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haemorrhage, adrenalectomy, Addison’s disease2, pituitary apoplexy (with loss of adrenocorticotrophic hormone, ACTH) or lack of corticosteroid replacement in
patients who have been on long-
Failure of aldosterone secretion results in volume
depletion and glucocorticoid deficiency, which
impairs autonomic responses. The ability to respond
to minor stress is severely compromised and may provoke an Addisonian crisis characterized by bradycardia and postural hypotension, which is responsive to
corticosteroid replacement. Adrenocortical failure
should be considered, and a bolus of hydrocortisone
given in all patients with unexplained hypotension.
term glucocorticoids.
Sympathetic interruption
This reduces the effective blood volume by widespread vasodilation. It follows transection of the
pinal cord (spinal shock), but may also occur after a
s
high spinal anaesthetic or thoracic epidural. It is not
unusual for patients undergoing open oesophagectomy with thoracic epidural to have vasopressor support to help perfusion of the anastomosis while
having epidural for analgesia.
The vasovagal syndrome (faint)
The vasovagal syndrome is produced by severe pain or
emotional disturbance, leading to vagal stimulation. It
is the result of reflex vasodilation together with cardiac
slowing owing to vagal activity. Hypotension is caused
by a fall in cardiac output due to both bradycardia and
reduced venous return, the latter being the result of
peripheral vasodilation. Clinically, it is recognized by
the presence of a bradycardia and responds to the simple measure of laying the patient flat with elevation of
the legs leading to less pooling and adequate preload.
Septic shock
Shock may be produced as the result of severe infection from either Gram- positive or, more commonly,
Gram-
negative organisms. The latter are seen particularly after colonic, biliary and urological surgery,
and with infected severe burns. The principal effect of
endotoxins is to cause vasodilation of the peripheral
circulation together with increased capillary perme-
2
omas Addison (1793–1860), Physician, Guy’s Hospital,
London, UK. His original specimens may still be seen in the
Gordon Museum at Guy’s Hospital.
ability. The effects are partly direct and partly due to
activation of normal tissue inflammatory responses
such as the complement system and release of
cytokines such as tumour necrosis factor (TNF). If
sepsis is identified, it is paramount to address this
with the Sepsis 6 approach (oxygen, fluid, antibiotics,
blood culture, blood tests including lactate and urine
output) in the early stages in order to prevent clinical
deterioration.
Disseminated intravascular coagulation (DIC)
results from activation of the clotting cascade and
may lead to blockage of the arterial microcirculation
by microemboli. Fibrin and platelets are consumed
excessively, with resultant spontaneous haemorrhages into the skin, gastrointestinal tract, lungs,
mouth and nose.
Sequelae ofshock
A continuous low blood pressure produces a series of
irreversible changes such that the patient may die in
spite of treatment. The lack of oxygen delivery affects
all the vital organs. The features of hypoperfusion are
as follows:
•
Cerebral hypoperfusion results in confusion or
coma.
•
Cutaneous hypoperfusion in all except septic
shock results in cold, clammy and pale skin.
Renal hypoperfusion results in reduced glomeru-
•
lar filtration, with oliguria or anuria. As renal
ischaemia progresses, tubular necrosis may occur,
and profound ischaemia may lead to cortical
necrosis (Chapter43).
•
Coronary hypoperfusion results in cardiac failure,
arrhythmia and arrest.
• Pulmonary capillaries may reflect the changes in
the systemic circulation with transudation of
fluid, resulting in pulmonary oedema, hampering
oxygen transfer and causing further arterial
hypoxaemia and thus tissue hypoxia. Pulmonary
capillary function may also be impaired following
multiple blood transfusions (transfusionacute lung injury, TRALI) and contusions resulting from chest trauma, a condition known as
acute lung injury (previously termed ‘shock
lung’).
