5: Electrolytes

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CHAPTER 5 Electrolytes

James Duke, MD, MBA

1 What is a normal sodium concentration? What degree of hyponatremia is acceptable to continue with a planned elective procedure?

A normal sodium level is between 135 and 145 mEq/L. Generally a sodium level of 130 mEq/L will not result in cancellation of a planned procedure as long as the patient is not symptomatic and hyponatremia is not an expected result of the procedure. It is important to note that recognizing hyponatremia should prompt an investigation as to the cause. Whether the investigation should take priority over the surgery depends on the urgency of the procedure and an overall assessment of the patient’s condition.

2 How is hyponatremia classified?

Hyponatremia may occur in the presence of hypotonicity, normal tonicity, or hypertonicity; thus it is important to measure serum osmolality to determine the cause of hyponatremia. Assessment of volume status is also important in determining the cause. An excess of total body water is more common than a loss of sodium in excess of water. Table 5-1 summarizes causes and treatment of hyponatremia.

TABLE 5-1 Causes of Hyponatremia

Total Sodium Content	Causes	Treatment (Always Treat Underlying Disorder)
Decreased	Diuretics (including osmotic diuretics); renal tubular acidosis; hypoaldosteronism; salt-wasting nephropathies, vomiting; diarrhea	Restore fluid and sodium deficits with isotonic saline
Normal	SIADH; hypothyroidism; cortisol deficiency	Water restriction
Increased	Congestive heart failure; cirrhosis; nephrotic syndrome	Water restriction, loop diuretics

SIADH, Syndrome of inappropriate antidiuretic hormone.

3 How should acute hyponatremia be treated?

The rate at which hyponatremia develops and the presence of symptoms determine the aggressiveness of treatment. If hyponatremia has developed quickly, the patient may develop nausea, vomiting, visual disturbances, muscle cramps, weakness, hypertension, bradycardia, confusion, apprehension, agitation, obtundation, or seizures; usually the sodium content is found to be less than 125 mEq/L. The aggressiveness of treatment depends on the extent of symptoms.

In the simplest cases fluid restriction may be sufficient. Administration of loop diuretics may also be indicated. Severe neurologic symptoms require careful administration of hypertonic (3%) saline. The dose of 3% saline (513 mEq Na/L) is determined as follows:

Correction should occur slowly, with serial sodium concentrations measured. Below 125 mEq/L, correct at a rate of about 1 mEq/L/hr. Once a concentration of 125 mEq/L has been achieved, the likelihood of continued severe neurologic symptoms has diminished. It should be noted that aggressive correction may result in central pontine myelinolysis.

Seizures require securing a protected airway, oxygenation, ventilation, and perhaps administration of anticonvulsants, although seizures are usually self-limited.

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

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

5 What may cause acute hyponatremia in the operating room?

Administration of hypotonic fluids or absorption of sodium-poor irrigants may result in hyponatremia. Such irrigants are used to facilitate transurethral resection of the prostate or distend the uterus during hysteroscopies. However, isotonic fluids are used increasingly in these settings when bipolar electrical cautery is used for the surgical procedure. Thus hyponatremia as a consequence of these procedures has been observed with decreasing frequency. However, some surgeons may still prefer monopolar cautery because the resection is more rapid. In this instance a hypotonic irrigation fluid is used to prevent dispersal of the electrical current, and in such a scenario hyponatremia is a risk. The most common cause of postoperative hyponatremia is syndrome of inappropriate antidiuretic hormone secretion and subsequent water retention.

6 Discuss hypernatremia and its causes

Hypernatremia is less common than hyponatremia and is always associated with hypertonicity. Hypernatremia can be associated with either low, normal, or high total body sodium content. Frequently hypernatremia is the result of decreased access to free water, as in elderly or debilitated patients with impaired thirst and decreased oral intake. Other causes include a lack of antidiuretic hormone (diabetes insipidus) and an excess sodium intake (either parenterally or intravenously such as with administration of sodium bicarbonate or 3% sodium chloride). Table 5-2 lists causes and treatment for each category.

