Hyponatremia (serum sodium <135 mEq/L) is the most common electrolyte disorder. The severity of symptoms is related to how rapidly the condition develops and the degree of cerebral edema that results from the low serum level of sodium. Hypertonic saline and the new vasopressin receptor antagonists are highly effective treatments for severe symptomatic hyponatremia, yet they can result in severe neurological complications if sodium levels are restored too quickly. Hyponatremia is classified as hypovolemic, euvolemic, and hypervolemic. Treatments include administration of high-risk medications and fluid restriction to restore fluid and electrolyte balance and relieve cerebral effects. Nursing care to ensure safe outcomes involves multidisciplinary collaboration, close monitoring of serum sodium levels and intake and output, and assessment for neurological changes.
Hyponatremia (serum sodium level <135 mEq/L) is the most common electrolyte disorder in hospitalized patients.1 In a study2 of 120000 patients, the prevalence of hyponatremia was 42%, and more than 25% of the patients had the abnormality at the time of admission to the hospital. The severity of neurological symptoms due to sodium deficiencies is related to the degree of cerebral edema caused by electrolyte and fluid imbalances and is correlated with the rate at which hyponatremia develops2 and the extent of the hyponatremia. Most patients do not have signs or symptoms unless the serum sodium level is less than 129 mEq/L, when nausea, vomiting, fatigue, irritability, disorientation, and headache may develop,3 although elderly patients with even mild hyponatremia may have cognitive problems and experience unsteadiness and/or falls.2 Elderly patients with hyponatremia also have prolonged reaction times and significantly more mental errors than do patients of a similar age who have normal serum sodium levels.4 A serum sodium level less than 125 mEq/L is a strong independent predictor of inpatient mortality for critical care patients.5 Critical care nurses must monitor electrolytes and take prompt actions to avoid marked decreases in sodium levels.
The standard treatments for hyponatremia are often not well tolerated and are potentially dangerous (see Figure). Hyponatremia creates relative hypo-osmolality, resulting in an osmolar gradient across the membranes of cells of the blood-brain barrier and other tissues. This gradient causes water to move into the cells, resulting in cellular overhydration.7 If sodium levels are adjusted too quickly, an irreversible neurological catastrophe can occur. Osmotic demyelination syndrome (ODS), also termed osmotic myelinolysis and formerly termed central pontine myelinolysis, and/or other neurological problems may develop because of rapid osmotic shifts of water out of the brain cells when sodium levels increase too quickly, and the damage might not be apparent for at least 4 days.9 ODS is due to a loss of oligodendrocytes and myelin in central and extrapontine sites; it rarely occurs if the serum sodium level remains greater than 120 mEq/L and when the onset of hyponatremia is rapid.3
Classifications of Hyponatremia
Hyponatremia is classified first as acute (<48 hours) or chronic (at least 48 hours) and then according to the severity of signs and symptoms and fluid balance (Table 1). Fluid balance, determined by serum osmolality and physical examination of edema, is categorized as hypovolemic, euvolemic, or hypervolemic.10
Among patients with hyponatremia, 50% have no physical indications of fluid overload, and the hyponatremia is classified as euvolemic2 ; syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause of euvolemic hyponatremia in critical care patients.2 SIADH occurs in response to multiple causes that result in excess release of vasopressin (antidiuretic hormone or arginine vasopressin) from the posterior part of the pituitary gland. The released antidiuretic hormone adheres to renal receptors, causing water to be reabsorbed by the kidneys and leading to increased intravascular volume.11 The excess volume causes a dilution of sodium and a hypo-osmolar state.7 Natriuresis (renal sodium excretion) occurs with SIADH, even in the presence of hyponatremia, and this excretion prevents the formation of edema. Urine osmolality is greater than 100 mOsm/kg in SIADH, indicating an inability of the kidneys to maximally dilute urine to correct hyponatremia.
