General Principles for Fluid Therapy in Critical Care
K. Gary Magdesian
Current guidelines for replacement fluid therapy in human critical care emphasize the “fluid challenge” method, believed to be more effective and safer than traditional estimates of percent dehydration.1 The author's protocol of fluid administration in horses follows this same algorithm.
Considerations for the fluid challenge technique incorporate four primary decision phases: (1) type of fluid, (2) rate and volume, (3) goals or end points of fluid therapy, and (4) safety limits to fluid therapy.1. Types of fluids include crystalloids (isotonic, hypotonic, and hypertonic) and natural and synthetic colloids. There is much controversy and no consensus as to whether crystalloids or colloids are more effective or advantageous in human critical care.1 The advantages of both fluid types are capitalized on by using them together in the treatment of some cases of hypovolemia that have concurrent hypoproteinemia. Otherwise, because of cost differences and lack of demonstrated benefit of colloids as compared with crystalloids in terms of mortality for fluid resuscitation in critically ill human patients, the use of colloids cannot be recommended over crystalloids.2 Recent publications have suggested increased mortality and complication rates in humans receiving hetastarch as compared to crystalloids. See the Fluid Therapy for Diarrhea and Colitis in Horses section later in this chapter. Table 44.1 lists the composition of several commercially available crystalloids that are used in equine practice.
2. The rate of fluid therapy for replacement (i.e., treatment of hypovolemia) is based on the “fluid challenge” principles, whereby a 30- to 60-minute bolus of 10 to 20 mL of isotonic crystalloid per kilogram is administered with subsequent reassessment of perfusion parameters.1 This rate would be faster for animals dying of hypovolemic shock, with pressure bags sometimes being used for rapid delivery.
This fluid challenge method assumes that uncontrolled hemorrhage is not present because that would warrant hypotensive resuscitation instead, where the goal is a mean arterial pressure of 60 mm Hg and just enough perfusion pressure to perfuse organs. Perfusion parameters on the physical examination of horses and foals include mentation, heart rate, mucous membrane color, capillary refill time, jugular fill, extremity temperature (limbs, ears), and pulse quality. Blood or plasma lactate concentration, arterial blood pressure, urine output, and urine specific gravity are additional monitoring tools that aid in assessment for further fluid challenges. After the initial bolus, additional boluses—over 30 to 60 minutes depending on the degree of hypovolemia present—would be administered if perfusion parameters dictate a need for more fluid volume. These are repeated until signs of shock abate, a lack of improvement is noted with subsequent boluses, or fluid limits are reached (see later). Most animals require one to three of these boluses, and rarely are four required. Alternatively, or in addition to isotonic crystalloids, hypertonic saline (7% to 7.5%) can be administered at a rate of 4 mL/kg intravenously (IV) once. Plasma sodium concentration should be monitored, as hypernatremia can result. Because of their distribution that is limited to the central compartment, colloids are bolused at lower volumes than isotonic crystalloids, such as 3 to 5 mL/kg for hetastarch. Up to 10 mL of hetastarch per kilogram may be administered per day, being limited by development of dose-dependent coagulopathies, although concerns over a mortality rate increase and renal injury in human patients has markedly reduced the use of hetastarch in those patients.If after reassessment of the perfusion parameters additional resuscitative fluids are deemed necessary, another similar bolus is given, although each subsequent bolus is usually provided at a slightly slower rate unless the patient is markedly hypovolemic.
