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The Korean Journal of Internal Medicine May 2023Hypernatremia is an occasionally encountered electrolyte disorder, which may lead to fatal consequences under improper management. Hypernatremia is a disorder of the... (Review)
Review
Hypernatremia is an occasionally encountered electrolyte disorder, which may lead to fatal consequences under improper management. Hypernatremia is a disorder of the homeostatic status regarding body water and sodium contents. This imbalance is the basis for the diagnostic approach to hypernatremia. We summarize the eight diagnostic steps of the traditional approach and introduce new biomarkers: exclude pseudohypernatremia, confirm glucose-corrected sodium concentrations, determine the extracellular volume status, measure urine sodium levels, measure urine volume and osmolality, check ongoing urinary electrolyte free water clearance, determine arginine vasopressin/copeptin levels, and assess other electrolyte disorders. Moreover, we suggest six steps to manage hypernatremia by replacing water deficits, ongoing water losses, and insensible water losses: identify underlying causes, distinguish between acute and chronic hypernatremia, determine the amount and rate of water administration, select the type of replacement solution, adjust the treatment schedule, and consider additional therapy for diabetes insipidus. Physicians may apply some of these steps to all patients with hypernatremia, and can also adapt the regimens for specific causes or situations.
Topics: Humans; Adult; Hypernatremia; Sodium; Osmolar Concentration; Body Water; Water
PubMed: 36578134
DOI: 10.3904/kjim.2022.346 -
American Family Physician Mar 2015Hyponatremia and hypernatremia are common findings in the inpatient and outpatient settings. Sodium disorders are associated with an increased risk of morbidity and...
Hyponatremia and hypernatremia are common findings in the inpatient and outpatient settings. Sodium disorders are associated with an increased risk of morbidity and mortality. Plasma osmolality plays a critical role in the pathophysiology and treatment of sodium disorders. Hyponatremia and hypernatremia are classified based on volume status (hypovolemia, euvolemia, and hypervolemia). Sodium disorders are diagnosed by findings from the history, physical examination, laboratory studies, and evaluation of volume status. Treatment is based on symptoms and underlying causes. In general, hyponatremia is treated with fluid restriction (in the setting of euvolemia), isotonic saline (in hypovolemia), and diuresis (in hypervolemia). A combination of these therapies may be needed based on the presentation. Hypertonic saline is used to treat severe symptomatic hyponatremia. Medications such as vaptans may have a role in the treatment of euvolemic and hypervolemic hyponatremia. The treatment of hypernatremia involves correcting the underlying cause and correcting the free water deficit.
Topics: Diagnosis, Differential; Diuresis; Fluid Therapy; Humans; Hypernatremia; Hyponatremia; Isotonic Solutions; Saline Solution, Hypertonic; Sodium
PubMed: 25822386
DOI: No ID Found -
Clinical Journal of the American... Mar 2019
Topics: Adult; Aged; Antimanic Agents; Biomarkers; Dehydration; Diuretics; Female; Fluid Therapy; Humans; Hypernatremia; Lithium Carbonate; Risk Factors; Sodium; Treatment Outcome; Up-Regulation; Water-Electrolyte Balance
PubMed: 30728169
DOI: 10.2215/CJN.12141018 -
Clinical Journal of the American... May 2019Hypernatremia is common in hospitalized, critically ill patients. Although there are no clear guidelines on sodium correction rate for hypernatremia, some studies...
BACKGROUND AND OBJECTIVES
Hypernatremia is common in hospitalized, critically ill patients. Although there are no clear guidelines on sodium correction rate for hypernatremia, some studies suggest a reduction rate not to exceed 0.5 mmol/L per hour. However, the data supporting this recommendation and the optimal rate of hypernatremia correction in hospitalized adults are unclear.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS
We assessed the association of hypernatremia correction rates with neurologic outcomes and mortality in critically ill patients with hypernatremia at admission and those that developed hypernatremia during hospitalization. We used data from the Medical Information Mart for Intensive Care-III and identified patients with hypernatremia (serum sodium level >155 mmol/L) on admission (=122) and hospital-acquired (=327). We calculated different ranges of rapid correction rates (>0.5 mmol/L per hour overall and >8, >10, and >12 mmol/L per 24 hours) and utilized logistic regression to generate adjusted odds ratios (aOR) with 95% confidence intervals (95% CIs) to examine association with outcomes.
RESULTS
We had complete data on 122 patients with severe hypernatremia on admission and 327 patients who developed hospital-acquired hypernatremia. The difference in in-hospital 30-day mortality proportion between rapid (>0.5 mmol/L per hour) and slower (≤0.5 mmol/L per hour) correction rates were not significant either in patients with hypernatremia at admission with rapid versus slow correction (25% versus 28%; =0.80) or in patients with hospital-acquired hypernatremia with rapid versus slow correction (44% versus 40%; =0.50). There was no difference in aOR of mortality for rapid versus slow correction in either admission (aOR, 1.3; 95% CI, 0.5 to 3.7) or hospital-acquired hypernatremia (aOR, 1.3; 95% CI, 0.8 to 2.3). Manual chart review of all suspected chronic hypernatremia patients, which included all 122 with hypernatremia at admission, 128 of the 327 hospital-acquired hypernatremia, and an additional 28 patients with ICD-9 codes for cerebral edema, seizures and/or alteration of consciousness, did not reveal a single case of cerebral edema attributable to rapid hyprnatremia correction.
