Fluid Therapy for Horses With Metabolic Acidosis (Box 44.11)
K. Gary Magdesian
Both organic and inorganic acidoses are found in horses with critical illness. A common cause of organic acidosis in horses is lactate (lactic acidosis). Hyperlactatemia occurs with hypovolemia, sepsis, and SIRSs such as endotoxemia, marked hypoxemia, heart failure, cytopathic hypoxia, and liver failure.1-4 Volume resuscitation can be performed with a combination of crystalloids and colloids, and possibly hypertonic saline.
Acetated crystalloids (such as Normosol-R or Plasma-Lyte 148/Plasma-Lyte A) do not contain lactate; however, even LRS (which contains sodium lactate) will correct hyperlactatemia when it is caused by hypoperfusion. Providing for hepatic perfusion will allow for clearance of the lactate previously accumulated. The exception is in liver failure, where fluids devoid of lactate should be administered because metabolism will be reduced. Other less common causes of organic (high anion gap) acidosis include ethylene glycol, salicylate toxicity, and uremic acidosis. The treatment of lactic acidosis is correction of the underlying pathogenesis. If the cause is hypoperfusion, reversal of that state should be the goal of therapy; this is accomplished through restoring blood volume, cardiac output, and finally systemic vascular resistance through the administration of fluids, dobutamine, and vasopressors, respectively. Sodium bicarbonate is therefore not a part of the routine treatment of lactic acidosis; its use in lactic acidosis is in fact controversial.5,6 In a canine model of lactic acidosis, the administration of sodium bicarbonate actually caused a decrease in pH and bicarbonate concentration and an increase in lactate.7 Similarly, in a model of endotoxemia in ponies, administration of sodium bicarbonate resulted in an increased blood lactate concentration.8 Despite these controversies with sodium bicarbonate and lactic acidosis, when the pH of the patient’s blood is below 7.2, administration of sodium bicarbonate until the pH reaches 7.2 is justified in order to prevent the detrimental effects of severe acidemia, even when the acidosis is a result of lactate. Severe acidosis can lead to life-threatening cardiovascular complications such as impaired contractility, sensitization to ventricular arrhythmias, and impaired responses to pressors.9 Small doses of sodium bicarbonate should be administered slowly to increase the pH to 7.2, at which point increasing perfusion should be the goal and sodium bicarbonate can be discontinued.Inorganic acidoses occur because of strong ion acidosis associated with electrolyte derangements. In horses these commonly result from hyperchloremia or hyponatremia, both of which decrease the strong ion difference. Common diseases associated with these metabolic abnormalities include enteritis, colitis, renal failure, and renal tubular acidosis (RTA). In these cases the acidosis is often caused by renal or gastrointestinal dysfunction of electrolyte homeostasis, whereas perfusion may be normal (i.e., normal plasma lactate). Chronic administration of carbonic anhydrase inhibitors, such as acetazolamide, is another cause of hyperchloremia. The fluid of choice for patients with hyperchloremic metabolic acidosis is one containing only strong cations without strong ions. Because sodium bicarbonate contains only strong cations (sodium), it is an ideal choice for patients with normal anion gap (hyperchloremic) acidosis. Sodium bicarbonate should be administered slowly to allow time for distribution and evaluation of its effects. As a fluid choice, rather than as a supplement, isotonic (1.3%) sodium bicarbonate can be used; this formulation contains 150 mEq each of sodium and bicarbonate ion per liter. Potential side effects of rapid or large-volume sodium bicarbonate therapy include hypernatremia, hypokalemia, ionized hypocalcemia, vasodilation, metabolic alkalosis (if in excess), and an increased affinity of hemoglobin for oxygen (left shift of the oxygen dissociation curve).8