ADULT TRAUMA CL IN ICAL PRACT ICE GU IDEL INES
:: Management of Hypovolaemic Shockin 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 areaimed at assisting clinicians in informed medical decision-making. They are not intended toreplace decision-making. The authors appreciate the heterogeneity of the patient populationand the signs and symptoms they may present with and the need to often modifymanagement in light of a patient's co-morbidities.
The guidelines are intended to provide a general guide to the management of specifiedinjuries. The guidelines are not a definitive statement on the correct procedures, rather theyconstitute 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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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 bleedingin 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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Algorithm 1 :: The management of hypovolaemic shock in the trauma patient
The Management of Hypovolaemic Shock in the Trauma PatientIf definitive care is not available in your facility make early contact with retrieval services
Primary surveyIncludes 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-spine1 Protect airway,
secure if unstable.
1 Airway adjunct as needed.
1 Control of c-spine.
Circulation1 Secure venous
access x 2 large bore cannula.
1 Bloods: – x-match – FBC – EUC's – Creatinine – ABG's – Blood ETOH.
1 Control external bleeding.
Disability1 Assess
neurological status.
1 AVPU: – alert – responds to vocal stimuli – responds to painful stimuli – unresponsive.
Exposure / Environment1 Undress
patient.1 Maintain
temperature.
Adjuncts1 X-ray:
– chest – pelvis – lateral c-spine.
Breathing1 Definitive
control of airway.
1 Oxygen.1 Bag and
mask.
External1 Careful visual
inspection.
Long bones1 Careful visual
inspection.
Chest1 Chest x-ray.
Abdomen1 DPA* and
/ or FAST**.
Retroperitoneum1 Pelvic x-ray.
External1 Apply direct
pressure.1 Suture
lacerations.
InterventionsLong bones1 Splint + / -
reduce #.
Chest1 Chest tube.
Abdomen1 Emergency
Laparotomy.
Retroperitoneum1 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, IVa 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-2who 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 Consensusfor 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 traumapatient 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-2of 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 Consensusof a normal mentation, heart rate, skin perfusion and urine output and maintaining 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 Itraumatic 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 immunefunction that, if prolonged, progresses to thesequential failure of multiple organ systems.1
Timely diagnosis, surgical control of on-going loss and physiologically directed fluid replacement remainthe cornerstones of management. In recent years,however, the practice of rapid fluid replacement has been questioned.
Early recognition of hypovolaemic shock is vitalfor optimal care of the injured patient. Ongoingcontroversy 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 thebleeding patient. This guideline aims to objectivelyanalyse the literature to provide the clinician withevidence-based options. The guidelines will also seekto establish the optimal care of the bleeding patientin the rural setting where resources may be lackingand access to definitive care is delayed.
This guideline has been developed to provideevidence-based recommendations for themanagement of hypovolaemic shock in the trauma patient.
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1 Introduction
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2.1 Scope of the guidelineThis guideline is intended for use by all clinicians who are involved in the initial care of patients withhypovolaemic shock: ambulance officers, emergencynurses, and physicians.
This guideline has been developed to assist cliniciansto provide a selective evidence based approach to themanagement of trauma patients with hypovolaemicshock. 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 ofindividuals. They aim to provide information onwhat 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 availableevidence to allow clinicians to make evidence-baseddecisions in the diagnosis and management of traumapatients with hypovolaemic shock.
A multidisciplinary team was consulted to aid in theidentification of the key clinical dilemmas that facedclinicians when caring for patients with hypovolaemicshock. By identifying the key clinical questions, theguideline should facilitate:
:: early diagnosis of hypovolaemic shock
:: identification of the source(s) of bleeding
:: enhancement of tissue perfusion while minimisingongoing haemorrhage.
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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 traumapatient 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 evidenceThe articles were classified according to their general purpose and study type.
Table 1. Levels of evidence2-4
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:: METHODS
2.4.2 Quality appraisalThe 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-2who 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
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3 How do you know when thepatient 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. Absolutehypovolaemia refers to the actual loss of volume that occurs in the presence of haemorrhage. Relative hypovolaemia refers to the inappropriateredistribution of body fluids such as that that occurs following major burn trauma.6
Acute blood loss is a very common problem followingtraumatic injury. Rapid recognition and restoration ofhomeostasis is the cornerstone of the initial care ofany seriously injured patient. Delay in recognising and quickly treating a state of shock results in aprogression from compensated reversible shock towidespread multiple system organ failure to death.Morbidity may be widespread and can include renalfailure, brain damage, gut ischaemia, hepatic failure,metabolic derangements, disseminated intravascularcoagulation (DIC), systemic inflammatory responsesyndrome (SIRS), cardiac failure, and death.
The standard physiological classification of acuteblood loss has been promulgated through theAdvanced Trauma Life Support Course developed by the American College of Surgeons.7 While a useful theoretical basis for understanding the stagesof 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 foundthat a systolic blood pressure (SBP) <90mmHg will only identify 61% of patients with activehaemorrhage (sensitivity 61% and specificity 79%).3.1% of patients with uncontrolled haemorrhagehad undisturbed physiological variables.8 Thesefindings are supported by others.9-11 Demetriadesexamined the incidence and prognostic value oftachycardia and bradycardia in the presence oftraumatic hypotension. The incidence of relativebradycardia (SBP <90mmHg and HR <90 minute) was present in 28.9% of hypotensive patients.11
The results of these studies suggest that commonlymonitored variables, in and of themselves, do notaccurately reflect or predict the circulating volume ofinjured patients.9 The accuracy of circulatory values(HR, BP, urine output and capillary return) in detectinghypovolaemia in trauma patients is hampered bycomplex neurohormonal mechanisms that cansuccessfully compensate for 15% loss of circulatingvolume, particularly considering the majority oftrauma patients are young, fit males.9 Confounderssuch as traumatic brain injury also decreases thesensitivity of SBP and HR to detect hypovolaemicshock.8
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Detecting hypovolaemic shock in the trauma patientwith normal haemodynamics is reliant on history,physical examination and pathology, including, base deficit, lactate, haematocrit and haemoglobin.However, these tests are only of value wheninterpreted 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 byKnottenbelt, in a review of 1000 trauma patients, tobe an indicator of serious ongoing haemorrhage.12
Lactate and base-deficit have also shown to correlatewell with vital signs and mortality.13,14 The ability and value of haemoglobin, lactate and base-deficit,however, to predict blood loss in haemodynamicallystable patients is unknown.
Oman examined the predictive power of haematocritdecrease of >5% as an indicator of ongoinghaemorrhage in trauma patients who receive IV fluids. The study found that haematocrit was notuseful in identifying patients who were bleeding, but was accurate 97% of the time for identifyingthose 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 assessmentIn a haemodynamically unstable trauma patient thereare five potential sites of major blood loss: externally,long bones, the chest, the abdomen and theretroperitoneum.7
4.2 Externally and long bonesBlood loss from fractures and lacerations can resultin a significant amount of blood loss. The scalp is ahighly vascular region and may be associated withsignificant blood loss. It is however, extremely difficultto estimate the volume of bleeding from scalp andother lacerations due to blood loss at the scene anden route to the hospital. External blood loss requirescareful visual inspection.
Clarke reported that a single long-bone fracture mayresult in 10-30% loss of total blood volume. Bleedingfrom long bone fractures is present in approximately40% 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 chestIntrathoracic haemorrhage is to be expected in 4-29% of cases16-19 and can be evaluated on a chestx-ray, which should be performed within 10 minutesof the patients arrival.20 There are minor limitations tofirst mobile supine chest x-ray. A small haemothoraxcan be initially missed in 5% of surviving patients andin up to 18% in non-surviving patients. However, a large haemothorax contributing to haemodynamicinstability should not be missed.
4.4 The pelvisThe next part of the decision tree is crucial, trying to decide whether the blood loss is in the abdomenor in the pelvic retroperitoneum or in both. At thispoint the AP pelvic radiograph should be reviewed. If a pelvic fracture with possible disruption of thepelvic ligaments causing an unstable fracture patternis seen or suspected, the probability of pelvic arterialbleeding is 52%.
The initial AP pelvic radiograph is the only guideto determine the probability of pelvic bleeding.Disruptions involving only the pubic rami do notvertically or rotationally unstabilise the pelvic ring, but when recognising a fracture of the pubic bone,posterior disruption and probability of arterialbleeding must always be suspected. One must alsobear in mind that bilateral inferior/superior pubicramus fractures (butterfly type fracture from APcompression mechanism), acetabular fractures andeven simple ramus fractures in the elderly can lead to arterial bleeding causing hypotension.
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4 How do you find the sources of bleeding in ahypotensive trauma patient?
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When the haemodynamically unstable patient enters the resuscitation room, IVa 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 abdomenThe abdomen is the most difficult to assess in therural and urban environment. Diagnostic PeritonealAspiration (DPA) and Focused Abdominal Sonographyin Trauma (FAST) are the preferred diagnostic meansto determine if there is intra-abdominal bleeding.Although the availability of FAST is increasing, it is not available in all urban and rural emergencydepartments. DPA is recommended if an EMSTaccredited clinician is available. If neither FAST norDPA can be undertaken, the clinician should examinethe other four sources for blood loss, upon exclusion of these it must be assumed that the patient hasintraabdominal 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 bowelmesentery (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-makingIn the face of continuing haemodynamic instabilityand in the absence of external blood loss, long boneor pelvic fractures or any evidence of bleeding onchest 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 externallystabilised in the resuscitation room. Please refer tothe ‘Adult Trauma Clinical Practice Guidelines The
Management of Haemodynamically Unstable Patients
with a Pelvic Fracture’ (which is available from theNSW Institute of Trauma and Injury Management,contact details listed on the inside cover).
4.7 TimeframesFor every three minutes of haemodynamic instability elapsed without haemorrhage control in the emergency department, there is a 1% increase in mortality. Therefore decision makingwithin 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 bleedingsources and long bone fractures should take placewithin the first five minutes. The chest x-ray andpelvic x-ray should be performed within 10 minutes of the patients arrival. Assessment of the abdomenwith FAST / DPA if possible, should be completedwithin 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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5 What is the best management of the bleeding patient?
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Management priorities in the bleeding patient include controlling blood loss, replenishingintravascular volume and sustaining tissue perfusion.1
When services are needed that exceed availableresources, it is of critical importance that earlyconsultation with a trauma specialist and rapidtransportation 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 lossAfter establishing a patent airway, ensuring adequateventilatory exchange and oxygenation and securingvenous access, the highest priority in the bleedingpatient is to control haemorrhage.21 Because patientsmay bleed from multiple sites, it is imperative that theattending medical officer establish strategies toaddress all sources of bleeding. Sources of bleedingmay be broadly classified as external or internal.
5.1.1 Controlling external bleedingThe Australian Resuscitation council advocates theuse of direct pressure to gain prompt control ofexternal bleeding.22 The recommended methodinvolves approximating the wound edges if possible,holding an absorbent dressing firmly over the areawith the heel of the hand, and elevating the bleedingpart. After bleeding is controlled the absorbentdressing may be secured with a bandage. If bleedingcontinues through the initial dressing, apply a seconddressing over the first and secure with a bandage. Do NOT disturb the dressing once the bleeding hasbeen controlled. Arterial tourniquets are reserved forlife-threatening bleeding and when direct pressure tothe wound has failed to stop the bleeding or whenprotruding 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 Itraumatic 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 bleedingEvidence from numerous studies over the past two decades indicates that immediate and definitiveoperative haemostasis is the optimal treatment for internal bleeding.23 To delay leaves the patientsusceptible to multi organ dysfunction and othercomplications. In the rural and remote settinghowever, immediate operative haemostasis is limitedby a lack of surgical presence and or operatingfacilities at the site, and or lengthy transport times to institutions capable of providing definitiveoperative haemostasis.
Given these limitations the challenge for the rural and remote physician is to rapidly identify patientswho would benefit from early transfer based onavailable local resources, manage any life-threateninginjuries, and establish prompt contact with the majorreferral centre, and the transport /retrieval service.Prolonged time spent in a local emergencydepartment 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 byMartin et al, up to 60% of the time delay pertainingto the transfer of injured patients was related to thetime taken to notify the retrieval team.25 In somecases this accounted for delays in excess of threehours. Numerous other studies have suggested thatprompt early contact with the retrieval service andsubsequent timely transfer of severely injured patientsis associated with increased survival rates.26-28
5.2 Repleting intravascular volumeIt is generally recognised that a depleted intravascularvolume robs the cardiovascular system of the preloadrequired for adequate cardiac output and peripheraloxygen delivery.29 Inadequate perfusion, even in theabsence of overt hypotension can result in aneurohumoral cascade that ultimately leads to sequential organ failure.30
Since the early 1900's the conventional approach to restoring intravascular volume and subsequentlysustaining tissue perfusion in the bleeding patient has focused on early aggressive fluid replacementwith large volumes of crystalloid and or bloodproducts.31 There is a growing body of evidence,however, that suggests that in the presence ofuncontrolled haemorrhage, fluid replacement mayresult in increased haemorrhage and subsequent
greater mortality.1;31-34 This is thought most likely to be the result of increased blood pressure and thesubsequent reversal of vasoconstriction, dislodgementof early thrombus and subsequent secondaryhaemorrhage, and the dilutional coagulopathy thatoccurs 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 aortaand aggressively resuscitated with lactated ringerssolution. 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 diedwithin 100 minutes. All of the control swine survived.The follow-up interval, however was only two hours.Kowalenko and his associates developed a moresevere model of aortic tear and similarlydemonstrated that animals aggressively resuscitatedwith high volumes of crystalloid had significantlylower survival rates than animals under-resuscitated.35
Data from Capone et al36, and Stern et al37 areconsistent with the study by Kowalenko.35
Several solid organ injury animal models ofuncontrolled haemorrhage demonstrate resultsthat also support low volume fluid resuscitation in the presence of uncontrolled haemorrhage37;38
In Krausz et al39 study of aggressive resuscitationfollowing moderate splenic injury in rats, untreatedcontrols sustained significantly less haemorrhagevolumes than treated animals. Similarly, Solomonov etal38 study of severe splenic injury in rats demonstratedthat animals aggressively resuscitated experiencedgreater haemorrhage volumes and a significantlylower survival time in comparison to untreatedanimals.
Findings from the animal models are substantiated by Bickell et al40 prospective controlled study ofpatients presenting with a penetrating torso injuryand a prehospital systolic blood pressure less than90mmHg. Patients received either immediate ordelayed fluid resuscitation following penetrating torsotrauma. The delayed resuscitation group (n = 289)had intravenous access secured, but received no fluidresuscitation until admission to the operating theatre.The immediate resuscitation group (n = 309) wereaggressively fluid resuscitated at the scene and duringtransport. The volume of fluid infused was 2,478mls.Survival to discharge rates was significantly higher inthe delayed resuscitation group compared to theimmediate 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 groupreceived fluids prior to operative intervention. Finally there was wide variation in the severity ofshock across both groups.31 Despite these limitations,Bickell's paper has led us to question traditional fluidresuscitation regimes.
A randomised study undertaken by Turner comparedearly and delayed fluid administration in traumapatients. Significant protocol violation (with only 31% of the fluid group actually receiving fluid)resulted in the inability of this study to find anytreatment affect (10.4% mortality early fluid group vs 9.8% mortality in delayed group).41
Dutton, in a randomised study evaluated fluidresuscitation titrated to a SBP of 100mmHg or70mmHg during a period of active haemorrhage on mortality. There was no difference in mortalitybetween the two groups (7% vs 7%).42 The lowpressure group appeared sicker than the higherpressure group (ISS in the conventional-pressuregroup was 19.65 ± 11.84, compared with 23.64 ± 13.82 in the low-pressure group). This may havehad a negative affect on survival in the low pressuregroup.
