Biomedical subjects
Publications and source records attributed to T H Glick.
The choice of objectives and content in neurologic education should be informed by evidence from patient outcomes and errors. Malpractice claims are proposed as one data source, although they only partially reflect health outcomes. Epidemiologic, statewide data suggest some provisional priorities for key topics and training targets, but require further research to assess their value for guiding neurologic education.
BACKGROUND: Major forces in society and within health systems are fragmenting patient care and clinical learning. The distancing of physician and trainee from the patient undermines learning about the patient-doctor relationship. The disconnection of care and learning from one successive venue to another impedes the ability of trainees to learn about illness longitudinally. METHODS: As a conceptual piece, our methods have been those of witnessing the experiences of patients, practitioners, and students over time and observing the impact of fragmented systems and changing expectations on care and learning. We have reflected on the opportunities created by digital information systems and interactive telemedicine to help renew essential relationships. RESULTS: Although there is, as yet, little in the literature on educational or health outcomes of this kind of technological enablement, we anticipate opportunities for a renewed focus on the patient in that patient's own space and time. Multimedia applications can achieve not only real-time connections, but can help construct a "virtual patient" as a platform for supervision and assessment, permitting preceptors to evaluate trainee-patient interactions, utilization of Web-based data and human resources, and on-line professionalism. CONCLUSIONS: Just as diverse elements in society are capitalizing upon digital technology to create advantageous relationships, all of the elements in the complex systems of health care and medical training can be better connected, so as to put the patient back in the centre of care and the trainee's ongoing relationship to the patient back in the centre of education.
The authors reviewed the occurrence in their emergency department of cases of serious neurologic problems initially thought to be conversion disorders or similar psychogenic conditions. Their aim is to indicate the significance of this issue for emergency physicians (EPs) because of its contribution to the incidence of medical errors. Although there are no national statistics, the authors estimate by extrapolation that thousands of such cases probably have occurred and large numbers may still occur each year in the United States, sometimes resulting in patient injury. They have identified ways of anticipating and attempting to prevent such occurrences. Proposed interventions focus on education regarding the difficulty of diagnosis, patient-based risk factors, and physician-based attitudes and thought processes. The authors also include suggestions for systemic "safety nets" that will help to ensure quality of care, such as appropriate imaging and consultation. Review of texts and journals readily accessible to EPs revealed little attention to this subject.
Emergency physicians need to understand the potential for false reassurance in the interpretation of reflex examination data. Neurologic consultation should be sought when classic signs are lacking, but other evidence causes suspicion. Changes in teaching emphasis and acute practice are needed, since the stakes may be high and time is of the essence. We have responded to the insights gained from this study by augmenting in-service and continuing medical education teaching and by implementing guidelines to assist EPs. We have emphasized the importance of spotlighting high-risk patients, as exemplified above, and of taking advantage of neurologic or neurosurgical consultation. Where in-person consultation is less available, the use of guidelines and remote consultation should be able to help direct further examination, diagnostic formulation, and the need for imaging decisions. Given the potential for severe negative outcome if spinal emergencies are not optimally managed, we must give the teaching of these issues high priority.
Clinical cases for problem-based learning should capture the relevance of patient encounters, and not serve merely as a 'take-off' point for scientific study. As a vehicle of learning, the case should drive the science and the science should drive the case. Decision points elicit intellectual commitment, and help to raise the level of inquiry. Our cases are focused, avoiding clinical complexity and reliance on pattern recognition. We emphasize formulation of evidence-based mechanistic hypotheses. The case does not stand alone, but must suit its position in the course and curriculum.
Ammonia metabolism in Reye syndrome was studied by quantitative analysis of the time course of hyperammonemia and the urinary excretion of ammonia, urea, and total nitrogen. These measures were then utilized to assess the effect of citrulline administration in 8 patients compared to results in 22 patients managed without citrulline. Two indices of the severity and duration of hyperammonemia correlated strongly with mortality: the half-time for decline of hyperammonemia and the area under the hyperammonemia curve (an index of the total burden of ammonia presented to the brain). These results suggest that the total amount of ammonia delivered to brain may be important to the pathogenesis of encephalopathy. Citrulline-treated patients had more severe disease at admission and greater abnormalities in indices of nitrogen and ammonia metabolism, though the latter did not reach significance. The urine ammonia/urea nitrogen excretion ratio, an index of the efficiency of ammonia conversion to urea, normalized more rapidly in the citrulline-treated group, evidence that citrulline may have improved urea cycle function. Overall mortality did not differ in the two groups. The deaths of 2 citrulline-treated patients in this small group were attributable to factors unrelated to treatment, however, so the possible effect of citrulline on mortality was not definitively tested. No indication was found that citrulline was harmful, nor that it increased ammonia levels.
The pathogenesis of Reye's syndrome encephalopathy was analyzed in terms of uniform criteria designed to clarify and assist evaluation of the leading hypotheses. Three of these hypotheses derive from known metabolic sequelae of hepatic mitochondrial dysfunction and the severe systemic catabolism of protein, fats, and carbohydrates that characterize the syndrome biochemically: hyperammonemia, hyperfattyacidemia, and hyperlactatemia. In addition, there is a fourth hypothesis of generalized mitochondrial insult affecting brain, muscle, and other organs as well as liver. The weight of evidence favors hyperammononemia as a sufficient factor while recognizing important interrelationships with the other observed biochemical derangements. How the catabolism and hepatic mitochondrial dysfunction are produced by the triggering viral infection remains unknown. Therapeutic efforts have thus far not succeeded in definitive metabolic intervention. Such reversal of the clinical syndrome would lead to confirmation of the necessary pathogenetic factors; this type of intervention remains the chief goal of metabolic research in Reye's syndrome.
In July 1968, an explosive epidemic of acute febrile illness occurred at a county health department facility in Pontiac, Michigan. Illness characterized principally by fever, headache, myalgia, and malaise affected at least 144 persons, including 95 of 100 persons employed in the health department building. The mean incubation period was approximately 36 hours. Illness was self-limited, generally lasting from two to five days. Secondary cases did not occur in family contacts and second attacks did not consistently follow re-exposure in the building. A defective air-conditioning system was implicated as the source and mechanism of spread of the causative factor. However, extensive laboratory and environmental investigations failed to identify the etiologic agent. Since these investigations a bacterium similar to or identical with the agent responsible for Legionnaires' Disease has been isolated from guinea pigs exposed to the Pontiac health department building in 1968 as well as from guinea pigs exposed to water from the evaporative condenser. Paired sera from 32 cases of Pontiac Fever showed seroconversion or diagnostic rises in antibody titers to this bacterium.
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