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Andrew M. Davis, MD
Rush-Presbyterian—St Luke's Medical Center Chicago

JAMA. 1987;257(5):626.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

The interesting review entitled "Hypocalcemia in Critical Illness" by Zaloga and Chernow¹ omits several important points in discussing rhabdomyolysis and hypocalcemia. These are worth discussing, since nontraumatic rhabdomyolysis may cause 7% of all cases of acute renal failure² and may be accompanied by dramatic hypocalcemia.³

Hyperphosphatemia is listed as the cause of hypocalcemia in this setting when in fact recent reviews single out calcium deposition in damaged muscle as the predominant mechanism in this complex process.^3,4 Calcium deposition in muscle has been demonstrated by biopsy and computed tomographic scan and may explain technetium 99 pyrophosphate bone scan uptake in damaged muscle. Moreover, a study of 87 episodes of rhabdomyolysis noted that 56% of hypocalcemic patients simultaneously had normal serum phosphorus levels.⁵

An important therapeutic point is that in this setting hypocalcemia is usually self-limited and rarely causes problems.³ My experience with . . . [Full Text PDF of this Article]

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