Management of hyponatremia.
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ABSTRACT:
SUBMITTER: Lee JJ
PROVIDER: S-EPMC4016091 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Aim:Treatment practices and effectiveness in cirrhotic patients with hyponatremia (HN) in the HN Registry were assessed. Methods:Characteristics, treatments, and outcomes were compared between patients with HN at admission and during hospitalization. For HN at admission, serum sodium concentration [Na] response was analyzed until correction to > 130?mmol/L, switch to secondary therapy, or discharge or death with sodium ? 130?mmol/L. Results:Patients with HN at admission had a lower [Na] and shorter length of stay (LOS) than those who developed HN (P < 0.001). Most common initial treatments were isotonic saline (NS, 36%), fluid restriction (FR, 33%), and no specific therapy (NST, 20%). Baseline [Na] was higher in patients treated with NST, FR, or NS versus hypertonic saline (HS) and tolvaptan (Tol) (P < 0.05). Treatment success occurred in 39%, 39%, 52%, 78%, and 81% of patients with NST, FR, NS, HS, and Tol, respectively. Relapse occurred in 55% after correction and was associated with increased LOS (9 versus 6 days, P < 0.001). 34% admitted with HN were discharged with HN corrected. Conclusions:Treatment approaches for HN were variable and frequently ineffective. Success was greatest with HS and Tol. Relapse of HN is associated with increased LOS.
| S-EPMC6180997 | biostudies-literature
Project description:Hyponatremia is a very common electrolyte abnormality, associated with poor short- and long-term outcomes in patients with heart failure (HF). Two opposite processes can result in hyponatremia in this setting: Volume overload with dilutional hypervolemic hyponatremia from congestion, and hypovolemic hyponatremia from excessive use of natriuretics. These two conditions require different therapeutic approaches. While sodium in the form of normal saline can be lifesaving in the second case, the same treatment would exacerbate hyponatremia in the first case. Hypervolemic hyponatremia in HF patients is multifactorial and occurs mainly due to the persistent release of arginine vasopressin (AVP) in the setting of ineffective renal perfusion secondary to low cardiac output. Fluid restriction and loop diuretics remain mainstay treatments for hypervolemic/ dilutional hyponatremia in patients with HF. In recent years, a few strategies, such as AVP antagonists (Tolvaptan, Conivaptan, and Lixivaptan), and hypertonic saline in addition to loop diuretics, have been proposed as potentially promising treatment options for this condition. This review aimed to summarize the current literature on pathogenesis and management of hyponatremia in patients with HF.
| S-EPMC8142352 | biostudies-literature
Project description:Hyponatremia is an electrolyte imbalance encountered commonly in the hospital and ambulatory settings. It can be seen in isolation or present as a complication of other medical conditions. It is therefore a challenge to determine the appropriate therapeutic intervention. An understanding of the etiology is key in instituting the right treatment. Clinicians must not be too hasty to correct a random laboratory value without first understanding the physiologic principle. We present such a case of a patient who presented with sodium of 98 mmol/L, the lowest recorded in the current literature, and yet was asymptomatic. Following appropriate management driven by an understanding of the underlying pathophysiologic mechanism, the patient was managed to full recovery without any clinically significant neurological sequelae.
| S-EPMC5551525 | biostudies-other
Project description:Hyponatremia is an electrolyte disorder frequently observed in several clinical settings and common in hospitalized patients with decompensated heart failure (HF). It is caused by deregulation of arginine vasopressin (AVP) homeostasis associated with water retention in hypervolemic or in euvolemic states. While hypervolemic hypotonic hyponatremia is also seen in advanced liver cirrhosis, renal failure, and nephrotic syndrome, the bulk of evidence associating this electrolyte disorder to increasing morbidity and mortality can be found in the HF literature. Hospitalized HF patients with low serum sodium concentration have lower short-term and long-term survival, longer hospital stay and increased readmission rates. Conventional therapeutic approaches, ie, restriction of fluid intake, saline and diuretics, can be effective, but often the results are unpredictable. Recent clinical trials have demonstrated the effectiveness of nonpeptide AVP receptor antagonists (vaptans) in the treatment of hyponatremia. The vaptans induce aquaresis, an electrolyte-sparing excretion of free water resulting in the correction of serum sodium concentrations and plasma osmolality, without activation of the renin-angiotensin-aldosterone system (RAAS) or changes in renal function and blood pressure. Further prospective studies in a selected congestive HF population with hyponatremia, using clinical-status titrated dose of tolvaptan, are needed to determine whether serum sodium normalization will be translated into a better long-term prognosis. This review will focus on recent clinical trials with tolvaptan, an oral V(2) receptor antagonist, in HF patients. The ability of tolvaptan to safely increase serum sodium concentration without activating the RAAS or compromising renal function and electrolyte balance makes it an attractive agent for treating hyponatremic HF patients.