Evidence from retrospective studies further supportsthe concept of delayed resuscitation. Sampalis et al43
reviewed the outcomes of 217 trauma patients whohad received intravenous fluid and compared themwith 217 controls who received no fluid. Correctionwas made for gender, age, mechanism of injury andinjury severity score. Patients who received on-sitefluid resuscitation had a higher mortality than thecontrol group, particularly when fluid resuscitationwas combined with prolonged prehospital times.Another study by Hambly and Dutton44 comparedpatients given fluids using a rapid infusion device with historical controls who had undergone standardresuscitation. Patient resuscitated with the rapidinfusion device had a higher mortality than thosereceiving standard resuscitation.
The advocates of early aggressive resuscitation of hypotensive bleeding patients argue that thetrauma population is too heterogenous to rely solelyon animal studies, and limited clinical trials. It shouldbe noted, however, that a systematic review on theeffects of early or large volume intravenous fluid in
uncontrolled bleeding by Kwan et al45 found noevidence to support the conventional practise of early aggressive fluid resuscitation in the presenceof uncontrolled haemorrhage.
From this data consensus opinion now recommendsa more discriminating approach to the conventionalpractice of delivering liberal volumes of intravenousfluids to patients with uncontrolled bleeding.46
The emerging evidence demonstrates that aggressivefluid resuscitation in the bleeding patient leads toadditional haemorrhage through soft clot dissolution,hydraulic acceleration of bleeding and dilution ofclotting factors. While aggressive fluid resuscitation it is still considered appropriate for unconsciouspatients with no palpable blood pressure, the latestrecommendations are to limit or delay intravenousfluid resuscitation preoperatively in those withuncontrolled haemorrhage, even if they are hypoperfusing, 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 hypotensionis crucial as a systolic blood pressure <90mmHg isassociated with poor outcomes. Infuse small aliquotsof fluid (100-200mls) to maintain systolic bloodpressure above 90mmHg.122
There is abundant data to suggest that hypotensive or limited resuscitation may be preferable toaggressive fluid resuscitation in the setting ofuncontrolled haemorrhage. There is, however, littleevidence suggesting the volume of fluid required tomaintain vital organ perfusion yet prevent thrombusdislodgment and subsequent secondary haemorrhageand coagulation dilution. At best the literaturesuggests that small aliquots of fluid (100-200mls)should be given to maintain the patients systolicblood 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.
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Although a wide variety of options are currently available for fluid resuscitation, most agree that the bestresuscitation 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 regardingcompatibility, 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?
bloodO-neg
:: Early use of blood, if available, remains the optimal resuscitation fluid Consensusfor 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 traumapatient 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
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The debate regarding the relative effectiveness ofcolloids compared to crystalloid continues severaldecades after it began. Despite numerous publicationsrecommending specific fluids, there is no evidencefrom randomised control trials that resuscitation withcolloids carries a reduced mortality in patients withtrauma, burns and following surgery.50;51 Becausecolloids 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 hypovolaemicpatient.50;51
A number of recent studies52-54 have suggested thatthe administration of hypertonic solutions, in theabsence of a head injury, allows for a more rapidstabilisation of macro and micro-haemodynamics. A recent systematic review by Alderson et al,50
suggests that there is no evidence that hypertoniccrystalloid is better than isotonic crystalloid. Due tothe clinically different outcomes identified during thereview, however, Bunn et al recommends furtherlarge-scale trials comparing hypertonic crystalloidswith isotonic crystalloids are required to informpractice.
Wade and colleagues undertook a meta-analysis ofrandomised trials examining the effects of HypertonicSaline (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 statisticsof the available data shows that HS does not provideany benefit over current practices in terms of survivaland that HSD may be superior.55
The optimal resuscitation fluid for the hypovolaemictrauma patient remains the early use of blood. In the absence of type specific blood, isotoniccrystalloids have an established safety record whenused appropriately.42 Isotonic crystalloids produce a relatively predictable increase in cardiac output andare generally distributed throughout the extracellularspace. Where blood is not available or delayed,Compound Sodium Lactate (Hartmanns) solution is the preferred alternative for the initial resuscitationof the hypovolaemic patient.7;56 Compound SodiumLactate solution contains a bicarbonate precursor thatwhen metabolised helps to correct metabolic acidosisand its attendant detrimental effects.56 Compoundsodium lactate may need to be discontinued in thepresence of liver disease. Normal Saline 0.9% is an acceptable alternative, however, large volumes of 0.9% Normal Saline may result in metabolicacidosis.56
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Traditional haemodynamic parameters do not adequately quantify the degree III-2of 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 Consensusof a normal mentation, heart rate, skin perfusion and urine output and maintaining 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 traumapatient involves limiting cellular oxygen deficits,anaerobic metabolism and resultant tissue acidosis.57
Resuscitation is complete when the cellular oxygendeficits have been corrected, tissue acidosis iseliminated and normal aerobic metabolism isrestored.58 Many patients may appear to beadequately resuscitated, but have occulthypoperfusion 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 restorationof a normal mentation, blood pressure, heart rate,skin perfusion and urine output signified the endpoints of resuscitation.59 Recent studies60;61 however,suggest that even after normalising these parameters,up to 85% of severely injured patients have evidenceof compensated shock. Compensated shock isdefined as the presence of ongoing inadequate tissueperfusion despite the normalisation of heart rate,blood pressure, skin perfusion and urine output.58
Recognition of compensated shock and its rapidreversal are critical to minimise the risk of multi organdysfunction or death. Consequently, the traditionalend points of fluid resuscitation in the hypovolaemictrauma patient need to be supplemented with globaland end organ markers that are sensitive to thesymptoms of compensated shock.
Global markers include: lactate levels and basedeficit.54 Arterial pH is not as sensitive as it is buffered by the body's compensatory mechanisms.54
End organ markers include: monitoring of gutperfusion with gastric tonometry, and direct measures of tissue oxygen tension.
7.1 Base deficitA recent study by Davis et al62 found that the initialbase deficit was a reliable early indicator of themagnitude of volume deficit. Patients were stratifiedaccording to the level of base deficit as mild (basedeficit 2 to -5mmol/L), moderate (base deficit -6 to -14) or severe (base deficit < -15). Patients with themore severe base deficit required a greater volume of fluid for resuscitation. Sixty-five per cent of patientswith an increasing base deficit had ongoing bloodloss. This is consistent with the findings of Canizaro et al63, and James et al64.
Kincaid and his associates65, further found thatamong trauma patients who normalised their lactatelevels, those with persistently higher base deficits had a significantly increased risk of multi-organdysfunction and death. Patients with persistentlyhigher base deficits also demonstrated impairedoxygen utilisation. In a similar study Rixen et al13
found that an increase in base deficit between the
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7 What are the endpoints of fluidresuscitation in the trauma patient?
bloodO-neg
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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 hightransfusion requirements, coagulation and metabolicderangements, 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 alterthe 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 guidefor identifying the magnitude of tissue oxygen debtand the adequacy of resuscitation. A persistently highor increasing base deficit indicates the presence ofongoing blood loss or inadequate volumereplacement.57
7.2 Lactate levelsRecent evidence suggests that serum lactate levelsaccurately reflect the degree of circulatory failure and level of oxygen debt in trauma patients.54
Abramson67 studied patients with a moderate injuryseverity score who were resuscitated to supranormalvalues of O2 transport. They found that patients whohad a normalised serum lactate level within 24 hourshad a significantly higher survival rate than thosewhose lactate levels did not return to normal within48 hours. Manikis and his associates68 in a study onthe correlation of serial blood lactate levels to organand mortality after trauma reported similar results.Sauaia et al69 found that a serum lactate of morethan 2.5mmol/L 12 hours post injury accuratelypredicted the onset of multiple organ failure.
When using lactate levels as an end point toresuscitation it is important to note that as the oxygendebt becomes normalised lactate maybe washed outinto the circulation, thus spuriously increasing lactatelevels. Nevertheless returning lactate levels to normal,and in particular normalising them in a short timeperiod, has proved to be a useful goal in theresuscitation of trauma patients.57
7.3 Gastric pHThe gastrointestinal circulation appears to beexquisitely 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 anearly warning sign of inadequate global oxygendelivery due to compensatory mechanism whichredistribute blood flow away from the gut, especiallythe splenic bed and intestinal mucosa. The resultingintestinal mucosal hypoxia may itself have deleteriouseffects, playing a role in the development of multi-organ failure as a result of increased intestinalpermeability and translocation of endotoxin andbacteria across the intestinal wall. Thus, correction oflow pHi by treatment aimed at correction of mucosalhypoxia should result in an improved outcome.
Ivatury and colleagues compared global oxygentransport indices versus organ-specific gastric mucosal pH as resuscitation endpoints in traumapatients 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 asimilar study undertaken by the same authors a yearlater found inconsistent results with survival beinghigher in the patients randomised to normalisationof gastric ph (90% vs 74.1%, p = 0.16) but organfailures 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 capnometryOne study was identified that included traumapatients and evaluated the predictive power ofsublingual capnometry for identifying peripheralhypoperfusion. Sublingual CO2 correlated stronglywith haemodynamic parameters and lactate (r2=0.84,p<0.01).72 The application of this instrument mayserve to diagnose and estimate the severity of shock,but does not appear to add any new information thatis not readily determined by standard monitoring ofheart, blood pressure and lactate.
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7.5 Supranormal circulatory valuesShoemaker, Bishop and colleagues have done a number of studies examining and evaluatingsupranormal circulatory values as resuscitation goals(based on cardiac index, oxygen delivery and oxygenconsumption) in severely injured patients.61;73-75
A quasi-randomised study compared global oxygenindices 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 mortalitybetween 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 observedmortality is much lower than the predicted mortalityin the control group whilst the observed mortality issimilar to the predicted mortality for the interventiongroup. Resuscitation to supranormal circulatory valuesdid not seem to improve survival when compared topredicted survival for this group. It is concerning as to why the observed mortality was 28% more thanpredicted. In conclusion, this study highlights thatfailure to achieve normal of supranormal circulatoryvalues is a predictor of a poor outcome, howeveraugmentation of survivor values in reducing mortalityis not conclusive from this study.
A randomised trial undertaken by Velmahos and colleagues also evaluated the effect earlyoptimisation on the survival of severely injuredpatients. However no difference in mortality (15% vs 11%), organ failure, sepsis or length ofintensive care unit stay was observed between thetwo groups. The authors conclude that patients whocan achieve optimal haemodynamic values are morelikely to survive than those who cannot, regardless ofresuscitation techniques.77
ConclusionMuch controversy exists regarding the optimum endpoints for resuscitation. What is agreed upon is thatvital signs are very poor indicators of the adequacy ofresuscitation. In recent times, ‘occult hypoperfusion’has dominated the literature on highlighting thatcurrent end points of resuscitation are inadequate.This has fuelled the development of GastricTonometry, Capnometry and goal directed therapies.Application of these tools in resuscitation of traumapatients has shown them to be powerful predictors of mortality, however the research has failed toconsistently demonstrate an improvement inoutcomes when used to direct therapy in comparisonto standard endpoints such as HR, BP, urine output,lactate and base deficit. There is compelling data forthe early recognition of compensated shock.
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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.
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::
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Evidence Table 1. How do you know when a trauma patient is in hypovolaemic shock?A
utho
rLe
vel o
fS
tud
y
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Vic
torin
o, G
P.B
attis
tella
, FD
.W
isne
r, D
H.
2003
78
III-2
Dia
gnos
ticte
st
B2
To d
eter
min
e th
e co
rrel
atio
nbe
twee
n ta
chyc
ardi
a an
dhy
pote
nsio
n.
Hea
rt r
ate
was
not
foun
d to
be
a go
odpr
edic
tor
of h
ypot
ensi
on, b
ut it
s se
nsiti
vity
an
d sp
ecifi
city
mak
e it
clin
ical
ly u
nrel
iabl
e in
dia
gnos
ing
hypo
vola
emic
hyp
oten
sion
.
***N
eed
to c
alcu
late
sen
sitiv
ity a
nd s
peci
ficity
.
Tach
ycar
dia
was
not
foun
d to
be
a re
liabl
e in
dica
tor
of h
ypot
ensi
on.
How
ever
, the
re a
re s
ome
limita
tions
of t
his
stud
y.H
ypot
ensi
on is
a s
urro
gate
or
late
out
com
e fo
rhy
povo
laem
ia. P
erha
ps t
he a
utho
rs s
houl
d ha
ve
mea
sure
d ci
rcul
atin
g vo
lum
e an
d ca
rdia
c ou
tput
to
dete
rmin
e th
e us
eful
ness
of t
achy
card
ia. A
s so
me
patie
nts
may
be
hypo
vola
emic
, tac
hyca
rdic
but
hav
e a
norm
al
bloo
d pr
essu
re d
ue t
o co
mpe
nsat
ory
mec
hani
sms.
Lech
leut
hner
,A
. Le
ferin
g, R
.O
uillo
n, B
.19
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III-2
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ATo
eva
luat
e sy
stol
ic b
lood
pres
sure
, cap
illary
ref
ill an
d tr
aum
a sc
ore
in id
entif
ying
unco
ntro
lled
haem
orrh
age
in p
atie
nts
with
blu
nt t
raum
a.
Sys
tolic
blo
od p
ress
ure
<90
mm
Hg
was
the
mos
t se
nsiti
ve p
aram
eter
, how
ever
onl
yid
entif
ied
50%
of b
lunt
tra
uma
patie
nts
with
unco
ntro
lled
haem
orrh
age.
The
sen
sitiv
ityim
prov
ed t
o 66
% w
ith a
SB
P<
60m
mH
g.
An
acco
mpa
nyin
g tr
aum
atic
bra
in in
jury
impa
ired
the
abilit
y of
SB
P t
o de
tect
unco
ntro
lled
haem
orrh
age.
The
sens
itivi
ty a
nd s
peci
ficity
of S
BP
<90
mm
Hg
is 6
1% a
nd 7
9% r
espe
ctiv
ely.
For
a S
BP
<70
mm
Hg
the
sens
itivi
ty d
rops
eve
n lo
wer
to
27%
but
spe
cific
ity in
crea
ses
to 9
4%.
3.1%
of p
atie
nts
with
unc
ontr
olle
d ha
emor
rhag
e ha
d un
dist
urbe
d ph
ysio
logi
cal v
aria
bles
.
A S
BP
<50
mm
Hg,
the
pre
senc
e of
TB
I im
pairs
th
e de
tect
ion
qual
ity.
No
para
met
er is
suf
ficie
ntly
pre
dict
ive
to d
iagn
ose
accu
rate
lyth
ose
patie
nts
with
unc
ontr
olle
d ha
emor
rhag
e.
The
stud
y w
as u
nder
take
n in
pat
ient
s w
ith tr
aum
a sc
ores
1-1
5.
Shi
ppy,
CR
.A
ppel
, PL.
Sho
emak
er,
WC
. 19
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III-2
Dia
gnos
ticte
st
B2
To e
valu
ate
the
relia
bilit
y of
clin
ical
mon
itorin
g to
ass
ess
bloo
d vo
lum
ein
crit
ical
ly il
l pat
ient
s.
In p
atie
nts
with
mea
sure
d hy
povo
laem
ia(~
1400
mls
) the
re w
ere
sign
ifica
nt r
educ
tions
in M
AP,
HR
, and
CI.
CV
P w
as n
ot s
igni
fican
tlyre
duce
d. N
one
of t
he c
orre
latio
n co
effic
ient
sbe
twee
n bl
ood
volu
me
and
thes
e co
mm
only
mea
sure
d va
riabl
es w
ere
sign
ifica
nt.
The
data
sug
gest
tha
t th
e co
mm
only
mon
itore
d va
riabl
es,
in a
nd o
f the
mse
lves
, do
not
refle
ct a
dequ
atel
y th
e bl
ood
volu
me
stat
us in
crit
ical
ly il
l pat
ient
s. C
omm
only
mon
itore
dva
riabl
es p
rovi
ded
adeq
uate
dat
a ne
eded
to
begi
nre
susc
itatio
n in
sho
ck, b
ut t
here
abs
olut
e va
lues
inde
pend
ently
are
not
a r
elia
ble
estim
atio
n of
blo
od
volu
me
stat
us.