Hypovolemic hyponatremia is the result of fluid shifts that create intravascular dehydration, such as the shift associated with severe hyperglycemia.10 Elevated glucose levels in diabetic ketoacidosis or a hyperosmolar hyperglycemic state dilute the serum level of sodium via an osmotic effect11 (Table 2 gives the formula for calculating the actual sodium level for patients with diabetic ketoacidosis or hyperosmolar hyperglycemic state). Other common causes of hypovolemic hyponatremia are use of diuretics, diarrhea, excessive diaphoresis,9 and cerebral salt wasting.1 Cerebral salt wasting, which can occur after a neurological injury, stimulates vasopressin secretion, leading to hyponatremia. Cerebral salt wasting may be mistaken for SIADH, but in the former, release of vasopressin is stimulated by volume depletion.1
Hypervolemic hyponatremia, the type of most concern in critical care, is the result of excess fluid causing sodium dilution10 ; about 25% of patients with hyponatremia have the hypervolemic type.2 Hypervolemic hyponatremia can be differentiated from euvolemic hyponatremia on the basis of physical signs of fluid overload, such as jugular venous distention, pulmonary edema, and/or pitting edema. The most common cause of hypervolemic hyponatremia is increased reabsorption of sodium by proximal nephrons3 (as in heart failure, hypothyroidism, nephritic syndrome, and cirrhosis). Another cause of dilutional hyponatremia is primary polydipsia, or water intoxication due to excessive fluid intake, a common condition in patients with schizophrenia.1 In psychogenic polydipsia, the volume of fluid intake may overwhelm normal renal functioning, creating a dilutional hyponatremia that often self-corrects with diuresis.1 Psychogenic polydipsia has an incidence of 4% to 20% in psychiatric patients.13 The actual mechanism is unknown, but one possibility is a malfunction of the thirst center in the hypothalamus and dysregulation of secretion of antidiuretic hormone due to a change in the hypothalamic-pituitary feedback loop.14 Many psychiatric medications cause xerostomia (dry mouth),15 which may also promote polydipsia.13
Several medications influence sodium excretion: diuretics, carbamazepine and other antiseizure medications, amiodarone, theophylline, selective serotonin reup-take inhibitors (antidepressants), vasopressin, and phenothiazine antipsychotics.16 Diuretics can result in hypovolemia, but most of the other medications that affect sodium excretion may cause SIADH, which can be reversed by discontinuing the medication.16
The initial goals in treatment of symptomatic hyponatremia are to reduce the cellular edema in the brain and improve the serum sodium concentration.11 However, in order to prevent ODS, sodium concentrations should be adjusted only to the level required to maintain normal respiration and prevent seizures.11 Treatment of hyponatremia is based on volume status, severity of neurological signs and symptoms (correlated with the degree of hyponatremia), onset of the hyponatremia (acute vs chronic), and consideration of the risks and benefits of the specific treatments (Table 1). Patients are at risk for ODS if the sodium concentration is corrected too quickly, especially patients with chronic hyponatremia. Sodium levels should be monitored every 2 to 4 hours until signs and symptoms abate and then every 4 to 8 hours to ensure that the serum sodium level is not adjusted too quickly.9
Traditional treatment options include fluid restriction (usually <1000 mL/d),1 infusion of isotonic (0.9%) or hypertonic saline, medications to reduce fluid retention, and—for patients with hypovolemia—discontinuation of diuretics.9 Hypertonic saline promotes osmosis of fluid from intracellular spaces into the vasculature so that the kidneys can excrete the excess fluid as urine. Isotonic saline suppresses vasopressin, a situation that permits rapid excretion of excess water, for most cases of hyponatremia that are not related to SIADH. A new drug class, vasopressin receptor antagonists (vaptans), now offers an alternative treatment for euvolemic and hypervolemic hyponatremia that directly targets excess arginine vasopressin, which is most often the reason for water disequilibrium10 and hyponatremia in hospitalized patients (see Sidebar, “Vasopressin Receptor Blockers”).
The hyponatremia treatment guidelines1 published in 2007 suggest that chronic hyponatremia should be corrected to less than 10 to 12 mEq/L over 24 hours and to less than 18 mEq/L over 48 hours to prevent neurological complications but that the goal for the first 24 hours should be 8 mEq/L to allow for absolute safety. Severe symptomatic hyponatremia, generally an acute sodium level less than 120 mEq/L, is a medical emergency9 because the osmotic movement of water into the cells of the brain can cause seizures or coma.10 Hypertonic saline or a vasopressin receptor antagonist may be prescribed initially in these critical cases to increase sodium levels by 1 to 2 mEq/L per hour7 until the serum sodium is 125 mEq/L or signs and symptoms subside or until the serum sodium concentration has increased by 25 mEq/L in the first 48 hours of treatment.1 A more rapid corrective rate of 3 to 5 mEq/L per hour can be used for up to 2 hours if imminent brainstem herniation is suspected.10 Loop diuretics can be given concurrently with hypertonic saline for patients with hypervolemia,10 but the combination must be used cautiously to avoid a too rapid reversal of the hyponatremia. Table 3 shows calculations for determining rates of administration for 3% saline.
