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Hypocalcemia

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Hypocalcemia

In medicine, hypocalcaemia (or hypocalcemia) is the presence of low serum calcium levels in the blood. Physiologically, blood calcium is tightly regulated within a narrow range for proper cellular processes. Calcium in the blood exists in three primary states: bound to proteins (mainly albumin), bound to anions such as phosphate and citrate, and as free (unbound) ionized calcium. Only the ionized calcium is physiologically active. Normal blood calcium level is between 8.5 to 10.5 mg/dL (2.12 to 2.62 mmol/L) and that of ionized calcium is 4.65 to 5.25 mg/dL (1.16 to 1.31 mmol/L). Common causes of hypocalcemia include hypoparathyroidism, vitamin D deficiency, and chronic kidney disease. Symptoms of hypocalcemia include neuromuscular irritability (including tetany as manifested by Chvostek's sign or Trousseau's sign, bronchospasm), electrocardiographic changes, and seizures. Treatment is dependent upon the cause, but most commonly includes supplementation of calcium and some form of vitamin D or its analogues.

Diagnosis

Because a significant portion of calcium is bound to albumin, any alteration in the level of albumin will affect the level of calcium is measured. 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]). Another way to determine the calcium level is to measure directly the ionized calcium level.

Causes

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, partial or total thyroidectomy, or neck dissection for head and neck cancers. Hypoparathyroidism may also be due to autoimmune destruction of the glands.


Symptoms

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, diminished calcium lowers the threshold for depolarization.[1] The symptoms can be recalled by the mnemonic "CATS go numb"- Convulsions, Arrhythmias, Tetany and numbness/parasthesias in hands, feet, around mouth and lips.

  • 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
  • Tendon reflexes are hyperactive
  • Life threatening complications
  • ECG changes include:
    • 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 fibrillation 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, as with any type of ventricular tachycardia, causes death, unless the patient can be electrically cardioverted, and returned to a normal cardiac rhythm.)

Management

  • Two ampoules of intravenous calcium gluconate 10% is given slowly in a period of 10 minutes, or if the hypocalcaemia is severe, calcium chloride is given instead. This is only appropriate if the hypocalcemia is acute and has occurred over a relatively short time frame. But if the hypocalcemia has been severe and chronic, then this regimen can be fatal, because there is a degree of acclimatization that occurs. The neuromuscular excitability, cardiac electrical instability, and associated symptoms are then not cured or relieved by prompt administration of corrective doses of calcium, but rather exacerbated. Such rapid administration of calcium would result in effective over correction – symptoms of hypercalcemia would follow.
  • However, in either circumstance, 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.

See also

References

External links

  • Hypocalcemia Cleveland Clinic
  • Endotext
  • EKG abnormalities associated with hypocalcemia
  • Seizures due to hypocalcaemia worsened by shifting towards alkalosis by bicarbonate therapy
  • Hypocalcemia eMedicine overview
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