Page 810 - Clinical Small Animal Internal Medicine

778 Section 8 Neurologic Disease

excess salt intake: salt poisoning, administration of IV with normovolemic or hypervolemic hyponatremia
●
VetBooks.ir hypertonic solutions (NaCl), sodium bicarbonate, or associated with excessive water intake or renal reten-
saline emetics
tion, water restriction (i.e., limiting water intake to less
insufficient water intake: lack of access, inability to
●
drink, CNS disease resulting in primary adipsia (absence than urine output) can be performed. In instances where
severe neurologic signs are seen associated with normal
of thirst), mental depression, congenital adipsia. or excessive intravascular fluid, frusemide (2–4 mg/kg
IV) can be used to promote renal water excretion.
Marked hypernatremia may induce cerebral signs, Chronic hyponatremia may be more difficult to treat
such as depression, weakness, irritability, uncharacteris- since overrapid correction of the deficit can result in a
tic aggression, confusion, propulsive circling, demen- worsening of clinical signs associated with central pon-
tia, seizures, coma, and death as the result of cellular tine myelinolysis. Lesions appear in white matter
dehydration of neurons. Neurologic signs may not associated with death of oligodendrocytes and loss of
occur until serum Na levels exceed 170–175 mEq/L myelin, resulting in bilaterally symmetric lesions in the
(>350 mOsm/kg), although the severity of neurologic pons and rarely (10% of cases) thalamus, subthalamic
signs depends especially on the rate of increase, with nuclei, striatum, internal capsule, amygdala, lateral
signs being most severe in animals with rapidly devel- geniculate body, white matter of the cerebellum and deep
oping hyperosmolality. layers of the cerebral cortex. The postulated hypothesis
Treatment depends on the rate at which hypernatremia
develops; overrapid correction can lead to worsening is that with chronicity, cells within the brain extrude
intracellular electrolytes followed by organic osmolytes
clinical signs (due to a relative hyponatremia and move- (“idiogenic osmoles”), in order to reduce the risk of brain
ment of water from the vascular spaces into the brain). edema. When sodium is replaced intravascularly as part
Replacement of the water deficit should be undertaken of fluid therapy, osmotic attraction of water out of cells
using 5% dextrose with the aim of correction of the deficit in the brain results in dehydration of brain tissue. Clinical
over 24 hours (or longer). In animals with acute‐onset signs occur several days after fluid treatment: ataxia,
hypernatremia, correction of Na levels at a rate of 1.0 weakness, hypermetria, visual deficits, depressed men-
mEq/h is acceptable. However, if the hypernatremia is ace response (with normal pupillary light response
more chronic, Na levels should not be allowed to change [PLR]), reduced proprioception, exaggerated licking
at more than 0.5 mEq/h. In animals with excess salt movements, episodic myoclonus, whole‐body spasms,
intake, diuretics should be given in conjunction with fluid obtundation, and tetraparesis. Prognosis for recovery is
therapy to avoid pulmonary edema.
reasonable; in one study of two dogs, one died but the
other recovered over 4–7 weeks. As a result, it is impor-
Hyponatremia tant to stick to the guideline of replacing Na at a rate no
Hyponatremia occurs when serum Na levels are less than greater than 0.5 mEq/L/h.
146 mEq/L in dogs (151 mEq/L in cats). Hyponatremia
can be further divided into true hyponatremia (associ-
ated with total body water in excess of Na – serum osmo- Neoplastic Causes
lality is low, <290 mOsm/L) and pseudohyponatremia
(low Na with normal or increased serum osmolality). Brain Tumors
Clinical signs of hyponatremia relate primarily to the
rate of onset of hyponatremia. In acute hyponatremia, Tumors affecting the brain can arise as one of several
sodium levels within the brain are relatively normal forms.
while sodium levels within the vascular spaces are low. Primary tumors arise from cells and structures of the
Water flows down its concentration gradient into the ● brain itself.
brain, producing cerebral edema and raised intracranial Secondary tumors arise from cells and structures adja-
pressure (ICP). Signs include generalized weakness, ● cent to the brain.
depression, stupor, coma, seizures, and dementia. Metastatic tumors arise from spread of a tumor at a
Treatment is aimed at increasing sodium levels: use ● distant site.
hypertonic saline (3–5%) when serum Na <115 mEq/L.
The Na deficit is calculated using: The most common tumors that affect dogs (and humans)
are primary tumors. They occur with a slightly greater inci-
Defect mEq /l 140 measured Na bodyweight kg . 03 dence than in people (14–15 per 100 000 dogs vs 8–9 per

The replacement fluid should be given slowly over 100 000 people at risk). The most common types include:
12–24 hours. For animals with hypovolemic hypona- ● meningiomas
tremia, normal isotonic saline can be used. For animals ● astrocytomas