Thrombosis Syndrome Research Articles

Treatment of Chronic Venous Stent Occlusion With a Wildcat Catheter

A 47-year-old female with an occluded iliac vein stent originally placed for deep venous thrombosis and May-Thurner syndrome presented to our clinic with complaints of left lower extremity pain and swelling. Multiple previous attempts had been made to cross this lesion with guidewire and catheter techniques without success. We were able to cross the lesion with the Wildcat catheter. Subsequent directional laser atherectomy and balloon angioplasty followed by stent placement resulted in a patent stent and resolution of her symptoms. This is the first reported use of the Wildcat catheter in chronic venous stent occlusions.

Investigational factor Xa inhibitors for thrombosis and acute coronary syndromes

Introduction: A number of new oral anticoagulant drugs that selectively and directly inhibit factor Xa (FXa) appear as promising alternatives to the existing anticoagulant agents. These compounds present a convenient route of administration with predictable pharmacokinetics and pharmacodynamics that allow fixed dosing regimens without requiring coagulation monitoring. Rivaroxaban is the first of this new class of drugs that was approved for the prevention of venous thromboembolism (VTE) after elective total hip replacement or total knee replacement surgery in the EU, Canada and several other countries. Clinical trials with rivaroxaban in patients with acute VTE and in patients with atrial fibrillation have been recently completed. Numerous other compounds are under different developing stages (apixaban, edoxaban, otamixaban, LY517717, PRT-054021, YM150).Areas covered: This review provides an overview of the two oral anti-FXa drugs at the most advanced stage of development (rivaroxaban and apixaban) and briefly describes and comments on the results of the most important studies.Expert opinion: Undoubtedly, these new drugs will offer several advantages over the previous compounds, but a number of issues still require some attention during the phase of translation from clinical trials into daily clinical practice.

Heparin-induced thrombocytopenia with iliacofemoropopliteal thrombosis in a patient operated for colorectal carcinoma liver metastases

We report a case of heparin-induced thrombocytopenia thrombosis (HITT) syndrome in a patient prophylactically treated with low molecular weight heparin. A 66-year-old men underwent radiofrequency-assisted partial liver resection for colorectal carcinoma liver metastases a year-and-a-half after he had been operated for rectal cancer. In the postoperative period, patient was prophilactically treated with reviparin sodium. On the 8th postoperative day, the platelet count decreased by more than 50% without clinical signs of thrombosis. HITT syndrome was suspected on the 19th postoperative day, after iliacofemoropopliteal thrombosis had developed, and related diagnosis was supported by the strongly positive particle gel agglutination technique immunoassay. Heparin was withdrawn and alternative anticoagulant, danaparoid sodium, was introduced in therapeutic doses. Despite delayed recognition, favorable clinical outcome was achieved. HITT syndrome should be considered with priority among the possible causes of thrombocytopenia in a surgical patient on heparin.

