You have just completed a major damage control operation with significant blood loss and ongoing resuscitation. As the patient rolls through the ICU doors, you are asked to write orders for the nurses to begin the postoperative care phase. You may or may not have an “intensivist” available to help you. Having a clear vision and plan for performing and monitoring the postoperative resuscitation is critical to avoid the twin evils of under-resuscitation and over-resuscitation. In combat surgery this is particularly critical as you often have to hand the patient off to the nurses or another physician and return to the ER or OR. Having a general approach or “philosophy” to resuscitation that the nurses, surgeons, and other physicians agree with and understand can make this process much smoother and less confusing.

The concepts of postoperative resuscitation and damage control surgery are inextricably linked in the combat environment. Presented with the critically injured patient, the surgeon in a combat environment must rely upon the guiding concepts of damage control surgery: stopping hemorrhage and controlling contamination. Definitive operations with anatomic reconstruction are delayed. Resuscitation and the restoration of normal physiology are the objectives, accomplished in the intensive care unit and aimed at either correcting or preventing the lethal triad of hypothermia, metabolic acidosis, and coagulopathy . Furthermore, resuscitation is a dynamic process, often occurring over hours or days, after injury. Combat resuscitation should be viewed as a continuum of care as outlined in Fig. 33.1.

The goals of therapy in the ICU after damage control surgery are well defined: (1) correct metabolic acidosis, (2) restore normothermia, (3) reverse coagulopathy , and (4) ensure adequate oxygen delivery and consumption. The components of the lethal triad act synergistically. Hypothermia and acidosis exacerbate coagulopathy by impairing clotting factor function. Each of the clotting factors is a protease that has enzyme kinetics dependent on an optimal pH and temperature. All three components of the triad must therefore be addressed simultaneously. The cornerstone of resuscitation in hemorrhagic shock (and the focus of this chapter) is ensuring adequate oxygen delivery by restoring an adequate circulating volume. Since the prior edition of Front Line Surgery , damage control resuscitation strategies utilizing plasma/platelets/PRBCs in a 1:1:1 ratio have been shown to improve early survival and reduce death from exsanguination compared to a 1:1:2 ratio in the PROPPR Trial published in 2015. Resuscitation is dynamic, and the goal is not merely to replenish circulating volume and restore oxygenation but to do so in a guided fashion, avoiding the complications of over-resuscitation. Indeed, fluid administration should be guided by the concept of volume responsiveness. Volume responsiveness refers to an increase in stroke volume of at least 10–15% after a fluid challenge of 250–500 mL or a passive leg raise. It should be noted that in normovolemic healthy patients, a volume challenge (increase in preload) will result in an increase in stroke volume, representing a reserve cardiac output capacity. Increasingly recognized is the need to prevent overloading with infused volume of any type; such overloading ultimately leads to tissue edema and more importantly pulmonary edema in the form of extravascular lung water (Fig. 33.2). In short, the goal of volume resuscitation is euvolemia: volume overloading with its attendant negative side effects is to be avoided.

Inherent to assessing volume responsiveness is the ability to measure cardiac output, preferably noninvasively. Various devices utilizing differing principles for the indirect measurement of cardiac output are available in the modern intensive care unit. They vary not only in the principles underlying their cardiac output measurements but also in their level of invasiveness. See Chap. 35 for a detailed discussion of monitoring devices, options, and applicability in the combat environment. Remember that no monitoring device can replace careful bedside assessment and good clinical judgment based on analysis of all of the available data. Do not go chasing some value on a monitor that does not agree with the rest of your assessment just to “normalize” the value.

A basic portable ultrasound and an anesthesia ventilator with end-tidal CO2 monitoring are available at all levels of surgical care throughout CENTCOM , including all far-forward GHOST (Golden Hour Offset Surgical Team) missions accompanying US Special Forces units. Facility with basic cardiac ultrasound views should allow static determinations of hypovolemia during resuscitation. Specifically, the parasternal long-and short-axis views (PLAX and PSAX, respectively) can provide nonquantitative information about volume status and global cardiac function during resuscitation. Additionally, although not validated in prospective studies, a subxiphoid inferior vena cava view (SIVC ) can assess IVC size and collapsibility during ventilation, providing some information regarding volume status. In the PLAX and PSAX views, left ventricular walls that touch during contraction are indicative of hypovolemia (ejection fraction >70%). On SIVC viewing, a decrease in IVC diameter with respiration of 75% or more indicates hypovolemia; 15% or less variation with respiration, determined quantitatively via M-mode, represents normovolemia. Again, the limitations of IVC collapsibility, especially during mechanical ventilation, remain an area of active investigation.

As previously described, the devices currently available to measure cardiac output and hence determine volume responsiveness are not available in the forward environment of the GHOST or even many Role 3 medical facilities. However, the availability of end-tidal CO2 (EtCO2) monitoring may provide some information regarding volume responsiveness, at least under stable ventilatory conditions. Recent studies have demonstrated that increases in EtCO2 of ≥5% after passive leg raise predict fluid responsiveness. One such study demonstrated that a passive leg raise-induced increase in EtCO2 of ≥5% predicted an increase in cardiac index of ≥15% (i.e., fluid responsiveness) on subsequent volume challenge (500 mL of normal saline infused over 30 min) with sensitivity of 71% and specificity of 100%. Moreover, changes in arterial pulse pressure were unable to predict fluid responsiveness in the same patients. When combined with echocardiographic assessments of left ventricular filling and IVC collapsibility , EtCO2 changes in response to volume challenges should enable the forward deployed surgeon to make informed decisions regarding initial and ongoing postoperative fluid resuscitation needs.

ATLS guidelines recommend the initial administration of 1–2 L of lactated Ringer’s solution (LR) or normal saline (NS) followed by an immediate assessment of the response of the arterial blood pressure as the preferred initial resuscitation maneuver in hemodynamically unstable patients. The goal is to differentiate patients into one of three categories: responder, transient responder, and nonresponder. If after the initial 2 L of crystalloid the patient fails to respond or transiently responds but then again develops hypotension, blood is transfused. Accordingly, several points regarding this approach and its application to the combat environment deserve mention.

The ATLS is geared toward blunt trauma, and the target audience is primarily those inexperienced in trauma or “amateurs.” You are not an amateur and should not approach trauma with a generic and basic algorithm. Do not spend 30 min in the emergency department with a critically injured patient trying to infuse liters of crystalloid to determine if the patient is a “responder” or trying to get the blood pressure up to some arbitrary level. In combat trauma this will get you way behind the power curve at the least or a dead patient. Combat trauma patients that are stable and mentating do not need any initial large fluid volumes, particularly cold crystalloid solutions. The vast majority of patients with compensated or uncompensated shock on presentation need resuscitation in tandem with operative intervention, and this resuscitation should start and end with blood products.

If you resuscitate postoperatively with standard crystalloid solutions (normal saline ), you may see several adverse effects due to the large sodium and chloride loads. The most immediate clinical consequence of this iatrogenic hyperchloremic metabolic acidosis is to confound the interpretation of blood gas pH and base deficit values obtained during the resuscitation. In the worst case, a persistently decreased pH or base deficit could be misinterpreted as ongoing hypoperfusion and treated with further volume expansion, thereby exacerbating the problem. This effect will be worse with normal saline compared to a more balanced solution like lactated Ringer’s (LR).