In hypovolemic shock, compensatory neuroendocrine responses are initiated to restore blood volume and meet metabolic demands that occur during acutely decreased cardiac output states, increasing ATP demands. When perfusion continues to be compromised despite these mechanisms, cells can no longer generate ATP, compensatory mechanisms become exhausted, and decompensatory shock ensues.
An adequate fluid resuscitation plan is necessary to optimize survival and should include the following steps:
Determine where the fluid deficit lies.
Select fluid(s) specific for the patient.
Determine resuscitation end points.
Determine the resuscitation technique to be used.
Determination of the Fluid Deficit in Fluid Resuscitation
Loss of fluid volume from the intravascular fluid compartment is manifested by poor perfusion (shock) and inadequate tissue oxygenation. This volume deficit results in lower vessel wall tension. Decreased wall tension in the aortic arch and carotid arteries results in decreased stimulation of the baroreceptors. This decreased rate of firing, sent via the glossopharyngeal and vagus nerves to the medulla oblongata, results in decreased inhibition (stimulation) of the sympathetic system.
Stimulation of the sympathetic nervous system is manifested by clinical changes in heart rate, pulse intensity, blood pressure, capillary refill time (CRT), mucous membrane color, level of consciousness, and rectal temperature. These physical perfusion parameters, combined with blood pressure, are used clinically to detect intravascular volume deficits.
Most animals with an intravascular deficit (poor perfusion) also have concurrent extravascular (interstitial and intracellular) deficits.
Fluid deficit in the interstitial and intracellular spaces causes clinical signs of dehydration. Physical findings are used to estimate the percentage of dehydration:
Semidry oral mucous membranes, normal skin turgor, and eyes maintaining normal moisture indicate 4–5% dehydration.
Dry oral mucous membranes, mild loss of skin turgor, and eyes still moist indicate 6–7% dehydration.
As dehydration becomes more severe, substantial quantities of fluid shift from the intravascular space into the interstitium, causing concurrent perfusion deficits with dehydration. Dry mucous membranes, considerable loss of skin turgor, retracted eyes, acute weight loss, and weak rapid pulses (concurrent intravascular deficit) indicate 8–10% dehydration.
Very dry oral mucous membranes, complete loss of skin turgor, severe retraction of the eyes, dull eyes, possible alteration of consciousness, acute weight loss, and thready, weak pulses indicate ≥ 12% dehydration.
Estimating dehydration in a patient is always, to some extent, subjective.
The physical guidelines to estimate dehydration are misleading in several clinical situations:
Chronically emaciated and geriatric animals may have metabolized fat from around their eyes and collagen in the skin, resulting in poor skin turgor and sunken eyes, despite normal hydration.
Animals with rapid fluid loss into a third body fluid space (a space within the body cavity where fluids from the local interstitial and intravascular spaces leak) have rapid fluid shifts from the intravascular compartments into these spaces before clinical evidence of interstitial fluid loss is observed.
Very young animals may have increased skin elasticity, making skin turgor a challenge to assess.
Nauseated animals may hypersalivate, which can alter mucous membrane dryness.
These situations require evaluation of the entire patient, including a review of their history and sometimes clinicopathological data such as PCV and total solids before dehydration can be estimated.
After the percentage of dehydration has been estimated, to determine the fluid volume deficit (in liters) using the estimated percentage, the patient's body weight in kilograms can be multiplied by the percentage of dehydration (as a decimal)—eg, a 12-kg dog that is 8% dehydrated has a fluid loss of 0.96 L (12 × 0.08 = 0.96 L). Multiplying by 1,000 will give the answer in milliliters instead of liters (960 mL).
Selection of Fluids in Fluid Resuscitation
Fluids to be administered must concentrate within the body fluid compartment where the volume deficit lies. Crystalloids are water-based solutions with small-molecular-weight particles, freely diffusible across the capillary membrane. Colloids are water-based solutions with a molecular weight too large to freely pass across the capillary membrane. Colloids are considered intravascular volume replacement solutions, and crystalloids as interstitial volume replacement solutions.
