Sodium hypernatremia

Sodium is contraindicated in patients with hypernatremia, fluid retention, and when the administration of sodium or chloride could be detrimental. Sodium is used cautiously in surgical patients and those with circulatory insufficiency, hypoproteinemia, urinaiy tract obstruction, congestive heart failure, edema, and renal impairment. Sodium is a Pregnancy Category C drug and is used cautiously during pregnancy. 

SODIUM When NaCl is administered by IV infusion, the nurse observes the patient during and after administration for signs of hypernatremia (see Display 58-2). The nurse checks the rate of IV infusion as ordered by the primary health care provider, usually every 15 to 30 minutes. More frequent monitoring of the infusion rate may be necessary when the patient is restless or confused. To minimize venous irritation during administration of sodium or any electrolyte solution, the nurse uses a small bore needle placed well within the lumen of a large vein. 

Hypovolemic hypernatremia (loss of water and sodium [water > sodium])... 

Hypervolemic hypernatremia (water and sodium gain [sodium > water])... 

Serum sodium in acute-onset hypernatremia may be lowered... 

Hypernatremia is a serum sodium concentration greater than 145 mEq/L (145 mmol/L) and can occur in the absence of a sodium deficit (pure water loss) or in its presence (hypotonic fluid loss).19 The signs and symptoms of hypernatremia are the same as those found in TBW depletion. Symptoms of hypernatremia are evident with a serum concentration greater than 160 mEq/L (160 mmol/L) and usually consist of thirst, mental slowing, and dry mucous membranes. Signs and symptoms become more profound as hypernatremia worsens, with the patient demonstrating confusion, hallucinations, acute weight... 

The neuromuscular junction and muscle are more resistant to changes in sodium concentration, to which they are minimally permeable at rest. In fact, the consequences of sodium disturbance relate instead to the role of this ion in maintaining the osmotic equilibrium between the brain and plasma and range from depression of consciousness, coma and seizures caused by hyponatremia, to brain shrinkage and tearing of superficial blood vessels due to excessive serum osmolarity due to hypernatremia. 

Hypernatremia and fluid retention commonly occur, necessitating restricting daily sodium intake to no more than 3 g. All sources of sodium, including antibiotics, need to be considered when calculating daily sodium intake. 

Hypernatremia can result from water loss (e.g., diabetes insipidus [DI]) hypotonic fluid loss or, less commonly, hypertonic fluid administration or sodium ingestion. 

Patients with sodium overload should be treated with loop diuretics (furosemide, 20 to 40 mg IV every 6 hours) and 5% dextrose at a rate that decreases serum sodium by approximately 0.5 mEq/L/hour or, if hypernatremia developed rapidly, 1 mEq/L/hour. 

Hypernatremia fluid retention when the administration of sodium or chloride could be clinically detrimental. 

Infusion of more than 1 L of isotonic (0.9%) sodium chloride may supply more sodium and chloride than normally found in serum, resulting in hypernatremia this may cause a loss of bicarbonate ions, resulting in an acidifying effect. 

Concentrated sodium chloride injection Inadvertent direct injection or absorption of concentrated sodium chloride injection may give rise to sudden hypernatremia and such complications as cardiovascular shock, CNS disorders, extensive hemolysis, cortical necrosis of the kidneys, and severe local tissue necrosis (if administered extravascularly). Do not use unless solution is clear. When administered peripherally, slowly infuse through a small bore needle placed well within the lumen... 

Neonates and children (younger than 2 years of age) - Rapid injection (10 mL/min) of hypertonic sodium bicarbonate solutions may produce hypernatremia, a decrease in cerebrospinal fluid pressure and possible intracranial hemorrhage. Do not administer more than 8 mEq/kg/day. A 4.2% solution is preferred for such slow administration. 

They have a synergistic effect with aminoglycosides (e.g. gentamicin or netilmicin) and hence should be given concomitantly in pseudomonas septicaemia. They should however, not be mixed in the same syringe. Owing to the sodium content, high doses may lead to hypernatremia. 

