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David M. Rothenberg, MD; Robert Barkin, PharmD; Russell H. Glantz, MD
Rush Medical College Rush-Presbyterian—St Luke's Medical Center Chicago, Ill

Arnold S. Berns, MD
St Francis Hospital Evanston, Ill

JAMA. 1990;264(4):455.

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In Reply.—

Drs Senecal and Osterloh raise concerns regarding the clinical correlation and the diagnosis of bromide intoxication in our patient. However, we still consider this diagnosis valid. As pointed out in our article, we also believe that this level of bromide is what would be considered by most to be below a toxic level. Although symptoms are not "usually" seen at this level, we believe that the temporal relationship of symptoms, as well as the peak negative anion gap, correlates with the high dose of pyridostigmine bromide and the bromide level measured. The normal half-life of bromide may have been easily reduced with the use of intravenous crystalloid solution, as was noted in our report, and this may have contributed to the rapid resolution of symptoms.

Drs Senecal and Osterloh also question whether an oral dose of 1 mg of levorphanol tartrate could have influenced the encephalopathic picture in . . . [Full Text PDF of this Article]

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