Study on Physician Ordering Behavior on Hypercoaguable Screening Tests

AbstractAbstract 4745 Background:We can now identify hereditary and acquired risk factors in patients with a venous thrombotic event. Hereditary factors include factor V Leiden; prothrombin G 20210A mutation; or deficiencies of antithrombin, protein C, or protein S. But considerable uncertainty exists in hypercoagulable testing. Clinical criteria (Bauer, 2002) guidelines are available and laboratory evaluation can confirm the diagnosis. But we know of anecdotal stories where physicians ignored the testing pathways. Even when correctly utilized, testing was inappropriately timed after the thrombotic event. There are many scenarios for thrombosis with no single test to identify these risk factors. We need to re-examine the use of these screening tests for inherited and acquired thrombosis syndromes. Materials and Methods:Retrospectively, 200 patient charts were reviewed on the use of hypercoagulable screening panels, patient characteristics, and physician characteristics. The hypercoaguable screening tests contain prothrombin time, partial thromboplastin time, thrombin time, fibrinogen, antithrombin, plasminogen, activated protein C resistance, protein C, protein S, and lupus anticoagulant. Factor V Leiden and prothrombin G 20210A mutation results were reviewed if available. Data reviewed included age, gender, location of thrombosis (arterial vs. venous), malignancy, connective tissue disorder, diabetes, hypertension, nephrotic syndrome, liver disease, active infections, recent surgery, trauma, anticoagulation medications, obstetric history, family history, hypercoaguable screening test results, physician specialty, training level, and indications for the tests. Results:Patient age range was 18–91; 79 males and 12 females. Among 200 cases, 23 were positive from the hypercoaguable screening tests but only 4 were true positive for hereditary thrombophilia (Factor V Leiden, prothrombin G 20210A, antithrombin deficiency and protein C and S deficiency, respectively). False positive results (low levels of antithrombin, protein C, protein S) were due to coumadin. Ordering physicians were diverse (internal medicine, general medicine, family medicine, hematology/oncology, cardiology, pulmonary, rheumatology, nephrology, neurology, general surgery, vascular surgery, and pediatrics). Reason for ordering tests were varied: family history of thrombosis, recurrent deep vein thrombosis, myocardial infarction, pulmonary embolus, stroke, malignancy, myeloproliferative disorders, connective tissue disorders, inflammatory bowel disease, liver disease, diabetes, nephrotic syndrome, arteriovenous shunt operation, and fetal loss. Few cases fit the clinical criteria. Ordering tests were inconsistent with the indications for hereditary thrombophilia, with no relation to the clinical history, physician training level, or specialty. Discussion and Conclusion:Why these irregularities in behavior exist, we are not sure. From our literature review, there were few papers available on discrepancies in physician reasoning for utilizing laboratory tests. Wertman (1980) identified no single reason for test ordering behavior of physicians. Axt-Adams (1993) suggested that motivators, other than physician education, had a higher correlation of influencing physician ordering behavior when over-utilizing laboratory tests. These motivators included 1) fear of failure to diagnose, 2) fear of criticism, 3) inability to cope with diagnostic uncertainty, 4) eagerness to complete the screening evaluation while in the hospital, 5) desire to be complete in evaluation, 6) hope that additional follow-up testing provides the correct diagnosis, 7) provide reassurance for patient, 8) collective ordering, and 9) ignorance of costs and diagnostic significance of tests and their sensitivity, specificity, and predictability. In many cases, the diagnostic criteria for ordering hypercoagulable screenings were not followed. We did not have the opportunity to interview the ordering physicians about their rationale which may have provided more insight. More education is necessary on hereditary thrombophilia, limitations of coagulation tests, acquired conditions for thrombosis, and the costs of these specialized tests. More studies are necessary to understand physician behaviors in ordering these expensive tests. Disclosures:No relevant conflicts of interest to declare.

Lower Extremity Manifestations and Treatment of Heparin-Induced Thrombocytopenia Syndromes: A Cohort Study

Heparin-induced thrombocytopenia (HIT) and heparin-induced thrombocytopenia with thrombosis (HITT) syndromes are the result of an adverse reaction to heparin that results in a spectrum of laboratory and end-organ manifestations secondary to thrombosis of both arterial and venous small and large vessels. HITT most often manifests in the extremities as acral ischemia and necrosis, with a spectrum of severity. The lower extremity surgical patient is at risk for deep venous thrombosis, and when exposed to heparin products, is also at risk for the development of a heparin-induced thrombocytopenic syndrome. This article reports on a cohort of patients from a tertiary referral lower extremity reconstruction practice with the HIT/HITT syndromes, with an analysis of the frequency, medical characteristics, clinical settings, lower extremity manifestations, management, and outcomes of patients with HIT/HITT.)

