Hyponatremia
last authored: Jan 2012, David LaPierre
last reviewed:
Introduction
Hyponatremia (plasma sodium <135 mmol/L)is a important and common electrolyte abnormality in many patients. It can occur for many reasons, with a clear diagnostic approach being very helpful. Hyponatremia, when mild, has minimal effects, though if it is severe, if can cause serious, life-threatening conditions. As such, all primary care providers should be familiar with this condition. Almost half of patients will also have other electrolyte abnormalities.
The Case of Mr WS
Mr S is a 48 year-old man who is admitted to the emergency department with confusion and a recent fall. His plasma sodium, amongst other lab abnormalities, is 118.
- what might be the cause of his low sodium?
- how do you correct it?
Pathophysiology
It is calculated in mmol per L by using this formula: 2 × [sodium] + [urea] + [glucose]
Sodium is primarily found in the extracellular space. Increased sodium acts on the brain to cause vasopressin, or anti-dieuretic hormone, from the posterior pituitary. This then acts on the kidney tubules and cortical collecting ducts to increase water absorption. Decrease sodium concentration accomplishes the opposite, with increased dieuresis.
Hyponatremia usually results when secretion of total body water decreases.
Causes and Risk Factors
Hyponatremia can be hypo- iso-, or hyper-osmolar.
Hypo-osmolar (dilutional) hyponatremia, is the most common cause, and is due to excess water in relation to sodium. The kidney is normally able to secrete large volumes of free water daily, but excretion may be impaired due to reduced GFR, reduced effective circulating volume, impaired sodium-chloride reabsorption in the renal diluting segments, or malfunction of the ADH axis.
Dilutional hyponatremia is further categorized according to volume status:
hypovolemic
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euvolemic
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hypervolemic
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Iso-osmolar hyponatremia is seen with conditions such as hyperlipidemia and paraproteins. These falsely cause hyponatremia though mechanical error.
Hyper-osmolar hyponatremia is due to extra extracellular osmoles which draw water and dilute plasma sodium. Glucose is the usual agent. Each 10 mmol increase in blood glucose leads to a 3 mm decrease in sodium. Mannitol may also cause hyperosmolar hyponatremia.
Signs and Symptoms
Signs and symptoms of brain swelling depend on degree and rapidity of onset.
- history
- physical exam
History
Most patients with hyponatremia are asymptomatic, though symptoms usually arise when the concentration falls below 120 mmol/L, or above this if the drop is acute.
Symptoms are primarily neurologic and gastrointestinal, and worsen as concentration drops. They include:
- headache
- nausea, loss of appetite, vomiting
- malaise
- lethargy
- weakness
- poor coordination
- muscle cramps
- somnolence
- disorientation
- personality change
Physical Exam
Volume status assessment is important to determine cause.
A neurological exam should be carried out to identify effects on the nervous system.
Decreased level of consciousness and depressed reflexes and may be seen.
Investigations
- lab investigations
- diagnostic imaging
Lab Investigations
Key tests to determine the cause of hyponatremia include:
- plasma osmolarity (may be low, normal (280-300 mOsM/kg), or high)
- creatinine (will rise in hypovolemic patients)
- blood urea nitrogen (BUN) and blood uric acid (usually low in SIADH)
- urine osmolality: urine will be concentrated if hypovolemic and dilute if euvolemic. If SIADH is present, however, it will be concentrated as well.
- urine sodium concentration: <10-20 mmol/L suggests volume depletion; >30mmol/L suggests SIADH, renal disease, hypothyroidism, and drugs
Potential causes of hyponatremia that may be assessed include:
- TSH
- 8 am cortisol
- glucose
- lipids
- serum electrophoresis for paraproteins
Diagnostic Imaging
If SIADH is suspected, a chest X-ray may be helpful to assess for potential lung malignancy.
Treatments
It is important to determine if the hyponatremia is acute or chronic, as this guides treatment. As levels are normalized, it is also important to treat the underlying cause of hyponatremia.
Acute
If hyponatremia is acute (<48 hrs), it is safe to increase the [sodium] to 130 mmol/L in 24h using IV hydration. In general, fluids with a tonicity greater than that of urine will increase serum concentrations.
Increase by 5mM/L over the first 3 hours, then continue the increase to 130 mmol/L in the first 24 hrs. Once there, stop.
Chronic (>48 hrs)
If hyponatremia has been present for >48 hours, this must be done gradually, at not more than 6-8 mM/day, or even less if the patient is elderly or cachectic. It is safe to initially increase by 1-2mM/hour if symptoms are severe. Restoring sodium too quickly can inhibit ADH secretion, causing prompt diuresis and dramatic increase in plasma sodium concentration. This may lead to central pontine myelinolysis, a catastrophic consequence described below.
To calculate the total sodium required:
- determine the deficit of sodium: 135 - [Naserum]
- multiply by total body water (0.6[weight] in men, 0.5[weight] in women)
- choose IV fluid and determine rate to increase per hour
- monitor sodium every six hours
Hypovolemia
Provide IV infusion. Oral water with salt added (ie OXO cubes) may be given. Hypertonic saline and IV Lasix may be used if the condition is severe.
Euvolemia
Restrict free water to <1-1.5L/d. Provide NS or hypertonic saline. Use Lasix if severe.
Hypervolemia
Restrict sodium and free water to <1-1.5L/d. Ensure bed rest. If hyponatremia is due to congestive heart failure or renal failure, treatment of the precipitating disease should be accompanied by loop diuretics to help with excretion of hypotonic urine, as well as fluid restriction.
If patient has both hyponatremia and hypokalemia, treat the hypokalemia first, then reassess. The extra potassium will increase the plasma sodium following shift out of cells.
Demeclocycline is a medication that works on the kidney to induce diabetes insipidus. This negative free-water balance results in a normalization of sodium. Caution is required for patients with kidney or liver disease.
Consequences and Course
Secere hyponatremia can be extremely serious, leading to seizures, coma, respiratory arrest, brainstem herniation, and death.
Hyponatremia is a poor prognosticator for CHF.
Asymptomatic hyponatremia can increase rates of falls.
Central pontine myelinolysis can result with too rapid correction of hyponatremia. The mechanism of this stems from electrolyte shift within the brain to accomodate for the difference in osmotic pressure (initially too high a sodium concentration intracellularly). A rapid rise in extracellular sodium leads to fluid shift FROM the cells and attending shrinkage. This leads to osmotic demyelination. Symptoms of this include dysarthria, dysphagia, paraperesis, lethargy, coma, and seizure. It has a very poor prognosis.
Resources and References
Lab. risk factors for hospital mortality in acutely admitted patients. QJM 2007.
Goh KP. 2004. Management of Hyponatremia. Am Family Physician. 69(10):2387-2394.
eMedicine - Hyponatremia in Emergency Medicine
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