Ovarian vein thrombosis (OVT), which generally occurs between 2 and 15 days postpartum, is a rare complication. OVT occurs in right ovarian vein in almost 90% of patients. It can easily be confused with acute appendicitis, pelvic infec- tion, ovarian torsion, tubo-ovarian abscess, and pyelonephri- tis. It may lead to fatal complications such as sepsis, inferior vena cava thrombosis (IVC), pulmonary emboli, and death [1–3].
Primary renal non-Hodgkin ’ s lymphoma (NHL) is thought to be rare, perhaps because of the lack of renal lymphatic tissue [10,11]. There have been a few case reports of intravascular extension of lymphomas. Rarely, NHL can present with focal intravascular lymphoma masses. This syndrome, termed intravascular large B-cell lymphoma, is generally characterized by proliferation of lymphoma cells in smaller blood vessels. In rare patients, intravascular large B-cell lymphoma can pre- sent as masses in large blood vessels. A single case of intravascular large B-cell lymphoma that presented initi- ally as superior vena cava syndrome has been reported . Rare additional case reports have described patients who presented with superior vena cava thrombosis which later revealed the presence of Burkitt ’ s lymphoma, lymphoblastic NHL  and a primary cardiac B-cell lymphoma that presented as superior vena cava syn- drome .
Medical management of renal vein thrombosis includes aggressive hydration and anti-coagulation. Nevertheless, previous studies report conflicting data regarding the benefit of anticoagulation with regard to long-term renal function, particularly in cases of bilateral renal vein thrombosis . Thrombolytic therapy may be considered in cases of bilateral renal vein thrombosis, especially if there is concomitant renal failure . Definitive surgical treatment consists of nephrectomy and thrombectomy on a non-urgent basis, provided there is no caval extension and obstruction. Thrombectomy for bilateral renal vein thrombosis with caval involvement and obstruction has been described once before, but with subsequent unilateral nephrectomy . Recently, Lee et al.  showed that bilateral renal vein thrombosis can be successfully managed with early surgical thrombectomy without the need for nephrectomy, thereby avoiding the Figure 4: Renal hemorrhagic infarction of the cortex (H&E,
and is 24/10,000 patients in neonatal intensive care units [6–8]. Several studies based on national and inter- national registries have evaluated the role of risk factors for thrombosis both in children and neonates [6–8]. While the vast majority of venous TEs in neonates and children are associated with the presence of central venous lines, renal vein thrombosis represents the most common non-catheter-related cause of venous TEs occurring during the neonatal period . The etiology of renal vein thrombosis is not precisely known. Reported as- sociated risk factors include perinatal asphyxia, maternal
This paper presents the results of the assessment of the adequacy of the inferior vena cava thrombosis model in rats with the definition of the main markers that can be used to study the efficacy of antithrombotic agents means at the stage of preclinical studies. The first stage of the study examined the processes of clottage and hemostasis system in rats exposed to total occlusion of inferior vena cava on the 1st and 7th days after the operation. The second phase of the experimental work through the example of pentoxifylline rated adequacy of inferior vena cava thrombosis of rats as a model for preclinical studies. The research work covered the functional activity of platelets, coagulation component of hemostasis, thrombosis markers, thromboelastograms and histological material of rats on the 1st and 7th days of acute thrombosis inferior vena cava. It is established that hemostasis system during modeling of the inferior vena cava thrombosis in rats is characterised by natural changes that are platelets hyperaggregation, the emergence of circulating platelet aggregates and hypercoagulation on coagulative component of hemostasis system. These indicators are recorded quite efficiently by method of classical aggregatometry, thromboelastometry and histological studies. The study of preventive effect of pentoxifylline demonstrates that inferior vena cava thrombosis model can be used in preclinical studies.