•
Raised lactate occurs as a result of a switch to
anaerobic metabolism in those tissues with
impaired cellular oxygenation.
related
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Principles inthe
management ofpatients
inshock
Assessment
The cause of shock may be clear from the history,
such as overt blood loss from trauma. Following history taking, which of necessity may be rapid, a thorough clinical examination is required to fully appraise
both the cause and degree of shock. This should
include assessment of the skin colour and perfusion,
heart rate and rhythm from the radial artery (or femoral/carotid if the radial is impalpable), blood pressure, jugular venous pulse (raised in cardiogenic and
obstructive shock, seldom visible in hypovolaemia
and sepsis), auscultation of the chest (is there a tension pneumothorax?), heart (quiet sounds of tamponade), and abdomen (peritonitis from diverticular
perforation in septic shock; tender and distended
with rupture aneurysm).
be administered with caution in the presence of
c ardiogenic shock. The nature of the fluid used is
discussed in Chapter3, but crystalloid solutions are
usually first choice unless the patient is actively
bleeding, when blood is the most appropriate
replacement fluid. The rate of fluid administration
should be titrated against the desired response; in a
patient who is shocked from fluid depletion rapid
infusion of 1L (or 20mL/kg) should be given immediately with monitoring for response and titration of
fluid thereafter. Overcause pulmonary oedema, and in patients who have
been bleeding, raising the blood pressure may
prompt further haemorrhage; permissive hypotension may be appropriate in such cases until the
cause of bleeding is addressed. Emphasis should be
on tissue perfusion, and if both the brain and heart
are well perfused with a good Glasgow Coma Score
(GCS) and good cardiac contractility after initial
infusion, further fluid can be closely titrated
accordingly.
Two causes of shock that merit mention for imme-
diate treatment are bleeding and anaphylaxis.
infusion is undesirable; it may
Immediate measures
Treatment is often started while the cause of shock is
being determined. Initial measures and management should include assessing the airway, breathing
and circulation. During airway assessment, 15 L of
oxygen should be administered via a non- rebreathing
mask and fluid resuscitation commenced by giving a
litre of crystalloid or 20 mL/kg immediately (Stat)
(Figure8.2). Once the cause of shock is identified, it
should be reversed as quickly as possible.
Ventilatory support
Emphasis should always be on delivering oxygen to tissues when managing shock. In most cases of shock, supplementary oxygen improves tissue oxygenation. The
efficacy of this should be assessed by blood gas monitoring, and severe breathlessness, persistent hypoxaemia
and worsening acidosis (pH<7.3) are indications to consider endotracheal intubation and ventilation.
Fluid resuscitation
Administration of fluids increases venous return
and thus improves cardiac output, but they should
Bleeding
Direct pressure should be applied to a bleeding
wound. Immediate surgical exploration is indicated
where continued bleeding is likely, such as in ruptured spleen, ruptured aortic aneurysm or ruptured
ectopic pregnancy. In these cases, resuscitation cannot overcome the losses until the rate of blood loss is
curtailed. While fluid replacement with crystalloid is
helpful, replacement of blood loss with blood is what
is required.
Anaphylaxis
In surgical practice, this may arise most commonly as an
allergic reaction to an antibiotic or radiological c ontrast
medium. In addition to hypotension (due to vasodilation), bronchospasm and laryngeal oedema may be present and warrant immediate therapy. The immediate
treatment for anaphylaxis is the administration of
adrenaline (epinephrine; 0.5mL of 1:1,000 concentration) intramuscularly or subcutaneously, repeated every
10–30 minutes as required. Subsequently, hydrocortisone and antihistamine agents (e.g. chlorphenamine)
may be given.
For milder reactions, aliquots of 1mL of 1:10,000
adrenaline are given and titrated to effect.
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Res
CO
2
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Pulmonary
artery
Veins
CO
2
elimination
Anatomy Initial assessment
Airway patent 15 L of O2 via
O
Intake
2
Trachea central
Air entry
Lung expansion
O
saturation
2
Heart rate
Blood pressure
JVP
Blood tests (Hb)
Blood gases
Shunts
Right
heart
Lungs
Pulmonary
veins
Left
heart
Artery
Treatment
non-rebreathing
mask
Consider chest
drain(s)
Large bone
cannula
IL Fluid STAT
(20 ml/kg)
Fluid challenge
response
t
Rest of the body
CO2 production
productio
O
metabolism
2
Figure8.2 Anatomical & physiological assessment and treatment of shock.
