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CHAPTER 99: Electrolyte Disorders in Critical Care 959

(>5 mg/dL), magnesium binds the calcium-sensing receptor on the para- surgical hypoparathyroidism had improved cardiac function with cal-
thyroid gland, imitating hypercalcemia, directly suppressing PTH release. cium infusions. Calcium should be repleted in cases of seizures, tetany,
186
187
Vitamin D Deficiency Acute hypocalcemia with vitamin D deficiency occurs laryngospasm, and hyperkalemia. Among asymptomatic patients, the
because of the inability to mobilize skeletal reserves of calcium. Vitamin risk of significant clinical symptoms rises as the ionized calcium falls
D deficiency is common among nursing home patients, alcoholics, below 3 mg/dL, and treatment is warranted in these patients. 156
and malnourished patients. Increased hepatic metabolism of vitamin The controversy regarding the treatment of ICU-H is due to in vitro data
D occurs in patients on phenytoin and phenobarbital. The nephrotic that show intracellular calcium to be a mediator of cell injury in reperfu-
188
syndrome is commonly associated with hypocalcemia. Though most of sion and sepsis models. In addition, animal studies have repeatedly
this is due to hypoalbuminemia, ionized hypocalcemia occurs due to shown that administering calcium to hypocalcemic septic rats improves
the loss of 25-hydroxyvitamin D and its binding protein in the urine. blood pressure but increases mortality. 189,190 The increased mortality was
Decreased activation of 25-hydroxyvitamin D occurs with renal failure not reproduced in septic pigs and more recent research has questioned the
and hypoparathyroidism. appropriateness of the rat as an animal model for human sepsis. 191
Critical Illness Hypocalcemia is a pervasive disorder in the ICU. While In critically ill hypocalcemic patients with life-threatening hypoten-
hypocalcemia was thought to be limited to patients with sepsis, Zivin sion that is resistant to other therapies (eg, pressors, volume resuscita-
tion, and inotropes), a trial of IV calcium may be considered. In a study
and associates have shown hypocalcemia to be common in all patients
with severe illness. However, despite careful assessment, a definitive of 12 hypocalcemic patients with bacterial sepsis, seven were hypoten-
168
sive despite volume resuscitation and dopamine and norepinephrine
etiology can be found in less than half of the patients. Some authors
167
believe that ICU-associated hypocalcemia (ICU-H) is an adaptive bene- infusions. Correcting hypocalcemia restored normal blood pressure
in all seven patients. Cardiac output, systemic vascular resistance, and
ficial response to critical illness, as it may prevent intracellular hypercal- 180,192
cemia and associated tissue damage. While not describing all patients urine output all improved following the calcium.
178
No studies have been done to assess whether treating ICU-H affects
with ICU-H, most patients have elevated levels of PTH and low levels
of calcitriol. 179,180 Elevated levels of procalcitonin have also been found mortality. However, a Cochrane review in 2008 concluded that there was
no clear evidence that parenteral calcium supplementation impacted the
in ICU-H, leading some authors to wonder if this supposedly calcium- 175,193
neutral precursor to calcitonin may exert a hypocalcemic effect. 180 outcome of critically ill patients.
It is important to note that all of the negative data on replacing
Clinical Sequelae: The primary manifestation of hypocalcemia is neu- calcium come from studies of sepsis in animals. The applicability to the
romuscular irritability. This can range from perioral numbness and human population with ICU-H is unclear. The multifactorial etiology of
acral paresthesias to severe tetany and seizures. Seizures can occur in ICU-H is accepted, and it is likely that benefits of treatment vary with
the absence of any other neuromuscular irritability. Both generalized the etiology.
and partial (simple and complex) seizures have been reported. How to Treat Patients with asymptomatic mild hypocalcemia (ionized calcium
Tetany classically affects the upper extremities followed by the lower >3.2 mg/dL) can be treated with increased dietary calcium (Table 99-9).
