46 research outputs found

    Hypertonic Saline for Hyponatremia: Meeting Goals and Avoiding Harm

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    Hypertonic saline has been used for the treatment of hyponatremia for nearly a century. There is now general consensus that hypertonic saline should be used in patients with hyponatremia associated with moderate or severe symptoms to prevent neurological complications. However, much less agreement exists among experts regarding other aspects of its use. Should hypertonic saline be administered as a bolus injection or continuous infusion? What is the appropriate dose? Is a central venous line necessary? Should desmopressin be used concomitantly and for how long? This article considers these important questions, briefly explores the historical origins of hypertonic saline use for hyponatremia, and reviews recent evidence behind its indications, dosing, administration modality and route, combined use with desmopressin to prevent rapid correction of serum sodium, and other considerations such as the need and degree for fluid restriction. The authors conclude by offering some practical recommendations for the use of hypertonic saline

    Pisse Prophecy and the BUMP

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    Basic Urine Metabolic Profile and the diagnosis of fluid and electrolyte disorders

    Estimating urine volume from the urine creatinine concentration

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    Spot determinations of the urine creatinine concentration are widely used as a substitute for 24-hour urine collections. Expressed as the amount excreted per gram of creatinine, urine concentrations in a single-voided sample are often used to estimate 24-hour excretion rates of protein, sodium, potassium, calcium, magnesium, urea, and uric acid. These estimates are predicated on the assumption that daily creatinine excretion equals 1 gm (and that a urine creatinine concentration of 100 mg/dl reflects a 1 Liter 24-hour urine volume). Such estimates are invalid if the serum creatinine concentration is rising or falling. In addition, because creatinine excretion is determined by muscle mass, the assumption that 24-hour urine creatinine excretion equals 1 gm yields a misleading estimate at the extremes of age and body size. In this review we evaluate seven equations for the accuracy of their estimates of urine volume based on urine creatinine concentrations in actual and idealized patients. None of the equations work well in patients who are morbidly obese or in patients with markedly decreased muscle mass. In other patients, estimates based on a reformulation of the Cockroft-Gault equation are reasonably accurate. A recent study based on this relationship found a high strength of correlation between estimated and measured urine output with chronic kidney disease (CKD) studied in the African American Study of Kidney Disease (AASK) trial and for the patients studied in the CKD Optimal Management with Binders and NictomidE (COMBINE) trial. However, the equation systematically underestimated urine output in the AASK trial. Hence, an intercept was added to account for the bias in estimated output. A more rigorous equation, derived from an ambulatory Swiss population, that includes body mass index and models the non-linear accelerated decline in creatinine excretion with age, could potentially be more accurate in overweight and elderly patients. In addition to extremes of body weight and muscle mass, decreased dietary intake or reduced hepatic synthesis of creatine, a precursor of creatinine, or ingestion of creatine supplements will also result in inaccurate estimates. These limitations must be appreciated to rationally use predictive equations to estimate urine volume. If the baseline urine creatinine concentration is determined in a sample of known volume, subsequent urine creatinine concentrations will reveal actual urine output as well as the change in urine output. Given the constraints of the various estimating equations, a single baseline timed collection may be more useful strategy for monitoring urine volume than entering anthropomorphic data into a calculator

    Managing electrolyte disorders: Order a basic urine metabolic panel

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    Fatal case of hospital-acquired hypernatraemia in a neonate: lessons learned from a tragic error

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    A 3-week-old boy with viral gastroenteritis was by error given 200 mL 1 mmol/mL hypertonic saline intravenously instead of isotonic saline. His plasma sodium concentration (PNa) increased from 136 to 206 mmol/L. Extreme brain shrinkage and universal hypoperfusion despite arterial hypertension resulted. Treatment with glucose infusion induced severe hyperglycaemia. Acute haemodialysis decreased the PNa to 160 mmol/L with an episode of hypoperfusion. The infant developed intractable seizures, severe brain injury on magnetic resonance imaging and died. The most important lesson is to avoid recurrence of this tragic error. The case is unique because a known amount of sodium was given intravenously to a well-monitored infant. Therefore the findings give us valuable data on the effect of fluid shifts on the PNa, the circulation and the brain\u27s response to salt intoxication and the role of dialysis in managing it. The acute salt intoxication increased PNa to a level predicted by the Edelman equation with no evidence of osmotic inactivation of sodium. Treatment with glucose in water caused severe hypervolaemia and hyperglycaemia; the resulting increase in urine volume exacerbated hypernatraemia despite the high urine sodium concentration, because electrolyte-free water clearance was positive. When applying dialysis, caution regarding circulatory instability is imperative and a treatment algorithm is proposed

    Allostasis and the Clinical Manifestations of Mild to Moderate Chronic Hyponatremia: No Good Adaptation Goes Unpunished

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    When homeostatic regulatory systems are unable to maintain a normal serum sodium concentration, the organism must adapt to demands of a disordered internal environment, a process known as allostasis. Human cells respond to osmotic stress created by an abnormal serum sodium level with the same adaptations used by invertebrate organisms that do not regulate body fluid osmolality. To avoid intolerable changes in their volume, cells export organic osmolytes when exposed to a low serum sodium concentration and accumulate these intracellular solutes when serum sodium concentration increases. The brain\u27s adaptation to severe hyponatremia (serum sodium \u3c 120 mEq/L) has been studied extensively. However, adaptive responses occur with less severe hyponatremia and other tissues are affected; the consequences of these adaptations are incompletely understood. Recent epidemiologic studies have shown that mild (sodium, 130-135 mEq/L) and moderate (sodium, 121-129 mEq/L) chronic hyponatremia, long thought to be inconsequential, is associated with adverse outcomes. Adaptations of the heart, bone, brain, and (possibly) immune system to sustained mild to moderate hyponatremia may adversely affect their function and potentially the organism\u27s survival. This review explores what is known about the consequences of mild to moderate chronic hyponatremia and the potential benefits of treating this condition

    Evidence for Managing Hypernatremia: Is It Just Hyponatremia in Reverse?

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    Where Do the Salt and Water Go? A Case of Profound Hyponatremia

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    Treatment of profound hyponatremia is challenging. Severe symptoms mandate correction by 4 to 6 mEq/L within hours, but with risk factors for osmotic demyelination, daily correction should be \u3c 8 mEq/L. With a therapeutic window this narrow, clinicians would like to know how serum sodium (SNa) concentration will respond to their therapy. Based on isotopic measurements, Edelman showed SNa level to be a function of exchangeable sodium and potassium divided by total-body water. Edelman defined this relationship with linear regression yielding an equation of the form y = mx + b, where y is SNa level, x is exchangeable sodium and potassium divided by total-body water, m is the slope, and b is the intercept. Edelman said that the intercept of his regression probably is a measure of the quantity of osmotically inactive exchangeable sodium and potassium per unit of body water. Predictive formulas are derived from Edelman\u27s original linear regression, some including and some omitting the regression\u27s intercept. We illustrate the performance and limitations of these formulas using comprehensive data for electrolyte and fluid balance obtained during the treatment of a critically patient who presented with an SNa concentration of 101 mEq/L
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