Resuscitation in the management of trauma

JICS Volume 10, Number 2, April 2009 109

Review articles The Intensive Care Society 2009

IntroductionTrauma is the leading killer of young people in the UnitedKingdom (UK).1 Death is commonly caused by hypovolaemicshock secondary to haemorrhage, shock being defined ascirculatory failure leading to inadequate perfusion andoxygenation of tissues. This may ultimately cause irreversibleorgan failure and death. The primary objective of trauma careis to minimise or reverse shock, thus saving life. The AmericanCollege of Surgeons Committee on Trauma teaches thatincreasing the circulating volume and blood pressure willimprove and maintain organ perfusion, thereby improvingpatient outcome and survival.2 This review outlines the animaland human data to support the strategy of hypotensiveresuscitation. Three subgroups of trauma will be considered penetrating trauma, blunt trauma and head injury.

Fluid resuscitationMost of the perceived benefits of fluid resuscitation wereestablished by animal experimentation using controlledhaemorrhage (CH) animal models in the 1950s and 1960s. TheWiggers preparation involved the insertion of an intravenous(IV) catheter from which the animal was bled and maintainedat a predetermined level of blood pressure (hypotension) forvarying periods before resuscitation was initiated.3 A markedextracellular fluid (ECF) deficit was observed, which couldonly be corrected with isotonic crystalloid 2-3 times thevolume of the estimated blood loss, hence the traditional fluid-replacement regimen of 3:1, crystalloid: blood.

Recommending aggressive volume replacement based onthese animal model experiments is problematic. Firstly, theWiggers model does not accurately reproduce thepathophysiology of the acutely exsanguinating trauma patient.The maintenance of blood pressure (BP) is controlled by theinvestigator rather than being a reflection of the animalsphysiological response to haemorrhage. Furthermore, the

animals are bled slowly from the catheter, which can be turnedoff instantaneously; again, this is not representative of themodern trauma patient who usually dies from rapidexsanguination or central nervous system (CNS) injury, notfrom protracted hypotension. Secondly, there is a lack ofrandomised controlled trials (RCTs) investigating aggressivevolume replacement in trauma patients with ongoinguncontrolled haemorrhage.

In an attempt to improve the physiological modelling oftrauma patients, models of haemorrhage from uncontrolledvascular injury were developed in the 1980s. The resultinghaemorrhage volume and duration were dependent on theanimals physiological response to haemorrhage, ie thrombusformation and vasoconstriction. The experiments with these models highlighted the fact that fluid resuscitation was harmful.4-6 Several mechanisms of harm werehypothesised, for example that increased blood pressure andcirculating volume resulting from fluid resuscitation, causedclot disruption, dilution of clotting factors from crystalloidadministration, and/or the reversal of the bodys naturalresponse to haemorrhage, ie vasoconstriction, which divertsblood from the peripheries and maintains perfusion of vital organs.

Solid-organ injury models of uncontrolled haemorrhage(UCH) were developed to simulate blunt trauma. In these,aggressive resuscitation with isotonic crystalloid increasedblood loss and increased blood pressure abruptly beforereducing it to less than or equal to the blood pressure of controlanimals and, most importantly, did not reduce mortality.7-9

Difficulties with trauma researchTrauma patients are a heterogeneous group. In the USA, deathsoccur commonly from both penetrating and blunt trauma,whereas in the UK deaths result primarily from blunt traumaand head injury. It is therefore difficult to devise a singleresuscitation strategy that is optimal for all healthcare

The role of hypotensive resuscitation inthe management of traumaK Jackson, J Nolan

The primary objective of trauma care is to minimise or reverse shock thus saving life. Aggressive fluid resuscitation may

be harmful in these patients because the resulting increased blood pressure and circulating volume may cause clot

disruption, dilution of clotting factors and/or the reversal of the bodys natural response to haemorrhage. The concept of

hypotensive resuscitation has evolved where small aliquots of fluid are infused, with hypovolaemia and hypotension

tolerated as a necessary evil until definitive haemorrhage control can be achieved. This review outlines the animal and

human data to support the strategy of hypotensive resuscitation.