Clin
icia
ns n
eed
to b
e m
indf
ul o
f the
com
plex
ne
uroh
orm
onal
mec
hani
sms
whi
ch p
rofo
undl
y ef
fect
th
e ci
rcul
atio
n in
gen
eral
whi
ch c
ould
lead
clin
icia
ns d
own
the
gard
en p
ath
of t
hink
ing
that
man
y pa
tient
s ar
e fu
llyre
susc
itate
d al
thou
gh t
hey
may
stil
l be
hypo
vola
emic
an
d at
ris
k of
dev
elop
ing
the
sequ
elae
of s
hock
.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 22
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 23
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Kno
tten
belt,
JD.
1991
12
III-2
Dia
gnos
ticte
st
B1
To e
valu
ate
the
impo
rtan
ce o
f alo
w in
itial
hae
mog
lobi
n an
d its
corr
elat
ion
with
sho
ck.
Initi
al h
aem
oglo
bin
corr
elat
ed w
ith v
ital s
igns
and
mor
talit
y.
In 3
1 pa
tient
s w
ith in
itial
Hb
leve
ls o
f les
s th
an 8
g/d
L, t
he o
vera
ll m
orta
lity
was
48.
4%,
com
pare
d w
ith 2
.6%
in 9
69 p
atie
nts
who
sein
itial
Hb
leve
l was
8 g
/dL
or m
ore
(p <
0.00
001)
.
A lo
w H
b le
vel o
bser
ved
soon
afte
r in
jury
is u
sual
ly
an in
dica
tor
of s
erio
us o
ngoi
ng h
aem
orrh
age
and
has
impo
rtan
t im
plic
atio
ns fo
r m
anag
emen
t an
d pr
ogno
sis.
Wo,
CC
J.S
hoem
aker
,W
C.
App
el, P
L.19
9310
III-2
B1
To e
valu
ate
the
relia
bilit
y of
the
vi
tal s
igns
to
eval
uate
circ
ulat
ory
stab
ility
as r
efle
cted
by
card
iac
inde
x.
In s
udde
n se
vere
hyp
ovol
aem
ic h
ypot
ensi
on,
the
low
est
mea
n ar
teria
l pre
ssur
e (M
AP
)ro
ughl
y co
rrel
ated
(r2
= .2
5) w
ith fl
ow, b
ut
ther
e w
as p
oor
corr
elat
ion
(r 2=
.000
1) w
hen
all p
ress
ure
and
flow
val
ues
wer
e ev
alua
ted.
Aut
hors
con
clud
e th
at b
lood
flow
can
not
relia
bly
be
infe
rred
from
art
eria
l pre
ssur
e an
d he
art
rate
mea
sure
men
tsun
til e
xtre
me
hypo
tens
ion
occu
rs.
75%
of t
he v
aria
tion
in M
AP
was
not
exp
lain
ed in
thi
s da
tase
t by
car
diac
inde
x.
Bis
hop,
MH
.S
hoem
aker
,W
C.
Ape
l, P
L.19
9380
III-2
Obs
erva
-tio
nal s
tudy
B2
To e
xam
ine
the
rela
tions
hip
betw
een
circ
ulat
ory
valu
es a
ndm
orta
lity
and
orga
n fa
ilure
.
Dat
a no
t pr
esen
ted.
MA
P a
nd h
eart
wer
e po
orly
cor
rela
ted
with
blo
od lo
ss a
ndth
e am
ount
of b
lood
tra
nsfu
sed.
The
est
imat
ed b
lood
loss
was
a m
ore
relia
ble
mea
ns t
han
MA
P a
nd H
R is
est
imat
ing
the
degr
ee o
f sho
ck. I
n th
e cu
tely
inju
red
patie
nt, w
idel
yva
riabl
e ca
tech
olam
ine
resp
onse
s to
hyp
ovol
aem
ia, p
ain,
or
dru
gs m
ade
MA
P a
nd H
R u
nrel
iabl
e pr
edic
tors
of
intr
avas
cula
r vo
lum
e.
Ard
agh,
MW
.H
odgs
on, T
.20
0181
III-2
Dia
gnos
ticTe
st
B2
To e
valu
ate
a ca
lcul
atio
n of
pu
lse
rate
ove
r pu
lse
pres
sure
as
a m
etho
d of
pre
dict
ing
deco
mpe
nsat
ion
in p
atie
nts
with
com
pens
ated
hae
mor
rhag
icsh
ock
in v
ictim
s of
maj
or
road
tra
uma.
RO
PE
is c
alcu
late
d by
: :: p
ulse
rat
e
:: S
BP
-DB
P.
Sen
sitiv
ity 5
5%.
Spe
cific
ity 7
9%.
A R
OP
E v
alue
of g
reat
er t
han
3.0
had
a po
sitiv
e pr
edic
tive
valu
e of
53%
and
a
valu
e le
ss t
han
3.0
had
a ne
gativ
e pr
edic
tive
valu
e of
86%
for
the
deve
lopm
ent
of d
ecom
pens
ated
sho
ck.
RO
PE
>3.
0 is
not
100
% a
ccur
ate
in id
entif
ying
tho
se w
how
ill or
will
not
deco
mpe
nsat
e in
the
em
erge
ncy
depa
rtm
ent,
how
ever
it m
ay p
rovi
de c
linic
ians
with
a u
sefu
l too
l to
incr
ease
sus
pici
on o
f tho
se w
ho m
ay.
:: 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 CL IN ICAL PRACT ICE GU IDEL INESH
YP
OV
OL
AE
MIC
SH
OC
K G
UID
EL
INE
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Tate
voss
ian,
RG
. W
o, C
CJ.
Velm
ahos
, GC
.20
0082
III-2
B1
To e
valu
ate
the
usef
ulne
ss o
ftr
ansc
utan
eous
oxy
gen
and
carb
on d
ioxi
de m
onito
ring
intr
aum
a pa
tient
s fo
r tis
sue
hypo
xia
and
poss
ible
sho
ck.
Com
pare
d w
ith s
urvi
vors
, pat
ient
s w
ho
died
had
sig
nific
antly
low
er P
tcO
2an
d hi
gher
Ptc
CO
2va
lues
beg
inni
ng w
ith t
he e
arly
sta
ge
of r
esus
cita
tion.
Tran
scut
aneo
us O
2co
rrel
ated
wel
l with
dea
than
d m
orbi
dity
.
How
ever
litt
le c
orre
latio
n w
as m
ade
with
alre
ady
mon
itore
d va
lues
suc
h as
HR
& B
P t
ote
st w
heth
er t
hese
val
ues
corr
elat
ed w
ith t
hem
.
Ther
e is
no
quan
tific
atio
n of
val
ues
in t
his
stud
y to
ref
lect
impe
ndin
g sh
ock
or d
ecom
pens
atio
n. V
alue
s ar
e co
rrel
ated
with
dea
th a
nd m
orbi
dity
.
Uns
ure
of t
he u
sefu
lnes
s of
thi
s te
st a
s it
take
~20
min
utes
to c
alib
rate
mac
hine
.
Om
an, K
S.
1995
15
III-2
B2
To v
alid
ate
Hae
mat
ocrit
as
anin
dica
tor
of o
ngoi
ng h
aem
orrh
age
in t
raum
a pa
tient
s w
ho r
ecei
veIV
flui
ds.
The
mea
n ha
emat
ocrit
cha
nge
was
-5
.3%
; in
grou
p 2
(hae
mor
rhag
e gr
oup)
the
haem
atoc
rit c
hang
e w
as -
8.3%
. (p
<0.
05).
A h
aem
atoc
rit d
ecre
ase
of 5
% h
as a
sen
sitiv
ity o
f 94%
,sp
ecifi
city
43%
, PP
V 2
6%, N
PV
97%
. Mea
ning
tha
tha
emat
ocrit
cha
nges
are
not
use
ful i
n id
entif
ying
pat
ient
sw
ho a
re h
aem
orrh
agin
g, b
ut a
re a
ccur
ate
97%
of t
he
time
in id
entif
ying
pat
ient
s w
ho a
re n
ot.
Rix
en, D
. R
aum
, M.
Bou
illon,
B.
Lefe
ring,
R.
2001
13
III-2
Ger
man
Abs
trac
ton
ly
N/A
To e
valu
ate
the
prog
nost
ic v
alue
of
bas
e de
ficit
in t
raum
a pa
tient
s.In
crea
sing
bas
e de
ficit
was
ass
ocia
ted
with
a s
igni
fican
t de
crea
se in
sys
tolic
blo
odpr
essu
re a
nd p
roth
rom
bin
time
as w
ell a
sin
crea
ses
in h
eart
rat
e, la
ctat
e le
vel a
ndm
orta
lity
(p <
0.00
01).
Mor
talit
y in
crea
sed
sign
ifica
ntly
(p <
0.00
01)
with
a w
orse
ning
of B
D fr
om h
ospi
tal t
o IC
Uad
mis
sion
.
Bas
e de
ficit
is a
n ea
rly a
vaila
ble
impo
rtan
t in
dica
tor
toid
entif
y tr
aum
a pa
tient
s w
ith h
aem
odyn
amic
inst
abilit
y,
high
tra
nsfu
sion
req
uire
men
ts, m
etab
olic
and
coa
gula
tory
deco
mpe
nsat
ion,
as
wel
l as
a hi
gh p
roba
bilit
y of
dea
th.
Ban
non
MP.
O'N
eill
CM
.M
artin
M.
1995
14
III-2
Dia
gnos
ticTe
st
B1
To e
xplo
re t
he u
sefu
lnes
s of
ce
ntra
l ven
ous
oxyg
en s
atur
atio
n,ar
teria
l bas
e de
ficit,
and
lact
ate
conc
entr
atio
n in
the
eva
luat
ion
in 4
0 pa
tient
s w
ith o
pera
tive
trun
cal i
njur
ies.
Pre
oper
ativ
e hy
pote
nsio
n oc
curr
ed in
12
.5%
of t
hese
initi
ally
sta
ble
patie
nts.
S
(cv)
O2
did
not
sign
ifica
ntly
cor
rela
te w
ith a
nyof
the
par
amet
ers
of b
lood
loss
and
sev
erity
of
inju
ry e
xam
ined
. How
ever
, bot
h ba
se d
efic
itan
d la
ctat
e co
ncen
trat
ion
corr
elat
ed w
ithtr
ansf
usio
n re
quire
men
ts; i
n ad
ditio
n, b
ase
defic
it co
rrel
ated
with
tra
uma
scor
e, a
ndla
ctat
e co
rrel
ated
with
per
itone
al s
hed
bloo
d vo
lum
e.
Bas
e de
ficit
and
lact
ate
wer
e in
dica
tors
of o
ngoi
ng
bloo
d lo
ss o
r in
adeq
uate
res
usci
tatio
n.
Nee
d to
che
ck s
ensi
tivity
and
spe
cific
ity in
full
text
.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 24
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 25
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Dem
etria
des,
D.
Cha
n, L
S.
Bha
si,
P.B
erne
, TV.
1998
11
III-2
B1
To e
xam
ine
the
inci
denc
e an
d pr
ogno
stic
sig
nific
ance
of
tac
hyca
rdia
and
rel
ativ
ebr
adyc
ardi
a in
pat
ient
s w
ithtr
aum
atic
hyp
oten
sion
.
(Rel
ativ
e br
adyc
ardi
a is
def
ined
SB
P <
or
= 9
0 m
m H
g an
d a
HR
<
or
= 9
0 be
ats
per
min
ute)
.
The
inci
denc
e of
rel
ativ
e br
adyc
ardi
a in
thi
sst
udy
was
28.
9% o
f hyp
oten
sive
pat
ient
s.
Pat
ient
s w
ith r
elat
ive
brad
ycar
dia
in t
hesu
bgro
ups
with
ISS
>16
sig
nific
antly
bet
ter
surv
ival
tha
n pa
tient
s w
ith s
imila
r in
jurie
spr
esen
ting
with
tac
hyca
rdia
.
Rel
ativ
e br
adyc
ardi
a in
hyp
oten
sive
tra
uma
patie
nts
is a
com
mon
hae
mod
ynam
ic fi
ndin
g. M
orta
lity
amon
gta
chyc
ardi
c pa
tient
s w
as m
ore
pred
icta
ble
than
am
ong
brad
ycar
dic
patie
nts
usin
g co
mm
only
use
d de
mog
raph
ican
d in
jury
indi
cato
rs.
:: 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 CL IN ICAL PRACT ICE GU IDEL INESH
YP
OV
OL
AE
MIC
SH
OC
K G
UID
EL
INE
Evidence Table 2. How do you find the sources of bleeding in a hypotensive trauma patient?A
utho
rLe
vel o
fS
tud
y
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Gith
aiga
, JW
.A
dwok
, JA
.20
0283
III-2
Dia
gnos
tic
B1
To d
eter
min
e th
e ac
cura
cy a
ndse
nsiti
vity
of d
iagn
ostic
per
itone
alla
vage
in t
he a
sses
smen
t of
in
tra-
abdo
min
al in
jury
usi
ng
the
dips
tick
met
hod.
DP
L us
ing
the
dips
tick
met
hod
had
anac
cura
cy a
nd s
ensi
tivity
of 9
3% a
nd s
peci
ficity
of 9
8%.
Dia
gnos
tic p
erito
neal
lava
ge is
a c
heap
, saf
e an
d re
liabl
em
etho
d fo
r as
sess
men
t of
abd
omin
al t
raum
a.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 26
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 27
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
Evidence Table 3. What is the best management of the bleeding patient?A
utho
rLe
vel o
fS
tud
y
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Kw
an, I
.B
unn,
F.
Rob
erts
, I.
2003
45
IB
2To
ass
ess
the
effe
cts
of e
arly
vers
us d
elay
ed, a
nd la
rger
ve
rsus
sm
alle
r vo
lum
e of
flui
dad
min
istr
atio
n in
tra
uma
patie
nts
with
ble
edin
g.
Due
to
thei
r he
tero
gene
ity, i
n te
rms
of t
ypes
of p
atie
nts
and
type
s of
flui
ds u
sed,
we
did
not
atte
mpt
to
perfo
rm a
met
a-an
alys
is o
f th
e st
udie
s.
Ther
e w
as n
o ev
iden
ce fo
r or
aga
inst
ear
ly o
r la
rger
volu
me
of in
trav
enou
s flu
id a
dmin
istr
atio
n in
unc
ontr
olle
dha
emor
rhag
e. A
larg
e, w
ell-c
ondu
cted
RC
T is
req
uire
d as
the
qua
lity
of t
he c
urre
nt e
vide
nce
is p
oor.
Bic
kell,
WH
.W
all,
MJ
Jr.
Pep
e, P
E.
Mar
tin, R
R.
1994
40
III-1
Qua
sira
ndom
ised
trial
B2
598
hypo
tens
ive
trau
ma
patie
nts
with
pen
etra
ting
tors
o in
jurie
s w
ere
quas
i-ran
dom
ised
(alte
rnat
e da
yal
loca
tion)
to
early
ver
sus
dela
yed
fluid
adm
inis
trat
ion.
Mor
talit
y w
as 3
8% in
ear
ly fl
uid
adm
inis
trat
ion
vs. 3
0% in
del
ayed
.
Pro
thro
mbi
n an
d pa
rtia
l thr
ombo
plas
tin
time
in e
arly
14.
1 an
d 31
.8 s
econ
ds a
nd
11.4
and
27.
5 se
cond
s in
del
ayed
gro
up.
RR
of d
eath
with
ear
ly fl
uid
adm
inis
trat
ion
is 1
.26
(95%
CI 1
.00-
1.58
).
