Clinical Semiology and Neuroradiologic Correlates of Acute Hypernatremic Osmotic Challenge in Adults: A Literature Review

Abstract

SUMMARY:The complex interplay between hypernatremic osmotic disturbances and cerebral lesions is yet to be clarified. In this review, we discuss, on the basis of the reported data of hypernatremic CNS challenge in the adult population, the clinical and radiologic features of the condition. Our search captured 20 case studies and 1 case series with 30 patients in total who acquired acute hypernatremia due to different etiologies and developed CNS lesions. We explored the associations between premorbid conditions, clinical presentation, hypernatremic state, correction rate, and radiologic appearance, including the localization of brain lesions and the outcomes. The results revealed that altered mental status was the most commonly reported symptom and osmotic demyelination syndrome in the form of extrapontine myelinolysis was the prevailing radiologic pattern. Finally, we contrasted, when appropriate, clinical and experimental data related to hypernatremic and hyponatremic osmotic insults to aid the understanding of the pathophysiology of CNS osmotic brain injury.ABBREVIATIONS: BG ϭ basal ganglia; CPM ϭ central pontine myelinolysis; EPM ϭ extrapontine myelinolysis; GCS ϭ Glasgow Coma Scale; ODS ϭ osmotic

Central and Extrapontine Myelinolysis after Alcohol Withdrawal and Correction of Hypernatremia in a Chronic Alcoholic: a Case Report

“…According to a recent report, clinical symptoms do not correlate with age, the presence of comorbid conditions, initial serum Na + levels, serum osmolality, or the serum Na + correction rate [1]. Apart from correction rates, the presence of additional metabolic derangements, such as serum K + levels and hyperglycemia, are considered to be independent risk factors for the development of ODS [1]. Therefore, an increase in serum sodium, as well as potassium levels, should not exceed 12 mEq/L in the first 24 hours and 18 mEq/L in the first 48 hours [4].…”

“…Frequently affected parts in ODS are the pons in CPM and the cerebellum, lateral geniculate body, external capsule, hippocampus, putamen, cerebral cortex, thalamus, and caudate nucleus and more infrequently, the claustrum, internal capsule, midbrain, and internal medullary lamella, in EPM [3]. EPM is more commonly observed with hypernatremia [1]. In particular, hippocampal involvement may be related to the high vulnerability of the hippocampus to the neurotoxic effects of osmotic derangement and general systemic stress [1].…”

“…EPM is more commonly observed with hypernatremia [1]. In particular, hippocampal involvement may be related to the high vulnerability of the hippocampus to the neurotoxic effects of osmotic derangement and general systemic stress [1].…”

“…It has been increasingly recognized that EPM can occur in the setting of other osmotic challenges, such as glycemic state and end-stage renal disease regardless of serum sodium levels [1]. According to a recent report, clinical symptoms do not correlate with age, the presence of comorbid conditions, initial serum Na + levels, serum osmolality, or the serum Na + correction rate [1].…”

“…CPM is classically described as the radiological manifestations of osmotic myelinolysis, and clinical symptoms range from subtle changes in cognitive functions to life-threatening autonomic and brainstem dysfunction and death [1]. EPM develops in extrapontine sites through mechanisms similar to CPM but the cases of EPM have been reported rarely than those of CPM [1,2].…”