Page 78 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

68 ELECTROLYTE DISORDERS

to increased plasma vasopressin concentrations and result suggesting that it was capable of suppressing vasopressin
in decreased renal excretion of water. These events may release in response to the water load.
result in postoperative hyponatremia, especially if the
patient receives hypotonic fluids. 6,38 In fact, routine use TREATMENT OF HYPONATREMIA
of hypotonic fluids in patients in whom water excretion The two main goals of treatment in hyponatremia are to
is impaired by nonosmotic stimulation of vasopressin diagnose and manage the underlying disease and, if nec-
release is thought to be the main contributing factor to essary, increase serum sodium concentration and plasma
hospital-acquired hyponatremia in human patients and osmolality. Severe, symptomatic hyponatremia of acute
can be prevented by administration of isotonic fluids such onset (<24 to 48 hours’ duration) may result in seizures,
as 0.9% NaCl. 114 cerebral edema, or death and requires prompt treatment.
Chlorpropamide potentiates the action of vasopressin, In human patients with acute hyponatremia, correction
possibly by inhibiting vasopressin-stimulated production of serum sodium concentration may be required at rates
of prostaglandin E 2 or by up-regulating vasopressin up to 12 mEq/L/day. 151 However, severe, symptomatic
35
receptors in the kidneys. Nonsteroidal anti-inflammatory hyponatremia of rapid onset is rare in small animal prac-
drugshaveasimilareffectbecauseoftheirinhibitionofpros- tice. Because of inexperience with the management of
taglandin production. The antineoplastic drugs vincristine acute hyponatremia in dogs and cats, and the known risks
and cyclophosphamide also impair water excretion. of overly rapid correction of hyponatremia, only use of
Figure 3-6 shows the effects of various drugs on the release conventional crystalloid solutions (e.g., lactated Ringer’s
and action of vasopressin. solution and 0.9% saline) is recommended. Use of 3%
NaCl is not recommended.
CLINICAL SIGNS OF Patients with chronic hyponatremia often have few or
HYPONATREMIA no clinical signs directly attributable to their
hypoosmolality. This is probably because the brain has
The clinical signs of hyponatremia are related more to the had sufficient time to adapt to plasma hypotonicity. In
rapidity of onset than to the severity of the associated fact, treatment of chronic hyponatremia can be more dan-
plasma hypoosmolality. In human patients, deaths and gerous than the disorder itself. In human patients,
severe complications of hyponatremia were most com- complications of treatment may occur when chronic
mon when the serum sodium concentration acutely (>48 hours’ duration) hyponatremia is corrected too rap-
decreased to less than 120 mEq/L or at a rate greater idly (i.e., when the serum sodium concentration is
than 0.5 mEq/L/hr. 25 Cerebral edema and water intoxi- increased by >10 to 12 mEq/L in 24 hours). 95,151
cation occur if hyponatremia develops faster than the When hyponatremia and hypoosmolality are
brain’s defense mechanisms can be called into play. corrected, potassium and organic osmolytes lost during
Reduction in plasma osmolality and influx of water into adaptation must be restored to the cells of the brain. If
the central nervous system cause the clinical signs replacement of these solutes does not keep pace with
observed in acute hyponatremia. A 30- to 35-mOsm/kg the increase in serum sodium concentration that occurs
gradient can result in translocation of water between as a result of treatment, brain dehydration and injury—
plasma and the brain in dogs. 61 Clinical signs are often called osmotic demyelination or myelinolysis—may
absent in chronic disorders characterized by slower result. 95,151 Experimental studies have confirmed that
decreases in serum sodium concentration and plasma this syndrome is a result of a rapid and large increase in
osmolality. During hyponatremia of chronic onset, brain serum sodium concentration and is not a consequence
volume is adjusted toward normal by loss of potassium of hyponatremia and hypoosmolality. Human patients
and organic osmolytes from cells. 6,134 with hyponatremia of more than 72 hours’ duration are
Acute water intoxication is likely only if the patient has more susceptible than those with hyponatremia of less
some underlying cause of impaired water excretion at the than 24 hours’ duration. 151 The neural lesions of
time a water load occurs. For example, water-loaded dogs myelinolysis develop several days after correction of
given repositol vasopressin developed signs of acute water hyponatremia and consist of myelin loss and injury to
intoxication. 69 Early signs were mild lethargy, nausea, and oligodendroglial cells in the pons and other sites in the
slight weight gain; more severe signs included vomiting, brain (e.g., thalamus, subcortical white matter, and cere-
coma, and a marked increase in body weight. One dog in bellum). Lesions may take several days to develop, but on
this study died from pulmonary and cerebral edema. Weak- magnetic resonance imaging they are hyperintense on
ness, incoordination, and seizures may also result from T2-weighted images, hypointense on T1-weighted
acute water intoxication. In one clinical report, a Labrador images, and are not enhanced after gadolinium injec-
retriever developed acute hyponatremia (125 mEq/L) and tion. 95 The ability to reaccumulate organic osmolytes
severe neurologic signs (i.e., coma) after swimming for may vary among different regions of the brain and thus
manyhoursinalake. 157 Thedogspontaneouslyunderwent account for why some regions (e.g., midbrain) are more
marked diuresis and recovered with supportive care, susceptible to osmotic demyelination.