Hypernatremia treatment

Treatment of hypernatremia. Treatment depends on the cause, but in most cases, the patient is hypovolemic and needs fluids. Caution Do not reduce the serum sodium level too quickly, because osmotic imbalance may cause excessive fluid shift into brain cells, resulting in cerebral edema. The correction should take place over 24-36 hours the serum sodium should be lowered about 1 mEq/L/h. 

Treatment of hypovolemic hypernatremia should begin with 0.9% saline. After hemodynamic stability is restored and intravascular volume is replaced, free-water deficit can be replaced with 5% dextrose or 0.45% saline solution. 

Vasopressin and desmopressin are treatments of choice for pituitary diabetes insipidus. The dosage of desmopressin is 10-40 meg (0.1-0.4 mL) in two to three divided doses as a nasal spray or, as an oral tablet, 0.1-0.2 mg two to three times daily. The dosage by injection is 1-4 meg (0.25-1 mL) every 12-24 hours as needed for polyuria, polydipsia, or hypernatremia. Bedtime desmopressin therapy, by intranasal or oral administration, ameliorates nocturnal enuresis by decreasing nocturnal urine production. Vasopressin infusion is effective in some cases of esophageal variceal bleeding and colonic diverticular bleeding. 

Kawahara C, Okada Y, Tanikawa T, Fukusima A, H, Tanaka Y. Severe hypercalcemia and hypernatremia associated with calcipotriol for treatment of psoriasis. J Bone Miner Metab 2004 22 159-62. 

After a valproate overdose a 27-year-old man developed seizures, hypernatremia, respiratory failure, metabolic acidosis, liver failure, and bone marrow depression (125). His plasma valproic acid concentration was 1414 pg/ml. Treatment with hemodialysis was effective in enhancing valproic acid clearance, while hemoperfu-sion was relatively less effective, because of saturation of the column. Overall, the half-Ufe of the drug was reduced from over 20 hours before treatment to less than 3 hours during hemodialysis/hemoperfusion drug removal was probably favored by saturation of drug binding to plasma proteins, which resulted in a low unbound fraction (32% at the start of treatment). He was comatose for 5 days but recovered fully thereafter. 

The polyuria which often accompanies lithium treatment is normally compensated for by drinking water, but when consciousness is impaired severe hypernatremia may develop. When any acute illness (particularly if associated with gastrointestinal symptoms) occurs or when new medication is given, lithium blood levels should be closely monitored, and the lithium dose adjusted. 

Mannitol, the most commonly employed osmotic diuretic, is a large polysaccharide molecule. It is often selected for use in the prophylaxis or treatment of oliguric ARF. It is not absorbed from the gastrointestinal tract and, therefore, is only administered i.v. with its elimination dependent on the GFR (within 30 to 60 min with normal renal function). Mannitol is distributed within the plasma and extracellular fluid spaces and produces an increase in the serum osmolality and expansion of the circulating volume. It is not generally used for the treatment of edema because any mannitol retained in the extracellular fluid can promote further edema formation. Furthermore, acute plasma volume expansion may challenge individuals with poor cardiac contractility and can precipitate pulmonary edema. Mannitol is commonly administered for the treatment of cerebral edema consequent to head trauma or to hypoxic-ischemic encephalopathy in neonatal foals. Because mannitol promotes water excretion, hypernatremia is a potential complication in patients that do not have free access to water (Martinez-Maldonado Cordova 1990, Wilcox 1991). 

Hyperphosphatemia occurs without specific clinical signs in horses with strangulating intestinal lesions (Arden Stick 1988) and severe colitis (Svendsen et al 1979). The clinical findings reported in small animals include diarrhea, hypocalcemia, hypernatremia and an increased propensity to metastatic soft-tissue calcification. The treatment recommended in small animals includes i.v. fluids to correct any acidosis and promote renal phosphorus excretion and dextrose-containing fluids to promote translocation of phosphorus into cells (Macintire 1997). 

FIGURE 49-4. Diagnostic and treatment algorithm for hypernatremia. D5W, 5% dextrose in water ECF, extracellular fluid H2O, water Na, sodium Uosm, urine osmolality Uvol, daily urine volume. See text for guidelines regarding calculations of infusion rates for intravenous solutions. 

The goals in treating patients with hypernatremia include correction of the serum sodium concentration at a rate that restores and maintains cell volume as close to normal as possible, as well as normalizing the ECF volume in states of ECF volume depletion and expansion. Adequate treatment should result in the resolution of symptoms associated with hypovolemia. Careful titration of fluids and medications should minimize the adverse effects from too rapid correction. Modulation of dietary sodium intake and sodium replacement may be necessary to prevent recurrence of hypernatremia. 

Treatment of sodium overload consists of administration of loop diuretics to facilitate excretion of the excess sodium, as well as intravenous D5W. The latter should be infused at a rate that will decrease the serum sodium at approximately 0.5 mEq/L per hour, or 1 mEq/L per hour in cases in which the hypernatremia developed rapidly over several hours. ° The volume of infusate may be estimated as described previously. Furosemide should be administered at a dose of 20 to 40 mg intravenously every 6 hours. 

In dehydrated patients, replace fluid deficits with intravenous crystalloid solutions. Initial treatment should Include repletion of sodium and water with 1-2 L of normal saline (children 10-20 mL/kg). Once fluid deficits are replaced, give hypotonic (eg, half-normal saline) solutions because continued administration of normal saline often leads to hypernatremia, especially in patients with lithium-induced nephrogenic diabetes insipidus. 

If dehydration is the underlying cause of hypernatremia, the primary treatment will be rehydration. Of particular concern is the rate of rehydration and use of hypotonic... 

The nurse would monitor for which of the following signs that the treatment provided to a patient for hypernatremia may be excessive ... 

The primary treatment for hyponatremia owing to excess free water in the body is to remove the excess water and, if indicated, to treat the source of water retention. If diuretics are used to remove water, the nurse must monitor intake and output and electrolytes closely. Most diuretics work by removing sodium and water thus sodium levels may remain low initially. If the patient is symptomatic, sodium supplement may be given. The nurse should monitor for signs of hypernatremia (e.g., thirst, agitation, and hyperreflexia), which indicates that too much fluid was removed or too much sodium was infused. Potassium loss may occur with diuretics as well, so the nurse should monitor for hypokalemia. 6... 

Use of diuretics and fluid restriction as treatment, and the nurse should monitor for excessive treatment and dehydration, including intake and output, weight loss, and hypernatremia, as stated earlier. 

Which of the following symptoms would indicate that the treatment for a patient with hypernatremia had been effective ... 

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