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General Principles in Older Adults
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Older adults are more vulnerable to developing sodium disorders as a result of age-related changes in water and sodium metabolism. Older adults may have an impaired ability to excrete water and to dilute urine because of reductions in the number of functioning nephrons and decreased renal blood flow with age, predisposing them to water overload and possible hyponatremia. Geriatric patients also tend to be on multiple medications that are associated with sodium disorders, such as diuretics and psychotropic medications (Table 37–1). Reviewing all medications is an integral part of evaluating patients with sodium disorders.
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Hyponatremia is commonly defined as a serum sodium concentration less than 135 mEq/L (or 135 mmol/L). This occurs in 7% to 11% of older patients and up to 50% of older hospitalized patients.
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Hypervolemic Hyponatremia
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In older adults, the most common etiology of hyponatremia is increased intake and subsequent retention of water. This type of hyponatremia is commonly described as dilutional or hypervolemic hyponatremia. These patients typically will exhibit edematous states, resulting from conditions such as congestive heart failure, cirrhosis, or the nephrotic syndrome. These conditions decrease effective circulating blood volume, leading to increased antidiuretic hormone (ADH) secretion, which results in water retention. Dilutional hyponatremia can also be iatrogenic, as a result of administration of excess IV fluids, especially in hospitalized patients.
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Hypovolemic Hyponatremia
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Although less common, salt depletion with or without loss of extracellular fluid, can cause depletional or hypovolemic hyponatremia. Hypovolemic hyponatremia can be caused by renal losses (eg, diuretic use) or from extrarenal losses, such as vomiting, diarrhea, laxative abuse, ostomies, or the presence of large burns. A particular etiology to consider in geriatric patients is restricted sodium intake, especially in the setting of tube feeding.
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Euvolemic Hyponatremia
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The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a disorder in which water excretion is partially impaired because of the inability to suppress secretion of ADH. Patients with SIADH will generally appear euvolemic. Many diseases that are common in older adults are associated with SIADH such as central nervous system disorders and malignancies (Table 37–2). In addition, although rare, older age itself may be a risk factor for SIADH. Medications (Table 37–1) are also an important cause of SIADH. As a result of multimorbidity, older adults are at higher risk for polypharmacy, typically defined as the use of 5 or more medications. In older patients, careful medication review is imperative. Other causes of euvolemic hyponatremia include hypothyroidism and adrenal insufficiency. An elevated serum potassium level in conjunction with hyponatremia should increase suspicion for adrenal insufficiency. Lastly, it is important to include pseudohyponatremia in the differential, which can occur in the setting of hyperlipidemia or hyperproteinemia.
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The primary symptoms for sodium disorders (hyper- or hyponatremia) are neurologic. Slow changes in serum sodium concentration (chronic hyponatremia) are more likely to be asymptomatic as the brain has had time to adapt to osmotic changes. Symptoms associated with hyponatremia include anorexia, nausea, vomiting, headache, weakness, loss of coordination, muscle cramps, agitation, tremors, disorientation, psychosis, delirium, seizures, and coma. Patients with chronic hyponatremia are more prone to have marked gait and attention impairments leading to increased risk of falls.
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Evaluation of Volume Status
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After obtaining the history, the next step in the work-up of a patient with hyponatremia is to evaluate the volume status. Patients who are hypovolemic may have dry mucous membranes, tachycardia, and/or relative or orthostatic hypotension. On the other hand, hypervolemic patients may have increased jugular vein pressures, crackles at lung bases, ascites, and/or peripheral edema.
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On laboratory exam, serum osmolality, urine osmolality, and urine sodium should be obtained. Hyponatremia secondary to pseudohyponatremia or hyperglycemia will have a normal serum osmolality while all other etiologies will demonstrate a low serum osmolality. Urine osmolality of more than 100 mOsm/kg is consistent with an inability to normally excrete water, which is generally caused by SIADH or low effective circulating volume depletion, such as true hypovolemia, heart failure, and cirrhosis. Urine sodium is useful in differentiating between the two. A urine sodium of less than 25 mEq/L suggests hypovolemia and more than 40 mEq/L suggests SIADH.
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Treatment of hyponatremia is based on the presence of symptoms, the severity of symptoms when present, and the acuity of the condition.
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Asymptomatic patients with acute hyponatremia may be treated like those with chronic hyponatremia (see below). Otherwise, therapy is aimed at correcting the major symptomatic consequences of hyponatremia while avoiding induction of central pontine myelinolysis (CPM). In patients with severe hyponatremia (serum sodium below 120 mEq/L) with severe neurologic symptoms such as seizures, the use of 3% hypertonic IV saline is recommended. In the first 2–3 hours, the saline should be infused to increase the serum sodium by 1–2 mEq/L per hour. Then the infusion should be slowed to increase the serum sodium an additional 8–12 mEq/L over the next 24 hours. The rate of infusion for each patient based on the desired change in the serum sodium can be calculated using the following formula:
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Change in serum sodium in older men = (infusate Na – serum Na)/[(0.50 × body weight) + 1]
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Change in serum sodium in older women = (infusate Na – serum Na)/[(0.45 × body weight) + 1]
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These equations have limitations and thus the actual change in serum sodium may differ. The equations should be used to guide the initial infusion rate, which should then be adjusted by obtaining frequent serum sodium levels to avoid rapid overcorrection, which can cause CPM. Symptoms of CPM include behavioral disturbances, movement disorders, and seizures, usually occurring several days after treatment. Furosemide can be used in conjunction with IV hypertonic saline to limit treatment-induced expansion of extracellular fluid volume.
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The goal is to identify underlying causes and intervene appropriately. For example, patients who are hyponatremic because of volume depletion secondary to diuretic use should hold their diuretics and receive volume repletion, such as IV isotonic saline. In contrast, patients with SIADH will not benefit from IV isotonic saline as the infused salt will be excreted in the concentrated urine, resulting in net retention of water and worsening of their hyponatremia. In these patients, long-term water restriction may be needed. Use of demeclocycline in patients who do not respond to water restriction is also an option.