H: Hyperosmolarity

Hyperosmolarity

BASICS

DEFINITION

Osmolarity—expressed in mOsm/L; represents the number of solute particles per liter of solution.
Osmolality—expressed in mOsm/kg; represents the number of solute particles per kilogram of solution.
Hyperosmolarity—a high concentration of solute particles per liter of solution.
Serum concentrations > 310 mOsm/L in dogs and > 330 mOsm/L in cats are usually considered hyperosmolar.

PATHOPHYSIOLOGY

Serum sodium is responsible for most of the osmotically active particles that contribute to serum osmolarity; serum glucose and urea also contribute to serum osmolarity.
Anything that causes water loss increases concentrations of solutes in plasma or serum, thereby increasing serum osmolarity.
Blood volume, hydration status, and ADH are intimately involved in controlling extracellular fluid volume.
Low circulating blood volume stimulates carotid and aortic baroreceptors to respond to changes in blood pressure, causing ADH secretion.
Hyperosmolarity affects the osmoreceptors in the hypothalamus and stimulates ADH secretion from the neurohypophysis; the hypothalamic thirst center is also stimulated and causes an increase in water consumption to counteract serum hyperosmolarity by solute dilution.
Rapid increases in serum osmolarity cause water movement along its concentration gradient from intracellular to extracellular spaces, resulting in neuronal dehydration, cell shrinkage, and cell death; cerebral vessels may weaken and hemorrhage.

SYSTEMS AFFECTED

Cardiovascular—hypotension and decreased ventricular contractility.
Nervous—excessive thirst may be the first sign of hyperosmolarity. Central nervous system depression may lead to coma.
Renal/Urologic—low urine output.

SIGNALMENT

Dogs and cats.
Hypodipsia and hyperosmolarity have been reported in young female miniature schnauzers.

SIGNS

General Comments

Primarily neurologic or behavioral.
Severity is related more to how quickly hyperosmolarity occurs than to the absolute magnitude of change.
Most likely to occur if serum osmolarity is > 350 mOsm/L and usually severe if > 375 mOsm/L.

Historical Findings

Anorexia, lethargy, vomiting, weakness, disorientation, ataxia, seizures, and coma; polydipsia followed by hypodipsia.

Physical Examination Findings

Normal, or abnormalities may reflect underlying disease.
In addition to historical findings, dehydration, tachycardia, hypotension, weak pulses, and fever may be detected.

CAUSES

Increased Solutes

Hypernatremia, hyperglycemia, severe azotemia, ethylene glycol toxicosis, salt poisoning, sodium phosphate enemas in cats and small dogs, mannitol, radiographic contrast solution, administration of ethanol, aspirin toxicosis, shock, lactate in patients with lactic acidosis, acetoacetate and β-hydroxybutyrate in patients with ketoacidosis, liquid enteral nutrition, and parenteral nutrition solutions.

Decreased Extracellular Fluid Volume

Dehydration—gastrointestinal loss, cutaneous loss, third space loss, low water consumption, and polyuria without adequate compensatory polydipsia.

RISK FACTORS

Medical conditions that predispose—renal failure, diabetes insipidus, diabetes mellitus, hyperadrenocorticism, hyperaldosteronism, and heat stroke.
Therapeutic hyperosmolar solutions—hypertonic saline, sodium bicarbonate, sodium phosphate enemas in cats and small dogs, mannitol, and parenteral nutrition solutions.
High environmental temperatures.
Fever.

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

Primary CNS disease and neoplasia may be characterized by altered mentation, but serum osmolarity is usually normal.
Physical evidence or history of injury usually helps to rule-out CNS depression caused by cranial trauma.
Perform a thorough physical examination to assess hydration status and obtain information regarding previous therapy that may have included sodium-containing fluids or hyperosmolar solutions.

LABORATORY FINDINGS

Drugs That May Alter Laboratory Results

Excessive administration of sodium-containing fluids or hyperosmolar solutions increase serum osmolarity.

