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Compendium December 2009 (Vol 31, No 12)

Perfusion Versus Hydration: Impact on the Fluid Therapy Plan

by Caroline Tonozzi, Elke Rudloff, DVM, DACVECC, Rebecca Kirby, DVM, DACVIM, DACVECC

    CETEST This course is approved for 3.0 CE credits

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    Creating a fluid therapy plan that is adequate to meet an individual patient's needs depends on identifying whether the animal has poor perfusion, is dehydrated, or both. This article reviews the body's fluid compartments, fluid dynamics, and the clinical parameters used to differentiate perfusion from hydration and create a fluid therapy plan.

    Water is the most important nutrient. It defines cell size and shape and provides necessary support for fibrin, collagen, and cells in tissue. In addition, it is the medium on which transport of nutrients, proteins, electrolytes, and cells throughout the body depends. The function of water is dynamic: it shifts from transport to support to intracellular metabolism, depending on the fluid compartment. When the body loses or redistributes water, the transportation, tissue support, and cellular processes can become impaired. The degree of impairment is typically proportional to the amount and rate of water loss.

    Fluid therapy is the principal method for correcting water deficits and blunting the effects of water imbalance. Inappropriate or inadequate fluid therapy can have a major effect on recovery and survival. Therefore, recognizing whether a fluid deficit is affecting transport of blood to the tissues (perfusion), tissue support and intracellular processes (hydration), or both is critical to implementing an effective fluid therapy plan for the patient.

    Knowledge of the normal composition and distribution of body water and the physiologic responses of the body to fluid deficits is essential to successful fluid therapy. This information is used to calculate the volume of fluid required, the rate of fluid administration, and the type of fluid needed.

    Body Water Composition and Distribution

    Water makes up 60% of the body weight of mammals.1 Total body water is mainly distributed between the intracellular and extracellular body compartments. The in-tracellular compartment contains 66% of the total body water, while the extracellular space contains 33%. The extracellular compartment is further divided into the interstitial and intravascular spaces. Of the total body water within the extracellular space, 75% is in the interstitium and 25% is in the intravascular compartment. The remaining 1% of total body fluid is trans-cellular, located in the synovial, peritoneal, pericardial, and intraocular spaces.2

    The intracellular and extracellular fluid compartments are separated by cell membranes. The vascular membrane, which separates the interstitial and intravascular spaces within the extracellular compartment, is composed of a thin layer of endothelial cells resting on a bed of collagen, fibrin, and sometimes smooth muscle, depending on the type of vessel. Most extracellular movement of water and solutes occurs at the capillary level.2

    The interstitial space comprises a macromolecular complex that contains water, collagenous molecules, glycoproteins, elastin, proteoglycans, and glycosaminoglycans. This matrix supports the capillaries and separates them from the cells, facilitates the transport or diffusion of oxygen and solutes between cells, and houses the lymphatic vessels (FIGURE 1). The interstitial environment gives organs their form.3

    Because the barriers separating the fluid compartments do not restrict water movement, additional forces must hold water within a compartment. Water moves across the vascular membrane as a result of the interaction of the physical forces represented in Starling's equation4:

    The characteristics of the vascular membrane, including the size of the interendothelial gaps (Σ) and the electrostatic charge of the gaps (filtration coefficient), also play a role in the movement of fluid and solutes between the capillaries and the interstitium. These traits become important in disease states because they can support or oppose the passage of large solutes across the vascular membrane.2

    Physiologic Responses to Fluid Deficits

    The volume and rate of fluid loss, as well as the composition of the fluid being lost, determine the severity of clinical signs associated with a deficit in any fluid compartment. Clinical signs can change as the equilibration shifts between body compartments. Small, slow isotonic volume losses, as with chronic, once-a-day vomiting, typically cause subtle clinical signs. Moderate or rapid isotonic volume losses, as with vomiting secondary to parvovirus or with hemorrhage, commonly manifest as obvious clinical signs reflecting the compartment(s) affected. Regardless of the rate of loss, large isotonic volume losses can be expected to lead to significant clinical signs.

