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CALCIUM HOMEOSTASIS


Too Much, Too Little or Not Sure???

Physiologic Role of Calcium
Hypocalcemia
Hypercalcemia
Pseudohypocalcemia

PHYSIOLOGIC FORMS AND ROLES OF CALCIUM

About 50% of calcium is bound to serum protein (80% of it to albumin). About 5-10% is complexed with anions like bicarbonate and the remainder is present as the free or ionized form. The ionized form is physiologically active.

Total Calcium

The total serum calcium is unreliable as a measure of the active form (ionized) fraction in certain situations. Using a correction factor that increases the total clcium by 0.8 mg/dl for each 1 mg/dl decrease in serum albumin can help estimate the serum calcium, from the physiological point of view, but it has not provenreliable to do so.Therefore, a direct measurement of ionized calcium is recommended to insure accuracy.

Ionized Calcium

Because many variables affect ionized calcium, the blood sample should be carefully obtained and handled.The following conditions affect ionized calcium levels:

Factors that increase ionized calcium:

Acid pH (increased time in tube)
Na+ >155
Increased temperature
Blood cell metabolism


Factors that decrease ionized calcium:

Alkaline pH
Heparin
Na+ <120
Decreased temperature (too long time in tube)


The blood should be collected anaerobically and processed as quickly as possible to minimize CO2 production (which decreases chances of acidity) and to prevent temp from dropping below body temperature. The tbe should not contain heparin or citrate (the later will chelate calcium).


HYPOCALCEMIA

Causes of Hypocalcemia

The most common causes of hypocalcemia are:

a) pseudohypocalcemia (low protein)
b) hypomagnesemia (depletion, even with normal Mg++ levels) (28% cases)
- inhibits parathormone secretion
- reduces end-organ response to parathormone
- hallmark: hypocalcemia with hypercalciuria when infusing calcium
c) alkalosis (6% of cases)
- with alkalosis, H+ becomes dissociated from albumin, leaving room for Ca++ ions to increasingly bind to it. The albumin correction factor will be misleading in this setting.
d) sepsis (50% of cases)
- presumably due to calcium eflux from a disrupted microcirculation - respiratory alkalosis may play a role
- exact cause not known
- marker of poor prognosis (more prone to hemodynamic instability and hypotension)
e) renal failure (8% of cases)
- hyperphosphatemia with cristallization
- decreased conversion of Vit. D to its active metabolite - associated acidosis reduces binding of calcium to albumin, so that it partically corrects the hypocalcemia expected for the degree of vitamin deficiency and hyperphosphatemia.
f) acute pancreatitis (3% of cases)

Clinical Manifestations a) frequently asymptomatic
b) neuromuscular irritability
1. hyperreflexia -rarely documented
2. tetany
3. seizures
4. Chvostek’s and Trousseau’s signs
- Chvostek’s sign is present in 25% of the general population and absent in 30% of patients with hypocalcemia. Trousseau’s sign is even less sensitive and less specific.
c) cardiovascular effect
- hypotension with vasodilatation
- prolonged QT segment
- left ventricular failure

The clinical significance of cardiovascular effects are questionable. For example, some cases of LVF improve with calcium infusion, but it is not a common phenomenon.

Calcium Infusion Therapy

Side effects:
a) vasoconstriction (may be detrimental in CHF or cardiogenic shock with severe vasoconstriction)
b) worsened diastolic dysfunction
c) “no-reflow” phenomenon of persistent hypoperfusion after hypotension or cardiac arrest

Do not treat hypocalcemia if it is asymptomatic. This seems to be a good general rule. If symptomatic, calcium infusion should be given IV, never intramuscularly.


HYPERCALCEMIA

Definition: levels above 13 mg/dl

Hypercalcemia is less frequent than hypocalcemia. It is present in 4% of all hospitalized patients.

Causes of Hypercalcemia

Most common cause in the general population is hyperparathyroidism, but in the ICU, the most common causes are malognancy and renal failure.

Clinical Manifestations:

a) altered mental status (as severe as coma)
b) ileus
c) hypotension
d) renal failure

Management and Therapy

1. Intravenous fluid (normal saline)
This not only promotes diuresis (secondary to natriuresis) and protects the kidney, but also replaces the fluid lost by calcium-induced osmotic diuresis.
2. Furosemide or any loop diuretic. Dose of furosemide is 40-100 mg q2 hours. Fluid lost as a result of diuretic therapy should be replaced every hour.
3. Calcitonin
Thyrocalcinonin reduces calcium by inhibiting bone reabsorption. Synthetic salcium calcitonin has the greatest potency and can return calcium to normal levels within 2-3 hours. The usual dose is 4 units/kg IM or SQ q 12h for two doses. If not completely iffective, the dose can be doubled after 2 days have elapsed. It is well tolerated, but may cause nausea and vomiting.
4. Mithramycin
An antineoplastic agent, used at lower doses, it inhibits bone reabsorption. It is more effective than calcitonin but the effects take 24036 hours. The usual dose is 25 mcg/kg given IV, as a bolus or as a 6-hour infusion.It may be repeated after 2 days if necessary. Because the dose is lower than for cancer, bone marrow depression should not develop. The drug is well tolerated if a time period of 2-3 days is allowed between doses.
5. Dialysis
Not practical for routine therapy, but indicated when all other measures fail. Hemodialysis more effective than peritoneal dialysis.


PSEUDOHYPOCALCEMIA

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