Rapid Correction Of Hyponatremia Research Articles

Hyponatremia With Anticonvulsant Medications: A Narrative Review.

Hyponatremia is an adverse effect of many antiseizure medications (ASMs). It occurs with interference with the normal balance of electrolytes within the body. Various risk factors associated with the development of hyponatremia in patients taking these medications include age, gender, dosage, and combinations with other drugs. ASMs such as carbamazepine (CBZ), oxcarbazepine (OXC), and valproic acid have a higher risk of hyponatremia. Hyponatremia induced by an antiseizure medication can occurthrough various mechanisms depending on the drug's specific mechanism of action.Hyponatremia can be a potentially fatal side effect. Patients taking these medications need to be monitored closely for the signs and symptoms of hyponatremia. Acute hyponatremia, defined as developing in <48 hours, is more likely to show symptoms than chronic hyponatremia. Signs of acute hyponatremia include delirium, seizures, decerebrate posturing, and cerebral edema with uncal herniation. Chronic hyponatremia, defined as developing in >48 hours, can cause lethargy, dizziness, weakness, headache, nausea, and confusion. Hyponatremia is associated with longer hospital stays and increased mortality. Treatment varies based on the degree of severity of hyponatremia. Choosing a treatment option should include consideration of the drug causing the electrolyte disturbance, the patient's risk factor profile, and the severity of symptoms as they present in the individual patient. Healthcare providers should be aware of hyponatremia as a potential side effect of ASMs, the signs and symptoms of hyponatremia,the different treatment options available, and the potential complications associated with rapid correction of hyponatremia.

Myelinolysis cases presenting with manic attack after rapid correction of hyponatremia: Two cases.

Myelinolysis is a neurological condition that can display diverse psychiatric symptoms, with electrolyte imbalance, alcoholism and malnutrition being the frequent causes. Rapid correction of hyponatremia may trigger pontine and extra-pontine myelinolysis. This paper examines two cases: one of hyponatremia after antihypertensive use and the other of myelinolysis due to rapid correction of hyponatremia. Since myelinolysis appeared as a manic episode, the patients sought treatment at the psychiatry outpatient clinic. Further tests were conducted to rule out organic causes and the diagnosis was confirmed prior to referring the patients to the neurology clinic. Psychiatrists should be meticulous in excluding organic causes in first-episode mania and consider these possibilities in the differential diagnosis for the pertinent patient group.

Diagnostic and Therapeutic Strategies to Severe Hyponatremia in the Intensive Care Unit.

Hyponatremia is the most common electrolyte abnormality encountered in critically ill patients and is linked to heightened morbidity, mortality, and healthcare resource utilization. However, its causal role in these poor outcomes and the impact of treatment remain unclear. Plasma sodium is the main determinant of plasma tonicity; consequently, hyponatremia commonly indicates hypotonicity but can also occur in conjunction with isotonicity and hypertonicity. Plasma sodium is a function of total body exchangeable sodium and potassium and total body water. Hypotonic hyponatremia arises when total body water is proportionally greater than the sum of total body exchangeable cations, that is, electrolyte-free water excess; the latter is the result of increased intake or decreased (kidney) excretion. Hypotonic hyponatremia leads to water movement into brain cells resulting in cerebral edema. Brain cells adapt by eliminating solutes, a process that is largely completed by 48 h. Clinical manifestations of hyponatremia depend on its biochemical severity and duration. Symptoms of hyponatremia are more pronounced with acute hyponatremia where brain adaptation is incomplete while they are less prominent in chronic hyponatremia. The authors recommend a physiological approach to determine if hyponatremia is hypotonic, if it is mediated by arginine vasopressin, and if arginine vasopressin secretion is physiologically appropriate. The treatment of hyponatremia depends on the presence and severity of symptoms. Brain herniation is a concern when severe symptoms are present, and current guidelines recommend immediate treatment with hypertonic saline. In the absence of significant symptoms, the concern is neurologic sequelae resulting from rapid correction of hyponatremia which is usually the result of a large water diuresis. Some studies have found desmopressin useful to effectively curtail the water diuresis responsible for rapid correction.

