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Featured, Insights in Electrolyte Disorders, Internal Medicine

Evaluation and Management of the Hypernatremic Patient

Acute salt toxicity resulting from the ingestion of large amounts of sodium chloride is a potential cause of hypernatremia.

Justin Heinz DVM, DACVECC

Dr. Heinz obtained his DVM from Purdue University. He completed an internship at LSU and a residency in emergency and critical care at Texas A&M University. After a year in private referral practice, Dr. Heinz joined the faculty at Texas A&M College of Veterinary Medicine & Biomedical Sciences. His clinical interests include transfusion medicine, sepsis, acute kidney injury, and renal replacement therapies.

Audrey CookBVM&S, MSc VetEd, MRCVS, DACVIM-SAIM, DECVIM-CA, DABVP (Feline)

Dr. Audrey Cook is a graduate of the University of Edinburgh. She completed an internship at NCSU and a residency in internal medicine at UC Davis. She is a Diplomate of the American and European Colleges of Veterinary Internal Medicine, and is one of the few internists with additional board certification in Feline Practice. After a decade in private referral practice, Dr. Cook joined the faculty at Texas A&M College of Veterinary Medicine. She is currently Professor and Chief of the Internal Medicine Service. Her clinical interests include canine and feline endocrinology and gastroenterology.

Evaluation and Management of the Hypernatremic Patient
Alex Zotov/shutterstock.com

Sodium (Na) is the most abundant extracellular fluid cation and the primary determinant of extracellular fluid osmolality.1 Serum sodium concentration (i.e., [Na]) is regulated by antidiuretic hormone (promotes renal water reclamation), thirst (drives water intake), and aldosterone (promotes renal sodium reabsorption). Hypernatremia is defined as a plasma or serum [Na] above the reference range and reflects the loss of water in excess of sodium, or the addition of sodium in excess of water. In healthy animals, central osmoreceptors will detect the associated increase in osmolarity and trigger water-seeking behaviors and antidiuretic hormone release. A patient with hypernatremia therefore must be unable or unwilling to consume adequate amounts of water or unable to retain adequate water. An [Na] measurement of 3 to 4 mmol/L above normal is of little concern, but [Na] >160 mmol/L should be specifically addressed. 

CAUSES OF HYPERNATREMIA

Addition of Sodium

The most common cause of true sodium excess is injudicious fluid therapy, in particular the prolonged administration of replacement fluids.2 Lactated Ringer’s solution administered at a maintenance rate provides 16 times the average animal’s daily sodium need. If water is provided, [Na] should stay within the reference range, but some patients are too anxious or otherwise compromised to take in sufficient water. The kidneys will attempt to mitigate hypernatremia by increasing sodium excretion, but these adaptations are modest, particularly if water intake is limited.

Salt toxicity reflects the ingestion of large amounts of sodium chloride (NaCl); the acute toxic dose in dogs is approximately 4 g/kg.3 This is rare but has been reported in dogs that drink from saltwater pools and oceans or secondary to the administration of saltwater to trigger emesis.4 Ingestion of homemade Play-Doh, which contains high concentrations of table salt, has also been associated with hypernatremia.5

Hyperaldosteronism is uncommonly associated with hypernatremia but should be considered if serum potassium concentration (i.e., [K]) is concurrently subnormal (typically <3 mmol/L).6

Water Loss

A substantial pure water loss occurs in patients with central or nephrogenic diabetes insipidus. Patients with other polyuric conditions such as acute kidney injury or liver dysfunction may also become hypernatremic, along with those on high doses of diuretics such as mannitol or furosemide.7 Vomitus and diarrhea have an [Na] of approximately 70 mmol/L; therefore, substantial gastrointestinal fluid loss (without compensatory water intake) may result in hypernatremia.

Hypodipsic Disorders

Various central nervous system disorders can result in inadequate water intake (hypodipsia).8,9 Affected animals do not experience feelings of thirst or lack the cognitive function needed to seek and ingest water.

