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Definition

Sodium bicarbonate is a fluid containing equal amounts of sodium and bicarbonate ions and can be indicated for correction of metabolic acidosis. Administration can result in undesired side effects such as hypernatremia or respiratory distress, and if used in the wrong patients without concurrent administration of isotonic fluids can result in worsening of the underlying acid–base abnormality.

Risk factors

 Patients with chronic hyponatremia receiving sodium bicarbonate

 Severely dehydrated animal with lactic acidosis receiving sole administration of sodium bicarbonate to correct metabolic acidosis

 Patients with severe respiratory failure (hypercapnia, pCO2 >60 mm Hg): administration of large amounts of sodium bicarbonate to these patients is believed to be contraindicated

Pathogenesis

Once infused, the sodium increases the strong ion difference and is shifting the equilibrium of the bicarbonate dissociation toward HCO₃, therefore in turn raising the pH concurrently with the sodium levels.

In chronic hyponatremia, intracellular sodium concentrations have adapted and are similar to extracellular (plasma) concentrations. When the plasma sodium concentration is increased rapidly due to the administration of NaHCO₃, the intracellular sodium concentration suddenly becomes lower than the plasma concentration. As water follows solute, water is drawn from the brain cells to extracellular fluid (plasma), causing osmotic demyelination syndrome (see also discussion on sodium above).

In severely dehydrated animals, the main acid–base disturbance is metabolic acidosis as a result of lactate accumulation because of hypoperfusion. If NaHCO₃ is erroneously administered in an attempt to raise the pH, along with an inadequate amount of fluid administered, hypoperfusion and metabolic acidosis due to lactate accumulation persists. Acute hypernatremia can be caused if large amounts of NaHCO₃ are infused in an attempt to rehydrate the animal with NaHCO₃.

In the traditional approach to acid–base disturbance, dissociation of HCO₃ produces CO₂, which then has to be eliminated via the lungs. In patients with respiratory compromise, elimination can be decreased and may lead to respiratory acidosis. Following the physicochemical approach to acid–base disturbance, CO₂ is an independent variable and therefore not influenced by the concentration of HCO₃. Infusion of Na‐HCO₃ therefore does not lead to elevated pCO₂ concentrations in the blood or lungs. To err on the side of caution, administration of Na‐HCO₃ to patients with respiratory compromise should be avoided.

Prevention

Determine acid–base and electrolyte status of patient and assess if Na‐HCO₃ is truly the fluid of choice. The origin of acidosis should be identified. In equine medicine, the most common cause for metabolic acidosis is due to increased serum L lactate concentrations due to hypovolemia and endotoxemia, and therefore Na‐HCO₃ is rarely indicated. These animals will benefit most from treatment of dehydration by administering replacement therapy of isotonic crystalloid fluids.

The second‐most common cause of metabolic acidosis is electrolyte derangements. The underlying electrolyte derangements should be identified and corrected. The most common causes of metabolic acidosis are hyponatremia and hyperchloremia. Sodium bicarbonate is therefore particularly useful in hyponatremic hyperchloremic patients where large amounts of sodium are needed without the addition of chloride. NaHCO₃ is indicated if:

 Hyponatremia concurrent with hyperchloremia

 pH <7.2

If possible, an isotonic formulation (1.3%) of NaHCO₃ should be administered:

 Add 150 mmoL (13 g) of NaHCO3 to 1 L of sterile water

 Alternatively, 150 mmol/L can be added to Lactated Ringer’s if sterile water is not available; note that this will result in a slightly hypertonic solution. There is no problem with Ca chelation.

Calculate the deficit based on:

 Deficit mmol/L NaHCO3 = BW × –BE × 0.3 (adults) or 0.5 (foals <2 months)

 Give half of the calculated amount over 30 min, the rest over 24 h

Alternatively, oral NaHCO₃ can be given 0.3–0.5 g/kg q 12–24 h.

Diagnosis

Repeat blood gas analysis should be performed after administration of NaHCO₃, every 6–12 hours, depending on severity of disease. Concentrations of pCO₂ and sodium should be particularly closely monitored.

Treatment

Immediately stop infusion of NaHCO₃ if signs or respiratory distress or tachypnea occur. Measure blood sodium levels and administer isotonic replacement fluids (e.g. Lactated Ringer’s) at a rate slightly higher than maintenance if Na levels are within normal limits; otherwise, follow recommendation in the paragraph on Sodium Imbalances.

Expected outcome

The outcome depends on the severity of the case. Animals can potentially die from respiratory failure or worsening of acid–base and electrolyte abnormalities. If treatment is instituted and the animal responds, full recovery is usually observed.