Early fluid resuscitation in severe trauma

Abstract

#### Summary points

Trauma is a global health problem that affects patients in both rich and poor countries and accounts for 10 000 deaths each day.1 2 Trauma is the second leading cause of death after HIV/AIDS in the 5-45 year old age group.w1 w2 Early triage and resuscitation decisions affect outcome in trauma situations.w3 w4 The two leading causes of mortality in trauma are neurological injury and blood loss.3 4 w5 w6 There has been considerable improvement in our understanding of trauma resuscitation in the past 20 years, and data from databases and observational trials suggests outcomes are improving.w7 For patients with severe traumatic injuries (defined as <15 by the injury severity score, an anatomical scoring system), the high volume fluid resuscitation promoted by early advanced trauma life support manuals,5 followed by definitive surgical care, has given way to a damage …

Full text

38 BMJ | 15 SEPTEMBER 2012 | VOLUME 345
CLINICAL REVIEW
of patients; however, physician decision and experience have
been found to be just as accurate.w9 w10 w11 w12 w13 Failure to
identify these patients early and to apply DCR is associated
with excess mortality.8
How can trauma patients in shock be identified?
Shock may be dened as a life threatening condition char-
acterised by inadequate delivery of oxygen to vital organs in
relation to their metabolic requirements.9 A systolic blood
pressure of 90 mm Hg is commonly used to dene both
hypotension and shock; however, oxygen delivery depends
on cardiac output rather than blood pressure. Homeostasis
with peripheral vasoconstriction acts to preserve blood pres-
sure even as circulating volume is lost. In patients who have
had trauma, adequate cardiac output cannot be inferred
from blood pressure. Only when blood loss approaches half
the circulating volume or occurs rapidly is there a relation
between the cardiac output and blood pressure.
10
Patients
presenting with hypotension, tachycardia, and obvious
blood loss are readily identied as being in a state of haem-
orrhagic shock. However, many patients will maintain their
pulse and blood pressure even aer massive blood loss and
tissue hypoxia. This condition is termed cryptic shock and
is associated with increased mortality.w14
The role of basic physiological parameters to estimate the
severity of blood loss has been popularised in the advanced
trauma life support courses and manuals.5 These materi-
als describe physiological deterioration with increasing
Trauma is a global health problem that aects patients
in both rich and poor countries and accounts for 10 000
deaths each day.1 2 Trauma is the second leading cause of
death aer HIV/AIDS in the 5-45 year old age group.w1 w2
Early triage and resuscitation decisions aect outcome in
trauma situations.w3 w4 The two leading causes of mortality
in trauma are neurological injury and blood loss.3 4 w5 w6
There has been considerable improvement in our under-
standing of trauma resuscitation in the past 20 years, and
data from databases and observational trials suggests out-
comes are improving.
w7
For patients with severe traumatic
injuries (dened as <15 by the injury severity score, an
anatomical scoring system), the high volume uid resus-
citation promoted by early advanced trauma life support
manuals,
5
followed by denitive surgical care, has given
way to a damage control resuscitation (DCR) strategy (box).
This DCR approach has seen a fall in the volume of
crystalloid delivered in the emergency department and an
associated fall in mortality.6 w8 In this review, we summa-
rise the evidence guiding the initial period of resuscitation
from arrival in the emergency department to transfer to
intensive care or operating theatre, focusing on trauma
in critically injured adults. This article emphasises newer
developments in trauma care. There is debate on whether
patients with brain injury should be resuscitated to higher
blood pressures, which is briey discussed later in the text.
How can patients who need DCR be identified?
