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June 2, 1917


Author Affiliations

Resident Physician, Cincinnati General Hospital CINCINNATI

From the Department of Medicine, University of Cincinnati, and the Medical Clinic, Cincinnati General Hospital.

JAMA. 1917;LXVIII(22):1618-1620. doi:10.1001/jama.1917.04270060026010

In recent years, undoubtedly as a result of sensational newspaper notoriety given to one or two cases, the frequency of mercuric chlorid poisoning has greatly increased. Cases of unintentional and suicidal poisoning are continually brought to notice. Naturally, the frequency of these cases has been productive of many studies, chemical, pathologic and therapeutic.

It has long been known that mercury, when introduced into the body, produces characteristic changes. Applied locally, necrosis and sloughing are produced. In the body, practically every organ is affected, the secretory and excretory organs bearing the brunt of the damage. The drug produces a cloudy swelling, leading to fatty degeneration and necrosis, frequently to hemorrhagic inflammation, and occasionally to subsequent calcification. As a part of these changes, an edema of the tissues takes place.

Kahn, Andrews and Anderson,1 in a chemical and pathologic study of a case of mercury poisoning, have shown that the metal

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