary cause of the cardiac arrest can sometimes also
be elucidated from information about past medical
history, events preceding the accident (if possible),
and a systematic post-ROSC assessment, including a
12-lead ECG.
Prognostic factors and
withholding resuscitation
There are no reliable predictors of survival for traumatic
cardiac arrest. Factors that are associated with survival
include the presence of reactive pupils, an organised
ECG rhythm and respiratory activity. Short duration of
CPR and pre-hospital times are also associated with
positive outcomes.
Current overall survival rate are 3.3% in blunt and
3.7% in penetrating trauma, with good neurological
outcome in 1.6% of all cases. Outcome is age
dependent, with children having a better prognosis
than adults. There is considerable variation in reported
mortality (range 0-27%) reflecting heterogeneity
in casemix and care in different systems. Pulseless
electrical activity (PEA), which in TCA may initially be a
low output state, and asystole are the prevalent heart
rhythms in TCA. Ventricular fibrillation (VF) is rare but
carries the best prognosis.
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One study reported good neurological outcome in Treatment

36.4% of patients with VF, but only in 7% with PEA
and 2.7% of those in asystole, but other studies of
patients in non-shockable rhythms have reported
100% mortality.
The prognosis is extremely poor in patients presenting
with apnoea, pulselessness and without organised
ECG activity. However, neurologically intact survivors
initially presenting in this state have been reported.
We therefore recommend the following approach:
Withholding resuscitation in TCA should be considered
in any of the following conditions:
Qno signs of life within the preceding 15 minutes
Qmassive trauma incompatible with survival (e.g.
decapitation, loss of brain tissue)
Termination of resuscitative efforts should be
considered if there is:
Qno ROSC after reversible causes have been
addressed
Qno detectable ultrasonographic cardiac activity
Emphasis on rapid treatment of all potentially reversible
pathology is the basis of treatment guidelines. Figure
5c.1 shows a traumatic cardiac (peri-) arrest algorithm,
which is based on the ERC universal ALS algorithm.
Effectiveness of chest compressions
In cardiac arrest caused by hypovolaemia, cardiac
tamponade or tension pneumothaorax, chest
compressions are unlikely to be as effective as in
normovolaemic cardiac arrest. Therefore, chest
compressions take a lower priority than the immediate
treatment of reversible causes, e.g. controlling
haemorrhage, thoracotomy.
Hypovolaemia
Uncontrolled haemorrhage is the cause of traumatic
cardiac arrest in 48% of all TCA. The main principle
is to achieve ‘haemostasis without delay’, usually with
surgical or radiological intervention. Temporary
haemorrhage control can be lifesaving.
QCompressible external haemorrhage can be treated

Trauma care systems throughout Europe vary with elevation, direct or indirect pressure, pressure
considerably and regional guidelines for treatment dressings, tourniquets and topical haemostatic
of TCA may help tailoring patient pathways to agents.
infrastructure and resources. QNon-compressible haemorrhage is more difficult and

splints (pelvic splint), blood products, intravenous

fluids and tranexamic acid can be used while moving
the patient to surgical haemorrhage control.

Traumatic Cardiac Arrest/Peri-arrest Algorithm

Trauma Patient in Arrest/Peri-Arrest

Non-traumatic Arrest likely? ALS

NO YES

Hypoxemia Address reversible causes

Start CPR

Tension pneumothorax simultaneously:

Tamponade 1. Control external catastrophic haemorrhage
Hypovolemia
2. Secure airway and maximise oxygenation
3. Bilateral chest decompression (thoracostomies) Expertise?
4. Relieve tamponade (penetrating chest injury) Equipment?
5. Proximal vascular control (manual aortic compression) Environment?
Elapsed time since loss
6. Pelvic splint of vital signs <10 min?

7. Blood products / Massive Haemorrhage Protocol

YES
8. REBOA

Resuscitative
ROSC? Thoracotomy
YES NO
Pre-hospital: immediate transport
to appropriate hospital Consider termination
In-hospital: damage control surgery of resuscitation
/ resuscitation

Figure 5c.1 The TCA algorithm focuses on the simultaneous treatment of reversible causes

