Annals of surgery
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Case Reports
Cerebral air embolism resulting from invasive medical procedures. Treatment with hyperbaric oxygen.
The introduction of air into the venous or arterial circulation can cause cerebral air embolism, leading to severe neurological deficit or death. Air injected into the arterial circulation may have direct access to the cerebral circulation. A patent foramen ovale provides a right-to-left shunt for venous air to embolize to the cerebral arteries. ⋯ Neurological symptoms included focal motor deficit, changes in sensorium, and visual and sensory deficits. Eight patients (50%) had complete relief of symptoms as a result of hyperbaric treatment, five (31%) had partial relief, and three patients (19%) had no benefit, two of whom died. The treatment of cerebral air embolism with hyperbaric oxygen is based upon mechanical compression of air bubbles to a much smaller size and the delivery of high doses of oxygen to ischemic brain tissue.
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Randomized Controlled Trial Clinical Trial
A single institution, randomized, prospective trial of cyclosporin versus azathioprine-antilymphocyte globulin for immunosuppression in renal allograft recipients.
Between September 26, 1980 and December 31, 1983, 230 splenectomized, transfused renal allograft recipients were randomized to treatment with either cyclosporin-prednisone (N = 121, 68 diabetic and 53 nondiabetic recipients; 73 cadaver and 48 related donor grafts) or azathioprine-prednisone-antilymphocyte globulin (N = 109, 61 diabetic and 48 nondiabetic recipients; 69 cadaver and 40 related donor grafts). The results were analyzed on March 31, 1984. Actuarial patient survival rates at 2 years were 88% in the cyclosporin and 91% in the azathioprine groups (p = 0.649). ⋯ D.) serum creatinine levels (mg/dl) at 1 year were higher in cyclosporin (2.0 +/- 0.6) than in azathioprine (1.5 +/- 0.5) treated recipients (p = less than 0.001). A reduction in cyclosporin dose because of nephrotoxicity was required in 96 of the cyclosporin-treated patients (70%), and 25 were switched to treatment with azathioprine (21%). The incidence of all infections in cyclosporin-treated patients was approximately half of that in azathioprine-treated patients, and only nine per cent of the cyclosporin-treated patients were diagnosed to have cytomegalovirus infections during the first post-transplant year vs. 28% in azathioprine-treated patients (p = 0.002).(ABSTRACT TRUNCATED AT 400 WORDS)
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Biography Historical Article
Lewis Stephen Pilcher, founding editor of the Annals of Surgery. Editor for 50 consecutive years.
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In an 11-year study of experimental insulin-deficient diabetes (IDDM) induced in rhesus monkeys by streptozotocin or total pancreatectomy, the authors have found that pathophysiologic changes occur in eye and kidney, which closely resemble the early stages of human insulin deficient diabetes mellitus (IDDM). In addition, morphologic changes of thickening of glomerular capillary basement membrane and expansion of mesangial matrix (by light microscopy) appear within 3 years of onset of hyperglycemia. However, progression to irreversible complications of advanced diabetic nephropathy or proliferative retinopathy, have not occurred. ⋯ The monkeys differ from humans in the absence of hypertension and hyperlipidemia. The authors suggest that the abnormalities in basement membrane form and function caused by hyperglycemia form the necessary background upon which other factors, such as hypertension and hyperlipidemia, then act to cause irreversible complications. The role of pancreatic transplantation is in prevention of these background changes.
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The authors previously have demonstrated axonal necrosis of autonomic nerves in the surgically resected ilea of patients with Crohn's disease both in grossly normal ileal resection margins and in diseased areas. The present study of ileal stomal biopsies was carried out to obviate the possibility that the observed axonal damage might be related to the prolonged surgical manipulations required for ileal resection. The authors present studies of biopsies of ileal stomas and of small bowel from patients with Crohn's disease and various control disorders, including ulcerative colitis. ⋯ Widespread, severe axonal necrosis of autonomic nerves was present in all Crohn's disease specimens, regardless of the patient's clinical status or the gross or routine microscopic evaluation of the same specimen. Controls either had no necrosis or displayed a minor degree of focal necrosis involving single axons. The authors conclude that Crohn's disease is accompanied by a severe and extensive necrosis of gut axons, and that such electron microscopic findings may serve to differentiate Crohn's disease from other inflammatory disorders.