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Section 5: Fluid Therapy in Ill Patients

Fluid therapy in sick patients requires a cautious, balanced approach and the ability to predict problems before they occur. The veterinary team faces complex challenges in fluid therapy when treating patients who present with conditions such as gastrointestinal, renal, or cardiac disease, anemia, electrolyte imbalances, traumatic brain injury (TBI), hypovolemic or vasodilatory shock, edema, thermoregulation disorders, and hypoglycemia.

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Dog with iv receiving fluid therapy
In This Resource:

Top Three Takeaways

  1. Do not forget about enteral routes of fluid delivery, including nasogastric, nasoesophageal, or esophageal, when treating sick patients. If tolerated by the patient, water can be mixed with food or administered separately.
  2. Do not withhold fluids in patients who are dehydrated or hypovolemic because of concurrent anemia. Monitor them closely to determine whether a transfusion is also indicated.
  3. Mitigate electrolyte derangements carefully. Never administer a bolus of fluids supplemented with potassium chloride (KCl). Thoroughly mix the fluids to ensure even dispersion of the KCl before administration. Intentionally manage sodium derangements to avoid potential life-threatening fluid shifts in the brain that can occur with rapid resolution of chronic (>24–48 hr) sodium alterations.

Nutritional Therapy as a Prompt for Enteral Fluid Therapy

Nutrition is one of the most neglected patient requirements during hospitalization. After 72 hr of anorexia, a patient’s metabolism shifts to alternate energy sources, such as ketones and fatty acids, instead of glycogen and glucose. Nasoesophageal, nasogastric, or esophageal feeding tubes facilitate caloric intake, and water can be mixed with food or administered separately. Use a canned diet to increase water intake.

The stomach’s capacity is 5–10 mL/kg at the time of starting enteral nutrition, and no consensus on canine and feline gastric emptying times exists (although prolonged emptying times have been reported). Use conservative calculations of fluid and food requirements for enteral nutrition and adjust based on a patient’s clinical signs of nausea, regurgitation, and vomiting.

Determine enteral water requirements based on daily maintenance rates and divide this amount between IV and enteral supplementation. It is important to continue to provide free access to water. Given that enteral nutrition rates typically start at one-third the resting energy requirement to avoid refeeding syndrome, enteral water administration may also aid in allowing the stomach capacity to accommodate increased volumes of subsequent enteral nutrition feedings.

Anemia

Do not withhold fluids in anemic patients. If an anemic patient is also dehydrated or hypovolemic, provide fluid therapy while recognizing that patients with a low hematocrit may require blood products. In healthy patients, fluid resuscitation has not been shown to decrease hemoglobin concentrations. Fluid therapy may result in a beneficial increase in microvascular flow and perfusion with an overall increase in oxygen delivery in patients with hypovolemic or distributive shock. However, fluid administration in non–fluid responders or fluid-overloaded patients can lead to a relative, but not absolute, reduction in hemoglobin concentration (“dilutional anemia”), which can cause a paradoxical decrease in oxygen delivery.

Carefully monitor anemic patients and thoroughly assess them for shock, hypovolemia, dehydration, and need for maintenance fluids. These needs should be addressed through an appropriate fluid prescription. These patients may become transfusion dependent when appropriately resuscitated or rehydrated. Transfusion triggers (e.g., heart rate, mucus membrane color, capillary refill time, respiratory rate and effort, pulse quality, blood pressure, mentation, and attitude) should be considered in conjunction with laboratory test results (e.g., packed red blood cell count and trends, hematocrit, hemoglobin levels, and blood lactate) to determine the need for a blood transfusion.,

Azotemia

Azotemic patients have varying fluid requirements that depend on factors such as their hydration status (including both dehydration and fluid overload), urine production levels, acute versus chronic onset, acid-base and electrolyte status, the underlying cause of the azotemia, and the extent of its severity. These patients present special monitoring challenges as they might experience xerostomia (dry mouth) secondary to uremia, prolonged skin tenting due to reduced skin elasticity associated with aging, concentrated retained urine, and inaccurate relative creatinine levels due to decreased muscle mass. Additionally, there may be a lack of a baseline creatinine concentration or previous body weight for comparison. Anecdotal techniques to assess dehydration include evaluating skin turgor over the rib cage, analyzing weight trends and sodium concentrations, fluid and food intake history, and identifying signs of fluid overload (see Section 6, Fluid Overload).

