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Infiltrative hepatocellular carcinoma (HCC) can be overlooked on imaging. Radiologists should have a high index of suspicion for this entity in patients with chronic liver disease. Careful evaluation of the portal vein may help the radiologist diagnose infiltrative HCC, due to the high association (68%-100%) of portal vein tumor thrombus with this condition. This article will review the imaging findings of infiltrative HCC, particularly its association with portal vein thrombus, and describe imaging pitfalls and mimickers. [ABSTRACT FROM AUTHOR]

Cerebral venous sinus thrombosis (CVST) is a rare cerebrovascular condition that affects approximately 5 per 1 million people annually, and develops in 0.5 % of all stroke patients. Herein we report a case involving a 31-year-old woman with CVST. She initially presented with a 2-month history of intermittent headaches at the nape of her neck with cervical pain. Other than these symptoms, she was in apparently good health and was a nonsmoker. She had no children and did not take contraceptives. She became comatose with unequal pupil size and CVST was diagnosed. An autopsy revealed CVST that extended from the confluence of the sinuses to the transverse sinuses and tip of the superior sagittal sinus, as well as a thrombus that obstructed the right internal jugular vein. A correct and early diagnosis of CVST combined with heparin-based therapy and/or interventional endovascular strategies may be of benefit by preventing intracerebral extension of jugular venous thrombosis and subsequent serious or even fatal neurological sequelae. [ABSTRACT FROM AUTHOR]

Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion. [ABSTRACT FROM AUTHOR]

The article focuses on the relationship between the use of direct thrombin inhibitor anticoagulants and increased frequency of thrombosis on abnormal cardiac endothelium. Topics discussed include cases of increased myocardial infarction and/or ischemia or coronary stent or cardiac valve thrombosis after direct thrombin inhibitor use particularly those who use dabigatran and the reason direct thrombin inhibitors are associated with higher cardiac thrombotic risk compared to warfarin or heparin.

External jugular vein thrombosis is a rare vascular event which may lead fatal complication such as sepsis and pulmonary embolism. Its relation to the visceral solid tumor as an etiologic factor has been established well. Although external jugular vein thrombosis may be seen in malignancy, it is unusual to see as a sign of breast cancer. Most of the external jugular vein thrombosis occurs secondary to compression of the vein. Vascular thrombosis due to hypercoagulability is known as Trousseau syndrome. Herein, we present a case of metastatic breast cancer which presented with external jugular vein thrombosis; Trousseau syndrome. [ABSTRACT FROM AUTHOR]

To evaluate in the setting of a stroke unit ward the usefulness of a prolonged (>6 h) video-EEG recording (PVEEG) in identifying non-convulsive status epilepticus (NCSE) in patients with an acute ischemic stroke. Predictors of NCSE were also evaluated. Patients with an acute ischemic stroke, referred to our unit, were included in this prospective observational study. A PVEEG recording was implemented after stroke in all patients during the first week: (a) promptly in those exhibiting a clear or suspected epileptic manifestation; (b) at any time during the routine activity in the remaining patients. After the first week, a standard EEG/PVEEG recording was hooked up only in presence of an evident or suspected epileptic manifestation or as control of a previous epileptic episode. NCSE was identified in 32 of the 889 patients (3.6 %) included in the study. It occurred early (within the first week) in 20/32 (62.5 %) patients and late in the remaining 12. Diagnosis was made on the basis of a specific clinical suspect ( n = 19, 59.4 %) or without any suspect ( n = 13, 40.6 %). In a multivariate analysis, a significant association of NCSE was observed with NIHSS score, infarct size and large atherothrombotic etiology. NCSE is not a rare event after an acute ischemic stroke and a delayed diagnosis could worsen patient prognosis. Since NCSE can be difficult to be diagnosed only on clinical grounds, implementation of a prompt PVEEG should be kept available in a stroke unit whenever a patient develop signs, although subtle, consistent with NCSE. [ABSTRACT FROM AUTHOR]