Pontine and extrapontine myelinolysis associated with rapid correction of hyponatremia - a review

Pontine and extrapontine myelinolysis associated with rapid correction of hyponatremia - a review

Osmotic Demyelinating Syndrome Secondary to Breast Cancer Chemotherapy: a Case Report (P10-5.024)

<h3>Objective:</h3> To report a case of osmotic demyelinating syndrome (ODS) secondary to chemotherapy for breast cancer. <h3>Background:</h3> ODS comprises both central pontine demyelination and extrapontine myelinolysis. This condition accounts for 0.4% to 0.56% of neurological admissions to tertiary referral hospitals and 0.06% of medical admissions. Although rapid correction of hyponatremia is the most common cause, other etiologies such as alcohol consumption, chronic renal failure, and organ transplantation are also reported. Chemotherapy can be an infrequent cause of this condition. Here we describe a case of ODS in a normonatremic patient in treatment with trastuzumab, pertuzumab, and docetaxel. <h3>Design/Methods:</h3> Not applicable. <h3>Results:</h3> A 71-year-old female with a history of breast cancer, with lung and brain metastases, is seen in the emergency room due to a decline in her functionality over the past three months, following the initiation of chemotherapy treatment with trastuzumab, pertuzumab and docetaxel. On neurological examination, she exhibited cognitive failures and a non-fluent aphasia without focal neurologic signs. In addition, right-sided focal seizures successfully managed with levetiracetam. On neuroimaging, there were signs of pontine myelinolysis and a reduction in the size of previous brain metastatic lesions. After discontinuing chemotherapy, the patient’s speech and gait significantly improved. <h3>Conclusions:</h3> ODS could be associated with combination chemotherapy treatment in the setting of a normonatremic patient. In 2014, Sungjae Lee and colleagues reported a similar case in a patient with colon cancer who received 5-fluorouracil, oxaliplatin, and leucovorin chemotherapy. In another study published by Cortes and colleagues, the development of osmotic demyelinating syndrome when using a combination of trastuzumab and pertuzumab for breast cancer was reported as a rare finding (one case of twenty-nine patients). To our knowledge, this is one of the first cases describing an ODS following therapy with pertuzumab, trastuzumab, and docetaxel. <b>Disclosure:</b> Dr. Gaitan Alfonso has nothing to disclose. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Scientific Advisory or Data Safety Monitoring board for Merck. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Scientific Advisory or Data Safety Monitoring board for Roche. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Scientific Advisory or Data Safety Monitoring board for BIIB. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Speakers Bureau for Merck. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Speakers Bureau for Novartis. Dr. Reyes has received personal compensation in the range of $0-$499 for serving on a Speakers Bureau for Biogen. Ms. Rodriguez has nothing to disclose. Dr. Salej has nothing to disclose. Dr. Otero has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for GSK. Dr. Otero has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Janssen . Dr. Otero has received personal compensation in the range of $10,000-$49,999 for serving as an officer or member of the Board of Directors for FICMAC. Dr. Toro has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Watch Neurology .

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.

Central Pontine Myelinolysis Secondary to Hyperglycemia: A Case Report

Centropontine myelinolysis (MCP) belongs to the osmotic demyelination syndrome, and occurs especially after the rapid correction of hyponatremia. In rare cases, it is caused by states of hyperosmolarity and it can be seen in hyperglycemia. Here, we report the case of a 28-year-old diabetic patient, admitted to intensive care unit for a disorder of consciousness and seizures. The physical examination found an apyretic patient with, Glasgow of 11, with quadriparesis and high blood pressure. Laboratory investigations showed hyperglycemia and metabolic ketoacidosis with chronic renal failure, natremia was normal, lumbar puncture was also normal. The diagnosis of MCP was retained on the MRI. Insulin therapy and rehydration were started and the patient showed a clinical improvement. However, he died because of ventilator-associated pneumonia. The aim of this work is to show that MCP can occur despite the absence of an abnormality of natremia and this diagnosis should be considered in diabetic patients with neurological disorders

Prediction of end-dialysis serum sodium concentration in severely hyponatremic kidney failure patients undergoing conventional hemodialysis using sodium kinetic equation