He was evaluated elsewhere and on basis of chest X-ray findings of consolidation and pleural effusion, anti-tuberculosis therapy (rifampicin, isoniazid, eth- ambutol and pyrazinamide) was started. Inspite of 3 months therapy his symptoms did not subside and he started noticing gradual abdominal distension. He was shifted to a tertiary care centre in Dehradun where he was found to have bilateral pleural effusion with ascites. Thoracocentesis was done which showed cell count—30 (polymorph 10 % and lymphocytes 90 %), glucose—92 mg/dl, protein—2800 mg/dl, adenosine deaminase—0.93. Cartridge-based nucleic acid ampli- fication test for tuberculosis was negative. Contrast enhanced computed tomography (CT) revealed gross ascites, bilateral pleural effusion, mild pericardial effu- sion and inferior vena cava thrombosis. He was then referred to another tertiary care centre at Delhi and he was re-evaluated. Intercostal drainage (ICD) tube was inserted and pus drained from the pleural cavity which was positive for acid fast bacilli (AFB) on Ziehl–Neelsen stain. Fine needle aspiration and cytology of right axil- lary lymphnode showed reactive lymphadenitis. Repeat CT of chest and abdomen revealed similar finding as before with additional thrombosis in superior and infe- rior vena cava, right internal jugular vein and bilateral brachiocephalic veins.
Sources agree that immediate anticoagulation improves morbidity and mortality by reducing risk of pulmonary embolism and propagation of clot. Catheter directed throm- bolysis has largely replaced surgical thrombectomy, and balloon dilation and endovascular stent placement are also alternatives. Thrombosed venous segments which fail to recanalize rapidly undergo subsequent fibrotic organization which leads to fixed stenosis or occlusion. This process of clot organization can lead to chronic obstructive symptoms or postphlebitic syndrome. Also, 15% of untreated deep venous thromboses will extend proximally . Our patient was treated with thrombolysis followed by anticoagulation and stenting. The accepted indications for this more aggressive treatment include young age, lack of comorbidities, and limb threatening thrombosis. Some reports suggest that valve patency is better maintained after thrombolysis . In this case, thrombolysis and stenting were chosen because of the size of his thrombosis and severity of symptoms, and because the patient wished to remain on active duty status, which chronic anticoagulation would preclude. He did not have any of these potentially deadly complications of acute caval thrombosis. He did however suffer from some of the known late complications, including pain, erythema, and swelling associated with postphlebitic syndrome, and recur- rent thrombosis. When stenting and anticoagulation fail,
Introduction: The Behcet’s disease is deemed to be scarce in Black Africa where data are still scattered. The purpose of our study is to describe the epidemiological, clinical, paraclinic and evolutive particularities of the pa- tients whose presenting symptoms of the Behcet’s diseases were a venous thrombosis. Patients and Methods: It was a descriptive, multicenter, and cross-sectional study lasting 15 months. We brought together all the cases of the Behcet’s disease revealed by venous thrombosis. The diagnosis was based on clinical criteria of the international group of study of the Behcet’s disease in 2007. Results: We have grouped 10 revealing thrombosis cases of the Beh- cet’s diseases during our study period. The average age was 34. The average wait period between the appearances of the early symptoms and the diagnosis of the very disease was 30 months. The admission motives were the abdomin- al pain (2 cases), a thrombophlebitis of the lower limb (2 cases), headaches (1 case), coma (1 case), a thrombophlebitis of the upper limb (3 cases). The thrombotic symptoms were exclusively venous-located. The seats of the thrombosis were the vena cava superior in 30% of the cases, the vena cava in- ferior in 20% of the cases, the veins of the lower limb in 20% of the cases, the cerebral vein in 20% of the cases, and the auxiliary vein in 10% of the cases. The treatment of the deep venous thrombosis consisted in all the cases of an effective anticoagulation associated with the colchicine. Primarily, the corti- cotherapy with a high dose was used in all the patients. One of them in the comatose stage, manifesting both cerebral thrombophlebitis and aseptic me- ningitis, had died. Conclusion: Behçet’s disease is a disease of the young adult, but it must be evoked even in old age, with a view to appropriate man- How to cite this paper: Fall, B.C., Ndao,
and assays for these antibodies are not a part of the standard evaluation when APS is suspected. Antibodies to prothrombin are associated with bleeding and throm- bosis . Thrombosis is the most common clinical mani- festation of APS, and the recurrence of thrombotic events is common as well. Thrombosis in APS can happen either spontaneously or with a triggering factor. Another com- mon clinical manifestation of APS is thrombocytopenia , but this does not preclude the occurrence of throm- botic complications of APS. It is common to treat throm- bosis associated with APS, but it is quite difficult to treat thrombosis and bleeding at the same time. In the litera- ture, only a few cases of APS have reported simultaneous bleeding and thrombosis [3-8], and only a few of these cases have reported thrombosis induced by norethisterone when used by patients with an underlying risk factor for thromboembolism .
