Section 2: General Fluid Therapy Principles

Fluid therapy involves administering prescribed fluids to restore a  patient’s body fluid homeostasis. As with any medication, the pharmacokinetics and pharmacodynamics of each fluid must be considered to attain therapeutic goals and minimize complications. However, fluid therapy alone cannot fix every abnormality, and using a standardized fluid rate for all patients can result in patient morbidity (see Box 1). To prescribe effective fluid therapy, veterinarians must have a basic understanding of the body’s fluid compartments and how water is distributed among them.

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Top three takeaways

  1. Fluids are drugs and must be prescribed accordingly to achieve the desired therapeutic goals promptly and minimize complications.
  2. Each body fluid compartment—intracellular, interstitial, and intravascular—may require a different fluid prescription tailored to a patient’s individual needs.
  3. Arbitrarily assigning a fluid rate or dose can contribute to patient morbidity and mortality and lead to missed fluid therapy goals.

Box 1: One Fluid Rate Does Not Fit All

A common misconception is that administering fluids at twice the maintenance rate will adequately treat most veterinary patients in need of fluid therapy. However, this approach may be inappropriate or inadequate in several scenarios, as shown in the following examples:

  • Interstitial dehydration. Using a twice maintenance fluid administration rate would take approximately 33 hr to rehydrate a patient who has 5% interstitial dehydration, far longer than the recommended 12–24 hr.
  • Uremia due to acute kidney injury (AKI). The primary goal in treating AKI is to ensure adequate renal perfusion and match the kidney’s ability to handle fluid volumes. The fluid input rate for normovolemic patients should be determined based on fluid output (see Section 5, Fluid Therapy in Ill Patients).
  • Intoxications. Administering an increased hourly fluid volume to force diuresis and urine output may not increase toxin excretion and can result in fluid overload. For example, although some animals with nonsteroidal anti-inflammatory drug (NSAID) toxicity may benefit from fluid therapy to treat dehydration or hypovolemia, high fluid rates (also known as forced diuresis) do not accelerate elimination of NSAIDs because most NSAIDs are highly protein-bound.

Fluid Distribution and Flow Among the Three Primary Fluid Compartments

The three main body compartments in mammals contain water. The intracellular and extracellular fluid compartments contain 67% and 33% total body water, respectively (Figure 1), and these sections are separated by cell membranes. The extracellular fluid compartment is further divided into interstitial (25% of the total body water, or 75% of the extracellular body water) and vascular (8% of the total body water, or 25% of the extracellular body water) compartments, and capillary walls separate these spaces (Figure 1).

Fluid intake by any route can affect the body fluid compartments. Administered fluids move between compartments based on:

  • Tonicity of the fluid
  • Tonicity of the patient’s extracellular compartment
  • Size of any macromolecules in the administered fluid

Sodium is the most abundant cation in the extracellular fluid compartment and is the most important molecule that supports extracellular tonicity. A fluid given IV that contains a sodium concentration similar to that of the extracellular fluid compartment will redistribute within 45 min based on a compartment’s percent total body water; i.e., in a normal animal, 25% of the administered fluid will remain in the intravascular space and 75% will move into the interstitial space. Fluid movement across the endothelial membrane depends on the contents of the administered fluid and the condition of the patient’s capillary membrane. The modified Starling hypothesis describes how fluid moves across the capillary membrane (Figure 2). Hydrostatic pressure, colloid osmotic pressure, and vascular permeability influence fluid movement.,

When increased capillary membrane permeability, elevated intravascular hydrostatic pressure, or decreased plasma colloid osmotic pressure occurs, more isotonic fluid can pass into the interstitium or body cavity and cause tissue edema, effusion, or both.

Administering a hypertonic fluid IV will cause water to move from the interstitial and intracellular spaces into the intravascular space. This can be desirable for rapid intravascular volume resuscitation. However, for this strategy to succeed, the interstitial and intracellular spaces must already be adequately hydrated. When administered IV, a hypotonic fluid will cause water to move from the extracellular space into the intracellular space, which is a suitable approach when treating a solute-free water deficit.

Figure 1: Normal distribution of body water
Figure 1 Bar graph of total body water

Figure 1: Normal distribution of body water

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Figure 2: Modified Starling hypothesis
Figure 2 Modified Starling hypothesis

Figure 2: Modified Starling hypothesisa

Modified Starting hypothesis of fluid flux across the capillary membrane. Filtration force = ([Pc – Pi] – s [pg]). Pc, Capillary hydrostatic pressure; Pi, Interstitial hydrostatic pressure; p, plasma oncotic pressure; i, interstitial oncotic pressure; g, glycocalyx oncotic pressure

a Reprinted from Silverstein DC and Hopper K, eds., Small Animal Critical Care Medicine, 3rd ed., Waddell L., Colloid osmotic pressure and osmolality, p. 1055, Elsevier (2022), with permission from Elsevier.