Argatroban in the management of heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia (HIT) is an immunoglobulin-mediated serious complication of heparin therapy characterized by thrombocytopenia and high risk for venous and arterial thrombosis: HIT and thrombosis syndrome (HITTS). Argatroban, a direct thrombin inhibitor, is indicated as the anticoagulant for the treatment and prophylaxis of thrombosis in patients with HIT and in patients undergoing percutaneous coronary intervention (PCI) who have HIT. The aim of this review is to examine the pharmacological characteristics and the clinical efficacy and safety of this drug in adults with HIT, including those undergoing PCI. Briefly, 2 prospective multicenter, nonrandomized, open-label studies evaluated the efficacy and safety of argatroban as an anticoagulant in patients with HIT or HITTS. Both studies showed that the incidence of the primary efficacy end point, a composite of all-cause death, all-cause amputation, or new thrombosis, was reduced in argatroban-treated patients vs control subjects with HIT or HITTS. In both studies, bleeding rates were similar between the groups. Argatroban was evaluated as the anticoagulant therapy in 3 prospective, multicenter, open-label studies in HIT patients who underwent PCI. The studies were similar in design with respect to patient inclusion and exclusion criteria, the argatroban dosing regimen, and primary efficacy outcomes. The investigators performed a pooled analysis of these studies, which showed that most (≥95%) patients achieved a satisfactory outcome from the procedure and adequate anticoagulation (coprimary end points).

Novel management of post varicella purpura fulminans owing to severe acquired protein S deficiency

Acquired protein S deficiency is a rare complication of varicella zoster infection often resulting in purpura fulminans, which is a potentially life-threatening syndrome of intravascular thrombosis and haemorrhagic infarction of the skin. Patients are presumed to develop crossreacting autoantibodies to the virus and protein S. There is no consensus on how best to manage these patients but previous recommendations focus on plasmapheresis and plasma exchange. We report the case of a 3-year-old girl with post varicella purpura fulminans owing to protein S deficiency, who was diagnosed promptly and made a full recovery following immediate treatment with anticoagulation and plasma support. This suggests that if anticoagulation is used, plasma exchange is not always necessary. As recovery occurred without plasmapheresis, we were able to track protein S levels. The timing of protein S recovery was consistent with the waning titre of an acquired immunoglobulin G autoantibody.

Polyarticular Gout Attacks Following Cerebrovascular Accidents

Cerebrovascular disease appears to have implications on rheumatic diseases, including gout. Accumulating evidence suggests that hemiparesis exerts a protective effect against gout via the down-regulation of mechanical and neural modulators of inflammation in neurologically impaired extremities. We present 2 divergent cases of unilateral gout following cerebrovascular events. One patient with a hemorrhagic stroke developed polyarticular gout only on the ipsilateral side to his hemiparesis, while another patient with basilar artery thrombosis and locked-in syndrome suffered a polyarticular gout flare only on the side that had regained limited function. As suggested by these cases, the effect of hemiparesis on gout is complex. Further insight into the interplay between gouty flares and hemiparesis may lead to novel therapeutic strategies for gout.

Endovenous therapy for deep venous thrombosis: The TORPEDO trial

We compared the efficacy and safety of percutaneous endovenous intervention (PEVI) plus anticoagulation with anticoagulation alone in the reduction of venous thromboembolism (VTE) and post-thrombotic syndrome (PTS) in acute proximal deep venous thrombosis (DVT). Recurrent VTE and PTS are common complications of DVT. There are no randomized trials investigating the efficacy of PEVI in the reduction of the above complications. Patients with symptomatic proximal DVT were randomized to receive PEVI plus anticoagulation or anticoagulation alone. Anticoagulation consisted of intravenous unfractionated heparin or subcutaneous low-molecular weight heparin plus warfarin. PEVI consisted of one or more of a combination of thrombectomy, balloon venoplasty, stenting, or local low-dose thrombolytic therapy. At 6 months follow-up, recurrent VTE developed in 2 of 88 patients of the PEVI plus anticoagulation group versus 12 of 81of the anticoagulation-alone group (2.3% vs. 14.8%, P = 0.003). PTS developed in 3 of 88 patients of the PEVI plus anticoagulation Group and 22 of 81 of the anticoagulation-alone group (3.4% vs. 27.2%, P < 0.001). In patients with symptomatic proximal DVT, PEVI plus anticoagulation may be superior to anticoagulation-alone in the reduction of VTE and PTS at 6 months.

