Optic nerve injury: role of the anesthesiologist?
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Biomedical subjects
Publications and source records attributed to M Roizen.
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Screening laboratory testing seemed logical: if you could spot abnormalities before overt disease occurred, you could prevent disability. But it has not worked out that way for the majority of preoperative tests. We are now spending over $40 billion a year in the United States on preoperative testing and evaluation; 60 per cent of it is wasted. This is like saying, "If a little epinephrine is good, more is better." That is wrong in the use of epinephrine and it can be wrong with too much testing. Worse than wasteful, I believe this extra testing is causing iatrogenic disease by pursuit and treatment of borderline and false-positive test results. It is increasing our medicolegal risk and decreasing the efficiency of practice. Fortunately, this history of too much testing can now be turned to our advantage. It provides an arena where we can demonstrate to our constituency, the patient, and our watchdog, the bureaucrat, that we can use inexpensive technology to reduce costs substantially and improve the quality of care.
To evaluate myocardial catecholamine balance in heart failure, systemic hemodynamics, coronary sinus blood flow, and arterial and coronary sinus venous norepinephrine (NE) and epinephrine (E) concentrations were determined in 30 patients with chronic left ventricular failure (CHF), and in 25 patients with angina pectoris (AP) but without heart failure. In the group with CHF, stroke work index was lower (CHF 20 +/- 9, AP 53 +/- 13 g-m/m2, p less than 0.001) and pulmonary capillary wedge pressure higher (CHF 28 +/- 8, AP 11 +/- 4 mm Hg, p less than 0.001), indicating depressed left ventricular function. Coronary sinus blood flow was similar in 2 groups (CHF 97 +/- 70, AP 73 +/- 32 ml/min, difference not significant). In the group with CHF, arterial (634 +/- 582 pg/ml) and coronary sinus venous (1,038 +/- 1,014 pg/ml) NE concentrations were significantly higher than in the group with AP (arterial 185 +/- 135, coronary sinus 231 +/- 167 pg/ml, p less than 0.001). The net myocardial NE release in patients with CHF was approximately 20 times higher than that in patients with AP (CHF 38,548 +/- 48,622, AP 2,245 +/- 10,242 pg/min, p less than 0.001). Arterial E and myocardial E uptake was similar in both groups. Although mechanisms for increased myocardial net NE release remains unknown, it probably represents enhanced cardiac sympathetic tone in response to heart failure.
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Retrospective study of the diagnosis and management of the 8 cases of thyroid storm in a series of 400 hyperthyroid patients led to conclusion that thyroid storm is a clinical diagnosis based on a life-endangering illness in a hyperthyroid patient whose hyperthyroidism has been severely exacerbated by a serious precipitating illness, and that storm is manifest by the symptoms of hyperpyrexia, tachycardia and striking alterations in consciousness. No laboratory tests were diagnostic of storm, and the underlying precipitating cause of thyroid storm was the major determinant of survival. Vigorous therapy must include blocking synthesis of thyroid hormones with antithyroid drugs, blocking release of preformed hormone with iodine, meticulous attention to hydration and supportive therapy, as well as correction of precipitating cause of storm. The blocking of the sympathetic nervous system with reserpine or guanethidine or with alpha and beta blocking drugs may be exceedingly hazardous and requires skillful management and constant monitoring in a critically ill patient.