Fluid therapy in clinical medicine is used to fulfill the following objectives: (1) to replace dehydration deficits, (2) to maintain normal hydration, (3) to replace essential electrolytes and nutrients, and (4) to serve as a vehicle for the infusions of certain intravenous medications. Except for the urgency of treatment, the same objectives apply in the critically ill animal. The methods for providing fluids often influence the eventual outcome of the case. The clinician and staff, therefore, should familiarize themselves with the pathophysiology of the diseases they are treating and how these conditions relate to the various types of fluids that are available for general use.

BODY WATER DISTRIBUTION

Total body water (TBW) accounts for approximately 60% of the body weight in kilograms (where 1 L H₂0 weighs 1.0 kg). Approximately two thirds of TBW is intracellular fluid (ICF) and one third is extracellular fluid (ECF). Three quarters of the ECF is interstitial fluid, and the remaining one quarter is intravascular fluid. Fluid administered intravenously is distributed between the intravascular and extravascular spaces in fractions determined by the compartments' protein and sodium contents.

ROUTES OF ADMINISTRATION

In general, fluids can be given by the following routes: (1) oral, (2) subcutaneous, (3) intraperitoneal, (4) intravenous, and (5) intraosseous. The two latter routes are preferred for the critically ill patient because they give direct access to the intravascular space.

Intravenous infusion is the preferred means of delivering fluids to severely dehydrated animals and medium to large dogs. It allows for a controlled delivery rate to meet the patient's changing needs. Intravenous treatment requires the insertion of a cannula into a vein using sterile technique and the subsequent sterile maintenance of the intravenous delivery system. Knowledge of these requirements and the complications that can result from this mode of therapy is important for a successful outcome. The more common complications include phlebitis, catheter sepsis, fluid overload, and the inadvertent flow of fluid into the surrounding perivascular subcutaneous tissue. Intravenous catheters should be changed and rotated to another site every 72 hours in order to avoid most of these iatrogenic complications. With proper technique, the advantages far outweigh the disadvantages.

Intraosseous fluid therapy is a preferred route for animals weighing less than 5 kg when the intravenous approach is impossible. Actually, because of the bone marrow's direct access to the systemic circulation, it can be considered as a large rigid vein through which most medications can be safely delivered. The intraosseous method for fluid therapy is a safe and efficacious route in the critically ill patient.^1,2 After adequate blood pressure is restored, the method for fluid delivery is switched to the intravenous route. A comparison of the various routes of fluid administration is provided in Table 1.

FLUID SELECTION--CRYSTALLOIDS

Parenteral fluid packages provide a list of the solute content and osmolality. This information is important when deciding which fluid to use in each particular clinical situation. Fluids can be conveniently classified on the basis of tonicity (Table 2).

Isotonic fluids contain the same osmolality as the extracellular fluids (approximately 290 to 310 mOsm/L). They are excellent solutions, therefore, for providing rehydration and maintenance needs, especially because they can be administered intravenously, intraosseously, subcutaneously, and intraperitoneally. Commonly used isotonic solutions include lactated Ringer's, .9 percent (normal or physiologic) saline; Ringer's, acetated Ringer's, and 2.5% dextrose in 0.45% saline.

Lactated Ringer's solution (LRS) is a polyionic, isotonic (273 mOsm/L) solution. It is more physiologic than isotonic saline because its electrolyte concentration is similar to that of plasma. The 28 mEq of lactate anions can help reverse metabolic acidosis because of their potential for conversion to bicarbonate ions by the patient's liver (in the absence of shock). Although each liter contains 4 mEq of potassium, supplementation with this cation is usually required for the patient's maintenance needs. Considerably more is required for treating hypokalemia. Because the bicarbonate derived from the lactate can promote alkalemia, this solution should not be used if the patient has a coexisting metabolic or respiratory alkalosis. LRS is commonly used as a routine rehydrating and maintenance solution, as a plasma space volume expander in the treatment of shock, and as the fluid of choice in the acidotic patient.

An acetated Ringer's solution is also available. Its uses and restrictions are similar to those for LRS. Theoretically, sodium acetate is preferable to sodium lactate because a significant part of the latter anion is converted into liver glycogen, whereas acetate ions are not metabolized by the liver but by muscles and other peripheral tissues. In addition, the acetate ions are metabolized differently than the lactate ions and require less oxygen for their metabolism to carbon dioxide and bicarbonate ions; this may be important if shock is present. Acetated solutions should not be used for treating ketoacidosis, because the acetate might promote acetoacetate production. Acetated Ringer's solution contains Mg⁺² which can benefit the patient with magnesium deficiency.

