Which clinical manifestations would the nurse monitor for potential development in a patient with hyponatremia?

Hypovolemic hyponatremia develops as sodium and free water are lost and replaced by inappropriately hypotonic fluids, such as tap water, half-normal saline, or dextrose in water. Sodium can be lost through renal or nonrenal routes. Nonrenal routes include GI losses, excessive sweating, third spacing of fluids (eg, ascites, peritonitis, pancreatitis, burns), and cerebral salt-wasting syndrome.

• Excess fluid losses (eg, vomiting, diarrhea, excessive sweating, GI fistulas or drainage tubes, pancreatitis, burns) that have been replaced primarily by hypotonic fluids

• Salt-wasting nephropathy

Cerebral salt-wasting syndrome seen in patients with traumatic brain injury, aneurysmal subarachnoid hemorrhage, and intracranial surgery. Cerebral salt-wasting must be distinguished from SIADH because both conditions can cause hyponatremia in neurosurgical patients, and yet the pathophysiology and treatment are different. [12]

Prolonged exercise in a hot environment, especially in patients who hydrate aggressively with hyposmolar fluids during exertion, is another cause of hyponatremia. Severe symptomatic hyponatremia has been reported in marathon runners and in recreational hikers in the Grand Canyon.

A study by Giordano et al found a significant increase in the prevalence of hyponatremia in elderly patients visiting a university hospital emergency department during the summer. Prevalence during the summer was 12.5% (zenith) in the elderly, compared with a mean monthly prevalence of 10.3% in these patients. The investigators suggested that factors such as reduced renal function, salt loss, a decline in salt intake, and increased water ingestion may play a role in the increased prevalence of hyponatremia in the elderly during hot-weather months. [13]

Similarly, a study by Huwyler et al found an increased incidence of adult patients with profound hyponatremia in a university hospital emergency department during the summer (1.29%, compared with 0.54% in the winter). Based on multivariate analysis, the investigators reported that the rise in incidence was related to patient age, the presence of psychiatric disorders, and the use of diuretics (either potassium-sparing or thiazide). [14]

Euvolemic hyponatremia implies normal sodium stores and a total body excess of free water. This occurs in patients who take in excess hypotonic fluids.

• Psychogenic polydipsia, often in psychiatric patients

• Administration of hypotonic intravenous or irrigation fluids during procedures or in the immediate postoperative period [15, 16]

• In one meta-analysis, administration of hypotonic maintenance intravenous fluids to hospitalized children has been associated with an increased incidence of acute hyponatremia compared with administration of isotonic maintenance fluids. [17]

• Infants who may have been given inappropriate amounts of free water

• Ingestion of sodium phosphate or sodium picosulfates and magnesium citrate combination as a bowel preparation before colonoscopy or colorectal surgery [18]

Hypervolemic hyponatremia occurs when sodium stores increase inappropriately. This may result from renal causes such as acute or chronic renal failure, when dysfunctional kidneys are unable to excrete the ingested sodium load. It also may occur in response to states of decreased effective intravascular volume. History of hepatic cirrhosis, congestive heart failure, or nephrotic syndrome, in which patients are subject to insidious increases in total body sodium and free water stores

• Uncorrected hypothyroidism or cortisol deficiency (adrenal insufficiency, hypopituitarism)

• Consumption of large quantities of beer or use of the recreational drug MDMA (ecstasy)

Hyponatremia can be caused by many medications. Known offenders include acetazolamide, amiloride, amphotericin, aripiprazole, atovaquone, thiazide diuretics, amiodarone, basiliximab, angiotensin II receptor blockers, angiotensin-converting enzyme inhibitors, bromocriptine, carbamazepine, carboplatin, carvedilol, celecoxib, cyclophosphamide, clofibrate, desmopressin, donepezil, duloxetine, eplerenone, gabapentin, haloperidol, heparin, hydroxyurea, indapamide, indomethacin, ketorolac, levetiracetam, loop diuretics, lorcainide, mirtazapine, mitoxantrone, nimodipine, oxcarbazepine, opiates, oxytocin, pimozide, propafenone, proton pump inhibitors, quetiapine, sirolimus, ticlopidine, tolterodine, vincristine, selective serotonin reuptake inhibitors, sulfonylureas, trazodone, tolbutamide, venlafaxine, zalcitabine, and zonisamide. [19]

