Management Of Hyponatremia Research Articles

Evidence-based hyponatremia management in liver disease.

Hyponatremia is primarily a water balance disorder associated with high morbidity and mortality. The pathophysiological mechanisms behind hyponatremia are multifactorial, and diagnosing and treating this disorder remains challenging. In this review, the classification, pathogenesis, and step-by-step management approaches for hyponatremia in patients with liver disease are described based on recent evidence. We summarize the five sequential steps of the traditional diagnostic approach: 1) confirm true hypotonic hyponatremia, 2) assess the severity of hyponatremia symptoms, 3) measure urine osmolality, 4) classify hyponatremia based on the urine sodium concentration and extracellular fluid status, and 5) rule out any coexisting endocrine disorder and renal failure. Distinct treatment strategies for hyponatremia in liver disease should be applied according to the symptoms, duration, and etiology of disease. Symptomatic hyponatremia requires immediate correction with 3% saline. Asymptomatic chronic hyponatremia in liver disease is prevalent and treatment plans should be individualized based on diagnosis. Treatment options for correcting hyponatremia in advanced liver disease may include water restriction; hypokalemia correction; and administration of vasopressin antagonists, albumin, and 3% saline. Safety concerns for patients with liver disease include a higher risk of osmotic demyelination syndrome.

Low-solute hyponatremia in a kidney transplant recipient.

Electrolyte and acid-base disturbances are common in kidney transplant recipients, but there are few reports of low-solute hyponatremia or beer potomania in this population. We report herein a case of low-solute hyponatremia in a kidney transplant recipient with impaired graft function, highlighting key issues in diagnosis and management of low-solute hyponatremia, as well as exploring the pathophysiology of hyponatremia after kidney transplantation. A 51-year-old man who had received a cadaveric renal transplant 18 years before presented with symptomatic hyponatremia and seizure. Workup for an underlying intracranial pathology was negative, and subsequent biochemical workup suggested low-solute hyponatremia with potomania, arising from dietary modifications taken by the patient while self-isolating during the COVID-19 pandemic. Correction of hyponatremia was successful with conservative management with close monitoring. This case illustrates key points in the diagnosis and management of low-solute hyponatremia and highlights the pathophysiology of hyponatremia after kidney transplantation.

Tolvaptan in the management of severe hyponatremia associated with acute intermittent porphyria

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

Hyponatremia in patients with arterial hypertension: pathophysiology and management.

Sodium is the main cation in the extracellular space. In physiological conditions, sodium concentration in plasma is 135-145 mmol/l. The kidneys play the most important role in the regulation of sodium homeostasis. In recent years, a significant role of glycosaminoglycans, localized mainly in the subcutaneous tissue, and the role of glycocalyx on the surface of vascular endothelial cells, have been documented in the regulation of sodium metabolism. Hyponatremia is defined by a plasma sodium concentration lower than 135 mmol/l. Hyponatremia significantly worsens the prognosis of patients with different chronic diseases. In patients with arterial hypertension, the risk of hyponatremia is 1.5 times higher than in the general population. One of the causes of hyponatremia in patients with arterial hypertension is the use of thiazide or thiazide-like diuretics. The symptoms of hyponatremia are caused mainly by the swelling of cells in the central nervous system. Treatment of hyponatremia depends on the degree and duration (acute or chronic) of hyponatremia as well as presence of clinical symptoms. Too rapid correction of hyponatremia might result in a potentially fatal osmotic demyelinating syndrome. In the present review paper, pathophysiology and management of hyponatremia in patients with arterial hypertension are discussed.

Hyponatremia and its Clinical Outcome Among Patients with Hepatic Encephalopathy Due to Liver Cirrhosis Presenting to ATH Abbottabad

