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Compendium June 2004 (Vol 26, No 6)

Hypernatremia in Critically Ill Cats: Evaluation and Treatment

by Kristen Temo, DVM, Elke Rudloff, DVM, DACVECC, Marla Lichtenberger, DVM, DACVECC, Rebecca Kirby, DVM, DACVIM, DACVECC

    Abstract

    It is vital to recognize trends in critically ill patients. Hypernatremia can arise as a life-threatening complication in many different disease processes and has been observed in critically ill cats. Careful initial evaluation and frequent reassessment of critically ill cats is vital to detect and treat sodium derangements.

    Acute hypernatremia requires immediate treatment. Successful therapeutic intervention depends on early recognition of an increased serum sodium concentration and administration of the correct therapy at the appropriate time and in the proper amount. Understanding normal sodium homeostasis, the mechanisms for alterations in sodium homeostasis in different diseases, and the reasons for resultant fluid shifts is essential for clinicians to formulate a therapeutic plan appropriate to the specific needs of each patient. The therapeutic approach to acute hypernatremia in cats should be individualized and can be determined after identifying the most likely underlying mechanism of the sodium and water disorder (see Figure 1 and Table 2).

    Evaluation

    Hypernatremia may be evident on presenting blood work in critically ill cats or, more com­monly, may appear during the course of therapy. History, physical examination, and initial laboratory evaluation can be used to detect underlying diseases or pathology that may lead to sodium or water imbalance. Carefully monitoring plasma electrolytes and urine specific gravity (USG) throughout hospitalization can lead to early intervention and a successful outcome.

    A thorough history may prompt a careful inves­ti­gation for hypernatremia. Owners may report the ­following in their pets: increased drinking and/or urination suggestive of diabetes mellitus or chronic renal disease, altered mentation, head trauma, diarrhea, vomiting, altered respiration, chronic nasal discharge, and vulvar discharge. These signs may suggest loss of water into a third space (e.g., respiratory or gastrointestinal tract, uterus, peritoneal cavity) from the intravascular, interstitial, or intracellular space. Medications that may influence action or secretion of antidiuretic hormone (ADH) or osmotic agents (e.g., mannitol, glucose) should be promptly discontinued.

    The most consistent physical examination findings suggestive of hypernatremia are dehydration and altered level of consciousness. When plasma sodium concentration increases rapidly and substantially (i.e., >165 mEq/L), signs of shock can include poor peripheral pulses, hypothermia, and prolonged capillary refill time. Carefully palpating the abdomen and examining the rectum may help detect fluid in the bowel or uterus, which suggests additional fluid losses that warrant aggressive volume replacement. Cats with evidence of brain pathology are at risk of developing hypernatremia and should have their electrolyte levels monitored closely.

    The initial complete blood cell count, biochemistry profile, and urinalysis should be evaluated to detect underlying diseases (e.g., diabetes mellitus, renal disease, pyometra, pyelonephritis, acute gastroenteritis) that may be associated with polyuria, third spacing of fluid, persistent vomiting or diarrhea, osmotic diuresis, or gram-negative bacterial infections. Measuring the serum electrolyte level at presentation not only provides a baseline from which to monitor trends of change but can also reveal preexisting hypernatremia that can lead to serious neurologic consequences if fluid resuscitation is administered indiscriminately.

    When hypernatremia persists despite volume replacement and rehydration, evaluation of urine osmolality (uOsm) and plasma osmolarity (pOsm) may be required to determine the underlying cause.1 Hypernatremia has been associated with elevated pOsm. When hypernatremia results from excessive sodium intake or water loss through third spacing of fluid or osmotic diuresis, increased uOsm is expected if ADH production and renal response to ADH are normal. The USG should reflect concentrated urine. Renal medullary washout that results from fluid therapy or underlying renal disease may prevent maximum urine concentration and should therefore be considered when evaluating USG.

    pOsm and uOsm measurements are frequently not available in veterinary patients. In humans, uOsm can be loosely correlated to USG2 (Table 1). This comparison can be made only if no osmotically active molecules such as glucose or mannitol are being excreted in the urine. In the absence of renal medullary washout, this correlation might prove beneficial in cats.

