Electrolyte Abnormalities Sodium

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Hypernatremia (>150 mEq/L) results from a total sodium excess or relative fluid loss. This can be from prolonged administration of excess sodium or excessive loss of free water. Hyperglycemia can also act as an osmotic diuretic increasing free water loss. Drugs such as amphoteracin B, methicillin and gentamicin can cause a nephro-genic diabetes and subsequent free water loss.

Patients present with restlessness, delirium, weakness, tachycardia, decreased saliva, dry sticky mucous membranes, flushed skin, oliguria, fever and or heatstroke. Treatment includes administration of free water and minimizing sodium intake (<3 g/day). One half of the free water deficit should be administered over a 24 hour period to minimize edema.

Hyponatremia is a common finding in the surgical patient and is usually the result of excessive administration of H2O or hypotonic fluids. Patients may be symptomatic with levels <130 mEq/L and develop seizures <120 mEq/L. The presentation is with muscle twitching, increased DTRs, increased ICP, convulsions, hypertension, increased salivation, watery diarrhea, oliguria. In many cases there are

| Table 1.1. Percent total body weight as water

Percent Body Water

Infants 75-80%

Children 65%

Lean adult males 60%

Lean adult females 50%

Obese adults 40-45%

Elderly adult 47-52%

no symptoms until sodium below 120 mEq/L. Symptoms appear earlier in head injured patients causing increased ICP. In severe hyponatremia, small amounts of hypertonic NaCl are administered IV, followed by normal saline IV. (Note: serum sodium should not increase more than 12 mEq/L per liter in the first 24 hours.) If volume is expanded, restrict free water intake to 1500 mL per 24 hours. Cirrhotic patients may also require spironolactone or furosemide to mobilize free water.


Hyperkalemia results from renal failure, acidosis, iatrogenic causes. Signs include nausea, vomiting, diarrhea, peaked T waves, widened QRS complex, depressed S-T segments. Fatal ventricular arrhythmias can result demanding rapid management. Diuresis with infusion of NaCl infusion with furosemide 40-80 mg can also decrease potassium levels over time. Hemodialysis may be required in extreme cases (Table 1.2).

Hypokalemia results from loop diuretics, vomiting, alkalosis, iatrogenic causes. It can also lead to atrial and ventricular arrhythmias but usually not until levels fall below 3 mEq/L. Treatment is with KCl IV if adequate urinary output is established (not to exceed 20 mEq per hour unless the patient is on a cardiac monitor). Each 10 mEq of KCl will only raise the serum potassium level by 0.1 mEq/L.

Table 1.2. Treatment of hyperkalemia



Calcium gluconate (10%)

Reduces electrical excitability of the heart


Drives potassium into cells by inducing

transient alkalosis


Drives potassium into cells

Sodium polystyrene sulfonate

Binds potassium


(0.1 mEq per gram)


Hypocalcemia is caused by necrotizing fasciitis, renal failure, intestinal fistulas, post-op from excision of parathyroid adenoma, hypoparathyroidism and magnesium depletion. In acute pancreatitis calcium is sequestered in saponified fat. Hypocalciemia can occur after massive transfusions and should routinely be replaced if >6 units of blood are given. Signs include hyperactive DTRs, muscle spasms, positive Chvostek sign, tetany, carpopedal spasm, convulsions, prolongation of the Q-T interval, numbness and tingling of the circumoral region and the tips of the digits. Treatment is by managing the underlying cause, administration of IV calcium gluconate or calcium chloride.

Hypercalcemia is found in hyperparathyroidism and malignancies with bony metastases and paraneoplastic syndromes. Signs include easy fatigue, weakness, anorexia, nausea, vomiting, weight loss, stupor, coma, body aches, headaches, thirst, polydipsia and polyuria. Treatment is with normal saline fluid resuscitation, furo-semide, sodium phosphate, corticosteroids, plicamycin, calcitonin. Surgical excision is employed for patients with hyperparathyroidism in hypercalcemic crisis.


Only 1% of magnesium is found in the extracellular space with the remaining in bone and muscle. Hypomagnesemia can result in hypermetabolic states, muscle wasting, starvation, malabsorption, fistula, primary aldosteronism, chronic alcoholism. Signs include hyperactive tendon reflexes, muscle tremors, tetany, positive Chvostek sign, delirium and convulsions. Treatment is with intravenous or oral administration of magnesium.

Hypermagnesemia is fairly rare with causes including renal failure, burns, massive trauma, volume deficit and acidosis. Patients will have lethargy, weakness, loss of DTRs, coma, paralysis, respiratory or cardiac arrest, widened QRS complex, elevated T waves and/or increased P-R interval. Treatment is with a brisk diuresis, hydration and correction of underlying disease process.

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