Crystalloids in Fluid Resuscitation
The small-molecular-weight particles in crystalloids are primarily electrolytes and buffers (see the table Crystalloid Fluid Types). When sodium concentration of the solution is equivalent to that of the blood plasma, the solution is called isotonic. Examples of isotonic crystalloids include the following:.
"physiological" or "normal" saline solution (0.9% NaCl)
lactated Ringer's solution (LRS), also known as Hartmann's solution
Plasma-Lyte A
Normosol-R
Intravascular administration of isotonic crystalloids will result in interstitial volume replacement and minimal intracellular fluid accumulation. More than 75% of the isotonic crystalloid administered IV will move into the extravascular space within 1 hour in a healthy animal because of normal fluid shifts between fluid compartments.
Hypotonic fluids will result in intracellular water accumulation and should not be used as resuscitation fluids. Examples of hypotonic crystalloids are 5% dextrose in water (D5W) and "half-strength" or "half-normal" saline solution (0.45% NaCl).
Hypertonic solutions contain higher concentrations of sodium and are best used when hydration is normal and concurrently with other fluids. Hypertonic saline solutions (eg, 7% NaCl) are examples of hypertonic crystalloids.
Crystalloids are considered buffered when they contain molecules (eg, acetate, gluconate, and lactate) that are converted to bicarbonate in the liver or other tissues, equilibrating the pH of the fluid to normal blood pH (7.4). Normal saline solution (0.9% NaCl) is isotonic but not buffered; it is used initially for specific clinical problems, including hyponatremia, hypernatremia, hypercalcemia, hypochloremic metabolic alkalosis, head trauma, and oliguric renal failure. Examples of buffered solutions include LRS and Plasma-Lyte A.
Crystalloids are considered balanced when they contain electrolytes (such as potassium, magnesium, calcium [K, Mg, Ca]), in addition to Na and Cl, making them similar to plasma. LRS and Plasma-Lyte A are examples of balanced solutions; normal saline solution is not balanced.
Which particular crystalloid to administer is determined by the measured or estimated sodium and potassium concentrations and by the osmolality of both the patient's serum and the fluid to be administered (see the table Crystalloid Fluid Types). Most clinical problems will benefit from the use of buffered, balanced, isotonic crystalloids (eg, LRS or Plasma-Lyte A) as part of the resuscitation fluid plan.
Crystalloid Fluid Types
Crystalloid | Tonicity | Sodium, mEq/L | Chloride, mEq/L | Potassium, mEq/L | Calcium, mEq/L | Osmolality, mOsm/L | pH |
|---|---|---|---|---|---|---|---|
Lactated Ringer’s solution | Isotonic | 130 | 109 | 4 | 3 | 273 | 6.7 |
Plasma-Lyte A | Isotonic | 140 | 103 | 5 | 0 | 294 | 7.4 |
Normosol-R | Isotonic | 140 | 98 | 5 | 0 | 295 | 7.4 |
Normal saline solution (0.9% NaCl) | Isotonic | 154 | 154 | 0 | 0 | 308 | 5.7 |
Dextrose (2.5% in 0.45% saline) | Hypotonic | 77 | 77 | 0 | 0 | 280 | 4.5 |
Dextrose (5%) in water | Hypotonic | 0 | 0 | 0 | 0 | 253 | 5.0 |
Hypertonic saline solution (7.5%) | Hypertonic | 1,232 | 1,232 | 0 | 0 | 2,464 | 5.2 |
Normosol-M with 5% dextrose | Hypertonic | 40 | 40 | 13 | 0 | 363 | 5.2 |
Abbreviations: mEq/L, milliequivalents per liter (concentration of electrolytes in solution); mOsm/L, milliosmoles per liter. | |||||||
Sodium Content in Fluid Resuscitation
When serum sodium measurements are normal, a balanced isotonic electrolyte solution can be used for volume replacement. Serum sodium concentrations that are moderately to severely decreased (< 130 mEq/L) or moderately to severely increased (> 170 mEq/L) may contribute to serum osmolality changes and result in neurological abnormalities.
Care must be taken not to increase or decrease the sodium concentration too quickly, because it may result in cerebral edema or dehydration (and can lead to intracranial hemorrhage). In affected patients, making a custom solution with a sodium content similar to the patient's during resuscitation phases may be necessary. In general, sodium concentrations should not be altered with fluid administration by > 0.5 mEq/L/h or 8–12 mEq/L/day. This allows for increased or decreased osmolality of neurons to adjust over time and avoids cerebral edema and dehydration.
