Figure 5-1 depicts the cat’s body fluid compartments. The body’s two main fluid compartments are the intracellular fluid (ICF) and the ECF. Approximately 66% of functional total body water is located within the ICF compartment, and 33% is in the ECF compartment.

FIGURE 5-1 Body fluid compartments of the cat. The body’s two main fluid compartments are the intracellular fluid (ICF) and the extracellular fluid (ECF). Approximately 66% of functional total body water is located within the ICF compartment, and 33% is in the ECF compartment.

The ICF is, of course, not a single compartment but rather a conceptualization of the result of combining the very small volumes of a body’s trillions of cells as one. This is useful for understanding physiology because of commonalities of ICF composition and behavior. The fluid inside cells is high in potassium (K⁺) and magnesium (Mg⁺⁺) and low in Na⁺ and chloride (Cl⁻) ions. Additionally, fluid inside all cells will respond similarly to tonicity changes in the ECF.

The ECF space is composed of four main subcompartments: interstitial, intravascular, transcellular, and bone and dense connective tissue. The intravascular fluid is that which is contained within blood vessels; it contributes only 8% to 10% of total body water (5% of body weight) and has been estimated to be approximately 45 mL/kg in cats.¹⁰

The interstitial compartment refers to that portion of the ECF located outside of the vascular space. Like the ICF, this is not a single space but rather a conceptualization, or “virtual space,” that would be created if all the interstitial fluid spaces were to be combined. It contributes approximately 22% to 24% to total body water (15% of total body weight).

The fluid of bone and dense connective tissue provides about 15% of the total body water. However, this fluid is mobilized very slowly, decreasing its importance when considering the effects of acute fluid interventions. Transcellular fluid is a normally small compartment that represents all those body fluids that are formed from the transport activities of cells. It is contained within epithelium-lined spaces. It includes cerebrospinal fluid (CSF), gastrointestinal fluids, urine in the bladder, aqueous humor, and joint fluid. The electrolyte compositions of the various transcellular fluids are dissimilar, but they are small in aggregate volume. However, fluid fluxes involving gastrointestinal fluid can be significant in disease.

The water in bone and dense connective tissue and the transcellular fluids, because of their slow mobilization, are subtracted from the total ECF volume to yield the functional ECF.

It is important to note that when excess fluid builds up in transcellular or interstitial compartments in which fluid volume are normally small, the process is termed third spacing. Excess fluid in the peritoneal space, pleural space, or gastrointestinal tract can add considerably to body weight, while diminishing the effective ECF volume.

Fluid Movement in the Extracellular Fluid Compartment

The water in the body’s ECF compartments is in a constant state of flux. Fluid moves across the capillary membrane, which is composed of endothelial cells that contain gap junctions through which fluid and solutes can flow. Solutes dissolved in fluid move from an area of higher to lower concentration along concentration gradients by the process of passive diffusion. The factors that regulate this transport of fluid and the electrolytes and other molecules it contains are called Starling forces (Box 5-1). The key factors are the hydrostatic and colloid oncotic pressure gradients between the intravascular and extravascular spaces. The hydrostatic pressure is greater in the capillary than in the interstitium, and the gradient favors fluid movement (filtration) out of the capillary. The colloid oncotic pressure, determined by protein concentration, is also greater in the capillary, and this tends to draw fluid into the capillary. Simplistically, at the beginning of the capillary the high hydrostatic pressure results in fluid egress into interstitium. As the fluid leaves along the length of the capillary, the hydrostatic pressure falls and the colloid oncotic pressure increases, resulting in fluid reentry into the capillary lumen toward the end of the capillary. Fluid also leaves the interstitial compartment by way of the lymphatics.

BOX 5-1 Starling Forces

The Starling forces are defined by the equation J_v = K_f([P_c − P_i] − σ[π_c − π_i]) relating to the following six variables: capillary hydrostatic pressure (P_c), interstitial hydrostatic pressure (P_i), capillary oncotic pressure (π_c), interstitial oncotic pressure (π_i), filtration coefficient (K_f), reflection coefficient (σ).

In the equation, ([P_c − P_i] − σ[π_c − π_i]) is the net driving force, K_f is the proportionality constant, and J_v is the net fluid movement between compartments.

By convention, outward force is defined as positive, and inward force is defined as negative. The solution to the equation is known as the net filtration or net fluid movement (J_v). If positive, fluid will tend to leave the capillary (filtration). If negative, fluid will tend to enter the capillary (absorption). This equation has a number of important physiologic implications, especially when pathologic processes grossly alter one or more of the variables.

Fluids in the ECF move continuously between the vascular space and the interstitial space across the capillary endothelium to achieve tissue perfusion. Edema results when the balance of the hydrostatic and colloid oncotic pressure gradients shifts such that fluid egress from the capillary is favored. All of the following promote edema formation: (1) decreased plasma oncotic pressure, (2) increased capillary hydrostatic pressure, (3) increased capillary permeability, and (4) lymphatic obstruction. The other key requirement for edema formation is Na⁺ retention: an increase in the ECF Na⁺ content.

