RESUSCITATION FLUIDS

CHAPTER 18 RESUSCITATION FLUIDS

Martin Schreiber, Brandon Tieu, Laszlo Kiraly, Michael Englehart

The practice of giving intravenous fluids or medication has been used since the 1600s. Slow progress was made after William Harvey provided a modern description of the circulatory system in 1638. William O’Shaughnessy theorized that patients suffering from volume loss secondary to cholera would benefit from restoration of blood to its natural specific gravity. This became the first concept of contemporary intravenous fluid therapy. Thomas Latta was credited with actually applying O’Shaughnessy’s theory and treating victims of cholera in 1832. Later in the century, Sydney Ringer described a physiologic solution with a focus on electrolyte concentrations in his animal models. Despite these early trials, application of these concepts was criticized and largely forgotten until the 20th century. The advent of modern surgery renewed interest in resuscitation as therapy to maintain intravascular volume.

World War I provided tremendous experience with resuscitation of hemorrhagic shock. Cannon’s work eloquently described the natural history and presentation of shock with primary accounts of battlefield victims. His work suggested that a delay in surgical control of bleeding was accompanied by a large increase in mortality. Furthermore, he indicated that aggressive resuscitation without surgical control could worsen hemorrhagic shock. He also indicated that resuscitation with saline could worsen existing acidosis. In subsequent decades, however, much of his work was forgotten or ignored. Then in World War II and the Korean War, practice shifted to resuscitation with plasma and blood. Blalock supported this based on his dog studies, suggesting that crystalloid fluids were rapidly lost from the intravascular space. In 1963, Shires showed that shock is accompanied by a shift of interstitial fluid into the vasculature. This discovery brought renewed interest in salt solution therapy. Subsequent decades have been characterized by further optimization in aggressive resuscitation. Specific gains have been made in the realm of intensive care, monitoring, intravenous access, and endpoints of resuscitation. Despite these advances, many controversies and questions remain. Choice of fluid has been largely unchanged and unexamined. The study of the mechanism of shock at a cellular and molecular level has yet to reveal any applicable treatments. More importantly, the complications of modern resuscitation are commonly seen in trauma intensive care units. Before discussing details on fluids, it is important to understand hemorrhage and the physiologic response.

CLASSES OF SHOCK

Shock is inadequate tissue perfusion. The humoral sympathetic response to shock causes vasoconstriction in the clinical appearance of the patient. These findings were observed by Cannon when he correlated the volume of blood loss with the patient’s clinical signs, symptoms, and blood pressure. His findings have since been validated with repeated observational studies in humans, as well as experimental studies in animals. The classes of shock are now well defined, and provide a quick means of assessing a patient’s blood loss and the level of resuscitation required (Table 1).

Table 1 Classes of Shock

AUTORESUSCITATION

The goal of the body’s compensatory mechanisms during shock is to preserve perfusion to vital organs. Bickell’s 1994 study of delayed fluid resuscitation for hypotensive patients with penetrating torso injuries demonstrated that, in the absence of resuscitation, blood pressure spontaneously increased prior to operative intervention. This finding validates observations made by Cannon, and has further been supported by subsequent data, which demonstrated that during hypotensive resuscitation blood pressure spontaneously rises toward normal in the absence of fluid therapy. Numerous mechanisms exist to account for these findings, specifically vasoconstriction, a reduction in capillary hydrostatic pressure, and hormonal responses. The sum of these responses is reflected in the phases of shock, which in turn help dictate the resuscitation strategy.

Vasoconstriction and Reduction of Capillary Hydrostatic Pressure

Peripheral and splanchnic vasoconstriction help to redirect blood flow away from muscle, skin, bowel, kidneys, and other nonvital organs. This is accomplished through the release of epinephrine, norepinephrine, and vasopressin. By increasing the peripheral vascular resistance, and effectively reducing the circulating volume through which the blood must pass, the mean arterial pressure is increased. Initially, during compensated shock, only the precapillary sphincter is constricted, reducing the capillary hydrostatic pressure and increasing the peripheral resistance. As the shock worsens, both the precapillary and postcapillary sphincters are constricted, leading to anaerobic metabolism, which results in excess lactate and acidosis. As the severity of shock increases, the postcapillary sphincter relaxes secondary to hydrogen ion buildup, releasing the metabolic byproducts into the circulation. The result is reperfusion injury. This is common when the system decompensates, and the patient shows signs of florid shock and global hypoperfusion.

