Cases reported "Postphlebitic Syndrome"

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1/11. Combined genetic defect (homogeneity for factor v Leiden and heterogeneity for prothrombin G20210A allele), in a young patient, with recurrent deep vein thrombosis and serious postphlebitic syndrome--a case report.

    Just a few years ago, resistance to activated protein c (APCR) was reported to be of high significance representing a strong predisposing factor in the development of venous thrombosis (VT). A little while later, APCR was established to be the result of a point mutation of the factor v gene (factor v Leiden: a G-to-A transition at position 1691). Up to today, it is not certain whether factor v Leiden is in itself able to lead to VT, or whether it acts in synergy with other factors. Nevertheless, heterozygous subjects have a tenfold increase in the risk of VT when compared to general population, whereas the risk is 80 times greater in homozygous individuals. In 1996, a prothrombin gene mutation (prothrombin G20210A allele), which is a single-nucleotide G-to-A transition at position 20210 in the sequence of the 3'-untranslated region (3'UTR) on chromosome 11, was discovered. The presence of this mutant gene results in elevated plasma prothrombin concentrations, increasing the possibility for the development of VT. However, the coexistence of these two abnormalities, as well as the clinical consequence, have not yet been studied. So far, only a few reports are found in the literature describing the coexistence of both mutations. The authors present a 25-year-old patient with a simultaneous double mutation of the FV and F II gene. The patient was homozygous for the factor v Leiden and heterozygous for the prothrombin G20210A allele. It is unclear whether the coexistence of the two predisposes more to the development of VT than the summation of the two as independent factors. ( info)

2/11. Post-thrombotic syndrome.

    Post-thrombotic syndrome (PTS) is a potentially disabling complication occurring in up to 67% of adult patients following deep venous thrombosis (DVT). PTS has recently been recognised in children. We present three cases of symptomatic PTS in children, which occurred following the use of central venous lines (CVLs). In two cases, no symptoms of acute thrombosis were noted. The cases highlight the clinical presentation of this syndrome. A review of the literature revealed two reports describing PTS occurring in children following DVT with an estimated incidence of 7-12%. It is concluded that PTS is an important complication of DVT in children. The clinical findings of pain, swelling, and brawny induration are similar to adult patients. The effect on growing limbs is not known. Paediatricians should be aware of the potential of PTS in all children who are at risk of DVT, including patients with malignancy, congenital heart disease, and children who have had previous CVLs, even in the absence of documented acute DVT. ( info)

3/11. The first experience with endovascular stenting of the iliac veins in patients suffering from post-thrombophlebitic disease.

    This paper describes the results of the first experience with endovascular stenting of the iliac veins in patients suffering from post-thrombophlebitic disease. During 11 months, the patient with a history of segmental venous thrombosis and involvement of the left iliac veins received conservative treatment which included phlebotropic therapy and elastic compression. Despite these measures the patient demonstrated the symptoms of venous insufficiency such as edema, and pains in the left lower extremity. In addition, control ultrasonography and radionuclide examinations revealed chronic occlusion of the left iliac veins. In view of this circumstance we performed endovascular dilatation and stenting of the iliac veins. The postoperative period was uneventful. After two months the pains in the left lower extremity and its edema were fully removed. Control radionuclide phleboscintigraphy demonstrated complete patency of the left iliac veins. So, endovascular stenting is an effective and safe modality for the treatment of the occlusive forms of post-thrombophlebitic disease. ( info)

4/11. Carotid artery dissection (literature review and a case report).

    The paper presents a literature review on the internal carotid artery (ICA) dissection and an original case report. The dissected ICA segment was resected and grafted. ( info)

5/11. Chronic femoral arteriovenous fistula masquerading as the postphlebitic syndrome.

