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Compendium April 2009 (Vol 31, No 4)


by Catherine Kasai, Robert King

    CETEST This course is approved for 3.0 CE credits

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    Salt toxicity can be fatal in dogs and cats. Whether toxicity occurs accidentally or iatrogenically, it is important to recognize the clinical signs of sodium toxicosis, which are mainly caused by hypernatremia and associated cerebral edema. Treatment involves prompt initiation of fluid therapy along with careful monitoring of neurologic status, serum and plasma electrolytes, and serum osmolarity. Salt was once recommended as an emetic for dogs and cats but has fallen out of favor because of the lethal complications that can arise from overzealous administration.

    Table salt (sodium chloride) was once recommended in the human medical and veterinary communities as an emetic agent. Older literature and some current information sources (e.g., the Internet) include statements regarding the use of table salt to induce vomiting in dogs and cats. Table salt taken orally causes pharyngeal irritation, which can lead to emesis.1 However, salt ingestion does not consistently produce emesis, and multiple cases have been reported in the veterinary and human literature in which the use of table salt and salt water led to acute hypernatremia followed by sodium toxicosis and death.2 As a result, sodium chloride is no longer recommended as an emetic in animals or humans.1,3,4

    Sodium toxicosis can also occur with ingestion of homemade modeling dough,1,5 seawater,6 or sodium chloride-containing ice-melt products7 and in the hospital setting after administration of hypertonic saline solution or resuscitation with intravenous (IV) sodium bicarbonate.8 BOX 1  provides a quick reference for the amounts of sodium and chloride in various forms of salt. In dogs, a sodium chloride dose of 2 to 3 g/kg (87 to 130 mmol/kg) has been shown to cause signs of toxicosis, whereas a dose of 4 g/kg (174 mmol/kg) is lethal.5,9 Hypernatremia is defined as a serum sodium concentration greater than 155 mEq/L in dogs and greater than 162 mEq/L in cats.8 Sodium levels that exceed 170 mEq/L usually result in neurologic signs in animals with acute hypernatremia of less than 4 hours' duration.8-10


    Hypernatremia can be classified as hypervolemic, euvolemic-isovolemic, or hypovolemic8-10 (TABLE 1).

    Hypervolemic Hypernatremia

    Salt intoxication increases the amount of sodium in the extracellular fluid space, causing a hyperosmolar state. As a result, the body moves water from the intracellular fluid space to the extracellular fluid space to restore osmotic equilibrium. This movement of fluid results in hypervolemia. The extracellular fluid compartment expands with the fluid shift, and in animals with a compromised cardiovascular system, the fluid can move into the interstitium of the lungs, leading to pulmonary edema.8 Other conditions (e.g., hyperaldosteronism, hyperadrenocorticism) can also cause hypervolemic hypernatremia.8,9

    Euvolemic-Isovolemic Hypernatremia

    Euvolemic or isovolemic hypernatremia occurs when there is water loss without significant electrolyte loss.8-10 For example, there may be excessive water loss from the lungs or skin in hot, dry climates.8 Dehydration can also occur during febrile illness or due to inadequate water intake caused by central nervous system depression or lack of access to water.8 This form of hypernatremia is readily corrected by providing ample access to water and addressing defects in the thirst mechanism.

    Hypovolemic Hypernatremia

    Hypovolemic hypernatremia occurs with severe water loss (e.g., vomiting, diarrhea, use of loop diuretics, nonoliguric acute renal failure, chronic renal failure).8,10 In these situations, the animal is not able to replace large amounts of hypotonic fluid and loses normal body osmolality.9 Hypotension results from water and salt loss from the extracellular space, which causes contraction of extracellular fluid volume.9


    In a hypernatremic animal, water leaves the intracellular space to correct the osmotic difference between the intracellular and extracellular compartments. This results in cellular shrinkage and crenation. Due to fine vascular attachments to the calvarium, the brain is most vulnerable to shrinkage.9 Brain shrinkage can lead to subarachnoid and subcortical hemorrhages, vascular rupture with cerebral bleeding, subdural hematomas, venous thrombosis, infarction of the cerebral vessels, permanent neurologic damage, and death.9,11

