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• W2032806445 abstract "Hyponatremia remains the most frequent electrolyte abnormality in hospitalized patients. Both neurological disease and the postoperative period are established risk factors contributing to the high prevalence of hyponatremia of more than 30%.1,2 Classically, central nervous system diseases favor the occurrence of both hypovolemic and isovolemic hyponatremia. The former is attributed to the cerebral salt wasting syndrome (CSW), and the latter results from the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Although both SIADH and CSW are both associated with hypotonic hyponatremia and increased natriuresis, the mechanism by which SIADH and CSW develop is considered to be quite distinct. SIADH is attributed to an excessive secretion of antidiuretic hormone, which is responsible for the impairment in urinary dilution (antidiuresis) and the retention of water. In patients with CSW, the major factor leading to an excessive natriuresis is thought to be an abnormal release of natriuretic hormones. Recent data, however, indicate that the separation between these two syndromes is less clear-cut as multiple abnormalities, including an increase in natriuretic peptide secretion, an inhibition of the renin-aldosterone system, and excessive adrenergic activity, together explain dysnatremia. Other peptides released after a subarachnoid hemorrhage (SAH) also possess profound vasoconstrictive or vasodilatory properties, for instance, adrenomedullin or endothelin. These peptides may explain the link between hyponatremia, natriuretic peptides, and the risk of vasospasm.3,4 In this issue of the journal, Audibert et al.5 report the results of a study in which relevant hormonal changes were measured at several periods after SAH in a homogeneous intensive care unit population. They clearly demonstrated an increased natriuresis associated with a low blood volume in the first 3 days after severe SAH. This result is in contrast to other studies showing no difference in blood volume between patients with or without hyponatremia.6 However, hyponatremia alone is not a reliable diagnostic criterion for CSW,7 and blood volume is notoriously difficult to assess at the bedside, which may explain why very few studies actually report a decreased blood volume, an essential feature of CSW diagnosis.7,8 In addition, Audibert et al. found changes in plasma concentration of several hormones (antidiuretic hormone, aldosterone, renin, angiotensin, atrial natriuretic peptide, and brain natriuretic peptide) during the first 12 days after SAH. As it is difficult to get rapid and accurate measurements of these hormones and their profile changes frequently, a pragmatic approach to the treatment of hyponatremia in acute neurological disorders is preferable. The study by Audibert et al.5 suggests that measurement of fluid and sodium balance at the bedside is still the least expensive and most valuable method of preventing and/or managing hyponatremia. In contrast to hypernatremia, hyponatremia may be associated with either isotonic, hypertonic or hypotonic states.2 Thus, hyponatremia first requires calculation of plasma tonicity (osmolality) to determine the intracellular volume. Depending on the plasma tonicity, completely opposite treatments may be appropriate, i.e., infusion of hypo- or hypertonic solutions. Although there is consistently an increase in intracellular volume, hypotonic hyponatremia may be associated with various changes in extracellular volume. In other words, whereas hypotonic hyponatremia always reflects an excess of extracellular water to extracellular sodium, the total body sodium content varies according to the cause of hyponatremia. Besides pathophysiological considerations, the most common severe complication of hypotonic hyponatremia is cerebral edema. In this situation, an incorrect or inappropriate treatment can lead to morbidity or mortality.9 As SIADH and CSW require different therapy, it is essential to distinguish them in order to administer the most appropriate treatment. Audibert et al.5 demonstrate the feasibility of maintaining plasma osmolality around 305 mOsm/L after severe SAH by giving 2–3 L of isotonic saline in the first 24 h, then adjusting the sodium intake to match the natriuresis measured every day. This is an easy to follow protocol in the intensive care unit but should one perhaps aim for a higher osmolality? Recent provocative experimental data suggest that a plasma osmolality >350 mOsm/L may be both safe and clinically sound in brain-injured patients.10 Infusion of considerable amounts of sodium would be needed to achieve and maintain this objective. This treatment objective has been refuted by retrospective studies showing that hypernatremia is independently associated with poorer outcomes.11 In a cohort study of 580 patients after SAH, hyponatremia was less frequent than hypernatremia and did not have any prognostic significance.12 Hypernatremia in contrast was associated with poor outcome in the univariate analysis, but not in the multivariate analysis, and was related to intracranial hypertension. Most probably, hypernatremia was due to the infusion of hyperosmolar fluids to control intracranial pressure in patients with severe brain injuries. For now, normonatremia should be considered the conservative but safe strategy. One must remember, however, that the relationships among sodium intake, plasma osmolality, and brain water content are not simple. Growing experimental evidence suggests that aquaporin-4 expression in the brain is critical for cerebral edema development.13,14 The pool of aquaporin-4 that mediates edema formation after a cerebral insult is probably a major route of water efflux from the brain in osmotherapy. Up- or down-regulation of the aquaporin-4 pool depends on multiple factors, including vasopressin and osmolality. Until we better understand the role of these and other water channels in brain edema, it is difficult to give clear guidelines on the appropriate use of sodium. The interactions among sodium and fluid intake, aquaporin-4 expression, cerebral edema and patient outcome may be a fruitful area of research. Another major finding in the study by Audibert et al.5 is the decrease in blood volume noted from day 2 to day 7 after SAH, despite adequate fluid and sodium intake and positive fluid balance. It shows that it is not possible to draw a parallel between sodium and water homeostasis and blood volume regulation. These data may add further support to the institution of hypervolemia for the prevention and management of symptomatic cerebral vasospasm. However, caution is required as the efficacy of this treatment in preventing delayed cerebral ischemia has not been demonstrated and brain-injured patients are prone to developing pulmonary edema.15 The putative beneficial effect of fluid loading to enhance the cerebral circulation should be weighted against potential detrimental effects on blood oxygenation. We clearly have to further improve our knowledge on easy diagnostic testing to find the appropriate balance between a good pinch of salt or two for the brain but not too much for the brain or the body." @default.
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• W2032806445 title "Hyponatremia and Subarachnoid Hemorrhage: Will That Be One Pinch or Two of Salt?" @default.
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