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Cerebral Venous Sinus Thrombosis samer kareem 5,776 ভিউ • 2 বছর আগে

Thrombosis of the venous channels in the brain is an uncommon cause of cerebral infarction relative to arterial disease, but it is an important consideration because of its potential morbidity. (See Prognosis.) Knowledge of the anatomy of the venous system is essential in evaluating patients with cerebral venous thrombosis (CVT), since symptoms associated with the condition are related to the area of thrombosis. For example, cerebral infarction may occur with cortical vein or sagittal sinus thrombosis secondary to tissue congestion with obstruction. (See Presentation.) Lateral sinus thrombosis may be associated with headache and a pseudotumor cerebri–like picture. Extension into the jugular bulb may cause jugular foramen syndrome, while cranial nerve palsies may be seen in cavernous sinus thrombosis as a compressive phenomenon. Cerebral hemorrhage also may be a presenting feature in patients with venous sinus thrombosis. (See Presentation.) Imaging procedures have led to easier recognition of venous sinus thrombosis (see the images below), offering the opportunity for early therapeutic measures. (See Workup.) Left lateral sinus thrombosis demonstrated on magn Left lateral sinus thrombosis demonstrated on magnetic resonance venography (MRV). This 42-year-old woman presented with sudden onset of headache. Physical examination revealed no neurologic abnormalities. View Media Gallery Axial view of magnetic resonance (MR) venogram dem Axial view of magnetic resonance (MR) venogram demonstrating lack of flow in transverse sinus. View Media Gallery The following guidelines for CVT have been provided by the American Heart Association and the American Stroke Association [1] : In patients with suspected CVT, routine blood studies consisting of a complete blood count, chemistry panel, prothrombin time, and activated partial thromboplastin time should be performed. Screening for potential prothrombotic conditions that may predispose a person to CVT (eg, use of contraceptives, underlying inflammatory disease, infectious process) is recommended in the initial clinical assessment. Testing for prothrombotic conditions (including protein C, protein S, or antithrombin deficiency), antiphospholipid syndrome, prothrombin G20210A mutation, and factor V Leiden can be beneficial for the management of patients with CVT. Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2-4 weeks after completion of anticoagulation. There is a very limited value of testing in the acute setting or in patients taking warfarin. In patients with provoked CVT (associated with a transient risk factor), vitamin K antagonists may be continued for 3-6 months, with a target international normalized ratio of 2.0-3.0. In patients with unprovoked CVT, vitamin K antagonists may be continued for 6-12 months, with a target international normalized ratio of 2.0-3.0. For patients with recurrent CVT, venous thromboembolism (VTE) after CVT, or first CVT with severe thrombophilia (ie, homozygous prothrombin G20210A; homozygous factor V Leiden; deficiencies of protein C, protein S, or antithrombin; combined thrombophilia defects; or antiphospholipid syndrome), indefinite anticoagulation may be considered, with a target international normalized ratio of 2.0-3.0. For women with CVT during pregnancy, low-molecular-weight heparin (LMWH) in full anticoagulant doses should be continued throughout pregnancy, and LMWH or vitamin K antagonist with a target international normalized ratio of 2.0-3.0 should be continued for ≥6 weeks postpartum (for a total minimum duration of therapy of 6 months). It is reasonable to advise women with a history of CVT that future pregnancy is not contraindicated. Further investigations regarding the underlying cause and a formal consultation with a hematologist or maternal fetal medicine specialist are reasonable. It is reasonable to treat acute CVT during pregnancy with full-dose LMWH rather than unfractionated heparin. For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the postpartum period is reasonable. Next: Etiology What to Read Next on Medscape Related Conditions and Diseases Quiz: Do You Know the Complications, Proper Workup, and Best Treatment Practices for Ischemic Stroke? Quiz: How Much Do You Know About Hypothyroidism? Quiz: Do You Know the Risk Factors, Symptoms, and Potential Treatments for Alzheimer Disease? Quiz: How Much Do You Know About Hypertension? 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Closed Reduction of a Distal Radius Fracture samer kareem 18,528 ভিউ • 2 বছর আগে

Closed Reduction of Distal Radius Fractures - Discussion: (distal radius fracture menu) - closed reduction & immobilization in plaster cast remains accepted method of treatment for majority of stable distal radius frx; - unstable fractures will often lose reduction in the cast and will slip back to the pre-reduction position; - patients should be examined for carpal tunnel symptoms before and after reduction; - carpal tunnel symptoms that do not resolve following reduction will require carpal tunnel release; - cautions: - The efficacy of closed reduction in displaced distal radius fractures. - Technique: - anesthesia: (see: anesthesia menu) - hematoma block w/ lidocaine; - w/ hematoma block surgeon should look for "flash back" of blood from hematoma, prior to injection; - references: - Regional anesthesia preferable for Colles' fracture. Controlled comparison with local anesthesia. - Neurological complications of dynamic reduction of Colles' fractures without anesthesia compared with traditional manipulation after local infiltration anesthesia. - methods of reduction: - Jones method: involves increasing deformity, applying traction, and immobilizing hand & wrist in reduced position; - placing hand & wrist in too much flexion (Cotton-Loder position) leads to median nerve compression & stiff fingers; - Bohler advocated longitudinal traction followed by extension and realignment; - consider hyper-extending the distal fragment, and then translating it distally (while in extended position) until it can be "hooked over" proximal fragment; - subsequently, the distal fragment can be flexed (or hinged) over the proximal shaft fragment; - closed reduction of distal radius fractures is facilitated by having an assistant provide counter traction (above the elbow) while the surgeon controls the distal fragment w/ both hands (both thumbs over the dorsal surface of the distal fragment); - flouroscopy: - it allows a quick, gentle, and complete reduction; - prepare are by prewrapping the arm w/ sheet cotton and have the plaster or fibroglass ready; - if flouroscopy is not available, then do not pre-wrap the extremity w/ cotton; - it will be necessary to palpate the landmarks (outer shaped of radius, radial styloid, and Lister's tubercle, in order to judge success of reduction; - casting: - generally, the surgeon will use a pre-measured double sugar sugar tong splint, which is 6-8 layers in thickness; - more than 8 layers of plaster can cause full thickness burns: - reference: Setting temperatures of synthetic casts. - position of immobilization - follow up: - radiographs: - repeat radiographs are required weekly for 2-3 weeks to ensure that there is maintenance of the reduction; - a fracture reduction that slips should be considered to be unstable and probably require fixation with (pins, or ex fix ect.) - there is some evidence that remanipulation following fracture displacement in cast is not effective for these fractures; - ultimately, whether or not a patient is satisfied with the results of non operative treatment depends heavily on th