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Monitoring andsubsequent
management
The severely shocked patient should be admitted to
an intensive care unit where continuous supervision
by specially trained nursing staff is available. Along
with careful clinical surveillance, the following
parameters need to be closely monitored:
•
Core temperature, pulse, respiration rate and
blood pressure.
•
Hourly urine output (via a urinary catheter).
• Central venous pressure.
• Pulse oximetry. Oxygen is administered to ensure
adequate oxygenation. Mechanical ventilation
may be required.
•
Electrocardiogram (ECG), looking at heart rate,
rhythm and signs of cardiac ischaemia.
Serum electrolytes, haemoglobin and white blood
•
cell count.
•
Arterial blood gases (PO
• Blood lactate is raised in tissue hypoxia and also in
septic shock through other mechanisms.
•
The cardiac output, and left atrial and pulmonary
arterial pressures (see later in this chapter).
The frequency of these measurements depends on
the patient’s condition and response to treatment. It is
particularly important to remember that if the patient
is conscious, he or she may well be terrified, in pain
and acutely aware of all that is going on. Proper explanations and appropriate analgesia must be provided.
, PCO2, [H+]).
2
Cardiac output measurement
Cardiac output can be measured by the direct Fick3
principle, indirect Fick principle, indicator dilution,
transoesophageal ECHO and several less invasive
procedures. Gold standard is the direct Fick principle,
although indicator dilution techniques are less invasive in providing accurate results with minimal complications. Until the past decade, the Swan–Ganz
4
catheter
ure cardiac output. Due to good accuracy, indicator
was used in intensive care settings to meas-
dilution techniques like transpulmonary lithium
dilution cardiac output (LiDCO™) measurement are
now more commonly used in intensive care settings.
Swan–Ganz measurement
ofcardiac output
The Swan–Ganz technique involves passing a
multipleright atrium. A small balloon on the end of the catheter is inflated, and the inflated balloon ‘floats’ with
the blood returning to the heart across the tricuspid
and pulmonary valves into the pulmonary artery.
Once there, the catheter is advanced until it wedges
itself in a small branch of the pulmonary arterial tree.
The balloon is then deflated. During insertion, the
position of the catheter can be monitored by the
changing pressure waveform recorded by a transducer connected to the lumen. Along with measuring
core temperature, a temperature probe at the tip of
the catheter facilitates the measurement of cardiac
output by the Fick principle: a bolus of cold is injected
through the catheter and the change in temperature
monitored. Importantly, the catheter also allows calculation of the systemic and pulmonary vascular
resistances.
lumen catheter via a central vein into the
LiDCO measurement ofcardiac
output
Cardiac output is now more commonly measured
using techniques like LiDCO: a very small amount of
lithium is injected into a central or peripheral vein.
An arterial line with a lithium sensor measures the
lithium, and this measurement is subsequently used
to calibrate pulse contour using software that provides continuous cardiac output data by analysing the
arterial pressure waveform. This technique is minimally invasive, requiring only arterial and venous
lines. A LiDCO monitor displays arterial pressure,
stroke volume and cardiac output.
3
Adolf Eugen Fick (1829–1901), German Physiologist
working rst in Zurich and then in Wurzburg.
4
Harold J C Swan (1922–2005), Cardiologist, Cedars of
Lebanon Hospital, Los Angeles, CA, USA. William Ganz
(1919–2009), Professor of Medicine, UCLA, and Senior
Research Scientist, Cedars of Lebanon Hospital, Los
Angeles, CA, USA.
Prevention ofhypothermia
Patients may cool down because of neglect, infusion
of cold fluids, particularly unwarmed blood, and
extracorporeal circulations such as haemodialysis or
haemofiltration circuits. Allowing a patient to cool
down to subnormal temperatures (35°C or below)
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impairs the coagulation cascades and platelet aggregation, and promotes fibrinolysis. To prevent this, all
infusions should be prewarmed, and the patient
actively warmed using convective (forced air) warm-
ing (e.g. Bair Hugger
).
