Page 1158 - Clinical Small Animal Internal Medicine

1096 Section 10 Renal and Genitourinary Disease

In veterinary medicine, because dialysis is not readily of randomized controlled trials supporting supplemen-
VetBooks.ir available, diuretic administration plays a large role in vol- tation of alkali in human AKI, it is recommended in vet-
erinary AKI when dialysis is not available.
ume management. Conversion from an oliguric or anuric
state to normal urine production or polyuria may
enhance the clinician’s ability to prevent or manage fluid
overload and thus allow administration of necessary par- Electrolyte Balance
enteral medications and nutrition that would otherwise Hyperkalemia can be an immediately life‐threatening
contribute to fluid overload. No class of diuretics has complication of AKI and is secondary to a decline in
been proven to be superior to another. However, the use renal excretory function. Excitable cells become refrac-
of loop diuretics predominates in both human and vet- tory to repolarization, thus resulting in decreased
erinary AKI due to the relatively high efficacy and safety conduction of both cardiac and neuromuscular tissue.
margin of these drugs, compared to the osmotic diuret- Typical electrocardiographic changes include bradycar-
ics. For this reason, the author does not recommend the dia, tall T‐waves, shortened QT intervals, wide QRS
use of mannitol as a diuretic for AKI.
complexes, and small, wide, or absent P‐waves. Severe
hyperkalemia can lead to sine waves, ventricular fibrilla-
Acid–Base Balance tion, or standstill. There are a variety of pharmacologic
Metabolic acidosis is a frequent complication in AKI of treatments available for emergent hyperkalemia, but
varying severities, and is due to the damaged nephron’s these therapies act to translocate potassium to the intra-
inability to excrete hydrogen ions and reabsorb bicarbo- cellular space or increase the resting membrane poten-
nate ions, as well as lactic acidosis secondary to compro- tial to allow repolarization of excitable cells, rather than
mised tissue perfusion (i.e., either volume deficit or enhance excretion of potassium. The efficacy of these
excess). Once perfusion has been restored, provision of treatments is typically modest and transient. Only
supplemental alkali, usually in the form of parenteral provision of dialysis or restoration of native renal excre-
sodium bicarbonate, should be considered if severe aci- tory function can significantly reduce the potassium
demia (pH <7.2, bicarbonate <12 mmol) persists. The burden in fulminant AKI.
bicarbonate dosage can be calculated from the formula: Expansion of the extracellular space with a nonpotas-
sium‐containing fluid (e.g., 0.9% sodium chloride) may
.
0 3 body weight kg base deficit be sufficient to at least partially correct hyperkalemia.
/
bicarbonate mEqL This maneuver should be implemented in cases of

suspected volume depletion, but should be used with
where the base deficit = 24 mEq/L – (patient bicarbonate caution or not at all if a patient is anuric or has volume
concentration). One‐fourth to one‐third of the dose overload.
should be given intravenously as a slow bolus, and an Administration of regular insulin is a common phar-
additional one‐fourth over the next 4–6 hours. macologic treatment for hyperkalemia. Insulin upregu-
Subsequent doses should be based on serial venous lates synthesis of subunits of the Na+/K+ATPase pump,
blood gas analyses. recruits the pump to the plasma cell membrane, and
Bicarbonate administration to a hypoventilating activates those pumps already located in the plasma
patient can further increase the partial pressure of car- membrane to stimulate intracellular translocation of
bon dioxide and can lead to paradoxical central nervous potassium. The potassium‐lowering effect of regular
system (CNS) acidosis. This phenomenon is due to the insulin may be observed within 20 minutes, but the effect
ability of carbon dioxide to diffuse across the blood– is typically modest (decline of 1–2 mmol/L) and tran-
brain barrier, while the charged bicarbonate molecule sient (redosing is frequently necessary within 4–6 hours).
diffuses across this barrier less readily. An additional A potentially catastrophic adverse effect associated with
drawback to parenteral sodium bicarbonate administra- regular insulin administration is hypoglycemia, so dex-
tion is that most formulations have high osmolality (e.g., trose must be administered concurrently with regular
8.4% solution = 1 mEq/mL = 2000 mosm/L). Therefore, insulin. If fluid overload is not present, the administra-
this solution must be diluted prior to administration, and tion of a continuous rate infusion of dextrose, following
the total volume administered must be factored into the the initial bolus, is recommended. Frequent assessment
fluid therapy plan. Provision of bicarbonate during dialy- of blood glucose concentrations is imperative, as dex-
sis is as effective in restoring extracellular acid–base sta- trose is metabolized more rapidly than insulin, and
tus as sodium bicarbonate infusion, and has the added redosing of dextrose is often required.
advantage of avoiding the fluid load necessary with the Calcium salts are frequently administered intrave-
latter treatment. While there is no evidence in the form nously to increase the threshold potential of polarized