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Over the past ten years the principle of ‘damage
control resuscitation’ (DCR) has been adopted in trauma
resuscitation for uncontrolled haemorrhage (see
chapter 5). DCR also is the guiding treatment principle
in trauma patients who are in a peri-arrest state or have
suffered cardiac arrest. Damage control resuscitation
combines permissive hypotension and haemostatic
resuscitation with damage control surgery. Permissive
hypotension allows intravenous fluid administration
to a volume sufficient to maintain a radial pulse.
Haemostatic resuscitation is the very early use of blood
products as primary resuscitation fluid to prevent
exsanguination and trauma-induced coagulopathy.
The recommended ratio of Packed Red Cells, Fresh
Frozen Plasma and Platelets is 1:1:1. Some services have
also started using blood products in the pre-hospital
phase of care.
Recent evidence suggests that Resuscitative
Endovascular Ballon Occlusion (REBOA) improves
survival in exsanguinating torso injuries. REBOA as
a temporary damage control procedure is a bridge
to surgical repair. REBOA can be carried out with
an embolectomy catheter advanced into the aorta
through a groin access to the femoral artery. Reduction
in blood flow below the balloon reduces perfusion
to the hemorrhagic focus. Thoracic aortic occlusion
(Zone I) can control bleeding from an abdominal
source, whereas infra-renal occlusion (Zone III) can
help controlling pelvic hemorrhage. REBOA is high-risk
procedure with the potential to cause fatal ischemic
damage to organ systems below the occlusion. Zone I
occlusion should not be longer than 30 minutes whereas
Zone III occlusion can be tolerated up to two hours.
Simultaneous damage control surgery and
haemostatic resuscitation using massive transfusion
protocols (MTP) are the principles of damage control
resuscitation in patients with exsanguinating injuries.
Hypoxaemia
Hypoxaemia due to airway obstruction and traumatic
asphyxia has been reported as cause of traumatic
cardiac arrest in 13% of all cases. Effective airway
management and ventilation can reverse hypoxic
cardiac arrest and it is essential to establish oxygenation
of the severely compromised trauma patient.
Tracheal intubation in trauma patients is a difficult
procedure with a high failure rate if carried out by less
experienced care providers. Basic airway manoeuvres
and second-generation supraglottic airways can be
used to maintain oxygenation if tracheal intubation
cannot be accomplished immediately.
Positive pressure ventilation worsens hypotension by
impeding venous return to the heart, particularly in
hypovolaemic patients. Low tidal volumes and slow
respiratory rates may help optimise cardiac preload.
Ventilation should be monitored with continuous
waveform capnography and adjusted to achieve
normocapnia.
Tension pneumothorax
Thirteen percent of all cases of TCA are caused by
tension pneumothorax.
To decompress the chest in TCA, perform bilateral
thoracostomies in the 4th intercostal space, extending
to a clamshell thoracotomy if required. In the presence
of positive pressure ventilation, thoracostomies are
likely to be more effective than needle thoracocentesis
and quicker than inserting a chest tube.
Cardiac tamponade and resuscitative
thoracotomy
Cardiac tamponade (chapter 4) is the underlying cause
of approximately 10% of cardiac arrest in trauma.
Where there is traumatic cardiac arrest and penetrating
trauma to the chest or epigastrium, immediate
resuscitative thoracotomy (RT) (via a clamshell incision,
Fig 5 c2) can be life saving. The chance of survival is
about 4 times higher in cardiac stab wounds than in
gunshot wounds.
Figure 5c.2 Resuscitation room emergency clamshell thoracotomy
Resuscitative thoracotomy is also applied for other
life threatening injuries; after arrival in hospital,
the decision to proceed with RT should include the
following criteria:
TABLE 5C.1
Indications for Resuscitative Thoracotomy
Q Penetrating torso trauma patients with less than
15 minutes of CPR
Q Patients with penetrating trauma to the neck or extremity
with less than 5 minutes of pre-hospital CPR
Q Blunt trauma patients with less than 10 minutes
of pre-hospital CPR
Q Peri-arrest state in patients with chest injuries refractory
to resuscitation
Survival rates for RT are approximately 15% for all
patients with penetrating wounds and 35% for patients
with a penetrating cardiac wound. In contrast, survival
from RT following blunt trauma is dismal, with survival
rates of 0 – 2% being reported.
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The prerequisites for a successful RT can be
summarized as “four Es rule” (4E):
QE xpertise: teams that perform RT must be led
by a highly trained and competent healthcare
practitioner. These teams must operate under a
robust governance framework.
QEquipment: adequate equipment to carry out RT and
to deal with the intrathoracic findings is mandatory.
QEnvironment: ideally RT should be carried out in an
operating theatre. RT should not be carried out if
there is inadequate physical access to the patient,
or if the receiving hospital is not easy to reach.
QElapsed time: the time from loss of vital signs to
commencing a RT should not be longer than 10
minutes
If any of the four criteria is not met, RT is futile and
exposes the team to risks that outweigh the benefits
The procedure
A bilateral anterior thoracotomy (clamshell incision)
gives access to the entire thoracic contents (figure
5c.2). This allows bleeding to be controlled with direct
pressure and the pericardium opened to evacuate
a tamponade. Internal cardiac compression can be
started and if necessary penetrating cardiac injury can
be made secure with either a stapler or a suture. Aortic
compression is used to redistribute the limited cardiac
output to the brain and myocardium, whilst at the same
time limit any abdominal bleeding while resuscitation
proceeds. The procedural aspects are summarized
in Fig 5c.3. Resuscitative thoracotomy is inevitably
Figure 5c.3 The ten top tips illustrate procedural key points of resuscitative thoracotomy (with kind permission from the ‘The Secret
Chest Cracker’, Jonathan Carter)
84 | EUROPEAN TRAUMA COURSE
associated with significant blood loss; it is therefore
essential that blood products are available and all the
team have appropriate personal protective equipment
(PPE) including eye protection.
Resuscitative Thoracotomy allows for:
Qpericardial incision and evacuation of pericardial
clotted blood causing tamponade;
Qlocal control of cardiac haemorrhage;
Qdirect control of exsanguinating thoracic
haemorrhage; open cardiac compression;
Qcross clamping of the descending aorta to maintain
cardiac and brain perfusion by stopping blood loss
below the diaphragm;
Qdirect repair of exsanguinating pulmonary
haemorrhage;
Qcross clamping of the pulmonary hila in
cases of massive pulmonary haemorrhage or
bronchovenous air embolism.
Pre-hospital care
Short pre-hospital times are associated with increased
survival rates for major trauma and traumatic cardiac
arrest. The time elapsed between injury and surgical
control of bleeding should therefore be minimised
and the patient should be immediately transferred to a
Trauma Centre for ongoing damage control resuscitation.
‘Scoop and run’ for these patients may be life saving.
Personal copy of eduard_razvan_toplicianu@yahoo.com [89962]

