Slight prolongation of CRT
Eyes possibly sunken inorbits
Possibly dry mucous membranes
Definite prolongation of CRT
Eyes sunken in orbits
Dry mucous membranes
Possible signs of shock(tachycardia, cool extremities, rapid and weak pulses)
From Muir, WW, DiBartola, SP. 1983. Fluid therapy. In Current Veterinary Therapy VIII, edited by Kirk, RW. Philadelphia: WB Saunders, p.33.
The same fluids can be used for both replacement and maintenance fluid therapy. However, adequate renal function should be present to ensure appropriate elimination of electrolytes in excess of daily requirements.
Isotonic saline, also known as normal saline or physiologic saline, can also be used as a replacement fluid. It is available as 0.9% NaCl and only the sodium is isotonic. It does not meet the patient’s daily electrolyte requirements when used as a maintenance fluid. It is used for rapid expansion of the extracellular fluid volume and is quickly redistributed throughout the extracellular space. Isotonic saline can have an acidifying effect because of its high chloride content and should be used cautiously in patients that are already acidemic.
Resuscitation fluid therapy
The patient’s clinical history and physical exam findings should determine whether the fluid resuscitation phase is needed. A patient in shock will usually present with pale mucous membranes and a prolonged to absent capillary refill time (CRT), tachycardia or severe bradycardia, cool extremities, weak to absent peripheral pulses, and hypotension. There are several different forms of shock that will be discussed more in depth later in the chapter. Hypovolemic and distributive types of shock typically respond better to rapid volume expansion. Obstructive shock responds better to moderate fluid therapy. Fluid therapy is contraindicated in most cases of cardiogenic shock (DiBartola and Bateman 2006). Shock fluid resuscitation can include crystalloids, colloids, and blood products if needed.
Hypochloremia can result due to a lipemic blood sample, vomiting of stomach contents, chronic respiratory acidosis, hyperadrenocorticism (Cushing’s disease), exercise, or sodium bicarbonate therapy. It can also be a result of thiazide (hydrochlorothiazide) or loop diuretic (furosemide) drug therapy (Autran de Morais and Biondo 2006).
Hyperchloremia can also be a result of a lipemic blood sample. Other causes are potassium bromide (KBr) therapy, which causes the analyzer to read bromide as chloride, high chloride-containing fluids, diarrhea, or an overall gain of chloride due to potassium supplementation or salt poisoning. Renal chloride retention can occur as a result of renal failure, hypoadrenocorticism (Addison’s disease), diabetes mellitus, chronic respiratory alkalosis, or spironolactone drug therapy.
The treatment for both hypochloremia and hyperchloremia is accomplished through finding and treating the underlying cause (Autran de Morais and Biondo 2006), although fluid therapy should be implemented in the meantime.
Sodium is a major extracellular cation. A serum sodium concentration tells the amount of sodium compared to the amount of water in the patient’s extracellular fluid. A patient is considered hyponatremic if its sodium is less than 140 mEq/L for a canine and less than 149 mEq/L for a feline. Hyponatremia will result when a patient is unable to excrete ingested water or when its urinary and insensible losses have a greater osmolality than that of the ingested or administered fluids (DiBartola, 2006).
A patient is considered hypernatremic when its sodium is greater than 155 mEq/L for a canine and greater than 162 mEq/L for a feline. Hypernatremia can result due to an inadequate intake of water, an excessive amount of sodium ingested or administered, a pure water deficit, hypotonic loss, or hemorrhagic shock.
Clinical signs of hyponatremia and hypernatremia are the same, but they have very different causes. In hypernatremia neurologic effects can be seen due to a rapid decrease in brain volume caused by rupture of cerebral vessels or focal hemorrhage. Hyponatremia leads to cerebral edema, which will also cause the patient to exhibit neurological signs. The severity of signs is related to the rapidity of onset, not to the magnitude. The neurologic signs can include weakness, behavioral changes, disorientation, ataxia, seizures, coma, and death. Anorexia, lethargy, and vomiting can also be seen (DiBartola 2006).
Acute hyponatremia can be corrected with LRS, 0.9% NaCl, or even hypertonic fluid administration. Chronic hyponatremia, as well as chronic hypernatremia must be treated much more slowly. Sodium levels must not be changed any more rapidly than 10–12 mEq/L in 24 hours (0.5 mEq/L/hr) for fear of causing some of the same neurologic effects that are trying to be resolved (DiBartola 2006). See Figure 12.2 for calculating fluid rates for sodium changes. When treating chronic hyponatremic patients, be sure to keep their water intake less than their urine output in the case of psychogenic polydipsia. Also be sure to discontinue any antidiuretic medications.
In the case of a pure water deficit leading to hypernatremia, the treatment is 5% dextrose in water (D5W) or 0.45% NaCl administration. When using DW the glucose will quickly enter the cells and be metabolized, leaving only water. Be sure to replace the water deficit slowly. If a hypotonic loss has occurred and signs of volume depletion are seen, rapid extracellular volume repletion with an isotonic fluid is necessary. In the case of hemorrhagic shock, whole blood, plasma, or colloid solutions can be administered in conjunction with crystalloids (DiBartola 2006). The important thing to remember is to closely monitor the sodium levels of your patient.
Potassium is a major intracellular cation. Hypokalemia can be caused by an insulin administration or glucose-containing fluids, vomiting of stomach contents, or diarrhea. Urinary losses can also occur. They are seen in chronic renal failure patients, postobstructive diuresis, dialysis, hyperadrenocorticism (Cushing’s disease), or primary hyperaldosteronism. Medications such as loop diuretics, thiazide diuretics, amphotericein B and pencillins can also lead to a hypokalemia (DiBartola and Autran de Morais 2006).
Signs of hypokalemia will vary patient to patient and also depend on the severity. Some patients will have no clinical signs. Other patients with values less than 3.0 mEq/L will exhibit signs such as polyuria/polydipsia (PU/PD), a decrease in urine-concentrating capabilities, and even muscle weakness possibly leading to respiratory paralysis. Cardiovascular signs may also be noted. These include delayed ventricular repolarization, increased duration of action potential, and an increased automaticity. Supraventricular and ventricular arrhythmias can be seen. A prolongation of the QT interval may be seen with potassium values less than 2.0 mEq/L, and they may become unresponsive to antiarrhythmic therapy (DiBartola and Autran de Morais 2006).
The treatment for hypokalemia is potassium supplementation. To avoid adverse cardiac effects during potassium supplementation do not administer potassium any faster than 0.5 mEq/kg/hr IV. Potassium is available as KCl (2 mEq/mL) or potassium phosphates (4.36 mEq K+/mL). If the hypokalemia is due to vomiting or diuretic administration, KCl is the treatment of choice. See Table 12.2 for an estimate on the amount of KCl to add to parenteral fluids based on the patient’s serum potassium value.
The effects of hyperkalemia, like hypokalemia, depend on the individual patient as well as the magnitude of the elevation. A potassium value greater than 6.5 mEq/L needs immediate treatment. Hyperkalemia is an uncommon finding in patients with normal renal function and urine output.
Hyperkalemia can have many causes. It can be due to calculation errors with constant rate infusions. It is seen in diabetic patients due to an insulin deficiency and hyperosmolality. Decreased urinary excretion from a urethral obstruction, ruptured bladder, or anuric/oliguric renal failure will also lead to an increased potassium. Hypoadrenocorticism will also cause hyperkalemia.