BACKGROUND: Osmotic demyelination syndrome (ODS), which embraces central pontine and extrapontine myelinolysis, is an uncommon neurological disorder that occurs due to plasma osmotic changes.
METHODS: We present the case of a 55-year-old man, who presented with severe hyponatremia due to repeated vomiting, antidepressant treatment and consumption of large amounts of water. Fifteen days after sodium correction, the patient showed fluctuation of vigilance, dysarthria and dysphagia, tremor, cogwheel rigidity, bilateral facial palsy, ophthalmoplegia and tetraparesis. A brain MRI scan revealed extrapontine and later on pontine myelinolysis. He received intravenous steroids and subsequently immunoglobulin. His status began to improve gradually after completion of immunoglobulin and at three month-follow-up had no neurological deficit.
METHODS: A comprehensive literature search of all reported ODS cases that received immunoglobulin, steroids or plasmapheresis was conducted in the electronic databases PubMed and Web of science.
CONCLUSIONS: Improvement was seen in most cases that received immunoglobulin either during treatment or in the first days after treatment. With regard to steroids, although most cases reported improvement in the following months their effect on the outcome is unclear. Most cases treated with plasmapheresis reported favorable outcome at variable follow-up time. Immunoglobulin and steroids have immunomodulatory effects, which could contribute to promotion of myelin repair in ODS. Plasmapheresis has effects on the immune system beyond removing myelinotoxins from the circulation. More evidence is required to support their use in ODS. However, in view of the disease severity, these therapeutic choices should be considered in the clinical management of ODS.

Hyponatremia is a common electrolyte disorder in patients with end-stage liver disease (ESLD) and is associated with increased mortality on the liver transplantation (LT) waiting list. The impact of hyponatremia on outcomes after LT is unclear. Ninety-day and one-year mortality may be increased, but the data are conflicting. Hyponatremic patients have an increased rate of complications and longer hospital stays after transplant. Although rare, osmotic demyelination syndrome (ODS) is a feared complication after LT in the hyponatremic patient. The condition may occur when the serum sodium (sNa) concentration increases excessively during or after LT. This increase in sNa concentration correlates with the degree of preoperative hyponatremia, the amount of intraoperative blood loss, and the volume of intravenous fluid administration. The risk of developing ODS after LT can be mitigated by avoiding large perioperative increases in sNa concentration . This can be achieved through measures such as carefully increasing the sNa pretransplant, and by limiting the intravenous intra- and postoperative amounts of sodium infused. SNa concentrations should be monitored regularly throughout the entire perioperative period.

UNASSIGNED: Osmotic demyelination syndrome (ODS) is a non-inflammatory process of the central nervous system caused by extracellular osmotic changes, which leads to oligodendrocyte apoptosis and disruption of myelin sheaths, usually affecting patients with underlying systemic conditions that impose susceptibility to osmotic stress. Description of ODS in patients with non-Hodgkin lymphoma (NHL) is limited to a few case reports.
UNASSIGNED: Here, we report a 44-year-old man with NHL that had an incidental diagnosis of ODS. We conducted a literature review of the published cases of ODS in NHL patients from 1959 to 2020, aiming to describe the characteristics of these patients.
UNASSIGNED: A total of seven patients were summarized (four men and three women), including our case and six patients from published reports. Risk factors such as weight loss and alcoholism were reported in five (71.4%) patients. Hyponatremia was found in six (85.7%) of the cases, and none of them had overly rapid sodium correction. Four cases were asymptomatic, and diffuse large B-cell lymphoma was the most common subtype of NHL (85.7%). The outcome was favorable in most cases; only two deaths not directly related to ODS were reported.
UNASSIGNED: We wish to suggest that systemic and metabolic stress induced by NHL may be associated with the development of central osmotic demyelination, and therefore, NHL may be a novel risk factor for ODS. Clinicians should be aware of ODS in patients with hematological malignancies, even in the absence of traditional risk factors.

Osmotic demyelination syndrome (ODS) is characterized by widespread degeneration of myelin within the central nervous system and has no established treatment. A limited number of cases have reported positive outcomes with plasma exchange in the treatment of ODS associated with chronic alcohol abuse or liver transplantation. We report the case of a 23-year-old female presenting with ODS following rapid correction of hyponatremia, which was attributed to hypoalbuminemia, volume overload, and malnutrition secondary to ulcerative colitis. Our patient received four plasma exchange sessions over the course of five days for a total plasma exchange of 15,500 mL. Unfortunately, the patient did not achieve significant neurologic recovery following completion of the plasma exchange regimen. This is the first report of the failure of this novel approach in the management of a patient with ODS, suggesting benefit in a limited patient population. We describe the proposed mechanism of plasma exchange in the treatment of ODS and provide a review of existing literature.

