Hypercalcemia

Pathophysiology

• Hypercalcemia slows cardiac conduction and decreases automaticity.
• Due to the creation of a tubular defect, hypercalcemia impairs the concentrating ability in the kidney. This leads to profound dehydration.
• Prolonged increases in calcium, especially in conjunction with increased phosphorus, leads to deposition of the solid phase in tissues throughout the body. Deposition in the conduction system of the heart and the renal parenchyma may cause permanent organ dysfunction.

Diagnosis and Evaluation

• Symptoms of hypercalcemia are varied and span multiple systems. They include weakness, lethargy, polyuria, renal calculi, bony and abdominal pain and other gastrointestinal symptoms. As calcium continues to rise, life-threatening manifestations are cardiac (dysrhythmias) and neurological (seizures, coma). Cardiac arrest may occur at levels above 20.

Laboratory/Studies

• STAT EKG should be performed, looking for signs of cardiac toxicity such as shortened QT interval, flattened T waves, conduction delays and blocks.
• EKG changes are of special concern in the presence of digitalis as digitalis effects are amplified.
• Measure STAT electrolytes, initially including Mg, PO4 and albumin and follow electrolytes every 1-2 h during correction.
• Consider head CT to rule out intracranial pathology

ED Management

• Decreased level of consciousness (LOC) may cause airway obstruction and may require airway adjuncts and/or intubation.
• Saline diuresis is the cornerstone of management in the ED, as most of these patients are significantly dehydrated. Fluid resuscitation with normal saline should commence prior to the initiation of loop diuretics, hypocalcemia.
• The clinician should not be misled by the presence of hypertension. Despite dehydration, hypercalcemic patients may be hypertensive secondary to arteriolar vasoconstriction.
• Thiazide diuretics are to be avoided as they raise calcium
• Dialysis may be necessary for renal patients
• Bisphosphanates, mithramycin, calcitonin and steroids are not usually necessary in the initial resuscitation, but may be considered after specialist consultation, hyperkalemia.
• Hyperreflexia, fasciculations and alteration of mental status progressing to coma may be present. Look for signs of focality on neurological examination and consider other causes of neurological deficits.