™
Pharmacological agents
The hypotensive patient may require significant vasopressor support. The principal drugs used are catecholamines or their derivatives, in addition to drugs
to treat specific causes such as antimicrobial therapy
for septicaemia. Patients in cardiogenic shock benefit
from positive inotropic agents, whereas patients with
low systemic vascular resistance due to sepsis require
agents to increase vascular resistance. The drugs used
in this context are sympathomimetics, with differing
degrees of α (peripheral vasoconstriction), β
tropic and chronotropic) and β
tion) effects. Examples of such drugs include the
following.
(peripheral vasodila-
2
(ino-
1
Noradrenaline (norepinephrine)
Noradrenaline has predominantly α effects, but with
modest β activity. It is used to increase systemic vascular resistance through its vasoconstrictor α effects,
while the β effects may help maintain cardiac output.
Metaraminol
Like noradrenaline, metaraminol has predominantly
α receptor agonist actions causing vasoconstriction
and inotropic effects on the heart increasing systemic
blood pressure (both the systolic and diastolic blood
pressure). It is weaker than noradrenaline but has a
more prolonged duration of action (20–60minutes).
Dopamine
Dopamine has three separate actions according to
dose:
1
At low doses (2 μg/kg/min), dopaminergic actions
dominate, causing increased renal perfusion. It
was thought to be useful in protecting the kidneys
from acute kidney injury, but its value in this setting has been disproved.
At moderate doses (5 μg/kg/min), β
2
dominate with positive inotropic activity (increasing myocardial contractility and rate).
3
At higher doses (over 5 μg/kg/min), α effects pre-
dominate with vasoconstriction.
Dopamine was once commonly used in shock, but
its lack of renal protective effect, increased incidence
of arrhythmias and association with a higher mortality in cardiogenic shock have reduced its usefulness.
effects pre-
1
Adrenaline (epinephrine)
Adrenaline has strong α and β actions, and may be
used to increase peripheral resistance while also
increasing cardiac output. The powerful vasoconstrictor actions of both adrenaline and noradrenaline
may result in ischaemia and infarction of peripheral
tissues, most commonly fingers, toes and the tips of
the nose and ears.
Vasopressin
Vasopressin (ADH) is a potent vasopressor, in addition to its effects on volume regulation in the kidney.
Infusion of vasopressin has been shown to be a useful
adjunct to noradrenaline in patients with septic
shock. Argipressin is an analogue of vasopressin,
with similar pressor properties.
Dobutamine
Dobutamine has predominantly β1 actions, increasing myocardial contractility and rate, thus increasing
cardiac output. It is used principally in cardiogenic
shock.
Dopexamine
Dopexamine has predominantly β2 actions, increasing myocardial contractility; it also acts on peripheral
dopamine receptors, increasing renal perfusion.
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Trauma surgery
Jonathan Morton
Learning objectives
✓ To understand the principles of initial trauma assessment.
✓ To understand the principles of damage control surgery.
✓ Gain knowledge of the trauma management of individual abdominal
organs.
Trauma is the commonest cause of death for those under
40 years of age in the UK. Trauma networks have been
associated with a reduction in mortality of between 10%
and 40% for those severely injured. In 2012, as part of
national trauma network systems, 27 designated major
trauma centres were created in the UK. As a result, there
has been a 19% increase in the odds of survival for trauma
victims for those who reach secondary care alive.
Trauma types
• Penetrating trauma is defined as a foreign object penetrating the skin or mucosal membranes of the body.
• Blunt trauma may be associated with no breaks in
the skin. However, it can result in deep tissue damage (including organs) depending on the forces
involved with the initial event.
Generally, timelines for penetrating trauma are
compressed, and physiology and injuries can evolve
and change far more rapidly compared with those of
blunt trauma. Management of time in the initial phase
of assessment and intervention for trauma patients is
critically important, especially for the team leader, as it
is easy to lose situational awareness (Chapter2).
