Compensation to a department of medicine and its faculty members for the teaching of medical students and house staff.

BACKGROUND: Changes in the organization and financing of health care threaten to alter the prevailing system of financing the teaching of medical students and residents. Little information is available from private medical schools and teaching hospitals about the extent of teaching by faculty members or the mechanisms and levels of reimbursement for teaching. METHODS: We surveyed faculty members in the Department of Medicine at Columbia-Presbyterian Medical Center to ascertain the extent of their teaching activities. A standard number of hours was assigned to each activity, and the total number of teaching hours was calculated for each faculty member. Teaching of fellows and in continuing medical education programs was excluded. We also determined how much money the Department of Medicine received in payment for faculty members' teaching activities, and the sources of this compensation. RESULTS: In the 1992-1993 academic year, the 188 full-time faculty members spent a total of 46,086 hours teaching (mean [+/- SD], 245 +/- 178 hours per faculty member); 10,780 hours (23.4 percent) were spent teaching medical students, and 35,306 hours (76.6 percent) teaching house staff. Eighty percent of faculty members taught for 137 or more hours each. In a multivariate analysis including faculty rank, subspecialty division, years since graduation from medical school, sex, and tenure or clinical track, senior faculty members (P = 0.02), members of certain subspecialty divisions (P < 0.001), and women (P = 0.05) contributed more than the average number of teaching hours. An additional 56 non-full-time faculty members contributed a total of 5684 hours. The net reimbursement to the department for teaching totaled $965,808, or about $16 per hour of teaching by full-time faculty members, after the cost of fringe benefits was excluded. CONCLUSIONS: Faculty members of the department of medicine at a major medical center contribute a large number of hours teaching medical students and house staff. This effort is poorly compensated. Cost-containment efforts have the potential to jeopardize fragile social contracts at academic health centers whereby the faculty participates in teaching by contributing unreimbursed or underreimbursed time.

Hydrocortisone choleresis in the dog.

Hydrocortisone sodium succinate (Solu-Cortef; Upjohn Co., Kalamazoo, Mich.) has been found to induce choleresis in unanesthetized fasting dogs fitted with Thomas duodenal cannulae for direct quantitative collection of bile. In all experiments, bile flow increased (average, 68%) 15-20 min after beginning hydrocortisone by infusion in association with an equivalent increment in the output of sodium, potassium, chloride, and bicarbonate. In five animals, the choleretic response occurred independently of, and apparently additive to, the effect of simultaneously administered sodium taurocholate. The fluid added to the bile resembled an ultrafiltrate of plasma. Erythritol clearance increased in proportion to flow, suggesting an effect at the hepatocellular rather than ductal level and probably independent, therefore, of endogenous secretin release. Hydrocortisone and its metabolites were excreted in amounts too small to induce choleresis osmotically. Simultaneous administration of sulfobromophthalein sodium blocked the choleretic response without preventing hydrocortisone excretion. The data suggest that a previously ill-defined mechanism of canalicular bile formation, not mediated by bile salt excretion, may be operative in choleretic response to a variety of agents.

Experimental viral hepatitis in the dog: production of persistent disease in partially immune animals.

Experimental infection with canine hepatitis virus has been studied in a series of 49 dogs. The pattern of response to infection was distinctly modified by the immune status of the animal. All of 19 fully susceptible dogs had an acute, fulminating fatal hepatitis when infected with a standard dose of virus, and all of 19 dogs with high levels of immunity to the virus survived without apparent illness. However, 11 dogs were spontaneously encountered with partial immunity to the infectious agent, and these animals developed different, prolonged forms of hepatitis following infection. In four animals death occurred in 8-21 days following what may be called a subacute course. The remaining seven dogs survived up to 8 months with evidence of chronic hepatic damage. The subacute and chronic forms of hepatitis were reproduced experimentally in seven of eight fully susceptible dogs which were passively immunized against the canine hepatitis virus by administration of hyperimmune serum. Although the virus could be found in sites of hepatic damage in the early stages of the subacute and chronic diseases, it could not be demonstrated in the later stages which were characterized by persistent hepatic damage and a marked chronic inflammatory reaction. Dogs with chronic hepatitis eventually developed extensive hepatic fibrosis. The pathologic, physiologic, virologic, and immunologic features of these experimental forms of viral hepatitis are described.