The subsequent decrease in capillary hydrostatic pressure reduces the volume of plasma lost from the vasculature into the interstitial space, and increases return of interstitial fluid into the vascular space. This is an additional method of increasing venous return to the heart. Given the large capacitance of the venous system, larger volumes of circulating blood are stored within the veins compared to the arteries. According to the Frank-Starling laws of cardiac performance, the cardiac output is directly proportional to the venous return to the heart (preload) (Figure 1). As venous return decreases, so does cardiac output, and thereby arterial pressure to perfuse vital organs.

Figure 1 The effect of increased right atrial pressure on cardiac output. Increases in right atrial pressure are accomplished through either an increase in circulating blood volume, or a decrease in venous compliance. Cardiac output increases linearly in response to increased right atrial pressure.

(Adapted from Berne RM, Levy MN: Cardiovascular Physiology, 3rd ed. St. Louis, MO, Mosby, 1977.)

Hormonal Response

In response to hypotension, numerous hormonal pathways are initiated to restore circulating plasma volume. Vasopressin plays a major role in peripheral vasoconstriction. Additionally, it acts to increase free water absorption in the collecting ducts of the kidneys. In response to lower pressures at the afferent arteriole within the kidney, renin is released, triggering the renin/angiotensin/aldosterone cascade. The effect is to increase the absorption of sodium, which in turn increases water absorption. Additionally, angiotensin-II acts as a potent peripheral vasoconstrictor. Finally, cortisol acts to increase extracellular osmolarity and increased lymphatic flow.

The reduction of capillary hydrostatic pressure and the hormonal response increase venous return during the first 1–2 hours following injury, but this may be inconsequential in the setting of severe hemorrhage. Cessation or slowing of ongoing hemorrhage also contributes to a spontaneous rise in blood pressure by limiting ongoing fluid losses. The remainder of the response is carried out through vasoconstriction and the redistribution of blood flow, accounting for the majority of increased venous return. If prolonged, this can have a damaging, and sometimes irreversible effect upon the tissues supplied by the splanchnic circulation. This will result in ischemia and potential reperfusion injury.

Phases of Shock

Combined, the aforementioned physiologic effects produce the classic signs and symptoms exhibited by patients in hypovolemic shock. The progression from compensated to uncompensated shock gives rise to the physical findings of the systemic insult (Figure 2). Initially, compensated shock affects the periphery, manifesting the symptoms of cool extremities, cyanosis, mottling of the skin, and decreased capillary reperfusion (blanching). As the severity of shock progresses, vasoconstriction affects the torso, producing oliguria as the main clinical sign. Finally, in severe classes of shock, perfusion of the heart and brain are affected, producing cardiac dysrhythmias and a reduced level of consciousness. Over the hours following injury, these mechanisms are in constant flux, in efforts to restore homeostasis to the injured system.

Figure 2 Signs and symptoms of shock.

Lower cardiac output, variable tachycardia, oliguria, and decreased capillary pressure define the initial phase following hemorrhagic shock. The interstitial space is contracted in efforts to preserve circulating plasma volume. This occurs typically in the prehospital phase and extends into the early portions of the patient’s initial resuscitation. During this period active replacement of blood loss is achieved through either crystalloid infusion or blood transfusion to restore circulating blood volume. The second phase is marked by extravascular fluid sequestration. This often occurs following surgical intervention and massive resuscitation. The intracellular and interstitial spaces expand as resuscitation continues, and blood pressure typically stabilizes. Crystalloids are given to maintain plasma volume based upon the patient’s observed hemodynamic status. The third and final stage is marked by diuresis and mobilization of fluids with an increase in blood pressure. This response occurs only after appropriate volume resuscitation, surgical correction of the cause of the hemorrhage, and resolution of organ failure with return to a more homeostatic state.

HYPOTENSIVE RESUSCITATION

Traditional resuscitation strategies have been directed toward restoring normal intravascular fluid volumes and arterial blood pressures to maintain perfusion to vital organs. Since the early 1990s, this approach has been re-examined. The strategy of hypotensive resuscitation dictates delivery of limited volumes of intravenous fluids to sustain blood pressures lower than normal. In delayed resuscitation, fluids are withheld until control of the hemorrhage has been established. Tissue injury from regional hypoperfusion is a risk of these strategies. It depends on both length of time and severity of hypoperfusion. A single accurate method to assess regional hypoperfusion has not been established. Rapid resuscitation can exacerbate bleeding by dislodging fragile clots, decreasing blood viscosity, and creating compartment syndromes of the cranial vault, abdomen, and extremities. It also exacerbates the “lethal triad” of hypothermia, acidosis, and coagulopathy.

