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Hyponatremia – Frequency, Causes, Pathobiochemistry, Clinics and Therapy.


Authors: A. Kazda
Authors‘ workplace: Ústav lékařské biochemie a laboratorní diagnostiky 1. LF UK a VFN, Praha
Published in: Klin. Biochem. Metab., 26, 2018, No. 4, p. 157-165

Overview

Objective:

Presentation of the current knowledge of hyponatremias in terms of their causes, frequency and pathobiochemical connections in development and treatment of these disbalances

Study type:

Synoptic

Settings:

Institute of Medical Biochemistry and Laboratory Diagnostics, First Faculty of Medicine and General University Hospital, Prague

Material and Methods: Based on the study of global literature is in the survey the frequency and prognostic importance of hyponatremia evaluated. Its hypotonic and non-hypotonic forms are described as well as pathophysiological consequences for the brain and clinical signs. The therapeutic proceedings are mentioned together with accompanying risks. It is referred about the problems of hyponatremia in neurointensive care, in older age and in the relation to the health of bones.

Results:

The frequency of hyponatremia in three large sets of patients admitted to ICU of various specialisations was between 10.0% till 17.1%. Its value is given by decreased relation of sodium supply in extracellular fluid (ECF) and size of ECF. Hyponatremia causes the decrease of osmolality – hypotonic form. If there are contemporary present another osmotically effective solutes in ECF (glucose, mannitol) they cause the shift of water from the cells to the ECF and natremia is diluted – non-hypotonic form. Decreased osmolality of ECF accompanying hyponatremia leads to the shift of water to the cells. The brain is therefore swelling and hyponatraemic encephalopathy develops. The clinical signs and prognostic significance of this evolution are described in relation to the categorization of natrium decrease. Brain compensates this disturbance by decreasing the content of ions and small organic molecules in its cells. Therapeutic proceedings are described. The rate of correction has to respect the time, necessary for the restoration if eliminated osmotically active particles back in brain cells. Maximal elevation of hyponatremia is 10 mmol/l/day and in risk patients yet less. More rapid correction is risk for brain demyelinisation. Differential diagnosis and treatment of hyponatremia is described in neurointensive care. It is referred about increased frequency of hyponatremia and its consequences in elder age and about its relation to bone fracture and osteoporosis.

Conclusion:

Hyponatremia is connected with more severe pathobiochemical changes and accompanied by elevated morbidity and mortality.

Keywords:

hyponatremia, encephalopathy, body fluids, cerebral salt-wasting syndrome, syndrome of inappropriate antidiuretic hormone secretion.


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