Fluid resuscitation in trauma: what are the best strategies and fluids?

Traumatic injuries account for nearly 10% of the global burden of disease [1]. The major cause of potentially preventable death among injured patients is uncontrolled post-traumatic hemorrhage [2]. In trauma patients, fluid resuscitation helps restore lost blood volume, regain tissue perfusion, and reduce mortality.

This review discusses the role of prehospital trauma care (PTC) in low-resource/remote settings; goals, principles and evolving strategies of fluid resuscitation, particularly those before blood products are available; and post-resuscitation fluid management. Management of fluid resuscitation in some special groups is also discussed.

PTC aims at the stoppage of bleeding to minimize further blood loss, initial resuscitation to maintain mental status and peripheral pulses, and fast transportation to hospital for definitive treatment [3]. Prehospital intravenous fluid administration decreases mortality in trauma patients, especially in major injuries and rural settings when prehospital transport time (PTT) is long [4‐7].

The goals of fluid resuscitation include controlling bleeding, restoring lost blood volume, and regaining tissue perfusion and organ function. Different target systolic blood pressure (SBP) values may be considered for different traumas: 60–70 mmHg for penetrating trauma; 80–90 mmHg for blunt trauma without traumatic brain injury (TBI); 100–110 mmHg for blunt trauma with TBI [8]. However, as clinical scenarios are complex and variable, adhering to evidence-based clinical practice guidelines and adapting according to local treatment and patient condition is likely to improve patient outcomes [2].

Fluid administration is beneficial only if it increases the stroke volume (SV) and thereby, the cardiac output. Patients are considered fluid responsive if SV increases by at least 10% after a fluid challenge of 500 mL of crystalloid [9]. Pulse pressure variation, passive leg raising test, and SV variation are some reliable markers for fluid responsiveness.

Resuscitation strategies are based on volume, rate, and time of fluid administration. Earlier, immediate aggressive fluid resuscitation in trauma patients was the standard approach to restore circulating volume and maintain organ perfusion. However, it may dislodge soft clots and cause dilutional coagulopathy thereby increasing hemorrhage and mortality [3]. Treating trauma patients with large crystalloid volumes leads to resuscitation injury, gastrointestinal and cardiac complications, increased extremity compartment pressures, coagulation disturbances, electrolyte imbalance, hypothermia, and abdominal compartment syndrome [3].

Two strategies were proposed to avoid clot disruption and dilutional coagulopathy: delayed resuscitation strategy where fluid is given after bleeding is controlled and permissive hypotension strategy, where fluid is given to increase SBP without reaching normotension. In penetrating trauma patients with hypotension (prehospital SBP < 90 mmHg), delayed resuscitation shows better survival rates compared to immediate resuscitation [10]. Increased mortality is seen with increased in-field procedures [11, 12], supporting “scoop and run” and delayed fluid resuscitation techniques. However, when PTT is long, simple life support measures reduce mortality in severely injured patients [4, 5] even when conducted in suburban and remote locations with long PTT [13].

The low volume fluid resuscitation during permissive hypotension maintains low tissue perfusion but is adequate for short periods. Permissive hypotension is achieved by goal-directed resuscitation [SBP/mean arterial pressure (MAP) is targeted based on patient physiology] or controlled resuscitation (predetermined fixed rates are infused such that normotension is not achieved) [3, 14]. In animal studies, controlled resuscitation of 60–80 mL/kg/h usually maintains SBP of 80–90 mmHg (MAP of 40–60 mmHg) in hemorrhagic shock patients [14].

Permissive hypotension is associated with decreased blood loss, intra-abdominal bleeding, risk of intra-abdominal hypertension, acidemia, hemodilution, thrombocytopenia, coagulopathy, apoptotic cell death, tissue injury, sepsis, volumes of crystalloid administration needed, and blood product utilization, and improved organ perfusion and survival [14, 15]. However, prolonged (8 h) hypotension (SBP < 65 mmHg or MAP around 65 mmHg) has been shown to increase metabolic stress, tissue hypoxia, and mortality in animal studies [14].

