Lets have a think about fluids in trauma.
Wildly different guidelines exist out there on the topic and we thought it might be wise to have a look back through some of the literature specifically on the fluid management in Haemorrhagic Shock (HS). We are talking about purely HS so these findings won’t fit all the other conditions we can have together with HS (e.g. Head Trauma and haemorrhage/ Spinal shock and Heamorrhage).
Now, in a perfect world, a patient presenting to the ED would have a clear picture of haemorrhagic shock without any other complicating factors but we know that in real life things are a little more tricky…..but lets say u=you’ve made it to that conclusion!
In your sick trauma patient in suspected haemorrhagic shock;
What are your priorities?
Will you give crystalloids aiming for a normal MAP, are you giving RBC/FFP/Platelets and your target MAP is definitely lower than a normal one?
Will you tailor your treatment to individual patients or will you follow a standard approach?
Let’s have a look to the literature and to help inform our approach to these critical patients
I reckon it is pivotal to start with the founding father of the major trauma management: ATLS, this breaks down the EBL in four distinct categories: the more the patient bleeds, the worse his/her physiology will be.
The classifications show a stepwise progression in physiology the greater the volume of blood lost. The treatment recommended by ATLS is 1-2 litres if i.v. warmed crystalloid based on the physiological response to the infusion in classes 1-2, class 3 should get crystalloids and blood and class 4 blood alone.
Recently, there have been some doubts about the accuracy of these shock classes and thanks to the Military research and experience in the battlefield, we already know that too many crystalloids do more harm than good to this category of patients.
Military benchmark: (2,3,4)
The military population is very different from the civilian one: young and fit adults who suffer from blast or blunt injuries (mainly IED or GSW). The leading but often treatable cause of death is caused by HS secondary to the devastating effects of their wounds. Due to their exposure, the military developed a deep knowledge and a broad experience in the treatment of major haemorrhages.
In the meantime, the concept of Damage Control Resuscitation (DCR) was born and while rapidly controlling the source of the bleeding was a focal point, they realised RBC/FFP and Platelets were the fluids of choice while crystalloids had to be limited during resuscitation.
DCR is a new concept but even in the WWI some surgeons highlighted that a limitation of fluids was beneficial unless the source of the bleeding had been already controlled by a trauma surgeon.
But DCR , which is composed by permissive hypotension+ early haemostatic resuscitation plus Damage control surgery, and subsequent restoration of organ perfusion & oxygen delivery with definitive resuscitation.
NB We have to be more cautious with Damage Control Resuscitation principles (DCR) when our patient has got a head injury. In that case, we have to be less strict and allow a MAP >90 or a SBP > 110 just to avoid any other secondary brain injury caused by hypotension.
Furthermore, also if our patient has got a suspected spinal cord injury we need to maintain a higher SBP/MAP to avoid any further spinal cord ischaemia. (10-11)
So how should we approach the early resuscitation in DCR with regards to fluids?
Civilian literature: (5,6,7,8,9)
Here it comes the pivotal article by Dutton (Haemostatic Resuscitation). In this article, the author breaks down and explains what happens to the human physiology when a major insult strikes and the pathophysiology of haemorrhagic shock is explained and discussed:
Fluid administration means increased venous return to the heart-> increased cardiac output-> reduces the reflex vasoconstriction of HS-> more bleeding allowed.
Increased output means increased blood pressure-> wash away of clots already formed + haemodiluition which leads to decreased blood viscosity and dilution of clotting factors/platelets and RBCs.
So, this is primarily an article about the pathophysiology of HS but I strongly suggest to have a look at it!
In the review by Harris, Rhys Thomas and Brohi (Early fluid resuscitation in severe trauma) other evidence is collated and the authors state “DCR approach has seen a fall in the volume of crystalloid delivered in the ED and an associated fall in mortality”.
In the retrospective analysis by Duke (Jan 2007 to May 2011) at a Level I Trauma Centre in the US, the authors suggest that a restricted fluid resuscitation (RFR) in combination with DCR conveys a survival benefit in patients with severe haemorrhage. 307 patients were included, all patients with penetrating torso injuries and Systolic BP <= 90mm Hg. They analysed 2 groups where the patients were either classifies as Standard fluid resuscitation (SFR 43% of total patients) where more than 150mL of crystalloids were given prior to DCR, or as Restricted fluid resuscitation (RFR 57% of total patients) where less than 150 mL were given before DCR. They found RFR held a statistically significant reduced mortality compared with SFR. The demographics and clinical characteristics were similar in both groups.
In a 2-year retrospective review by Duchesne, the authors compared patients treated in the post-DCR institution with patients treated in the conventional way pre-DRC at the same centre, a historical cohort. They included 1866 patients with both blunt and penetrating injuries. Again they found a significant mortality reduction in those undergoing DCR
Similar results can be seen in the retrospective study by Ley where data collected from a Level I Trauma Centre between January 2000 and December 2008 were analysed. They demonstrated the more crystalloids administered to trauma victims the higher the associated mortality, this was not proof of causation but certainly one of association.
Last but not least in August 2015 NICE released the new guidelines “Major Trauma: assessment and initial management”(draft).
The key points relating to this part of the story;
So it’s fair to say that the literature base isn’t perfect, there’s no big multi centre RCT that will be generalisable to your patients showing crystalloids to have an adverse effect on morbidity and mortality. But there is a good scientific basis for why they may be harmful, there is softer evidence to align with this and NICE’s new draft guideline on Major Trauma certainly helps to unify the anti-crystalloid approach to haemorrhagic shock.
And what do we do if we find ourselves stuck without the blood products available? Well Harris, Thomas and Brohi suggested very small boluses (250mL) in the absence of central pulses (as per prehospital management) until blood products can be obtained is probably the most pragmatic approach.
And most importantly gain definitive control of that bleeding!
(2) WB Cannon, J. Fraser, Cowell EM. The preventive treatment of wound shock. JAMA.1918; 70:618-621
(3) R. Dawes, G.O.R.Thomas. Battlefield reuscitation. Curr. Op. Crit. Care 200915:527-535
(4) BA Cotton, JS Guys, Morris JA et al. The cellular, metabolic and systemic consequences of aggressive fluid resuscitation strategies. Shock 2006;26:115-121.
(5) R.P. Dutton. Haemostatic Resuscitation. BJA 2012;10(1):39-46
(6) T.Harris, GO Rhys Thomas, K.Brohi. Early fluid resuscitation in severe trauma. BMJ 2012;e345
(7) MD Duke, C. Guidry, J Guice, L Stuke et al. Restrictive Fluid Resuscitation in combination with damage control resuscitation: Time for adaptation. J Trauma Acute Care Surg 2012,73;(3)674-678.
(8) J.C. Duchense, J.M. Barbeau, T.M. Islam et al. Damage control resuscitation: from Emergency Department to the Operating Room. The American Surgeon 2011;77(2):201-206.
(9) EJ Ley, MA Clond, MK Srour et al. Emergency Department Crystalloid Resuscitation of 1.5 L or more is associated with Increased mortality in elderly and non elderly trauma patients. J Trauma 2011;70:398-400.
(10) European Trauma Course- The Team Approach Ed 3.1
(11) D.M. Stein, V. Roddy, J.Marx. Emergency Neurological Life Support: Traumatic Spine Injury. Neurocrit Care (2012);17:S102-S111