| S-EPMC3108784 | biostudies-other
Project description:IntroductionHyponatremia is a common electrolyte disorder in critically ill patients. Rapid correction of chronic hyponatremia may lead to osmotic demyelination syndrome. Management of severe hyponatremia in patients with acute or chronic kidney disease who require continuous renal replacement therapy (CRRT) is limited by the lack of commercially available hypotonic dialysate or replacement fluid solutions.MethodsThis was a single-center quality improvement project that consisted of the development and implementation of a multidisciplinary protocol for gradual correction of severe hyponatremia in patients who were admitted to the intensive care unit (ICU) and required CRRT. The protocol utilized a simplified method based on single-pool urea kinetic modeling and a hybrid technique of volume exchange, and addition of sterile water for sodium dilution of commercially available dialysate and replacement fluid solutions.ResultsWe report data of the first 3 ICU patients who required CRRT for acute kidney injury management, had severe hyponatremia (serum sodium <120 mEq/l), and were treated under the protocol. Targeted and gradual hyponatremia correction was achieved in all 3 patients. The observed versus the predicted serum sodium correction in each patient was concordant. No complications related to the protocol were reported. We detailed facilitators of and hindrances to the development and successful implementation of our multidisciplinary protocol.ConclusionWe demonstrated gradual and individualized rates of severe hyponatremia correction utilizing customized (sodium dilution) dialysate/replacement fluid solutions in ICU patients who required CRRT. It is not known whether the use of customized solutions to prevent hyponatremia overcorrection has a significant impact on patient outcomes. Further research in this susceptible population is needed.
| S-EPMC6308919 | biostudies-literature
Project description:BackgroundHyponatremia is a frequent and potentially life-threatening adverse side effect of thiazide diuretics. This sub-analysis of the Hyponatremia Registry database focuses on current management practices of thiazide-associated hyponatremia (TAH) and compares differences between TAH and syndrome of inappropriate antidiuretic hormone secretion (SIADH).MethodsWe analyzed 477 patients from 225 US and EU sites with euvolemic hyponatremia ([Na+] ?130 mEq/L) who were receiving a thiazide diuretic. Of these, 118 met criteria for true thiazide-induced hyponatremia (TIH).ResultsThiazide was withdrawn immediately after hyponatremia was diagnosed only in 57% of TAH; in these patients, the median rate of [Na+] change (?daily[Na+]) was significantly higher than those with continued thiazide treatment (3.8 [interquartile range: 4.0] vs. 1.7 [3.8] mEq/L/day). The most frequently employed therapies were isotonic saline (29.6%), fluid restriction (19.9%), the combination of these two (8.2%), and hypertonic saline (5.2%). Hypertonic saline produced the greatest ?daily[Na+] (8.0[6.4] mEq/L/day) followed by a combination of fluid restriction and normal saline (4.5 [3.8] mEq/L/day) and normal saline alone (3.6 [3.5] mEq/L/day). Fluid restriction was markedly less effective (2.7 [2.7] mEq/L/day). Overly rapid correction of hyponatremia occurred in 3.1% overall, but in up to 21.4% given hypertonic saline. Although there are highly significant differences in the biochemical profiles between TIH and SIADH, no predictive diagnostic test could be derived.ConclusionsDespite its high incidence and potential risks, the management of TAH is often poor. Immediate withdrawal of the thiazide is crucial for treatment success. Hypertonic saline is most effective in correcting hyponatremia but associated with a high rate of overly rapid correction. We could not establish a diagnostic laboratory-based test to differentiate TIH from SIADH.
| S-EPMC5452281 | biostudies-literature
Project description:PurposeHyponatremia secondary to SIADH is frequent in cancer patients and potentially deleterious. The aim of this sub-analysis of the Hyponatremia Registry database is to analyze current diagnostic and therapeutic management practices in cancer patients with SIADH.MethodsWe analyzed 358 cancer patients who had serum sodium concentration ([Na+]) ? 130 mEq/L and a clinical diagnosis of SIADH from 225 sites in the USA and EU.ResultsPrecise diagnostic testing was performed in only 46%. Almost 12% of all patients did not receive any hyponatremia treatment. The most frequent therapies were fluid restriction (20%), isotonic saline (14%), fluid restriction/isotonic saline (7%), tolvaptan (8%), and salt tablets (7%). Hypertonic saline was used in less than 3%. Tolvaptan produced the greatest median rate of [Na+] change (IQR) (3.0 (4.7) mEq/L/day), followed by hypertonic saline (2.0(7.0) mEq/L/day), and fluid restriction/isotonic saline (1.9(3.2) mEq/L/day). Both fluid restriction and isotonic saline monotherapies were significantly less effective (0.8(2.0) mEq/L/day and 1.3(3.0) mEq/L/day, respectively) and were associated with clinically relevant rates of treatment failure. Only 46% of patients were discharged with [Na+] ? 130 mEq/L. Overly rapid correction of hyponatremia occurred in 11.7%.ConclusionsAlthough essential for successful hyponatremia management, appropriate diagnostic testing is not routinely performed in current practice. The most frequently employed monotherapies were often ineffective and sometimes even aggravated hyponatremia. Tolvaptan was used less often but showed significantly greater effectiveness. Despite clear evidence that hyponatremia is associated with poor outcome in oncology patients, most patients were discharged still hyponatremic. Further studies are needed to assess the beneficial impact of hyponatremia correction with effective therapies.