Fluid Movement Between the Intracellular Fluid and Extracellular Fluid Compartments

The ICF and ECF are separated by cellular membranes. The protein components of these membranes give them substantial and rapid permeability to water while carefully controlling their permeability to solutes such as ions. Cell membranes are also flexible. Thus, when water flows into or out of cells, those cells expand or shrink, respectively. Hydrostatic pressure, therefore, does not play a significant role in fluid movement between ECF and ICF compartments, because osmosis results in water flow rather than the development of pressure. Osmotic water flow occurs wherever there is a gradient of impermeable solute (such as Na⁺) across a water-permeable membrane (the body cell membranes).

In the body the ECF and ICF compartments are always in osmotic equilibrium, even though the composition of the fluids within them is very different. Water flows into or out of cells and changes their volume when an osmotic gradient exists between the ICF and ECF compartments.

Perfusion

Perfusion refers to the process in which blood carries oxygen and nutrients to body tissues and organs and transports waste products of cellular metabolism away. Perfusion is optimized when an animal is in a state of normal fluid balance. Oxygen delivery is a critical part of perfusion and is dependent on the animal’s cardiac output and the oxygen-carrying capacity of the blood. Cardiac output is a function of heart rate and stroke volume. Stroke volume depends on ventricular preload, ventricular afterload, and contractility. The amount of blood that enters the ventricle, causing the ventricular wall to stretch, thus affects the ventricular preload because the amount of wall stretch is directly proportional to the force of contraction. When there is adequate circulating volume, cardiac preload on the healthy ventricle results in a contraction of appropriate force. By contrast, in a cat with hypovolemia cardiac preload will be diminished, thus decreasing the force of ventricular contraction. Intravenous fluid therapy can affect cardiac preload by replenishing intravascular fluid volume in a hypovolemic animal.

Salt Balance: Disorders of ECF Volume

Sodium Content

The Na⁺ content of the body determines the volume of the ECF and total body fluid volume. It does this because the osmolality of body fluids is regulated within a very narrow range. If Na⁺ ions (always with an accompanying anion) are added to the ECF space, more water molecules must be added to ECF space in the same proportion or the osmolality will increase beyond the relatively narrow range compatible with health and normal cellular function. Thus increasing the number of Na⁺ ions in the ECF (the Na⁺ content) increases the ECF volume. Similarly, if Na⁺ ions are removed from the ECF space, water molecules must leave in proportion, resulting in a decreased ECF volume, or the fluid’s osmolality would decrease beyond that which the body’s regulatory mechanisms will allow in health. In that sense, the Na⁺ content of the ECF fluid space determines its volume.

Regulation of Sodium Balance

Regulatory mechanisms exist to control both Na⁺ content and Na⁺ concentration ([Na⁺]), and they are interrelated. Body Na⁺ content is regulated by mechanisms that control the renal excretion of Na⁺ and which operate in response to body fluid volume and not [Na⁺].⁹ Control of [Na⁺] is determined by the osmoregulatory control mechanisms.

Evolutionarily, it appears that salt was a scarce commodity. Thus the kidney has evolved mechanisms to conserve salt. Na⁺ excretion in the urine can vary over 500-fold depending on Na⁺ intake and body need. The homeostatic mechanisms that control Na⁺ content are poorly understood. Regulation is generally a comparatively slow process. For example, many hours will pass before excesses in Na⁺ content (e.g., when isotonic saline is infused) are corrected by increased renal Na⁺ excretion. In contrast, excesses or deficiencies of water relative to Na⁺ (changes in [Na⁺]) activate the osmoregulatory mechanisms and are dealt with very rapidly. Many physiologists believe that a set point for Na⁺ regulation does not exist. Rather, Na⁺ is retained in low volume states until the volume deficit is corrected.¹²

Sodium excess results in augmented ECF volume, which increases urinary Na⁺ excretion. A useful analogy is a bucket with a hole in its side: When volume is at or below the hole, Na⁺ excretion is minimal while the bucket fills to the level of the hole. Once there, the inflow equals the outflow. When the volume of the bucket is above the hole (ECF expansion), the pressure of fluid in the bucket drives the fluid to flow out of the hole more quickly. For example, when dietary Na⁺ intake is increased, it takes several days to reach a new steady state of neutral Na⁺ balance.

The following factors are known to affect renal Na⁺ excretion:

1 Arterial hypertension

2 Tubuloglomerular feedback

3 Circadian rhythm

It is suspected that others also exist. The sensors (afferent signals) in the regulation of Na⁺ excretion are thought to include intrathoracic volume receptors, atrial pressure receptors, arterial baroreceptors, intrarenal baroreceptors, the macula densa, hepatic volume receptors, CSF volume receptors, and possibly tissue receptors. The mediators of Na⁺ conservation or excretion include the sympathetic nervous system, the renin–angiotensin–aldosterone system (RAAS), vasopressin, atrial natriuretic peptide (ANP), renal prostaglandins, the kallikrein–kinin system, nitric oxide, and renal pressure and flow phenomena (glomerular filtration rate [GFR], renal blood flow, and arterial pressure).

Salt excess states include congestive heart failure, nephrotic syndrome, hepatic cirrhosis, hyperaldosteronism, Na⁺ channel defects, and pregnancy. In the pathogenesis of certain salt-retaining states, reference is made to the effective plasma volume. This is not a measurable quantity, and the concept lacks a precise definition. It refers to the “fullness” of the vascular volume. It is the portion of the vascular volume that is being sensed by those mechanisms that regulate body fluid volume. An inadequate effective circulating volume is inferred when salt-retaining mechanisms are activated.