In the aforementioned Swiss-Austrian study, major risk factors for hyponatremia in emergency patients with AKI included the use of potassium-sparing or thiazide diuretics, a medical cause for emergency referral, and AKI stage. [4]

A study by Poddighe of 328 pediatric emergency department patients indicated that a systemic inflammatory condition is associated with mild hyponatremia during acute illnesses, finding, in the 98 patients determined to have (mostly mild) hyponatremia, a link between lower plasma sodium levels and higher levels of C-reactive protein. [20]

Overall, the above causes are not mutually exclusive, with hyponatremia often resulting from multiple factors. [21]

Sodium is an electrolyte that helps maintain the volume and concentration of extracellular fluid and affects water distribution between intracellular fluid and extracellular fluid. It is vital in the generation and transmission of nerve impulses, muscle contractility, and the regulation of acid-base balance. 

The ratio of sodium to water is reflected by the serum sodium level. Changes in the serum sodium level can indicate primary sodium imbalance, primary water imbalance, or both. 

Hypernatremia or elevated serum sodium greater than 145 mEq/L occurs when there is excess water loss, inadequate water intake, or excess sodium gain. This condition causes hyperosmolarity, making the patient excessively thirsty. 

Signs and symptoms of hypernatremia occur due to the shifting of water out of the cells causing cell shrinkage and dehydration. Symptoms include:

• Restlessness
• Agitation
• Lethargy
• Intense thirst
• Muscle cramps
• Weakness
• Postural hypotension
• Tachycardia

Hyponatremia or low serum sodium of less than 135 mEq/L results from a loss of sodium-containing fluids often caused by diarrhea, vomiting, and draining wounds. This condition can also result from excess water in relation to sodium levels like the inappropriate use of sodium-free IV fluids. 

Clinical manifestations of hyponatremia occur because of cellular swelling. Symptoms include:

• Irritability
• Confusion
• Seizures
• Headache
• Dizziness
• Nausea and vomiting
• Edema

The Nursing Process

The management of hypernatremia and hyponatremia will depend on the underlying cause. Hypernatremia management will include fluid replacement either orally or through intravenous access and diuretics to promote sodium excretion. Hyponatremia management involves fluid replacement using sodium-containing fluids, increased oral intake, and other salt-replacing medications. 

Nurses are responsible for monitoring sodium levels and identifying clinical manifestations that can indicate further complications of underlying medical conditions. Electrolyte management requires serious assessment and delicate treatment. Nurses can educate patients and families on the important role electrolytes play in the body and how to prevent future imbalances.

Nursing Care Plans Related to Hypernatremia and Hyponatremia

Deficient Fluid Volume Care Plan

Either hyponatremia or hypernatremia occurs when there are severe deficits in fluid volume, depending on the ratio of sodium to water.

Nursing Diagnosis: Deficient Fluid Volume

Related to:

• Hypernatremia
• Hyponatremia 
• Active fluid volume loss 
• Compromised regulatory mechanisms

As evidenced by:

Expected Outcomes:

• The patient will maintain normal hydration status as evidenced by urine output and concentration within normal limits

Deficient Fluid Volume Assessment

1. Assess for signs of hypovolemia.
Early signs of hypovolemia include thirst, headaches, restlessness, and inability to concentrate. Late signs include thready pulses, cold and clammy skin, oliguria, and confusion. These symptoms occur after the body has attempted to compensate for the loss of fluids.

2. Assess factors that contribute to fluid volume deficit.
Factors like vomiting, diarrhea, diuretic drug therapy, fever, hemorrhage, and decreased oral fluid intake can influence hyponatremia from deficient fluid volume.

Deficient Fluid Volume Interventions

1. Monitor intake and output accurately.
Ensure a balance between oral and IV intake compared with urine output. Inspect urine clarity and concentration.

2. Administer IV fluids as indicated.
5% dextrose or 0.45% normal saline can be used to fluid volume deficit without worsening hypernatremia.

3. Administer medications as ordered.
Antidiarrheals or antiemetics may be ordered as appropriate to treat symptoms of the underlying cause.

4. Encourage salt-containing foods and fluids.
Encourage free water as applicable. Encourage soups, broths, and Pedialyte to enhance fluid intake and correct hyponatremia.