Hyponatremia is the most common electrolyte disturbance amongst hospitalized patients. An overly rapid rate of correction of chronic hyponatremia is believed to increase the risk of poor clinical outcomes including osmotic demyelination syndrome (ODS). There is disagreement in the literature regarding the definition of hyponatremic overcorrection.
We performed a systematic review of all English language studies to identify those that calculated sodium correction rate and classified patients\' overcorrection status. We then identified all patients who presented to our hospital\'s emergency department between 2003 and 2015 with a corrected serum sodium ≤ 116 mmol/L. All methods from the systematic review for sodium correction rate calculation and overcorrection status were applied to this cohort.
We identified 24 studies citing 9 distinct sodium correction rate methods and 14 criteria for overcorrection. Six hundred twenty-four patients presenting with severe hyponatremia (median initial value 113 mMol) were identified. Depending on the method used, the median sodium correction rates in our cohort ranged from 0.271 to 1.13 mmol/L per hour. The proportion of patients classified with overcorrection with the different criteria varied almost 11-fold, ranging from 8.5 to 89.9%.
Published methods disagree regarding the calculation of sodium correction rates and the definition of hyponatremic overcorrection. This leads to wide variations in sodium correction rates and the prevalence of overcorrection in patient cohorts. Definitions based on ODS risk are needed.

Osmotic demyelination syndrome is classically associated with a swift adjustment of previously low serum sodium levels which lead to cellular dehydration and subsequent neurological insult. We also review the epidemiology, different postulations to explain the underlying pathophysiology, current diagnostic modalities, subsequent therapeutic interventions used to manage this phenomenon, and the resultant prognosis of this ailment.

Beer potomania, a unique syndrome of hyponatremia, was first reported in 1972. It is described as the excessive intake of alcohol, particularly beer, together with poor dietary solute intake that leads to fatigue, dizziness, and muscular weakness. The low solute content of beer, and suppressive effect of alcohol on proteolysis result in reduced solute delivery to the kidney. The presence of inadequate solute in the kidney eventually causes dilutional hyponatremia secondary to reduced clearance of excess fluid from the body. Early detection of hyponatremia due to beer potomania in the hospital is necessary to carefully manage the patient in order to avoid neurological consequences as this syndrome has unique pathophysiology. We are reporting two cases, presenting to the emergency department with severe hyponatremia. After a detailed initial evaluation of the patients and labs for hyponatremia, a diagnosis of beer potomania was established in both cases. Considering the unique pathophysiology of beer potomania syndrome, the patients were closely monitored and treated appropriately to prevent any neurological sequelae.

Hyponatremia is the most frequently occurring electrolyte abnormality and can lead to life-threatening complications. This disorder may be present on admission to the intensive care setting or develop during hospitalization as a result of treatment or multiple comorbidities. Patients with acute hyponatremia or symptomatic chronic hyponatremia will likely require treatment in the intensive care unit (ICU). Immediate treatment with hypertonic saline is needed to reduce the risk of permanent neurologic injury. Chronic hyponatremia should be corrected at a rate sufficient to reduce symptoms but not at an excessive rate that would create a risk of osmotic injury. Determination of the etiology of chronic hyponatremia requires analysis of serum osmolality, volume status, and urine osmolality and sodium level. Correct diagnosis points to the appropriate treatment and helps identify risk factors for accelerated correction of the serum sodium level. Management in the ICU facilitates frequent laboratory draws and allows close monitoring of the patient\'s mentation as well as quantification of urine output. Overly aggressive correction of serum sodium levels can result in neurological injury caused by osmotic demyelination. Therapeutic measures to lower the serum sodium level should be undertaken if the rate increases too rapidly.

OBJECTIVE: Central and extrapontine myelinolysis are collectively known as osmotic demyelination syndrome. This encephalopathic illness has been well documented in the adult literature, occurring most commonly in the context of chronic alcoholism, correction of hyponatraemia and liver transplantation. Aetiology and outcome in the paediatric population are less well understood.
METHODS: Two cases of osmotic demyelination syndrome occurring in children with transient severe hypophosphataemia during the course of their illness are presented. Both had very different neurological outcomes, but the changes of central and extrapontine myelinolysis were apparent on neuroimaging. Sixty-one cases in the paediatric literature were then reviewed.
RESULTS: We summarize aetiology and outcome in paediatric cases of osmotic demyelination syndrome and postulate a role for hypophosphataemia as a contributing factor in the development of these sometimes devastating conditions.
CONCLUSIONS: Hypophosphataemia may contribute to the risk of developing osmotic demyelination syndrome in at-risk paediatric patients and further study of this association should be undertaken.