[Thrombosis of the jugular veins].
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Biomedical subjects
Publications and source records attributed to A Kriessmann.
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Intermittent claudication is the principal symptom in stage II of peripheral arterial occlusive disease. As this is a multilocular manifestation of atherosclerosis, a distinction must be drawn between treatment of the underlying disease with consideration of the individual risk factors and improvement and abolition of the intermittent claudication. Various therapeutic principles exist, and drug therapy is the subject of controversial discussion. On the basis of eight controlled, randomized studies, it was demonstrated that in comparison with placebo a statistically significant increase in the pain-free walking distance can be achieved by oral drug administration within 3-6 months. This drug therapy should be considered for those patients with intermittent claudication who cannot undergo revascularization, angioplasty, or walking training.
In a controlled multicenter study 70 patients with chronic arterial occlusive disease stage IV according to Fontaine's classification were randomised to treatment with prostaglandin E1 (PGE1) or pentoxifylline (PX), administered over 4 weeks. Parameters of effectiveness were the reduction of analgesics, the relief of rest pain according to an analogue scale, the improvement of the ulceration according to an ulcer score and the healing of necrotic area. The results show that both forms of treatment produced a significant reduction in analgesic consumption and rest pain. Moreover in both groups a significant reduction of the ulcer score and healing of the necrotic area were observed. Side effects occurred in six patients of the PGE1-group and in ten patients of the PX-group, which required premature discontinuation of treatment in four patients of the PX-group. The study also demonstrated that PGE1 is more effective in the treatment of severe arterial occlusive disease than PX. With respect to the analgesic consumption, the reduction of ulcer score and the healing of necrotic area a significant difference was found in favour of PGE1. In accordance the six months follow-up examinations showed a marked deterioration in the PX-group opposed to the PGE1-group. The intravenous application of PGE1 over a period of 4 weeks in patients with severe arterial occlusive disease seems to be an effective therapeutical principle.
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In a prospective, randomized trial 33 patients with deep vein thrombosis were treated either with 2,200 or 1,100 IU/kg/h urokinase or with 100,000 IU/h streptokinase for at least 6 days. While streptokinase was given continuously, urokinase was administered intermittently (12 hr urokinase alternating with 12 hr heparin). Urokinase treatment resulted in a dose-dependent fibrinolytic state with shortening of the euglobulin clot lysis time, easily demonstrable amidolytic activity and moderate decrease of plasminogen. At the end of each urokinase-free interval the fibrinolytic activity had mostly faded, but was reproducibly elicited again by each new urokinase administration. Streptokinase immediately evoked the customary, intense fibrinolytic state, which progressively tapered off as plasminogen fell to 1% of its pretreatment concentration. In all treatment groups alpha-2-antiplasmin dropped to approximately 40% of its initial value during the first 12 hr with a further decrease to about 20% after 6 days. alpha-2-macroglobulin fell only moderately with either urokinase regimen, whereas it decreased progressively to 45% under streptokinase. While the fibrinolytic activity decreased under streptokinase over the 6-day infusion period, it appeared to increase with each successive urokinase infusion particularly with 1100 IU/kg/h. Thus the final euglobulin clot lysis times and the final fibrinogen concentrations were similar in all three treatment groups on the sixth day.
Thirty-three patients with acute iliofemoral thrombosis were randomly assigned to three treatment groups in a pilot dose-ranging study of thrombolytic therapy in deep vein thrombosis. One group received tissue culture urokinase in a dose of 2,200 I.U./kg/hr, and a second group in a dose of 1,100 I.U./kg/hr following a loading dose of 4,400 I.U./kg given in ten min. Urokinase was administered for 12 hr periods, alternating with 12 hr periods of heparin. A third group received an initial dose of 250,000 I.U. of streptokinase in 20 min, followed by 100,000 I.U./hr. Treatment of all patients continued for three days. At the end of this period little improvement, evaluated by "blinded" interpretation of pre- and post-treatment phlebograms, was found in five out of ten of the higher-dose urokinase patients, seven out of eleven of lower-dosage urokinase patients, and six out of ten of streptokinase patients. Optional treatment for another three days showed little further improvement of urokinase-patients and moderate further improvement in the streptokinase-patients. Neither of the 2 dosage schemes at intermittent application of urokinase appeared to be advantageous. Urokinase treated patients experienced fewer adverse reactions.
In 107 consecutive patients the frequency of peripheral arterial occlusive disease in coronary heart disease was assessed by selective coronary angiography and sonographic Doppler pressure estimation. Among 75 patients with coronary heart disease 21 (28%) had arterial occlusive disease, among 32 patients without coronary heart disease only one (3%). There was no statistically significant correlation between the severity of both diseases. 40 out of 75 patients with coronary heart disease had suffered from cardiac infarction. Infarction frequency showed a highly significant correlation with increasing severity of the coronary heart disease, but none with increasing severity or frequency of arterial occlusive disease. When there was no arterial occlusive disease all degrees of severity of coronary heart disease were found. Analysing the literature it becomes evident that coronary heart disease is frequently an isolated or premature manifestation of arteriosclerosis.
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Fibrinolytic therapy was carried out in 59 patients suffering from a total of 60 deep venous thromboses of the iliac segment (n = 24), the femoropopliteal segment (n = 18), the deep calf veins (n = 2), or the subclavian vein (n = 16). 46 patients received streptokinase (SK), 4 were given urokinase (UK), and 10 were treated with streptokinase followed by urokinase (SK + UK). The duration of fibrinolytic therapy was between 19 and 596 hours (x = 166 +/- 111 hrs). Phlebographic examination was used to determine the location of the thrombotic occlusion as well as to evaluate therapeutic results. To assure sufficient anticoagulatory protection during therapy with streptokinase the dose of streptokinase was either reduced by steps of 20,000 U/hr to a minimum of 40,000 U/hr or heparin was added as a continuous infusion. Urokinase was administered with a mean loading dose of 75,000 IU followed by an average maintenance dose of 40,000 IU/hr; it was always given in combination with heparin. When therapeutic success was graded as complete/partial/no recanalisation, the following results were obtained: thrombotic occlusion up to 1 week old 35%/48%/17%; up to 2 weeks old 57%/14%/29%; 3 or 4 weeks old 12%/38%/50%; older than 4 weeks 13%/37%/50%. The two most common side effects were a fall of the hemoglobin and a rise of body temperature. Treatment with SK had to be interrupted for bleeding in two cases. One patient diet after rupture of the liver and of the spleen following development of subcapsular hematoma in these organs, 3 patients survived pulmonary embolism without major long-term impairment. Considering medical and social aspects (preservation of capability for working in young adults) it appears justified to administer fibrinolytic agents up to a thrombus age of 14 days, in some cases even up to a thrombus age of 28 days. Good results in cases of deep vein thrombosis of the lower limbs are often obtained only when fibrinolytic therapy is extended beyond 96 hours. It should be performed in intensive care units only. Follow-up examinations of the venous drainage capacity up to 2 years after fibrinolytic therapy document the good therapeutic effect that is warrented by streptokinase or urokinase induced complete recanalisation.
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