extremities. Patients typically demonstrate elbow extension, wrist flexion, Increases of 1000 mg per day are appropriate. The 25-hydroxyvitamin
and metacarpophalangeal flexion. Tetany can cause laryngospasm or D level should be checked and patients placed on vitamin D if low. In
171
bronchospasm, resulting in respiratory failure. The classic signs of latent patients with renal failure, treating the hyperphosphatemia and decreased
tetany are Trousseau sign (carpal spasm after inflation of a blood pres- calcitriol levels will help correct the hypocalcemia.
sure cuff on the arm and leaving it in place for 3 minutes) and Chvostek Severe or symptomatic hypocalcemia should be treated with an infu-
sign (facial spasm induced by tapping on the facial nerve anterior to the sion of 100 to 200 mg of elemental calcium. This should be given over
ear). The sensitivity of both is poor (both may be negative in hypo- 10 to 20 minutes to avoid cardiac toxicity. This initial infusion tends to
181
calcemia) and the specificity of Chvostek is particularly poor (a partial suppress symptoms longer than it maintains a normal calcium level. In
Chvostek sign is found in 25% of eucalcemic individuals). 92,181,182 Tetany order to prevent rebound hypocalcemia, a calcium infusion should be
may be masked by anticonvulsant therapy. started at 0.5 to 1.5 mg elemental calcium/kg per hour (Table 99-10).
Acute hypocalcemia can cause reversible heart failure. 183,184 Even Two forms of parenteral calcium are commonly available: calcium
modest hypocalcemia can precipitate heart failure and hypotension in gluconate and calcium chloride. Concerns that calcium gluconate
patients with latent cardiac damage. These serious findings can precede requires hepatic metabolism have not been borne out. In a random-
194
tetany. The classic electrocardiogram findings of hypocalcemia are ized, double-blind trial of the two calcium salts in critically ill chil-
185
bradycardia, prolonged QT interval, and inversion of the T wave. dren, the chloride salt resulted in a higher and more consistent rise in
175
Heart block and cardiac arrest have also been documented. The elec- ionized calcium levels. All of the patients receiving the chloride salt had
trocardiogram is not a sensitive marker of hypocalcemia and may be an increase in ionized calcium versus 65% of the gluconate group.
195
normal during life-threatening hypocalcemia. Calcium chloride is caustic to veins and should be reserved for central
Acute hypocalcemia may result in loss of vascular tone and
hypotension. In one ICU study, decreased ionized calcium correlated
175
with decreased mean arterial pressures. Digitalis acts by increasing TABLE 99-9 Oral Formulations for Hypocalcemia
intracellular calcium, thus hypocalcemia is a cause of digitalis resistance. Agent Elemental Calcium How Supplied
Patients can sometimes tolerate toxic digitalis levels with concurrent
hypocalcemia. Correction of this protective hypocalcemia can precipi- Calcium glubionate 64 mg/g 1.8 g/5 mL
tate arrhythmias due to digitalis toxicity. Calcium gluconate 90 mg/g 500-1000 mg tab
Treatment Calcium lactate 130 mg/g 325-650 mg tab
When to Treat Unique to calcium among all electrolyte disorders is the Calcium citrate 211 mg/g 950 mg tab
theory that hypocalcemia may be an adaptive response to critical ill-
ness, and because of this the treatment of ICU-associated hypocalcemia Calcium acetate 253 mg/g 667 mg tab
(ICU-H) was long deemed controversial. Care must be taken not to Calcium carbonate 400 mg/g 650-1500 mg tab
178
extrapolate this controversy to patients in whom the etiology of their Vitamin D requirements 1 µg = 40 IU
hypocalcemia is understood (eg, acute hypoparathyroidism, tumor lysis
syndrome, or acute renal failure). Patients with chronic hypocalcemia RDA 10 µg 400 IU
and myocardial dysfunction should be given a trial of calcium supple- For D deficiency 40-50 µg/d 1600 IU/d
mentation. Patients with asymptomatic hypocalcemia secondary to RDA, recommended daily allowance.

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