Water, water everywhere: Fluid choices in the hospitalized patient

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Danielle Thomas, DVM, DACVECC
Massachusetts Veterinary Referral Hospital, Woburn, MA
Posted on 2017-01-31 in Emergency & Critical Care
 

Fluid therapy is a crucial part of the treatment of patients in the emergency room and the critical care unit. Though it has great ability to help our patients, like any medical intervention, it has the potential to do harm as well. Having a greater understanding of the fluid balance within the body, the effect of different disease states on this fluid balance, and the fluid choices available for treating our patients is vital to maximizing patient benefit, while minimizing side effects of therapy.

Bone, water, and ions

Sixty percent of an adult animal’s body weight is water (referred to as total body water). This composition will vary with age, sex, species, and body condition score. Water has a multitude of roles within an animal’s body including transport of red blood cells, electrolytes, and nutrients, carrying substrates across cellular membranes, facilitating evaporative cooling, acting as a solvent, and participating in metabolic functions and reactions. It is the major component of all body fluids and is distributed into distinct compartments within the body. The intracellular fluid (ICF) makes up 40% of body weight, or two-thirds of total body water. The remaining third of total body water is contained in the extracellular fluid (ECF) compartment which makes up roughly 15-30% of body weight. The extracellular fluid is further compartmentalized into the interstitial fluid which makes up ¾ of the ECF and the intravascular fluid which comprises the remaining ¼ of ECF. This portion is primarily plasma. The easiest way to remember these proportions is the 60:40:20 rule. Sixty percent of weight is water. Forty percent of body weight is intracellular fluid. Twenty percent of body weight is extracellular fluid. These compartments are separated by membranes. The endothelial membrane and endothelial glycocalyx separate the intravascular from the interstitial space and the cell membranes separate the ICF from the ECF. Fluid movement across these membranes depends on the characteristics of the membrane, hydrostatic pressure, colloid oncotic pressure, and osmolarity. The ECF and ICF have very distinct ionic compositions which are maintained primarily through the activity of the sodium / potassium ATPase pump. The activity of this pump maintains a high extracellular sodium concentration and a low extracellular potassium concentration, which is evident in the electrolyte composition of plasma in the healthy patient.

Fluid balance

In addition to maintaining a balance between the fluid compartments within the body, the animal must also maintain fluid balance with the outside world. Fluid enters the body in the form of water consumed by the animal. Some water is also produced via metabolic processes. Fluid is lost from the body under normal conditions from the respiratory system, the feces, and the urine. Disease states can lead to fluid losses from additional sources such as pyrexia, cutaneous injury, gastrointestinal disease, respiratory disease, third spacing of fluid, and hemorrhage. Disruption in the balance between fluid intake and loss can result in disorders of hydration and perfusion. These imbalances may be evident on physical examination, laboratory data, or assumed based on signalment and history.

Terminology

When fluid losses exceed fluid intake a fluid imbalance develops. The type of fluid that is lost from the body, as well as the fluid compartment from which it is lost is important for determining a strategy for treating the patient. It is necessary to clarify certain terms which are relevant for the discussion of compartment specific losses. Hydration is the process of water intake and a patient’s hydration status is a reflection of their total body water and the role of this water in tissue support and cellular processes. Dehydration results from decreased water intake relative to losses. The term “perfusion” refers to the transport of blood to the tissues. Hypovolemia is a condition of reduced intravascular volume which can result from losses of plasma water or whole body blood loss.

Intravascular fluid deficits lead to changes in perfusion which can manifest as the clinical signs of shock. Interstitial and intracellular fluid losses change hydration status and lead to clinical signs associated with dehydration. In the event of interstitial fluid losses interstitial COP increases and hydrostatic pressure decreases which leads to movement of fluid from the intravascular to interstitial space. This is clinically evident as an increased plasma sodium concentration and packed cell volume. Interstitial fluid losses are common through the loss of hypotonic fluid through many common disease processes (i.e. gastroenteritis, diabetes mellitus, or fever). Intracellular water deficits are associated with diseases that result in intravascular or interstitial hypernatremia, loss of solute free water (diabetes insipidus), or a large increase in impermeable solutes (mannitol administration).

