Bridget M. Lyons, VMD
Lori S. Waddell, DVM, DACVECC
University of Pennsylvania
GO WITH THE FLOW
Fluid therapy is a mainstay of care in the hospitalized small animal patient. Assessment of a patient’s fluid deficits and ongoing needs will help determine what variety of fluid and rate to use.
Fluid therapy is an essential component of the treatment plan in many hospitalized small animal patients. Choice of fluid type and dose depends on available resources as well as the patient’s interstitial hydration status, hemodynamic stability, and electrolyte balance. This article reviews fluid distribution, hydration assessment, types of body fluid losses, types of fluids available, and calculation of fluid needs. A second article will focus on calculating free water deficit, monitoring fluid therapy, when to discontinue fluids, and the approach to fluid therapy in patients with electrolyte abnormalities and specific fluid balance states.
DISTRIBUTION OF BODY WATER
Total body water (TBW) is commonly described in terms of individual fluid compartments. Although fluid balance in the body is a dynamic process—water is constantly being lost through elimination and metabolic processes and gained from food and water intake—it is useful to use compartments to understand how water is distributed in the body and thus how fluid therapy affects overall hydration.
TBW makes up approximately 60% of total body weight in adults (FIGURE 1) and 80% in pediatric animals.1 This percentage is lower in overweight patients because fat contains less water than other body tissues.1 Intracellular fluid accounts for two-thirds of TBW.1 Of the remaining third, approximately 75% is in the interstitial space and 25% is in the intravascular space1; a small amount is contained in the transcellular space (eg, cerebrospinal fluid, synovial fluid).
Separating the intracellular and extracellular compartments are cell membranes, through which water can move freely by osmosis.1 The intravascular space is partitioned off from other compartments by the vascular endothelium. Within the capillaries is the endothelial glycocalyx, a web of membrane-bound glycoproteins and proteoglycans that plays an important role in fluid dynamics.2
The classic Starling model of fluid dynamics did not take into account the endothelial glycocalyx, and it was previously thought that fluid was filtered at the arteriolar end of the capillary and subsequently resorbed on the venule side, with the rate of filtration and absorption related to both the hydrostatic pressure and the colloid oncotic pressure (COP) in the capillary and the interstitial space.2 Newer research has shown that the COP of the subglycocalyx space replaces interstitial COP and that fluids are not absorbed on the venule side but rather are returned to the circulation via the lymphatic system.2,4
TYPES OF FLUID LOSS
Fluid loss in small animals can be isotonic, hypotonic, or hypertonic. While osmolality is a measure of all solutes in solution, tonicity refers only to the effective solutes in solution; that is, those that cannot cross a membrane and so exert an osmotic pressure.
Isotonic losses, such as those observed with vomiting and diarrhea, occur when the fluid being lost has an osmolality similar to that of plasma. With isotonic fluid loss, sodium concentrations are typically normal; however, if the animal is able to drink water, hyponatremia may result from replacement with a hypotonic fluid.
Hypotonic losses occur when the type of fluid being lost has a higher concentration of water than plasma, such as with diabetes insipidus and panting. The loss of a hypotonic fluid, or water in excess of sodium, can result in hypernatremia. Although isotonic replacement fluids may benefit some patients with hypotonic losses, others benefit from fluids that contain more free water.
Hypertonic losses, or loss of sodium in excess of water, are uncommon but can be seen with hypoadrenocorticism, third-space loss of fluid (such as pleural or peritoneal effusion), and diuretic administration.1 Excess loss of hypertonic fluid can result in hyponatremia. Treatment of hypernatremia and hyponatremia will be discussed in Fluid Therapy: Part 2.
DETERMINING FLUID DEFICITS
Assessment of Hydration
Dehydration refers to lack of fluid in the interstitial compartment, whereas hypovolemia describes lack of fluid in the intravascular compartment. Intracellular dehydration cannot be detected on physical examination and is primarily assessed via changes in sodium concentration.
