Hypernatremia caused

Parenteral phosphorus supplementation is associated with risks of hyperphosphatemia, metastatic soft tissue deposition of calcium-phosphate product, hypomagnesemia, hypocalcemia, and hyperkalemia or hypernatremia (caused by intravenous phosphorus salt) (Table 49-9). Inappropriate administration of large doses of parenteral phosphorus over relatively short time periods has resulted in symptomatic hypocalcemia and soft-tissue calcification. The rate of infusion and choice of initial dosage should therefore be based on severity of hypophosphatemia, presence of symptoms, and coexistent medical conditions. Patients should be closely monitored with frequent (every 6 hours) serum phosphorus determinations for 48 to 72 hours after starting intravenous therapy. It may be necessary to continue administration of intravenous phosphorus for several days in some patients, while other patients may be able to tolerate an... 

Hypernatremia occurs in water deficiency, caused by reduced water supply or elevated water loss, corresponding to hypertonic dehydration. Hypernatremia caused by excessive intake of sodium or reduced elimination of sodium results in hypertonic hyperhydration. Elevated serum sodium may also occur in endocrine dysregulations (e.g., hyperaldosteronism. Conn s syndrome, Cushing s syndrome) and in chronic kidney disease. 

Hyponatremia, hypernatremia, hyperkalemia, hypocalcemia, hypomagnesemia, and hypoglycemia can cause SE... 

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. 

Symptoms of hypernatremia are primarily caused by decreased neuronal cell volume and can include weakness, restlessness, confusion, and coma. 

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. 

Excessive dosage may cause hypokalemia, hypervolemia, and hypernatremia. 

Acid-base and electrolyte balance High therapeutic dose especially when used in rheumatic fever, stimulates respiration and causes respiratory alkalosis. Reduction in bicarbonate and potassium level reduces the buffering capacity of the extracellular and intracellular fluid. Hypokalemia may lead to dehydration and hypernatremia. They also interfere with carbohydrate metabolism resulting in accumulation of pyruvic acid and lactic acid. 

If serum Na+ is not monitored closely, ADH antagonists can cause severe hypernatremia and nephrogenic diabetes insipidus. If lithium is being used for a psychiatric disorder, nephrogenic diabetes insipidus can be treated with a thiazide diuretic or amiloride. 

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. 

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. 

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). 

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. 

Hypernatremia (plasma Na >150 mmol/L) is always hyperosmolar, Symptoms of hypernatremia are primarily neurological (because of intraneuronal loss of H2O to the ECF) and include tremors, irritability, ataxia, confusion, and coma. As with hyponatremia, the rapidity of the development of hypernatremia wiU determine the plasma Na value at which symptoms occur. Acute development may cause symptoms when Na reaches 160 mmol/L, although in chronic hypernatremia, overt symptoms may not occur until Na exceeds 175 mmol/L. In chronic hypernatremia, the intracellular osmolality of CNS cells wiU increase to protect against intracellular dehydration. Because of this, rapid correction of hypernatremia can cause dangerous cerebral edema, as CNS cells will take up too much water if the ICF is hyperosmotic when normonatremia is achieved. ... 

Hypernatremia in the setting of decreased ECF is caused by the renal or extrarenal loss of hypoosmotic fluid leading to dehydration. Thus once hypovolemia is established, measurement of urine Na" " and osmolality is used to determine the source of fluid loss. Patients who have large extrarenal losses have a concentrated urine (>800 mOsmol/L) with low urine Na (<20 mmol/L), reflecting the proper renal response to conserve Na and water as a means to restore ECF volume. Extrarenal causes include diarrhea, skin (burns or excessive sweating), or respiratory losses coupled with failure to replace the lost water. When gastrointestinal loss is excluded, and the patient has normal mental status and access to H2O, a hypothalamic disorder (tumor or granuloma) should be suspected, because the normal thirst response should always replace insensible water losses. 

The presence of excess TBW and hypernatremia indicates a net gain of water and Na, with Na gain in excess of water (see Figure 46-3). This condition is commonly observed in hospital patients receiving hypertonic saline or sodium bicarbonate. Other causes of hypervolemic hypernatremia include hyperaldosteronism and Cushing s syndrome (see Chapters 24 and 51). Excess aldosterone and cortisol (which also act as ligands for the distal tubule aldosterone receptor) results in excess Na and water retention. Corticosteroid therapy can have similar effects as weh. 

The unmeasured anion is commonly known as the anion gap, which is normally 12 4 mEq/L. This value is useful in assessing the acid-base status of a patient and in diagnosing metabolic acidosis. Disorders that cause a high anion gap are metabolic acidosis, dehydration, therapy with sodium salts of strong acids, therapy with certain antibiotics (e.g., carbenicillin), and alkalosis. A decrease in the normal anion gap occurs in various plasma dilution states, hypercalcemia, hypermagnesemia, hypernatremia, hypoalbuminemia, disorders associated with hyperviscosity, some paraproteinemias, and bromide toxicity. 

Potential adverse effects associated with hypertonic fluid administration for circulatory insufficiency include cellular crenation and damage caused by the dramatic fluid shifts, as well as peripheral vein destruction from their high osmolality. Also, in the case of hypertonic sodium chloride solutions, there are the possibilities of neurologic damage from hypernatremia and hyperchloremic metabolic acidosis from hyperchloremia. In the limited number of studies conducted in humans to date, such adverse effects have been uncommon and apparently of little clinical importance. ... 

Two-thirds of total body water is distributed intracellularly while one-third is contained in the extracellular space. Sodium and its accompanying anions, chloride and bicarbonate, comprise more than 90% of the total osmolality of the extracellular fluid (ECF), while intracellular osmolality is primarily dependent on the concentration of potassium and its accompanying anions (mostly organic and inorganic phosphates). The differential concentrations of sodium and potassium in the intra- and extracellular fluid is maintained by the Na+-K+-ATPase pump. Most cell membranes are freely permeable to water, and thus the osmolality of intra- and extracellular body fluids is the same. Symptoms in patients with hypo- and hypernatremia are primarily related to alterations in cell volume. It is therefore essential to understand the factors that cause changes in cell volume. 

The symptoms of hypernatremia are primarily caused by a decrease in neuronal cell volume, and may include weakness, restlessness, confusion, and coma. Hypernatremia results in movement of water from the intracellular space to the extracellular fluid. Neurons can adapt to hypertonicity in the ECF by generating intracellular organic osmolytes within 24 hours of onset. This increase in intracellular fluid tonicity then draws water into the neurons, thus limiting the decrease in cell volume. Patients with chronic hypernatremia are less likely to present with symptoms caused by this cerebral adaptation. 

Chapter 6). Prolonged or excessive losses of fluid via the GI tract will affect packed cell volume (hematocrit), plasma total protein, albumin, electrolytes, acid-base balance, and osmolality values as the circulating blood volume adjusts to the fluid loss. Excessive and prolonged salivation may also cause electrolyte perturbations, but to a much smaller extent. Hypo- or hypernatremia may occur depending on the proportional losses of electrolyte to water these electrolyte changes are also reflected by plasma osmolality. There may be significant differences between the measured and calculated plasma osmolality in the presence of hyperlipidemia and hyperproteinemia. 

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