Keywords: hypotensive resuscitation; shock, haemorrhagic; shock, traumatic; head injuries; fluid therapy

Volume 10, Number 2, April 2009 JICS110

Review articles

situations. The ultimate goal of trauma therapy is definitivehaemorrhage control followed by normalisation of tissueperfusion, as rapidly as possible. The severity of haemorrhagedetermines the extent that hypoperfusion will be tolerated.Thus the concept of hypotensive resuscitation has evolved,where small aliquots of fluid are infused, with hypovolaemiaand hypotension tolerated as a necessary evil until definitivehaemorrhage control can be achieved. In 2004, the Joint RoyalColleges Ambulance Liaison Committee (JRCALC) guidelinesindicated that IV infusions should be commenced en route tohospital and fluid given (eg 500 mL of IV crystalloid) justsufficient to maintain a systolic BP of 80-90 mm Hg.10

Definition of hypotensive resuscitation The concept of hypotensive resuscitation in the literature isclear; however, how much of which fluid to which endpoint(MAP or other) should be given is not defined precisely.

Walter B Cannon is credited with the first proposal ofdeliberate hypotension (controlled hypotension) as amechanism to reduce internal haemorrhage duringuncontrolled haemorrhage before control of bleeding vessels isachieved.11

There are two possible strategies in trauma:1. Delayed resuscitation, where the hypotensive period is

deliberately prolonged by withholding fluid therapy untiloperative intervention achieves definitive haemostasis, or

2. Permissive hypotension, where fluid is given but theendpoint for resuscitation is lower than normotension(normotension is defined as a MAP of 80 mm Hg or higher).In practical terms, these two approaches may be combined

and adjusted to meet the needs of the individual patient, sothat the differences between them are not clearly defined. In areview of emergency procedures performed by UK paramedics,23% of resuscitation protocols were based on hypotensiveresuscitation principles.12

Effect of hypotensive resuscitation on survivalrates

Animal evidence

Mapstones well conducted systematic review13 of nine RCTs inswine and rat models of uncontrolled haemorrhage produced apooled risk ratio of 0.37 (95% CI 0.27-0.52) for hypotensiveresuscitation, concluding that hypotensive resuscitationreduces the risk of death in vascular injury models of UCH.

There are no direct comparison studies in animal blunttrauma models. However, aggressive fluid resuscitation afterblunt trauma has been shown to increase bleeding anddecrease survival.7, 14

Two randomised laboratory trials demonstrated thathypotensive resuscitation improves outcome in uncontrolledhaemorrhagic shock (simulating penetrating trauma andextremity injury) with head injury.15,16 However, a third studyevaluating uncontrolled haemorrhage (blunt injury) with headinjury failed to demonstrate any benefit of delayedresuscitation.17

Evidence from human studies

Penetrating trauma

There are no RCTs directly comparing hypotensive versusnormotensive resuscitation. A Cochrane systematic reviewperformed by Kwan and colleagues18 in 2003 assessed theeffects of early versus delayed fluids, and large- versus small-volume fluid therapy in trauma patients (penetrating andblunt) with bleeding. Three papers reported increasedmortality when comparing early versus late fluid therapy.

The landmark study by Bickell and colleagues is the largestto date, which compared immediate fluid resuscitation withdelayed fluid resuscitation.19 This single centre, prospectiverandomised controlled trial was carried out in Houstonbetween 1989 and 1992. Five hundred and ninety eight adulttrauma patients with penetrating torso injury presenting with asystolic blood pressure (SBP) 90 mm Hg were randomlyassigned (by day of the month) to two study groups. Animmediate fluid resuscitation group (even numbered days) (IRgroup; n=238), received standard fluid therapy until theyreached theatre. The delayed resuscitation group (oddnumbered days) (DR group; n=289), were cannulated butreceived no intravenous fluids until they reached the operatingroom (OR). On average, patients in the IR group received870 mL fluid before reaching the hospital and 1,608 mL in theemergency department (ED) versus 92 and 283 mL in the DRgroup. On arrival at the ED, SBP was significantly higher in theIR group, 7946 versus 7243 mm Hg (DR), p=0.02, but thiseffect was not sustained by the time of arrival in the OR.

