section name header

Info


A. Hyponatremic Encephalopathy navigator

  1. Early
    1. Anorexia
    2. Headache
    3. Nausea
    4. Vomiting
    5. Myalgias and Muscle Cramps
    6. Weakness
  2. Moderate to Advanced
    1. Impaired verbal and pain responses
    2. Inappropriate behavior
    3. CNS Depression / Lethargy
    4. Confusion
    5. Asterixis
    6. Obtundation
    7. Incontinence (urinary or fecal)
  3. Advanced and Progressive
    1. Decorticate and/or decerebrate posturing
    2. Respiratory center depression / respiratory arrest
    3. Bradycardia
    4. Autonomic dysfunction (hypotension, hypertension, abnormal thermoregulation)
    5. Seizures
    6. Coma
    7. Death

B. Pathogenesis of Neurologic Changes with Hyponatremianavigator

  1. Nerve cell dysfunction caused by abnormal sodium currents in setting of hyponatremia
  2. Decrease in extracellular sodium (osmotic strength) leads to cell swelling and edema
  3. This cerebral edema leads to CNS depression and can cause coma and death
  4. Development of symptoms and signs is related to rapidity of developing hyponatremia
  5. Symptoms generally occur in all patients with sodium < 125mM

C. Syndrome of Osmotic Demyelination [1,2,3,4]navigator

  1. Non-inflammatory destruction of myelin in central nervous system
    1. Most commonly affects the pons (bilaterally) and all pontine nerve tracts
    2. Extrapontine involvement is fairly common
    3. Related to rapid correction of hyponatremia
    4. Rapid correction leads to brain dehydration and intramyelinic edema
  2. Recommended correction of serum sodium in hyponatremic patients
    1. Slow correction for hyponatremia, even with severe signs of hyponatremia
    2. Serum sodium should be elevated by less than 10-12mEq/L/day in early stages
    3. Decrease correction rate after reaching serum sodium around 120-125 mEq/L
  3. Contributing Factors
    1. Hypokalemia
    2. Orthotopic liver transplantation
    3. Alcoholism
    4. Malnutrition
  4. Neurological Symptoms
    1. Early - mutism and dysarthria
    2. Lethargy, changes in affect
    3. Severe - spastic quadraparesis and pseudobulbar signs
    4. Extrapontine involvement can lead to other cranial nerve signs and ataxia
    5. Positive Babinski signs (dorsiflexed toes) and decreased deep tendon reflexes common
    6. Pseudobulbar signs: Dysarthria, dysphagia, respiratory muscle weakness
  5. Differential Diagnosis
    1. Inflammatory - encephalitis, possibly multiple sclerosis
    2. Non-inflammatory: alcoholism, intoxication, dehydration, malnutrition
  6. Diagnosis
    1. Clinical setting, signs and symptoms
    2. MRI scanning shows enhanced T2 signal throughout pons (possibly extrapontine also)
  7. Prognosis is variable and ranges from death to full recovery

References navigator

  1. Fraser CL and Arieff AI. 1997. Am J Med. 102(1):67 abstract
  2. Laureno R and Karp BI. 1997. Ann Intern Med. 126(1):57 abstract
  3. Sterns RH, Riggs JE, Schochet SS Jr. 1986. NEJM. 314:1535 abstract
  4. Kumar S and Berl T. 1998. Lancet. 352(9123):220 abstract