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.
Chlorpropamide-Induced ADH Release, Hyponatremia and Central Pontine Myelinolysis in Diabetes Mellitus.