Ringer's solution is an isotonic saline solution (309 mOsm/L), with potassium and calcium ion concentrations approximately equal to those normally found in blood and extracellular water. The chloride concentration, however; is supraphysiologic (155 mEq/L). Potassium and calcium ions should be added when patients are depleted of these cations.

"Physiologic," 0.9% saline (NS) is also isotonic (310 mOsm/L) and is commonly used for rehydration. However, because of its supraphysiologic levels of sodium and chloride ions (154 mEq/L), it is not recommended for maintenance. This solution is mainly used for plasma volume expansion, for the correction of hyponatremia, and, along with potassium chloride supplementation for the treatment of metabolic alkalosis. Once plasma volume deficits are restored to normal, NS should not be used in animals with congestive heart failure or other conditions in which sodium restrictions are imposed.

Dextrose 2.5% in 0.45% saline is nearly isotonic (280 mOsm/L). Once rehydration has been accomplished and normal electrolyte balance has been restored, it is a useful maintenance solution when supplemented with potassium chloride. It is also the fluid of choice for patients whose sodium intake is restricted and those that tend to develop hypernatremia with NS (as seen in some azotemic cats with urethral obstruction).

The osmolality of hypotonic solutions is less than that of plasma and extracellular water. The most commonly used product is 5% dextrose solution (D-5-W; 253 mOsm/L). It is mainly used (1) in patients with hypernatremia, because the dilutional effects will lower the serum sodium level; (2) as a carbohydrate source when another polyionic electrolyte solution is used concomitantly, and (3) as a fluid supplement for patients with sodium intolerance. D-5-W should not be the sole intravenous fluid for maintenance therapy because electrolyte depletion states hyponatremia, hypochloremia, hypokalemia, and hypomagnesemia can result. In addition, this solution should not be administered subcutaneously, because extracellular electrolytes tend to diffuse down the concentration gradient into the area of hypodermoclysis. When this happens the subsequent reduction of plasma solute can lower the circulating blood volume and cause hypotension.³ D-5-W should not be given to correct extracellular volume depletion because two thirds of the infused volume will enter the intracellular space within the first hour of infusion; the expanded plasma space is therefore not maintained. Isotonic saline and LRS, on the other hand, remain in the extracellular space for a considerably longer period of time. Eight percent of administered D-5-W stays in the intravascular space, whereas with isotonic saline, at least a quarter of the volume administered remains in the intravascular space.

Hypertonic solutions have a higher osmolality than plasma and extracellular fluid. The most commonly used hypertonic solution is dextrose 5% in 0.9% saline (560 mOsm/L). It can be used as a partial maintenance solution once the patient is completely rehydrated. It is best administered slowly IV. This solution should never be used in a dehydrated animal because it will promote cellular dehydration and intensify the hypovolemia by stimulating diuresis before adequate plasma volume expansion has been achieved. This fluid can be used as an energy source and as a sodium supplement in the well hydrated, hyponatremic patient.

Small-volume hypertonic saline solution (7.5%) has recently been suggested as a means of effective initial resuscitation from hemorrhagic shock.^4,5 Infusion of 4 to 5 ml/kg of sodium chloride 7.5% (2400 mOsm/L) in hemorrhagic shock can rapidly increase systemic blood pressure and cardiac output and produce elevated renal, total splanchnic, and coronary blood flow. The effect of hypertonic saline treatment has also been attributed to its action on the cardiovascular system, including vasodilation, increase in myocardial contractility, and redistribution of fluid from the extravascular to the intravascular compartments, leading to a transient rise in the circulating volume.⁵

COLLOIDS

Whole blood, plasma, and colloidal plasma expanders are valuable for increasing the circulating blood volume when shock is present. Most of the solution is retained within the vascular system, where it increases the osmotic pressure of the blood above that of the extravascular fluid spaces. Consequently, water passes from the interstitial fluid space into the blood, increasing the circulating blood volume.

Plasma is the most commonly used colloid solution in veterinary medicine. Its main advantage stems from the colloid osmotic pressure provided by plasma proteins. It is useful for treating hypoproteinemic conditions such as chronic liver disease, protein-losing enteropathy, and glomerulopathy. The main disadvantages of plasma are that its availability is limited, its effects are temporary, and it is expensive.