Euvolemic hyponatremia, most commonly due to SIADH, is primarily treated with fluid restriction.9 Normal saline is not corrective in patients with euvolemic hyponatremia, so hypertonic saline or vaptans are necessary if more aggressive treatment is needed.1 The goal of treatment is to maintain fluid intake of 500 mL less than urine output, but fluid restriction is difficult in critical care patients because of nutrition and treatment needs, and patients often do not comply with the restriction in other settings.23 Standard treatment of hypovolemic hyponatremia includes fluid restriction, electrolyte replacement, and discontinuation of diuretics. Ideally, fluid balance and sodium deficits are replaced simultaneously, with the primary focus on fluid for the first 48 hours and then slow sodium replacement in the next 48 hours.9 An increase of 0.5 mEq/L per hour in the serum level of sodium may be sufficient unless signs and symptoms are severe. In severe cases, a higher rate may be targeted until signs and symptoms resolve or the sodium level is greater than 120 mEq/L.9 Vaptans are contraindicated in hypovolemia because they cause profound renal aquaresis.18
Hypervolemic hyponatremia requires a reduction of fluid volume. Hypertonic saline and/or intravenous loop diuretics or vasopressin receptor blockers are effective. The new vaptans create aquaresis, in which water is excreted and electrolytes are retained. Renal damage, which may occur with loop diuretics, has not been detected with the vaptans. Currently, 2 vaptans have been approved by the Food and Drug Administration. Conivaptan (Vaprisol) is for intravenous administration only, and tolvaptan (SAM-SCA) is for oral administration (see Sidebar for more information on vasopressin receptor blockers). With both vaptans, patients must be monitored because sodium levels can be corrected too quickly, creating the potential for ODS (see Sidebar, “Osmotic Demyelination Syndrome”).
The nursing care of patients with hyponatremia begins with an understanding of the relationship between sodium and fluid balance and the role of vasopressin, recognition of a patient’s volume status, onset of the of sodium deficit (acute or chronic), severity of signs and symptoms, and degree of the sodium deficit.
Critical care patients being treated for hyponatremia require diligent monitoring. Depending on the severity of the condition and the selected treatments, serum sodium levels should be measured every 1 to 2 hours during initial treatment and then at least every 4 hours until signs and symptoms resolve.28 Levels should be measured every 1 to 2 hours while hypertonic saline is being infused.20 The serum concentration of sodium, especially for patients with chronic hyponatremia, must be adjusted slowly to prevent the development of ODS (Table 1). A key nursing responsibility is to ensure that laboratory tests are ordered, blood samples are obtained, and results of tests are reported in a timely manner. Results should be reported to the ordering physician per written parameters or hospital policy. Generally, the goal of serum sodium adjustment is for a maximum of 8 mEq/L, and definitely less than 12 mEq/L, in the first 24 hours of treatment, and less than 18 mEq/L in the first 48 hours. Strict intake and output are necessary because the kidneys excrete both water and electrolytes.
Table 3 shows the calculations to determine the sodium deficiency and dosage of hypertonic saline for severe euvolemic or hypervolemic hyponatremia. Hospitals may have a policy to guide administration of hypertonic saline to ensure patient safety. Hypertonic saline should be administered cautiously, and safety features should be followed, such as using independent double verification and an intravenous pump that provides a drug library and limits for high-risk medications and tubing that prevents free flow of fluids.29
Patients who are symptomatic have neurological signs and symptoms of brain cellular edema, so assessments should include determining the progress of the neurological condition, such as level of consciousness, mental status, and reflexes (Table 4). Safety precautions are important. Severe hyponatremia can lead to seizures or coma, so side rails may need to be padded, and nurses should be prepared to provide suctioning and airway support. Patients who are ambulatory may be weaker than normal, and precautions should be taken to prevent falls.
Oral care is important because patients are likely to have a dry mouth, exacerbated by fluid restrictions. Fluid restriction may be difficult when critical care patients receive their nutrition and medications in liquid forms. Collaboration with nutritionists and pharmacists can help maximize concentrations of medications and limit the volume of tube feedings or intravenous fluids, although this intervention may require a central catheter to accommodate the more concentrated solutions and to reduce the risk of infiltration.