A DCR strategy applies to patients who present with sus-
pected major haemorrhage. While many denitions exist,
the most practical in the acute trauma setting is for estimated
blood transfusion volumes of over four units in the initial 2-4
h. Identifying these patients can be a challenge because they
are oen young with good physiological reserve and may
have no physiological evidence of hypovolaemic shock.7 A
number of tools have been developed to identify this group
1Barts and the London School of
Medicine and Dentistry, Queen
Mary University of London,
London, UK
2Barts Health NHS Trust, London
316 Air Assault Medical Regiment
4Royal London and Queen Victoria,
East Grinstead, UK
Correspondence to
: T Harris,
Department of Emergency
Medicine, Royal London Hospital,
Whitechapel, London E11BB
tim.harris@bartshealth.nhs.uk
Cite this as: BMJ 2012;345:e5752
doi: 10.1136/bmj.e5752
Early fluid resuscitation in severe trauma
Tim Harris,1 2 G O Rhys Thomas,3 4 2 Karim Brohi1 2
SUMMARY POINTS
Critically injured trauma patients may have normal cardiovascular and respiratory
parameters (pulse, blood pressure, respiratory rate), and no single physiological or
metabolic factor accurately identifies all patients in this group
Initial resuscitation for severely injured patients is based on a strategy of permissive
hypovolaemia (hypotension) (that is, fluid resuscitation delivered to increase blood
pressure without reaching normotension, aiming for cerebration in the awake patient, or
70-80 mm Hg in penetrating trauma and 90 mm Hg in blunt trauma) and blood product
based resuscitation
This period of hypovolaemia (hypotension) should be kept to a minimum, with rapid
transfer to the operating theatre for definitive care
Crystalloid or colloid based resuscitation in severely injured patients is associated with
worse outcome
Once haemostasis has been achieved, resuscitation targeted to measures of cardiac output
or oxygen delivery or use improves outcome
Tranexamic acid administered intravenously within 3 h of injury improves mortality in patients
who are thought to be bleeding
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KEY COMPONENTS OF DCR
Permissive hypovolaemia (hypotension) (see summary
points)
Haemostatic transfusion (resuscitation)—that is, fresh
frozen plasma, platelets, or packed red blood cells,
and tranexamic acid. Avoidance of crystalloids (normal
saline, Hartmann’s, Ringer’s lactate solutions), colloids (a
substance microscopically dispersed evenly throughout
another substance; with resuscitation fluids, this term
refers to larger molecules dispersed most usually in normal
saline, such as gelofusion, haemaccel, or volulyte), and
vasopressors
Damage control surgery or angiography to treat the cause
of bleeding
Restore organ perfusion and oxygen delivery with definitive
resuscitation
SOURCES AND SELECTION CRITERIA
We searched Medline, Embase, the Cochrane database,
and Google for randomised controlled trials, meta-analyses,
and peer reviewed articles, limiting the search to adults.
The search was performed once by the lead author (TH) and
once by a professional librarian. All articles were shared
and supplemented by the author’s own libraries. The
main search terms used were “trauma,” “resuscitation,”
“fluid,” and “goal directed therapy.” Ongoing studies were
identified from www.clinicaltrials.gov.

BMJ | 15 SEPTEMBER 2012 | VOLUME 345 39
CLINICAL REVIEW
volumes of blood loss, and categorise four stages of shock.
But data from a 1989-2007 analysis of the United Kingdom
Trauma Audit Research Network database suggest that this
model is not reected in practice. Patients with progressive
levels of blood loss to stage 4 haemorrhagic shock (equating
to >2 L blood loss) were found to increase their pulse rates
from 82 to 95 beats per minute, not to change respiratory
rates or Glasgow coma scale, and maintain systolic blood
pressures above 120 mm Hg.11 Although an important part
of the initial assessment, physiological derangement alone
is neither sensitive nor specic as a tool to identify shock in
trauma patients.7
There is observational evidence from large datasets in
the UK and United States that mortality increases in trauma
patients in both blunt and penetrating trauma, while s ystolic
blood pressure falls below 110 mm Hg.12 w15 w16 w17 w18 w19 A
US review of 870 634 sets of trauma records identied that
for every 10 mm Hg below 110 mm Hg, mortality increased
by 4.8%.
12
Shock index does not improve aer risk stratica-
tion of trauma patients.w20
Metabolic assessment with lactatew21 w22 and base
excessw23 w24 also predicts blood loss and mortality. Fur-
thermore, these parameters may be increased from exer-
cise around the time of injury (running, ghting) or may be
(falsely) low if the hypoxic tissues are not being perfused
suciently to wash anaerobic products into the circulation
(for example, when a tourniquet is applied). For patients
in whom central access is obtained, mixed venous oxygen
saturation is also a good indicator of blood loss, with levels
below 70% suggesting inadequate oxygen delivery.w25
Estimated injuries and associated blood loss are an import-
ant part of the initial trauma assessment. Clinical examina-
tion is augmented by focused ultrasound assessment of the
chest, pericardium, and peritoneal cavity (extended focused
assessment with sonography in trauma (eFAST), a specic
but insensitive test for blood loss); and computed tomo-
graphy (a sensitive and specic test for blood loss).