    In cases of chronic hypernatremia, the brain promptly produces three major groups of organic osmolytes or idiogenic osmoles (amino acids [e.g., glutamine, glutamate, taurine], polyols [e.g., myoinositol], and methylamines [e.g., phosphocreatinine]) to counteract shrinkage of the brain cells and restore lost water.8,9,11 Animals that are producing osmolytes may have no neurologic signs.8 Osmoles allow the brain cells to maintain water balance in the presence of peripheral sodium elevation. Production of idiogenic osmoles starts soon after the onset of hypernatremia.9 In a study of rabbits and rats, production of idiogenic osmoles began as early as 1 hour after the hypernatremic insult.12 In one rabbit population, the concentration of amino acids and idiogenic osmoles in the brain accounted for 42% to 49% of the total increase in brain osmolality 1 to 4 hours after the induction of hypernatremia.12 In another rabbit population in the same study, the higher levels of amino acids and idiogenic osmoles accounted for 71% of the total increase in brain osmolality after 1 week of hypernatremia.12 When osmolytes are present during chronic hypernatremia, free water must be reintroduced slowly to allow the brain cells to reequilibrate the water they contain.8-11 Introducing water too rapidly can cause brain cells to swell and lead to severe cerebral edema, convulsions, and death.8-11 The rate at which the idiogenic osmolyte levels in the brain return to normal varies depending on the osmolyte.13

    Clinical Signs

    Signs of acute hypervolemic hypernatremia are related to central nervous system dysfunction caused by loss of water from the brain cells and brain shrinkage.8,9,11 The earliest clinical signs include lethargy, depression, and inappropriate vocalization. Signs progress to muscle rigidity, tremors, myoclonus, and generalized hyperreflexia.9 Seizures, coma, and death will follow if appropriate therapy is not instituted. Signs of chronic hypervolemic hypernatremia tend to be similar to those seen with acute disease, but they may be less dramatic due to the presence of idiogenic osmoles in the brain.

    Diagnostic Evaluation

    The initial evaluation in cases of suspected salt toxicity includes obtaining a thorough history from the owner (including environment and access to water), performing a physical examination, and conducting tests, including a complete blood count, a complete chemistry panel with electrolyte levels, and urinalysis. Patients with hypernatremia may have erythrocytes that appear crenated on peripheral blood smear assessment.

    The following formula may be applied to calculations of plasma osmolality:

    In this equation, conversion factors of 2.8 and 18 are used to convert urea and glucose, respectively, from mg/dL to mmol/L.  BOX 2 gives a clinical example of calculation and use of plasma osmolality.

    Gross and Histologic Changes

    Cerebral and pulmonary edema can be seen on gross necropsy of animals that die of hypernatremia (BOX 3). Histopathologic changes in the central nervous system include intracranial hemorrhage, hematoma, thrombosis, infarction, and various degrees of edema. Vascular congestion, hemorrhage, and perivascular hemorrhage may also be evident in the brain, lungs, liver, and kidneys.3,12,13


    The goal of treatment for hypervolemic hypernatremia is to bring sodium levels back into the normal range without causing adverse neurologic signs. If the animal is conscious and able to drink and swallow, oral water replacement is preferred9; hypernatremia is rare in healthy animals with free access to fresh water. The volume and rate of free water replacement are similar to those for intravenous fluid administration. The total replacement volume should be divided into small amounts given frequently throughout the day.9 Ideally, the speed at which sodium levels are corrected should parallel the speed of hypernatremia onset.

    Acute Hypervolemic Hypernatremia

    It is very important to note that the treatment for acute hypervolemic hypernatremia (less than 2 to 4 hours since salt ingestion or administration) is different from that for chronic hypervolemic hypernatremia (more than 4 hours since salt ingestion or administration). If sodium ingestion is known to be acute, rapid correction of sodium levels improves the outcome. These patients have not had a chance to form idiogenic osmoles; therefore, a rapid decrease of peripheral osmolarity to normal will not result in fluid movement into the brain.11

    In animals with no access to fresh water or with impaired thirst or swallowing mechanisms, IV fluids should be started immediately. Patients must be monitored carefully during the fluid therapy for any change in neurologic status. It is recommended that the serum or plasma sodium concentration be reduced at a rate of not more than 1 to 2 mEq/L/hr.11,14 Administration of 5% dextrose in water (D5W) solution combined with a loop diuretic (e.g., furosemide) facilitates the excretion of sodium. In addition to the water already present in the solution, D5W serves to replace free water when the glucose enters the cells and is metabolized into carbon dioxide and water.

    Chronic Hypervolemic Hypernatremia

    Patients with chronic hypervolemic hypernatremia may have a significant concentration of idiogenic osmoles in their brain that could promote cerebral edema if the sodium balance is corrected too quickly. Therefore, these patients should be treated more cautiously with a sodium correction rate of not more than 0.5 mEq/L/hr.8 The following formulas can be used to calculate the fluid rates for both acute and chronic conditions, using the selected infusate (TABLE 2).  BOX 2 provides a clinical example.

