Hypocalcemia

In medicine, hypocalcemia is the presence of low serum calcium levels in the blood, usually taken as less than 2.1 mmol/L or 9 mg/dl or an ionized calcium level of less than 1.1 mmol/L (4.5 mg/dL). It is a type of electrolyte disturbance. In the blood, about half of all calcium is bound to proteins such as serum albumin, but it is the unbound, or ionized, calcium that the body regulates. If a person has abnormal levels of blood proteins, then the plasma calcium may be inaccurate. The ionized calcium level is considered more clinically accurate in this case. In the setting of low serum albumin (frequently seen in patients with chronic diseases, hepatic disease or even long term hospitilization), the formula for corrected calcium is: CorrCa = Measured serum Ca + [(4.0 - measured serum albumin) * 0.08]. Thus, if the albumin is low, the measured calcium may appear low when in fact it is physiologically within normal limits.

Cause
It manifests as a symptom of a parathyroid hormone deficiency/malfunction, a Vitamin D deficiency, or unusually high magnesium levels hypermagnesemia, or low magnesium levels hypomagnesemia.

More specifically, hypocalcemia may be associated with low PTH levels as seen in hereditary hypoparathyroidism, acquired hypoparathyroidism (surgical removal MCC of hypoparathyroidism), and hypomagnesemia. Hypocalcemia may be associated with high PTH levels when the parathyroid hormone is ineffective; in chronic renal failure, the hydroxylation of vitamin D is ineffective, calcium levels in the blood fall, and high PTH levels are produced in response to the low calcium, but fail to return calcium levels to normal.


 * Eating disorders
 * Excessive dietary magnesium, as with supplementation.
 * Prolonged use of medications/laxatives containing magnesium
 * Absent parathyroid hormone (PTH)
 * Hereditary hypoparathyroidism
 * Acquired hypoparathyroidism
 * Hypomagnesemia
 * Following parathyroidectomy, "Hungry Bone Syndrome"
 * Following thyroidectomy, the parathyroid glands are located very close to the thyroid and are easily injured or even accidentally removed during thyroidectomy
 * In DiGeorge Syndrome, a disease characterized by the failure of the third and fourth pharyngeal pouches to develop, the parathyroid glands do not form and there is thus a lack of PTH.
 * Ineffective PTH
 * Chronic renal failure
 * Absent active vitamin D
 * Decreased dietary intake
 * Decreased sun exposure
 * Defective Vitamin D metabolism
 * Anticonvulsant therapy
 * Vitamin-D dependent rickets, type I
 * Ineffective active vitamin D
 * Intestinal malabsorption
 * Vitamin-D dependent rickets, type II
 * Pseudohypoparathyroidism
 * Deficient PTH
 * Severe acute hyperphosphatemia
 * Tumor lysis syndrome
 * Acute renal failure
 * Rhabdomyolysis (initial stage)
 * Osteitis fibrosa following parathyroidectomy
 * Exposure to hydrofluoric acid
 * As a complication of pancreatitis
 * As a result of hyperventilation
 * Alkalosis, often caused by hyperventilation
 * Chelation Therapy
 * Neonatal hypocalcemia
 * Very low birth weight (less than 1500 grams)
 * Gestational age less than 32 weeks

Symptoms

 * Petechia which appear as one-off spots, then later become rashes.
 * Perioral tingling and parasthesia, 'pins and needles' sensation over the extremities of hands and feet. This is the earliest symptom of hypocalcemia.
 * Tetany, carpopedal spasm 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 zygoma will produce facial spasms)
 * Tendon reflexes are hyperactive
 * Life threatening complications
 * Laryngospasm
 * Cardiac arrhythmias
 * EKG changes
 * Prolonged QTc
 * Prolonged ST interval

Management

 * Two ampoules of intravenous calcium gluconate 10% is given slowly in a period of 10 minutes, or if the hypocalcemia is severe, calcium chloride is given instead.
 * Maintenance doses of both calcium and vitamin-D (often as 1,25-(OH)2-D3, i.e. calcitriol) are often necessary to prevent further decline.

Animals
Farm animals, mainly cows, can suffer hypocalcaemia (or milk fever) after calving. This is due to a large calcium demand and a slow response from the animal in terms of intestinal absorption or bone resorption. If a cow or other animal is affected it will collapse and have muscle spasms. It will eventually enter a coma and can die.

The treatment is an injection of calcium gluconate. It can be prevented in part by avoiding excess calcium, or more commonly, by regulating potassium in the diet before calving.

Alkalosis
As blood plasma hydrogen ion concentration decreases, caused by respiratory or metabolic alkalosis, freely ionized calcium concentration decreases. This freely ionized calcium is the biologically active component of blood calcium. Since a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, 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 hypocalcemia related to alkalosis is partially responsible for the cerebral vasoconstriction that causes the lightheadedness, fainting, and parasthesia often seen with hyperventilation.