Management Of Hyponatremia Research Articles

Electrolyte derangement in cerebral malaria: a case for a more aggressive approach to the management of hyponatraemia.

Although hyponatraemia has been consistently shown to occur in a large proportion of children with cerebral malaria, no statistical relationship has been established between the incidence of hyponatraemia and that of malaria-attributable mortality. However, hyponatraemia is not a benign state in other conditions (such as meningitis) or in surgical patients, and is likely to add to malarial deaths. The high mortality rate seen among cases of cerebral malaria, despite all efforts to curb it, therefore calls for a more aggressive approach to the management of hyponatraemia. Current methods for the administration of hypotonic saline and isotonic glucose solutions need review. In addition, children admitted with cerebral malaria should have their electrolyte status monitored to identify new or ongoing hyponatraemia. When hyponatraemia is discovered, it should be quickly and actively corrected.

Diuretic therapy in congestive heart failure--new views on spironolactone therapy

Cardiac pump failure leads to a reduction of the effective arterial volume. This is sensed by the kidney via afferent sympathetic fibres. The renal response to the perceived lack of volume is the retention of sodium and water. Although initially homeostatic, this renal counterregulation is maladaptive later on and may contribute to further cardiac compromise by increasing preload (volume retention) and afterload (hyperreninism). The renal sodium retention in congestive heart failure is a consequence of the activation of the sympathetic nervous system and of the renin-angiotensin-aldosterone system. The retention of osmotically free water is partly caused by the nonosmotic secretion of antidiuretic hormone from the posterior pituitary and partly by a diminished osmoregulatory capacity of the kidney due to diuretic therapy and/or (pre-)renal insufficiency. In the near future specific blocking drugs of vasopressin receptors should become available which could make a significant contribution to the management of hyponatremia in this setting. For the management of extracellular volume overload a negative sodium balance is the central objective. A moderate reduction of sodium intake is helpful to achieve this goal and has the additional benefit of reducing thirst and renal potassium loss. However, the majority of patients require (loop) diuretics in addition. Patients who are refractory to high and repeated doses of loop diuretics may respond to a combination of diuretics which act on different nephron segments. Diuretics increase the risk of hypokalemia which can trigger life-threatening tachyarrhythmia, particularly in patients with cardiac dysfunction. Hypokalemia is therefore an indicator of an adverse outcome. Secondary hyperaldosteronism--which can persist despite effective therapy with ACE-inhibitors--is the major cause of hypokalemia in this setting. The randomized aldactone evaluation study (RALES) has shown that spironolactone (25 mg/day) reduced the risk of hypokalemia and decreased morbidity, mortality and clinical symptoms in patients with heart failure. The recent encouraging results with vasopressin receptor antagonists and spironolactone point to the fact that the therapeutic modification of maladaptive homeostatic renal mechanisms plays an increasingly important role in the modern diuretic management of heart failure beyond symptomatic relief from volume overload.

The urine/plasma electrolyte ratio: a predictive guide to water restriction.

Patients with hypotonic hyponatremia are encountered commonly in the general practice of medicine. Nearly all strategies for the management of subacute or chronic hyponatremia call for some amount of water restriction. The considerations for such a prescription have not been addressed in the literature. We describe therefore a simple approach grounded in the physiology of electrolyte-free water clearance that can be used at the bedside.

The treatment of hyponatraemia using vasopressin antagonists.

Hyponatraemia is a frequent electrolyte disorder. It is primarily attributable to vasopressin excess plus sustained fluid intake. Hyponatraemia causes CNS symptoms, especially during the first 2-4 days; these symptoms are related to brain swelling. Hyponatraemia occurs in the setting of liver cirrhosis and congestive cardiac failure, in which it is related to stimulation by low arterial blood pressure acting through baroreceptors. Hyponatraemia also occurs in the syndrome of inappropriate antidiuretic hormone secretion, usually from neoplasms releasing vasopressin. The conventional treatment of hyponatraemia used to be fluid restriction and treatment of the underlying disorder. This kind of treatment has been unreliable, cumbersome and difficult to comply with for the patient. In the future, effective vasopressin V2 antagonists will become available for clinical use in the treatment of hyponatraemia, and are expected to improve the management of hyponatraemia. Pharmacological characteristics and observations of biological effects of three antagonists are reported in the present article.

Management and outcome of symptomatic hyponatremia in emergency department

Management and outcome of symptomatic hyponatremia in emergency department

Review of investigation and management of severe hyponatraemia in a hospital population.