 Kumar, S., Singh, S. and Garg, N. (2015) Right Sided Double Inferior Vena Cava with Obstructed Retrocaval Ureter: Managed with Single Incision Multiple Port Laparoscopic Technique Using “Santosh Postgraduate Institute Tacking Ureteric Fixation Technique”. Korean Journal of Urology , 56, 330-333.
Fistula formation to the inferior vena cava is a rare complication of abdominal aorta aneurysm (AAA). The incidence of aortocaval fistulae (ACF) varies between 0.2% and 0.9% as a complication of AAA . Spontaneous erosion of the aneurysm into the vena cava is the major cause of the primary ACF. Most of these aneurysms are atherosclerotic in nature.
The hepatic portal and pancreas head are rich blood supply regions where vessels around are dense; many im- portant vessels are distributed here, such as the portal vein (PV), superior or inferior mesenteric vein (SMV/ IMV), vena cava, etc. Thus, it is common that space-occupying lesions originating from these regions or nearby (such as liver, gallbladder or pancreas head cancer) are easy to invade vessels nearby; for instance, ashilar cho- langiocarcinoma invades the main trunk or branch of portal vein; the hepatic cancer or echinococcosis invades one or more hepatic veins, etc. Once occurred, the success rate of integrity/radical resection was low, even re- garded as surgical contraindication in the past.
divided with cautery. This incision was made up to the right superior coronary ligament before it bypassed to the left side, thereby dividing the left triangular ligament. In the proposed modified and simplified liver-mobilization technique, we simply divided the falciform ligament to ex- pose the whole suprahepatic IVC without having to incise the entire right superior coronary and left triangular liga- ments. Dissection of the suprahepatic IVC is usually per- formed during liver transplantation to enable the use of a father clamp, which blocks the suprahepatic IVC. During liver mobilization, the right inferior coronary and hepator- enal ligaments are both incised to make the liver roll to the left, as described for liver transplantation. Minimally invasive procedures are achieved with this technique. Opening the lesser omentum would allow for the control of the porta hepatis with a tourniquet loop when neces- sary. This tourniquet loop temporarily occludes the blood inflow to the liver. Surgeons are advised to wait and allow the liver to decompress before applying other vascular clamps. The tourniquet loops were placed in the proper order. First, the infrarenal vena cava and the left renal vein were controlled (Figure 1), before a father clamp was placed vertically across the IVC (Figure 2). The IVC wall was incised upward from the opening of the renal vein to the third hepatic hilum. The tumor was then removed (mobile tumor thrombus) or dissected from the IVC wall (adherent tumor thrombus). After the removal of the tumor thrombus, the vena cava was closed with 4-0 poly- propylene. Heparin saline was first injected into the opened IVC to wash out tumor tissue residues before clos- ing the incision. Normal blood flow was thereafter reestab- lished in the liver.
Introduction: Transthoracic echocardiography (TTE) is a useful tool for minimally invasive hemodynamic monitoring in the ICU. Dynamic indices (such as the inferior vena cava distensibility index (dIVC)) can be used to predict fluid responsiveness in mechanically ventilated patients. Although quantitative use of the dIVC has been validated, the routinely used qualitative (visual) approach had not been assessed before the present study. Methods: Qualitative and quantitative assessments of the dIVC were compared in a prospective, observational study. After operators with differing levels in critical care echocardiography had derived a qualitative dIVC, the last (expert) operator performed a standard, numeric measurement of the dIVC (referred to as the quantitative dIVC). Two groups of patients were separated into two groups: group (dIVC < 18%) and group (dIVC ≥ 18%).
Although persistent left superior vena cava (PLSVC) itself is a common venous anomaly in congenital heart disease, PLSVC with absent right superior vena cava (RSVC) is a rare venous congenital malformation. Due to the lack of symptoms, this malformation is often detected fortuitously when patients undergo central venous catheter placement, pacemaker implantation, or open cardiac surgery. We present a case of PLSVC with absent RSVC in visceroatrial situs solitus detected by transesophageal echocardiography during emergent coronary artery bypass grafting surgery.
