Risk Factors for Overly Rapid Correction in Patients with Profound Hyponatremia: A Retrospective Cohort Study.

Objective Overly rapid correction of profound hyponatremia can lead to osmotic demyelination syndrome; however, the incidence of and risk factors for overly rapid correction in patients with profound hyponatremia have not been thoroughly examined. Therefore, this study examined the incidence of and risk factors for overly rapid correction in patients with profound hyponatremia. Methods This single-center, retrospective cohort study conducted at an 865-bed teaching hospital analyzed data from 144 new inpatients with profound hyponatremia (initial serum sodium [Na+] level of <125 mEq/L) treated in our department between January 2014 and December 2022. Overly rapid correction was defined as serum Na+ correction of >10 mEq/L at 24 h. We examined the incidence of and risk factors for overly rapid correction.Results Thirty (20.8%) patients met the overly rapid correction criteria; however, none developed osmotic demyelination syndrome. A low initial serum Na+ level, female sex, primary polydipsia, and low frequency of follow-up in 24 h were significant independent risk factors for overly rapid correction in the multivariable analysis (p=0.020, p=0.011, p=0.014, and p=0.025, respectively). Conclusion Our study shows that a low initial serum Na+ level, female sex, primary polydipsia, and low frequency of follow-up within 24 h are associated with an increased risk for overly rapid correction of profound hyponatremia. Therefore, we suggest that physicians perform careful management when managing patients with profound hyponatremia with the risk factors for overly rapid correction identified in this study.

Intensive Care Management of Severe Hyponatraemia-An Observational Study.

Background and Subject: Hyponatraemia is a common electrolyte disorder. For patients with severe hyponatraemia, intensive care unit (ICU) admission may be required. This will enable close monitoring and allow safe management of sodium levels effectively. While severe hyponatraemia may be associated with significant symptoms, rapid overcorrection of hyponatraemia can lead to complications. We aimed to describe the management and outcomes of severe hyponatraemia in our ICU and identify risk factors for overcorrection. Materials and Methods: This was a retrospective single-centre cohort that included consecutive adults admitted to the ICU with serum sodium < 120 mmol/L between 1 January 2017 and 8 March 2023. Anonymised data were collected from electronic records. We included 181 patients (median age 67 years, 51% male). Results: Median admission serum sodium was 113 mmol/L (IQR: 108-117), with an average rate of improvement over the first 48 h of 10 mmol/L/day (IQR: 5-15 mmol/L). A total of 62 patients (34%) met the criteria for overcorrection at 48 h, and they were younger, presented with severe symptoms (seizures/arrythmias), and had lower admission sodium concentration. They were more likely to be treated with hypertonic saline infusions. Lower admission sodium was an independent risk factor for overcorrection within 48 h, whereas the presence of liver cirrhosis and fluid restriction was associated with normal correction. No difference was identified between the normal and overcorrected cohorts for ICU/hospital length of stay or mortality. Conclusions: In some patients with severe hyponatraemia, overcorrection is inevitable to avoid symptoms such as seizures and arrhythmias, and consequently, we highlight the key factors associated with overcorrection. Overall, we identified that overcorrection was common and concordant with the current literature.

Rate of Sodium Correction and Osmotic Demyelination Syndrome in Severe Hyponatremia: A Meta-Analysis.

Introduction: Current guidelines recommend limiting the rate of correction in patients with severe hyponatremia to avoid severe neurologic complications such as osmotic demyelination syndrome (ODS). However, published data have been conflicting. We aimed to evaluate the association between rapid sodium correction and ODS in patients with severe hyponatremia. Materials and methods: We searched PubMed, Embase, Scopus, Web of Science, and Cochrane Central Register of Controlled Trials from inception to November 2023. The primary outcome was ODS and the secondary outcomes were in-hospital mortality and length of hospital stay. Results: We identified 7 cohort studies involving 6,032 adult patients with severe hyponatremia. Twenty-nine patients developed ODS, resulting in an incidence rate of 0.48%. Seventeen patients (61%) had a rapid correction of serum sodium in the first or any 24-hour period of admission. Compared with a limited rate of sodium correction, a rapid rate of sodium correction was associated with an increased risk of ODS (RR, 3.91 [95% CI, 1.17 to 13.04]; I2 = 44.47%; p = 0.03). However, a rapid rate of sodium correction reduced the risk of in-hospital mortality by approximately 50% (RR, 0.51 [95% CI, 0.39 to 0.66]; I2 = 0.11%; p < 0.001) and the length of stay by 1.3 days (Mean difference, -1.32 [95% CI, -2.54 to -0.10]; I2 = 71.47%; p = 0.03). Conclusions: Rapid correction of serum sodium may increase the risk of ODS among patients hospitalized with severe hyponatremia. However, ODS may occur in patients regardless of the rate of serum sodium correction.

