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July 1933


Author Affiliations


From the Laboratories of the Mount Sinai Hospital and the Medical Division, service of Dr. George Baehr.

Arch Intern Med (Chic). 1933;52(1):16-29. doi:10.1001/archinte.1933.00160010023002

The occurrence of jaundice in cases of heart failure was first attributed to mechanical pressure of the blood stasis in the liver. This supposition has been supplanted recently by the theory advocated by Rich and his co-workers1 that jaundice in these cases is the result of anoxemia of the liver cells. The chief support for the hypothesis of anoxemia lies in the experimental observations of Binger, Brow and Branch2 that pulmonary infarction is attended by anoxemia and in the numerous clinical observations3 that jaundice often supervenes on pulmonary infarction. According to Rich and his co-workers, the retention of bile pigment in the blood which occurs in practically every case of outspoken passive congestion of the liver is caused by two factors, impairment of the excretory function of the liver by anoxemia and the increased burden placed on the functionally impaired liver by the demand for the excretion

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