Making a plan

Once you have established that a fluid imbalance exists in your patient it is time to develop a fluid therapy plan. There are three phases of fluid therapy: resuscitation, rehydration, and maintenance. To construct your therapy plan it is necessary to ask several questions: Is the patient in shock? Is the patient dehydrated? Can the patient drink? If your patient can drink, can it drink enough to replace losses and sustain itself? What type of fluid are you going to administer to your patient? By what route will the fluids be administered, what volume of fluids should you give, and how rapidly should they be administered?

One of the most important questions to ask in designing your treatment plan is what are your goals of fluid administration? Are you attempting to correct clinical dehydration or achieve targeted end points of resuscitation? By establishing objective goals of fluid therapy such as correcting electrolyte abnormalities, normalizing lactate, or improving blood pressure you establish markers by which you can evaluate your treatment plan and determine the next steps of therapy. In human and veterinary medicine achieving specific end points of resuscitation such as normo-lactatemia, improved base deficit, and correcting hypotension has been shown to improve outcome in the critically ill.

Types of fluids

When selecting a fluid for treating your patient, choosing a fluid with a composition similar to that of what was lost by your patient is ideal. There are several types of fluid options which can be considered including crystalloids, colloids, blood products, and hemoglobin based oxygen carriers. Transfusion medicine is a large topic which will be touched on when necessary in this discussion, but is generally beyond the scope of this talk. Hemoglobin based oxygen carriers are products derived from isolated bovine hemoglobin and are intended solely for the transport of oxygen. These products are sporadically available in this country and will therefore not be discussed in any detail here.

Crystalloids and colloids are the mainstays of fluid therapy and an understanding of their properties will allow the most effective use in our patients. Crystalloids contain small solutes with a molecular weight less than 500g/mole. The majority of these solutes are electrolytes and readily cross the capillary endothelium and equilibrate throughout the extracellular fluid compartment. Crystalloids can be categorized as balanced or unbalanced fluids. Balanced fluids have a composition similar to extracellular fluid (relatively high sodium and low potassium), whereas unbalanced fluids do not (0.9% saline). Further classification divides crystalloids into replacement or maintenance solutions. Lactated ringers solution, Plasmalyte -148, and Normasol R are all replacement solutions. Replacement solutions, aka isotonic crystalloids, are similar in composition to the extracellular fluid and are intended to be used to correct fluid deficits. Maintenance crystalloid solutions replicate the fluid lost daily through normal physiologic functions. These fluids may be hypotonic to plasma and contain lower concentrations of sodium and higher concentrations of potassium than replacement solutions. It is not necessary to use these solutions, as you can often get by using a replacement solution throughout hospitalization if you supplement potassium and monitor for iatrogenic hypernatremia.

Five percent dextrose in water (D5W) is another crystalloid that may be considered in certain cases. This solution uses dextrose molecules to make it isosmotic to plasma. When administered, this dextrose is quickly metabolized so that you are essentially administering water. D5W is used to replace free water deficits. It should not be used to correct dehydration, but can be given in concert with an isotonic replacement crystalloid to correct free water deficits and correct interstitial dehydration.

Crystalloids exert their effect on the interstitial and intracellular compartments primarily. Because they rapidly equilibrate throughout the ECF, after 30 minutes only half of the administered dose remains in the vasculature. This is important if you are intending to use them for a volume expanding effect. This effect rapidly declines and you may require repeated dosing, increasing the risk of fluid overload.

Advantages to the use of crystalloids in fluid therapy include their ready accessibility, relative affordability, and their ease of use. Because crystalloid usage is so prevalent there is also a large body of literature concerning their use. Conversely, because crystalloids readily equilibrate with the interstitium their benefit in resuscitation and therapy can be short lived. As a result, large volumes of fluids may be required to sustain hemodynamic endpoints, increasing the risk for fluid overload. Large volume crystalloid infusion can also lead to a dilutional coagulopathy, hypothermia, damage to the endothelial glycocalyx, cardiac arrhythmias, and alteration of immune function. The risk of fluid overload, resulting in pulmonary edema, abdominal, and extremity compartment syndrome is substantial with aggressive crystalloid usage, especially in critically ill or traumatized patients. The hemostatic impact of crystalloid infusion will be discussed further in the discussion of resuscitation in trauma.

