scholarly journals Unpredictable Nature of Tolvaptan in Treatment of Hypervolemic Hyponatremia: Case Review on Role of Vaptans

2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
Ishan Malhotra ◽  
Shilpa Gopinath ◽  
Kalyana C. Janga ◽  
Sheldon Greenberg ◽  
Shree K. Sharma ◽  
...  
Keyword(s):  
Volume Status ◽  
Case Review ◽  
Osmotic Demyelination Syndrome ◽  
Sodium Deficiency ◽  
Neurologic Recovery ◽  
Vasopressin Antagonists ◽  
Low Sodium ◽  
Osmotic Demyelination ◽  
Sodium Correction

Hyponatremia is one of the most commonly encountered electrolyte abnormalities occurring in up to 22% of hospitalized patients. Hyponatremia usually reflects excess water retention relative to sodium rather than sodium deficiency. Volume status and serum osmolality are essential to determine etiology. Treatment depends on several factors, including the cause, overall volume status of the patient, severity of hyponatremic symptoms, and duration of hyponatremia at presentation. Vasopressin antagonists like tolvaptan seem promising for the treatment of euvolemic and hypervolemic hyponatremia in heart failure. Low sodium concentrations cause cerebral edema, but the overly rapid sodium correction can also lead to iatrogenic cerebral osmotic demyelination syndrome. Demyelination may occur days after sodium correction or initial neurologic recovery from hyponatremia. The following case report analyzes the role of vasopressin antagonists in the treatment of hyponatremia and the need for daily dosing of tolvaptan and the monitoring of serum sodium levels to avoid rapid overcorrection which can result in osmotic demyelination syndrome (ODS).

Osmotic demyelination syndrome following slow correction of hyponatraemia

2021 ◽  
Vol 14 (8) ◽  
pp. e241407
Author(s):  
Isabel Saunders ◽  
David M Williams ◽  
Aliya Mohd Ruslan ◽  
Thinzar Min
Keyword(s):  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Inflammatory Markers ◽  
Urine Osmolality ◽  
Fluid Restriction ◽  
Osmotic Demyelination Syndrome ◽  
Electrolyte Disturbance ◽  
Osmotic Demyelination ◽  
Sodium Correction ◽  
Hospital Inpatients

Hyponatraemia is the most common electrolyte disturbance observed in hospital inpatients. We report a 90-year-old woman admitted generally unwell following a fall with marked confusion. Examination revealed a tender suprapubic region, and investigations observed elevated inflammatory markers and bacteriuria. Admission investigations demonstrated a serum sodium of 110 mmol/L with associated serum osmolality 236 mmol/kg and urine osmolality 346 mmol/kg. She was treated for hyponatraemia secondary to syndrome of inappropriate antidiuretic hormone (SIADH) and urosepsis. However, her serum sodium failed to normalise despite fluid restriction, necessitating treatment with demeclocycline and hypertonic saline. Despite slow reversal of hyponatraemia over 1 month, the patient developed generalised seizures with pontine and thalamic changes on MRI consistent with osmotic demyelination syndrome (ODS). This case highlights the risk of ODS, a rare but devastating consequence of hyponatraemia treatment, despite cautious sodium correction.

scholarly journals Osmotic Demyelination: From an Oligodendrocyte to an Astrocyte Perspective

2019 ◽  
Vol 20 (5) ◽  
pp. 1124 ◽  
Author(s):  
Charles Nicaise ◽  
Catherine Marneffe ◽  
Joanna Bouchat ◽  
Jacques Gilloteaux
Keyword(s):  
Glial Cells ◽  
Serum Sodium ◽  
Brain Regions ◽  
Osmotic Demyelination Syndrome ◽  
Brain Areas ◽  
Osmotic Demyelination ◽  
Central Myelin ◽  
Barrier Breakdown ◽  
Blood Brain Barrier Breakdown

Osmotic demyelination syndrome (ODS) is a disorder of the central myelin that is often associated with a precipitous rise of serum sodium. Remarkably, while the myelin and oligodendrocytes of specific brain areas degenerate during the disease, neighboring neurons and axons appear unspoiled, and neuroinflammation appears only once demyelination is well established. In addition to blood‒brain barrier breakdown and microglia activation, astrocyte death is among one of the earliest events during ODS pathology. This review will focus on various aspects of biochemical, molecular and cellular aspects of oligodendrocyte and astrocyte changes in ODS-susceptible brain regions, with an emphasis on the crosstalk between those two glial cells. Emerging evidence pointing to the initiating role of astrocytes in region-specific degeneration are discussed.

scholarly journals Osmotic Demyelination Syndrome Following Correction of Hyponatremia by ≤10 mEq/L per day