TABLE 5-2 Causes of Hypernatremia

Total Sodium Content	Causes	Treatment (Always Treat Underlying Disorder)
Decreased	Osmotic diuresis; increased insensible losses	First restore intravascular volume with isotonic fluids; then correct Na with hypotonic fluids
Normal	Diabetes insipidus (neurogenic nephrogenic); diuretics; renal failure	Correct water loss with hypotonic fluids
Increased	Excessive Na administration (NaHCO₃; 3% NaCl); hyperaldosteronism	Slowly correct fluid deficits with D₅W, loop diuretics

7 What problems does hypernatremia pose for the anesthesiologist?

Most often hypernatremia is associated with fluid deficits, and the hypovolemia poses the greater challenge to the anesthesiologist. Complicating this, fluid deficits must be corrected slowly lest cellular edema ensue. Generally elective surgery should be delayed if serum sodium levels exceed 150 mEq/L. Hypernatremia increases minimal alveolar concentration.

8 Review hypokalemia and its causes

A serum level of less than 3.5 mEq/L defines hypokalemia. Hypokalemia may be the result of total body loss of potassium (gastrointestinal and renal), transcellular shifts in potassium, or inadequate intake. Diuretics frequently cause hypokalemia, as do gastrointestinal losses and renal tubular acidosis. β-Adrenergic agonists, insulin, and alkalosis (respiratory and metabolic) shift potassium to the intracellular space. Hypokalemia is not uncommon in pregnant women receiving tocolytic therapy or in patients requiring inotropic support because β-agonists are used in both instances.

9 What are the risks of hypokalemia?

Hypokalemia produces electrocardiogram abnormalities (ST segment and T wave depression and onset of U waves) and cardiac arrhythmias (often premature ventricular contractions and atrial fibrillation). It also impairs cardiac contractility. These cardiac abnormalities are usually not seen until serum K decreases to 3 mEq/L. Hypokalemia is especially worrisome in patients taking digitalis or with ischemic heart disease or preexisting arrhythmias. Hypokalemia renders muscles weak and sensitive to muscle relaxants. But no definitive data suggest that patients having surgery with potassium levels as low as 2.6 mEq/L have adverse outcomes.

10 A patient takes diuretics and is found to have a potassium level of 3 mEq/L. Why not give the patient enough potassium to restore the serum level to normal?

The total body deficit of potassium, primarily an intracellular cation, is not reflected by serum concentrations. A patient with a serum potassium of 3 mEq/L may have a total body potassium deficit of 100 to 200 mEq. Rapid attempts to correct hypokalemia poorly address the problem and have resulted in cardiac arrest. Hypokalemic patients without the risk factors previously discussed who are not undergoing major thoracic, vascular, or cardiac procedures can tolerate modest hypokalemia (certainly 3 and possibly as low as 2.8 mEq/L).

11 If potassium is administered, how much should be administered and how fast should it be administered?

Potassium should be administered at a rate no greater than 0.5 to 1 mEq/L. As a safety measure, no more than 20 mEq of potassium, diluted in a carrier and run through a controlled infusion pump, should be connected into a patient’s intravenous lines at any one time.

12 Define hyperkalemia and review its symptoms

Hyperkalemia is defined as serum concentration greater than 5.5 mEq/L. Hyperkalemia may produce profound weakness. Cardiac conduction manifestations include enhanced automaticity and repolarization. T waves become peaked, and there is PR interval and QRS prolongation and an increased risk for severe ventricular arrhythmias.

13 What are some causes of hyperkalemia?

Hyperkalemia may be either acute or chronic in etiology and secondary to increased intake, decreased excretion, or intracellular shifts related to acid-base status. Hyperkalemia may be iatrogenic (e.g., potassium supplementation, potassium-containing medications) and associated with massive transfusion, metabolic acidosis, and renal failure (acute and chronic); it may also occur after massive tissue trauma or rhabdomyolysis. Medications that may cause hyperkalemia include angiotensin antagonists and receptor blockers, potassium-sparing diuretics (spironolactone and triamterene), and succinylcholine.

