Ruminations of a teaching surgeon.
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Biomedical subjects
Publications and source records attributed to R A Chase.
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Overwhelming pneumonia may be caused by a large number of different organisms in both immunocompetent and compromised hosts. In this article, the most common etiologies of overwhelming pneumonia are considered from an epidemiologic and clinical point of view.
We have evaluated a new enzyme immunoassay (EIA) to measure IgG antibodies (Abs) to HIV in patients with AIDS, AIDS-related complex (ARC), AIDS contacts (AC), and low risk controls. Twenty-nine (94%) of 31 AIDS, 27 (96%) of 26 ARC, 12 (54%) of 22 AC, and 1 (2%) of 60 control patients were anti-HIV Ab positive by this assay. Positive results were confirmed by Western blot analysis. The EIA for anti-HIV evaluated in this study is sensitive and specific in identifying individuals who have been infected by this retrovirus.
The transfer of autogenous tissues in man has its origins in antiquity. Movement of composite tissues using pedicle techniques, which assured that such tissues were never deprived of vital blood supply, preceded free grafting. The ultimate refinement of carrying pedicles was reached in the vascularized island pedicle flap, which carried composite tissues solely on an intact vascular leash. An enormous increase in the versatility of composite transfers occurred when microvascular surgery made transfer with immediate vascularization a reliable procedure. This opened the door to free functioning muscle and musculocutaneous transfers with motor reinnervation at the recipient site--the supreme tissue transfers.
The present state of human gross anatomy in medical education can generally be characterized as the presentation of a large bolus of information that is swallowed and only partly digested during the first year of medical school. The subject is often taught in a depth beyond that which would be relevant to all physicians irrespective of their future professional careers. This condition has resulted from adaptive adjustments to the escalating discrepancy between a rapidly expanding knowledge base in science and technology and the relatively fixed time period for education of a physician. Initially, traditional courses retained their comprehensive character, and new information was simply piled on top of existing departmental offerings. It soon became obvious that there would have to be a reduction in time devoted to established courses and a reciprocal expansion of time to accommodate newly developing sciences. Such adjustments were painful and often led to conflicts about what comprises essential knowledge in medical education. Thus, the curriculum time devoted to human gross anatomy has been significantly reduced to accommodate new knowledge in cellular and sub-cellular structures and other disciplines. That common foundation of knowledge, skills, values, and attitudes essential to all physicians regardless of specialty is ever-changing and often debated by medical school faculty members. However, two facts are generally agreed upon: that today's medical student with a broad but perhaps thin base in science and limited direct clinical experience is not competent upon graduation to assume patient care responsibilities without supervision and that as a result, the formal education of a physician has expanded into the graduate domain.(ABSTRACT TRUNCATED AT 250 WORDS)
An 87-year-old woman with a known atherosclerotic thoracic aneurysm died suddenly from a massive esophageal hemorrhage. Prior to death, tuberculous esophagitis was diagnosed by biopsy. At autopsy, a fistulous tract was found extending from the esophagus to the aortic aneurysm; this fistula proved to be the site of fatal hemorrhage. The tract was surrounded by a granulomatous inflammatory reaction, in which acid-fast bacilli were found. To our knowledge, this is the first reported case of tuberculous esophagitis extending to an aortic aneurysm resulting in hemorrhage and death.
alpha- and beta-N-oxalyl-L-alpha, beta-diaminopropionic acids, isolated from Lathyrus sativus seed, which is implicated in the pathogenesis of human neurolathyrism, were injected into rat lumbar cerebrospinal fluid. The alpha-isomer was neither acutely nor chronically toxic, whereas the beta-isomer was both an acute and a chronic neurotoxin in this test system. These results are relevant to the aetiology of neurolathyrism and suggest that the conversion of the beta- to the alpha-isomer that occurs during boiling of the seed prior to human consumption reduces the neurotoxicity of the seed.
This review recounts the known historical development of techniques to achieve soft tissue coverage using free skin grafts, pedicle flaps of various types, and composite tissue transfers with immediate revascularization. There is documentation of an incremental emphasis on muscle-containing pedicle flaps and free revascularized composite tissue transfers in the world literature.