Intr
aven
ous
fluid
adm
inis
trat
ion
shou
ld b
e w
ithhe
ld u
ntil
defin
itive
sur
gica
l man
agem
ent
is a
vaila
ble
as e
arly
flui
dad
min
istr
atio
n is
ass
ocia
ted
with
incr
ease
d ris
k of
dea
th
and
prol
onga
tion
of c
oagu
latio
n ca
scad
e.
The
stud
y ho
wev
er is
not
con
clus
ive,
met
hods
of a
lloca
tion
usin
g qu
asi-r
ando
mis
ed m
etho
ds is
not
idea
l. A
pro
per
rand
omis
ed t
rail
is n
eede
d to
dra
w d
efin
ite c
oncl
usio
ns.
Turn
er.
2000
41
IIB
21,
309
hypo
tens
ive
trau
ma
patie
nts
rand
omis
ed t
o re
ceiv
e flu
ids
or
no fl
uids
.
Ear
ly fl
uid
adm
inis
trat
ion
mor
talit
y 10
.4%
vs
. 9.8
% in
del
ayed
/no
fluid
gro
up.
Rel
ativ
e ris
k fo
r de
ath
was
1.0
6 (9
5% C
I 0.7
7-1.
47).
Ther
e w
as s
igni
fican
t no
n-co
mpl
ianc
e to
stu
dy p
roto
col
with
31%
of f
luid
gro
up r
ecei
ving
flui
d an
d 80
% o
f no
n flu
id g
roup
not
rec
eivi
ng fl
uid.
Kaw
eski
, SM
.S
is,
MJ.
Virg
ilio, R
W.
1990
84
III-2
cas
eco
ntro
lB
2Th
e ou
tcom
es o
f 6,8
55
trau
ma
patie
nts
wer
e st
udie
dre
tros
pect
ivel
y to
eva
luat
e th
eim
pact
of p
re-h
ospi
tal i
ntra
veno
usflu
id o
n m
orta
lity.
Mor
talit
y w
as s
imila
r be
twee
n th
e tw
o gr
oups
. Th
is s
tudy
faile
d to
sho
w a
n in
fluen
ce o
f flu
id a
dmin
istr
atio
non
sur
viva
l.
Ham
bly,
PR
.D
utto
n, R
P.19
9644
III-3
His
toric
alco
ntro
l
To a
ddre
ss t
he im
pact
of r
apid
infu
sion
dev
ices
on
patie
ntou
tcom
e.
Com
pare
d to
mat
ched
con
trol
pat
ient
s in
jure
d to
the
sam
e ex
tent
dur
ing
the
sam
etim
e pe
riod,
pat
ient
s w
ho r
ecei
ved
fluid
s vi
a th
e R
IS h
ad a
4.8
tim
es g
reat
er c
hanc
e of
dyin
g (9
5% c
onfid
ence
inte
rval
2.4
-7.1
).
Act
ual v
ersu
s ex
pect
ed m
orta
lity
was
als
ohi
gher
tha
n ex
pect
ed m
orta
lity
(52.
9% v
s.61
.8%
, p <
0.00
1).
B2
This
stu
dy r
aise
s th
e qu
estio
n of
the
saf
ety
of r
apid
in
fusi
ng d
evic
es. T
his
anec
dota
l evi
denc
e su
gges
ts t
hene
ed fo
r a
pros
pect
ive
rand
omis
ed t
rial t
o de
term
ine
its
true
impa
ct. H
owev
er, i
n th
e lig
ht o
f cur
rent
evi
denc
e th
atsu
gges
ts s
mal
l vol
ume
hypo
tens
ive
resu
scita
tion
this
is
unl
ikel
y to
occ
ur.
:: 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 CL IN ICAL PRACT ICE GU IDEL INESH
YP
OV
OL
AE
MIC
SH
OC
K G
UID
EL
INE
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Dut
ton,
RP.
Mac
kenz
ie, C
F.S
cale
a, T
M.
2002
42
IIB
2To
eva
luat
e th
e af
fect
of f
luid
resu
scita
tion
titra
ted
to a
low
erth
an n
orm
al S
BP
(100
mm
Hg
vs.
70m
mH
g) d
urin
g th
e pe
riod
ofac
tive
haem
orrh
age
on s
urvi
val i
ntr
aum
a pa
tient
s pr
esen
ting
to t
heho
spita
l in
hem
orrh
agic
sho
ck.
Mor
talit
y be
twee
n th
e tw
o gr
oups
was
the
sam
e (7
% v
s. 7
%).
Titr
atio
n of
initi
al fl
uid
ther
apy
to a
low
er t
han
norm
al
SB
P d
urin
g ac
tive
haem
orrh
age
did
not
affe
ct m
orta
lity
in t
his
stud
y.
Kw
an, I
. B
unn,
F.
Rob
erts
, I.
2003
45
I
B2
To a
sses
s th
e ef
fect
s of
ear
lyve
rsus
del
ayed
, and
larg
er
vers
us s
mal
ler
volu
me
of fl
uid
adm
inis
trat
ion
in t
raum
a pa
tient
s w
ith b
leed
ing.
Due
to
thei
r he
tero
gene
ity, i
n te
rms
of t
ypes
of
pat
ient
s an
d ty
pes
of fl
uids
use
d, w
e di
d no
t at
tem
pt t
o pe
rform
a m
eta-
anal
ysis
of
the
stud
ies.
Ther
e w
as n
o ev
iden
ce fo
r or
aga
inst
ear
ly o
r la
rger
vo
lum
e of
intr
aven
ous
fluid
adm
inis
trat
ion
in u
ncon
trol
led
haem
orrh
age.
A la
rge,
wel
l-con
duct
ed R
CT
is r
equi
red
as t
he q
ualit
y of
the
cur
rent
evi
denc
e is
poo
r.
Bic
kell,
WH
.W
all,
MJ
Jr.
Pep
e, P
E.
1994
40
IIB
2Th
e pu
rpos
e of
thi
s st
udy
was
to
dete
rmin
e th
e ef
fect
s of
del
ayin
gflu
id r
esus
cita
tion
until
the
tim
e of
ope
rativ
e in
terv
entio
n in
hypo
tens
ive
patie
nts
with
pene
trat
ing
inju
ries
to t
he t
orso
.
598
hypo
tens
ive
trau
ma
patie
nts
with
pene
trat
ing
tors
o in
jurie
s w
ere
quas
i-ra
ndom
ised
(alte
rnat
e da
y al
loca
tion)
to
early
ver
sus
dela
yed
fluid
adm
inis
trat
ion.
Mor
talit
y w
as 3
8% in
ear
ly fl
uid
adm
inis
trat
ion
vs. 3
0% in
del
ayed
.
Pro
thro
mbi
n an
d pa
rtia
l thr
ombo
plas
tin t
ime
in e
arly
14.
1 an
d 31
.8 s
econ
ds a
nd 1
1.4
and
27.5
sec
onds
in d
elay
ed g
roup
.
RR
of d
eath
with
ear
ly fl
uid
adm
inis
trat
ion
is 1
.26
(95%
CI 1
.00-
1.58
)
Intr
aven
ous
fluid
adm
inis
trat
ion
shou
ld b
e w
ithhe
ld u
ntil
defin
itive
sur
gica
l man
agem
ent
is a
vaila
ble
as e
arly
flui
dad
min
istr
atio
n is
ass
ocia
ted
with
incr
ease
d ris
k of
dea
th
and
prol
onga
tion
of c
oagu
latio
n ca
scad
e.
Turn
er.
2000
41
IIB
2E
arly
flui
d ad
min
istr
atio
n vs
. no
fluid
.E
arly
flui
d ad
min
istr
atio
n m
orta
lity
10.4
%
vs. 9
.8%
in d
elay
ed/n
o flu
id g
roup
.
Rel
ativ
e ris
k fo
r de
ath
was
1.0
6 (9
5% C
I 0.7
7-1.
47).
Ther
e w
as h
ug n
on-c
ompl
ianc
e to
stu
dy p
roto
col w
ith
31%
of f
luid
gro
up r
ecei
ving
flui
d an
d 80
% o
f non
flui
d gr
oup
not
rece
ivin
g flu
id.
Kaw
eski
, SM
.S
ise,
MJ.
Virg
ilio, R
W.
1990
84
IITh
e ou
tcom
es o
f 6,8
55
trau
ma
patie
nts
wer
e st
udie
dre
tros
pect
ivel
y to
eva
luat
e th
eim
pact
of p
re-h
ospi
tal i
ntra
veno
usflu
id o
n m
orta
lity.
Mor
talit
y w
as s
imila
r be
twee
n th
e tw
o gr
oups
.B
2Th
is s
tudy
faile
d to
sho
w a
n in
fluen
ce o
f flu
id
adm
inis
trat
ion
on s
urvi
val.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 28
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 29
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Bla
ir, S
D.
Janv
rin, S
B.
McC
ollu
m, C
.19
8686
IIB
1E
arly
ver
sus
dela
yed
bloo
dtr
ansf
usio
n fo
r pa
tient
s w
ithga
stro
inte
stin
al b
leed
ing.
Mor
talit
y w
as 8
% in
the
ear
lyve
rsus
0%
in t
he la
te. T
he e
arly
bloo
d tr
ansf
usio
n gr
oup
was
5.4
(95%
CI 0
.3 t
o 10
7.1)
.
The
wer
e ni
ne p
atie
nts
in t
he t
rans
fuse
d gr
oup
that
re-
bled
com
pare
d w
ith o
nly
one
in t
he n
on-t
rans
fuse
d gr
oup
(p <
0.01
).
The
auth
ors
conc
lude
tha
t ea
rly b
lood
tra
nsfu
sion
app
ears
to r
ever
se t
he h
yper
coa
gula
ble
resp
onse
to
haem
orrh
age
ther
eby
enco
urag
ing
re-b
leed
ing
and
henc
e th
e ne
ed fo
r an
ope
ratio
n.
Dun
ham
, CM
.B
elzb
erg,
H.
Lyle
s, R
.W
eire
ter,
L.19
9187
IIC
Rap
id in
fusi
ng d
evic
e vs
.co
nven
tiona
l flu
id a
dmin
istr
atio
nTh
e re
lativ
e ris
k fo
r de
ath
is 0
.80
(95%
CI 0
.28-
2.29
).
Lact
ate
leve
ls w
ere
low
er in
the
RIS
gro
up a
tvi
rtua
lly a
ll tim
es fr
om h
ours
1 t
o 24
(4.3
/5.3
mM
/l, t
-val
ue =
3.3
, DF
= 2
79, p
= 0
.001
).
Pos
t-ad
mis
sion
hyp
othe
rmia
was
gre
ater
in
the
CFA
gro
up a
t al
l tim
es d
urin
g th
e fir
st
24 h
(35.
2 /
36.4
deg
rees
C, t
-val
ue =
5.6
, D
F =
250
, P =
0.0
01).
The
mea
n pa
rtia
lth
rom
bopl
astin
tim
e w
as s
igni
fican
tly h
ighe
rin
the
CFA
gro
up (4
7.3/
35.1
s, t
-val
ue =
3.1
,D
F =
279
, P =
0.0
02).
The
PTT
and
PT
wer
e re
late
d to
the
deg
ree
of la
ctic
aci
dosi
s (p
= 0
.000
1) a
nd h
ypot
herm
ia (p
= 0
.001
) bu
t no
t to
the
am
ount
of F
FP g
iven
(p =
0.1
4).
Hyp
ovol
aem
ic t
raum
a pa
tient
s re
susc
itate
d w
ith
the
RIS
less
coa
gulo
path
y; m
ore
rapi
d re
solu
tion
ofhy
pope
rfusi
on a
cido
sis;
bet
ter
tem
pera
ture
pre
serv
atio
n;
and
few
er h
ospi
tal c
ompl
icat
ions
tha
n th
ose
resu
scita
ted
with
con
vent
iona
l met
hods
of f
luid
/ b
lood
pro
duct
adm
inis
trat
ion.
Dut
ton,
RP.
Mac
kenz
ie, C
F.20
0242
IIB
2La
rge
vs s
mal
l flu
id r
esus
cita
tion.
Mor
talit
y w
as 4
/55
(7.3
%) i
n th
e gr
oup
adm
inis
tere
d a
larg
er v
olum
e an
d 4/
55 (7
.3%
)in
the
gro
up a
dmin
iste
red
a sm
alle
r vo
lum
e(1
000m
l les
s th
an in
the
inte
rven
tion
grou
p).
The
rela
tive
risk
for
deat
h is
1.0
0 (9
5% C
I 0.
26-3
.81)
.
Ther
e w
as n
o ev
iden
ce fo
r or
aga
inst
larg
e vo
lum
ead
min
istr
atio
n in
pat
ient
s w
ith t
raum
atic
hyp
oten
sion
.
:: 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 CL IN ICAL PRACT ICE GU IDEL INESH
YP
OV
OL
AE
MIC
SH
OC
K G
UID
EL
INE
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Nef
f, TA
.D
oelb
erg,
M.
Jung
hein
rich
C.
2003
88
IIB
1To
inve
stig
ate
the
safe
ty o
fre
petit
ive
larg
e-do
se in
fusi
on
of a
nov
el h
ydro
xyet
hyl s
tarc
hso
lutio
n (6
% H
ES
130
/0.4
) in
cran
io-c
ereb
ral t
raum
a pa
tient
s.
Ther
e w
ere
no d
iffer
ence
s be
twee
n gr
oups
in m
orta
lity,
ren
al fu
nctio
n, b
leed
ing
com
plic
atio
ns, a
nd u
se o
f blo
od p
rodu
cts.
Ther
e w
ere
also
no
maj
or d
iffer
ence
s in
coag
ulat
ion
varia
bles
.
Pre
viou
sly,
the
effe
ct o
f hyd
roxy
ethy
l sta
rch
(HE
S) t
ypes
for
plas
ma
volu
me
expa
nsio
n on
coa
gula
tion
and
rena
lfu
nctio
n. H
owev
er, t
his
stud
y su
gges
ts t
hat
HE
S 1
30/0
.4ca
n sa
fely
be
used
in c
ritic
ally
ill h
ead
trau
ma
patie
nts
over
seve
ral d
ays
at d
oses
of u
p to
70
mL
x kg
(-1)
x d
(-1)
.
Buc
hman
, TG
.M
enke
r, JB
.Li
pset
t, PA
.19
9189
IVC
To e
valu
ate
the
effe
ct o
f rap
idin
fuse
r on
uns
uspe
cted
sur
viva
lra
tes
in h
ypot
ensi
ve p
enet
ratin
gtr
aum
a pa
tient
s.
Ther
e w
as a
sta
tistic
ally
sig
nific
ant
impr
ovem
ent
in c
linic
al fl
ow r
ates
, dec
rem
ent
in r
esus
cita
tion
times
and
une
xpec
ted
surv
ival
.
Sta
tistic
al s
umm
ary
not
pres
ente
d in
pap
er,
unab
le t
o de
term
ine.
Use
of r
apid
infu
sion
dev
ice
in t
his
smal
l ser
ies
of
patie
nts
is h
ypot
hesi
sed
by t
he a
utho
rs t
o im
prov
edun
expe
cted
sur
viva
l.
Rem
mer
s, D
E.
Wan
g, P
. C
ioffi
, WG
.19
9890
Sci
entif
icA
nim
alN
/ATo
det
erm
ine
whe
ther
pro
long
ed(c
hron
ic) r
esus
cita
tion
has
any
bene
ficia
l effe
cts
on c
ardi
ac o
utpu
tan
d he
pato
cellu
lar
func
tion
afte
rtr
aum
a-ha
emor
rhag
e an
d ac
ute
fluid
rep
lace
men
t.
Chr
onic
res
usci
tatio
n w
ith 5
mL/
kg/h
r re
stor
edca
rdia
c ou
tput
, hep
atoc
ellu
lar
func
tion,
and
hepa
tic m
icro
vasc
ular
blo
od fl
ow a
t 20
hou
rsaf
ter
haem
orrh
age.