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
Mechanisms ofinjury
The mechanism of injury is of great importance for
trauma patients. Understanding the forces involved
(and how these were transferred to the patient) can
help anticipate injuries and injury patterns. For example, an unrestrained front seat passenger of a vehicle
impacting the steering wheel at 50mph may well have
threatening injuries to their thorax and abdomen.
lifeIn contrast, the same patient who was restrained with
deployed airbags at the scene may have significantly
less severity in their injury pattern(s).
Principles oftrauma management
• Rapid assessment.
• Avoidance of secondary injuries.
• Interventions to stop the fatal triad of death in
trauma.
The triad ofdeath
intrauma
A common pathway of eventual mortality has been
described for critically injured trauma patients: the
so- called trauma triad of death, which refers to the
vicious cycle of evolving acidosis, hypothermia and
coagulopathy (Figure9.1).
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Hypoperfusion
+ve
Acidosis
+ve
+ve
Loss of
intrinsic
thermoregulation
Figure9.1 The triad of death in trauma care.
The positive feedback from each component of the
triad promotes further worsening of physiology.
Haemorrhage promotes loss/consumption of
factors and contributes to hypothermia. This also
reduces oxygen delivery to tissues (hypoxia), with
anaerobic respiration predominating. This results in
lactic acid production and an increase in acidosis. This
acidosis, together with hypothermia, adversely impacts
the clotting cascade, further
thy and promoting further haemorrhage.
Most interventions and trauma objectives are directed
at minimizing or stopping the propagation of the triad,
and by so doing, minimizing secondary injuries and
improving patient outcomes. The surgical approach
used to stop this positive feedback loop is generally
referred to as damage control surgery (see later).
For critically injured trauma patients, interventions
to prevent worsening physiology are made at different
stages of the patient pathway. Figure9.2 summarizes a
critically ill trauma patient’s journey from the incident
to definitive surgical intervention. During these different phases of care, interventions are made to arrest or
reverse the effects of the triad of death.
exacerbating coagulopa-
clotting
+ve
Haemorrhage
+ve
CoagulopathyHypothermia
+ve
advanced care teams for critically ill patients will be
sent to the scene of incidents to initiate treatment
interventions at the earliest opportunity. Some prehospital teams travel with blood products and other
advanced medications to progress the early resuscitation of patients. These teams also assess where
trauma patients should be transferred to minimize
time to definitive management of injuries.
As part of the transfer process to definitive care,
alerts are given to the appropriate emergency
precentres to enable trauma teams to prepare appropriately for the imminent arrival of a critically ill patient.
The acronym ATMIST (Table 9.1) is often used to
standardize communication, summarizing the
patient’s situation. As part of this preparation of the
receiving trauma centre, a team will be established
(frequently utilizing a trauma call/page) and led by a
team leader. A briefing will be given to the team on
the mechanism of injury, understanding of current
physiology and anticipated equipment needed. Roles
within the team are established as different aspects of
the primary survey (see below) are typically conducted simultaneously by various team members.
Phase 1: Pre- hospital
trauma care andinitial
assessment
Care of the trauma patient starts from the time of the
first call for help. Calls are screened, and the likely
severity of traumatic injuries is assessed. Pre- hospital
Table9.1 ATMIST Communication acronym
ATMIST
Age
Time of incident
Mechanism of injury
Injuries (top to toe)
Signs (vitals)
Treatment
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Pre-Hospital/
Initial
Assessment
Resuscitation
DCS ICU Surgery
Abdominal
Closure
PHASE I II III IV V
Figure9.2 Phases of damage control. DCS: damage control surgery; ICU: intensive care unit.
Advanced Trauma Life Support
Phase 2: Initial
assessment withongoing
resuscitation
Assessment oftrauma patients
The initial assessment of trauma victims as they arrive in
the hospital is a critical aspect of trauma care. Great
emphasis is on the mechanism of injury (MOI), which
helps establish the transmitted forces involved with the
accident/incident and enable the receiving hospital team
to anticipate injuries and their severity. Upon arrival,
there is a focused handover between the pre- hospital and
trauma teams. An initial assessment of the trauma patient
is performed: the primary survey (Table9.2).
