How fast sodium correction




















All children should have a strict fluid balance including weight minimum daily, but maybe hourly for more unwell children. Remember to treat the underlying cause. Fluid Overloaded. Administration of hypertonic fluids e. If there are no inputs, the sodium should stay roughly stable.

The patient's fluid intake must be strictly controlled. To begin with, restrict any fluid intake dry foods are OK. After hours you may liberalize a bit. Note that the patient's sense of thirst is due to hyponatremia, so there is no safe way to get rid of this immediately. Figure out how much more you want the sodium to increase over the next 24 hours. Follow electrolytes every hours to ensure that the sodium is on track.

If the sodium is too high, calculate the amount of free water required to decrease it back to target using this formula. This volume of free water may be given intravenously as D5W or orally if the patient is able to drink. This is tedious, but effective. About 10 hours later, the patient's diet may be gradually liberalized. One of two things will happen at this point: a If the cause of hyponatremia has been eliminated e. You're all set.

The kidneys will excrete any exogenous urea in the urine, along with water. Thus, oral urea intake functions as an aquaretic that forces the net elimination of water from the body.

The volume of water removed is proportional to the amount of urea administered, leading to a finite and controlled removal of water equation above.

Recently, several studies have confirmed that oral urea is a safe and effective therapy for SIADH , , , Contraindications to urea are as follows: Inability to tolerate PO intake. Cirrhosis with hepatic encephalopathy. Severe renal failure. Dosing and monitoring is outlined in the figure below.

However, it's generally not preferred compared to oral urea for the following reasons: Combination therapy is trickier if the doses of loop diuretic and sodium aren't balanced correctly, this may provoke volume overload or volume depletion.

Frequent doses of loop diuretic may cause frequent urination at night, interfering with sleep. Nonetheless, this treatment may be useful in situations where oral urea is contraindicated, or unavailable.

General concept: i These patients are usually in sodium balance, so they shouldn't retain sodium. As sodium is excreted, it will pull water out of the body along with it. The amount of water loss is equal to the osmotic load of the sodium divided by the urine osmolarity. Washing out the kidney concentration gradient will increase the amount of water which is pulled out of the body due to sodium administration in part i.

As patients stabilize, this may be weaned down or off furosemide will augment the efficacy of the NaCl, but it's not mandatory for it to work. As chronic maintenance therapy or in less emergent situations, oral salt tabs may also be used a typical dose would be 3 grams TID with meals. Hyponatremia due to heart failure is usually chronic and is not a life-threatening process.

Exactly when treatment is beneficial is unclear. The best approach to chronic, asymptomatic hyponatremia is often to provide no specific therapy for the hyponatremia. Instead, the primary focus of therapy should remain the heart failure. There is a risk of focusing too much energy on treating the hyponatremia, and not enough energy on treating the underlying heart failure. For example: It's counter-productive for a cardiology service to refuse admission of a heart failure patient solely due to moderate hyponatremia.

Thus, hyponatremia in heart failure is a reflection of poor systemic perfusion. This may explain why hyponatremia is a prognostic sign of poor long-term outcome. For example: 1 Sometimes acute hyponatremia may be a feature of cardiogenic shock deteriorating systemic perfusion. Treatment here will depend on systemic hemodynamic assessment.

Sometimes hypoperfusion may be due to volume depletion — such patients may benefit from judicious volume repletion. Some hypoperfused patients could benefit from therapies such as inotropes or withdrawal of beta-blockers.

For more on this, see the chapter on cardiogenic shock. For patients with marked volume overload, furosemide is an excellent therapy.

Furosemide stimulates the production of dilute urine, causing loss of both water and sodium but generally more water than sodium. This will improve the volume status and also increase the sodium concentration. For patients with mild volume overload and substantial hyponatremia, oral urea could be a consideration.

Urea will cause a pure water loss aquaresis , so it will increase the sodium level with less volume loss. A figure describing how to use oral urea is shown above. For patients with hyponatremia and severe refractory congestion that doesn't respond to conventional doses of loop diuretics, a combination of simultaneous loop diuretic and hypertonic saline may be trialed i.

This is usually chronic and not a life-threatening process. The best approach to chronic, asymptomatic hyponatremia could be to do nothing. Rare patients may be hypovolemic, in which case judicious volume resuscitation may be considered. Furosemide diuresis is often a good option for patients with volume overload. This should improve the volume status and also increase the sodium concentration.

Oral lactulose is a good option for patients with any degree of hepatic encephalopathy. Lactulose causes wasting of water via the gut which will improve the hyponatremia , while simultaneously treating hepatic encephalopathy more on this here. Oral urea might be considered in patients without any history of hepatic encephalopathy, but its use in cirrhosis is controversial. There is concern that urea could be converted into ammonia by gut bacteria, promoting the development of hepatic encephalopathy.

Overall, urea is probably a 2nd or 3rd line agent here and potentially inferior to lactulose. In one of the few published studies on real-world treatment of hyponatremia and incidence of ODS, authors looked back at almost 1, patients with severe hyponatremia at seven hospitals associated with a single health care system. Eight patients 0. The new neurologic symptoms attributed to osmotic demyelination were persistent in three of the eight patients with identified ODS, and resolved in the other five patients.

Almost all of the patients with ODS had their sodium corrected too quickly. Part of the problem is published expert guidance on correction of hyponatremia. With such a low threshold to use powerful osmotic agents for relatively non-threatening hyponatremia, it's unsurprising that over-correction of serum sodium is so common. The increasing pressure inside hospital systems to discharge patients sooner, along with our general impatience, likely also contribute.

A complex process like sodium homeostasis doesn't respond consistently to simplistic total body water calculations taught in training programs. Acute, severe hyponatremia can rapidly shift fluid into brain cells, causing cerebral edema with symptoms of seizures or brain herniation. Few patients who are admitted with hyponatremia present this way, or require such dramatic and potentially dangerous interventions.



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