Colloids are large molecular weight substances (> 10,000 Da) which are restricted to the vascular compartment in patients with an intact endothelial membrane. These substances can be synthetic (synthetic starch compounds) or natural (albumin, allogenic blood products). Colloids exert their effect within the intravascular compartment by increasing intravascular colloid oncotic pressure and pulling fluid into the vascular space from the interstitium. Because of this ability to move fluid between compartments the vascular expansion achieved by colloids is reported to be 1.4 to 1.5 times greater than the volume of colloid administered. This volume expansion is maintained for several hours suggesting that the clinical impact of colloid administration has a greater duration than that of crystalloids. As a result, you theoretically can resuscitate a patient using a smaller volume of colloids than you would need of crystalloids. A multitude of studies in human medicine have investigated this question and this hypothesis has not been supported.

Synthetic colloids in the form of synthetic starches are the colloids most often available in veterinary practice. These colloid solutions are polydiverse and hyperoncotic to plasma. Hydroxyethylstarches are characterized by their concentration in solution, their molecular weight and their degree of hydroxyl substitutions at the C2 vs C6 position. These characteristics determine the half-life of these colloids with a larger molecular weight, higher degree of substitution, and higher C2:C6 ratio being associated with a longer half-life. Synthetic starches are removed from the body via amylase activity and the reticuloendothelial system. The break down products are eliminated by the kidneys in what is a saturable elimination process, with a higher dose leading to a prolonged half-life.

The most important natural colloid is the protein albumin. In health, albumin contributes more than 70% of colloid oncotic pressure (COP) in the blood. Albumin has many other functions including wound healing, coagulation, and transport of hormones, toxins, drugs, and cations. It also binds free radicals and acts as a weak buffer by binding hydrogen ions.

Isolated human albumin, available as isooncotic 5% or hyperoncotic 25% solutions, is the colloid most commonly used in human medicine and its role in resuscitation has been extensively studied. The use of human albumin in critically ill veterinary patients has also been reported. Because canine and human albumin share only 79% homology, there is the risk for delayed or immediate hypersensitivity reactions when this product is given to veterinary patients. Retrospectives reporting the use of human albumin in critically ill dogs have reported a relatively low rate of reactions when the product is given only once. The reaction rate was much higher when healthy dogs received the product in single or repeated doses.

Isolated canine albumin has recently become available and its use has been reported in veterinary medicine in patients with septic peritonitis. Craft et al demonstrated that this product increased albumin, COP, and Doppler blood pressure, but that this change was not maintained until discharge. Higher albumin was associated with improved survival, which has been shown in several other studies. No adverse reactions were reported to the product in this study.

Albumin can be dosed either by calculating the albumin deficit or based on body weight. Fresh frozen plasma or frozen plasma can also be used to supplement albumin. The dose of plasma required to raise a patient’s albumin 1g/dL is 45ml/kg. This rapidly becomes cost prohibitive in medium to large sized dogs.

In addition to their effect on colloid oncotic pressure both synthetic colloids and albumin are reported to help reduce fluid extravasation in the critically ill by sealing leaks in the vascular endothelium. In what is called the “COP paradox” these molecules have been shown to reduce fluid extravasation in excess of what is expected by just the increase in COP. This is attributable to their effect on the endothelium and endothelial glycocalyx. For instance, HES causes a greater increase in COP than albumin, but albumin has a greater effect on reducing fluid extravasation due to its greater ability to bind to the endothelial glycocalyx.