In cases in which patients are not hypotensive, the fluid prescription should provide a gradual correction of dehydration, whereas patients with significant renal compromise should receive fluids at slower rates. Fluid therapy is not the mainstay of treating azotemic patients. Rather, it is to support the kidneys by correcting treatable abnormalities associated with renal compromise so that the kidneys can heal themselves. Key aspects entail reducing sodium and chloride load, managing blood pressure, treating anemia, and infections, ensuring adequate short-term nutrition (without protein restriction), and addressing primary conditions that may trigger secondary AKI (e.g., acute pancreatitis) or acute-on-chronic kidney disease presentations. Fluid requirements for patients with chronic kidney disease vary depending on the severity of polyuria and polydipsia along with other clinical signs.

Heart Disease

The most important consideration for fluid therapy in patients with cardiac disease is to prevent the onset of heart failure. For cardiac patients, therapeutic goals include increasing myocardial contractility, decreasing preload and afterload, counteracting the pathological effects of the renin-angiotensin-aldosterone system, improving vasodilation, and optimizing diastolic filling.,

Cardiac patients may experience dehydration, relative hypovolemia, electrolyte disturbances, moderate to severe azotemia, and metabolic imbalances caused by heart failure and medications. Fluid therapy is frequently avoided in cardiac patients owing to its potential to increase preload in left-sided heart failure, increase afterload, and decrease venous return in right-sided heart failure (especially in the presence of increased intra-abdominal pressure from ascites).,, Whenever possible, fluid intake should be provided enterally, such as through water and a canned diet. When fluid therapy is necessary, administer 0.45% NaCl with 2.5% dextrose IV at half to daily maintenance rates (See Table 9 for maintenance rates), depending on the patient’s needs and tolerance of supplemental fluids. Hypotension in patients with congestive heart failure should be addressed by considering positive inotropes.

Cardiorenal Disorders

The cardiorenal axis is an important consideration because a pathological state in either the cardiovascular or renal system has the potential to affect the other. Renal disease treatment focuses on maintaining hydration with enteral water, so less conflict exists with heart disease treatment; however, the administration of additional fluid therapy presents challenges. Cardiac medications may potentially lead to mild azotemia through diuresis (e.g., furosemide) and decreased glomerular filtration rate (GFR) (e.g., enalapril and telmisartan). It is crucial to consistently monitor for fluid overload, severe progressive azotemia, worsening of heart failure, changes in blood pressure, and other relevant indicators to ensure that these patients do not decline as a result of fluid therapy. Even with the best possible therapy, this can be a significant challenge.

Patients with Hypovolemia and Edema

Alterations in Starling’s forces (hydrostatic and oncotic pressure) (Figure 2) may contribute to the development of edema in veterinary patients. Common causes of edema include vasculitis, hypoalbuminemia, heart failure, kidney failure, lymphatic obstruction, and thrombosis. Fluid therapy in hypovolemic, edematous patients presents a therapeutic challenge, and the underlying cause of the edema must be taken into consideration in order to safely provide fluids.

When edema results from hypoalbuminemia, intravascular volume resuscitation and restoration are paramount, and colloids can be used to raise the colloid oncotic pressure. This can be accomplished with rapid administration of synthetic colloids (e.g., hetastarch and tetrastarch [although their use is controversial; see Section 7, Questions and Controversies in Fluid Therapy]), canine specific albumin (CSA) in dogs, human serum albumin in dogs or cats (which may predispose patients to allergic reactions or anaphylaxis), and veterinary plasma products (e.g., fresh frozen plasma, frozen plasma, and cryoprecipitate-poor plasma [CPP]).

Although plasma products are less prone to induce allergic reactions, large plasma volumes are needed to significantly change albumin concentrations (~22 mL/kg plasma to increase serum albumin by 0.5 g/dL), which results in higher costs of care and risk of volume overload. In one study, there was no difference in mean serum albumin concentrations before and after transfusion with fresh frozen plasma (median dose of 15–18mL/kg). Thus, although a plasma bolusmay be used to treat hypovolemia in edematous patients, its use for this purpose is controversial.

A continuous rate infusion (CRI) of canine CPP, administered at a rate of 1.1–2.2 mL/kg/hr, has been described in a case report for treating hypoalbuminemia. This may be a more reasonable approach to treating hypoalbuminemia because CPP has a higher album in concentration than other plasma products, although CPP is less widely available.

