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Hypotonic hyponatremia

Hyponatremia is very common in hospitalized patients and is defined as a serum sodium concentration below 136 mEq/L (136 mmol/L). Clinical signs and symptoms appear at concentrations below 120 mEq/L (120 mmol/L) and typically consist of agitation, fatigue, headache, muscle cramps, and nausea. With profound hyponatremia (less than 110 mEq/L [110 mmol/L]), confusion, seizures, and coma maybe seen. Because therapy is also influenced by volume status, hyponatremia is further defined as (1) hypertonic hyponatremia (2) hypotonic hyponatremia with an increased ECF volume (3) hypotonic hyponatremia with a normal ECF volume and (4) hypotonic hyponatremia with a decreased ECF volume.16... [Pg.409]

Hypotonic hyponatremia with an increase in ECF is also known as dilutional hyponatremia. In this scenario, patients have an excess of total body sodium and TBW however, the excess in TBW is greater than the excess in total body sodium. Common causes include CHF, hepatic cirrhosis, and nephrotic syndrome. Treatment includes sodium and fluid restriction in conjunction with treatment of the underlying disorder—for example, salt and water restrictions are used in the setting of CHF along with loop diuretics, angiotensin-converting enzyme inhibitors, and spironolactone.15... [Pg.409]

In hypotonic hyponatremia with a decreased ECF volume, patients usually have a deficit of both total body sodium and TBW, but the sodium deficit exceeds the TBW deficit. Common causes include diuretic use, profuse sweating,... [Pg.409]

Possible intestinal leak/perforation, diffuse peritonitis, sepsis, mild dehydration, and hypovolemic hypotonic hyponatremia... [Pg.1495]

Depending on serum osmolality, hyponatremia is classified as isotonic, hypertonic, or hypotonic (Fig. 78-1). [Pg.894]

Hypotonic hyponatremia, the most common form of hyponatremia, can be further classified as hypovolemic, euvolemic, or hypervolemic hyponatremia. [Pg.894]

Patients with hypovolemic hypotonic hyponatremia should be treated with 0.9% saline, initially at infusion rates of200 to 400 mL/hour until symptoms... [Pg.895]

Patients with hypervolemic hypotonic hyponatremia should be treated with 3% saline and prompt initiation of fluid restriction. Loop diuretic therapy will also likely be required to facilitate urinary excretion of free water. [Pg.895]

Treatment of asymptomatic hypervolemic hypotonic hyponatremia involves correction of the underlying cause and restriction of water intake to less than 1,000 to 1,200 mL/day. Dietary intake of sodium chloride should be restricted to 1,000 to 2,000 mg/day. [Pg.895]

A potential risk of desmopressin is of water intoxication with resultant hyponatremia (48), and rapid falls in serum sodium concentration can result in seizures. The risk is increased in infants and patients receiving hypotonic intravenous fluids, and such patients need to be carefully monitored. [Pg.482]

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. [Pg.881]

The most common cause of hyponatremia in hospital patients is SIADH. However, other disorders can cause dilutional hyponatremia and must be differentiated from SIADH. These conditions include (1) congestive heart failure, (2) renal insufficiency, (3) nephrotic syndrome, (4) liver cirrhosis, and (5) hypothyroidism. Excessive administration of hypotonic fluids and treatment with drugs that stimulate AVP (e.g., chlorpropamide, vincristine, clofibrate, carbamazepine, nicotine, phenothiazines, and cyclophosphamide) can cause dilutional hyponatremia as well. Hyponatremia may also occur from renal or extrarenal sodium losses (depietional hyponatremia) as a result of vomiting, diarrhea, excessive sweating, diuretic abuse, saltlosing nephropathy, or mineralocorticoid deficiency. [Pg.1994]

Proper attention to plasma expansion must be continued into the intraoperative and postoperative periods. A number of neurohormonal changes take place that affect urine output, and patients may have substantial third-spacing of fluid depending on the operation and the preexisting condition of the patient. Furthermore, postoperative patients are prone to hyponatremia from renal generation of electrolyte-free water and from antidiuretic hormone release. As in acute resuscitation, the administration of hypotonic solutions in the perioperative period does not prevent the decrease in extracellular volume that often occurs. Therefore, although excess fluid administration is to be avoided in the perioperative setting, isotonic crystalloid solutions should be used when fluids are indicated to prevent intravascular depletion and circulatory insufficiency. [Pg.489]

In patients with the syndrome of inappropriate secretion of antidiuretic hormone and symptomatic hypotonic hyponatremia, the most efficient means of correcting the hyponatremia involves the administration of 3% saline in conjunction with a loop diuretic. [Pg.937]

Patients with hypotonic hyponatremia caused by volume depletion should initially receive normal saline followed by 0.45% saline once signs of extracellular fluid volume depletion abate in order to avoid overly rapid correction of the serum sodium concentration. [Pg.937]

In patients with a low plasma osmolality (hypotonicity), the most important step in the diagnostic evalnation of hyponatremia is the clinical assessment of the extraceUnlar flnid volume. Categorization of patients with hypotonic hyponatremia into one of three gronps (decreased, increased, or clinically normal ECF volnme) is crucial in order to identify the pathophysiologic mechanisms responsible for the hyponatremia and thereby propose an appropriate treatment regimen (Fig. 49-2). [Pg.939]

This includes patients with fluid losses caused by diarrhea, excessive sweating, and diuretics. This transient hypernatremic hyperosmolality results in osmotic release of ADH and stimulation of thirst. If sodium and water losses continue, more ADH is released as a result of hypovolemia. Patients who then drink water or who are given hypotonic fluids intravenously retain water and develop hyponatremia. Urine osmolality is generally greater than 450 mOsm/kg, reflecting the presence of ADH and formation of a concentrated urine. The urine sodium concentration is <20 mEq/L when sodium losses are extrarenal, as in patients with diarrhea, and >20 mEq/L in patients with renal sodium losses, as occurs in the setting of diuretic use or adrenal insufflciency. °... [Pg.940]

The differential diagnosis of euvolemic hypotonic hyponatremia also includes primary or psychogenic polydipsia. Patients with this... [Pg.940]


See other pages where Hypotonic hyponatremia is mentioned: [Pg.229]    [Pg.169]    [Pg.410]    [Pg.1497]    [Pg.1504]    [Pg.88]    [Pg.895]    [Pg.895]    [Pg.527]    [Pg.882]    [Pg.882]    [Pg.2647]    [Pg.1217]    [Pg.1994]    [Pg.1995]    [Pg.939]    [Pg.940]    [Pg.940]    [Pg.940]    [Pg.941]   
See also in sourсe #XX -- [ Pg.169 ]

See also in sourсe #XX -- [ Pg.409 ]




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