Dehydration hypernatremia

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. 

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. 

Excessive use of mannitol without adequate water replacement can ultimately lead to severe dehydration, free water losses, and hypernatremia. As water is extracted from cells, intracellular K+ concentration rises, leading to cellular losses and hyperkalemia. 

A 78-year-old man who had taken lithium for 30 years who presented with dehydration, azotemia, hypernatremia, hypercalcemia, and increased PTH concentrations (669). 

Hypernatremia can occur secondary to dehydration in patients taking lithium and is not uncommon in association with lithium poisoning. Lithium-induced diabetes insipidus is often a contributing factor. 

A 77-year-old woman who had taken lithium for 10 years developed delirium, hypernatremia, prerenal azotemia, and a serum lithium concentration of 1.4 mmol/1 her condition was attributed to dehydration related to partial nephrogenic diabetes insipidus (381). 

A 76-year-old man developed severe intractable diabetes insipidus which was attributed to lithium (395). He was hospitalized for over 2 weeks and eventually died from intestinal hemorrhage. Vigorous efforts were made to treat his polyuria, electrolyte disturbances, hypernatremia, and dehydration. He had been taking chlorpromazine, lithium, and furosemide, along with other medications, and the diagnosis of lithium-induced nephrogenic diabetes insipidus was considered because of a lack of alternative explanations. 

Clinical signs associated with hypo- and hypernatremia result from changes in the plasma osmolality. Sodium is the major cation in plasma, and sodium and glucose concentrations are the main determinants of plasma osmolality (Brownlow Hutchins 1982). Changes in plasma osmolality can lead to CNS edema or dehydration (Rose 1994), because the CSF equilibrates slowly with the plasma but will change rapidly if osmotic gradients are high. 

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 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. 

Because of concerns about hypernatremia, physicians continue to hospitalize and intravenously correct fluid and electrolyte deficits in severe dehydration. Oral solutions are strongly recommended. In developing countries, the World Health Organization Oral Rehydration Solution (WHO-ORS) saves the lives of millions of children annually. 

Hypernatremia Dehydration, net relative sodium excess Increase fluid intake, decrease sodium intake... 

The low plasma PCO2 leads to decreased renal tubular reabsorption of bicarbonate and increased renal excretion ofNa , K, and water. Water also is lost by salicylate-induced sweating (especially in the presence of hyperthermia) and hyperventilation dehydration, which can be profound, particularly in children, rapidly occurs. Because more water than electrolyte is lost through the lungs and by sweating, the dehydration is associated with hypernatremia. Prolonged exposure to high doses of salicylate also causes depletion ofK due to both renal and extrarenal factors. 

C. Nephrogenic diabetes insipidus (see p 35) is a recognized complication of chronic lithium therapy and may lead to dehydration and hypernatremia. 

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. 

C. Use of charcoal-sorbitol mixtures should be avoided in children (risk of hypernatremia and dehydration). 

C. Diarrhea, dehydration, hypermagnesemia, and hypernatremia resulting from co-administered cathartics, especially with repeated doses of charcoal and cathartics, or even after a single large dose of a premixed, sorbitol-containing charcoal product. 

Mineral balance Hypernatremia, hypokalemia, and acidosis have been reported after incorrect administration of oral rehydration solutions to two infants [lOS ]. In both cases the parents had diluted 21 g of each oral rehydration solution packet in 200 ml of water. In one case the electrolyte abnormalities were corrected and the losses were replaced with properly reconstituted oral rehydration solution. In the other case there was severe dehydration and the child died. 

Decreased intake of fluids—the elderly are at risk for hypernatremia owing to a decreased thirst mechanism that results in decreased fluid intake and dehydration. 

Thus hypernatremia occurs in diabetes insipidus because the disease causes excessive urine production and dehydration. 2... 

In hypernatremia, fluid moves out of the cells in an attempt to dilute the high concentration of sodium in the extracellular fluid. This causes cell dehydration with shrinkage, resulting in dry tissues, particularly evident in mucous membranes, loss of skin elasticity (turgor), and thirst (stimulated by ADH release). 

Some symptoms of hypernatremia may vary depending on the underlying cause. If dehydration is present owing to vomiting or diarrhea or failure to drink fluids, the urine output will be low (< 30 mL/h) with dark yellow appearance. However, if a hyperosmotic state or a condition causing decreased ADH release, such as diabetes insipidus, is... 

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... 

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. 

Fluid loss and dehydration are the most common causes of hypernatremia. 

Bailey McIntosh, age 34, was admitted with dehydration and hypernatremia after a marathon race. The nurse would watch closely for which of the following signs of a likely magnesium imbalance ... 

The potential for hypernatremia is increased owing to dehydration and hemoconcentration. AlA... 

The dehydration is aggravated by the lack of thirst response in the elderly, resulting in decreased intake of fluids and increased serum osmolality and hypernatremia. 

Sodium deprivation increases aldosterone secretion, probably by modifying the volume of the body fluids. This conclusion was reached because of observations that (1) the administration of water (with Pitressin to prevent diuresis) depresses aldosterone secretion in spite of the hyponatremia (2) if the body fluids are expanded by administering normal saline, aldosterone excretion is stimulated although the sodium levels of the blood are not modified and (3) dehydration leads to aldosterone secretion, although the reduction in body fluid volume resulting from dehydration is associated with hypernatremia. From these observations, changes in body fluid volume appear to affect aldoster-rone secretion, and it has been stated that the expansion of the body fluids reduces aldosterone secretion. This conclusion, which is based on experimental obser-... 

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