The purpose of this study was to assess retrospectively the prevalence of severe hyponatraemia in a hospital population and its laboratory investigation, treatment and clinical outcome. Over a 6-month period 47 patients (27 women and 20 men) were found to have a plasma sodium concentration of < or = 120 mmol/L (this number made up less than 0.17% of all plasma sodium requests over that time period). The mean patient age was 75 +/- 16 years and the average hospital stay was 37 +/- 45 days (1-179 days). Patient mortality was 51% (women 57% and men 43%). The mean initial plasma sodium concentration was 116 +/- 4.5 mmol/L, rising after therapeutic intervention to a mean of 130 +/- 4.2 mmol/L. The mean plasma sodium correction rate was 4.7 +/- 4.3 mmol/L/24 h (0.9-17.5 range). Twelve per cent of the patients had their plasma sodium raised at a rate of greater than 10 mmol/L/24 h after their initial presentation. Two patients may have had symptoms and signs suggestive of cerebral oedema/cortical dysfunction: in one patient the sodium concentration was raised at a rate of 9.5 mmol/L/24 h and in the other at 12.0 mmol/L/24 h. Sixty-one per cent of the patients had a chest infection, 44% were on diuretics, 28% had congestive cardiac failure, 28% were post-operative (9% orthopaedic procedures), 19% had carcinoma and 9% were on a selective serotonin re-uptake inhibitor. Regarding laboratory investigations, 56% had liver function tests, 41% had thyroid function tests, 36% had plasma osmolality determination, 36% had urinary electrolytes including urinary osmolality and < 2% had tests to exclude hypoadrenalism.

Extra pontine myelinolysis in a tetraplegic patient: Case report

Hyposmolar hyponatremia (serum sodium < 130 mmol/l) is a common phenomenon in the spinal cord injury (SCI) patient population and in most cases, it is of relatively little consequence. However, rapid correction or over correction of hyponatremia (a change in serum sodium > 25 mmol/l within 48 h) has been linked to Central Pontine Myelinolysis (CPM) and Extra Pontine Myelinolysis (EPM), usually along with other recognized predisposing factors. We report the first case of isolated Extra Pontine Myelinolysis in an SCI patient without any of the recognized predisposing factors, following correction of hyponatremia. The signs and symptoms of Extra Pontine Myelinolysis were not very remarkable in our patient because of prior spinal cord injury. The diagnosis was confirmed by the typical finding of myelinolysis in the basal ganglion region on MRI. Hyponatremia occurs frequently in the SCI patient population, thus placing them at increased risk for Extra Pontine Myelinolysis. Therefore, we emphasize the importance of watching for this entity during the management of hyponatremia in the SCI patient population and recommend the use of MRI scans to confirm the clinical diagnosis.

Epidemiology, Pathophysiology, and Management of Hyponatremic Encephalopathy

Hyponatremia is the most common electrolyte abnormality among hospitalized patients. Death or brain damage associated with hyponatremia has been described since 1935, and it is now evident that hyponatremia can lead to death in otherwise healthy individuals. In the past, it had been assumed that the likelihood of brain damage from hyponatremia was directly related to either a rapid decline in plasma sodium or a particularly low level of plasma sodium. Recent studies have demonstrated that other factors may be more important. These factors include the age and gender of the individual, with children and menstruant women the most susceptible. Although many clinical settings are associated with hyponatremia, those most often associated with brain damage are postoperative, polydipsia, pharmacological agents, and heart failure. Morbidity and mortality associated with hyponatremia are primarily a result of brain edema, hypoxemia, and associated hormonal factors. Management of hyponatremia is largely determined by symptomatology. If the patient is asymptomatic, discontinuation of drugs plus water restriction is often sufficient. If the patient is symptomatic, active therapy to increase the plasma sodium with hypertonic NaCl is usually indicated. Although inappropriate therapy of hyponatremia can lead to brain damage, such an occurrence is rare. Thus, the risk of not treating a symptomatic patient for exceeds that of improper therapy.

Hyponatremia: focus on therapy.

Hyponatremia can be a serious medical problem, and severe hyponatremia can be a medical emergency. Nevertheless, considerable controversy remains with respect to the best way to avoid the important sequelae of hyponatremia, while minimizing the complications of its treatment. Unquestionably, severe hyponatremia may cause life-threatening and/or permanent neurologic abnormalities. The risk of these untoward events, however, is much greater with acute than with chronic hyponatremia. The adaptive changes in the brain that reduce the hazards of a low serum sodium concentration for patients with chronic hyponatremia increase the risk for therapy-induced central pontine myelinolysis. In general, acute, symptomatic hyponatremia should be corrected more rapidly than chronic hyponatremia, at least until severe symptoms abate. Detailed guidelines are provided for the management of acute and chronic hyponatremia. But regardless of guidelines, therapy must be individualized, with adjustments based on frequent assessments of clinical condition and laboratory data.

Management of symptomatic hyponatraemia: dependence on the duration of development

Serious neurological symptoms are common in patients with a serum sodium concentration below 115 mmol l-1. The treatment is controversial and the most adequate rate of sodium correction to avoid both morbidity due to residual hypo-osmolality and therapy-induced neurological sequelae is debated. The management of symptomatic hyponatraemia is discussed here against the background of two cases and a literature review. It is concluded that the treatment should be based on whether the electrolyte disturbance is acute (< 24-36 h) or has developed insidiously. Slow sodium correction (< 0.5 mmol l-1 h-1) in patients with chronic hyponatraemia and rapid correction (1-2 mmol l-1 h-1) to a moderately hyponatraemic level in those with an acute development are recommended. If available data do not permit differentiation between the two conditions in a patient with seizures or in coma, rapid correction with sodium chloride and furosemide for 3-4 h followed by slow correction therapy is suggested.