Salt-deficient states are secondary to a number of disease conditions that result in losses of Na⁺ or inadequate intake. Extrarenal losses are localized to diseases of the gastrointestinal tract, skin, respiratory tract, and third space losses. Renal salt loss may occur with the following:

1 Diuresis (e.g., diuretic phase of acute tubular necrosis, postobstructive diuresis, or the use of diuretic medications)

2 Intrinsic renal disease (e.g., chronic renal failure, Fanconi syndrome, Bartter syndrome)

3 Defects in the RAAS system (e.g., hypoadrenocorticism, hyporeninemic hypoaldosteronism)

4 Disorders resulting in excesses of ANP

The use of high-sodium, isotonic fluid types in fluid therapy is thus primarily for the administration of Na⁺. They augment the total ECF Na⁺ content and thus expand the functional ECF volume, both vascular and interstitial.

Water Balance: Disorders of Sodium Concentration

Permeant and Impermeant Solutes

The next important concept to be understood is that of water balance. Cells must be in osmotic equilibrium with the fluid that surrounds them, insofar as their membranes are permeable to water. Although extracellular and intracellular fluids have very different compositions, they must have the same total solute concentrations because of the free movement of water. Looking at this concept “in reverse,” the water concentration of the ECF and the ICF must be the same. Inequalities of water concentrations in body fluid compartments can exist only transiently because water movement occurs rapidly to correct these inequalities. This basic concept underlies an understanding of fluid movement between intracellular and extracellular compartments during intravenous fluid therapy.

The concentration of solutes in fluid defines the solution’s osmolality. Because cell membranes are water permeable and water movement will occur until solutions on either side of a membrane are iso-osmolar, the osmolality of plasma reflects the osmolality of the body fluid in total. It is important to distinguish between permeant and impermeant solutes. Permeant solutes (e.g., urea) move freely across cellular membranes and thus do not induce net water movement across cell membranes when they are introduced into a solution; they are termed ineffective osmoles. Impermeant solutes (e.g., Na⁺) do not freely move across cell membranes and do induce water movement when introduced into a solution; thus they are effective osmoles.

Tonicity

The term tonicity refers to the effect a solution has on cellular volume. Hypertonicity results when impermeant solutes are added to the ECF; this promotes cellular dehydration. Hypotonicity results from a decrease in the concentration of impermeant solutions; this results in water movement into cells and cellular swelling. Hypertonic solutions are always hyperosmolar. The reverse is not always the case: Hyperosmolar solutions are not necessarily hypertonic because ineffective osmoles contribute to osmolality but not tonicity.

Plasma [Na⁺] is the key determinant of the osmolality of body fluids. Glucose and urea make minor contributions under normal circumstances. Plasma osmolality may be calculated using the following equation:

The preceding equation is a simplification because it does not take into account the fact that plasma is only 93% water; that sodium salts are not completely dissociated in solution; or that calcium, magnesium, and potassium salts also contribute. However, these factors appear to cancel out because experimental evidence demonstrates that calculated osmolality and measured osmolality are in close agreement in normal patients.

Plasma [Na⁺] reflects the plasma tonicity very well in normal patients. Urea is an ineffective osmole because it equilibrates freely across cell membranes and does not induce fluid shifts. Glucose normally can move across cell membranes in normal patients in the presence of insulin; therefore it is usually an ineffective osmole, similar to urea. In diabetic patients lacking insulin, it becomes an effective osmole. Thus plasma [Na⁺] predicts plasma tonicity when the glucose concentration is known. In hyperglycemia water leaves the cells because of the hypertonicity of the ECF. This serves to dilute the Na⁺, and hyponatremia is observed.

It is important to remember that serum [Na⁺] does not reflect body salt balance. Salt balance determines ECF volume. Serum [Na⁺], instead, reflects the state of water balance. The term osmoregulation refers to the control of body fluid tonicity. By stabilizing body fluid tonicity, osmoregulation thus controls cell volume. Osmoreceptors are, in fact, hypothalamic cells that sense their own cell volume. Changes in plasma osmolality sensed by these cells affect secretion of arginine vasopressin (antidiuretic hormone; ADH). ADH is the primary regulator of renal water excretion. Changes in plasma osmolality also strongly affect the thirst mechanism. This is why patients with central diabetes insipidus, who thus lack ADH, are able to maintain a relatively normal osmolality provided they have access to water and the ability to drink.

Regulation of Water Balance

In contrast to salt balance, which is controlled by many factors and has a relatively slow response to changes in effective plasma volume, plasma osmolality is very tightly regulated. When plasma osmolality is altered, changes in thirst and ADH secretion, and the resulting renal response, are brisk.

In addition to plasma osmolality, hypotension and hypovolemia also stimulate ADH release and thus this is a point where regulation of salt and water balance are interrelated. ADH release is not as sensitive to hemodynamic stimuli as it is to changes in osmolality; however, when the hemodynamic stimulus is sufficiently strong, the ADH response will be of higher magnitude. In the presence of a significant volume deficit, decreased water excretion by the kidney will in fact act to increase volume at the expense of a decrease in plasma osmolality.

The primary function of ADH is to increase the water permeability of the luminal membrane of the collecting duct of the nephron. ADH, through a second-messenger system, causes water channels called aquaporins to be inserted into the cell membrane. Water reabsorption in the collecting duct occurs through these channels, thus allowing the kidney to conserve water.

