Mechanisms of thrombosis in spinal cord injury.
Hematol Oncol Clin North Am
; 14(2): 401-16, 2000 Apr.
Article
in En
| MEDLINE
| ID: mdl-10806563
ABSTRACT
Many studies failed to identify a hypercoagulable imbalance in the blood factors or decreased anticoagulant activity. On the other hand, fibrinolysis, a process unrelated to hypercoagulability but closely related to endothelial cell integrity, is predictably altered and contributes to the persistence of venous occlusion by thrombosis. There is considerable evidence that interruption of neurologic impulses and the ensuing paralysis cause metabolic changes in blood vessels and that blood vessel changes are accountable for venous thrombosis. Altered venous competence with complete spinal cord injury manifests by a decrease in venous distensibility and capacity and an increase in venous flow resistance. Vascular adaptations to inactivity and muscle atrophy, rather than the effect of a nonworking leg-muscle pump and sympathetic denervation, seem to lead to the thrombosis; indicating that thrombosis resulting from venous incompetence cannot be reversed by anticoagulation alone.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Spinal Cord Injuries
/
Venous Thrombosis
Type of study:
Etiology_studies
/
Prognostic_studies
Limits:
Humans
Language:
En
Journal:
Hematol Oncol Clin North Am
Journal subject:
HEMATOLOGIA
/
NEOPLASIAS
Year:
2000
Document type:
Article
Affiliation country:
Estados Unidos