    A patient with a traumatic femoral arteriovenous fistula was misdiagnosed for 11 years as having "postphlebitic syndrome." angiography revealed diffuse dilatation of the veins and arteries of the right lower extremity with the iliac vein measuring 16.0 cm in diameter and the cava 6.0 cm in diameter. Operative repair of the fistula has resulted in marked clinical improvement and return of the patient to fulltime employment. A history of trauma should be sought when a patient presents with unilateral chronic venous insufficiency. ( info)

6/11. Occult antithrombin iii deficiency: a potentially lethal complication of the postphlebitic limb.

    Chronic venous insufficiency is a frequent sequel to lower extremity venous thrombosis. A relatively uncommon, but potentially lethal, cause of the thrombosis is congenital antithrombin iii deficiency. Recognition and treatment of this occult deficiency is critical. The following report describes a family treated by the authors for this problem. In one generation of nine siblings, three males had documentation of the disease with functional antithrombin III levels in the range of 50% to 60%. Before evaluation for the deficiency one female sibling died at the age of 20 years as a consequence of a proven pulmonary embolus. Antithrombin III levels in another female sibling, who was free of symptoms, were normal (80% to 120%). Four other siblings who were free of symptoms (one female, three males) refused evaluation. All three men with the deficiency had severe, chronic, bilateral, lower extremity, venous insufficiency manifested by pain, varicosities, edema, pigmentation, and ulceration. Despite chronic warfarin therapy, one experienced recurrent pulmonary embolization with eventual loss of perfusion of the entire right lung. Ascending venography in the symptomatic males with the deficiency revealed evidence of recurrent and diffuse venous thrombosis with partial recanalization. Recurrent lower extremity venous thrombosis consequent to antithrombin iii deficiency causes a particularly fulminant postphlebitic syndrome with characteristic venographic findings. Although potentially lethal if unrecognized and treated simply as venous insufficiency, chronic therapy with warfarin offers palliation and prolongs life. ( info)

7/11. Intermittent compression units for the postphlebitic syndrome. A pilot study.

    The postphlebitic syndrome is a common affliction with limited therapeutic options. patients who fail to respond to treatment with graded elastic compression stockings often develop a chronic pain syndrome manifested by intractable pain and swelling. Because lymphedema, a condition also associated with leg pain and swelling, has been successfully treated by intermittent compressive therapy with an extremity pump, we conducted a pilot study of compressive therapy in patients with severe postphlebitic syndrome. All five patients studied had dramatic improvement in symptoms and functional status without side effects. Although a large randomized trial is needed to properly evaluate compressive therapy, it appears to be very effective in selected patients. ( info)

8/11. Anticardiolipin syndrome in plastic surgery of the breast.

    A 38-year-old female patient had bilateral silicone-made prosthesis implantation performed 17 years ago. Three years after surgery, she had a series of spontaneous miscarriages, later she developed recurrent venous and arterial thromboses. Laboratory tests detected antibodies against cardiolipin and the diagnosis of cardiolipin syndrome was established. The authors discuss the possible association between surgery and the patient's current disease. ( info)

9/11. Causalgic form of postphlebitic syndrome. A variety of reflex sympathetic dystrophy caused by acute deep thrombophlebitis.

    The causalgic form of the postphlebitic syndrome or reflex sympathetic dystrophy resulting from acute deep thrombophlebitis is a relatively uncommon and, unfortunately, frequently unrecognized form of the postphlebitic syndrome. The usual signs of venous insufficiency are minimal, but severe burning pain is characteristic, usually increased by dependency. The diagnosis is confirmed by phlebography and the response to a lumbar sympathetic block. A lumbar sympathectomy produces permanent pain relief. ( info)

10/11. Deep vein thrombosis: recovery or recurrence?

    As many as two thirds of patients with new symptoms after documented DVT have postphlebitic syndrome, not DVT. Noninvasive imaging is central to the differentiation so that unnecessary anticoagulation therapy can be avoided. Recent changes in heparin and warfarin protocols for DVT are also outlined. ( info)
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