Hyponatremia treatment

In mild cases of hyponatremia, treatment typically focuses on water restriction (< 800 mL/day) however this approach suffers from poor patient compliance due to thirst brought on by increasing serum osmolality.1,10 In cases of extreme hyponatremia, infusions of hypertonic saline are used to elevate serum sodium concentrations. Loop diuretics (e.g., furosemide) are often used as an adjunct to such treatment to offset potential volume overload.1 Hypertonic saline therapy is also suboptimal, as it carries a risk of overly rapid adjustment of plasma sodium levels, which can result in the rapid shift of water from brain tissue to the vascular space, triggering neural demyelination that can result in seizures, coma, quadriplegia, and even death.1... 

The use of fixed combination of a thiazide and a potassium-sparing drug, often Moduretic (hydrochlorothiazide 50 mg with amiloride 5 mg), has been consistently implicated in diuretic-induced hyponatremia. Treatment with chlorpropamide (200-800 mg/day) along with Moduretic has precipitated hyponatremia in several cases (96). Simultaneous use of Moduretic with trimethoprim has also been reported to increase the risk (97). The mechanism appears to be impairment of the clearance of free water, resulting in dilutional hyponatremia. Whether... 

Sterns RH. Severe symptomatic hyponatremia Treatment and outcome A study of 64 cases. Ann Intern Med 1987 107 656-664. 

Treatment of hyponatremia. Treatment depends on the cause, the patient s volume status, and most important, the patient s clinical condition. Caution Avoid overly rapid correction of the sodium, because brain damage (central pontine myelinolysis) may occur if the sodium is increased by more than 25 mEq/L in the first 24 hours. Obtain frequent measurements of serum and urine sodium levels and adjust the rate of infusion as needed to inorease the serum sodium by no more than 1-1.5 mEq/h. Arrange consultation with a nephrologist as soon as possible. For patients with profound hyponatremia (serum sodium < 110 mEq/L) accompanied by coma or seizures, administer hypertonic (3% sodium chloride) saline, 100-200 mL. 

In long-term treatment, the thia2ides may produce hypokalemia, hyperglycemia, hypemricemia, and a 5% increase in plasma cholesterol indapamide has been shown not to increase plasma cholesterol or Hpids at therapeutic doses (21—23). The decrease of plasma potassium, ie, hypokalemic effect, is dose-dependent, and can be avoided if high doses are avoided (24,25). Thia2ides can cause hyponatremia in patients with large water intake while on the dmg (26,27) hyponatremia may be associated with nausea, vomiting, and headaches. 

The use of V2 antagonists is promising in the treatment of the hyponatremia that usually accompanies congestive heart failure and cirrhosis, two edematous conditions in which the use of diuretics is indicated. In addition, V2 antagonists may be beneficial in the treatment of polycystic kidney disease. 

Several nonpeptidic, orally active vasopressin receptor antagonists have been developed. The dual V1A/V2R antagonist conivaptan is used in the treatment of hyponatraemia and could also become useful for diseases such as congestive heart failure, in which increased peripheral resistance and dilutional hyponatremia both are present [4]. Side effects of conivaptan include headache, injection site reactions, vomiting, diarrhoea, constipation and thirst. 

Hypertonic hyponatremia is usually associated with significant hyperglycemia. Glucose is an osmotically active agent that leads to an increase in TBW with little change in total body sodium. For every 60 mg/dL (3.33 mmol/L) increase in serum glucose above 200 mg/dL (11.1 mmol/L), the sodium is expected to decrease by approximately 1 mEq/L (1 mmol/L). Appropriate treatment of the hyperglycemia will return the serum sodium to normal.15... 

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... 

Carbamazepine Manufacturer recommends CBC and platelets (and possibly reticulocyte counts and serum iron) at baseline, and that subsequent monitoring be individualized by the clinician (e.g., CBC, platelet counts, and liver function tests every 2 weeks during the first 2 months of treatment, then every 3 months if normal). Monitor more closely if patient exhibits hematologic or hepatic abnormalities or if the patient is receiving a myelotoxic drug discontinue if platelets are less than 100,000/mm3, if white blood cell (WBC) count is less than 3,000/mm3 or if there is evidence of bone marrow suppression or liver dysfunction. Serum electrolyte levels should be monitored in the elderly or those at risk for hyponatremia. Carbamazepine interferes with some pregnancy tests. 

Treatment of hyponatremia involves the use of hypertonic saline. However, care is required since correction at rates in excess of 1 mEq/l/h may result in central pontine myelinolysis (CPM) [5], Symptoms of CPM include progressive weakness leading to quadriparesis, pseudobulbar palsy and altered mental status. CPM is often fatal and is characterized neuropathologically by demyelinating lesions in the central pons. 