Although dehydrated patients have some hypovolemia, clinical changes do not occur until dehydration exceeds 10%.1 The minimum percentage dehydration that can be detected on physical examination is 5%, and dehydration greater than 12% is likely to be fatal.1 Percentage dehydration can be estimated by examining mucous membrane moisture, skin turgor (FIGURE 2), eye position (FIGURE 3), and corneal moisture, as described in TABLE 1.1
TABLE 1 Subjective Estimation of Percentage Dehydration Based on Physical Examination Parameters5
|ESTIMATED DEHYDRATION||PHYSICAL EXAMINATION FINDINGS|
|5% – 6%||Tacky mucous membranes|
|6% – 8%||Decreased skin turgor Dry mucous membranes|
|8% – 10%||Retracted globes within orbits|
|10% – 12%||Persistent skin tent Dull corneas Evidence of hypovolemia|
|>12%||Hypovolemic shock Death|
|Data adapted from reference 5.|
Overhydration of the interstitial compartment, which occurs in cases of fluid overload, can also be detected on physical examination. Signs of overhydration include chemosis, serous nasal discharge, increased skin turgor, peripheral edema, ascites, pleural effusion, and pulmonary edema.
Hydration status should be interpreted with the clinical status of the patient in mind. For example, hypersalivation in a nauseated patient may result in moist mucous membranes, but the patient may still have decreased skin turgor, indicating dehydration. Conversely, decreased skin turgor may be present in emaciated or older animals regardless of hydration status. In pediatric animals, skin turgor is often maintained because of increased skin elasticity, making this finding more difficult to interpret in this population.
The 4 primary means of fluid delivery are intravenous (IV), intraosseous, subcutaneous (SC), and enteral. IV fluid administration is generally preferred for hospitalized patients because the delivery rate can be controlled and changed quickly depending on patient requirements.
Assessment of Intravascular Volume
Intravascular volume can also be assessed on physical examination. Signs of decreased intravascular volume, or hypovolemia, include increased heart rate, fair or weak pulses, coolness of the distal limbs, weakness, and pale mucous membranes. Although blood pressure can initially be normal or even high in the early stages of hypovolemic shock, a normal blood pressure in conjunction with physical examination findings consistent with hypovolemia should not dissuade clinicians from considering hypovolemia and treating appropriately because compensated shock will eventually progress to the uncompensated stage.
METHOD OF DELIVERY
The 4 primary means of fluid delivery are intravenous (IV), intraosseous, subcutaneous (SC), and enteral. IV fluid administration is generally preferred for hospitalized patients because the delivery rate can be controlled and changed quickly depending on patient requirements. Intraosseous catheters can be placed in neonates, exotic patients, and other small animals in which IV access cannot be obtained, but these catheters may not be tolerated for extended periods once patients have been resuscitated.
SC fluids are not recommended for hospitalized patients because they are more difficult to titrate. In addition, patients with intravascular deficits require more aggressive support; SC fluids are not adequately absorbed because of peripheral vasoconstriction and so are not indicated for treating shock. Patients that are easily overloaded may receive too much fluid with no means of discontinuation once fluids are administered, resulting in fluid overload. In patients that are being discharged from the hospital, SC fluids may become a component of home care if they are well tolerated and there are ongoing excessive fluid losses.
Enteral fluids are ideal in patients that can tolerate them because enteral delivery is the most physiologic method to provide water. Many hospitalized patients cannot take in adequate water for various reasons (eg, vomiting, nausea, hypotension). If a patient can tolerate enteral water but is not willing to drink an adequate amount, a feeding tube can be used to provide fluids. An esophagostomy tube placed for feeding can also be used for water intake. Alternatively, a nasoesophageal tube can be placed to provide water and liquid diets (FIGURE 4). This is particularly useful in patients that cannot tolerate IV fluids, such as those with cardiac and/or renal disease.
TYPES OF FLUIDS
Crystalloids are fluids containing small solutes (<500 Da), most of which are electrolytes, in particular sodium and chloride.3 The electrolytes and water in these solutions move easily across the endothelium into the interstitial space. More than 60% to 80% of a crystalloid solution distributes out of the intravascular space within 20 to 30 minutes.3,4 Crystalloid solutions can be classified as isotonic, hypotonic, or hypertonic.