The
reg
imen
abo
ve a
lso
redu
ced
plas
ma
IL-6
leve
ls.
Chr
onic
flui
d re
susc
itatio
n in
add
ition
to
acut
e flu
idre
plac
emen
t sh
ould
be
rout
inel
y us
ed in
exp
erim
enta
lst
udie
s of
tra
uma-
hae
mor
rhag
e.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 30
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 31
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
Evidence Table 4. If fluid resucitation is indicated, what type of fluids should be used?A
utho
rLe
vel o
fS
tud
y
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Ald
erso
n, P
.S
chie
rhou
t, G
.R
ober
ts, I
.B
unn,
F.
2004
50
I Not
spec
ifica
llytr
aum
apa
tient
s,bu
tin
clud
esst
udie
s on
trau
ma
patie
nts.
ATo
ass
ess
the
effe
cts
on m
orta
lity
of c
ollo
ids
com
pare
d to
cry
stal
loid
sfo
r flu
id r
esus
cita
tion
in c
ritic
ally
ill pa
tient
s.
– C
ollo
ids
com
pare
d to
cry
stal
loid
s: R
R1.
52(9
5% c
onfid
ence
inte
rval
1.0
8 to
2.1
3).
– H
ydro
xyet
hyls
tarc
h: R
R1.
16 (0
.68
to 1
.96)
.
– M
odifi
ed g
elat
in: R
R0.
50 (0
.08
to 3
.03)
.
– D
extr
an: R
R1.
24 (0
.94
to 1
.65)
.
– C
ollo
ids
in h
yper
toni
c cr
ysta
lloid
com
pare
dto
isot
onic
cry
stal
loid
: RR
0.88
(0.7
4 to
1.0
5).
Ther
e is
no
evid
ence
from
ran
dom
ised
con
trol
led
tria
ls
that
res
usci
tatio
n w
ith c
ollo
ids
redu
ces
the
risk
of d
eath
com
pare
d to
cry
stal
loid
s in
pat
ient
s w
ith t
raum
a, b
urns
an
d fo
llow
ing
surg
ery.
As
collo
ids
are
not
asso
ciat
ed w
ith
an im
prov
emen
t in
sur
viva
l, an
d as
the
y ar
e m
ore
expe
nsiv
eth
an c
ryst
allo
ids,
it is
har
d to
see
how
the
ir co
ntin
ued
use
in t
hese
pat
ient
typ
es c
an b
e ju
stifi
ed o
utsi
de t
he c
onte
xt
of r
ando
mis
ed c
ontr
olle
d tr
ials
.
Wilk
es, M
M.
Nav
icki
s, R
J.20
0191
I Not
spec
ifica
llytr
aum
apa
tient
s,bu
tin
clud
esst
udie
s on
trau
ma
patie
nts.
B2
To t
est
the
hypo
thes
is t
hat
albu
min
adm
inis
trat
ion
is n
ot a
ssoc
iate
dw
ith e
xces
s m
orta
lity.
Alb
umin
adm
inis
trat
ion
did
not
sign
ifica
ntly
affe
ct m
orta
lity
in a
ny c
ateg
ory
of in
dica
tions
.Fo
r al
l tria
ls, t
he r
elat
ive
risk
for
deat
h w
as 1
.11
(95%
Cl,
0.95
to
1.28
).
No
effe
ct o
f alb
umin
on
mor
talit
y w
as d
etec
ted;
an
y su
ch e
ffect
may
the
refo
re b
e sm
all.
This
find
ing
supp
orts
the
saf
ety
of a
lbum
in.
Aut
hors
con
clud
e th
at o
vera
ll m
etho
dolo
gica
l qua
lity
of s
tudi
es is
poo
r an
d ef
fect
s st
udy
resu
lts. A
larg
e w
ell-e
xecu
ted
RC
T is
nee
ded.
Wad
e, C
E.
Kra
mer
, GC
.G
rady
, JJ.
1997
55
I Trau
ma
To e
valu
ate
the
effe
cts
ofH
yper
toni
c S
alin
e an
d H
yper
toni
cS
alin
e /
Dex
tran
on
surv
ival
unt
ildi
scha
rge
or fo
r 30
day
s.
HS
was
not
effe
ctiv
e in
impr
ovin
g su
rviv
al.
HS
D r
esul
ted
in a
n in
crea
se in
sur
viva
l in
7/8
tria
ls. O
R 1
.20
(95%
CI 0
.94-
1.57
)
B2
Hyp
erto
nic
Sal
ine
alon
e do
es n
ot o
ffer
any
bene
fit
in t
erm
s of
30-
day
surv
ival
ove
r is
oton
ic c
ryst
allo
ids.
Hyp
erto
nic
Sal
ine
with
Dex
tran
may
impr
ove
mor
talit
y.
The
met
a-an
alys
is o
f the
ava
ilabl
e da
ta s
how
s th
at H
S is
not
diffe
rent
from
the
sta
ndar
d of
car
e an
d th
at H
SD
may
be s
uper
ior.
Wad
e, C
E.
Gra
dy, J
J.K
ram
er, G
C.
Youn
es, R
N.
1997
92
IITo
eva
luat
e im
prov
emen
ts
in s
urvi
val a
t 24
hou
rs a
nddi
scha
rge
afte
r in
itial
tre
atm
ent
with
Hyp
erto
nic
Sal
ine
Dex
tros
e in
pat
ient
s w
ho h
ad t
raum
atic
br
ain
inju
ry.
HS
D r
esul
ted
in a
sur
viva
l unt
il di
scha
rge
of 3
7.9%
(39
of 1
03) v
s. 2
6.9%
(32
of 1
19)
with
sta
ndar
d of
car
e (p
= 0
.080
). U
sing
logi
stic
regr
essi
on, a
djus
ting
for
tria
l and
pot
entia
lco
nfou
ndin
g va
riabl
es, t
he t
reat
men
t ef
fect
ca
n be
sum
mar
ised
by
the
odds
rat
io o
f 2.
12 (p
= 0
.048
) for
sur
viva
l unt
il di
scha
rge.
B2
Pat
ient
s w
ho h
ave
trau
mat
ic b
rain
inju
ries
in t
he p
rese
nce
of h
ypot
ensi
on a
nd r
ecei
ve H
SD
are
abo
ut t
wic
e as
like
ly t
osu
rviv
e as
tho
se w
ho r
ecei
ve s
tand
ard
of c
are.
:: 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 CL IN ICAL PRACT ICE GU IDEL INESH
YP
OV
OL
AE
MIC
SH
OC
K G
UID
EL
INE
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Mat
tox,
KL.
Man
inga
s, P
A.
Moo
re, E
E.
1991
93
IIA
To c
ompa
re 2
50 m
L of
HS
D
vers
us 2
50 m
L of
nor
mal
crys
tallo
id s
olut
ion
adm
inis
tere
dbe
fore
rou
tine
preh
ospi
tal a
ndem
erge
ncy
cent
re r
esus
cita
tion.
Ther
e w
as n
o di
ffere
nce
in s
urvi
val b
etw
een
the
two
grou
ps.
The
HS
D g
roup
had
an
impr
oved
blo
odpr
essu
re (p
= 0
.024
). H
aem
atoc
rit, s
odiu
mch
lorid
e, a
nd o
smol
ality
leve
ls w
ere
sign
ifica
ntly
elev
ated
in t
he e
mer
genc
y ce
ntre
.
This
stu
dy s
how
ed t
he s
afet
y of
HS
D, b
ut fa
iled
to s
how
an
y be
nefit
of t
his
solu
tion
in r
educ
ing
mor
talit
y. In
ligh
t of
the
cos
t of
thi
s so
lutio
n in
com
paris
on t
o st
anda
rdth
erap
y, u
ntil
prov
en e
ffica
ciou
s is
not
rec
omm
ende
d.
Man
inga
s, P
A.
Mat
tox,
KL.
Pep
e, P
E.
Jone
s, R
L.19
8994
IIB
1P
ilot
stud
y to
ass
ess
the
safe
ty o
fsa
line-
dext
ran
solu
tions
in t
raum
apa
tient
s w
ith p
enet
ratin
g in
jurie
san
d a
preh
ospi
tal s
ysto
lic b
lood
pres
sure
< 9
0 m
m H
g.
Ther
e w
ere
no c
ompl
icat
ions
ass
ocia
ted
with
the
infu
sion
of t
he h
yper
toni
c sa
line-
dext
ran
solu
tion,
and
exe
cutio
n of
the
pro
toco
l by
para
med
ic p
erso
nnel
was
bot
h sa
fe a
ndun
iform
ly s
ucce
ssfu
l.
The
resu
lts o
f thi
s fe
asib
ility
stud
y ju
stify
the
initi
atio
n of
a la
rger
pro
spec
tive,
ran
dom
ised
clin
ical
tria
l on
the
effic
acy
of t
his
solu
tion
in t
he p
reho
spita
l set
ting.
Slo
an, E
P.K
oeni
gsbe
rg,
M.
Gen
s, D
.C
ipol
le, M
.19
9995
IITo
det
erm
ine
if th
e in
fusi
on o
f up
to 1
000
mL
of d
iasp
irin
cros
s-lin
ked
haem
oglo
bin
(DC
LHb)
du
ring
the
initi
al h
ospi
tal
resu
scita
tion
coul
d re
duce
28
-day
mor
talit
y in
tra
umat
iche
mor
rhag
ic s
hock
pat
ient
s.
At
28 d
ays,
24
(46%
) of t
he 5
2 pa
tient
s in
fuse
d w
ith D
CLH
b di
ed, a
nd 8
(17%
) of
the
46
patie
nts
infu
sed
with
the
sal
ine
solu
tion
died
(p =
.003
). A
t 48
hou
rs, 2
0 (3
8%)
of t
he 5
2 pa
tient
s in
fuse
d w
ith D
CLH
b di
edan
d 7
(15%
) of t
he 4
6 pa
tient
s in
fuse
d w
ith
the
salin
e so
lutio
n di
ed (p
= .0
1).
B2
Mor
talit
y w
as h
ighe
r fo
r pa
tient
s tr
eate
d w
ith D
CLH
b.D
CLH
b do
es n
ot a
ppea
r to
be
an e
ffect
ive
resu
scita
tion
fluid
.
Bou
wm
an, D
L.W
eave
r, D
W.
Vega
, J. e
t al
.19
7896
IITo
stu
dy t
he e
ffect
s of
alb
umin
on
ser
um p
rote
in h
omeo
stas
is
in 5
2 se
rious
ly in
jure
d pa
tient
s.
Alte
red
haem
osta
sis
and
depr
esse
d im
mun
ere
spon
se a
re t
wo
poss
ible
effe
cts
with
cl
inic
al s
igni
fican
ce e
xper
ienc
ed in
the
al
bum
in-r
ecei
ving
gro
up.
B1
Add
ition
al in
vest
igat
ion
of s
econ
dary
hom
eost
atic
resp
onse
s ar
e ne
cess
ary
to m
ore
com
plet
ely
eval
uate
the
effe
cts
of a
lbum
in in
fusi
on.
Wu,
JJ.
H
uang
, MS
.Ta
ng, G
J.
Kao
, WF.
2001
97
IITo
com
pare
the
car
diac
and
haem
odyn
amic
res
pons
es t
o a
rapi
d in
fusi
on o
f 100
0 m
l of
mod
ified
flui
d ge
latin
(gro
up A
) or
100
0 m
l of l
acta
ted
Rin
ger'
sso
lutio
n (g
roup
B) i
n em
erge
ncy
room
pat
ient
s su
fferin
g fro
m s
hock
.
In b
oth
grou
ps t
he m
ean
arte
rial b
lood
pres
sure
(MA
P),
syst
olic
and
dia
stol
ic p
ress
ure,
cent
ral v
enou
s pr
essu
re (C
VP
), an
d pu
lmon
ary
arte
ry o
cclu
sion
pre
ssur
e (P
AO
P) i
ncre
ased
sign
ifica
ntly.
The
CV
P a
nd P
AO
P in
crea
sed
sign
ifica
ntly
mor
e in
the
mod
ified
flui
d ge
latin
resu
scita
tion
grou
p.
B1
Mod
ified
Flu
id G
elat
in w
as m
ore
effe
ctiv
e th
an L
R in
incr
easi
ng B
P, M
AP
and
CO
imm
edia
tely
afte
r in
fusi
on
(<15
min
utes
) (p
<0.
05).
Ther
e w
as n
o di
ffere
nce
in s
urvi
val b
etw
een
the
two
grou
ps.
Exc
lude
d pa
tient
s th
at w
ere
mec
hani
cally
ven
tilat
ed.
This
stu
dy in
clud
es p
atie
nts
with
neu
roge
nic
shoc
k.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 32
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 33
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Wad
e, C
E.
Gra
dy, J
J.K
ram
er, G
C.
2003
98
IIA
To a
sses
s w
heth
er t
head
min
istr
atio
n of
hyp
erto
nic
salin
ede
xtra
n (H
SD
) was
det
rimen
tal
whe
n ad
min
iste
red
to p
atie
nts
who
wer
e hy
pote
nsiv
e be
caus
e of
pen
etra
ting
inju
ries
to t
he t
orso
.
82.5
% t
reat
ed w
ith H
SD
sur
vive
d vs
. 75
.5%
pat
ient
s w
ho r
ecei
ved
norm
al s
alin
e.Th
e di
ffere
nce
in s
urvi
val r
ates
bet
wee
n gr
oups
was
not
sta
tistic
ally
sig
nific
ant
(p =
0.1
89).
For
the
patie
nts
with
tru
ncal
inju
ries
that
did
not
rece
ive
surg
ery,
the
re w
as n
o si
gnifi
cant
diffe
renc
e (p
= 0
.09)
bet
wee
n flu
id t
reat
men
tsin
sur
viva
l unt
il di
scha
rge.
For
pat
ient
s tr
eate
dw
ith H
SD
, 77.
8% s
urvi
ved
24 h
ours
whe
reas
,of
tho
se r
ecei
ving
SO
C, 9
1.9%
sur
vive
d un
tildi
scha
rge.
For
pene
trat
ing
trun
cal i
njur
ies
that
req
uire
dsu
rger
y, t
here
was
a s
tatis
tical
ly s
igni
fican
tef
fect
(p =
0.0
1) o
f tre
atm
ent
on o
vera
ll su
rviv
alun
til d
isch
arge
. Of t
he 8
4 pa
tient
s tr
eate
d w
ithH
SD
, 84.
5% s
urvi
ved,
whe
reas
sur
viva
l was
67.1
% in
the
73
patie
nts
rece
ivin
g S
OC
.
The
incr
ease
in b
leed
ing
and
mor
talit
y as
soci
ated
with
the
infu
sion
of H
SD
res
ulte
d in
ani
mal
stu
dies
was
not
foun
d in
this
stu
dy. A
utho
rs h
ypot
hesi
s th
at t
his
is b
ecau
se t
he r
ate
of in
fusi
on a
nd t
imin
g of
infu
sion
afte
r in
jury
was
diff
eren
t in
this
stu
dy p
erha
ps h
ighl
ight
ing
the
timin
g of
the
initi
atio
n of
fluid
infu
sion
and
the
rat
e m
ay in
fluen
ce o
utco
me.
The
resu
lts o
f thi
s st
udy
sugg
est
that
the
adm
inis
trat
ion
of h
yper
toni
c sa
line
is n
ot d
etrim
enta
l to
patie
nts
with
pene
trat
ing
trun
cal w
ound
s de
spite
the
incr
ease
in S
BP.
Ther
e is
som
e ev
iden
ce t
o su
gges
t th
at H
SD
impr
oves
mor
talit
y to
hos
pita
l dis
char
ge.