Of the 598 patients, 70 died before they reached the OR and528 underwent operative intervention: 268 (IR) and 260 (DR).The overall survival rate in the DR group was significantlyhigher, 203/289 (70%) versus 193/309 (62%), p=0.04, whichdid not alter after adjustment for the pre-hospital and trauma-centre intervals. The explanation for this may be inferred fromthe trend toward increased intraoperative blood loss in the IRgroup (p=0.11) and increased intraoperative fluid infusionrates to maintain a SBP of 100 mm Hg. Furthermore, a trendtowards more complications (ARDS, sepsis, ARF, coagulopathy,wound infection, pneumonia) was noted in the IR group (30%versus 23%), with an associated longer total hospital length ofstay, but not ICU length of stay.

The results do not justify the recommendation to withholdany infusion until bleeding is controlled; information about thecause and timing of patient deaths is unavailable, and 70patients died before reaching the OR. Common sense dictatesthat patients with a MAP of


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its increased mortality risk. The fact that 22 patients in the DRgroup did receive some fluid infers that they were treated witha hypotensive strategy and had a better outcome, rather thanhaving fluids withheld completely.

Blunt injury

Turner randomised paramedics into two groups, who gaveeither immediate fluids (IR) or no prehospital fluids (DR).20

Patients, all over 16 years old, were recruited (699 IR and 610DR). No significant differences in mortality or complicationswere found between the groups. However, protocol compliancewas poor: only 30.9% of the IR group received prehospital fluidand only 79.8% of the DR group had fluids withheld, makingthe number of patients in each group receiving fluids verysimilar.

A retrospective matched pairs case-controlled study wasundertaken, using records of blunt trauma patients with on-scene SBP 500 mL pre-hospital fluids were matched by Injury Severity Score (ISS) andSBP on scene with those who did not receive any pre-hospitalfluids. There were 75 patients in each group. Those whoreceived fluids were more likely to have an increased SBP uponarrival at the ED, but there was no significant difference insurvival to discharge or length of hospital stay.

Head injury

There are no human studies investigating the effect on survivalof hypotensive resuscitation in trauma patients with concurrenthead injury.

Conclusion

Animal studies demonstrate the superiority of hypotensiveresuscitation compared to aggressive fluid resuscitation aimingto restore normotension. Human studies are very limited, withno RCTs directly comparing hypotensive strategies to normo-tensive resuscitation. Although Bickells RCT demonstratedbetter survival with delayed resuscitation, it has limitations inapplication to patients other than those who are young withpenetrating trauma. Aggressive fluid infusion appears to beharmful, resulting in the pop-the-clot scenario and cyclicalhyper-resuscitation. But it is unclear whether intravenous fluidshould be withheld completely until haemostasis is achieved(delayed regimen), or whether low volumes should be infusedto hypotensive endpoints. Further RCTs are needed to confirmimproved survival and to investigate blunt trauma and headinjury resuscitation strategies.

Effect of hypotensive resuscitation on blood loss

There is copious animal data to support the view thathypotensive resuscitation strategies reduce blood loss and

consequently reduce transfusion requirements for allsubgroups of trauma in animal studies.


Penetrating trauma

In the Houston study, the IR group had significantly lowerhaemoglobin levels on arrival at the trauma centre(11.2 g/dL2.6 versus 12.9 g/dL2.2; p


Review articles

deficit (BD) has been shown to be a reliable measure of: the degree and duration of hypoperfusion the oxygen debt changes in oxygen delivery (DO2) in haemorrhagic shock.

Reversal of BD may be considered a reliable marker ofadequacy of resuscitation.22-24 Others also feel that lactate andbase excess are the best indicators of metabolic function inhaemorrhagic shock and trauma.25

Evidence from animal studies

Penetrating trauma

Worse metabolic derangements were observed in the shortterm and longer term follow-up demonstrated evidence ofischaemic organ damage. Moderate under-resuscitation, aiming for a MAP of 60 mm Hg, seems to be a compromisebetween increasing haemorrhage volumes and maintainingtissue perfusion in animal models simulating penetratingtrauma.15,26-30

Blunt trauma and head injuryThere is no evidence31,32 to suggest that hypotensiveresuscitation has detrimental effects in blunt trauma, but thereare few data.

The fact that the two randomised controlled animal studiesexamining this subject both selected higher target MAPs fortheir hypotensive strategy demonstrates the apprehensionabout applying it to those with head injuries. However, thesestudies have not demonstrated any detrimental effect of ahypotensive strategy. If anything, they call into question thetraditional strategy of aggressive fluid resuscitation in closedhead injury.


The Bickell study19 found no significant difference in pH andvenous bicarbonate on arrival in the trauma room or OR.There was, however, a trend towards more complications in theIR group (p=0.08).