CSA appears to be a relatively safe alternative to synthetic colloids and increases albumin concentrations more efficiently than plasma products., In one study, CSA administration improved the shock index in hypovolemic canine patients.

In another study, CSA increased arterial blood pressure within 2 hr of administration in dogs with septic peritonitis.

Giving colloids to patients with edema due to vasculitis may be controversial, as colloids may leak into the interstitial space and worsen interstitial edema. In these patients, judicious colloid use combined with lower volumes of crystalloids is recommended. Overall, regardless of the cause of edema, use crystalloids judiciously in all affected patients.

Low-dose diuretics may be considered in patients with edema, but only in normotensive, normovolemic patients.

Traumatic Brain Injury

The primary fluid therapy goal in treating veterinary patients who have TBI is optimizing cerebral perfusion pressure and mean arterial blood pressure. The Brain Trauma Foundation guidelines for human patients recommend maintaining systolic arterial blood pressure between 100 and 110 mm Hg to reduce mortality and improve outcomes.

Studies that evaluate the ideal fluid choice for veterinary patients with TBI are limited. However, information based on human clinical studies and swine and rodent research studies supports the use of packed red blood cells, plasma, and platelets over crystalloid fluids because of better outcomes in patients with ongoing hemorrhage.,

Osmotherapy—using osmotic agents (e.g., hypertonic saline or mannitol) to reduce intracranial content volume—is common in treating patients who have TBI (Figure 10). Various studies and a meta-analysis in human medicine suggest that both mannitol and hypertonic saline effectively lower intracranial pressure, but there is no evidence to recommend one over the other.,, Hypertonic saline may have the advantage of avoiding diuresis, increasing cardiac preload, and positively impacting cerebral perfusion. In dogs and cats, mannitol is usually dosed at 0.5–1 g/kg IV given over 15 min with a microfilter, whereas hypertonic saline (NaCl 7.2%) is dosed at 1–6 mL/kg IV given over 15 min. Continuous infusion of hypertonic saline has been described in human patients, but it is not thought to significantly affect outcome.

Figure 10: Approach to Fluid Therapy for Dogs and Cats with Traumatic Brain Injury
Figure 10 Approach to Fluid Therapy for Traumatic Brain Injury

Figure 10 Approach to Fluid Therapy for Dogs and Cats with Traumatic Brain Injury

* Fluid resuscitation techniques can be any one of the following or a combination thereof: (1) 10–20 mL/kg crystalloids (Plasma Lyte or Normosol-R) IV rapid infusion up to 60–90 mL/kg. (2) 5–10 mL/kg 6% HES (tetrastarch) IV rapid infusion up to 40–50 mL/kg. (3) 5–10 mL/kg plasma rapid infusion IV up to 20–30 mL/kg. (4) 3–4 mL/kg 7% HTS IV over 10–15 min. (5) Whole blood or pRBC, if indicated.

**Altered level of consciousness with or without bilateral or unilateral miotic pupils; unresponsive mid range pupil(s) or mydriasis; loss of the oculocephalic reflex; bradycardia with hypertension (Cushing reflex); posturing (opisthotonus, decerebellate, decerebrate); alteration of the respiratory pattern.

***1 g/kg mannitol IV up to 3 doses q 60–90 min OR 3–4 mL/kg 7% HTS IV.

dReprinted with permission from Pigott A, Rudloff E. Traumatic brain injury–a review of intravenous fluid therapy. Front Vet Sci. 2021;8:643800.

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Electrolyte Disturbances

Electrolyte imbalances are common in ill patients. Proper fluid selection and, if necessary, supplementation of electrolytes aid in restoring balance.

Hypokalemia

Dogs and cats in poor health often experience hypokalemia. This may be due to increased urinary or gastrointestinal loss, prolonged anorexia, alkalemia, an aldosterone-secreting tumor, or treatment with potassium-poor replacement fluids. Clinical signs of hypokalemia may include weakness, cardiac arrhythmias, and respiratory muscle impairment.

Treat hypokalemia with KCl supplementation in IV fluids (Table 11). Determine the KCl dosage based on the patient’s serum potassium concentration. For IV KCl administration, calculate the total mEq/kg/hr to be administered, ensuring that the supplementation rate does not exceed 0.5 mEq/kg/hr, as rapid administration can be fatal. Never bolus fluids supplemented with KCl. Before administration, invert the bag and thoroughly mix the fluids to ensure uniform dispersion of the KCl. Exercise caution with highly supplemented fluids or KCl CRIs to prevent inadvertent bolus or over administration to the patient. Use appropriate fluid pump settings or syringe pumps as safeguards and educate staff on the risks of over administration. In cases of persistent hypokalemia even after KCl supplementation, check magnesium levels to determine whether magnesium supplementation is needed.