| S-EPMC5445151 | biostudies-literature
Project description:Hyponatremia is a common electrolyte disorder, with prevalence as high as 20% in inpatient settings. It is classified based on volume status, urine sodium and osmolality results. While this approach might help narrow down the differential diagnoses, it can leave other diagnoses unentertained. In this case, we report recurrent and refractory hyponatremia secondary to hypocortisolism due to non-functioning pituitary macroadenoma. Interestingly, urine studies mimicked syndrome of inappropriate antidiuresis, but exclusively responded to hydrocortisone replacement. Hospital course was also complicated by hyponatremia-induced rhabdomyolysis, which is a rare complication of severe hyponatremia. We also discuss the role of anchoring heuristics and how they influence the physician's decision leading to possible diagnostic errors. One way to minimise the effect of anchoring bias on physicians is their cognitive awareness of such bias. In addition, discussing complicated cases with all members of medical team can highlight the clinician's thought processes, share uncertainty and help broaden differential diagnoses.
| S-EPMC6169692 | biostudies-literature
Project description:Background and objectivesCurrent therapies for hyponatremia have variable effectiveness and tolerability, and in certain instances, they are very expensive. We examined the effectiveness, safety, and tolerability of urea for the treatment of inpatient hyponatremia.Design, setting, participants, & measurementsWe identified all patients hospitalized at the University of Pittsburgh Medical Center between July 2016 and August 2017 with hyponatremia (plasma sodium <135 mEq/L) who received urea, including a subgroup of patients who received urea as the sole drug therapy for hyponatremia (urea-only treated). We matched urea only-treated patients to a group of patients with hyponatremia who did not receive urea (urea untreated) and compared changes in plasma sodium at 24 hours and the end of therapy as well as the proportion of patients who achieved plasma sodium ?135 mEq/L. We abstracted data on adverse events and reported side effects of urea.ResultsFifty-eight patients received urea (7.5-90 g/d) over a median of 4.5 (interquartile range, 3-8) days and showed an increase in plasma sodium from 124 mEq/L (interquartile range, 122-126) to 131 mEq/L (interquartile range, 127-134; P<0.001). Among 12 urea only-treated patients, plasma sodium increased from 125 mEq/L (interquartile range, 122-127) to 131 mEq/L (interquartile range, 129-136; P=0.001) by the end of urea therapy. There was a larger increase in plasma sodium at 24 hours in urea only-treated patients compared with urea-untreated patients (2.5 mEq/L; interquartile range, 0-4.5 versus -0.5 mEq/L; interquartile range, -2.5 to 1.5; P=0.04), with no difference in change in plasma sodium by the end of therapy (6 mEq/L; interquartile range, 3.5-10 versus 5.5 mEq/L; interquartile range, 3-7.5; P=0.51). A greater proportion of urea only-treated patients achieved normonatremia, but this difference was not statistically significant (33% versus 8%; P=0.08). No patients experienced overly rapid correction of plasma sodium, and no serious adverse events were reported.ConclusionsUrea seems effective and safe for the treatment of inpatient hyponatremia, and it is well tolerated.
| S-EPMC6237061 | biostudies-literature
Project description:Understanding and applying pathophysiological concepts to patient care is an important skill for physicians in the clinical setting. Here, we present a case that demonstrates how the application of common physiological concepts relating to the widely accepted hyponatremia algorithm led to an accurate diagnosis of hyponatremia. This case documents iso-osmolar hyponatremia caused by orally administered polyethylene glycol absorption in the gastrointestinal tract. Herein, we discuss the workup and differential diagnosis for iso-osmolar hyponatremia in juxtaposition with the pathophysiological mechanisms unique to this case. We discuss these pathophysiological mechanisms based on the patients' laboratory data and responses to therapeutic interventions.
| S-EPMC7886577 | biostudies-literature