Page 1013 - Cote clinical veterinary advisor dogs and cats 4th

498 Hypernatremia

Nutrition/Diet Recommended Monitoring • Hypercholesterolemia may indicate the pres-
• Hypertriglyceridemia • Monitor plasma TGs 4-8 weeks after initia- ence of an underlying disorder but rarely
VetBooks.ir metabolizable energy [ME]; cat: < 25% • Monitor hematologic/biochemical parameters Prevention
○ Dietary fat restriction (dog: < 20%
tion of low-fat diet, then every 6-12 months.
causes clinical disease.
with fibrates, niacin, or lovastatin.
ME)
○ If a low-fat diet is unsuccessful, a
nutritionist can design an ultralow-fat PROGNOSIS & OUTCOME • Treat predisposing disorders.
• Monitor TG concentrations in susceptible
(10%-12% ME) diet. breeds.
• Hypercholesterolemia • Successful management depends on adequate
○ Low-fat diet with increased amounts of control of underlying disease(s) and reduction Technician Tips
soluble fiber of plasma lipid concentrations. • Alert the attending veterinarian if the
• Cats with peripheral neuropathies generally supernatant in a hematocrit tube or serum
Drug Interactions have clinical signs resolve within 4-12 weeks or plasma in a centrifuged tube is cloudy
• Statins should not be used concurrently with of instituting diet change. and the patient has not eaten in > 12 hours.
azole antifungals, cyclosporine, diltiazem, or • Lipemia can increase total solids measured by
gemfibrozil. PEARLS & CONSIDERATIONS refractometry and can interfere with multiple
• Statins may increase the toxicity of digoxin. biochemical tests.
Comments
Possible Complications • Hyperlipidemia in patients fasted > 12 hours SUGGESTED READING
• Fibrates may cause myalgia and hepatopathy. is abnormal. Xenoulis PG, et al: Canine hyperlipidaemia. J Small
• Niacin may cause hyperglycemia, erythema, • Lipemic plasma is an indication of hypertri- Anim Pract 56:595-605, 2015.
pruritus, myalgia, and hepatopathy. glyceridemia, not hypercholesterolemia.
• Statins may cause lethargy, diarrhea, myalgia, • Hypertriglyceridemia often signals underlying AUTHOR: Karen M. Tefft, DVM, MVSc, DACVIM
EDITOR: Ellen N. Behrend, VMD, PhD, DACVIM
and hepatopathy. disease and may cause clinical disease.

Hypernatremia

BASIC INFORMATION hypernatremia; volume status provides clues • Acute hyperosmolality can cause brain cells
about the cause to shrink because intracellular water is pulled
Definition into the extracellular fluid space, resulting in
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A serum sodium (Na ) concentration above HISTORY, CHIEF COMPLAINT rupture of vessels and intracranial bleeding.
the reference range; caused by net water loss • Clinical signs (e.g., vomiting, diarrhea, • If hypernatremia comes about more slowly,
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(most common) or Na gain polyuria/polydipsia [PU/PD]) often related the brain can adapt through production of
to the underlying cause of hypernatremia idiogenic osmoles, which hold water volume
Epidemiology • Severity and rapidity of onset correlate in the brain cells.
SPECIES, AGE, SEX with severity of signs attributed directly to ○ Overly rapid correction of long-standing
No species, age, or sex predisposition hypernatremia, which can include hypernatremia causes water to be pulled
○ Mental dullness/ inappropriate mentation into the brain cells by idiogenic osmoles,
GENETICS, BREED PREDISPOSITION ○ Ataxia resulting in brain swelling and neurologic
Essential adipsic hypernatremia rarely reported ○ Stupor/coma damage.
in schnauzers, other dog breeds, and cats; may ○ Seizures • Causes of hypernatremia (p. 1237)
have a genetic basis ○ Muscle weakness ○ Pure water deficit: normovolemic hyperna-
tremia (e.g., water deprivation [especially
RISK FACTORS PHYSICAL EXAM FINDINGS with diabetes insipidus], adipsia)
• Diuresis in the absence of adequate available • Findings often relate to the underlying cause ○ Hypotonic fluid loss (most common):
water replacement of hypernatremia. hypovolemic hypernatremia (e.g., dia-
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• Excessive water loss from nonrenal sources • When Na > 170 mEq/L, findings directly betes mellitus, postobstructive diuresis,
(e.g., vomiting, diarrhea, burns) attributed to hypernatremia can become gastrointestinal (GI) fluid loss, burns,
• Acute administration/consumption of large apparent (see Chief Complaint). chronic kidney disease)
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amounts of Na (e.g., sea water consumption) • Evidence of volume depletion or excess ○ Increased Na retention or intake: hyper-
○ Hydration usually adequate (from movement volemic hypernatremia (e.g., hypertonic
ASSOCIATED DISORDERS of water from intracellular space to extracel- enema solutions, sea water consumption,
Essential adipsic hypernatremia, diabetes lular space) until extreme water loss occurs excess hypertonic saline infusion)
insipidus, central nervous system (CNS) ○ Volume depletion: loss of skin turgor, weak
damage pulse, tachycardia, delayed capillary refill DIAGNOSIS
time
Clinical Presentation ○ Volume excess: serous nasal discharge, Diagnostic Overview
DISEASE FORMS/SUBTYPES tachypnea, harsh lung sounds Hypernatremia may be suspected in depressed
• Can be acute or chronic; accumulation of animals with conditions known to predispose
idiogenic osmols in chronic hypernatremia Etiology and Pathophysiology to hypernatremia, or it can be an incidental
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impact treatment • Na and its anions account for ≈95% of finding on serum biochemical profile. Signs of
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• Categorized by volume status as hypovo- osmotic activity in extracellular fluids; there- hypernatremia may not be apparent until Na
lemic, normovolemic, or hypervolemic fore, hypernatremia causes hyperosmolality. > 175-180 mEq/L.
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