    Intravascular Water Deficits

    A reduction in intravascular fluid volume (hypovolemia) can be a serious complication of a number of disease processes (TABLE 1). Hypovolemia manifests as abnormalities in perfusion, the process of nutrient and oxygen delivery by arterial blood to capillary beds in tissue. Changes in physical perfusion parameters include altered heart rate, capillary refill time (CRT), mucous membrane color, and pulse quality (TABLE 2). The loss of whole blood or plasma water results in reduced intravascular hydrostatic pressure and decreased baroreceptor stretch. The sympathetic system becomes the dominating force as vagal activity is decreased, leading to increased heart rate and contractility, together with peripheral vasoconstriction, in dogs.5

    In dogs with mild to moderate volume loss, clinical signs include red mucous membranes, rapid CRT (<1 second), and bounding pulses (i.e., compensatory shock,TABLE 2). When this response fails to improve oxygen delivery or there is a large volume loss, the sympathetic response intensifies, causing selective peripheral vasoconstriction with shunting of blood flow and tachycardia with increased cardiac contractility. Clinical signs associated with early decompensatory shock include tachycardia, weak/absent peripheral pulses, pale to white mucous membranes, and a CRT of <2 seconds. Late decompensatory shock manifests as organ malfunction (e.g., loss of tachycardic response, altered mentation, oliguria/anuria, hypothermia).6

    In contrast to dogs, cats with hypovolemic shock often present with bradycardia and hypothermia. Cats with underlying conditions such as significant pain, hyperthermia, tachyarrhythmia, or hyperthyroidism may present with tachycardia or normal body temperature (TABLE 2). It is postulated that hypothermia results in a reduced response of adrenergic receptors to catecholamines, playing an important role in fluid resuscitation techniques for cats.7 Rapidly infusing large volumes of fluid can result in signs of fluid intolerance after the body temperature returns to normal (BOX 1). Therefore, we recommend actively warming hypothermic cats after initiating fluid resuscitation. This practice minimizes the volume of fluid necessary for reaching perfusion end points.

    When plasma water loss causes an increase in the concentration of plasma solutes, an osmotic gradient develops between the plasma and interstitium (FIGURE 2). Water mobilizes from the interstitial space and redistributes into the plasma space. While correcting the osmotic gradient, this fluid shift can also cause an interstitial water deficit.

    Interstitial Water Deficits

    Interstitial water content is responsible for signs of tissue hydration and dehydration. Examples of disease processes complicated by interstitial dehydration are listed in TABLE 1 . Fluid loss from the interstitium raises the interstitial colloid osmotic pressure (COP) and electrolyte concentration and lowers the interstitial hydrostatic pressure. This favors the movement of fluid from intravascular and intracellular spaces into the interstitium (FIGURE 2).

    Clinical manifestations of interstitial dehydration are listed in TABLE 3 . Perfusion deficits do not typically result from mild to moderate interstitial dehydration. Acute interstitial fluid loss may not allow time for physical changes in interstitial compliance and shape. Ongoing interstitial water deficits reduce the support medium and alter the elasticity and shape of the tissues, causing them to become less compliant. This results in tenting of the skin when stretched and dryness of the mucous membranes and corneas.

    As fluids shift from the intravascular to the interstitial space, dehydration can also be associated with increasing packed cell volume (PCV) and total protein (TP). Plasma sodium and chloride concentrations can increase with the loss of hypotonic fluids or solute-free water. When extracellular water loss causes an increased concentration of interstitial solutes that cannot permeate the cell membrane, intracellular water moves into the extracellular spaces, leaving an intracellular water deficit (FIGURE 2).

    Intracellular Water Deficits

    Intracellular water deficits (intracellular dehydration) cannot be measured directly or determined by physical parameters. Intracellular fluid loss of any magnitude is associated with diseases that result in intravascular or interstitial hypernatremia due to loss of solute-free water or a dramatic increase in impermeable solutes. Clinical signs of altered mentation and seizures occur when brain cell function has been altered by cellular fluid shifts. Diseases that can result in intracellular dehydration with or without hypernatremia are listed in TABLE 1 .

    Clinical Signs Without Fluid Deficits

    There are several clinical situations in which changes in perfusion and physical parameters of hydration do not accurately reflect fluid balance in the intravascular or interstitial spaces. Adequate intravascular volume or hypervolemia may be present. Cardiac dysfunction, hypoxia, brain injury, and profound pain can result in signs typical of poor perfusion in the absence of an intravascular fluid deficit. The contributions of the heart, lungs, brain, and pain response to the cardiovascular system must be determined before initiating aggressive fluid resuscitation to avoid volume overload. Monitoring the central venous pressure or administering a small "test" fluid bolus can aid in determining whether hypovolemia is playing a role in the initiation and maintenance of poor perfusion (see Restoration of Perfusion Deficits).

