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ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES

:: Management of Hypovolaemic Shock


in the Trauma Patient
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Suggested citation:
Ms Sharene Pascoe, Ms Joan Lynch 2007, Adult Trauma Clinical Practice Guidelines,
Management of Hypovolaemic Shock in the Trauma Patient,
NSW Institute of Trauma and Injury Management.
Authors
Ms Sharene Pascoe (RN), Rural Critical Care Clinical Nurse Consultant
Ms Joan Lynch (RN), Project Manager, Trauma Service, Liverpool Hospital
Editorial team
NSW ITIM Clinical Practice Guidelines Committee
Mr Glenn Sisson (RN), Trauma Clinical Education Manager, NSW ITIM
Dr Michael Parr, Intensivist, Liverpool Hospital
Assoc. Prof. Michael Sugrue, Trauma Director, Trauma Service, Liverpool Hospital
This work is copyright. It may be reproduced in whole or in part for study
training purposes subject to the inclusion of an acknowledgement of the source.
It may not be reproduced for commercial usage or sale. Reproduction for purposes
other than those indicated above requires written permission from the NSW Insititute
of Trauma and Injury Management.
NSW Institute of Trauma and Injury Management
SHPN (TI) 070024
ISBN 978-1-74187-102-9
For further copies contact:
NSW Institute of Trauma and Injury Management
PO Box 6314, North Ryde, NSW 2113
Ph: (02) 9887 5726
or can be downloaded from the NSW ITIM website
http://www.itim.nsw.gov.au
or the
NSW Health website http://www.health.nsw.gov.au
January 2007
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Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE i
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Important notice!
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'Management of Hypovolaemic Shock in the Trauma Patient clinical practice guidelines are
aimed at assisting clinicians in informed medical decision-making. They are not intended to
replace decision-making. The authors appreciate the heterogeneity of the patient population
and the signs and symptoms they may present with and the need to often modify
management in light of a patient's co-morbidities.
The guidelines are intended to provide a general guide to the management of specified
injuries. The guidelines are not a definitive statement on the correct procedures, rather they
constitute a general guide to be followed subject to the clinicians judgement in each case.
The information provided is based on the best available information at the time of writing,
which is December 2003. These guidelines will therefore be updated every five years and
consider new evidence as it becomes available.
These guidelines are intended for use in adults only.
All guidelines regarding pre-hospital care should be read and
considered in conjunction with NSW Ambulance Service protocols.
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Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE iii
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Contents
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Algorithm 1 ::
The management of hypovolaemic
shock in the trauma patient ......................................1
Summary of guidelines.....................................3
1 Introduction................................................5
2 Methods.....................................................6
3 How do you know when the
patient is in hypovolaemic shock? ............8
4 How do you find the sources of bleeding
in a hypotensive trauma patient? ............10
5 What is the best management
of the bleeding patient?...........................12
6 If fluid resuscitation is indicated,
what type of fluid should be given? ........15
7 What are the endpoints of fluid
resuscitation in the trauma patient?........17
Evidence tables
Evidence Table 1. How do you know when
a trauma patient is in
hypovolaemic shock?...................22
Evidence Table 2. How do you find the sources
of bleeding in a hypotensive
trauma patient?...........................26
Evidence Table 3. What is the best management
of the bleeding patient? ..............27
Evidence Table 4. If fluid resucitation
is indicated, what type
of fluids should be used?.............31
Evidence Table 5. What are the endpoints
of fluid resuscitation in
the trauma patient?.....................37
Appendices
APPENDIX A ::
Search Terms used for the identificaion of studies ...44
References .....................................................46
List of tables
Table 1. Levels of evidence ......................................11
Table 2. Codes for the overall assessment
quality of study checklists ...........................11
Table 3. Complications of blood transfusions...........15
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Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 1
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Algorithm 1 :: The management of hypovolaemic shock in the trauma patient
The Management of Hypovolaemic Shock in the Trauma Patient
If definitive care is not available in your facility make early contact with retrieval services
Primary survey
Includes organising the trauma team, calling the surgeon and notifying the blood bank.
Also consider early call to Retrieval Services (AMRS 'formerly MRU' 1800 650 004).
REMEMBER BP and HR will not identify all trauma patients who are in shock.
ASSESS History and perfusion indices ABG's, base deficit, lactate, Hb and HCT.
In the presence of uncontrolled haemorrhage and a delay of greater than 30 minutes to operative haemostasis,
infuse small aliquots (100-200mls) of fluid to maintain systolic blood pressure between 80-90mmHg. Use caution in
the elderly. Contraindicated in the unconscious patient without a palpable blood pressure. Maintain the systolic blood
pressure >90mmHg for those with a traumatic brain injury.
SIGNS OF SHOCK? Perform Secondary Survey
Identify the source of haemorrhage
Airway /
C-spine
1
Protect airway,
secure if
unstable.
1
Airway adjunct
as needed.
1
Control of
c-spine.
Circulation
1
Secure venous
access x 2
large bore
cannula.
1
Bloods:
x-match
FBC
EUC's
Creatinine
ABG's
Blood ETOH.
1
Control
external
bleeding.
Disability
1
Assess
neurological
status.
1
AVPU:
alert
responds
to vocal
stimuli
responds
to painful
stimuli
unresponsive.
Exposure /
Environment
1
Undress
patient.
1
Maintain
temperature.
Adjuncts
1
X-ray:
chest
pelvis
lateral
c-spine.
Breathing
1
Definitive
control of
airway.
1
Oxygen.
1
Bag and
mask.
External
1
Careful visual
inspection.
Long bones
1
Careful visual
inspection.
Chest
1
Chest x-ray.
Abdomen
1
DPA* and
/ or FAST**.
Retroperitoneum
1
Pelvic x-ray.
External
1
Apply direct
pressure.
1
Suture
lacerations.
Interventions
Long bones
1
Splint + / -
reduce #.
Chest
1
Chest tube.
Abdomen
1
Emergency
Laparotomy.
Retroperitoneum
1
Externally
stabilise pelvis.
1
Emergency
angiogram.
* Diagnostic Peritoneal Aspiration (DPA). >10mls of frank blood = positive DPA.
** Focused Abdominal Sonography in Trauma (FAST). Free fluid = positive FAST.
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Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 3
Summary of guidelines
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When the haemodynamically unstable patient enters the resuscitation room, IV
a primary survey with full exposure takes place. Carefully inspect for external
bleeding sources and examine the long bones. If x-ray facilities are available,
a supine chest x-ray and pelvic x-ray should be obtained within 10 minutes
of arrival. The CXR will identify any large haemothorax. If the pelvic x-ray
shows a pelvic fracture, the remaining two sites of significant bleeding are
the abdomen and the pelvic retroperitoneum. The options for assessing
the abdomen are DPA and / or FAST.
GUIDELINE LEVEL OF EVIDENCE
Blood pressure and heart rate will not identify all trauma patients III-2
who are in shock. Assessment of the trauma patient should include:
:: arterial blood gases and assessment of base deficit
:: haemoglobin
:: lactate
:: haematocrit.
