Hypocalcemia in Emergency Medicine
- Author: Christopher B Beach, MD, FACEP, FAAEM; Chief Editor: Erik D Schraga, MD more...
Background
Calcium regulation is critical for normal cell function, neural transmission, membrane stability, bone structure, blood coagulation, and intracellular signaling. The essential functions of this divalent cation continue to be elucidated, particularly in head injury/stroke and cardiopulmonary effects. Depending on the cause, unrecognized or poorly treated hypocalcemic emergencies can lead to significant morbidity or death.
Pathophysiology
Metabolic and endocrine emergencies require an understanding of normal physiology.
Calcium regulation is maintained by parathyroid hormone (PTH), vitamin D, and calcitonin through complex feedback loops. These compounds act primarily at bone, renal, and GI sites. Calcium also is affected by magnesium and phosphorus.[1]
Distribution
Approximately 99% of calcium is found in bone, and 1% is found in extracellular fluid. Of this 1%, 50% is in the free (active) ionized form (1-1.15 mmol/L), 40% is bound to protein (predominantly albumin), and 10% is complexed with anions (eg, citrate).
Homeostasis is maintained by an extracellular to intracellular gradient, which is largely due to abundant high-energy phosphates intracellularly.
Intracellular calcium regulates cAMP-mediated messenger systems and most cell organelle functions. Ion pumps control levels.
Extracellular calcium levels are maintained at 8.7-10.4 mg/dL. Variations depend upon serum pH, protein and anion levels, and calcium-regulating hormone function.
Total body levels of calcium are controlled by a complex feedback system. PTH directly targets the bone and the kidneys to increase serum calcium levels. Indirectly, through vitamin D, it causes intestinal calcium absorption. Vitamin D directly targets GI absorption of calcium to increase calcium levels. Calcitonin lowers calcium by targeting bone, renal, and GI losses.
Epidemiology
Frequency
United States
Epidemiology of hypocalcemia versus other electrolyte abnormalities has not been performed. During the last 20 years, laboratory tests have quantified serum and ionized calcium and PTH levels, enabling easier diagnosis. The incidence of ionized hypocalcemia is difficult to quantify, but it has been reported to be 15-50% for ICU patients. In a series of 500 postsurgical patients operated on for hyperparathyroidism, 2% had permanent hypocalcemia.[2]
International
Similar standards exist in other industrialized nations throughout the world.
Mortality/Morbidity
Severe, symptomatic hypocalcemia may result in cardiovascular collapse, hypotension unresponsive to fluids and vasopressors, and dysrhythmias. Clinically evident hypocalcemia generally presents in milder forms and is usually the result of a chronic disease state. Chronic or subacute complaints secondary to mild or moderate hypocalcemia are more likely to be a chief complaint in the ED than severe symptomatic hypocalcemia.
- Neurologic sequelae (eg, tetany, seizures) may occur.
- Death is rare but has been reported.
- The disease causing hypocalcemia may have greater impact on morbidity than hypocalcemia itself.
Sex
The incidence in males and females is equal.
Age
Hypocalcemia spans all ages. The differential diagnosis varies depending on the age of the patient and the coexistent medical illnesses.
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