Pseudohypernatremia

Depending on the methodology used, hypoproteinemia can cause spurious hypernatremia.10 If necessary, serum [Na] should be verified using a direct ion selective electrode.1

CONSEQUENCES OF HYPERNATREMIA

Acute hypernatremia (i.e., occurring over ≤24 hours) causes cellular shrinkage but is particularly deleterious within the central nervous system, with widespread intracranial hemorrhages and irreversible brain injury. Clinical signs are not usually noted until [Na] is >170 mmol/L.3 Patients can be profoundly obtunded or twitching, or they may present with seizures and hyperthermia. Massive oral salt intake also results in gastrointestinal upset, which may cause confusion regarding the etiology of the hypernatremia.4

In contrast, chronic hypernatremia (i.e., lasting for >24 hours) is often well tolerated because it triggers the production of osmotically active chemicals (“idiogenic” osmoles) within neurons.11 These prevent the efflux of water and maintain normal cellular volume. However, rapid correction of established hypernatremia can be problematic, as water will be drawn into the intracellular compartment and result in cerebral edema with potentially devastating consequences. 

INITIAL PATIENT ASSESSMENT

Owners should be questioned regarding their pet’s current medical therapy; recent water intake and urine output; gastrointestinal status, including any vomiting or diarrhea; and the potential for exposure to sources of salt or saltwater. The physical examination should include an assessment of the patient’s general status and neurologic function, along with an estimation of hydration status. It can be challenging to identify subtle (<5%) dehydration or volume overload; clinicians should pay close attention to skin turgor and recent changes in body weight. If necessary, the fractional excretion of sodium (FeNa) can be used to differentiate patients with sodium excess (FeNa ≥2%) versus those with hypernatremia secondary to hypotonic fluid loss (FeNa <2%):1

FeNa = 100 × {(Urine [Na] × Plasma [creatinine])/(Plasma [Na] × Urine [creatinine])} 

It is important to bear in mind that this calculation is unreliable in patients being treated with diuretics or fluid therapy and those with chronic kidney disease or urinary tract obstruction.

See FIGURE 1 for an algorithm showing evaluation of the hypernatremic patient.

TREATMENT OF HYPERNATREMIA

If a hypernatremic patient presents with signs of shock and an obvious need for resuscitative fluids, the safest option is to administer a fluid with [Na] within 10 mmol/L of the patient’s measured serum [Na]. Physiologic saline (0.9% NaCl) has an [Na] of 154 mmol/L and is an acceptable option if the patient’s [Na] is ≤164 mmol/L. If necessary, a suitable fluid can be created by adding hypertonic saline (e.g., 3%; [Na] = 513 mmol/L) to a replacement fluid. This approach will mitigate issues related to ineffective perfusion but is unlikely to cause a significant shift in [Na]. The impact of fluid administration can be calculated using the Adrogué-Madias formula:12

Expected change in [Na] with 1 liter of fluids = (Fluid [Na + K] – Patient [Na])/(TBW + 1)

TBW = Total body water = Weight in kg × 0.6

Some versions of this formula discount the K contribution because this is negligible in unsupplemented, replacement-type fluids.

In hemodynamically stable patients, the first step is to determine the free water deficit (FWD):

FWD (in liters) = {(Patient [Na] – Target [Na])/Target [Na]} × TBW

Target [Na] = Midrange of the reference interval

It is important to note that dehydration and body composition (i.e., lean versus fatty tissue) can impact TBW estimation.13 Calculations of FWD that rely on measurements of plasma osmolality may be more reliable but require access to specialized equipment. 

The time required to replace the FWD depends on chronicity of the hypernatremia, with a target decrease in [Na] of 1 mmol/hr in acute cases and 0.5 mmol/hr in chronic cases:1

FWD replacement time (hr) for acute hypernatremia = Patient [Na] – Target [Na] 

FWD replacement time (hr) for chronic hypernatremia = (Patient [Na] – Target [Na]) × 2

If other fluids are not needed, the FWD should be replaced using 5% dextrose.

Concurrent dehydration can be simultaneously addressed using a standard buffered replacement fluid; this volume deficit should ideally be corrected over at least 12 hours. Bear in mind that the [Na] of this fluid may be substantially lower than that of the patient, and it may provide a small amount of free water. Maintenance needs should also be included in any fluid plan; the composition of this component should be carefully considered because any free water will also contribute to changes in the patient’s serum [Na]. As a general rule, drinking water should be limited until the patient’s serum [Na] is close to the target value.