Pearls & Pitfalls
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Crystalloids are also classified as either replacement or maintenance fluids:
Replacement fluids are intended to replace fluids lost from the body (through hemorrhage, vomiting, diarrhea, etc) and often contain a sodium concentration near that of plasma (such as LRS or 0.9% saline solution); these fluids result in excessive concentrations of sodium if given over prolonged periods of time (> 24–72 hours) or for animals with free water loss; however, they are ideal resuscitation fluids for animals with sodium-rich fluid losses.
Maintenance fluids contain considerably less sodium (such as half-strength saline solution or D5W) and are intended for animals that have free water loss or require prolonged fluid administration. Replacement fluids given to an animal with free water deficits or for prolonged periods of time (without access to water) will result in hypernatremia and hyperosmolarity.
Serum sodium alterations with fluid administration (Delta[Na]) can be estimated using the following formula:
Delta[Na] = ([Na]fluid − [Na]patient ) / (total body water + 1 L), in which total body water = 0.6 × kg.
In animals with decreased serum sodium content, volume replacement should be with isotonic saline solution (0.9% NaCl) or other replacement/isotonic fluids. Increased serum sodium values most commonly reflect a loss of solute-free water. The animal should be perfused and hydrated using isotonic saline solution (0.9% NaCl) or other replacement/isotonic fluids. The free water can then be replaced, if necessary, using 2.5% dextrose in half-strength LRS, 2.5% dextrose in half-strength saline solution (0.45% NaCl), or D5W when hypernatremia persists. This must be done carefully and the sodium concentration lowered slowly. Desmopressin may be required if hypernatremia persists after appropriate fluid therapy, especially when the patient has hyposthenuria or head injury.
Potassium Content in Fluid Resuscitation
When serum potassium concentration estimates are normal, a balanced electrolyte solution can be used. Unless severe, hypokalemia can be difficult to recognize clinically.
Few clinical situations warrant potassium supplementation beyond the content of LRS or Plasma-Lyte A during initial volume replacement. Once the patient has been stabilized, potassium chloride should be added to the fluids, administered at ≤ 0.5 mEq/kg/h, IV. This rate may be increased when severe hypokalemia (< 2 mEq/L) is associated with catastrophic clinical signs (eg, respiratory distress/hypoventilation from paresis of the diaphragm or generalized lower motor paresis or paralysis); one case reported infusions of 0.7–2 mEq/kg/h, but there is not a consensus on these higher rates (1). The serum potassium concentration must be closely monitored with more rapid infusions. Patients with refractory hypokalemia may benefit from concurrent magnesium supplementation (MgSO4 at 1.6–2.5 mg/kg/h, CRI).
More commonly, potassium chloride is added to 1 L of balanced isotonic crystalloids administered as maintenance fluids based on serum potassium concentration (see the table Guideline for Potassium Supplementation in Dogs and Cats). Serum potassium concentration should be monitored closely during continued therapy. Potassium phosphates may be used if a concurrent phosphorus deficiency is present.
Guideline for Potassium Supplementation in Dogs and Cats
Serum Potassium Concentration, mEq/L | Amount of KCl to Add to 1 L of Maintenance Fluids, mEq |
|---|---|
< 2.0 | 80 |
2.1–2.5 | 60 |
2.6–3.0 | 40 |
3.1–3.5 | 25–30 |
3.6–5.0 | 20 |
> 5.0 | none |
Abbreviations: KCl, potassium chloride; mEq/L, milliequivalents per liter (concentration of electrolytes in solution). | |
In animals with hyperkalemia, fluids should be selected carefully. When oliguric renal failure is suspected as the cause of hyperkalemia, potassium-free solutions, such as saline solution (0.9% NaCl), are used for volume replacement. Clinical conditions requiring potassium-free solutions include oliguric renal failure, heatstroke, adrenal insufficiency (Addison disease), and massive muscle breakdown.