Table 11: Guidelines for Potassium Supplementation in Fluids
Serum Potassium Concentration Suggested Potassium Dose Suggested Potassium Added to Isotonic Crystalloids at 60 mL/kg/Day for a 10-kg Dog (25 mL/hr)
<2.0 mEq/L 0.5 mEq/kg/hr 200 mEq/L
2.0–2.5 mEq/L 0.3–0.4 mEq/kg/hr 120–160 mEq/L
2.6–3 mEq/L 0.2–0.25 mEq/kg/hr 80–100 mEq/L
3.1–3.5 mEq/L 0.1–0.15 mEq/kg/hr 40–60 mEq/L
>3.5 mEq/L 0.05 mEq/kg/hr 20 mEq/L

Table 11
Guidelines for Potassium Supplementation in Fluids

Download Table 11 PDF

Sodium imbalances

Sodium concentration disturbances are common. These cases should be managed with deliberate care to prevent potentially life-threatening fluid shifts in the brain that may occur after rapid correction, faster than 0.5 mEq/kg/hr, of chronic (greater than 24–48 hr) sodium alterations.

Hyponatremia. Patients with acute euvolemic hyponatremia (e.g., primary polydipsia) may present with neurologic signs and should be treated with 2–6 mL/kg of 3–7.5% hypertonic saline over 10–15 min.,, In symptomatic chronic hyponatremia, a similar approach using hypertonic saline should be taken. Once neurological clinical signs resolve, treatment should continue similarly to that in asymptomatic chronic hyponatremia patients. In asymptomatic chronic hyponatremia patients, isotonic crystalloids (Table 12C) that have a sodium content ~10 mEq/L higher than the patient’s sodium should be selected. A rate of correction should be calculated that does not exceed 0.5 mEq/L/hr or a maximum sodium increase of 10–12 mEq/L/day to prevent osmotic demyelination syndrome (Tables 12A, 12D).

Patients with hypovolemic hyponatremia should be resuscitated with a crystalloid that contains a similar sodium content to the patient’s current sodium concentration., Depending on the severity of the hyponatremia, commercial isotonic crystalloids may not be available with similar sodium contents. In these cases, custom fluids can be tailored by adding sterile water to an isotonic crystalloid to achieve the desired sodium content. These fluids should be used exclusively for bolus administration until hypovolemia is resolved. Hypotonic fluids should not be used in patients with hyponatremia.

Hypernatremia. The strategies to treat hypernatremia are similar to those taken with hyponatremia regarding the considerations of chronicity and rate of correction of 0.5 mEq/L/hr. Sodium concentration drops that are faster than this rate in patients with chronic hypernatremia may cause abrupt fluid shifts that lead to cerebral edema. However, patients with acute hypernatremia can undergo rapid sodium concentration correction without the risk of cerebral edema, by using hypotonic IV fluids. Calculate the free water deficit and administer fluids at an appropriate rate while monitoring sodium concentrations frequently to allow for a safe resolution of hypernatremia (Table 13A).

Hypochloremia. Relative shifts in chloride usually occur with shifts in sodium. To assess true chloride disturbances in the face of sodium derangements, chloride should be corrected using the following equation:

Corrected Cl = (normal Na/measured Na) x measured Cl

In patients with true hypochloremia that have developed metabolic alkalosis, 0.9% NaCl has historically been the fluid of choice because of its high chloride concentration (154 mEq/L). Recently, concerns have been raised about the effect of 0.9% NaCl on kidney function owing to the potential risk of causing hyperchloremia, which has been shown to cause renal vasoconstriction and reduced renal blood flow., To safely use 0.9% NaCl in hypochloremic renal patients, recheck chloride concentrations frequently, and once chloride levels have been corrected, use a buffered isotonic crystalloid (e.g., lactated Ringer’s solution or Plasma-Lyte) instead.

Hypocalcemia. Use calcium gluconate to treat patients with clinical signs of hypocalcemia (e.g., weakness, tachycardia, and tremors). Lactated Ringer’s solution contains a very small amount of calcium, and it will not resolve hypocalcemia.

