Page 1159 - Clinical Small Animal Internal Medicine

120 Acute Kidney Injury 1097

cells, thus allowing depolarization at high extracellular Nutritional Support
VetBooks.ir potassium concentrations. The membrane‐stabilizing Nutritional support is an important component of sup-
effects of calcium salts are rapid and dramatic but the
portive care for AKI. Enteral feeding is the preferred
beneficial effects are even more transient than those of
regular insulin. Readministration is typically necessary method of nutrient delivery, but is often limited by
vomiting and ileus. For those patients that are not vom-
within 1–4 hours. The patient should be monitored iting, esophageal, gastric, and jejunal feeding devices
with an electrocardiogram during administration to can be used. If vomiting cannot be controlled, partial or
identify worsening bradycardia, a shortened QT inter- total parenteral nutrition should be considered. In
val, a widened T‐wave, or alterations in the ST ampli- patients which are anuric or oliguric, the volume and
tude. If any of these changes are recognized, the calcium osmolality of nutritional product, whether adminis-
infusion should be discontinued. Calcium gluconate is tered enterally or parenterally, must be taken into con-
favored over calcium chloride, due to the severe sideration and may constitute a relative contraindication
extravasation injuries that can occur with calcium unless there is a method of excess fluid and solute
chloride administration. It should be noted, however, removal (e.g., dialysis).
that calcium gluconate can also cause extravasation The optimal dietary composition for veterinary AKI
injuries (albeit less severe), so care must be taken patients has not been determined. The author is una-
to ensure intravenous catheter patency prior to ware of any particular diet that is appropriate in all sce-
administration. narios of AKI. Rather, each individual patient should be
Lastly, theoretical concerns regarding promotion of
calcium‐phosphorus/phosphate precipitation and soft evaluated for the following factors, as each may influ-
ence the choice of diet to be fed: degree of uremia, avail-
tissue mineralization exist with repeated administration ability of dialysis, volume status and volume of urine
of calcium salts. produced, electrolyte balance, and availability of
Alternative treatments for hyperkalemia exist, but
each has limitations in efficacy and side‐effects, com- assisted feeding (e.g., esophagostomy or gastrostomy
tube). Patients with severe uremia may benefit from a
pared with provision of dialysis. These treatments protein‐restricted diet because a reduced protein con-
include beta‐2 agonist drugs, polystyrene sodium sul- tent may decrease the endogenous production of ure-
fonate, sodium bicarbonate, and loop diuretics. mic toxins. However, a negative protein balance may
While ionized hypocalcemia occurs frequently in AKI,
clinical signs (e.g., tetany) associated with this problem hinder renal repair/recovery. Patients treated with dial-
ysis may actually require more protein than patients
are rare. When manifestations of hypocalcemia do occur, with extrarenal disease, due to loss of amino acids in
the minimum dose of supplemental calcium that con- dialysate. Patients with feeding tubes that are prone to
trols clinical signs should be used to minimize precipita- volume overload should be fed the most calorically
tion with phosphorus. As with the treatment of dense diet that will pass through the tube to minimize
hyperkalemia, the electrocardiogram should be moni- the amount of fluid administered. Some commercially
tored closely during infusion. available recovery diets have caloric contents of approx-
Additional electrolyte abnormalities may be present or
develop during the course of disease, the most common imately 2 kcal/mL and easily pass through most 14 Fr
red rubber catheters or feeding tubes. These diets typi-
of which are hyponatremia and hyperphosphatemia. cally have a high protein and potassium content, the lat-
Hyponatremia may be the result of gastrointestinal or ter of which may be problematic in hyperkalemic
urinary losses, with or without the contribution of patients. There are multiple appropriate, commercially
decreased excretion of free water. Hyponatremia, if available diets from which to select, depending on the
severe (<120 mmol/L), may result in neurologic sequelae. individual patient’s clinical status.
Hyperphosphatemia contributes to acidosis and renal However, a common misconception among veteri-
secondary hyperparathyroidism. However, the use of nary personnel is that commercial renal diets, formu-
phosphate‐binding drugs has not been shown to improve lated and marketed for patients with chronic kidney
outcome in human or veterinary cases of AKI. disease, are also appropriate for patients with AKI.
Furthermore, administration of aluminum hydroxide While these diets have reduced protein content, which
(the most commonly used phosphate‐binding drug in may be desirable in certain situations, they require dilu-
veterinary medicine) may result in acute aluminum tion and blending with water, which reduces their
intoxication, which manifests as encephalopathy, a con- caloric density and increases the amount of fluid that
dition which may not be readily recognizable in a patient must be administered with each feeding. Furthermore,
severely affected with AKI. Therefore, aluminum‐con- these diets have a low sodium content, which is reduced
taining phosphate‐binding drugs should be used with even further when they are diluted with water. Many
caution in cases of AKI.