South African Equine Veterinary Association Congress 2015 Protea Hotel Stellenbosch
than 48 hours and in patients that are losing large amounts of fluid in the form of ongoing gastric
reflux or profuse diarrhoea. In these patients, acid-base status and serum electrolyte
concentrations often need to be reassessed daily and these results are used to modify the fluid
therapy plan.
A common practice to address the anticipated Ca++ deficit in anorectic horses is to add 125 ml of
a 23% calcium borogluconate solution to each 5 litre intravenous fluid bag. This addition of
calcium borogluconate provides about 2.7 g of Ca++ in each 5 liter bag that would replace about
one-eighth of the exchangeable Ca++ pool in a 500 kg horse. Although hypercalcemia may
occasionally develop with this type of supplementation, adverse effects of transient hypercalcemia
have not been reported and the problem is rapidly reversed once Ca++ supplementation is
discontinued. Monitoring for excessive Ca++ supplementation is a further reason that follow-up
measurement of serum electrolytes should be considered for horses that are receiving fluid
therapy for more than 48 hours, especially when initial laboratory results were outside of the
reference ranges for one or more values. The borogluconate added with this Ca++ supplementation
also provides some carbohydrate substrate, equal to about a 0.5% dextrose solution. Although the
benefit is small, this amount of carbohydrate may at least replace some of the energy expended to
warm room temperature fluids to body temperature.
Most crystalloid rehydration fluids contain relatively modest amount of K+ (5 mEq/L or less for
most polyionic solutions); thus, addition of supplemental K+ to the base fluid may be needed in
some instances. Because K+ is the most abundant cation in body fluids (Figure 1),
supplementation is usually not necessary unless horses have been off feed for several days or have
been on fluid therapy for more than 48 hours. In these instances, depletion of total body K+ stores
can be substantial yet serum K+ may still be within the normal range because <0.5% of
exchangeable K+ is in plasma. Again, with prolonged support (>48 hours) with fluids designed for
rehydration, excessive replacement of body Na+ stores may increase urine output and further
exacerbate K+ depletion by increasing obligate K+ loss in urine. Assuming that the fluid therapy
plan at the time a decision to add K+ is made is to administer about 35 litres of intravenous fluid
over the subsequent 12 hours (1 litre/hour for maintenance and 2 litres/hour for anticipated losses
in diarrhoea, after rehydration has been accomplished), only about 175 mEq of K+ would be
replaced using a typical polyionic crystalloid fluid. This would represent replacement of <1% of
body K+ stores at the same time that urine K+ losses could result in further depletion of as much
as 3-4% of body K+ stores through production of 10 litres of urine (~3-fold increase in urine flow
due to a Na+ diuresis) with a K+ concentration as low as 100 mEq/L. To simply match this
estimated urine K+ loss, 25 mEq of additional K+ would need to be added to each of the 35 litres
of fluid administered. As can be seen, addition of 20 mEq/L of K+ per litre of fluid, usually in the
form of KCl, is generally safe (with the exception of horses with hyperkalaemia accompanying
uroperitoneum and acute renal failure) and is often of benefit to horses receiving fluid support for
more than a couple of days. An alternative to adding KCl to the intravenous fluids is to administer
KCl in enteral fluids or as an oral paste. For example, to provide 1500 mEq of KCl daily (5% of
body K+ stores), 110 g of KCl (1 g of KCl provides 13.4 mEq of both K+ and Cl-) could be
administered as 4 doses of 25-30 g KCl via a nasogastric tube or as an oral paste.
In critically ill patients, most commonly those with profuse diarrhoea and poor perfusion,
metabolic acidosis (decreased pH with a decrease in serum bicarbonate concentration, [HCO3-])
may also have to be addressed. Initially, rehydration with crystalloid fluids (administered
intravenously and enterally) is the treatment for both dehydration and acidosis. Volume expansion
with this treatment alone may improve perfusion and correct the acidosis. However, when
acidosis is severe (pH<7.2 or serum tCO2 <15 mEq/L) and unresponsive to initial rehydration,
9