The primary advantages to using colloids in fluid therapy is their greater and sustained impact in intravascular volume relative to the administered dose. Compared to crystalloids, you get a greater bang for the buck in this respect. Disadvantages to using colloids include their cost, availability, and risk of extravasation in vascular leak conditions. Recently, significant concerns have been raised in human (and veterinary medicine) regarding the use of synthetic starches such as Hetastarch for fluid support. These concerns include increased risk of acute kidney injury, induced coagulopathy, and increased mortality. Impaired coagulation has been demonstrated following Hetastarch administration in dogs experimentally. This topic will be addressed further later in this presentation.

Dose and rate

Determining the dose of fluids to administer and the rate at which to administer them is the next step in your treatment plan. The route of fluid administration should also be considered. As this discussion is focused on the critically ill and hospitalized patient, we will confine our discussion of the route of fluid administration to the intravenous route. The intraosseus route is also an excellent option for neonatal or pediatric patients or in the hemodynamically unstable patient in whom venous access cannot be rapidly obtained. The subcutaneous route of fluid administration is appropriate only for hemodynamically stable patients with mild dehydration. Venous access should be obtained by placing the shortest IV catheter with the largest diameter possible. Because flow through the catheter is inversely proportional to the length of the catheter and directly proportional to the radius of the tube raised to the fourth power you can see how important the diameter of the catheter is to insuring proper fluid administration. Large animals or animals that are unstable and require a large amount of resuscitation may require multiple intravenous catheters.

The dose of IV fluids to administer depends on the hemodynamic stability of your patient, the degree of dehydration, and the amount of ongoing losses that they are experiencing. In the dehydrated patient one can make a calculation of fluid deficit based on their estimated degree of dehydration as a percentage of body weight based on the following calculation: Fluid deficit in milliliters = (percent dehydration/ 100) x (body weight in kilograms) x 1000. To determine the patient’s total fluid needs you must also take into account the maintenance fluid requirements based on the patient’s signalment. There are a multitude of ways to calculate these requirements based on body weight and body surface area. Generally, these requirements approximate the animal’s daily caloric requirements which may be calculated by the following equation: Daily maintenance requirements in milliliters = 70 x (body weight in kg)0.75 . The last, and potentially most challenging component to the fluid therapy dose is an estimate of the patient’s ongoing losses. This can be evaluated by quantifying urine output or weighing bedding, or estimated based on body weight. Patients that are hyperthermic, drooling excessively, or panting heavily will have excessive fluid losses that may not be as evident as a pool of vomit on the floor. Because this part of the assessment is challenging to quantify, it underscores the importance of reassessing the patient and adjusting your plan as needed.

Having determined your patient’s fluid deficit, maintenance requirements, and estimated ongoing losses you next determine the speed at which you plan to replenish the deficit and therefore the fluid rate for your patient. The speed at which fluids are administered depends on the hemodynamic instability of your patient, the chronicity of any dehydration that is present, and the underlying cardiac and renal function of your patient. In an otherwise healthy, dehydrated, vomiting patient for example, you may elect to replace the fluid deficit rather fast, say, over a period of 4-6 hours. If you have a geriatric pet with heart disease and renal dysfunction who is chronically dehydrated due to poorly controlled diabetes mellitus, it is more appropriate to replace the fluid deficit over a period of 18-24 hours. In both of these cases, the volume of the fluid deficit is divided by the number of hours over which you plan to replace it, to give a milliliters / hour rate. This volume is in addition to the maintenance rate dictated by your patient’s daily fluid requirements. Special attention must be paid to conditions involving derangements of sodium and potassium. Fluid resuscitation in cases of severe elevations or deficits of either of these electrolytes, resulting in rapid changes in plasma concentrations can have severe consequences.

Monitoring

No fluid resuscitation plan will be perfect, therefore reassessment of the plan based on objective patient parameters and therapeutic endpoints is crucial. Patient assessment should include physical examination, urine output assessment and urine specific gravity, body weight monitoring, and bloodwork including PCV/TS, electrolyte assessment, and potentially evaluation of perfusion parameters such as plasma lactate, and central venous oxygen saturation. Central venous pressure can also be measured if your patient possesses an appropriately placed jugular venous catheter. The patient should be monitored for signs of fluid overload such as weight gain in excess of replaced fluid deficit, chemosis, gelatinous subcutaneous tissue, limb edema, or signs of pulmonary edema such as pulmonary crackles or tachypnea.

