ArticleBMC nephrology2014
Plasma exchange successfully treats central pontine myelinolysis after acute hypernatremia from intravenous sodium bicarbonate therapy.
Article in BMC nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 37 citations in OpenAlex.
- Renal tubular acidosis as the initial presentation of Sjögren syndrome complicated by iatrogenic central pontine myelinolysis: a case report.Encephalitis (Seoul, Korea) · 2026Article
- Central pontine myelinolysis caused by hyperglycemia: A case report and mechanistic review.The Journal of international medical research · 2025Review
- Article
- Central Pontine Myelinolysis and Hypokalemic Paralysis as Presenting Manifestations of Sjogren's Syndrome.Cureus · 2023Article
- A rare presentation of central pontine myelinolysis secondary to hyperglycaemia.BMC endocrine disorders · 2023Article
- Effective treatment of osmotic demyelination syndrome with plasmapheresis: a case report and review of the literature.Journal of medical case reports · 2021Review
- Extrapontine myelinolysis caused by rapid correction of pituitrin-induced severe hyponatremia: A case report.World journal of clinical cases · 2020Article
- Favorable Outcomes Following the Use of Triple Therapy in a Patient with Osmotic Demyelination Syndrome.Kansas journal of medicine · 2020Article
- Excessive Sodium Bicarbonate Infusion May Result in Osmotic Demyelination Syndrome During Treatment of Diabetic Ketoacidosis: A Case Report.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2019Article
- How Dangerous Is Hyperkalemia?Journal of the American Society of Nephrology : JASN · 2017Review
- Osmotic demyelination syndrome: plasmapheresis versus intravenous immunoglobulin?Internal and emergency medicine · 2017Article
- The Improvement of the Outcome of Osmotic Demyelination Syndrome by Plasma Exchange.Internal medicine (Tokyo, Japan) · 2017Article
- A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2016Review
- Atypical bromethalin intoxication in a dog: pathologic features and identification of an isomeric breakdown product.BMC veterinary research · 2015Article
- Plasmapheresis for Extrapontine Myelinolysis: A Case Series and a Literature Review.Case reports in neurologyArticle
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6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundOsmotic demyelination syndrome (ODS) primarily occurs after rapid correction of severe hyponatremia. There are no proven effective therapies for ODS, but we describe the first case showing the successful treatment of central pontine myelinolysis (CPM) by plasma exchange, which occurred after rapid development of hypernatremia from intravenous sodium bicarbonate therapy. CASE PRESENTATION: A 40-year-old woman presented with general weakness, hypokalemia, and metabolic acidosis. The patient was treated with oral and intravenous potassium chloride, along with intravenous sodium bicarbonate. Although her bicarbonate deficit was 365 mEq, we treated her with an overdose of intravenous sodium bicarbonate, 480 mEq for 24 hours, due to the severity of her acidemia and her altered mental status. The next day, she developed hypernatremia with serum sodium levels rising from 142.8 mEq/L to 172.8 mEq/L. Six days after developing hypernatremia, she exhibited tetraparesis, drooling, difficulty swallowing, and dysarthria, and a brain MRI revealed high signal intensity in the central pons with sparing of the peripheral portion, suggesting CPM. We diagnosed her with CPM associated with the rapid development of hypernatremia after intravenous sodium bicarbonate therapy and treated her with plasma exchange. After two consecutive plasma exchange sessions, her neurologic symptoms were markedly improved except for mild diplopia. After the plasma exchange sessions, we examined the patient to determine the reason for her symptoms upon presentation to the hospital. She had normal anion gap metabolic acidosis, low blood bicarbonate levels, a urine pH of 6.5, and a calyceal stone in her left kidney. We performed a sodium bicarbonate loading test and diagnosed distal renal tubular acidosis (RTA). We also found that she had Sjögren's syndrome after a positive screen for anti-Lo, anti-Ra, and after the results of Schirmer's test and a lower lip biopsy. She was discharged and treated as an outpatient with oral sodium bicarbonate and potassium chloride.
conclusionThis case indicates that serum sodium concentrations should be carefully monitored in patients with distal RTA receiving intravenous sodium bicarbonate therapy. We should keep in mind that acute hypernatremia and CPM can be associated with intravenous sodium bicarbonate therapy, and that CPM due to acute hypernatremia may be effectively treated with plasma exchange.
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