Background and ObjectivesConventional hemodialysis (HD) for kidney failure patients with severe hyponatremia may be complicated by rapid correction of hyponatremia, which increases the risk of osmotic demyelination syndrome. A simple sodium kinetic equation was effective in prediction of end-dialysis serum Na+ in severely hyponatremic kidney failure patient treated with continuous venovenous hemofiltration, but was not tested in conventional HD. The aim of this study was to assess the validity of this equation when used in conventional HD.MethodsTwenty conventional HD sessions were delivered to 12 kidney failure patients with severe hyponatremia (serum Na+ < 120 mEq/L). The target change in serum Na+ was 4 mEq/L. The DNa.t/V that obtained this change was predetermined according to the sodium kinetic equation and monitored in real time by online clearance monitoring software embedded in dialysis machine. The dialysis session was terminated once the target DNa.t/V was achieved.ResultsThe mean observed and predicted serum Na+ were 119.80 ± 3.42 mEq/L and 119.45 ± 3.12 mEq/L, respectively. Bland–Altman plot analysis revealed a mean difference ± SD of 0.33 ± 1.26 mEq/L, and 95% limits of agreement of − 2.13 to 2.83. The imprecision in prediction of end-dialysis serum Na+ was 2.52 mEq/L. The small difference and clinically insignificant 95% limits of agreement indicate a good agreement between the observed and predicted serum Na+.ConclusionThe sodium kinetic equation was effective in prediction of end-dialysis serum Na+ in kidney failure patients with severe hyponatremia.

Myélinolyse centropontine réversible sans hyponatrémie chez un enfant atteint de leucémie aigue lymphoblastique: à propos d’un cas

Central pontine myelinolysis is a demyelinating disorder mainly affecting the central pons. In some cases, it is associated with extrapontine myelinolysis. It is usually caused by rapid correction of hyponatremia and osmotic shock. We here report the case of a 3.5-year-old girl diagnosed with acute lymphoblastic leukemia admitted to our Oncology Unit with neutropenic fever and diarrhea. Laboratory tests showed mild neutropenia, normochromic normocytic anemia. Electrolyte tests were normal without hyponatremia. She received antibiotic therapy with Metronidazole. Five days later, she developed flaccid quadriparesis with mutism. Computerized tomography (CT) scan was normal, cerebrospinal fluid (CSF) examination was normal (there was no evidence of leukemic cells) and ophthalmological examination did not show any abnormalities. Brain MRI found hyperintense signal in the pons. The child improved without specific treatment, and clinical and complete neurological recovery was noted. This case highlights that myelinolysis can occur under some circumstances not related with hyponatremia such as malignancy, chemotherapy.

Centropontine myelinolysis after rapid correction of hyponatremia: a case report

Centropontine myelinolysis after rapid correction of hyponatremia: a case report

An observational study on the effectiveness of tolvaptan in patients with euvolemic and hypervolemic hyponatremia admitted to a tertiary care center

Background: Hyponatremia is a common electrolyte abnormality encountered in hospital wards. Even mild hyponatremia can result in significant morbidity and mortality especially in elderly. Treatment of the condition depends on the volume status of the patient, duration and severity of hyponatremia, and clinical condition of the patient. Aims and Objectives: Tolvaptan is an oral vasopressin receptor antagonist approved for use in euvolemic and hypervolemic hyponatremia. The present study aimed to assess the effectiveness and safety of tolvaptan 15 mg daily for 3 days in patients with euvolemic and hypervolemic hyponatremia. Materials and Methods: This study was a prospective observational study conducted on 82 patients with euvolemic and hypervolemic hyponatremia in whom tolvaptan was given in the Department of General Medicine in a tertiary care teaching hospital in south India. History, clinical examination findings, and baseline laboratory values were recorded in the structured proforma. Serum sodium levels were done daily along with other laboratory parameters such as renal function test, serum electrolytes, liver function tests, and random blood sugar. The rise in serum sodium level and the occurrence of overcorrection was noted. Adverse effects developing during treatment were recorded. Results: By day 3, 27% of patients achieved normonatremia and hence tolvaptan was stopped after 2 doses. By day 4, 84% of patients who took tolvaptan achieved normonatremia. Overly rapid correction of hyponatremia was observed in 9.8% of patients. There was a significant correlation between day 1 sodium and day 4 sodium as well as day 1 sodium and total correction. The mean increase in serum sodium with 3 doses of tolvaptan was 18.24 mEq/L with a P &lt; 0.0001. The adverse events during the study period were mild and included increased thirst, dry mouth, and polyuria. There was no significant change in transaminase levels during treatment. Conclusion: Tolvaptan is highly effective in increasing serum sodium level in hyponatremia with minimal adverse effects. The risk of an overly rapid correction is present with its use and is more in severe hyponatremia. This can be minimized by frequent monitoring of sodium level and ensuring adequate fluid intake.