After volume replacement and fluid diuresis resolve hyperkalemia, a balanced electrolyte solution should be used. These solutions have a normal pH and promote potassium excretion. Evidence suggests that with hyperkalemia secondary to feline urinary obstruction, any isotonic balanced fluid can be used, with minimal concern for increasing serum potassium as long as the underlying obstruction is treated.
Osmolality in Fluid Resuscitation
Osmolality is defined as the number of solute particles per unit of solvent. Several formulas are used to calculate serum osmolality; however, the most accurate formula, even in the face of azotemia and hyperglycemia, is as follows:
Osmolality (mOsm / kg) = 2(Na+) + [glucose / 18] + [BUN / 2.8].
Normal serum osmolality is 290–310 mOsm/L. Fluids that do not contribute substantially to serum osmolality should be used for volume replacement.
Hyperosmolar solutions include hypertonic saline solution, Normosol-M with 5% dextrose, or any isotonic fluid that has glucose or hypertonic saline solution added. Except for hypertonic saline solution, the hyperosmolar glucose-containing solutions are meant to be maintenance solutions used in animals in which fluids are not shifting rapidly from the vascular compartment to a third body fluid space. They are usually not used as volume replacement solutions.
Hypertonic saline solution provides a supranormal concentration of sodium and is generally given in a 3%, 7%, or 7.5% IV solution. The effect is to rapidly draw water from the interstitial space into the intravascular space, expanding the intravascular volume. Hypertonic saline solution may also decrease cellular swelling and improve myocardial contractility in sepsis and hemorrhagic shock. If the animal has concurrent interstitial fluid deficits (dehydration) or a disease that results in free water loss (eg, hyperthermia, diabetes), administration of hypertonic saline solution could result in severe hyperosmolality with neurological complications. Because hypertonic crystalloid solution will leak into the interstitium in < 1 hour, combining hypertonic saline solution with a colloid is recommended to offset the interstitial edema resulting from interstitial extravasation, keeping in mind the potential adverse effects associated with synthetic colloid administration.
Colloids in Fluid Resuscitation
When colloids are to be administered, a natural colloid (eg, plasma, albumin, or whole blood) or a synthetic colloid must be selected.
When the patient requires RBCs, clotting factors, antithrombin III, or albumin, blood products are the colloids of choice.
When the initial goal is to rapidly improve perfusion in an animal with adequate RBCs, a synthetic colloid can achieve the desired volume expansion rapidly. Choices of synthetic colloids include dextran, hydroxyethyl starch (HES), and stroma-free hemoglobin (see the table Synthetic Colloid Fluid Types). Synthetic colloids are generally less expensive than natural colloids but are not without concern for adverse events, which are discussed below.
Synthetic Colloid Fluid Types
Colloid | In Solution With | Average Molecular Weight, kDa | Average (and Range of) Molecular Weight, kDa | C2:C6 Ratio | Colloid Oncotic Pressure, mm Hg | Suggested Upper Limit, dose/kg/d | Concentration, % |
|---|---|---|---|---|---|---|---|
Dextran 70 | 0.9% NaCl | 70 | 10–80 | NA | 59 | 20 mL | 6 |
Hextend (670/0.7) x | Lactated electrolyte solution | 670 | 20–2,500 | 5:1 | 25–30 | 20 mL | 6 |
VetStarch/Voluven (130/0.4) | 0.9% NaCl | 130 | 110–150 | 9:1 | 36 | 50 mL | 6 |
HESPAN (600/0.4) | 0.9% NaCl | 600 | 450–800 | 5:1 | 25–30 | 20 mL | 6 |
Stroma-free hemoglobin | Modified lactated Ringer's solution | 65–130 | Up to 500 | NA | 20 | See text | 13 |
Abbreviations: kDa, kilodaltons; NA, not applicable. C2:C6 ratio describes the position of the hydroxyethyl groups on the glucose units; a higher ratio indicates a greater resistance to degradation by amylase, indicating a longer plasma half-life. | |||||||
Dextrans are polysaccharides composed of linear glucose residues. They are produced by the enzyme dextran sucrase during growth of various strains of Leuconostoc bacteria in media containing sucrose. Dextrans are isotonic and can be stored at room temperature. Dextran is broken down completely to CO2 and H2O by dextranase present in spleen, liver, lung, kidney, brain, and muscle at a rate approaching 70 mg/kg every 24 hours. In normal dogs, dextran 70 increases plasma volume 1.38 times (138%) the volume infused.