Prolonged extracellular low sodium concentrations and subsequent their rapid correction modulate nitric oxide production dependent on NFAT5 in microglia.

Hyponatremia is the most common clinical electrolyte disorder. Chronic hyponatremia has been recently reported to be associated with falls, fracture, osteoporosis, neurocognitive impairment, and mental manifestations. In the treatment of chronic hyponatremia, overly rapid correction of hyponatremia can cause osmotic demyelination syndrome (ODS), a central demyelinating disease that is also associated with neurological morbidity and mortality. Using a rat model, we have previously shown that microglia play a critical role in the pathogenesis of ODS. However, the direct effect of rapid correction of hyponatremia on microglia is unknown. Furthermore, the effect of chronic hyponatremia on microglia remains elusive. Using microglial cell lines BV-2 and 6-3, we show here that low extracellular sodium concentrations (36 mmol/L decrease; LS) suppress Nos2 mRNA expression and nitric oxide (NO) production of microglia. On rapid correction of low sodium concentrations, NO production was significantly increased in both cells, suggesting that acute correction of hyponatremia partly directly contributes to increased Nos2 mRNA expression and NO release in ODS pathophysiology. LS also suppressed expression and nuclear translocation of nuclear factor of activated T cells-5 (NFAT5), a transcription factor that regulates the expression of genes involved in osmotic stress. Furthermore, overexpression of NFAT5 significantly increased Nos2 mRNA expression and NO production in BV-2 cells. Expressions of Nos2 and Nfat5 mRNA were also modulated in microglia isolated from cerebral cortex in chronic hyponatremia model mice. These data indicate that LS modulates microglial NO production dependent on NFAT5 and suggest that microglia contribute to hyponatremia-induced neuronal dysfunctions.

Hyponatremia in the emergency department: an overview of diagnostic and therapeutic approach.

INTRODUCTION: Hyponatremia, defined as a serum sodium concentration <135 mmol/l, is a frequent electrolyte disorder in patients presenting to an emergency department (ED). In this context, appropriate diagnostic and therapeutic management is rarely performed and challenging due to complex pathophysiologic mechanisms and a variety of underlying diseases. OBJECTIVE: To implement a feasible pathway of central diagnostic and therapeutic steps in the setting of an ED. METHODS: We conducted a narrative review of the literature, considering current practice guidelines on diagnosis and treatment of hyponatremia. Underlying pathophysiologic mechanisms and management of adverse treatment effects are outlined. We also report four cases observed in our ED. RESULTS: Symptoms associated with hyponatremia may appear unspecific and range from mild cognitive deficits to seizures and coma. The severity of hyponatremia-induced neurological manifestation and the risk of poor outcome is mainly driven by the rapidity of serum sodium decrease. Therefore, emergency treatment of hyponatremia should be guided by symptom severity and the assumed onset of hyponatremia development, distinguishing acute (<48 hours) versus chronic hyponatremia (>48 hours). CONCLUSIONS: Especially in moderately or severely symptomatic patients presenting to an ED, the application of a standard management approach appears to be critical to improve overall outcome. Furthermore, an adequate work-up in the ED enables further diagnostic and therapeutic evaluation during hospitalization.

Effects of hypernatremia on the microglia.