Introduction: Hepatic encephalopathy (HE) is a potentially reversible complication of liver cirrhosis causing significant mortality. Hyponatremia in cirrhosis is caused by hampered renal function to eliminate free water that results in water retention disproportionate to sodium retention leading to reduced plasma osmolality and is associated with significant morbidity and mortality. The purpose of study was to determine the frequency of hyponatremia among patients of liver cirrhosis with hepatic encephalopathy. Methods: The design of this study was an observational study design which was hospital-based survey and was conducted on 130 patients of liver cirrhosis. A specialized questionnaire was designed to collect all the study information. All data was analyzed using SPSS Statistics version 24. Chi-square test and Spearman's rank test were employed to correlate hyponatremia with HE and its severity. A p-value of <0.05 was considered statistically significant. Results: Among the patients, 92 (71%) males and 38 (29%) females; the mean age of the patients was 56±11.3 years. Hyponatremia was present in 48 (36.9%) patients. Among these, 25 (52%) were male and 23 (48%) were female; 12 (25%) patients had mild Hyponatremia, 28(58.3%) had moderate, and 8 (16.6%) had severe Hyponatremia. HE was significantly associated with hyponatremia with p value of lea than 0.001. Practical Implication: The benefit of our study was undertaken to determine the frequency of hyponatremia among patients of liver cirrhosis with hepatic encephalopathy to provide evidence for hyponatremia as a prognostic factor in HE so that early detection and management of hyponatremia in such patients will help reduce disease burden and mortality in liver cirrhosis. Conclusion: Patients with lower levels of sodium had higher grades/severity of HE. Significant association of hyponatremia was seen with liver cirrhosis and encephalopathy. Keywords: Abbottabad, Cirrhosis, Hepatic encephalopathy, Hyponatremia, Liver.

Treatment algorithm: management of hyponatremia in acute and emergency medicine

Treatment algorithm: management of hyponatremia in acute and emergency medicine

Study on Quality of Life and Management of Hyponatremia and Hypertension in Stroke Patients in the Neurology Department of a Tertiary Care Teaching Hospital in South India

A stroke or cerebrovascular accident is an abrupt onset of a neurologic deficit that lasts for at least 24 hours and is mainly of vascular origin. Stroke is one of the leading causes of death and disability in our country and leads to long-term disability and functional dependency. Hyponatremia is one of the common electrolyte abnormalities seen in patients with neurological disorders which may be due to SIADH or CSWS. Hypertension is one of the important risk factors and it is proven that anti-hypertensive therapy can reduce the risk of developing stroke. The various scales that have proved reliability and valid in stroke trials are the National Institutes of Health Stroke Scale (NIHSS), the modified Rankin scale (Mrs), the Barthel index (BI),

Hyponatremia Related to Neurocritical Care: Focus on Diagnosis and Therapy: A Systematic Review.

Hyponatremia is the most frequently occurring electrolyte disorder in neurocritical care and traumatic brain injury, aneurysmal subarachnoid hemorrhage (SAH), neurosurgery, and ischemic stroke are the clinical conditions more often associated with this condition. SIADH and CSWS are the main causes of hyponatremia in neurologically ill patients. Since hyponatremia is a negative prognostic factor for neurocritical patients, early diagnosis and consequent targeted therapy are of fundamental importance. The present review was carried out to provide a brief recap on the main causes and management of hyponatremia in the neurocritical patient. A methodical search of the medical literature using the online database MEDLINE was carried out and studies comprising case reports, prospective and retrospective observational studies, or randomized controlled clinical trials in which there is a diagnosis of hyponatremia in neurocritical patients were included. 18 articles were analyzed, consisting of 8 case reports, 4 case series, 3 prospective trials, 1 retrospective study, and 1 multicenter trial. A total of 1371 patients from 18 studies were included. Patients' average age was 29.28 ± 20.9, respectively. TBI was the main cause of hyponatremia in the literature reviewed; 12 studies were about the relationship between TBI and hyponatremia, 2 studies about stroke, 2 studies about SAH and 1 about hyponatremia postneurosurgical procedure. Hyponatremia is the most common electrolyte disorder in hospitalized patients and the main scenarios of hyponatremic neurocritical patients are subarachnoid hemorrhage, ischemic stroke, traumatic brain injury and iatrogenic hyponatremia due to neurosurgical cases. Hyponatremia is a frequent finding in neurocritical care and is also a recognized negative prognostic factor leading to increased mortality and ICU length hospitalization. Its diagnosis and therapy are essential for correct neurocritical management. The most common cause of serum sodium abnormality is SIADH, and an early diagnosis for target treatment is paramount to prevent delayed symptoms and complications.

Management of Hyponatremia in Heart Failure: Practical Considerations.

