MATTER FOR DEBATE

Fluid Resuscitation in Pre-Hospital Trauma Care: a Consensus View

I. GREAVES, K.M. PORTER and M.P. REVELL
 

Introduction

Cannulation

Choice of fluid for resuscitation

 

Quantity of fluid used in resuscitation

Summary

References

J.R.Coll.Surg.Edinb., 47, April 2002, 451-457

List of participants: Brian Steggles, Keith Porter, Philip Munrow, Andrew Thurgood, Tim Hodgetts, Ian Greaves, Lee Turner, Ian Robertson-Steel, Mark Gough, John McDonald, Keith Allison, Tim Coates, Mark Turner, Janette Turner, Matthew Revell, Professor Ann-Marie Kelly (Professor of Emergency Medicine in Melbourne).

Groups represented: Faculty of Pre-hospital Care & Faculty of Accident & Emergency Medicine, Royal College of Surgeons of Edinburgh, The United Kingdom Military Defence Forces, Ambulance Service Association with Paramedics representatives, British Association for Immediate Care (BASICS), London Helicopter Emergency Medical Service (HEMS) and Researchers with an interest in Pre-hospital Care

Fluid administration for trauma in the pre-hospital environment is a challenging and controversial area. The available evidence does not clearly support any single approach. Nevertheless, some provisional conclusions may be drawn. It was with this intention that the Faculty of Pre-Hospital Care (RCSEd) arranged to meet in August 2000 in an attempt to reach a working consensus. The following guidelines are the result of those discussions. It is intended that they will be modified as future research brings clarity to the area. When treating trauma victims in the pre-hospital arena cannulation should take place en route, where possible. Only two attempts at cannulation should be made. Transfer should not be delayed by attempts to obtain intravenous access. Entrapped patients require cannulation at the scene. Normal saline may be titrated in boluses of 250 ml against the presence or absence of a radial pulse (caveats; penetrating torso injury, head injury, infants).

Keywords: fluid resuscitation, trauma care, clinical practice

INTRODUCTION

Evidence-based medicine describes clinical practice in which patient care and therapeutic decisions are supported by information gained from a careful consideration of the available worldwide research literature. Ideally, unequivocal clinical conclusions should be drawn based on the results of carefully conducted studies. Unfortunately, even at the beginning of the twenty-first century, in many areas this evidence is patchy or contradictory. Furthermore, a number of the most fundamental questions confronting present day clinicians may never be answered by suitably conducted studies. Initial evidence might suggest, for example, that a particular treatment offers a small survival advantage compared with another, but the number of recruits required to ensure a meaningful trial may render it impractical in terms of logistics and cost. In addition, an increasingly complex ethical framework makes it likely that many definitive clinical studies would not gain ethical approval.

In the meantime, practitioners in all disciplines have to try to base their clinical decisions on whatever sound evidence is available. Most clinicians also find it helpful to discuss experiences and ideas. Although such exchanges tend to be anecdotal, they often fill the gaps in our present scientific knowledge, allowing decisions to be made regarding patient care on the basis of shared experience, where firm evidence is inconclusive or absent.

It is with the aim of reconciling clinical experience and current evidence in the pre-hospital trauma setting that the following article has been prepared. Evidence from the scientific literature is cited where possible. The remainder is a consensus reached by experienced trauma personnel from a variety of backgrounds (Pre-hospital Fluid Resuscitation in Trauma: a consensus meeting. Faculty of Pre-hospital Care, University Hospital Birmingham, August 2000). The concept of value being added to raw data through the input of acknowledged authorities is a well-established process in evidence-based medicine.1

These guidelines provide one simple strategy applied to the use of fluids for trauma patients in the pre-hospital setting. Three main areas have been addressed -cannulation, the choice of fluid and the quantity of fluid given. It is intended that these issues should continue to be debated and, where ideas and concepts are put forward, it is expected that they will evolve or change as experience and evidence accumulate.

CANNULATION

Issues

Early venous access in trauma patients has traditionally been regarded as of great importance.2,3  It allows administration of fluids, where necessary, or other drugs such as anaesthetic, analgesic and resuscitation agents.4 Placement of a venous line is likely to be technically easier in the early stages of shock than when hypovolaemia has progressed and compensatory mechanisms have resulted in peripheral vasoconstriction. As a consequence, paramedics have been encouraged to use such skills in trauma.