A prospective study in hypotensive, blunt-trauma patientssuggested that metabolic acidosis and coagulopathy werereduced by the rapid infusion of reduced resuscitation volumesearly in the post-shock period.33

ConclusionAnimal studies suggest that prolonged hypotension makes themetabolic state worse during the hypotensive period, but thatit is recoverable. Follow-up has not been long enough to knowwhat this would mean in the long term, although there is someevidence of ischaemic damage to organs. The limited humandata did not reproduce these findings of metabolic disturbancesor later organ failure.

Irreversible organ failure

Evidence from animal studies

Hypotensive resuscitation can be applied for two hours in dogsresuscitated with 30% of haemorrhaged blood, with complete

cessation of bleeding and full resuscitation at two hours beforeorgan damage ensues.34 The duration of tolerating hypotensiveresuscitation is species- and trauma-injury dependent.34,35


The only data relevant to this question come from the Bickellstudy, in which the average time from injury to commencingfluid resuscitation was 79 minutes. However, during this time,the SBP of patients in the delayed resuscitation group increasedfrom an average of 59 mm Hg at the scene to 113 mm Hg onarrival in the OR. Therefore, they were not hypotensive for theentire 79 minutes.

What are resuscitation end points?


Dutton compared a target SBP of 70 mm Hg with that of>100 mm Hg. However, the observed mean SBP in each groupwas 100 mm Hg and 114 mm Hg respectively. He failed todemonstrate a mortality difference between the two groups,36

but that may well reflect the inaccuracies of measurement ofSBP in comparison with MAP and a global tendency toovershoot the target blood pressures as patients homeostaticmechanisms act to correct hypotension.

Bickell did not target blood pressures at all with hisprotocol. However, the observed SBPs on arrival at the traumacentre were 7946 mm Hg (IR) and 7243 mm Hg (DR)p=0.02. On arrival in the OR, there was no significantdifference between the two groups in SBP (112 versus113 mm Hg) or diastolic blood pressure (57 versus60 mm Hg).

Recent guidelines are based on expert opinion,pathophysiological rationale and the results of observationalcohort studies in humans and controlled studies in animals.They aim to limit the volume of fluid given and maintain theSBP as low as is considered safe in the specific situation.Titration of aliquots of fluid from 25 mL to 500 mL has beensuggested. This contrasts markedly with traditional fluidresuscitation (give 2 L of crystalloid and aim fornormotension) or delayed resuscitation (no fluid given untilsurgery). The Israeli military commence hypotensiveresuscitation when one of the following three conditions isdocumented: 37

Altered sensorium Radial pulse cannot be palpated Systolic blood pressure less than 80 mm Hg.

Repeated aliquots of 250 mL are infused with continuousmonitoring, aiming for restoration of consciousness, a radialpulse and SBP of 80 mm Hg.

The Brain Trauma Foundation, the American Association ofNeurological Surgeons, and the Joint Section on Neurotraumaand Critical Care all recommend that in CNS injuries withhaemorrhagic shock, fluid is infused with the aim of achieving

How long can the strategy be applied before irreversibleorgan failure ensues?

1. Penetrating trauma 80-90 mm Hg, or presence of radialpulse.

2. Blunt trauma 80-90 mm Hg, or presence of radial pulse.3. Head injury 100 mm Hg.


Review articles

a SBP of 100 mm Hg.38 The JRCALC guidelines state thatintravenous infusions should only be commenced en route tohospital and only sufficient fluid (500 mL of crystalloid) begiven to maintain a systolic blood pressure of 80-90 mm Hg,and effects on the circulatory system be assessed before furtherfluids are administered.10

Conclusion

There are no randomised controlled trials in humans thatevaluate the blood pressure (mean arterial or systolic) thatshould be targeted during hypotensive resuscitation.Guidelines suggesting titrating small volumes of crystalloids toa SBP target of between 80-90 mm Hg, or 100 mm Hg if headinjury is suspected, are based on indirect evidence thataggressive fluid infusion is detrimental.38

DiscussionThe way in which animal models relate to human traumaticinjuries is unclear. Animal models fail to reproduce thecomplexity of multiple injuries, the contradictory treatmentgoals, and the pre-existing co-morbidities which commonlyoccur in the trauma population. Mortality outcomes assessedwithin the first three days may be comparable to early humantrauma deaths but certainly not to the late deaths caused bysepsis and multi-organ failure.