Dextrans are synthetic colloids derived from sugar beets. Dextran 70 and 40 are available in 5% dextrose or saline solutions. Dextran 40 has the advantage of retarding formation of rouleaux and sludging of red blood cells, thus improving microcirculation above and beyond simple volume expansion.⁶ Disadvantages include coagulopathies as a result of decreased platelet function and altered fibrin clot formation. Other problems include renal failure, anaphylaxis, and depressed immune function.⁴

Hydroxyethyl starch (Hetastarch) is a synthetic polymer derived from a waxy starch composed mostly of amylopectin. Like albumin, it expands the circulating plasma volume. Its osmolality is approximately 310 mOsm/L. The expanded plasma volume may last for 24 hours or longer. Hydroxyethyl starch is available as a 6% solution in saline. It should be infused slowly at a rate of 10 to 20 ml/kg/day.

FLUID VOLUME REPLACEMENT

The animal requires fluids for (1) rehydration, (2) maintenance, (3) replacement of insensible loss volumes, and (4) replacement of ongoing loss volumes. Clinically, the amount of fluid needed to correct dehydration deficits can be assessed from the degree of skin turgor, capillary refill time, and pulse rate and quality. The degree of dehydration ranges from 5% to 12% (Table 3). Skin turgor assessment can sometimes be misleading in the obese animal, because adipose tissue replaces subcutaneous interstitial water and maintains elasticity despite negative water balance. Also, old, cachectic patients that have lost skin resiliency may give a false impression of marked dehydration. To clarify the diagnosis in such questionable situations, clinicians can check for the elevated packed red cell volume and plasma total solids that accompany the hemoconcentration caused by volume depletion. Discretion should be used when interpreting these clinicopathologic parameters, because lab values in an anemic animal with concomitant hypoproteinemia may seem normal even if the animal is dehydrated.

The volume of fluid needed to correct dehydration is calculated from either of the following formulas:

1.  Volume (ml) of fluid needed = % dehydration x body weight (lb) x 500

2.  Volume (ml) of fluid needed = % dehydration x body weight (kg) x 1000

The maintenance volume is that amount normally required in a 24-hour period by a well hydrated patient. Taking insensible fluid loss into consideration, the 24-hour maintenance volume for a dog or cat whose urine output is normal is approximately 50 to 60 ml/kg (25 to 30 ml/lb) per day. The total 24-hour fluid requirement for the dehydrated animal is the sum of maintenance volume and volume required to correct dehydration.

The initial rate and route of fluid delivery depend on the patient's status. Mildly to moderately dehydrated small dogs and cats that require short-term fluid treatment can be adequately managed with subcutaneous fluids (Table 1).

Any severely (>10%) dehydrated patient should initially receive fluids intravenously. Because of the accompanying vasocollapse, medications injected subcutaneously may not be adequately absorbed into the systemic circulation. For the mildly to moderately hypovolemic patient, it is recommended that one fourth to one half of the estimated dehydration deficit be replaced over the first two to four hours with the remaining dehydration deficit and maintenance isotonic volumes administered over the subsequent 20 to 22-hour period. The amount of subsequent fluid infusion will depend on the patient's response to treatment.

Exceptions to the recommended maintenance doses of fluids occur under the following circumstances:

1.  Oliguria and anuria. After dehydration deficits are replaced, the patient's maintenance needs depend on urinary output, which should be estimated or quantitated. Providing full normal maintenance fluid volumes to oliguric and anuric patients can lead to fatal pulmonary edema or pleural effusion because of iatrogenic intravascular fluid overload. Specific treatment for low output renal failure is provided in the next section.

2.  Polyuria. Polyuric animals require fluid volumes in excess of normal maintenance needs. Failure to provide these volumes can result in a sustained negative water balance if the patient is unable to drink. The maintenance needs for polyuria consist of exact urinary losses plus insensible and ongoing losses. Assurance of adequate treatment is made by weighing the patient each day as well as by assessing the physical and laboratory parameters for hydration. An acute loss of 1 kg of body weight suggests a 1 L fluid deficit.

3.  Rapid internal shifts of fluid, which can occur in pancreatitis, extensive burns, enteritis, and gastrointestinal obstructions. In these conditions, the fluid needs of the patient will exceed the usual maintenance volumes by as much as three times.