    A factor of 0.6 is used because water makes up 60% of the animal's body weight.

    A sampling catheter should be placed in a jugular or saphenous vein to allow fluid administration and more convenient access for repeated blood sampling. The plasma sodium level should be checked every 2 to 4 hours if the animal can tolerate multiple samplings.

    Fluid correction is more complex in hypervolemic hypernatremic patients with pulmonary edema because of the increased fluid volume in the pulmonary interstitium. Treatment with water or hypotonic fluids will expand the extracellular compartment and worsen pulmonary edema. To balance the increase in extracellular fluid and decrease the sodium content, a loop diuretic (e.g., furosemide, 2 to 4 mg/kg three times a day for dogs and 1 to 4 mg/kg one to three times a day for cats) given orally, IV, or subcutaneously may be used in conjunction with IV fluid therapy.9 Fluid choices for hypervolemic hypernatremic patients are listed in TABLE 2 .

    Animals with heart failure or oliguric renal failure and hypernatremia may develop volume overload resulting in pulmonary edema and thus would benefit from the use of loop diuretics.10

    Gastrointestinal Tract Decontamination

    Due to the severe neurologic signs and mortality that can arise from sodium toxicosis, current literature no longer recommends using table salt as an emetic for gastrointestinal decontamination after toxin ingestion. Alternative decontaminants have been shown to more safely promote emesis in dogs and cats1 (TABLE 3). When gastrointestinal decontamination is necessary, practitioners must thoroughly evaluate the animal and substance ingested to choose the appropriate emetic. If activated charcoal products containing sorbitol are used during the gastrointestinal decontamination process, hydration status should be monitored closely, as sorbitol-containing products have been found to cause hypernatremia and dehydration in people.1


    Sodium toxicosis in small animals, although rare, can lead to death if not treated promptly and appropriately. It is important to recognize the signs of hypernatremia and to obtain a detailed history from the owner to ensure timely initiation of therapy. Patients with acute hypervolemic hypernatremia should be distinguished from those with chronic hypervolemic hypernatremia because the treatment protocols are very different. Animals undergoing treatment to correct acute or chronic hypervolemic hypernatremia should have sodium levels and plasma osmolality checked every 2 hours and monitored closely during and after therapy. In toxicity cases that require an emetic for decontamination, the use of an emetic other than table salt is urged to prevent iatrogenic hypernatremia.

    Downloadable PDF

    1. Rosendale ME. Decontamination strategies. Vet Clin North Am Small Anim Pract 2002;32:311-321.

    2. Johnston JG, Robertson WO. Fatal ingestion of table salt by an adult. West J Med 1977;126:141-143.

    3. Tí¼rk EE, Schulz F, Koops E, et al. Fatal hypernatremia after using salt as an emetic—report of three autopsy cases. Legal Med 2005;7:47-50.

    4. Casavant MJ, Fitch JA. Fatal hypernatremia from saltwater used as an emetic. J Toxicol Clin Toxicol 2003;41(6):861-863.

    5. Barr JM, Khan SA, McCullough SM, et al. Hypernatremia secondary to homemade play dough ingestion in dogs: a review of 14 cases from 1998-2001. J Vet Emerg Crit Care 2004;14(3):196-202.

    6. Ellis RJ. Severe hypernatremia from sea water ingestion during near-drowning in a hurricane. West J Med 1997;167:430-433.

    7. Foss TS. The hazards of ice melts to dogs and cats. Vet Tech 2002;23(2):94-95.

    8. DiBartola SP. Disorders of sodium and water: hypernatremia and hyponatremia. Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice. 3rd ed. St. Louis: Saunders Elsevier; 2006:47-79.

    9. Hardy RM. Hypernatremia. Vet Clin North Am Small Anim Pract 1989;19(2):231-240.

    10. Marks S, Taboada J. Hypernatremia and hypertonic syndromes. Vet Clin North Am Small Anim Pract 1998;28(3):533-543.

    11. Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med 2000;324(20):1493-1499.

    12. Ayus JC, Armstrong DL, Arieff AI. Effects of hypernatraemia in the central nervous system and its therapy in rats and rabbits. J Physiol 1996;492:243-255.

    13. Lee JH, Arcinue E, Ross BD. Organic osmolytes in the brain of an infant with hypernatremia. N Engl J Med 1994;331(7):439-442.

    14. Pouzot C, Descone-Junot C, Loup, J, et al. Successful treatment of severe salt intoxication in a dog. J Vet Emerg Crit Care 2007;17(3):294-298.

    References »

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