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Federal government websites often end in. Before sharing sensitive information, make sure you’re on a federal government site. The site is secure. NCBI Bookshelf. Taimur Saleem ; Donald T. Authors Taimur Saleem 1 ; Donald T. Baril 2. Paget Schroetter syndrome PSS is effort-induced thrombosis of the axillary and subclavian veins associated with compression of the subclavian vein at the thoracic outlet. It is the venous variant of thoracic outlet syndrome TOS , the syndrome of symptoms associated with compression of the subclavian vein, subclavian artery, or brachial plexus as they pass through the thoracic outlet.

This activity reviews the evaluation and management of Paget Schroetter syndrome and highlights the role of the interprofessional team in the care of patients with this condition. Objectives: Describe the pathophysiology of Paget Schroetter syndrome.

Review the evaluation of a patient with Paget Schroetter syndrome. Summarize the treatment options for a patient with Paget Schroetter syndrome. Explain modalities to improve care coordination among interprofessional team members in order to improve outcomes for patients affected by Paget Schroetter syndrome. Access free multiple choice questions on this topic. The description of this entity dates back to when Sir James Paget reported a case of spontaneous thrombosis of the subclavian vein in a patient.

In , von Schroetter hypothesized that the condition was a consequence of injury to the vein from repetitive musculoskeletal motion. The subclavian vein travels in the proximity of the clavicle, first rib, anterior scalene, and subclavius muscles. PSS is related to the compression and subsequent thrombosis of the subclavian vein due to these structures. PSS is more commonly seen in younger patients in their 20s and 30s with a male to female ratio of Often these patients will not have any other significant medical comorbidities.

The incidence ranges from 1 to 2 per , individuals per year in various studies. It is more commonly encountered on the right side. Often affected individuals with PSS will be athletes, specifically, those engaged in the repetitive over-the-head motion of their arms, including baseball or softball pitchers, swimmers, rowers, or weightlifters.

Repetitive strain from vigorous physical activity and compression of the subclavian vein from adjacent anatomic structures leads to venous injury and subsequent thrombosis. This impedes the venous return from the affected extremity leading to edema. Over time, the body forms collaterals to bypass the venous obstruction.

In the chronic phase, the vein becomes fibrotic. Surrounding inflammatory changes from the thrombosis lead to scar tissue formation. Patients may present with upper extremity swelling and pain. The presentation of these symptoms can be acute, subacute, or chronic. For the onset of symptoms in PSS, a history of an antecedent strenuous exercise can usually be elicited from the patients. On examination, the upper extremity will demonstrate edema with an enlarged girth of the extremity compared to the contralateral side.

The upper extremity may be tense and cyanotic. A convenient non-invasive first test is ultrasonography of the upper extremities. This will demonstrate thrombus in the deep venous system.

Acute thrombus will be non-compressible on ultrasound. A vein with chronic thrombus will have an irregular and more collapsed appearance with the development of collaterals on ultrasound.

Ultrasonography will not allow for complete demonstration of the central veins. Computed tomography CT venography and magnetic resonance MR venography can demonstrate thrombus in the venous system as well.

Contrast venography is a more invasive test that can demonstrate patency of the central venous system. Laboratory workup includes a thrombophilia panel protein C and S levels, antithrombin levels, prothrombin gene mutation analysis, factor V Leiden mutation testing, among others and D-dimer levels.

D-dimer levels will be elevated in a patient with deep venous thrombosis; however, this elevation can also be seen in other infectious, inflammatory, and physiologic conditions.

If the patients have any symptoms concerning for a pulmonary embolism, a CT angiogram CTA thorax with pulmonary embolism protocol should be obtained. Alternatively, a ventilation-perfusion study can diagnose pulmonary embolism as well, but CTA thorax remains the study of choice. PSS is a deep venous thrombosis, and, as such, the first step in the management is to initiate anticoagulation therapy, typically, via an intravenous IV heparin drip.

Patients are given an initial bolus of intravenous IV heparin and then kept on a maintenance IV heparin drip. The dose of the bolus and maintenance heparin drip is weight-based. The affected extremity should be elevated to mitigate edema. If the patient presents within 2 weeks of the onset of symptoms, it is reasonable to consider a venogram and catheter-directed thrombolysis to reduce the clot burden.

Under fluoroscopic guidance, a lysis catheter is placed to drip a thrombolytic agent such as alteplase for 24 to 48 hours. Alternatively, a pharmacomechanical thrombectomy system can be used. When using alteplase, the fibrinogen levels should be monitored closely to direct the dosing and duration of the catheter-directed lysis. When using pharmacomechanical thrombectomy, one should be mindful of the risk of acute kidney injury associated with hemolysis.