Shock resuscitation

Fluid therapy of a patient in shock deserves special attention. Shock is a specific physiologic condition characterized by inadequate production of energy at the cellular level which is typically due to inadequate delivery of oxygen and nutrients. In most cases, shock is a reflection of poor perfusion leading to the partial pressure of oxygen at the tissue level falling below a critical level. In certain cases, shock can be due to the inability of the cells to extract oxygen from the blood, but this is beyond the scope of this discussion. Shock can be further categorized by etiology. Cardiovascular shock results from an absolute decrease in intravascular circulating volume (hypovolemic shock). Anemia and hypoxemia lead to shock by decreasing the oxygen content of the blood. Distributive shock is the result of inappropriate generalized vasoconstriction or vasodilation leading to the maldistribution of the circulating volume. Cardiogenic shock refers to the failure of the cardiac pump as we see in cases of congestive heart failure.

Patients in shock may display clinical signs of poor perfusion including pale mucus membranes, prolonged capillary refill time, weak peripheral pulses, hypotension, and altered mentation as well as clinical signs associated with the triggering disease process. Tachycardia and tachypnea may also be present as these are associated with the body’s attempt to compensate for decreased cardiac output and tissue oxygenation. Lab work in patients with shock may show hyperlactatemia, decreased central venous oxygen saturation, hemoconcentration, or anemia as well as electrolyte abnormalities.

Fluid therapy is an important part of treatment of shock in cases of cardiovascular shock or distributive shock. The goal of fluid therapy in shock is to reestablish tissue perfusion and nutrient delivery to the cells, allowing them to resume function and preventing cell death and end organ injury. Improvement in hypotension in dogs in the emergency room has been shown to improve outcome, but the best way to provide resuscitation in shock remains open for debate.

Isotonic crystalloids are an appropriate choice for a patient with a volume deficit, but they must be given rapidly and their effect on intravascular volume is short lived. It can be challenging to give the needed dose of these fluids to a large animal in a timely fashion to achieve intravascular expansion before fluid redistribution. If resuscitation with isotonic crystalloids is attempted it is appropriate to consider the blood volume of your patient, 90ml/kg for a dog and 50ml/kg for a cat. This volume has been called the “shock dose” of fluids, which is inappropriate, because not every patient in shock needs this dose of fluids. Instead, start with ¼ of this dose of fluids and assess your patient’s response. These small doses can be repeated depending on your patient’s status. Giving crystalloids in a titrated fashion reduces the chance of fluid overload.

Hypertonic crystalloids, specifically hypertonic saline, are another choice for resuscitation in shocky patients. These solutions have a high osmolarity, up to 2400mOsm/L, which creates an osmotic gradient from the interstitium to the intravascular fluid compartment. As a result, like colloids, the volume expansion achieved with hypertonic saline is greater than the dose given. Typically, these solutions are administered in doses of 3-4ml/kg. Hypertonic saline is good choice for patients that were normovolemic prior to going into shock, therefore they don’t need a large volume of fluid replaced. A good example of this is an otherwise healthy dog who was acutely hit by a car. This dog is not dehydrated, but may be in shock. Hypertonic saline has other perks including benefits for patients with traumatic brain injury, immunomodulatory effects, improved rheologic properties of blood, reduced endothelial swelling, and positive ionotropic effects. Hypertonic saline also rapidly redistributes between the fluid compartments, so the volume expansion that it achieves will be short lived if it is not followed with another type of fluid. Commonly, hypertonic saline is followed by a similar dose of colloid, to help maintain volume expansion. The use of hypertonic saline in profoundly dehydrated patients or patients that may not be able to regulate their total body water appropriately is not recommended. Dehydration is not a contraindication for use as long as isotonic crystalloid therapy is also part of the plan. Hypertonic saline must be given slowly (usually over 10 -15 minutes) as rapid infusion can cause a vagal response.