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Goal-Directed Fluid Therapy

Goal-directed fluid therapy requires creating a fluid prescription that replaces fluid deficits that may exist in each fluid compartment, using the following steps:

  1. Recognize which fluid compartment deficit(s) exists.
  2. Understand which fluid type and administration route will best replace each deficit.
  3. Calculate the fluid dose and administration rate.
  4. Monitor patients for response to therapy and signs of complications.,,

Assessing Patients: General Principles Before and During Fluid Therapy

The extracellular fluid compartment (i.e., the vascular and interstitial spaces) must have adequate volume before intracellular fluid compartment deficits can be addressed. Therefore, assess and address alterations in volume homeostasis in the following order:

  1. Assess the intravascular fluid space by evaluating:
    • Patient history
    • Perfusion parameters (mentation, heart rate, capillary refill time, mucous membrane color, extremity temperature, skin turgor, and pulse quality)
    • Monitored parameters (blood pressure, electrocardiogram findings)
    • Laboratory test results (Table 1)
    • Diagnostic imaging findings (Tables 1, 2)
  2. Assess the interstitial space by evaluating:
    • Patient hydration parameters (Tables 3, 4, 5)
  3. Assess the intracellular space by evaluating:
    • Patient sodium concentration
    • Solute-free water deficit (FWD) (Box 2)

Replace deficits and monitor response

  • To replace extracellular fluid space deficits (i.e., vascular and interstitial fluid space deficits):
  • Administer a buffered isotonic crystalloid fluid that contains a sodium concentration similar to the patient’s.
  • For rapid intravascular volume replacement, a hypertonic crystalloid, a colloid solution, or both can also be used.
  • Closely monitor patient parameters until fluid homeostasis is achieved and maintained (Tables 1, 3, 4, 5).
  • Monitoring may also be achieved by assessing the relative variation in the caudal vena cava during one respiratory cycle using ultrasonography and calculating the Caudal Vena Cava Collapsibility Index., See Table 6 for some conditions that pose additional challenges in addressing individual fluid compartment needs. For more information on addressing fluid therapy challenges, see Section 5, Fluid Therapy in Ill Patients.
Box 2: Calculating Free Water Deficit

Free Water Deficit (FWD) in Liters (L) = [Patient Na/Desired Na) -1] x (0.6 3 Weight [kg])

Table 1: Intravascular Volume Assessment
Criteria Hypovolemia Hypervolemia*
Patient history Vomiting, diarrhea, decreased water intake, anorexia or hyporexia, respiratory signs, fever, blood loss and hemorrhage Iatrogenic fluid overload, polydipsia, salt intoxication, osmotic agent administration
Physical examination findings See Table 2
Can occur with severe dehydration (>12%) May see evidence of hemorrhage (bleeding, epistaxis, etc.)
Bounding pulse quality, new cardiac murmur, wet lung sounds, ocular/nasal discharge, jugular vein distention, peripheral edema
Blood pressure or electrocardiogram findings Hypotension, arrhythmia Arrhythmia
Laboratory test results Hyperlactatemia, metabolic acidosis, acute anemia, hypoproteinemia (may be secondary to hemorrhage) Hemodilution of packed cell volume, blood urea nitrogen, and electrolytes
Diagnostic imaging results (e.g., radiography, ultrasonography, computed tomography) Microcardia, small caudal thoracic vena cava, caudal vena cava collapsibility index >27% Abdominal venous distension, caudal vena cava collapsibility index <27%, pleural effusion, ascites, retroperitoneal effusion, perirenal effusion

*Usually occurs in conjunction with signs of overhydration of the interstitial space (see Tables 4 and 5).

