Management Of Hyponatremia Research Articles

1828P - ASSERT: A prospective, observational study measuring sodium improvement and outcomes in patients treated for moderate to severe hyponatremia secondary to syndrome of inappropriate antidiuretic hormone secretion (SIADH) in Italy (lung cancer cohort)

BackgroundHyponatremia (serum sodium concentration [Na+] <135mmol/L), is the most common electrolyte disorder in lung cancer patients (incidence 20–44%) with SIADH a frequent cause, particularly in small cell lung cancer (SCLC). MethodsASSERT was a prospective, observational, non-interventional study conducted from October 2015 to June 2017 in cancer patients requiring treatment for hyponatremia secondary to SIADH at 18 Italian oncology centres. Management of hyponatremia primarily included water restriction, tolvaptan and hypertonic saline, in accordance with local standard of care/guideline recommendations. The primary endpoint was change in serum [Na+] from baseline visit to end of the first month of the observational period, or earlier discontinuation. ResultsThe full analysis set (FAS) included 68 adult cancer patients (lung cancer, n=48, SCLC, n=33). Group 1 patients received ≥1 dose of tolvaptan during the observational period; Group 2 patients did not receive tolvaptan. Overall survival (FAS) was significantly higher in Group 1 vs Group 2 (median 123 vs 56 days; p=0.001), as was mean survival (299.4 vs 74.9 days; p=0.001). In a linear regression analysis of the relationship between sodium levels and tolvaptan dose intensity for the lung cancer and SCLC cohorts, dose intensity correlated significantly with clinical response after 6 months of treatment in both cohorts (p=0.005 and p=0.023, respectively). In the lung cancer cohort, a significantly higher percentage of patients achieved serum [Na+] ≥130mmol/L in Group 1 vs Group 2 during 6 months of follow-up (Group 1, 87.5% vs Group 2, 62.5%; p=0.033). These results were similar to those observed in the FAS. ConclusionsHyponatremia secondary to SIADH is a potentially modifiable risk factor, which might be implicated in the survival of lung cancer patients. Correction of hyponatremia may be preferentially achieved with pharmacological treatment, rather than the non-pharmacological approaches routinely used in clinical practice. Clinical trial identificationNCT102573077. Editorial acknowledgementSarah Stowell PhD, CMPP of Ashley Medical Communications, funded by Otsuka Pharmaceutical Europe Ltd. Legal entity responsible for the studyOtsuka Pharmaceutical Italy Srl. FundingOtsuka Pharmaceutical Italy Srl. DisclosureR. Berardi: Honoraria (self), Advisory / Consultancy: Otsuka Pharmaceutical. C. Ferrara: Full / Part-time employment: Otsuka Pharmaceutical Italy. M.G. Giustra: Full / Part-time employment: Otsuka Pharmaceutical Italy. R. Evans: Full / Part-time employment: Otsuka Pharmaceutical Europe. All other authors have declared no conflicts of interest.