Con
side
r pr
ehos
pita
l and
ED
sta
ff ab
ility
to id
entif
y ea
rly
hose
req
uirin
g O
T.
Mau
ritz,
W.
Sch
imet
ta, W
.O
berr
eith
er, S
.P
olz,
W.
2002
99
IV Pro
spec
tive
Cas
e se
ries
To d
eter
min
e th
e sa
fety
of
hype
rton
ic h
yper
onc
otic
sol
utio
nsfo
r pr
ehos
pita
l sm
all-v
olum
ere
susc
itatio
n.
Ther
e w
ere
smal
l inc
reas
es in
ser
um s
odiu
man
d ch
lorid
e (7
and
12
mm
ol/l,
med
ians
;p
<0.
001)
. On
arriv
al o
xyge
n sa
tura
tion
and
syst
olic
and
dia
stol
ic b
lood
pre
ssur
e ha
din
crea
sed
(5%
, 30
and
20 m
mH
g, r
espe
ctiv
ely)
,w
here
as h
eart
rat
e ha
d dr
oppe
d by
15
b.p.
m.
(med
ians
; p <
0.00
1).
5% o
f pat
ient
s ex
perie
nced
mild
sid
e ef
fect
s(h
eat
sens
atio
ns, v
omiti
ng)
B2
Hyp
erto
nic
hype
r on
cotic
sol
utio
ns w
ere
foun
d to
be
safe
and
effe
ctiv
e in
thi
s se
ries
of p
atie
nts.
How
ever
with
no
com
paris
on g
roup
the
affe
cts
of t
his
inte
rven
tion
are
not
conc
lusi
ve.
Sha
tney
, CH
.D
eepi
ka, K
.M
ilitel
lo, P
R.
1983
100
IITo
eva
luat
e 6%
het
asta
rch
(HE
S)
v 5%
pla
sma
prot
ein
fract
ion
(PP
F)as
the
col
loid
com
pone
nt o
fin
trav
enou
s (IV
) flu
id r
esus
cita
tion
in 3
2 pa
tient
s w
ith m
ultis
yste
mtr
aum
a an
d/or
hem
orrh
agic
sho
ck.
No
inte
rgro
up d
iffer
ence
s w
ere
note
d in
inde
xes
of h
epat
ic, p
ulm
onar
y, o
r re
nal f
unct
ion
or in
the
inci
denc
e of
infe
ctio
n. T
he fr
eque
ncy
of o
ther
com
plic
atio
ns, i
nclu
ding
ble
edin
gdi
athe
ses,
and
mor
talit
y w
ere
iden
tical
in
the
two
grou
ps.
B1
Res
ults
of t
his
pilo
t st
udy
sugg
est
that
, com
pare
d w
ith
PP
F, H
ES
in la
rge
volu
mes
is a
saf
e, e
ffect
ive
collo
idso
lutio
n in
the
res
usci
tatio
n of
pat
ient
s w
ith m
ultis
yste
mtr
aum
a an
d /
or h
emor
rhag
ic s
hock
.
Cos
t of
col
loid
s gr
eate
r th
an c
ryst
allo
ids,
is t
here
any
bene
fit.
:: 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 CL IN ICAL PRACT ICE GU IDEL INESH
YP
OV
OL
AE
MIC
SH
OC
K G
UID
EL
INE
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Vass
ar, M
J.P
erry
, CA
.G
anna
way
,W
L.
1991
101
IIB
17.
5% N
aCl/D
extr
an (H
TS) v
s.La
ctat
ed R
inge
rs (L
R) s
olut
ion
for
fluid
res
usci
tatio
n in
hyp
oten
sive
trau
ma
patie
nts.
Sur
viva
l at
hosp
ital d
isch
arge
w
as 6
4% v
s. 5
9% fo
r H
TS a
ndLR
res
pect
ivel
y.
The
rate
of s
urvi
val t
o ho
spita
l dis
char
ge
for
the
pat
ient
s w
ith s
ever
e he
ad in
jurie
s w
as 3
2% f
or
the
HT
S g
roup
vs.
16%
fo
r th
eLR
sol
utio
n gr
oup.
(thi
s di
d no
t re
ach
stat
istic
alsi
gnifi
canc
e).
Hyp
erto
nic
salin
e/D
extr
an w
as s
how
n to
dec
reas
e m
orta
lity
at h
ospi
tal d
isch
arge
in t
his
stud
y; R
R18
.3(9
5% C
I 0.6
0-1.
30).
Vass
ar, M
J.Fi
sche
r, R
P.O
'Brie
n, P
E.
Bac
hulis
, BL.
1993
102
IITo
eva
luat
e th
e us
e of
250
mL
of a
7.5
% s
odiu
m c
hlor
ide
solu
tion,
both
with
and
with
out
adde
dde
xtra
n 70
, for
the
pre
hosp
ital
resu
scita
tion
of h
ypot
ensi
ve
trau
ma
patie
nts.
Cha
nge
in s
ysto
lic b
lood
pre
ssur
e on
arr
ival
inth
e em
erge
ncy
depa
rtm
ent
was
sig
nific
antly
high
er in
the
hyp
erto
nic
salin
e so
lutio
n gr
oup
than
tha
t in
the
lact
ated
Rin
ger'
s so
lutio
ngr
oup
(34
plus
or
min
us 4
6 vs
. 11
plus
or
min
us 4
9 m
m H
g, p
<.0
3).
Ther
e w
as n
o di
ffere
nce
in s
urvi
val b
etw
een
the
grou
ps. R
R09
7 (0
.68-
1.37
).
B1
Pre
hosp
ital i
nfus
ion
of 2
50 m
L of
7.5
% s
odiu
m c
hlor
ide
is a
ssoc
iate
d w
ith a
n in
crea
se in
blo
od p
ress
ure.
How
ever
no
stat
istic
ally
sig
nific
ant
diffe
renc
e w
as n
oted
betw
een
the
grou
ps.
Vass
ar, M
J.P
erry
, CA
.H
olcr
oft,
JW.
1993
52
IITo
eva
luat
e th
e co
ntrib
utio
n of
the
dext
ran
com
pone
nt in
res
usci
tatio
nof
hyp
oten
sive
tra
uma
patie
nts.
Ther
e w
as n
o di
ffere
nce
in m
orta
lity
betw
een
the
grou
ps.
RR
1.42
(0.7
7-2.
6)
B1
The
addi
tion
of a
col
loid
, in
the
form
of 6
% d
extr
an 7
0,
did
not
offe
r an
y ad
ditio
nal b
enef
it, a
t le
ast
in t
his
sett
ing
of r
apid
urb
an t
rans
port
.
Tran
baug
h, R
F.Le
wis
, FR
.19
8310
3
III-2
To e
valu
ate
the
effe
cts
of c
ryst
allo
idflu
id r
esus
cita
tion
on lu
ng w
ater
(pul
mon
ary
oede
ma)
.
Ext
ra-v
ascu
lar
lung
wat
er r
emai
ned
in t
heno
rmal
ran
ge o
f 7.0
+/-
1.0
ml/k
g du
ring
the
first
five
hos
pita
l day
s fo
r al
l pat
ient
s de
spite
prof
ound
dec
reas
e in
PC
OP
(les
s th
an
15m
m H
g).
Sci
entif
icC
ryst
allo
id r
esus
cita
tion
clea
rly is
not
har
mfu
l to
the
lung
and
it is
equ
ally
as
effe
ctiv
e as
col
loid
res
usci
tatio
n.C
ryst
allo
id is
mar
kedl
y le
ss e
xpen
sive
tha
n co
lloid
and
,gi
ven
the
grea
ter
cost
of c
ollo
id w
ithou
t ev
iden
t be
nefit
.
Hol
crof
t, JW
.Va
ssar
, MJ.
Per
ry, C
A.
1989
104
IITo
eva
luat
e th
e ef
fect
s of
ahy
pert
onic
7.5
% N
aCl /
6%
D
extr
an 7
0 (H
SD
) sol
utio
n in
the
resu
scita
tion
of p
atie
nts
in t
heem
erge
ncy
room
.
Ther
e w
as n
o di
ffere
nce
in m
orta
lity
betw
een
the
two
grou
ps, o
r in
the
phy
siol
ogic
al v
aria
ble
that
wer
e m
easu
red.
AH
yper
toni
c so
lutio
n w
as s
afe
to u
se, b
ut t
he d
ata
pres
ente
d in
thi
s st
udy
show
no
affe
ct o
n m
orta
lity
on b
leed
ing
trau
ma
patie
nts.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 34
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 35
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
:: EVIDENCE TABLES
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
John
son,
JL.
Moo
re, E
E.
Offn
er, P
J.H
aene
l, JB
.19
9810
5
IIB
2To
tes
t th
e va
soco
nstr
ictio
nfo
llow
ing
adm
inis
trat
ion
ofte
tram
eric
hae
mog
lobi
ns in
tr
aum
a pa
tient
s.
Ther
e w
as n
o di
ffere
nce
in a
ny o
f the
mea
sure
dha
emod
ynam
ic p
aram
eter
s be
twee
n pa
tient
sre
susc
itate
d w
ith p
olym
eriz
ed h
aem
oglo
bin
vers
us b
lood
.
Pol
ymer
ised
hae
mog
lobi
n gi
ven
in la
rge
dose
s to
inju
red
patie
nts
lack
s th
e va
soco
nstr
ictiv
e ef
fect
s re
port
ed in
th
e us
e of
oth
er h
aem
oglo
bin-
base
d bl
ood
subs
titut
es.
This
sup
port
s th
e co
ntin
ued
inve
stig
atio
n of
pol
ymer
ised
haem
oglo
bin
in in
jure
d pa
tient
s re
quiri
ng u
rgen
t tr
ansf
usio
n.
Ker
ner,
T.A
hler
s, O
. Ve
it, S
. R
iou,
B.
2003
106
II (Eur
opea
n‘O
n-S
cene
’m
ultic
entr
est
udy)
To t
est
the
hypo
thes
is t
hat
the
early
adm
inis
trat
ion
of a
n ox
ygen
carr
ier
may
red
uce
the
occu
rren
ceof
org
an fa
ilure
s an
d im
prov
esu
rviv
al.
(10%
dia
spiri
n cr
oss-
linke
dha
emog
lobi
n (D
CLH
b) v
s.
stan
dard
IVF.
)
Org
an fa
ilure
s an
d su
rviv
al r
ates
unt
il da
y fiv
ean
d da
y 28
sho
wed
no
sign
ifica
nt d
iffer
ence
s.B
2Th
e ea
rly a
pplic
atio
n of
an
oxyg
en c
arrie
r (D
CLH
b) t
op
atie
nts
wit
h se
vere
hem
orr
hag
ic s
hock
follo
win
gtr
aum
a ha
d no
sig
nific
ant
effe
ct o
n th
e oc
curr
ence
of
orga
n fa
ilure
or
on 5
- an
d 28
-day
sur
viva
l in
this
abbr
evia
ted
tria
l.
(Thi
s st
udy
was
sto
pped
afte
r in
terim
ana
lysi
s,
spon
sors
exp
ress
ed s
ome
conc
ern
on t
he lo
ng-t
erm
ef
fect
s of
thi
s dr
ug.)
John
son,
JL.
Moo
re, E
E.
Offn
er, P
J.20
0110
7
IITo
com
pare
the
impa
ct o
f RB
C
or B
lood
sub
stitu
tes
on n
eutr
ophi
lac
tivity
.
(Pac
ked
red
bloo
d ce
lls h
ave
the
pote
ntia
l to
exac
erba
te e
arly
post
inju
ry h
yper
infla
mm
atio
nan
d m
ultip
le o
rgan
failu
re t
hrou
ghpr
imin
g of
circ
ulat
ing
neut
roph
ils[P
MN
s]).
Pol
yhem
e di
d no
t re
sult
in t
he a
ggra
vatio
n of
circ
ulat
ing
neut
roph
ils in
con
tras
t to
PR
BC
.B
1Th
e us
e of
a b
lood
sub
stitu
te in
the
ear
ly p
ost
inju
ry
perio
d av
oids
PM
N p
rimin
g an
d m
ay t
here
by p
rovi
de
an a
venu
e to
dec
reas
e th
e in
cide
nce
or s
ever
ity o
f po
st in
jury
mul
tiple
org
an fa
ilure
.
Hirs
hber
g, A
.D
ugas
, M.
Ban
ez, E
I.20
0310
8
Sci
entif
ic/
Com
pute
rsi
mul
atio
n
To c
alcu
late
the
cha
nges
inpr
othr
ombi
n tim
e (P
T), f
ibrin
ogen
,an
d pl
atel
ets
with
ble
edin
g.
Pro
long
atio
n of
PT
is t
he s
entin
el e
vent
of
dilu
tiona
l coa
gulo
path
y an
d oc
curs
ear
ly in
the
oper
atio
n. T
he k
ey t
o pr
even
ting
coag
ulop
athy
is p
lasm
a in
fusi
on b
efor
e P
T be
com
essu
bhem
osta
tic. T
he o
ptim
al r
epla
cem
ent
ratio
sw
ere
2:3
for
plas
ma
and
8:10
for
plat
elet
s.
CE
xist
ing
prot
ocol
s un
dere
stim
ate
the
dilu
tion
of c
lott
ing
fact
ors
in s
ever
ely
blee
ding
pat
ient
s.
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 CL IN ICAL PRACT ICE GU IDEL INESH
YP
OV
OL
AE
MIC
SH
OC
K G
UID
EL
INE
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Gou
ld, S
A.
Moo
re, E
E.
Hoy
t, D
B.
1998
109
IIB
1To
com
pare
dire
ctly
the
the
rape
utic
bene
fit o
f Pol
yHem
e w
ith t
hat
ofal
loge
neic
red
blo
od c
ells
(RB
Cs)
inth
e tr
eatm
ent
of a
cute
blo
od lo
ss.
Ther
e w
as n
o di
ffere
nce
in t
otal
[Hb]
bet
wee
nth
e gr
oups
bef
ore
infu
sion
(10.
4 +
/- 2
.3 g
/dL
cont
rol v
s. 9
.4 +
/- 1
.9 g
/dL
expe
rimen
tal).
At
end-
infu
sion
the
exp
erim
enta
l RB
C [H
b]fe
ll to
5.8
+/-
2.8
g/d
L vs
. 10.
6 +
/- 1
.8 g
/dL
(p <
0.05
) in
the
cont
rol.
Pol
yHem
e is
saf
e in
acu
te b
lood
loss
, mai
ntai
ns t
otal
[Hb]
in li
eu o
f red
cel
ls d
espi
te t
he m
arke
d fa
ll in
RB
C [H
b],
and
redu
ces
the
use
of a
lloge
neic
blo
od. P
olyH
eme
appe
ars
to b
e a
clin
ical
ly u
sefu
l blo
od s
ubst
itute
.
Gou
ld, S
A.
Moo
re, E
E.
Moo
re, F
A.
1997
110
IITo
ass
ess
the
ther
apeu
tic b
enef
it of
Pol
y S
FH-P
in a
cute
blo
od lo
ssin
39
inju
red
patie
nts.
Pol
y S
FH-P
mai
ntai
ned
tota
l [H
b], d
espi
te t
hem
arke
d fa
ll in
red
cel
l [H
b] d
ue t
o bl
ood
loss
.Th
e ut
ilisat
ion
of O
2 (e
xtra
ctio
n ra
tio) w
as
27 +
/- 1
6% fr
om t
he r
ed c
ells
and
37
+/-
13%
from
the
Pol
y S
FH-P
. Tw
enty
-thr
ee p
atie
nts
(59%
) avo
ided
allo
gene
ic t
rans
fusi
ons
durin
g th
e fir
st 2
4 ho
urs
afte
r bl
ood
loss
.