These tests are only of value when interpreted in a series,
therefore should be repeated.
GUIDELINE LEVEL OF EVIDENCE
How do you know when the patient is in hypovolaemic shock?
GUIDELINE LEVEL OF EVIDENCE
What is the best management of the bleeding patient?
:: Establish patent airway. III-2
:: Ensure adequate ventilation and oxygenation.
:: Secure venous access large bore cannula x 2.
:: Control any external bleeding by applying direct pressure.
:: Rapidly identify patients requiring operative haemostasis.
:: Establish prompt contact with the major referral hospital and retrieval service.
In the presence of uncontrolled haemorrhage and a delay of greater than II
30 minutes to operative haemostasis, infuse small aliquots of fluid (100-200mls)
to maintain systolic blood pressure between 80-90mmHg. Use caution in the
elderly. Contraindicated in unconscious patients without a palpable blood
pressure and those with traumatic brain injury (see over leaf).
How do you find the sources of bleeding in a hypotensive trauma patient?
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PAGE 4 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
Summary of guidelines
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:: Early use of blood, if available, remains the optimal resuscitation fluid Consensus
for the hypovolaemic patient. Use with caution due to numerous complications.
:: Where blood is not available or delayed, Compound Sodium Lactate II
(Hartmanns) is the preferred alternative for the initial resuscitation of the
hypovolaemic trauma patient. Caution should be exercised in the trauma
patient with liver disease.
:: 0.9% Normal Saline is also an acceptable alternative. Large volumes,
however may result in metabolic acidosis.
GUIDELINE LEVEL OF EVIDENCE
If fluid resuscitation is indicated, what type of fluid should be given?
Traditional haemodynamic parameters do not adequately quantify the degree III-2
of physiological derangement in hypovolaemic trauma patients. If point of care
blood gas analysis is available base deficit and lactate levels should be used to
identify the magnitude of tissue oxygen debt and the adequacy of resuscitation.
These tests are only of value when interpreted in a series, therefore should
be repeated.
A persistently high or increasing base deficit indicates the presence of ongoing
blood loss or inadequate volume replacement.
In the absence of point of care blood gas analysis capability the restoration Consensus
of a normal mentation, heart rate, skin perfusion and urine output and maintain
ing the systolic blood pressure at 80-90 mmHg serve as the end point of
resuscitation.
GUIDELINE LEVEL OF EVIDENCE
What are the endpoints of fluid resuscitation in the trauma patient?
GUIDELINE LEVEL OF EVIDENCE
What is the best management of the bleeding patient? continued...
In the presence of uncontrolled haemorrhage in the patient with a concurrent I
traumatic brain injury, prevention of secondary brain injury from hypotension
is crucial as a systolic blood pressure <90mmHg is associated with poor outcomes.
Infuse small aliquots of fluid (100-200mls) to maintain systolic blood pressure
above 90mmHg.
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Despite significant advances in the management
of trauma victims, traumatic injury remains
the fifth leading cause of death in Australia.
A significant number of these deaths are the result
of hypovolaemic shock. Acute blood loss following
injury leads to a depression of organ and immune
function that, if prolonged, progresses to the
sequential failure of multiple organ systems.
1
Timely diagnosis, surgical control of on-going loss
and physiologically directed fluid replacement remain
the cornerstones of management. In recent years,
however, the practice of rapid fluid replacement
has been questioned.
Early recognition of hypovolaemic shock is vital
for optimal care of the injured patient. Ongoing
controversy exists regarding the diagnosis of
occult shock and the ideal resuscitation scheme.
Advancement in technology and pharmacology
has added more treatment options to care for the
bleeding patient. This guideline aims to objectively
analyse the literature to provide the clinician with
evidence-based options. The guidelines will also seek
to establish the optimal care of the bleeding patient
in the rural setting where resources may be lacking
and access to definitive care is delayed.
This guideline has been developed to provide
evidence-based recommendations for the
management of hypovolaemic shock in
the trauma patient.
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1 Introduction
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2.1 Scope of the guideline
This guideline is intended for use by all clinicians
who are involved in the initial care of patients with
hypovolaemic shock: ambulance officers, emergency
nurses, and physicians.
This guideline has been developed to assist clinicians
to provide a selective evidence based approach to the
management of trauma patients with hypovolaemic
shock. It is recognised that this guideline will not
suit all clinical situations.
These guidelines are not prescriptive, nor are
they rigid procedural paths. The guidelines rely
on individual clinicians to decipher the needs of
individuals. They aim to provide information on
what decisions can be made, rather than dictate
what decisions should be made.
2.2 Aims and objectives
of the guideline
This guideline aims to summarise the available
evidence to allow clinicians to make evidence-based
decisions in the diagnosis and management of trauma
patients with hypovolaemic shock.
A multidisciplinary team was consulted to aid in the
identification of the key clinical dilemmas that faced
clinicians when caring for patients with hypovolaemic
shock. By identifying the key clinical questions, the
guideline should facilitate:
:: early diagnosis of hypovolaemic shock
:: identification of the source(s) of bleeding
:: enhancement of tissue perfusion while minimising
ongoing haemorrhage.
PAGE 6 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
2 Methods
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The clinician using this guideline can identify:
:: when the patient is in hypovolaemic shock
:: how to find the sources of bleeding
in a hypotensive trauma patient
:: what is the best management of the
bleeding patient
:: over what timeframe a hypovolaemic trauma
patient should be fluid resuscitated
:: what type of fluids should be used if required
:: what the endpoints of fluid resuscitation
in the hypovolaemic trauma patient.
2.3 Inclusion and exclusion
Inclusion criteria
Meta-analysis
Randomised control trials
Controlled clinical trials
Case series
Population aged >16 years
Traumatic hypovolaemic shock
Exclusion criteria
Case reports
Paediatric <15 years
Hypovolaemic shock secondary to burns
or non-traumatic (sepsis, dehydration)

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2.4 Strength of the evidence
2.4.1 Level of evidence
The articles were classified according to their general purpose and study type.
Table 1. Levels of evidence
2-4
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:: METHODS
2.4.2 Quality appraisal
The included articles were appraised according to the NHMRC. The MERGE assessment tool.
5
The articles were rated for quality on a 4-point scale as follows:
Table 2. Codes for the overall assessment quality of study checklists
Level I Evidence obtained from a systematic review of all relevant randomised control trials
Level II Evidence obtained from at least one properly-designed randomised control trial.
Level III-1 Evidence obtained from well-designed pseudo-randomised controlled trials
(alternate allocation or some other method).
Level III-2 Evidence obtained from comparative studies (including systematic reviews of such studies) with concurrent controls
and allocation not randomised, cohort studies, case-control studies, or interrupted time series with a control group.
Level III-3 Evidence obtained from comparative studies with historical control, two or more
single arm studies or interrupted time series without a parallel control group.
Level IV Evidence obtained from a case-series, either post-test or pre-test / post-test
Low risk of bias A All or most evaluation criteria from the checklist are fulfilled,
the conclusions of the study or review are unlikely to alter.
