Chapter 64 Daily Intravenous Fluid Therapy
Intravenous fluid therapy is vital for the management of shock, dehydration, and maintenance in animals that require parenteral fluid therapy (see Chapters 61, 62, and 63, Peripheral Venous Catheterization, Intraosseous Catheterization, and Central Venous Catheterization, respectively, and Chapter 65 and 66, Shock Fluids and Fluid Challenge and Transfusion Medicine, respectively). This chapter focuses primarily on the distribution of total body water, patient assessment, and the delivery of synthetic intravenous fluids to maintain normal water, electrolyte, and acid-base status in critically ill dogs and cats that are hemodynamically stable. Because critically ill animals often have fluid and electrolyte balance derangements, overall recovery often depends on recognition and appropriate treatment of these disorders, in addition to diagnosing and treating the primary disease process.
Living organisms are predominantly composed of water. Total body water content is approximately 60% of body weight in a nonobese adult dog or cat. Total body water is distributed between two main compartments: intracellular fluid (ICF) and extracellular fluid (ECF) (Figure 64-1). Each compartment consists of solutes, primarily electrolytes, dissolved in water. The most important determinant of the size of each body fluid compartment is the quantity of solutes contained in that compartment.1,2
The ICF compartment is the larger of the two and comprises 66% of the total body water and 40% of body weight. It is separated from the ECF compartment by the cell membrane, which is very permeable to water but impermeable to most solutes. Cell membranes contain numerous proteins, including ion channels and active solute pumps. The most important active pump is the sodium-potassium ATPase pump, which extrudes three sodium ions out of the cell in exchange for bringing two potassium ions into the cell. This pump is responsible for generation of the electrochemical gradient across cell membranes, typified by a high intracellular potassium concentration, high extracellular sodium concentration, and a negative resting membrane potential.Therefore the most prevalent cation in the ICF is potassium, with much smaller contributions made by magnesium and sodium. The most prevalent anions in the ICF are phosphate and the polyanionic charges of the intracellular proteins.1,2
The ECF comprises the remaining 33% of the total body water and 20% of body weight. The ECF is subdivided into the plasma (25% of ECF) and interstitial (75% of ECF) fluid compartments. The interstitial fluid bathes all cells and includes lymph. The primary cation in the ECF is sodium and the most prevalent anions are Cl− and HCO3−. The proteins in plasma and the interstitial space also contribute to the negative charges. The oncotic pressure gradient between the intravascular and interstitial spaces is determined by the ratio of proteins in these two compartments.1,2
Water moves freely within most compartments in the body. Small particles such as electrolytes move freely between the intravascular and interstitial compartment, but cannot enter or leave the cellular compartment without a transport system. Larger molecules (>20,000 daltons) do not easily cross the vascular endothelial membrane and may attract small, charged particles, thus creating the colloid osmotic pressure (COP). There are three main natural colloid particles: albumin, globulins, and fibrinogen. An increase in the pressure of fluid within a compartment that pushes against a membrane is known as hydrostatic pressure.
In health, fluid balance is determined by the balance between forces that favor reabsorption of fluid into the vascular compartment (increased COP or decreased hydrostatic pressure) and those that favor filtration out of the vascular space (decreased COP or increased hydrostatic pressure).1 Changes in the osmolality between any of the fluid compartments within the body will cause free water movement across the respective membrane.
In disease states, both increased fluid losses and decreased intake may lead to dehydration. The nature of the fluid loss (hypotonic, isotonic, or hypertonic) will determine the subsequent changes in osmolality. This will in turn dictate the relative impact on the ICF and ECF compartments.
Isotonic fluid losses, as seen in animals with polyuric renal failure or bleeding, will lead to depletion of the ECF compartment and dehydration. If severe ECF losses are not replaced, hypovolemia may become clinically apparent. Because isotonic losses will not alter ECF osmolality, there will be no movement of water across the cell membrane and ICF volume will remain unchanged. In order to replace the ECF deficit, isotonic crystalloids should be administered (see Fluid Deficit).
Hypotonic fluid losses, as seen with diabetes insipidus or excessive panting, will cause hypernatremia and an increase in ECF osmolality. This will lead to movement of water out of the ICF space. Consequently, there is a depletion of both the ICF and ECF compartments. Isotonic fluid therapy may be sufficient if the hypernatremia is not severe, but in animals with significant hypotonic fluid losses, free water administration is indicated. Care must be taken to lower serum sodium slowly to avoid causing potentially life-threatening cerebral edema (see Chapter 54, Sodium Disorders).
Loss of hypertonic fluid, such as with heat exhaustion or highly concentrated urine, may cause hyponatremia and hypoosmolality. This maybe a direct result of the loss of high solute–containing fluid or may be exacerbated by a combination of isotonic or hypertonic fluid loss with hypotonic fluid replacement (i.e., oral water intake). Hypoosmolality will lead to water movement into the ICF compartment, resulting in dehydration and intracellular edema. Significant hyponatremia or hypoosmolality will require careful fluid therapy to avoid rapid (>0.5 mEq/L increase per hour) changes in sodium concentration and subsequent central pontine myelinolysis.
Disease processes that cause an increase in vascular permeability may lead to high-protein fluid extravasation from the intravascular space. This can lead to a decrease in intravascular volume, possibly associated with interstitial edema. Because this will not alter the osmolality of the ECF compartment, increased vascular permeability alone is not expected to alter the ICF volume.
Patient history, physical examination, and laboratory data can provide useful information concerning the route of fluid losses, timeline of these losses, food and water consumption, and current clinical status. This will guide formulation of an appropriate fluid therapy plan.