Signs and symptoms of hypernatremia largely indicate central nervous system dysfunction. Acute hypernatremia can cause demyelinating lesions similar to that observed in osmotic demyelination syndrome (ODS). We have previously demonstrated that microglia accumulate in ODS lesions and minocycline protects against ODS by inhibiting microglial activation. However, the direct effect of rapid rise in the sodium concentrations on microglia is largely unknown. In addition, the effect of chronic hypernatremia on microglia also remains elusive. Here, we investigated the effects of acute (6 or 24 h) and chronic (the extracellular sodium concentration was increased gradually for at least 7 days) high sodium concentrations on microglia using the microglial cell line, BV-2. We found that both acute and chronic high sodium concentrations increase NOS2 expression and nitric oxide (NO) production. We also demonstrated that the expression of nuclear factor of activated T-cells-5 (NFAT5) is increased by high sodium concentrations. Furthermore, NFAT5 knockdown suppressed NOS2 expression and NO production. We also demonstrated that high sodium concentrations decreased intracellular Ca2+ concentration and an inhibitor of Na+/Ca2+ exchanger, NCX, suppressed a decrease in intracellular Ca2+ concentrations and NOS2 expression and NO production induced by high sodium concentrations. Furthermore, minocycline inhibited NOS2 expression and NO production induced by high sodium concentrations. These in vitro data suggest that microglial activity in response to high sodium concentrations is regulated by NFAT5 and Ca2+ efflux through NCX and is suppressed by minocycline.

A Case Report in the Management of Dysphagia in Osmotic Demyelination Syndrome Using Mann Assessment of Swallowing Ability (MASA).

Osmotic Demyelination Syndrome (ODS) is one of the primary cause of demyelination in alcoholics and malnourished resulting in various kind of clinical manifestations in pontine symptoms, neuro-behavioural symptoms movement disorders as well as speech and language and swallowing difficulties. The study was done to introspect the prognosis of swallowing therapy in a patient with ODS using MASA (Mann Assessment of Swallowing Ability). A 36 years old male with a history of regular alcohol intake and hypertensiom reported in our healthcare centre with hypoaklemia and speech, language and swallowing difficulty. Magnetic resonance imaging of the brain showed bilateral symmetrical T2 and T2 FLAIR (fluid attenuated inversion recovery) hyperintensity lesion in the bilateral basal ganglia involving the caudate nuclei, putaminal region and bilateral thalami with similar lesion along the mid brain. There were no areas of acute restriction in diffusion study. The findings suggested of Osmotic Demyelination Syndrome (ODS).When accessed with N-DAT, WAB and MASA; patient was diagnosed with Spastic Dysarthria, Transcortical Motor Aphasia and Moderate Dysphagia. Intervention was provided using speech and swallowing therapy and when introspected with MASA scores, improvement was seen within 5 days and statistically 97% of variance was seen inferring the progressing trend in the MASA scores. This study concludes that MASA can be an effective tool in introspecting the prognosis of Dysphagia in ODS and early intervention in the management of dysphasia shows positive results.

The Response of Osmotic Demyelination Syndrome to Plasmapheresis in a Patient Presenting with Catatonia after Correction of Hyponatraemia in Hyperemesis Gravidarum.

Osmotic demyelination syndrome (ODS) is a disorder characterised by the widespread development of demyelination in both pontine and extrapontine regions. It has been recognised as a complication arising from the rapid correction of hyponatraemia. This study presents the case of a 20-year-old Thai female patient at 10 weeks gestation, exhibiting an initial presentation of catatonia - an uncommon manifestation of ODS. The patient developed symptoms following the rapid correction of hyponatraemia in the context of hyperemesis gravidarum. Magnetic resonance imaging (MRI) of the brain revealed a trident or bat-wing-shaped pattern in T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences at the central pons. The patient underwent five cycles of plasmapheresis and received rehabilitation, leading to clinical improvement. LEARNING POINTS: Osmotic demyelination syndrome (ODS) is a rare but potentially devastating neurological complication, such as catatonia, resulting from the correction of hyponatraemia.Pregnancies complicated by hyperemesis gravidarum tend to exhibit hyponatraemia and hypokalaemia, which serve as contributing risk factors for ODS.Plasmapheresis is considered as an option in the treatment of ODS for the removal of inflammatory substances.

Hand knob sign in osmotic demyelinating syndrome.

