Fluid Resuscitation in Trauma

Couple of articles worth reading.

The first paper is an evidence based review of fluid management of traumatic hemorrhagic shock. Take home points:

1.    How little we really know, how bad the science is, and that some conventional dogma is incorrect.

2.    In the bleeding patient, lost time is lost blood. Minimise delays (pre-hospital and in-hospital) prior to definitive control of hemorrhage. A common statement is that the best pre-hospital fluid is a bolus of diesel to the engine of the ambulance (ie get moving).

3.    Fluid choice doesn’t seem to have any significant impact on morbidity or mortality.

a.    No advantage to colloid. The best study here is SAFE, which concludes that crystalloids and colloids should be considered equivalent. There may be a minor logistic advantage to colloid in remote or military environments (when someone has to carry the IV fluids on their back).

b.    No clear advantage to either Saline or Hartmanns. Theoretical considerations favor Hartmanns, and some studies suggest that Hartmanns may be better (these studies are poor quality however).

c.    No advantage to hypertonic saline. Theoretically you would expect hypertonic saline to be of greatest benefit in head injuries (due to its ability to reduce ICP). However the best study addressing this (from Melbourne) failed to find a benefit.

4.    Trend towards using less fluid and less “resuscitation” than previously.

a.    Theoretical concerns of large volumes of IV fluid include increased bleeding due to hydrostatic disruption of hemostasis (“popping the clot”), dilution of hemoglobin (reduced oxygen transport), dilution of clotting factors and platelets (more bleeding), hypothermia (more bleeding) and tissue edema (including lung injury, pulmonary edema, and intra-abdominal compartment syndrome).

b.    The most famous study here is 1994 US study by Bickell et al. This showed significantly higher mortality in patients who got aggressive prehospital fluids. Note the setting of this study – inner-urban USA (= short prehospital times), and lots of penetrating trauma (ie big holes in big vessels). Care therefore needs to be taken extrapolating this data to all trauma patients.

c.    However minimizing fluids has become accepted practice. Our thinking now is that a patient does not immediately require fluid resuscitation if he has normal mentation (and therefore presumably normal tissue perfusion).

5.    Above all else, significant head injuries require normal BP. A single episode of hypotension doubles the mortality in head injury. In the setting of traumatic brain injury, the need to give fluids to maintain BP outweighs concerns about increased bleeding from a co-existing splenic injury.

6.    There is a trend to using more and earlier FFP and platelets in trauma resuscitation. There is a lot of evidence favoring this approach, although the studies are not perfect (mostly US military from Iraq and Afghanistan. However the believers are firm believers, and we are increasingly using FFP and platelets pre-emptively rather than waiting until clotting times become abnormal. Hospital based massive transfusion protocols recommending agreed fixed ratios of red cells:FP:platelets have been shown to be helpful in achieving this goal of early and more FFP and platelets.

7.    Tranexamic acid is definitely in following CRASH-2.


The second paper by Brohi is interesting in view of the current trend towards minimum volume fluid resuscitation. This paper is hard going unless you have a particular interest in coagulation! However the conclusion is that hypotension has been shown to induce activation of Protein C, and hence lead to anticoagulation! This happens very quickly (hence “acute”), and is frequently present by the time the patient has arrived in Emergency. This process has been termed “Acute Coagulopathy of Trauma”. This ACT appears to be more important than other traditional explanations for coagulopathy in trauma (eg dilutional, hypothermia). It seems strange that we would have a mechanism to initiate endogenous anti-coagulation when in a state of hemorrhagic shock. If there is an evolutionary rationale for this, it presumably lies in avoiding widespread sludging, thrombosis and ischemia when in a low perfusion state.

So we seem to be saying that excessive fluids can increase bleeding, and that insufficient fluids and uncorrected shock can induce a coagulopathy which will presumably increase bleeding. A delicate balance, especially in the early management of a seriously injured patient with lots of unknowns. What is this patients normal BP? Where is he bleeding? Does he have a significant brain injury, or is he just intoxicated?

Bottom line: Trauma is a complex entity, and we don’t know it all. Treatment decisions (including resuscitation strategy) need to be individualized taking into account the patient’s particular circumstances and competing priorities.

You can download the articles below for further reading.

Paper 1: Fluid Management in Traumatic Hemorrhagic Shock

Paper 2: Acute Coagulopathy of  Trauma (ACT)

Happy reading,

Steve Walker

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