Understanding Fluid Losses

Sensible and Insensible Fluid Losses

Sensible fluid losses are those that can be measured and include fluid lost in the form of urine, feces, vomitus, body cavity effusions, and wound exudates. It is important in seriously ill patients actually to quantify these losses and incorporate them into the fluid prescription. For example, urine output can be determined by collecting voided urine or by weighing the bedding or litter when dry and again after urination. Similarly, vomitus or diarrhea can be weighed to allow the clinician to estimate fluid loss, given that 1 g is approximately equivalent to 1 mL water. For wounds with large volumes of exudate, an animal’s bandage material can be weighed before and after use to create a fluid loss estimate. For patients with drains or chest tubes in place, the amount of fluid produced from these devices can also be measured.

Insensible losses are those that cannot directly be measured. They include largely solute-free water in evaporative respiratory, sweat, and salivary losses. This classical definition of insensible losses is sometimes replaced with a clinical definition that includes fecal water loss. This is because the amount of normal daily fecal water loss is small and is rarely measured.¹⁶

As a gross approximation, sensible fluid losses account for half of a healthy animal’s daily fluid requirement and insensible losses account for the other half. However, this partitioning is variable and is species and environment dependent. For example, dogs as a species may have a higher percentage of insensible losses compared with cats because of the greater use of panting for thermoregulation. However, cats may have considerable salivary losses if they have increased grooming or lick their fur to promote evaporative cooling in hot weather.⁷

Insensible fluid losses are generally considered to be solute-free water because respiratory losses are the major contributor in small animal species, including cats. Insensible losses are estimated to be 12 to 30 mL/kg/day, depending on the study and definition.¹⁶

In contrast to insensible losses, sensible fluid losses do contain solutes. Although a necessary oversimplification, this explains why maintenance fluid types are hypotonic. They replace the solute-free water of insensible losses and the solute-containing water of sensible losses. As a matter of practicality, given these estimates and variable definitions, it is reasonable to assume that half of daily maintenance fluids are to offset normal levels of obligate urine output required for daily solute excretion and are solute-containing fluid losses, and the other half, accounting for everything else, are solute-free water losses. This is important clinically when adjusting the fluid prescription for “ins and outs” because it provides a method to estimate how much of measured hourly urine production is abnormal losses in polyuric patients (who have excessive ongoing urinary fluid loss that must be met by the replacement portion of the fluid prescription) and how much is normal obligate urine (and thus met by maintenance portion of the fluid prescription).

Body Weight and Fluid Losses

Total body water remains essentially the same day to day in a healthy animal. However in disease, excessive loss of fluid can occur associated with hemorrhage, vomiting, diarrhea, burns, fever, effusions, wound exudates, polyuria, and panting. Because rapid changes in body weight, over the span of hours to a few days, are largely due to changes in total body water, changes in an animal’s weight are an invaluable tool in the assessment of an animal’s hydration status. Because of the relative small size of cats, weighing animals on scales that can accurately detect changes of a few ounces or several grams (human pediatric scales) are very important.

Relationship to Lean Body Mass

Because lean body mass is so important in determining an animal’s daily fluid need, resting energy requirement (RER), or daily caloric requirement, is used to calculate an animal’s metabolic water requirements: To metabolize 1 kilocalorie of energy, 1 mL of water is consumed. As such, calculation of an animal’s RER can be extrapolated to determine the volume of fluid in mL required in a 24-hour period. Several equations may be used to calculate RER and hence water requirement.⁵ The following is one of the most commonly used:

This formula is accurate for animals weighing more than 2 kg and less than 25 kg and thus is applicable to adult domestic cats. Kittens and cats weighing less than 2 kg require the use of a different formula:

Terminology of Body Fluid Balance

The terminology used to describe body fluid balance is at times unfortunately vague. Dehydration refers to a decrease in total body water: loss of fluid from the ICF and ECF compartments. However, the physical examination findings used to assess hydration, such as skin tenting and mucous membrane dryness, are specifically assessments of the ECF volume and subject to significant individual variation and inaccuracy. Thus when clinicians suggest that a patient “appears dehydrated,” they are referring specifically to clinical signs of ECF volume depletion. This is to be distinguished from hypovolemia, which refers to inadequate circulating intravascular fluid volume. The distinction is important because hypovolemia is a much more time-sensitive condition requiring rapid, aggressive treatment.

Assessment of Fluid loss

Patients can be assumed to have a decrease in total body water in the presence of known excessive net losses, such as those produced by vomiting, diarrhea, anorexia, and marked polyuria, even without a demonstrable increase in skin tenting and mucous membrane dryness, which are detectable only when 4% to 5% of total body weight has been lost. Humans report headaches with dehydration, and presumably this may reflect some of the general lethargy seen in volume-depleted cats. At 7% total body weight loss, mild tachycardia could also be present. At 10% total body weight loss, the patient might also have a palpably decreased pulse pressure. Signs of very severe total body water loss are sunken eyes, dry corneas, and altered mentation. Overt hypovolemia will occur with severe fluid loss (>12% body weight), even when chronic. It is important to note at this time that lethargy can be present with both underhydration and overhydration. This is particularly important in cats with oliguria because they are readily susceptible to overhydration.