Creating an appropriate plan can be challenging in patients with multiple needs (i.e., free water, volume replacement, and maintenance). It can be simpler to determine the total volume of fluid needed over a fixed time period and then decide the appropriate fluid [Na] to meet these requirements by reworking the Adrogué-Madias formula:

Fluid [Na + K] = Patient [Na] – {TD × (TBW + Volume of fluid in liters)}

TD = Target decrease in patient [Na]

Because factors such as obesity and ongoing losses can impact the reliability of the assumptions behind these calculations, serum [Na] should be rechecked every 4 to 6 hours. Clinical signs associated with too rapid a drop in [Na] and cerebral edema include obtundation, limb rigidity, and seizures. Cerebral edema should be immediately addressed with mannitol (0.5 g/kg IV over 15 to 20 minutes); 3% NaCl (3 to 5 mL/kg IV over 15 to 20 minutes) may be used if mannitol is unavailable. The fluid plan should then be adjusted to slow down the rate of decrease in [Na]. The therapeutic objective in treating chronic hypernatremia is to raise the serum [Na] no more than 8 to 12 mm/L during the first 24 hours and then continue with slow correction with close monitoring over the next 24 to 48 hours.

See FIGURE 2 for an algorithm of the management of the hypernatremic patient.

CASE SCENARIO

History

A 10-year-old spayed female domestic shorthair cat was evaluated for a 3-day history of anorexia, hiding, and vomiting. A tentative diagnosis of pancreatitis was made, and 150 mL of 0.9% NaCl was administered subcutaneously. The cat was discharged with transmucosal buprenorphine, and the owner was instructed to administer 150 mL of 0.9% NaCl SC q24hr. Four days later, the cat was presented to an emergency hospital with persistent anorexia and vomiting; she had not been observed to drink since last examined and had only urinated 5 times. On presentation, she weighed 3.6 kg and was assessed to be 8% dehydrated. Serum [Na] was 167 mmol/L (reference range, 144 to 155 mmol/L); [K] was 3.5 mmol/L (reference range, 3.5 to 5.1 mmol/L).

Assessment

This cat was probably somewhat volume depleted when initially evaluated. This loss was replaced with a fluid containing 154 mmol/L of sodium. In addition to ongoing hypotonic losses through vomiting, this cat was expected to lose approximately 1 mL/kg/hr (i.e., ≈90 mL/day) of pure water across her respiratory tract. Because the cat was persistently hypodipsic, she was unable to balance the surplus sodium provided by the repeated doses of 0.9% NaCl with adequate amounts of water and became progressively hypernatremic. Furthermore, robust aldosterone secretion in response to hypovolemia would have furthered the cat’s renal tubular sodium retention. It is not unusual for sick/painful/stressed cats to fail to drink enough water to meet their physiologic needs.

Calculations

Target [Na]: 150 mmol/L

TBW: Weight in kg × 0.6 = 3.6 × 0.6 = 2.16 L
(Note: This will change when the cat is rehydrated.)

FWD: {(Patient [Na] – Target [Na])/Target [Na]} × TBW = {(167 – 150)/150} × 2.16 = 0.245 L (245 mL)

Target time to replace FWD: (Patient [Na] – Target [Na]) × 2 = (167 – 150) × 2 = 34 hr

Volume of free water/hr: FWD/Target time = 245/34 ≈ 7 mL/hr

Patient’s volume deficit: % dehydration × Weight in kg = 0.08 × 3.6 = 0.288 L (288 mL)

Target time to replace volume deficit: 12 hours

Rate to address volume deficit: Deficit/Target time = 288/12 = 24 mL/hr

Maintenance fluid need: Weight in kg0.75 × 70 = 183 mL/day ≈ 8 mL/hr

For the first 12 hours:

Total volume needed: (24 mL for replacement + 8 mL for maintenance) × 12 = 384 mL (0.384 L)

Target decrease in [Na] over 12 hours: 0.5 × 12 = 6 mmol

Adrogué-Madias formula to predict appropriate [Na] in the fluid: Fluid [Na + K] = Patient [Na] – {TD × (TBW + Volume of fluid in liters)} = 167 – {6 × (2.16 + 0.384)} = 167 – 15.3 = 152 mmol/L

As this patient’s [K] is 3.5 mmol/L, we need to provide 20 mmol of potassium chloride (KCl)/L.

