One Too Many: Severe Hyponatremia

1University of Kansas Medical Center, Kansas City, KS

Meeting: Hospital Medicine 2011, May 10-13, Dallas, Texas.

Abstract number: 277

Case Presentation:

A 57‐year‐old man was “found down” at home. The patient reported seizures for 2 days. He denied chronic medical conditions including history of seizures. He reported drinking a case of beer daily. Physical exam was remarkable for confusion and visual hallucinations. Labs included: sodium 102 mmol/L, creatinine 0.6 mg/dL, creatine kinase 4948 U/L, alcohol 6 mg/dL, AST 187 U/L, ALT 96 U/L, lactic acid 2.4 mmol/L, serum osmolality 219 mOsm/kg, urine sodium < 10 mmol/L. Initially, he was treated with normal saline for rhabdomyolysis and hyponatremia. Frequent labs showed sodium 106 mmol/L at 10 hours, 110 mmol/L at 16 hours. After 21 hours, sodium was 111, and intravenous fluids were changed to lactated Ringer's solution. After 26 hours of treatment, sodium was 119 mmol/L. Sodium increased to the mid‐120s over the next 1–2 days. On day 6 of hospitalization, he developed acute dysphagia, dysarthria, and left‐sided weakness. CT of the head, CT arteriogram, and electroencephalogram were unremarkable. MRI showed mild pontine changes. Repeat MRI on day 21 of hospitalization showed changes consistent with osmotic demyelination syndrome in the pons, thalamus, basal ganglia, and external capsule.


Hyponatremia has myriad causes and is frequently encountered by the hospitalist. Severe hyponatremia can cause significant neurologic symptoms including cerebral edema and seizures. Caution must be taken in treating hyponatremia, as rapid correction can cause osmotic demyelination syndrome. Goal rates for correcting sodium are 10–12 mmol/L in 24 hours and 18 mmol/L in 48 hours. Antidiuretic hormone (ADH) can play an important role in hyponatremia. ADH levels can be increased because of inappropriate release, medications, or volume depletion. As ADH decreases due to correction of the underlying cause, the collecting tubules of the kidney become less permeable to water, and urine becomes more dilute. This can lead to a more rapid increase in sodium than anticipated. Osmotic demyelination syndrome occurs 2–6 days after correction of sodium, and symptoms include dysarthria, paresis, behavioral changes, and coma. Reversibility of these symptoms is variable. Additional risk factors for developing osmotic demyelination syndrome include hypokalemia, liver failure, and malnutrition. Radiographic changes may not be apparent for up to 4 weeks after onset of symptoms.

FIGURE . This MRI image shows central pontine demyelination with sparing of the periphery.


The purpose of this vignette is to present an extreme case of a common medical problem seen by hospitalists and to highlight the features of its treatment as well as features of osmotic demyelination syndrome.


S. Folscroft ‐ none

To cite this abstract:

Folscroft S. One Too Many: Severe Hyponatremia. Abstract published at Hospital Medicine 2011, May 10-13, Dallas, Texas. Abstract 277. Journal of Hospital Medicine. 2011; 6 (suppl 2). Accessed September 20, 2019.

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