Page 958 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Urinary system 933

VetBooks.ir AKI, regardless of the cause. Fluid therapy will phase of AKI, i/v or oral electrolyte/salt supple-
In the later stages, during the polyuric recovery
Fluid therapy is essential for the treatment of
restore fluid and acid–base deficits and prevent/
reduce intrinsic renal lesions. It is important to mentation is required. Most horses with AKI do not
require specialised dietary support. Feeding grass
consider whether pre-renal, renal or post-renal fail- forage can provide a diet low in protein, phospho-
ure and polyuria, normouria, oliguria or anuria are rous and calcium. Concentrated feed is not necessary
present. Fluid therapy in oliguric or anuric patients in most horses, but if necessary may be fed at not
should be conservative initially and set at 50% of the more than 0.6–0.7 kg/100 kg of body weight per day.
calculated requirements (estimated level of dehydra- If oliguria or anuria persists after rehydration,
tion × body weight = amount of fluid required in more aggressive therapy is indicated. Furosemide
litres). Pulmonary sounds and body weight should be (1–4 mg/kg i/v q6 h), mannitol (0.25–1.0 g/kg i/v
monitored to prevent the development of overhydra- as 20% solution q4–6 h) and dopamine (120 mg in
tion and pulmonary oedema. Conjunctival oedema 1 litre of 0.9% NaCl or 5% dextrose given at the rate
is often observed in overhydrated horses. Uraemia of 12.5 ml per minute to achieve 3 µg/kg/min) can be
should decrease rapidly following rehydration in given in concert with fluid therapy. Treatment with
cases of pre-renal failure. mannitol and dopamine should be reserved for situ-
If hypernatraemia is not present, i/v adminis- ations where close monitoring is available, because
tration of physiological saline (0.9% NaCl solu- of the higher likelihood of adverse effects compared
tion) should be started. In acutely hypernatraemic with furosemide administration. Mannitol is rec-
patients a 0.45% NaCl/2.5% dextrose solution ommended, along with vigorous volume replace-
should be used. A slower volume correction is pru- ment and sodium bicarbonate, for the prevention
dent in patients with hypernatraemia of longer or and treatment of early myoglobinuric AKI. NSAIDs
unknown duration. In such patients, reducing the diminish the response to loop and thiazide diuretics,
serum sodium concentration at a maximal rate of because they increase electrolyte and water resorp-
0.5 mmol/l per hour or 10 mmol/l per day helps tion at the thick ascending limb of the loop of Henle.
prevent cerebral oedema. If hyperkalaemia is pres- Peritoneal dialysis may sometimes be helpful in
ent (serum K+ >5.5 mmol/l), sodium bicarbon- relieving severe azotaemia. The procedure is labour-
ate should be given (1–2 mEq/kg i/v over 10–15 intensive and has a short-term benefit.
minutes). Alternatively, calcium borogluconate Surgical intervention may be indicated with uri-
(0.5 ml/kg of 10% solution slowly i/v or added to nary tract obstruction or rupture. Stabilisation of
5 litres of fluids and infused over 1 hour) may be the horse with fluid therapy and gradual drainage
administered to counteract the cardiotoxic effects of peritoneal fluid are indicated if uroperitoneum is
of hyperkalaemia. Sodium bicarbonate is also indi- present.
cated when myoglobulinuria is associated with
AKI, as alkalisation of the urine increases urinary Prognosis
myoglobin solubility and reduces intrinsic damage The prognosis is affected by the duration of AKI
to the kidney. before the initiation of therapy. The prognosis for
Once the azotaemia begins to resolve, fluid ther- pre-renal failure is good if the primary disease pro-
apy should be continued at a rate that maintains cess can be controlled and appropriate fluid therapy
normal hydration of the horse (maintenance rate can be provided. There is always a degree of tubu-
of 55–65 ml/kg/day). It should not be discontinued lar and/or interstitial damage present in AKI. Rapid
until the patient’s mentation is normal, creatinine resolution of azotaemia (decrease in urea of 25–50%
values are not more than 10–15% over the high nor- within 24 hours) is usually associated with a favour-
mal reference interval and other serum biochemical able prognosis. The prognosis becomes less favour-
values are normal. Fluid therapy should be discon- able if azotaemia does not resolve over a prolonged
tinued gradually, and serum creatinine monitored period of time. Horses that are oliguric for 48 hours
regularly following cessation of fluid therapy. or more before the initiation of therapy, horses that