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Hypernatremia is defined as an increase in serum Na above 145 mmol/L. The problem accompanying this condition are osmotic, not a direct effect of the ion.
Independent marker for mortality.
a simple case introducing clincial presentation and calling for a differential diagnosis to get students thinking.
Hypernatremia is usually due to net water loss, rather than because of excess sodium. Accordingly, it is synonymous with dehydration. Common causes include:
Mild hypernatremia normally induces a strong thirst response, making the condition rare. It accordingly occurs in people unable to sense this drive or respond to it, such as:
Most people with hypernatremia also have a primary problem with urine concentrating ability. Osmotic diuresis can occur with hyperglycemia, after ingesting mannitol, or in the context of massive excretion of amino acids or urea.
Hypervolemic causes are rare. They include:
Diabetes Insipidus (DI) reflects impermeability of the collecting tubule to water, either because of an absence of ADH (central DI) or absence of response (nephrogenic DI).
Central DI can be caused by surgery, maligancy, trauma, vascular events, or granulomatous diseases
Nephrogenic DI can be due to lithium, hypokalemia, hypercalcemia, or congenital.
Hypernatremia often presents with subtle symptoms such as lethargy, weakness, irritability, and edema.
Diabetes insipidus (see below) reveals an inappropriately low urine osmolality (ie <750 mOsm/d)
Dehydration test: deprive of water for 12-18h. If urine fails to concentrate, it is most likely DI.
DDAVP is exogenous ADH. It can be used to separate central form nephrogenic DI.
Salt restrict and provide free water, either PO or IV. Oral intake is preferred. Monitor the patient to ensure correction is not occurring too rapidly.
Water deficit: [TBW x (serum Na - 140) ] / 140
Treat the underlying cause.
If the person is hemodynamically unstable, first correct volume depletion with NS bolus.
Change is serum Na = infusate[Na] - serum[Na] / TBW + 1L
Rapid correction can lead to cerebral edema due to ongoing brain hyperosmolarity. Lower Na no more than 12 mmol/L over 24 hours.
Hypotonic IV solutions (D5W, half- or quarter-normal saline) administration is the primary treatment. The body may adapt to higher sodium concentrations, and a rapid lowering of sodium concentration may result in cellular swelling. This can cause serious cerebral edema. It is criticial to therefore proceed carefully.
Hypernatremia along with hypovolemia suggests sodium deficit and requires isotonic saline infusion.
With more severe elevations (above 158 mMol/L) seizures and coma may occur.
Levels above 180 mmol/L often result in death, potentially due to coexisting medical conditions.
There is an increased risk of vascular rupture, resulting in intracranial hemorrhage.
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