Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1969 to 1971 the authors treated 1360 injured patients, eight of which suffered serious injuries of the thigh; fractured femur complicated by a severed Femoral Popliteal Artery, and lesions of the Sciatic Nerve. Six patients were injured at work, one in an automobile accident, and one was a gunshot victim. In approximately 1000 fractures one is complicated by an injured neurovascular bundle. The clinical picture of such a case is characteristic. The arteriograph is used only to locate the lesion. Reconstruction of the artery must be accomplished some eight to twelve hours following the injury. In all of the authors' cases, this was done one to eight hours following the trauma. After twelve hours, ischemic necrosis of the soft tissue (musculature) sets in requiring amputation. The remaining segment of the damaged artery is usually resected. In one case, a segment 8 cm. long was removed. Following the termino-terminal anastomosis, the injured extremity was placed in a flexed position whlich alleviated the tension on the sutures. The result of vein autographs are worse than those of the termino-terminal anastomoses. Thrombosis later begins to restrict blood flow through the reconstructed artery, but by this time, adequate collateral circulation has been established. The limb has thus been saved. Heparin is administrated immediately before and during the operation in a dosage of 5000 units per 500 ml. of physiological solution. Postoperatively, it is not used as it acts on the fibrin thrombi, and not on the thrombocyte thrombi which are formed postoperatively in the areas where the tunica intima has been damaged. Heparin is indicated in the prophylaxis of venous thrombosis. In these cases in which the femur was fractured, the question asked is whether to perform the osteosynthesis and anastomosis simultaneously, or to perform the former at a later time. The authors chose both methods for various reasons. Only a few cases permitted the authors to decide which approach would be better. Usually they performed a temporary fixation of the bone with Rusch's Pin, and sutured the artery. Four months later, a compressive osteosynthesis using an L-plate, was performed. In four cases, the Sciatic Nerve was injured, which, according to the circumstances was sutured either immediately, or 3 to 4 weeks later. In 3 patients, good functional results were obtained. Three cases resulted in a contracture of the knee, two of which also had residual Sciatic Paresis. One case resulted in permanent venous stasis (edema of the legs, and two cases results in amputation.
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PMID:[Injuries of the thigh bone with a destruction of the neuro-vascular bundle]. 99 30

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.
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PMID:[Neurologic principles of edema in inactivity]. 128 27

The value of the vascular examination cannot be over-estimated. Symptoms of vascular disease present in the foot and lower extremity may actually be manifestations of severe life-threatening disease. Symptoms, their location, and the frequency and quality of the patient's pain often provide valuable clues for the clinician's diagnosis. Central nervous system symptoms, ocular disturbances, cardiac symptoms, impotence, or constitutional disturbances may all indicate systemic arterial disease. Risk factors for this disease include smoking, hypertension, hyperlipidemia, genetic predisposition, diabetes, emotional stress, and physical inactivity. Those factors attributable to hypercoagulability and venous disease are birth control pill use, estrogen chemotherapy, obesity, prolonged immobilization, paralysis, previous thrombotic episodes, venous stasis disease, and varicose veins. An accurate bilateral assessment of blood pressure, pulses, and capillary perfusion is of critical importance. Careful inspection of the extremity for trophic changes, skin color, texture, temperature, edema, ulceration, atrophy, or paresis, will provide clues of vasculopathy. A relatively accurate assessment of circulatory status may be obtained without the use of exotic instruments. Simple tests such as the elevation and dependency tests, capillary bed return test, venous filling time test, along with blood pressure, pulse, and possibly oscillometry data are valuable in arterial evaluation. Such venous tests as inspection, percussion, Homan's sign, Trendelenburg, and Perthes' tourniquet are useful in the determination of the presence of venous disease. Fortunately, over the past few years tremendous advances have been made in the technology of the vascular laboratory. If symptoms are discovered during the vascular history and physical examination, the complete noninvasive study will provide impressive data to quantitate and specifically establish the diagnosis.
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PMID:The vascular history and physical examination. 173 54

Three patients with spinal dural arteriovenous fistula presented with acute and/or progressive myelopathy. The thoracic cord was focally enlarged and poorly defined on MR images in two of the patients. One individual showed focal cord atrophy, and one demonstrated abnormal intrathecal vessels. In all patients MR studies revealed cord enhancement after IV administration of gadopentetate dimeglumine. The MR findings are believed to represent disruption of the blood-cord barrier associated with cord ischemia and/or infarction, which, in turn, is caused by venous stasis resulting from the fistula. The diagnosis in each case was confirmed by the combined results of myelography, spinal arteriography, and surgery. Surgical excision or embolization of the fistula produced a poor return of lost function but an arrest in the progression of paresis. One of the patients had constant severe back and leg pain postoperatively, and a follow-up MR study 5 months after surgery showed focal atrophy and persistent enhancement of the thoracic cord. The patient with preoperative focal cord atrophy had an MR examination 1 year prior to surgery, which revealed enhancement of the cord similar to that seen on the immediate preoperative MR study. This patient also had severe pain in the back and lower extremities preoperatively, which accompanied her progressive paraparesis. It is believed that long-standing enhancement of the spinal cord in patients with dural arteriovenous fistula probably results from chronic progressive venous ischemia, which may be irreversible and cause pain of a central type.
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PMID:Venous infarction of the spinal cord resulting from dural arteriovenous fistula: MR imaging findings. 188 56