A novel mechanism of thrombosis in antiphospholipid antibody syndrome

Antiphospholipid antibody syndrome (APS) is an autoimmune thrombophilia mediated by autoantibodies directed against phospholipid-binding plasma proteins, mainly β2 Glycoprotein I (β2GPI)-a plasma apolipoprotein and prothrombin (PT). A subgroup of these antibodies termed “Lupus Anticoagulant” (LA) elongate in vitro the clotting times, this elongation not corrected by adding normal plasma in the detection system. The exact mechanism by which these autoantibodies induce thrombosis is not well understood. Resistance to natural anticoagulants such as protein C, impaired fibrinolysis, activation of endothelial cells to a pro-coagulant phenotype and activation of platelets, are among the mechanisms partially supported by experimental evidence. Artificially dimerized β2GPI binds tightly to platelet membrane activating them. We search for mechanisms of natural dimerization of β2GPI by proteins of the platelet membranes and found that platelet factor 4 (PF4) assembled in homotetramers binds two molecules of β2GPI and this complex is recognized by anti-β2GPI antibodies, the whole complexes being thrombogenic in terms of activating platelets as confirmed by p38MAP kinase phosphorylation and thromboxane B2 production. Of note PF4/heparin complexes are also immunogenic triggering the production of anti-PF4/heparin antibodies which activate also platelets (the so-called “heparin-induced thrombocytopenia and thrombosis syndrome”, HITT). The anti-β2GPI antibodies activate platelets by their F(ab)2, while the anti-PF4/heparin by their Fc fragments. Thus PF4 is a common denominator in the pathogenesis of APS and HITT which share also clinical characteristics such as thrombocytopenia and thrombosis.

Thrombotic microangiopathy: new insights

In the following study new aspects and insights into the epidemiology, pathogenesis and typical morphology of kidney involvement in thrombotic microangiopathy (TMA) are discussed. TMA comprises a spectrum of microvascular thrombosis syndromes associated with multiple pathogenetic factors, that is, typical and atypical haemolytic uraemic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), malignant hypertension, drugs or systemic autoimmune diseases or antibody-mediated rejection. The present article will put particular emphasis on new pathophysiological insights into the development of TMA in the various settings. In addition, new options in the therapeutic management of TMA in atypical HUS are discussed. The pathogenesis of TMA in atypical HUS primarily involves hereditary or acquired deficiencies and disturbances of the complement system. Eculizumab is a promising new therapeutic option that has been discovered recently. In HUS/TTP the kidney shows characteristic vascular changes due to endothelial damage, that is, TMA, which should be clinically and morphologically differentiated from other diseases. Recent genetic and molecular studies have shed more light on the pathogenesis of TMA in atypical HUS, that is, disturbances of various aspects of the complement system, and in TTP, that is, von Willebrand factor regulation by ADAMTS13, which are also helpful in the differential diagnosis.

Anticoagulant Therapy for Percutaneous Coronary Intervention

Received June 2, 2009; accepted November 16, 2009. Percutaneous coronary intervention (PCI) is the most commonly performed invasive therapeutic cardiac procedure and plays an important role in the treatment of ischemic heart disease. Since the first description of coronary angioplasty in a human by Gruntzig,1 the technique, equipment, and associated pharmacotherapy have undergone substantial evolution, leading to significant improvements in periprocedural complications.2 In particular, procedural anticoagulant therapy has been the focus of numerous clinical trials, and several options are now available and supported by practice guidelines; each agent has both advantages and disadvantages, and procedural pharmacotherapy continues to be a focus of drug development. The purpose of this review is to summarize the goals of anticoagulant therapy during PCI, the pharmacokinetics and pharmacodynamics of available agents, and the clinical data surrounding each agent and to identify new agents in development. The goals of pharmacotherapy during PCI are 2-fold: (1) to mitigate the sequelae of iatrogenic plaque rupture from balloon angioplasty or stenting and (2) to reduce the risk of thrombus formation on intravascular PCI equipment. Central to these thrombotic events is thrombin (factor IIa). Iatrogenic damage to the endothelium during PCI leads to increased expression of tissue factor, activation of the coagulation cascade, and formation of activated factor Xa. This ultimately leads to the generation of thrombin, conversion of fibrinogen to fibrin, and thrombus formation.3 In addition to its effects on fibrin, thrombin also directly activates platelets, enhances platelet aggregation, and is proinflammatory.4 Because of its multiple actions in promoting thrombosis, the focus of most anticoagulant agents is thrombin inhibition. Available agents for use include unfractionated heparin (UFH), low-molecular-weight heparins (LMWH, of which enoxaparin has the largest body of clinical data), the synthetic pentasaccharides (of which fondaparinux has the largest body of clinical data), and the …

