Page 493 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Fluid, Electrolyte, and Acid-Base Disturbances in Liver Disease 481

Hepatic function portosystemic shunting
impaired intrahepatic circulation

Toxin production Toxin accumulation

Toxin degradation and elimination

NH 3
Altered neuron function
Altered vascular autoregulation
Neuronal vasodilatation Abnormal
glutaminase CO 2 -responsivity cerebral
perfusion
Altered permeability of the blood-brain-barrier
Glutamine Glutamate Intracranial
Impaired brain
Altered glutamatergic blood
neurotransmission energy production pressure
Altered astrocyte function
Altered
Altered
neuroreceptors neurotransmitter Cytotoxic cerebral
balance NH 3 detoxification Glucose uptake edema
Glutamate uptake Lactate production
Altered
False
neurotransmitters neurotransmitter Altered membrane Alanine accumulation
storage transporters
Aquaporin-IV
Altered cerebral Systemic vasopressin
sensitivity to expression
sedative and analgesics
Figure 19-16 Diagram demonstrating pathomechanisms contributing to hepatic encephalopathy, as
discussed in the text.

in various types of liver injury, including those associated coagulopathies associated with its deficiency. Since vita-
197,198
with cholestasis. The amount of vitamin E needed min K is a fat-soluble vitamin, its enteric availability
to protect membrane polyunsaturated fatty acids may be substantially reduced by impaired enterohepatic
(PUFAs) from oxidative damage ranges from 0.4 to bile acid circulation. Consequently, intramuscular or sub-
0.8 mg of vitamin E/g of dietary PUFA. 233 However, cutaneous administration of vitamin K is recommended.
patients on diets rich in long-chain PUFA may require A vitamin K 1 dosage of 0.5 to 1.5 mg/kg, repeated three
more than 1.5 mg of vitamin E/g of dietary PUFA. times at 12-hour intervals, has been clinically shown to
The complex relationship between vitamin E status and ameliorate coagulation abnormalities in most cats and
dietary PUFA intake makes definitive recommendations many dogs with liver disease. 44 The dose of vitamin K
difficult. 141 Vitamin E uptake by enterocytes is depen- should be calculated carefully because excessive amounts
dent on the presence of enteric bile acids, and cholestasis can cause oxidant damage to the liver, erythrocytes, and
may increase vitamin E requirement because of impaired other organs (especially in sick cats). The risk of anaphy-
enterohepatic bile acid circulation. 62 Using a water-solu- laxis should be considered when administering vitamin
ble form of a-tocopherol can circumvent problems cre- K 1 , but the incidence of anaphylaxis due to intravenous
ated by impaired enteric bile acid circulation (e.g., phytonadione (vitamin K 1 ) injection in humans was 3
a-tocopherol formulated with polyethylene glycol-1000 per 10,000 doses in a retrospective study over 5 years. 177
succinate, Eastman Chemical Company, Kingsport, The subcutaneous route is preferred over other routes,
Tenn.). A dosage of at least 10 U/kg body weight per especially intravenous.
day is recommended but has not been critically evaluated
for efficacy in dogs and cats with spontaneous liver Maintenance of Euglycemia
disorders. Patients with hepatic dysfunction may have insufficient
Vitamin K 1 is given to all jaundiced patients during liver and muscle glycogen reserves to maintain glycogen-
the first 12 hours of hospitalization to prevent olysis. If hepatic gluconeogenesis also is impaired, these