Surgery
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General surgical chief residents in all approved training programs were surveyed to evaluate the influence of fellowships, specialization, and research. Respondents represented 76% of programs and 60% of residents. Most chief residents plan to take post-residency fellowships. ⋯ This survey suggests that general surgery is predominant among residents in independent training programs who then enter private practice. University programs produce subspecialists who are predominant among future academic surgeons. This trend has vital implications for the future of academic general surgery.
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Data were collected for 163 students completing a surgical clerkship including scores on patient write-ups, ward performance evaluations, oral examinations, and National Board of Medical Examiners (NBME) Surgery subscores. Oral examination scores and patient write-ups were rated from 74 (failing) to 100 (honors) by faculty members. The ward performance evaluation included ratings on nine components of ward performance from 1 (unsatisfactory) to 4 (superior) and an overall ward score of 74 (failing) to 100 (honors). ⋯ Although these results suggest that residents are better evaluators of a clerk's performance than are faculty members, other studies indicated the opposite. The elimination of participation of either faculty or residents in the grading of students is unwise. Periodic monitoring of evaluation practices is necessary to ensure fairness in grading procedures.
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Activated complement, thromboxane A2, prostacyclin, and activated granulocytes have been implicated in hemodynamic dysfunction after trauma, in sepsis, and in hypovolemic and septic shock. This study evaluated the interaction of plasma concentrations of complement components C3a and C5a, thromboxane B2 (TxB), prostaglandin 6-keto-F1 alpha (PGI), and granulocyte aggregation in clinical sepsis and hypotension. Forty-eight critically ill patients were followed clinically for as long as 10 days. ⋯ PaO2/FiO2 ratios correlated directly with PGI and inversely with C3a and TxB/PGI. Plasma PGI and C3a are increased in septic shock. C3a and TxB/PGI imbalances are involved in hypovolemic and septic shock.
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Juxtahepatic venous injuries are usually fatal. The optimal method of dealing with these injuries remains controversial, but most experience has been with the insertion of an atriocaval shunt. However, the mortality rate with atriocaval shunting remains prohibitively high (60% to 100%). ⋯ One additional patient died in the operating room before any definitive repair could be undertaken. Four steps are considered essential to the successful management of these patients: (1) compression of the injury site until adequate resuscitation has been achieved; (2) early recognition that a juxtahepatic venous injury exists, as indicated by failure of the Pringle maneuver to adequately arrest hemorrhage; (3) prolonged portal triad occlusion with hepatocyte protection by means of large doses of steroids and topical hypothermia (portal triad occlusion time in the nonshunted group ranged from 20 to 64 minutes with a mean occlusion time of 46 minutes; although a transient rise in liver function test results seemed to correlate with the length of ischemia time, neither hepatic dysfunction nor hepatic necrosis occurred; and (4) extensive finger fracture of the liver to the site of vascular injury for primary repair or ligation; the extent of the finger fracture varied from 15 to 30 cm in length and from 5 to 15 cm in depth. The successful results achieved in five consecutive patients who sustained juxtahepatic venous injuries treated without a shunt serve as a basis for recommending this operative approach.
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To assess the relative importance of cardiac versus peripheral vascular failure in patients dying of septic shock, a series of 42 patients with documented septic shock was retrospectively evaluated. Patients were included in the study if serial hemodynamic and metabolic studies had been performed: the first one within 12 hours after onset of septic shock and the last one within 12 hours (median 2 hours; range 0.1 to 12 hours) before death in nonsurvivors. Nonsurvivors were included only if they died in shock. ⋯ The nonsurvivors showed progressive lactic acidemia. Even group IIb patients showed persistent vasodilation despite a decrease in CI. Our data suggest that many patients in septic shock die as a result of peripheral vascular rather than cardiac failure, since persistent vasodilation, irrespective of CI, was a major hemodynamic determinant in nonsurvivors, of whom 57% maintained a high CI until shortly before death.