Hemostatic changes in healthy experimental dogs given dextran 70 include an increase in the buccal mucosal bleeding time and partial thromboplastin time and a decrease in von Willebrand factor antigen and factor VIII coagulant activity, without clinical bleeding. Dextran copolymerizes with the fibrin monomer, destabilizing clot formation. Blood glucose concentration may be increased during dextran metabolism. Dextran 70 may cause a change in the total solids value that does not reflect actual protein content and may interfere with blood crossmatching.
Moderate to life-threatening reactions in dogs have been rare. Due to their adverse effects, dextrans are rarely used clinically in favor of other colloids; dextran 40 is not recommended because it is known to cause renal injury.
Hydroxyethyl starch is the parent name of a polymeric molecule made from waxy species of corn and potatoes and is composed primarily of amylopectin (98%). HES molecules vary in size from 10,000 to several million daltons (average 70–670 thousand daltons). The disappearance of HES molecules from the body depends primarily on their rate of enzymatic degradation by alpha-amylase and subsequent renal excretion. Other methods of elimination include absorption by tissues (liver, spleen, kidney, and heart), uptake by the reticuloendothelial system, and clearance through bile. Blood alpha-amylase–mediated hydrolysis (primarily at the C6 position) decreases the molecular weight to < 72,000 Da; these smaller particles are more osmotically active but eliminated at a faster rate through the kidney. Metabolism of HES retained in tissue is likely performed by cytoplasmic lysosomes. An increase in serum amylase is to be expected without alteration in pancreatic function.
Along with molecular weight, the degree of molar substitution, which is the number of glucose units on the starch molecule that have been replaced by hydroxyethyl units, is the major determinant of how long different types of HES survive in the blood. Molar substitution rates vary from 0.35 to 0.7, and the higher the molar substitution, the longer the half-life in blood. The position of the molar substitution also impacts half-life; this can occur at the C2, C3, and C6 positions. Stereotactically, substitution at the C2 site impedes degradation by amylase, prolonging the half-life of HES; this is often referred to as the C2:C6 ratio. Higher ratios imply impeded breakdown and therefore longer half-lives in blood.
When hetastarch (the most common HES) is infused at 25 mL/kg, IV, in healthy dogs, the initial increase in plasma volume is 1.37 times (137%) the volume infused; most hetastarches will expand plasma volume 100–150%. Intravascular persistence is significantly greater than that of dextran 70, with 38% of hetastarch remaining, compared with 19% of dextran, 24 hours after infusion. Administration by CRI may provide a constant supply of larger-molecular-weight particles, perhaps maintaining and augmenting plasma colloid oncotic pressure (COP) and intravascular volume in animals with albumin loss or increased capillary permeability. Most HES molecules may persist in the body for 2–7 days.
Hydroxyethyl starches favor retention of intravascular fluid and prevent washout of interstitial proteins. In hypo-oncotic situations, HES infusion has a great advantage over other colloids because the larger molecules remain intravascular, limiting pulmonary fluid flux. HES infusion is nontoxic and nonallergenic in dosages as high as 100 mL/kg in dogs. Many cats have a moderate reaction—nausea and occasional vomiting—with rapid infusion. However, when hetastarch is given slowly (throughout 5–15 minutes), this adverse effect is minimal.
More serious adverse effects associated with synthetic colloid use include the development of acute kidney injury (AKI) and coagulopathy. Renal injury, reported to occur from an osmotic nephrosis in humans, has been poorly documented in dogs and cats. Although there has been much controversy and decreased use of HES solutions due to concern for kidney injury, more recent evidence does not suggest that kidney injury develops with 7% or lower solutions (2). Synthetic colloid–associated AKI is seemingly of low risk when colloids are administered in small doses (< 20 mL/kg) or for short durations (< 24 hours); however, administering synthetic colloids to patients with preexisting azotemia is not advised.