Low-moderate risk of bias B1 Some evaluation criteria from the checklist are fulfilled. Where evaluation
criteria are not fulfilled or are not adequately described, the conclusions
of the study or review are thought unlikely to occur.
Moderate High risk of bias B2 Some evaluation criteria from the checklist are fulfilled. Where evaluation criteria
are not fulfilled conclusions of the study or review are thought likely to alter.
High risk of bias C Few or no evaluation criteria fulfilled. Where evaluation criteria are not fulfilled
or adequately described, the conclusion of the study or review are thought
very likely to alter.
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Blood pressure and heart rate will not identify all trauma patients III-2
who are in shock. Assessment of the trauma patient should include:
:: arterial blood gases and assessment of base deficit
:: haemoglobin
:: lactate
:: haematocrit.
These tests are only of value when interpreted in a series,
therefore should be repeated.
GUIDELINE LEVEL OF EVIDENCE
PAGE 8 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
3 How do you know when the
patient is in hypovolaemic shock?
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Acute blood loss or the redistribution of blood,
plasma, or other body fluid predisposes the
injured patient to hypovolaemic shock. Absolute
hypovolaemia refers to the actual loss of volume
that occurs in the presence of haemorrhage.
Relative hypovolaemia refers to the inappropriate
redistribution of body fluids such as that that
occurs following major burn trauma.
6
Acute blood loss is a very common problem following
traumatic injury. Rapid recognition and restoration of
homeostasis is the cornerstone of the initial care of
any seriously injured patient. Delay in recognising
and quickly treating a state of shock results in a
progression from compensated reversible shock to
widespread multiple system organ failure to death.
Morbidity may be widespread and can include renal
failure, brain damage, gut ischaemia, hepatic failure,
metabolic derangements, disseminated intravascular
coagulation (DIC), systemic inflammatory response
syndrome (SIRS), cardiac failure, and death.
The standard physiological classification of acute
blood loss has been promulgated through the
Advanced Trauma Life Support Course developed
by the American College of Surgeons.
7
While a
useful theoretical basis for understanding the stages
of shock, the physiological changes said to occur as
a patient progresses through the four stages are
not supported by evidence.
Lechleuthner et al in a study of blunt trauma found
that a systolic blood pressure (SBP) <90mmHg
will only identify 61% of patients with active
haemorrhage (sensitivity 61% and specificity 79%).
3.1% of patients with uncontrolled haemorrhage
had undisturbed physiological variables.
8
These
findings are supported by others.
9-11
Demetriades
examined the incidence and prognostic value of
tachycardia and bradycardia in the presence of
traumatic hypotension. The incidence of relative
bradycardia (SBP <90mmHg and HR <90 minute)
was present in 28.9% of hypotensive patients.
11
The results of these studies suggest that commonly
monitored variables, in and of themselves, do not
accurately reflect or predict the circulating volume of
injured patients.
9
The accuracy of circulatory values
(HR, BP, urine output and capillary return) in detecting
hypovolaemia in trauma patients is hampered by
complex neurohormonal mechanisms that can
successfully compensate for 15% loss of circulating
volume, particularly considering the majority of
trauma patients are young, fit males.
9
Confounders
such as traumatic brain injury also decreases the
sensitivity of SBP and HR to detect hypovolaemic
shock.
8
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Detecting hypovolaemic shock in the trauma patient
with normal haemodynamics is reliant on history,
physical examination and pathology, including,
base deficit, lactate, haematocrit and haemoglobin.
However, these tests are only of value when
interpreted in a series. Initial haemoglobin (Hb)
of <=6g/l correlated well with mortality (48.4%)
and vital signs. A low level Hb (<8g/l) was found by
Knottenbelt, in a review of 1000 trauma patients, to
be an indicator of serious ongoing haemorrhage.
12
Lactate and base-deficit have also shown to correlate
well with vital signs and mortality.
13,14
The ability
and value of haemoglobin, lactate and base-deficit,
however, to predict blood loss in haemodynamically
stable patients is unknown.
Oman examined the predictive power of haematocrit
decrease of >5% as an indicator of ongoing
haemorrhage in trauma patients who receive IV
fluids. The study found that haematocrit was not
useful in identifying patients who were bleeding,
but was accurate 97% of the time for identifying
those who were not (sensitivity 94%, specificity
43%, PPV 26%, NPV 97%).
15
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:: HOW DO YOU KNOW WHEN THE PATIENT IS IN HYPOVOLAEMIC SHOCK?
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4.1 Probabilities and assessment
In a haemodynamically unstable trauma patient there
are five potential sites of major blood loss: externally,
long bones, the chest, the abdomen and the
retroperitoneum.
7
4.2 Externally and long bones
Blood loss from fractures and lacerations can result
in a significant amount of blood loss. The scalp is a
highly vascular region and may be associated with
significant blood loss. It is however, extremely difficult
to estimate the volume of bleeding from scalp and
other lacerations due to blood loss at the scene and
en route to the hospital. External blood loss requires
careful visual inspection.
Clarke reported that a single long-bone fracture may
result in 10-30% loss of total blood volume. Bleeding
from long bone fractures is present in approximately
40% of cases and is usually evident from swelling
due to haematoma formation. This is usually
a contribution, not a major ongoing cause of
blood loss.
16-18
4.3 The chest
Intrathoracic haemorrhage is to be expected in
4-29% of cases
16-19
and can be evaluated on a chest
x-ray, which should be performed within 10 minutes
of the patients arrival.
20
There are minor limitations to
first mobile supine chest x-ray. A small haemothorax
can be initially missed in 5% of surviving patients and
in up to 18% in non-surviving patients. However,
a large haemothorax contributing to haemodynamic
instability should not be missed.
4.4 The pelvis
The next part of the decision tree is crucial, trying
to decide whether the blood loss is in the abdomen
or in the pelvic retroperitoneum or in both. At this
point the AP pelvic radiograph should be reviewed.
If a pelvic fracture with possible disruption of the
pelvic ligaments causing an unstable fracture pattern
is seen or suspected, the probability of pelvic arterial
bleeding is 52%.
The initial AP pelvic radiograph is the only guide
to determine the probability of pelvic bleeding.
Disruptions involving only the pubic rami do not
vertically or rotationally unstabilise the pelvic ring,
but when recognising a fracture of the pubic bone,
posterior disruption and probability of arterial
bleeding must always be suspected. One must also
bear in mind that bilateral inferior/superior pubic
ramus fractures (butterfly type fracture from AP
compression mechanism), acetabular fractures and
even simple ramus fractures in the elderly can lead
to arterial bleeding causing hypotension.
PAGE 10 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
4 How do you find the
sources of bleeding in a
hypotensive trauma patient?
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When the haemodynamically unstable patient enters the resuscitation room, IV
a primary survey with full exposure takes place. Carefully inspect for external
bleeding sources and examine the long bones. If x-ray facilities are available,
a supine chest x-ray and pelvic x-ray should be obtained within 10 minutes
of arrival. The CXR will identify any large haemothorax. If the pelvic x-ray
shows a pelvic fracture, the remaining two sites of significant bleeding are
the abdomen and the pelvic retroperitoneum. The options for assessing the
abdomen are DPA and / or FAST.
