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Updated: Jan 1, 2026
Continuous Video Electroencephalogram during Hypoxia-Ischemia in Neonatal Mice
Published on: June 11, 2020
Retrospective evaluation of the association between hyponatremia and neurological dysfunction in hospitalized foals
Bettina Dunkel1, Fiona Dodson1, Yu-Mei Chang2
1Department of Clinical Science and Services, The Royal Veterinary College, Herts, UK.
Objective:
Hyponatremia and rapid correction of hyponatremia can lead to neurological abnormalities. The objective of the study was to determine whether plasma sodium concentrations (Na+ ) and speed of correction of hyponatremia are significantly associated with neurological abnormalities in foals.
Design:
Retrospective cohort study 2012 to 2016.
Setting:
Equine hospital.
Animals:
One hundred and nine foals <6 months old with hyponatremia (Na+ concentration ≤125 mmol/L).
Interventions:
Case records were reviewed for any foal with hyponatremia. Clinicopathological findings, presence or absence of neurological signs on the day of the lowest Na+ concentration measured and the following 5 days, diagnosis and outcome were recorded, and changes in Na+ concentration per hour were calculated for up to 5 subsequent days. Logistic regression was used to assess the association between presence or absence of neurological signs, Na+ concentration, other known risk factors for neurological dysfunction in foals, and possible confounders.
Measurements And Main Results:
In the final multivariable model, only Na+ (odds ratio [OR]: 0.86; 95% CI 0.79-0.95; P = 0.002) and BUN concentrations (OR: 1.04; 95% CI: 1.02-1.06; P = 0.001) were significantly associated with neurological signs. Changes in Na+ concentrations per hour were not associated with neurological signs on any day after the lowest Na+ concentration had been measured (P = 0.18-0.82), and development of new neurological signs following correction of hyponatremia was not reported in any foal.
Conclusions:
Na+ concentrations were associated with the development of neurological signs in hyponatremic foals. Increased BUN concentrations might contribute to neurological dysfunction, but further studies are necessary to confirm or refute these findings.