Isotonic crystalloids have an osmolarity and sodium concentration similar to those of plasma. They are commonly used to treat interstitial dehydration and hypovolemia because fluid losses are typically isotonic or hypotonic.
Isotonic solutions are considered balanced (or buffered) if their electrolyte composition and pH closely mirror those of plasma. Common balanced isotonic crystalloids include Plasmalyte-A (baxter.com), Normosol-R (hospira.com), and lactated Ringer’s solution (LRS) (TABLE 2). Metabolism of these buffers consumes hydrogen ions, resulting in an alkalinizing effect. The lactate in LRS is metabolized by the liver; thus, it is a suboptimal choice for patients with hepatic dysfunction or diabetic ketoacidosis because they will not be able to convert lactate to bicarbonate. Neonates are able to use lactate as a fuel source, making LRS the preferred fluid choice for young patients.
TABLE 2 Comparison of Various Crystalloid Solutions7
|CRYSTALLOID||OSMOLARITY, MOSM/L||SODIUM, MEQ/L||CHLORIDE, MEQ/L||POTASSIUM, MEQ/L||MAGNESIUM, MEQ/L||BUFFER (MEQ/L)|
|Plasmalyte-A||295||140||98||5||3||Acetate (27) Gluconate (23)|
|Plasmalyte-56 and 5% dextrose||362||40||40||13||3||Acetate (16)|
|Normosol-R||295||140||98||5||3||Acetate (27) Gluconate (23)|
|Normosol-M and 5% dextrose||363||40||40||13||3||Acetate|
Many available crystalloids are buffered solutions meant for fluid replacement (eg, Plasmalyte-A, Normosol-R). For longer-term treatment of patients receiving IV fluids, maintenance fluids (eg, Plasmalyte-56, Normosol-M) are solutions that contain lower sodium and higher potassium concentrations to meet maintenance needs. These solutions use dextrose to increase the osmolality of what would otherwise be a hyposmolar fluid. In practice, replacement fluids are frequently used as maintenance fluids and are often well tolerated in patients that do not have underlying conditions, such as cardiac or renal disease, that make them unable to handle the excess sodium.
In contrast, 0.9% saline is an unbuffered isotonic crystalloid. Although the tonicity of 0.9% saline is similar to that of plasma, the pH is relatively low (5.5) and the solution contains no electrolytes other than sodium and chloride. Isotonic saline is the fluid of choice for treating hypochloremic metabolic alkalosis because the acid–base disturbance cannot be resolved without correction of chloride. It also promotes calciuresis and so can be used in the treatment of hypercalcemia.
Hypotonic crystalloids are useful for treating patients with hypotonic fluid losses that result in hypernatremia or patients that have renal disease and cannot excrete the salt load of balanced isotonic solutions. Two commonly used hypotonic solutions are 0.45% saline and 5% dextrose in water (D5W). The former has an osmolarity of 154 mOsm/L, approximately half the normal plasma osmolarity in dogs and cats. D5W has a high osmolarity at 250 mOsm/L, but the dextrose in solution is rapidly metabolized upon infusion, resulting in infusion of what is essentially free water.
Hypertonic saline is the primary hypertonic fluid administered in small animal medicine. Hypertonic saline from 3-7.5% is primarily used during resuscitation in hypovolemic shock and to decrease intracranial pressure. Administration of hypertonic saline results in free water shifting from the interstitial space into the intravascular space, expanding the extracellular volume by approximately 3 times the volume administered.3,6 Movement of fluid into the intravascular space results in interstitial and intracellular dehydration, so a hypertonic saline bolus should be followed by a bolus of isotonic crystalloid, although this is not necessary if used to treat cerebral edema.
The intravascular expansion is short lived, lasting approximately 30 minutes before redistribution.3 Because the effect is transient, hypertonic saline can be combined with colloid solutions to prolong time present in the intravascular space.
