scholarly journals A Rare Case of Central Pontine Myelinolysis in Overcorrection of Hyponatremia with Total Parenteral Nutrition in Pregnancy

2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
Kalyana C. Janga ◽  
Tazleem Khan ◽  
Ciril Khorolsky ◽  
Sheldon Greenberg ◽  
Priscilla Persaud
Keyword(s):  
Parenteral Nutrition ◽  
Total Parenteral Nutrition ◽  
Serum Sodium ◽  
Rare Case ◽  
Central Pontine Myelinolysis ◽  
Graph Representation ◽  
Radiological Findings ◽  
Complicated Case ◽  
Pontine Myelinolysis ◽  
Central Pontine

A 42-year-old high risk pregnant female presented with hyponatremia from multiple causes and was treated with total parenteral nutrition. She developed acute hypernatremia due to the stage of pregnancy and other comorbidities. All the mechanisms of hyponatremia and hypernatremia were summarized here in our case report. This case has picture (graph) representation of parameters that led to changes in serum sodium and radiological findings of central pontine myelinolysis on MRI. In conclusion we present a complicated case serum sodium changes during pregnancy and pathophysiological effects on serum sodium changes during pregnancy.

scholarly journals A Case of Central Pontine Myelinolysis Caused by Hypophosphatemia Secondary to Refeeding Syndrome

2015 ◽  
Vol 7 (3) ◽  
pp. 196-203 ◽  
Author(s):  
Chikara Yamashita ◽  
Hiroshi Shigeto ◽  
Norihisa Maeda ◽  
Takako Torii ◽  
Yasumasa Ohyagi ◽  
...  
Keyword(s):  
Serum Sodium ◽  
Central Pontine Myelinolysis ◽  
Rapid Change ◽  
Serum Biochemistry ◽  
Refeeding Syndrome ◽  
Pontine Myelinolysis ◽  
History Of ◽  
Biochemistry Test ◽  
Magnetic Resonance Imaging Mri ◽  
Central Pontine

Central pontine myelinolysis (CPM), which was originally considered to be the result of rapid correction of chronic hyponatremia, is not necessarily accompanied by hyponatremia or drastic changes in serum sodium level. Here, we report a case of an anorexic 55-year-old male with a history of pharyngo-laryngo-esophagogastrectomy, initially hospitalized with status epilepticus. Although his consciousness gradually recovered as we were controlling his convulsion, it deteriorated again with new onset of anisocoria, and magnetic resonance imaging (MRI) at this point revealed CPM. Rapid change of serum sodium or osmolarity, which is often associated with CPM, had not been apparent throughout his hospitalization. Instead, a review of the serum biochemistry test results showed that serum phosphate had drastically declined the day before the MRI first detected CPM. In this case, we suspect that hypophosphatemia induced by refeeding syndrome greatly contributed to the occurrence of CPM.

scholarly journals Relowering of Serum Na for Osmotic Demyelinating Syndrome

2012 ◽  
Vol 2012 ◽  
pp. 1-2 ◽  
Author(s):  
Hideomi Yamada ◽  
Koji Takano ◽  
Nobuhiro Ayuzawa ◽  
George Seki ◽  
Toshiro Fujita
Keyword(s):  
Serum Sodium ◽  
Central Pontine Myelinolysis ◽  
Supportive Therapy ◽  
Chronic Hyponatremia ◽  
Pontine Myelinolysis ◽  
Extreme Care ◽  
The Brain ◽  
Osmotic Demyelinating Syndrome ◽  
Central Pontine ◽  
Rapid Correction

We report a case in whom slow correction of hyponatremia (5 mmol/day for 3 days) induced central pontine myelinolysis (CPM). After the diagnosis was confirmed by imaging, we started to relower serum Na that completely recovered the sign and symptoms of CPM. Rapid correction of serum sodium is known to be associated with CPM. However, it may occur even after slow correction of hyponatremia. Currently, there is no standard therapy for CPM other than supportive therapy. Other therapy includes sterioid, plasmaphresis and IVIG, but these therapies have not been shown to be particularly effective. The pathophysiology of CPM is related to a relative dehydration of the brain during the correction of hyponatremia, resulting in cell death and demyelination, therefore gentle rehydration with lowering serum sodium may not be an unreasonable therapy. The present case provides supportive evidence that reinduction of hyponatremia is effective in treating CPM if started immediately after the diagnosis is suggested. The present case tells us that severe chronic hyponatremia must be managed with extreme care especially in patients with chronic debilitating illness and that relowering serum Na is a treatment of choice when CPM is suggested.