Key Points TCA: Summary

QFollow ALS guidelines if underlying medical Having worked through this chapter, you are now
cause of TCA is suspected ready to apply the following knowledge in the
QIf TCA is confirmed, identify and treat reversible shock workshop:
causes simultaneously without delay Qhow to assess, manage and monitor trauma

QIf indicated Resuscitative Thoracotomy is part victims with shock;

of the primary survey and should be carried out Qwhen to apply the principles of haemostatic

without delay provided the ‘Four E’ criteria are resuscitation;

met. Qthe indications for activating the major

haemorrhage protocol;
Qunderstand how medical conditions can
Suggested Readings complicate shock management;
Qhow to assess, manage and monitor burned

QWise D, Davies G , Coats T, Lockey D, Hyde L, Good victims.

A Emergency thoracotomy: "how to do it". Emerg Qhow to assess and mange patients in traumatic

Med J 2005 Jan;22(1):22-4. cardiac arrest

QTruhlář A, Deakin CD, Soar J, Khalifa GE, Alfonzo These cognitive abilities will be integrated with
A, Bierens JJ, Brattebø G, Brugger H, Dunning the practical skills during the course workshops.
J, Hunyadi-Antičević S, Koster RW, Lockey DJ,
Lott C, Paal P, Perkins GD, Sandroni C, Thies KC,
Zideman DA, Nolan JP; Cardiac arrest in special
circumstances section Collaborators. European
Resuscitation Council Guidelines for Resuscitation
2015: Section 4 .Cardiac arrest in special
circumstances. Resuscitation. 2015 Oct; 95:148-201.
QKleber C, Giesecke MT, Lindner T, Haas NP,

Buschmann CT Requirement for a structure

algorithm in cardiac arrest following major
trauma: Epidemiology, management errors,
and preventability of traumatic deaths in Berlin.
Resuscitation. 2014 Mar;85(3):405-10
QManzano Nunez R, Naranjo MP, Foianini E, Ferrada

P, Rincon E, García-Perdomo HA, Burbano P,

Herrera JP, García AF, Ordoñez CA. A meta-analysis
of resuscitative endovascular balloon occlusion of
the aorta (REBOA) or open aortic cross-clamping
by resuscitative thoracotomy in non-compressible
torso hemorrhage patients. World J Emerg Surg.
2017 Jul 14;12:30

CHAPTER 5 SHOCK | 85