    Chronic weight loss without dehydration can cause the loss of skin elasticity and metabolism in the fat pad around the eye, leading to skin tenting and retraction of the eyes within the sockets. However, mucous membrane and corneal moisture should remain normal, with any changes in the PCV and TP reflecting the underlying disease process rather than hemoconcentration.

    The Fluid Therapy Plan

    When the fluid compartments have been assessed and a fluid deficit has been identified, a fluid therapy plan is constructed by (1) selecting the appropriate fluids (crystalloids, colloids, or both) to administer; (2) determining patient-specific resuscitation end points or goals; (3) assigning the route and rate of infusion; (4) determining the time frame over which replacement is needed; and (5) employing appropriate monitoring techniques. Perfusion deficits are more life-threatening than dehydration; therefore, perfusion deficits must be corrected first. The decision regarding the rate and volume of fluids to administer is guided by monitoring physical parameters to achieve the desired clinical goals. This is called early goal-driven, goal-oriented, or end-point resuscitation.8,9 BOX 2 presents four case examples of fluid therapy plans and goals.

    Fluid Selection

    Crystalloids, natural colloids, and/or synthetic colloids can be used to replace fluid volume, depending on which fluid compartments have deficits and the rate of volume replacement required ( FIGURE 3 andFIGURE 4). Crystalloids are water-based solutions with small particles that permeate freely across the capillary membrane. A colloid solution is a crystalloid-based fluid that also contains molecules that are too large to pass through the endothelial gaps of the capillary membrane.


    The cornerstone of fluid resuscitation is the infusion of isotonic replacement crystalloids. "Isotonic" implies that the solutes (primarily sodium) are in concentrations similar to those of normal plasma and will not cause an osmolar water shift from blood cells to the plasma. "Replacement" implies that the fluid has sodium and chloride concentrations similar to those of the extracellular space. Buffer-containing crystalloids (e.g., Plasmalyte-A, Normosol-R, lactated Ringer's solution) contain gluconate and acetate, or lactate for metabolism to bicarbonate, and may restore the acid-base balance more rapidly than buffer-free isotonic crystalloids (e.g., 0.9% sodium chloride). Buffered replacement crystalloids are a reasonable choice when fluid therapy is first initiated and until an emergency laboratory database (e.g., PCV, TP, blood urea nitrogen, glucose, venous blood gases, electrolyte panel, lactate) can be obtained. Metabolic alkalosis, hyperkalemia, hyponatremia and hypernatremia, hypochloremia, and hypercalcemia may be better treated with 0.9% sodium chloride. Compared with other isotonic solutions, 0.9% sodium chloride causes less of an osmotic shift when treating animals with hypernatremia. In addition, the higher chloride concentration can rapidly correct hypochloremic metabolic alkalosis. Normal saline does not contain supplemental electrolytes that can exacerbate hyperkalemic and hypercalcemic conditions.

    Intravenous hypertonic crystalloids such as 7% hypertonic saline produce an osmotic gradient that promotes water movement into the intravascular space from the interstitium and intracellular space. The use of hypertonic crystalloids can cause profound and immediate intravascular volume expansion that dissipates at the same rate as expansion produced by isotonic crystalloids. If the interstitium or intracellular compartments are dehydrated, the use of hypertonic crystalloids is not recommended.

    The infusion of crystalloids immediately increases intravascular hydrostatic pressure and lowers the intravascular COP (through dilution), favoring movement of fluid through the capillary membrane into the interstitium. In normal vessels, 75% or more of infused crystalloids redistribute into the interstitial space within 1 hour.10 This property makes isotonic crystalloids ideal for interstitial volume replacement and maintenance.


    Colloid fluids augment intravascular fluid and increase intravascular volume.11,12 A colloid that contains molecules large enough to remain within the vessel and increase the vascular COP over the anticipated increase in hydrostatic pressure from fluid infusion can be beneficial in critical illnesses associated with endothelial cell dysfunction.13 The ideal colloid would contain molecules larger than the gaps between the endothelial cells and be readily available, affordable, hypoallergenic, and free of adverse effects. No single colloid fulfills all these criteria; however, available natural and synthetic colloids fulfill some.