GUIDELINE LEVEL OF EVIDENCE
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4.5 The abdomen
The abdomen is the most difficult to assess in the
rural and urban environment. Diagnostic Peritoneal
Aspiration (DPA) and Focused Abdominal Sonography
in Trauma (FAST) are the preferred diagnostic means
to determine if there is intra-abdominal bleeding.
Although the availability of FAST is increasing,
it is not available in all urban and rural emergency
departments. DPA is recommended if an EMST
accredited clinician is available. If neither FAST nor
DPA can be undertaken, the clinician should examine
the other four sources for blood loss, upon exclusion
of these it must be assumed that the patient has
intraabdominal bleeding until proven otherwise.
Seventy-eight per cent of intraperitoneal injuries
result in haemorrhage including; the spleen (22%),
the liver (20%), the bladder (15%), the bowel
mesentery (10%) and diaphragmatic lesions (4%).
Renal haemorrhage is found in 7% of cases.
The other 22% are intraperitoneal injuries
not associated with bleeding.
4.6 Decision-making
In the face of continuing haemodynamic instability
and in the absence of external blood loss, long bone
or pelvic fractures or any evidence of bleeding on
chest x-ray, immediate laparotomy is warranted.
If an unstable pelvic fracture is seen on x-ray
the chance of pelvic arterial bleeding is 52%.
The patient should have their pelvis externally
stabilised in the resuscitation room. Please refer to
the Adult Trauma Clinical Practice Guidelines The
Management of Haemodynamically Unstable Patients
with a Pelvic Fracture (which is available from the
NSW Institute of Trauma and Injury Management,
contact details listed on the inside cover).
4.7 Timeframes
For every three minutes of haemodynamic
instability elapsed without haemorrhage control
in the emergency department, there is a 1%
increase in mortality. Therefore decision making
within pre-determined timeframes is crucial.
The haemodynamically unstable pelvic fracture
patient should leave the resuscitation room
within 45 minutes heading for either angiography
or laparotomy. Assessment of external bleeding
sources and long bone fractures should take place
within the first five minutes. The chest x-ray and
pelvic x-ray should be performed within 10 minutes
of the patients arrival. Assessment of the abdomen
with FAST / DPA if possible, should be completed
within 30 minutes.
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:: HOW DO YOU FIND THE SOURCES OF BLEEDING IN A HYPOTENSIVE TRAUMA PATIENT
Performance indicators
Assessment of external bleeding sources and long bone
fractures should take place within the first five minutes.
The chest x-ray and pelvic x-ray should be performed
within 10 minutes (if x-ray facilities are available).
FAST / DPA within 30 minutes.
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PAGE 12 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
5 What is the best management
of the bleeding patient?
blood
O-neg
Management priorities in the bleeding patient
include controlling blood loss, replenishing
intravascular volume and sustaining tissue perfusion.
1
When services are needed that exceed available
resources, it is of critical importance that early
consultation with a trauma specialist and rapid
transportation to definitive care occurs.
(Refer to NSW Department of Health Circular 2002/105
Early Notification of Severe Trauma in Rural NSW)
5.1 Controlling blood loss
After establishing a patent airway, ensuring adequate
ventilatory exchange and oxygenation and securing
venous access, the highest priority in the bleeding
patient is to control haemorrhage.
21
Because patients
may bleed from multiple sites, it is imperative that the
attending medical officer establish strategies to
address all sources of bleeding. Sources of bleeding
may be broadly classified as external or internal.
5.1.1 Controlling external bleeding
The Australian Resuscitation council advocates the
use of direct pressure to gain prompt control of
external bleeding.
22
The recommended method
involves approximating the wound edges if possible,
holding an absorbent dressing firmly over the area
with the heel of the hand, and elevating the bleeding
part. After bleeding is controlled the absorbent
dressing may be secured with a bandage. If bleeding
continues through the initial dressing, apply a second
dressing over the first and secure with a bandage.
Do NOT disturb the dressing once the bleeding has
been controlled. Arterial tourniquets are reserved for
life-threatening bleeding and when direct pressure to
the wound has failed to stop the bleeding or when
protruding objects prevent direct pressure.
GUIDELINE LEVEL OF EVIDENCE
What is the best management of the bleeding patient?
:: Establish patent airway. III-2
:: Ensure adequate ventilation and oxygenation.
:: Secure venous access large bore cannula x 2.
:: Control any external bleeding by applying direct pressure.
:: Rapidly identify patients requiring operative haemostasis.
:: Establish prompt contact with the major referral hospital and retrieval service.
In the presence of uncontrolled haemorrhage and a delay of greater than II
30 minutes to operative haemostasis, infuse small aliquots of fluid (100-200mls)
to maintain systolic blood pressure between 80-90mmHg. Use caution in the
elderly. Contraindicated in unconscious patients without a palpable blood
pressure and those with traumatic brain injury (see below).
In the presence of uncontrolled haemorrhage in the patient with a concurrent I
traumatic brain injury, prevention of secondary brain injury from hypotension
is crucial as a systolic blood pressure <90mmHg is associated with poor outcomes.
Infuse small aliquots of fluid (100-200mls) to maintain systolic blood pressure
above 90mmHg.
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5.1.2 Controlling internal bleeding
Evidence from numerous studies over the past
two decades indicates that immediate and definitive
operative haemostasis is the optimal treatment
for internal bleeding.
23
To delay leaves the patient
susceptible to multi organ dysfunction and other
complications. In the rural and remote setting
however, immediate operative haemostasis is limited
by a lack of surgical presence and or operating
facilities at the site, and or lengthy transport times
to institutions capable of providing definitive
operative haemostasis.
Given these limitations the challenge for the rural
and remote physician is to rapidly identify patients
who would benefit from early transfer based on
available local resources, manage any life-threatening
injuries, and establish prompt contact with the major
referral centre, and the transport /retrieval service.
Prolonged time spent in a local emergency
department poses a significant risk of mortality
for the internally bleeding patient.
24
In a prospective analysis of the interhospital
transfer of injured patients to a tertiary centre by
Martin et al, up to 60% of the time delay pertaining
to the transfer of injured patients was related to the
time taken to notify the retrieval team.
25
In some
cases this accounted for delays in excess of three
hours. Numerous other studies have suggested that
prompt early contact with the retrieval service and
subsequent timely transfer of severely injured patients
is associated with increased survival rates.
26-28
5.2 Repleting intravascular volume
It is generally recognised that a depleted intravascular
volume robs the cardiovascular system of the preload
required for adequate cardiac output and peripheral
oxygen delivery.
29
Inadequate perfusion, even in the
absence of overt hypotension can result in a
neurohumoral cascade that ultimately leads
to sequential organ failure.
30
Since the early 1900's the conventional approach
to restoring intravascular volume and subsequently
sustaining tissue perfusion in the bleeding patient
has focused on early aggressive fluid replacement
with large volumes of crystalloid and or blood
products.