Colloids may have a role in resuscitation from shock because of their volume expanding effects and the prolonged duration of this effect relative to crystalloids. Small doses of colloids such as Hetastarch (4-5ml/kg) used in combination with hypertonic saline is known as low volume resuscitation and is a good option for normovolemic shock patients. These doses can be repeated based on patient response. The previously mentioned risks associated with colloids should be considered.

Fluid resuscitation in shock patients should continue until the patient’s clinical signs have improved and until endpoints of resuscitation have been achieved. In hemodynamically unstable patients it is not always clear if their cardiovascular instability is due to a fluid volume deficit, or other factors (i.e. vasoplegia). A fluid challenge may be performed in these patients. When performing a fluid challenge objective resuscitative end points are selected (lactate, heart rate, blood pressure) and a dose of fluid is administered for a specific period of time (10-30 minutes). Once this dose of fluids has been received, the patient is reassessed to determine if the previously abnormal hemodynamic parameters have improved. The potential for fluid overload exists in these exercises and patient monitoring is very important.

A large volume of human literature has attempted to determine which fluid is most appropriate for patient resuscitation. These studies have not shown crystalloids or colloids to be most beneficial. They have shown that in certain patient populations colloids may help patients reach hemodynamic stability faster, but that this benefit is not maintained throughout hospitalization. It can be difficult to extrapolate from human resuscitation papers because the patients are hospitalized for months, the colloid used most commonly is human albumin, and fluid overload can be more easily corrected through the use of hemodialysis. There is a similar lack of clarity in the veterinary literature regarding the best choice, though the positive effect of successful resuscitation in improving outcome has been clinically supported.

Fluid therapy in trauma

Trauma is another special condition which warrants discussion in the realm of fluid therapy. In human patients, hemorrhage is responsible for the majority of deaths in the first hours following injury. This hemorrhage can be due to the primary injury, but increasingly there has developed an awareness of an acute hypocoagulable state, Acute Traumatic Coagulopathy, which contributes to hemorrhage in these patients. This coagulopathy can be due to physiologic factors such as endothelial disruption, hyperfibrinolysis, and anticoagulant activation, but iatrogenic factors including hypothermia, hemodilution of coagulation factors, and metabolic acidosis also contribute.

Previously, it has been recommended that, in the face of trauma, crystalloid fluids be administered in a 3:1 ratio relative to the volume of blood lost. Subsequent studies have shown that animals receiving large volumes of crystalloids have increased mortality in the face of uncontrolled hemorrhage. Large volume fluid resuscitation has been shown to lead to the following: dislodgement of hemostatic plugs, a rapid increase in intravascular hydrostatic pressure, and dilution of coagulation factors. In addition, the use of synthetic starch-based colloids in resuscitation may contribute to coagulopathy due to their negative impact on Von Willebrand’s factor, factor VIII, and platelet receptors.

New treatment strategies have developed for resuscitation in trauma including the concepts of delayed resuscitation and hypotensive resuscitation. Hypotensive resuscitation, also called controlled resuscitation, is achieved by fluid administration to maintain a mean arterial blood pressure around 40mmHg. This endpoint is lower than the normally recommended 80mmHg. When an accurate mean arterial pressure cannot be obtained, fluids are administered at a predetermined rate such that normotension would be unlikely. These patients have been shown to have decreased blood loss, better splanchnic perfusion, less severe acidosis, thrombocytopenia, and coagulopathy.

Delayed resuscitation entails withholding resuscitation fluid entirely until definitive hemorrhage control is achieved. Experimental models have supported this strategy, but clinical support has been less definitive, though one meta-analysis has shown that a restrictive (vs liberal strategy) in trauma showed a better outcome. Because delayed resuscitation reflects a “scoop and run” approach to human trauma care, this may more closely parallel the presentation of veterinary patients to the emergency room. There is not veterinary literature evaluating either of these strategies. Despite the lack of clear evidence to advocate restrictive resuscitation in veterinary patients, a measured, step-wise, approach to resuscitation in our bleeding patients is recommended until hemostasis can be achieved.