Hyponatremia is commonly encountered in the setting of heart failure, especially in decompensated, fluid-overloaded patients. The pathophysiology of hyponatremia in patients with heart failure is complex, including numerous mechanisms: increased activity of the sympathetic nervous system and the renin-angiotensin-aldosterone system, high levels of arginine vasopressin and diuretic use. Symptoms are usually mild but hyponatremic encephalopathy can occur if there is an acute decrease in serum sodium levels. It is crucial to differentiate between dilutional hyponatremia, where free water excretion should be promoted, and depletional hyponatremia, where administration of saline is needed. An inappropriate correction of hyponatremia may lead to osmotic demyelination syndrome which can cause severe neurological symptoms. Treatment options for hyponatremia in heart failure, such as water restriction or the use of hypertonic saline with loop diuretics, have limited efficacy. The aim of this review is to summarize the principal mechanisms involved in the occurrence of hyponatremia, to present the main guidelines for the treatment of hyponatremia, and to collect and analyze data from studies which target new treatment options, such as vaptans.

A step-by-step guide for the diagnosis and management of hyponatraemia in patients with stroke.

Hyponatraemia is common in patients with stroke and associated with adverse outcomes and increased mortality risk. The present review presents the underlying causes and provides a thorough algorithm for the diagnosis and management of hyponatraemia in stroke patients. Concomitant diseases and therapies, such as diabetes, chronic kidney disease and heart failure, along with diuretics, antidepressants and proton pump inhibitors are the most common causes of hyponatraemia in community. In the setting of acute stroke, the emergence of hyponatraemia might be attributed to the administration of hypotonic solutions and drugs (ie. mannitol and antiepileptics), poor solute intake, infections, as well as stroke-related conditions or complications, such as the syndrome of inappropriate secretion of antidiuretic hormone, cerebral salt wasting syndrome and secondary adrenal insufficiency. Diagnostically, the initial step is to differentiate hypotonic from non-hypotonic hyponatraemia, usually caused by hyperglycaemia or recent mannitol administration in patients with stroke. Determining urine osmolality, urine sodium level and volume status are the following steps in the differentiation of hypotonic hyponatraemia. Of note, specific parameters, such as fractional uric acid and urea excretion, along with plasma copeptin concentration, may further improve the diagnostic yield. Therapeutic options are based on the duration and symptoms of hyponatremia. In the case of acute or symptomatic hyponatraemia, hypertonic saline administration is recommended. Hypovolaemic chronic hyponatremia is treated with isotonic solution administration. Although fluid restriction remains the first-line treatment for the rest forms of chronic hyponatraemia, therapies increasing renal free water excretion may be necessary. Loop diuretics and urea serve this purpose in patients with stroke, whereas sodium-glucose transport protein-2 inhibitors appear to be a promising therapy. Nevertheless, it is yet unclear whether the appropriate restoration of sodium level improves outcomes in such patients. Randomized trials designed to compare therapeutic strategies in managing hyponatraemia in patients with stroke are required.

Editorial introductions.

Editorial introductions.

Effects of Short-Term Human Albumin Infusion for the Prevention and Treatment of Hyponatremia in Patients with Liver Cirrhosis.

Background: Human albumin (HA) infusion is potentially effective for the management of hyponatremia in liver cirrhosis, but the current evidence is very limited. Methods: In this retrospective study, 2414 cirrhotic patients who were consecutively admitted to our hospital between January 2010 and June 2014 were included in the Hospitalization outcome cohort, and 339 cirrhotic patients without malignancy who were consecutively admitted to our department between December 2014 and April 2021 were included in the Long-term outcome cohort. The development and improvement of hyponatremia were compared between patients who received HA infusion during hospitalizations and did not. Logistic and Cox regression analyses were performed to evaluate the association of development and improvement of hyponatremia during hospitalizations with the outcomes. Odds ratios (ORs) and hazard ratios (HRs) were calculated. Results: In the two cohorts, HA infusion significantly decreased the incidence of hyponatremia and increased the rate of improvement of hyponatremia in cirrhotic patients during hospitalizations. In the Hospitalization outcome cohort, the development of hyponatremia during hospitalizations was significantly associated with increased in-hospital mortality (OR = 2.493, p < 0.001), and the improvement of hyponatremia during hospitalizations was significantly associated with decreased in-hospital mortality (OR = 0.599, p = 0.014). In the Long-term outcome cohort, the development of hyponatremia during hospitalizations was significantly associated with decreased long-term survival (HR = 0.400, p < 0.001), and the improvement of hyponatremia during hospitalizations was not significantly associated with long-term survival (HR = 1.085, p = 0.813). Conclusions: HA infusion can effectively prevent the development of hyponatremia and improve hyponatremia in cirrhotic patients during hospitalizations, which may influence the patients’ outcomes.