International guidelines recommend restrictive volume replacement approach to achieve target blood pressure (BP) until bleeding is controlled [2]. Penetrating trauma patients have better outcomes with SBP of 60–70 mmHg. In blunt trauma, higher SBP of 80–90 mmHg is permitted but slower infusions are preferred over large boluses [15]. In patients with traumatic hemorrhagic shock, permissive hypotension is safe and feasible, and reduces mortality [16]. However, large crystalloid volumes are not advisable and should be cautiously administered.

Mortality is increased in patients with head injury and low cerebral perfusion pressures [17]. Small aliquots of fluid (100–200 mL) should be administered to maintain SBP > 90 mmHg [18] or MAP > 80 mmHg [15]. Permissive hypotension is contraindicated in TBI [18].

When PTT to definitive care is shorter (< 10–15 min) and patients are well-selected, delayed resuscitation seems a good option [13, 14]. Advanced life support interventions provide no added benefit and may delay the time to definitive care [19]. When PTT is longer than 10–15 min, mortality is increased and goal-directed resuscitation with low-volume crystalloid and basic/advanced life support interventions are better [4, 5, 13, 14]. As clinical scenarios are complex and variable, adhering to evidence-based clinical practice guidelines and individualizing the patient’s SBP/MAP goals are important.

In severely injured patients, the lethal triad of hypothermia, acidosis, and coagulopathy exacerbates hemorrhage. Damage control resuscitation combats this and comprises of permissive hypotension, hemostatic resuscitation, and damage control surgery (DCS).

Permissive hypotension, as discussed, prevents further bleeding from recently clotted vessels. Hemostatic resuscitation involves early use of blood and blood products to minimize coagulopathy, prevent dilutional coagulopathy, and improve survival [20, 21]. It entails the use of plasma, platelets, and red blood cells in an optimal ratio of 1:1:1 as well as the use of antifibrinolytic agents such as tranexamic acid in addition to limiting the use of crystalloids [22]. Hemostatic monitoring is applied so that when bleeding slows, a goal-directed approach for resuscitation can be adopted [22]. Massive transfusion protocol (MTP) should be activated in patients requiring continued resuscitation [3] and started as early as possible to avoid rapid administration of crystalloids [23] and post-injury complications such as organ failure and abdominal compartment syndrome [24].

DCS restores physiology instead of providing definitive anatomical repair. It consists of bleeding control, decontamination, quick body cavity closure to rewarm the patient, and planned re-operation for definitive repair [20].

Though crystalloids and colloids are widely used for fluid resuscitation, the ideal choice of fluid is debated. Hypotonic fluids do not stay intravascular. Therefore, isotonic and hypertonic crystalloids are used for fluid resuscitation. Lactated Ringer’s (LR) or normal saline (NS) is the primary resuscitation fluids [18]. Albumin and gelatin solutions are protein colloids whereas starches and dextrans are non-protein colloids.

The Saline versus Albumin Fluid Evaluation (SAFE) study compared 4% albumin and NS. Both showed clinically equivalent efficacy. The volume of fluid administered was less with albumin than with NS (1:1.4) [25]. However, in TBI patients, albumin resuscitation was associated with higher mortality compared to NS [26]. In trauma patients who required > 10 units of packed red blood cells and underwent DCS, permissive hypotension with hypertonic saline (HTS) involved less fluid requirements, reduced 30-day mortality, increased urine output, and reduced risk of acute respiratory distress syndrome, sepsis, and organ failure compared to standard resuscitation with isotonic crystalloids. However, there was no difference in renal failure [27].

A multicenter randomized controlled trial called the Colloids Versus Crystalloids for the Resuscitation of the Critically Ill (CRISTAL) trial compared mortality in critically ill patients who received colloids (n = 1414; gelatins, dextrans, hydroxyethyl starches, or 4% or 20% of albumin) or crystalloids (n = 1443; isotonic or hypertonic saline or LR solution) for fluid resuscitation [28]. Therapy was open-label but the outcome assessment was blinded to treatment assignment. There was no difference in 28-day mortality, need for renal replacement therapy, development of organ failure, and number of hospital days between the two groups [28]. The 90-day mortality was slightly lower with colloids. This needs further evaluation [28].

