Case Studies: Hypernatremia
ACVIM 2008
Columbia, MO, USA


Disorders of serum sodium concentration are commonly seen in critically ill patients and present a diagnostic and therapeutic challenge to the veterinarian. Clinical signs may be subtle and often masked by the primary disease process and there are significant risks associated with aggressive or inappropriate treatment. This presentation will focus on an approach to the diagnosis and treatment of patients with sodium disorders.


The volume and tonicity of body fluids are normally maintained within a narrow range by regulation of sodium and water balance. Abnormalities in extracellular fluid volume reflect changes in total body sodium content. Abnormalities in serum concentration are caused by changes in water balance. The maintenance of a normal serum sodium concentration is dependent on the balance between water intake and water excretion. An appreciation of the physiologic effects of changes in plasma osmolarity is important when dealing with hyponatremic or hypernatremic patients. Total body water is estimated to be 60% of lean body weight. The distribution of this water is 1/3 extracellular (intravascular and interstitial) and 2/3 intracellular. Each fluid compartment has one major solute restricted primarily to that compartment that acts to hold water within the compartment. The extracellular fluid compartment (ECF) volume is maintained by sodium salts while the intracellular fluid compartment (ICF) is maintained by potassium salts. Because the cell membrane is freely permeable to water, the ECF and ICF spaces are in osmotic equilibrium. If an osmotic gradient is established, water will flow from the compartment of low osmolarity to the compartment with high osmolarity until the osmotic pressures are equalized. An increase in osmolarity of the ECF results in cellular dehydration and conversely a decrease in ECF osmolarity results in cellular overhydration.1

In contrast to regulation of ECF volume by changes in urinary sodium excretion, plasma osmolarity is maintained within narrow limits by balancing water intake (drinking, the water content of food and the water of oxidation) with water losses from urine, feces and insensible loss from the skin and respiratory tract. Small changes in plasma osmolarity are sensed by osmoreceptors in the hypothalamus which affect both thirst and water excretion via the secretion of ADH.1

Clinical Signs

The flow of water in and out of cells, particularly brain cells, is primarily responsible for the symptoms of both hyponatremia and hypernatremia. Symptoms of sodium disorders are nonspecific and may be difficult to separate from the underlying disease. Central nervous system signs are most common ranging from lethargy and weakness to ataxia, seizure, coma and death. The severity of neurologic dysfunction is related to the rapidity, as well as the degree of the change in serum sodium concentration.


Hypernatremia (serum sodium concentration >155 mEq/L in dogs and >162 mEq/L in cats) represents a deficit of water in relation to the body's sodium stores. It can result from a net water loss or a hypertonic sodium gain. Common causes of hypernatremia are listed in Table 1. Net water loss is more often the cause than is sodium gain. Water loss can occur in the absence of a sodium deficit (pure water loss) or with sodium loss (hypotonic fluid loss).2

Brain shrinkage secondary to movement of water out of brain cells is minimized by an adaptive response that begins within 24 hours of the development of hyperosmolarity. Initially there is movement of sodium and potassium into the brain cells followed by the generation of solutes called osmolytes ("idiogenic osmoles"). This response leads to normalization of brain volume and accounts for the milder symptoms of hypernatremia that develop slowly. This adaptive response also explains the development of cerebral edema and neurologic deterioration that can occur with overly rapid correction of hypernatremia. When the osmolytes are no longer needed to protect the central nervous system from dehydration, they are slowly metabolized over a few days. When chronic peripheral osmolarity is reduced to normal too quickly, the osmotic effect of the remaining CNS osmolytes can cause fluid to shift into the CNS until the osmolytes are metabolized.

Therapy for hypernatremia includes identification and treatment of the underlying cause and correcting the hypertonicity. Because of the adaptive development of osmolytes with brain cells, rapid correction of hypernatremia can cause cerebral edema, seizures, permanent neurologic damage and death. If hypernatremia has developed rapidly (over hours), the sodium can be lowered more rapidly. In patients with acute hypernatremia, serum sodium can safely be lowered by 1 mmol/liter/hour. If the hypernatremia is more chronic, the hypernatremia should be correctly more slowly. A targeted fall in the serum sodium concentration of 10 mmol/liter/day has been recommended in these patients. Alternatively, a decrease of 0.5 mmol/L/hour can be attempted. Various methods of free water replacement have been described in the literature over time. One method of replacement which is outlined here involves estimating the sodium-lowering effect of various fluid infusates on patient sodium level. Table 2 provides sodium content of certain fluid infusates. The formula in Table 3 can be used to estimate the effect of one liter of any infusate on serum sodium concentration.2 Hypoperfusion should be corrected with an isotonic fluid such as 0.9% sodium chloride before replacement of the calculated water deficit. If possible the patient's water deficit should be replaced enterally by allowing oral access to water or by placing an enteral feeding device. If the patient with chronic hypernatremia is alert enough to rapidly consume large quantities of water, oral intake can be limited judiciously until hypernatremia resolves. In patients with ongoing fluid losses, the fluid therapy plan should include an estimation of ongoing fluid losses.

Table 1. Causes of hypernatremia.

1. Net water loss

Pure water loss

Unreplaced insensible losses


Inadequate access to water


Diabetes insipidus

Neurogenic (Central)


Hypotonic fluid loss



Intrinsic renal disease




Gastric suction

Osmotic cathartic agents

Cutaneous burns

2. Hypertonic sodium gain



Sea water


Sodium bicarbonate

Hypertonic saline


Sodium phosphate enema

3. Reset osmostat

Primary hyperaldosteronism

Essential hypernatremia

Table 2. Sodium content of various fluid infusates.

Fluid infusate

Sodium content:

0.9% NaCl (Normal saline, NS)


Normosol R®


Lactated Ringer's solution (LRS)


5% dextrose in water (D5W)


Table 3. Correction of hypernatremia, with example.2

Part 1. The effect of fluid infusate on patient sodium

 Change in serum sodium from infusing 1 L of X fluid infusate = (infusate Na+ - serum Na+) / total body water + 1

 Total body water = Body weight (Kg) x 0.6

Part 2. Example of a 10 kg dog with serum sodium of 200 mmol/L treating with 5% dextrose in water (D5W)

 Change in serum sodium from infusing 1 L of D5W = (0 - 200) / (10 kg x 0.6) + 1

 Change in serum sodium from infusing 1 L of D5W = - 28, therefore 1 liter of D5W will lower the serum sodium in this dog by 28 mmol/L

Part 3. The amount b-y which to lower sodium

 Example: 10 kg dog with serum sodium of 200 mEq/L, goal is to lower Na+ to the high end of the reference range (155 mmol/l), therefore sodium needs to be reduced by 45 mEq

Part 4. Fluid dose

 The amount of sodium reduction desired is divided by the amount of reduction that 1 liter of the desired infusate will accomplish to determine the number of liters to administer of the desired fluid type.

 Example: 45 mEq/l desired reduction / 28 mEq/l reduction from 1 L D5W = 1.6 L of D5W needed in this patient.

Part 5. Rate of administration

 If this patient had chronic hypernatremia, the goal for sodium reduction is 0.5 mmol/L/hr. Therefore, the 1.6 L of D5W would be administered over 90 hours. In addition, sodium should be monitored every 6-12 hours to monitor response, and oral water can be administered if there is no restriction to GI intake of water.


1.  Rose BD. Clinical Physiology of Acid-Base and Electrolyte Disorders. 4 ed. New York: McGraw-Hill, 1994;261.

2.  Adrogue HJ, et al. New Engl J Med 2000;342(20):1493

Speaker Information
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Fulton, MO