14 Describe the patterns of hyperkalemia observed after the administration of succinylcholine

Mild hyperkalemia (an increase of approximately 0.5 mEq/L) occurs after routine administration of succinylcholine, but susceptible patients may experience life-threatening hyperkalemia. Examples of such patients include those with chronic spinal cord or denervation injuries, head injuries, and unhealed significant burns, and patients who have been immobile (e.g., patients in intensive care). I am aware of an otherwise healthy patient who experienced hyperkalemic cardiac arrest after administration of succinylcholine. His only risk factor was that he was a hospitalized prisoner chained to the bed day after day.

15 A patient with chronic renal failure requires an arteriovenous fistula for hemodialysis. Potassium is measured as 7 mEq/L. What are the risks of general anesthesia?

Hyperkalemia >6 mEq/L should be corrected before elective procedures. Usually dialysis is the treatment. Always consider hyperkalemia when a patient with renal failure suffers cardiac arrest.

16 How is hyperkalemia treated?

Emergent treatment of hyperkalemia is threefold. Treat cardiotoxicity with intravenous calcium chloride. Potassium can be quickly shifted intracellularly by hyperventilation, β-adrenergic stimulation (e.g., β-agonist nebulizer), sodium bicarbonate, and insulin (if insulin is given, one should consider glucose supplementation). Bodily excretion of potassium is more time-consuming but is accomplished using diuretics, Kayexalate, and dialysis.

17 What are the major causes and manifestations of hypocalcemia?

The major causes of hypocalcemia are hypoparathyroidism, hyperphosphatemia, vitamin D deficiency, malabsorption, rapid blood transfusion (chelated by citrate), pancreatitis, rhabdomyolysis, and fat embolism. Hypocalcemia is a concern after thyroidectomy if no parathyroid tissue is left, and the patient may develop laryngeal spasms and stridor. This must be differentiated from other causes of postoperative stridor, including wound hematoma and injury to the recurrent laryngeal nerves. Hypocalcemia also impairs cardiac contractility, resulting in hypotension, a not uncommon event during massive transfusion. Patients may also be confused.

KEY POINTS: Electrolytes

1. Rapid correction of electrolyte disturbances may be as dangerous as the underlying electrolyte disturbance.

2. Electrolyte disturbances cannot be corrected without treating the underlying cause.

3. Acute hyperkalemia is life threatening and associated with ventricular tachycardia and fibrillation. It should always be suspected when cardiac collapse follows succinylcholine administration or in any patient with chronic renal disease.

4. When other causes have been ruled out, persistent and refractory hypotension in trauma or other critically ill patients may be caused by hypocalcemia or hypomagnesemia.

18 How is hypocalcemia treated?

Treatment of acute hypocalcemia is straightforward: administer calcium chloride. Volume to volume this provides more calcium than the gluconate preparation. Always remember to address the primary disturbance.

19 Does hypomagnesemia pose a problem for the anesthesiologist?

Hypomagnesemia is increasingly recognized in critically ill patients, often in association with hypokalemia and hypophosphatemia. It is common in alcoholic patients. Hypokalemia cannot be corrected unless hypomagnesemia is also treated. Hypomagnesemic patients have increased susceptibility to muscle relaxants and may be weak after surgery, including having respiratory insufficiency. They may have impaired cardiac contractility and dysrhythmias. Trauma patients having massive blood resuscitations may also become hypomagnesemic, and such patients should be administered magnesium chloride, 1 to 2 g, if dysrhythmias develop or refractory hypotension ensues.

20 Hyperchloremia has been increasingly recognized after administration of what standard resuscitation fluid?

Hyperchloremia is associated with massive resuscitation with normal saline and with metabolic acidosis caused by dilution of sodium bicarbonate, and it should be part of the differential diagnosis of metabolic acidosis in this setting. Besides after trauma, it has been noted during aortic, gynecologic, and cardiopulmonary bypass surgeries and during the management of sepsis.

SUGGESTED READING

1. Palmer B.F. Approach to fluid and electrolyte disorders and acid-base problems. Prim Care Clin Pract. 2008;35:195-213.

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