The aforementioned physical findings that are used to determine an animal’s total body fluid status are not used to assess hypovolemia. Peripheral perfusion should instead be assessed by capillary refill time (CRT), mucous membrane color, arterial blood pressure, pulse quality and rate, and temperature of extremities.

The body responds to fluid loss by redistributing the functional ECF volume—that is, by pulling fluid into the intravascular space from the interstitial space to maintain circulating blood volume as the first priority. When the interstitial space can no longer replenish intravascular volume depletion, clinical signs of hypovolemia will result. In decompensated shock, severe hypovolemia results in a marked worsening of perfusion parameters. Hypotension, bradycardia, prolonged CRT, pale pink to gray or cyanotic mucous membranes, hypothermia, decreased central venous pressure, altered mentation, and decreased urine output will be present in decompensated shock. Table 5-1 gives examples of the types of fluid losses that would be expected with selected medical problems.

TABLE 5-1 Examples of the Types of Fluid Losses that Would Be Expected with Selected Medical Problems

Condition	Dehydration	Hypovolemia
Blood loss		X
Vomiting	X	X (if severe)
Diarrhea	X	X (if severe)
Sepsis/vasodilation		X
Hypoadrenocorticism		X
Polyuria	X (depending on cause)	X (depending on cause)
Hypodipsia or water deprivation	X

Assessment of Fluid Excess

Overhydration, like dehydration, is detrimental to patients and should be avoided in patients on fluid therapy. Human and canine patients with ECF volume excess can have pulmonary edema, ascites, and generalized peripheral edema. Unique to the cat, possibly because of a difference in the anatomy of pulmonary venous drainage, pleural effusion may develop more readily than pulmonary edema or ascites. Cats with preexisting cardiac disease are more susceptible to pleural effusion or pulmonary edema with volume overload, depending on their underlying disease. Cats with oliguria or markedly decreased GFRs are also particularly at risk for overhydration, and measurement of urinary output is essential in such patients. Early signs of overhydration may include the more subtle findings of loss of appetite and mental dullness. An astute clinician will notice tachypnea or crackles on auscultation, insofar as pleural effusion or pulmonary edema develops before the onset of overt dyspnea. Careful and repeated weighing is important for prevention of volume overload, particularly in cats, because of their small size.

Body Response to Hypovolemia

Intravascular volume status is sensed by baroreceptors in the carotid body and aortic arch. In euvolemic cats, stimulation of the stretch receptors triggers the vagus nerve to maintain an appropriate heart rate. In hypovolemia the baroreceptors sense a decrease in wall tension, and the sympathetic nervous system is activated. Norepinephrine and epinephrine release results in vasoconstriction, improved cardiac contractility, and an increase in heart rate. These effects are designed to compensate for decreased intravascular fluid volume by improving cardiac output and maintaining systemic blood pressure and, ultimately, perfusion. Hypovolemic shock results when intravascular volume is sufficiently reduced that these compensatory mechanisms are overwhelmed and decreased tissue perfusion results. Perfusion parameters that can be assessed include capillary refill time, blood pressure, heart rate, and temperature of extremities.

Cats are unique in that the vasoconstrictor response to volume loss is blunted in the presence of hypothermia.^13,¹⁴ For this reason, cats are more prone than other species to fluid overload when they have been volume resuscitated while hypothermic. Once body temperature returns to normal, the vasoconstrictor response returns and intravascular pressure rises. For this reason, hypothermia in cats is a potentiator of shock, as well as a result of shock. Cautious fluid resuscitation must coincide with aggressive rewarming efforts to prevent volume overload. Specific therapy and therapeutic endpoints for resuscitation are discussed in subsequent sections.

General Considerations for Fluid Therapy

Fluid therapy choices are often the product of educated guesswork. They certainly rely on the physiologic abilities of a normally functioning kidney for fine-tuning. Although there are many useful guidelines for selection of fluid types and rates, good fluid management demands careful monitoring of body weight, physical examination, and electrolyte concentrations. The veterinarian must be prepared to alter the fluid therapy prescription in response to changes in these parameters, and should understand that the initial fluid therapy plan merely provides a starting point. The clinician must also be more vigilant with fluid therapy monitoring in patients with cardiovascular or renal disease. It should be remembered that cats may have cardiac disease in the absence of a detectable murmur.

As fluid bag sizes are not scaled down to the size of feline patients, it is helpful to use fluid pumps, burettes, and other devices to prevent fluid overload and pulmonary edema or pleural effusion (Figure 5-2).

FIGURE 5-2 Because fluid bag sizes are not scaled down to the size of feline patients, it is helpful to use fluid pumps (A and B), burettes (C), and other devices to prevent fluid overdosing.

Fluid Types

The two main types of parenteral fluids, crystalloids and colloids, have fundamental differences that affect the way fluid distributes among body fluid compartments. Crystalloids are composed of smaller molecules that diffuse readily; therefore approximately 80% of the fluid infused will leave the intravascular space within 1 hour. Colloids, made of larger molecules, stay within the intravascular space longer, which is an important advantage when managing hypovolemia. The tonicity of fluids determines distribution rates to the intracellular and extracellular spaces. When the [Na⁺] of a fluid approximates that of plasma (145 mEq/L), it will equilibrate rapidly with the interstitial space. Remaining fluid that is not lost in urine or as other ongoing losses will distribute to the ICF in proportion to the normal size of those compartments: two thirds ICF and one third ECF.