While early successful cannulation will save time when the patient arrives in hospital, it is also clear that repeated unsuccessful attempts or access with a cannula of insufficient gauge will hinder progress at the same stage.5

Recently, interventions made by paramedics before the patient arrives in hospital have come under close scrutiny. In a retrospective study, Demetriades et al (1996) found that outcome was worse in a group of 4856 patients brought to hospital by paramedics than in 926 patients brought in by bystanders, relatives and the police.6 Assuming the results are truly representative, it is has been suggested that poor outcomes relate to detrimental effects of pre-hospital advanced life support (ALS) measures. There is other evidence suggesting ALS methods improve survival, but the aggressive use of fluid, in particular, has been called into question.7

Independent of the use of intravenous fluids, however, transfer time to hospital appears to be an important predictor of out-come.8 Improvements may be possible here. Cannulating ambulance crews appear to spend a longer time on scene and this extra time does appear to be related to the interventions they perform.9-11 If the administration of fluid pre-hospital is open to question, then this apparent delay in transfer in order to obtain circulatory access should also come under scrutiny.

One way to balance the benefits to be gained by obtaining pre-hospital venous access, with the risk of lengthening transfer times, is to attempt cannulation en route.12 This approach has both training and Health and Safety implications, but has received strong support.13,14

The management of entrapped patients is a special situation.15 Here again, the focus should be on keeping the time to arrival in hospital as short as possible. The coordinated roles of all the emergency services are critical in keeping delays to a minimum.16 It is likely that efforts to cannulate in these situations will not extend the time of transfer. In addition, there are usually compelling reasons for obtaining a venous line on scene; principally, the need for analgesia but on occasion, for infusion of specific drugs for resuscitation and fluids.

Consensus View

Cannulation at an early stage is desirable. However, in most situations, priority should be given to transfer of the patient to a centre where definitive care can be provided. The on scene time should not be prolonged by attempts to gain a line. Intravenous access during transit has been employed success-fully and should be considered where appropriate expertise and training are available. A limit of two attempts en route is reasonable.

In cases of entrapment, circulatory access should be gained on scene. This reflects the unique demands of this area of pre-hospital medicine.

CHOICE OF FLUID FOR RESUSCITATION

Issues

This area continues to be one in which, despite an increasing body of evidence, no consensus regarding choice of fluid has been reached. Broadly, the choice of options includes:

• no fluid

• crystalloids (isotonic and hypertonic)

• colloids (mainly gelatins and starch solutions)

• oxygen carrying solutions (blood and blood substitutes)

The decision is a complex one and includes consideration of the factors listed in table 1

early haemodynamic effects
effects on haemostasis
oxygen carriage 
distribution and capillary endothelial leak
modulation of inflammatory response
safety
pH buffering
method of elimination

practicality and cost

Table 1: Factors influencing choice of fluids

Early haemodynamic effects: The aim of administering fluids is to restore end-organ perfusion and, therefore, oxygen delivery. An increase in circulating volume will have a tendency to increase cardiac output and blood pressure. The rapidity with which a given fluid will produce its effect will largely be determined by its volume of distribution within the body and how quickly it equilibrates. A sudden increase in blood flow may not be beneficial because it has the potential to precipitate rebleeding from sites where physiological mechanisms have brought about cessation of haemorrhage.

Haemostasis: In general, administration of fluid has a detrimental effect on haemostasis and a tendency to increase bleeding.17,18 To begin with, primary haemostatic thrombus may be dislodged from a vessel causing rebleeding, as outlined above. Most fluids will cause vasodilatation, at least as a result of reversing hypovolaemia, with similar risks. With the obvious exception of fresh frozen plasma, most will also reduce blood viscosity and dilute clotting factors to the detriment of haemostatic mechanisms.