31
There is a growing body of evidence,
however, that suggests that in the presence of
uncontrolled haemorrhage, fluid replacement may
result in increased haemorrhage and subsequent
greater mortality.
1;31-34
This is thought most likely
to be the result of increased blood pressure and the
subsequent reversal of vasoconstriction, dislodgement
of early thrombus and subsequent secondary
haemorrhage, and the dilutional coagulopathy that
occurs in the presence of large volumes of fluid.
1
Bickell et al studied the outcomes of swine that
were bled from a 5mm tear in the infrarenal aorta
and aggressively resuscitated with lactated ringers
solution. Control swine were not resuscitated.
33
A significant elevation of mean arterial pressure
(MAP) in the resuscitated swine was observed.
One-hundred per cent of resuscitated swine died
within 100 minutes. All of the control swine survived.
The follow-up interval, however was only two hours.
Kowalenko and his associates developed a more
severe model of aortic tear and similarly
demonstrated that animals aggressively resuscitated
with high volumes of crystalloid had significantly
lower survival rates than animals under-resuscitated.
35
Data from Capone et al
36
, and Stern et al
37
are
consistent with the study by Kowalenko.
35
Several solid organ injury animal models of
uncontrolled haemorrhage demonstrate results
that also support low volume fluid resuscitation
in the presence of uncontrolled haemorrhage
37;38
In Krausz et al
39
study of aggressive resuscitation
following moderate splenic injury in rats, untreated
controls sustained significantly less haemorrhage
volumes than treated animals. Similarly, Solomonov et
al
38
study of severe splenic injury in rats demonstrated
that animals aggressively resuscitated experienced
greater haemorrhage volumes and a significantly
lower survival time in comparison to untreated
animals.
Findings from the animal models are substantiated
by Bickell et al
40
prospective controlled study of
patients presenting with a penetrating torso injury
and a prehospital systolic blood pressure less than
90mmHg. Patients received either immediate or
delayed fluid resuscitation following penetrating torso
trauma. The delayed resuscitation group (n = 289)
had intravenous access secured, but received no fluid
resuscitation until admission to the operating theatre.
The immediate resuscitation group (n = 309) were
aggressively fluid resuscitated at the scene and during
transport. The volume of fluid infused was 2,478mls.
Survival to discharge rates was significantly higher in
the delayed resuscitation group compared to the
immediate resuscitation group (70% versus 62%;
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:: WHAT IS THE BEST MANAGEMENT OF THE BLEEDING PATIENT?
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p = 0.04). A number of methodological flaws,
however, have led some to question the study.
First the causes of death were not well defined.
Second, there were a number of protocol violations.
Eight per cent of the delayed resuscitation group
received fluids prior to operative intervention.
Finally there was wide variation in the severity of
shock across both groups.
31
Despite these limitations,
Bickell's paper has led us to question traditional fluid
resuscitation regimes.
A randomised study undertaken by Turner compared
early and delayed fluid administration in trauma
patients. Significant protocol violation (with only
31% of the fluid group actually receiving fluid)
resulted in the inability of this study to find any
treatment affect (10.4% mortality early fluid
group vs 9.8% mortality in delayed group).
41
Dutton, in a randomised study evaluated fluid
resuscitation titrated to a SBP of 100mmHg or
70mmHg during a period of active haemorrhage
on mortality. There was no difference in mortality
between the two groups (7% vs 7%).
42
The low
pressure group appeared sicker than the higher
pressure group (ISS in the conventional-pressure
group was 19.65 11.84, compared with 23.64
13.82 in the low-pressure group). This may have
had a negative affect on survival in the low pressure
group.
Evidence from retrospective studies further supports
the concept of delayed resuscitation. Sampalis et al
43
reviewed the outcomes of 217 trauma patients who
had received intravenous fluid and compared them
with 217 controls who received no fluid. Correction
was made for gender, age, mechanism of injury and
injury severity score. Patients who received on-site
fluid resuscitation had a higher mortality than the
control group, particularly when fluid resuscitation
was combined with prolonged prehospital times.
Another study by Hambly and Dutton
44
compared
patients given fluids using a rapid infusion device
with historical controls who had undergone standard
resuscitation. Patient resuscitated with the rapid
infusion device had a higher mortality than those
receiving standard resuscitation.
The advocates of early aggressive resuscitation
of hypotensive bleeding patients argue that the
trauma population is too heterogenous to rely solely
on animal studies, and limited clinical trials. It should
be noted, however, that a systematic review on the
effects of early or large volume intravenous fluid in
uncontrolled bleeding by Kwan et al
45
found no
evidence to support the conventional practise of
early aggressive fluid resuscitation in the presence
of uncontrolled haemorrhage.
From this data consensus opinion now recommends
a more discriminating approach to the conventional
practice of delivering liberal volumes of intravenous
fluids to patients with uncontrolled bleeding.
46
The emerging evidence demonstrates that aggressive
fluid resuscitation in the bleeding patient leads to
additional haemorrhage through soft clot dissolution,
hydraulic acceleration of bleeding and dilution of
clotting factors. While aggressive fluid resuscitation
it is still considered appropriate for unconscious
patients with no palpable blood pressure, the latest
recommendations are to limit or delay intravenous
fluid resuscitation preoperatively in those with
uncontrolled haemorrhage, even if they are hypo
perfusing, although caution should be used with
the elderly.
In the presence of uncontrolled haemorrhage in
the patient with a concurrent traumatic brain injury,
prevention of secondary brain injury from hypotension
is crucial as a systolic blood pressure <90mmHg is
associated with poor outcomes. Infuse small aliquots
of fluid (100-200mls) to maintain systolic blood
pressure above 90mmHg.
122
There is abundant data to suggest that hypotensive
or limited resuscitation may be preferable to
aggressive fluid resuscitation in the setting of
uncontrolled haemorrhage. There is, however, little
evidence suggesting the volume of fluid required to
maintain vital organ perfusion yet prevent thrombus
dislodgment and subsequent secondary haemorrhage
and coagulation dilution. At best the literature
suggests that small aliquots of fluid (100-200mls)
should be given to maintain the patients systolic
blood pressure between 80-90mmHg.
47;48
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Performance indicators
Primary Survey completed.
Initial stabilisation of life threatening injuries.
Early transfer to definitive care..
Fluid administration <600mls/hr.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 14
Although a wide variety of options are currently available for fluid resuscitation, most agree that the best
resuscitation fluid is blood. It provides simultaneous volume expansion and oxygen carrying capacity.
49
However,
there are a number of disadvantages to blood as a resuscitation fluid (Table 1, p.7). In addition, issues regarding
compatibility, cost and storage requirements make blood and its derivates in the rural setting unlikely options as
a permanent solution for the rural physician. This limits the choice in the rural setting to crystalloid and or colloid.
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6 If fluid resuscitation is indicated,
what type of fluid should be given?
blood
O-neg
:: Early use of blood, if available, remains the optimal resuscitation fluid Consensus
for the hypovolaemic patient. Use with caution due to numerous complications.
:: Where blood is not available or delayed, Compound Sodium Lactate II
(Hartmanns)is the preferred alternative for the initial resuscitation of the
hypovolaemic trauma patient. Caution should be exercised in the trauma
patient with liver disease.
