LITMIR.BIZ

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       Pathogenesis

      Changes in blood sodium concentrations are often due to underlying diseases or incorrect fluid therapy and result from abnormal water and sodium intake or loss. Blood sodium is always in distribution equilibrium with the total ECF. Abrupt changes in blood sodium concentration cause shifts in the intracellular and interstitial fluid concentrations.

      In hyponatremia, water shifts from the extracellular fluid compartment intracellularly to maintain osmolal equality between the compartments. Water accumulation in brain cells leads to cerebral swelling and neurological abnormalities. Hyponatremia is uncommon in horses, but can occur in association with diarrhea, bladder rupture, acute renal failure, and severe sweat losses and more rarely with excessive water consumption. Adrenal insufficiency and rhabdomyolysis are rare causes of hyponatremia [14–18].

      In hypernatremia, osmolality of the extracellular fluid increases. In acute cases, water shifts from the intracellular fluid compartment extracellular to maintain osmolal equality between the compartments. Cerebral cell dehydration can lead to neurological signs. Hypernatremia is rare in horses.

       Prevention

       Monitor the amount of sodium administered via fluid therapy.

       Sodium levels (in combination with other electrolytes) should be measured every 24–48 h during fluid therapy.

       In hypo‐ or hypernatremic animals, the rate and speed of correction is crucial to avoid complications.

       If high or low sodium fluids are used, or correction of existing hypo‐ or hypernatremia is performed, plasma sodium concentrations should be measured every 12–24 hours.

       High risk patients (small patients, neonates undergoing abdominal or colon lavage with water) should have blood sodium levels measured 1–2 hours after the procedure.

      When replacement fluid therapy is administered to a normonatremic animal, a fluid containing concentrations of sodium equal or close to plasma (~130–150 mmol/L) should be used, e.g. Lactated Ringer’s solution (130 mmol/L). For maintenance, solutions with lower sodium concentration (~40 mmol/L) can be used. As these are not widely available in 3–5 L bags, replacement fluid is often used for maintenance as well. As long as renal function is adequate, the increased sodium load is simply excreted by the kidney. In foals, or animals with impaired renal function, this should be taken into account and a true maintenance solution containing lower amounts of sodium and chloride (e.g. Normosol‐M^TM Na 40 mmol/L) should be considered.

       Diagnosis

      Diagnosis is based on clinical signs and blood sodium concentrations. Clinical signs occur only in moderate to severe hyponatremia and include restlessness, focal and general seizures and death. Clinical signs of acute hyponatremia occur in humans at concentrations of 125 mmol/L [19], while concentrations as low as 110 mmol/L can be without clinical signs in chronic hyponatremia [20]. The concentrations at which horses show clinical signs have not been experimentally determined; however, it is known from case reports that foals with Na <100 mmol/L showed severe signs [15, 16]. Signs of hypernatremia in horses are unclear, but seizures are reported in humans.

       Treatment

      For recommendations regarding treatment of hypo‐and hypernatremia, the reader is referred to an excellent review (Equine Fluid Therapy, 1st ed. Fielding, Magdesian eds, Wiley).

      Acute hyponatremia (<24–48 h) can be corrected rapidly, while long‐standing hyponatremia (>48 h) has to be corrected slowly. It is often difficult to determine the duration of hyponatremia; if duration cannot be determined from history, underlying disease and clinical examination, chronic hyponatremia should be assumed.

      For patients with acute hyponatremia displaying severe signs of neurological side effects (seizures), hypertonic saline can be used. The rate of correction is based on data from humans, which showed that demyelinating syndrome was avoided when correction rates were limited to an increase of <12 mmol/L in 24 hours and <18 mmol/ in 48 hours [21]. In equine practice, the most common formulation of hypertonic saline is 7.2%. The concentration is not as important as the overall rate of sodium administered (slower rate for more concentrated solutions, faster rate for less concentrated).

       Administer NaCl (0.9%) 2 ml/kg over 10 minutes then recheck blood sodium concentrations.

      Note that these patients will often also have hypochloremia and metabolic acidosis due to decreased strong ion difference. Sodium bicarbonate should not be used in these patients, as this will only supply sodium.

      In chronic cases, the change of sodium concentration should not exceed 0.5 mmol/h. The expected change in sodium concentration when administering 1 L of fluid can be determined using this formula [22]:

       Change in serum Na (mmol/L) = (Nainfusate/Napatient)/(kg Body weight × 0.6) +1

Using this calculation, one can determine how many liters are required to correct the abnormality and using the maximum correction rate of 0.5 mmol/h, how quickly to administer the amount. A rather conservative approach should be used in animals with severe abnormalities, as this formula tended to underestimate the final serum sodium concentrations in humans with severe abnormalities [23].

      In horses with chronic hyponatremia and dehydration, the following protocol can be attempted:

       Administer an isotonic crystalloid (e.g. Lactated Ringer’s Na 130 mmol/L or equivalent) at maintenance rate 2–4 mL/kg/h.

       Recheck sodium blood concentrations frequently (every 2 h) and aim for a correction rate of 0.5 mmol/h. If the correction is too fast, add sterile water to the infusion; if the correction rate is too slow, switch to a crystalloid containing more sodium (e.g. Normosol‐Na 140 mmol/L, NaCl 0.9% Na 154 mmol/L).

      In hypernatremia, controversy exists over the type of fluid that should be used. In severely hypernatremic animals, it might be feasible to start using saline (Na 154 mmol/L), followed by Lactated Ringer solution (Na 130 mmol/L) and then switching to 5% dextrose in water (Na 0 mmol/L) to avoid rapid correction of hypernatremia.

      In dehydrated hypernatremic animals, the following protocol can be used:

       Use an isotonic or slightly hypertonic crystalloid fluid (e.g. saline Na 154 mmol/L or Lactated Ringer solution Na 130 mmol/L) at 4 ml/kg/h.Recheck sodium concentrations frequently (every 2 h) and aim for a correction rate of 0.5 mmol/h. In severe cases fluid might have to be spiked with hypertonic saline to achieve concentration approx. 20 mmol less than the patient’s serum concentrations.

      Once dehydration is resolved or in animals with normal total body water, the following protocol can be followed:

       Use a slightly hypotonic crystalloid fluid (e.g. 0.45% saline Na 77 mmol/L or 5% dextrose in water 0 mmol/L) at 4 ml/kg/h.

       Expected outcome

       Depends on severity

       Animals can die from neurological side effects

       If treatment is instituted and the animal responds, full recovery is possible

       Overzealous and quick correction of chronic hyponatremia can cause central pontine myelinolysis and permanent neurological deficits

      Potassium Imbalance

       Definition

      Increased (hyperkalemia) or decreased (hypokalemia) blood potassium levels outside the reference range 3.1–4.1 mmol/L [24, 25]

       Risk factors

       Administration of potassium containing

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