Severe Hyponatremia

 3/18/02 (Gala)

Question: What are the diagnostic and therapeutic considerations in severe hyponatremia?

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Unique Identifier:11251026

Authors: Gross P. Reimann D. Henschkowski J. Damian M.

Institution: Department of Medicine, Universitatsklinikum Carl Gustav Carus, Dresden, Germany. peter.gross@mailbox.tu-dresden.de

Title: Treatment of severe hyponatremia: conventional and novel aspects. [Review] [43 refs]

Source: Journal of the American Society of Nephrology. 12 Suppl 17:S10-4, 2001 Feb.

Abstract: Hyponatremia is a frequent electrolyte disorder. A hyponatremia is called acute severe (<115 mM) when the duration has been <36 to 48 h. Such patients often have advanced symptoms as a result of brain edema. Acute severe hyponatremia is a medical emergency. It should be corrected rapidly to approximately 130 mM to prevent permanent brain damage. In contrast, in chronic severe hyponatremia (>4 to 6 d), there is no brain edema and symptoms are usually mild. In such patients, a number of authors have recommended a correction rate <0.5 mM/h to approximately 130 mM to minimize the risk of cerebral myelinolysis. Sometimes it is not possible to diagnose whether a severe hyponatremia is acute or chronic. In such cases, an initial imaging procedure is helpful in deciding whether rapid or slow correction should be prescribed. The modalities of treatment of severe hyponatremia have so far consisted of infusions of hypertonic saline plus fluid restriction. In the near future, vasopressin antagonists will become available. Preliminary experience has already demonstrated their efficiency of inducing a sustained water diuresis and a correction of hyponatremia. [References: 43] CAS Registry/EC Number 0 (Receptors, Vasopressin).

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Unique Identifier:9475480

Authors: Gross P. Reimann D. Neidel J. Doke C. Prospert F. Decaux G. Verbalis J. Schrier RW.

Institution: Department of Medicine, Universitatsklinikum C.G. Carus, Dresden, Germany.

Title: The treatment of severe hyponatremia.

Source: Kidney International - Supplement. 64:S6-11, 1998 Feb.

Abstract: Severe hyponatremia may be chronic (days) or acute (hours), symptomatic or asymptomatic. Severe chronic symptomatic hyponatremia (serum sodium concentration < 110 to 115 mM/liter) occurs most commonly in the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The treatment of this hyponatremia is a challenge to practicing physicians, in part because an overly rapid correction of hyponatremia may cause brain damage. The latter sometimes takes the form of central pontine myelinolysis (CPM). On the basis of available clinical and experimental literature, the rate of correction of this symptomatic hyponatremia should be no more than 0.5 mM per liter per hour, and the initial treatment should be halted once a mildly hyponatremic range of the serum sodium concentration has been reached (approximately 125 to 130 mM/liter). In contrast, severe chronic asymptomatic hyponatremia may be treated sufficiently by a fluid restriction. On the other hand, severe symptomatic acute hyponatremia should be treated promptly and rapidly, using hypertonic saline, to initially reach a mildly hyponatremic level. CAS Registry/EC Number 7440-23-5 (Sodium). 7732-18-5 (Water).

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Unique Identifier:8879850

Authors: Soupart A. Decaux G.

Institution: Research Unit for the Study of Hydromineral Metabolism, Erasmus University Hospital, Free University of Brussels, Belgium.

Title: Therapeutic recommendations for management of severe hyponatremia: current concepts on pathogenesis and prevention of neurologic complications. [Review] [174 refs]

Source: Clinical Nephrology. 46(3):149-69, 1996 Sep.

