Complications in Equine Surgery. Группа авторов

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.

      Complications Due to Glucose‐/Dextrose‐Containing Fluids

       Definition

      Abnormal blood glucose levels (reference range: 3.7–6.7 mmol/L). The terms glucose and dextrose can be used interchangeably. Glucose exists as two isomers. L‐glucose is the isomer circulating in the blood of animals and humans, while D‐glucose (known as dextrose) is the isomer occurring widely in nature.

       Risk factors

       Neonates (hypoglycemia)

       Patients with metabolic disease are at high risk of hyperglycemia (Equine metabolic syndrome, pituitary pars intermedia dysfunction)

       Sepsis (both hypo‐ and hyperglycemia can occur)

       Pathogenesis

      Carbohydrate‐containing solutions are commonly used to provide additional energy as a simple means of parenteral nutrition. If administration of glucose exceeds the utilization by tissues, hyperglycemia ensues. Animals with metabolic disease or sepsis have impaired glucose uptake by cells due to insulin resistance contributing to hyperglycemia. Hypoglycemia very rarely occurs in adult horses. Neonates however, have low glucose storage capability and are at risk of hypoglycemia if glucose intake is reduced. In septic animals, particularly neonates, glucose consumption by bacteria and increased cell demands due to inflammatory mediators leads to hypoglycemia.

       Prevention

      Recommendations are to maintain serum glucose within narrow margins and avoid hypo‐ or hyperglycemia [27]. To avoid hyperglycemia, glucose‐containing fluids should not be administered for initial large‐volume fluid resuscitation. This can lead to profound hyperglycemia with a diuretic effect causing massive diuresis. If milk is withheld for more than 12 hours in neonatal foals, glucose‐containing fluids should be administered. In horses, it is reasonable to use a 2.5–5% dextrose‐containing polyionic fluid as maintenance therapy. Isotonic Glucose (5% glucose in water) should not be used as a general maintenance fluid due to the absence of electrolytes. This solution is useful for providing large amounts of water to patients with hyperosmolar syndrome but does have in vivo acidifying effects.

      If a fluid amount higher than the maintenance rate has to be administered to a horse or foal to cover additional losses or treat dehydration, it is often better to give a glucose‐free polyionic crystalloid solution separately and to add 50% dextrose as a separate infusion set using an infusion pump. In this way, the amount of glucose can be titrated properly and separately from the amount of other fluids infused. Polyionic crystalloid glucose‐free fluids should always be given simultaneously through the same catheter as the 50% dextrose, to dilute the hyperosmolar solution and avoid endothelial injury. An infusion pump should always