In addition to intravascular expansion, hypertonic saline increases cardiac output and tissue perfusion through a weak positive inotropic effect, reduction of endothelial swelling, and arteriolar vasodilation.3
Colloid solutions contain large molecules (>10,000 Da) and tend to remain in the intravascular space longer than crystalloids.3,4 The most commonly used colloid solutions in veterinary medicine contain hydroxyethyl starch (HES).8 HES solutions are thought to be most effective in treating hypovolemia because the colloid should theoretically remain in the intravascular space, although some extravasation does occur. The half-life of various colloids depends on their molecular properties. As mentioned above, the lack of absorption at the venules means that administration of a colloid does not necessarily “pull” interstitial water into the intravascular space but opposes filtration out of the intravascular space.2
Signs of overhydration include chemosis, serous nasal discharge, increased skin turgor, peripheral edema, ascites, pleural effusion, and pulmonary edema.
The use of HES has been under debate—the risk for acute kidney injury (AKI) and increased mortality in humans has resulted in a “black box” warning from the Food and Drug Administration.8,9 A retrospective study evaluating the occurrence of AKI and death in dogs receiving HES showed an increased risk for both; however, this study evaluated a 10% HES solution, which is thought to be associated with increased risk for AKI compared with 6% solutions.10 Other potential adverse effects of HES include coagulopathy, pruritus, reticuloendothelial dysfunction, proinflammatory effects, volume overload, hepatopathy, and anaphylaxis.2,4 The incidence of AKI and increased mortality in humans has been associated with longer infusion times and higher volumes than are used in most veterinary patients,4 and further research is needed in animal patient populations to determine the risk-to-benefit ratio. HES is still used in our institution, although with somewhat more caution than previously.
Other colloids include fresh or fresh frozen plasma, canine albumin, and human serum albumin. Plasma provides albumin and coagulation factors. Because the concentration of albumin present is similar to that in plasma, large volumes must be administered to have an oncotic effect. Approximately 40 to 50 mL/kg must be administered to raise the serum albumin by 1 g/dL.1,4
Although the administration of an albumin solution would be preferable, species-specific albumin is expensive and is only intermittently available.1,4 Concentrated human serum albumin can be administered to dogs for the treatment of hypoalbuminemia, but because it is not completely homologous with canine albumin, there is potential for an immediate or delayed hypersensitivity reaction, which can result in death.1,4 Immediate hypersensitivity reactions are more common in healthy patients. Although immediate hypersensitivity reactions are rare in critically ill patients that receive human serum albumin, delayed hypersensitivity is observed as a serious complication in this population.
DETERMINING A FLUID RATE
When deciding if fluid therapy is appropriate for a patient, a few basic questions should be asked before determining a fluid therapy plan (BOX 1). These questions can be answered based on assessment of the patient for hypovolemia and dehydration (see Determining Fluid Deficits). Once the patient’s volume status and hydration needs have been determined, a fluid therapy plan can be developed.
BOX 1 Questions to Ask When Formulating a Fluid Plan
- Is the patient hypovolemic? Does it need a bolus?
- Is the patient dehydrated?
- What type of fluid should be given?
- What route?
- How much fluid should be given, and over what time period?
- When can the fluids be discontinued?
Fluid Therapy for Shock Patients
The goal of fluid therapy in patients with hypovolemic and distributive shock is to rapidly restore effective circulating volume and improve cellular oxygenation. Cardiogenic shock should be ruled out before the administration of crystalloid and colloid fluids because of the risk for exacerbation of pulmonary vasculature fluid overload.
The “shock bolus” of fluids is based on the estimated blood volume of the patient: 60 to 90 mL/kg in dogs and 40 to 60 mL/kg in cats. This amount of fluid is typically not administered because most patients have not lost their entire blood volume and respond to lower volumes of fluids. In dogs, recommendations are to start by administering 10-20ml/kg boluses of isotonic crystalloids over 15 to 30 minutes and reassessing the patient’s intravascular volume status after each bolus. Subsequent boluses can be administered according to whether perfusion parameters (eg, heart rate, blood pressure, capillary refill time, mucous membrane color) are improved. Cats are typically less tolerant of fluid boluses than dogs, so slightly lower volumes (10 to 15 mL/kg) are recommended. If a synthetic colloid is used, 5 mL/kg in dogs and 3 mL/kg in cats should be administered over 15 to 30 minutes.