With a grain of salt; A cautionary reminder. A case report of osmotic demyelination syndrome

Osmotic Demyelination Syndrome (ODS) is a demyelinating disease typically seen in the central pons, often associated with a rapid correction of hyponatraemia.

Central Pontine Myelinolysis Complicating Hodgkin Lymphoma: A Case Report &amp; Review of Literature

Central Pontine myelinolysis is a demyelinating disorder generally caused by rapid correction of hyponatremia and is a debilitating condition. Here we describe an interesting case of a 38 year old man diagnosed with Hodgkin lymphoma who developed CPM prior to start of the first cycle of chemotherapy with no antecedent hyponatremia and had complete neurological recovery.

Osmotic demyelination syndrome despite appropriate gradual correction of moderate hyponatraemia.

Osmotic demyelination syndrome characteristically follows rapid correction of hyponatraemia. We present a young woman with a subacute progressive brainstem syndrome and diffuse pontine signal abnormality on MR imaging, diagnosed as osmotic demyelination syndrome. The case posed a diagnostic challenge due to comorbid Behçet's disease and the absence of significant fluctuation in her serum sodium concentration. Osmotic demyelination syndrome is not limited to patients with rapidly corrected hyponatraemia, especially when there are other risk factors. These factors, all present in this patient, include hypokalaemia, hypophosphataemia, malnutrition, harmful alcohol use and liver dysfunction.

Osmotic demyelination syndrome and overly rapid correction of hyponatremia

Hyponatremia is a frequent condition in hospitalized patients and is associated with significant morbidity and mortality. An association between rapid correction of hyponatremia and the occurrence of osmotic demyelination syndrome has been reported. Osmotic demyelination syndrome may present with severe neurologic symptoms, including in rare cases locked-in. Therefore, rapid correction of hyponatremia is recommended only in the presence of severe symptoms. In those cases, hypertonic saline (NaCl 3% 2 ml/Kg over 20 minutes) is recommended with close plasma sodium monitoring. After symptoms improvement, increases in sodium concentration should not exceed 8 mmol/l/24h. In cases without severe neurologic symptoms, the use of 3% NaCl solution should be avoided, and management should target the underlying causes of hyponatremia.

MRI Findings in Osmotic Demyelination Syndrome- A Report of Two Cases

Osmotic demyelination syndrome is a condition seen due to the loss of normal myelin in the central nervous system. Multiple etiologies have been identified as causing this condition, however, the most reported cause is the rapid correction of hyponatremia. Different levels of the central nervous system are involved in the condition. Despite variable etiologies and clinical outcomes of the disease, the Magnetic Resonance Imaging (MRI) findings are well-established and characteristic. Hereby, two cases (45 years and 25 years old males) of Osmotic demyelination syndrome are described, to demonstrate the characteristic magnetic resonance imaging findings of the brain. Both cases were chronic alcoholics with a history of few episodes of vomiting, who later developed neurological symptoms. Their biochemical investigations showed severe hyponatremia. The hyponatremia was corrected rapidly, following which they developed neurological symptoms. Non-contrast MRI brain was done for both patients, which showed abnormal hyperintense T2/Fluid-attenuated Inversion Recovery (FLAIR) signals in central Pons. Both cases showed variable, however characteristics findings of osmotic demyelination syndrome on MRI. Despite, multiple causative factors and clinical outcomes of Osmotic demyelination syndrome, MRI with its characteristic findings plays a key role in diagnosis.

Extra-pontine osmotic demyelination syndrome and membranous nephropathy

Rapid correction of hyponatremia can increase the risk of osmotic demyelination syndrome (ODS) involving the central pons and extrapontine (basal ganglia) brain areas. We described a patient who developed extrapontine ODS after rapid correction of profound hyponatremia in the setting of severe nephrotic syndrome (NS).

