5. DETERMINE (13–15)
8.3 SODIUM
Essentially all of the body’s sodium is located in the extracellular fluid volume (ECFV) or space, so that total body sodium can be closely estimated just by multi- plying the serum sodium concentration times the ECFV. However, while the serum sodium concentration is easy to measure, ECFV is difficult to estimate. Sodium is the primary cation in the ECFV and is hydrophilic attracting osmotically obligated water that, in turn, is responsible for the maintenance of plasma and extracellular volume.
While there are no recommended dietary intakes for sodium, current US dietary guidelines recommend that persons greater than 2 years of age consume less than
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2300 mg of sodium per day (5.8 g of salt) as high dietary sodium intakes increase the development of hypertension and the atherosclerotic vascular diseases(5). Persons with normal renal function, when placed on severely restricted salt intakes, can very effectively conserve salt; however, older persons do so less effectively than younger persons(6).
When primary salt depletion occurs (the causes will be discussed below), there is with it a loss of osmotically obligated water so that plasma volume and ECFV initially decrease at a rate proportionate to the sodium loss. If this sodium loss continues unabated, forces come into play, e.g., stimulation of release of antidiure- tic hormone (ADH) in response to volume depletion that increases water reabsorp- tion by the kidneys and stimulation of thirst that increases the ingestion of water, so that the concentration of sodium in the ECFV begins to drop (hyponatremia). This causes a decrease in the osmolality (osmotic pressure) of the serum and ECFV. Since sodium and other ions cannot move freely out of the cells to reach an equilibrium with concentrations of ions outside the cell, water instead shifts (is osmotically pulled) from the ECFV back into the cells producing swelling of the cells, further depleting the ECFV. As water shifts into the cell, however, it creates an osmotic equilibrium with the lower serum osmolality outside the cell. With depletion of serum and ECFV, subjective signs and symptoms of dehydration begin to develop (postural hypotension, tenting of the forearm skin, dryness of the mucous membranes).
A low serum sodium concentration may result from a loss of sodium in excess of osmotically obligated water (primary salt depletion), a retention of water in excess of sodium (dilutional hyponatremia ), or a combination of both, as seen in the syndrome of inappropriate antidiuretic hormone (SIADH). Older persons studied in both acute and chronic care facilities have a higher prevalence of hyponatremia (serum sodium concentration less than 135 mEq/L)(7,8). Even in an ambulatory geriatric clinic, 11% of the patients had evidence of hyponatremia (9). SIADH appeared to be the etiology in over half the cases with no apparent underlying cause other than age found in seven patients (idiopathic). Reasons why older subjects are more prone to the development of hyponatremia, more specifically SIADH, are discussed elsewhere(10).
A reduction in serum sodium concentration to below 120 mEq/L, regardless of etiology, produces symptoms ranging from mild non-specific complaints, such as malaise, apathy, irritability, muscle weakness, and change in personality, to marked central nervous system (CNS) impairment, often ending with seizures. The CNS symptoms result from shifts of fluid along osmotic gradients from the hypotonic ECFV into the isotonic brain cells, thereby increasing brain volume and intracranial pressure. Although this fluid shift occurs throughout the body, e.g., producing ‘‘finger printing’’ (pressure over the sternum leaves finger prints due to the increase in intracel- lular water), those tissues not entrapped in a bony structure (cranium) are little affected.
8.3.1 Hyponatremia with Contracted ECFV
The causes of hyponatremia are listed in Table 8.2. When primary salt depletion with contraction of ECFV is suspected, a measure of urinary sodium concentration is most helpful. A concentration less than 10 mEq/L suggests inadequate intake of Chapter 8/ Hydration, Electrolyte, and Mineral Needs 141
salt, excessive sweating, or, most often, excessive gastrointestinal losses (diarrhea, bowel, or biliary fistulas). If urinary sodium excretion exceeds this level, one must think of excessive use of diuretics, adrenal or pituitary insufficiency, or intrinsic renal causes, e.g., renal tubular acidosis, salt-losing nephritis, or renal insufficiency.
Severe vomiting with resultant metabolic alkalosis can result in loss of sodium bound to the increased amounts of bicarbonate filtered and not reabsorbed in the proximal tubules, despite hyponatremia and hypovolemia.