    Cats that present with a normal electrolyte level and head trauma, brain dysfunction, diabetes mellitus, renal failure, gram-negative bacterial infections, and/or gastroenteritis require vigilant monitoring for an increasing plasma sodium concentration throughout hospitalization. Hypernatremia that develops from metabolic causes has most commonly been related to insufficient volume resuscitation from using a fluid containing higher concentrations of sodium during continued, large, hypotonic fluid losses. When iatrogenic and metabolic causes of hypernatremia have been eliminated, an investigation for ADH deficiency must be conducted.

    In critically ill cats, an elevated serum sodium concentration with a dilute USG warrants an investigation for diabetes insipidus (Figure 1). In humans, when hypernatremia (sodium concentration: >145 mEq/L) or elevated pOsm (>295 mOsm/L) occurs despite polyuria and urine hypoosmolality (uOsm: <200 mOsm/kg water), diabetes insipidus is suspected.3,4 Because ADH deficiency can manifest at any time after a head injury, serial testing of serum sodium concentration and uOsm or USG throughout hospitalization in a cat with a head injury can help recognize this life-threatening complication early. In humans with head trauma, laboratory evidence of central diabetes insipidus reportedly occurs between 10 and 240 hours after the initial traumatic event.5,6 However, in the four cats with head injury and hypernatremia that we have seen, hypernatremia occurred 2 to 13 days after the traumatic event. In one cat, the USG measured 1.023.

    Water deprivation testing has been described as the classic diagnostic test for diabetes insipidus but has not been recommended in critically ill cats. Even under ideal circumstances, a specific diagnosis may not be obtained from water deprivation testing alone, and such tests can lead to life-threatening dehydration. In addition, chronic polyuria and medullary washout may prevent the kidneys from optimizing water reabsorption and urine concentration.5

    Partial ADH impairment has been reported in humans, dogs, and cats.5,7 Urine-concentrating abilities in these patients may not exceed 300 mOsm/L during significant dehydration. Water deprivation testing is considered unnecessary in humans who have a lower uOsm than pOsm when pOsm is greater than 295 mOsm/L and serum sodium concentration is greater than 145 mEq/L.8 Finding low serum ADH levels in the presence of high pOsm and low uOsm provides a higher accuracy in diagnosing diabetes insipidus.5 However, ADH levels may not be readily available to most veterinary practitioners.

    Administering exogenous ADH (vasopressin) can be both diagnostic and therapeutic (Table 2). Results of subcutaneously administering vasopressin have proven extremely variable in animals; thus IV aqueous or intranasal administration of vasopressin is preferred.7 In cats, vasopressin should be administered at 0.5 U/kg IM and USG and osmolality values obtained at 0, 30, and 60 minutes. Alternatively, oral tablets are available, as is intranasal desmopressin acetate (100 µg/ml administered in the conjunctival sac [1 to 2 drops, equaling about 1.5 to 4 µg bid for 5 days]). However, when clinical signs are severe and the level of hypernatremia is considered life threatening, IM or IV administration of vasopressin is preferred. If administering either of these drugs results in improved clinical signs, such as a 50% reduced water intake or increased uOsm or USG, a diagnosis of diabetes insipidus can be made.7,9,10

    Treatment

    Figure 1 presents a general diagnostic and therapeutic approach to cats with hypernatremia. Although treating underlying problems (e.g., insulin therapy for diabetes mellitus, managing intracranial pressure or bleeding) is required to prevent or definitively resolve the pathology leading to hypernatremia, this discussion is directed only at treating sodium and water disorders in cats.

    The goal of therapy is to slowly lower the serum sodium concentration while minimizing the rate of transcellular fluid shifts (Figure 2). Intracellular osmolality increases in response to hypernatremia. Lowering the serum sodium concentration or osmolality too rapidly causes fluid to shift into the cells, with subsequent cellular swelling and death. In this case, neurologic signs may worsen with treatment efforts. If hypernatremia is diagnosed or anticipated, all drugs that can interfere with ADH production, release, or action as well as osmotic diuretics must be discontinued immediately. The treatment plan for hypernatremia gives priority to fluid therapy, with careful consideration given to the choice of fluid and rate of administration (Table 2 and Table 3). The fluid therapy plan has two phases: resuscitation of hypovolemic hypernatremia and maintenance of eu­volemic hypernatremia. When central diabetes insipidus has been determined to be the most likely cause of hypernatremia, administering exogenous ADH (vasopressin) may be a necessary part of the maintenance treatment plan for stabilization.

