Superficial vein thrombosis (SVT) is a blood clot formed in a superficial vein, a vein near the surface of the body. Usually there is thrombophlebitis, which is an inflammatory reaction around a thrombosed vein, presenting as a painful induration (thickening of the skin) with redness. SVT itself has limited significance (in terms of direct morbidity and mortality) when compared to a deep vein thrombosis (DVT), which occurs deeper in the body at the deep venous system level. However, SVT can lead to serious complications (as well as signal other serious problems, such as genetic mutations that increase ones risk for clotting), and is therefore no longer regarded as a benign condition. If the blood clot is too near the saphenofemoral junction there is a higher risk of pulmonary embolism, a potentially life-threatening complication. SVT has risk factors similar to those for other thrombotic conditions and can arise from a variety of causes. Diagnosis is often based on symptoms. There are multiple possible treatments, with the goal of providing symptomatic relief and preventing complications. Signs and symptoms
SVT is recognized by the presence of pain, warmth, redness, and tenderness over a superficial vein. The SVT may present as a "cord-like" structure upon palpation. The affected vein may be hard along its entire length. SVTs tend to involve the legs, though they can affect any superficial vein (e.g. those in the arms). Complications
SVT in the lower extremities can lead to a dangerous complication in which the clot travels to the lungs, called pulmonary embolism (PE).
The cause is thought to be predominantly related to abnormal ammonia metabolism. Asterixis is seen most often in drowsy or stuporous patients with metabolic encephalopathies, especially in decompensated cirrhosis or acute liver failure. It is also seen in some patients with kidney failure and azotemia. It can also be a feature of Wilsons disease. Asterixis is also seen in respiratory failure due to carbon dioxide toxicity (hypercapnia). Some drugs are known to cause asterixis, particularly phenytoin (when it is known as phenytoin flap). Other drugs implicated include benzodiazepines, salicylates, barbiturates, valproate, gabapentin, lithium, ceftazidime, and metoclopramide. History
R.D. Adams and J.M. Foley first described asterixis in 1949 in patients with severe liver failure and encephalopathy. Initially Foley and Adams referred to asterixis simply as "tremor" but realized that they needed a more appropriate term. On a literature search they found a poorly described phenomenon in similar patients mentioned by German physicians called “jactitations” but the reference was vague. Foley consulted Father Cadigan, a Jesuit classics scholar, who suggested “anisosterixis” (an "negative"–iso "equal"–sterixis "firmness") but Foley shortened this to asterixis due to the former being too difficult to pronounce. They introduced the term in 1953 by way of a medical abstract and later Adams solidified its medical use as he was an author and editor of the widely influential Harrisons Principles of Internal Medicine. References
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