Self-leveling device for holding cup of barium sulfate.
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Biomedical subjects
Publications and source records attributed to D Silver.
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Heparin is usually administered to patients with intra-aortic balloon pumps (IABP) to prevent thromboembolism. In addition to thrombocytopenia caused by IABP mechanical damage to platelets, exposure to heparin can cause heparin induced thrombocytopenia (HIT). Heparin induced thrombocytopenia is caused by an immune mechanism in which heparin antibodies are produced, causing platelet aggregation, leading to bleeding or thromboembolic complications. Over a 9 year period, 35 of 764 (4.5%) patients with IABPs have been diagnosed as having HIT. Surgical procedures included coronary artery bypass (CABG) in 14 (40%), valve repair or replacement in 7 (20%), and CABG and other cardiac procedure in 14 (40%). Lowest platelet counts ranged from 17,000-114,000/mm3 (median, 44,000/mm3). Thirty-three of 35 (94.3%) had mediastinal hemorrhage requiring infusion of multiple blood products, and 6 of these 35 (17%) required return to the operating room. Seventeen of 35 (48.6%) experienced thromboembolic complications. Hospital mortality was 15 of 35 (42%). Etiology of thrombocytopenia in patients on IABPs is multifactorial. Patients on an IABP who develop thrombocytopenia should be tested for heparin dependent anti-platelet antibodies to rule out HIT. When a heparin antibody is present, heparin must be discontinued and alternate forms of anticoagulation/platelet inhibition initiated to reduce morbidity and mortality.
One hundred and eight patients were studied with fluid-filled oculoplethysmography and carotid phonoangiography (OPG-CPA) and by arteriography. Thirty-two patients also had "Doppler evaluation" of supraorbital arterial flow. The OPG-CPA correctly predicted the degree of occlusion in 76% of the involved vessels, including the degree of occlusion of each carotid for each patient (63%). The OPG-CPA identified at least one obstructing carotid lesion in 51 of the 56 (91%) patients with obstructing lesions demonstrated by arteriography. On a per patient basis, which requires that both carotids be correctly assessed, the OPG-CPA had a false negative rate of 9.6% and false positive rate of 50%. The supraorbital artery "Doppler evaluation" had an accuracy rate of 66%, a per patient false negative rate of 50%, and a per patient false positive rate of 12%. The OPG-CPA and supraorbital artery "Doppler evaluation" are adjunctive tests for evaluating patients with cerebral vascular insufficiency and should not, at present, replace arteriography in symptomatic patients or in certain asymptomatic patients.
PURPOSE: This study was conducted to determine whether recommendations from the Diabetes Control and Complications Trial (DCCT) could be implemented in a large pediatric population using a diabetes clinical nurse specialist program coordinator dedicated to intensive management. METHODS: Patients' charts were reviewed to examine HbA1c levels from before the results of the DCCT were published and again 1 year after the recommendations were implemented. Patients who met the following criteria (N = 124) were enrolled: type 1 diabetes, less than 18 years old, followed at Yale for 1 year prior to the results of the DCCT and 1 year after, and HbA1c level recorded in the medical chart. RESULTS: HbA1c levels were significantly lower 1 year after implementing the DCCT protocol; 3 years later these same patients improved even further as evidenced by another decrease in HbA1c levels. The patients were taking more insulin (more Ultralente and regular insulin and less NPH) and had an increased number of injections at both the 1-year and 3-year follow-up points. CONCLUSIONS: The DCCT protocol can be implemented in a large population of pediatric patients with the help of a nurse who is dedicated and available to the patients for ongoing adjustments and provides creative ways to overcome the barriers to achieving normoglycemia.
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Skeletal muscle contraction and metabolism was evaluated using an in vivo, intact autoperfused canine hindlimb model during 7 hours of reperfusion following 4 hours of complete ischemia, with and without bolus administration of superoxide dismutase (SOD) and catalase (CAT) at the start of reperfusion. Contractile tension of paw dorsiflexion during reperfusion demonstrated small but statistically non-significant increases of recovery towards pre-ischemic baseline with SOD/CAT (i.e. 43% +/- 10 vs 32% +/- 9 with muscle-stimulated tetanic tension). Oxygen utilization by the hindlimb rose during reperfusion from a baseline in the control group of 2.4 +/- 0.3 ml 02/min to 5.4 +/- 1.1 during the first 10 minutes and plateaued at 3.5 +/- 1.3 by the first hour with no differences in the SOD/CAT group. Lactate clearance was prompt (increase from a pre-ischemia value of zero to 0.93 +/- .14 mM/min by 5 minutes and return to near-zero by 1 hour in controls) exhibiting no sustained anaerobic metabolism and was not affected by SOD/CAT. These finding demonstrate irreversible loss of 60-70% of skeletal muscle contraction with preservation of aerobic metabolic capacity at 225% of basal activity. Bolus administration of SOD/CAT at the start of reperfusion offered no significant improvement in metabolic or contractile function. These observations, in a model simulating the in vivo setting, necessitate evaluating alternate ischemia reperfusion conditions and modified free-radical inhibitor protocols before any clinical benefit can be assumed.
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