IMPORTANCE Venous thromboembolism (VTE), comprising deep vein thrombosis (DVT) and pulmonary embolism (PE), is a common, potentially lethal condition with acute morbidity. OBJECTIVE To review the etiology of VTE and the 3 phases of VTE treatment: acute (first 5-10 days), long-term (from end of acute treatment to 3-6 months), and extended (beyond 3-6 months). EVIDENCE REVIEW Cochrane reviews, meta-analyses, and randomized controlled trials, as well as other clinical trials for topics not covered by the former, were reviewed. Literature searches using broad terms were used to find meta-analyses published in the last 15 years. The ninth edition of the American College of Chest Physicians Antithrombotic Therapy Guidelines was used to supplement the literature search. Guidelines from specialty organizations were consulted when relevant. The Canadian Agency for Drugs and Technologies in Health was searched for relevant cost-effectiveness studies. We also searched our own literature database of 8386 articles for relevant research. FINDINGS Low-molecular-weight heparin (LMWH) along with with vitamin K antagonists and the benefits and proven safety of ambulation have allowed for outpatient management of most cases of DVT in the acute phase. Development of new oral anticoagulants further simplifies acute-phase treatment and 2 oral agents can be used as monotherapy, avoiding the need for LMWH. Patients with PE can also be treated in the acute phase as outpatients, a decision dependent on prognosis and severity of PE. Thrombolysis is best reserved for severe VTE; inferior vena cava filters, ideally the retrievable variety, should be used when anticoagulation is contraindicated. In general. DVT and PE patients require 3 months of treatment with anticoagulants, with options including LMWH, vitamin K antagonists, or direct factor Xa or direct factor IIa inhibitors. After this time, decisions for further treatment are based on balancing the risk of VTE recurrence, determined by etiology of the VTE (transient risk factors, unprovoked or malignancy associated), against the risk of major hemorrhage from treatment. Better prediction tools for major hemorrhage are needed. Experience with new oral anticoagulants as acute, long-term, and extended therapy options is limited as yet, but as a class they appear to be safe and effective for all phases of treatment. CONCLUSIONS AND RELEVANCE The mainstay of VTE treatment is anticoagulation, while interventions such as thrombolysis and inferior vena cava filters are reserved for limited circumstances. Multiple therapeutic modes and options exist for VTE treatment with small but nonetheless important differential effects to consider. Anticoagulants will probably always increase bleeding risk, necessitating tailored treatment strategies that must incorporate etiology, risk, benefit, cost, and patient preference. Although great progress has been made, further study to understand individual patient risks is needed to make ideal treatment decisions. [ABSTRACT FROM AUTHOR]