Kidney360 ◽  
2021 ◽  
pp. 10.34067/KID.0004402021
Author(s):  
Srijan Tandukar ◽  
Richard H. Sterns ◽  
Helbert Rondon-Berrios
Keyword(s):  
Risk Factors ◽  
Serum Sodium ◽  
Alcohol Use Disorder ◽  
Neurological Deficits ◽  
Osmotic Demyelination Syndrome ◽  
European Guidelines ◽  
Osmotic Demyelination ◽  
Chronic Hyponatremia ◽  
The Mean ◽  
Sodium Correction

Background: Overly rapid correction of chronic hyponatremia may lead to osmotic demyelination syndrome. European guidelines recommend a correction to ≤10 mEq/L in 24 hours to prevent this complication. However, osmotic demyelination syndrome may occur despite adherence to these guidelines. Methods: We searched the literature for reports of osmotic demyelination syndrome with rates of correction of hyponatremia <10 mEq/L in 24 hours. The reports were reviewed to identify specific risk factors for this complication. Results: We identified 19 publications with a total of 21 patients that were included in our analysis. The mean age was 52 years of which 67% were male. All of the patients had community acquired chronic hyponatremia. Twelve patients had an initial serum sodium <115 mEq/L, of which seven had an initial serum sodium ≤105 mEq/L. Other risk factors identified included alcohol use disorder (n=11), hypokalemia (n=5), liver disease (n=6), and malnutrition (n=11). The maximum rate of correction in patients with serum sodium <115 mEq/L was at least 8 mEq/L in all but 1 patient. In contrast, correction was <8 mEq/L in all but 2 patients with serum sodium >115 mEq/L. Among the latter group, osmotic demyelination syndrome developed before hospital admission or was unrelated to hyponatremia overcorrection. Four patients died (19%), 5 had full recovery (24%) and 9 (42%) had varying degrees of residual neurological deficits. Conclusions: Osmotic demyelination syndrome can occur in patients with chronic hyponatremia with a serum sodium <115 mEq/L despite rates of serum sodium correction <10 mEq/L in 24 hours. In patients with severe hyponatremia and high risk features, especially those with serum sodium <115 mEq/L, we recommend limiting serum sodium correction to <8 mEq/L. Thiamine supplementation is advisable for any hyponatremic patient whose dietary intake has been poor.

scholarly journals Role of Risk Factors in Developing Osmotic Demyelination Syndrome During Correction of Hyponatremia: A Case Study

Cureus ◽  
2020 ◽  
Author(s):  
Tom D.Y. Reijnders ◽  
Wilbert M.T. Janssen ◽  
S.M. Laila Niamut ◽  
Andrea B Kramer
Keyword(s):  
Risk Factors ◽  
Osmotic Demyelination Syndrome ◽  
Osmotic Demyelination

scholarly journals A case of Osmotic demyelination syndrome despite normal rate of Sodium correction with good recovery

2018 ◽  
Vol 17 (3) ◽  
pp. 160-163
Author(s):  
Shiva Mongolu ◽  
Keyword(s):  
Risk Factors ◽  
Sodium Concentration ◽  
Good Recovery ◽  
Osmotic Demyelination Syndrome ◽  
Good Clinical Outcome ◽  
Osmotic Demyelination ◽  
Severe Hyponatraemia ◽  
Sodium Correction ◽  
Hospital Inpatients ◽  
Rapid Correction

The Osmotic demyelination syndrome (ODS) primarily occurs with rapid correction of severe hyponatraemia that has been present for more than two or three days. Some patients are, however at risk and can develop ODS at higher sodium concentration and lower rates of correction. A case of Osmotic demyelination Syndrome which developed despite an ‘optimal’ rate of correction of serum Sodium with good clinical outcome is described. The risk factors that contribute to development of ODS and strategies to prevent this complication are discussed, along with recommendations on how to manage this condition in hospital inpatients.

scholarly journals Osmotic demyelination syndrome following slow correction of hyponatremia: Possible role of hypokalemia

2013 ◽  
Vol 17 (4) ◽  
pp. 231-233 ◽  
Author(s):  
Mohammed Ashraf ◽  
Parvaiz A. Koul ◽  
Umar Hafiz Khan ◽  
Rafi A. Jan ◽  
Sanaullah Shah ◽  
...  
Keyword(s):  
Osmotic Demyelination Syndrome ◽  
Osmotic Demyelination

scholarly journals Treatment response in osmotic demyelination syndrome presenting as severe parkinsonism, ptosis and gaze palsy