CONCLUSIONS
We did not find any evidence that rapid correction of hypernatremia is associated with a higher risk for mortality, seizure, alteration of consciousness, and/or cerebral edema in critically ill adult patients with either admission or hospital-acquired hypernatremia.
Topics: Aged; Aged, 80 and over; Cohort Studies; Critical Illness; Female; Hospital Mortality; Humans; Hypernatremia; Male; Middle Aged; Sodium
PubMed: 30948456
DOI: 10.2215/CJN.10640918 -
Clinical Endocrinology Jul 2019Copeptin is secreted in an equimolar amount to arginine vasopressin (AVP) but can easily be measured in plasma or serum with a sandwich immunoassay. The main stimuli for... (Review)
Review
Copeptin is secreted in an equimolar amount to arginine vasopressin (AVP) but can easily be measured in plasma or serum with a sandwich immunoassay. The main stimuli for copeptin are similar to AVP, that is an increase in osmolality and a decrease in arterial blood volume and pressure. A high correlation between copeptin and AVP has been shown. Accordingly, copeptin mirrors the amount of AVP in the circulation. Copeptin has, therefore, been evaluated as diagnostic biomarker in vasopressin-dependent disorders of body fluid homeostasis. Disorders of body fluid homeostasis are common and can be divided into hyper- and hypoosmolar circumstances: the classical hyperosmolar disorder is diabetes insipidus, while the most common hypoosmolar disorder is the syndrome of inappropriate antidiuresis (SIAD). Copeptin measurement has led to a "revival" of the direct test in the differential diagnosis of diabetes insipidus. Baseline copeptin levels, without prior thirsting, unequivocally identify patients with nephrogenic diabetes insipidus. In contrast, for the difficult differentiation between central diabetes insipidus and primary polydipsia, a stimulated copeptin level of 4.9 pmol/L upon hypertonic saline infusion differentiates these two entities with a high diagnostic accuracy and is clearly superior to the classical water deprivation test. On the contrary, in the SIAD, copeptin measurement is of only little diagnostic value. Copeptin levels widely overlap in patients with hyponatraemia and emphasize the heterogeneity of the disease. Additionally, a variety of factors lead to unspecific copeptin elevations in the acute setting further complicating its interpretation. The broad use of copeptin as diagnostic marker in hyponatraemia and specifically to detect cancer-related disease in SIADH patients can, therefore, not be recommended.
Topics: Diabetes Insipidus; Glycopeptides; Humans; Hypernatremia; Hyponatremia; Polydipsia, Psychogenic
PubMed: 31004513
DOI: 10.1111/cen.13991 -
Journal of Clinical Monitoring and... May 2021Dysnatremia-either hyponatremia or hypernatremia-is frequently encountered in the clinical practice and often poses a diagnostic and therapeutic challenge for...
Dysnatremia-either hyponatremia or hypernatremia-is frequently encountered in the clinical practice and often poses a diagnostic and therapeutic challenge for physicians. Despite their frequent occurrence, disorders of the water and sodium balance in the human body have puzzled many physicians over the years and often remain elusive for those lacking experience in their interpretation and management. In this article, we derive a transparent governing equation that can be used by clinicians to describe how a change in relevant physiological parameters will affect the plasma sodium concentration. As opposed to many existing models, our model takes both input and output into account, and integrates osmolarity and tonicity. Our governing equation should be considered a means for clinicians to get a better qualitative understanding of the relationship between the plasma sodium concentration and the variables that influence it for a wide range of scenarios.
Topics: Humans; Hypernatremia; Hyponatremia; Sodium; Water
PubMed: 32382841
DOI: 10.1007/s10877-020-00512-z -
American Journal of Nephrology 2012Understanding hypernatremia is at times difficult for many clinicians. However, hypernatremia can often be deciphered easily with some basic understanding of water and... (Review)
Review
Understanding hypernatremia is at times difficult for many clinicians. However, hypernatremia can often be deciphered easily with some basic understanding of water and sodium balance. Here, the basic pathophysiological abnormalities underlying the development of sodium disorders are reviewed, and case examples are given. Hypernatremia often arises in the hospital, especially in the intensive care units due to the combination of (1) not being able to drink water; (2) inability to concentrate the urine (most often from having kidney failure); (3) osmotic diuresis from having high serum urea concentrations, and (4) large urine or stool outputs.
