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3 Experience with and Complications of Fluid Resuscitation
Pages 47-78

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From page 47...
... Despite the impact of salt solutions on survival in shock, numerous questions and concerns persist regarding the composition, rate, and quantity of fluid resuscitation. This chapter gives an overview of colloid and crystalloid resuscitation, examines the complications of fluid resuscitation in general, and then describes the complications of crystalloid and colloid resuscitation specifically.
From page 48...
... Considerable controversy arose, however, regarding the formula or the clinical criteria used to determine the adequacy of fluid resuscitation; in addition, questions arose regarding the type of fluid that was most appropriate for volume replacement. Several studies suggested that normal saline and lactated Ringer's solution were equally effective in maintaining intravascular volume after hemorrhage (Cervera and Moss, 1975; Siegel et al., 1973; Wright, 1974)
From page 49...
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From page 50...
... Despite the lessons learned in Vietnam (increased incidence ot pulmonary failure and ARDS with aggressive fluid resuscitation from shock) , crystalloid solutions gained increasing acceptance in both clinical and military areas for fluid resuscitation from trauma.
From page 51...
... Effects of Fluid Resuscitation on Coagulation Prolonged bleeding time has been described in patients with severe anemia (Hellem et al., 1961~. A decrease in hematocrit as a consequence of largevolume crystalloid resuscitation produces anemia, thrombocytopenia, reduced plasma, and oncotic, clotting, and opsonic proteins.
From page 52...
... Aggressive fluid resuscitation from hemorrhage and the resulting anemia increase the blood flow but also increase the shear stress on vascular endothelial cells, promoting the release of endothelium-derived nitric oxide (Duke and Abelmann, 1969; Griffith, 1987; Ignarro, 1987; Loscalzo, 1995; Palmer et al., 1987~. Shear stress on the endothelium is related to both shear rate and whole-blood viscosity.
From page 53...
... Although trauma patients with hemorrhagic shock may receive oxygen therapy during transport and in the emergency department, these patients seldom require supraphysiologic concentrations of oxygen. A primary concern in the treatment of the trauma patient with hemorrhagic shock is aggressive fluid resuscitation and the potential for reperfusion injury related to (1)
From page 54...
... The toxic effects of oxygen in animals and humans has been well recognized, but oxygen toxicity has been best characterized with regard to reperfusion injury, in which the return of molecular oxygen to previously ischemic tissues contributes to oxygen free-radical generation via xanthine oxidase activation. Reperfusion-Mediated Injury A major concern with regard to fluid resuscitation, that is, the reintroduction of molecular oxygen into previously ischemic tissues, the production of excess oxygen-derived free radicals, and subsequent tissue damage, has been investigated extensively.
From page 55...
... This phenomenon has been described as the "oxygen paradox" and describes the fact that although the restoration of oxygen delivery to ischemic tissue is essential to the maintenance of function and survival, this oxygen may initiate a cascade of deleterious events, producing tissue injury. The free radicals produced during reperfusion or fluid resuscitation from hemorrhagic shock attack multiple components of the cell, including lipids, nucleic acids, and proteins.
From page 56...
... These factors are major contributing factors to the development of multiple-organ failure after traumatic injury with shock, despite aggressive fluid resuscitation. Other studies have described no significant changes in either superoxide dismutase or catalase levels during hemorrhage alone (Uzuner et al., 19954; however, in those studies, a reduced catalase level after resuscitation suggested reperfusion-mediated injury via the generation of free radicals as well as a fall in antioxidant capacity.
From page 57...
... , there is abundant evidence that nitric oxide interaction with superoxide radical yields peroxynitrite, exacerbating the injury produced by either nitric oxide or superoxide alone. Peroxynitrite generation occurs particularly during fluid resuscitation from hemorrhagic shock in which the level of production of the superoxide radical exceeds the scavenging capacity of endogenous enzymes.
From page 58...
... cascade, which triggers DNA fragmentation and cellular apoptosis (Endres, 1998; Szabo, 1998; Virag et al., 1998; Yaoita et al., 1998~. Clearly, hemorrhagic shock produces local and whole-body ischemia; and fluid resuscitation, regardless of the type of fluid administered, increases perfusion of previously ischemic or hypoperfused tissues, triggering the production of numerous free radicals and likely contributing to cellular injury.
From page 59...
... Such transgenic and pharmacologic approaches have been shown to decrease free radicalmediated injury, as indicated by decreased lipid peroxides and malondialdehyde levels and have confined that the activated neutrophil is one source of free radicals in resuscitated hemorrhagic shock. Complications of Late Resuscitation of Shock In the late phase of shock resuscitation, emphasis is placed on continued volume replacement as well as nutritional support delivered via the enteral or the parenteral route.
From page 60...
... However, these agents are cheap to manufacture, are stable with storage at room temperature, and eliminate the infectious risks associated with blood products. Recent studies have shown that artificial colloids increased the levels of expression of adhesion molecules, increased the levels of synthesis of several proinflammatory cytokines, and promoted cellular apoptosis (Coimbra et al., 1996; Junger et al., 1997a,b; Rhee, 1998~.
From page 61...
... Resuscitation with a minimal volume of hypertonic saline has been discussed, but it is important to note that hard evidence of the effectiveness of this strategy exists primarily from the early resuscitation of patients with ruptured aortic abdominal aneurysms and penetrating truncal trauma. Alternative synthetic colloids like hydroxyethyl starch (and other high-molecular-weight starches)
From page 62...