Ultrasound Molecular Imaging of Cardiovascular Disease

Molecular imaging with ultrasound contrast agents relies on the detection of microbubbles within diseased tissue. Microbubbles produce an acoustic signal owing to their resonant properties in an ultrasound field. Microbubble targeting is accomplished by either manipulating the microbubble shell for attachment of microbubbles to activated leukocytes, or by conjugation of disease-specific ligands to the microbubble surface. Inflammation, angiogenesis, and thrombus formation are central pathophysiologic processes in many cardiovascular diseases and produce phenotypic changes in the vascular compartment that can be imaged with targeted ultrasound contrast agents. In the future, targeted contrast ultrasound could aid in the diagnosis of atherosclerosis, myocardial ischemia, transplant rejection, and thrombosis syndromes and could be used for assessing angiogenesis.

Pathophysiology of Anti-PL Syndrome in Thrombosis.

Abstract SCI-45The antiphospholipid (aPL) syndrome (APS) is an enigmatic autoimmune thrombotic disorder that was initially identified through astute clinical observations and the development of a quantitative test for aPL antibodies. The condition is marked by 2 types of assays: 1) immunoassays that were derived from the “biologic false positive syphilis” test and 2) coagulation assays that detect “lupus anticoagulants” (LAs), which are inhibitors of phospholipid-dependent coagulation reactions. The most recent consensus investigational criteria for diagnosing APS require that patients have evidence for thrombosis and/or pregnancy complications attributable to placental insufficiency and also laboratory evidence for persistent (aPL) antibodies, detected by high levels of IgG or IgM antibodies against cardiolipin and β2-glycoprotein I (β2GPI) and/or through abnormal LA assays. The thrombotic disorder requires long term anticoagulant treatment, which is accompanied by the risk of bleeding complications. Several mechanisms have been postulated and can be classified as involving: 1) aPL antibody-mediated inhibition of endogenous anticoagulant mechanisms; 2) aPL antibody-triggered signaling events on target cells (vascular endothelial cells, monocytes, platelets and trophoblasts) that promote proadhesive and prothrombotic phenotypes; and 3) aPL antibody-mediated complement activation. At present, it appears that the APS diagnostic entity actually includes several distinct subsets that reflect the actions of heterogeneous antibodies directed against different epitopes of phospholipid-binding proteins which then may yield different clinical sequelae. We have accumulated significant data indicating that a major one of these mechanisms involves aPL antibody-mediated disruption of annexin A5 (AnxA5) activity. AnxA5 is a potent anticoagulant protein whose anticoagulant properties are a consequence of its high affinity for anionic phospholipid. The protein forms 2-dimensional crystals on phospholipid surfaces that shield the phospholipids from availability for coagulation reactions. AnxA5 appears to play a thrombomodulatory role on the surfaces of cells lining the placental and systemic vasculatures. It is highly expressed on the apical membranes of placental syncytiotrophoblasts, the location where maternal blood interfaces with fetal cells. aPL antibody-antigen complexes disrupt the ordered crystallization of AnxA5, displace the protein from phospholipid membrane surfaces and thereby accelerate coagulation reactions. This effect of the antibodies has been demonstrated on artificial bilayers, on cultured trophoblasts and on endothelial cells and platelets. This disruption has been appears to be a consequence of aPL antibodies that recognize a specific epitope within domain I of β2GPI, the key antigen recognized by aPL antibodies. Based upon these data, we developed a novel clinical assay “the AnxA5 resistance (A5R) test” to identify patients who have antibodies that interfere with the anticoagulant activity of AnxA5. Initial studies indicate that a large proportion of APS patients have evidence for A5R. It therefore appears possible that measurement for A5R may provide a mechanistic assay for APS. We are also developing treatments to target this mechanism and protect AnxA5 from antibody-mediated disruption which may open novel nonanticoagulant approaches to treating APS. DisclosuresOff Label Use: The presentation will include research on in vitro effects of hydroxychloroquine; the drug is not FDA approved for the treatment of patients with antiphospholipid syndrome who do not also have concurrent systemic lupus erythematosus or rheumatoid arthritis.