Disorders That May Alter Laboratory Results

N/A

Valid if Run in Human Laboratory?

Yes

CBC/BIOCHEMISTRY/URINALYSIS

High PCV, hemoglobin, and plasma proteins in dehydrated patients; serum electrolytes may also be increased.
Hyperosmolarity is an indication to evaluate serum sodium and glucose concentrations.
Without the presence of excessive unmeasured osmoles, estimated serum osmolarity may be calculated from serum chemistries as follows:
Normally, calculated osmolarity should not exceed measured osmolarity; if it does, consider laboratory error.
If measured osmolarity exceeds the calculated osmolarity, determine the osmolar gap.
Osmolar gap = measured osmolarity − calculated osmolarity.
High measured osmolarity and normal calculated osmolarity with a high osmolar gap indicate the presence of unmeasured solutes (not Na, K, glucose, BUN).
High measured osmolarity and high calculated osmolarity with a normal osmolar gap usually indicate that the hyperosmolarity is caused by hyperglycemia or hypernatremia.
Serum sodium concentration may be artificially low in patients with severe hyperglycemia and hyperosmolarity.
Fasting hyperglycemia and glucosuria support a diagnosis of diabetes mellitus.
Numerous calcium oxalate crystals in the urine suggest ethylene glycol toxicosis.
High urinary specific gravity rules-out diabetes insipidus.
Low urinary specific gravity, especially hyposthenuria, suggests diabetes insipidus.

OTHER LABORATORY TESTS

Urinary osmolarity lower than serum osmolarity suggests diabetes insipidus; concentrated urine rules-out diabetes insipidus.

IMAGING

Renal ultrasonography may reveal bright hyperechoic kidneys in patients with ethylene glycol toxicosis.

DIAGNOSTIC PROCEDURES

N/A

TREATMENT

Mild hyperosmolarity without clinical signs may not warrant specific treatment, but diagnose and treat underlying diseases.
Hospitalize patients with moderate-to-high osmolarity (> 350 mOsm/L) and patients exhibiting clinical signs and gradually lower serum osmolarity with intravenous fluids while a definitive diagnosis is pursued.
Administer D5W or 0.45% saline slowly IV.
Free water deficit can be calculated by the following formula:
The goal is to not drop sodium more than 15 mEq/L in an 8-hour period; that is, the ultimate goal is to not drop the sodium by more than 2 mEq/L/hour.
Initially, 0.9% saline may be used to restore normal hemodynamics and replace dehydration deficits; replace one-half of dehydration deficits over 12 hours and the remainder over 24 hours; then switch to D5W or 0.45% saline.

MEDICATIONS

DRUG(S) OF CHOICE

Seizures can be controlled with diazepam, phenobarbital, propofol, or pentobarbital.

CONTRAINDICATIONS

Hypertonic saline and hyperosmolar solutions

PRECAUTIONS

May use normal saline initially, but rapid administration may worsen neurologic signs.
Rapid administration of hypotonic fluids (e.g., D5W and 0.45% saline) may also cause cerebral edema and worsen neurologic signs.

POSSIBLE INTERACTIONS

N/A

ALTERNATIVE DRUG(S)

Regular insulin 0.1 unit/kg IM or IV can be administered if a hyperglycemic crisis occurs secondary to parenteral nutrition administration.

FOLLOW-UP

PATIENT MONITORING

Hydration status; avoid overhydration.
Bladder size, urine output, and breathing patterns during IV fluid administration.
Anuria, irregular breathing patterns, worsening depression, coma, or seizures may be signs of deterioration.

POSSIBLE COMPLICATIONS

Altered consciousness and abnormal behavior

MISCELLANEOUS

ASSOCIATED CONDITIONS

Hypernatremia and hyperglycemia

AGE-RELATED FACTORS

None

ZOONOTIC POTENTIAL

None

PREGNANCY/FERTILITY/BREEDING

N/A