Electrolyte Imbalances: Part 4

   In February EMS World began a four-part look at electrolyte imbalances. This month we conclude with calcium balance disorders.

   Calcium is essential for many body functions, including cell membrane permeability, hormone secretion, growth and ossification of bones, muscle contraction and, most important, the transmission of nerve impulses. Unlike sodium and potassium, total body calcium is measured in mg/dl (milligrams per deciliter). Normal levels are 8.7 to 10.4 mg/dl. Of the body's calcium, 99% is stored in the bones, teeth and nails, and the remaining 1% is found in the serum. Approximately 50% of the calcium located in the serum is unbound and ionized. It is this that is used for the various chemical reactions involving calcium. Its normal range is 2.1 to 2.6 mEq/L. Hypocalcemia indicates total calcium levels below 8.7 mg/dl or ionized calcium levels below 2.0 mEq/L, while hypercalcemia indicates total calcium levels above 10.4 mg/dl or ionized calcium levels above 2.6 mEq/L.

   Calcium is ingested daily, and a healthy diet generally contains enough calcium to meet an individual's needs. Calcium is absorbed in the small intestine and excreted through the urine and feces. A small amount of calcium can also be excreted through the skin.

   Calcium levels are closely regulated by parathyroid hormone, calcitonin and metabolized vitamin D (calcitriol). In the setting of hypocalcemia, PTH promotes the release of stored calcium from the bones and teeth in an attempt to raise serum calcium levels. Additionally, intestinal and renal absorption of calcium is enhanced in the presence of PTH. Calcitriol further promotes the release of calcium from the bones and teeth and absorption of calcium from the small intestine, and impairs calcium excretion by the kidneys. In the setting of hypercalcemia, calcitonin is released from the thyroid gland and promotes the movement of calcium into the bones and teeth.

   As with potassium, changes in pH can have an effect on calcium. In the presence of alkalosis, the binding of calcium to plasma proteins is enhanced, thereby reducing ionized calcium, leading to the effects of hypocalcemia. During acidosis, this binding is inhibited, increasing ionized calcium and resulting hypercalcemia. These conditions can occur even in the absence of changes in total calcium levels, as it is the amount of ionized calcium being affected.

   Hypocalcemia can have a multitude of causes, including factors that affect PTH, calcitonin and vitamin D levels (Figure 1). Although many of the signs and symptoms of hypocalcemia generally present through the neuromuscular system, cardiovascular function can be affected in severe cases. In these situations patients often present similarly to patients who have overdosed on calcium channel blockers, including with hypotension refractory to fluids, bradycardia and cardiovascular collapse, all of which may lead to hypoperfusion of the brain For signs and symptoms of hypocalcemia, see Figure 2.

   Prehospital treatment for hypocalcemia is generally limited to recognition of the condition and transport to an appropriate facility. Life-threatening conditions must be addressed, and associated conditions are treated symptomatically with standard interventions. Calcium levels are rarely corrected in the field through the administration of calcium-containing solutions. However, the IV administration of 10 ml of 10% calcium chloride or calcium gluconate may be appropriate in the setting of suspected hypocalcemia associated with seizures, hypotension, cardiac dysrhythmias or other significant signs and symptoms.

   Hypercalcemia is a fairly common condition, but emergency treatment is generally not indicated or needed unless the patient enters a hypercalcemic crisis, defined as a calcium level of greater than 14 mg/dl. Primary hyperparathyroidism and malignant tumors are two of the more common causes of hypercalcemia, although medications and endocrine disorders can also cause it (Figure 3). When associated with malignant tumors, the mortality rate of acute hypercalcemia can be as high as 50% to 75%.