Hyponatremia is the most common electrolyte disorder encountered in neurosurgical patients. The aggressive treatment of hyponatremia in this group is critical, as hyponatremia can lead to mental status changes, seizures, vasospasm, cerebral edema, and even death. When it occurs, it represents a failure of one of several homeostatic mechanisms that tightly regulate serum sodium. In these patients, hyponatremia is most commonly due to the syndrome of inappropriate antidiuretic hormone (SIADH) or cerebral salt wasting (CSW). It can be problematic to differentiate between these 2 as they share key features, including low serum sodium, low serum osmolality, a higher urine osmolality than serum osmolality, and an elevated urinary sodium concentration. Furthermore, distinctions between CSW and SIADH, namely extracellular fluid (ECF) volume and total sodium balance, are often difficult to establish. Syndrome of inappropriate antidiuretic hormone is characterized by a volume-expanded state, whereas CSW is characterized by a volume-contracted state. Determining the exact cause remains a clinical imperative as the treatment for each is different. The rate at which serum sodium is corrected must be attended to, as rapid shifts in serum sodium pose potential risk of cerebral pontine myelinolysis.
"Considering that diuretics or excessive amount of fluids were not administrated, the most probably diagnoses remained SIAD or C/RSWS, which differ mainly for the extracellular volume (ECV) status, normal in SIAD while reduced in C/RSWS . "
[Show abstract][Hide abstract] ABSTRACT: It is important to ensure an adequate sodium and volume balance in neurosurgical patients in order to avoid the worsening of brain injury.Indeed, hyponatremia and polyuria, that are frequent in this patient population, are potentially harmful, especially if not promptly recognized.Differential diagnosis is often challenging, including disorders, which, in view of similar clinical pictures, present very different pathophysiological bases, such as syndrome of inappropriate antidiuresis, cerebral/renal salt wasting syndrome and diabetes insipidus.
Here we present the clinical report of a 67-year-old man with a recent episode of acute subarachnoid haemorrhage, admitted to our ward because of severe hyponatremia, hypokalemia and huge polyuria.We performed a complete workup to identify the underlying causes of these alterations and found a complex picture of salt wasting syndrome associated to primary polydipsia. The appropriate diagnosis allowed us to correct the patient hydro-electrolyte balance.
The comprehension of the pathophysiological mechanisms is essential to adequately recognize and treat hydro-electrolyte disorders, also solving the most complex clinical problems.
"Hyponatremia involves several clinical conditions that affect as much as 22% of hospitalized patients (see Loh and Verbalis 2008). Hyponatremia results in decreased sodium plasma levels from approximately 150 to \135 mM and is often associated with hypo-osmolarity caused by excessive renal water retention (Wakil et al. 2011; Upadhyay and Gormley 2011). Hyponatremia and generally cell swelling have been associated with increased oxidative stress (Barsony et al. 2011; Haussinger and Schliess 2008; Friis et al. 2008). "
[Show abstract][Hide abstract] ABSTRACT: The present work was initiated to investigate regulation of the taurine transporter TauT by reactive oxygen species (ROS) and the tonicity-responsive enhancer binding protein (TonEBP) in NIH3T3 mouse fibroblasts during acute and long-term (4 h) exposure to low-sodium/hypo-osmotic stress. Taurine influx is reduced following reduction in osmolarity, keeping the extracellular Na+ concentration constant. TonEBP activity is unaltered, whereas TauT transcription as well as TauT activity are significantly reduced under hypo-osmotic conditions. In contrast, TonEBP activity and TauT transcription are significantly increased following hyperosmotic exposure. Swelling-induced ROS production in NIH3T3 fibroblasts is generated by NOX4 and by increasing total ROS, by either exogenous application of H2O2 or overexpressing NOX4, we demonstrate that TonEBP activity and taurine influx are regulated negatively by ROS under hypo-osmotic, low-sodium conditions, whereas the TauT mRNA level is unaffected. Acute exposure to ROS reduces taurine uptake as a result of modulated TauT transport kinetics. Thus, swelling-induced ROS production could account for the reduced taurine uptake under low-sodium/hypo-osmotic conditions by direct modulation of TauT.
Electronic supplementary material
The online version of this article (doi:10.1007/s00232-012-9416-8) contains supplementary material, which is available to authorized users.
[Show abstract][Hide abstract] ABSTRACT: Cerebral edema is a common finding in a variety of neurological conditions, including ischemic stroke, traumatic brain injury, ruptured cerebral aneurysm, and neoplasia. With the possible exception of neoplasia, most pathological processes leading to edema seem to share similar molecular mechanisms of edema formation. Challenges to brain-cell volume homeostasis can have dramatic consequences, given the fixed volume of the rigid skull and the effect of swelling on secondary neuronal injury. With even small changes in cellular and extracellular volume, cerebral edema can compromise regional or global cerebral blood flow and metabolism or result in compression of vital brain structures. Osmotherapy has been the mainstay of pharmacologic therapy and is typically administered as part of an escalating medical treatment algorithm that can include corticosteroids, diuretics, and pharmacological cerebral metabolic suppression. Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(-) co-transporter (NKCC1) and the SUR1-regulated NC(Ca-ATP) (SUR1/TRPM4) channel. These two ion channels have been demonstrated to be critical mediators of edema formation in brain-injured states. Their specific inhibitors, bumetanide and glibenclamide, respectively, are well-characterized Food and Drug Administration-approved drugs with excellent safety profiles. Directed inhibition of these ion transporters has the potential to reduce the development of cerebral edema and is currently being investigated in human clinical trials. Another class of treatment agents for cerebral edema is vasopressin receptor antagonists. Euvolemic hyponatremia is present in a myriad of neurological conditions resulting in cerebral edema. A specific antagonist of the vasopressin V1A- and V2-receptor, conivaptan, promotes water excretion while sparing electrolytes through a process known as aquaresis.
Journal of the American Society for Experimental NeuroTherapeutics 11/2011; 9(1):65-72. DOI:10.1007/s13311-011-0087-4 · 5.05 Impact Factor
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