Excess Fluid Volume Care Plan

Hyponatremia can occur with excess fluid intake without solute replacement and when there is excessive water intake versus water excretion in the kidneys. This results in sodium concentration in the blood being diluted.

Nursing Diagnosis: Excess Fluid Volume

Related to:

• Compromised regulatory mechanisms (SIADH)
• Excessive fluid intake
• Deviations affecting fluid elimination
• Excess sodium intake

As evidenced by:

• Altered mental status 
• Altered urine-specific gravity
• Intake exceeds output
• Oliguria
• Edema
• Weight gain over a short period

Expected Outcomes:

• The patient will be free of edema, abnormal lung sounds, and maintain normal intake and output
• The patient will identify causes of excess fluid volume and resulting hyponatremia

Excess Fluid Volume Assessment

1. Assess signs of excess fluid volume.
Anasarca can occur when the kidneys are unable to excrete excess fluid.

2. Monitor lab values.
Monitor kidney function, albumin, electrolytes, and urine specific gravity and osmolality to assess for imbalances and underlying issues.

Excess Fluid Volume Interventions

1. Monitor lung sounds.
Excess fluid volume can cause acute pulmonary edema as an underlying cause.

2. Restrict fluids.
Excess fluid volume can be treated by restricting oral and IV fluid intake. Most restrictions are 1-1.5 L.

3. Restrict diuretic medications as indicated.
Diuretics rid the body of water which is useful in treating fluid volume overload but may perpetuate hyponatremia.

4. Administer salt tablets.
Patients with severe hyponatremia may require sodium chloride tablets which are essentially salt tablets to increase sodium levels.

Acute Confusion Care Plan

Both hypernatremia and hyponatremia manifest neurologic symptoms. Severe hyponatremia (<115 mEq/L) can cause confusion, seizures, coma, and death. Hypernatremia can cause lethargy, personality changes, and confusion.

Nursing Diagnosis: Acute Confusion

Related to:

• Dehydration
• Electrolyte imbalance
• Impaired metabolism
• Urinary retention 

As evidenced by:

• Cognitive dysfunction 
• Difficulty initiating goal-directed behavior 
• Difficulty initiating purposeful behavior
• Neurobehavioral manifestations 
• Psychomotor agitation
• Seizure activity

Expected Outcomes:

• The patient will remain oriented to person, place, and time
• The patient will not experience seizure activity

Acute Confusion Assessment

1. Assess the patient’s mental status.
Establishing the patient’s baseline mental status and performing frequent cognitive assessments can help identify subtle changes in cognition and behavior.

2. Assess risk factors and underlying conditions that contribute to an altered mental state.
Identifying risks and possible causes helps formulate a care plan that will prevent confusion and changes in mentation.

Acute Confusion Interventions

1. Assist in correcting fluid and electrolyte imbalance.
Fluid and electrolyte imbalances can cause acute confusion. Addressing and correcting these imbalances will help resolve acute confusion.

2. Constantly reorient the patient.
Confusion can cause agitation and present a safety issue. Continually orient the patient to person, place, and situation.

3. Provide a calm environment.
Prevent overstimulating the patient and offer plenty of rest periods with minimal interruptions.

4. Implement seizure precautions.
Severely low sodium levels can cause seizures due to the shift of water into brain cells causing cerebral swelling. Patients at risk for seizures should have safety precautions in place.

References and Sources

1. Diagnosis and Management of Sodium Disorders: Hyponatremia and Hypernatremia. American Family Physician. Am Fam Physician. 2015;91(5):299-307. MICHAEL M. BRAUN, DO, CRAIG H. BARSTOW, MD, AND NATASHA J. PYZOCHA, DO. From: https://www.aafp.org/pubs/afp/issues/2015/0301/p299.html
2. Difference Between Hypernatremia and Hyponatremia. WebMD. Dan Brennan, MD. Updated May 16, 2021. From: https://www.webmd.com/a-to-z-guides/difference-between-hypernatremia-hyponatremia
3. Friedler, R. M., Koffler, A., & Kurokawa, K. (1977). Hyponatremia and hypernatremia. Clinical nephrology, 7(4), 163–172. From: https://pubmed.ncbi.nlm.nih.gov/870270/