Calcium hypocalcemia

Low total serum calcium (hypocalcemia) may be due to either a reduction in the albumin-bound calcium, the free firaction of calcium, or both (Box 49-Hypoalbu-minemia is the most common cause of pseudohypocalcemia (decreased total and norma free calcium) because 1 g/dL of albumin binds approximately 0.8 mg/dL of calcium. Common clinical conditions associated with low serum... 

PTH deficiency can cause h5 ocalcemia, which is a deficit of serum calcium. Hypocalcemia can also be caused by vitamin D deficiency, renal impairment, or diuretic therapy. 

Severe exposure to hydrogen fluoride by any route will cause the lowering of serum calcium (hypocalcemia), which can be fatal if not treated. Hypocalcemia is possible in all instances of inhalation or ingestion and whenever skin bums exceed 25 in (164 cm ). 

Mild exposure to HF via inhalation can irritate the nose, throat, and respiratory system. The onset of symptoms may be delayed for several hours. Severe exposure via inhalation can cause nose and throat bums, lung inflammation, and pulmonary edema, and can also result in other systemic effects including hypocalcemia (depletion of body calcium levels), which if not promptly treated can be fatal. Permissible air concentrations are (42) OSHA PEL, 3 ppm (2.0 mg/m ) as E OSHA STEL, 6 ppm (5.2 mg/m ) as E and ACGIH TLV, 3 ppm (2.6 mg/m ) as E. Ingestion can cause severe mouth, throat, and stomach bums, and maybe fatal. Hypocalcemia is possible even if exposure consists of small amounts or dilute solutions of HE. 

Other Calcium Disorders. In addition to hypocalcemia, tremors, osteoporosis, and muscle spasms (tetary), calcium deficiency can lead to rickets, osteomalacia, and possibly heart disease. These, as well as Paget s disease, can also result from faulty utilization of calcium. Calcium excess can lead to excess secretion of calcitonin, possible calcification of soft tissues, and kidney stones when combined with magnesium deficiency. 

Magnesium ion is essential for normal Ca " and K" metaboHsm. In acute experimental magnesium deficiency in humans, hypocalcemia occurs despite adequate calcium intake and absorption and despite normal renal and parathyroid functions. Negative K" balance is also observed. AH biochemical and clinical abnormaHties disappear upon restoration of adequate amounts of magnesium to the diet (64). 

Calcium is readily abundant in the mammalian diet. A 70 kg human contains approximately 1200 g of calcium and has a daily intake of 1100 mg/day. There are no pubHshed exposure limits (38). Low levels of calcium in the blood, hypocalcemia, can lead to tetany high levels, hypercalcemia, can lead to coma and death. Calcium toxicity, above 160 mg/L in the blood, is not related to an excessive intake of calcium. 

Monitor for hypernatremia or hyperkalemia, hypocalcemia, and metastatic soft tissue deposition of calcium-phosphate crystals... 

Severe hyperphosphatemia, presenting as hypocalcemia and tetany should be treated with hemodialysis and possibly careful intravenous calcium administration (see management of hypocalcemia)... 

Parathyroidectomy is a treatment of last resort for sHPT, but should be considered in patients with persistently elevated iPTH levels above 800 pg/mL (800 ng/L) that is refractory to medical therapy to lower serum calcium and/or phosphorus levels.39 A portion or all of the parathyroid tissue may be removed, and in some cases a portion of the parathyroid tissue may be transplanted into another site, usually the forearm. Bone turnover can be disrupted in patients undergoing parathyroidectomy whereby bone production outweighs bone resorption. The syndrome, known as hungry bone syndrome, is characterized by excessive uptake of calcium, phosphorus, and magnesium for bone production, leading to hypocalcemia, hypophosphatemia, and hypomagnesemia. Serum ionized calcium levels should be monitored frequently (every 4 to 6 hours for the first 48 to 72 hours) in patients receiving a parathyroidectomy. Calcium supplementation is usually necessary, administered IV initially, then orally (with vitamin D supplementation) once normal calcium levels are attained for several weeks to months after the procedure. 

Cinacalcet is a calcimimetic that increases the sensitivity of receptors on the parathyroid gland to serum calcium levels to reduce PTH secretion. Cinacalcet maybe beneficial in patients with an increased Ca-P product who have elevated PTH levels and cannot use vitamin D therapy. Because the effects of cinacalcet on PTH can reduce serum calcium levels and result in hypocalcemia, cinacalcet should not be used if serum calcium levels are below normal. 