Oversulfated Chondroitin Sulfate Does Not Cause Augmentation in HIT Antibody Mediated Heparin-Induced Platelet Aggregation (HIPA).

Abstract 2417Poster Board II-394Heparin is one of the widely used anticoagulants for the prophylaxis and treatment of thrombotic disorders. Heparin, a linear polysaccharide belonging to a family of glycosaminoglycans (GAGS) consists of repeating disaccharide units of 1-4 linked iduronic acid and glucosamine residues. Heparin is a mixture of low, medium and high molecular fractions and is heterogeneous not only in terms of molecular weight but also sites and degree of sulfation. Oversulfated chondroitin sulfate, one of the important toxic contaminants in certain batches of heparins manufactured during 2007 to 2008 resulted in deaths of some patients following intravenous administration that led to the recall of these heparins by the FDA. An increased incidence of heparin-induced thrombocytopenia (HIT) and thrombosis syndrome (HITTS) was reported as a result of contaminated heparins. It was hypothesized that OSCS interacts with heparins and other LMWHs increasing their HIT/HITTS potential. In order to validate this hypothesis blood was drawn from healthy volunteers (n=5) and mixed with 3.2% sodium citrate solution (9 parts of whole blood to 1 part of citrate). The citrated blood samples were centrifuged at 800 rpm to obtain platelet rich plasma (PRP) and further centrifuged at 3000 rpm to obtain platelet poor plasma (PPP). Apheresis fluid was collected from confirmed cases of HIT and pooled. The platelet aggregometers (Biodata) were blanked with individual PPP. The PRP (300ml) was mixed with HIT positive pooled apheresis fluid (200ml) and platelet aggregation was recorded using Gentium Heparin, Enoxaparin, and Bemiparin at a final concentration of 10mg/ml, either alone or in mixtures of 10%, 20% and 30% OSCS. The Heparin-induced platelet aggregations (HIPA) were run for a period of 30 minutes and the tracings obtained. While OSCS alone at a final concentration of 10 mg/ml caused an average of 29.5% platelet aggregation, it did not cause an augmentation of platelet aggregation in 10%, 20% and 30% mixtures with Heparin, Enoxaparin, Bemiparin and AVE 5026 (see table). This data suggests that drugs like heparin, and low molecular weight heparins such as Enoxaparin, and Bemiparin did not augment HIT/HITTS response when combined in various proportions with OSCS. Based on HIPA the reported increase in HIT response may therefore be due to in vivo interactions of the OSCS with platelets and endothelial cells. Corroborative evidence from clinical studies are warranted to validate these preliminary results.Drugs (FC10mg/ml)Drug Alone10%OSCS mixture20%OSCS mixture30%OSCS mixtureOSCS aloneSalineHeparin52.3%60%58.3%58.6%21.6%8.3%Enoxaparin56%58%60.5%60.5%31%7%Bemiparin60%59.6%63%60%37.6%9.3% Disclosures:No relevant conflicts of interest to declare.