Daily Fluid Therapy
In stable dehydrated patients, the goal of fluid therapy is to replace interstitial losses while simultaneously taking into account the patient’s baseline fluid requirements and any excessive losses. Thus, daily crystalloid fluid needs are calculated on the basis of 3 values:
- Maintenance needs
- Ongoing losses
The volume of crystalloid needed to correct dehydration can be calculated using the following formula:
Body weight (kg) × [% dehydration/100] = fluid deficit (L)
Dehydration can be corrected over 24 to 48 hours. Once the deficit has been determined, the total volume can be divided by the number of hours over which the dehydration is to be corrected to obtain a mL/h rate.
Maintenance fluid needs are based on both sensible and insensible losses. These can be estimated as 40-60 ml/kg per day or 2-3 ml/kg per hour in adults (pediatric patients require slightly higher rates).
Because of alterations in lean body mass, these estimates may not be as accurate for animals that weigh <2 or >40 kg.1 Because daily water requirements parallel resting energy requirements (RERs), the formula to determine RER can be used:
Body weight (kg)0.75 × 70 = RER ≈ daily fluid requirement
Ongoing losses include excessive urine output in polyuric animals, vomiting, diarrhea, blood loss, and third spacing. These losses vary by patient and may be difficult to calculate. A general rule is to estimate the amount of ongoing loss in a patient in mL/h and then reassess the patient in 4 to 6 hours to determine whether this amount needs to be adjusted.
As an example, the daily fluid needs of a 5-kg patient that is estimated to be 6% dehydrated (to be corrected over 24 hours) and has estimated ongoing losses of 1 mL/kg per hour can be calculated as follows:
- Dehydration deficit: 5 kg × 0.06 = 0.3 L × 1000 = 300 mL to be corrected over 24 hours (300 mL/24 h) = 12.5 mL/h
- Maintenance rate: 2 mL/kg/h × 5 kg = 10 mL/h
- Ongoing losses: 1 mL/kg/h × 5 kg = 5 mL/h
- Total rate (dehydration + maintenance + losses): 12.5 + 10 + 5 = 27.5 mL/h
Fluid therapy is a mainstay of care in the hospitalized small animal patient. Assessment of a patient’s fluid deficits and ongoing needs will help determine what variety of fluid and rate to use.
- Rudloff E. Assessment of hydration. In: Silverstein D, Hopper K, eds. Small Animal Critical Care Medicine. 2nd ed. St. Louis. MO: Elsevier; 2015:302-311.
- Woodcock TE, Woodcock TM. Revised Starling equation and the glycocalyx model of transvascular fluid exchange: an improved paradigm for prescribing intravenous fluid therapy. Br J Anaesthes 2012;108(3):384-394.
- Liu DT, Silverstein DC. Crystalloids, colloids, and hemoglobin-based oxygen carrying solutions. In: Silverstein D, Hopper L, eds. Small Animal Critical Care Medicine. 2nd ed. St. Louis, MO: Elsevier; 2015:311- 315.
- Cazolli D, Prittie J. The crystalloid-colloid debate: consequences of resuscitation fluid selection in veterinary critical care. J Vet Emerg Crit Care 2015;25(1):6-19.
- Muir WW, DiBartola SP. Fluid therapy. In: Kirk RW, ed. Current Veterinary Therapy VIII. Philadelphia: WB Saunders; 1983:33.
- Silverstein DC, Aldrich J, Haskins SC, et al. Assessment of changes in blood volume in response to resuscitative fluid administration in dogs. J Vet Emerg Crit Care 2005;15(3):185-192.
- Mathews KA. The various types of parenteral fluids and their indications. Vet Clin N Am 1998;28(3):483-513.
- Glover PA, Rudloff E, Kirby R. Hydroxyethyl starch: a review of pharmacokinetics, pharmacodynamics, current products, and potential clinical risks, benefits, and use. J Vet Emerg Crit Care 2014;24(6):642-661.
- Perel P, Roberts I, Ker K. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2013;2:1-64.
- Hayes G, Benedecenti L, Mathews K. Retrospective cohort study on the incidence of acute kidney injury and death following hydroxyethyl starch (HES 10% 250/0.5/5:1) administration in dogs (2007-2010). J Vet Emerg Crit Care 2016;26(1):35-40.