If the presentation is more than 2 to 4 weeks from the onset of symptoms, heparinization alone may be initiated without thrombolytic therapy as the success of thrombolytic therapy is low beyond that window of time.

Another option for treatment is mechanical catheter-directed thrombectomy. This must be done early in the course of the disease. Decompression of the thoracic outlet is the definitive management of PSS. The surgical approach can either be transaxillary or supra, infra, or para-clavicular. The timing of decompression after thrombolytic therapy is widely debated. The role of long-term anticoagulation in these patients after adequate decompression remains unclear.

Some clinicians perform a venogram, often with intravascular ultrasound, 2 weeks postoperatively and decide about the duration of anticoagulation at that time. In this setting, venoplasty can be used for any residual stenosis since decompression has been achieved surgically. The use of stents is discouraged in this anatomic location due to the repetitive motion and risk of stent fracture and thrombosis.

The duration of anticoagulation in patients with underlying hypercoagulability disorders after decompression also remains unclear. In most patients, anticoagulation for 3 to 6 months following an episode of deep venous thrombosis such as PSS is reasonable.

This can be achieved either via warfarin or direct oral anticoagulants DOAC. In the case of recurrent thrombosis after decompression surgery, thrombolysis and venography are usually attempted again with the maintenance of long-term anticoagulation therapy afterward.

In some patients with PSS, chronic total occlusion of the subclavian vein may persist despite adequate decompression maneuvers. Depending on the severity of the symptoms, venous reconstruction should be considered. This can be achieved with a bypass or jugular vein turndown procedure with or without medial claviculectomy. Upper extremity swelling may be present in patients with lymphatic disorders or systemic conditions such as end-stage renal disease and congestive heart failure.

Upper extremity deep venous thrombosis can be seen with indwelling catheters as well. Anticoagulation with decompression is less successful than thrombolysis and decompression but still yields better results than anticoagulation alone. Patients should be encouraged to adhere to all medication recommendations and have close follow up with all of their healthcare providers. Activity and lifestyle modification may reduce the risk of recurrent thrombosis.

Patients with hypercoagulable states should be made aware that they may need long-term anticoagulation. The diagnosis and management of PSS are best accomplished with an interprofessional team that consists of a primary care provider, sports medicine clinician, vascular surgeon, and radiologist. Patients with venous obstruction do need treatment or the arm will remain swollen and painful.

After anticoagulation, decompression of the thoracic outlet is often required. Most patients do have a good outcome with treatment but depending on the state of the subclavian vein, some degree of arm swelling may persist. Today, for some cases of PSS, endovascular therapy is available. Patient with bilateral first rib resection. Contributed by StatPearls. The right subclavian artery and surrounding structures. Contributed by Gray’s Anatomy Public domain. This book is distributed under the terms of the Creative Commons Attribution 4.

Turn recording back on. Help Accessibility Careers. StatPearls [Internet]. Search term. Affiliations 1 St. Dominic Hospital. Continuing Education Activity Paget Schroetter syndrome PSS is effort-induced thrombosis of the axillary and subclavian veins associated with compression of the subclavian vein at the thoracic outlet.

Introduction Paget Schroetter syndrome PSS is effort-induced thrombosis of the axillary and subclavian veins associated with compression of the subclavian vein at the thoracic outlet. Etiology The subclavian vein travels in the proximity of the clavicle, first rib, anterior scalene, and subclavius muscles. Epidemiology PSS is more commonly seen in younger patients in their 20s and 30s with a male to female ratio of Pathophysiology Repetitive strain from vigorous physical activity and compression of the subclavian vein from adjacent anatomic structures leads to venous injury and subsequent thrombosis.

 
 

Usa jobs government jobs login paget schroetter s syndrome angelman –

 
It occurs in conjunction with oat cell carcinoma of the lung and certain other malignant tumors and is caused by production of vasopressin by the tumor. See. Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treat- ment and drug therapy are required. The. Before sharing sensitive information, make sure you’re on a federal government site. The site is secure. The https:// ensures that you are connecting to the.

 

– StatPearls – NCBI Bookshelf

 
Here, we show that Arc interacts with dynamic chromatin and closely associates with histone markers for active enhancers and transcription in. Research points to two distinct regions within the Prader-Willi chromosome region: one for Prader Willi syndrome and one for Angelman syndrome.

 
 

Usa jobs government jobs login paget schroetter s syndrome angelman. Brain site-specific proteome changes in aging-related dementia

 
 

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