Hypotonic fluids, with a [Na⁺] lower than that of plasma, will dilute the plasma and drive water into cells to equilibrate the water concentration inside and outside cells. The decreasing plasma osmolality (pOsm) will also result in a decreased ADH production and, thus, increased water excretion by the kidney. Most of the Na⁺-free fluid thus either enters cells or is excreted. Hypertonic fluids with a [Na⁺] higher than plasma will draw water out of cells and into the ECF, thus increasing the intravascular and interstitial volumes but at the expense of taking water from the ICF compartment. Thus an understanding of which body compartments need to be replenished in any given patient is essential in fluid selection. This is true not only regarding fluid types selected but also in terms of route of administration. For example, fluids instilled into the subcutaneous space cannot be used readily to replenish the intravascular blood volume because they will be absorbed too slowly in a patient with hypovolemia.

Crystalloids

A crystalloid is a solution that is able to pass through a semipermeable membrane, including the vascular endothelium. The ability of crystalloids to pass through the capillary endothelium allows them to replenish fluid losses both in the intravascular and interstitial compartments, making them ideal for rehydration therapy. All crystalloid fluids are true solutions, meaning that they are homogeneous and transparent, diffuse rapidly, and do not settle. Substances that are dissolved in crystalloids are termed solutes; these are predominantly electrolytes and dextrose.

Solutes contained in crystalloid fluids move freely from the intravascular space to the interstitial space. Movement of impermeant solutes such as ions and glucose into the intracellular compartment is comparatively slower, occurring by facilitated diffusion or active transport. As parenteral fluid solutions, most crystalloids are formulated with a solute concentration close to that of plasma to avoid osmotic cell damage, particularly red blood cell damage from tonicity-induced osmotic water movement. Some parenteral intravenous solutions, such as 0.45% NaCl and 5% dextrose in water (D5W) are hypotonic and can cause hemolysis if given too rapidly.

The three categories of crystalloids are isotonic high-sodium, hypotonic low-sodium, and hypertonic saline; they differ primarily in their sodium concentrations.

Isotonic High-Sodium Crystalloids

General Characteristics and Indications for Isotonic High-Sodium Crystalloids

Isotonic high-sodium fluids are commonly referred to as replacement fluids because they are often used for rapid replacement of ECF volume deficits caused by vomiting and diarrhea. They have a [Na⁺] near that of ECF, ranging from approximately 130 mEq/L (e.g., lactated Ringer’s solution [LRS]) to a high of 154 mEq/L (e.g., 0.9% saline). Table 5-2 includes additional examples of replacement fluids, highlighted in red.

TABLE 5-2 Composition of Common Crystalloids *

* High-sodium “replacement” fluids are in red. Low-sodium “maintenance” fluids are in green.

Isotonic high-sodium fluids are used both for hypovolemia and for less severe ECF volume depletion, such as dehydration. When given rapidly, they can be used to restore the intravascular fluid volume in cats with hypovolemia. They are also used, when administered more slowly, to replace ECF volume in states of isotonic dehydration that are not immediately life threatening, such as occurs in patients with gastrointestinal or urinary fluid losses when oral intake is insufficient to balance losses.

Isotonic high-sodium fluids are not suited for use as maintenance fluids. They lack sufficient solute-free water content to offset ongoing solute-free water loss, such as through respiratory evaporation. When used on a short-term basis, most patients with normal renal function will tolerate the excess Na⁺ that these fluids contain when they are being used primarily to compensate normal daily ongoing hypotonic fluid loss. This is particularly true when patients are able to drink some water in addition to their intravenous fluid therapy. Some patients can become hypernatremic after therapy with high-sodium fluid. There are also some patients for whom the use of high-sodium fluids is contraindicated, including those with congestive heart failure, oliguric renal disease, and some edema states.

Isotonic high-sodium fluids are used to maintain patients with ongoing isotonic fluid losses, as, for example, in vomiting or diarrhea. However, in these patients the fluids are in fact being used for replacement of these losses, rather than for true maintenance. It is critical to understand this distinction. Maintenance is a term used to reflect what is needed to replace only normal sensible and insensible losses, and such losses are not isotonic. Isotonic fluids may work to maintain fluid balance in animals with additional pathologic losses because such patients need the additional sodium and chloride. However, such patients need to drink to provide solute-free water; otherwise, hypernatremia will develop. In addition to the relative solute-free water deficit of high-sodium isotonic fluids, all of these fluids are also too low in potassium to be used as true maintenance fluids, unless K⁺ is added to the fluids. Patients with continuing ongoing losses for more than 1 to 2 days that stay on high-sodium fluids are likely to need nutritional support, which will also replace their hypotonic maintenance fluid needs.

Some patients with readily corrected deficits and no ongoing losses will need to be transitioned to a maintenance-type solution, such as Normosol-M-D5 or Plasmalyte-56-D5, after their rehydration and electrolyte needs have been corrected and before the start of enteral or parenteral nutrition. The need to change to a true maintenance fluid will be indicated by a progressive increase in serum [Na⁺] in these patients. Changes should be made well in advance of the development of hypernatremia.

