Central Pontine Myelinolysis in a Patient with Hyperosmolar Hyperglycemia and Consistently Normal Serum Sodium

Burns, Joseph D.; Kosa, Steven C.; Wijdicks, Eelco F. M.

doi:10.1007/s12028-009-9241-9

Cited by 53 publications

(49 citation statements)

References 8 publications

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“…Also inherent to this physiology is the understanding that plasma osmolality is more than just sodium and BUN and includes glucose. In a prior publication in this journal, a case of hyperglycemia (relative hypertonic insult) with rapid correction led to central pontine myelinolysis (CPM) [9].…”

mentioning

confidence: 99%

A Brain–Kidney Connection: The Delicate Interplay of Brain and Kidney Physiology

Freeman

Wadei

2015

Neurocrit Care

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mentioning

confidence: 99%

A Brain–Kidney Connection: The Delicate Interplay of Brain and Kidney Physiology

Freeman

Wadei

2015

Neurocrit Care

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“…Hyperglycemia and osmolality were corrected within 24 hours and 2 days after presentation he developed marked gait ataxia and mild dysarthria. MRI confirmed the diagnosis of ODS and at 1-month follow-up showed marked improvement in his gait unsteadiness 18 . More recently, Mao et al reported the case of a 55-year-old man who had a history of multiple focal seizures 3 weeks before hospitalization.…”

Section: Discussionmentioning

confidence: 67%

“…In all cases a growing body of evidence demonstrates that more than sodium per se, the key factor, in ODS pathogenesis, is a rapid change in serum osmoles. The association of ODS with hyperosmolar hyperglycemic state (HHS) has been seldom reported with less than five cases in the literature [16][17][18][19][20] . Previous cases have been in the clinical scenario of concomitant hypernatremia, chronic hyperglycemia/epilepsy, and after HHS treatment.…”

Section: Introductionmentioning

confidence: 99%

Osmotic Demyelination Syndrome Occurs Early in The Course of Hyperosmolar Hyperglycemic State.

Das¹,

A.S²,

Mossang³

et al. 2017

IOSR JDMS

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Osmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome. The association of ODS with hyperosmolar hyperglycaemic state (HHS) has been seldom reported. The aim of this study was to show that Osmotic Demyelination Syndrome occurs early in the course of Hyperosmolar I. BackgroundOsmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome, which usually occurs in the setting of a rapid correction of severe chronic hyponatremia 1,2 .ODS is a clinical syndrome characterized by altered mental status, quadriparesis, dyspnoea, dysarthria, and dysphagia which all occur characteristically five to seven days after the correction of serum sodium 3 . The pathogenesis is still to be clearly understood, it is known that rapidly increasing serum osmolality shifts water out of the cells as a response to correct solute imbalance resulting in shrinkage of glial cells that can consequently lead to disruption of the blood-brain barrier allowing inflammatory mediators to enter the central nervous system damaging oligodendrocytes and myelin 4-7 . Even though ODS has been classically thought to be exclusively secondary to a rapid correction of hyponatremia, it has also been described, even though rarely, in various other situations such as malnutrition, liver transplantation, alcoholism, hypokalemia, hypophosphatemia, AIDS, lithium toxicity, hypoglycemia, and folate deficiency, among others [8][9][10][11][12][13][14][15] . In all cases a growing body of evidence demonstrates that more than sodium per se, the key factor, in ODS pathogenesis, is a rapid change in serum osmoles. The association of ODS with hyperosmolar hyperglycemic state (HHS) has been seldom reported with less than five cases in the literature [16][17][18][19][20] . Previous cases have been in the clinical scenario of concomitant hypernatremia, chronic hyperglycemia/epilepsy, and after HHS treatment.Herein we present the case of a patient with HHS who presented with ODS early in the course of her illness. A review of previous cases and pathophysiological mechanisms involved in ODS secondary to HHS will be presented and discussed. Case PresentationA 45 year old female with poorly controlled Type2 Diabetes Mellitus came to the emergency room due to loss of consciousness. She was a known case of Type2 Diabetes Mellitus on Tab.Glipizide 5mg and Metformin 500mg for 10years and long acting Isophane Insulin(30:70) for 5years and she was a known Hypertensive on Tab Amlodipine 5mg for 5 years. She had irregular Medication.On Physical examination, her BP was 100/60 mmHg. Heart rate was 140/min and SpO 2 was 90% in Room air. Her BMI was 27.2. Mucus membranes were dry. ECG showed Right Axis Deviation. She had a Glasgow Coma Scale of 3/15 and muscle power was 0/5 in all the limbs and plantars were flexor B/L.There was no neck rigidity. Blood Glucose levels were 600mg%. Plasma and urinary ketones were negetive. ABG analysis showed pH 7.31. HbA1C was 14.1%, Serum Calcium 7.9mg/dL. Serum creatinine was 4.5mg/dL. Her eGFR

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“…There are a number of previous case reports of neurological sequelae resulting from rapid glucose correction in HHS. [6][7][8][9] Joint British Diabetes Societies (JBDS) guidelines on management of DKA These guidelines were published in 2010, and present a new paradigm for the diagnosis and management of DKA in the UK. 10 Diagnostic criteria for DKA remained unchanged (plasma glucose >11 mmol/l, ketonaemia >3 mmol/l, acidosis [bicarbonate<15 mmol/l] and/or pH <7.3).…”

Section: Discussionmentioning

confidence: 99%

Managing hyperglycaemic emergencies: an illustrative case and review of recent British guidelines

Gouveia

Chowdhury

2013

Clinical Medicine

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-Diabetic ketoacidosis and hyperosmolar hyperglycaemic syndrome are important hyperglycaemic emergencies seen in patients with diabetes. Occasionally, differentiation between the two conditions can be difficult. We present the case of a patient whose hyperglycaemic emergency was managed in a way that could have adversely influenced the outcome. We also discuss important aspects of the new Joint British Diabetes Societies Guidelines on the management of hyperglycaemic emergencies.

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Central Pontine Myelinolysis in a Patient with Hyperosmolar Hyperglycemia and Consistently Normal Serum Sodium

Cited by 53 publications

References 8 publications

A Brain–Kidney Connection: The Delicate Interplay of Brain and Kidney Physiology

A Brain–Kidney Connection: The Delicate Interplay of Brain and Kidney Physiology

Osmotic Demyelination Syndrome Occurs Early in The Course of Hyperosmolar Hyperglycemic State.

Managing hyperglycaemic emergencies: an illustrative case and review of recent British guidelines

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