The severity of signs and symptoms depends greatly on the rapidity of the fall in calcium. The more acute the drop in the serum calcium, the more likely are significant pathophysiologic changes. As serum calcium levels fall, neuronal membranes become increasingly more permeable to sodium, enhancing excitation. Potassium and magnesium have an antagonizing effect on this excitation.
Decreased ionized calcium levels reduce the strength of myocardial contraction primarily by inhibiting relaxation. They also decrease the sensitivity of the heart to digitalis. Hypocalcemia should be considered in patients with refractory heart failure.
Low ionized calcium levels increase PTH secretion, which mobilizes calcium from bone and decreases renal tubular absorption of phosphate and bicarbonate. This, in turn, may cause an increased absorption of chloride, producing a tendency to hyperchloremic hypophosphatemic renal tubular acidosis. A ratio of chloride to phosphate greater than 35 to 1 in meq/mg in the plasma is sometimes considered to be highly suggestive of hyperparathyroidism.
Increased cytoplasmic calcium activates phospholipase, which increases prostaglandin production and alters cell lipids. Increased cytoplasmic calcium also interferes with cell metabolism. Efforts by mitochondria to pump the excess calcium from the cytoplasm into the mitochondrial matrix greatly reduce adenosine triphosphate (ATP) formation. Consequently, giving calcium during shock or sepsis may transiently improve hemodynamics, but if cell metabolism does not also improve, some of the additional calcium moves into the cytoplasm within 30 to 40 min and further impairs cell metabolism.
Movement of calcium into ischemic cerebrovascular smooth muscle cells may cause persistent cerebral vasoconstriction with resultant failure of cerebral reperfusion after strokes or cardiac arrest. This may be a major cause of the poor results in management of these problems. Consequently, there has been some interest in the use of calcium blockers for cerebral resuscitation.
DIAGNOSIS Symptoms The most characteristic initial symptom of hypocalcemia following thyroid or parathyroid surgery is paresthesias around the mouth or in the fingertips. Hypocalcemia should be suspected in any patient who is irritable and has hyperactive deep tendon reflexes following neck surgery. It should also be suspected in patients who have seizures particularly if they have ever had thyroid surgery, even if many years previously.
Signs A positive Chvostek or Trousseau sign is generally considered to be good clinical evidence of hypocalcemia. A positive Chvostek sign is a twitch at the corner of the mouth when the examiner taps over the facial nerve just in front of the ear. However, it is present in about 10 to 30 percent of normal individuals. Nevertheless, eyelid muscle contraction with the Chvostek maneuver is said to be almost diagnostic of hypocalcemia.
Trousseau sign, which is generally a more reliable indicator of hypocalcemia, is positive if carpal spasm is produced when the examiner applies a blood pressure cuff to the upper arm and maintains a pressure above systolic for 3 min. The fingers are spastically extended at the interphalangeal joints and flexed at the metacarpophalangeal joints. The wrist is flexed and the forearm is pronated.
Laboratory Findings Signs of hypocalcemia may be found with normal total serum calcium levels if a patient is very alkalotic. Each 0.1 rise in pH lowers ionized calcium levels by about 3 to 8 percent. Consequently, a very alkalotic patient may have normal total serum calcium levels with ionic hypocalcemia. Similar signs and symptoms may be caused by hypomagnesemia, strychnine, or tetanus toxin.
Decreased plasma levels of ionized calcium are diagnostic, but one should also suspect ionic hypocalcemia if a patient has decreased levels of total calcium in the presence of normal plasma proteins. Primary hypoparathyroidism is characterized by a low serum PTH concentration, hyperphosphatemia, and hypocalcemia.
ECG The most characteristic ECG finding in hypocalcemia is prolonged QT intervals. However, the T wave is of normal width, and it is the ST segment that is really prolonged. This finding is usually seen with total serum calcium levels less than 6.0 mg/dL.
X-rays Radiologically, rickets is characterized by craniotabes, frontal skull bossing, rachitic rosary ribs, widened rib cage (Harrison groove), bowed legs, and, often, fractures. Other radiographic changes include cupping and splaying of the metaphyseal ends of long bones, widening between the metaphyses and epiphysis, bone demineralization, and thinning of cortical bone.
TREATMENT Treatment of hypocalcemia is tailored to the individual and directed toward the underlying cause. If a patient is asymptomatic, oral calcium therapy with or without vitamin D may be all that is required. Calcium lactate, calcium glubionate, calcium ascorbate, calcium carbonate, and calcium gluconate are available in oral preparations. Milk, because of the large amount of phosphate present, is not really a very good source of calcium, except in normal growing children who also need the phosphate.
Symptomatic patients following thyroid or parathyroid surgery are often treated with parenteral calcium. With severe acute hypocalcemia, 10 mL of 10% CaCl 2 (or 10 to 30 mL of 10% calcium gluconate) may be given intravenously (IV) over 10 to 20 min followed by a continuous IV drip providing 1 g of CaCl 2 over a period of 6 to 12 h. If the patient is not asymptomatic or if the hypocalcemia is not severe and prolonged for more than 10 to 14 days, treatment with calcium may not be required. One should not administer calcium rapidly IV to asymptomatic patients with mild to moderate hypocalcemia because it can cause severe unnecessary cardiovascular, neuromuscular, and renal complications.
During massive transfusions, if the blood is being given faster than 1 unit every 5 min, 10 mL of 10% calcium chloride can be given after every 4 to 6 units of blood if a patient is in shock or heart failure in spite of adequate volume replacement therapy. Calcium is seldom required during transfusions for elective surgery.
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