SODIUM DEFICIT (HYPONATREMIA)
Hyponatremia refers to a serum sodium level that is below nor-mal (less than 135 mEq/L [135 mmol/L]). Plasma sodium con-centration represents the ratio of total body sodium to total body water. A decrease in this ratio can occur from a low quantity of total body sodium with a lesser reduction in total body water, normal total body sodium content with excess total body water, and an excess of total body sodium with an even greater excess of total body water. However, a hyponatremic state can be super-imposed on an existing FVD or FVE.
Sodium may be lost by way of vomiting, diarrhea, fistulas, or sweating, or it may be associated with the use of diuretics, parti-cularly in combination with a low-salt diet. A deficiency of aldo-sterone, as occurs in adrenal insufficiency, also predisposes the patient to sodium deficiency.
In water intoxication (dilutional hyponatremia), the patient’s serum sodium level is diluted by an increase in the ratio of water to sodium. This causes water to move into the cell, so that the pa-tient develops an ECF volume excess. Predisposing conditions for this type of hyponatremia include syndrome of inappropriate antidiuretic hormone (SIADH), hyperglycemia, and increased water intake through the administration of electrolyte-poor parenteral fluids, the use of tap-water enemas, or the irrigation of naso-gastric tubes with water instead of normal saline solution.
Water may be gained abnormally by the excessive parenteral administration of dextrose and water solutions, particularly dur-ing periods of stress. It may also be gained by compulsive water drinking (psychogenic polydipsia).
The basic physiologic disturbances in SIADH are excessive ADH activity, with water retention and dilutional hyponatremia, and inappropriate urinary excretion of sodium in the presence of hyponatremia. SIADH can be the result of either sustained se-cretion of ADH by the hypothalamus or production of an ADH-like substance from a tumor (aberrant ADH production).
Conditions associated with SIADH include oat-cell lung tu-mors, head injuries, endocrine and pulmonary disorders, physio-logic or psychological stress, and the use of medications such as oxytocin, cyclophosphamide, vincristine, thioridazine, and ami-triptyline.
Clinical manifestations of hyponatremia depend on the cause, mag-nitude, and speed with which the deficit occurs. Poor skin turgor, dry mucosa, decreased saliva production, orthostatic fall in bloodpressure, nausea, and abdominal cramping occur. Neurologic changes, including altered mental status, are probably related to the cellular swelling and cerebral edema associated with hyponatremia. As the extracellular sodium level decreases, the cellular fluid be-comes relatively more concentrated and pulls water into the cells (Fig. 14-4). In general, patients with an acute decrease in serum sodium levels have more severe symptoms and higher mortality rates than do those with more slowly developing hyponatremia.
Features of hyponatremia associated with sodium loss and water gain include anorexia, muscle cramps, and a feeling of ex-haustion. When the serum sodium level drops below 115 mEq/L (115 mmol/L), signs of increasing intracranial pressure, such as lethargy, confusion, muscle twitching, focal weakness, hemipare-sis, papilledema, and seizures, may occur.
Regardless of the cause of hyponatremia, the serum sodium level is less than 135 mEq/L; in SIADH it may be quite low, such as 100 mEq/L (100 mmol/L) or less. Serum osmolality is also de-creased, except in azotemia or ingestion of toxins. When hypo-natremia is due primarily to sodium loss, the urinary sodium content is less than 20 mEq/L (20 mmol/L), suggesting increased proximal reabsorption of sodium secondary to ECF volume de-pletion; the specific gravity is low, such as 1.002 to 1.004. When hyponatremia is due to SIADH, however, the urinary sodium content is greater than 20 mEq/L and the urine specific gravity is usually over 1.012. Although the patient with SIADH retains water abnormally and thus gains body weight, there is no pe-ripheral edema; instead, fluid accumulates inside the cells. This phenomenon is sometimes manifested as “fingerprinting” when the finger is pressed over a bony prominence, such as the sternum.
The key to treating hyponatremia is assessment; this includes the speed with which hyponatremia occurred rather than relying only on the patient’s actual serum sodium value (Fall, 2000).
