All of the following are appropriate therapies for suppurative thrombophlebitis EXCEPT:
Treatment of superficial vein thrombophlebitis (SVT) is quite variable. A Cochrane Review reported that lowmolecular-weight heparins (LMWHs) and nonsteroidal anti-inflammatory drugs both reduce the rate of SVT extension or recurrence. Topical medications appear to improve local symptoms. Surgical treatment, combined with the use of graduated compression stockings, is associated with a lower rate ofVTE and SVT progression. The treatment is individualized and depends on the location of the thrombus and the severity of symptoms. In patients with SVT not within 1 cm of the saphenofemoral junction, treatment consists of compression and administration of an anti-inflammatory medication such as indomethacin. In patients with suppurative SVT, antibiotics and removal of any existing indwelling catheters are mandatory. Excision of the vein may be necessary but is usually reserved for patients with systemic symptoms or when excision of the involved vein is straightforward. If the SVT extends proximally to within 1 cm of the saphenofemoral junction, extension into the common femoral vein is more likely to occur. In these patients, anticoagulation therapy for 6 weeks and great saphenous vein ( GSV) ligation appear equally effective in preventing thrombus extension into the deep venous system.
Which of following statements regarding injection sclerotherapy for varicose veins is true?
Interventional management includes injection sclerotherapy, surgical therapy, or a combination of both techniques. Injection sclerotherapy alone can be successful in varicose veins <3mm in diameter and in telangiectatic vessels. Sclerotherapy acts by destroying the venous endothelium. Sclerosing agents include hypertonic saline, sodium tetradecyl sulfate, and polidocanol. Concentrations of 1 1.7 to 23.4% hypertonic saline, 0.125 to 0.250% sodium tetradecyl sulfate, and 0.5% polidocanol are used for telangiectasias. Larger varicose veins require higher concentrations: 23.4% hypertonic saline, 0.50 to 1% sodium tetradecyl sulfate, and 0.75 to 1 .0% polidocanol. Elastic bandages are wrapped around the leg after injection and worn continuously for 3 to 5 days to produce apposition of the inflamed vein walls and prevent thrombus formation. After the bandages are removed, elastic compression stockings should be worn for a minimum of 2 weeks. Complications from sclerotherapy include allergic reaction, local hyperpigmentation, thrombophlebitis, DVT, and possible skin necrosis.
Heparin-induced thrombocytopenia (HIT) is characterized by which of the following?
Heparin-induced thrombocytopenia (HIT) results from heparin-associated antiplatelet antibodies (HAAbs) directed against platelet factor 4 complexed with heparin. HIT occurs in 1 to 5% of patients being treated with heparin. In patients with repeat heparin exposure (such as vascular surgery patients), the incidence ofHAAbs may be as high as 21%. HIT occurs most frequently in the second week of therapy and may lead to disastrous venous or arterial thrombotic complications. Therefore, platelet counts should be monitored periodically in patients receiving continuous heparin therapy. HIT is diagnosed based on previous exposure to heparin, platelet count less than 100,000, and/or platelet count decline of 50% following exposure. All heparin must be stopped and alternative anticoagulation initiated immediately to avoid thrombotic complications, which may approach 50% over the subsequent 30 days in affected individuals.
Direct thrombin inhibiting medications include which of the following:
Direct thrombin inhibitors (DTis) include recombinant hirudin, argatroban, and bivalirudin. These antithrombotic agents bind to thrombin, inhibiting the conversion of fibrinogen to fibrin as well as thrombin-induced platelet activation. These actions are independent of antithrombin. The DTis should be reserved for (a) patients in whom there is a high clinical suspicion or confirmation of HIT, and (b) patients who have a history of HIT or test positive for heparin -associated antibodies. In patients with established HIT, DTis should be administered for at least 7 days, or until the platelet count normalizes. Warfarin may then be introduced slowly, overlapping therapy with a DTI for at least 5 days.
Which of the following is a true statement about lymphedema?
The original classification system, described by Allen, is based on the cause of the lymphedema. Primary lymphedema is further subdivided into congenital lymphedema, lymphedema praecox, and lymphedema tarda. Congenital lymphedema may involve a single lower extremity, multiple limbs, the genitalia, or the face. The edema typically develops before 2 years of age and may be associated with specific hereditary syndromes (Turner syndrome, Milroy syndrome, Klippel-TrenaunayWeber syndrome). Lymphedema praecox is the most common form of primary lymphedema, accounting for 94% of cases. Lymphedema praecox is far more common in women, with the gender ratio favoring women 10:1. The onset is during childhood or the teenage years, and the swelling involves the foot and calf. Lymphedema tarda is uncommon, accounting for < 10% of cases of primary lymphedema. The onset of edema is after 35 years of age. Secondary lymphedema is far more common than primary lymphedema. Secondary lymphedema develops as a result of lymphatic obstruction or disruption. Axillary node dissection leading to lymphedema of the arm is the most common cause of secondary lymphedema in the United States. Other causes of secondary lymphedema include radiation therapy, trauma, infection, and malignancy. Globally, filariasis (an infection caused by Wuchereria bancrofti, Brugia malayi, and Brugia timori) and environmental exposure to minerals in volcanic soil resulting in podoconiosis in barefoot populations are the most common causes of secondary lymphedema. Control of chronic limb swelling through compression is the mainstay of therapy for lymphedema.
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