:: 0.9% Normal Saline is also an acceptable alternative. Large volumes,
however may result in metabolic acidosis.
GUIDELINE LEVEL OF EVIDENCE
Table 3. Complications of blood transfusions
Complication Mechanism
Impaired oxygen The ability of red blood cells to store and release oxygen is impaired after storage.
2,3
release from DPG levels fall rapidly resulting in a shift to the left of oxygen disassociation curve,
haemoglobin and subsequent impaired oxygen release.
Dilutional Stored blood contains all coagulation factors except factors V and VIII. Microvascular bleeding and
coagulopathy coagulopathy can occur in the setting of massive transfusion due to decreased levels of Factor V, VIII
and fibrinogen and associated increased prothrombin times.
Thrombocytopenia Dilutional thrombocytopenia is inevitable following massive transfusion as platelet function declines
to zero after a few days of storage.
Hypothermia Cold blood is associated with major coagulation derangements, peripheral vasoconstriction, metabolic acidosis,
and impaired immune response.
Citrate toxicity / Each unit of blood contains approximately 3g of citrate. Citrate toxicity is caused by acutely decreasing serum
Hypocalcaemia levels of ionised calcium, which occurs because citrate binds to calcium
Hyperkalaemia The plasma potassium concentration of stored blood increases during storage and may be over 30mmols/l.
The potential for Hyperkalaemia occurs with infusion rates of blood greater than 120ml/min and in patients
with severe acidosis.
Acid-base Lactic acid levels in the blood pack give stored blood an acid load of up to 30-40mmols/l. This along with
abnormalities citrate is metabolised rapidly. Citrate in turn is metabolised to bicarbonate, and a profound metabolic alkalosis
may result.
Haemolytic Reactions that result in destruction of the transfused cells may occur from errors involving ABO incompatibility,
transfusion or when the recipients antibody coats and immediately destroys the red blood cells.
reactions
Source: Adapted from Trauma.Org, Transfusion for Massive Blood Loss, http://www.trauma.org/resus/massive.html, accessed 27 April 2004
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 15
The debate regarding the relative effectiveness of
colloids compared to crystalloid continues several
decades after it began. Despite numerous publications
recommending specific fluids, there is no evidence
from randomised control trials that resuscitation with
colloids carries a reduced mortality in patients with
trauma, burns and following surgery.
50;51
Because
colloids are not associated with an increase in
survival and they carry a significant cost compared
to crystalloids there is no apparent benefit to their
use in the initial management of the hypovolaemic
patient.
50;51
A number of recent studies
52-54
have suggested that
the administration of hypertonic solutions, in the
absence of a head injury, allows for a more rapid
stabilisation of macro and micro-haemodynamics.
A recent systematic review by Alderson et al,
50
suggests that there is no evidence that hypertonic
crystalloid is better than isotonic crystalloid. Due to
the clinically different outcomes identified during the
review, however, Bunn et al recommends further
large-scale trials comparing hypertonic crystalloids
with isotonic crystalloids are required to inform
practice.
Wade and colleagues undertook a meta-analysis of
randomised trials examining the effects of Hypertonic
Saline (HS) and Hypertonic Saline/Dextran (HSD)
on survival of trauma patients until discharge or
for 30 days. The study found that HS alone does
not offer any benefit in terms of 30-day survival
over isotonic crystalloids. HSD may improve mortality
(OR 1.20 [95% CI 0.94-1.57]). The summary statistics
of the available data shows that HS does not provide
any benefit over current practices in terms of survival
and that HSD may be superior.
55
The optimal resuscitation fluid for the hypovolaemic
trauma patient remains the early use of blood.
In the absence of type specific blood, isotonic
crystalloids have an established safety record when
used appropriately.
42
Isotonic crystalloids produce
a relatively predictable increase in cardiac output and
are generally distributed throughout the extracellular
space. Where blood is not available or delayed,
Compound Sodium Lactate (Hartmanns) solution
is the preferred alternative for the initial resuscitation
of the hypovolaemic patient.
7;56
Compound Sodium
Lactate solution contains a bicarbonate precursor that
when metabolised helps to correct metabolic acidosis
and its attendant detrimental effects.
56
Compound
sodium lactate may need to be discontinued in the
presence of liver disease. Normal Saline 0.9% is
an acceptable alternative, however, large volumes
of 0.9% Normal Saline may result in metabolic
acidosis.
56
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Traditional haemodynamic parameters do not adequately quantify the degree III-2
of physiological derangement in hypovolaemic trauma patients. If point of care
blood gas analysis is available base deficit and lactate levels should be used to
identify the magnitude of tissue oxygen debt and the adequacy of resuscitation.
These tests are only of value when interpreted in a series, therefore should
be repeated.
A persistently high or increasing base deficit indicates the presence of ongoing
blood loss or inadequate volume replacement.
In the absence of point of care blood gas analysis capability the restoration Consensus
of a normal mentation, heart rate, skin perfusion and urine output and maintain
ing the systolic blood pressure at 80-90 mmHg serve as the end point of
resuscitation.
GUIDELINE LEVEL OF EVIDENCE
The challenge of caring for the hypovolaemic trauma
patient involves limiting cellular oxygen deficits,
anaerobic metabolism and resultant tissue acidosis.
57
Resuscitation is complete when the cellular oxygen
deficits have been corrected, tissue acidosis is
eliminated and normal aerobic metabolism is
restored.
58
Many patients may appear to be
adequately resuscitated, but have occult
hypoperfusion and ongoing tissue acidosis
(compensated shock).
57
Failure to recognise
this may result in organ dysfunction and death.
Traditionally it has been assumed that the restoration
of a normal mentation, blood pressure, heart rate,
skin perfusion and urine output signified the end
points of resuscitation.
59
Recent studies
60;61
however,
suggest that even after normalising these parameters,
up to 85% of severely injured patients have evidence
of compensated shock. Compensated shock is
defined as the presence of ongoing inadequate tissue
perfusion despite the normalisation of heart rate,
blood pressure, skin perfusion and urine output.
58
Recognition of compensated shock and its rapid
reversal are critical to minimise the risk of multi organ
dysfunction or death. Consequently, the traditional
end points of fluid resuscitation in the hypovolaemic
trauma patient need to be supplemented with global
and end organ markers that are sensitive to the
symptoms of compensated shock.
Global markers include: lactate levels and base
deficit.
54
Arterial pH is not as sensitive as it is
buffered by the body's compensatory mechanisms.
54
End organ markers include: monitoring of gut
perfusion with gastric tonometry, and direct
measures of tissue oxygen tension.
7.1 Base deficit
A recent study by Davis et al
62
found that the initial
base deficit was a reliable early indicator of the
magnitude of volume deficit. Patients were stratified
according to the level of base deficit as mild (base
deficit 2 to -5mmol/L), moderate (base deficit -6 to
-14) or severe (base deficit < -15). Patients with the
more severe base deficit required a greater volume
of fluid for resuscitation. Sixty-five per cent of patients
with an increasing base deficit had ongoing blood
loss. This is consistent with the findings of Canizaro
et al
63
, and James et al
64
.