Direct interference with the clotting cascades is seen with some starches.19 Finally, hypothermia-induced coagulopathy should be avoided, if possible, and the fluids should be warmed prior to infusion.20, 21

pH buffering: Acidosis results from anaerobic metabolism of energy substrate, producing lactic acid, phosphoric acids and unoxidised amino acids. This can have negative ino-tropic effects and predispose to arrhythmias. Manipulating pH per se, with the use of bicarbonate, for example, is not presently advised since it impairs oxygen delivery to the tissues by its effect on the dissociation of oxygen from haemoglobin. Some protein-based fluids, such as albumin and fresh frozen plasma, have pH buffering properties, which may be beneficial.22

Oxygen carriage: High flow oxygen is administered routinely to trauma patients. The main thrust of fluid administration is directed towards reversing hypovolaemia. In the early stages, the relative anaemia caused by blood loss is compensated for by the decrease in blood viscosity, which allows improved peripheral oxygen delivery. Anaemia associated with haemorrhage is considered to be secondary in importance to hypovolaemia in the accumulation of oxygen debt. To date, no artificial oxygen carrying solutions have reached widespread use.

Modulation of the inflammatory response and capillary leak: Critically ill patients exhibit increased capillary permeability which can allow molecules such as albumin and water to pass into the interstitium exacerbating oedema and impeding oxygen transfer.23,24 Molecular size is a major determinant of whether a fluid will remain primarily in the intravascular space or be distributed more widely within the extracellular space. Both low molecular weight synthetic colloids and exogenous albumin solutions leave the circulation to a variable degree.25,26 Conversely, high molecular weight colloids, which remain in the intravascular space, exert an oncotic effect which can result in cellular dehydration. Accordingly, these should be administered with adequate amounts of water.27 Evidence suggests that high molecular weight starches may have a secondary direct down-regulatory action on capillary leak via an action on endothelial surface molecules.28

Safety: The fluid of choice must be one that can be administered safely in all patient groups. Some starches and haemoglobin solutions have detrimental effects on renal function. Anaphylaxis has been seen with blood products in particular, but also with gelatins. The introduction of viral and prion infections is a risk associated with blood and its derivatives. The possible consequences on a cross-match sample in the later stages of treatment have also been raised with the use of dextran; new dextran preparations are believed not to give rise to these problems.29

Practicality and cost: The ideal resuscitation fluid should be cheap, with a long shelf life. It should be easy to store and to warm when required. In the rarest of circumstances, pre-hospital administration of blood is almost never achievable.

Consensus View

Modern perfluourocarbons and haemoglobin-b oxygen carriers are currently still largely experimental.30,31 Blood (together with human albumin solution and fresh frozen plasma) is costly and difficult to store, having a relatively short shelf life. In addition, issues regarding compatibility and disease transmission make blood and its derivatives unlikely candidates as a permanent solution in the pre-hospital situation.

The debate as to the superiority of crystalloid or colloid continues, several decades after it began.32,33 Many recent publications advocating specific solutions, emphasize the heterogeneity within both categories of resuscitation fluids.34,35 Resuscitation fluids should be evaluated on an individual basis and not in terms of generic groupings.

Isotonic crystalloid solutions are cheap, easy to store and warm and have an established safety record when they are used appropriately. They produce a relatively predictable rise in cardiac output and are generally distributed evenly throughout the extracellular space. They do not draw water out of the intravascular space. The use of Ringers solution as the fluid of choice in burns has been documented.36 It offers some buffering capacity but carries a possible risk of iatrogenically increasing lactic acidosis, when given in large doses or to patients with liver failure. 37 Saline in large quantities may produce a hyperchloraemic acidosis.38 The case for hypertonic solutions in head injury has not yet been conclusively established in a randomised controlled trial. A meta-analysis by Wade et al (1997) strongly suggests a survival advantage and such a trial is urgently required.39

At present, isotonic saline is recommended as the first line fluid in the resuscitation of a hypovolaemic trauma patient.