B1
Hum
an p
olym
eris
ed h
aem
oglo
bin
effe
ctiv
ely
load
s an
dun
load
s O
2an
d m
aint
ains
tot
al h
aem
oglo
bin
in li
eu o
f re
d ce
lls a
fter
acut
e bl
ood
loss
, the
reby
red
ucin
g al
loge
neic
tra
nsfu
sion
s.
Youn
es, R
N.
Aun
, F.
Acc
ioly,
CQ
.19
9254
IITo
com
pare
the
imm
edia
teha
emod
ynam
ic e
ffect
s of
a
bolu
s in
fusi
on o
f 7.5
% N
aCl o
r7.
5% N
aCl p
lus
6% d
extr
an 7
0(b
oth
2400
mO
sm/L
) in
seve
rehy
povo
laem
ia.
Mor
talit
y w
as s
imila
r be
twee
n th
e gr
oups
.H
yper
toni
c so
lutio
ns a
cted
fast
er in
res
torin
gbl
ood
pres
sure
tha
n is
oton
ic s
olut
ions
. Gre
ater
volu
me
was
req
uire
d fo
r is
oton
ic s
olut
ions
to
achi
eve
the
sam
e B
P.
AW
hils
t th
e sa
fety
of h
yper
toni
c so
lutio
ns is
sup
port
edby
thi
s st
udy,
hyp
erto
nic
solu
tions
did
not
pro
ve t
o be
of
any
ben
efit
in r
educ
ing
mor
talit
y.
Knu
dson
, MM
.Le
e, S
.E
ricks
on, V
.20
0311
1
II Ani
mal
Stu
dy
Sm
all-v
olum
e re
susc
itatio
n w
ith H
BO
C-2
01 (B
iopu
re) v
s.la
ctat
ed R
inge
r's
(LR
) sol
utio
n vs
hy
pert
onic
sal
ine
dext
ran
(HS
D)
in h
aem
orrh
agic
sho
ck.
Ther
e w
ere
no s
igni
fican
t di
ffere
nces
inm
easu
red
liver
or
mus
cle
PO
2va
lues
afte
rre
susc
itatio
n w
ith a
ny o
f the
thr
ee s
olut
ions
.
The
card
iac
outp
ut w
as in
crea
sed
from
sh
ock
valu
es in
all
thre
e an
imal
gro
ups
with
resu
scita
tion,
but
was
sig
nific
antly
hig
her
inth
e, a
nim
als
resu
scita
ted
with
HS
D. S
imila
rly,
MA
P w
as in
crea
sed
by a
ll so
lutio
ns d
urin
gre
susc
itatio
n, b
ut r
emai
ned
sign
ifica
ntly
bel
owba
selin
e ex
cept
in t
he g
roup
of a
nim
als
rece
ivin
g H
BO
C-2
01 (p
< 0
.01)
.
N/A
HB
OC
-201
is s
igni
fican
tly m
ore
effe
ctiv
e th
an H
SD
and
LR s
olut
ion
in r
esto
ring
MA
P a
nd s
ysto
lic b
lood
pre
ssur
e to
nor
mal
val
ues
alth
ough
its
abilit
y to
res
tore
tis
sue
oxyg
enat
ion
is n
o di
ffere
nt fr
om c
onve
ntio
nal f
luid
th
erap
ies.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 36
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 37
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
Evidence Table 5. What are the endpoints of fluid resuscitation in the trauma patient?A
utho
rLe
vel o
fS
tud
y
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Bis
hop,
MH
.S
hoem
aker
,W
C.
App
el, P
L.19
9576
III-I
B1
To t
est
pros
pect
ivel
y su
pran
orm
alva
lues
of c
ardi
ac in
dex
(CI),
oxy
gen
deliv
ery
inde
x (D
O2I)
, and
oxy
gen
cons
umpt
ion
inde
x (V
O2I)
as
resu
scita
tion
goal
s to
impr
ove
outc
ome
in s
ever
ely
trau
mat
ised
patie
nts.
Sup
rano
rmal
val
ues
to a
chie
ved
usin
g vo
lum
e lo
adin
g to
PC
WP
18m
mH
g an
d th
en d
obut
amin
ein
fusi
on.
Mor
talit
y in
sup
rano
rmal
val
ues
grou
p 18
% v
s.37
% in
nor
mal
circ
ulat
ory
valu
es (p
<0.
027)
.
Org
an fa
ilure
074
+/-
0.28
vs.
1.6
2 +
/- 0
.28
(p <
0.00
2) in
sup
rano
rmal
and
nor
mal
circ
ulat
ory
grou
ps r
espe
ctiv
ely.
Res
usci
tatio
n to
sup
rano
rmal
circ
ulat
ory
valu
es
decr
ease
d m
orta
lity
and
orga
n fa
ilure
in t
his
stud
y.
Dur
ham
, RM
.N
euna
ber,
K.
Maz
uski
, JE
.19
9611
2
IITo
eva
luat
e th
e ef
ficac
y of
O
xyge
n co
nsum
ptio
n (V
O2I)
an
d de
liver
y (D
O2I)
indi
ces
asen
dpoi
nts
of r
esus
cita
tion
in
58 c
ritic
ally
ill p
atie
nts.
Mor
talit
y w
as n
ot d
iffer
ent
betw
een
the
grou
ps e
ven
with
exc
lusi
on o
f the
gro
up 1
patie
nts
who
faile
d to
mee
t V
O2I/
DO
2I go
als
(p =
0.6
6). O
F oc
curr
ed in
18
of 2
7 (6
7%) i
ngr
oup
1 an
d in
22
of 3
0 (7
3%) i
n gr
oup
2 (p
= 0
.58)
. Len
gth
of v
entil
ator
sup
port
,in
tens
ive
care
uni
t st
ay, a
nd h
ospi
tal s
tay
wer
e no
t di
ffere
nt b
etw
een
grou
ps.
B1
No
diffe
renc
e w
as fo
und
in t
he in
cide
nce
of o
r de
ath
in p
atie
nts
resu
scita
ted
base
d on
oxy
gen
tran
spor
tpa
ram
eter
s co
mpa
red
to c
onve
ntio
nal p
aram
eter
s.
Aut
hors
sug
gest
tha
t ox
ygen
-bas
ed p
aram
eter
s ar
e m
ore
usef
ul a
s pr
edic
tors
of o
utco
me
than
as
endp
oint
s fo
r re
susc
itatio
n.
Dut
ton,
RP.
Mac
kenz
ie, C
F.S
cale
a, T
M.
2002
42
IITo
eva
luat
e th
e ef
ficac
y of
flui
dre
susc
itatio
n tit
rate
d to
a lo
wer
than
nor
mal
SB
P d
urin
g th
e pe
riod
of a
ctiv
e ha
emor
rhag
e on
sur
viva
lin
tra
uma
patie
nts.
Dur
atio
n of
act
ive
haem
orrh
age
(2.9
7 +
/- 1
.75
hour
s vs
. 2.5
7 +
/- 1
.46
hour
s, p
= 0
.20)
was
not
diffe
rent
bet
wee
n gr
oups
.
Mor
talit
y be
twee
n th
e gr
oups
was
the
sam
e.(7
.3%
vs.
7.3
%).
B2
Titr
atio
n of
initi
al fl
uid
ther
apy
to a
low
er t
han
norm
al
SB
P (<
70m
mH
g) d
urin
g ac
tive
haem
orrh
age
did
not
affe
ct m
orta
lity
in t
his
stud
y.
Ivat
ury,
RR
.S
imon
, RJ.
Isla
m, S
.19
9611
3
IIG
loba
l oxy
gen
tran
spor
t in
dice
sve
rsus
org
an-s
peci
fic g
astr
icm
ucos
al p
H in
tra
uma
patie
nts.
Ther
e w
as n
o si
gnifi
cant
diff
eren
ce in
mor
talit
ybe
twee
n th
ose
who
res
usci
tatio
n go
al w
asop
timis
ing
oxyg
en d
eliv
ery
vs o
ptim
isat
ion
of g
astr
ic p
H (7
4.1%
vs
90%
, p =
0.1
6).
B2
Sur
viva
l was
sim
ilar
betw
een
the
two
grou
ps.
:: 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 CL IN ICAL PRACT ICE GU IDEL INESH
YP
OV
OL
AE
MIC
SH
OC
K G
UID
EL
INE
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Flem
ing,
A.
Bis
hop,
M.
Sho
emak
er, W
.A
ppel
, P.
1992
114
III-2
B1
To e
valu
ate
the
early
pos
t in
jury
atta
inm
ent
of s
upra
norm
al v
alue
sof
car
diac
inde
x (>
= 4
.52
L/m
in),
oxyg
en d
eliv
ery
(> =
670
mL/
min
),an
d ox
ygen
con
sum
ptio
n (>
= 1
66 m
L/m
in) o
n ou
tcom
e in
tra
umat
ised
pat
ient
s w
ith
an e
stim
ated
blo
od lo
ss
of 2
000
mL
or m
ore.
Mor
talit
y w
as 2
4% v
s. 4
4% in
pro
toco
l an
d co
ntro
l res
pect
ivel
y.
The
prot
ocol
pat
ient
s ha
d fe
wer
mea
n or
gan
failu
res
per
patie
nt (0
.76
+/-
1.2
1 vs
. 1.5
9 +
/-1.
60),
shor
ter
stay
s in
the
inte
nsiv
e ca
re u
nit
(5 +
/ -3
vs
12 +
/- 1
2), a
nd fe
wer
mea
n da
ysre
quiri
ng v
entil
atio
n (4
+/-
3 v
s 11
+/-
10)
tha
ndi
d th
e co
ntro
l pat
ient
s (P
<.0
5 fo
r ea
ch).
This
non
-ran
dom
ised
stu
dy d
ispl
ayed
att
aini
ng
supr
anor
mal
circ
ulat
ory
valu
es im
prov
es s
urvi
val a
ndde
crea
ses
mor
bidi
ty in
the
sev
erel
y tr
aum
atis
ed p
atie
nt.
Velm
ahos
, GC
.D
emet
riade
s,D
.20
0077
II Trau
ma
To e
valu
ate
the
effe
ct o
f ear
lyop
timis
atio
n in
the
sur
viva
l of
sev
erel
y in
jure
d pa
tient
s.
Ther
e w
as n
o di
ffere
nce
in r
ates
of d
eath
(1
5% o
ptim
al v
s 11
% c
ontr
ol),
orga
n fa
ilure
,se
psis
, or
the
leng
th o
f int
ensi
ve c
are
unit
or h
ospi
tal s
tay
betw
een
the
two
grou
ps.
B2
Sev
erel
y in
jure
d pa
tient
s w
ho c
an a
chie
ve o
ptim
alha
emod
ynam
ic v
alue
s ar
e m
ore
likel
y to
sur
vive
tha
n th
ose
who
can
not,
rega
rdle
ss o
f the
res
usci
tatio
nte
chni
que.
In t
his
stud
y, a
ttem
pts
at e
arly
opt
imis
atio
n di
d no
t im
prov
e th
e ou
tcom
e of
the
exa
min
ed s
ubgr
oup
of s
ever
ely
inju
red
patie
nts.
Sho
emak
er,
WC
. Fl
emin
g, A
W.
1986
79
III-2
Trau
ma
To c
ompa
re o
utco
mes
in t
raum
apa
tient
s w
ho h
ad r
esus
cita
tion
aim
ed a
t im
prov
ing
circ
ulat
ory
valu
es a
nd c
hem
istr
y vs
. tho
seai
med
at
optim
isin
g ‘p
hysi
olog
icpa
tter
ns’.
Cou
ld n
ot d
eter
min
e re
sults
.
Dat
a w
as n
ot p
rese
nted
cle
arly.
B2
–
Bis
hop,
MH
.S
hoem
aker
,W
C.
App
el, P
L.19
9380
III-2
To d
escr
ibe
the
tem
pora
l pat
tern
sof
hae
mod
ynam
ics
and
oxyg
entr
ansp
ort
in s
urvi
vors
and
nons
urvi
vors
of s
ever
e tr
aum
ain
rel
atio
n to
tim
e de
lays
, m
orta
lity,
and
mor
bidi
ty.
Dur
ing
the
first
24
hour
s, t
he m
ean
valu
es
of C
I (4.
52 +
/- 1
.45
vs 3
.8 +
/- 1
.20l
/min
/m2 ;
p<0.
05),
DO
2(6
70 +
/- 2
30 v
s 54
0+/-
200m
l/min
/m2 ;
p<
0.01
) and
VO
2(1
66 +
/-
48 v
s 13
4 +
/- 4
7ml/m
in/m
2 ; p
<0.
01) o
f the
60
sur
vivo
rs w
ere
sign
ifica
ntly
hig
her
than
th
e 30
non
-sur
vivo
rs.
Pat
ient
s w
ho a
chie
ved
surv
ivor
val
ues
in le
ssth
an 2
4 ho
urs
had
a m
orta
lity
of12
% v
s 54
%fo
r th
ose
who
did
not
rea
ch s
urvi
vor
valu
es a
tal
l or
took
long
er t
han
24 h
ours
.
B2
Rea
chin
g su
rviv
or v
alue
s (o
r su
pran
orm
al c
ircul
ator
y va
lues
)w
ithin
24
hour
s of
inju
ry m
ay g
reat
ly im
prov
e su
rviv
al a
sde
mon
stra
ted
in t
his
obse
rvat
iona
l stu
dy.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 38
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 39
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Wax
man
, K.
Ann
as, C
.D
augh
ters
, K.
Tom
inag
a, G
T.19
9411
5
III-2
Dia
gnos
ticte
st
B1
To t
est
the
hypo
thes
is t
hat
chan
gein
tis
sue
PO
2in
res
pons
e to
an
incr
ease
d in
spire
d O
2ch
alle
nge
may
be
rela
ted
to t
he s
tate
of
cellu
lar
oxyg
enat
ion,
and
hen
ceth
e ad
equa
cy o
f res
usci
tatio
n.
(Tis
sue
PO
2is
mea
sure
d th
roug
h a
prob
e in
sert
ed in
the
del
toid
mus
cle)
.
Pat
ient
s w
ere
dete
rmin
ed t
o ha
ve in
adeq
uate
resu
scita
tion
if a
rise
in t
issu
e P
O2
did
not
occu
r w
ith a
n in
crea
se in
insp
ired
oxyg
en.
Nin
e tr
aum
a pa
tient
s di
d no
t ex
hibi
t an
incr
ease
in t
issu
e P
O2.
Flui
d re
susc
itatio
nco
rrec
ted
thes
e fin
ding
s in
5/9
. Fou
r pa
tient
sdi
d no
t re
spon
d af
ter
repe
ated
flui
dad
min
istr
atio
n.
The
usef
ulne
ss o
f thi
s te
st is
not
dem
onst
rate
d co
nclu
sive
lyin
thi
s ar
ticle
. The
re is
insu
ffici
ent
data
sup
plie
d to
det
erm
ine
if th
ere
is a
n ab
solu
te t
issu
e ox
ygen
cut
off.
Fur
ther
wor
k is
need
ed b
efor
e th
is t
ool c
an b
e ro
utin
ely
inco
rpor
ated
incl
inic
al p
ract
ice.
Dav
is, J
W.
Sha
ckfo
rd, S
R.
Mac
kers
ie, R
C.
1988
62
IVTo
eva
luat
e B
ase
Def
icit
(BD
)as
an
inde
x fo
r flu
id r
esus
cita
tion
in t
he in
jure
d pa
tient
s.
A r
etro
spec
tive
revi
ew o
f 209
cha
rts
reve
aled
as B
ase
Def
icit
beca
me
mor
e ne
gativ
e M
AP
decr
ease
d si
gnifi
cant
ly a
nd t
he v
olum
e of
flu
id r
equi
red
for
resu
scita
tion
incr
ease
d w
ithin
crea
sing
sev
erity
of B
D g
roup
. (p
<0.
001)
A
BD
tha
t be
cam
e m
ore
nega
tive
with
resu
scita
tion
was
ass
ocia
ted
with
ong
oing
haem
orrh
age
in 6
5%. (
p <
0.00
2).