    Resuscitation Phase

    For hypovolemia during hypernatremia, the circulating plasma should be resuscitated using the least amount of fluid possible to correct volume and pressure deficits. Fluid selection depends on whether the fluid deficit is intravascular (due to poor perfusion), interstitial (due to dehydration), or both and whether cardiac dysfunction is contributing to hypotension. To avoid rapid transcellular fluid shifts, using an isosodium fluid is recommended (i.e., the sodium concentration of the fluid administered should be similar to the serum sodium concentration; Table 2).

    Poor perfusion in cats is characterized by weak or absent peripheral pulses, a slow or normal heart rate, hypothermia, depressed mentation, gray mucous membranes, prolonged capillary refill time, and low arterial blood pressure. Careful auscultation of the heart for a murmur, gallop, or arrhythmia and of the thorax for pulmonary edema or pleural fluid can help determine whether cardiac failure is contributing to hypotension. If no abnormalities are auscultated during the initial examination, thoracic radiographs should still be indicated in critically ill cats. It is important to repeat the examination during the fluid resuscitation process to detect volume overload.

    Poor perfusion due to hypovolemia, with normal cardiac function, may benefit from low-volume infusion of high molecular weight synthetic colloids (e.g., hetastarch), titrated to effect, to help retain administered fluids within the intravascular space11 (Table 2). Crystalloids with a relatively higher sodium concentration (e.g., 0.9% sodium chloride [NaCl]) should be administered to begin replacing interstitial volume deficits (Table 3). When cardiac failure is suspected to contribute significantly to hypotension, crystalloids containing a more conservative sodium concentration (e.g., lactated Ringer's solution, Plasmalyte-A, Normosol-R) should be used for resuscitation.

    Maintenance Phase

    Once perfusion and hydration have been restored, an electrolyte panel should be repeated; maintenance fluid selection should be based on these results. If serum sodium levels remain elevated (>160 mEq/L), the solute-free water deficit should be calculated4 (Table 2Figure 1). When a patient has altered mentation, this volume should be replaced over 24 to 48 hours to slowly lower the serum sodium concentration (about 1 to 2 mEq/L/hr) and minimize transcellular fluid shifts. When a patient's mentation is normal, this volume may be replaced more rapidly (over 12 to 24 hours). Maintenance fluid volumes should be administered simultaneously using isotonic crystalloids, and the total volume of fluids administered should meet ongoing losses while preventing fluid overload.

    The most common reason for mild to moderate hypernatremia during hospitalization is that the patient's water intake is failing to meet metabolic needs or correct ongoing losses. Hypernatremia can develop when sufficient water is not available and sodium is reabsorbed by the kidneys. This occurs more frequently when osmotic diuresis associated with diabetes mellitus or third spacing of fluid associated with gastroenteritis or peritonitis is present. Cats with these conditions benefit from administering larger volumes of low-sodium crystalloids and replacing solute-free water as outlined in Table 2 . Hetastarch administered at a maintenance rate can also help maintain intravascular volume despite ongoing crystalloid losses.

    If a cat is isovolemic but has persistent hypernatremia, administering low-dose furosemide (about 0.5 mg/kg IV) may stimulate renal sodium and water excretion. Renal volume loss can simultaneously be replaced using isotonic crystalloids with a lower sodium content (e.g., half-strength lactated Ringer's solution with 2.5% dextrose or 0.45% NaCl with 2.5% dextrose).

    Symptomatic hypernatremia associated with oliguric renal failure may require peritoneal dialysis for slow electrolyte equilibration. The dialysate should contain a sodium concentration similar to that of normal plasma. The technique for peritoneal dialysis in dogs and cats has been described elsewhere.12

    Vasopressin Therapy

    Cats with hypernatremia that is not responsive to adjustments in fluid therapy might benefit from vasopressin administration (Figure 2). Hypernatremia associated with head trauma or brain dysfunction may likely be due to abnormalities of ADH release and receptor responsiveness. In humans who are hypernatremic and hemodynamically unstable, it has been recommended that a vasopressin trial be instituted immediately by continuous IV infusion of aqueous vasopressin (2.5 U/hr; 0.036 U/kg/hr [extrapolated for a 70-kg human]) titrated to obtain a urine output of approximately 100 ml/hr (1.4 ml/kg/hr [extrapolated for a 70-kg human]).13 This type of vasopressin administration has not been described in cats. Aqueous vasopressin administration in cats has been reported as 0.5 U/kg IM, or one to two drops of desmopressin acetate nasal spray in the conjunctival sac, q12h.7,10,14 Overdosing can result in water intoxication (hyponatremia) and reduced renal blood flow, with signs ranging from listlessness or depression to coma and seizures.