A Review on Central Pontine Myelinolysis and Correction of Hyponatremia in Hospitalized Patients

Pontine myelinolysis (PM) can be a nerve disorder represented by pons demyelination. it is characterized by damage to regions of the brain, most commonly tracts pontine substantia alba, after rapid correction of metabolic disorders such as hyponatremia. PM (Pontine Myelinolysis) is categorized into Central pontine myelinolysis (CPM) and extra pontine myelinolysis (EPM). The various studies revealed that quick correction of hyponatremia plays a vital role in the pathogenesis of ODS. Prevention of ODS must be conducted by gradually increasing sodium concentration of 4–6 mmol/Lin in any 24-h period. PubMed and Medline literature search was done using CPM and hyponatremia as keywords. The principal aim of this review is to encapsulate, the recent evidence from literature about the association between rapid correction of hyponatremia and central pontine myelinolysis.&#x0D; Keywords: Demyelination syndrome, EPM, CPM, Serum tonicity, Hyponatremia, Demyelination

A Stepwise Multidisciplinary Rehabilitation Approach of Central Pontine and Extra Pontine Myelinosis in Locked-in Syndrome: A Case Report

Central Pontine Myelinosis (CPM) and Extra Pontine Myelinosis (EPM) are debilitating conditions, resulting from the rapid correction of hyponatremia. The outcome and prognosis of this medical condition are variable; mainly involving functional decline from neuro-musculoskeletal upset. An intensive, multidisciplinary rehabilitation has played an essential role in facilitating and hasten recovery, promoting a favorable outcome. We reported our experience in rehabilitating a patient with a rare condition of comorbid CPM and EPM. The reported patient presented with disabling Locked-in Syndrome (LIS) and Parkinsonism movement disorder. We highlighted the stepwise rehabilitation approach according to Patterson and Grabois Motor Recovery scale for LIS in preventing and reversing the complications and disabilities caused by CPM and EPM that may facilitate favorable therapeutic outcomes.

Diabetes Induced Osmotic Demyelination of the Pons in a Patient on Peritoneal Dialysis

Introduction: Osmotic demyelination of the pons as a result of uncontrolled diabetes is a rare event. Here we present a unique case of central pontine myelinolysis in a patient with poorly controlled type 2 diabetes mellitus in the setting of peritoneal dialysis.Clinical Case: A 48-year-old male with a history of insulin-dependent diabetes mellitus, hypertension, non-ischemic cardiomyopathy, and end-stage renal disease, treated with peritoneal dialysis, presented to the hospital for slurred speech, inability to walk, and persistent hyperglycemia for 3 days. Approximately 2 years prior to admission, peritoneal dialysis was initiated for ESRD and poor cardiac function. The patient’s outpatient pharmacologic regimen was 30 units of glargine daily and glimepiride. On physical exam, there was evidence of aphasia, dysarthria, and muscle weakness (2/5 in bilateral upper and lower extremities) without muscle rigidity. Deep tendon reflexes were absent in the lower extremities, but sensation to light touch was intact throughout. On admission, the patient was found to be in a hyperosmolar hyperglycemic state without ketosis. Initial lab tests were significant for serum sodium: 138mmol/L (n=134–145 mmol/L), serum sodium corrected for hyperglycemia: 143 mmol/L, serum glucose: 419mg/dL (n=75–99 mg/dL), beta-hydroxybutyrate 2.1 mg/dL (n<4.4 mg/dL), and serum osmolality: 330mosmol/kg (n=275–305 mosmol/kg). Urinalysis showed glucosuria without ketonuria. The cerebrospinal fluid analysis showed protein 57, glucose 109, and WBC 3. Lab studies for meningitis/encephalitis panel were negative. During his 2 years of dialysis, his HbA1C increased from 7.6% to 14.3% (n<5.6%). CT brain without contrast showed midline hypoattenuation of the inferior pons without edema. Magnetic resonance imaging without contrast of the brain demonstrated a lobulated lesion in the pons measuring 1–2 cm that shows T2 hyperintensity without surrounding edema. He was then diagnosed with central pontine myelinolysis in the setting of chronic glycemic changes.Conclusion: Osmotic demyelination of the pons is typically associated with rapid correction of hyponatremia. We describe osmotic demyelination of the pons as a result of poorly controlled diabetes with normal sodium. To our knowledge, this is the first report of this event in association with worsening diabetes after the initiation of peritoneal dialysis.