Electrolyte Imbalances—Part 4: Calcium Balance Disorders

   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%.

   Hypercalcemia presents with nonspecific signs and symptoms (Figure 4). They can manifest through the musculoskeletal, neurological, gastrointestinal, cardiovascular and renal systems. Realize that each patient presents differently, and all systems may not be affected in any one person. Therefore, the history and physical are crucial elements in determining the presence of this condition. Hypovolemia is commonly associated with hypercalcemia and can result in hypotension. It is more likely that blood pressure will be normal or elevated in this setting, though, as hypercalcemia results in vasoconstriction. Hypercalcemia potentiates digoxin, which may result in toxicity in hypercalcemic patients taking this medication. Uncommonly, severe hypercalcemia can cause atrioventricular and bundle branch blocks.

   Aside from symptomatically treating any conditions that exist, treatment of hypercalcemia in the prehospital setting is generally limited to recognition of the condition and transport to an appropriate facility. The administration of normal saline promotes renal excretion of calcium, as does administration of loop diuretics. The latter should be used with caution and are generally reserved for severe cases, as hypovolemia, hypokalemia and hypomagnesemia may exist and be worsened by loop diuretics.

Series Summary

   Although the technology currently exists to measure electrolyte levels in the prehospital setting, it is not widely used. However, in many cases the prehospital professional can determine the likely presence of electrolyte abnormalities. In most cases treatment is limited to recognition, supportive care and transport to an appropriate facility. However, in the setting of imminent arrest, aggressive treatment may be required.

   When faced with a patient who has a history conducive to and signs or symptoms consistent with the development of electrolyte imbalances, treatment decisions cannot be made arbitrarily. This can pose more risk to the patient than simply monitoring their condition. In the absence of actual electrolyte levels, decisions must be based on an appropriate history and physical, solid understanding of body processes, and knowledge of anatomy, physiology, pathophysiology and pharmacology, including home medications. With this knowledge appropriate treatment can be administered when indicated, and, more important, inappropriate treatment can be avoided when the patient is not in a periarrest condition.

   BIBLIOGRAPHY

   Braunwald E, Fauci AS, Kasper DL, et al. Harrison's Principles of Internal Medicine, 15th ed. New York, NY: McGraw-Hill, 2001.

    Marx JM, Hockberger RS, Walls RM, et al. Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed. Philadelphia, PA: Mosby, 2006.

   Tintinalli JE, Kelen GD, Stapczynski JS. Emergency Medicine: A Comprehensive Study Guide, 6th ed. New York, NY: McGraw-Hill, 2004.

 Robert Vroman, BS, NREMT-P, has been involved in all levels of EMS for almost 20 years, working with both rural and urban services as a provider and educator. He has a Bachelor’s degree in Emergency Medical Care from Western Carolina University, and is currently pursuing a Master’s of Education, specializing in Adult Education and Training at Colorado State University.