Symptoms Of Low Blood Sodium In Elderly

Symptoms Of Low Blood Sodium In Elderly – Hyponatremia is a common electrolyte disorder defined as a serum sodium level of less than 135 mEq per L.

A Dutch systematic review of 53 studies showed that the prevalence of mild hyponatremia was 22.2% in geriatric wards, 6.0% in non-geriatric wards, and 17.2% in the intensive care unit.

Symptoms Of Low Blood Sodium In Elderly

The prevalence of severe hyponatremia (serum sodium level less than 125 mEq per L) was 4.5%, 0.8%, and 10.3%, respectively. It is estimated that hyponatremia occurs in 4% to 7% of the ambulatory population, with rates of 18.8% in nursing homes.

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In patients with severe symptomatic hyponatremia, the rate of sodium correction should be 6 to 12 mEq per L in the first 24 hours and 18 mEq per L or less in 48 hours.

A bolus of 100 to 150 mL of hypertonic 3% saline may be given to correct severe hyponatremia.

Vaptans appear to be safe for the treatment of severe hypervolemic and euvolemic hyponatremia but should not be used routinely.

Chronic hypernatremia should be corrected at a rate of 0.5 mEq per L per hour, with a maximum change of 8 to 10 mEq per L in a 24-hour period.

Hyponatremia In Elderly|causes|symptoms|treatment

In patients with heart failure undergoing cardiac surgery, hyponatremia increases rates of postoperative complications, length of hospital stay, and mortality.

Mild hyponatremia in the ambulatory setting is associated with increased mortality (hazard ratio = 1.94) compared with normal sodium levels.

Patients who develop hyponatremia during hospitalization have increased mortality rates compared with those who have hyponatremia during admission.

It is unclear whether hyponatremia is a marker for poor prognostic outcomes or just a reflection of disease severity. Its presence indicates a worse prognosis in patients with liver cirrhosis, pulmonary hypertension, myocardial infarction, chronic kidney disease, hip fractures and pulmonary embolism.

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The most common classification system for hyponatremia is based on volume status: hypovolemic (decreased total body water with a greater decrease in sodium level), euvolemic (increased total body water with a normal sodium level), and hypervolemic (increased total body water compared to sodium).

Plasma osmolality has a role in the pathophysiology of hyponatremia. Osmolality refers to the total concentration of solutes in water. Effective osmolality is the osmotic gradient created by solutes that do not cross the cell membrane. Effective osmolality determines the osmotic pressure and the flow of water.

Plasma osmolality is maintained by tight regulation of the arginine vasopressin (also called antidiuretic hormone [ADH]) system and thirst. If plasma osmolality increases, ADH is secreted and water is retained by the kidneys, thus decreasing serum osmolality. If plasma osmolality decreases, ADH also decreases, resulting in diuresis of free water and a return to homeostasis.

Symptoms of hyponatremia depend on its severity and the rate of sodium depletion. Gradual decreases in sodium usually result in minimal symptoms, while rapid decreases can result in severe symptoms. Polydipsia, muscle cramps, headaches, falls, confusion, altered mental status, obtundation, coma and status epilepticus may indicate the need for emergency intervention. Most patients with hyponatremia are asymptomatic, and hyponatremia is noted incidentally. Volume status should be assessed to help determine the underlying cause

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The diagnostic workup should include history and physical examination with specific attention to cardiac, cancer, pulmonary, surgical, endocrine, gastrointestinal, neurological, and renal histories (Table 1).

Diuretics, carbamazepine (Tegretol), and selective serotonin reuptake inhibitors can cause hypovolemia; therefore, medications should be reviewed. Alcohol and illegal drugs (especially beer and 3, 4-methylenedioxymethamphetamine [“Ecstasy”) can cause hyponatremia.

Low aldosterone and morning cortisol levels, hyperkalemia, increased plasma renin level, low or increased adrenocorticotropic hormone level (cause-dependent), urinary sodium > 20 mEq per L, positive results on cosyntropin stimulation test, 21-hydroxylase autoantibodies (Addison’s disease ), computed tomography of adrenal glands to rule out infarction

Urine osmolar gap, increased urine pH, urine sodium > 25 mEq per L, fractional excretion of bicarbonate > 15% to 20%, hyperchloremic acidosis, decreased serum bicarbonate level, potassium abnormalities (type dependent)

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Decreased osmolality, urine osmolality > 100 mOsm per kg, euvolemia, urine sodium > 20 mEq per L, absence of thyroid disorders or hypocortisolism, normal renal function, no diuretic use.

SIADH secondary to medication use (eg, barbiturates, carbamazepine [Tegretol], chlorpropamide, diuretics, opioids, selective serotonin reuptake inhibitors, tolbutamide, vincristine)

Clinical (eg, jugular vein distention, edema), elevated B-type natriuretic peptide level, echocardiography, urine sodium < 20 mEq per L

Serum osmolality and fractional excretion of sodium should be calculated (eTable A). Measurement of thyroid-stimulating hormone, uric acid, adrenocorticotropic hormone, plasma cortisol, and brain natriuretic peptide may be considered in selected patients to rule out other causes.