Abby (a pseudonym) was a 40-year-old man with paranoid schizophrenia who lived in a group home. He came to the emergency department at 10:30 AM because he was “getting a kidney stone.” Vital signs were as follows: body temperature 37ºC (98.6ºF), pulse rate 104/min, respirations 16/min, blood pressure 140/88 mm Hg, and oxygen saturation 95% on room air. Abby weighed 142 kg (312 lb) and was 1.8 m (6 ft) tall. He appeared bloated and had some edema in his hands and ankles. His initial score on the Glasgow Coma Scale (GCS) was 15. He was placed in a room near the nurses’ station in the emergency department.
Abby was initially cooperative, but during a short period, he became increasingly labile, paranoid, and delusional. He paced in his room or sat on the bed and rapidly rocked back and forth. He refused to have laboratory tests and would not speak with the emergency department staff. He refused to let a physician examine him. Abby was given ziprasidone hydrochloride (Geodon) 20 mg intramuscularly after striking at a nurse. Within moments of receiving the medication, Abby experienced a generalized seizure that lasted 3 minutes; during the seizure he was incontinent of urine and bit his tongue. He was given lorazepam (Ativan) 2 mg intravenously to prevent further seizures and to sedate him to allow computed tomography of the brain. Blood specimens for a chemical profile, complete blood cell count, and drug screen were obtained immediately after the seizure. Table 5 gives the initial laboratory values.
Abby’s GCS score decreased to 8 from the initial 15, and he vomited. He was intubated to protect his airway, and mechanical ventilation was started. A nasogastric tube was placed for low continuous suctioning. Once the laboratory results indicated hypervolemic hypona-tremia (serum sodium level 115 mEq/L, urea nitrogen 52 mg/dL [to convert to millimoles per liter, multiply by 0.357], serum osmolality 238 mOsm/kg), an immediate nephrology consultation was requested to manage the electrolyte and fluid imbalances. An indwelling urinary catheter was inserted to monitor urinary output, and an arterial catheter was used to monitor blood pressure. A central vascular access device was placed, and central venous pressure was monitored for fluid balance. The nephrologist ordered an infusion of 3% saline at 30 mL/h, which was to continue until the serum concentration of sodium reached 125 mEq/L. The rate of 30 mL/h was based on the hospital’s policy not to exceed an infusion rate of 30 to 40 mL/h for 3% hypertonic saline and a maximum increase of 8 mEq/L in the serum sodium level in the first 24 hours.
Upon transfer to the intensive care unit, Abby was agitated and thrashing in the bed. He localized painful stimuli, and he did not follow commands. His score on the Riker Sedation-Agitation Scale (SAS; Table 6) was 7, indicating a dangerous level of agitation.
Propofol (Diprivan) was administered at 5 μg/kg per minute. Vital signs remained stable. Pupils were equal and reactive. Central venous pressure was 25 mm Hg, markedly greater than the normal 5 to 10 mm Hg. Breath sounds were clear. Abby had 2+ bilateral pedal edema.
During the first 24 hours of hospitalization, Abby excreted more than 10000 mL of urine. Although specimens for assays of serum sodium levels were obtained every 4 hours, 16 hours after the initial value was obtained, Abby’s serum sodium level had increased to 130 mEq/L. The physician was notified immediately, and the hypertonic saline was replaced with normal saline 150 mL/h in an attempt to allow the sodium concentration to return to normal levels more slowly.
Throughout day 2 in the intensive care unit, the sodium levels continued to increase, but at a much slower rate. Just 24 hours after admission, the serum sodium concentration was normal at 135 mEq/L. Abby’s weight was down to 133 kg (293 lb), a loss of 9 kg (20 lb). Attempts were made to minimize sedation to better assess neurological status, but Abby was agitated, with an SAS score of 6, and he required frequent doses of lorazepam and haloperidol (Haldol) and continued use of restraints simply to keep him in the bed. Ziprasidone hydrochloride was not given again because it can cause seizures. Unfortunately, Abby had no family or close friends who might have been able to calm him and allow a reduction in the number of medications. A psychiatric consultation offered no additional solutions. Abby’s vital signs remained stable, and his hemodynamic values were normalizing. Abby was turned every 2 hours and given passive range-of-motion exercises. Chest radiographs showed that his lungs remained clear.
