FLUID MANAGEMENT IN TRAUMA PATIENTS
What made me interested in the topic is this extract from Fragile Lives by Prof Stephan Westaby
"Research from Washington, DC, even showed that patients with penetrating chest wounds had better survival rates when brought to hospital by private car rather than by paramedics who spent time putting up drips and pushing in cold fluid ... What I didn't want was aggressive fluid infusion to replace the blood loss. Clear fluid simply raises the blood pressure, promotes bleeding and impairs the blood's ability to clot, risking catastrophic haemorrhage."
TRAUMA AND SHOCK
Is defined as a life threatening condition during which there is inadequate delivery of oxygen to vital organs in relation to their metabolic requirements. Major trauma almost always results in prolonged disability or death. Trauma can be caused by blunt and penetrating wounds, including falls, motor vehicle collisions, stabbing wounds, and gunshot wounds.
Trauma is accompanied by severe blood loss: haemorrhage. The lost blood is often replaced with fluids, the goal of which is to raise the falling blood pressure, promote micro-circulatory perfusion, decreasing blood viscosity to increase blood flow.
Often, the patient may seem to be stable, but is in hemorrhagic shock.
This is because even with a blood pressure of 60mmHg (under 90mmHg is defined as hypotension) the patient can still be talking. Even as circulatory volume of blood can be greatly lost, through a combination of the following, blood pressure and circulatory volume can be maintained:
- peripheral vasoconstriction
- adrenalin in the body
- release of stress hormones
- fluid shifts into the intravascular space
- administration of fluids to increase blood volume
The graph below follows the deterioration of a trauma patient in shock  :
The graph tracks the systolic blood pressure of the patient with time.
"The saw-tooth BP pattern of recurring normo- and hypo-tension often reflects ongoing haemorrhage in the setting of intermittent fluid resuscitation."
The blood pressure was measured every five minutes. There are constant valleys in the systolic BP, seen in the graph, where the pressure drops, and after which fluid bolus is routinely administered (the transfusion of large quantities of fluid into a trauma patient has been the standard approach to such cases for many decades).
The graph shows that the valleys are getting lower and lower with passing time, showing that the patient's ability to cope with the blood loss is becoming worse and worse, until ultimately, the patient dies.
Often, death is immediate, in this case, coming within five minutes of it being at 100mmHg.
So, what is happening to the body and how have fluids and our attempts to help affected it?
PATHOPHYSIOLOGY OF TRAUMA
Severe blood loss causes hypovolemia: a decreased volume of circulating blood in the body. Insufficient micro-circulation results in inadequate oxygen availability for most of the cells in the human body: the mitochondria can no longer carry out the process of oxidative phosphorylation in a rhythm that would be sufficient to keep up with the cell's metabolic needs for energy.
In this condition of insufficient oxygen availability, the cell resorts to utilising anaerobic respiration to produce energy, a byproduct of which is lactic acid. Lactic acid can rapidly accumulate in tissues, resulting in a drop of body's pH, acidosis.
Acidosis can also impair heart function. 
One of the most harmful effects of acidosis on a trauma patient is a severe impairing of their coagulation system, which can be reduced by 55-70% in functionality when pH drops from 7.4 to 7.0. 
Hypothermia is defined as the core body temperature being lower than 35degrees Celsius (the normal human body temperature being between 35.6-37degrees C) . With vasoconstriction and lowered circulation, hypothermia is very common in trauma patients.
Coagulopathy: is a condition in which the blood's ability to clot is impaired, leading to prolonged or excessive bleeding, exacerbating haemorrhage.
Haemorrhage itself causes coagulopathy through the physical loss of clotting factors during bleeding, leaving the body depleted of both platelets and clotting factors.
Coagulation disorders in trauma have a complex pathophysiology including activation or dysfunction of fibrin generation or both, platelet and endothelium dysfunction, relative inhibition of stable clot formation by anticoagulant and fibrinolytic pathways and either consumption or inhibition of coagulation proteases. 