QUANTITY OF FLUID USED IN RESUSCITATION

Issues

The dilemma that faces medical personnel confronted with a hypovolaemic, trauma patient is essentially the balance between:

• administering fluid and, thereby, risking delay in transfer, rebleeding and increased blood loss, and

• withholding fluid and, thereby, allowing the possibility of organ ischaemia and death from hypovolaemia, prior to arrival   in hospital

This quandary is not new. Cannon et al (1918) based on experience in the First World War, considered administration of fluids before the surgical control of bleeding to be dangerous.40 The same outlook governed thinking on fluid replacement in the Second World War. 41

There is evidence that in penetrating torso trauma, aggressive use of intravenous fluids is detrimental to outcome.42 In a randomised controlled trial, patients received either no fluid pre-hospital or immediate fluid resuscitation. Reduced mortality and complications were seen if fluid resuscitation was delayed until surgery. Although methodological criticisms have been raised about the study, it remains extremely influential because it is a rare prospective, randomised study in this area.43 There are also animal studies that raise similar doubts about the effectiveness or safety of early fluid replacement. 44,45

The majority of trauma seen in the United Kingdom is blunt trauma. Unfortunately, there is little available data from human studies regarding whether blunt trauma differs significantly from penetrating trauma in its behaviour. In a retrospective case-matched review of severe trauma victims, 217 patients who had on-site fluid replacement fared worse, in terms of mortality, than controls receiving no fluid. 46 Increased pre-hospital times and fluid administration were identified as risk factors, requiring further investigation.

Enthusiasm for aggressive fluid resuscitation during the second half of the twentieth century probably had its roots in early animal haemorrhage experiments conducted by Wiggers and other workers in the 1950’s and 1960’s. 47 In the classic model used, blood was taken out through a catheter until a set pressure was reached, after which withdrawal ceased. Administration of fluid following this improved outcome. Traverso et al (1986) employed a similar porcine model, but this time a fixed volume was removed. 48,49 The problem with both studies is that haemorrhage had ceased prior to resuscitation and would not recommence due to its controlled nature. In the trauma patient, there are no such guarantees.

More recently, animal experiments have attempted to replicate the possibility of uncontrolled haemorrhage more closely. There are two main groups of experiments; external haemorrhage models (e.g. rat tail amputation) and internal haemorrhage models, where a controlled injury to a great vessel or major abdominal artery produces hypovolaemia. Overall, the external haemorrhage models suggest that bleeding and mortality will increase if fluid is administered prior to haemostasis.45, 50-52 Some authors, however, found improved survival in resuscitated rats, though Sindlinger et al (1993) noted increased blood loss. 53 Soucy et al (1995) identified anaesthetic agents as an important confounding factor and there are many methodological arguments, which make extrapolation to human trauma difficult. 54,55  Internal haemorrhage experiments on rats and pigs appear to provide clearer evidence that aggressive fluid administration reduces survival.17, 56-58

Many of the ways in which fluid may worsen bleeding have been outlined already. Bickell et al (1991) discuss these mechanisms in some detail. 17 They suggest that a major danger in penetrating large vessel injury is that the improvement in haemodynamics, brought about by administration of fluid, will cause primary extraluminal thrombus to be dislodged. Using a porcine aortotomy model, they confirmed that aggressive replacement of blood loss with three times the volume of crystalloid increased haemorrhage and decreased survival.

Attention, therefore, has become focused on resuscitation strategies. Stern et al (1995) bled pigs rapidly through a fem-oral catheter then produced an aortotomy using a steel wire. Animals haemorrhaged down to a pulse pressure of 5 torr. They were then resuscitated to a systolic pressure of 40, 60 or 80 torr. The most bleeding and the highest mortality were seen in the 80 torr group. The 60 torr group were less acidotic than the 40 torr group. Riddez et al (1998) performed a standardised aortotomy in dogs. 59 There were four resuscitation groups; no fluid, 1:1 volume ratio Ringers, 2:1 Ringers and 3:1 Ringers replacement. Aortic blood flow increased with the amount of fluid used. Blood loss also increased. The highest mortality was seen in the no fluid and the 3:1 groups. The authors felt that the deaths in the less aggressive fluid replacement groups were due to shock and those in the more vigorously resuscitated dogs were due to re-bleeding. Similar findings in rats were noted by other groups.52,60 These findings appear to suggest that the best strategy is not to withhold fluid altogether, but that a moderate replacement policy is likely to be most successful.

