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Biomedical subjects

R N Rubin

Publications and source records attributed to R N Rubin.

At least 19 recordsLinked to original sources
PubMed1998

Feasibility and pharmacokinetics of carbamazepine oral loading doses.

The pharmacokinetics and adverse effects of an oral loading dose of carbamazepine administered in tablet or suspension form were studied. Patients on a hospital epilepsy unit who were to receive carbamazepine as a discharge medication were randomly assigned to receive either an oral 8-mg/kg loading dose of the tablet formulation or the same dose of the suspension on an empty stomach. Blood samples were drawn before and at intervals up to 12 hours after the loading dose. Adverse effects were evaluated subjectively and objectively. Total and free serum carbamazepine and carbamazepine-10, 11-epoxide (CBZE) concentrations were determined by high-performance liquid chromatography. Six adult patients were enrolled in and completed the study. All the patients achieved therapeutic total carbamazepine levels; the suspension group did so within two hours and the tablet group within five hours. Maximum serum carbamazepine concentrations ranged from 7.10 to 9.92 mg/L, area under the concentration-versus-time curve from 54.85 to 82.23 micrograms.hr/L, and terminal elimination half-life from 14.05 to 15.71 hours. Adverse effects were mild, few, and short-lived; none of the patients developed gastrointestinal toxicity. Adverse effects were not associated with total or free carbamazepine and CBZE concentrations or with total or free CBZE:carbamazepine ratios. An oral loading dose of carbamazepine 8 mg/kg achieved therapeutic levels within two hours when given as a suspension and within five hours when given as tablets and was well tolerated in all patients.

Adult↗
PubMed1995

Techniques for evaluating the cause of bleeding in the ICU. Diagnostic clues and keys to interpreting hemostatic tests.

Begin by obtaining both a bleeding and a family history to help ascertain whether the disorder is acquired or inherited. On physical examination, look for multiple bleeding sites or profuse bleeding; these can indicate a systemic bleeding diathesis. Order hemostatic tests. Prolonged aPTT points to a defect in the intrinsic or common coagulation pathway; prolonged PT, to a defect in the extrinsic or common pathway. Thrombin time is abnormal when hypofibrinogenemia, afibrinogenemia, or thrombin inhibitors are present. Bleeding time is prolonged in thrombocytopenia, platelet dysfunction, severe hypofibrinogenemia, and von Willebrand's disease. Factor assays also may be needed to further define the defect.

Blood Coagulation Tests↗
PubMed1992

Disseminated intravascular coagulation. Approach to treatment.

Disseminated intravascular coagulation (DIC) is a syndrome caused by the systemic generation of thrombin. Most cases are due to pathological activation of the intrinsic coagulation systems (e.g. in sepsis), and/or the extrinsic system (e.g. in malignancy and head trauma). Diagnosis is made by finding abnormalities in at least 3 of 4 laboratory values, namely prothrombin time, platelet count, fibrinogen and fibrinogen/fibrin degradation products. The most common clinical manifestation of DIC is bleeding, with thrombosis in less than 10% of acute cases but more frequently encountered in chronic DIC associated with malignancy. Acute DIC must first be treated by specific therapy of the underlying disease and general support measures. If serial clinical and laboratory monitoring improves, no further treatment is required. If severe or life-threatening haemorrhage occurs or a thrombotic event ensues, heparin anticoagulation followed by aggressive replacement with platelets, fresh plasma and possibly cryoprecipitate is indicated. Heparin doses should be 'therapeutic' (i.e. adequate to overcome the coagulant forces that may have produced a relative heparin-resistant state in the blood). Chronic DIC with haemorrhage, or more usually thrombosis, should also be treated with heparin; warfarin is ineffective. If DIC persists because, for example, a tumour does not regress, long term outpatient subcutaneous heparin therapy may be required.

Disseminated Intravascular Coagulation↗
PubMed1989

Government.

Explore the source record for details and available documents.

Delivery of Health Care↗
PubMed1988

Reform of the Medicare program.

Financing of the Medicare program is under stress because of national economic and demographic trends. A comprehensive overview of the required changes is imperative. The American Medical Association has proposed to place Medicare funding out of the political arena and to place it under the administration of an independent commission such as the Federal Reserve Board. Further, the plan would initiate a voucher system financed by a tax on adjusted gross income during the working years invested through a new public trust fund.

American Medical Association↗
PubMed1987

Enterobronchial fistula.

An unusual case of a fistula originating from the jejunum and crossing the diaphragm to involve the pleura and bronchial tree is presented. The presence of the fistula was first suggested on a computed tomographic examination of the chest. An upper gastrointestinal series verified the origin of the fistula.

Barium Sulfate↗
PubMed1987

Physician reimbursement: the environment for change.

Escalation of costs for physician care services in the Medicare program has elicited measures to rein in these expenditures. These include freeze and control of physician fees, limits on reimbursement for certain procedures, and mandated assignment of clinical laboratory service charges. An important step in rationalizing physician fees lies in the resource cost-based relative value study undertaken by the American Medical Association together with Harvard University economists. The results should redress inequities inherent in the current reimbursement system and allow a more suitable distribution of funds within the profession.

