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October 22, 2020#

hyponatremia flowchart

2014; 170(3):G1-47. Developed by: The European Society of Endocrinology, the European Society of Intensive Care Medicine (ESICM), and the European Renal Association – European Dialysis and Transplant Association. Hyponatremia, defined as a serum sodium concentration below 135 mEq/L, is usually caused by a failure to excrete water normally [].In healthy individuals, the ingestion of water does not lead to hyponatremia because suppressed release of antidiuretic hormone (ADH), also called vasopressin, allows excess water to be excreted in a dilute urine (). In diuretic-induced hyponatremia, elimination of the diuretic may be enough; some patients need some sodium or potassium replacement. Both of these drugs are strong inhibitors of CYP3A (cytochrome P450, family 3, subfamily A) and as such have multiple drug interactions. Hyperkalemia suggests adrenal insufficiency. Decreased total body water (TBW) and sodium, with a relatively greater decrease in sodium, Osmotic diuresis (glucose, urea, mannitol), Salt-losing nephropathies (eg, interstitial nephritis, medullary cystic disease, partial urinary tract obstruction, polycystic kidney disease), Increased TBW with near-normal total body sodium, Thiazide diuretics, barbiturates, carbamazepine, chlorpropamide, clofibrate, opioids, tolbutamide, vincristine, 3,4-Methylenedioxymethamphetamine (MDMA [ecstasy]), Possibly cyclophosphamide, nonsteroidal anti-inflammatory drugs (NSAIDs), oxytocin, selective serotonin reuptake inhibitors (SSRIs), Adrenal insufficiency as in Addison disease, Syndrome of inappropriate antidiuretic hormone (ADH) secretion, States that increase nonosmotic release of vasopressin(ADH), Increased total body sodium with a relatively greater increase in TBW. Serum sodium concentration and serum osmolality that are low and urine osmolality that is inappropriately high (120 to 150 mmol/L [120 to 150 mOsm/kg]) with respect to the low serum osmolality suggest volume overload, volume contraction, or SIADH. Its effectiveness can be limited by increased thirst. Ltd 2019 | All Rights Reserved, View and share this diagram and more in your device, Varnish Behind the Amazon Elastic Load Balance - AWS Example, AWS Cloud for Disaster Recovery - AWS Template, 10 Best Social Media Tools for Entrepreneurs, edit this template and create your own diagram. Severe cerebral edema may occur in premenopausal women with acute hyponatremia, perhaps because estrogen and progesterone inhibit brain Na+,K+-ATPase and decrease solute extrusion from brain cells. Among the many potential contributing factors are, Nonosmotic vasopressin release due to intravascular volume depletion, Administration of drugs that impair renal water excretion. Overtly hypervolemic patients usually have a readily recognizable condition, such as heart failure or hepatic or renal disease. In addition, adrenal insufficiency has become increasingly common among AIDS patients as the result of cytomegalovirus adrenalitis, mycobacterial infection, or interference with adrenal glucocorticoid and mineralocorticoid synthesis by ketoconazole. Am J Med 2007; 120 (II Suppl. SIADH may be present because of coexistent pulmonary or central nervous system infections. In some situations, hypertonic saline may be used with a loop diuretic. Serum sodium concentration falls about 1.6 mEq/L (1.6 mmol/L) for every 100-mg/dL (5.55-mmol/L) rise in the serum glucose concentration above normal. Thus, the intracellular environment becomes relatively hypertonic compared to the serum, causing intracellular fluid shifts that can rapidly cause cerebral edema, potentially progressing to brain stem herniation and death. Fluid restriction alone is frequently is not enough to prevent recurrence of hyponatremia. Renal causes of hypovolemic hyponatremia can usually be differentiated from extrarenal causes by the history. Investigation and Management of Hyponatraemia. Euvolemic patients and patients with equivocal volume status require more laboratory testing to identify a cause. Newer methods of measuring serum electrolytes with ion-selective electrodes circumvent this problem. However, because findings are nonspecific, hyponatremia is often recognized only after serum electrolyte measurement. This group includes interstitial nephritis, medullary cystic disease, partial urinary tract obstruction, and, occasionally, polycystic kidney disease. Osmotic demyelination syndrome (previously called central pontine myelinolysis) may follow too-rapid correction of hyponatremia. Tolvaptan use is limited to 30 days because of the risk of liver toxicity. Hyponatremia can be life threatening and requires prompt recognition and proper treatment.

The degree, duration, and symptoms of hyponatremia are used to determine how quickly to correct the serum sodium. Am J Med 2007; 120 (II Suppl. BUN (blood urea nitrogen) and creatinine values are normal, and serum uric acid is generally low. When the serum sodium is < 120 mEq/L (< 120 mmol/L), hyponatremia may not completely correct upon restoration of intravascular volume; restriction of free water ingestion to 500 to 1000 mL/24 hours may be needed. These drugs are potentially dangerous because they may correct serum sodium concentration too rapidly; they are typically reserved for severe (< 121 mEq/L [< 121 mmol/L]) and/or symptomatic hyponatremia that is resistant to correction with fluid restriction.

Laboratory tests should include serum and urine osmolality and electrolytes. When sodium is replaced too rapidly (eg, > 14 mEq/L/8 hour [14 mmol/L/8 hours]) and neurologic symptoms start to develop, it is critical to prevent further serum sodium increases by stopping hypertonic fluids. Diuretics may also cause hypovolemic hyponatremia. Many experts recommend that, in general, serum sodium be raised no faster than 1 mEq/L/hour (1 mmol/L/hour).