Topics: Body Fluids; Diuresis; Electrolytes; Feces; Humans; Hypernatremia; Kidney Diseases; Models, Biological; Osmolar Concentration; Potassium; Sodium; Urea; Urine
PubMed: 22739333
DOI: 10.1159/000339625 -
International Journal of Molecular... Jun 2022Specific antibody responses to subfornical organs, including Na antibody, have been reported in patients with adipsic hypernatremia of unknown etiology who do not have... (Review)
Review
Specific antibody responses to subfornical organs, including Na antibody, have been reported in patients with adipsic hypernatremia of unknown etiology who do not have structural lesions in the hypothalamic-pituitary gland. The subfornical organ, also referred to as the window of the brain, is a sensing site that monitors sodium and osmotic pressure levels. On the other hand, ROHHAD syndrome is a rare disease for which the etiology of the hypothalamic disorder is unknown, and there have been some reports in recent years describing its association with autoimmune mechanisms. In addition, abnormal Na levels, including hypernatremia, are likely to occur in this syndrome. When comparing the clinical features of adipsic hypernatremia due to autoimmune mechanisms and ROHHAD syndrome, there are similar hypothalamic-pituitary dysfunction symptoms in addition to abnormal Na levels. Since clinical diagnoses of autoimmunological adipsic hypernatremia and ROHAD syndrome might overlap, we need to understand the essential etiology and carry out precise assessments to accurately diagnose patients and provide effective treatment. In this review, I review the literature on the autoimmune mechanism reported in recent years and describe the findings obtained so far and future directions.
Topics: Autoimmunity; Autonomic Nervous System Diseases; Endocrine System Diseases; Humans; Hypernatremia; Hypothalamic Diseases; Rare Diseases; Respiration Disorders; Sodium; Syndrome
PubMed: 35805903
DOI: 10.3390/ijms23136899 -
Brain and Behavior May 2022Hypernatremia often occurs in patients with brain death. This study summarizes its characteristics.
OBJECTIVES
Hypernatremia often occurs in patients with brain death. This study summarizes its characteristics.
METHODS
We recorded 57 patient's highest blood sodium value, as well as daily NT-proBNP, blood creatinine, and urine output. Further, we analyzed the time of the first rise in blood sodium, and the relationship between NT-proBNP, serum creatinine, urine output, and serum sodium.
RESULTS
There was no hyponatremia in these patients, and only seven of the 53 patients registered blood sodium between 137 and 150 mmol/L. We found that blood sodium started to rise at 36.0 (28.5-52.3) h, reaching the highest value in 79.0 (54.0-126.0) h. Urine volume and creatinine have no correlation with serum sodium level, while NT-proBNP has a significant correlation with serum sodium level.
CONCLUSION
It is necessary to conduct volume assessments and urine electrolyte testing on patients with brain death. BNP has a protective effect on water and electrolytes to prevent hypernatremia.
Topics: Brain; Brain Death; Creatinine; Humans; Hypernatremia; Sodium
PubMed: 35452564
DOI: 10.1002/brb3.2574 -
Clinical Journal of the American... Mar 2023In children with hypernatremia, current clinical guidelines recommend a reduction in serum sodium of 0.5 mmol/L per hour or less to avoid complications of cerebral...
BACKGROUND
In children with hypernatremia, current clinical guidelines recommend a reduction in serum sodium of 0.5 mmol/L per hour or less to avoid complications of cerebral edema. However, no large-scale studies have been conducted in the pediatric setting to inform this recommendation. Therefore, this study aimed to report the association between the rate of correction of hypernatremia, neurological outcomes, and all-cause mortality in children.
METHODS
A retrospective cohort study was conducted from 2016 to 2019 at a quaternary pediatric center in Melbourne, Victoria, Australia. All children with at least one serum sodium level ≥150 mmol/L were identified through interrogation of the hospital's electronic medical record. Medical notes, neuroimaging reports, and electroencephalogram results were reviewed for evidence of seizures and/or cerebral edema. The peak serum sodium level was identified and correction rates over the first 24 hours and overall were calculated. Unadjusted and multivariable analyses were used to examine the association between the rate of sodium correction and neurological complications, the requirement for neurological investigation, and death.
RESULTS
There were 402 episodes of hypernatremia among 358 children over the 3-year study period. Of these, 179 were community-acquired and 223 developed during admission. A total of 28 patients (7%) died during admission. Mortality was higher in children with hospital-acquired hypernatremia, as was the frequency of intensive care unit admission and hospital length of stay. Rapid correction (>0.5 mmol/L per hour) occurred in 200 children and was not associated with greater neurological investigation or mortality. Length of stay was longer in children who received slow correction (<0.5 mmol/L per hour).
CONCLUSIONS
Our study did not find any evidence that rapid sodium correction was associated with greater neurological investigation, cerebral edema, seizures, or mortality; however, slow correction was associated with a longer hospital length of stay.
Topics: Humans; Child; Hypernatremia; Retrospective Studies; Brain Edema; Sodium; Seizures
PubMed: 36888887
DOI: 10.2215/CJN.0000000000000077