Permissive hypotension describes the approach in which the blood pressure is allowed to remain below the normal levels seen in health, with the aim of maintaining vital organ perfusion without exacerbating haemorrhage. A review of hypotensive resuscitation is provided by Hyde et al (1998). 61

If hypotensive resuscitation is the best paradigm, the problem will be translating its use practically into the field. One prescription will not be suitable for all trauma victims. It is also vital that in the pre-hospital phase of patient care, strategies are straightforward, reflecting the difficulties of treating trauma victims on scene and in transit, without detailed diagnostic information. One method to minimise the risk of excessive fluid administration is to give small boluses of fluid at a time. The number of these could even be limited unless authorisation was sought by means of a call to a control centre. Boluses of 250ml are easy to administer from 500ml or 1 litre bags.

Protocols can be based around easily available physiological measures. The presence or absence of a radial pulse gives an approximate guide to whether the blood pressure is above or below 80-90 mmHg. Brachial pulse corresponds to about 70-80 mmHg and a central (femoral or carotid) to 60-70 mmHg. 62 Deakin (2000, 2001) has recently criticised these figures. 63-65 It is known that a degree of hypotension in trauma can be tolerated and that this tolerance is linked to physiological compensation mechanisms, especially to haemostasis. Differing limits on the degree of hypotension that should be permitted can be found. 66,67 However, it is likely that subgroups tolerate hypotension differently. The head-injured patient may require a higher pressure in order to maintain cerebral perfusion and reduce secondary brain injury. 68 Patients with penetrating torso trauma probably require lower pressures. The elderly are known to tolerate hypotension badly. However, no evidence has been found, so far, that that these patients should receive qualitatively different treatment from the population at large.

Consensus View

Fluid should not be administered to trauma victims prior to haemorrhage control if a radial pulse can be felt. Judicious aliquots of 250 mls should be titrated for other patients. If the radial pulse returns, fluid resuscitation can be suspended for the present and the situation monitored. In penetrating torso trauma the presence of a central pulse should be considered adequate. In children less than 1 year old, the use of a brachial pulse is more practical as it is easier to feel.

SUMMARY

Fluid administration for trauma in the pre-hospital environment is a challenging and controversial area. There is, as yet no equivocal answer or view, which can be supported by clear, well-documented and reliable evidence. Nevertheless, a careful evaluation of what evidence is available does allow some provisional conclusions to be drawn. We believe that the following represent the best possible current expert consensus on pre-hospital fluids in trauma. As future evidence brings clarity to this area, these guidelines can be modified, and further consensus statements will be issued taking into account such information.

When treating trauma victims in the pre-hospital setting:

• Cannulation should take place en route, where possible

• Only two attempts at cannulation should be made

• Transfer should not be delayed by attempts to obtain intravenous access

• Entrapped patients require cannulation at the scene

• Normal saline is recommended as a suitable fluid for administration to trauma patients

• Boluses of 250 ml fluid may be titrated against the presence or absence of a radial pulse (caveats; penetrating torso injury, head injury, infants)

