in the Trauma Patient - Avoiding the Lethal Triad · PDF fileManagement of Hypovolaemic Shock in the Trauma Patient:: NSW ITIM PAGE iii HYPOVOLAEMIC SHOCK GUIDELINE Contents blood

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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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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Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE iii

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Contents

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Algorithm 1 :: The management of hypovolaemic

shock in the trauma patient ......................................1

Summary of guidelines.....................................3

1 Introduction................................................5

2 Methods.....................................................6

3 How do you know when the patient is in hypovolaemic shock? ............8

4 How do you find the sources of 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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Management of Hypovolaemic Shock in the Trauma Patient :: NSW ITIM PAGE 1

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Algorithm 1 :: The management of hypovolaemic shock in the trauma patient

The Management of Hypovolaemic Shock in the Trauma 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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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.


How do you know when the patient is in hypovolaemic shock?


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.


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.


What are the endpoints of fluid resuscitation in the trauma patient?


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.


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)

�

✕


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.


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.



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


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?


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.


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.


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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.



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.


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?


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


ADULT TRAUMA CL IN ICAL PRACT ICE GU IDEL INESH

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Primary Survey completed.

Initial stabilisation of life threatening injuries.

Early transfer to definitive care..

Fluid administration <600mls/hr.


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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:: 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.


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


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.


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


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?


Arterial blood gases and lactate measured

to assess degree of shock.

Urinary catheter inserted to assess urine output.


::





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Evidence Table 1. How do you know when a trauma patient is in hypovolaemic shock?A

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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




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

.



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




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.



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




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.



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




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.



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




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.



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




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.



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.




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.



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




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.



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




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.

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tric

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may

be

usef

ul in

iden

tifyi

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atie

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with

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hat

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entif

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by r

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onito

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ury,

RR

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, RJ.

1995

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com

pare

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tric

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pH

and

glob

al o

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n va

riabl

es (D

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as

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rs o

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ere

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itatio

n in

tra

uma

patie

nts.

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talit

y w

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for

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orm

aliz

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nof

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tric

pH

(`7.

30) c

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to 3

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in t

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o gr

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aybe

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l, M

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vest

igat

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edic

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pat

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s w

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mon

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g.

:: EVIDENCE TABLES


::



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


Search strategy for the identification of studies

HY

PO

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blood

O-neg

APPEND IX A


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


HY

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:: SEARCH TERMS USED FOR THE IDENTIFICATION OF STUDIES


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2 National Health and Medical Research Council2000, How to use the scientific evidence:

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3 National Health and Medical Research Council1999, How to review the evidence: systematic

identification and review of the scientific literature.

Biotext Canberra, editor.

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

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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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IC S

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blood

O-neg


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22 Australian Resuscitation Council 2003, Principles for controlling bleeding for first aiders; Guideline 8.1.

23 Shoemaker WC, Peitzman AB, Bellamy RF,Bellomo R, Bruttig SP, Capone A, et al 1996,Resuscitation from severe hemorrhage,

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of Trauma-Injury Infection & Critical Care,

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27 Sloan EP, Callahan E, Duda J, Sheaff C, Robin A1989, The effect of urban trauma system hospitalbypass on prehospital times and level 1 traumapatient survival, Annals of Emergency Medicine,

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29 Scalea TM 1998, Massive transfusion and

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30 Dantzker D 1989, Oxygen Delivery and utilisationin sepsis, Critical Care Clinics, 5:81-98.

31 Stern SA 2001, Low-volume fluid resuscitationfor presumed hemorrhagic shock: helpful orharmful? Current Opinion in Critical Care,

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32 Bickell WM 1993, Are victims of injury sometimesvictimised by attempts at fluid resuscitation?Annals of Emergency Medicine 1993;22:225-6.

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34 Burris D, Rhee P, Kaufman C, al e 1999,Controlled resuscitation for uncontrolledhemorrhagic shock, Journal of Trauma –

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33:349-53.

36 Capone AC, Safar P, Stezoski W, al e 1995,Improved outcome with fluid restriction intreatment of uncontrolled haemorrhagic shock,Journal of the American College of Surgeons,

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37 Stern SA, Dronen SC, Birrer P, al e 1993, The effect of blood pressure on haemorrhagevolume and survival in a near-fatal haemorrhagemodel incorporating a vascular injury, Annals of

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and control of hemorrhage in the trauma patient.



YP

OV

OL

AE

MIC

SH

OC

K G

UID

EL

INE


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75 Shoemaker WC 1996, Temporal physiologicpatterns of shock and circulatory dysfunctionbased on early descriptions by invasive andnoninvasive monitoring, New Horizons,

4(2):300-18.

76 Bishop MH, Shoemaker WC, Appel PL et al 1995,Prospective, randomized trial of survivor values of cardiac index, oxygen delivery, and oxygenconsumption as resuscitation endpoints in severe trauma, Journal of Trauma-Injury Infection

& Critical Care, 38(5):780-7.

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232(3):409-18.

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1986;15(12):1437-44.

80 Bishop MH, Shoemaker WC, Appel PL, Wo CJ, Zwick C, Kram HB, et al 1993,Relationship between supranormal circulatoryvalues, time delays and outcome in severelytraumatized patients, Critical Care Medicine

1993;21(1):56-63.

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