Treatment is generally best accomplished by giving isotonic (0.9%) saline as the replacement; however, in individuals with symptomatic conditions, small amounts of hypertonic (5%) saline can be utilized. Caution needs to be exercised to avoid correcting the hyponatremia too rapidly as devastating demyelinating syndromes (cerebropontine myelinosis) can occur. The differential diagnosis between primary salt loss syndromes and SIADH can be problematic as edema is generally absent and urinary sodium excretions are high in both situations. The classic signs of dehydration may be unreliable, e.g., skin turgor in the normally hydrated older persons may appear poor due to loss of subcutaneous fat allowing ‘‘tenting’’ of skin over the backs of hands rather than being evidence of dehydration. An important clue in making the correct diagnosis can be serum urea nitrogen (SUN or BUN); it tends to be high in the former, and low, even sub-normal, in patients with SIADH, unless pre-existing renal impairment is present.
Table 8.2
Hyponatremic syndromes
1.Hyponatremia with contracted extracellular volume (ECFV)
A. Urinary sodium<10 mEq/L (inadequate intake, excessive sweating, excessive gastrointestinal loss, e.g., diarrhea, bowel, and biliary fistulas)
B. Urinary sodium>10 mEq/L
1. Severe metabolic alkalosis due to vomiting 2. Excessive urinary losses (salt wasting)
(a) Adrenal insufficiency (Addison’s disease, hypoaldosteronism) (b) Renal disease (renal tubular acidosis, interstitial nephritis) (c) Diuretic induced
2.Hyponatremia with normal ECFV
A. Displacement syndromes (hyperglycemia, hyperlipidemia, hyperproteinemia) B. Syndrome of inappropriate antidiuretic hormone (SIADH)
1. Malignancies, especially small cell carcinoma of lung 2. Pulmonary diseases, including positive pressure breathing 3. Cerebral conditions (trauma, infection, tumor, stroke)
4. Drugs (sulfonylureas, thiazides, antitumor agents, psychotropics, antidepressants)
5. Other (myxedema, porphyria, idiopathic) C. Water intoxication (schizophrenia)
3.Hyponatremia with expanded ECFV (dilutional hyponatremia) (congestive heart failure, cirrhosis, nephrotic syndrome, hypoalbuminemia, renal failure)
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8.3.2 Hyponatremia with Expanded ECFV (Dilutional Hyponatremia) Impairment of water excretion commonly occurs in conditions where salt excretion also is severely impaired. Patients with advanced cardiac, hepatic, and renal failure, and with generalized edema often are placed on diets that sharply curtail salt intake with little attention placed on putting limitations on fluid intake. When dilutional hyponatremia develops, considerations need to be given to also restricting fluid intake. Although total ECFV is increased, the blood flow returning to the heart and delivered to the arterial system is decreased, stimulating baroreceptors in the right atrium and arterial system to help the kidneys retain sodium, and baroreceptors in the left atrium and arterial system to stimulate ADH release and retain water. A marked increase in sodium and water reabsorption in the proximal tubule further limits water excretion by limiting the delivery of water and sodium to the distal nephron where dilution of urine below isotonic levels can take place. Although potent diuretics, e.g., furosemide, are available to increase sodium excretion, vasopressin antagonists that will block ADH effect on the distal nephron and increase water excretion are still in the investigative stages. One can use furosemide to increase salt excretion (this also creates a hypotonic urine), and give a hypertonic salt solution back to increase serum sodium concentration. As mentioned earlier, one must exercise caution in attempting to correct the hypona- tremia too rapidly.
8.3.3 Hyponatremia with Normal ECFV (Syndrome of Inappropriate ADH) Persistence of high levels of circulating ADH is considered inappropriate when neither hyperosmolality of serum nor volume depletion is present. The diagnosis of SIADH is usually made after other causes of hyponatremia are excluded. This means the urine remains concentrated and a high urinary sodium excretion persists after adrenal, renal, cardiac, and hepatic functions are determined to be normal.
The inability to excrete water because of high levels of circulating ADH causes volume expansion that, in turn, increases sodium loss with its osmotically obligated water, thereby returning ECFV to near normal. The causes of SIADH are shown in Table 8.2, and include patients with different neoplasms, most notably oat cell carcinoma of the lung, where an ADH-like molecule is secreted by the tumor.
Conditions limiting blood flow through the pulmonary circulation, including posi- tive pressure breathing, limit filling of the left atrium thereby stimulating ADH release in the presence of normal or increased volumes elsewhere. A number of drugs also have been implicated in causing this syndrome.
Normovolemic hyponatremia also can result from addition to the serum of an uncharged solute, e.g., glucose or mannitol. This will increase serum osmotic pressure drawing water from inside the cell to expand and dilute the ECFV. This increases urinary sodium loss, thereby lowering serum and body stores of sodium. A pseudohyponatremia also can develop from displacement of water in serum/plasma with abnormal amounts of high molecular weight solute, e.g., proteins or lipids.
While the concentration of sodium in the serum water is normal, the volume of water is less in the sample so that when further diluted prior to the assay, it gives a low serum sodium value.
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