This is repeated until signs of hypoperfusion resolve (end points are achieved) or safety limits are reached and there is no further positive clinical response to fluid bolus administration, at which point inotrope and/or vasopressor therapy is indicated if hypoperfusion persists.3. The goals or end points of fluid therapy include both replacement and maintenance of fluid balance. Replacement refers to the replenishment of fluid deficits, primarily referring to those in the extracellular fluid compartment. Maintenance fluid therapy refers to the provision of maintenance fluid requirements to account for metabolism, insensible losses, growth, and ongoing losses. In general terms, replacement refers to replenishment of circulating volume and secondarily of interstitial fluid deficits; maintenance refers to provision of fluids after hypovolemia and dehydration have been corrected. Maintenance fluid therapy maintains both circulating volume and hydration status, including that of the intracellular compartment. In this section, replacement fluid
■ TABLE 44.1
Composition of Commercial Replacement and Maintenance Fluids
| Crystalloid | Sodium (mEq/L) | Potassium | Chloride | Calcium | Magnesium | Osmolarity (mOsm/L) | Organic Salt |
| Replacement | |||||||
| Lactated Ringer’s solution | 130 | 4 | 109 | 3 | 0 | 272-273 | 28 lactate |
| Saline (0.9%) | 154 | 0 | 154 | 0 | 0 | 308 | 0 |
| Ringer’s solution | 147-148 | 4 | 156 | 4.5 | 0 | 310 | 0 |
| Plasma-Lyte 148 or Plasma-Lyte A | 140 | 5 | 98 | 0 | 3 | 294 | 27 acetate 23 gluconate |
| Normosol-R | 140 | 5 | 98 | 0 | 3 | 294 | 27 acetate 23 gluconate |
| Maintenance | |||||||
| Plasma-Lyte 56 | 40 | 13 | 40 | 0 | 3 | 111 | 16 acetate |
| Normosol-M | 40 | 13 | 40 | 0 | 3 | 110 | 16 acetate |
| 45% NaCl + 2.5% dextrose | 77 | 0 | 77 | 0 | 0 | 280 | 0 |
| 5% dextrose | 0 | 0 | 0 | 0 | 0 | 252-253 | 0 |
is emphasized; the goals of replacement fluid therapy include rapid correction of hypovolemia by reversal of the signs of shock, including improvement or correction of seven perfusion parameters: tachycardia (except in some neonatal foals, which may not demonstrate tachycardia as a manifestation of hypovolemia), pale mucous membranes, prolonged capillary refill time, cold extremities, poor pulse quality, depressed mentation, and, in horses, reduced jugular fill time. Urine production is another positive sign indicating correction of fluid deficits and subsequent perfusion of the kidneys.
Dehydration, or the extravascular fluid deficit, is corrected more slowly than hypovolemia and is marked by reduced skin turgor (increased skin tent), dry mucous membranes, and dry corneal surface (reduced tear production). Additional goals of volume replacement include correction of hypotension, tachycardia, oliguria, and blood lactate concentration.1 A decrease in urine specific gravity (in the absence of renal failure), an increase in arterial blood pressure and CVP, and improvement in venous oxygen saturation are specific end points. The goals of maintenance fluid therapy are different than those of replacement fluid therapy; they are to maintain a normal degree of hydration by providing for ongoing losses, including insensible losses (respiratory, cutaneous evaporative losses) and any abnormal ongoing losses such as diarrhea or reflux. Maintenance fluid rates for horses vary with ambient temperature, use, diet, and metabolic status. In general, a reasonable starting point for maintenance fluid requirements includes 2 to 3 mL/kg/h for adult horses (possibly slightly lower if off feed) and 4 to 6 mL/kg/h for neonatal foals.3,44. The safety limits to fluid therapy are indicators of intravascular volume overload, including supranormal CVP, a decrease in arterial oxygen saturation (PaO2), and clinical indicators of volume overload and overhydration. Once maximal CVP is achieved (10 to 12 cm H2O in neonatal foals and 15 cm H2O in adult horses), replacement bolus fluid therapy must stop; if continued, edema may form as systemic and capillary hydrostatic pressures increase in response to further fluid boluses. A decrease in oxygen saturation in serial arterial blood samples, or in SpO2 measured with pulse oximetry, in a horse receiving fluid boluses may be consistent with the possible development of pulmonary edema; this may precede development of tachypnea, increased respiratory effort, or frank edema in large airways or nostrils.
Although no published reports address fluid overload in clinical equine patients, one experimental study evaluating hyperhydration before moderate-intensity exercise in horses suggested the development of arterial hypoxemia during exercise.5 These animals were administered oral fluids equivalent to 6% of body weight (approximately 26 L of isotonic fluid by nasogastric tube). Hyperhydration resulted in arterial hypoxemia, suspected to be caused by pulmonary edema associated with hyperhydration, during moderate-intensity exercise.5 Clinical indicators serving as limits to fluid therapy include visible subcutaneous edema and tachypnea; with optimal monitoring, fluid therapy will not be allowed to continue to this point. Another end point or limitation to fluid therapy is a lack of further improvement in perfusion parameters despite repeated fluid boluses. This would indicate that hypoperfusion is not solely due to hypovolemia and may require inotropes and/or pressor agents (e.g., dobutamine and norepinephrine, respectively). If safety limits are reached before the goals of fluid therapy are achieved, the next step is also to turn to inotrope and vasopressor therapy.Prevention of fluid overload should be emphasized to the same degree as provision of fluid therapy. Fluid overload and tissue edema are very detrimental to tissue and organ health, as are dehydration and hypovolemia.
See the Fluid Therapy for Diarrhea and Colitis in Horses section later in this chapter.