ODP184 Diabetic Postural Dizziness,Hyperlactatemia,Hyponatremia-Role of Fludrocortisone

Abstract Background Fludrocortisonehas been used in the management of idiopathic postural hypotension and occasionally in diabetic postural hypotension. [1]Enhanced sympathetic nervous system(SNS) activity consequent upon autonomic dysfunction has been linked with the development and maintenance of hyperlactatemia and lactic acidosis(converted to lactate at physiological pH). [2]The mineralocorticoid property of fludrocortisone is utilized inthe management of hyponatremia and hypovolemia. [3] Clinical Cases: Hereby,two T2DM patients are being discussed where fludrocortisone(0.1 mg/d) provided symptomatic relief in postural dizziness. The first patient was a 60 year-old obese, euthyroid,hypertensive male having diabetes(insulin requiring)for the last 30 years with normal kidney function and complaints of frequent postural dizziness and occasional fainting attacks,although,there was no postural drop of blood pressure or tachycardia. He had lactate levels of 4 to 5 mmol/L with normal pH and bicarbonate. He had symptomatic relief with fludrocortisone(being taken for the last four years) with no rise of blood pressure or change in electrolytes or lactate levels. He had associated epigastric fullness and erectile dysfunction(suggestive of autonomic neuropathy). The other patient was an 80 year-old male, euthyroid,normotensive,insulin requiring diabetic for last 27 years with normal kidney function. He was operated for right adrenocortical carcinoma almost 30 years ago which was uneventful till three years ago when he presented with breathlessness and was diagnosed as having adrenal metastasis(immunohistochemistry)in lungs. Thereafter,he developed postural dizziness(despite being on ivabradine),cognitive decline along with abdominal fullness and urinary incontinence(suggestive of autonomic neuropathy). He had hyponatremia(possibly due to SIADH) which rose from 117 mmol/L on 15 mg/d tolvaptan to 123 mmol/L on 30 mg/d. There was significant relief in postural dizziness and slight improvement in serum sodium(rose to 124mmol/L)with 0.10 mg/d fludrocortisone. A lower dose of fludrocorisone is required for symptomatic relief in diabetic postural hypotension (efferent fibre lesion affecting SNS, possibly with reduced renin secretion in response to erect posture) as compared to idiopathic postural hypotension(afferent or central lesion). Fludrocortisone has been reported to increase serum sodium in short-term studies whereas serum sodium remained in normal range and there was no increase in blood pressure in long-term studies. [1] Conclusion: These cases highlight the benefit of fludrocortisone in the management of diabetic postural dizziness and hyponatremia and the rare association of hyperlactatemia with autonomic dysfunction.

Management of Severe Hyponatremia With Modified Continuous Venovenous Hemodiafiltration (CVVHDF) Solutions

Management of Severe Hyponatremia With Modified Continuous Venovenous Hemodiafiltration (CVVHDF) Solutions

PSAT361 Severe Hyponatremia in a Patient with Myxedema Coma

Abstract Introduction Patients with myxedema coma present with hypothermia, bradycardia, hypotension, altered mental status, and hyponatremia. We present an interesting case of myxedema coma with severe hyponatremia and discuss hyponatremia management. Case presentation Patient is a 67-year-old female with history of hypothyroidism following thyroidectomy for papillary thyroid carcinoma, hypertension, and medication nonadherence who was found down and brought to the hospital for altered mental status. On presentation she had a temperature of 35 °C, heart rate of 49, BP of 130/105, and intermittent O2 desaturations due to hypoventilation. On exam she was somnolent with nystagmus and lateral gaze deviation. She was moving all extremities. Lung and heart exam were normal. Labs showed sodium of 102 mEq/L (135-145 mEq/L) and serum osmolality of 243 mOsm/kg (280-300 mOsm/kg). TSH was 35U/mL (0.4-5 U/mL), and free T4 was &amp;lt;0.2 ng/dL (4.8-10.8 ug/dL). CBC and creatinine were normal. Head CT and chest XR were unremarkable. In the ER, she received hypertonic saline 3% as a 150mL bolus along with 1L of isotonic saline. Her sodium rapidly corrected to 117 mEq/L over 2.5 hours. She was given 3 doses of desmopressin 2mcg to control the overcorrection. She received hydrocortisone 100mg IV followed by 50mg IV q8hr. After the first dose of hydrocortisone, she was given levothyroxine 100mcg IV once followed by 75mcg IV daily. Hydrocortisone was discontinued after her cortisol level returned at 49 ug/dL (5.0-22.6 mcg/dL). Plasma sodium stabilized at 114meq/L in 48hrs. With continued IV levothyroxine alone, plasma sodium increased to 122 mEq/L by day 3 and then rose to 134 mEq/L on day 4. Free T4 improved to 0.4 ng/dL on day 3. Her mentation improved slowly and returned to baseline by day 6. Discussion In patients with chronic, severe hyponatremia, treatment usually entails hypertonic saline delivered either by bolus or continuous infusion with a targeted sodium correction rate of ≤8 mEq/L in any 24-hour period. However, when hyponatremia is due specifically to hypothyroidism, hypertonic saline confers high risk of overcorrection, as was evident in this patient. The pathogenesis of hyponatremia in myxedema coma is multifactorial, involving reduced free water clearance due to lower renal perfusion, inappropriately elevated ADH levels due to decreased cardiac output, and tubular dysfunction. Therefore, isotonic IV fluids and levothyroxine therapy directly address the mechanisms underlying hyponatremia and avoid the undue risk of hypertonic saline. Myxedema coma constitutes a unique context for the etiology and treatment of severe hyponatremia. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