Importantly, coagulation is a process closely regulated by both the body temperature and it's pH. As the body's temperature goes down, so does its ability to coagulate, as result of inhibition of platelet function, inhibition of clotting factors and inappropriate activation of clotting breakdown. 
WHAT ARE THESE FLUIDS?
Already familiar with the problems the body is experiences during trauma, the requirements for the ideal administered fluid are:
1) the same oxygen carrying capacity and and volume expansion of blood (to increase the blood pressure, provide oxygen all body cells to reduce acidosis and hypothermia, and to make up for the lost blood during haemorrhage)
2) no need for cross-matching between blood groups
3) maintains a normal composition and distribution of body fluid compartments (it will allow the blood to normally clot)
4*) ideally it would also be cheap and easily accessible (trauma can occur anywhere so it could be used by emergency care units too)
More realistically, the fluids listed in the table below  are those that can be used for resuscitation. Most commonly, lactate ringer and normal saline are used.
THE NEGATIVE EFFECTS OF THESE FLUIDS
Great care should be taken that the blood and fluids administered are not at room temperature, but heated to normal body temperature. If a saline solution is at (20-25degrees C), then it could worsen hypothermia.
Normal saline has a pH of around 5.5, and is far more acidic than normal blood, therefore normal saline administration worsens the blood pH.
Administering fluids or blood products that do not themselves contain clotting factors dilutes the remaining blood in the body, making haemorrhage control even more difficult. Increased blood flow due to fluid administration can also disrupt any clotting that was being formed.
Referring back to the first graph , the patient was continuously administered bolus fluid, which kept raising his blood pressure seen as the peaks in the graph. The patient was also actively haemorrhaging, the valleys in the graph. With time, the body loses its ability to cope with the blood loss, severe acidosis triggers myocardial compromise, ongoing blood loss causes coagulopathy, and death ensues.
It is therefore dangerous to administer aggressive amounts of IV fluids to a patient in trauma. Although it may improve a number by increasing their blood pressure, by diluting their clotting factors and worsening acidosis they may damage the patient in the long run. 
FLUID ADMINISTRATION IN TRAUMA
Debate continues regarding the strategy of fluid management in trauma. Although no certain fluid has been shown to be more or less effective than the others, administration of large volumes of IV fluids should be avoided. Tranexamic acid (an antifibrinolytic that prevents clot breakdown and thus decreases blood loss) should be given to all the patients with penetrating trauma who need transfusion.
 Trauma: Emergency Resuscitation, Perioperative Anesthesia, Surgical Management, Volume I: Volume 1, 5 Feb 2007 by William C. Wilson and Christopher M. Grande
 Meng ZH, Wolberg AS, Monroe DM, et al. The effect of temperature and pH on the activity of factor VIIa: Implications for the efficacy of high-dose factor VIIa in hypothermic and acidotic patients. J Trauma. 2003;55(5):886–891.
 Soreide E, Smith CE. (2005.) Hypothermia in trauma victims—friend or foe? Trauma Care International. Retrieved Feb. 10, 2014, from www.itaccs.com/traumacare/archive/05_01_Winter_2005/friendorfoe.pdf .
 The coagulopathy of trauma: a review of mechanisms.Hess JR, Brohi K, Dutton RP, Hauser CJ, Holcomb JB, Kluger Y, Mackway-Jones K, Parr MJ, Rizoli SB, Yukioka T, Hoyt DB, Bouillon BJ Trauma. 2008 Oct; 65(4):748-54.
 J Anaesthesiol Clin Pharmacol. 2015 Jul-Sep; 31(3): 308–316. doi: 10.4103/0970-9185.161664
 Functional significance of cell volume regulatory mechanisms. Lang F, Busch GL, Ritter M, Völkl H, Waldegger S, Gulbins E, Häussinger D Physiol Rev. 1998 Jan; 78(1):247-306.
 Low-volume fluid resuscitation for presumed hemorrhagic shock: helpful or harmful? Stern SA Curr Opin Crit Care. 2001 Dec; 7(6):422-30.