Hypoparathyroidism is a common cause of hypocalcemia. Calcium is tightly regulated by the parathyroid hormone (PTH). In response to low calcium levels, PTH induces the kidneys to reabsorb calcium, the kidneys to increase production of calcitriol (the active form of vitamin D) thereby increasing intestinal absorption of calcium, and the bones to release calcium. These actions lead to a re-balance in the blood calcium levels. However, in the setting of absent, decreased, or ineffective PTH hormone, the body loses this regulatory function, and hypocalcemia ensues. Hypoparathyroidism is commonly due to surgical destruction of the parathyroid glands via parathyroidectomy or neck dissection for head and neck cancers. Hypoparathyroidism may also be due to autoimmune destruction of the glands.
- Eating disorders
- Prolonged vomiting (e. G. With a viral illness)
- Exposure to mercury, including infantile acrodynia
- Excessive dietary magnesium, as with supplementation.
- Excessive dietary zinc, as with supplementation (causes rapid hypocalcemia).
- Prolonged use of medications/laxatives containing magnesium
- Chelation therapy for metal exposure, particularly EDTA
- Osteoporosis treatment or preventive agents, such as bisphosphonates and denosumab.
- Agents for the treatment of hypercalcemia, such as Calcitonin.
- Chronic kidney failure
- Absent active vitamin D Decreased dietary intake Decreased sun exposure Defective Vitamin D metabolism Anticonvulsant therapy Vitamin-D dependent rickets, type I
- Decreased dietary intake
- Decreased sun exposure
- Defective Vitamin D metabolism Anticonvulsant therapy Vitamin-D dependent rickets, type I
- Anticonvulsant therapy
- Vitamin-D dependent rickets, type I
- Ineffective active vitamin D Intestinal malabsorption Vitamin-D dependent rickets, type II
- Intestinal malabsorption
- Vitamin-D dependent rickets, type II
- Pseudohypoparathyroidism
- Severe acute hyperphosphataemia
- Tumour lysis syndrome
- Acute kidney failure Rhabdomyolysis (initial stage)
- Rhabdomyolysis (initial stage)
- Exposure to hydrofluoric acid which can be fatal if 2.5% of skin is exposed
- As a complication of pancreatitis
- Alkalosis, often caused by hyperventilation As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic alkalosis, the concentration of freely ionized calcium, the biologically active component of blood calcium, decreases. Because a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium. For every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L. This hypocalcaemia related to alkalosis is partially responsible for the cerebral vasoconstriction that causes the lightheadedness, fainting, and paraesthesia often seen with hyperventilation. Tetany may also be seen with this condition.
- As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic alkalosis, the concentration of freely ionized calcium, the biologically active component of blood calcium, decreases. Because a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium. For every 0.1 increase in pH, ionized calcium decreases by about 0.05 mmol/L. This hypocalcaemia related to alkalosis is partially responsible for the cerebral vasoconstriction that causes the lightheadedness, fainting, and paraesthesia often seen with hyperventilation.
- Tetany may also be seen with this condition.
- Neonatal hypocalcemia Very low birth weight (less than 1500 grams) Gestational age less than 32 weeks
- Very low birth weight (less than 1500 grams)
- Gestational age less than 32 week.
Because a significant portion of calcium is bound to albumin, any alteration in the level of albumin will affect the measured level of calcium. A corrected calcium level based on the albumin level is: Corrected calcium (mg/dL) = measured total Ca (mg/dL) + 0.8 * (4.0-serum albumin g/dL).
The neuromuscular symptoms of hypocalcemia are caused by a positive bathmotropic effect due to the decreased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, reduced calcium lowers the threshold for depolarization. The symptoms can be recalled by the mnemonic "CATs go numb"-convulsions, arrhythmias, tetany, and numbness in the hands and feet and around the mouth.
- Petechiae which appear as on-off spots, then later become confluent, and appear as purpura (larger bruised areas, usually in dependent regions of the body).
- Oral, perioral and acral paresthesias, tingling or 'pins and needles' sensation in and around the mouth and lips, and in the extremities of the hands and feet. This is often the earliest symptom of hypocalcaemia.
- Carpopedal and generalized tetany (unrelieved and strong contractions of the hands, and in the large muscles of the rest of the body) are seen.
- Latent tetany Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic) Chvostek's sign (tapping of the inferior portion of the cheekbone will produce facial spasms)
- Trousseau sign of latent tetany (eliciting carpal spasm by inflating the blood pressure cuff and maintaining the cuff pressure above systolic)
- Chvostek's sign (tapping of the inferior portion of the cheekbone will produce facial spasms)
- Tendon reflexes are hyperactive
- Life-threatening complications Laryngospasm Cardiac arrhythmias
- Laryngospasm
- Cardiac arrhythmias
- Effects on cardiac output Negative chronotropic effect, or a decrease in heart rate. Negative inotropic effect, or a decrease in contractility
- Negative chronotropic effect, or a decrease in heart rate.
- Negative inotropic effect, or a decrease in contractility
- - ECG changes include the following: Intermittent QT prolongation, or intermittent prolongation of the QTc (corrected QT interval) on the EKG (electrocardiogram) is noted. The implications of intermittent QTc prolongation predisposes to life-threatening cardiac electrical instability (and this is therefore a more critical condition than constant QTc prolongation). This type of electrical instability puts the patient at high risk of torsades de pointes, a specific type of ventricular tachycardia which appears on an EKG (or ECG) as something which looks a bit like a sine wave with a regularly increasing and decreasing amplitude. (Torsades de pointes can cause death, unless the patient can be medically or electrically cardioverted and returned to a normal cardiac rhythm.)
- Intermittent QT prolongation, or intermittent prolongation of the QTc (corrected QT interval) on the EKG (electrocardiogram) is noted. The implications of intermittent QTc prolongation predisposes to life-threatening cardiac electrical instability (and this is therefore a more critical condition than constant QTc prolongation). This type of electrical instability puts the patient at high risk of torsades de pointes, a specific type of ventricular tachycardia which appears on an EKG (or ECG) as something which looks a bit like a sine wave with a regularly increasing and decreasing amplitude. (Torsades de pointes can cause death, unless the patient can be medically or electrically cardioverted and returned to a normal cardiac rhythm.