The Bickell paper is the only RCT which enables tentativeconclusions to be drawn and suggests there is some harmassociated with pre-hospital fluid infusion. Hypotensiveresuscitation reduces blood loss and transfusion requirements.Animal studies show consistently that excessive crystalloidsincrease the circulating volume and SBP, and increase or restartbleeding. The evidence supporting hypotensive resuscitation inblunt trauma and head injury is extremely limited and thiswarrants further investigation.

Detrimental effects and the length of time that thestrategy can be applied

As with most treatments in medicine, there are alwaysassociated unwanted effects. Hypotensive resuscitation mayimprove short-term survival but there has been insufficientlength of follow-up to determine the longer-term effects oforgan ischaemia and the potential for permanent organ failureand perhaps late deaths. Anecdotally, we commonly see non-trauma patients on the intensive care unit who arehypovolaemic and hypotensive and are in pre-renal failure.They seem to be able to tolerate several hours of hypovolaemiaand hypotension before renal failure becomes established.Perhaps trauma patients will similarly be able to tolerateseveral hours of organ hypoperfusion without long-termconsequences.

Endpoints of hypotensive resuscitation

Successful resuscitation from haemorrhagic shock andelimination of the oxygen debt is impossible withouthaemostasis. There is no clear endpoint to resuscitation ofuncontrolled haemorrhage, but clinical signs and laboratoryresults can indicate that tissue hypoperfusion and ischaemiaare not severe enough to cause permanent organ failure.

The measured SBP is determined by cardiac output,

peripheral vascular resistance and the measurement techniqueused oscillometry or auscultation or, the gold standard,invasively. The associated inaccuracy and variability make it aless than ideal target endpoint during hypotensiveresuscitation. A substitute endpoint is the presence of a radialpulse, which is equivalent to a SBP of no less than 80 mm Hg.Although the accuracy of this is debatable, there appears to bereasonable clinical agreement between the extent ofhaemorrhagic shock and the presence of a peripheral pulse.Thus, it has been suggested that the combination of alteredmental state, or unconsciousness, combined with cool, clammyskin and an absent radial pulse is a triad that confirmshypovolaemic shock.39

Bishop and colleagues performed a prospective, randomisedtrial of survivor values of cardiac index, oxygen delivery andoxygen consumption as resuscitation endpoints.40 All wereadult patients with an estimated blood loss 2,000 mL or apelvic fracture and/or two or more major long bone fractureswith >4 units of blood given within six hours of admission.They targeted cardiac index (CI) 4.5 L/min/m2, oxygendelivery index (DO2I) 670 mL/min/m2, and oxygenconsumption index 166 mL/min/m2 within 24 hours ofadmission. The 50 patients treated according to the protocoldemonstrated lower mortality compared with the control group(18% versus 37%). They suggest that the increased CI, DO2Iand oxygen consumption found in survivors of severe traumaare primary physiological compensations, therefore their use astargets may reduce shock-related organ failures and perhapsmortality. Currently, it would be impractical to use these on theintensive care unit, let alone at the roadside. But as technologyadvances perhaps a device will be developed enabling moreadvanced prehospital monitoring of trauma patients.

The ideal endpoint for resuscitation would be reliable, easyto use (in the field), non-invasive, safe and cheap. Furtherwell-controlled trials are needed, but they will always sufferfrom lack of blinding, bias and protocol violations. Even whenthe optimal endpoints are determined, the question of how toachieve them still needs to be answered. For hypotensiveresuscitation before haemorrhage is controlled, it may not beenough to use simple blood pressure targets but instead toadjust them individually based on the information available atthe time. An end-point is not a realistic goal whilehaemorrhage continues; thus, the objective is rapid transfer toa trauma facility capable of stopping the bleeding.

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Kathryn Jackson Specialist Registrar Anaesthetics, UniversityHospital Bristol

[email protected]

Jerry Nolan Consultant Anaesthetics and Intensive CareMedicine, Royal United Hospital, Bath

Work performed while Dr Jackson was an Advanced Trainee in

Intensive Care Medicine at Royal United Hospital, Bath. Part of a

dissertation for the UK Diploma of Intensive Care Medicine

Resuscitation in the management of trauma

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