Calcium and Phosphorus
Calcium and phosphorus are responsible for much of the structural integrity of the bony skeleton. Although neither is found in abundance in the soft tissues, both have an important role in vital cell functions. Phosphorus participates in energy storage and utilization, while calcium participates in blood coagulation, neuromuscular transmission, and smooth muscle contraction.
I. Calcium in Plasma
Calcium is the most abundant electrolyte in the human body (the average adult has more than half a kilogram of calcium), but 99% is in bone (1,2).
A. Plasma Fractions
About half of the calcium in plasma is ionized (biologically active), and the other half is either bound to albumin (80%) or complexed to phosphates and sulfates (20%) (1).
The concentration of total and ionized calcium in plasma is shown in Table 30.1.
Hypoalbuminemia decreases the total plasma calcium without changing the ionized calcium. A variety of correction factors have been proposed for adjusting the total plasma calcium in patients with hypoalbuminemia, but none are reliable (3,4). However, this adjustment
is not necessary, since the ionized calcium fraction is not altered by hypoalbuminemia.
Ionized calcium can be measured in whole blood, plasma, or serum with ion-specific electrodes that are now available in most clinical laboratories.
Table 30.1 Normal Ranges for Calcium and Phosphate in Blood | ||||||||||||||||||||
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II. Ionized Hypocalcemia
Ionized hypocalcemia is extremely common in ICU patients (with an incidence of 88% in one study) (5), and there are several predisposing conditions.
A. Etiologies
The common disorders associated with hypocalcemia in ICU patients are listed in Table 30.2. Hypoparathyroidism is a leading cause of hypocalcemia in outpatients, but is not a consideration in the ICU unless neck surgery has been performed recently.
Table 30.2 Causes of Ionized Hypocalcemia in the ICU | ||||||||
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Magnesium depletion promotes hypocalcemia by inhibiting parathormone secretion, and reducing end-organ responsiveness to parathormone (see References 21 and 22 in Chapter 29). The hypocalcemia in these cases is refractory to calcium replacement, and correction requires magnesium replacement.
Alkalosis promotes the binding of calcium to albumin, and thereby reduces the fraction of ionized calcium in blood.
Ionized hypocalcemia has been reported in 20% of patients receiving blood transfusions (6). The culprit is citrate anticoagulant in banked blood, which binds calcium.
A number of drugs can bind calcium and reduce ionized calcium levels (6). These include aminoglycosides, cimetidine, heparin, and theophylline.
Ionized hypocalcemia can accompany renal failure as a
result of phosphate retention and impaired conversion of vitamin D to its active form in the kidneys. Treatment is aimed at lowering phosphate levels in blood.
The acidosis in renal failure can decrease the binding of calcium to albumin, so a decrease in total serum calcium in renal failure does not always indicate the presence of ionized hypocalcemia.
Necrotizing pancreatitis can produce hypocalcemia via several mechanisms. The appearance of hypocalcemia in pancreatitis carries a poor prognosis (8).
B. Clinical Manifestations
The potential consequences of hypocalcemia include increased neuromuscular excitability, and reduced contractile force in cardiac muscle and vascular smooth muscle. However, most cases of ionized hypocalcemia have no adverse consequences (5,9).
1. Neuromuscular
Hypocalcemia is reported to cause tetany (of peripheral or laryngeal muscles), hyperreflexia, paresthesias, and seizures (10).
Chvostek’s and Trousseau’s signs are often listed as manifestations of hypocalcemia, but Chvostek’s sign is nonspecific (and present in 25% of normal adults), and Trousseau’s sign is insensitive (absent in ≥30% of cases of hypocalcemia) (11).
2. Cardiovascular
The cardiovascular complications of hypocalcemia, which include hypotension, decreased cardiac output, and ventricular ectopic activity, are reported only in cases of severe ionized hypocalcemia (<0.65 mmol/L) (6).
C. Calcium Replacement Therapy
The treatment of ionized hypocalcemia should be directed at the underlying cause of the problem. Calcium replacement should be reserved only for symptomatic hypocalcemia, which is uncommon.
The available calcium solutions and a recommended replacement regimen are shown in Table 30.3 (6).
Note that the calcium chloride solution contains three times more elemental calcium than calcium gluconate.
Calcium gluconate is usually preferred because it has a lower osmolarity, and is less irritating when injected. However, both calcium solutions are hyperosmolar, and should be given via a large central vein, if possible.
Table 30.3 Intravenous Calcium Replacement Therapy
Intravenous Solution
Elemental Calcium
Unit Volume
Osmolarity (mosm/L)
10% calcium chloride
27 mg/mL
10 mL
2,000
10% calcium gluconate
9 mg/mL
10 mL
680
For symptomatic hypocalcemia:
1. Give a bolus dose of 200 mg elemental calcium in 100 mL isotonic saline over 10 minutes.
2. Follow with a continuous infusion of 1–2 mg/kg/hr for 6–12 hrs.
3. Monitor ionized calcium levels hourly for the first few hours.
CAUTION: Intravenous calcium can be risky; i.e., calcium infusions can promote vasoconstriction and ischemia in
vital organs (12), and intracellular calcium accumulation can produce lethal cell injury (13). These risks emphasize the importance of avoiding calcium replacement therapy un-less there is evidence of an adverse effect of hypocalcemia.
III. Ionized Hypercalcemia
In one large survey, 23% of ICU patients had at least one episode of ionized hypercalcemia (5). The source of hypercalcemia in ICU patients has not been adequately studied, but common causes of hypercalcemia outside the ICU are hyperparathyroidism and malignancy (14,15,16).
A. Clinical Manifestations
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