Osmotic demyelination syndrome: Difference between revisions
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===Risk Factors=== | ===Risk Factors=== | ||
*Chronic heart failure | *Chronic [[heart failure]] | ||
*[[Alcoholism]] | *[[Alcoholism]] | ||
*[[Cirrhosis]] | *[[Cirrhosis]] | ||
| Line 12: | Line 12: | ||
*[[Malnutrition]] | *[[Malnutrition]] | ||
*Treatment with vasopressin antagonists (e.g. tolvaptan) | *Treatment with vasopressin antagonists (e.g. tolvaptan) | ||
===Risk Factors for Over-correction<ref>George, J. C., Zafar, W., Bucaloiu, I. D., & Chang, A. R. (2018). Risk Factors and Outcomes of Rapid Correction of Severe Hyponatremia. Clinical Journal of the American Society of Nephrology: CJASN, 13(7), 984–992.</ref>=== | |||
*Lower initial sodium | |||
*[[Schizophrenia]] | |||
*Lower baseline urine sodium | |||
==Clinical Features== | ==Clinical Features== | ||
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*[[Dysarthria]] | *[[Dysarthria]] | ||
*[[Dysphagia]] | *[[Dysphagia]] | ||
*Lethargy | *[[Lethargy]] | ||
*Behavioral disturbances/ confusion | *Behavioral disturbances/ confusion | ||
*Paraparesis or quadriparesis | *[[weakness|Paraparesis]] or quadriparesis | ||
*[[Seizures]] | *[[Seizures]] | ||
*"Locked in" syndrome | *"Locked in" syndrome | ||
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==Evaluation== | ==Evaluation== | ||
*MRI can be used to visualize the pontine lesion, with a characteristic "batwing" lesion of the pons appearing in typical cases | *Evaluate for alternative/reversible causes of AMS or exacerbating factors | ||
*[[brain MRI|MRI]] can be used to visualize the pontine lesion, with a characteristic "batwing" lesion of the pons appearing in typical cases | |||
==Management== | ==Management<ref>Sterns RH and Hix JK. Overcorrection of hyponatremia is a medical emergency. Kidney International. Volume 76, Issue 6, 2 September 2009, Pages 587-589.</ref>== | ||
*[[Desmopressin]] at 2 mcg q6 hrs IV/SC | |||
*6 mL/kg of 5% dextrose in water, repeated until serum sodium rise back below 9 mEq in 24 hrs | |||
*If concerns for iatrogenic rapid increase in serum Na concentration (IV crystalloid bolus before Na lab comes back): | |||
**Stop IV fluids, send urine osmolality, repeat serum Na | |||
**If uOsm is < 100 mOsm/L, this suggests free water diuresis | |||
**Or if sodium appears to be on a trajectory to increase >8mEq/L in 24hrs | |||
**Administer DDAVP 1 mcg x1 | |||
==Disposition== | ==Disposition== | ||
*Admit | *Admit | ||
==Prevention== | |||
See [[hyponatremia]] for safe correction rate | |||
==See Also== | ==See Also== | ||
*[[Hyponatremia]] | |||
*[[Hypernatremia]] | |||
==References== | ==References== | ||
Latest revision as of 23:19, 27 August 2021
Background
- Formerly called "central pontine myelinolysis"
- A neurologic condition caused by rapid correction of hyponatremia, with starting serum sodium normally 120 meq/L or less
- Caused by rapid correction of hyponatremia (>12 mEq/L/24 h), as water moves from cells to extracellular fluid, yielding intracellular dehydration.
- Symptoms are often irreversible or only partially reversible
Risk Factors
- Chronic heart failure
- Alcoholism
- Cirrhosis
- Hypokalemia
- Malnutrition
- Treatment with vasopressin antagonists (e.g. tolvaptan)
Risk Factors for Over-correction[1]
- Lower initial sodium
- Schizophrenia
- Lower baseline urine sodium
Clinical Features
Symptoms can be present 2-6 days after rapid correction of serum sodium
- Dysarthria
- Dysphagia
- Lethargy
- Behavioral disturbances/ confusion
- Paraparesis or quadriparesis
- Seizures
- "Locked in" syndrome
- Coma and death
Differential Diagnosis
Altered mental status
Diffuse brain dysfunction
- Hypoxic encephalopathy
- Acute toxic-metabolic encephalopathy (Delirium)
- Hypoglycemia
- Hyperosmolar state (e.g., hyperglycemia)
- Electrolyte Abnormalities (hypernatremia or hyponatremia, hypercalcemia)
- Organ system failure
- Hepatic Encephalopathy
- Uremia/Renal Failure
- Endocrine (Addison's disease, Cushing syndrome, hypothyroidism, myxedema coma, thyroid storm)
- Hypoxia
- CO2 narcosis
- Hypertensive Encephalopathy
- Toxins
- TTP / Thrombotic thrombocytopenic purpura
- Alcohol withdrawal
- Drug reactions (NMS, Serotonin Syndrome)
- Environmental causes
- Deficiency state
- Wernicke encephalopathy
- Subacute Combined Degeneration of Spinal Cord (B12 deficiency)
- Vitamin D Deficiency
- Zinc Deficiency
- Sepsis
- Osmotic demyelination syndrome (central pontine myelinolysis)
- Limbic encephalitis
Primary CNS disease or trauma
- Direct CNS trauma
- Diffuse axonal injury
- Subdural/epidural hematoma
- Vascular disease
- SAH
- Stroke
- Hemispheric, brainstem
- CNS infections
- Neoplasms
- Paraneoplastic Limbic encephalitis
- Malignant Meningitis
- Pancreatic Insulinoma
- Seizures
- Nonconvulsive status epilepticus
- Postictal state
- Dementia
Psychiatric
Evaluation
- Evaluate for alternative/reversible causes of AMS or exacerbating factors
- MRI can be used to visualize the pontine lesion, with a characteristic "batwing" lesion of the pons appearing in typical cases
Management[2]
- Desmopressin at 2 mcg q6 hrs IV/SC
- 6 mL/kg of 5% dextrose in water, repeated until serum sodium rise back below 9 mEq in 24 hrs
- If concerns for iatrogenic rapid increase in serum Na concentration (IV crystalloid bolus before Na lab comes back):
- Stop IV fluids, send urine osmolality, repeat serum Na
- If uOsm is < 100 mOsm/L, this suggests free water diuresis
- Or if sodium appears to be on a trajectory to increase >8mEq/L in 24hrs
- Administer DDAVP 1 mcg x1
Disposition
- Admit
Prevention
See hyponatremia for safe correction rate
See Also
References
- ↑ George, J. C., Zafar, W., Bucaloiu, I. D., & Chang, A. R. (2018). Risk Factors and Outcomes of Rapid Correction of Severe Hyponatremia. Clinical Journal of the American Society of Nephrology: CJASN, 13(7), 984–992.
- ↑ Sterns RH and Hix JK. Overcorrection of hyponatremia is a medical emergency. Kidney International. Volume 76, Issue 6, 2 September 2009, Pages 587-589.