P948 A case report of heparin-induced thrombocytopenia and thrombosis syndrome (HITTS) post uterine fibroid embolisation at University College Hospital Galway, Ireland, December 2008

P948 A case report of heparin-induced thrombocytopenia and thrombosis syndrome (HITTS) post uterine fibroid embolisation at University College Hospital Galway, Ireland, December 2008

Chronic thrombotic scarring in patients with acute deep venous thrombosis of the lower limbs

Some patients with acute deep venous thrombosis of the lower limbs may present risk factors for recurrent disease. Aims: To analyze the most important conditions related to recurrent deep venous thrombosis of the lower limbs, other than thrombophilias. Patients and methods: We examined 88 consecutive patients (47 males-53.41%, average age 64.9±13.9 years) admitted to a Medical Clinic in 2007. Duplex ultrasonography was performed to assess acute deep venous thrombosis and post-thrombotic syndrome. Anamnesis and physical examination were used to detect risk factors for recurrent disease. The 28 subjects with acute deep venous thrombosis and post-thrombotic syndrome were included in group A (31.82%). Group B comprised 60 patients (68.18%) with acute deep venous thrombosis without postthrombotic syndrome. Results: Risk factors for recurrent disease in groups A and B were the following: personal history of deep venous thrombosis of the lower limbs (17 subjects versus 7, p<0.0001), varicose veins (14 vs 24, p=0.51), obesity (13 vs 18, p=0.21), malignancy (6 vs 8, p=0.25), chronic obstructive lung disease (5 vs 6, p=0.24), prolonged immobilization (1 vs 7, p=0.21), major surgery (1 vs 1, p=0.54), stroke (0 vs 3, p=0.62), family history of deep venous thrombosis, immobilizing plaster cast, and congestive heart failure (0 vs 1, p=0.54). Location of thrombi in patients in groups A and B was as follows: 18 patients in group A vs 25 subjects in group B on the left side and 13 patients in group A vs 20 patients in group B on the right side (p=0.02). Conclusion: Post-thrombotic syndrome correlated with personal history of deep venous thrombosis and previous deep venous thrombosis located in the left lower limb.

Axillary vein thrombosis and compartment syndrome in upper limb trauma

Axillary thrombophlebitis and compartment syndrome are potential complications of upper limb trauma with significant morbidity and mortality. A 25 year old man presented 24 hours following an isolated limb injury with these synchronous complications. Early systemic anticoagulation and fasciotomy resulted in significant bleeding and anaemia. Renal function remained normal despite evidence of significant rhabdomyolysis (CK>16 000U/L). Several attempts at closure of fasciotomies were frustrated by major swelling and finally, devitalised biceps brachii was debrided in toto. He was discharged with residual sensory and motor deficits. Three months later, he had marked disability from weakness, sensory disturbance and post-phlebitic swelling.

Argatroban

Argatroban, a highly selective direct thrombin inhibitor, is indicated for use as an anticoagulant for the treatment and prophylaxis of thrombosis in patients with heparin-induced thrombocytopenia (HIT), and in patients undergoing percutaneous coronary intervention (PCI) who have, or are at risk for, HIT. Intravenous argatroban improved clinical outcomes and was generally well tolerated in adults with HIT or HIT with thrombosis syndrome (HITTS). In two pivotal, open-label, historically controlled studies in adults with HIT, the incidence of the primary composite endpoint (all-cause death, all-cause amputation, or new thrombosis) was significantly lower in argatroban recipients than in historical controls, and more argatroban recipients than historical controls stayed event-free during the study according to a Kaplan-Meier analysis. In adults with HITTS in these trials, although the incidence of the primary composite endpoint did not differ significantly between argatroban recipients and historical controls, a Kaplan-Meier analysis showed that more patients receiving argatroban than historical controls remained event-free during the study. Major and minor bleeding rates in argatroban recipients were generally similar to those in historical controls in these studies. Argatroban was also an effective anticoagulant in patients with HIT undergoing PCI in three small, uncontrolled trials, pooled data from which showed that most (>or=95%) patients achieved a satisfactory outcome of the PCI procedure and adequate anticoagulation (coprimary endpoints). It was generally well tolerated in these patients, with the incidence of major bleeding being <or=1.1%. The efficacy and safety of argatroban in pediatric patients has not been established. However, a small uncontrolled, preliminary study suggests that it may be useful in seriously ill pediatric patients requiring nonheparin anticoagulation.

Cerebral vein thrombosis and Guillain-Barre syndrome: a challenging association

Cerebral vein thrombosis and Guillain-Barre syndrome: a challenging association