Korean Society of Nephrology 2022 recommendations on controversial issues in diagnosis and management of hyponatremia.

The Korean Society for Electrolyte and Blood Pressure Research, in collaboration with the Korean Society of Nephrology, has published a clinical practice guideline (CPG) document for hyponatremia treatment. The document is based on an extensive evidence-based review of the diagnosis, evaluation, and treatment of hyponatremia with the multidisciplinary participation of representative experts in hyponatremia with methodologist support for guideline development. This CPG consists of 12 recommendations (two for diagnosis, eight for treatment, and two for special situations) based on eight detailed topics and nine key questions. Each recommendation begins with statements graded by the strength of the recommendations and the quality of the evidence. Each statement is followed by rationale supporting the recommendations. The committee issued conditional recommendations in favor of rapid intermittent bolus administration of hypertonic saline in severe hyponatremia, the use of vasopressin receptor antagonists in heart failure with hypervolemic hyponatremia, and syndrome of inappropriate antidiuresis with moderate to severe hyponatremia, the individualization of desmopressin use, and strong recommendation on the administration of isotonic fluids as maintenance fluid therapy in hospitalized pediatric patients. We hope that this CPG will provide useful recommendations in practice, with the aim of providing clinical support for shared decision-making to improve patient outcomes.

The diagnosis and management of acute hyponatraemia in critical care.

Nurses working in critical care, consisting of the intensive care and high dependency units, will encounter a broad range of diseases and conditions. Therefore, a comprehensive knowledge and understanding of common presentations is required, especially for advanced clinical practitioners (ACPs). One of the most common electrolyte disturbances seen within these areas is hyponatraemia, affecting around 40% of patients in critical care and 30% of inpatients. It is important that ACPs working in this area are aware of the symptoms and recommended diagnosis and management.

Hyponatremia and homoeopathy

The normal serum sodium level →135–145 mEq/L. Hyponatremia is elucidated as serum sodium levels of >135 mEq/L, but may change to a little extent according to different evaluating laboratories. Edelman found that serum sodium ion concentration doesn’t depend on total body sodium volume but to the ratio of total body solutes to total body water/solvent. Serum sodium of > 120 mEq/L is severe. Classification1.Hypertonic (translocational) type of Hyponatremia2.Hypotonic (dilutional) type of Hyponatremiaa.Hypovolemic hypotonic type of Hyponatremiab.Euvolemic or normovolemic hypotonic type of Hyponatremiac.Hypervolemic hypotonic type of HyponatremiaHomeopathic management of Hyponatremia is based on individualization of patient and therapeutic approaches for restoration of the patient with Hyponatremia.

Risk of pre-existing hyponatremia and mortality in patients with traumatic brain injury across age groups

Traumatic brain injurySodiumClinical outcomes.

Prospective, multicentre study of screening, investigation and management of hyponatraemia after subarachnoid haemorrhage in the UK and Ireland

BackgroundHyponatraemia often occurs after subarachnoid haemorrhage (SAH). However, its clinical significance and optimal management are uncertain. We audited the screening, investigation and management of hyponatraemia after SAH.MethodsWe prospectively identified consecutive...