Pearls & Pitfalls
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Hetastarch is associated with minor alterations in laboratory coagulation measurements but not with clinical bleeding unless daily minimal dosages (20–50 mL/kg/day, depending on the type) are exceeded. Molecular weight seems to have the biggest impact on coagulation, with larger-molecular-weight starches impacting coagulation to a greater degree. The proposed mechanisms of impact on coagulation include "coating" platelets or impeded platelet receptor signaling, dilution of coagulation factors, and interference with von Willebrand factor/factor VIII interaction. Dilutional effects on coagulation, cells, and proteins are produced in response to the volume expansion of the plasma. Animals that receive large volumes of HES solutions may have more oozing if surgery is performed, and diligent hemostasis is warranted.
Current recommendations for administration of HES solutions include minimizing the dose and duration while monitoring coagulation parameters, platelet count, hematocrit, and renal function. A variety of HES solutions are currently available, each with its own advantages and disadvantages based on its molecular composition.
Stroma-free hemoglobin, also called hemoglobin-based oxygen carrier (HBOC), is a polymerized bovine hemoglobin-based solution that increases plasma and total hemoglobin concentration. HBOCs are not currently available in the US. These solutions are indicated for treatment of anemia and hypovolemia with tissue hypoxia. Stroma-free hemoglobin has colloidal properties similar to those of hetastarch and exerts mild vasopressor activity, believed to be through scavenging of nitric oxide, a potent constitutive and inducible vasodilator. The solution's dark hue causes discoloration of serum (and sometimes urine) that can interfere with some serum biochemical tests, depending on the type of analyzer and reagents used. Bilirubinuria will be present.
HBOC (≤ 30 mL/kg/day, IV, at an infusion rate of < 10 mL/kg/h) has been approved for dogs. When given to an animal with normal blood volume, HBOC must be administered slowly and carefully monitored to avoid volume overload resulting from the colloidal and pressor properties of the solution. HBOC has also been used in cats (4–25 mL/kg/day, IV infusion, and as a rapid infusion of 1–5 mL/kg over a mean of 25 minutes) (3). Anecdotally, the pressor effects in cats seem pronounced, and blood pressure should be monitored. HBOC has been associated with development of pulmonary edema, pleural effusion, and respiratory distress, particularly in cats with underlying heart disease.
Lyophilized canine albumin is available and can be reconstituted to a 5% solution. It has been administered to dogs with septic peritonitis and hypoalbuminemia and has been demonstrated to increase oncotic pressure, measured albumin concentration, and Doppler-measured blood pressure, with increased albumin concentration persisting for up to 24 hours. Minimal adverse effects have been noted. Replacement volume in milliliters of albumin 5% solution (50 mg/mL) can be calculated using the following formula:
body weight (kg) × 90 mL/kg × (target albumin concentration [eg, 2 mg/dL] − patient's current albumin concentration) × 0.2 g/dL
Lyophilized canine albumin may also be administered to hypotensive patients as a more concentrated solution (up to 25% or 250 mg/mL; 450–800 mg/kg, slow IV over several hours). Human serum albumin is available as well and has been used with success in critically ill veterinary patients; however, when it is administered to healthy animals, severe adverse effects, including multiple organ failure, have been noted, so its use in critically ill animals remains controversial.
Blood products are important in many situations. Animals that need clotting proteins may require frozen (or fresh frozen) plasma or cryoprecipitate, which contains concentrated amounts of factor VIII and von Willebrand factor; platelet-rich plasma or lyophilized platelets may be necessary for platelet deficiencies. Animals with severe anemia or blood loss may require whole blood or packed RBCs. Cavitary hemorrhage may allow collection of blood, either with centesis or in surgery, for autologous blood administration when banked blood is not available. More information is available in Blood Transfusions in Dogs and Cats.
Fluid Selection in Fluid Resuscitation
Interstitial and intracellular volume deficits (dehydration) are replaced by the administration of crystalloids. Intravascular volume (perfusion) deficits can also be replaced with crystalloids alone. However, when large quantities of isotonic crystalloids are rapidly administered IV, there is an immediate increase in intravascular hydrostatic pressure, a decrease in intravascular COP, and extravasation of large fluid quantities into the interstitial spaces; negative effects of the endothelial glycocalyx have also been reported. By administering colloids in conjunction with crystalloids during fluid resuscitation of perfusion deficits, less total fluid volume is required (crystalloids decreased by 40–60%), there is less tendency toward fluid overload, and resuscitation times are shorter.