Fluid [Na]: 152 – 20 = 132 mmol/L

Lactated Ringer’s solution has a sodium of 130 mmol/L; therefore, this would be an appropriate choice for this cat.

Plan: Lactated Ringer’s solution plus 16 mEq/L of KCl at 32 mL/hr

After the first 12 hours:

Hydration is adequate.

New weight: 3.9 kg; [Na] = 161 mmol/L; [K] = 3.6 mmol/L

TBW: 3.9 × 0.6 = 2.34 L

FWD: {(161 – 150)/150} × 2.34 = 0.172 L (172 mL)

Time to replace FWD: (161 – 150) × 2 = 22 hr

Plan: Dextrose 5% plus 20 mEq/L of KCl at 8 mL/hr

Note: These calculations are designed to provide an appropriate starting point, but an individual patient’s response may differ significantly from the calculated course. Frequent monitoring and adjustments are therefore necessary. 

References

1. DiBartola SP. Disorders of sodium and water: hypernatremia and hyponatremia. In: Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice. 4th ed. St. Louis, MO: Saunders Elsevier; 2011:45-75.

2. Ueda Y, Hopper K, Epstein SE. Incidence, severity and prognosis associated with hypernatremia in dogs and cats. J Vet Intern Med. 2015;29(3):794-800. doi: 10.1111/jvim.12582

3. Thompson LJ. Sodium chloride (salt). In: Gupta RC, ed. Veterinary Toxicology: Basic and Clinical Principles. 3rd ed. St. Louis, MO: Elsevier; 2018:476-482.

4. Khanna C, Boermans HJ, Wilcock B. Fatal hypernatremia in a dog from salt ingestion. JAAHA 1997;33(2):113-117. doi: 10.5326/15473317-33-2-113

5. Barr JM, Khan SA, McCullough SM, Volmer PA. Hypernatremia secondary to homemade play dough ingestion in dogs: a review of 14 cases from 1998 to 2001. J Vet Emerg Crit Care. 2004;14(3):196-202. doi: 10.1111/j.1534-6935.2004.04027.x

6. Ash RA, Harvey AM, Tasker S. Primary hyperaldosteronism in the cat: a series of 13 cases. J Feline Med Surg. 2005;7(3):173-182. doi: 10.1016/j.jfms/2004.08.007

7. Guillaumin J, DiBartola SP. A quick reference on hypernatremia. Vet Clin North Am Small Anim Pract. 2017;47(2):209-212. doi: 10.1016/j.cvsm.2016.10.002

8. Bach J, Claus K. Primary hypodipsia in a cat with severe hypernatremia. J Feline Med Surg. 2014;16(3):240-242. doi: 10.1177/1098612X13515260

9. Miyama TS, Iwamoto E, Umeki S, et al. Magnetic resonance imaging and clinical findings in a miniature Schnauzer with hypodipsic hypernatremia. J Vet Med Sci. 2009;71(10):1387-1391. doi: 10.1292/jvms.001387

10. Evans SJM, Truelove MP, Tebbe NA, et al. Formulae to correct sodium concentrations for serum water fraction in cases of hypo- and hyperproteinemia in cats. Vet Clin Pathol. 2020;49(1):100-105. doi: 10.1111/vcp.12833

11. Wilson CS, Mongin AA. Cell volume control in healthy brain and neuropathologies. Curr Top Membr. 2018;81:385-455. doi: 10.1016/bs.ctm.2018.07.006

12. Adrogué HJ, Madias NE. Aiding fluid prescription for the dysnatremias. Intensive Care Med. 1997;23(3):309-316. doi: 10.1007/s001340050333

13. Cheuvront SN, Kenefick RW, Sollanek KJ, et al. Water-deficit equation: systematic analysis and improvement. Am J Clin Nutr. 2013;97(1):79-85. doi: 10.3945/ajcn.112.046839

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