Heparin binds fibrin and, by bridging thrombin onto fibrin, promotes the formation of a ternary heparin-thrombin-fibrin complex that protects thrombin from inhibition by antithrombin. Because thrombin binds γA/γ′-fibrin, a variant with an extended γ-chain, with higher affinity than the bulk γA/γA-fibrin, γA/γ′-fibrin affords bound thrombin more protection from inhibition by antithrombin–heparin. We examined the effect of Zn+ on heparin–thrombin–fibrin complex formation because Zn+ modulates heparin–protein interactions. Zn+ increased the affinity of heparin for γA/γA- and γA/γ′-fibrin by 4.3- and 3.7-fold, respectively, but had no effect on the affinity of thrombin for either form of fibrin. In contrast, in the presence of heparin, Zn+ increased the affinity of thrombin for γA/γA-fibrin 4-fold (from a Kd value of 0.8 to 0.2 μM) and slowed the rate of thrombin dissociation from γA/γA-fibrin clots. These findings suggest that Zn+ enhances the formation of ternary heparin–thrombin–fibrin complexes with γA/γA-fibrin but does not influence the already high affinity interaction of thrombin with γA/γ′-fibrin. Consistent with this concept, in the presence of Zn+, γA/γA-fibrin protected thrombin from inhibition by antithrombin–heparin to a similar extent as γA/γ′-fibrin. Therefore, by enhancing the binding of heparin to fibrin, physiological concentrations of Zn+ render fibrin-bound thrombin more protected from inhibition by antithrombin. Because fibrin-bound thrombin can trigger thrombus expansion, these findings help to explain why recurrent thrombosis can occur despite heparin treatment. Heparin binds fibrin and, by bridging thrombin onto fibrin, promotes the formation of a ternary heparin–thrombin–fibrin complex that protects thrombin from inhibition by antithrombin. Because thrombin binds γA/γ′-fibrin, a variant with an extended γ-chain, with higher affinity than the bulk γA/γA-fibrin, γA/γ′-fibrin affords bound thrombin more protection from inhibition by antithrombin–heparin. We examined the effect of Zn+ on heparin–thrombin–fibrin complex formation because Zn+ modulates heparin–protein interactions. Zn+ increased the affinity of heparin for γA/γA- and γA/γ′-fibrin by 4.3- and 3.7-fold, respectively, but had no effect on the affinity of thrombin for either form of fibrin. In contrast, in the presence of heparin, Zn+ increased the affinity of thrombin for γA/γA-fibrin 4-fold (from a Kd value of 0.8 to 0.2 μM) and slowed the rate of thrombin dissociation from γA/γA-fibrin clots. These findings suggest that Zn+ enhances the formation of ternary heparin–thrombin–fibrin complexes with γA/γA-fibrin but does not influence the already high affinity interaction of thrombin with γA/γ′-fibrin. Consistent with this concept, in the presence of Zn+, γA/γA-fibrin protected thrombin from inhibition by antithrombin–heparin to a similar extent as γA/γ′-fibrin. Therefore, by enhancing the binding of heparin to fibrin, physiological concentrations of Zn+ render fibrin-bound thrombin more protected from inhibition by antithrombin. Because fibrin-bound thrombin can trigger thrombus expansion, these findings help to explain why recurrent thrombosis can occur despite heparin treatment. [ABSTRACT FROM AUTHOR]

The endothelial protein C receptor (EPCR) limits thrombus formation by enhancing activation of the protein C anticoagulant pathway, and therefore may play a role in the etiology of thrombotic disorders. The rs867186 single-nucleotide polymorphism in the PROCR gene (g.6936A > G, C.4600A > G), resulting in a serine-to-glycine substitution at codon 219, has been associated with reduced activation of the protein C pathway, although its association with thrombosis risk remains unclear. The present study is a highly comprehensive systematic review and meta-analysis, including unpublished genome-wide association study results, conducted to evaluate the evidence for an association between rs867186 and 2 common thrombotic outcomes, venous thromboembolism (VTE) and myocardial infarction (Ml), which are hypothesized to share some etiologic pathways. MEDLINE, EMBASE, and HuGE Navigator were searched through July 2011 to identify relevant epidemiologic studies, and data were summarized using random-effects metaanalysis. Twelve candidate genes and 13 genome-wide association studies were analyzed (11 VTE and 14 Ml, including 37 415 cases and 84 406 noncases). Under the additive genetic model, the odds of VTE increased by a factor of 1.22 (95% confidence interval, 1.11-1.33, P<.001) for every additional copy of the G allele. No evidence for association with Ml was observed. [ABSTRACT FROM AUTHOR]

A young male was referred to us for evaluation of fever of unknown origin (FUO). He had history of recurrent painful oral ulcers for one year and moderate to high grade fever, pustulopapular rash, and recurrent genital ulcers for 6 months and hemoptysis for 3 days. He was detected to have intracardiac thrombi and pulmonary arterial thrombosis along with underlying Behcet’s disease (BD). Patient responded to high dose prednisolone (1 mg/Kg/day) along with monthly parenteral cyclophosphamide therapy. This case highlights the fact that BD is an important cause for pulmonary artery vasculitis with intracardiac thrombus formation, and such patients can present with FUO. [ABSTRACT FROM AUTHOR]