Hypercalcemia. Historically, 0.9% NaCl has been recommended for calciuresis in hypercalcemic patients, but its effects are generally mild. Because of concerns regarding kidney injury with 0.9% NaCl, consider using a balanced isotonic crystalloid instead in patients at risk of or with current kidney disease.

Table 12A: Approach to Fluid Therapy in Hyponatremic Patients
1. Is hyponatremia acute or chronic?
ACUTE CHRONIC
  1. Raise the serum sodium concentration as quickly as possible.
  2. Administer isotonic crystalloids with a sodium concentration greater than the patient’s serum sodium concentration.
  3. Recheck serum sodium concentrations 2–4 hr after starting therapy to assess therapeutic response, then recheck them every 6–8 hr afterward.
  1. It takes 24–48 hr for the brain to compensate for hyponatremia.
  2. Correct chronic hyponatremia slowly to prevent osmotic demyelination syndrome.
  3. Increase the serum sodium concentration by no more than 0.5 mEq/L/hr for a maximum total correction of 10–12 mEq/L/day.
2. Does the patient have clinical signs of hyponatremia?
  1. Clinical signs include vomiting, disorientation, and seizures secondary to cerebral edema.
  2. If symptomatic, treat with 3, 5, or 7.5% hypertonic saline at a recommended dose of 2–6 mL/kg given over 10–15 min.1
  3.  In human patients, serum sodium concentration increases of 4–6 mEq/L are often enough to alleviate clinical signs.1
3. Is the patient hypovolemic?
  1. Perform fluid resuscitation: 5-10 mL/kg (cats) or 15-20 mL/kg (dogs) given rapidly over 15–30 min with a buffered isotonic solution capable of expanding the intravascular space (Table 12c).1
  2. Repeat as needed until perfusion parameters are restored. Maintenance or hypotonic fluids (0.45% NaCl, 5% dextrose in water) have low sodium concentrations and are not indicated to treat hypovolemia.1
4. Does the patient have chronic hyponatremia without neurologic signs?
  1. Slowly correct the sodium concentration at a maximum rate of 0.5 mEq/L/hr or 10-12 mEq/L/day.
  2. Treat asymptomatic patients with mild water restriction and monitor their serum sodium concentrations.
  3. Use the Adrogue-Madias formula below to calculate the expected change in sodium concentration when 1 L of a specific fluid type is administered (see Table 12c).2

Expected change in serum sodium concentration with 1 L of fluid =
Fluid sodium concentration − serum sodium concentration / (total body water + 1)
Where total body water = body weight in kg × 0.6

1. Adrogué HJ, Tucker BM, Madias NE. Diagnosis and management of hyponatremia: a review. JAMA. 2022;328(3):280-91.
2. Heinz J, Cook A. Evaluation and management of the hyponatremia patient. Today’s Veterinary Practice. 2022;12(2). February 10, 2022. Available at https://todaysveterinarypractice.com/internal-medicine/evaluation-and-management-of-the-hyponatremic-patient/. Accessed January 4, 2024.

Download Table 12A PDF

Table 12B: Common Causes of Acute and Chronic Hyponatremia in Dogs and Cats
Acute Chronic*
  • Consumption of large amounts of fresh water leading to acute water intoxication
  • Infusion of significant volumes of non replacement fluids (e.g., administering a 5% dextrose in water solution to a dehydrated patient)
  • Congestive heart failure
  • Hypoadrenocorticism
  • Liver dysfunction
  • Nephrotic syndrome
  • Renal and gastrointestinal sodium loss

*Consider that patients with vague clinical signs for longer than 24–48 hours likely have chronic hyponatremia.

Download Table 12B PDF

Table 12C: Sodium Concentration of Isotonic Crystalloids
Lactated Ringer’s solution 130 mEq/L
Plasma-Lyte A 140 mEq/L
Normosol R 140 mEq/L
0.9% NaCl* 154 mEq/L

* Evidence in human patients suggests that 0.9% NaCl may be detrimental to kidney health.1,2

1. Ostermann M, Randolph AG. Resuscitation fluid composition and acute kidney injury in critical illness. New England Journal of Medicine.
2022;386(9):888-889.
2. Sigmon J, May CC, Bryant A, Humanez J, Singh V. Assessment of acute kidney injury in neurologically injured patients receiving hypertonic
sodium chloride: does chloride load matter? Annals of Pharmacotherapy. 2020;54(6):541-546.

