[Neurologic principles of edema in inactivity].
Identifieur interne : 005845 ( PubMed/Curation ); précédent : 005844; suivant : 005846[Neurologic principles of edema in inactivity].
Auteurs : H. TrettinSource :
- Zeitschrift fur Lymphologie. Journal of lymphology [ 0343-8554 ] ; 1992.
Descripteurs français
- KwdFr :
- MESH :
- physiopathologie : Lymphoedème, Système nerveux autonome.
- innervation : Drainage, Humains, Immobilisation, Lymphoedème, Système lymphatique.
English descriptors
- KwdEn :
- MESH :
- innervation : Lymphatic System.
- physiopathology : Autonomic Nervous System, Lymphedema.
- therapy : Lymphedema.
- Drainage, Humans, Immobilization.
Abstract
The complete immobilisation of a limb alone can lead to the formation of oedema. Whereas the oedema secondary to inactivity induced by immobilisation is completely reversible, and will only lead to tissue damage in the longterm, neglect of oedema secondary to inactivity in the presence of central and peripheral paresis (apoplectic insult, paraplegia, damage to the plexus brachialis) may entail serious consequences due to the danger of tissue fibrosis. With paresis of an extremity, the lymphovenous return is impaired by two decisive factors: increased hydrostatic pressure in the distal limb segment, and absence of the muscle pump. In flaccid paresis, where there is low muscle tone and no muscle pump action, there is also a low venous tone and the resultant hydrostatic pressure is especially high. Venous stasis in the sub- and prefascial veins leads to increased protein loss from the venous limb of the capillaries and the venules. Compensation initially occurs in the prefascial lymph outflow region (latent oedema) which becomes decompensated if overloaded (visible oedema). Fibrosis of the subcutis and trophic skin changes are the result. In spastic paresis the regional subfascial lymphatic system responds with lymphangiospasm. Where the sympathetic innervation is interrupted (e.g. brachial plexus paralysis) there is passive hyperaemia of the terminal vessels with vascular dilatation and lymphangioparalysis. Insufficiency of the vascular walls results in an accumulation of protein in the tissues, which ultimately ends in fibrosis with ankylosis and shortening of the tendons and muscles. The early administration of complex physical decongestion therapy with manual lymphatic drainage can prevent this state.
PubMed: 1288027
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H. Trettin<affiliation><nlm:affiliation>Neurologischen Abteilung, REHA-Klinik Damp.</nlm:affiliation><wicri:noCountry code="subField">REHA-Klinik Damp</wicri:noCountry></affiliation>Le document en format XML
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Whereas the oedema secondary to inactivity induced by immobilisation is completely reversible, and will only lead to tissue damage in the longterm, neglect of oedema secondary to inactivity in the presence of central and peripheral paresis (apoplectic insult, paraplegia, damage to the plexus brachialis) may entail serious consequences due to the danger of tissue fibrosis. With paresis of an extremity, the lymphovenous return is impaired by two decisive factors: increased hydrostatic pressure in the distal limb segment, and absence of the muscle pump. In flaccid paresis, where there is low muscle tone and no muscle pump action, there is also a low venous tone and the resultant hydrostatic pressure is especially high. Venous stasis in the sub- and prefascial veins leads to increased protein loss from the venous limb of the capillaries and the venules. Compensation initially occurs in the prefascial lymph outflow region (latent oedema) which becomes decompensated if overloaded (visible oedema). Fibrosis of the subcutis and trophic skin changes are the result. In spastic paresis the regional subfascial lymphatic system responds with lymphangiospasm. Where the sympathetic innervation is interrupted (e.g. brachial plexus paralysis) there is passive hyperaemia of the terminal vessels with vascular dilatation and lymphangioparalysis. Insufficiency of the vascular walls results in an accumulation of protein in the tissues, which ultimately ends in fibrosis with ankylosis and shortening of the tendons and muscles. The early administration of complex physical decongestion therapy with manual lymphatic drainage can prevent this state.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1288027</PMID><DateCreated><Year>1993</Year><Month>03</Month><Day>15</Day></DateCreated><DateCompleted><Year>1993</Year><Month>03</Month><Day>15</Day></DateCompleted><DateRevised><Year>2008</Year><Month>02</Month><Day>26</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0343-8554</ISSN><JournalIssue CitedMedium="Print"><Volume>16</Volume><Issue>1</Issue><PubDate><Year>1992</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Zeitschrift fur Lymphologie. Journal of lymphology</Title><ISOAbbreviation>Z Lymphol</ISOAbbreviation></Journal><ArticleTitle>[Neurologic principles of edema in inactivity].</ArticleTitle><Pagination><MedlinePgn>14-6</MedlinePgn></Pagination><Abstract><AbstractText>The complete immobilisation of a limb alone can lead to the formation of oedema. Whereas the oedema secondary to inactivity induced by immobilisation is completely reversible, and will only lead to tissue damage in the longterm, neglect of oedema secondary to inactivity in the presence of central and peripheral paresis (apoplectic insult, paraplegia, damage to the plexus brachialis) may entail serious consequences due to the danger of tissue fibrosis. With paresis of an extremity, the lymphovenous return is impaired by two decisive factors: increased hydrostatic pressure in the distal limb segment, and absence of the muscle pump. In flaccid paresis, where there is low muscle tone and no muscle pump action, there is also a low venous tone and the resultant hydrostatic pressure is especially high. Venous stasis in the sub- and prefascial veins leads to increased protein loss from the venous limb of the capillaries and the venules. Compensation initially occurs in the prefascial lymph outflow region (latent oedema) which becomes decompensated if overloaded (visible oedema). Fibrosis of the subcutis and trophic skin changes are the result. In spastic paresis the regional subfascial lymphatic system responds with lymphangiospasm. Where the sympathetic innervation is interrupted (e.g. brachial plexus paralysis) there is passive hyperaemia of the terminal vessels with vascular dilatation and lymphangioparalysis. Insufficiency of the vascular walls results in an accumulation of protein in the tissues, which ultimately ends in fibrosis with ankylosis and shortening of the tendons and muscles. The early administration of complex physical decongestion therapy with manual lymphatic drainage can prevent this state.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Trettin</LastName><ForeName>H</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Neurologischen Abteilung, REHA-Klinik Damp.</Affiliation></AffiliationInfo></Author></AuthorList><Language>ger</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><VernacularTitle>Neurologische Grundlagen des Inaktivitätsödems.</VernacularTitle></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Z Lymphol</MedlineTA><NlmUniqueID>7805527</NlmUniqueID><ISSNLinking>0343-8554</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CitationSubset>S</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001341" MajorTopicYN="N">Autonomic Nervous System</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004322" MajorTopicYN="N">Drainage</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007103" MajorTopicYN="Y">Immobilization</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008208" MajorTopicYN="N">Lymphatic System</DescriptorName><QualifierName UI="Q000294" MajorTopicYN="Y">innervation</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1992</Year><Month>12</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1992</Year><Month>12</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1992</Year><Month>12</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1288027</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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