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Cerebral edema has now been noted to occur frequently in patients dying of fulminant hepatic failure. In the present study, intracranial pressure was monitored in an animal model of acute liver failure. Acute liver failure was induced surgically by hepatic devascularization. Serial monitoring of the electroencephalogram revealed progressive slowing of the frequency with decreasing amplitude. Elevation of the blood ammonia was also observed from baseline values of 64 +/- 12 SE to 744 +/- 97 mumol/liter. Monitoring of the intracranial pressure with a subdural pressure transducer demonstrated a progressive and reproducible rise from 12.8 +/- 2.5 mm Hg immediately after the operation to a mean value of 51.6 +/- 11.8 mm Hg just before death 6--12 hr later. At autopsy, the brains of the test animals were found to be swollen with flattened cortical gyri. In the control animals, intracranial pressure rose slightly but returned toward normal levels (8.0 +/- 2.5 mm Hg) 8 hr after laparotomy and remained normal until their death. There was a statistically significant difference between intracranial pressure levels of the test animals and those of the controls (P less than 0.01). Intravenous methylprednisolone (2.0 g initially followed by 0.5 g every 2 hr) administered immediately before and after hepatic devascularization prevented rises in intracranial pressure but had no effect when given 4 hr after operation. The early and progressive increase in intracranial pressure was an unexpected finding, and an assessment of such a sequence in patients with fulminant hepatic failure is currently in progress.
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24 patients with fulminant hepatic failure who had deteriorated to grade-IV coma were treated by repeated periods of haemodialysis with a polyacrylonitrile membrane. 9 patients fully recovered consciousness, and 8 (33%) survived to leave hospitals. These results are to be compared with those of conservative management alone (15% survival in 53 cases) and those obtained initially with charcoal haemo-perfusion (38%). Of the 16 treatment failures, cerebral oedema was found at necropsy in 13 (18%). Whether this would have been less of problem if treatment had been started earlier in the course of the illness remains to be determined.
Over the past half decade, there has been an increment in forces moving the profession toward recertification and a decrement in the restraining forces. The whole process will be catalyzed by available funding through grants to implement continuing medical education, development of performance-, and competency-based assessment measures and recertification. Specialty boards serving relatively small numbers of candidates have serious difficulty funding certification, to say nothing of recertification. An adequate mechanism to implement recertification can emerge only from the profession itself, working through the American Board of Medical Specialties and specialty boards. The means to discharge this responsibility should, at the outset, come from public and private sources. Eventually the system may become self-supporting through evaluation and certification fees. The public interest will be best served when there are adequate mechanisms to assess continuing competence of all physicians. As a minimum, there must be a system to guard against incompetence through obsolescence of any of the practicing professionals.
1. An investigation was carried out into the mechanism of unexplained hypotension in patients with fulminant hepatic failure. The cardiac output and peripheral resistance were compared in normotensive and hypotensive patients. In addition, the serum concentration of the false neurotransmitter octopamine and the pressor response to noradrenaline, and to the indirectly acting sympathomimetic agent tyramine, were measured in hypotensive and normotensive patients with fulminant hepatic failure and in healthy subjects. 2. The cardiac output and the peripheral resistance were decreased in the hypotensive patients, and their mean heart rate was slower than in the normotensive patients. Although the serum octopamine concentration was significantly elevated in the patients compared with the control subjects, the highest octopamine concentrations were unexpectedly found in the normotensive patients and a significant positive correlation could be demonstrated between the resting blood pressure and the serum octopamine concentration. The pressor response to tyramine and noradrenaline were similar in the hypotensive patients, the normotensive patients and control subjects. 3. These results suggest that neither increased serum concentrations of the false neurotransmitter octopamine, nor end-organ insensitivity to released noradrenaline are responsible for the hypotension. A more likely explanation is toxic depression of the vasomotor centre. The opening of peripheral arteriovenous shunts, possibly as a result of endotoxaemia, might be an additional factor.
Serum octopamine levels were significantly higher in twenty patients with fulminant hepatic failure (FHF) during the first 48 h of grade IV coma than in health control subjects (3.38 +/- 0.20 ng/ml and 1.75 +/- 0.19 ng/ml respectively, P less than 0.001). Serial measurements in five patients who died without regaining consciousness showed serum octopamine to remain raised, and concentrations in the cerebrospinal fluid at death reflected serum levels. In five patients who regained consciousness, improvement in encephalopathy was associated with a significant reduction in serum octopamine. Renal failure in patients with FHF was found to contribute to raised serum octopamine but could not alone account for the observed levels. Patients given neomycin therapy did not have significantly lower serum octopamine levels than an untreated group. There was, however, a significant correlation between elevated serum octopamine and the occurrence of gestrointestinal bleeding during the previous 24 h. Charcoal haemoperfusion did not appreciably reduce serum octopamine levels.