Calcium Disorders
Total serum calcium comprises three different fractions in equilibrium: 50% circulates in the form of free active calcium ion (ionized calcium), 40% nonspecifically bound to plasma albumin and 10% complexed to anions such as phosphates and citrates.
Mechanism
Calcium Calculation Corrected by Albumin
Because the traditional laboratory reports total serum calcium, any decrease in plasma albumin artificially decreases the reported concentration of calcium, without altering the actual levels of physiologically active ionized calcium. In the event of hypoalbuminemia, it is mandatory to correct the measured calcium value using the following mathematical equation:
Cacorrected (mg/dL) = Cameasured (mg/dL) + 0.8 · ( 4.0 - [Albumin] (g/dL) )
Severe hypercalcemia
Defined as a corrected calcium concentration greater than 14 mg/dL (or ionized calcium > 1.5 mmol/L). The main causes include primary hyperparathyroidism and malignant neoplasms (through paraneoplastic secretion of parathyroid hormone-related protein - PTHrP).
Security
Infusion Alert: Danger of Calcium Tissue Necrosis
The correction of severe symptomatic hypocalcemia or with prolongation of the QT interval of the ECG requires the intravenous administration of calcium in a controlled manner:
- Administer 1 to 2 ampoules of 10% Calcium Gluconate (equivalent to 90-180 mg of elemental calcium) diluted in 100 mL of 5% glucose serum to pass over a period of 10 to 20 minutes.
- Strictly avoid calcium extravasation into soft tissues: Calcium solution, especially calcium chloride, is extremely hyperosmolar and caustic to the peripheral venous endothelium. Its subcutaneous extravasation invariably induces severe tissue vasospasm, chemical cell necrosis and destructive cutaneous calcinosis. Venous access of adequate caliber and perfectly permeable must be guaranteed, preferring central lines.
Clinical
Clinical Protocol for the Treatment of Severe Hypercalcemia
1. Volume Expansion and Restoration of the Glomerular Filtration Rate: It is the fundamental initial pillar of the treatment. Patients with severe hypercalcemia present with profound dehydration due to a direct effect of calcium on the calcium-sensing receptor in the collecting duct, inducing transient nephrogenic diabetes insipidus.
Administer 2 to 4 liters of 0.9% Physiological Saline Solution in the first 24 hours. The massive intake of sodium competitively decreases passive calcium reabsorption at the branch of the loop of Henle, directly stimulating calciuresis.
2. Calcitonin: Administer 4 to 8 IU/kg subcutaneously every 12 hours. Inhibits osteoclastic bone resorption rapidly in a period of 4 to 6 hours. Its use is self-limited to the first 48 hours of evolution due to the development of tachyphylaxis due to internalization of its cellular receptors.
3. Long-Acting Bisphosphonates: They persistently inhibit systemic osteoclastic activity. The drug of choice is Zoledronic Acid in a single dose of 4 mg slowly intravenously to be administered over a period of 15 minutes. Its maximum calcium control effect is achieved between 2 and 4 days after its administration.
Symptomatic Hypocalcemia
Defined as corrected calcium less than 8.5 mg/dL (or ionized calcium < 1.1 mmol/L). It is clinically associated with an increase in peripheral neuromuscular excitability, classically manifesting by painful muscle spasms (tetany) and physical signs of nervous hyperreactivity:
- Chvostek sign: Reflex and involuntary contraction of the ipsilateral facial muscles when gently percussing the course of the facial nerve in front of the external auditory canal.
- Trousseau's sign: Painful spasm of the carpus (midwife's hand) induced by inflating the cuff of the sphygmomanometer above the patient's systolic blood pressure for a continuous period of 3 minutes.
Epistemis is educational review material. It is not a medical device, does not diagnose or prescribe treatment, and does not replace formal medical training, current clinical guidelines, or professional clinical judgment.
- System
- Fluid therapy, Electrolytes and Acid-Base
- Cluster
- Cation Homeostasis