REFERENCES

1. American College of Physicians, BMJ Publishing. Purpose and Procedure. Evidence-based Medicine 1998;3(1):34-35
2. American College of Surgeons Committee on Trauma, editor. American College of Surgeons Committee on Trauma: ATLS - Advanced Trauma Life Support for Doctors; 1997
3. Pons PT, Moore EE, Cusick JM, Brunko M, Antuna B, Owens L. Pre-hospital venous access in an urban paramedic system-a prospective on-scene analysis. Journal of Trauma-Injury Infection & Critical Care 1988;28(10):1460-3
4. Mahoney P, Haji-Michael PJ. Therapeutics. In: Greaves I, Porter KM, editors. Pre-Hospital Medicine: Arnold; 1999.p.167-177
5. Wears RL, Winton CN. Load and go versus stay and play: analysis of pre-hospital fluids therapy by computer simulation.Ann Emerg Med 1990;19(2):163
6. Demetriades D, Chan L, Cornwell E, Belzberg H, Berne TV, Asensio J, et al. Paramedic vs. private transportation of trauma patients. Effect on outcome. Archives of Surgery 1996;131(2):133-8
7. Jacobs LM, Sinclair A, Beiser A, D’Agostino RB. Pre-hospital advanced life support: benefits in trauma. Journal of Trauma-Injury Infection & Critical Care 1984;24(1):8-13
8. Pepe PE, Wyatt CH, Bickell WH, Bailey ML, Mattox KL. The relationship between total pre-hospital time and out-come in hypotensive victims of penetrating injuries. Annals of Emergency Medicine 1987;16(3):293-7
9. Powar M, Nguyen-Van-Tam J, Pearson J, Dove A. Hidden impact of paramedic interventions. Journal of Accident & Emergency Medicine 1996;13(6):383-5
10. Nicholl J, Hughes S, Dixon S, Turner J, Yates D. The costs and benefits of paramedic skills in pre-hospital trauma care. Health Technology Assessment (South Hampton, NY) 1998;2(17):i-iv, 1-72
11. Johnson GS, Guly HR. The effect of pre-hospital administration of intravenous nalbuphine on on-scene times. Journal of Accident & Emergency Medicine 1995;12(1):20-2 tee. Guidelines for Cannulation
12. Joint Royal Colleges Ambulance Service Liaison Commit
13. O’Gorman M, Trabulsy P, Pilcher DB. Zero-time pre-hospital i.v. Journal of Trauma-Injury Infection & Critical Care 1989;29(1):84-6
14. Slovis CM, Herr EW, Londorf D, et al. Success rates for initiation of intravenous therapy en-route by pre-hospital care providers. Am J Emerg Med 1990;8:305-7
15. Scott J. Immobilisation and extrication. In: Greaves I, Porter KM, editors. Pre-Hospital Medicine: Arnold; 1999. p. 634-5
16. Wilmink AB, Samra GS, Watson LM, Wilson AW. Vehicle entrapment rescue and pre-hospital trauma care. Injury 1996;27(1):21-5
17. Bickell WH, Bruttig SP, Millnamow GA, O’Benar J, Wade CE. The detrimental effects of intravenous crystalloid after aortotomy in swine. Surgery 1991;110(3):529-36
18. Dries DJ. Hypotensive resuscitation. Shock 1996;6(5):311-6
19. Franz A, Braunlich P, Gamsjager T, Felfernig M, Gustorff B, Kozek-Langenecker SA. The effects of hydroxyethyl starches of varying molecular weights on platelet function. Anaesthesia & Analgesia 2001;92(6):1402-7
20. Ferrara A, MacArthur JD, Wright HK, Modlin IM, McMillen MA. Hypothermia and acidosis worsen coagulopathy in the patient requiring massive transfusion. Am J Surg 1990;160(5):515-8
21. Watts DD, Trask A, Soeken K, Perdue P, Dols S, Kaufmann C. Hypothermic coagulopathy in trauma: effect of varying levels of hypothermia on enzyme speed, platelet function, and fibrinolytic activity. Journal of Trauma-Injury Infection & Critical Care 1998;44(5):846-54
22. Traverso LW, Medina F, Bolin RB. The buffering capacity of crystalloid and colloid resuscitation solutions. Resuscitation 1985;12(4):265-70
23. Zakria B, Bascom J. Mechanisms of Multiple Organ Failure. In: Zakria B, Oz M, Carlson R, editors. Reperfusion Injuries and Clinical Capillary Leak Syndrome. New York: Futura; 1994. p. 443-492