RESOLUTION OF AKI AFTER LARGE VOLUME PARACENTESIS AND CORRECTION OF INTRA-ABDOMINAL HYPERTENSION

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Intra-abdominal pressure (IAP) is the pressure within the abdominal cavity. Elevated IAP can lead to Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS). This is caused by a wide variety of causes including ascites. This entity can cause low abdominal perfusion pressures (AAP) and result in end organ damage. We present a case of AKI caused by tense ascites, which resolved after drainage CASE PRESENTATION: A 52-year-old man was transferred to our ICU for the management of hyponatremia and AKI. He presented initially with confusion, weakness, and fall. He has a history of systolic heart failure and alcohol abuse. On presentation, he was significantly volume overloaded with ascites, pitting lower extremity edema and significant electrolyte abnormalities including severe hyponatremia, hypokalemia and an AKI with creatinine of 1.35mg/dL (baseline = 0.6). Urine electrolytes were consistent with pre-renal AKI and his echo showed a normal LV function, RV and RA dilation with no signs of pulmonary hypertension. He was initially treated with hypertonic saline infusion. He was found to have liver cirrhosis on abdominal ultrasound. Given his tense abdomen, a paracentesis was performed in conjunction with IAP monitoring via an arterial line monitoring system. After zeroing the pressure at the insertion of the paracentesis catheter, an initial IAP of 22 mmHg was obtained. IAPs were documented at end expiration following each liter of ascites fluid removed (figure 1). A total of 8.75L were removed and a final IAP of 6mmHg was recorded. Mean arterial pressure prior to paracentesis was 73mmHg and AAP was 51mmHg. Over the following 24 hours, patient’s urinary output increased dramatically to over 4L without diuretics and his creatinine normalized (figure 2). Over the course of the hospital stay, the patient’s electrolyte abnormalities, volume overload, weakness and confusion resolved and he was discharged without complication DISCUSSION: We demonstrate a case of a patient who developed AKI and electrolyte derangements from tense ascites causing IAH that resolved after fluid removal. We illustrate that there may be a linear decrease in IAP with ascites volume removal. The most likely cause the the dramatic increase in UOP following the paracentesis is restoration of renal blood flow with normalization of IAP. CONCLUSIONS: IAH and ACS can be dramatic consequences of elevated IAP and clinicians should be aware of more subtle presentations of organ damage that are due to IAH Reference #1: Papavramidis, Theodossis S et al. “Abdominal compliance, linearity between abdominal pressure and ascitic fluid volume” Journal of emergencies, trauma, and shock vol. 4,2 (2011): 194-7. Reference #2: Caldwell CB, Ricotta JJ. Changes in visceral blood flow with elevated intraabdominal pressure.J Surg Res. 1987;43(1):14. Reference #3: Caldwell CB, Ricotta JJ.Changes in visceral blood flow with elevated intraabdominal pressure. J Surg Res. 1987 Jul;43(1):14-20. DISCLOSURES: No relevant relationships by Amit Chopra, source=Web Response No relevant relationships by Kurt Hu, source=Web Response No relevant relationships by Ali Wazir, source=Web Response No relevant relationships by Robert Wilcott, source=Web Response

Recent developments in the management of acute and chronic hyponatremia.

The aim of the study is to review recent studies on the management of acute and chronic hyponatremia. In acute symptomatic hyponatremia, bolus infusion of hypertonic saline improves hyponatremia and neurological status more quickly than continuous infusion. In chronic hyponatremia, newly identified predictors of nonresponse to fluid restriction include a high urine osmolality (>500 mOsm/kg) and high urine sodium (>133 mmol/l). Vasopressin-receptor antagonists effectively raise the serum sodium concentration in patients with euvolemic or hypervolemic hyponatremia but have a risk of overcorrection, even at low doses. Several observational studies now support the use of urea for a more gradual correction of hyponatremia without a risk of overcorrection. Recently identified risk factors for overcorrection include lower serum sodium at presentation, polydipsia, hypovolemia, and early urine output during treatment. Specific treatments with potential efficacy are the use of intravenous albumin for hyponatremia because of liver cirrhosis, and fludrocortisone for hyponatremia in tuberculous meningitis. The recent data will help to further optimize and personalize the management of patients with acute and chronic hyponatremia. However, most data are still observational and retrospective. Therefore, the field is in need of prospective studies comparing interventions for chronic hyponatremia and focusing on patient-relevant outcomes.

Hyponatremia in Heart Failure: Pathogenesis and Management.

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.

MON-LB693: Management of Hyponatremia in Patients with Total Enteral Tube Feeding (TEN), are we Doing it Right?

MON-LB693: Management of Hyponatremia in Patients with Total Enteral Tube Feeding (TEN), are we Doing it Right?

Severe Hyponatremia in a 6-month-old Infant.

Letter to the Editor in response to the article ‘ Transient Pseudohypoaldosteronism in an Infant: A Case Report ’ by T. Latt et al. To the Editor, We want to congratulate Latt and colleagues on the article describing a case of a patient with transient pseudohypoaldosteronism. 1 Electrolyte derangements in course of this rare entity may be much more severe, as in our patient presenting with hyponatremia of 103 mmol/L. We feel that we can contribute to the topic by reporting our patient and discussing hyponatremia management.

Hyponatremia in children under 100days old: incidence and etiologies.