Consequently, a right lower extremity ascending veno- gram was performed via the right popliteal vein with the patient in prone position (Figure 4). The venogram confirmed Doppler imaging and the diagnosis of extensive venous thrombosis involving the right superficial femoral, common femoral, and right iliac veins. A thrombus was also noted involving the left iliac vein.
Case presentation: A 43-year-old Iranian (Persian) woman was admitted to our hospital with palpitation of 2 years ’ duration and mild to moderate dyspnea of 10 days ’ duration. Her past medical history, basic laboratory test results, and cardiac enzyme measurements were unremarkable. Imaging studies revealed a 1.4-cm × 7.4-cm multilobulated, hypermobile mass in the right atrium, extending into the right ventricle, that appeared to be emanating from the superior vena cava. Moreover, partial filling defects were visible in the distal parts of both right and left pulmonary arteries extending to their branches, suggesting massive pulmonary emboli. The patient ’ s huge mass and emboli were removed by surgery, and pathologic evaluations confirmed that all of the specimens were thrombosis. A number of mutations known as risk factors of thrombosis were detected during genetic evaluations. However, mild symptoms of the patient along with a huge mass in the right atrium, thrombosis in the superior vena cava, and massive
We searched the PubMed database from the National Library of Medicine using the keywords “renal vein thrombosis” and “neonates” with the limits set to only English-language articles and those that involved hu- man subjects. An additional search was performed via the Cochrane Central Register of Controlled Trials and the Cochrane database of systemic reviews (Issue 4, 2006). We included all case reports and case series that were published in English from January 1992 to Decem- ber 2006 that reported neonates with RVT. We excluded studies that contained discussion related to neonatal RVT but did not report on an actual case and those reports with 2 or fewer patients. Because the diagnostic criteria of RVT were not clearly stated in every study, we could not scrutinize the accuracy of the diagnosis of each reported case.
The developmental cause of AIVC is debated: it’s maybe caused by embryonic dysgenesis or by an intrauterine in- sult during the perinatal period [6,33]. AIVC have been associated with other congenital anomalies, like renal hy- poplasia/agenesis. This anatomic anomaly for the right kidney was found in our research in 6% of AIVC, but not in NoAIVC patients. The right renal hypoplasia is suggest- ive of a defect in the formation of the IVC in these seg- ments, since the embryologic right SV does not drain the mesonephros . A hypoplastic left kidney was also found here in AIVC (2.7%). However, it is not clear whether this represents a true congenital malformation or atrophy of a previously normal kidney due to long- standing poor perfusion or thrombosis secondary to vascu- lar malformation. The question of hereditary is not clearly answerable, but two cases in our collective direct to this hypothesis. In one case, the son of a patient with AIVC was diagnosed with DVT bilateral. Computed tomography showed here also an AIVC in the same segment like his father. The second remarkable case was the asymptomatic twin-brother of an AIVC patient, who received imaging for other reasons. His AIVC pattern was identical to his twin brother. The thrombophilic patterns were identical in- between the relatives. Of course, these relatives with AIVC cannot be representative, but both give rise to a hereditary hypothesis of AIVC. Interestingly, factor-V-deficiency is caused by mutations in the F5 gene, located on the long (q) arm of chromosome 1 at position 23, nearby LEFTY2 (Left-Right Determination Factor 2), playing a role in left- right asymmetry determination of organ systems during development at cytogenetic location 1q42.1 . Renal dysgenesis and MTHFR-mutation is also located on this chromosome . Further genetic investigations could here emblaze the hereditary genesis of AIVC.
The abdominal CT excluded the suspicion of a renal tumor. Having ruled out the most likely suspect that can cause renal vein thrombosis, we started to look for more unusual causes. All the tumor markers came back negative. But the extended coagulation testes revealed elevated D- dimers (980 𝜇g), present PDF, and a protein S deficiency (45%). However, the protein S deficiency alone is not enough to cause the massive vein thrombosis. We also tested for a genetic hypercoagulability state, which included tests for