Abstract: Patients with hyponatremia are exposed to major neurological complications. On the one hand hyponatremia itself produces brain edema, increased intracranial pressure which potentially leads to subsequent neuropathological sequelae or death. On the other hand excessive correction could be followed by development of brain demyelinating lesions (central pontine or extrapontine myelinolysis) with major disability or fatal outcome. Understanding of brain adaptative mechanisms to changes in osmolality largely contributes to explain these neurological events. When serum sodium decreases, the brain prevents swelling by extruding electrolytes and organic osmolytes, a process almost fully achieved after 48 h. Conversely, during subsequent increase in serum sodium, reestablishment of intracerebral osmolytes occurs but their reuptake is more delayed (+/- 5 days). In both circumstances, these mechanisms can be overwhelmed, leading to brain damage. Acute hyponatremia (< 48 h) is generally hospital-acquired, mainly in the postoperative state and/or after excessive fluid administration. After abrupt fall in serum sodium, seizure, respiratory arrest and coma may develop and these manifestations are sometimes explosive in nature. Recognition of even minor symptoms is crucial and implies prompt correction. There is generally no risk of brain myelinolysis in acute hyponatremia. Some factors are suspected to aggravate the prognosis of hyponatremic encephalopathy, including female gender (menstruant women), hypoxia and young age. Chronic hyponatremia (> 48 h) usually develops outside the hospital and is generally better tolerated. The risks of brain myelinolysis can be largely reduced by limiting the correction level to < or = 15 mEq/1/24 h. However, if necessary, the initial rate of correction can be rapid provided that the final correction remains < 15 mEq/1/24 h. However, when other recognized risk factors for myelinolysis (hypokalemia, liver disease, poor nutritional state, burns) are present, correction should not exceed 10 mEq/1/24 h. Demyelinization is also observed in hypernatremia but it follows greater (50%) increase in serum sodium than from hyponatremic baseline. For symptomatic hyponatremia, rapid correction is usually obtained by hypertonic saline (3%) infusion. Another option consists in administration of intravenous or oral urea. Urea allows a rapid reduction of brain edema and intracranial pressure which is followed by subsequent correction of hyponatremia. Experimental data also suggest that treatment of hyponatremia with urea is associated with a lower incidence of myelinolysis. In hyponatremic patients without symptoms, there is no need for rapid correction and the treatment should be more conservative. Close monitoring of the serum sodium is indicated initially and if necessary, correction must be stopped and diuresis interrupted with dDAVP. Given recent experimental data, in patients overly corrected (delta SNa > 15 mEq/1/24 h), the risk of myelinolysis could be greatly reduced by rapidly decreasing the serum sodium through hypotonic fluids administration and dDAVP. [References: 174]

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Unique Identifier:2405660

Authors: Cluitmans FH. Meinders AE.

Institution: Department of General Internal Medicine, University Hospital of Leiden, The Netherlands.

Title: Management of severe hyponatremia: rapid or slow correction? [see comments.]. [Review] [79 refs]

Source: American Journal of Medicine. 88(2):161-6, 1990 Feb.

Abstract: Case reports and the literature on the treatment of severe hyponatremia were reviewed. It appeared that the conflicting opinions with respect to the rate of correction of severe hyponatremia could be reduced to not differentiating between acute and chronic hyponatremia, to using different criteria for this distinction, and to differences in treatment strategy. After reviewing the available data in the literature, it is suggested that hyponatremia should be classified as acute whenever the rate of decrease of serum sodium exceeds 0.5 mmol/L/hour. If it is unknown at which rate the hyponatremia has developed, it can be assumed to be acute if within a short period of time (two to three days), large quantities of fluid are ingested orally or administered parenterally, especially hypotonic fluids in the presence of impaired water excretion. In other cases, chronic hyponatremia is probable. It is concluded that acute hyponatremia should be treated without delay and rapidly at a rate of at least 1 mmol/L/hour, to prevent severe neurologic damage or death. With respect to chronic hyponatremia, it appeared that severe neurologic complications almost exclusively occurred in patients who were treated with hypertonic or isotonic saline without the addition of furosemide or an osmotic diuretic agent, resulting in a (rapid) correction rate of 0.5 mmol/L/hour or more. In contrast, patients with severe chronic hyponatremia treated with furosemide and isotonic or hypertonic saline almost uniformly did well after rapid correction. Uneventful recovery is also the rule when severe chronic hyponatremia is corrected slowly, at a rate less than 0.5 mmol/L/hour. On pathophysiologic grounds, and bearing in mind that slow correction was used in the majority of reported patients in the literature with severe chronic hyponatremia who recovered without neurologic complications, this treatment modality is preferable. Whenever the available data do not permit a differentiation between acute or chronic hyponatremia, rapid correction has to be pursued by means of administration of hypertonic or isotonic saline together with furosemide. [References: 79]

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