In the Crystalloid versus Hydroxyethyl Starch Trial (CHEST), hydroxyethyl starch (HES) was associated with increased renal failure, need for renal-replacement therapy [29], and mortality [30]. However, risks of renal injury and mortality related to colloids were observed only in critically ill patients with sepsis [31].

Crystalloids are generally readily available and inexpensive [32]. They are preferred in TBI [26] and in initial resuscitation of trauma patients [18]. Compared to non-balanced fluids, L-isomer of LR causes less inflammation, immune dysfunction [33], and mortality in critically ill patients [34] and is recommended fluid of choice in hemorrhagic shock patients [18]. HTS is beneficial in patients with brain edema [35], TBI [36], or massive hemorrhage requiring DCS [27]. Though HTS contributes to renal failure, it significantly decreases the fluid requirement and consequent acute respiratory distress syndrome related to interstitial fluid overload [27, 35]. Chloride-restrictive fluids reduce the risk of renal failure and the need for renal replacement therapy [37]. They may be used as adjuncts to blood products and other therapies.

Colloids remain intravascular longer, rapidly expand plasma volume, and achieve similar goals quickly with less volume than crystalloids. However, they come with added expense and lack of survival benefit over crystalloids [38]. Colloid use is recommended when patients cannot tolerate large crystalloid volumes and overload is of concern [25]. Albumin is contraindicated in TBI [26], and HES and other starches are not recommended [29‐31]. Owing to the increased risk of kidney injury, colloids should be cautiously used in patients with renal impairment. Renal effects are colloid-specific; albumin displays renoprotection while HES shows nephrotoxicity [39].

Gelatins are low molecular weight, cheaper than albumin and other synthetic colloids, rapidly excreted by kidneys, associated with less renal impairment than HES, and have no upper limit of volume that can be infused unlike starches and dextran [40]. They have a lower risk of dilutional coagulopathy than dextrans and starches [41]. Though gelatins are associated more with anaphylactoid reactions than albumin, some recent studies showed no anaphylactic reactions with polygeline [42, 43]. New generation gelatins may have a significant role in remote/rural settings to prevent crystalloid overuse until definitive care is available and also in low-income settings where albumin may not be available/affordable. In India, polygeline is routinely used in hypovolemic trauma patients. Polygeline has a short half-life of 4–6 h and is readily excreted in the urine and does not seem to adversely affect renal function [42]. It does not accumulate in patients with renal failure [43]. Though polygeline seems to be safe and effective to treat hypovolemic trauma patients [42, 43], further large and multicenter comparative studies are warranted to validate results and elucidate outcome benefits.

Both under-resuscitation and over-resuscitation are fatal. Transitioning from the initial resuscitation to post-resuscitation phase is important to improve outcomes. The post-resuscitation phase is the period after coagulopathy is corrected, microcirculatory flow is improved, and hemodynamic parameters are stabilized (SBP > 100 mmHg; MAP > 65 mmHg in most cases) [15]. During this phase, markers for fluid responsiveness are normalized. Patients are no longer fluid responsive. If a patient is fluid responsive but the risks of fluid challenge outweigh the hemodynamic benefits, then other options should be considered such as inotropic support and hemodialysis with net ultrafiltration. Awareness of Resuscitation, Organ support, Stabilization, Evacuation (ROSE) concept [15] is essential for timely and appropriate decisions. Maintenance fluids should be given such that they stay intravascular for longer periods to avoid tissue edema. During this phase, crystalloids are used for both supplementing the fluid and administering medicines. Fluids used for administering medicines and supplementing nutrition together should not exceed 2 mL/kg/h [15]. Balanced fluids are better than 0.9% NS especially if sodium and chloride overload is of concern [15].

Fluid resuscitation strategies have evolved with time. Different traumas need different fluids and different resuscitation strategies. Prehospital trauma care reduces mortality in rural/remote settings. Delayed fluid resuscitation is preferred when transport time to definitive care is shorter whereas goal-directed resuscitation with low-volume crystalloid is preferred if transport time is longer. Adhering to evidence-based clinical practice guidelines and local modifications based on patient population, available resources, and expertise may improve patient outcomes.