Page 809 - Clinical Small Animal Internal Medicine

71 Disorders of the Forebrain 777

Other theories pertaining to the pathogenesis of HE associated with disease can be abolished if parathyroid-
VetBooks.ir include perturbed monoamine neurotransmission as a ectomy is performed before induction of uremia.
Prognosis is poor as a result of the underlying renal dis-
result of altered plasma amino acid metabolism; imbal-
ance between excitatory amino acid neurotransmission
(glutamate) and inhibitory amino acid neurotransmis- ease but treatment with calcitriol (1.5–3.4 ng/kg/day
PO) can reduce signs of neurologic depression in animals
sion (gamma‐aminobutyric acid, GABA); and increased with chronic uremia, as long as phosphate levels are nor-
cerebral concentration of an endogenous benzodiaze- mal to prevent renal mineralization.
pine‐like substance.
Clinical signs relate to prosencephalic disease:
behavioral changes (vocalizing, aggression), dullness, Electrolyte Disturbances
ataxia, circling, aimless wandering, blindness, seizures, Hypoglycemia
and head pressing. In severe cases this can progress to There are two main causes for hypoglycemia: insulin‐
stupor or coma. Diagnosis is made on biochemistry secreting tumors (insulinomas) of the pancreas, and
panels together with pre‐ and postprandial bile acid overdosage of diabetic patients with insulin (especially
tolerance tests. Ammonia levels can also be measured when not eating). Young puppies (less than 3 months of
but are very labile and should only be relied on if qual- age) are also prone to hypoglycemia in association with
ity control standards associated with performing the cold, starvation or gastrointestinal (GI) disease, and
test are high. If imaging studies are performed, MRI hypoglycemia may also be seen in animals with porto-
may show (precontrast) T1‐weighted hyperintensities systemic shunts. Clinical signs associated with hypogly-
in the caudate nucleus, amgydala and hippocampus cemia include behavioral changes, weakness, ataxia,
and/or cingulate gyrus. Treatment is directed at the collapse, transient blindness, and seizures. Signs are
underlying hepatic disease. Ligation of portosystemic often intermittent, becoming more frequent as the dis-
shunts (or coil embolism) is the treatment of choice for ease progresses, and may be associated with periods of
animals with congenital shunts. fasting, exercise or excitement. Rarely, polyneuropathies
It is also important to note that when treating animals may also occur with hypoglycemia; tetraparesis/plegia,
with seizures secondary to hepatic insufficiency, anti- facial nerve signs, hyporeflexia, and hypotonia are the
convulsants that are metabolized by the liver should be most commonly seen signs associated with these. Central
avoided (e.g., phenobarbitone, diazepam). Potassium nervous system (CNS) signs occur because neurons are
bromide or levetiracetam are preferable as first‐line unable to synthesize or store glucose and rely almost
therapy. In addition, animals that have portosystemic entirely on glucose derived from the blood.
shunts ligated may develop seizures shortly postopera- Diagnosis of hypoglycemia secondary to insulinoma
tively, for reasons that are poorly understood (and inde- requires demonstration of hypoglycemia in a fasting
pendent of whether the patient has HE prior to shunt blood sample, together with elevated insulin levels (from
ligation). Various causes have been postulated, including paired samples). Treatment is directed at removing the
the existence of endogenous benzodiazepine‐like ligands underlying cause of hypoglycemia plus administration of
within the brain of these patients. These seizures are fre- dextrose solutions (5%). In animals with inoperable
quently very difficult to control if they occur; potassium insulinomas, prednisolone and diazoxide can be used
bromide at 100 mg/kg PO QID for 24 hours followed by but the prognosis is guarded to poor, with survival of
30 mg/kg PO SID dosing has been recommended but is 90 days only (vs 12–14 months for resectable tumors).
not always effective, and levetiracetam has also been
proposed as a useful treatment. Propofol constant‐rate Sodium Abnormalities
infusions (CRIs) have also been reported to be effective. Neurologic signs may be seen in association with both
In addition to HE, a rare encephalopathy associated
with end‐stage renal disease is also reported, with clinical hypernatremia and hyponatremia.
signs including depression or stupor, seizures, muscle Hypernatremia
fasciculations, and myoclonic head‐bobbing movements. Hypernatremia occurs with sodium >156 mEq/L (dogs)
The diagnosis is usually straightforward, with profound or >161 mEq/L (cats). Causes include:
uremia evident on biochemistry panels, usually with
accompanying hyperphosphatemia. The underlying ● excess water loss: diabetes insipidus (central or nephro-
cause is unknown, with suggested mechanisms including genic), burns, fever, osmotic diuresis (acute/chronic
depressed cerebral oxygen consumption, cerebral renal failure, diabetes mellitus, diuretics, or IV solute
hypoxia, increased brain calcium levels, and increased administration such as mannitol, glucose or urea),
blood levels of parathyroid hormone (PTH). In experi- osmotic diarrhea (lactulose therapy, malabsorption
mental uremia, the electroencephalogram (EEG) changes syndromes, infectious enteritides), hot weather