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Biomedical subjects

G Rudofsky

Publications and source records attributed to G Rudofsky.

At least 109 records · Page 6Linked to original sources
PubMed1989

[Pathogenesis, diagnosis and therapy of thrombophlebitis and varicophlebitis].

Thrombophlebitis is defined as thrombotic inflammation of a previously healthy superficial vein, varicophlebitis as that occurring in varicosities. The latter appears responsible for the majority of thrombotic venous occlusions. In contrast to venous thrombosis, the thrombotic involvement of deep veins, thrombophlebitis usually resolves without sequel and, in general, thrombophlebitis nor varicophlebitis are associated with the risk of pulmonary embolism. The clinical presentation of thrombophlebitis is that of a tender, hardened superficial vein which, in the presence of inflammation, may be very painful. The lower extremities are most frequently involved. Differential diagnostic considerations include bacterial cellulitis and lymphangitis. The cause of thrombophlebitis, which is rare without precipitating factors, may be a mechanical lesion such as kinking of the vein or trauma to the wall of the vein as well as other primary disease such as auto-immune afflictions, endangiitis obliterans or malignancy; in particular, with localization in the area of the rump, with concomitant occurrence in various regions or extending phlebitis, paraneoplastic syndromes and hemoblastoses should be ruled out. Rarely, phlebitis may be associated with tuberculosis and syphilis. Thrombophlebitis may be caused iatrogenically by improper application of chemical substances which cause damage to the venous walls as well as by indwelling catheters or cannulas. This form can progress to sepsis and pulmonary embolism may be incurred. Varicophlebitis, in contrast, accounts for about 90% of all cases of phlebitis and can be regarded as a typical late complication of varicosities in the superficial venous system.(ABSTRACT TRUNCATED AT 250 WORDS)

Bandages↗
PubMed1989

Intravenous prostaglandin E1 in the treatment of venous ulcers--a double-blind, placebo-controlled trial.

To assess the clinical efficacy of i.v. PGE1 in the treatment of refractory venous ulcers a double-blind, placebo-controlled study was carried out. 42 patients were given at random either one i.v. infusion of 3 ampoules of Prostavasin (60 micrograms PGE1) or 3 ampoules of placebo (1940.1 micrograms alpha-CD) daily, soluted in 250 ml saline over 3 h. The treatment period was 6 weeks. In the PGE1 group (n = 20) there was a significant improvement in the ulcer status compared to placebo (n = 22) (p less than 0.001) being assessed by a detailed, multivariated score. Ulcers healed completely in 8 out of 20 patients on PGE1 (40%) compared to only 2 out of 22 patients on placebo (9%). Concomitant clinical symptoms improved accordingly. Whereas in the PGE1 group edema were completely resolved in 17 out of 20 patients (85%) this was the case in 7 out of 20 patients of the placebo group (35%). Calf cramps and eczema vanished in 80% and 87.5% respectively under PGE1, but only in 50% and 9% respectively under placebo. Parallel to this an increase of the tcPO2 in the ulcer area of a mean of 45.9% was observed. Throughout the whole treatment period no side effects were noted after PGE1 infusion.

Adult↗
PubMed1988

[Intra-arterial infusion treatment with prostaglandin E1 in patients with intermittent claudication].

In a double-blind, placebo-controlled study 50 patients with peripheral arterial occlusive disease stage IIb were given daily or intra-arterial infusion of either 1 ampoule of Prostavasin (20 micrograms PGE 1) or 1 ampoule of placebo (646.7 micrograms alpha-cyclodextrin), each dissolved in 50 ml saline, over 60-120 min. Weekends excepted, the therapy was continued for three weeks. Under PGE 1 therapy the maximum ergometric walking distance increased by 146% (mean: from 109 m to 268 m), as opposed to 40% in the placebo group (mean: from 101.5 m to 142 m). Furthermore, significant improvements were seen with regard to painfree walking capacity (PGE 1: + 170%; placebo: + 49%). Free maximum and pain-free walking distances were increased as well (PGE 1: + 131% and 48%; placebo: + 26% and 27%). Haemorrheological parameters, e.g. plasma and whole blood viscosity, haematocrit and erythrocyte aggregation decreased (p less than 0.01) after PGE 1, whereas a significant increase (p less than 0.01) in acral digital temperature, blood flow and ultrasonic Doppler values was seen. No side-effects were observed.

Alprostadil↗
PubMed1988

[Epidemiology and pathophysiology of primary varicose veins].

Epidemiological investigations in German-speaking countries have covered over 14,000 people. Chronic venous insufficiency (edema, dermal alteration) was found in 13% and extensive varicosis in 15%. Thus, nearly 30% must be regarded as afflicted with varicose veins. The major pathophysiology, the absence of a directed blood flow due to venous dilatation and valve incompetence, becomes relevant hemodynamically and clinically if the proximal valves of the saphenous veins and/or perforating veins are also incompetent. Chronic venous insufficiency develops.

Cross-Sectional Studies↗
PubMed1987

[Non-invasive diagnosis of the venous system of the leg in pregnancy].

During pregnancy one should largely avoid invasive and radiological diagnostic methods. However, real-time sonography and venous occlusion plethysmography yield non-hazardous information on venous morphology and venous function. It became possible to demonstrate by means of these examination methods that the diameters of the veins are enlarged in pregnancy compared to the situation post partum. The difference in significant. Venous occlusion plethysmography points to a deterioration of venous function post partum, since the difference to the values in the third trimenon is not significant. Venous function measurement often pointed to the existence of an obstacle to flow during pregnancy, whereas sonographically a dilatation of the veins was revealed the existence of an obstacle to flow represented by the pregnant uterus. Hence, it appears meaningful to combine both investigation methods to confirm the occurrence of venous changes during pregnancy.

Blood Flow Velocity↗
PubMed1987

[Intravascular pressure measurements and phlebography of the renal vein: a contribution to the etiology of varicocele].

Phlebography of the left renal vein was performed in 80 patients with left-sided varicocele demonstrating the nutcracker phenomenon. In 39 cases we could prove a compression of the left renal vein. In 10 varicocele patients additional intravascular pressure measurements were studied in both renal veins in the supine and erect position. We found no significant difference between the pressure in the left and right renal vein in the supine position: values varied with respiration. Changing from the supine to the erect position one can note a significantly elevated pressure, higher on the left side than on the right side due to the longer excursion of the left kidney. Urine investigations were done in 153 patients before and in 191 after sclerotherapy to detect protein or blood. Only in 4 patients we found proteinuria but no microhematuria. The results suggest that the aetiology of the varicocele formation is not the nutcracker phenomenon or renal vein hypertension; the predominant cause is a congenital incompetence of the valves in the left testicular vein. The driving force for the retrograde blood flow from the left renal vein into the testicular vein was the increase in pressure: in the supine position caused by respiration, the continuous reflux in the erect position caused by the hydrostatic pressure. The varicocele does not cause a congested kidney with hematuria and proteinuria.

Humans↗