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Table 12D: Calculating Expected Changes in Sodium Concentration
Stevie, a 10 kg, 5-year-old, male neutered Jack Russell terrier, presented for evaluation of vomiting and diarrhea of 72 hours duration. Stevie was mildly lethargic, but all perfusion parameters (heart rate, capillary refill time, blood pressure, pulse quality) were normal, and no other abnormalities were found on physical examination. Stevie’s serum sodium concentration was 115 mEq/L.

Stevie is presumed to have chronic hyponatremia because clinical signs have been present for longer than 48 hours. Stevie does not have neurologic signs, so treatment with a hypertonic saline bolus is not indicated. An isotonic crystalloid bolus is also not indicated because Stevie’s perfusion parameters are normal.
To correct the hyponatremia, the Adrogue-Madias formula was used with Normosol R as the fluid of choice:
Expected change in serum sodium concentration with 1 L of Normosol R =

140 mEq/L − 115 mEq/L = 3.57 mEq/L
(10 kg × 0.6) + 1

Therefore, 1 L of Normosol R will change Stevie’s sodium concentration by ~3.5 mEq/L.

If Stevie is treated at 25 mL/hr (60 mL/kg/day), ~600 mL of Normosol R will be administered over 24 hours, which will estimate the sodium change at 2.1 mEq/L.

For a faster correction rate, hypertonic saline may be infused into Normosol R to increase fluid sodium concentration using this formula:

Fluid Na = Patient Na + [Target increase in patient’s NA over set time x (TBW + Volume of fluids administered over set time)]1
TBW = body weight in kg × 0.6

1. Heinz J, Cook A. Evaluation and management of the hyponatremia patient. Today’s Veterinary Practice. 2022;12(2). February 10, 2022
Available at https://todaysveterinarypractice.com/internal-medicine/evaluation-and-management-of-the-hyponatremic-patient/. Accessed
January 4, 2024.

Download Table 12D PDF

Table 13A: Approach to Fluid Therapy in Hypernatremic Patients
1. Is hypernatremia acute or chronic?
ACUTE CHRONIC
  • Use hypotonic intravenous fluids to correct.
  • Can undergo rapid sodium concentration correction without the risk of cerebral edema.
  • Calculate the free water deficit and administer at an appropriate rate (see #3 below).
  • Monitor sodium concentrations every 4-6 hours.
  • It takes 24–48 hours for the brain to compensate for hypernatremia.
  • Correct chronic hypernatremia slowly to prevent cerebral edema.
  • Decrease serum sodium concentration by no more than 0.5 mEq/L/hr for a maximum total correction of 10–12 mEq/L/day (see #3 below).
2. Is the patient hypovolemic?
  • Perform fluid resuscitation with a buffered isotonic solution capable of expanding the intravascular space.
  • Maintenance or hypotonic fluids (0.45% NaCl, 5% dextrose in water) have low sodium concentrations and are not indicated to treat hypovolemia.
  • Fluids listed in Table 12c are suitable options to treat hypovolemia (5-10 mL/kg [cat] and 15-20 mL/kg [dog] given over 15–30 minutes and repeated as needed) until perfusion parameters are restored.
3. Calculations for chronic and acute hypernatremia
Estimate the amount of water lost (free water deficit). Administer fluids that are relatively dilute compared with plasma.

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

 Modify the calculation of the free water deficit according to whether hypernatremia is acute or chronic, using the subsequent formulas:

FWD replacement time (hr) for acute hypernatremia = Patient Na − Target Na1

FWD replacement time (hr) for chronic hypernatremia = (Patient Na − Target Na) × 21

In general, replace the free water deficit by administering 5% dextrose in water.
4. Is the patient dehydrated?
  • Simultaneously treat by administering a buffered isotonic crystalloid (Table 12c).
  • Correct dehydration over 12–24 hours to minimize shifts in sodium.1
  • Recheck sodium concentrations every 4–6 hours to prevent dramatic changes.
  • Limit drinking water until the patient’s sodium is close to the target concentration.

1. Heinz J, Cook A. Evaluation and management of the hyponatremia patient. Today’s Veterinary Practice. 2022;12(2). February 10, 2022.
https://todaysveterinarypractice.com/internal-medicine/evaluation-and-management-of-the-hyponatremic-patient/.
Accessed January 4, 2024.