The incidence of venous thromboembolism exceeds 1 per 1000; over 200,000 new cases occur in the United States annually. Of these, 30% die within 30 days; one-fifth suffer sudden death due to pulmonary embolism. Despite improved prophylaxis, the incidence of venous thromboembolism has been constant since 1980. Independent risk factors for venous thromboembolism include increasing age, male gender, surgery, trauma, hospital or nursing home confinement, malignancy, neurologic disease with extremity paresis, central venous catheter/transvenous pacemaker, prior superficial vein thrombosis, and varicose veins; among women, risk factors include pregnancy, oral contraceptives, and hormone replacement therapy. About 30% of surviving cases develop recurrent venous thromboembolism within ten years. Independent predictors for recurrence include increasing age, obesity, malignant neoplasm, and extremity paresis. About 28% of cases develop venous stasis syndrome within 20 years. To reduce venous thromboembolism incidence, improve survival, and prevent recurrence and complications, patients with these characteristics should receive appropriate prophylaxis.
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PMID:The epidemiology of venous thromboembolism in the community. 1148 36

Venous thromboembolism is a major health problem, with an incidence that exceeds 1 per 1000. Over 200,000 new cases occur in the United States annually. Of these, 30% of patients die within 30 days; one-fifth suffer sudden death due to pulmonary embolism. Despite improved prophylaxis, the incidence of venous thromboembolism has not changed significantly since 1980. Independent risk factors for venous thromboembolism include increasing age, male gender, surgery, trauma, hospital or nursing home confinement, malignancy, neurologic disease with extremity paresis, central venous catheter/ transvenous pacemaker, prior superficial vein thrombosis, and varicose veins; among women, the risk factors include pregnancy, oral contraceptives, and hormone replacement therapy. About 30% of surviving patients develop recurrent venous thromboembolism within 10 years. Independent predictors for recurrence include increasing age, obesity, malignant neoplasm, and extremity paresis. About 28% of patients develop venous stasis syndrome within 20 years. To reduce venous thromboembolism incidence, improve survival, and prevent recurrence and complications, patients with these characteristics should receive appropriate prophylaxis.
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PMID:Venous thromboembolism epidemiology: implications for prevention and management. 1207 75

Deep vein thrombosis (DVT) and pulmonary embolism (PE) are distinct but related aspects of the same dynamic disease process known as venous thromboembolism (VTE). An estimated 200,000 new cases occur in the United States every year, including 94,000 with PE, resulting in an incidence of 23 per 100,000 patients per year-cases. Without treatment, pulmonary embolism is associated with a mortality rate of approximately 30%, causing nearly 50,000 deaths per year. Moreover, based on post-mortem studies, two-thirds of the patients with pulmonary emboli remain undiagnosed. Clinically, PE may present as (1) isolated dyspnea, (2) pleuritic pain and/or hemoptysis, and (3) circulatory collapse. However, clinical history and examination can be notoriously misleading in reaching a diagnosis. A number of acquired etiologic risk factors (predispositions) are associated with a tendency to develop VTE. These include increasing age, immobilization, surgery, trauma, hospital or nursing home confinement, malignancy, neurologic disease with extremity paresis, as well as certain types of oral contraception and hormone replacement therapy. In addition, a variety of genetic risk factors, such as factor V Leiden, protein S or C deficiency have also been identified. However, in at least half of the instances, no predisposing factors can be identified (idiopathic PE). In the majority of cases thromboemboli originate in the deep veins of the calf or pelvis. The pathogenic conditions for VTE comprise a triad of factors and include (1) venous stasis, (2) hypercoagulable states, and (3) vascular endothelium injury. Occlusion of pulmonary arteries has variable and transient clinical and pathophysiologic consequences, involving both mechanical and reflex effects of vascular occlusion with a consecutive perfusion defect as well as the release of vasoactive and other inflammatory mediators. The objectives of this article are to present an overview of the etiologic and pathogenic factors promoting VTE as well as the pathophysiologic and inflammatory processes following PE.
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PMID:Principle mechanisms underlying venous thromboembolism: epidemiology, risk factors, pathophysiology and pathogenesis. 1258 87

The epidemiology of venous thromboembolism (VTE) in the community has important implications for VTE prevention and management. This review describes the incidence, survival, recurrence, complications and risk factors for deep vein thrombosis and pulmonary embolism occurring in the community. VTE incidence among whites of European origin exceeds 1 per 1000; the incidence among persons of African and Asian origin may be higher and lower, respectively. VTE incidence over recent time remains unchanged. Survival after VTE is worse than expected, especially for pulmonary embolism where one-quarter of patients present as sudden death. Of those patients who survive, 30% develop VTE recurrence and venous stasis syndrome within 10 and 20 years, respectively. Common independent VTE risk factors include surgery, hospitalization for acute medical illness, nursing home confinement, trauma, active cancer, neurologic disease with extremity paresis, superficial vein thrombosis, central venous catheter/transvenous pacemaker, and among women, oral contraceptives, pregnancy and the puerperium, and hormone and SERM therapy. Exposures can identify populations at risk but have a low predictive value for the individual person. An acquired or familial thrombophilia may predict the subset of exposed persons who actually develop symptomatic VTE. In conclusion, VTE is a common, lethal disease that recurs frequently and causes serious long-term complications. To improve survival and prevent complications, VTE occurrence must be reduced. Better individual risk stratification is needed in order to modify exposures and target primary and secondary prophylaxis to the person who would benefit most.
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PMID:The epidemiology of venous thromboembolism in the community: implications for prevention and management. 1647 38