Sick cats that have been anorexic for 2 to 3 days or longer should receive nutritional support. Generally, the provision of enteral or parenteral nutrition sufficient to meet the patient’s caloric needs will also provide maintenance fluid needs. Thus the use of additional isotonic, high-sodium fluids in this setting will be to replace excessive isotonic losses, such as those associated with gastrointestinal loss or polyuria. Intravenous fluid rates can be greatly reduced in patients receiving either enteral or parenteral nutrition to a rate sufficient to meet additional ongoing losses only. In other words, the fluid therapy recipe should account for all sources of fluid intake (Table 5-3; also see Table 5-8).

TABLE 5-3 Calculation Worksheet for Fluid Therapy*†

TABLE 5-8 Case Example Using the Calculation Worksheet for Fluid Therapy

Acidifying and Alkalinizing Fluids

Sick cats requiring fluid therapy may also have acid–base disorders, and fluid therapy can be used to mitigate these disturbances. Restoration of ECF volume will improve tissue perfusion and correct lactic acidosis. The replenishment of water and electrolytes in appropriate concentrations will also improve renal perfusion and normalize renal electrolyte handling, thus promoting an improved acid–base balance. The volume expansion and improved perfusion seen with appropriate fluid therapy will also promote the peripheral utilization of glucose and decrease production of lactate. The end result of this can be the normalization of acid–base balance without the need to resort to the use of sodium bicarbonate, which can have adverse effects, such as hypernatremia and central nervous system acidosis.

High-sodium crystalloids will have a primary effect on the patient’s acid–base status, depending on their composition. As such, they can be classified as either acidifying or alkalinizing solutions. High-sodium fluids that contain more Cl⁻ than is present in the patient’s ECF are acidifying. Although 0.9% saline has a high Na⁺ content and thus is frequently used to restore intravascular fluid in hypovolemic patients, it also has a high Cl⁻ content and will be acidifying. This fluid is most appropriate for treatment of patients with hypochloremic metabolic alkalosis because it provides the necessary Cl⁻. A common clinical scenario associated with hypochloremic metabolic acidosis is the vomiting of gastric contents. It is important to point out that although the measured pH of parenteral fluid solutions ranges from about 4 to 6.5, they are extremely weak acids. These low measured in vitro pH values will not reflect their effect on pH in the patient because of buffering.

Alkalinizing fluids, by contrast, do not have a higher Cl⁻ concentration than ECF fluid. Some of the chloride is replaced with another anion such as lactate, acetate, or gluconate. The anions are metabolized by the liver to bicarbonate. One example of a commonly used alkalinizing fluid is LRS.

Supplements

In some situations fluids must be supplemented with additional electrolytes; this decision is based on an assessment of the history, physical examination findings, and measured electrolyte values. Commonly added electrolytes are listed in Table 5-4. Electrolyte additives may be appropriate for replacing deficits, providing replacement for normal maintenance losses in anorexic patients, compensation for transcellular movement of ions, or replacement of ongoing gastrointestinal or urinary losses. Potassium and magnesium are found in some low-sodium hypotonic fluids formulated as maintenance fluids. If not, they can be added to fluids to maintain homeostasis in animals that are not depleted.

TABLE 5-4 Concentration of Common Fluid Additives

Product	Concentration per mL
KCl	2 mEq each
KPO₄	4.4 mEq K⁺, 3 mM PO₄
MgCl	1.97 mEq each
MgSO₄	4.06 mEq each
Ca gluconate 10%	0.465 mEq Ca⁺⁺
CaCl₂	1.36 mEq Ca⁺⁺
NaPO₄	4 mEq Na⁺, 3 mM PO₄
Dextrose 50%	500 mg

From Abbott Animal Health Fluid Therapy Module 2, courtesy Dr. Steve Haskins.

Potassium

All of the isotonic high-sodium fluids, apart from 0.9% NaCl, contain 4 or 5 mEq/L of potassium. Although this amount of potassium is within the normal range of plasma [K⁺], it is not in fact sufficient for maintenance of the patient. This is because therapy with intravenous isotonic high-sodium fluids typically causes a solute diuresis. The rate of flow of filtrate through the renal tubule is one of the factors regulating renal potassium excretion. As urine flow rate increases in response to intravenous fluid administration, K⁺ loss in the urine will also increase. The loss of K⁺ from the body will be further compounded by decreased intake in patients that are anorexic or hyporexic and by increased losses of K⁺ in gastrointestinal secretions in patients with vomiting or diarrhea. Thus when isotonic high-sodium fluids are used for maintenance of patients that are drinking or for support of patients with ongoing isotonic fluid losses, it is necessary to supplement the fluids with additional K⁺. A common level of supplementation for a cat that is normokalemic is the addition of 20 mEq/L of KCl to the isotonic high-sodium fluid. This amount is typically added to the K⁺ already present in the fluids; it is not necessary to subtract the small amount that is already present in the fluid. If K⁺ is not added to these fluids when they are used for more than a short time in normokalemic patients, hypokalemia will result.

For patients that are hypokalemic, a sliding scale is used to calculate how much potassium to add to the fluid. One such scale is shown in Table 5-5. When using the potassium-containing replacement fluids for fluid resuscitation, it must be remembered that if the K⁺ concentration of the fluid exceeds 5 mEq/L, the fluid must not be infused rapidly for intravascular volume restoration because of the risk of hyperkalemia.

