Hyponatremia in a volume-depleted patient is caused by a deficit in total body sodium and total body water, with a disproportionately greater sodium loss, whereas in euvolemic hyponatremia, the total body sodium level is normal or near normal. Differentiating between hypovolemia and euvolemia may be clinically difficult, especially if the classic features of volume depletion such as postural hypotension and tachycardia are absent.
Laboratory markers of hypovolemia, such as a raised hematocrit level and blood urea nitrogen BUN -to-creatinine ratio of more than 20, may not be present. In fact, results of one study 15 showed an increased BUN-to-creatinine ratio in only 68 percent of hypovolemic patients. Two useful aids for evaluating euvolemic or hypovolemic patients are measurement of plasma osmolality and urinary sodium concentration.
Plasma osmolality testing places the patient into one of three categories, normal, high, or low plasma osmolality, while urinary sodium concentration testing is used to refine the diagnosis in patients who have a low plasma osmolality.
The combination of hyponatremia and normal plasma osmolality to mOsm per kg [ to mmol per kg] of water can be caused by pseudohyponatremia or by the post-transurethral prostatic resection syndrome. The phenomenon of pseudohyponatremia is explained by the increased percentage of large molecular particles, such as proteins and fats in the serum, relative to sodium.
These large molecules do not contribute to plasma osmolality, resulting in a state in which the relative sodium concentration is decreased, but the overall osmolality remains unchanged. Severe hypertriglyceridemia and hyperproteinemia are two causes of this condition in patients with pseudohyponatremia. These patients usually are euvolemic. The post-transurethral prostatic resection syndrome consists of hyponatremia with possible neurologic deficits and cardiorespiratory compromise.
Although the syndrome has been attributed to the absorption of large volumes of hypotonic irrigation fluid intraoperatively, its pathophysiology and management remain controversial. Increased plasma osmolality more than mOsm per kg of water in a patient with hyponatremia is caused by severe hyperglycemia, such as that occurring with diabetic ketoacidosis or a hyperglycemic hyperosmolar state.
It is caused by the presence of glucose molecules that exert an osmotic force and draw water from the intracellular compartment into the plasma, with a diluting effect.
Osmotic diuresis from glucose then results in hypovolemia. Fortunately, hyperglycemia can be diagnosed easily by measuring the bedside capillary blood glucose level. Patients with low plasma osmolality less than mOsm per kg of water can be hypovolemic or euvolemic. The level of urine sodium is used to further refine the differential diagnosis. Excess renal sodium loss can be confirmed by finding a high urinary sodium concentration more than 30 mmol per L.
In these patients, the main causes of hyponatremia are renal disorders, endocrine deficiencies, reset osmostat syndrome, syndrome of inappropriate antidiuretic hormone secretion SIADH , and drugs or medications. Because of their prevalence and importance, SIADH and drugs deserve special mention, and the author will elaborate on these causes later in the article. Renal disorders that cause hyponatremia include sodium-losing nephropathy from chronic renal disease e.
Endocrine disorders are uncommon causes of hyponatremia. Diagnosing hypothyroidism or mineralocorticoid deficiency i. In either case, the serum levels of thyroid-stimulating hormone TSH , cortisol, and adrenocorticotropic hormone ACTH should be measured, because hypothyroidism and hypoadrenalism can coexist as a polyendocrine deficiency disorder i. The reset osmostat syndrome occurs when the threshold for antidiuretic hormone secretion is reset downward.
Patients with this condition have normal water-load excretion and intact urine-diluting ability after an oral water-loading test. The condition is chronic—but stable—hyponatremia. Patients with extra-renal sodium loss have a low urinary sodium concentration less than 30 mmol per L as the body attempts to conserve sodium.
Causes include severe burns and gastrointestinal losses from vomiting or diarrhea. Diuretic therapy, on the other hand, can cause either a low or a high urinary-sodium concentration, depending on the timing of the last diuretic dose administered, but the presence of concomitant hypokalemia is an important clue to the use of a diuretic. Medications and drugs that cause hyponatremia are listed in Table 1. Diuretics cause a hypovolemic hyponatremia. Fortunately, in most cases, stopping the offending agent is sufficient to cause spontaneous resolution of the electrolyte imbalance.
