SAT-596 - An Underrecognized Complication of Hyperosmolar Hyperglycemic State: Central Pontine Myelinolysis without Sodium Overcorrection

Osmotic demyelination syndrome (ODS), particularly central pontine myelinolysis (CPM), is classically associated with rapid correction of chronic hyponatremia. However, emerging evidence suggests that severe hyperosmolar states may independently precipitate demyelination, even in the absence of rapid sodium shifts.
A 53-year-old woman with insulin-dependent type 2 diabetes mellitus, hypertension, hyperlipidemia, and stage IV chronic kidney disease presented with nausea, vomiting, hyperglycemia, and acute bilateral lower extremity weakness in the setting of insulin noncompliance. Laboratory evaluation was consistent with hyperosmolar hyperglycemic state (HHS), with a serum glucose of 687 mg/dL, an anion gap of 16, venous pH of 7.26, bicarbonate of 21 mmol/L, lactate of 2.5 mmol/L, and normal beta-hydroxybutyrate levels. The serum sodium level was 129 mmol/L. She was treated with a brief insulin infusion and transitioned to subcutaneous insulin.
Neurologic evaluation revealed profound proximal lower extremity weakness with preserved distal strength, marked sensory deficits involving proprioception, temperature, and vibration, mild right ankle clonus, and a crossed adductor reflex, consistent with upper motor neuron involvement. Upper extremity strength and reflexes were intact. Initial differential diagnoses included transverse myelitis, Valsalva-associated spinal cord injury, and central nervous system infection. Computed tomography of the brain was unremarkable. Magnetic resonance imaging of the brain and spine demonstrated T2- and FLAIR-hyperintensity within the pons, consistent with central pontine myelinolysis. The patient underwent lumbar puncture, and cerebrospinal fluid analysis was unremarkable, making infectious or inflammatory etiologies unlikely.
This case illustrates the development of CPM as a complication of HHS in the absence of rapid sodium correction. Severe hyperosmolarity itself may disrupt the blood–brain barrier and contribute to oligodendrocyte injury, highlighting an underrecognized mechanism of ODS in uncontrolled diabetes.
CPM is a rare but potentially devastating complication of HHS, even without rapid serum sodium shifts. Deficits may be long-lasting or permanent, and any recovery, if it occurs, is typically slow and unpredictable. Clinicians should maintain a high index of suspicion for ODS in patients with poorly controlled diabetes who develop acute neurologic deficits. Early recognition and prompt management of hyperosmolar states are critical to reducing the risk of permanent neurologic injury.

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