What is permissive hypotension (hypovolaemic)
resuscitation?
Permissive (hypotension) hypovolaemic resuscitation is
used to describe a process that minimises administration
of uid resuscitation until haemorrhage control has been
achieved, or is deemed unnecessary on denitive imaging.
Resuscitation is the restoration of oxygen delivery and organ
perfusion to match requirements. In the 1960s and 1970s,
a strategy of high volume crystalloid resuscitation in a ratio
of 3 mL per 1 mL of blood loss was promoted, which was
thought to replace intravascular and interstitial losses and
reduce the risk of organ failure.13 However, vigorous uid
resuscitation increases blood pressure, the eect of which
increases hydrostatic forces on newly formed clot, dilutes
clotting factors and haemoglobin, and reduces body temper-
ature. These eects could promote further bleeding. In per-
missive hypotension, denitive resuscitation is deferred until
haemostasis is obtained. It is now recognised that aggressive
crystalloid resuscitation also impairs organ perfusion.14 w26
What evidence do we have for hypovolaemic
resuscitation?
Considerable animal work has informed our understanding
of hypovolaemic resuscitation. In summary, this research
found that withholding uid resuscitation from animals
with critical blood loss (about half their circulating vol-
ume) was associated with death, whereas animals with
less severe blood loss had a lower mortality with no uid
resuscitation.15
The table summarises three randomised controlled trials
exploring the risks and benets of hypovolaemic resusci-
tation.16 17 w27 These trials provide evidence of a mortality
advantage in favour of this resuscitation strategy for trun-
cal penetrating trauma and evidence of no harm in blunt
trauma.
The National Institute for Health and Clinical Excellence
has recommended that in older children and adults with
blunt trauma, no uid be administered in the prehospi-
tal resuscitation phase if a radial pulse can be felt, or for
penetrating trauma if a central pulse is palpable.18 In the
absence of this, 250 mL crystalloid uid boluses are admin-
istered and the patient is reassessed until these pulses, as
described, return.
Much of the evidence for hypovolaemic resuscitation was
developed before the advent of haemostatic resuscitation,
as described below. This period of hypovolaemic resuscita-
tion is maintained for as short a period as possible, until the
injury complex is dened and any sites of blood loss treated
surgically or embolised.
Untreated hypovolaemic shock leads to microvascular
hypoperfusion and hypoxia, leading to multiorgan failure.19
Hypovolaemic resuscitation sacrices perfusion for coagula-
tion and haemorrhage control. The trauma team carefully
balances the resuscitation process to maintain organ per-
fusion but at lower than normal blood pressure to regulate
bleeding. Based on the evidence available, we suggest that
uid resuscitation before haemorrhage control should aim
to maintain a systolic blood pressure of 80 mm Hg or a
Randomised trials of permissive hypotension in trauma
Trial Intervention Patient group Setting Findings Comments
Pseudo-randomised
controlled trial16
No fluid resuscitation before
surgical intervention in
operating theatre v crystalloid
based resuscitation
Penetrating truncal trauma and
systolic blood pressure >90 mm
Hg (n=598)
Prehospital and
in emergency
department
Lower mortality in group with no
fluid resuscitation than in group
with crystalloid based resuscitation
(survival 70% v 62%, P=0.04)
Short transport distances, mortality
benefit predominantly vascular injuries,
young cohort (mean age 31 years), 8% in
no fluid group received fluids
Randomised controlled
trial17
Resuscitation to target systolic
blood pressure 100 mm Hg v
70 mm Hg
Blunt or penetrating trauma and
systolic blood pressure <90 mm
Hg in first hour (n=110)
Urban trauma centre
resuscitation room
No mortality difference, low
mortality of four (7.3%) patients in
each group
Low mortality, study underpowered to
show mortality difference, observed
systolic blood pressures were 114 mm
Hg and 100 mm Hg despite targets
Randomised controlled
trial: interim analysisw27
Intraoperative resuscitation to
mean arterial pressure 50 mm
Hg v 65 mm Hg
Traumatic injuries excluding
traumatic brain injury with at least
one episode of systolic blood
pressure <90 mm Hg (n=90)
Operating theatre No mortality difference Observed blood pressures did not differ
significantly despite targets; results may
not translate to preoperative environment
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40 BMJ | 15 SEPTEMBER 2012 | VOLUME 345
CLINICAL REVIEW
p alpable radial pulse or cerebration by using small volume
boluses of 250 mL. This value is arbitrary with little evidence
to support it. The 250 mL boluses are able to increase blood
pressure, since the circulation is highly constricted with a
small volume of distribution. In practice, achieving target
blood pressures is challenging. Patients with severe injuries
will probably need blood product based resuscitation, as
described below.
