Page 498 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

486 FLUID THERAPY

Selection of commercially available solutions with decreased by redirection of ammonia into urine rather
restricted sodium content or mixing of commercially than into the renal vein. Volume expansion in well-
available solutions to achieve restricted sodium content compensated human patients with cirrhosis also decreases
is necessary for these patients. Slow infusion of both a plasma renin activity and angiotensin II production. The
crystalloid and a colloid is a useful approach for many latter effect may be important because angiotensin II
of these patients because it expands intravascular volume, enhances ammoniagenesis in the proximal tubules. 107
limits the requirement for crystalloids, and reduces the Improved systemic perfusion increases uptake of NH 3
tendency for third-space fluid sequestration. Crystalloid by liver, skeletal muscle, and brain where it can be
administration is reduced to 33% of normal maintenance detoxified.
requirement when administered with 20 mL/kg/day of Enhanced sodium reabsorption in the ascending limb
synthetic colloid. The potential bleeding complications of Henle’s loop and distal tubule is a disturbance
associated with synthetic colloid use and their cost must associated with cirrhosis that may cause resistance to con-
be carefully considered. (See Chapter 27 for more ventional doses of furosemide. Decreased response to
information on colloid therapy). furosemide also may reflect impaired drug access to the
Hypoalbuminemic patients with tense ascites require tubular lumen where it achieves its pharmacologic effect.
individually tailored fluid therapy combined with a syn- When very large doses of furosemide are administered to
thetic colloid or plasma, large-volume paracentesis, and initiate diuresis, the risk of hypovolemia and excessive loss
þ

diuretics (furosemide and spironolactone). Simply of Cl (in excess of Na ) is increased. Although retention

adjusting fluid sodium intake or restricting water intake of HCO 3 maintains electroneutrality, it contributes to
is not efficacious. Water restriction is hazardous because metabolic alkalosis that can increase NH 3 flux through
of inadequate home monitoring. Although providing a an impaired urea cycle. Collectively, these effects promote
synthetic colloid may seem reasonable, this approach persistent hyperammonemia in the patient with hepatic
alone will not interrupt the complex physiologic signals insufficiency. Dopamine may act synergistically with furo-
impairing renal water excretion. Low plasma oncotic semide in this setting because dopamine inhibits proximal

pressure is not the sole driving force of ascites in these renal tubular Na / HCO 3 cotransport. 122
þ
patients. Administration of a carbonic anhydrase inhibitor (e.g.,
Hyponatremia presents a therapeutic challenge in acetazolamide) or a thiazide (e.g., chlorothiazide)
patients with liver disease because the underlying physiol- diuretic can indirectly augment hyperammonemia
ogy is complex and involves increased secretion of AVP by inhibiting HCO 3 generation in the renal tubular
(see Figure 19-10). Availability of aquaretic agents, such epithelium. Bicarbonate is necessary for mitochondrial
as conivaptan (an AVP receptor antagonist) may facilitate synthesis of carbamoyl phosphate (an essential urea cycle
management of water retention in the future.* An angio- substrate) and urea cycle function may be impaired (see
tensin II type one receptor antagonist (e.g., Losartan) Figure 19-2). 100
may improve the blunted natriuresis observed in cirrhotic
human patients with or without ascites. 87,91,236,239 This Fluid Therapy Aggravating Electrolyte
natriuretic effect appears to be more pronounced in Depletions and Transcellular Shifts
ascitic than in nonascitic patients. Low doses are preferred Hyperglycemia caused by oral carbohydrate loading, dia-
because higher doses may substantially lower mean betes mellitus, or glucose-supplemented fluids aggravates
arterial blood pressure. 87 The appropriate dosage and electrolyte depletion by osmotic diuresis. During the ini-
benefit of losartan in dogs and cats with liver disease tial stages of refeeding in cats with HL, hyperglycemia
are not established. also may provoke symptomatic hypothiaminosis (in
patients with marginal thiamine reserves) because thia-
Influence of Diuresis, Fluid Expansion, and mine is a cofactor for several enzymatic reactions involv-
Diuretics on Ammonia Concentration ing glucose use. Provision of thiamine is mandatory
Hyperammonemia in patients with hepatic insufficiency during refeeding of cats with HL and is accomplished
can be attenuated by systemic volume expansion because using a water-soluble B-complex vitamin supplement.
volume expansion reduces renal and hepatic Glucose supplementation is contraindicated in cats with
ammoniagenesis. Renal ammoniagenesis is curtailed by HL because it favors metabolic adaptations that precipi-
increased renal plasma flow and the GFR, which increases tate refeeding syndrome, compromises adaptation
fractional NH 3 excretion. Enhanced renal NH 3 elimina- to fatty acid oxidation, and may potentiate hepatic
tion occurs secondary to increased glutamine delivery to triglyceride accumulation via enhanced lipogenesis.
the proximal tubules, increased urine flow rate (i.e., Carbohydrates should not be used to increase the energy
decreased NH 3 reabsorption), and suppression of density of diets fed to cats with HL. However, carbohy-
antidiuretic hormone secretion. Total body NH 3 load is drate supplementation of parenteral fluids may be neces-
sary in very small or young dogs with PSVA because they
*References 9, 78, 89, 160, 235, 240. may have inadequate gluconeogenic and glycolytic