Treatment of hyponatremia is associated with a risk of osmotic demyelina-tion syndrome, a severe neurologic complication that can develop if the rate of serum sodium correction exceeds 8 to 12 mEq/L within 24 hours. 

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. 

The activity of the renin-angiotensin system is reduced with age (Muhlberg and Platt 1999). The ability of the kidney to concentrate urine maximally after water deprivation decreases with age, as does the ability to excrete a water and salt load, particularly during the night. Nocturnal polyuria is common in the elderly (Lubran 1995). Diuretics are commonly used in the elderly. There is an increased risk for hypokalemia and hyponatremia from diuretics in the elderly (Passare et al. 2004). Electrolyte disturbances may also be caused by several types of drugs in the elderly and it is important to monitor serum electrolyte levels in the elderly. Treatment with... 

Hyponatremia/Hypochloremia - A chloride deficit is generally mild and usually does not require specific treatment, except in extraordinary circumstances (as in liver or renal disease). Thiazide-induced hyponatremia has been associated with death and neurologic damage in elderly patients. 

Hyponatremia Clinically significant hyponatremia generally occurred during the first 3 months of treatment with oxcarbazepine, although there were patients who first developed a serum sodium less than 125 mmol/L greater than 1 year after initiation of therapy. Most patients who developed hyponatremia were asymptomatic, but patients in the clinical trials were frequently monitored and some had their oxcarbazepine dose reduced or discontinued or had their fluid intake restricted for hyponatremia. When oxcarbazepine was discontinued, normalization of serum sodium generally occurred within a few days without additional treatment. 

A toxicity that is unique to cyclophosphamide and ifosfamide is cystitis. Dysuria and decreased urinary frequency are the most common symptoms. Rarely, fibrosis and a permanently decreased bladder capacity may ensue. The risk of development of carcinoma of the bladder also is increased. Large intravenous doses have resulted in impairment of renal water excretion, hyponatremia, and increased urine osmolarity and have been associated with hemorrhagic subendocardial necrosis, arrhythmias, and congestive heart failure. Interstitial pulmonary fibrosis may also result from chronic treatment. Other effects of chronic drug treatment include infertility, amenorrhea, and possible mutagenesis and carcinogenesis. 

ADH antagonists, including nonpeptide analogues that may be taken orally, have been developed with specificity for each of the receptor types. In the future, those that block Vj receptors may be useful in treating hypertension, and those that block Vj receptors may be useful in any condition of excessive water retention or hyponatremia, for which so far there is no satisfactory therapeutic treatment. 

A vasopressin V2 receptor antagonist, lixivaptan, is currently being developed (Phase 11) for the treatment of hyponatremia. This agent blocks the effect of the antidiuretic hormone arginine-vasopressin. 

Enuresis 10-40 ag qhs/bid Headache nausea Hyponatremia and water intoxication at toxic doses Can be useful for acute situations (e.g., sleepaways) or as maintenance treatment DDAVP 0.1, 0.2 mg t nasal spray 10 Hg/ spray... 

Case reports have indicated an association between SSRIs and the syndrome of inappropriate secretion of antidiuretic hormone. Symptoms include lethargy, headache, hyponatremia, increased urinary sodium excretion, and hyperosmotic urine. Acute treatment of this syndrome should consist of discontinuation of the drug as well as restriction of fluid intake. Patients experiencing severe confusion, convulsions, or coma should receive intravenous sodium chloride. Elderly persons may he at a higher risk for developing this syndrome. 

The syndrome of inappropriate antidiuretic hormone secretion, with resultant hyponatremia, may be induced by carbamazepine treatment. Alcoholic patients may be at greater risk for hyponatremia. 

Oxcarbazepine is typically started at a dosage of 150 mg twice a day and titrated by 300 mg/day at weekly intervals. Therapeutic dosages are in the range of 450 mg twice a day to 1,200 mg twice a day. The conversion from carbamazepine to oxcarbazepine is approximately 1 to 1.5. Oxcarbazepine has a higher risk of hyponatremia than does carbamazepine. Serum sodium should be monitored in patients at risk for hyponatremia, such as the elderly or patients who are also taking diuretics. Stevens-Johnson syndrome and toxic epidermal necrolysis may occur between 3 and 10 times more frequently in oxcarbazepine-treated patients than in the general population. Median time from starting treatment to the development of these serious reactions is 19 days. 

Antidiuretic hormone is also elevated in response to diminished effective circulating blood volume, as often occurs in congestive heart failure. When treatment by volume replacement is not desirable, hyponatremia may result. As for SIADH, water restriction is often the treatment of choice. In patients with congestive heart failure, this approach is often unsuccessful in view of increased thirst and the large number of oral medications being used. In these patients, conivaptan may be particularly useful because it has been found that... 

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