Fluid resuscitation in traumatic brain injury
This review does not deal in detail with the complexities
of resuscitation in brain injury; however, retrospective
observational data for patients with traumatic brain injury
suggest that any single reduction in mean arterial blood
pressure below 90 mm Hg is associated with a doubling in
mortality.
w28 w29
Guidelines published by the Brain Trauma
Foundation advocate maintaining a systolic blood pressure
above 90 mm Hg but do not specically state whether this is
during active haemorrhage.w30 Currently, there is controversy
about whether the guidelines for permissive hypotension
should be changed in the presence of head injury because
there is no human evidence from prospective studies.
What is the role of blood products in trauma resuscitation?
Severe bleeding in trauma patients can result in disordered
blood clotting. Until recently, this eect was thought to be
a late phenomenon arising primarily from loss of coagula-
tion factors during haemorrhage and dilution from resus-
citation uids. However, it is now recognised that trauma
induced coagulopathy occurs within minutes of injury, and
is as sociated with a fourfold increase in mortality.20 The
process is multifactorial21 but is partly due to an endogenous
coagulo pathy that occurs as a result of tissue damage in
severe shock.w31 This understanding has led to changes in
the management of trauma haemorrhage.
Haemostatic resuscitation
Haemostatic resuscitation is a combination of strategies
targeting trauma induced coagulopathy to reduce bleeding
and improve outcomes.w32 w33
How do blood products aid in resuscitation?
The main strategy to treat trauma induced coagulopathy is
to provide volume replacement that augments coagulation.
This replacement has been achieved by the transfusion of
fresh frozen plasma, platelets, and packed red blood cells.
A retrospective observational study performed on military
personnel with similar injuries but diering resuscitation
uid strategies suggested that the use of higher ratios of
fresh frozen plasma to packed red blood cells may improve
outcomes.22 Similar results have been seen in other ret-
rospective studies and a few small prospective cohort
studies,
23
although the retrospective studies are subject to
survival bias.
It is also unclear whether the benet from these strate-
gies comes from the coagulation factors present in fresh
frozen plasma or from reducing the amount of crystalloid
and colloid administered. Nevertheless, it seems clear that
the usual 1-2 units of plasma previously administered aer
massive transfusions was insucient to prevent dilutional
coagulopathy. Current consensus is that plasma should be
given from the beginning of the resuscitation, alongside
transfusions of packed red blood cells, in a ratio of 1 “unit”
of plasma for each 1-2 units of packed red blood cells.24
Very little is known about platelet function in trauma
induced coagulopathy or the effectiveness of platelet
transfusions.w34 w35 Although these early strategies of blood
product in high doses seem eective, they are based on
limited evidence. These regimens also place substantial
resource demands on blood banks and are logistically dif-
cult to implement owing to the requirements for rapid
thawing and delivery.
Research is also being undertaken to look at alterna-
tives to blood component therapy for the management
of trauma induced coagulopathy. Fibrinogen is the cen-
tral substrate of blood clotting, and levels are low in this
patient group.
