Professor and Associate Chair, University of Florida, College of Veterinary Medicine
Gainesville, FL, USA
Conditions Requiring Special Fluid Therapy Considerations
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. Hypervolemia amounting to 20-30% in water excess can cause pulmonary edema.
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 (PLE), beneficial effects are usually temporary at best because of continued protein losses especially with PLE.
Heart failure patients receiving intravenous fluids should be closely observed for weight gain and respiratory distress caused by intravascular fluid overload. A rapid respiratory rate will often be the earliest sign of overload therefore calling for close patient observation. 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.
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. 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.
The loss of 30-40% of intravascular volume will cause severe hypovolemia and hypotension. Cardiac arrest occurs when 50-60% of blood volume is lost.
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. 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. 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.
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. After volume loading an HGE patient with crystalloid solution, the plasma proteins will decrease substantially. In most cases this will begin to correct itself after the first 24-hour period of treatment.
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/kgBW every 24-hours) is the fluid of choice.
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. 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 (13-20 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.
The fluid deficit from massive diarrhea can be efficiently corrected with LRS 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).
The common causes of extreme hyperosmolality in the dog and cat include hyperosmolar nonketotic diabetes mellitus, hypernatremia associated with water deprivation in diabetes insipidus patients, and essential hypernatremia (in dogs). 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. 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. 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. This gradual water replacement will prevent cerebral edema and death, which can be caused by too rapid correction of the serum sodium level.
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. 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.
Chronic hyponatremia is more common than the acute form and occurs when the rate of decline is less than 0.5 mEq/L/hr. Slow correction, essential for preventing central pontine myelinosis, is accomplished by administering NS and furosemide at a rate of less than 0.5 mEq/L/hr.
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.