Page 499 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Fluid, Electrolyte, and Acid-Base Disturbances in Liver Disease 487

enzyme activity and insufficient muscle and liver glycogen causing hypoperfusion) or acute fulminant hepatic fail-
stores to maintain euglycemia during anorexia or recov- ure. At a normal rate of lactate production, abrupt cessa-
ery from anesthesia and surgery. tion of hepatic lactate metabolism does not result in
clinically significant lactate accumulation because of a
TREATMENT OF ACID-BASE compensatory increase in lactate extraction by extrahe-
DISTURBANCES IN LIVER DISEASE 237
patic tissues. As a result of lack of correlation between
Respiratory and Metabolic Alkalosis systemic and CNS lactate concentrations, however, it is
Respiratory alkalosis usually does not cause clinical difficult to determine which patients may suffer from lac-
158
complications or require intervention. Amelioration of tate administration (see Figure 19-13). Therefore
HE often attenuates hyperventilation. If loss of acid-rich acetated Ringer’s solution (or a comparable crystalloid
gastric juice underlies development of metabolic alkalosis, solution) has been recommended as an alternative
treatment with an H 2 blocker or acid pump inhibitor alkalinizing solution for patients with serious hepatic dys-
13,211
(e.g., omeprazole) may allow normalization of systemic function. As a bicarbonate precursor, acetate is
pH. In patients with hypokalemia, KCl supplementation more readily metabolized by peripheral tissues than is lac-
of fluids is required for recovery from alkalosis. In the tate (acetate combines with CoA, forming acetyl CoA).
absence of impending ascites or edema, 0.9% NaCl may This process consumes one hydrogen ion from carbonic
be administered to replace the chloride deficit. In the acid and yields one bicarbonate ion for each millimole
presence of ascites or edema, infusion of 0.45% NaCl in of acetate metabolized. Although acetate usually is con-
2.5% dextrose is preferable. Induction of a bicarbonate sidered nontoxic, excessive administration of acetate
myocardial
diuresis by administration of the carbonic anhydrase may impair 8,229 contraction and induce
inhibitor acetazolamide can also be effective if conven- vasodilatation.
67 It is unclear whether treatment with bicarbonate or a
tional therapy fails.
bicarbonate precursor is beneficial in patients with liver
Metabolic Acidosis disease and lactic acidosis. 7,94 Administration of bicar-
If alkalinization is necessary, a bicarbonate- or acetate- bonate to dogs with hypoxic lactic acidosis does not facil-
containing polyionic solution (e.g., Normosol-R, itate recovery but rather increases blood lactate
Plasma-Lyte) can be used for patients with hepatic insuf- concentrations. Administered bicarbonate may have det-
ficiency. Consideration of the patient’s sodium tolerance rimental effects on hepatic and splanchnic circulation,
is essential because sodium bicarbonate delivers a sodium increasing CO 2 delivery to the liver and decreasing
load that may increase ascites formation. In general, treat- hepatic intracellular pH. 94,166
ment with alkalinizing solutions or medications should be Respiratory Acidosis
avoided in patients with signs of HE because alkalosis
worsens hyperammonemia and increases NH 3 delivery Respiratory acidosis is a grave prognostic finding in
to the CNS. If lactic acidemia is suspected, identification patients with liver disease and requires diagnostic investi-
and correction of systemic hypoperfusion are warranted. gation. Ventilatory support should be provided if
An important potential cause of metabolic acidosis in hypoventilation is present, but caution should be
animals with severe liver disease is renal dysfunction, exercised to prevent hyperventilation and hypocapnia,
which may develop as a result of hemodynamic which can decrease cerebral blood flow and metabolic
disruptions associated with portal hypertension and sys- rate. Calculation of the PA-Pao 2 gradient identifies
temic hypoperfusion or the underlying cause of liver impaired gas diffusion and ventilation-perfusion mis-
injury (e.g., copper toxicosis, immune-mediated injury, match in patients with normal arterial Po 2 values.
infectious disease), chronic interstitial nephritis, A PA-Pao 2 gradient greater than 15 mm Hg warrants
or glomerulonephropathy. Renal tubular acidosis also consideration of oxygen therapy. Respiratory acidosis
has been recognized in dogs with copper-associated hep- and increased PA-Pao 2 gradient justify a grave prognosis
atotoxicity, drug-induced fulminant hepatic failure (e.g., in animals with hepatic disease.
carprofen or other NSAIDs), and in cats with HL. 33,48
MANAGEMENT OF ASCITES IN
Lactic Acidosis PATIENTS WITH LIVER DISEASE
With the exception of cats with HL and animals in fulmi- Increased abdominal pressure caused by tense ascites can
nant hepatic failure, the importance of lactic acidosis in increase portal venous pressure. This effect can potentiate
patients with spontaneous liver disease remains unclear. gastrointestinal hemorrhage from newly expanded vari-
High anion gap metabolic acidosis, in the absence of renal ces, ectatic vessels, or ulcerative lesions, as well as protein
failure or administration of unusual drugs, suggests lactic loss from the intestines. Tense ascites also has negative
acidemia. Marked lactic acidosis in a patient with liver dis- hemodynamic effects on cardiac output. Studies of
ease suggests the presence of some other complicating patients before and after fluid removal have shown a pro-
condition (i.e., endotoxemia, severe infection, disorders gressive increase in cardiac output, stroke volume, and