Electrolytes

1

How is hyponatremia classified?

Classification is primarily based on the patient’s serum osmolality and volume status. Hyponatremia may occur in the presence of low serum osmolality (< 285 mOsm/kg), normal osmolality (285–295 mOsm/kg), or high osmolality (> 295 mOsm/kg). Elevated total body water is more common than a loss of sodium disproportionate to free water losses. This elevation is typically caused by impaired renal excretion of water, but it can occasionally be caused by excessive intake of water (e.g., primary polydipsia). Additional workup with urine sodium and urine osmolality may be helpful in determining the cause of hyponatremia. Many patients with hyponatremia have a single etiology, although complex or critically-ill patients may have multiple contributing factors. Table 9.1 summarizes causes of hyponatremia and their recommended treatments.

2

List the possible causes of acute hyponatremia in the operating room

Administration of hypotonic fluids or absorption of sodium-poor irrigation solutions may result in hyponatremia. Irrigation solutions like glycine and sorbitol can be used to facilitate transurethral resection of the prostate or distend the uterus during hysteroscopies. These solutions are hypotonic to prevent dispersal of the electrical current when monopolar cautery is used.

The intraoperative use of mannitol, especially in patients with renal dysfunction, may also cause hyponatremia by increasing plasma osmolality. Water moves out of cells, resulting in intravascular volume expansion and a drop in serum sodium. Mannitol is more commonly associated with intracranial surgeries, but can also be used as a flushing solution during transurethral resection of the prostate or bladder, or to promote urine output following renal transplant.

3

What are the symptoms of acute hyponatremia?

Symptoms often present based on the rate of change, as well as the absolute level of sodium. Typical symptoms include: nausea, vomiting, visual disturbances, muscle cramps, weakness, and bradycardia. Patients may also develop elevated intracranial pressure resulting in mental status changes. These changes can run the spectrum from apprehension and agitation to confusion and obtundation. Patients with severe hyponatremia, usually at levels less than 120 mEq/L, are also at risk for seizures.

4

What degree of hyponatremia is acceptable to continue with a planned elective procedure?

A normal sodium level is between 135 and 145 mEq/L. Recognizing hyponatremia should prompt an investigation of the cause. In addition to its etiology, the acuity and trajectory of the sodium change will also have an impact on management. Whether the investigation and treatment of hyponatremia should take priority over the surgery depends on the urgency of the procedure and an overall assessment of the patient's condition. In general, mild hyponatremia with a sodium level of at least 130 mEq/L should not result in cancellation of a planned procedure, as long as the patient is not symptomatic, and worsening hyponatremia is not an expected result of the procedure.

5

How should acute hyponatremia be treated?

The aggressiveness of treatment depends on the extent of symptoms and the rate at which hyponatremia has developed. In the simplest cases, fluid restriction is usually sufficient. Administration of loop diuretics may also be indicated. Correction should occur slowly, with serial sodium concentrations measured. For asymptomatic patients with a sodium concentration of less than 130 mEq/L, serum sodium should be corrected at less than or equal to a rate of 0.5 mEq/L/h.

Administration of hypertonic saline is reserved for patients with refractory hyponatremia or severe, neurological symptoms, including seizures or coma. For neurological symptoms, the patient can be treated with an initial bolus of 100 mL of 3% saline followed by, if symptoms have not resolved, two additional 100 mL boluses over a total course of 30 minutes. The goal is to rapidly increase the serum sodium by 4 to 6 mEq/L over a few hours, which should be sufficient to decrease intracranial pressure, stop seizure activity, and reduce the risk of herniation.

6

What daily rate of correction for hyponatremia is safe, and what is the risk if this rate is exceeded?

The rate of sodium increase should not exceed 10 to 12 mEq/L/day. Aggressive correction may result in osmotic demyelination syndrome. As there may be differences between intended and actual correction, it may be safer to target lower rates of correction (e.g., 4–6 mEq/L/day), especially in asymptomatic patients. Of note, it is the daily change rather than the hourly change in serum sodium that is associated with osmotic demyelination syndrome. This allows some level of safety for rapid correction in the setting of neurological symptoms, as long as the rapid correction rate does not continue past a period of a few hours. Lastly, osmotic demyelination syndrome is rare in patients who have an initial sodium level higher than 120 mEq/L.

7

What are the symptoms of osmotic demyelination syndrome? When do they typically develop?

Clinical manifestations of osmotic demyelination syndrome typically develop 2 to 6 days following rapid sodium changes. Neuromuscular symptoms are the most common and include: confusion, movement disorders, obtundation, seizures, weakness, and myoclonic jerks. Typically, these symptoms are either partially or completely irreversible.

8

Is there a subset of patients who tend to have residual neurological sequelae from a hyponatremic episode?

Females of reproductive age, especially during menstruation, have been noted to be at the greatest risk for residual sequelae. There may be an estrogen-related impairment in the ability of the brain to adapt to hyponatremia.

Brain adaptations that help minimize cerebral edema during hyponatremia also place the brain at risk in the setting of rapid sodium correction. Patients who have had hyponatremia for more than 2 days are especially vulnerable to osmotic demyelination syndrome, because the brain has been given more time to adapt.

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