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 fluids (hyperkalemia)
Administration of low potassium fluids (>48 h, hypokalemia)
Administration of Na‐HCO3 (hypokalemia)
Non‐oliguric renal failure (hyperkalemia)
Pre‐existing potassium abnormalities such as rhabdomyolysis, ruptured bladder or hemolysis (hyperkalemia)
Long‐term administration of diuretics (azetazolamide, e.g. for HYPP, hypokalemia)
Anorexia for several days (hypokalemia, total body deficit of potassium)
Reflux or diarrhea (usually hypokalemia)
Pathogenesis
Potassium is the most important intracellular electrolyte, as more than 98% of the body potassium is located intracellularly. Equine veterinarians are usually most interested in the extracellular amount of potassium. Potassium concentrations in blood are generally low and tightly maintained. Increases and decreases can occur rapidly. Small changes in serum potassium concentrations can lead to severe clinical signs that can be fatal. Potassium is important for cell membrane polarization. Abnormal serum concentrations of potassium therefore lead to changes in cell membrane potential, which affects primarily muscle and heart cells.
Prevention
Monitor blood potassium levels q24–48 h while administering fluid therapy. If a pre‐existing potassium abnormality is present and being corrected, aim for more frequent monitoring, every 6–12 hours. Fluids with adequate amounts of potassium should be administered.
Replacement therapy can contain a potassium concentration similar to equine plasma (e.g. Lactated Ringer’ solution K+: 5 mmol/L). Fluids with higher amounts of potassium should not be used as replacement fluids as inadvertent administration of potassium can cause severe signs of hyperkalemia.
Maintenance fluids should contain higher amounts of potassium (13–20 mmol/L), particularly if the horse is not eating to avoid hypokalemia. If available, a commercial maintenance solution (e.g. NormosolTM K+ 13 mmol/L) can be used; if unavailable, replacement fluids can be spiked with potassium chloride (20 mmol/L). Note that adding 20 mmol/L of KCl to Lactated Ringer’s will result in a total potassium concentration of 25 mmol/L, as LRS contains 5 mmol/L of potassium. Maintenance fluid should not be administered in volumes or rates higher than 2–4 ml/kg/day to avoid side effects due to potassium.
Oral KCl administration assists in reestablishing body homeostasis of potassium in depleted anorexic horses (e.g. acute colitis and diarrhea) (500 kg horse, 30–50 g KCl PO q 12 h).
Diagnosis
Diagnosis is based on clinical signs and determination of blood concentrations of potassium. Hyperkalemia is clinically more relevant than hypokalemia. Clinical signs of hypokalemia are not well documented in horses and vary. Muscle weakness, diaphragmatic flutter, and intestinal hypomotility have been described. Clinical signs of hyperkalemia are mainly related to electrical conduction in the myocardium. Tall or peaked T‐waves, flattened P‐waves and prolongations of the QRS complexes appear on ECG and can lead to asystole. Initial changes can be detected at serum potassium levels of 6.2 mmol/L, and more pronounced and consistent signs are seen at serum potassium concentrations of 7–8 mmol/L [26].
Treatment
General hydration status and all other electrolytes should be assessed, as abnormalities in blood potassium concentrations rarely occur alone. In hypokalemia, the recommended potassium supplementation in the administered fluids depends on serum potassium levels.
Serum K+ <2.5 mmol/L – substitute at 40 mmol/L
Serum K+ 2.5–3 mmol/L – substitute at 30 mmol/L
Serum K+ 3.0–3.5 mmol/L – substitute at 15–20 mmol/L
In mild hyperkalemia (5–7 mmol/L), potassium free fluids should be administered and potassium levels monitored closely. If severe hyperkalemia (>7 mmol/L) is present and abnormalities are seen on ECG analysis, emergency treatments should be instituted and include:
Intravenous 23% calcium gluconate, 0.5 ml/kg, given over 20 minutes diluted in isotonic IV fluids
Intravenous dextrose 50%, 10 mg/kg/minutes, diluted to 5% (isotonic) in fluids and given over 30 minutes
Intravenous insulin, 0.1–0.2 IU/kg/h, diluted in fluids and given over 30 minutes
Expected outcome
Depends on severity.
Animals can die from cardiac effects.
If treatment is instituted and the animal responds, full recovery is possible.
Other Electrolyte Imbalances
