Page 494 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

482 FLUID THERAPY

patients are prone to symptomatic hypoglycemia. requirements may be present in hepatic insufficiency
Animals with portosystemic shunting and those with (i.e., reduced hepatic storage or activation); (9)
fulminant hepatic failure are at greatest risk. identifying and eliminating infectious complications
Neuroglycopenia must be avoided in animals with PSVA including enteric parasites that may provoke catabolism
during surgical and anesthetic procedures because neuro- and nitrogenous waste production; and (10) using meta-
logic recovery can be permanently impaired. In HE, bolic strategies to improve NH 3 metabolism or amelio-
hypoglycemia can intensify neurologic signs by rate NH 3 toxicity (e.g., supplementing L-carnitine
augmenting ammonia-associated brain energy deficits. [L-CN], L-ornithine, L-aspartate, and possibly
Intravenous fluids initially should be supplemented with branched-chain amino acids).
2.5% dextrose with sequential determinations of blood Adjusting the enteric bacterial flora, providing ferment-
glucose concentration guiding maintenance treatment. able carbohydrates, and avoiding constipation are common
Symptomatic hypoglycemia is managed by administra- strategies used to modify enteric factors contributing to
tion of 0.5 to 1.0 mL/kg of a 50% dextrose solution given HE. Constipation is detrimental because many encephalo-
by bolus intravenous injection (diluted 1:2 to 1:8 in pathic toxins are produced and absorbed in the large intes-
saline). Thereafter, glucose supplementation is sustained tine. Excessively aggressive nitrogen restriction and failure
by adding glucose to fluids to effect using a continuous to provide enough energy for maintenance requirements
24-hour infusion. encourages a catabolic state and muscle wasting, which
impair protein and NH 3 tolerance. Cachexia, starvation,
TREATMENT OF HEPATIC and glucocorticoid administration increase nitrogenous
ENCEPHALOPATHY waste production from muscle catabolism, including
NH 3 and other toxic metabolites.
General Considerations Antianabolic effects of certain drugs (e.g.,
Treatment of HE is based on clinical signs and a compre- tetracyclines) may promote release of nitrogenous waste
hensive understanding of the underlying pathophysio- products, exceeding hepatic capacity for detoxification.
logic mechanisms. Syndrome severity is difficult to Avoiding hypokalemia and metabolic alkalosis are crucial
quantify with biochemical tests and does not correlate because these disturbances favor high blood NH 3
with hepatic histologic lesions. The degree of HE reflects concentrations. Metabolic alkalosis facilitates brain
circulatory complications, portosystemic shunting, fluid uptake and intracerebral trapping of NH 3 . Hypokalemia
and electrolyte disturbances, hypoglycemia, accumula- promotes renal ammoniagenesis and H loss, promoting
þ
tion of toxins associated with HE (especially ammonia), metabolic alkalosis and increasing renal tubular NH 3
systemic complications caused by liver dysfunction, and reabsorption. Severe hypokalemia also may impair urinary
concurrent disease processes. Stratification of patients concentrating ability, leading to diuresis and dehydration.
into two major categories facilitates therapeutic decisions. Persistence of either hypokalemia or hypophosphatemia
The first category consists of patients with episodic can lead to weakness and anorexia, compromising ade-
HE that are relatively normal between episodes and quate nutritional support and fluid balance. In some
likely have a resolvable precipitating circumstance (see animals, hypoglycemia precipitates encephalopathic
Table 19-3). The second category consists of patients signs. While hypoglycemia can directly or indirectly pro-
with spontaneous acute encephalopathy in which an voke neurologic and systemic signs (e.g., weakness, leth-
underlying cause cannot be found. Management of HE argy, confusion) and increased neuronal susceptibility to
involves detection and treatment of precipitating events, cerebral neurotoxins, hyperglycemia can contribute to an
modulation of causative mechanisms, and treatment of increase in astrocyte osmolal load thereby provoking
the underlying liver disease. cerebral edema. A number of neuroactive drugs (e.g.,
Major treatment strategies for HE include (1) reduc- sedatives, analgesics, anesthetics) can directly interact
ing systemic and cerebral NH 3 concentrations by thera- with dysfunctional neuroreceptors causing encephalo-
peutically targeting the gastrointestinal tract (the pathic signs. Maintaining adequate hydration is impor-
primary source of NH 3 production); (2) maintaining sta- tant in preventing prerenal azotemia, which can
ble systemic blood pressure; (3) ensuring euhydration increase enteric NH 3 production and hyperammonemia.
(i.e., avoiding dehydration or overhydration); (4) Volume expansion can attenuate hyperammonemia
correcting or avoiding detrimental electrolyte caused by enteric hemorrhage when NH 3 arises largely
disturbances (e.g., hypokalemia, hypophosphatemia); from enhanced renal ammoniagenesis. However,
(5) maintaining euglycemia; (6) controlling hemorrhage avoiding overhydration also is important because it can
(especially enteric bleeding); (7) avoiding catabolic events promote ascites, cerebral edema, or pulmonary edema
and maintaining body condition and muscle mass by associated with occult cardiopulmonary complications
feeding a diet tailored to the patient’s nitrogen tolerance of hepatic insufficiency. Fluid volumes and drug dosages
and energy requirements; (8) providing supplemental must be calculated based on estimated lean body mass in
vitamins and micronutrients in the event that increased patients with ascites. Failure to do so can lead to fluid