Kincaid and his associates
65
, further found that
among trauma patients who normalised their lactate
levels, those with persistently higher base deficits
had a significantly increased risk of multi-organ
dysfunction and death. Patients with persistently
higher base deficits also demonstrated impaired
oxygen utilisation. In a similar study Rixen et al
13
found that an increase in base deficit between the
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time the patient arrived at the hospital to the time
of admission to intensive care identified patients
who were haemodynamically unstable, had high
transfusion requirements, coagulation and metabolic
derangements, and an increased risk of death.
It is important to note that base deficit may
be confounded by a number of factors. Firstly,
approximately 12-16 hours following resuscitation,
base deficit may no longer correlate with lactate.
66
Secondly, the administration of bicarbonate may alter
the base deficit without correcting the oxygen debt.
57
Underestimation of base deficit may occur in
the hypocapnic or hypothermic trauma patient,
whereas an elevated base deficit may be present
in the presence of excess heparin in the blood.
Finally, alcohol intoxication can worsen base deficit
for similar levels of injury severity after trauma.
In summary, although base deficit has its limitations,
it is apparent that base deficit levels are a useful guide
for identifying the magnitude of tissue oxygen debt
and the adequacy of resuscitation. A persistently high
or increasing base deficit indicates the presence of
ongoing blood loss or inadequate volume
replacement.
57
7.2 Lactate levels
Recent evidence suggests that serum lactate levels
accurately reflect the degree of circulatory failure
and level of oxygen debt in trauma patients.
54
Abramson
67
studied patients with a moderate injury
severity score who were resuscitated to supranormal
values of O
2
transport. They found that patients who
had a normalised serum lactate level within 24 hours
had a significantly higher survival rate than those
whose lactate levels did not return to normal within
48 hours. Manikis and his associates
68
in a study on
the correlation of serial blood lactate levels to organ
and mortality after trauma reported similar results.
Sauaia et al
69
found that a serum lactate of more
than 2.5mmol/L 12 hours post injury accurately
predicted the onset of multiple organ failure.
When using lactate levels as an end point to
resuscitation it is important to note that as the oxygen
debt becomes normalised lactate maybe washed out
into the circulation, thus spuriously increasing lactate
levels. Nevertheless returning lactate levels to normal,
and in particular normalising them in a short time
period, has proved to be a useful goal in the
resuscitation of trauma patients.
57
7.3 Gastric pH
The gastrointestinal circulation appears to be
exquisitely sensitive to changes in perfusion.
Measuring gastric pH has been attributed to
detect intestinal hypoxia to determine both the
depth of shock and the adequacy of resuscitation.
The potential value of detecting intestinal hypoxia
is two-fold. Intestinal mucosal hypoxia may be an
early warning sign of inadequate global oxygen
delivery due to compensatory mechanism which
redistribute blood flow away from the gut, especially
the splenic bed and intestinal mucosa. The resulting
intestinal mucosal hypoxia may itself have deleterious
effects, playing a role in the development of
multi-organ failure as a result of increased intestinal
permeability and translocation of endotoxin and
bacteria across the intestinal wall. Thus, correction of
low pHi by treatment aimed at correction of mucosal
hypoxia should result in an improved outcome.
Ivatury and colleagues compared global oxygen
transport indices versus organ-specific gastric
mucosal pH as resuscitation endpoints in trauma
patients and found a large reduction in mortality
in patients resuscitated to achieve a gastric pH >7.3
(mortality 9.1% vs 31.3%, p = 0.27).
70
However in a
similar study undertaken by the same authors a year
later found inconsistent results with survival being
higher in the patients randomised to normalisation
of gastric ph (90% vs 74.1%, p = 0.16) but organ
failures also being higher (56.7% vs 29.6%).
71
Both studies, however were underpowered to
draw any conclusions. Larger studies are warranted.
7.4 Sublingual capnometry
One study was identified that included trauma
patients and evaluated the predictive power of
sublingual capnometry for identifying peripheral
hypoperfusion. Sublingual CO
2
correlated strongly
with haemodynamic parameters and lactate (r
2
=0.84,
p<0.01).
72
The application of this instrument may
serve to diagnose and estimate the severity of shock,
but does not appear to add any new information that
is not readily determined by standard monitoring of
heart, blood pressure and lactate.
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7.5 Supranormal circulatory values
Shoemaker, Bishop and colleagues have done
a number of studies examining and evaluating
supranormal circulatory values as resuscitation goals
(based on cardiac index, oxygen delivery and oxygen
consumption) in severely injured patients.
61;73-75
A quasi-randomised study compared global oxygen
indices as resuscitation goals to resuscitation based
on standard variables (HR, BP, U/O, BD, and Lactate).
Bishop and colleagues found a lower mortality
for patients who were resuscitated to achieve supra-
normal circulatory values (18% vs 37%, p<0.027)
and a lower incidence of organ failures per patient
(0.74 +/- 0.28 vs 1.62 +/- 0.28, p<0.002).
76
It is notable that predicted and observed mortality
between the two groups is different with 81%
observed survival vs 84% predicted survival in
the intervention group versus 63% observed vs
91% predicted in the control group. The observed
mortality is much lower than the predicted mortality
in the control group whilst the observed mortality is
similar to the predicted mortality for the intervention
group. Resuscitation to supranormal circulatory values
did not seem to improve survival when compared to
predicted survival for this group. It is concerning as
to why the observed mortality was 28% more than
predicted. In conclusion, this study highlights that
failure to achieve normal of supranormal circulatory
values is a predictor of a poor outcome, however
augmentation of survivor values in reducing mortality
is not conclusive from this study.
A randomised trial undertaken by Velmahos
and colleagues also evaluated the effect early
optimisation on the survival of severely injured
patients. However no difference in mortality
(15% vs 11%), organ failure, sepsis or length of
intensive care unit stay was observed between the
two groups. The authors conclude that patients who
can achieve optimal haemodynamic values are more
likely to survive than those who cannot, regardless of
resuscitation techniques.
77
Conclusion
Much controversy exists regarding the optimum end
points for resuscitation. What is agreed upon is that
vital signs are very poor indicators of the adequacy of
resuscitation. In recent times, occult hypoperfusion
has dominated the literature on highlighting that
current end points of resuscitation are inadequate.
This has fuelled the development of Gastric
Tonometry, Capnometry and goal directed therapies.
Application of these tools in resuscitation of trauma
patients has shown them to be powerful predictors
of mortality, however the research has failed to
consistently demonstrate an improvement in
outcomes when used to direct therapy in comparison
to standard endpoints such as HR, BP, urine output,
lactate and base deficit. There is compelling data for
the early recognition of compensated shock.
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 19
H
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G
U
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:: WHAT ARE THE ENDPOINTS OF FLUID RESUSCITATION IN THE TRAUMA PATIENT?
Performance indicators
Arterial blood gases and lactate measured
to assess degree of shock.
