Ramin Sam

The diagnosis and treatment of hyponatremia present challenges to clinicians and opportunities to improve our understanding of body water, sodium and potassium homeostasis and disorders. The first step in the diagnosis of every case of hyponatremia is to categorize it as hypotonic hyponatremia, hypertonic hyponatremia, or pseudohyponatremia. The diagnostic steps that follow the verification of hypotonic hyponatremia include: (a) the identification of the medical condition that caused the hyponatremia; (b) the evaluation of the mechanism of hyponatremia, including the computation of the magnitude of the changes in body water, sodium, and potassium that were responsible for the hyponatremia. Whether the extracellular volume is low, normal, or high provides key information for the determination of the mechanism of hyponatremia and the choice of its treatment method; and (c) the determination of the duration of hyponatremia. Whether hyponatremia is acute or chronic (i.e., lasting more than 48 h) has important implications for its manifestations and management. This perspective reviews the diagnostic categories and various aspects of treatment strategies of hypotonic hyponatremia, including choosing the method(s) for increasing the electrolyte-free renal water clearance, decreasing this clearance during treatment to prevent excessively rapid correction of hyponatremia, determining the type and amount of saline infused for correction of the hyponatremia (choice of isotonic versus hypertonic saline and of the target rise in serum sodium, which determines, along with other parameters, the volume of saline infused), and dialytic methods for correcting hyponatremia. The aim of this perspective is to identify topics that require further research, including diagnostic topics and treatment areas.

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Patients in the intensive care unit often develop anion gap metabolic acidosis most commonly from lactic acidosis. Clinicians routinely measure serum lactate levels, but it is not clear if one is able to use the measured serum lactate level to determine if there is a second cause for anion gap metabolic acidosis in these critically ill patients. In this report, 503 episodes of lactic acidosis with serum lactate levels greater than 5 mmol/L at a single institution over two years were analyzed. The average serum anion gap minus serum lactate level in these patients was 6.9 ± 0.21 mEq/L, the average corrected anion gap was −1.3 ± 0.23 mEq/L and the average strong ion gap was 5.1 ± 0.3 mEq/L. The majority of the episodes with anion gap—serum lactate concentration >8.0 mEq/L were explained by elevated serum albumin concentration, elevated serum phosphorus concentration, presence of ketones in the urine or high β-hydroxybutyrate concentrations. The above data suggest that one can use the measured serum lactate concentration and subtract from the serum anion gap to determine if there is a second reason for anion gap metabolic acidosis.

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Background/Objectives: Hyperglycemic emergencies cause significant losses of body water, sodium, and potassium. This report presents a method for computing the actual losses of water and monovalent cations in these emergencies. Methods: We developed formulas for computing the losses of water and monovalent cations as a function of the presenting serum sodium and glucose levels, the sum of the concentrations of sodium plus potassium in the lost fluids, and body water at the time of hyperglycemia presentation as measured by bioimpedance or in the initial euglycemic state as estimated by anthropometric formulas. The formulas for computing the losses from hyperglycemia were tested in examples of hyperglycemic episodes. Results: The formulas were tested in two patient groups, those with or without known weight loss during the development of hyperglycemia. In the first group, these formulas were applied to estimate the losses of body water and monovalent cations in (a) a previously published case of a boy with diabetic ketoacidosis and known weight loss who, during treatment not addressing his water deficit, developed severe hypernatremia and (b) a comparison of water loss computed by this new method with the reported average fluid gained during treatment of the hyperglycemic hyperosmolar state in a published study. In the second group, the formulas were applied in hypothetical subjects with varying levels of initial body water, serum sodium, and glucose at the time of hyperglycemia and sums of sodium and potassium concentrations in the lost fluids. Conclusions: Losses of body water and monovalent cations, which determine the severity of dehydration and hypovolemia, vary significantly between patients with hyperglycemic emergencies presenting with the same serum glucose and sodium concentrations. These losses can be calculated using estimated or measured body water values. Prospective studies are needed to test this proof-of-concept report.

In hyperglycemia, the serum sodium concentration ([Na]_S) receives influences from (a) the fluid exit from the intracellular compartment and thirst, which cause [Na]_S decreases; (b) osmotic diuresis with sums of the urinary sodium plus potassium concentration lower than the baseline euglycemic [Na]_S, which results in a [Na]_S increase; and (c), in some cases, gains or losses of fluid, sodium, and potassium through the gastrointestinal tract, the respiratory tract, and the skin. Hyperglycemic patients with hypernatremia have large deficits of body water and usually hypovolemia and develop severe clinical manifestations and significant mortality. To assist with the correction of both the severe dehydration and the hypovolemia, we developed formulas computing the fractional losses of the body water and monovalent cations in hyperglycemia. The formulas estimate varying losses between patients with the same serum glucose concentration ([Glu]_S) and [Na]_S but with different sums of monovalent cation concentrations in the lost fluids. Among subjects with the same [Glu]_S and [Na]_S, those with higher monovalent cation concentrations in the fluids lost have higher fractional losses of body water. The sum of the monovalent cation concentrations in the lost fluids should be considered when computing the volume and composition of the fluid replacement for hyperglycemic syndromes.

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Pseudohyponatremia remains a problem for clinical laboratories. In this study, we analyzed the mechanisms, diagnosis, clinical consequences, and conditions associated with pseudohyponatremia, and future developments for its elimination. The two methods involved assess the serum sodium concentration ([Na]_S) using sodium ion-specific electrodes: (a) a direct ion-specific electrode (ISE), and (b) an indirect ISE. A direct ISE does not require dilution of a sample prior to its measurement, whereas an indirect ISE needs pre-measurement sample dilution. [Na]_S measurements using an indirect ISE are influenced by abnormal concentrations of serum proteins or lipids. Pseudohyponatremia occurs when the [Na]_S is measured with an indirect ISE and the serum solid content concentrations are elevated, resulting in reciprocal depressions in serum water and [Na]_S values. Pseudonormonatremia or pseudohypernatremia are encountered in hypoproteinemic patients who have a decreased plasma solids content. Three mechanisms are responsible for pseudohyponatremia: (a) a reduction in the [Na]_S due to lower serum water and sodium concentrations, the electrolyte exclusion effect; (b) an increase in the measured sample’s water concentration post-dilution to a greater extent when compared to normal serum, lowering the [Na] in this sample; (c) when serum hyperviscosity reduces serum delivery to the device that apportions serum and diluent. Patients with pseudohyponatremia and a normal [Na]_S do not develop water movement across cell membranes and clinical manifestations of hypotonic hyponatremia. Pseudohyponatremia does not require treatment to address the [Na]_S, making any inadvertent correction treatment potentially detrimental.