Many conditions can increase capillary permeability, including disruption of the endothelial glycocalyx layer (EGL), and result in systemic inflammation response syndrome (SIRS):
parvoviral diarrhea
severe GI disease
pancreatitis
septic shock
massive trauma
heatstroke
cold exposure
burns
systemic neoplasia
Hetastarch and blood products are the colloids of choice for intravascular volume resuscitation when there is increased capillary permeability and loss of albumin through the capillary membrane. Using crystalloids alone in animals that require large volumes for resuscitation or that have increased capillary permeability and disruption of the EGL will often result in notable interstitial and organ edema, which can lead to organ dysfunction. When hypotension is concurrent, a vasopressor to increase vascular tone (blood pressure) is often indicated as well.
Many affected animals also have third-space fluid losses, most likely due to substantial regional inflammation, that result in massive fluid requirements and make it difficult to predict the volume required to maintain fluid balance.
Determination of Resuscitation End Points
There are no standard formulas for crystalloid or colloid infusion that will guarantee complete volume resuscitation in a small animal. Variables such as renal function, presence of a third body fluid space, brain injury, lung injury, heart disease or failure, continued losses, or closed cavity hemorrhage require that fluid resuscitation rate and volumes be individualized for the patient.
Sufficient volumes of fluid should be administered to reach desired resuscitation end points. This process has also been termed early goal-directed therapy. The end points typically reflect perfusion status and include heart rate, blood pressure, central venous pressure, mucous membrane color, CRT, and pulse intensity. A resolution of an increased blood lactate concentration to < 2 mmol/dL supports adequate tissue oxygenation. Supplementary end points may be used but require additional patient instrumentation and are used less commonly; they include central venous pressure of 5–8 cm H2O, central venous oxygen saturation > 70%, and a urine output ≥ 1–2 mL/kg/h.
Shock depletes cellular energy stores, with subsequent cellular and organ dysfunction. Restoring the circulation to “normal,” with normal oxygenation and perfusion parameters, may not be enough to allow sufficient ATP production for repair as well as maintenance.
When an animal is suspected of having a disease process related to SIRS, such as vasodilation, increased capillary permeability, or depressed cardiac output, resuscitation end points are chosen for supranormal resuscitation (see the table Resuscitation End Points). The goal is to deliver oxygen and glucose to the cells in higher-than-normal concentrations to promote sufficient energy production for both repair and maintenance of the cells.
Resuscitation End Points
Monitored Parameter | Supranormal (high-volume resuscitation) | Hypotensive (low-volume resuscitation) |
|---|---|---|
Blood pressure | ||
- Systolic - Mean arterial | 90–120 mm Hg 80–90 mm Hg | 80–90 mm Hg 60–80 mm Hg |
Central venous pressure | 6–8 cm H2O | 3–5 cm H2O |
Heart ratea | ||
- Dog - Cat | < 140 bpm 160–200 bpm | < 140 bpm 160–200 bpm |
Capillary refill time | 1–2 seconds | 1–2 seconds |
Pulse intensity (femoral) | Strong | Strong |
Resuscitation technique | ||
- Dog - Cat | Large volume Small volume | Small volume Small volume |
Clinical indications | SIRS diseases Cortisol deficiency (hypoadrenocorticism, critical illness-related corticosteroid insufficiency) Anaphylaxis | Heart failure Closed cavity hemorrhage Ongoing hemorrhage Brain disease Lung edema Oliguric renal failure |
a After appropriate analgesia. | ||
In certain situations, however, supranormal resuscitation can be detrimental. Increased vessel wall tension can dislodge a lifesaving clot in the vasculature of a traumatized animal, exacerbating hemorrhage. Brain and lung edema or hemorrhage can be worsened by aggressive and sudden increases in hydrostatic pressure.
Hypotensive resuscitation provides end points that are at the lower limit of normal. The goal is to administer the smallest volume of fluids possible to successfully resuscitate the intravascular compartment while minimizing extravasation of fluids into the interstitium (especially brain or lungs), titrating the amount of preload to minimize excess fluid load to a potentially disabled heart, and decreasing the probability of dislodging clots. Small-volume resuscitation techniques should be used to reach hypotensive resuscitation end points.
