Page 495 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Fluid, Electrolyte, and Acid-Base Disturbances in Liver Disease 483

overload or life-threatening drug toxicities. Administra- metabolism. 123 Antimicrobials should be administered
tion of a highly protein-bound drug to a patient with to prevent enteric organisms from gaining access to the
hypoalbuminemia without dosage adjustment potentially systemic circulation. Patients with cirrhosis and HE
can lead to an inadvertent drug overdose that could may have increased endogenous benzodiazepines or ben-
be lethal. zodiazepine-like substances, which can bind to this recep-
tor complex and lead to neuroinhibitory effects from
Acute Severe Hepatic Encephalopathy or activation of the GABA portion of the receptor complex.
Liver Injury Flumazenil, a drug that acts as an antagonist of the
Treatments should be targeted at controlling benzodiazepine-g-aminobutyric acid (GABA) receptor
hyperammonemia and cerebral edema. Critical support- complex located in the brain has been proposed to ame-
ive care should address circumstances that increase cere- liorate HE in the short term. 82 However, recent findings
bral blood flow and compromise cerebral or hepatic have not supported its routine use in human medicine. 130
metabolism. Effort should be made to attenuate systemic
inflammatory responses and provoking causative factors. Chronic Hepatic Encephalopathy
Although acute hepatic failure usually is associated with Dietary Management
high blood NH 3 concentrations, strategies targeting The mainstay of nutritional support is judicious protein
enteric NH 3 production generally are less effective in restriction taking care to avoid a catabolic state. 49 Nitro-
patients with acute HE than in those with episodic HE gen allowances should be tailored individually for each
caused by chronic liver disease or portosystemic shunting. patient. Excessively severe protein restriction can contrib-
Careful management of systemic blood pressure is ute to malnutrition patients with chronic liver disease,
important; both hypotension and hypertension must be increasing catabolic loss of muscle. Positive nitrogen bal-
prevented. Analogs of AVP used to counteract splanchnic ance should be maintained and catabolism should be
hypoperfusion and enteric bleeding in severe hepatic avoided because muscle is an important site for transient
insufficiency are contraindicated in patients with signs NH 3 detoxification. Vegetable and dairy sources of pro-
of cerebral edema based on experimental studies and tein are superior to meat, fish, or egg sources in dogs. A
observations in human patients. 50 Body temperature recent study showed that a soy-based, low-protein diet
should be monitored, and hyperthermia should be had more impact in decreasing plasma ammonia concen-
avoided. Hyperthermia increases metabolic rate and cere- tration when compared with a poultry-based, low-protein
bral blood flow, which can increase intracranial pressure. diet after 4 weeks of treatment. Despite the difference in
Modest hypothermia may prevent emerging cerebral plasma ammonia concentration, both diets improved HE
edema in acute HE but cannot be maintained long term. scores, increased serum fibrinogen concentration, and
Glucose infusion may ensure euglycemia, but hyperglyce- increased prothrombin times. 172 Whether the lower
mia and hyponatremia may provoke cerebral edema in plasma ammonia concentration reflected better control
acute hepatic failure. Hypercapnia must be avoided of HE has been a topic of debate. 232 Some dogs devel-
because it may increase cerebral blood flow and intracra- oped very low albumin concentration, likely due to the
nial pressure. However, hyperventilation must also be negative energy balance. 172,232 Recent studies in animals
avoided because severe hypocapnia may decrease cerebral and humans suggest that the main source of ammonia in
perfusion. Monitoring blood pH to prevent alkalemia or the portal blood is the glutaminase activity of small intes-
acidemia is essential. Alkalemia can facilitate diffusion of tinal enterocytes, which use glutamine as their main
NH 3 across the blood-brain barrier, and acidemia may energy source. 192 The issue of whether or not the
indicate the presence of unmeasured anions, especially standard treatment approach of a low-protein diet and
lactate. Hyperlactatemia should be avoided because it lactulose actually benefits patients with HE has been
192
contributes to cerebral edema, increased cerebral blood debated. Although no double-blinded, placebo-con-
flow, and increased intracranial pressure. Infusion of trolled studies have been done to date, clinical experience
branched-chain amino acids and supplemental L-CN still supports the use of these treatments in human
may be appropriate in patients with acute severe patients. 29,57,230 Cats are strict carnivores and require
HE and suspected cerebral edema, but these treatments meat-derived protein as part of their restricted protein
remain controversial. Supplemental vitamin K and allowance. Energy requirements may be increased
water-soluble vitamins should be given, and some in hepatic insufficiency, and the patient’s body condition
clinicians believe that fluids containing lactate should and behavior at home should be evaluated sequentially to
be avoided. However, the benefit of avoiding lactate- assess the adequacy of nutritional support.
containing fluids may be more theoretical than Conventional recommendations for chronic manage-
practical. 15,123 An investigation of endogenous lactate ment of hyperammonemia and HE in dogs include limit-
production in septic human patients with acute renal ing dietary protein intake to between 14% and 16% of
failure found that an acute exogenous load of lactate energy intake with a minimum of 2.5 g protein/kg body
did not affect basal endogenous lactate production and weight per day. Recommendations for cats include