The assessment of the animal's fluid requirements must always be made within the pathophysiologic context.

CONDITIONS REQUIRING SPECIAL FLUID THERAPY CONSIDERATIONS (See Table 4)

Anemia

Intravenous fluids are sometimes used excessively in the anemic patient when the decrease in red blood cell mass is misinterpreted as total blood volume depletion, when in fact the plasma volume might even be expanded. To compensate for decreased tissue oxygen delivery, the heart rate increases, and if these patients are subjected to large fluid volumes over a short period of time, pulmonary edema can occur.

Anemic cats in particular are susceptible to intravenous overload from crystalloid infusions. The dehydration deficit and maintenance fluid volumes should be gradually replaced over a 24-hour period with an isotonic crystalloid solution, while fresh whole blood is used to replace the red blood cells. The volume of whole blood infused should be considered when calculating the volume of crystalloid for infusion.

Extracellular Fluid Volume Excess

This condition is associated with an increase in total body salt and water and occurs in a variety of clinical settings including congestive heart failure, glomerulopathies, liver fibrosis, and protein-losing enteropathy. These conditions are associated with a decrease in "effective arterial volume," which stimulates the renin-angiotensin-aldosterone cycle and the release of antidiuretic hormones to promote renal salt and water retention, respectively. Because of increased venous pressure from heart failure and cirrhosis or because of decreased plasma oncotic pressure associated with hypoalbuminemia, the retained salt and water move into the interstitial and other body spaces, causing edema, ascites, or pleural effusion.

Patients with any of these conditions are extremely sensitive to intravenous overload with crystalloid solutions. Treatment should be directed toward improving the underlying primary pathologic process. Fresh or fresh frozen plasma should be used to volume expand animals with hypoalbuminemia, although in glomerulopathies and protein-losing enteropathy, beneficial effects are usually temporary at best because of continued protein losses.

Heart failure patients receiving intravenous fluids should be closely observed for weight gain and respiratory distress caused by intravascular fluid overload. Under optimal conditions, monitoring of central venous and pulmonary wedge pressures is helpful for avoiding this potentially fatal complication. The reader is referred to other sources for details regarding these techniques.^7,8

When parenteral fluid therapy is indicated in the cardiac patient, solutions containing little or no sodium are given after dehydration and hypovolemia are corrected with isotonic solutions.^6,7 Either 0.45% saline or D-5-W can be used. Efforts should be made to avoid hypokalemia by adding potassium chloride solution to the fluids at a dose of 7 to 10 mEq/250 ml. Periodic monitoring of serum electrolytes is necessary for accurate treatment adjustments.

Hypovolemic Shock

Isotonic crystalloid solutions (NS, acetated Ringer's or LRS)are the most commonly used replacement fluids because they are usually effective, readily available, easily administered, and relatively inexpensive.^6,9 Severely hypotensive patients might require at least one whole blood volume of replacement fluids during the first hour of treatment. Initial rapid infusion for dogs should be 20 to 40 ml/kg IV (one half this amount for cats) for 15 minutes, followed by 70 to 90 ml/kg (dogs) or 30 to 50 ml/kg (cats) administered over one hour. This loading volume is followed by administration of maintenance fluids at a rate of 10 to 12 ml/kg/hr for dogs and 5 to 6 ml/kg/hr for cats.¹⁰ The patient's heart and respiratory rates and urine volume are monitored every 15 minutes during vascular volume resuscitation. Any signs of fluid overload necessitate prompt decreases in fluid delivery and consideration of diuretic therapy. Optimally, central venous or pulmonary arterial wedge pressure determinations should be used to monitor the patient's hemodynamic status.⁸

This particular fluid regimen is especially useful for treating dogs and cats with trauma-induced peracute blood loss. It has also been proved efficacious for treating other conditions in which plasma volume is depleted rapidly, such as the canine hemorrhagic gastroenteritis (HGE) syndrome.

Vomiting

Vomiting is the principle sign of gastric disease, but it can also accompany disorders of the small or large bowel, liver, and pancreas, as well as disorders occurring outside of the digestive system. Vomiting can deplete the body of a substantial volume of fluids and electrolytes. The specific types of electrolyte deficiencies and acid-base abnormalities depend on the location of the primary disorder. Vomiting caused by pyloric outflow obstructions typically can lead to dehydration, metabolic alkalosis, hypochloremia, hypokalemia, and hyponatremia. NS supplemented with potassium chloride (3 to 10 mEq/kg_BW every 24-hours) is the fluid of choice.¹¹

Fluid losses through vomiting associated with systemic illness or intestinal disease are best replaced with lactated or acetated Ringer's solutions. The patient's serum electrolyte status should be monitored and corrected when indicated.