Table9.2 The primary survey
Primary survey:
(C) Catastrophic haemorrhage control (not part of
ATLS)
A Airway, with cervical spine control (hard collar or
equivalent device/method)
B Breathing, with ventilation (oxygen application with
a non- rebreathing mask)
C Circulation, with haemorrhage control (intravenous
access and blood for analysis)
D Disability assessment (neurological assessment)
E Exposure, with environmental control
(ATLS)
Advanced Trauma Life Support is a training course
and ethos in assessing trauma patients. In ATLS, an
A to E assessment of patients is conducted in rigid
sequential steps, simulating the worstof an individual doctor alone looking after trauma
patients. In most trauma centres, however, this initial
assessment is conducted by multiple team members
simultaneously while there is ongoing resuscitation.
Catastrophic haemorrhage control is listed at the
top of the primary survey. While not part of the ATLS
mantra, it has been added in recognition of the
importance of haemorrhage control in the context of
catastrophic haemorrhage (Table9.2).
If at any stage interventions are required during the
primary survey, or there is a significant change in the
patient’s physiology, repeated assessment(s) using
this primary survey sequence are often performed.
This ensures that no life- threatening conditions
evolve unrecognized, requiring further intervention.
Catastrophic haemorrhage
control
The principle of controlling catastrophic haemorrhage has evolved from recent military conflicts. For
individuals who have lost limbs and are at risk of
immediate exsanguination, temporizing haemorrhage
case scenario
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control is required before starting the A to E assessment. This is typically achieved with either direct pressure or tourniquets. These will often be applied in the
pre-
hospital setting with a record of the time of when
they were applied (either in medical notes or directly
on the tourniquet). These are generally not removed
until the patient is in the operating room environment.
The same principle applies to any objects such as a
knife that may still be in the patient on arrival to the
hospital after an incident. These are also not removed
until surgery/definitive management has either commenced or will do so imminently.
A: Airway withadequate cervical
spine control
Before examining the patient, a simple question such
as asking their name with an appropriate response
confirms airway patency and indicates a good level of
consciousness. In this scenario, a more formal airway
assessment may not be required.
The airway should be inspected to exclude airway
obstruction from foreign bodies (e.g. dentures). Signs
that might suggest impending airway obstruction,
such as evidence of inhalational injuries (carbonaceous material in the airways), often require preemptive/early intubation and ventilation. While
controlling the cervical spine in recognition that
there is often concurrent cervical spine trauma, simple airway manoeuvres can be performed to improve
relative airway obstruction (e.g. jaw thrust / chin lift).
Adjuncts to airway control include oro/nasopharyngeal airways and, should the conscious level,
as measured by the Glasgow Coma Score (GCS,
Table 17.3), be 8 or below, a definitive airway is
required. A definitive airway is defined as a secured,
cuffed tube in the trachea.
Some penetrating injury patterns such as gunshot
wounds to the face or complex facial fractures are also
associated with significant difficulties in securing airways on occasion. It should be noted that there are
specific anatomical differences between adults and
children, and as such, different approaches and
equipment to assist with the airway are required in
the paediatric population.
B: Breathing withadequate
ventilation
Combining these two aspects of ‘B’ alludes to the
importance of the patient being able to breathe and
the adequacy of that attempted ventilation/gas
exchange. Supplemental oxygen should be placed on
the patient at 100% unless the patient is already intubated and ventilated. A pulse oximeter should also be
applied.
Life- threatening chest injuries such as massive haemothorax (IV access recommended before intervention), tension pneumothorax, tracheal or bronchial
injuries should be identified, and treatment instigated/
planned at this stage of the primary survey.
Tension pneumothorax is an immediate lifethreatening clinical situation. The classical description
of clinical presentation is the patient having a deviated
trachea away from the side of the pneumothorax, distended neck veins (which can be hard to assess with a
hard collar in situ) and the physiological state of shock.
In reality, these are often quite late signs of a tension
pneumothorax. Clinical examination should be sufficient to diagnose the condition as waiting for radiological confirmation is not appropriate from a time
perspective. Treatment is rapid needle decompression. This is achieved by inserting a cannula into the
fourth or fifth intercostal space (inferior to the pectoralis major muscle) just posterior to the anterior axillary
line. The second intercostal space in the midclavicular
line is advocated in paediatric populations.