Management of acute symptomatic hyponatraemia

EDITOR, - Christopher Heneghan and colleagues discuss the management of hyponatraemia during transurethral resection of the prostate.1 Having been a urologist throughout my career, since my retirement I have acted as reviewer for legal assessment firms. I have been impressed by certain recurring patterns that may be important. Acute hyponatraemia …

Management of hyponatraemia: Differentiate between acute and chronic: Author's reply

Management of hyponatraemia: Differentiate between acute and chronic: Author's reply

Management of hyponatraemia. Differentiate between acute and chronic.

Management of hyponatraemia. Differentiate between acute and chronic.

Fatal Acute Glycine and Sorbitol Toxicity During Operative Hysteroscopy

Four cases of severe hyponatremia occurring during operative hysteroscopy and resulting in a 50% death rate are presented. Either glycine 1.5% or sorbitol 3% was used for uterine irrigation in each circumstance. Although careful monitoring of fluid intake and output is important, more precise methods of tracking medium intrusion into the vascular space may be required. Serial serum sodium, central venous pressure, and plasma osmolality determinations are recommended to establish a timely diagnosis of hyponatremia and hypoosmolality. Rapid and aggressive management of significant hyponatremia (Na < 120 mmol/liter) should be instituted using 3%-5% sodium chloride solution and furosemide to attain the goal of elevating serum sodium to 130–135 mmol/liter with 24 h. Young women appear to be more susceptible to the sequelae of postoperative hyponatremia, e.g., cerebral edema, than are their male counterparts because of efficiency differences in their cerebral sodium pump function. Liquid distending media with osmolalities in the range of 280 mOsm/liter would offer a greater margin of patient safety than either sorbitol or glycine for operative hysteroscopy. (J GYNECOL SURG 9:137, 1993)

Limits of brain tolerance to daily increments in serum sodium in chronically hyponatraemic rats treated with hypertonic saline or urea: advantages of urea

1. At present there is no consensus about the optimal management of hyponatraemia to prevent demyelinating brain lesions. We have evaluated in a large series of rats (n = 136) the protective role of urea for the brain in the treatment of severe chronic hyponatraemia. Urea (group I, n = 51) was compared with hypertonic saline in boluses (group II, n = 46) and with hypertonic saline in divided doses (group III, n = 39). Treatment was administered intraperitoneally over 48 h. The severity of brain lesions was assessed by histological scoring. 2. For 95% of the injured animals treated with hypertonic saline, brain lesions appeared for an absolute increment in serum Na+ concentration (delta SNa+) of 20 mmol day-1 l-1. Above this limit neurological injuries gradually worsened, and beyond a transition zone (delta SNa+ greater than or equal to 20 less than or equal to 23 mmol day-1 l-1) 89% (group III) to 100% (group II) of the animals were injured. This limit can be reached rapidly, as attested by the comparable severity of brain lesions observed in group II (mean delta SNa+ 1 h after a bolus injection, 19 mmol/l) and in group III (mean delta SNa+ 1 h after an injection, 2 mmol/l), both groups achieving similar daily delta SNa+. 3. A correction above the threshold of 20 mmol day-1 l-1 is as toxic during the first 24 h as during the second day of the treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

The management of symptomatic hyponatremia.

The management of symptomatic hyponatremia.

The management of hyponatraemia

The management of hyponatraemia

Management of severe hyponatremia: Rapid or slow correction?

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.

Diagnosis and Management of Hyponatremia

Appropriate treatment of hyponatremic disorders is de pendent on an understanding of the mechanisms that cause these abnormalities. This article offers a patho physiological approach to hypoosmolar syndromes. Common causes of hyponatremia are reviewed with particular emphasis on congestive heart failure, ad vanced liver disease, diuretic use, and the syndrome of inappropriate antidiuretic hormone secretion. New con cepts in treatment are discussed with the aid of clinical examples that emphasize critical information. A number of recent studies have questioned the safety of rapidly correcting hyponatremia; recommendations based on our current understanding of these risks are proposed. Pitfalls in the diagnosis and management of patients with hyponatremic disorders are also discussed.

Urea treatment for water retention in hyponatremic congestive heart failure

We have studied the efficiency of urea in the treatment of hyponatremia and hydrosaline retention in a 76-year-old man with chronic ischemic congestive heart failure. Since increase of furosemide worsened the hyponatremia (120 mmol/l), 30 g/day of urea was added and induced the following changes: progressive weight loss (6.5 kg in one week), increased diuresis (from 0.750 to 1.950 l/day), increased salt excretion (from 40 to 165 mmol sodium/day) and correction of the hyponatremia (120 to 136 mmol/l). Blood urea and creatinine serum concentrations rose moderately without significant change in creatinine clearance (32 to 38 ml/min). No adverse effects related to urea administration were observed. Urea intake seems to be useful in the management of hyponatremia in our patient with cardiac failure.