Why can’t we all agree on colloids?

In the last decade there has been increasing concern regarding the use of synthetic starch colloids for fluid therapy in human medicine. Several studies have shown that patients receiving these fluids did not require lower volumes of fluids compared to those receiving crystalloids, but they did demonstrate higher levels of acute kidney injury, renal replacement therapy requirements, and mortality. Specifically, septic patients were examined and shown to be at risk. There have been two, large human studies looking at trauma and hypovolemic shock which did not replicate these findings. These studies evaluated HES use for a shorter period of time relative to previous studies, perhaps more closely mimicking how these fluids are used in veterinary medicine. Given the fact that there has not been a demonstrated benefit in human medicine to resuscitation with tetrastarches, the risks appear to outweigh the benefits. As a result, hetastarch has been banned from use in the European Union and carries a black box warning in the United States.

Extrapolating these findings to veterinary patients is challenging. Dogs possess greater amylase activity than humans and our patients do not receive tetrastarches for weeks on end, in contrast to human patients. In addition, with the relatively limited availability and expense of canine albumin, veterinarians lack a viable alternative to synthetic colloids in some cases. Until recently, there was no evidence to suggest that veterinary patients may suffer the same risks as humans with HES administration. Hayes et al recently published a retrospective study assessing the risk of mortality and acute kidney injury in a heterogeneous population of hospitalized dogs receiving HES (250/0.5/5:1) compared to the general population. When disease severity was controlled for, patients receiving HES had an increased risk of acute kidney injury and mortality. Though this is a retrospective study, it does suggest that our patients may run similar risks to human patients when receiving tetrastarches. Given these concerns and the need for additional studies in veterinary medicine a prudent approach to synthetic colloid administration in veterinary patients is warranted. Veterinary specific guidelines are lacking, but the Pharmacovigilance Risk Assessment Committee guidelines recommend using tetrastarches for acute hypovolemia for periods of 24 hours or less at the lowest possible dose. The Surviving Sepsis Campaign 2012 guidelines recommend against their use in septic patients.

Conclusion

Unfortunately, there is no ideal resuscitation fluid, nor a formulaic fluid resuscitation strategy for all veterinary patients. An understanding of the underlying disease process and available resuscitation options allows a clinician to make sensible choices for their patient. Given the dynamic nature of critical illness, patient reassessment and the identification of resuscitation endpoints helps ensure successful fluid therapy while minimizing the risk of adverse events.

 