BACKGROUND: Osmotic demyelinating syndrome, commonly recognized as a consequence of the rapid correction of hyponatremia, has been known to cause motor, neuropsychiatric, or extrapyramidal symptoms. We reported a patient with an unusual presentation involving bilateral hand weakness, and pseudobulbar affect. The imaging was compatible with osmotic demyelinating syndrome with bilateral hand knob lesions, despite no history of overcorrection of hyponatremia. CASE PRESENTATION: A 44-year-old female presented with three weeks of emotional lability, spastic dysarthria, and bilateral hand weakness following ankle surgery and a mild head injury. Physical examination revealed weakness in the intrinsic hand muscles, leading to a claw-like deformity of the hands, although sensation remained unimpaired. Magnetic resonance imaging (MRI) of the brain revealed several hyperintensities on fluid-attenuated inversion recovery imaging involving various areas, including the hand knob area of the bilateral precentral gyri, caudate, lentiform nuclei, and pons, suggestive of osmotic demyelinating syndrome. Clinical improvement was observed following a trial of intravenous pulse methylprednisolone and plasmapheresis. CONCLUSIONS: Bilateral hand weakness is an unusual manifestation of osmotic demyelinating syndrome. The precentral gyrus, specifically in the hand knob area, is the vulnerable region that can result from osmotic demyelinating syndrome.

Extra-pontine Myelinolysis After Rapid Correction of Hyponatremia Responding to Levodopa.

Osmotic demyelinating disease of the central nervous system has two variants: central pontine myelinolysis and extra-pontine myelinolysis (EPM). Up to 10% of cases of osmotic demyelination syndrome are associated with EPM, which mostly affects the thalamus and basal ganglia. It is commonly associated with the rapid correction of hyponatremia. An elderly woman in her 60s presented with complaints of acute gastroenteritis and giddiness and visited the emergency ward. On examination, she was conscious and oriented to time but disoriented to place and person and had slurring of speech with signs of dehydration. Her serum sodium levels were 100 meq/L, and her brain MRI was normal. After shifting her to the intensive care unit, she was treated with 200 ml of 3% NaCl bolus to correct her hyponatremia. On day three, she began developing rigidity in both lower limbs, which progressed to the upper limbs with hyperreflexia and mutism. A brain MRI was done, which showed subtle hyperintensities in the caudate lobe with no other new findings. Her serum aldosterone and cortisol were on the lower side of the normal range. Treatment of tablet levodopa-carbidopa (100/25) combination thrice a day (TDS) led to an improvement in her health condition.

[Consensus recommendations on the diagnosis and treatment of hyponatremia from the Austrian Society for Nephrology 2024]. / Konsensusempfehlungen zur Diagnose und Therapie der Hyponatriämie der Österreichischen Gesellschaft für Nephrologie 2024.

Hyponatremia is a disorder of water homeostasis. Water balance is maintained by the collaboration of renal function and cerebral structures, which regulate thirst mechanisms and secretion of the antidiuretic hormone. Measurement of serum-osmolality, urine osmolality and urine-sodium concentration help to diagnose the different reasons for hyponatremia. Hyponatremia induces cerebral edema and might lead to severe neurological symptoms, which need acute therapy. Also, mild forms of hyponatremia should be treated causally, or at least symptomatically. An inadequate fast increase of the serum sodium level should be avoided, because it raises the risk of cerebral osmotic demyelination. Basic pathophysiological knowledge is necessary to identify the different reasons for hyponatremia which need different therapeutic procedures.

A machine learning approach for predicting treatment response of hyponatremia.

Hyponatremia leads to severe central nervous system disorders and requires immediate treatment in some cases. However, a rapid increase in serum sodium (s-Na) concentration could cause osmotic demyelination syndrome. To achieve a safety hyponatremia treatment, we develop a prediction model of s-Na concentration using a machine learning. Among the 341 and 47 patients admitted to two tertiary hospitals for hyponatremia treatment (s-Na <130 mEq/L), those who were admitted to the general unit with urine sodium <20 mEq/L or treated with desmopressin were excluded. Ultimately, 74 and 15 patients (342 and 146 6-hourly datasets) were included in the learning and validation data, respectively. We trained the prediction model using three regression algorithms for shallow machine learning to predict s-Na every 6 h during treatment with the data of patients with hyponatremia (median s-Na: 112.5 mEq/L; range: 110.0-116.8 mEq/L) from one hospital. The model was validated externally using the data of patients with hyponatremia (median s-Na: 117.0 mEq/L; range: 112.9-120.0 mEq/L) from another hospital. Using 5-7 predictors (water intake, sodium intake, potassium intake, urine volume, s-Na concentration, serum potassium concentration, serum chloride concentration), the support vector regression model showed the best performance overall (root mean square error = 0.05396; R2 = 0.92), followed by the linear regression and regression tree models. The predicted s-Na levels, using explainable machine learning algorithms and clinically accessible parameters, correlated well with the actual levels. Thus, our model could be applied to the treatment of hyponatremia in clinical practice.

