Page 1134 - Small Animal Clinical Nutrition 5th Edition

1180 Small Animal Clinical Nutrition

VetBooks.ir Box 68-4. Adjunctive Lactulose for Patients with Hepatic Encephalopathy.

Administration of lactulose is considered one of the treatments of Lactulose also is highly effective when added to water (30%
choice for hepatic encephalopathy (HE). Lactulose is a synthetic lactulose and 70% water) and given as a retention enema.
disaccharide that is hydrolyzed by colonic bacteria principally to Approximately 20 to 30 ml/kg body weight are infused and
lactic and acetic acids. Lactulose probably exerts its beneficial retained in the colon for 20 to 30 minutes before evacuation.
effects by: 1) increasing intraluminal nitrogen retention by increas- Lactulose requires intestinal bacteria for activation. Although neo-
ing the colonic flora, 2) increasing intestinal transit rate due to its mycin and other nonabsorbable antibiotics are used in the treat-
cathartic properties and 3) decreasing ammonia generation from ment of HE in people, their use is limited to cases that do not
glutamine in the intestinal wall by providing acetic acid as an alter- respond to lactulose alone. Furthermore, patients should be mon-
native energy source. The dosage required to achieve these goals itored carefully. Moreover, evidence of their effectiveness in the
varies greatly, with a range of 2.5 to 25 ml, three times daily for treatment of dogs and cats with HE is lacking.
dogs and 1.0 to 3.0 ml, three times daily for cats. The dosage
should be titrated to produce a “porridge-like” stool and should be The Bibliography for Box 68-4 can be found at
reduced if watery diarrhea develops. www.markmorris.org.

occurs. Studies involving people with hepatic failure have electrolyte levels within 12 to 72 hours after feeding.
shown that nitrogen balance can be improved if the food is Hypophosphatemia can result in muscle weakness, hemolytic
divided into small, frequent meals, including a snack at bedtime anemia, leukocyte dysfunction, platelet dysfunction and de-
(Swart et al, 1989). Nauseated patients may also better tolerate creased tissue oxygenation as a result of decreased levels of
multiple small meals. 2,3,-diphosphoglycerate. Electrolyte abnormalities should be
Appetite stimulants and force feeding moist food can be corrected before feeding hepatic lipidosis patients. Ap-
used to encourage caloric intake, but these strategies often fail proximately one-fourth of the patient’s caloric needs should
to ensure enough food is consumed to meet the patient’s be provided by tube feeding on Day 1, then the amount
nutrient requirements and typically frustrate the owner. Ap- should be gradually increased to provide the caloric need
petite stimulants such as anabolic steroids and benzodi- within the first week of feeding (Justin and Hohenhaus,
azepine derivatives are not recommended and should be used 1995; Center et al, 1993).
cautiously in patients with hepatic disease, because of the
potential for hepatotoxicity and, benzodiazepines may possi- REASSESSMENT
bly be involved in the pathogenesis of HE (Wilson, 1990;
Meyer, 1998). The owner and veterinarian should monitor the appetite, body
Many patients may develop learned aversion to the foods weight and condition of the patient, while observing the fre-
they are offered if GI disturbances accompany liver disease. quency and severity of GI disturbances (i.e., vomiting, diar-
This is the classic scenario in cats with hepatic lipidosis. Cats rhea), icterus and neurobehavioral signs. One of the most
that refuse to eat a food they associate with nausea may contin- important clinical findings is improvement in the patient’s atti-
ue to avoid that food even after a complete recovery.Therefore, tude and activity level. This finding is highly correlated with
tube feeding should be started in cats immediately after a diag- nutritional success.Serial laboratory evaluations (every few days
nosis of hepatic lipidosis is made. Such an approach is preferred to weeks) of serum liver enzyme activity, bile acids and potassi-
to offering several commercial foods and possibly having the um and blood ammonia concentrations are useful. Serial hepat-
cat develop an aversion to them.The prognosis for hepatic lipi- ic biopsy specimens (i.e., every four to six months) can be eval-
dosis is influenced largely by the ability of the veterinarian and uated for hepatic copper concentrations and assessed for in-
owner to aggressively meet the nutrient requirements of the cat flammatory hepatopathies. Body weight, abdominal configura-
via enteral feeding. tion and ultrasonography can be used to monitor patients with
Managing cats with hepatic lipidosis that are starved or ascites.
severely malnourished can be complicated by a refeeding syn- Assisted-feeding tubes for cats with hepatic lipidosis and/or
drome, a condition that results in metabolic electrolyte distur- cholangitis can often be removed after several weeks to
bances that can lead to neurologic, pulmonary, cardiac, neuro- months. Enteral tubes are usually removed after the cat has
muscular and hematologic complications. Cats with hepatic shown clinical improvement and has begun eating two-thirds
lipidosis often have hypophosphatemia and hypokalemia to three-fourths of its normal DER on its own. Many of these
from low food intake, decreased intestinal absorption or patients can be fed typical adult maintenance-type foods after
increased renal loss. With the introduction of food and a sud- hepatobiliary disease is resolved. These include patients that
den shift to carbohydrate metabolism, stimulation of insulin have recovered from an acute hepatic insult or hepatic lipido-
secretion promotes intracellular uptake of phosphorus, potas- sis and patients that have undergone successful (partial or
sium, magnesium, water and glucose and further lowers serum total) closure of PSS.