The obvious treatment for hyponatremia is careful administration of sodium by mouth, nasogastric tube, or the parenteral route. For patients who can eat and drink, sodium is easily replaced, be-cause sodium is consumed abundantly in a normal diet. For those who cannot consume sodium, lactated Ringer’s solution or iso-tonic saline (0.9% sodium chloride) solution may be prescribed. Serum sodium must not be increased by greater than 12 mEq/L in 24 hours, to avoid neurologic damage due to osmotic de-myelination. This condition may occur when the serum sodium concentration is overcorrected (above 140 mEq/L) too rapidly or in the presence of hypoxia or anoxia (Pirzanda & Imran, 2001). It may produce lesions in the pons that cause paraparesis, dysarthria, dysphagia, and coma. Table 14-5 describes the components of selected water and electrolyte solutions. The usual daily sodium requirement in adults is approximately 100 mEq, provided there are no abnormal losses.
In SIADH, the administration of hypertonic saline solution alone cannot change the plasma sodium concentration. Excess sodium would be excreted rapidly in a highly concentrated urine. With the addition of the diuretic furosemide (Lasix), urine is not concentrated and isotonic urine is excreted to effect a change in water balance. In patients with SIADH, in whom water restric-tion is difficult, lithium or demeclocycline can antagonize the os-motic effect of ADH on the medullary collecting tubule.
In a patient with normal or excess fluid volume, hyponatremia is treated by restricting fluid to a total of 800 mL in 24 hours. This is far safer than sodium administration and is usually effective. When neurologic symptoms are present, however, it may be nec-essary to administer small volumes of a hypertonic sodium solu-tion, such as 3% or 5% sodium chloride. Incorrect use of these fluids is extremely dangerous because 1 L of 3% sodium chloride solution contains 513 mEq of sodium, and 1 L of 5% sodium chloride solution contains 855 mEq of sodium. If edema exists alone, sodium is restricted; if edema and hyponatremia occur together, both sodium and water are restricted.
The nurse needs to identify patients at risk for hyponatremia so that they can be monitored. Early detection and treatment of this disorder are necessary to prevent serious consequences. For patients at risk, the nurse monitors fluid intake and output as well as daily body weights. Abnormal losses of sodium or gains of water are noted. GI manifestations, such as anorexia, nausea, vomiting, and abdominal cramping, are also noted. The nurse must be particularly alert for central nervous system changes, such as lethargy, confusion, muscle twitching, and seizures. In general, more severe neurologic signs are associated with very low sodium levels that have fallen rapidly because of fluid over-loading. Serum sodium levels are monitored very closely in pa-tients at risk for hyponatremia; when indicated, urinary sodium levels and specific gravity are also monitored.
Hyponatremia is a frequently overlooked cause of confusion in elderly patients. The elderly are at increased risk for hypona-tremia because of changes in renal function and subsequent de-creased ability to excrete excessive water loads. Administration of medications causing sodium loss or water retention is a pre-disposing factor.
For patients experiencing abnormal losses of sodium who can consume a general diet, the nurse encourages foods and fluids with a high sodium content. For example, broth made with one beef cube contains approximately 900 mg of sodium; 8 oz of tomato juice contains approximately 700 mg of sodium. The nurse also needs to be familiar with the sodium content of par-enteral fluids (see Table 14-5).
For patients taking lithium, the nurse observes for lithium tox-icity, particularly when sodium is lost by an abnormal route. In such instances, supplemental salt and fluid are administered. Be-cause diuretics promote sodium loss, patients taking lithium are instructed not to use diuretics without close medical supervision. For all patients on lithium therapy, adequate salt intake should be ensured.
Excess water supplements are avoided in patients receiving isotonic or hypotonic enteral feedings, particularly if abnormal sodium loss occurs or water is being abnormally retained (as in SIADH). Actual fluid needs are determined by evaluating fluid in-take and output, urine specific gravity, and serum sodium levels.
When the primary problem is water retention, it is safer to restrict fluid intake than to administer sodium. Administering sodium to a patient with normovolemia or hypervolemia predisposes the pa-tient to fluid volume overload. As stated previously, the nurse must monitor patients with cardiovascular disease very closely.
In severe hyponatremia, the aim of therapy is to elevate the serum sodium level only enough to alleviate neurologic signs and symptoms. It is generally recommended that the serum sodium concentration be raised no higher than 125 mEq/L (125 mmol/L) with a hypertonic saline solution.
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