w36
Some retrospective evidence suggests
that patients who receive more brinogen replacement
(in the form of cryoprecipitate and plasma) have bet-
ter outcomes in terms of total use of packed red blood
cells and mortality.w37 Fibrinogen is also available as a
powdered concentrate and could be a replacement ther-
apy that can be easily administered in trauma induced
coagulopathy.w38 w39
ADDITIONAL EDUCATIONAL RESOURCES
Resources for healthcare professionals
Trauma.org (www.trauma.org/)—an independent, non-profit organisation providing global
education and information for professionals involved in trauma care
Eastern Association for Surgery of Trauma guidelines (www.east.org/research/treatment-
guideline)—provides a series of evidence based guidelines for trauma care
Online lectures from massive transfusion and coagulopathy state of the art symposium at the
London Trauma Conference in 2008 (www.trauma.org/index.php/main/articles/)—provides a
series of lectures on blood transfusion, resuscitation, and trauma induced coagulopathy
Resources for patients
Patient.co.uk website (www.patient.co.uk/)—UK patient website providing wide range of
information and discussing a variety of injuries
Cohen D. Code red: repairing blood in the emergency room. New Scientist 2011. www.
newscientist.com/article/mg21228352.900-code-red-repairing-blood-in-the-emergency-
room.html
Trauma information pages (www.trauma-pages.com/)—provides simply worded information
specifically for non-healthcare professionals concerning traumatic injuries
National Institute of Neurological Disorders and Stroke. Information page on traumatic
brain injury. 2012. www.ninds.nih.gov/disorders/tbi/tbi.htm—provides clearly written
information directed at members of the public and healthcare professionals on a variety of
neurological insults, including traumatic brain injuries
ONGOING RESEARCH
PROPPR (pragmatic, randomised optional platelets and plasma ratios): randomised controlled
trial of 1:1:1 v 1:1:2 of red blood cells to platelets to plasma in patients requiring massive
transfusion, seeking to better define the ratio of plasma to packed red blood cells for damage
control resuscitation (NCT01545232)
MP4OX phase IIb trial for ischaemia rescue (lactate clearance): trial exploring the use of an
oxygen carrying colloid in trauma resuscitation (NCT01262196)
VITRIS (vasopressin for therapy of persistent traumatic hemorrhagic shock): multicentre
randomised controlled trial further exploring the role of vasopressin in fluid resistant shock
(NCT00379522)
CIST (colloids in severe trauma): multicentre pilot study of volume resuscitation based on
crystalloid only versus crystalloid-colloid (starch based) in trauma; this randomised controlled
trial has just been completed, looking particularly at the incidence of intra-abdominal
hypertension (NCT00890383)
HypoResus (field trial of hypotensive v standard resuscitation for hemorrhagic shock after
trauma): randomised controlled trial comparing standard resuscitation with hypotensive
resuscitation prehospital and in the first 2 h in the emergency department (NCT01411852)

BMJ | 15 SEPTEMBER 2012 | VOLUME 345 41
CLINICAL REVIEW
controlled trial of 229 patients with hypotension and severe
traumatic brain injury (Glasgow coma scale <9) who received
prehospital resuscitation with hypertonic or normal saline
had almost identical survival and neurological function six
months aer injury.28 Furthermore, a recent randomised con-
trolled trial of prehospital use of hypertonic solutions was
terminated by the data and safety monitoring board aer ran-
domisation of 1331 patients, having met prespecied futility
criteria. Among patients with severe traumatic brain injury
not in hypovolaemic shock, initial resuscitation with either
hypertonic saline or hypertonic saline or dextran, compared
with normal saline, did not result in improved neurological
outcome or survival at six months.29 Thus, we suggest the
use of crystalloid based uid administration in this cohort
of patients who are less severely injured.
Once haemostasis is achieved, what should be done to
ensure adequate resuscitation in severe trauma?
Once haemostasis has been achieved with surgical inter-
vention, fracture splintage or angiography, or the require-
ment for these interventions identied as not necessary,
then denitive resuscitation is required. If patients are
resuscitated to normal blood pressure and pulse with-
out further parameters being used to evaluate for tissue
hypoxia, over half of patients would be inadequately
resuscitated, with increased morbidity and mortality.30 w42
Resuscitation to targets of oxygen delivery or use is termed
goal directed therapy, and good quality evidence from ran-
domised trials indicates that this approach should be used
in trauma; indeed, the original evidence for this approach
came from trauma studies.w43 w44 w45 w46 w47 31 32
What other agents should be used in the initial
resuscitation period?