2018 ◽  
pp. bcr-2018-225751 ◽  
Author(s):  
Sanihah Abdul Halim ◽  
Nur Aida Mohd Amin
Keyword(s):  
Intravenous Immunoglobulin ◽  
Osmotic Demyelination Syndrome ◽  
Bilateral Ptosis ◽  
Extrapontine Myelinolysis ◽  
Osmotic Demyelination ◽  
Severe Hyponatraemia ◽  
Experimental Therapies ◽  
Sodium Correction ◽  
Central Pontine ◽  
Gaze Palsy

Osmotic demyelination syndrome commonly affects the pons and infrequently involves the extrapontine region. We report a patient with severe hyponatraemia who developed osmotic demyelination syndrome as a consequence of rapid sodium correction. The condition manifested as acute severe parkinsonism, bilateral ptosis and gaze impairment. MRI revealed typical features of central pontine and extrapontine myelinolysis. The patient improved gradually after treatment with a combination of levodopa, intravenous immunoglobulin and dexamethasone. However, it is important to emphasise that the improvement of neurological symptoms is not necessarily causal with these experimental therapies.

scholarly journals A primary cilium in oligodendrocytes: a fine structure signal of repairs in thalamic Osmotic Demyelination Syndrome (ODS)

2021 ◽  
pp. 1-30
Author(s):  
Jacques Gilloteaux ◽  
Joanna Bouchat ◽  
Valery Bielarz ◽  
Jean-Pierre Brion ◽  
Charles Nicaise
Keyword(s):  
Fine Structure ◽  
Primary Cilium ◽  
Osmotic Demyelination Syndrome ◽  
Osmotic Demyelination

Osmotic demyelination syndrome in patients with non-Hodgkin lymphoma: A case report and literature review

2021 ◽  
pp. 1-6
Author(s):  
Miguel García-Grimshaw ◽  
Amado Jiménez-Ruiz ◽  
José Luis Ruiz-Sandoval ◽  
Carlos Cantú-Brito ◽  
Erwin Chiquete
Keyword(s):  
Case Report ◽  
Literature Review ◽  
Hodgkin Lymphoma ◽  
Osmotic Demyelination Syndrome ◽  
Non Hodgkin Lymphoma ◽  
Osmotic Demyelination

scholarly journals Role of diuretics on long-term mortality may differ in volume status in patients with acute myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T Kawai ◽  
D Nakatani ◽  
T Yamada ◽  
T Watanabe ◽  
T Morita ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Propensity Score ◽  
Plasma Volume ◽  
Cox Regression ◽  
Volume Status ◽  
Increased Risk ◽  
Long Term Mortality

Abstract Background Diuretics has been reported to have a potential for an activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system, leading to a possibility of poor clinical outcome in patients with cardiovascular disease. However, few data are available on clinical impact of diuretics on long-term outcome in patients with acute myocardial infarction (AMI) based on plasma volume status. Methods To address the issue, a total of 3,416 survived patients with AMI who were registered to a large database of the Osaka Acute Coronary Insufficiency Study (OACIS) were studied. Plasma volume status was assessed with the estimated plasma volume status (ePVS) that was calculated at discharge as follows: actual PV = (1 − hematocrit) × [a + (b × body weight)] (a=1530 in males and a=864 in females, b=41.0 in males and b=47.9 in females); ideal PV = c × body weight (c=39 in males and c=40 in females), and ePVS = [(actual PV − ideal PV)/ideal PV] × 100 (%). Multivariable Cox regression analysis and propensity score matching were performed to account for imbalances in covariates. The endpoint was all-cause of death (ACD) within 5 years. Results During a median follow-up period of 855±656 days, 193 patients had ACD. In whole population, there was no significant difference in long-term mortality risk between patients with and without diuretics in both multivariate cox regression model and propensity score matching population. When patients were divided into 2 groups according to ePVS with a median value of 4.2%, 46 and 147 patients had ACD in groups with low ePVS and high ePVS, respectively. Multivariate Cox analysis showed that use of diuretics was independently associated with an increased risk of ACD in low ePVS group, (HR: 2.63, 95% confidence interval [CI]: 1.22–5.63, p=0.01), but not in high ePVS group (HR: 0.70, 95% CI: 0.44–1.10, p=0.12). These observations were consistent in the propensity-score matched cohorts; the 5-year mortality rate was significantly higher in patients with diuretics than those without among low ePVS group (4.7% vs 1.7%, p=0.041), but not among high ePVS group (8.0% vs 10.3%, p=0.247). Conclusion Prescription of diuretics at discharge was associated with increased risk of 5-year mortality in patients with AMI without PV expansion, but not with PV expansion. The role of diuretics on long-term mortality may differ in plasma volume status. Therefore, prescription of diuretics after AMI may be considered based on plasma volume status. Funding Acknowledgement Type of funding source: None

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