Hyponatremia is one of the most common electrolyte disorders in hospitalized children. The underlying mechanisms are poorly understood and potentially multifactorial, making management difficult, particularly in neonates. This retrospective study aimed to determine the incidence and etiologies of hyponatremia in hospitalized children under the age of 100days, in our pediatric tertiary care hospital over a 1-year period. The etiology of hyponatremia was determined by reviewing the data noted in each patient's medical reports. Neonatal hyponatremia had a prevalence of 4.3% (86/2012 patients) and was mostly hospital-acquired (74/86 patients). Fifty-nine patients (68.9%) were preterm neonates. The etiology was iatrogenic in 26 cases (30.2%). In other cases, hyponatremia was due to transient (23 patients, 26.7%) or genetic abnormalities of the renal mineralocorticoid pathway (3 patients, 3.4%), SIADH (12 patients, 14%), digestive disease (3 patients, 3.5%), acute renal failure (3 patients, 3.5%), or heart failure (1 patient, 1.2%).Conclusion: Our findings confirm that hyponatremia is a frequent electrolyte disorder in neonates. Various mechanisms underlie this condition, most of which could be prevented by optimized management. The prevalence of genetic hypoaldosteronism and pseudohypoaldosteronism was higher than expected. We provide a simple diagram to help physicians identify the mechanisms underlying neonatal hyponatremia. What is Known: • In neonates, hyponatremia may be multifactorial, making it difficult to treat. • Newborns display partial resistance to aldosterone, and preterms have a defect in aldosterone secretion. What is New: • Four percent of hospitalized neonates had hyponatremia, 86% hospital-acquired. Hyponatremia was due to a transient or constitutional defect of the mineralocorticoid pathway in 26/86 patients (30%) which is higher than expected. • We propose a tree diagram for improving the management of hyponatremia in neonates.

Hyponatremia Is Protective Against the Development of Portal Vein Thrombosis in Patients Undergoing Liver Transplant

BackgroundBoth hyponatremia and portal vein thrombosis (PVT) reflect the severity of liver dysfunction and are independently associated with increased morbidity in cirrhotic patients. In this study, we analyzed effects of hyponatremia on PVT development. MethodsData on adult liver transplants (LTs) in the Model for End-Stage Liver Disease era through September 2016 were obtained. Receiver operating curves and multivariable logistic regression models were constructed to evaluate the association between serum sodium level and PVT. Based on the receiver operating curves, hyponatremia was defined as a sodium level below 125 mEq/L. ResultsOf the 49,155 recipients included, 16% had hyponatremia (n = 7828) and 9% had PVT (n = 4414) at transplant. Subjects with hyponatremia had lower rates of PVT at the time of LT (4.4% vs 10.1%, P < .001), incidence of nonalcoholic steatohepatitis (10.8% vs 16.5%, P < .001), diabetes (19.7% vs 24.3%, P < .001), and need for dialysis (8.8% vs 16.0%, P < .001) as well as higher rates of chronic hepatitis C and B (37.6% vs 29.1%, P < .001 and 2.9% vs 1.7%, P < .001). Multivariable regression analysis confirmed that hyponatremia was independently associated with a decreased likelihood of PVT (odds ratio [OR], 0.44, P < .001). African American patients had a lower incidence of PVT (OR, 0.70; P < .001). Variables associated with a higher incidence of PVT were: nonalcoholic steatohepatitis (OR, 1.15; P = .005), moderate-to-severe ascites (OR, 1.10; P = .008), and Hispanic ethnicity (OR, 1.2; P < .001). ConclusionHyponatremia is associated with a lower rate of PVT independent of severity of liver disease and other thrombotic risk factors. This protective effect should be taken into consideration during the perioperative management of hyponatremia in patients undergoing LT.

Practical document on the management of hyponatremia in critically ill patients

Hyponatremia is the most prevalent electrolyte disorder in Intensive Care Units. It is associated with an increase in morbidity, mortality and hospital stay. The majority of the published studies are observational, retrospective and do not include critical patients; hence it is difficult to draw definitive conclusions.Moreover, the lack of clinical evidence has led to important dissimilarities in the recommendations coming from different scientific societies.Finally, etiopathogenic mechanisms leading to hyponatremia in the critical care patient are complex and often combined, and an intensive analysis is clearly needed. A study was therefore made to review all clinical aspects about hyponatremia management in the critical care setting. The aim was to develop a Spanish nationwide algorithm to standardize hyponatremia diagnosis and treatment in the critical care patient.

Management of Persistent Hyponatremia after Off-Pump Coronary Artery Bypass Grafting: A Case Report

Management of Persistent Hyponatremia after Off-Pump Coronary Artery Bypass Grafting: A Case Report

Approach to Hyponatremia in Cirrhosis.