    A protocol has been proposed for fluid therapy in humans with head injury to prevent the consequences of rapidly reduced serum sodium concentration15 (Figure 2). Twenty humans with head injury and hypoosmolar urine (suggestive of diabetes insipidus) were administered ADH intravenously and crystalloid infusion in which the sodium content was adjusted every 8 hours to match the patient's serum sodium concentration. If polyuria was observed (i.e., urine output >500 ml/hr or >7 ml/kg/hr), vasopressin (continuous IV infusion 0.02 U/hr or 0.003 U/kg/hr) was administered. The vasopressin dose was increased by 0.05 U/hr (or 0.007 U/kg/hr) until uOsm exceeded pOsm. This protocol has not been reported in treating critically ill hypernatremic cats suspected of having diabetes insipidus. However, it warrants consideration when the serum sodium concentration rises with concurrent low Osm or USG.

    Monitoring

    Closely monitoring physical and biochemical parameters is essential to establish and maintain sodium and water balance in critically ill cats. Physical parameters that reflect perfusion and hydration should be assessed throughout hospitalization and fluid deficits replaced. Central venous pressure can be used to reflect central vascular volume. Deteriorating mentation and neurologic signs during therapy requires reassessment of fluid choice and rate of administration, with adjustments made as indicated. Serum electrolyte levels and renal parameters reflect the progress made during therapy. Measuring water intake and urine output as well as uOsm and/or USG can reveal polyuria, polydipsia, and hyposthenuria associated with abnormal ADH mechanisms and excessive water loss, which require interventional therapy.

    Downloadable PDF

    1. Palevsky PM: Hypernatremia. Semin Nephrology 18(1):20-30, 1998.

    2. Rose BD, Post T: Clinical Physiology of Acid-Base and Electrolyte Disorders, ed 5. New York, McGraw-Hill, 2001.

    3. Kern KB, Meislin HW: Diabetes insipidus: Occurrence after minor head trauma. J Trauma 24(1):69-72, 1984.

    4. Geheb MA: Clinical approach to the hyperosmolar patient. Crit Care Clin 5:797-815, 1987.

    5. Ober KP: Diabetes insipidus. Crit Care Clin 7(1):109-125, 1991.

    6. Keren G, Barzilay Z, Schreiber M, et al: Diabetes insipidus indicating a dying brain. Crit Care Med 10:798-799, 1982.

    7. Feldman EC, Nelson RW: Canine and Feline Endocrinology and Reproduction, ed 2. Philadelphia, WB Saunders, 1996.

    8. Blevins LS, Wand GS: Diabetes insipidus. Crit Care Med 20(1):69-79, 1992.

    9. Nichols R, Thompson L: Pituitary-hypothalamic disease, in Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine. Philadelphia, WB Saunders, 1995, pp 1422-1436.

    10. Plumb DC: Veterinary Drug Handbook. Ames, Iowa State University Press, 1999.

    11. Rudloff E, Kirby R: The critical need for colloids: Maintaining fluid balance. Compend Contin Educ Pract Vet 19(6):705-718, 1997.

    12. Garcia AM, Rudloff E, Kirby R: Peritoneal dialysis: Not just for renal failure. Compend Contin Educ Pract Vet 24(10):758-770, 2002.

    13. Levitt MA, Fleischer AS, Meislin HW: Acute post-traumatic diabetes insipidus: Treatment with continuous intravenous vasopressin. J Trauma 24(4):532-535, 1984.

    14. Kraus KH: The use of desmopressin in diagnosis and treatment of diabetes insipidus in cats. Compend Contin Educ Pract Vet (9)7:752-758, 1987.

    15. Mizobata Y, Yokota J, Matsuoka T, et al: Volume supplementation with iso-sodium solution prevents hypernatremia after head injury. J Trauma 50(5):871-877, 2001.

    References »

    NEXT: Hypernatremia in Critically Ill Cats: Pathophysiology

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