TABLE 5-5 Sliding Scale for the Amount of KCl Added to Intravenous Fluids Depending on the Serum [K⁺]*

Measured Serum K+ (mEq/L)	KCl Added (mEq/L)
>5.5	None
3.6-5.5	20
3.1-3.5	30
2.6-3	40
2-2.5	60
<2	80

* If the [K⁺] of the fluid exceeds 5 mEq/L, the fluid must not be infused rapidly for intravascular volume restoration because of the risk of hyperkalemia.

Cats with anorexia, gastrointestinal losses, or polyuria are particularly at risk for K⁺ depletion. As an alternative to the sliding scale, a constant-rate infusion (CRI) is typically used to give K⁺ separately when the patient seems resistant to “normal” amounts of K⁺ supplementation, particularly in diabetic ketoacidosis (DKA) (Figure 5-3). This allows K⁺ to be adjusted separately from the remainder of the fluid prescription. If CRI is used, it must be monitored very carefully. The usual dose range to replace normal ongoing losses of potassium is 0.05 to 0.1 mEq/kg per hour. The dosage for cats with severe whole body potassium depletion, severe symptomatic hypokalemia, or both can be as high as 0.5 mEq/kg per hour, known as KMax. Administration at rates higher than 0.5 mEq/kg per hour can cause serious or fatal cardiac arrhythmias. Administration of undiluted KCl (2 mEq/mL) through a programmable syringe pump is possible, but should only be done with extreme care, reserved for intensive care situations in patients with life-threatening hypokalemia (generally levels below 1.5 mEq/L).

FIGURE 5-3 A constant-rate infusion is typically used to give K⁺ separately when the patient seems resistant to “normal” amounts of K⁺ supplementation, particularly in diabetic ketoacidosis.

Phosphate

Hypophosphatemia may develop rapidly during insulin therapy for DKA. For hypophosphatemia a portion or all of the phosphate (PO₄⁻) can be administered as potassium phosphate (KPO₄) when the [PO₄⁻] is less than 2 mEq/L or when serum [PO4⁻] is observed to be decreasing rapidly and a drop below that level is expected. This also provides K⁺ for concurrently hypokalemic patients. Hemolysis can occur when the [PO₄⁻] is less than approximately 1.5 mEq/L in cats. Sodium phosphate is used in the unusual case of phosphate-depleted patients that do not require potassium. The usual dose range to replace normal ongoing losses of phosphate is 0.01 to 0.03 mmol/kg per hour. Dose rates as high as 0.12 mmol/kg per hour may be necessary in some patients being treated for DKA.

Magnesium

Magnesium depletion is common in critically ill patients, particularly those with decreased dietary intake and polyuria, such as patients with diabetes mellitus. Supplementation is generally recommended when serum total magnesium concentration is less than 1.5 mg/dL. Because total serum magnesium concentration does not represent the physiologically active form of the element, measurement of ionized magnesium should be performed when possible; however, this assay is not readily available in most veterinary hospitals.

Replacement doses are 0.03 to 0.04 mEq/kg per hour for severe cases requiring rapid replacement and 0.013 to 0.02 mEq/kg/hour for more mild deficiency. MgCl₂ or MgSO₄ may be given but not mixed with calcium- or bicarbonate-containing fluids.² Patients with reduced GFR are at greater risk for hypermagnesemia during supplementation and require more frequent monitoring. Magnesium is a cofactor for potassium homeostasis, and magnesium supplementation should be considered in any patient with refractory hypokalemia.

Hypotonic Low-Sodium Crystalloids

Maintenance

Low-sodium crystalloid fluids are indicated for the short-term support of water and electrolyte homeostasis by replacing normal ongoing losses in patients in which oral intake is not appropriate or possible. Thus hypotonic low-sodium fluids have historically been referred to as maintenance fluids. These crystalloids have a lower [Na⁺] than the ECF. Given that normal insensible fluid losses (respiratory and other evaporative loss) do not contain Na⁺, these fluids are indicated when the patient needs a supply of solute-free water to replace daily requirements normally met through drinking and metabolism of food. The [Na⁺] concentration of low-sodium crystalloid fluids ranges from 0 mEq/L in the case of 5% dextrose in water to 77 mEq/L in the case of a half-strength, or 0.45%, saline solution. Solutions with less than 77 mEq/L of Na⁺ contain 2.5 or 5% dextrose to raise the osmolality closer to that of ECF. Nonetheless, maintenance fluids are hypotonic and must be given slowly to allow for equilibration and to prevent hemolysis. It is important to note that dextrose, when present in these fluids, does not provide significant calories. The addition of dextrose is merely a way to raise the osmolality of the fluid (to make it isotonic with plasma) with a readily metabolized solute that will allow sodium-free water to be administered intravenously without causing hemolysis. It should be noted that the potassium content of the hypotonic low-sodium crystalloids is highly variable. As previously discussed, a potassium concentration of 20 mEq/L is the minimum that is usually considered necessary for true maintenance of a normokalemic patient.

Table 5-2 lists some examples of low-sodium crystalloid fluids in green. The rate of administration of IV fluids used for maintenance is based on the metabolic body size and will only change when patients begin to eat and drink. Low-sodium crystalloids are contraindicated in patients requiring rapid administration, such as for hypovolemia, as doing so will rapidly reduce the ECF [Na⁺] and cause cell swelling due to rapid reduction in osmolality.

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Aug 26, 2016 | Posted by admin in INTERNAL MEDICINE | Comments Off

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