Further reading

  1. Adamik K,Yozova I. Controversies in the use of hydroxyethyl starch solutions in small animal emergency and critical care. J Vet Emerg Crit Care 2015;25:20-47.
  2. Annane D, Siami S, Jaber S, et al. Effects of fluid resuscitation with colloids vs crystalloids on mortality in critically ill patients presenting with hypovolemic shock: the CRISTAL randomized trial. J Am Med Assoc 2013;310:1809–1817.
  3. Bunn F, Trivedi D. Colloid solutions for fluid resuscitation. Cochrane Database Syst Rev 2012; 7:CD001319.
  4. Cazzolli D, Prittie J; The crystalloid-colloid debate: Consequences of resuscitation fluid selection in veterinary critical care. J Vet Emerg Crit Care 2015;25:6-19.
  5. Craft EM, Powell LL. The use of canine-specific albumin in dogs with septic peritonitis. J Vet Emerg Crit Care 2012;22:631–639.
  6. Delaney AP, Dan A; The role of albumin as a resuscitation fluid for patients with sepsis: a systemic review and meta-analysis: Crit Care Med 2011;39:386-391.
  7. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012. Crit Care Med 2013;41:580–637.
  8. Dibartola S. Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Medicine. 4th Edition. Elsevier Saunders. St. Louis, 2012.
  9. Driessen B. Fluid therapy for the traumatized patient. J Vet Emerg Crit Care 2006;16:276-299.
  10. Francis AH, Martin LG, Haldorson GJ, et al. Adverse reactions suggestive of type III hypersensitivity in six healthy dogs given human albumin. J Am Vet Med Assoc 2007;230:873–879.
  11. Guidet B, Martinet O, Boulain T, et al. Assessment of hemodynamic efficacy and safety of 6% hydroxyethylstarch 130/0.4 vs. 0.9%NaCl fluid replacement in patients with severe sepsis: the CRYSTMAS study. Crit Care 2012;16:R94.
  12. Hayes G, Benedicenti L; 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. J Vet Emerg Crit Care 2016;26:35-46.
  13. Holowaychuk MK, Hanel RM, Darren Wood R, et al. Prospective multicenter evaluation of coagulation abnormalities in dogs following severe acute trauma. J Vet Emerg Crit Care 2014;24:93–104.
  14. James MF, Michell WL, Joubert IA, et al. Resuscitation with hydroxyethyl starch improves renal function and lactate clearance in penetrating trauma in a randomized controlled study: the FIRST trial (Fluids in Resuscitation of Severe Trauma). Br J Anaesth 2011;107:693–702.
  15. Kyes J, Johnson JA; Hypertonic saline solutions in shock resuscitation. Compend Contin Educ Vet 2011;33:E1-8.
  16. Mathews KA, Barry M. The use of 25% human serum albumin: outcome and efficacy in raising serum albumin and systemic blood pressure in critically ill dogs and cats. J Vet Emerg Crit Care 2005;15:110-118.
  17. Mutter TC, Ruth CA, Dart AB. Hydroxyethyl starch (HES) verses other fluid therapies: effects on kidney function. Cochrane Database Syst Rev 2013: CD007594.
  18. Myburgh JA, Finfer S, Bellomo R, et al. Hydroxyethyl starch or saline for fluid resuscitation in intensive care. N Engl J Med 2012;367:1901-1911.
  19. Perel P, Roberts I, Ker K. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2013; 2:CD000567.
  20. Perner A, Haase N et al. Hydroxyethyl starch (130/0.42) versus Ringers acetate in severe sepsis (the 6S trial): N Engl J Med 2012;367:124-134.
  21. Prittie J.Optimal endpoints of resuscitation and early goal-directed therapy. J Vet Emerg Crit Care 2006;16:329-339.
  22. SAFE Study Investigators. A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004;350:2247–2256.
  23. Santry HP, Alam HB. Fluid resuscitation: past, present and future. Shock 2010;33:229-241.
  24. Silverstein D. Small Animal Critical Care Medicine, 2nd Edition. Elsevier Saunders. St. Louis, 2015.
  25. 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;15:185-192.
  26. Silverstein et al; Effectiveness of intravenous fluid resuscitation in the emergency room for treatment of hypotension in dogs. J Vet Emerg Crit Care 2012;22:666-673.
  27. Trow AV, Rozanski EA, de Laforcade AM, et al. Evaluation of the use of human albumin in critically ill dogs: 73 cases (2003–2006). J Am Vet Med Assoc 2008;233:607-612.
  28. Vigano F, Perissinotto L, Bosco VRF. Administration of 5% human serum albumin in critically ill small animal patients with hypoalbuminemia: 418 dogs and 170 cats (199–2008). J Vet Emerg Crit Care 2010;20:237-243.
  29. Wang CH, Hsieh W; Liberal versus restricted fluid resuscitation strategies in trauma patients: a systemic review and meta-analysis of randomized controlled trials and observational studies. Crit Care Med 2014;42:954-961.
  30. 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 Anaesth 2012;108:384-394.

 

About the author

Dr. Danielle Thomas received her undergraduate degree from Swarthmore College and her veterinary degree from Virginia Tech. She then completed a small animal rotating internship, followed by a 3 year residency in Emergency and Critical Care Medicine at Angell Animal Medical Center in Boston. Dr. Thomas became a diplomate of the American College of Veterinary Emergency and Critical Care in 2013. She joined the Emergency and Critical Care team at MVRH in 2015.

When she is not in the hospital, Dr. Thomas can be found running along the Charles, cheering for the UConn Huskies, or acting as the Seeing Eye Human for her blind Boston Terrier Bugsy.