SAEVA Proceedings 2016 | Page 216

  In metabolic disturbances, the change in anion gap should approximate the change in bicarbonate. If that is not the case, then mixed acid-base disturbances should be suspected. Yet another parameter that you will encounter on blood-gas analyses is the Base Excess, which is defined as the amount of strong acid (such as HCl) needed to titrate 1L of blood to pH 7.40 at 37°C with PCO2 constant at 40 mm Hg. It only changes with non-volatile / fixed acids and is therefore also a measure of metabolic disturbances. Production of lactate under hypoxic conditions leads to lower strong ion difference (SID) and high [H+] (lower pH). Compensation to maintain pH neutral blood includes chemical buffering (immediate response), respiratory compensation through hyperor hypoventilation (fast response) and renal compensation by altering the amount of bicarbonate absorption or excretion (delayed response). Hypovolaemic foals frequently exhibit a metabolic acidosis due to hyperlactataemia associated with poor tissue perfusion. This typically resolves without specific treatment when normovolemia is restored. Thus, alkalinizing therapy is not indicated in foals unless severe acidosis persists after volume resuscitation. In severely and persistently acidotic horses or foals, such as those with a blood pH < 7.1 or ongoing bicarbonate losses in diarrhea, alkalinizing therapy with sodium bicarbonate may be indicated. The bicarbonate deficit is calculated for foals as follows: HCO3- deficit (mEq) = (25 – patient HCO3-) x 0.5 x body weight (kg) The author prefers to provide bicarbonate as an isotonic solution, which can easily be made by adding 150mEq bicarbonate to 1L sterile water. Intravenous nutritional support All compromised neonates, and especially those with gastrointestinal dysfunction (e.g. premature, septic or enterocolitis) benefit from exogenous nutritional support. A constant rate infusion of glucose assists in resolution of metabolic acidosis, supports cardiac output, and prevents postasphyxial or sepsis associated hypoglycemia. Intravenous glucose is the first line of exogenous support, but should be monitored closely, because intolerance is not uncommon. Best results are achieved by starting with a low glucose infusion rate (4mg/kg/min) and then gradually increasing the dose. Aiming for 4-8mg/kg/min, which is the rate of glucose supply by the placenta. Low initial glucose infusion rates yield better results even in severely hypoglycaemic patients. Thiamine is essential for carbohydrate metabolism and may be added to the glucose infusion. In the event of hyperglycaemia in excess of the renal threshold (>14mmol/L or 250 mg/dL), glucose diuresis with fluid and electrolyte wasting occurs. If blood glucose remains below the renal threshold, one may give the foal more time to mount its own insulin response. Once this threshold is breached, insulin therapy should be initiated (0.00125-0.2 u/kg/hr regular insulin). Changes should only be made every 4-6 hours to avoid a glucose rollercoaster. If a foal is not going to be fed for > 12-14 hours, administration of total parenteral nutrition is preferable to plain dextrose to provide more balanced nutritional support. Be sure to account for any sodium in the parenteral nutrition preparation when Proceedings  of  the  South  African  Equine  Veterinary  Association  Congress  2016   215