Download 13A PDF

Table 13B: Common Causes of Acute and Chronic Hypernatremia in Dogs and Cats
ACUTE CHRONIC
Intake of large amounts of sodium chloride (ingestion of salt water, homemade playdough, or salt) Hypotonic fluid losses (diarrhea, peritonitis, vomiting, kidney disease)
Nephrogenic diabetes insipidus
Heatstroke
Infusion of replacement fluids or hypertonic fluids may lead to acute or chronic hypernatremia, depending on how often the patient’s sodium concentration is rechecked during hospitalization.

Download Table 13B PDF

Vasodilatory States

Patients may exhibit signs of poor perfusion or shock (such as tachycardia, hypotension, weak peripheral pulses, or elevated lactate concentrations) due to generalized vasodilation, also referred to as vasodilatory or maldistributive shock. In vasodilatory shock, there is excessive dilation of blood vessels, leading to a significant decrease in blood pressure and inadequate perfusion of vital organs., Common clinical conditions that can lead to vasodilation include acute pancreatitis, anaphylaxis, sepsis, trauma, and parvoviral enteritis. Historically, vasodilatory shock treatment has revolved around rapid administration of fluids, the administration of broad-spectrum antibiotics, establishing source control, and using pharmacologic interventions to maintain adequate mean arterial blood pressure.,

Because distinguishing between hypovolemic and vasodilatory shock based solely on physical examination findings is challenging, and because patients with vasodilatory shock may have some degree of hypovolemia, a fluid challenge is a reasonable treatment approach in these situations. Poor or limited response to fluid boluses may suggest vasodilation. In cases in which there is a poor response to fluid therapy, vasopressor therapy should be considered. In patients with suspected anaphylaxis, it is crucial to administer epinephrine, a vasopressor, as soon as possible.

Thermoregulation Disturbances

Hypothermia. Whenever possible, use warm fluids for resuscitation or rehydration in hypothermic patients for active core rewarming. The task force believes warm fluids will at least mitigate worsening hypothermia compared with the administration of room temperature fluids. It has been recommended to warm IV fluids to 40–42°C (104–107.6°F). Fluids can be warmed using numerous methods, including immersion of IV tubing in warm water, microwaving of the fluid bag, in-line fluid warmers, and prewarming of fluids in a convection oven. However, the effect of warm fluids in producing an increase in body temperature is controversial.,,

Hypothermia is commonly observed in cats in shock. Aggressive fluid resuscitation with the aim of restoring normal blood pressure in hypotensive, hypothermic cats will often lead to interstitial fluid overload, pulmonary edema, and pleural effusion. Administering conservative fluid volumes (e.g., 5 mL/kg IV boluses at a time) concurrent with active rewarming is an essential part of shock resuscitation therapy in cats.

Hyperthermia. Fluid therapy is important in treating hyperthermia in dogs and cats. Administering room temperature fluids may assist with cooling and maximize volume expansion.

Hypoglycemia

Administer dextrose to patients exhibiting clinical signs related to hypoglycemia, such as lethargy, weakness, ataxia, or seizures. For a bolus, use 0.5–1 mL/kg (0.25–0.5 g/kg) of 50% dextrose, which should be diluted at a ratio of 1:2–1:4 and administered over 2–5 min. In most cases, the bolus should be followed by a CRI of 1.25–5% dextrose (Table 14) until the patient can maintain normoglycemia. The concentration of dextrose instilled in fluids depends on the severity of the patient’s hypoglycemia and fluid administration rate. It is advisable to administer dextrose concentrations exceeding 5% through a central line to avoid phlebitis.

Note that in patients with insulinoma, dextrose administration may perpetuate hypoglycemia. Therefore, dextrose should only be given when patients present with clinical indications of hypoglycemia, and the lowest effective concentration should be used to prevent the manifestation of clinical signs.

Table 14: How to Formulate Dextrose-Containing Fluids
Amount of 50% Dextrose Solution Added to 1L Bag of Isotonic Crystalloids* Final Dextrose Concentration
25 mL 1.25%
50 mL 2.5%
100 mL 5%

*Remove an equivalent amount of the isotonic crystalloid fluid from the bag before adding dextrose.

Download Table 14 PDF

Citations
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  8. Chan DL. Nutritional support of the critically ill small animal patient. Vet Clin North Am Small Anim Pract 2020;50(6):1411–22.
  9. Grathwohl KW, Bruns BJ, LeBrun CJ, et al. Does hemodilution exist? Effects of saline infusion on hematologic parameters in euvolemic subjects. South Med J 1996;89(1):51–5.
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