Hypernatremia, like hyponatremia, is a disorder of water balance, most frequently arising from a combination of excess loss of water or hypotonic fluid with an insufficient compensatory intake. In medical literature, hypernatremia is frequently eclipsed by its more prevalent counterpart, hyponatremia, receiving comparatively less attention in scholarly discussions. Hypernatremia may exist at admission (community-acquired hypernatremia) or develop 24 hours after admission (hospital-acquired hypernatremia). The prevalence of hypernatremia among hospitalized patients has been reported to be between 1% and 6% (1–3). A report by Tsipotis et al. (4) found that the hypernatremia spectrum in unselected hospitalized patients is independently associated with increased in-hospital mortality and is often associated with inappropriate correction (5, 6).
A study recently published in CJASN (7) explored the outcomes and discharge dispositions of various levels of hospital-acquired hypernatremia in patients with or without chronic kidney disease. This was a retrospective study, using data from the Cerner Health Facts database (2000–2018), which analyzed 1.7 million patients with normal serum sodium (Na) levels of 135 to 145 mEq/L up to 24 hours after admission. Of this cohort, only 6% of patients developed hypernatremia after hospitalization. The patients with hypernatremia were older and had a lower estimated glomerular filtration rate (eGFR) at presentation. In addition to analyzing the in-hospital mortality, discharge dispositions (to hospice, to a nursing facility, or home) and length of hospital stay were primary outcomes. The risk of all outcomes was significantly greater for a serum Na >145 mEq/L when compared with the reference interval (serum Na, 135–145 mEq/L). The in-hospital mortality and discharge to nursing facilities were 12% and 25%, respectively, in the hypernatremia group, whereas they were only 0.6% and 9%, respectively, in the normonatremic group. Patients with hypernatremia had higher odds for in-hospital mortality (odds ratio [OR], 14.04), discharge to hospice (OR, 4.35), and discharge to nursing facilities (OR, 3.88; p = 0.001 for all). Furthermore, the adjusted models showed that the ORs of in-hospital mortality became significantly higher as serum Na increased >145 mEq/L and as eGFR decreased <90 mL/min/1.73 m2 when compared with the reference groups.
A previous study on “community-acquired hypernatremia” from the same database found similar results (8). The risk of in-hospital mortality and discharge to a hospice or nursing facility was highest among those with a serum Na >155 mEq/L. The community-acquired hypernatremia study addressed the knowledge gap by examining the association between various degrees of hospital-acquired hypernatremia and specific outcomes in a sizable and diverse population, focusing on kidney function status. Although associations between hypernatremia and adverse outcomes were identified, the study appropriately underscored the need for caution in inferring direct causation.
Although it offers valuable insights, a nuanced examination reveals limitations that necessitate careful consideration in interpreting its findings. The Sequential Organ Failure Assessment score is a crucial tool for assessing the severity of illness in predicting outcomes, particularly among patients who are critically ill. The lack of use of this assessment in this study is a notable limitation. Furthermore, without a granular examination of specific diagnoses, the study may have overlooked the heterogeneity within the hypernatremic population. The complex interplay of various factors influencing outcomes makes it challenging to eliminate the possibility of confounding variables affecting the reported results. The high mortality in these patients may just mean that they were terminally ill, and the high Na was a bystander “marker.”
Thus, optimizing outcomes in hypernatremia necessitates a multifaceted approach involving the identification of the vulnerable population at heightened risk, early diagnostic interventions, discernment of underlying etiologies, and judicious correction of hypernatremia at a rate aligned with established guidelines.
Footnotes
References
- 1.↑
Palevsky PM, et al. Hypernatremia in hospitalized patients. Ann Int Med 1996; 124:197–203. doi: 10.7326/0003-4819-124-2-199601150-00002
- 2.
Felizardo Lopes I, et al. Prevalence, risk factors and prognosis of hypernatraemia during hospitalisation in internal medicine. Neth J Med 2015; 73:448–454. https://www.njmonline.nl/article_ft.php?a=1647&d=1093&i=189
- 3.↑
Ranjan R, et al. Progression to severe hypernatremia in hospitalized general medicine inpatients: An observational study of hospital-acquired hypernatremia. Medicina (Kaunas) 2020; 56:358; doi: 10.3390/medicina56070358
- 4.↑
Tsipotis E, et al. Hospital-associated hypernatremia spectrum and clinical outcomes in an unselected cohort. Am J Med 2018; 131:72–82.e1. doi: 10.1016/j.amjmed.2017.08.011
- 5.↑
Alshayeb HM, et al. Severe hypernatremia correction rate and mortality in hospitalized patients. Am J Med Sci 2011; 341:356–360. doi: 10.1097/MAJ.0b013e31820a3a90
- 6.↑
Feigin E, et al. Rate of correction and all-cause mortality in patients with severe hypernatremia. JAMA Netw Open 2023; 6:e2335415. doi: 10.1001/jamanetwork-open.2023.35415
- 7.↑
Arzhan S, et al. Outcomes of hospital-acquired hypernatremia. Clin J Am Soc Nephrol 2023; 18:1396–1407. doi: 10.2215/CJN.0000000000000250
- 8.↑
Arzhan S, et al. Hypernatremia in hospitalized patients: A large population-based study. Kidney360 2022; 3:1144–1157. doi: 10.34067/KID.0000702022