Incr
easi
ng B
ase
Def
icit
was
ass
ocia
ted
with
dec
reas
ing
MA
P, a
nd d
ecre
asin
g Tr
aum
a S
core
(p <
0.00
1 fo
r bo
th).
B2
This
stu
dy in
dica
tes
that
bas
e de
ficit
may
be
a re
liabl
ein
dica
tor
of t
he r
elat
ive
mag
nitu
de o
f vol
ume
defic
it.
BD
may
be
a us
eful
gui
de t
o vo
lum
e re
plac
emen
t in
the
res
usci
tatio
n of
tra
uma
patie
nts.
Hus
ain,
FA
.M
artin
, MJ.
Mul
leni
x, P
S.
2003
116
III-2
To d
eter
min
e w
heth
er la
ctat
e le
vels
and
bas
e de
ficits
in c
ritic
ally
ill su
rgic
al in
tens
ive
care
uni
t (S
ICU
)pa
tient
s co
rrel
ate
and
whe
ther
eith
er m
easu
re is
a s
igni
fican
tin
dica
tor
of m
orta
lity
and
mor
bidi
ty.
Initi
al a
nd 2
4-ho
ur la
ctat
e le
vel w
as s
igni
fican
tlyel
evat
ed in
non
surv
ivor
s ve
rsus
sur
vivo
rs(p
= 0
.002
). In
itial
bas
e de
ficit
was
not
sign
ifica
ntly
diff
eren
t; 24
-hou
r ba
se d
efic
it di
d ac
hiev
e st
atis
tical
sig
nific
ance
(p =
0.0
2).
Mor
talit
y if
lact
ate
norm
alis
ed w
ithin
24
hour
sw
as 1
0%, c
ompa
red
with
24%
for
>48
hou
rsan
d 67
% if
lact
ate
faile
d to
nor
mal
ise.
B1
Ele
vate
d in
itial
and
24-
hour
lact
ate
leve
ls a
re s
igni
fican
tlyco
rrel
ated
with
mor
talit
y an
d ap
pear
to
be s
uper
ior
toco
rres
pond
ing
base
def
icit
leve
ls. L
acta
te c
lear
ance
tim
em
ay b
e us
ed t
o pr
edic
t m
orta
lity
and
is a
ssoc
iate
d w
ithou
tcom
e at
dis
char
ge. I
nitia
l bas
e de
ficit
was
a p
oor
pred
icto
r of
mor
talit
y bu
t di
d co
rrel
ate
with
lact
ate
leve
lsin
tra
uma
nons
urvi
vors
.
:: 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 CL IN ICAL PRACT ICE GU IDEL INESH
YP
OV
OL
AE
MIC
SH
OC
K G
UID
EL
INE
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Wei
l, M
H.
Nak
agaw
a, Y
.W
anch
un, T
.S
ato,
Y.
1999
117
III-2
B2
To c
linic
ally
val
idat
e su
blin
gual
PC
O2
for
diag
nosi
ng s
hock
inpa
tient
s w
ith c
ircul
ator
ydi
sarr
ange
men
t.
Sub
lingu
al C
O2
corr
elat
ed s
tron
gly
with
art
eria
lbl
ood
lact
ate
and
mea
n ar
teria
l pre
ssur
e.
Incr
ease
s in
Psl
CO
2co
rrel
ated
with
incr
ease
s in
arte
rial b
lood
lact
ate
(r =
084
, p<
0.00
1). W
hen
Psl
CO
2ex
ceed
ed a
thr
esho
ld 7
0mm
Hg
itspo
sitiv
e pr
edic
tive
valu
e of
circ
ulat
ory
shoc
kw
as 1
.0. W
hen
it w
as <
70m
mH
g its
pre
dict
edsu
rviv
al w
as 0
.93.
The
valid
ity o
f ele
vate
d S
ublin
gual
PC
O2
as a
mar
ker
ofsh
ock
is s
how
n in
thi
s st
udy.
How
ever
abs
olut
e va
lues
of
Psl
CO
2ar
e no
t de
term
ined
. The
re s
till r
emai
ns a
n ov
erla
p of
read
ings
in p
atie
nts
who
did
and
did
not
hav
e cl
inic
al s
hock
.
Larg
er tr
ials
are
war
rant
ed a
s th
is te
chni
que
may
pro
ve to
be
a us
eful
, sim
ple
and
non-
inva
sive
tech
niqu
e fo
r qu
antif
ying
perfu
sion
in tr
aum
a pa
tient
s. T
he s
tudy
nee
ds to
inco
rpor
ate
patie
nts
with
and
with
out c
linic
al s
igns
of s
hock
to d
eter
min
e if
subl
ingu
al C
O2
is a
mor
e ac
cura
te m
arke
r of
sho
ck th
atre
adily
mea
sure
d va
riabl
es s
uch
as H
R, B
P a
nd u
rine
outp
ut.
One
of t
he p
robl
ems
with
det
erm
inin
g th
e cl
inic
al u
tility
of
sub
lingu
al C
O2
is t
hat
ther
e is
no
‘gol
d st
anda
rd’ w
ithw
hich
to
com
pare
.
Kirt
on, O
C.
Win
dsor
, J.
1998
118
III-2
To c
ompa
re g
astr
ic p
H a
nd
oxyg
en v
aria
bles
in s
urvi
vors
and
non-
surv
ivor
s of
tra
uma
in a
ICU
.
Sen
sitiv
ity o
f gas
tric
pH
<7.
32 in
pre
dict
ing
mor
talit
y w
as 8
3% a
nd s
peci
ficity
61%
.In
pre
dict
ing
mul
ti-or
gan
failu
re 8
6%
sens
itivi
ty a
nd s
peci
ficity
66%
.
The
risk
of d
eath
with
a p
Hi <
7.32
4.5
(p<
0.01
) and
ris
k of
MO
F 5.
4 (p
<0.
01).
The
risk
of d
eath
ass
ocia
ted
with
an
abno
rmal
lact
ate
at 2
4 ho
urs
was
3.0
.
The
risk
of M
OF
was
3.6
.
B1
A g
astr
ic p
H<
7.32
and
lact
ate
>2.
3mm
ol a
t 24
hou
rsis
ass
ocia
ted
with
hig
h m
orta
lity
rate
s an
d in
cide
nce
of m
ulti-
orga
n fa
ilure
.
Rou
men
, RM
.Vr
eugd
e, J
P.19
9411
9
IVTo
exa
min
e th
e po
sttr
aum
atic
gast
ric p
H in
15
mul
tiply
inju
red
trau
ma
patie
nts.
No
corr
elat
ion
betw
een
gast
ric p
H a
nd s
hock
,IS
S, l
actic
aci
dosi
s, o
r A
PAC
HE
II s
core
s on
adm
issi
on w
ere
foun
d.
25%
of p
atie
nts
with
a p
Hi <
7.32
die
d.
All
patie
nts
with
nor
mal
pH
i sur
vive
d.
B1
Gas
tric
pH
may
be
usef
ul in
iden
tifyi
ng p
atie
nts
with
spl
anch
ic m
alpe
rfusi
on t
hat
is n
ot id
entif
ied
by r
outin
e m
onito
ring.
HypovolaemicShock_FullRep.qxd 3/2/07 12:36 PM Page 40
Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 41
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
Aut
hor
Leve
l of
Stu
dy
& y
ear
evid
ence
Qua
lity
que
stio
n /
po
pul
atio
nR
esul
tsC
onc
lusi
on
Ivat
ury,
RR
.S
imon
, RJ.
1995
70
IIB
2To
com
pare
gas
tric
muc
osal
pH
and
glob
al o
xyge
n va
riabl
es (D
O2l
/ V
O2l)
as
indi
cato
rs o
f ade
quat
ere
susc
itatio
n in
tra
uma
patie
nts.
Mor
talit
y w
as 9
.1%
for
patie
nts
in n
orm
aliz
atio
nof
gas
tric
pH
(`7.
30) c
ompa
red
to 3
1.3%
(p
= 0
.27)
.
The
cont
rol g
roup
in t
his
stud
y w
as s
icke
r th
an
the
inte
rven
tion
grou
p as
indi
cate
d by
initi
al la
ctat
e (5
.2+
/- 3
.4 v
s 8.
3+/-
5.7)
and
bas
e de
ficit
(7.0
+/-
3.9
vs 1
1.7
+/-
8.3
), al
thou
gh IS
S w
as s
imila
r be
twee
n th
e tw
o gr
oups
(24.
4 vs
24.
3).
Gas
tric
pH
may
be
an im
port
ant
mar
ker
to a
sses
s th
ead
equa
cy o
f res
usci
tatio
n. F
ailu
re t
o no
rmal
ise
ph in
thi
sst
udy
was
ass
ocia
ted
with
hig
h or
gan
failu
re a
nd d
eath
.H
owev
er, t
he a
bilit
y to
man
ipul
ate
pHi t
hrou
gh o
xyge
nin
dice
s an
d in
otro
pes
has
yet
to b
e de
mon
stra
ted.
The
resu
lts d
o no
t re
ach
stat
istic
al s
igni
fican
ce b
ut t
his
may
be d
ue t
o sm
all s
tudy
num
bers
. A la
rger
stu
dy is
war
rant
edto
val
idat
e th
e re
sults
of t
his
stud
y.
Cha
ng, M
C.
Che
atha
m,
ML.
19
9412
0
III-2
To a
sses
s th
e co
rrel
atio
n be
twee
nga
stric
pH
and
oth
er m
arke
rs o
fha
emod
ynam
ic s
tatu
s an
dm
orta
lity
in c
ritic
ally.
Ther
e w
as p
oor
corr
elat
ion
betw
een
gast
ric
pH a
nd g
loba
l mar
kers
of h
aem
odyn
amic
func
tion
and
oxyg
en t
rans
port
var
iabl
es.
PH
tha
t di
d no
t co
rrec
t its
elf w
ithin
24
hour
sw
as a
ssoc
iate
d w
ith a
hig
her
mor
talit
y (5
0% v
s 0%
, p =
0.0
3) a
nd o
rgan
failu
re
(2.6
org
ans
/ pa
tient
vs
0.62
org
ans
/ pa
tient
).
B1
Gas
tric
pH
sup
plem
ents
info
rmat
ion
prov
ided
by
stan
dard
haem
odyn
amic
var
iabl
es a
nd m
aybe
use
ful i
s id
entif
ying
patie
nts
at r
isk
of m
ulti-
orga
n fa
ilure
and
dea
th. T
reat
men
tim
plic
atio
ns a
re n
ot id
entif
ied
by t
his
stud
y.
Hey
wor
th, J
.19
9212
1
IVTo
eva
luat
e th
e us
e of
con
junc
tival
oxyg
en t
ensi
on
mon
itor
(PC
JO2)
durin
g th
e ea
rly a
sses
smen
t of
inju
red
patie
nts.
A P
CJO
2le
ss t
han
45m
mH
g w
as a
ssoc
iate
dw
ith h
ypov
olae
mia
, red
uced
car
diac
out
put
and
ches
t in
jury
.
B1
Th
e us
eful
ness
of P
CJO
2as
a m
onito
ring
tool
for
occu
lthy
pope
rfusi
on is
not
dem
onst
rate
d in
thi
s ar
ticle
.
Wei
l, M
H.
Nak
agaw
a, Y
.19
9911
7
III-2
To in
vest
igat
e th
e pr
edic
tive
valu
e of
sub
lingu
al c
apno
met
ry(P
(SL)
CO
2) as
an
early
indi
cato
r of
sys
tem
ic p
erfu
sion
failu
re in
46
pat
ient
s w
ith a
cute
life
-th
reat
enin
g illn
esse
s or
inju
ry.
P(S
L)O
2>
70m
mH
g ha
d a
posi
tive
pred
ictiv
eva
lue
of 1
.00
for
the
pres
ence
of
clin
ical
sig
nsof
sho
ck.
B2
Sub
lingu
al c
apno
met
ry c
orre
late
s w
ith s
igns
of s
hock
. Th
is s
tudy
doe
s no
t sh
ow t
hat
PS
LCO
2w
ould
add
any
info
rmat
ion
that
is n
ot a
lread
y ro
utin
ely
colle
cted
thr
ough
stan
dard
circ
ulat
ory
mon
itorin
g.
:: 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 Medline1 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
HY
PO
VO
LA
EM
IC S
HO
CK
GU
IDE
LIN
E
blood
O-neg
APPEND IX 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
HY
PO
VO
LA
EM
IC S
HO
CK
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IDE
LIN
E
:: 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 Council2000, How to use the scientific evidence:
assessment and application of scientific
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3 National Health and Medical Research Council1999, How to review the evidence: systematic
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4 National Health and Medical Research Council1998, A guide to the development, implementation
and evaluation of clinical practice guidelines,
Biotext Canberra, editor.
5 Liddle J, Williamson M, Irwig L 1996, Method for
Evaluating Research Guideline Evidence (MERGE),NSW Department of Health.
6 Jordan KS 2000, Fluid resuscitation in acutelyinjured 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
Manual Book 1, First Impression: USA.
8 Lechleuthner A, Lefering R, Bouillon B, Lentke E,Vorweg M 1994, T. T. Prehospital detection ofuncontrolled 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 bloodvolume in critically ill patients, Critical Care
Medicine, 12(2):107-12.
10 Wo CC, Shoemaker WC, Appel PL, Bishop MH,Kram HB, Hardin E 1993, Unreliability of bloodpressure and heart rate to evaluate cardiacoutput in emergency resuscitation and criticalillness, Critical Care Medicine, 21(2):218-23.
11 Demetriades D, Chan LS, Bhasin P, Berne TV,Ramicone E, Huicochea F, et al 1998, Relative bradycardia in patients with traumatichypotension, Journal of Trauma Injury, Infection
and Critical Care, 45(3):534-9.
12 Knottenbelt JD 1991, Low initial hemoglobin levels in trauma patients: an important indicator of ongoing hemorrhage, Journal of Trauma-Injury
Infection & Critical Care, 31(10):1396-9.
13 Rixen D, Raum M, Bouillon B, Lefering R,Neugebauer E 2001, Unfallchirurgie. APotDGf.Base deficit development and its prognosticsignificance in posttraumatic critical illness: an analysis by the trauma registry of the Deutshce Gesellschaft fur unfallchirurgie, Shock 2001;15(2):83-9.
14 Bannon MP, O'Neill CM, Martin M, ilstrup DM, Fish NM, Barrett J 1995, Central venous oxygensaturation, arterial base deficit, and lactateconcentration in trauma patients, American
Surgeon 61(8):738-45.
15 Oman KS 1995, Use of hematocrit changes as an indicator of blood loss in adult traumapatients who receive intravenous fluids,Journal of Emergency Nursing, 21(5):395-400.
16 McMurtry R, Walton D, Dickinson D, Kellam J, Tile M 1980, Pelvic disruption in thepolytraumatized patient: a management protocol. Clinical Orthopaedics & Related
Research (151):22-30, 1980 Sep.
17 Klein SR, Saroyan RM, Baumgartner F, Bongard FS 1992, Management strategy ofvascular injuries associated with pelvic fractures,Journal of Cardiovascular Surgery 33(3):349-57,May-Jun.
18 Looser KG, Crombie HD, Jr 1976, Pelvic fractures: an anatomic guide to severity of injury,Review of 100 cases, American Journal of Surgery
132(5):638-42.
19 Flint L, Babikian G, Anders M, Rodriguez J,Steinberg S 1990, Definitive control of mortalityfrom severe pelvic fracture, Annals of Surgery
211(6):703-6; discussion 706-7, 1990 Jun.
20 Lu W, Kolkman K, Seger M, Sugrue M 2000, An evaluation of trauma team response in a major trauma hospital in 100 patients withpredominantly minor injuries, ANZ Journal
of Surgery, (5):329-32.
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