The patient in the case presented with hypervolemic hyponatremia associated with ascites and edema. The sNa concentration of 120 mmol/L is bordering severe hyponatremia and is associated with renal insufficiency. The management of this patient includes free water restriction, holding diuretics, and consideration of albumin infusion (Fig. ​(Fig.1).1). Tolvaptan is not recommended in patients with liver disease. Furthermore, hyponatremia and renal dysfunction are associated with poor prognosis. If the hyponatremia is persistent, liver transplant evaluation should be considered. Open in a separate window Figure 1 Algorithm depicting suggested management of hyponatremia in the patient with cirrhosis.

Successful management of severe hyponatremia in CKD‐VD: In a cost limited setting

Patients with end stage renal disease (ESRD) and severe hyponatremia always pose a challenge to manage. It is necessary to correct biochemical parameters, advanced azotemia, and fluid overload with conventional haemodialysis (HD) but it may correct serum sodium (Na) rapidly resulting in neurological complications like seizures and osmotic demyelination syndrome. Continuous renal replacement therapy (CRRT) is an ideal modality to manage such patients. However, most of the centers in the developing or underdeveloped nations do not have CRRT facility. We present two cases of ESRD, who had advanced azotemia requiring dialysis, also had persistent vomiting and severe hyponatremia (one with Na 107, another with Na 109 mEq/L), both cases were managed with conventional HD using dialysate Na concentration of 128 mEq/L (lowest permissible level of Na in a traditional HD machine) and keeping the blood flow of 50 mL/min. The serum Na increased by 1 mEq/L/h during first HD session, during the next session blood flow increased to 100 mL/min, and serum Na increased by two mEq/L/h. At the end of 48 hours, we were able to successfully correct serum Na by 18 mEq/L, with complete resolution of uremic manifestations and no neurological deficits. The current reports highlight management of hyponatremia in newly diagnosed ESRD in a cost limited setting.

Follow-up observation on short-term efficacy of low dose tolvaptan in the management of cirrhotic hyponatremia

多周期间断性低剂量托伐普坦应用于肝硬化失代偿期并低钠血症的血钠管理，具备一定的疗效性和安全性。本研究拟对部分住院失代偿期肝硬化并稀释性低钠血症患者采用多周期间断性低剂量托伐普坦管理方案，旨在探讨针对该并发症的托伐普坦合理应用方案。.

The prognostic effects of hyponatremia and hyperchloremia on postoperative NSCLC patients

Electrolytic disorders are common in lung cancer patients. But the association between serum electrolytes levels and survival in patients undergoing lung cancer resections for non–small-cell lung cancer (NSCLC) has been poorly investigated. A retrospective study was conducted on consecutive postoperative NSCLC patients. Pearson's test was used to determine the association between serum sodium and chlorine levels and clinical characteristics, and cox regression and Kaplan-Meier model were applied to analyze risk factors on overall survival. We found that hyponatremia was an independent prognostic factor associated with poor prognosis in NSCLC patients undergoing complete resection (log-rank test, P = 0.004). In addition, we found that hyperchloremia predicted a poor clinical outcome in patients with non-anion-gap (log-rank test, P = 0.011), whereas it predicted a favorable clinical outcome in patients with high-anion-gap (log-rank test, P = 0.002). The serum electrolytes levels may reflect the prognosis of NSCLC patients who receive complete resection. Early detection, monitoring, and management of hyperchloremia and hyponatremia might improve patients’ prognosis.

Hypovolemic Hyponatremia.

The etiology of hyponatremia is often multifactorial. The most common causes include hypovolemia from gastrointestinal (GI) or other fluid losses, thiazide diuretics, and SIAD [<citeref rid="ref1">1</citeref>]. In this chapter, we will discuss hypovolemic hyponatremia, as well as the clinical parameters that help distinguish between hypovolemic and euvolemic states. These include not only the urine [Na+] concentration but also the fractional uric acid excretion, a parameter that can be employed even when diuretics have been prescribed [<citeref rid="ref2">2</citeref>,<citeref rid="ref3">3</citeref>,<citeref rid="ref4">4</citeref>,<citeref rid="ref5">5</citeref>,<citeref rid="ref6">6</citeref>,<citeref rid="ref7">7</citeref>]. Among the common causes of hypovolemic hyponatremia are GI fluid loss, a range of endocrinopathies [<citeref rid="ref7">7</citeref>], and thiazide-induced hyponatremia, which is best considered as a distinct entity, in particular because recent data suggest that it has a genetic predisposition. Also, the discontinuation of thiazide is a key step in treatment [<citeref rid="ref2">2</citeref>,<citeref rid="ref7">7</citeref>]. The management of hypovolemic hyponatremia starts with confirming its presence and determining the underlying cause. Correction focuses on the appropriate use of isotonic fluid to effect volume repletion while avoiding an overly rapid rise in serum [Na+] concentration.