Experience of Rehabilitation Treatment for Osmotic Demyelination Syndrome with Locked-in Syndrome / The Japanese Journal of Rehabilitation Medicine

Osmotic demyelination syndrome is a pathological condition that leads to electrolyte imbalances and rapid correction, resulting in pseudobulbar palsy, quadriplegia, and altered consciousness. Approximately 33-55％ of affected patients experience residual functional impairment. Herein, we describe a case of a patient with osmotic demyelination syndrome who developed locked-in syndrome during the disease course, underwent rehabilitation treatment, and achieved complete remission without sequelae.The patient was a 47-year-old man who was admitted to hospital A owing to weakness in the lower extremities and dysarthria. He had severe hyponatremia and received sodium correction. However, on hospital day 9, dysarthria redeveloped and involuntary finger movements were noted. Osmotic demyelination syndrome was suspected based on the findings of magnetic resonance imaging of the head and clinical course, leading to his transfer to hospital B. Steroid pulse and rehabilitation therapies were initiated at hospital B. By the 19th day of symptom onset, his limb and facial muscle paralysis progressed, leading to locked-in syndrome. Thereafter, the patient was transferred to hospital C, where he received physiotherapy, occupational therapy, and eating training, markedly improving his physical functions. He was discharged from hospital C, 4 months after the symptom onset, with limited range of motion of the fingers and weakness of the extremities and continued to receive outpatient rehabilitation treatment. His symptoms improved further, and 1 year after the onset of symptoms, he returned to work without any sequelae.

Osmotic Demyelination Syndrome in a High-Risk Patient Despite Cautious Correction of Hyponatremia.

Hyponatremia is a common electrolyte disorder requiring careful management to prevent severe complications. Osmotic demyelination syndrome (ODS) is a serious neurological disorder that can develop from rapid correction of hyponatremia. Herein, is a description of the case of a 61-year-old man with multiple risk factors, including alcoholism, hypokalemia, malnutrition, and alcoholic liver cirrhosis, who developed ODS despite adherence to the recommended correction rate for hyponatremia. The patient presented to the emergency department with generalized weakness, gait disturbance, and decreased muscle strength. Initial laboratory investigations revealed severe hyponatremia, hypokalemia, and dehydration. The patient was treated with cautious correction of the hyponatremia below 8 mmol/L per day. However, on the seventh hospital day, he developed tremors, rigidity, and decreased consciousness and was diagnosed with osmotic demyelination syndrome. Despite receiving general supportive care, desmopressin, and dextrose 5% in water to reduce the serum sodium levels, the patient did not show significant improvement and was transferred to a nursing home for long-term conservative care on day 35 of hospitalization. This case report highlights the challenges associated with the diagnosis and management of osmotic demyelination syndrome and the importance of identifying patients at high risk of developing this neurological disorder.

Osmotic Demyelination Syndrome: A Rare Clinical Image.

The term "Osmotic Demyelination Syndrome" (ODS) is synonymous with central pontine myelinolysis (CPM), denoting a condition characterised by brain damage, particularly affecting the white matter tracts of the pontine region. This damage arises due to the rapid correction of metabolic imbalances, primarily cases of hyponatremia. Noteworthy triggers encompass severe burns, liver transplantations, anorexia nervosa, hyperemesis gravidarum, and hyperglycaemia, all linked to the development of CPM. Clinical manifestations encompass a spectrum of signs and symptoms, including dysphagia, dysarthria, spastic quadriparesis, pseudobulbar paralysis, ataxia, lethargy, tremors, disorientation, catatonia, and, in severe instances, locked-in syndrome and coma. A recent case involving a 45-year-old woman illustrates these complexities. Upon admission to the Medicine Intensive Care Unit, she presented with symptoms indicative of diminished responsiveness and bilateral weakness in the upper and lower limbs. Of significance, the patient had a pre-existing medical history of hyperthyroidism. Extensive diagnostic investigations were undertaken, revealing compelling evidence of profound hyponatremia through blood analyses. Furthermore, magnetic resonance imaging (MRI) was performed, unveiling conspicuous areas of abnormal hyperintensity located in the central pons, intriguingly accompanied by spared peripheral regions. These radiological findings align with the characteristic pattern associated with osmotic demyelination syndrome, illuminating the underlying pathology.