C: Circulation withhaemorrhage
control
A rapid assessment of circulation can be achieved by
assessing the patient’s pulse, capillary refill time and
level of consciousness. Blood pressure monitoring, if
not already applied, should be commenced.
Consideration needs to be given to the physiological
state of shock for the individual and its cause while
initiating resuscitation of the patient.
Intravenous access
Two large- bore intravenous catheters are typically
placed in both antecubital fossae. If intravenous
access is challenging, the trauma team may place
either an interosseous needle or a long line (central line). Blood is taken and sent to the laboratory
(Table 9.3) and rapidly analysed on a blood gas
machine to obtain a lactate, which will indicate
the degree of physiological shock. Once intravenous access has been successful, resuscitation can
commence with either crystalloid (warmed normal saline or Hartmann’s solution) or blood
products.
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Volume replacement
Consideration should be given to initiating the major
transfusion protocol within the hospital. This protocol
typically releases multiple resources within the hospital as well as blood products to help the trauma
team. A 1:1 ratio for the various blood components,
including red cells, fresh frozen plasma, platelets and
cryoprecipitate, is typically delivered within the
packs.
Haemorrhage control
Reversal of any anticoagulation should be considered
as part of this phase of the primary survey. There is
also evidence that tranexamic acid (an antifibrinolytic that stabilizes clot), given within 3 hours
of injury, improves the longpatients. As discussed above, tourniquets/splints/
direct pressure can be used for peripheral limb
haemorrhage control, and pelvic binders are frequently used to control bleeding from pelvic
fractures.
term outcomes of trauma
D: Disability andneurological
assessment
A rapid neurological assessment of the patient is
made. This phase of the primary survey aims to
establish the patient’s conscious level, identify any
potential spinal cord injuries and initiate the assessment of these. Pupillary size and blood glucose are
also assessed at this stage. The conscious level is
assessed using the GCS scale (Table 17.3), which
divides assessment of consciousness into responses
of the eyes, speech and movement. Each of the
three domains of the GCS are added together to
obtain a result out of 15. The maximum score is 15
and the minimum 3 (assuming all aspects can be
tested).
E: Exposure withenvironmental
control
Exposure has to be adequate so that additional injuries are identified, documented and assessed
promptly is critical. This is particularly the case for
penetrating trauma wounds, where exit wounds or
other injuries can be hidden on the posterior aspect
of the body.
Hypothermia has a profound adverse effect on
coagulation; it inhibits the clotting cascade, impairs
platelet aggregation and enhances fibrinolysis,
resulting in a coagulopathy as well as an acidosis.
Therefore, it is essential to maintain an adequate
core temperature for the patient during this phase of
the primary survey. In modern emergency rooms
and operating theatres, it should be possible to rapidly increase the temperature of the rooms to facilitate adequate environmental control (minimizing
the risk of hypothermia). Forced air warming devices
(e.g. Bair huggers™) are frequently used to help
maintain patients’ core temperatures.
Submersion andexposure injuries
In submersion or exposure injuries, where the patient
is profoundly hypothermic, more aggressive and/or
controlled warming may be required either utilizing
trans-
vesical warming or, in extremes, cardiac or
veno- venous bypass systems.
Spinal injury andthermoregulation
Patients with high spinal cord injuries often lose the
ability to thermoregulate due to inappropriate vasodilation in the peripheries contributing to heat loss
(with the loss of sympathetic tone).
Table9.3 Blood tests fortrauma patients
Typical blood tests for trauma patients
Full blood count (FBC)
Urea and Electrolytes (creatinine, potassium and
sodium)
Metabolic/Endocrine tests (liver function and bone
profile, including calcium)
Clotting studies
Beta- HCG
Group and save or cross- match samples
Amylase
The AMPLE history
Following the A to E assessment of the primary survey, a targeted medical history is taken, known as an
AMPLE history. This involves
Allergy history.
•
• Medical history.
• Past medical history.
• Last: ate / drank / menstrual period / tetanus
injection.
• Events leading to the trauma.
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