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Table 2: Stages and Clinical Signs of Hypovolemic Shock
Heart rate CRT MM color Peripheral pulses Peripheral blood pressure Extremities Body temperature
Cat Rarely recognized (seconds to a few minutes in duration)
Dog Normal or increased 1-2 s Normal or red Bounding Normal or increased Normal temperature to touch Hypothermic, hyperthermic or normothermic
Early decompensatory
Cat Normal or decreased >2 s Pale Weak Low Cool to touch Hypothermic
Dog Increased >2 s Pale to white Weak Normal or decreased Cool to touch Hypothermic, hyperthermic or normothermic
Late decompensatory
Cat Decreased >2 s or absent White Absent Low or unable to obtain Cool to cold to touch Hypothermic
Dog Normal or decreased >2 s or absent White Absent Low or unable to obtain Cool to cold to touch Hypothermic, hyperthermic or normothermic

CRT, capillary refill time; MM, mucous membrane

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Table 3: Estimated Interstitial Dehydration (%) Based on Physical Examination Findings
Estimated % Dehydration Physical Examination Finding
  • Not detectable
  • Some change in skin turgor
  • Mild decreased skin turgor
  • Dry mucous membranes*
  • Obvious decreased skin turgor
  • Retracted globes within orbits
  • Persistent skin tent due to complete loss of skin elasticity
  • Dull corneas**
  • Evidence of hypovolemia
  • Hypovolemic shock
  • Death

Note: There is substantial clinical variation in the correlation between clinical signs and degree of dehydration, so this is an estimate only.

Reprinted from Silverstein DC and Hopper K, eds., Small Animal Critical Care Medicine, 3rd ed., Rudloff, E, Assessment of hydration, p. 1054-58, Elsevier (2022), with permission from Elsevier.

*Xerostomia can be present in AKI and CKD patients without dehydration.

**Retracted globes may also be present.

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Table 4: Extracellular Hydration Status Assessment Parameters and Expected Changes from Baseline in Patients Receiving Hypo- or Over-hydration
Parameter Hypohydration Overhydration
Skin turgor
Mucous membrane moisture
Packed cell volume
Total protein
Blood urea nitrogen
Urine osmolality
Urine specific gravity

Reprinted from Silverstein DC and Hopper K, eds., Small Animal Critical Care Medicine, 3rd ed., Rudloff, E, Assessment of hydration, p. 1054-58, Elsevier (2022), with permission from Elsevier.

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Table 5: Additional Clinical and Diagnostic Findings That May Indicate Overhydration/Fluid Overload

Acute weight gain

Respiratory signs

  • Tachypnea
  • Cough
  • Moist lung sounds
  • Labored breathing
  • Diagnostic imaging findings consistent with pleural effusion, ascites, and/or pulmonary edema


  • Chemosis
  • Subcutaneous edema
  • Organ edema and dysfunction (e.g., gastrointestinal signs, altered mentation, arrhythmia)

Serous nasal discharge

Cavitary effusion

Polyuria in the absence of renal failure



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Table 6: Conditions That Pose Challenges When Addressing Individual Fluid Compartment Needs
Condition Challenge
Hypovolemic shock in cats
  • Cats typically develop bradycardia, hypothermia, and hypotension.
  • This triad of events makes cats more susceptible to hypervolemia and overhydration compared with dogs, when similar fluid resuscitation strategies are used (see Table 2).
Increased capillary permeability (e.g., due to systemic inflammation, burns, trauma)
  • Can result in both hypovolemia and overhydration.
Acute congestive heart failure in a patient receiving diuretics and afterload reducers
  • Can result in poor perfusion and signs of shock due to cardiovascular dysfunction.
Osmotic diuretic therapy or uncontrolled hyperglycemia
  • Can lead to hypervolemia and reduced interstitial and intracellular water volume.

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  1. Waddell L. Colloid osmotic pressure and osmolality. In: Silverstein DC, Hopper K, eds. Small Animal Critical Care Medicine. 3rd ed. St. Louis: Elsevier; 2022:1054–58.
  2. Woodcock TE, Michel CC. Advances in the Starling principle and microvascular fluid exchange; consequences and implications for fluid therapy. Front Vet Sci 2021;8:623671.
  3. Boysen SR, Gommeren K. Assessment of volume status and fluid responsiveness in small animals. Front Vet Sci 2021;8:630643.
  4. Rudloff E, Hopper K. Crystalloid and colloid compositions and their impact. Front Vet Sci 2021;8:639848.
  5. Rudloff E. Assessment of hydration. In: Silverstein DC, Hopper K, eds. Small Animal Critical Care Medicine. 3rd ed. St. Louis: Elsevier; 2022:373–77.
  6. Rudloff E, Hopper K. Crystalloid and colloid compositions and their impact. Front Vet Sci 2021;8:639848.
  7. Marshall KA, Thomovsky EJ, Brooks AC, et al. Ultrasound measurements of the caudal vena cava before and after blood donation in 9 greyhound dogs. Can Vet J 2018;59(9):973-980.
  8. Donati PA, Guevara JM, Ardiles V, et al. Caudal vena cava collapsibility index as a tool to predict fluid responsiveness in dogs. J Vet Emerg Crit Care (San Antonio) 2020;30(6):677–86.
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