... Flow cytometry was used to detect superoxide burst activity as a measure of neutrophil activation. Hemorrhage-mediated neutrophil activation was exacerbated by lactated Ringer's solution resuscitation, whereas shed blood or hypertonic saline infusion returned neutrophil activity to baseline values.
From page 63...
... In a subsequent study, Rhee and colleagues (in press) diluted whole blood from healthy volunteers with various resuscitation fluids to examine the hypothesis that neutrophil adherence and activation correlates with the type of fluid resuscitation used as well as with the degree of hemodilution.
From page 64...
... Although many trauma patients with hemorrhagic shock have received larger volumes than necessary for adequate resuscitation with no evidence of inflammatory activation, the data suggest that fluid resuscitation from hemorrhagic shock is not innocuous and that the type of resuscitation twirl nice, ~- -the inflammatory syndrome.
From page 65...
... In contrast, resuscitation with neither shed blood nor hypertonic saline produced significant changes in apoptotic staining in either the mucosa, the bowel wall, or the liver (see Figure 3-6~. Furthe~ore, the mucosa walls and bowel walls of sham-hemorrhaged rats given lactated Ringer's solution produced high levels of apoptotic staining, confirming that large-volume lactated Ringer's solution infusion, even in the absence of hemorrhage, pro ~rr~ ~¢ BAA a- -- 1 &'
From page 66...
... examined the effects of various fluid resuscitation regimens on the upregulation of the Bax protein, a member of the Bc1-2 protein family and a potent inducer of apoptosis (see Chapter 2~. In their study, Sprague-Dawley rats were hemorrhaged and maintained through a 75-minute hemorrhagic shock phase; fluid resuscitation consisted of either 5 percent albumin, whole blood, 6 percent hetastarch, dextran 40, or lactated Ringer's solution.
From page 67...
... The absence of evidence-based research in this regard suggests that additional studies are needed to examine both the immune consequence of small-volume lactated Ringer's resuscitation and the immune consequences of small-volume hypertonic saline resuscitation followed by lactated Ringer's resuscitation. Effects of Crystalloid Resuscitation on Cytokine Response Recently Hierholzer and colleagues (1998)
From page 68...
... However, studies examining the effects of colloid resuscitation, reduced-volume lactated Ringer's solution resuscitation, or hypertonic saline resuscitation from hemorrhagic shock on cytokine response are lacking. Adverse Effects of Large-Volume Crystalloid Resuscitation Although Shires' work proposed that volume resuscitation after hemorrhagic shock should consider extracellular fluid deficits (Shires et al., 1960a, 1961, 1964)
From page 69...
... , a 10 to 20 percent weight gain in a 70-kilogram (kg) man represents "a 2-3 gallon increase in the intracellular and extracellular fluid compartments." These studies collectively suggest that reassessment of both the composition and the rates of fluid resuscitation in the patient with hemorrhagic shock is warranted.
From page 70...
... However, the cardiotoxicity of lactated Ringer's solution resuscitation from hemorrhagic shock has been examined in adult Sprague-Dawley rats. Ringer's solutions containing ~-lactate, D-lactate, or the racemate were compared in conscious unrestrained rats after hemorrhage to a mean arterial blood pressure of 40 millimeters of mercury (mm Hg)
From page 71...
... to initiate fluid resuscitation from hemorrhagic shock in a sheep model. In their study, the infusion of HSD was followed by the infusion of lactated Ringer's solution to maintain hemodynamic function and urine output at prehemorrhage levels.
From page 72...
... Hypertonic saline solutions were shown to provide immunologic protection, whereas hypoosmolar lactated Ringer's solution as well as artificial colloids unregulated adhesion molecule expression, increased proinflammatory cytokine synthesis, and promoted cellular apoptosis (Coimbra et al., 1996; Junger et al., 1997a,b; Rhee, 1998~. The limits of hypertonic saline resuscitation include the fact that its efficacy is lessened in patients who receive an initial bolus of isotonic lactated Ringer's solution.
From page 73...
... In light of the continuing concerns of transportation of large crystalloid volumes required for resuscitation, the ability to recover mean arterial pressure and cardiac output in the field with small-volume HSD resuscitation confirms the value of this regimen as the initial treatment for hemorrhagic shock in the field. The added benefits of HSDrelated reductions in the total volume of fluid used for resuscitation may contribute to a decrease in the incidence of ARDS, MODS, and systemic inflammatory response syndrome currently associated with crystalloid resuscitation.
From page 74...
... The finding that lactated Ringer's solution and artificial colloids increase the levels of expression of adhesion molecules, promote the release of proinflammatory cytokines, and promote cellular apoptosis suggests that fluid resuscitation has significant immunologic consequences. It was of interest that hypertonic saline solutions, shown to stabilize arterial blood pressure and cardiac output with small-volume infusion, have been shown to have no deleterious effects on immune function or to promote programmed cell death.
From page 75...
... proposed modification of existing regimens of fluid resuscitation to more nearly mimic the composition of intravascular fluid. For example, the use of parenteral normochloremic carbonate (HCO3+~/CO2 saline would have a more physiologic ratio of sodium chloride, thus avoiding the risk of hyperchloremia.
From page 76...
... . Recommendation 3.3 Previous concerns regarding the detrimental effects of aggressive fluid resuscitation with large volumes of crystalloids suggested the need to examine both the immunologic as well as hemodynamic consequences of small-volume lactated Ringer's resuscitation.


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