Hypernatremia water/sodium

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

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

Hypernatremia is rare in horses (Brownlow Hutchins 1982). It is usually a result of water loss in excess of electrolytes and is accompanied by hyperchloremia. Iatrogenic hypernatremia may occur in horses in which resuscitation formulas are used for maintenance and is not an uncommon sequela in neonates. To correct hypernatremia, low sodium fluids such as 5% dextrose or 2.5% dextrose and 0.45% sodium chloride should be given. Again, in other species, it is recommended that hypernatremia not be corrected too rapidly sodium should be lowered by 0.5 mEq/1 per h, not to exceed 12 mEq/1 in the first 24 h (Schaer 1999). 

Hypernatremia (serum sodium > 145 mEq/L) may be caused by excessive sodium intake, excessive free water loss, or impaired renal concentrating ability. 

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... 

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

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. 

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. 

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. 

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 proper assessment of a patient with an abnormal serum sodium concentration requires recognition that the serum sodium level may bear no relationship to the ECF volume and sodium content. Hypernatremia and hyponatremia may be associated with conditions of high, low, or normal ECF sodium and volume. Abnormahties in the serum sodium concentration are thus a result of an alteration in the normal ratio between the total sodium and water content in the ECF... 

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. 

Hypernatremia occurs when the patient s semm sodium is greater than 145 mEq/L. This happens for one of two reasons The patient s sodium concentration has increased while the volume of water remains unchanged or the patient s water volume has decreased while the sodium concentration remains unchanged. 

Sodium bicarbonate is a systemic antacid that has many side effects including sodium excess that causes hypernatremia and water retention. Sodium bicarbonate also causes metaboMc alkalosis related to the excess bicarbonate. Therefore, sodium bicarbonate is seldom used to treat peptic ulcers. 

E. Hypernatremia and hyponatremia. Sodium disorders occur infrequently in poisoned patients (see Table 1-26). More commonly they are associated with underlying disease states. Antidiuretic hormone (ADH) is responsible for concentrating the urine and preventing excess water loss. 

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. 

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. 

Electrolyte balance Hypernatremia has been reported in a 44-year-old woman with normal renal function who was given too much sodium polystyrene sulfonate she was also taking furosemide, spironolactone, and lisinopril [39 ]. The authors attributed this to net intestinal water loss because of profuse osmotic diarrhea. 

Hypernatremia, that is, sodium levels of 146 mEq/L (146 mmol/L) or higher, results from excessive sodium intake or sodium retention with excessive loss of water owing to diarrhea, diurehc medicahon use, vomiting, sweating, heavy respirahon, or severe bums. Therefore, these pahents are at highest risk and should be monitored closely. Elderly hospitalized pahents should be watched most carefully because many have chronic diseases that may be fatal in combinahon with excessive sodium and fluid loss. 

Excessive ingestion of high-sodium solutions, such as sea water, or medications containing sodium (rarely causes hypernatremia because of the intestinal control of absorption of sodium). 

Diuretics that cause the kidneys to excrete more water than sodium are a common cause of hypernatremia. Additionally, pathology of the pituitary or hypothalamus can result in a deficiency of ADH, resulting in diabetes insipidus and excessive diuresis (with extremely high urine output). 

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... 

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-... 

The nutritional requirement is a reflection of obligatory losses (maintenance) and the needs of growth, pregnancy, and lactation. Abnormal losses owing to disease, or in animals such as humans and horses which sweat extensively, raise the requirement. The impact of equine sweating is different from that in humans. Human sweat always contains sodium at concentrations well below plasma levels (and when aldosterone secretion is raised, levels of sweat sodium fall very low) horse sweat is hypertonic but this helps to offset the osmotic effect of the increased respiratory water loss during exertion, i.e., it may be a defense against hypernatremia, rather than a potential cause of sodium depletion. Similarly hypernatremia in many species induces dehydration natriuresis - an appropriate defense. 

Excess salt intake does not raise plasma sodium concentration (hypernatremia) if water is available and the patient can drink the excess sodium is diluted. The resulting increase in ECF volume then stimulates increased sodium excretion. Sodium also enables ECF to hold water against the osmotic pull of the solutes in ICE and sodium thus functions as the osmotic skeleton of ECF it is the main determinant of its volume. 

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