Hyperbrinolysis is common aer trauma, owing to associ-
ated hypovolaemic shock and tissue injury.w48 In a recent,
large, multinational randomised controlled trial research-
ers targeted a specic component of trauma induced coag-
ulopathy—hyperbrinolysis. They showed a reduction in
mortality with the use of tranexamic acid, which has anti-
brinolytic properties (1 g delivered over 15 min, then 1 g
over 4 h, commenced within 3 h of injury).33
Contributors
: TH conceived the review and wrote the introduction,
sections of permissive hypovolaemia, resuscitation endpoints, and fluid
resuscitation. RT wrote the sections contrasting colloids and crystalloids
with hypertonic saline. KB wrote the sections on blood product use and
trauma induced coagulopathy. The contributions were correlated by TH,
and all authors reviewed the paper. TH is guarantor.
Competing interests
: KB has received unrestricted research funding from
Octapharma and Thromboelastometry and has consulted for Haemonetics
and Sangart; no other relationships or activities that could appear to have
influenced the submitted work.
Provenance and peer review
: Commissioned; externally peer reviewed.
1 Roberts I, Shakur H, Edwards P, Yates D, Sandercock P. Trauma care research
and the war on uncertainty. BMJ 2005;331:1094-6.
2 Kauvar DS, Lefering R, Wade CE. Impact of haemorrhage on trauma outcome:
an overview of epidemiology, clinical presentations and therapeutic
considerations. J Trauma 2006;60:S3-11.
3 Chesnut RM, Marshall LF, Klauber MR, Blunt BA, Baldwin N, Eisenberg HM,
et al. The role of secondary brain injury in determining outcome from severe
head injury. J Trauma 1993;34:216-22.
4 Bratton SL, Chestnut RM, Ghajar J, McConnell Hammond FF, Harris OA, Hartl
R, et al. Guidelines for the management of severe traumatic brain injury. I.
Blood pressure and oxygenation. J Neurotrauma 2007;24(suppl 1):S7-13.
How do I identify patients with trauma induced coagulopathy?
Standard clotting tests from laboratories such as the pro-
thrombin time do not show any of the key derangements in
trauma induced coagulopathy, such as reduced clot strength
and brinolysis.25 Furthermore, in a trauma setting, it is
impractical to wait for tests that can take up 1 h to process.
The point of care versions of these tests (such as the pro-
thrombin time) are prone to be under-read in the presence
of low haematocrits. These diculties have led to a renewed
interest in the use of thromboelastography—a point of care
assessment of clot generation, strength, and breakdown.
This procedure has the potential to provide a rapid assess-
ment of the whole clotting process, but it has not yet been
validated in the acute setting.25 In the absence of a validated
diagnostic test at the point of care, management is therefore
blind to the status of the coagulation system and relies on
clinical judgment and empiric therapy.
What fluids should be used to resuscitate trauma patients
who do not need DCR?
Patients who do not need DCR need no immediate resuscita-
tion until denitive imaging has identied the underlying
injuries. These patients should be observed carefully for signs
of physiological and metabolic deterioration, consequent
on disease progression with blood loss, visceral injury, and
pericardial or pleural tamponade. Debate continues on the
relative merits of colloid or crystalloid based resuscitation
strategies, with a recent Cochrane review concluding that
there was no evidence that survival was better with one or
the other solution.26
However, a subgroup analysis of 460 patients with trau-
matic brain injury (Glasgow coma scale ≤13) from a large ran-
domised controlled trial comparing the safety of albumin in
normal saline with normal saline identied a survival advan-
tage in the crystalloid group (33.2% v 20.4%, P=0.003).27
Hypertonic solutions have been proposed to improve cer-
ebral perfusion and reduce cerebral oedema, and have been
advocated for resuscitation of patients with traumatic brain
injury.
w40
A meta-analysis of eight randomised trials identi-
ed a survival advantage in this group,w41 but a randomised
TIPS FOR NON-SPECIALISTS
Doctors and nurses who care for trauma patients who are severely injured need to be
familiar with the principles of resuscitation strategies for damage control, as outlined in this
review
A clearly written protocol for massive transfusion facilitates rapid access to and delivery of
blood product based resuscitation
Transfer patients with severe traumatic injuries to a dedicated trauma unit
Trauma teams bring together doctors and nurses from a range of disciplines, and scenario
based practice is likely to facilitate smooth teamwork
QUESTIONS FOR FUTURE RESEARCH
How do we balance the risks of impaired organ perfusion consequent on hypovolaemic
resuscitation with clot preservation?