Carbamazepine Tegretol Chlorpromazine Thorazine Vasopressin analogs Indapamide Natrilix Selective serotonin reuptake inhibitors Amiodarone Cordarone Ecstasy 3,4-methylenedioxymethamphetamine Information from references 20 through Antidiuretic hormone causes water retention, so hyponatremia then occurs as a result of inappropriately increased water retention in the presence of sodium loss.
SIADH is a diagnosis of exclusion and should be suspected when hyponatremia is accompanied by urine that is hyperosmolar compared with the plasma.
This situation implies the presence of a low plasma osmolality with an inappropriately high urine osmolality, although the urine osmolality does not necessarily have to exceed the normal range.
Another suggestive feature is the presence of hypouricemia caused by increased fractional excretion of urate. The treatment of hyponatremia can be divided into two steps.
First, the physician must decide whether immediate treatment is required. This decision is based on the presence of symptoms, the degree of hyponatremia, whether the condition is acute arbitrarily defined as a duration of less than 48 hours or chronic, and the presence of any degree of hypotension. The second step is to determine the most appropriate method of correcting the hyponatremia. Shock resulting from volume depletion should be treated with intravenous isotonic saline.
Acute severe hyponatremia i. In patients with chronic hyponatremia, overzealous and rapid correction should be avoided because it can lead to central pontine myelinolysis. In patients who have difficulty adhering to fluid restriction or who have persistent severe hyponatremia despite the above measures, demeclocycline Declomycin in a dosage of to 1, mg daily can be used to induce a negative free-water balance by causing nephrogenic diabetes insipidus.
Loop diuretics can be used in severe cases. Newer agents such as the arginine vasopressin receptor antagonists have shown promising results 39 and may be useful in patients with chronic hyponatremia. In all patients with hyponatremia, the cause should be identified and treated.
Some causes, such as congestive heart failure or use of diuretics, are obvious. Other causes, such as SIADH and endocrine deficiencies, usually require further evaluation before identification and appropriate treatment. The initial rate of sodium correction with hypertonic saline should not exceed 1 to 2 mmol per L per hour.
Overzealous correction of chronic hyponatremia can lead to central pontine myelinolysis. Demeclocycline Declomycin in a dosage of to 1, mg daily is effective in patients with refractory hyponatremia.
Arginine vasopressin receptor antagonists may be useful in patients with chronic hyponatremia. Already a member or subscriber?
Log in. Interested in AAFP membership? Learn more. Address correspondence to Kian Peng Goh, M. Reprints are not available from the author. The author indicates that he does not have any conflicts of interest. Sources of funding: none reported. The author thanks Evelyn Koay, S. Response of thiazide-induced hypokalemia to amiloride.
Barclay L, Nainggolan L. Medscape Medical News. Accessed 01 March Clinical practice guideline on diagnosis and treatment of hyponatraemia. Ghose RR. Plasma arginine vasopressin in hyponatraemic patients receiving diuretics. Postgrad Med J. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia.
N Engl J Med. User Username Password Remember me. Font Size. Notifications View Subscribe. Article Tools Print this article. Indexing metadata. Thiazide diuretic prescription and electrolyte abnormalities in primary care. Br J Clin Pharmacol. Mann SJ. The silent epidemic of thiazide-induced hyponatremia. J Clin Hypertens Greenwich. Thiazide-associated hyponatremia in the elderly: what the clinician needs to know.
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Thiazide-induced hyponatremia: reproducibility by single dose rechallenge and an analysis of pathogenesis. Ann Intern Med. To sign up for updates or to access your subscriber preferences, please enter your email address below. We want to hear from our users about how we can improve the PSNet experience. Please select your preferred way to submit a case. Note that even if you have an account, you can still choose to submit a case as a guest.
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