In each of these disorders, a decrease in effective circulating volume results in the release of vasopressin and angiotensin II. In these patients, rapid correction with hypertonic saline is indicated even when neurologic symptoms are mild (eg, forgetfulness). When SIADH is present, severe water restriction (eg, 250 to 500 mL/24 hours) is generally required. N Engl J Med. A newer oral formulation of urea has been developed to enhance palatability. Ltd. All rights reserved. Flaccid paralysis, dysarthria, and dysphagia can evolve over a few days or weeks after a hyponatremic episode. If the decision is made to go ahead with treatment, keep the following principles in in mind. Conivaptan is indicated for treatment of hypervolemic and euvolemic hyponatremia. This site complies with the HONcode standard for trustworthy health information: verify here. Damage often is permanent. Volume overload and volume contraction are differentiated clinically. In patients with hypovolemia and normal renal function, sodium reabsorption results in a urine sodium of < 20 mEq/L (20 mmol/L). Joel Topf, a nephrologist and the author of the staff review of this article, also provided a flowchart of his basic approach to hyponatremia. Spasovski G, Vanholder R, Allolio B, et al. The selective vasopressin (V2) receptor antagonists conivaptan (IV) and tolvaptan (oral) are relatively new treatment options for severe or resistant hyponatremia. Pseudohyponatremia with normal serum osmolality may occur in hyperlipidemia or extreme hyperproteinemia, because the lipid or protein occupies space in the volume of serum taken for analysis; the concentration of sodium in serum itself is not affected. An excellent summary of the literature. Lasting correction depends on successful treatment of the underlying disorder. The resulting water retention increases plasma dilution and hyponatremia. Euvolemic patients should also have thyroid and adrenal function tested. Euvolemic hyponatremia may also result from excessive water intake in the presence of Addison disease, hypothyroidism, or nonosmotic vasopressin release (eg, due to stress; postoperative states; use of drugs such as chlorpropamide, tolbutamide, opioids, barbiturates, vincristine, clofibrate, or carbamazepine). Symptoms mainly involve central nervous system dysfunction. INTRODUCTION: Severe chronic hyponatremia (<120 mEq/L) remains the #1 reason nephrologists lose sleep on call nights and rightly so. Hypertonic (3%) saline (containing 513 mEq sodium/L (513 mmol/L)) use requires frequent (every 2 hours) electrolyte determinations. Close monitoring is recommended especially during initiation and dosage changes. This amount (in mEq OR mmol) may be calculated using the sodium deficit formula as. European journal of endocrinology. Treatment should be focussed on the individual patient, not lab values. Symptoms are also more severe with faster-onset hyponatremia. In such cases, inducing hyponatremia with hypotonic fluid may mitigate the development of permanent neurologic damage. Similarly, when mild hyponatremia results from inappropriate hypotonic parenteral fluid administration in patients with impaired water excretion, merely altering fluid therapy may suffice.

Patients with SIADH need chronic treatment for hyponatremia. Other strong CYP3A inhibitors (eg, ketoconazole, itraconazole, clarithromycin, retroviral protease inhibitors) should be avoided. When the underlying disorder is not correctable, as in metastatic cancer, and patients find severe water restriction unacceptable, demeclocycline 300 to 600 mg orally every 12 hours may be helpful by inducing a concentrating defect in the kidneys. Copyright © 2008-2019 Cinergix Pty. Rarely, hyponatremia occurs in nephrotic syndrome, although pseudohyponatremia may be due to interference with sodium measurement by elevated lipids. Hyponatremia may occur with normal, increased, or decreased extracellular fluid volume. Developed by: The European Society of Endocrinology, the European Society of Intensive Care Medicine (ESICM), and the European Renal Association – European Dialysis and Transplant Association. 1) : S1-21 [PMID : 17981159] 2. Older patients may have increased sodium diuresis and are especially susceptible to thiazide-induced hyponatremia, particularly when they have a preexisting defect in renal capacity to excrete free water. IV conivaptan, a vasopressin receptor antagonist, causes effective water diuresis without significant loss of electrolytes in the urine and can be used in hospitalized patients for treatment of resistant hyponatremia. Creately is an easy to use diagram and flowchart software built for team collaboration. Rarely, such patients develop severe, life-threatening hyponatremia within a few weeks after the initiation of a thiazide diuretic. Severe or resistant hyponatremia generally occurs only when heart or liver disease is near end-stage.

Patients affected include those with psychosis or more modest degrees of polydipsia plus renal insufficiency.

Equations are available to help predict the sodium response to a given amount of hypertonic saline, but these formulas are only rough guidelines and do not decrease the need to monitor electrolyte levels frequently. Levels of 130-133mmol/L are considered mild and do not require investigation. Tolvaptan use is limited to less than 30 days due to the potential for liver toxicity and it should not be used in patients with liver or kidney disease. Clinicians should review the other drugs the patient is taking for potentially dangerous interactions with V2 receptor antagonists before initiating a treatment trial. Tolvaptan use is also limited by excessive cost. However, when hyponatremia is accompanied by disturbances in total body sodium content, signs of ECF volume depletion or volume overload also occur. For patients with rapid-onset hyponatremia and neurologic symptoms, rapid correction is accomplished by giving 100 mL of hypertonic saline IV over 15 minutes. Even with severe hyponatremia, serum sodium concentration should not be increased by more than 8 mEq/L (8 mmol/L) over the first 24 hours.

Another recommendation includes administration of desmopressin 1 to 2 mcg every 8 hours concurrently with hypertonic saline. Significant ECF fluid losses also cause release of vasopressin, causing water retention by the kidneys, which can maintain or worsen hyponatremia. Deficiencies in both total body water and total body sodium exist, although proportionally more sodium than water has been lost; the sodium deficit causes hypovolemia.

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