Analyze Diet

Retrospective evaluation of the association between hyponatremia and neurological dysfunction in hospitalized foals (2012-2016): 109 cases.

Abstract: 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. Methods: Retrospective cohort study 2012 to 2016. Methods: Equine hospital. Methods: One hundred and nine foals <6 months old with hyponatremia (Na concentration ≤125 mmol/L). Methods: 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. 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.
Publication Date: 2019-12-17 PubMed ID: 31845521DOI: 10.1111/vec.12906Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
  • Journal Article

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research examined if there was a significant relationship between plasma sodium levels and the speed of hyponatremia correction with neurological abnormalities in foals. The findings indicated a considerable link between sodium levels and neurological signs in hyponatremic foals. However, the change in sodium levels per hour did not influence the neurological signs, and no new neurological symptoms appeared post-hyponatremia correction.

Objective of the Study

  • The study aims to establish if there is a significant correlation between plasma sodium concentrations and the speed of correction of hyponatremia (a condition characterized by low sodium levels in the blood) with neurological abnormalities in foals (young horses).

Research Methodology

  • The researchers conducted a retrospective cohort study from 2012 to 2016 at an equine hospital.
  • The study observed 109 foals under six months old with hyponatremia, denoted by a sodium concentration of 125 mmol/L or less.
  • The researchers reviewed the case records of each foal, noting clinical findings, the presence or absence of neurological signs on the day of the lowest sodium level, and the following five days. They also recorded the diagnosis and outcome.
  • The average change in sodium concentration per hour for the subsequent five days was determined and logistic regression was used to assess the correlation between neurological signs and sodium concentration, alongside other known risk factors for neurological dysfunction in foals and potential confounders.

Study Findings

  • The multivariable model showed that only sodium concentrations and Blood Urea Nitrogen (BUN) levels were significantly associated with the occurrence of neurological signs.
  • However, hourly changes in sodium levels were not linked to neurological signs any day after recording the lowest sodium level.
  • No new neurological signs were observed after correcting hyponatremia in any of the foals in the study.

Conclusion of the Study and Further Research

  • The study concluded that the sodium concentrations in the blood are significantly associated with the development of neurological signs in hyponatremic foals.
  • Additionally, elevated BUN levels might contribute to neurological dysfunction. However, further studies would be necessary to substantiate or refute these findings.

Cite This Article

APA
Dunkel B, Dodson F, Chang YM, Slovis NM. (2019). Retrospective evaluation of the association between hyponatremia and neurological dysfunction in hospitalized foals (2012-2016): 109 cases. J Vet Emerg Crit Care (San Antonio), 30(1), 66-73. https://doi.org/10.1111/vec.12906

Publication

ISSN: 1476-4431
NlmUniqueID: 101152804
Country: United States
Language: English
Volume: 30
Issue: 1
Pages: 66-73

Researcher Affiliations

Dunkel, Bettina
  • Department of Clinical Science and Services, The Royal Veterinary College, Herts, UK.
Dodson, Fiona
  • Department of Clinical Science and Services, The Royal Veterinary College, Herts, UK.
Chang, Yu-Mei
  • Research Support Office, The Royal Veterinary College, Herts, UK.
Slovis, Nathan Marc
  • Hagyard Equine Medical Institute, McGee Medicine Center, Lexington, KY.

MeSH Terms

  • Animals
  • Animals, Newborn / blood
  • Blood Urea Nitrogen
  • Cohort Studies
  • Female
  • Horse Diseases / blood
  • Horses
  • Hyponatremia / blood
  • Hyponatremia / complications
  • Hyponatremia / veterinary
  • Male
  • Odds Ratio
  • Retrospective Studies
  • Risk Factors
  • Seizures / blood
  • Seizures / etiology
  • Seizures / veterinary
  • Sodium / blood

