Page 906 - Cote clinical veterinary advisor dogs and cats 4th

Hepatic Encephalopathy 441

atrophy, attenuation of portal vasculature, ■ N-acetylcysteine 140 mg/kg slow • Body weight and body condition score
lobular collapse) seen with all forms of IV initially followed by 70 mg/kg as • Serum albumin
VetBooks.ir hypoperfusion. Necroinflammatory changes ■ Glucocorticoids of no benefit and may PROGNOSIS & OUTCOME Diseases and Disorders
hepatic disease associated with chronic
needed; may correct disturbances in
microcirculation
with chronic hepatitis/fibrosis. Hepatic
necrosis with acute liver failure. Dysplastic
be detrimental
causing HE:
bile duct proliferation with ductal plate ■ Hypoglycemia may require infusion Depends on nature of underlying liver disease
malformation. of high concentrations of dextrose- • Hepatic vascular disease (PSS, microvascular
• Urea cycle disorders diagnosed by enzyme containing solutions (monitor q 4h). dysplasia, arteriovenous malformation): signs
activity in hepatic tissue. • Address fluid and electrolyte imbalances; often respond quickly and fully to appropri-
avoid lactated solutions if acute liver ate drug and dietary intervention. Long-term
TREATMENT failure; sodium-restricted fluids if ascites prognosis depends on response to medical
present; potassium, glucose, and B vitamins management or correction of the vascular
Treatment Overview (especially thiamine and cobalamin in cats) defect.
Goals of treatment are to lower levels of circu- supplementation as needed • Acquired chronic hepatic disease: clinical
lating neurotoxins by modulating GI protein • Control precipitating factors signs of HE generally abate with proper inter-
metabolism, maintain optimal nutritional plane, ○ Oral protein burden: GI hemorrhage, vention, but long-term prognosis depends on
and control precipitating factors. high-protein meals nature and severity of the underlying hepatic
○ Catabolic conditions: infection, dehydra- disorder. Patients with signs of severe HE due
Acute and Chronic Treatment tion, azotemia to acquired hepatic diseases generally have
• Nothing per os if stupor or coma is present ○ Alkalosis with hypokalemia: increases renal a very poor prognosis unless the underlying
• Medications that increase GI protein toler- ammonia production disease can be reversed.
ance (first line of therapy) ○ Synergistic neural inhibition with seda- • Acute liver failure: HE is more refractory
○ Lactulose is drug of choice. Nonabsorbable tives, tranquilizers, or anesthetic agents; to therapy, probably reflecting a more
disaccharide is broken down by colonic use these with caution if at all (e.g., complex underlying cerebral lesion or
bacteria into short-chain fatty acids. Traps diazepam) process. Encephalopathy progressing to
soluble ammonia (NH 3 ) as ammonium ○ Transfusion with stored blood products coma or stupor (grade 3-4) is considered
+
(NH 4 ), which is nonabsorbable and (high ammonia concentrations) a grave prognostic sign and is one of the
excreted in the feces. Alters bacterial ○ Constipation criteria used for determining the need for
metabolism so that less ammonia is ○ Concurrent azotemia liver transplantation in human patients.
generated • Correct underlying disorder if possible • Ductal plate malformation: poor if portal
○ Lactulose is titrated from an initial dose (e.g., surgical correction of CPSS after hypertension and HE present
of 0.5-1 mL/kg PO q 8-12h to a dose stabilization)
that produces 3-4 soft stools per day. If PEARLS & CONSIDERATIONS
stupor or coma is present, may be given Nutrition/Diet
rectally in a retention enema (p. 1099) • Adequate calories to avoid catabolism of Comments
○ Antibiotics alter bacterial metabolism, muscle (highly ammoniagenic; may make • Normal blood ammonia concentration does
synergistic with lactulose control of HE difficult) not rule out the presence of HE.
Metronidazole 7.5 mg/kg PO q 8-12h, • Modulation of protein content: high-quality • Initial treatment of HE involves nonab-
■
low dose to avoid neurotoxicosis second- protein derived preferably from plant and sorbable disaccharides and antibiotics in
ary to decreased hepatic metabolism, or dairy products. Start with diet containing combination with dietary protein modulation
Neomycin 10-22 mg/kg PO q 12h; can minimum daily protein requirements (cat: but not excessive protein restriction.
■
be given orally or as a retention enema, 6.5 g/100 kcal; dog: 5.1 g/100 kcal) in • Be aware of common comorbid conditions
or combination with medications to increase that can complicate control of HE, such
Amoxicillin 22 mg/kg PO q 12h, or protein tolerance, and decrease protein only as GI bleeding, dehydration, hypokalemia,
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Rifaximin 10 mg/kg PO q 12h; if necessary. azotemia, constipation, and alkalosis.
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antibiotic of choice in humans with • Increase fiber content of diet. • HE accompanying acute liver failure differs
HE but limited veterinary experience • Vitamin supplementation: in cats, thiamine from that accompanying congenital vascular
• Control seizure activity 50-100 mg/CAT PO q 24h; if associated disorders or chronic hepatic failure in that it
○ Barbiturates (e.g., phenobarbital 6-10 mg/ coagulopathy, vitamin K 0.5 mg/kg SQ q involves the development of overt cerebral
kg slow IV to effect); patient should 12h for 5-7 days initially parenterally, then edema and an initial neuroexcitatory state
be monitored closely for respiratory once weekly often refractory to therapeutic intervention.
depression • Sodium restriction necessary only with • Development of HE is determined by the
○ Propofol is useful for controlling HE- ascites: 0.04-0.05 g/100 kcal amount of functional hepatic tissue and the
induced status epilepticus. Because it is presence of intrahepatic and extrahepatic
metabolized by the liver, small doses may Drug Interactions shunting of blood away from the hepatic
be effective and may have a long dura- • Neuroinhibitory drugs (e.g., sedatives, vascular system.
tion of action. Maintain an anesthetized anesthetics, and tranquilizers) should be used
state for several hours before tapering and cautiously because they may potentiate the Technician Tips
observe for recurrence. Monitor for apnea neuroinhibition of HE. • Note changes in mentation or the appearance
during use. • Avoid drugs that depend heavily on of abnormal behavior because they may
○ Cerebral edema is likely if seizures hepatic metabolism and/or excretion if indicate increasing grade of HE.
observed with acute liver failure; prog- possible. • Avoid feeding high-protein meals and limit
nosis is grave (seizures often refractory to intake of snacks containing protein.
treatment). Recommended Monitoring • Lactulose is expected to cause soft stools,
Mannitol 0.5 g/kg IV over 10-15 • Blood ammonia concentration although overt diarrhea warrants a decreased
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minutes • Mentation and appetite at home dose.

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