24. Traylor R, Pearl R. Crystalloid vs. colloid. Anaesthesia & Analgesia 1996;83:443-492
25. Sutcliffe A. Crystalloids and colloids for volume replacement. Trauma 1999;1(2):115-123
26. Watts J, Gosling P, Makin A, Plenderleith L, McAnulty G, Grounds R, et al. Fluid resuscitation with colloid or crystalloid solutions. BMJ 1998;317:277
27. Gosling P. Albumin: Friend or Foe? Trauma 2000;2(2):125-134
28. Boldt J, Heesen M, Padberg W, Martin K, Hempelmann G. The influence of volume therapy and pentoxifylline infusion on circulating adhesion molecules in trauma patients. Anaesthesia 1996;51:529-35
29. Ljunstrom K. Colloid Safety: fact and fiction. Ballieres Clinical Anaesthesiology 1997;11:163-177
30. Cohn SM. Is Blood Obsolete? J Trauma 1997;42:730-2
31. Conhaim RL, Harms BA. Hemoglobin therapeutics in hemorrhagic shock. Current Opinion in Critical Care 1998;4:442-6
32. Schierhout G, Roberts I. Fluid resuscitation with colloid or crystalloid solutions in critically ill patients: a systematic review of randomised trials. BMJ 1998;316(7136):961-4
33. Alderson P, Schierhout G, Roberts I, Bunn F. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database of Systematic Reviews [computer file] 2000(2):CD000567
34. Bunn F, Alderson P, Hawkins V. Colloid solutions for fluid resuscitation. Cochrane Database of Systematic Reviews [computer file] 2000(2):CD001319
35. Choi PT, Yip G, Quinonez LG, Cook DJ. Crystalloids vs. colloids in fluid resuscitation: a systematic review. Critical Care Medicine 1999;27(1):200-10
36. Shirani KZ, Vaughan GM, Mason AD, Jr., Pruitt BA, Jr. Update on current therapeutic approaches in burns. Shock 1996;5(1):4-16
37. Veech RL. Immediate versus delayed fluid resuscitation in patients with trauma. New England Journal of Medicine 1995;332(10):681-2; discussion 682-3
38. Williams EL, Hildebrand KL, McCormick SA, Bedel MJ. The effect of intravenous lactated Ringer’s solution versus 0.9% sodium chloride solution on serum osmolality in human volunteers. Anaesthesia & Analgesia 1999;88(5):999-1003
39. Wade CE, Grady JJ, Kramer GC, Younes RN, Gehlsen K, Holcroft JW. Individual patient cohort analysis of the efficacy of hypertonic saline/dextran in patients with traumatic brain injury and hypotension. Journal of Trauma-Injury Infection & Critical Care 1997;42(5 Suppl):S61-5
40. Cannon W, Fraser J, Cowell E. The Preventative Treatment of Wound Shock. JAMA 1918:618-621
41. Office of the Surgeon General. Surgery in World War II, General Surgery: US Government Printing Office; 1952
42. Bickell WH, Wall MJ, Jr., Pepe PE, Martin RR, Ginger VF, Allen MK, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries [see comments]. New England Journal of Medicine 1994;331(17):1105-9
43. Various authors. Correspondence. Immediate versus delayed nal of Medicine 1995;332(10):681-3fluid resuscitation in patients with trauma. New England Jour
44. Chudnofsky CR, Dronen SC, Syverud SA, Hedges JR, Zink BJ. Early versus late fluid resuscitation: lack of effect in porcine hemorrhagic shock. Annals of Emergency Medicine 1989;18(2):122-6
45. Krausz MM, Landau EH, Klin B, Gross D. Hypertonic saline treatment of uncontrolled hemorrhagic shock at different periods from bleeding. Archives of Surgery 1992;127(1):93-6
46. Sampalis JS, Tamim H, Denis R, Boukas S, Ruest SA, Nikolis A, et al. Ineffectiveness of on-site intravenous lines: is pre-hospital time the culprit? Journal of Trauma-Injury Infection & Critical Care 1997;43(4):608-15; discussion 615-7
47. Wiggers CJ. Experimental Haemorrhage Shock. In: Physiology of Shock: The Commonwealth Fund, New York;1950. p. 121-143
48. Traverso LW, Lee WP, Langford MJ. Fluid resuscitation after an otherwise fatal haemorrhage: I. Crystalloid solutions. Journal of Trauma-Injury Infection & Critical Care 1986;26(2):168-75