In a swine aortotomy model, Sondeen noted the average mean arterial pressure at which rebleeding occurred following uncontrolled hemorrhagic shock and spontaneous clotting was 64 mm Hg. This was independent of time of resuscitation. In addition, crystalloid solutions reduce the oxygen carrying capacity of the blood by dilution. The optimal volume of intravenous fluid administered is a balance between improving tissue perfusion and increasing blood loss by raising systolic blood pressure. Cannon stated that early control of hemorrhage was paramount and attempts at fluid resuscitation prior to this would result in increased bleeding and mortality. This concept has been evaluated in both animal and human studies. Previous animal studies used controlled hemorrhage models where hemostasis was achieved early allowing rapid restoration to a normovolemic state. Unfortunately, in the clinical setting the bleeding source may not be immediately known or immediate control is not possible. Using an aortotomy model in immature swine, Bickell and colleagues showed unfavorable outcomes in those swine resuscitated with lactated Ringer’s or hypertonic saline/dextran compared with no fluid.

In a prospective randomized study, Bickell compared immediate and delayed fluid resuscitation in hypotensive patients (systolic blood pressure [SBP] <90 mm Hg) with penetrating injuries to the torso. There was a statistically significant difference in survival between the two groups, 62% versus 70% (p=0.04), suggesting delayed resuscitation improved outcomes in penetrating injuries to the torso. The study was criticized for its predominantly young, male patient population, and its urban setting with short transfer times. Subsequent subgroup analysis showed survival benefits only in patients with cardiac injuries and no difference in survival when deaths were divided into preoperative, intraoperative, and postoperative time periods. Dutton compared fluid resuscitation to SBP 70 mm Hg versus SBP of greater than 100 mm Hg in actively hemorrhaging patients. Resuscitation to a lower SBP did not affect overall mortality. Both blunt and penetrating trauma patients were included in this study.

Further randomized controlled trials are needed before a hypotensive resuscitation strategy can be defined. Currently, patients suffering from blunt injuries should be managed with traditional strategies. Although the ideal target blood pressure remains elusive, in penetrating injuries an SBP of 80–90 mm Hg may be adequate. A significant association exists between prehospital hypotension (SBP <90) and worse outcomes in severe traumatic brain injury (TBI). Attempts to maintain SBP above 90 may decrease adverse outcomes in head-injured patients, although no class I evidence is available to corroborate this.

The current literature on hypotensive resuscitation cannot be extrapolated to all trauma patients but it emphasizes the importance of rapid diagnosis and treatment. Early identification of bleeding sources and control of hemorrhage will lead to more rapid replacement of intravascular volume and decreased morbidity and mortality.

Choice of Fluids

The use of crystalloids versus colloids has been an ongoing debate for decades. In the Vietnam War, isotonic crystalloids were used when laboratory work from the 1960s by Shires and others showed larger volume resuscitation with isotonic crystalloids resulted in the best survival. They also noted that extracellular fluid redistributed into both intravascular and intracellular spaces during shock, and rapid correction of this extracellular deficit required an infusion of a 3:1 ratio of crystalloid fluid to blood loss. Figure 3 shows the influence of fluids on the extracellular fluid compartments. Using this resuscitation strategy, the rate of mortality and acute renal failure decreased but a new entity of shock lung, now better known as acute respiratory distress syndrome (ARDS), was discovered. In reviewing studies comparing crystalloids and colloids with respect to pleural effusions and pulmonary dysfunction, two trials reported no differences. Two other series showed more pulmonary complications among patients resuscitated with colloid. When mortality was used as an endpoint, the use of crystalloids in trauma patients was associated with increased survival.

Figure 3 The influence of colloid and crystalloid fluids on the volume of the extracellular fluid compartments.

(Data from Imm A, Carlson RW: Fluid resuscitation in circulatory shock. Crit Care Clin 9:313, 1993.)

There are advantages and disadvantages to the use of both crystalloids and colloids. Crystalloids replace interstitial as well as intravascular fluid loss, do not cause allergic reactions, and are inexpensive. Possible disadvantages include limited intravascular expansion and tissue edema, which can impair gas exchange in the lungs and diminish bowel perfusion. Colloids have a longer intravascular half-life, which may improve organ perfusion and may cause less tissue edema. This may be a short-term effect as the interstitial oncotic pressure increases from diffusion of the colloid over time. Also, the choice of colloid may affect blood loss. Other possible disadvantages include increased incidence of allergic reactions, impaired blood cross matching due to dextrans, altered platelet function (dextrans, hetastarches), hyperchloremic acidosis due to high chloride content (hetastarch), and greater expense. A meta-analysis of clinical studies comparing crystalloids and colloids for fluid resuscitation failed to show any evidence of improved outcome with the use of colloids. In summary, there is no clear basis to give colloid products over crystalloid solutions for fluid resuscitation.

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Tags: Current Therapy of Trauma and Surgical Critical Care

Jul 7, 2016 | Posted by admin in CRITICAL CARE | Comments Off

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