For acute symptomatic hypocalcemia, 200 to 300 mg of elemental calcium is administered IV and repeated until symptoms are fully controlled. This is achieved by infusing 1 g of calcium chloride or 2 to 3 grams of calcium at a rate no faster than 30 to 60 mg of elemental calcium per minute. More rapid administration is associated with hypotension, bradycardia, or cardiac asystole. Total calcium concentration is commonly monitored in critically ill patients. Under normal circumstances, about half of calcium is loosely bound to serum proteins while the other half is free. Total calcium concentration measures bound and free calcium. Ionized calcium measures free calcium only. Under usual circumstances, a normal calcium level implies a normal free ionized calcium level. Ionized calcium should be obtained in patients with comorbid conditions that would lead to inconsistency between total calcium and free serum calcium (abnormal albumin, protein, or immunoglobulin concentrations). For chronic asymptomatic hypocalcemia, oral calcium supplements are given at doses of 2 to 4 g/day of elemental calcium. Many patients with calcium deficiency have concurrent vitamin D deficiency that must also be corrected in order to restore calcium homeostasis.2,37,38... 

Because the severity of symptoms and the absolute serum concentration are poorly correlated in some patients, institution of therapy should be dictated by the clinical scenario. All patients with hypercalcemia should be treated with aggressive rehydration normal saline at 200 to 300 mL/hour is a routine initial fluid prescription. For patients with mild hypocalcemia, hydration alone may provide adequate therapy. The moderate and severe forms of hypercalcemia are more likely to have significant manifestations and require prompt initiation of additional therapy. These patients may present with anorexia, confusion, and/or cardiac manifestations (bradycardia and arrhythmias with ECG changes). Total calcium concentrations greater than 13 mg/dL (3.25 mmol/L) are particularly worrisome, as these levels can unexpectedly precipitate acute renal failure, ventricular arrhythmias, and sudden death. 

Hyperphosphatemia is generally benign and rarely needs aggressive therapy. Dietary restriction of phosphate and protein is effective for most minor elevations. Phosphate binders such as aluminum-based antacids, calcium carbonate, calcium acetate (PhosLo , Nabi), sevelamer (Renagel , Genzyme), and lanthanum carbonate (Fosrenol , Shire) may be necessary for some patients.43 If patients exhibit findings of hypocalcemia (tetany), IV calcium should be administered empirically. 

Patients with tumor lysis syndrome experience a wide range of metabolic abnormalities. The massive cell lysis that occurs leads to the release of intracellular electrolytes, resulting in hyperkalemia and hyperphosphatemia. High concentrations of phosphate bind to calcium, leading to hypocalcemia and calcium phosphate precipitation in the renal tubule. Purine nucleic acids are also released that are subsequently metabolized to uric acid... 

Electrolyte disturbances that develop in patients with tumor lysis syndrome should be managed aggressively to avoid renal failure from hyperphosphatemia and hypocalcemia and cardiac signs from hyperkalemia. One exception pertains to the use of intravenous calcium for hypocalcemia. Adding calcium may cause further calcium phosphate precipitation in the presence of hyperphosphatemia and should be used cautiously. 

Foscarnet Pentamidine IV Increased risk of severe nephrotoxicity/hypocalcemia Monitor renal functiorVserum calcium... 

HYPOCALCEMIA (TOTAL SERUM CALCIUM LESS THAN 8.5 MG/DL)... 

Hypomagnesemia can be associated with severe symptomatic hypocalcemia that is unresponsive to calcium replacement therapy. 

Hypocalcemia associated with hypoalbuminemia requires no treatment because ionized plasma calcium concentrations are normal. 

Acute, symptomatic hypocalcemia requires IV administration of soluble calcium salts (Fig. 78-3). 

Oral calcium supplementation (e.g., 1 to 3 g/day of elemental calcium) is indicated for chronic hypocalcemia due to hypoparathyroidism and vitamin D deficiency. If serum calcium does not normalize, a vitamin D preparation should be added. 

The major effect of hyperphosphatemia is related to the development of hypocalcemia and damage resulting from calcium phosphate deposits. 

Severe symptomatic hyperphosphatemia manifesting as hypocalcemia and tetany is treated by the IV administration of calcium salts. 

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