Gastric Dilatation--Volvulus (GDV)

The GDV complex causes hypovolemic shock as well as gastric sequestration of fluids and electrolytes. Although the hypovolemia can cause tissue hypoxia and eventually metabolic acidosis, there are several instances in which the gastric hydrogen and chloride ion sequestration can offset the acidosis and perhaps even cause a metabolic alkalosis.¹² Although most dogs with GDV are initially volume resuscitated with LRS, their acid-base parameters should be monitored if possible in order to detect any need for a change in fluid type.

Oliguric and Anuric Renal Failure

The urine output of all critically ill patients should be monitored, especially during periods of intensive fluid therapy. Fortunately, many oliguric patients will begin producing urine after they receive one half of their estimated dehydration deficit values during the first one to two hours of treatment. If urine production is inadequate, the following protocol is recommended:

1.  Insert an indwelling urethral catheter and empty the urinary bladder of any residual urine.

2.  Administer the calculated dehydration deficit fluid volume over the first two to four hours of treatment.

3.  Once rehydration has occurred, administer furosemide (4 mg/kg IV push) and/or mannitol (0.5 gm/kg IV) over a 10-minute period.

4.  If no urine flow occurs, readminister furosemide (8 mg/kg IV push) or administer dopamine (1 to 2 µg/kg/min IV).

5.  If oliguria or anuria persists, the amount of fluids infused per day will consist of the sum of the measured urine output, the insensible water loss (5 ml/kg/day), and the extra losses caused by vomiting or diarrhea. Peritoneal dialysis will be required to rid the body of uremic toxins.

Plasma volume expansion should be accomplished with LRS or NS; the latter is preferred if hyponatremia is present. Maintenance fluids can initially consist of Ringer's lactate or acetate but can eventually be reduced in concentration to one-half strength in the absence of any renal sodium-losing disorder.

Diarrhea

The fluid deficit from massive diarrhea can be efficiently corrected with LRS or acetated Ringer's because it resembles the type of fluid lost, is readily available, and provides uniformly good results. In markedly hypotensive patients, the intravenous fluids should be given as described previously (see Hypovolemic Shock).

Hyperosmolar Conditions

The common causes of extreme hyperosmolality in the dog and cat include hyperosmolar nonketotic diabetes mellitus,⁶ hypernatremia associated with water deprivation in diabetes insipidus patients,¹³ and essential hypernatremia (in dogs).¹⁴ In hyperosmolar diabetes, dehydration is easily detectable through skin turgor evaluation; in the latter two conditions, the interstitial water is often retained because of a shift of fluid from the intracellular space, thereby allowing for normal skin turgor.¹⁵ Eventually, however, the subcutaneous water will become depleted. In each of these conditions, hypovolemia can be life-threatening.

It would seem logical that a hypotonic solution such as D-5-W (252 mOsm/L) would be the fluid of choice; however, this solution rapidly exits from the intravascular space (two thirds of the infused volume exits within the first hour), and thereby does little to expand the intravascular fluid space. The preferred initial fluid, therefore, is NS because of its isotonicity, its tendency to persist within the intravascular space for a reasonable length of time, and its hypotonicity relative to the patient's hyperosmolar plasma.¹⁵ After adequate plasma space resuscitation, the infusion can be changed to 0.45% saline with or without 2.5% dextrose added.

In marked hypernatremia (serum Na⁺ > 165 mEq/L), the goal of treatment is reduction of the serum sodium level by 0.5 to 1.0 mEq/L per hour, replenishing one half of the water deficit in 12 to 24 hours and the remainder in another 24 hours.¹⁵ This gradual water replacement will prevent cerebral edema and death, which can be caused by too rapid correction of the serum sodium level.¹⁶

Hypotonic Disorders

A hypotonic disorder is one in which the serum osmolality and sodium levels are reduced in parallel. Clinically significant hyponatremia is most often due to an inability to excrete a maximally dilute urine.