Determination of Appropriate Resuscitation Technique
Large- and small-volume techniques are used to reach end points discussed above. These doses of fluids should be administered throughout 15–30 minutes as a rapid IV infusion, and then the patient should be reassessed for restoration of normal clinical perfusion parameters and objective measurements of perfusion. Continual reassessment and titration of fluid doses will achieve resuscitation from shock in most cases (while the underlying disease is investigated and therapy instituted).
Dogs in hypovolemic shock that require supranormal end point values can benefit from large-volume resuscitation techniques. Typically, an initial IV infusion of 20–50 mL/kg of buffered, balanced isotonic crystalloids is given, followed by 5–15 mL/kg of an HES solution, if indicated. When stroma-free hemoglobin is selected as the colloid, the dosage is 5 mL/kg. Additional colloids (such as blood products) can be administered using small-volume intravascular resuscitation techniques if perfusion has not improved to the desired supranormal end points after the initial large-volume dose of fluids. Colloids should be added immediately in any animal with proteinaceous fluid losses (SIRS disease, GI fluid losses, etc). For patients with hemorrhage, blood products are often the ideal choice for resuscitation, and with catastrophic hemorrhage, large volumes may be required.
Pearls & Pitfalls
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Small-volume resuscitation techniques are recommended in hypovolemic cats and any dog with closed cavity hemorrhage, head injury, pulmonary contusions or edema, cardiogenic shock, or oliguric renal failure. An initial IV dosage of balanced isotonic crystalloids (10–15 mL/kg for dogs; 5–10 mL/kg for cats) is given. A colloid solution (dogs: 5 mL/kg; cats: 2–5 mL/kg) can be administered IV over 5 minutes as well. The perfusion parameters are reassessed, and the initial bolus dose repeated as needed until the resuscitation end point is reached. When stroma-free hemoglobin is used as the colloid in dogs, the dosage is 2–5 mL/kg. HBOCs have not been approved for use in cats; however, they have been used successfully at a dosage of 1–5 mL/cat (0.25–1 mL/kg) slow IV over 5 minutes.
Hypothermia, especially in cats, can greatly limit the cardiovascular response to endogenous sympathetic stimulus (catecholamines) and to fluid resuscitation. Active external warming with circulating water blankets should be done concurrently with fluid resuscitation for hypothermic patients. Additional warming techniques, such as fluid line warmers, warm air blowers, and temperature-controlled blankets, can be used as well; water bottles or electric blankets can result in burns and should be avoided. Aggressive volume administration without active warming of hypothermic cats can result in pulmonary edema despite continued hypotension.
Key Points
The fluid resuscitation plan should include determining where the fluid deficit lies (intravascular, interstitial, or intracellular) based on history and physical exam findings, the appropriate fluid for the patient, appropriate resuscitation end points, and appropriate resuscitation technique.
Crystalloid solutions are classified as isotonic, hypotonic, or hypertonic, based upon their osmolarity in relation to blood plasma, each with utility for specific clinical situations.
Colloid solutions are natural or synthetic, with adverse effects associated with synthetic colloid administration, including acute kidney injury and coagulation abnormalities reported most commonly with hydroxyethyl starch solutions.
Resuscitation end points can be classified as either supranormal or hypotensive, with large- and small-volume resuscitation techniques used to reach these end points, depending on clinical indications for each individual patient.
For More Information
2024 AAHA Fluid Therapy Guidelines for Dogs and Cats. American Animal Hospital Association.
Transfusion guidelines. Association of Veterinary Hematology and Transfusion Medicine.
DiBartola SP, de Morais HA. Disorders of potassium: hypokalemia and hyperkalemia. In: DiBartola SP, ed. Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice. 4th ed. Saunders Elsevier; 2012:92-119. doi:10.1016/B978-1-4377-0654-3.00012-3
Bateman S. Disorders of magnesium: magnesium deficit and excess. In: DiBartola SP, ed. Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice. 4th ed. Saunders Elsevier; 2012:212-229. doi:10.1016/B978-1-4377-0654-3.00015-9
References
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