    Natural colloids increase the COP mainly through albumin. Albumin infusion using species-specific plasma products (5% albumin) can be cost prohibitive and carries a risk for transfusion reaction. In addition, these fluids pass into the interstitium when the endothelial gap size is larger than the albumin molecule, and large volumes are required to effectively increase the COP.14 Plasma products are useful as adjuncts to other colloids to provide albumin, coagulation proteins, and antithrombin.15 Although its use in veterinary medicine has been limited, concentrated human albumin (25% albumin; 0.1 to 0.25 mL/kg IV) can be an effective colloid in dogs and cats.16,17 The strong COP effect (200 mm Hg) can initially cause interstitial fluid depletion when the product is given without crystalloids.18 Human albumin has also been associated with a risk of type III hypersensitivity in dogs.19

    Synthetic colloids such as dextran 70 and 6% hetastarch (HES) are readily available, require no preparation, are less expensive than blood products, and rarely cause immunologic reactions. When vasculitis and hypoalbuminemia are prominent features of the disease process (e.g., systemic inflammatory response syndrome [SIRS]), the colloid molecular size must be larger than albumin (62,000 to 69,000 Da).20 Dextran 70 (average molecular weight: 70,000 Da) might extravasate in this situation.21 HES contains a large proportion of high-molecular-weight colloid molecules (average 450,000 Da) as well as smaller colloid molecules. The larger molecules can sustain intravascular COP when the gaps between the endothelial cells increase.20

    The use of synthetic colloids has been associated with adverse effects in patients with hemostatic abnormalities (e.g., von Willebrand's disease). In patients with coagulation abnormalities, large doses of these fluids can interfere with platelet function and prolong clotting times.22 In cases of increased vascular permeability, plasma proteins and small synthetic colloid molecules leak into the interstitium, raising the interstitial COP. It is important to maintain the intravascular COP above the interstitial COP to avoid the movement of intravascular fluid into the interstitial space.

    The use of colloid therapy in situations of increased lung permeability is hotly debated in human medicine. Recent recommendations concerning fluid management in sepsis-related acute lung injury and respiratory distress syndrome have stressed the need for judicious fluid support to maintain organ perfusion, and the use of colloids in hypoproteinemic patients is now considered an acceptable adjunct to therapy.23

    The administration of high-molecular-weight synthetic colloids results in the intravascular retention of large colloid molecules, an elevation in intravascular COP, and a fluid shift from the interstitium into the intravascular space. The intravascular volume increases by more than the volume of synthetic colloid administered. This allows the estimated necessary crystalloid volume to be decreased by 40% to 60%.24 When multiple colloid fluids are needed, they should be administered consecutively rather than simultaneously to avoid sudden, dramatic elevations in hydrostatic pressure.

    Hemoglobin-Based Oxygen-Carrying Solutions

    Hemoglobin-based oxygen-carrying solutions such as Oxyglobin (Biopure, Cambridge, MA; average molecular weight: 150,000 Da) have a colloid osmotic effect and transport hemoglobin-bound oxygen into tissue beds where the flow of erythrocytes may have been obstructed.25,26 Veterinarians who have access to Oxyglobin should consider its use for volume expansion and oxygen transport in patients with circulatory shock, anemia, or maldistribution of blood flow (e.g., trauma, SIRS). Oxyglobin can also cause mild vasoconstriction, which may be of benefit in hypovolemic and distributive shock. It has universal compatibility and is unlikely to transmit hematogenous diseases. Erythrocyte replacement may still be required if significant anemia is present, and the red color of the solution can interfere with enzyme chemistry analyses. Adverse effects may include pulmonary edema, vomiting, and diarrhea; associated hypertension can be minimized by slow administration, titrated to effect.

    Restoration of Perfusion Deficits

    Clinical signs of perfusion abnormalities (TABLE 2) reflect an intravascular volume deficit in the absence of cardiac dysfunction, hypoxia, brain injury, and profound pain. Adequate perfusion of peripheral tissue depends on sufficient intravascular volume. Perfusion parameters must be monitored to evaluate the effectiveness of the fluid therapy plan. Intravascular volume loss through hemorrhage reduces intravascular hydrostatic pressure. Intravascular plasma protein and water loss through increased capillary permeability (e.g., SIRS) reduces intravascular COP and hydrostatic pressure. Losses of fluid into a third body fluid compartment (not the interstitium) cause fluid to translocate from the interstitial compartment into the vascular compartment, resulting in concurrent interstitial fluid deficit and dehydration.