Evaluation Studies as Topic↗
PubMed1987

Intra-arterial thrombolytic therapy in peripheral vascular disease.

This is a prospective analysis of patients undergoing 34 treatments for arterial thromboses and emboli with intra-arterial thrombolytic therapy. These included acute arterial thromboses, graft thromboses, arterial emboli and pulmonary emboli. Twenty-seven of 34 patients treated had evidence of lysis, 14 had complete lysis, 13 had partial lysis and seven had no lysis. Both patients with occlusions for longer than three weeks failed to respond to treatment. Thirty-two patients presented with ischemia of the extremity. Twenty-four of 32 patients had limb salvage with eight subsequently undergoing amputation. No patient who was treated for claudication or who had a patent popliteal artery distal to the acute thrombosis failed to respond. Extensive tibioperoneal occlusion generally responded poorly compared with femoropopliteal or more proximal thrombi. Complications are divided into direct (drug related) and indirect (technique related). Four of 34 patients had an extensive hemorrhagic event with two suffering intracranial bleeding who ultimately died. All of the patients with extensive hemorrhagic episodes had serum fibrinogen levels of less than 50 milligrams per cent. During infusion, extensive distal emboli occurred in three with two of these patients requiring thrombectomy; one instance resolved with infusion. Minor distal emboli occurred in three and all resolved with continued infusion. We believe that intra-arterial thrombolytic therapy is a valuable adjunct in the treatment of acute arterial occlusion. The local infusion of lytic agents appears to be more efficient than systemic therapy. The tip of the infusion catheter should be placed into the thrombus for optimal lysis, but not advanced too far. The fibrinogen level is a sensitive indicator of systemic lysis and should be maintained above 50 milligrams per cent. Systemic lysis is obtained even with low dose infusion when therapy exceeds six hours. Intra-arterial infusion of thrombolytic agents can be performed safely in the immediate postoperative period as well as intraoperatively if specific guidelines are followed. Patients with massive unilateral pulmonary embolism can be efficiently treated with intra-arterial lytic therapy.

Fibrinogen↗
PubMed1984

Fibrinogenolytic afibrinogenemia after envenomation by western diamondback rattlesnake (Crotalus atrox).

The absence of fibrinogen and the presence of plasmic fragments X, Y, D, and E were demonstrated in a patient bitten by a western diamondback rattlesnake, Crotalus atrox. The factor VIII level and the platelet count were within normal limits. There were distinct changes of protease inhibitors in the patient's plasma. Alpha-1-protease inhibitor was elevated. Antithrombin-III was only slightly decreased after the envenomation, but alpha 2-antiplasmin and alpha 2-macroglobulin were initially significantly lowered, returning to normal values in 38 and 3 days, respectively. Plasmin-alpha 2-antiplasmin complex was present until day 10 after the envenomation. However, purified plasminogen was not activated in vitro by the venom. Cultured endothelial and smooth muscle cells from human blood vessels released an increased amount of plasminogen activator upon incubation with the venom. The release did not result from cell lysis. Platelets in normal human platelet-rich plasma were aggregated by 10 micrograms/ml of the venom, without serotonin secretion. The aggregation kinetics and serotonin secretion induced by adenosine diphosphate (ADP) or arachidonate were not significantly affected by the venom at 1-10 micrograms/ml. It is concluded that the predominant mechanism of afibrinogenemia in the patient after Crotalus atrox bite resulted from primary fibrinogenolysis and not from a consumptive coagulopathy. The lytic state seemed to be induced through an indirect activation of plasminogen by vascular plasminogen activator, which was probably released from endothelial cells and smooth muscle cells by the snake venom.

Adult↗
PubMed1983

Unique degradation of human fibrinogen by proteases from western diamondback rattlesnake (Crotalus atrox) venom.

Thrombin-coagulability of both human fibrinogen and plasma was rapidly lost upon incubation with western diamondback rattlesnake (Crotalus atrox) venom. The dose- and time-dependent effect was due to direct proteolytic degradation of fibrinogen (Mr 340,000) by venom enzymes. Using purified fibrinogen as the substrate it was demonstrated that the venom degraded the A alpha chain first and then the B beta chain. The degradation pattern of fibrinogen in plasma was different to that of purified fibrinogen, since only the B beta chain was cleaved. A fibrinogen derivative isolated from venom-treated plasma had impaired thrombin-coagulability, Mr 325,000 +/- 10,000, its A alpha and gamma chains appeared intact and only the B beta chain was degraded to a species of Mr 52,000 +/- 1,500. The venom contained three proteolytic enzyme fractions as revealed by gel filtration chromatography. All abolished coagulability of purified fibrinogen, however, only one enzyme fraction rendered plasma incoagulable. The proteolytic enzyme with anticoagulant activity against plasma degraded only the B beta chain of purified fibrinogen, generating a derivative of Mr 325,000, which was identical to that obtained upon incubation of the crude venom with plasma. The polypeptide chain structure of the derivative indicates that the intact B beta chain of fibrinogen plays an important role in the formation of fibrin clots.

Anticoagulants↗