49. Traverso LW, Hollenbach SJ, Bolin RB, Langford MJ, DeGuzman LR. Fluid resuscitation after an otherwise fatal haemorrhage: II. Colloid solutions. Journal of Trauma-Injury Infection & Critical Care 1986;26(2):176-82
50. Krausz MM, Bar-Ziv M, Rabinovici R, Gross D. “Scoop and run” or stabilize hemorrhagic shock with normal saline or small-volume hypertonic saline? Journal of Trauma-Injury Infection & Critical Care 1992;33(1):6-10
51. Rabinovici R, Krausz MM, Feuerstein G. Control of bleeding is essential for a successful treatment of hemorrhagic shock with 7.5 per cent sodium chloride solution. Surgery, Gynecology & Obstetrics 1991;173(2):98-106
52. Capone A, Safar P, Stezoski SW, Peitzman A, Tisherman S. Uncontrolled hemorrhagic shock outcome model in rats. Resuscitation 1995;29(2):143-52
53. Sindlinger JF, Soucy DM, Greene SP, Barber AE, Illner H, Shires GT. The effects of isotonic saline volume resuscitation in uncontrolled haemorrhage. Surgery, Gynaecology & Obstetrics 1993;177(6):545-50
54. Soucy DM, Sindlinger JF, Greene SP, Barber A, Illner H, Shires GT. Effects of anaesthesia on a model of uncontrolled haemorrhage in rats. Critical Care Medicine 1995;23(9):1528-32
55. Soucy DM, Sindlinger JF, Greene SP, Barber AE, Illner HP, Shires GT. Isotonic saline resuscitation in uncontrolled haemorrhage under various anesthetic conditions. Ann Surg 1995;222(1):87-93
56. Bickell WH, Bruttig SP, Millnamow GA, O’Benar J, Wade CE. Use of hypertonic saline/dextran versus lactated Ringer’s solution as a resuscitation fluid after uncontrolled aortic haemorrhage in anaesthetised swine. Annals of Emergency Medicine 1992;21(9):1077-85
57. Craig RL, Poole GV. Resuscitation in uncontrolled haemorrhage. American Surgeon 1994;60(1):59-62
58. Stern SA, Dronen SC, Wang X. Multiple resuscitation regimens in a near-fatal porcine aortic injury haemorrhage model [see comments]. Academic Emergency Medicine 1995;2(2):89-97
59. Riddez L, Johnson L, Hahn RG. Central and regional hemodynamics during crystalloid fluid therapy after uncontrolled intra-abdominal bleeding. Journal of Trauma-Injury Infection & Critical Care 1998;44(3):433-9
60. Kim SH, Stezoski SW, Safar P, Capone A, Tisherman S. Hypothermia and minimal fluid resuscitation increase survival after uncontrolled hemorrhagic shock in rats. Journal of Trauma-Injury Infection & Critical Care 1997;42(2):213-22
61. Hyde JAJ, Rooney SJ, Graham TR. Hypotensive Resuscitation. Trauma 1998:177-185
62. Anonymous. Shock. In: Greaves I, Porter KM, Ryan JM, editors. Trauma Care Manual: Arnold; 2000. p. 71-86
63. Deakin CD, Low JL. Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: observational study. BMJ 2000;321(7262):673-4
64. Russell IS. Accuracy of ATLS guidelines for predicting systolic blood pressure: Authors’ core assertion was wrong. BMJ 2001;322:552
65. Deakin CD. Accuracy of ATLS guidelines for predicting systolic blood pressure: Authors’ reply. BMJ 2001;322:552
66. Stern SA, Dronen SC, Birrer P, Wang X. Effect of Blood Pressure On Haemorrhage Volume and Survival In Near-Fatal Haemorrhage Model Incorporating A Vascular Injury. Ann Emerg Med 1993;22:155-163
67. Bock BF, Berk WA, Bonner SC, Wilson RF. Pre-Hospital Medical Care of the Injured Patient. In: Wilson RF, Walt AJ, editors. Management of Trauma: Pitfalls and Practice. 2 ed: Williams and Wilkins; 1996. p. 8-9
68. Miller JD, Becker DP. Secondary Insults to the Injured Brain. J R Coll Surg Edinb 1982;27:292-298

Copyright date: 18 March 2002

Correspondence: Mr Keith Porter, Consultant in Trauma and Orthopaedics, Selly Oak Hospital, Raddleburn Road, Birmingham, B29 6JD, UK Tel: +44 (121) 627 8751 E-mail: kp999uk@aol.com