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Biomedical subjects

N Kluken

Publications and source records attributed to N Kluken.

11 recordsLinked to original sources
PubMed1980

[Diagnostic problems posed by acute inflammatory exacerbations of lymphoedema. Isotopic methods of investigation (author's transl)].

With the help of isotope examination methods as isotope angiography, -phlebography, particle-scintigraphy and isotope lymphography it is possible to differ the oedemaproductive component, i.e. the increase of perfusion in the inflammation area and the lymphostatic oedema. In an inflammatory pushes the non equilibrium between increased plasma filtration and increasing lymphostasis due to destruction of the still capable lymphatics conducts to an accelerated progression of the chronic lymphostatic oedema.

Angiography↗
PubMedDate not supplied

[Does the success of thrombolysis depend on the age of the patient?].

This study raises the question whether the age of the patient has any influence on the results of the treatment of the post-phlebitic syndrome of the lower extremities by thrombolysis. Our study demonstrates that elderly patients respond to thrombolysis as well as young patients.

Adult↗
PubMedDate not supplied

[Micromorphological and clinical aspects of angiodysplasias].

As is known, 1900 Klippel and Trenaunay summarized naevus teleangiectatisuc lateralis, vein ectasias and isolated gigantism to a triad. Seven years later Weber described the same syndrom adding the symptom of arterio-venous fistulas, that he clinically diagnosed. Some authors deduce from this symptomatology two syndroms ; on one hand the Klippel and Trenaunay syndrom and on the other the P. F. Weber-syndrom. As it is shown, in spite of an immense variability of symptoms, arterio-venous short circuits can regularly be demonstrated-clinically, arteriographically or histomorphologically. In addition to this some casuistical examples are presented. Referring to this reports the authors do not agree on separation of Klippel-Trenaunay and Weber syndrom. Considering to therapeutical consequences -- namely surgical -- it should be always cleared up angiographically if hemodynamically relevant arterio-venous fistulas are present. (Due to this fact a divergence to Weber's characterization is given). Relative to the authors opinion the presence of hemodynamically and so therapeutically relevant or obviously hemodynamically non-relevant arterio-venous fistulas does not allowed the separation in two syndroms. Out of this reason the authors nomenclature the described symptomatology as Klippel-Trenaunay-Weber-Syndrom.

Angiomatosis↗
PubMedDate not supplied

[Physico-mechanical treatment of chronic arterial obliterations in the extremities. Attempt to objectify its efficacy].

This study shows the objective value of a physico-mechanical high pressure/low pressure therapy using the Vasculator. Until recently, the supposition that such a treatment would improve the blood circulation was based purely on clinical observation. We have been able to define ergometric parameters confirming the improvement of the circulation effected by the Vasculator. This ergometric equipment enables us to measure pace and distance and, at the same time, to check with precision the effort required. Our experiment proves that the Vasculator treatment induces increased muscular effort, approximately 20-25 p. cent, and the quantitative analysis has shown that our results may be considered fully significant. Taking into account the values obtained before and after each treatment, increased parameters lead us to believe that the Vasculator gives not only short-term results, but also effects a long-term improvement of the blood-circulation.

Arterial Occlusive Diseases↗
PubMedDate not supplied

[Possibilities of drug therapy in the fight against deep venous thrombosis].

The aim of treatment of this illness should be recovery of the circulation, i.e. the suppression of thrombi in the deep venous network. This goal may currently be reached, in the same way as embolic lysis, by the early administration of streptokinase and urokinase, whose mechanisms, dosage-problems and chances of success are discussed here. This thrombolytic treatment is charged with major risks. If it is not to be used then anticoagulants are indicated. These have only a prophylactic effect, that is: they prevent the growth of thrombi. Heparin is the most active anticoagulant but it can only be administered parenterally. The author discusses the mechanism and efficiency of heparin and the antagonists of vitamin K1. Anti-aggregates rather show prophylactic action in the formation of arterial thromboses. Their spectacular effect in vitro on coagulation in vivo has not always been clearly proved in the venous system. It can be seen from the varied effects on thrombocytes and the vascular wall why anti-aggregates are not ideal anti-coagulants.

Anticoagulants↗
PubMedDate not supplied

[Do the clinical symptoms described by Raynaud correspond to a nosological entity or a syndrome with multiple etiologies?].

In considering this problem, our opinion concerning Raynaud's phenomenon is as follows: The symptomatology described by Raynaud includes among other things a local asphyxia and gangrene. All the patients in whom these two signs are not found should not therefore be included under the label of Raynaud's disease. It is preferable in such cases to use Reil's term of "dead fingers". But our experience shows that if there is local asphyxia or even gangrene, in addition to the syncopal episodes, there is always a causal disease. However it is not justifiable here to speak of Raynaud's disease, but rather of Raynaud's syndrome or Raynaud's phenomenon complicating some causal disorder, such as progressive scleroderma or obstructive arterial disease with digital localisation. The phenomenon of "dead fingers" is very common and most marked at the time of puberty. The symptoms regress in the years following. It is rare to see Raynaud's phenomenon at the time of puberty, this being commoner in later decades, with a course which is more or less pronounced and progressive according to the underlying disease. The prognosis is also a function of the underlying disease and is likely to be unfavourable, even threatening life, in cases of progressive scleroderma.

Humans↗