Turning complexity into clarity: polyuria and hypernatremia

Turning complexity into clarity: polyuria and hypernatremia

Hyponatremia in Oncology Patients.

Hyponatremia is frequent in cancer patients and potentially deleterious. Cancer patients have specific requirements due to the nature and treatment of their disease, which can directly impact the occurrence and severity of hyponatremia, and limit treatment choices. Although essential for successful hyponatremia management, appropriate diagnostic testing is not routinely performed in the current practice. Despite clear evidence that hyponatremia is associated with poor outcome in oncology patients, most patients are still hyponatremic while under observation. Guidance on specific treatment of cancer patients with hyponatremia is needed to optimize patient care in the face of these challenges.

Investigation and management of moderate to severe inpatient hyponatraemia in an Australian tertiary hospital

BackgroundHyponatraemia is the most common electrolyte disturbance amongst hospitalised patients. Both American and European guidelines recommend fluid restriction as first line treatment for SIADH, however differ on second line recommendations. The objective of this study was to examine investigation and management of hyponatraemia in hospitalised patients in an Australian tertiary hospital.MethodsA retrospective audit was conducted of electronic medical records and laboratory data of inpatients with serum sodium (Na) ≤125 mmol/L, admitted over a 3 month period to the Princess Alexandra Hospital, Brisbane, Australia. The main outcomes measured included: demographic characteristics, investigations, accuracy of diagnosis, management strategy, change in Na and patient outcomes.ResultsThe working clinical diagnosis was considered accurate in only 37.5% of cases. Urine Na and osmolality were requested in 72 of 152 patients (47.4%) and in 43 of 70 euvolaemic patients (61.4%). Thyroid function tests (67.1%) and morning cortisol (45.7%) were underutilized in the euvolaemic group. In the SIADH cohort, fluid restriction resulted in a median (IQR) 7.5 mmol/L (4–10.5) increase in Na after 3 days; no treatment resulted in a median 0 mmol/L (− 0.5–1.5) change. Oral urea was utilized in 5 SIADH patients where Na failed to increase with fluid restriction alone. This resulted in a median 10.5 mmol/L (3.5–13) increase in Na from baseline to day 3. There were no cases of osmotic demyelination. The median length of stay was 8 days (4–18.5). Mortality was 11.2% (17 patients). There was a weak but significant correlation between nadir serum Na and mortality (R = 0.18, P = 0.031).ConclusionInpatient hyponatraemia is often inadequately investigated, causing errors in diagnosis. Treatment is heterogeneous and often incorrect. In cases with hyponatraemia refractory to fluid restriction, oral urea presents an effective alternative treatment.

Active management of severe hyponatraemia by endocrinologists is associated with lower mortality

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Hyponatremia in Cirrhosis: Implications for Liver Transplantation.

Hyponatremia in cirrhosis is defined as a serum sodium level ≤130 mEq/L and occurs in approximately 22% of patients with cirrhosis. The appearance of hyponatremia in patients with cirrhosis portends a poor prognosis before liver transplantation (LT), independent of the Model for End-Stage Liver Disease (MELD) score. With the development of the MELD-sodium score, the management of hyponatremia has become more relevant than ever before. Overcorrection of hyponatremia before LT or perioperatively can lead to the devastating neurologic condition known as osmotic demyelination syndrome, which is often irreversible and fatal. Therefore, the most important tenet of hyponatremia is to avoid correcting the serum sodium by ≥8 mEq/L in a 24-hour period. Treatment of hyponatremia is highly challenging. The vast majority of patients with cirrhosis have chronic hypervolemic hyponatremia. Fluid restriction increases serum sodium levels, but tolerance and compliance are significant barriers. Diuretic withdrawal is helpful but contributes to worsening fluid overload. There are limited data to support use of intravenous concentrated albumin solutions. The use of the arginine vasopressin antagonists ("vaptans") is contentious; however, they may have a limited role. Risk factors for intraoperative overcorrection of serum sodium include increased utilization of packed red blood cell and fresh frozen plasma transfusions, which are often unavoidable. Intraoperative management is evolving, and more data are needed in regard to the use of sodium-reduced continuous venovenous hemofiltration and the use of trishydroxymethylaminomethane (Tris) to avoid excess sodium rebound. A thorough discussion of the current treatment options before and during LT is given in this review.