The goal of treatment in hyponatremia is to correct body water osmolality and restore cell volume by raising the sodium-to-water ratio of extracellular fluid. Acute hyponatremia occurs when the decline in serum sodium exceeds 0.5 mEq/L/hr.¹⁷ When levels fall below 120 mEq/L, with associated brain dysfunction, the condition should be treated immediately. Hypertonic saline (3% or 5% is administered at a rate of at least 1 mEq/L/hr to replace sodium.¹⁷

Chronic hyponatremia is more common than the acute form and occurs when the rate of decline is less than 0.5 mEq/L/hr.^17,18 Slow correction, essential for preventing central pontine myelinosis,^17-19 is accomplished by administering NS and furosemide at a rate of less than 0.5 mEq/L/hr.¹⁷

Hypercalcemia

Many patients with hypercalcemia are volume depleted. Initially, NS should be infused to normalize intravascular volume. Because the renal excretions of sodium and calcium are linked, a forced saline diuresis using furosemide and isotonic saline will accelerate calciuresis. Close monitoring of serum electrolyte levels, especially potassium, is essential to detect and correct possible hypokalemia. All patients receiving rapid saline diuresis should be monitored for signs of intravascular fluid overload.

Table 1. Routes of Fluid Administration the Dogs and Cats

Modified from Schaer M: General principles of fluid therapy. Vet Clin North Am 19:203, 1989.

Table 2. Comparison of Commonly Used Parenteral Fluids in the Dog and Cat

From Covington TR, Dipalma JR, Hussar DA, et al (eds): Drug Facts and Comparisons, 1985 edition. St. Louis, JB Lippincott, 1984

Table 3. Estimating the Degree of Dehydration

Table 4. Fluid Therapy for Special Circumstances

References

1.  Otto CM, Kaufman GM, Crowe DT 1989. Intraosseous infusions of fluids and therapeutics. Compendium on Continuing Education (Small Anim Pract) 11:421.

2.  Orlowski JP, Julius CJ, Petras RE, et al 1989. The safety of intraosseous infusions: Risks of fat and bone marrow emboli to the lungs. Ann Emerg Med 18:1062.

3.  Goldberger E 1986. A Primer of Water, Electrolyte, and Acid-Base Syndromes. Philadelphia, Lea & Febiger.

4.  Garvey MS 1989. Fluid and electrolyte balance in critical patients. Vet Clin North Am 19: 1021.

5.  Landau EH, Gross D, Assalia A, et al 1989. Treatment of uncontrolled hemorrhagic shock by hypertonic saline and external counterpressure. Ann Emerg Med 18:1039.

6.  Wolfsheimer KJ 1989. Fluid therapy in the critically ill patient. Vet Clin North Am 19:361.

7.  Bonagura JD 1982. Fluid management of the cardiac patient. Vet Clin North Am 12:501.

8.  Haskins SC 1989. Monitoring the critically ill patient. Vet Clin North Am 19:1059.

9.  Webb AI 1982. Fluid therapy in hypotensive shock. Vet Clin North Am 12:515.

10. Goodwin JK, Schaer M 1989. Septic shock. Vet Clin North Am 19:1239.

11. Twedt DC, Grauer GF 1982. Fluid therapy for gastrointestinal, pancreatic and hepatic disorders. Vet Clin North Am 12:463.

12. Wingfield WE, Twedt DC, Moore RW, et al 1982. Acid-base and electrolyte values in dogs with acute gastric dilatation volvulus. J Am Vet Med Assoc 180:1070.

13. Reidarson TH, Weis DJ and Hardy RM 1990. Extreme hypernatremia in a dog with central diabetes insipidus: a case report. J Am Anim Hosp Assoc 26:89.

14. Crawford MA, Kittleson MD 1984. Hypernatremia and adipsia in a dog. J Am Vet Med Assoc 184:818.

15. Hardy RM 1980. Hypernatremia. Vet Clin North Am 19:231.

16. Snyder NA, Feigal DW, Arieff AI 1987. Hypernatremia in elderly patients, a heterogeneous, morbid and iatrogenic entity. Ann Intern Med 108:309.

17. Cluitmans FHM, Meinders AE 1990. Management of severe hyponatremia: Rapid or slow correction? Am J Med 88:161.

18. DiBartola SP 1989. Hyponatremia. Vet Clin North Am 19:215.

19. Sterns RH 1990. The treatment of hyponatremia: First, do no harm. Am J Med 88:557.