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Excerpt
We appreciate the comments of Dr. Montero and would like to respond to several of his points. First, he infers that the authors felt that the observed rhabdomyolysis was not a result of acute muscular injury. On the contrary, we explicitly stated that we thought it was due to muscular injury, but not at the instant of impact. Rather, it seems more likely to have been due to the patient's relative immobility during the first several days after injury, analogous to the majority of cases of rhabdomyolysis whose etiology is a period of immobility secondary to decreased levels of consciousness after alcohol and drug ingestion. [1]
In regard to other sources of serum CPK elevation, Dr. Montero's discussion is thorough. However, the references cited do not support CPK levels as high as 6000-7000 IU/L due to cardiac or cerebral sources, especially without clinical manifestations. [2,3] The patient's normal neurologic exam (above the spinal cord injury) and normal electrocardiographic monitoring in the ICU argue against a lesion of the magnitude necessary to elevate CPK levels significantly.
Although CK-BB has been found in a variety of tissues outside the central nervous system, including intestines, prostate and uterus, [3,4] limitations on the contribution of this isoenzyme to total serum CPK levels arise from an intact blood-brain barrier and a serum half-life as short as 1 hour. [5] Total CPK elevations above 5000 IU/L are essentially unheard of except in hemispheric contusion/infarction. [3] Other reports have recorded serum CPK-BB levels ranging from 8 to 40 ng/mL in cases of mild to fatal traumatic brain injury, respectively, all of which returned to baseline values within 48 hours. [6] The same inability to produce this high an elevation of serum CPK applies even to large, completed myocardial infarctions. The magnitude of total CPK elevation in this case report is simply inconsistent with clinically occult brain or myocardial injury. The question of spinal cord CPK has yet to be answered; however, in no case in our collective experience at this center have we encountered a patient with an isolated spinal cord or brain injury who developed rhabdomyolysis. Finally, the patient did not receive intramuscular injections at any point in his hospital course.
In summary, although we were and still are unable to absolutely exclude the various sources of CPK elevation suggested by Dr. Montero, our own experience as well as that of others cited leads us to maintain our impression that immobilization, with a contribution from relative hypotension/hypovolemia, was the most likely etiology of rhabdomyolysis in this patient. We thank Dr. Montero for his interest in this topic.