A Misleading Case of Central Pontine Myelinolysis

1992 ◽  
Vol 160 (4) ◽  
pp. 550-552 ◽  
Author(s):  
Peter McColl ◽  
Christopher Kelly
Keyword(s):  
British Journal ◽  
Schizophrenic Patient ◽  
Serum Sodium ◽  
Psychiatric Patients ◽  
Central Pontine Myelinolysis ◽  
Review Of The Literature ◽  
Psychiatric Referral ◽  
Chronic Schizophrenic Patient ◽  
Pontine Myelinolysis ◽  
Central Pontine

Central pontine myelinolysis (CPM) is an uncommon disorder initially described in alcoholic or malnourished patients. Recent reports suggest an aetiological association with abnormalities of serum sodium. A physically unwell non-alcoholic chronic schizophrenic patient, whose symptoms led to psychiatric referral, died of CPM. A review of the literature reveals that psychiatric patients may indeed be at risk for CPM.British Journal of Psychiatry (1992), 160, 550–552

Association between rise in serum sodium and central pontine myelinolysis

1982 ◽  
Vol 11 (2) ◽  
pp. 128-135 ◽  
Author(s):  
Michael D. Norenberg ◽  
Kevin O. Leslie ◽  
Andrew S. Robertson
Keyword(s):  
Serum Sodium ◽  
Central Pontine Myelinolysis ◽  
Pontine Myelinolysis ◽  
Central Pontine

scholarly journals Severe hypokalaemia in diabetic ketoacidosis: a contributor to central pontine myelinolysis?

2019 ◽  
Vol 2019 ◽  
Author(s):  
A Chinoy ◽  
N B Wright ◽  
M Bone ◽  
R Padidela
Keyword(s):  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Serum Sodium ◽  
Management Strategies ◽  
Central Pontine Myelinolysis ◽  
Central Line ◽  
List Type ◽  
Pontine Myelinolysis ◽  
Central Pontine

Summary Hypokalaemia at presentation of diabetic ketoacidosis is uncommon as insulin deficiency and metabolic acidosis shifts potassium extracellularly. However, hypokalaemia is a recognised complication of the management of diabetic ketoacidosis as insulin administration and correction of metabolic acidosis shifts potassium intracellularly. We describe the case of a 9-year-old girl with newly diagnosed type 1 diabetes mellitus presenting in diabetic ketoacidosis, with severe hypokalaemia at presentation due to severe and prolonged emesis. After commencing management for her diabetic ketoacidosis, her serum sodium and osmolality increased rapidly. However, despite maximal potassium concentrations running through peripheral access, and multiple intravenous potassium ‘corrections’, her hypokalaemia persisted. Seventy two hours after presentation, she became drowsy and confused, with imaging demonstrating central pontine myelinolysis – a rare entity seldom seen in diabetic ketoacidosis management in children despite rapid shifts in serum sodium and osmolality. We review the literature associating central pontine myelinolysis with hypokalaemia and hypothesise as to how the hypokalaemia may have contributed to the development of central pontine myelinolysis. We also recommend an approach to the management of a child in diabetic ketoacidosis with hypokalaemia at presentation. Learning points: Hypokalaemia is a recognised complication of treatment of paediatric diabetic ketoacidosis that should be aggressively managed to prevent acute complications. Central pontine myelinolysis is rare in children, and usually observed in the presence of rapid correction of hyponatraemia. However, there is observational evidence of an association between hypokalaemia and central pontine myelinolysis, potentially by priming the endothelial cell membrane to injury by lesser fluctuations in osmotic pressure. Consider central pontine myelinolysis as a complication of the management of paediatric diabetic ketoacidosis in the presence of relevant symptoms with profound hypokalaemia and/or fluctuations in serum sodium levels. We have suggested an approach to the management strategies of hypokalaemia in paediatric diabetic ketoacidosis which includes oral potassium supplements if tolerated, minimising the duration and the rate of insulin infusion and increasing the concentration of potassium intravenously (via central line if necessary).

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

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A375-A375
Author(s):  
Sri Mandava ◽  
Lucas Pfeifer ◽  
Gretel D’Souza ◽  
Mark Wilson
Keyword(s):  
Diabetes Mellitus ◽  
Peritoneal Dialysis ◽  
Serum Sodium ◽  
Central Pontine Myelinolysis ◽  
Rare Event ◽  
Lower Extremities ◽  
Muscle Rigidity ◽  
Osmotic Demyelination ◽  
Pontine Myelinolysis ◽  
Central Pontine

Abstract 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.

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