For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
6
views
63
references
 Top references
cited by
8
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      523
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Hyponatraemia in older patients: a clinical and practical approach

      Read this article at

      ScienceOpenPublisher
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Summary

          Hyponatraemia is frequent in older people and induces marked motor and cognitive dysfunction, even in patients deemed ‘asymptomatic’. Nutritional status is worse than in euvolaemic-matched controls, and the risk of fracture is increased following incidental falls. Yet hyponatraemia is undertreated, in spite of the fact that its correction is accompanied by a clear improvement in symptoms. Both evaluation of neurological symptoms and classification by volaemia are essential for a correct diagnosis and treatment of the hyponatraemic elderly patient. The syndrome of inappropriate anti-diuretic hormone secretion (SIADH) is the most common cause of hyponatraemia in older people. Nutritional status and chronicity of SIADH should be taken into account when deciding therapy. We propose an 8-step approach to the management of the elderly patient with hyponatraemia.

          Related collections

          Most cited references63

          • Record: found
          • Abstract: found
          • Article: not found

          Hyponatremia: evaluating the correction factor for hyperglycemia.

          T A Hillier, R D Abbott, E J Barrett (1999)
          There are no controlled experimental data that assess the accuracy of the commonly used correction factor of a 1.6 meq/L decrease in serum sodium concentration for every 100 mg/dL increase in plasma glucose concentration. The purpose of this study was to evaluate experimentally the hyponatremic response to acute hyperglycemia. Somatostatin was infused to block endogenous insulin secretion in 6 healthy subjects. Plasma glucose concentrations were increased to >600 mg/dL within 1 hour by infusing 20% dextrose. The glucose infusion was then stopped and insulin given until the plasma glucose concentration decreased to 140 mg/dL. Plasma glucose and serum sodium concentrations were measured every 10 minutes. Overall, the mean decrease in serum sodium concentration averaged 2.4 meq/L for every 100 mg/dL increase in glucose concentration. This value is significantly greater than the commonly used correction factor of 1.6 (P = 0.02). Moreover, the association between sodium and glucose concentrations was nonlinear. This was most apparent for glucose concentrations >400 mg/dL. Up to 400 mg/dL, the standard correction of 1.6 worked well, but if the glucose concentration was >400 mg/dL, a correction factor of 4.0 was better. These data indicate that the physiologic decrease in sodium concentration is considerably greater than the standard correction factor of 1.6 (meq/L Na per 100 mg/dL glucose), especially when the glucose concentration is >400 mg/dL. Additionally, a correction factor of a 2.4 meq/L decrease in sodium concentration per 100 mg/dL increase in glucose concentration is a better overall estimate of this association than the usual correction factor of 1.6.
          Article 0 comments Cited 131 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Hyponatremia-Induced Osteoporosis

            Joseph Verbalis, Julianna Barsony, Yoshihisa Sugimura … (2009)
            There is a high prevalence of chronic hyponatremia in the elderly, frequently owing to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Recent reports have shown that even mild hyponatremia is associated with impaired gait stability and increased falls. An increased risk of falls among elderly hyponatremic patients represents a risk factor for fractures, which would be further amplified if hyponatremia also contributed metabolically to bone loss. To evaluate this possibility, we studied a rat model of SIADH and analyzed data from the Third National Health and Nutrition Examination Survey (NHANES III). In rats, dual-energy X-ray absorptiometry (DXA) analysis of excised femurs established that hyponatremia for 3 months significantly reduced bone mineral density by approximately 30% compared with normonatremic control rats. Moreover, micro-computed tomography (µCT) and histomorphometric analyses indicated that hyponatremia markedly reduced both trabecular and cortical bone via increased bone resorption and decreased bone formation. Analysis of data from adults in NHANES III by linear regression models showed that mild hyponatremia is associated with increased odds of osteoporosis (T-score –2.5 or less) at the hip [odds ratio (OR) = 2.85; 95% confidence interval (CI) 1.03–7.86; p < .01]; all models were adjusted for age, sex, race, body mass index (BMI), physical activity, history of diuretic use, history of smoking, and serum 25-hydroxyvitamin D [25(OH)D] levels. Our results represent the first demonstration that chronic hyponatremia causes a substantial reduction of bone mass. Cross-sectional human data showing that hyponatremia is associated with significantly increased odds of osteoporosis are consistent with the experimental data in rodents. Our combined results suggest that bone quality should be assessed in all patients with chronic hyponatremia. © 2010 American Society for Bone and Mineral Research.
            Article 0 comments Cited 83 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Development of severe hyponatraemia in hospitalized patients: treatment-related risk factors and inadequate management.

              Ewout J. Hoorn, Jan W. Lindemans, Robert Zietse (2005)
              Although hyponatraemia [plasma sodium (PNa) 122+/-4 mmol/l). In hospital-acquired hyponatraemia, treatment started significantly later (1.0+/-2.6 vs 9.8+/-10.6 days, P<0.001) and the duration of hospitalization was longer (18.2+/-11.5 vs 30.7+/-23.4 days, P=0.01). The correction of PNa in hospital-acquired hyponatraemia was slower after both 24 h (6+/-4 vs 4+/-4 mmol/l, P=0.009) and 48 h (10+/-6 mmol/l vs 6+/-5 mmol/l, P=0.001) of treatment. Nineteen patients (26%) from both groups were not treated for hyponatraemia and this was associated with a higher mortality rate (seven out of 19 vs seven out of 55, P=0.04). Factors that contributed to hospital-acquired hyponatraemia included: thiazide diuretics (none out of 38 vs eight out of 36, P=0.002), drugs stimulating antidiuretic hormone (two out of 38 vs eight out of 36, P=0.04), surgery (none out of 38 vs 10 out of 36, P<0.001) and hypotonic intravenous fluids (one out of 38 vs eight out of 36, P=0.01). Symptomatic hyponatraemia was present in 27 patients (36%), and 14 patients died (19%). The development of severe hyponatraemia in hospitalized patients was associated with treatment-related factors and inadequate management. Early recognition of risk factors and expedited therapy may make hospital-acquired severe hyponatraemia more preventable.
              Article 0 comments Cited 65 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (publisher-id): applab
                Title: Reviews in Clinical Gerontology
                Abbreviated Title: Rev. Clin. Gerontol.
                Publisher: Cambridge University Press (CUP)
                ISSN (Print): 0959-2598
                ISSN (Electronic): 1469-9036
                Publication date Created: February 2015
                Publication date (Print): January 16 2015
                Volume: 25
                Issue: 01
                Pages: 31-52
                Article
                DOI: 10.1017/S0959259814000197
                SO-VID: a105da28-96c4-47fa-9b04-0093ccbdfe33
                Copyright © © 2015
                History

                Data availability:

                Comments

                Comment on this article

                scite_

                Similar content523

                See all similar

                Cited by8

                See all cited by

                Most referenced authors677

                See all reference authors