Sodium is the primary extracellular cation in the body. It regulates osmotic forces, it is involved in membrane transport systems, it helps regulate many chemical reactions as well as aid in acid-base balance.
The picture shown here is of a cell membrane. The Green box in the center is the Na/K pump. This is an enzyme that acts as a pump to pump Sodium out of cells while pumping potassium into cells. Both of these ions are moving AGAINST their concentration gradient, and this movement requires energy which is formed by cleaving a phosphate from the molecule ATP.
The movement of these ions gives energy for other transport systems that move amino acids, glucose and other nutrients into cells, it controls signaling within many cells, controls cell volume and controls neuron activity. This small electrolyte shift is important to so many mechanisms in the body, that you can hopefully appreciate the importance that Sodium, Potassium and even phosphorus play in cellular function. The normal range of Sodium is typically 138-146 mmol/L. Values outside this range can have detrimental effects on many cellular functions throughout the body.
HYPERNATREMIA
Hypernatremia, or sodium that is too high can be seen with dehydration, where the concentration of sodium is elevated in relation to the amount of water in the body, with excess saline administration. It can be seen with renal loss of water, such as aggressive diuretic use or Diabetes Insipidus. In the setting of dehydration, a decrease is blood pressure is sensed by the kidneys and the RAAS system is activated, increasing the absorption of water in the kidneys. Further, the chemoreceptors in the brain sense a higher sodium concentration, and the pituitary will secrete ADH, causing more free water to be reabsorbed. It also activates the thirst centers, causing the patient to feel thirsty. As clinicians, we can help this process by giving the patient free water. What that means is, we are giving water in the pure form, without sodium. If the patient can tolerate oral fluids, we can give them water to drink. It is not uncommon the amount of free water that they are deficient is quite large, in the 7-10-liter range. This deficit is a calculated value based on a patients gender, age, weight and sodium level. If they need more free water than they can drink, or they are unable to tolerate PO, we can give them free water through the IV. However, it is not safe to infuse free water into an IV. So IV free water is given in the form of Dextrose and water, or D5W.
Symptoms
Clinical Pearls
- 30% will have permanent neurological deficits
- Documenting a good neurologist exam is important
- DDAVP is safe in pregnancy (transient DI of pregnancy)
- Pediatric mortality is as high as 50%
Admission Criteria
- New diagnosis with Na+ > 150
- ICU admit if > 160
Discharge Criteria
- Na+ level < 150 and asymptomatic or known history of hypernatremia
Diagnosis and Management
HYPONATREMIA
Hyponatremia, or a sodium concentration that is too low can be caused by excessive vomiting or diarrhea, where sodium is expelled from the body before it can be absorbed, or reabsorbed by the GI tract, by certain diuretics, by inadequate salt intake or by drinking too much free water as is seen in patients with diabetes insipidus. Hyponatremia can cause headaches, confusion, lethargy and if the levels drop below 120 mEq/L, the patient is at risk for seizures, coma and death. Treatment for this is typically a gradual increase in the sodium concentration by slow infusion of 0.9% normal saline. If sodium is corrected too rapidly, a devastating phemonenon called Central Pontine Myolinolysis can occur, where the myelin sheath on neuronal cells in the pons of the brainstem degenerates, and results in irreversible paralysis, difficulty swallowing, difficulty speaking and other neurological symptoms. A 1 liter bag of normal saline will increase sodium by about 1 mEq/L. Our goal in treatment is an increase in serum sodium by 1-2 mEq/L/hr in acute hyponatremia, and no more than 0.5 mEq/L/hr in patients with chronic hyponatremia to avoid central Pontine myolinolysis. Now, If a patients sodium drops too low, and they start to have significant neurological changes and certainly if they develop seizures, the treatment is to give a higher concentration of sodium. This is done with 3% hypertonic saline given at 25-100 mL/hr with very close monitoring of rate correction. If seizures occur, treatment of the seizure with benzodiazepines should be attempted, but unlikely to respond until the sodium is brought up to a safer level, typically > 120 mEq/L
Symptoms
Clinical Pearls
- Risk factors for osmotic demyelination syndrome include females, alcoholics, hypokalemia, history of liver transplant and chronic malnourishment.
- Thiazide diuretics may cause persistent hyponatremia up to 2 weeks after discontinuation.
Whenever hyponatremia is seen on laboratory evaluation, it is extremely important to look at the glucose and ensure that the glucose is not significantly elevated. Significant elevations in glucose will cause sodium concentrations to appear low, and this is actually a falsely low reading even though the actual sodium concentration may be normal. Therefore, if you notice a significantly elevated glucose level (like in the hundreds) and the sodium is low, you must correct the sodium level with the mathematical equation shown. If you don’t like equations, there is another way to calculate this. Typically, sodium will falsely read low by 1.6 mEq/L for every 100 mg/dL of glucose AFTER 100. So for example, if the patients blood glucose is 300, you would add 1.6 for every 100 mg/dL of glucose AFTER 100. So in this case, we use a glucose level of 200. So we will have to add 1.6 twice (so, 3.2) to the patients measured sodium to get the corrected, and accurate sodium level. So if the patient had a measured sodium of 129, the corrected sodium for a glucose of 300 would be 132.2 (round it to 132). An even easier method, is to just download the app MDCalc where all of the equations I will talk about today are located, and you can just plug the numbers in.
Admission Criteria
- Any symptomatic hyponatremia
- Asymptomatic and mild (120-127) with comorbid factors
Discharge Criteria
- Na+ levels > 130 and asymptomatic or chronic state
- Asymptomatic and mild (120-129) with no co-morbid factors
- Patient has close follow-up
Diagnosis
Caveat...
This calculation assumes entire infusate is retained without any output of Na+ or H2O. This assumption can be detrimental in the setting of SIADH.
SIADH
Clinical Pearls
- Na+ reabsorption is handled by Aldosterone
- Water reabsorption is handled by ADH
- In SIADH, Na+ handling is intact, while H2O handling is NOT.
- If Uosm > is > infusateOsm – SerumNa will worsen.
- This is because all Na will be excreted, while water is still reabsorbed
Example:
- 1 L NS (154 mEq of Na or 308 mOsm of solute in 1 L free H2O
- In an SIADH patient has Uosm 616 – 308 mOsm solute will be excreted in 0.5 L H2O for a net gain 0.5 L free H2O leading to a ↓ in [Na+]
SIADH Specific Treatment:
- Free water restriction to < 1 L/day & treat the underlying cause (meds, malignancy, TB, CNS infection, etc.)
- If this fails à Hypertonic saline (1,025 mOsm) with Lasix
- Aquaresis: Conivaptan (IV) or Tolvaptan (PO) vasopressin antagonists (caution as rate of correction can be very rapid)
- Demeclocycline: a tetracycline that acts on collecting tubule cells to ↓ responsiveness to ADH à induces nephrogenic DI
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