Thalamic Neuron Resilience during Osmotic Demyelination Syndrome (ODS) Is Revealed by Primary Cilium Outgrowth and ADP-ribosylation factor-like protein 13B Labeling in Axon Initial Segment.

A murine osmotic demyelinating syndrome (ODS) model was developed through chronic hyponatremia, induced by desmopressin subcutaneous implants, followed by precipitous sodium restoration. The thalamic ventral posterolateral (VPL) and ventral posteromedial (VPM) relay nuclei were the most demyelinated regions where neuroglial damage could be evidenced without immune response. This report showed that following chronic hyponatremia, 12 h and 48 h time lapses after rebalancing osmolarity, amid the ODS-degraded outskirts, some resilient neuronal cell bodies built up primary cilium and axon hillock regions that extended into axon initial segments (AIS) where ADP-ribosylation factor-like protein 13B (ARL13B)-immunolabeled rod-like shape content was revealed. These AIS-labeled shaft lengths appeared proportional with the distance of neuronal cell bodies away from the ODS damaged epicenter and time lapses after correction of hyponatremia. Fine structure examination verified these neuron abundant transcriptions and translation regions marked by the ARL13B labeling associated with cell neurotubules and their complex cytoskeletal macromolecular architecture. This necessitated energetic transport to organize and restore those AIS away from the damaged ODS core demyelinated zone in the murine model. These labeled structures could substantiate how thalamic neuron resilience occurred as possible steps of a healing course out of ODS.

Central pontine myelinolysis: a rare finding in hyperosmolar hyperglycemia.

Central pontine myelinolysis (CPM) is a heterogeneous nervous system disease of pontine demyelination, usually caused by rapid correction of hyponatremia. In the present study, we report a unique case of a 46-year-old man with a hyperglycemic state complicated with CPM. MRI demonstrated a high signal on T2 and symmetric restricted diffusion in the pontine. In conclusion, the clinical case described confirmed that the hyperosmolar state inherent in hyperglycemia was a likely cause of CPM.

Osmotic Demyelination Syndrome in a Normonatremic Patient Under Treatment With Proton Pump Inhibitors.

A 66-year-old woman was admitted to the emergency department with diarrhea, nausea, and vomiting as well as low-grade fever. She was initially treated with ciprofloxacin and metronidazole with symptomatic improvement and was discharged. One week later, she returned to the emergency department for gait instability, dizziness, and vomiting and had a witnessed generalized tonic-clonic seizure in the hospital. During both admissions, the presence of ionic alterations such as severe hypomagnesemia, hypophosphatemia, and hypokalemia stood out, while sodium levels remained normal. Among her antecedents, she had a hiatal hernia and had been receiving treatment with omeprazole for years.

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.

Osmotic Demyelination Syndrome in a Patient with Diabetic Ketoacidosis Despite No Rapid Sodium Correction.

Osmotic demyelination syndrome (ODS) occurs in patients with diabetes and hyponatremia. We herein report a case of ODS with chorea detected on serial magnetic resonance imaging (MRI), despite no prompt hyponatremia correction. A 74-year-old man with cirrhosis and uncontrolled type 2 diabetes developed an altered mental status and chorea during treatment for diabetic ketoacidosis (DKA). Despite no rapid sodium correction and normal initial brain MRI findings, serial MRI revealed ODS-related abnormalities. Clinicians should consider ODS in patients with DKA and a hyperosmolar hyperglycemic state displaying unconsciousness and neurological manifestations, including chorea, even without substantial changes in serum sodium levels. An MRI re-examination can help capture missing ODS complications.