    Pain management with analgesics is an important part of the initial resuscitation and monitoring plan. When present, severe hypoxia, cardiac arrhythmias, and central nervous system disease must be treated early in the course of resuscitation. If hypovolemia is suspected in a dog with cardiac or neurologic dysfunction or hypoxia, we recommend a fluid challenge. This involves a "test" intravenous bolus infusion of 10 to 15 mL/kg of isotonic replacement crystalloids and 3 to 5 mL/kg of HES to see whether perfusion parameters improve. If the fluid challenge is effective and the parameters improve, careful fluid resuscitation is continued (FIGURE 3).

    A combination of synthetic colloids and crystalloids can provide prolonged and rapid intravascular volume replacement, which can lead to resolution of interstitial dehydration ( FIGURE 3 and FIGURE 4 ). To avoid fluid overload, the minimum volume of each fluid necessary to reach the desired end points should be used. If hypertonic (7%) saline solution is used for rapid intravascular volume replacement, a 4-mL/kg dose can be combined with a colloid to improve intravascular volume expansion.27

    If hypotension persists despite adequate volume replacement and return of body temperature to normal, vasopressors and/or positive inotropes should be considered. We have successfully used infusion of small volumes of Oxyglobin, based on its colloidal and vasoconstrictive properties, to augment arterial blood pressure and oxygen delivery in persistently hypotensive dogs and cats. In dogs, Oxyglobin can be titrated in 3- to 5-mL/kg increments to desired end points, up to a total of 30 mL/kg; in cats, 1- to 3-mL/kg increments can be administered slowly to effect, up to 10 mL/kg. As with any colloid therapy, careful monitoring is necessary to identify early signs of fluid intolerance.

    Once the desired end points of resuscitation have been reached, we use a constant-rate infusion of HES (20 mL/kg/d) or Oxyglobin (10 mL/kg/d in cats; 30 mL/kg/d in dogs) in conjunction with crystalloids as part of the intravascular fluid maintenance program until recovery is certain.28,29 The crystalloid infusion rate is reduced when the end points are met to the minimum amount required to provide rehydration, maintenance fluid needs, and replacement of ongoing losses.


    Interstitial Dehydration

    Common clinical parameters used to estimate interstitial dehydration include mucous membrane moisture, skin turgor, eye position within the orbit, changes in body weight, and emergency laboratory database results, including the PCV/TP (TABLE 3). Isotonic replacement crystalloids are used to replenish interstitial fluid deficits. The ideal route for rapid rehydration is intravenous or intraosseous administration, but the subcutaneous route can be used when the fluid deficit is minimal. The volume of isotonic replacement crystalloid fluids necessary to rehydrate the interstitial space is estimated using the following calculation:

    The volume of fluid is divided by the number of hours needed to replenish the interstitial fluid. Acute losses can be corrected over 6 to 12 hours, whereas more chronic conditions causing dehydration should be corrected over 12 to 48 hours.13 When interstitial dehydration occurs in a patient with cardiac and renal disease, careful administration of fluids is warranted, with repeated evaluation for signs of volume overload (BOX 1).30 Low urine output and heart failure or polyuric renal failure with hypertension may require less fluid to be administered over a longer period of time. Some experts advocate the use of low-sodium fluids (e.g., 0.45% saline solution + 2.5% dextrose) to rehydrate patients with cardiac disease.31

    Intracellular Dehydration

    Treatment of intracellular dehydration requires the administration of intravenous fluids that will primarily move into the intracellular compartment, such as solute-free water. To prevent hemolysis from intravenous infusion of solute-free water, 5% dextrose (D5W) is added to create an osmotic gradient sufficient to prevent movement of water into the circulating blood cells. As the dextrose is metabolized, 66% of the water moves into the interstitium and then the intracellular compartment. Other solutions with solutes that are metabolized (e.g., partial parenteral nutrition fluids) can be used to provide more water than solutes. Half-strength crystalloid solutions (e.g., 0.45% saline solution or 50%-strength lactated Ringer's solution) can also be used to slowly restore water in the intracellular space without causing cell lysis.