Sodium phosphate is available as a nonprescription liquid formulation and by prescription as a tablet formulation. When taking these agents, it is very important that patients maintain adequate hydration by taking increased oral liquids to compensate for fecal fluid loss. Sodium phosphate frequently causes hyperphosphatemia, hypocalcemia, hypernatremia, and hypokalemia. Although these electrolyte abnormalities are clinically insignificant in most patients, they may lead to cardiac arrhythmias or acute renal failure due to tubular deposition of calcium phosphate (nephrocalcinosis). Sodium phosphate preparations should not be used in patients who are frail or elderly, have renal insufficiency, have significant cardiac disease, or are unable to maintain adequate hydration during bowel preparation. 

Aldosterone and other steroids with mineralocorticoid properties promote the reabsorption of sodium from the distal convoluted and cortical collecting renal tubules, loosely coupled to the excretion of potassium and hydrogen ion. Sodium reabsorption in the sweat and salivary glands, gastrointestinal mucosa, and across cell membranes in general is also increased. Excessive levels of aldosterone produced by tumors or overdosage with synthetic mineralocorticoids lead to hypernatremia, hypokalemia, metabolic alkalosis, increased plasma volume, and hypertension. 

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. 

Sodium When patients present with hypernatremia and elevated serum osmolality, they are suffering from severe fluid deficits. Depending on the patient s hemodynamic stability, fluid therapy should generally be instituted as a moderate-to-slow intravenous infusion of 0.9% normal saline over a period of 48-72 h to avoid cerebral edema. Patients with evidence of circulatory compromise will require more aggressive fluid resuscitation. Estimated plasma osmolality and corrected serum sodium concentrations are calculated using the following formulas ... 

Eight years after stopping lithium because of polydipsia and polyuria, a 55-year-old woman was hospitalized with lethargy, coma, and hypernatremia (sodium concentration 156 mmol/1) after her fluid intake had been restricted (391). 

A 67-year-old man with bipolar disorder became confused, delirious, and manic (99). His only medications were olanzapine 10 mg/day and divalproex sodium 500 mg bd. On day 6, typical neuroleptic malignant syndrome developed. He had a fever (39.9°C), obtundation, rigidity, tremor, sweating, fluctuating pupillary diameter, labile tachycardia and hypertension, hypernatremia, and raised serum creatine kinase. Olanzapine was withdrawn and the syndrome resolved by day 12. 

Adding an isotonic solution to the extracellular fluid (ECF) does not change intracellular volume. Adding a hypertonic solution to the ECF decreases cell volume, whereas adding a hypotonic solution increases it (Table 78-1). Hypernatremia and hyponatremia can be associated with conditions of high, low, or normal ECF sodium and volume. Both conditions are most commonly the result of abnormalities of water metabolism. 

Since beta-lactam antibiotics contain sodium or potassium, they can cause or at least aggravate electrolyte disturbances when given in sufficiently high doses. The most frequent manifestations are hypernatremia and hypokalemia. The sodium content of injectable beta-... 

Potassium penicUhn G can significantly alter potassium balance when given in very high doses 20 mUhon units of potassium penicUhn G contains about 30 mmol of potassium, and in patients with renal insufficiency this amount can decisively aggravate potentially lethal hyperkalemia. Similarly, large doses of sodium penicillin G, carbenicil-lin, or ticarcUhn can cause hypernatremia (29,30). 

A 46-year-old woman, with hepatic encephalopathy complicating cirrhosis due to hepatitis B and C infection, developed fatal hypernatremia, hyperphosphatemia, and hypocalcemia following the erroneous administration of a total of six sodium phosphate enemas (133 ml each) over 36 hours (16). 

Sodium polystyrene sulfonate can cause hypokalemia, hypocalcemia, and hypernatremia (4,5). 

In addition to vasodilatory responses, PGs have a number of other effects in the kidney. For example, PGs stimulate adenylate cyclase in juxtaglomerular cells, resulting in an increase in cAMP production this, in turn, increases renin release. Renin stimulates the release of aldosterone, which increases renal tubular secretion of potassium (Stillman Schlesinger 1990). PGs also enhance tubular excretion of sodium and water (Patrono Dunn 1987). By causing these effects in the kidneys, PGs can alter electrolyte homeostasis. Therefore, other renal side-effects of NSAID therapy can include hyperkalemia, hypernatremia and edema. Often these metabolic changes are not observed in individuals with normal renal function, but in the presence of pre-existing disease they can become clinically significant. 

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