Pdf) Hyponatremia In Elderly In Patients

The diagnosis of reset osmostat (a variant of syndrome of inappropriate antidiuretic hormone secretion [SIADH] in which ADH secretion occurs despite low plasma osmolality) can be aided by using fractional excretion of urate (uric acid) in non-edematous patients who have unresponsive hyponatremia. to usual treatment.

Online calculators for the infusion rate and the required sodium concentration are available at http://www.mdcalc.com/sodium-correction-rate-in-hyponatremia, http://www.medcalc.com/sodium.html, and http://www.nephromatic.com/sodium_correction.php

Serum sodium correction should generally not proceed faster than 0.5 mEq per L per hour during the first 24 to 48 hours; however, in severely symptomatic patients, the rate may be 1.0 to 2.0 mEq per L per hour; these situations typically require the use of 3% saline

The goal is to raise the serum sodium to not exceed 10 to 12 mEq per L in the first 24 hours and 18 mEq per L in the first 48 hours.

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Isotonic saline contains 154 mEq of sodium per L, and 3% saline contains 513 mEq of sodium per L.

Example: for a 70-kg man with a serum sodium level of 120 mEq per L and a desired serum sodium level of 140 mEq per L, the calculation is 0.6 × 70 (140 − 120) = 42 × 20 = 840 mEq.

For total body water%, use 0.45 for women older than 65, 0.5 for women 65 and younger and for men older than 65, and 0.6 for men 65 and younger and for children

Example: for a 70-kg man with a serum sodium level of 120 mEq per L, the calculation is 0.6 × 70 × ([120 − 140] / 140) = 42 × (−20 / 140) = 42 × (−1) / 7) = −6 L

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Pseudohyponatremia occurs when apparently low sodium levels are actually normal. Causes include hyperglycemia, hyperproteinemia, mannitol use, or laboratory errors. Osmolality remains unchanged, and patients are usually euvolemic.

Patients typically have signs and symptoms associated with volume depletion (eg, vomiting, diarrhea, tachycardia, elevated blood urea nitrogen-to-creatinine ratio). Urine sodium levels are typically less than 20 mEq per L unless the kidney is the site of sodium loss. Fractional excretion of sodium is often inaccurately elevated in patients receiving diuretics due to diuretic-induced natriuresis; fractional excretion of urea can be used in these patients instead. Fractional excretion of urea less than 35% is more sensitive and specific for diagnosing prerenal azotemia in this setting.

Treatment generally consists of volume repletion with isotonic (0.9%) saline, occasional use of salt tablets, and treatment of the underlying condition.

Monitoring of urine output is recommended as output of more than 100 mL per hour may be a warning sign of overcorrection.

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Euvolemic hyponatremia is most commonly caused by SIADH, but can also be caused by hypothyroidism and glucocorticoid deficiency. Euvolemia is diagnosed by history and physical examination findings, low serum uric acid levels, a normal blood urea nitrogen-to-creatinine ratio, and a point urine sodium greater than 20 mEq per L. Diuretic therapy can artificially raise urine sodium, while low -sa diet can artificially lower urinary sodium, thus obfuscating the diagnosis of hypovolemia versus euvolemia. Treatment generally consists of fluid restriction and correction of the underlying cause. Fluid restriction should be limited to 500 ml less than the daily urine volume.

The consumption of salt and protein should not be limited. Predictors of failure with fluid restriction include urine osmolality greater than 500 mOsm per kg, 24-hour urine volume less than 1.5 L, an increase in the serum sodium level of less than 2 mEq per L within 24 to 48 hours, and serum sodium. level less than the sum of the urinary sodium and potassium levels.

Sodium levels in patients with SIADH will decrease further with intravenous fluid administration. The use of demeclocycline (Declomycin) and lithium is not recommended due to an increased risk of damage.

Hypervolemic hyponatremia occurs when the kidneys cannot excrete water effectively. In volume overload states, the effective arterial blood volume is decreased compared to venous volume, resulting in excessive ADH secretion. The most common causes of hypervolemic hyponatremia are heart failure, cirrhosis, and kidney injury. Treatment consists of correcting the underlying cause, sodium and fluid restriction, and diuretic therapy to increase excretion of undissolved water.

Hypernatremia And Hyponatremia Notes: Diagrams & Illustrations

A randomized controlled trial of 46 patients with heart failure showed that limiting fluid intake to 1 L per day improved quality of life 60 days after discharge.

Severe symptomatic hyponatremia occurs when sodium levels decrease for less than 24 hours. Severe symptoms (eg, coma, seizures) typically occur when the sodium level falls below 120 mEq per L, but can occur as low as 125 mEq per L. Severe symptomatic hyponatremia must be corrected promptly because it can lead to cerebral edema, irreversible neurological . damage, respiratory arrest, brainstem herniation, and death. Treatment includes

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