How do we identify and target trauma induced coagulopathy in the acute phase?
What is the most effective combination of blood products for initial trauma resuscitation?
Should patients with traumatic brain injury be subject to different initial resuscitation
strategies?
Does therapeutic hypothermia have a role in trauma resuscitation or traumatic brain injury
in the acute phase?

42 BMJ | 15 SEPTEMBER 2012 | VOLUME 345
CLINICAL REVIEW
21 Hess JR, Brohi K, Dutton RP, Hauser CJ, Holcomb JB, Kluger Y, et al. The
coagulopathy of trauma: a review of mechanisms. J Trauma 2008;65:
748-54.
22 Borgman MA, Spinella PC, Perkins JG, Grathwohl KW, Repine T, Beekley AC,
et al. The ratio of blood products transfused affects mortality in patients
receiving massive transfusions at a combat support hospital. J Trauma
2007;63:805-13.
23 Rajasekhar A, Gowing R, Zarychanski R, Arnold DM, Lim W, Crowther MA,
et al. Survival of trauma patients after massive red blood cell transfusion
using a high or low red blood cell to plasma transfusion ratio. Crit Care Med
2011;39:1507-13.
24 Davenport R, Curry N, Manson J, De’Ath H, Coates A, Rourke C, et al.
Hemostatic effects of fresh frozen plasma may be maximal at red cell ratios
of 1:2. J Trauma 2011;70:90-5.
25 Davenport R, Manson J, De’Ath H, Platton S, Coates A, Allard S, et al.
Functional definition and characterization of acute traumatic coagulopathy.
Crit Care Med 2011;39:2652-8.
26 Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in
critically ill patients. Cochrane Database Syst Rev 2011;3:CD000567.
27 SAFE Study Investigators; Australian and New Zealand Intensive Care Society
Clinical Trials Group; Australian Red Cross Blood Service; George Institute
for International Health, Myburgh J, Cooper DJ, et al. Saline or albumin
for fluid resuscitation in patients with traumatic brain injury. N Engl J Med
2007;357:874-84.
28 Cooper JD, Myles PS, McDermott FT, Murray LJ, Laidlaw J, Cooper G, et al.
Pre-hospital hypertonic saline resuscitation of patients with hypotension
and severe traumatic brain injury: a randomized controlled trial. JAMA
2004;291:1350-7.
29 Bulger EM, May S. Out-of-hospital hypertonic resuscitation following severe
traumatic brain injury: a randomized controlled trial. JAMA 2010;304:
1455-64.
30 Claridge JA, Crabtree TD, Pelletier SJ, Butler K, Sawyer RG, Young JS. Persistent
occult hypoperfusion is associated with a significant infection rate and
mortality in major trauma patients. J Trauma 2000;48:8-13.
31 McKinley BA, Valdivia A, Moore FA. Goal-orientated shock resuscitation
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ANSWERS TO ENDGAMES, p 48
For long answers go to the Education channel on bmj.com
CASE REPORT
Ear pain and facial palsy
1 Necrotising (malignant) otitis externa.
2 The House-Brackmann grading system.
3 Admission for intravenous antibiotics, aural microsuction, eye care, pain management, and
occasionally surgical debridement.
STATISTICAL QUESTION
Hazards and hazard ratios
Statements a and d are true, whereas b
and c are false.
Echocardiogram showing evidence of a
pericardial effusion (white arrow)
PICTURE QUIZ
Signs of shock and raised jugular venous pressure
1 The chest radiograph shows a globular cardiac silhouette, possibly as a result of fluid
surrounding the heart. The echocardiogram shows a large pericardial effusion (figure).
2 Cardiac tamponade. Electrocardiography classically shows diffuse decreased QRS voltages and
may display electrical alternans.
3 In view of the slow onset, associated weight loss, and other systemic symptoms, cancer is the
most likely diagnosis. In developing countries tuberculosis should also be considered.
4 Beck’s triad and Kussmaul’s sign were seen in this patient. Pulsus paradoxus could be
looked for.
5 Urgent pericardiocentesis under fluoroscopy or echocardiographic guidance should be
undertaken. Fluid should be sent for cytology, protein count, and microbiology. The underlying
cause of the tamponade will need appropriate management.