Urinary catheter inserted to assess urine output.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 19
::
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 20
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 21
PAGE 22 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES
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HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 22
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 23
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:: EVIDENCE TABLES
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 23
PAGE 24 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES
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HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 24
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 25
H
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:: EVIDENCE TABLES
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 25
PAGE 26 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES
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Evidence Table 2. How do you find the sources of bleeding in a hypotensive trauma patient?
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HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 26
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 27
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:: EVIDENCE TABLES
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 27
PAGE 28 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES
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HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 28
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 29
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:: EVIDENCE TABLES
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 29
PAGE 30 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES
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Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 31
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:: EVIDENCE TABLES
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 31
PAGE 32 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES
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HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 32
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 33
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:: EVIDENCE TABLES
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 33
PAGE 34 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES
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HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 34
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 35
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HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 35
PAGE 36 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES
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HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 36
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 37
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:: EVIDENCE TABLES
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 37
PAGE 38 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES
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Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 39
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:: EVIDENCE TABLES
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 39
PAGE 40 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
ADULT TRAUMA CLI NI CAL PRACTI CE GUI DELI NES
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HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 40
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 41
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:: EVIDENCE TABLES
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 41
::
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 42
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 43
The following search terms were used in Medline
1 Shock/
2 1 and hypovol?emi$.mp. [mp=title, abstract, subject headings, drug trade name, original title, device manufacturer,
drug manufacturer name]
3 hypovol?emic shock.mp.
4 shock, hemorrhagic/
5 exp Hemorrhage/
6. (hemorrhag$ or haemorrhag$).mp. [mp=title, abstract, subject headings, drug trade name, original title, device manufacturer,
drug manufacturer name]
7 Hypotension/
8 low blood pressure.mp.
9 or/2-8
10 "Wounds and Injuries"/
11 trauma.mp.
12 or/10-11
13 exp resuscitation/
14 Fluid Therapy/
15 fluid resuscitation$.mp.
16 blood transfusion/ or exp blood component transfusion/
17 exp Blood Substitutes/
18 blood expand$.mp.
19 exp colloids/
20 crystalloids.mp.
21 (volume expansion or volume expand$ or blood expansion or blood expand$).mp. [mp=title, abstract, subject headings,
drug trade name, original title, device manufacturer, drug manufacturer name]
22 exp Monitoring, Physiologic/
23 Time Factors/
24 endpoint determination/
25 (endpoint$ or end point$).mp. [mp=title, abstract, subject headings, drug trade name, original title, device manufacturer,
drug manufacturer name]
26 (or/2-4) and 12 and di.fs.
27 (or/5-6) and (or/7-8) and 12 and et.fs.
28 (or/5-6) and (th.fs. or manage$.mp.) and (rural$ or remote$ or non?urban$).mp. [mp=title, abstract, subject headings,
drug trade name, original title, device manufacturer, drug manufacturer name]
29 (or/13-16) and 9 and 12 and 23
30 (or/13-16) and 9 and 12 and (or/17-21)
31 (or/13-16) and 12 and (or/24-25)
32 9 and 12 and 22
33 or/26-32
34 9 and 12 and (dt,th.fs. or manage$.mp.) [mp=title, abstract, subject headings, drug trade name, original title, device manufacturer,
drug manufacturer name]
35 limit 35 to english language
36 33 or 36
37 limit 37 to human
PAGE 44 Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM
Search strategy for
the identification of studies
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APPENDI X A
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 44
The following search terms were used in Embase-
1 Hypovolemic Shock/
2 Hemorrhagic Shock/
3 ((hypovol?emic or hemorrhagic or haemorrhagic) adj shock).mp. [mp=title, abstract, cas registry/ec number word,
mesh subject heading]
4 exp Bleeding/
5 (hemorrhag$ or haemorrhag$).mp. [mp=title, abstract, cas registry/ec number word, mesh subject heading]
6 hypotension/ or hemorrhagic hypotension/
7 low blood pressure.mp.
8 or/1-7
9 Injury/
10 trauma.mp.
11 or/9-10
12 resuscitation/
13 exp fluid therapy/
14 fluid resuscitation.mp.
15 exp blood transfusion/
16 Blood Substitute/
17 (volume expansion or volume expand$ or blood expansion or blood expand$).mp. [mp=title, abstract,
cas registry/ec number word, mesh subject heading]
18 exp colloid/
19 crystalloid/
20 exp monitoring/ or hemodynamic monitoring/ or patient monitoring/
21 (time or timing).mp.
22 (endpoint$ or end point$).mp. [mp=title, abstract, cas registry/ec number word, mesh subject heading]
23 (or/1-3) and 11 and di.fs.
24 (or/4-5) and (or/6-7) and 11 and et.fs.
25 (or/4-5) and (th.fs. or manage$.mp.) and (rural$ or remote$ or non?urban$).mp. [mp=title, abstract,
cas registry/ec number word, mesh subject heading]
26 (or/12-15) and 8 and 11 and 21
27 (or/12-15) and 8 and 11 and (or/16-19)
28 (or/12-15) and 11 and 22
29 8 and 11 and 20
30 or/23-29
31 8 and 11 and (dt,th.fs. or manage$.mp.) [mp=title, abstract, cas registry/ec number word, mesh subject heading]
32 limit 31 to (english language)
33 30 or 32
34 limit 33 to human
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 45
H
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:: SEARCH TERMS USED FOR THE IDENTIFICATION OF STUDIES
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 45
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2 National Health and Medical Research Council
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3 National Health and Medical Research Council
1999, How to review the evidence: systematic
identification and review of the scientific literature.
Biotext Canberra, editor.
4 National Health and Medical Research Council
1998, A guide to the development, implementation
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5 Liddle J, Williamson M, Irwig L 1996, Method for
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6 Jordan KS 2000, Fluid resuscitation in acutely
injured patients, Journal of Intravenous Nursing
23(2):81-7, 2000 Mar;-Apr.
7 American College of Surgeons 1997, Advanced
Trauma life support for Doctors Instruction Course
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8 Lechleuthner A, Lefering R, Bouillon B, Lentke E,
Vorweg M 1994, T. T. Prehospital detection of
uncontrolled haemorrhage in blunt trauma,
European Journal of Emergency Medicine 1(1):13-8.
9 Shippy CR, Appel P, Shoemaker WC 1984,
Reliability of clinical monitoring to assess blood
volume in critically ill patients, Critical Care
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10 Wo CC, Shoemaker WC, Appel PL, Bishop MH,
Kram HB, Hardin E 1993, Unreliability of blood
pressure and heart rate to evaluate cardiac
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11 Demetriades D, Chan LS, Bhasin P, Berne TV,
Ramicone E, Huicochea F, et al 1998,
Relative bradycardia in patients with traumatic
hypotension, Journal of Trauma Injury, Infection
and Critical Care, 45(3):534-9.
12 Knottenbelt JD 1991, Low initial hemoglobin
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13 Rixen D, Raum M, Bouillon B, Lefering R,
Neugebauer E 2001, Unfallchirurgie. APotDGf.
Base deficit development and its prognostic
significance in posttraumatic critical illness:
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