On day 3 in the intensive care unit, Abby was less agitated, with an SAS score of 5, and his neurological and respiratory conditions allowed extubation. After extubation, Abby’s GCS score was 14. Slowly Abby improved during the next several hours until his GCS score returned to 15 and his SAS remained at 5. Previous medical records indicated that Abby’s baseline behavior matched his pacing his room and repeatedly asking the same questions with rapid speech. A nurse helped calm Abby by simply assuring him that he had space to pace without dislodging his intravenous catheter and sitting with him. By the end of the day 4, Abby was transferred to the progressive care unit. Eventually, he was able to tell us that he did not want to get another kidney stone, so he drank large amounts of water in a short time “to flush out my system.” Thus, Abby’s hyponatremia was the result of self-induced water intoxication (psychogenic polydipsia), and he had stopped taking his medications several months ago, a situation that led to the delusions about kidney stones. Often hyponatremia-induced psychogenic polydipsia self-corrects, but no history was initially available for Abby and the seizures and reduced level of consciousness required prompt treatment. Concerns continued about the possibility of neurological damage from the rapid improvement in the serum concentration of sodium because signs and symptoms may not appear for 4 or more days. Abby was monitored, and at the end of hospitalization day 6, he was transferred to the behavioral health unit for stabilization of antipsychotic medications and behavior. Several days later, Abby was discharged back to his group home, still showing no deterioration in neurological status.
Abby’s treatment required the collaboration of nurses, specialty physicians, pharmacists, respiratory therapists, laboratory technologists, and chaplains. Abby was a challenging patient because his schizophrenic behavior both contributed to and delayed detection of the hyponatremia and the reason for the hypervolemic hyponatremia. Hyponatremia, with treatments dependent on a multitude of variables, is a complex condition fraught with potential life-threatening and/or disabling consequences. The rapid diuresis and resulting quick increase in Abby’s serum sodium level placed him at risk for neurological complications such as ODS, although this syndrome is more common in patients with chronic hyponatremia. Nurses caring for patients with hyponatremia must monitor the patients’ urine output and sodium levels and adhere rigorously to treatment orders to ensure a slow adjustment in the serum concentration of sodium and maximize the opportunity for a safe recovery. Once the hyponatremia was resolved, Abby’s schizophrenic behaviors made it difficult to determine his mental status and neurological condition. For example, the health care staff could not tell whether Abby was choosing not to follow commands or that he did not understand the commands, a finding that might indicate neurological damage. Fortunately, Abby had no residual neurological problems. Once his psychiatric condition was stabilized with medications, he was able to return to his group home, where his fluid intake would be monitored.
Hyponatremia is a common electrolyte disorder and has several causes. Nurses must recognize the degree of sodium deficiency, the fluid status, and whether the hyponatremia developed acutely or chronically because this information correlates with the severity of signs and symptoms and determines the best treatment options. Correction of hyponatremia requires collaboration of the entire health care team to ensure patient safety. The hyponatremia treatment guidelines1 suggest that chronic hyponatremia be corrected to less than 10 to 12 mEq/L over 24 hours and less than 18 mEq/L over 48 hours to prevent neurological complications, but the goal for the first 24 hours should be 8 mEq/L to allow for absolute safety. Severe symptomatic hyponatremia, generally with an acute serum sodium level less than 120 mEq/L, is a medical emergency,9 because the osmotic movement of water into the cells of the brain can cause seizures or coma.10
Hypertonic saline, or intravenous vasopressin receptor blockers, when ordered, should be administered with meticulous care via a pump with safety features. Strict intake and output, careful administration of medications, neurological assessments, and assays of serum sodium levels every 1 to 4 hours are the basic components of care for patients with severe hyponatremia.
Figure and Tables
I am grateful for the assistance of Christina Amidei, rn, msn, cnrn, faan, of the University of Central Florida, College of Nursing, Orlando, Florida.
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To learn more about hyponatremia, read “Central Neurogenic Diabetes Insipidus, Syndrome of Inappropriate Secretion of Antidiuretic Hormone, and Cerebral Salt-Wasting Syndrome in Traumatic Brain Injury” by John and Day in Critical Care Nurse, April 2012;32:e1-e7. Available at www.ccnonline.org.
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