References

This article includes 35 references
  1. Hardefeldt LY. Hyponatraemic encephalopathy in azotaemic neonatal foals: four cases. Aust Vet J 2014;92(12):488-491.
  2. Wong DM. Neurologic deficits associated with severe hyponatremia in 2 foals. J Vet Emerg Crit Care 2007;17(3):275-285.
  3. Dunkel B, Palmer JE, Olson KN. Uroperitoneum in 32 foals: influence of intravenous fluid therapy, infection, and sepsis. J Vet Intern Med 2005;19(6):889-893.
  4. Perkins G, Valberg SJ, Madigan JM. Electrolyte disturbances in foals with severe rhabdomyolysis. J Vet Intern Med 1998;12(3):173-177.
  5. Magdesian KG. Neonatal foal diarrhea. Vet Clin North Am Equine Pract 2005;21(2):295-312.
  6. Collins NM, Axon JE, Carrick JB. Severe hyponatraemia in foals: clinical findings, primary diagnosis and outcome. Aust Vet J 2016;94(6):186-191.
  7. Andrews FM, Matthews HK. Seizures, narcolepsy, and cataplexy. 2004:560-566.
  8. Verbalis JG, Goldsmith SR, Greenberg A. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med 2013;126(10 Suppl 1):S1-42.
  9. Hoorn EJ, Zietse R. Diagnosis and treatment of hyponatremia: compilation of the guidelines. J Am Soc Nephrol 2017;28(5):1340-1349.
  10. Diez E, Estepa JC, Lopez I. Hyponatremia and metabolic alkalosis in a foal with gastroesophageal reflux: a case report. Veterinarni Medicina 2009;54(10):501-506.
  11. Centor RM. Clinical Methods. 1990.
  12. Wong DM, Wilkins PA. Defining the systemic inflammatory response syndrome in equine neonates. Vet Clin North Am Equine Pract 2015;31(3):463-481.
  13. Li Q, Chen H, Hao JJ. Agreement of measured and calculated serum osmolality during the infusion of mannitol or hypertonic saline in patients after craniotomy: a prospective, double-blinded, randomised controlled trial. BMC Anesthesiol 2015;15:138.
  14. Guglielminotti J, Pernet P, Maury E. Osmolar gap hyponatremia in critically ill patients: evidence for the sick cell syndrome?. Crit Care Med 2002;30(5):1051-1055.
  15. Sterns RH, Silver SM. Brain volume regulation in response to hypo-osmolality and its correction. Am J Med 2006;119(7 Suppl 1):S12-16.
  16. Baumgaertel MW, Kraemer M, Berlit P. Neurologic complications of acute and chronic renal disease. Handb Clin Neurol 2014;119:383-393.
  17. Frye MA, Johnson JS, Traub-Dargatz JL. Putative uremic encephalopathy in horses: five cases (1978-1998). J Am Vet Med Assoc 2001;218(4):560-566.
  18. Bouchard PR, Weldon AD, Lewis RM, Summers BA. Uremic encephalopathy in a horse. Vet Pathol 1994;31(1):111-115.
  19. Sterns RH, Silver SM, Hix JK. Urea for hyponatremia?. Kidney Int 2015;87(2):268-270.
  20. Gankam Kengne F, Couturier BS, Soupart A, Decaux G. Urea minimizes brain complications following rapid correction of chronic hyponatremia compared with vasopressin antagonist or hypertonic saline. Kidney Int 2015;87(2):323-331.
  21. Soupart A, Penninckx R, Stenuit A, Decaux G. Azotemia (48 h) decreases the risk of brain damage in rats after correction of chronic hyponatremia. Brain Res 2000;852(1):167-172.
  22. Dhrolia MF, Akhtar SF, Ahmed E. Azotemia protects the brain from osmotic demyelination on rapid correction of hyponatremia. Saudi J Kidney Dis Transpl 2014;25(3):558-566.
  23. Trefz FM, Feist M, Lorenz I. Hypoglycaemia in hospitalised neonatal calves: prevalence, associated conditions and impact on prognosis. Vet J 2016;217:103-108.
  24. Funk GC, Lindner G, Druml W. Incidence and prognosis of dysnatremias present on ICU admission. Intensive Care Med 2010;36(2):304-311.
  25. Ueda Y, Hopper K, Epstein SE. Incidence, severity and prognosis associated with hypernatremia in dogs and cats. J Vet Intern Med 2015;29(3):794-800.
  26. Nicolini EA, Nunes RS, Santos GV. Could dysnatremias play a role as independent factors to predict mortality in surgical critically ill patients?. Medicine (Baltimore) 2017;96(9):e6182.
  27. Achinger SG, Ayus JC. Treatment of hyponatremic encephalopathy in the critically ill. Crit Care Med 2017;45:1762-1771.
  28. Dembek KA, Hurcombe SD, Frazer ML. Development of a likelihood of survival scoring system for hospitalized equine neonates using generalized boosted regression modeling. PLoS One 2014;9(10):e109212.
  29. Rohrbach BW, Buchanan BR, Drake JM. Use of a multivariable model to estimate the probability of discharge in hospitalized foals that are 7 days of age or less. J Am Vet Med Assoc 2006;228(11):1748-1756.
  30. Brewer BD, Koterba AM. Development of a scoring system for the early diagnosis of equine neonatal sepsis. Equine Vet J 1988;20(1):18-22.
  31. Elmer J, Callaway CW. The brain after cardiac arrest. Semin Neurol 2017;37(1):19-24.
  32. Gillam-Krakauer M, Gowen C Jr. Birth asphyxia. StatPearls 2017.
  33. Millar LJ, Shi L, Hoerder-S꯭issen A, Molnar Z. Neonatal hypoxia ischaemia: mechanisms, models, and therapeutic challenges. Front Cell Neurosci 2017;11:78.
  34. Chesler M. Regulation and modulation of pH in the brain. Physiol Rev 2003;83(4):1183-1221.
  35. Baba R, Zwaal JW. Severe metabolic acidosis after a single tonic-clonic seizure. Anaesthesia 2005;60(6):623-624.

Citations

This article has been cited 1 times.
  1. Urgibl-Bauer A, Lorch A, Badura D, Zablotski Y, Constable PD, Trefz FM. Retrospective evaluation of acid-base imbalances, clinicopathologic alterations, and prognostic factors in hospitalized calves with Eimeria-associated diarrhea. Front Vet Sci 2024;11:1467583.
    doi: 10.3389/fvets.2024.1467583pubmed: 39834917google scholar: lookup