    Perfusion and hydration must be restored before the volume of water needed to replace intracellular losses is determined. The serum sodium level reflects the concentration of solute-free water, with hypernatremia in a normally perfused and interstitially hydrated patient indicating a deficit of solute-free water. The volume of solute-free water necessary to restore the cellular water balance is calculated by determining the amount of sodium excess and the volume of water distribution32:

    This calculated deficit should be replaced very slowly (over 24 to 48 hours) with D5W or half-strength solutions to avoid cellular swelling and lysis. A general rule of thumb is to decrease sodium levels by 0.5 mEq/L/h.33 If hypernatremia occurs in conjunction with congestive heart failure or oliguric renal failure, loop diuretic administration may also be indicated.31



    Bedside methods of monitoring perfusion parameters can be invasive or noninvasive, continuous or intermittent, physical, and biochemical (TABLE 2). Heart rate can be checked using cardiac auscultation, continuous electrocardiography, or Doppler monitoring. Pulse rate is compared with heart rate to identify dysrhythmias. A "bounding" or weak pulse may indicate increased systemic vascular resistance, decreased stroke volume, or decreased cardiac performance.34

    Arterial blood pressure, urine output, lactate levels, and central venous pressure can be tracked in patients that need more extensive monitoring. Arterial blood pressure should always be assessed in conjunction with heart rate. A normal arterial blood pressure does not signify normal perfusion when the heart rate is elevated. When the heart rate is normal, the optimal arterial blood pressure is approximately 120/60 mm Hg, with a targeted mean arterial pressure of approximately 80 mm Hg. Indirect blood pressure measurements can be obtained with Doppler or oscillometric monitors. Patients that are subject to rapid decompensation require intensive monitoring and may benefit from direct arterial catheterization to track blood pressure.

    Urine output provides an indirect estimate of renal perfusion when renal function is adequate. Normal urine production depends on a mean arterial pressure >60 mm Hg. Lower mean arterial pressures result in oliguria, which can progress to acute renal failure. Target urine output in critical patients is 1 to 2 mL/kg/h, depending on the patient's urine concentrating ability. This volume increases if fluid diuresis is prescribed or polyuric renal disease is present. Patients with decreased urine output must be evaluated for oliguric/anuric renal failure, hypotension, hypovolemia, and urinary tract obstruction.

    The plasma lactate concentration has been used in human and veterinary medicine as a marker of global tissue perfusion.35,36 Hyperlactatemia in a critically ill animal is usually associated with conditions causing inadequate tissue perfusion, hypoxemia, increased tissue oxygen demands, decreased hemoglobin concentration, or a combination of these factors. The lactate level can also increase with severe hepatic dysfunction and intense muscle activity. A goal of resuscitation is to return the blood lactate value to normal; however, a normal serum lactate concentration does not guarantee adequate regional tissue perfusion.

    Central venous pressure (CVP) measurement can provide information for estimating intravascular volume. Placement of a central venous catheter early in resuscitation can help guide fluid therapy. In the absence of cardiac disease, hypovolemia causes low CVP (<1 to 2 cm H2O). Elevated CVP (>8 to 10 cm H2O) can indicate volume overload, pleural space disease, right heart dysfunction, or pulmonary artery obstruction. The ideal CVP after fluid resuscitation is 5 to 8 cm H2O. When the CVP is normal or elevated and clinical signs of poor perfusion persist, causes of nonresponsive shock should be evaluated and vasoactive or inotropic agents administered to further promote perfusion.


    Interstitial hydration status is monitored by evaluating changes in mucous membrane and corneal moisture, skin turgor, body weight, respiratory rate and effort, and PCV and TP levels. Signs of interstitial fluid overload are listed in BOX 1 .

    Intracellular hydration is monitored by ob-taining serial serum sodium values. The serum sodium concentration is monitored frequently to prevent rapid changes. Consequences of correcting serum sodium concentrations too quickly include mental dullness, seizures, coma, and death.37 Chronic need (>48 hours) for crystalloid infusion to maintain hydration may necessitate a change to maintenance fluid therapy using Normosol-M or partial parenteral nutrition, which contain less sodium and potassium.


    Perfusion and hydration parameters are used to assess the intravascular, interstitial, and intracellular body water compartments. Perfusion deficits related to hypovolemia must be corrected before rehydration of the interstitial and intracellular compartments. Isotonic crystalloids are used during fluid replacement, and colloids can be added for intravascular volume replacement. When end-point parameters have been achieved, close monitoring is necessary to identify early signs of decompensation or fluid intolerance.

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    Dr. Rudloff discloses that she has received financial support from Abbott Animal Health.

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