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      Excessive Sodium Bicarbonate Infusion May Result in Osmotic Demyelination Syndrome During Treatment of Diabetic Ketoacidosis: A Case Report

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          Abstract

          Introduction

          We present a case wherein diabetic ketoacidosis (DKA) was treated with a large amount of sodium bicarbonate and potassium chloride, resulting in the development of osmotic demyelination syndrome (ODS).

          Case presentation

          Our patient was a 29-year-old male with a history of post-surgical repair for ventricular septal defect. Upon arrival, the patient’s Glasgow Coma Scale (GCS) score was E2M4V3. Laboratory examinations revealed leukocytosis, severe metabolic acidosis, hypokalemia, and hyperglycemia. His consciousness status and hemodynamics improved after resuscitation (GCS: E3M6Ve). However, they declined at the 40th hour of admission and dropped to GCS E2M2Ve. Magnetic resonance imaging revealed multifocal abnormal signal intensity changes in the whole brain stem. The diagnosis of type 1 diabetes mellitus was made during the hospitalization period. The patient exhibited improved consciousness status after 17-day medical care at the ICU.

          Conclusions

          We recommend that in the case of DKA, the correction of hypokalemia should be prioritized during treatment. Sodium bicarbonate infusion should be reserved for pH < 6.9. In addition, close monitoring of the serum sodium level and prompt actions to lower it if it exceeds the threshold may be necessary.

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          Most cited references15

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          Risk factors for cerebral edema in children with diabetic ketoacidosis. The Pediatric Emergency Medicine Collaborative Research Committee of the American Academy of Pediatrics.

          Cerebral edema is an uncommon but devastating complication of diabetic ketoacidosis in children. Risk factors for this complication have not been clearly defined. In this multicenter study, we identified 61 children who had been hospitalized for diabetic ketoacidosis within a 15-year period and in whom cerebral edema had developed. Two additional groups of children with diabetic ketoacidosis but without cerebral edema were also identified: 181 randomly selected children and 174 children matched to those in the cerebral-edema group with respect to age at presentation, onset of diabetes (established vs. newly diagnosed disease), initial serum glucose concentration, and initial venous pH. Using logistic regression we compared the three groups with respect to demographic characteristics and biochemical variables at presentation and compared the matched groups with respect to therapeutic interventions and changes in biochemical values during treatment. A comparison of the children in the cerebral-edema group with those in the random control group showed that cerebral edema was significantly associated with lower initial partial pressures of arterial carbon dioxide (relative risk of cerebral edema for each decrease of 7.8 mm Hg [representing 1 SD], 3.4; 95 percent confidence interval, 1.9 to 6.3; P<0.001) and higher initial serum urea nitrogen concentrations (relative risk of cerebral edema for each increase of 9 mg per deciliter [3.2 mmol per liter] [representing 1 SD], 1.7; 95 percent confidence interval, 1.2 to 2.5; P=0.003). A comparison of the children with cerebral edema with those in the matched control group also showed that cerebral edema was associated with lower partial pressures of arterial carbon dioxide and higher serum urea nitrogen concentrations. Of the therapeutic variables, only treatment with bicarbonate was associated with cerebral edema, after adjustment for other covariates (relative risk, 4.2; 95 percent confidence interval, 1.5 to 12.1; P=0.008). Children with diabetic ketoacidosis who have low partial pressures of arterial carbon dioxide and high serum urea nitrogen concentrations at presentation and who are treated with bicarbonate are at increased risk for cerebral edema.
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            Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patients.

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              Osmotic demyelination syndrome.

              The osmotic demyelination syndrome (ODS) has been a recognized complication of the rapid correction of hyponatremia for decades. However, in recent years, a variety of other medical conditions have been associated with the development of ODS, independent of changes in serum sodium. This finding suggests that the pathogenesis of ODS may be more complex and involve the inability of brain cells to respond to rapid changes in osmolality of the interstitial (extracellular) compartment of the brain, leading to dehydration of energy-depleted cells with subsequent axonal damage that occurs in characteristic areas. Features of the syndrome include quadriparesis and neurocognitive changes in the presence of characteristic lesions found on magnetic resonance imaging of the brain. Although slow correction of hyponatremia seems to be the best way to prevent development of the syndrome, there are new data that suggest reintroduction of hyponatremia in those patients who have undergone inadvertent rapid correction of the serum sodium and corticosteroids may play a role in prevention of ODS.
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                Author and article information

                Contributors
                garykou@gmail.com
                Journal
                Diabetes Ther
                Diabetes Ther
                Diabetes Therapy
                Springer Healthcare (Cheshire )
                1869-6953
                1869-6961
                6 March 2019
                6 March 2019
                April 2019
                : 10
                : 2
                : 765-771
                Affiliations
                [1 ]ISNI 0000 0004 0572 7372, GRID grid.413814.b, Division of Critical Care, Department of Internal Medicine, , Changhua Christian Hospital, ; Changhua, Taiwan
                [2 ]ISNI 0000 0004 0572 7372, GRID grid.413814.b, Department of Neurology, , Changhua Christian Hospital, ; Changhua, Taiwan
                [3 ]ISNI 0000 0004 0572 7372, GRID grid.413814.b, Division of Nephrology, Department of Internal Medicine, , Changhua Christian Hospital, ; Changhua, Taiwan
                Article
                592
                10.1007/s13300-019-0592-8
                6437239
                30843157
                fe5b4def-e01d-470e-be19-0a5496862539
                © The Author(s) 2019
                History
                : 28 January 2019
                Categories
                Case Report
                Custom metadata
                © The Author(s) 2019

                Endocrinology & Diabetes
                case report,diabetic ketoacidosis,hypernatremia,osmotic demyelination syndrome,sodium bicarbonate

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