Formation Of Collateral Veins Research Articles

May Thurner Syndrome: Diagnostic and Therapeutic Outcomes in an Institutional Setting

Introduction: May-Thurner syndrome (MTS), a chronic compression of left common iliac vein (CIV) against the lumbar vertebrae by overlying common iliac artery is an underappreciated contributor to left leg deep venous thrombosis. Even though the estimated prevalence of MTS is high in left-leg deep vein thrombosis (DVT) cases per autopsy studies, the clinical association remains low. Since the screening for MTS in patients with recurrent left-leg DVTs is not a common practice, diagnosis can either be incidental or a combination of clinical presentation and objective testing. Diagnosis is challenging via ultrasound (US) due to the deep anatomical location of iliac veins; therefore, invasive imaging including Contrast venography (CTV) is needed for confirmation. The management of MTS has been reformed over the years with the advances in minimally invasive therapeutic tools. We sought to review the management and outcomes of the MTS adult population by conducting a retrospective review to identify all adult cases of MTS at our academic safety net hospital between 2010 and 2022. Methods: Data was extracted and analyzed for baseline parameters including age, gender, ethnicity, and body mass index (BMI). Presenting symptoms, imaging used for MTS diagnosis (including US Doppler, magnetic resonance venography or CTV), and interventional approaches (catheter or systemic thrombolysis, thrombectomy, balloon angioplasty and/or stent placement) were additionally documented. SAS v9.4 (Cary, NC) was used for statistical analysis. Results: A total of 19 cases, predominantly females 68% (13/19), with a median age of 48 years and a mean BMI of 28.84 kg/m 2 diagnosed with MTS were identified. The predominant initial presentation was left lower extremity edema and pain 36% (7/19) later found to have a DVT, followed by non-healing venous ulcer 15% (3/19) and pelvic congestion syndrome 0.05 % (1/19). Whereas 42% (8/19) of the patients were diagnosed with MTS while undergoing evaluation for chronic and recurrent DVTs. All patients were diagnosed following CTV using transvenous pressures with the formation of collateral veins and a pressure gradient of more than 2 mm Hg across iliofemoral stenosis at rest. Sixteen patients (84%) underwent endovascular stent placement, while one patient underwent Balloon Angioplasty only. One patient refused any intervention for MTS however underwent great saphenous vein ablation for chronic venous wounds. In view of anticoagulation therapy, the initial choice in the most cases was low molecular weight heparin (LMWH), which was later transitioned to other choices, 81 % (10/16) were switched to direct oral anticoagulants, (apixaban= 10, rivaroxaban=3) due to ease of administration and compliance, while 19 % (3/16) were continued on LMWH for patient preference and pregnancy. Post-intervention complications consisted of stent failure in 25% (4/16) patients; related to stent thrombosis and Post-thrombotic Syndrome (PTS) in 12.5 % (2/16) patients. No bleeding complications were seen post any case of endovascular stent placement. Conclusion: This review was a highly educational experience giving us insight into this unacknowledged syndrome. Multiple factors could be contributing to this underdiagnosis, including invasive gold standard imaging for MTS, more easily recognizable risk factors for DVTs that can overshadow MTS, and a smaller number of data and studies. Some authorities have advocated a need to rule out MTS in young women with acute left lower extremity DVT, a clear female predominance was also noted (68%) in our analysis. Post-stent placement, systemic anticoagulation for 3-6 months is recommended, in our review, all patients (100%) who underwent stent placement were started on anticoagulation for at least 3 months. A small sample size, patients lost to follow-up (poor outcomes and complications could have been missed) and a single institutional review were some limitations of our study, however with a rare disease such as MTS with 2-3% prevalence it is difficult to conduct a large size, multi- institutional analysis. This study contributes to the limited literature available on MTS.

Endovascular Venous Stenosis and Thrombosis Large Animal Model: Angiographic, Histological, and Biomechanical Characterizations

PurposeTo characterize an ovine endovascular radiofrequency (RF) ablation-based venous stenosis and thrombosis model for studying venous biomechanics and response to intervention. Materials and MethodsUnilateral short-segment (n = 2) or long-segment (n = 6) iliac vein stenoses were created in 8 adult sheep using an endovenous RF ablation technique. Angiographic assessment was performed at baseline, immediately after venous stenosis creation, and after 2-week (n = 6) or 3-month (n = 2) survival. Stenosed iliac veins and the contralateral healthy controls were harvested for histological and biomechanical assessment. ResultsAt follow-up, the short-segment RF ablation group showed stable stenosis without occlusion. The long-segment group showed complete venous occlusion/thrombosis with the formation of collateral veins. Stenosed veins showed significant wall thickening (0.28 vs 0.16 mm, P = .0175) and confluent collagen deposition compared with the healthy controls. Subacute nonadherent thrombi were apparent at 2 weeks, which were replaced by fibrous luminal obliteration with channels of recanalization at 3 months. Stenosed veins demonstrated increased longitudinal stiffness (448.5 ± 5.4 vs 314.6 ± 1.5 kPa, P < .0001) and decreased circumferential stiffness (140.8 ± 2.6 vs 246.0 ± 1.6 kPa, P < .0001) compared with the healthy controls. ConclusionEndovenous RF ablation is a reliable technique for creating venous stenosis and thrombosis in a large animal model with histological and biomechanical attributes similar to those seen in humans. This platform can facilitate understanding of venous biomechanics and testing of venous-specific devices and interventions.

Resection of the inferior vena cava in different neoplasm

Purpose: The involvement of the inferior vena cava (IVC) in advanced abdominal tumors is a surgical challenge, given the high postoperative morbidity and poor long-term prognosis. IVC reconstruction is not always required due to the formation of collateral veins. Our goal was to analyze our experience, perioperative management, and results. Methods: We retrospectively evaluated short and long-term results of surgical resections of tumors with associated inferior vena cava resection performed in our facilities between 2012 and 2020. Results: 15 patients were selected for our retrospective study: 1 with renal carcinoma, 4 with sarcoma, 7 with colorectal metastases, 2 with adrenal tumors, and 1 with hepatocellular carcinoma. 7 were male with an average age of 59.06 years. The postoperative severe complications (Dindo-Clavien ≥ IIIa) affected 40% of patients and the mortality rate was 13.3%. Partial resection with primary repair was performed in 7 patients (46.7%), with patch reconstruction in 1 (6.7%), thrombectomy in 2 (13.3%), and vascular reconstruction with prosthesis in 5 patients (33.3%). The average follow-up was 30.62 months. The 1, 3 and 5-year OS rates were 100%, 91% and 43%, respectively; excluding the postoperative mortality. The mean DFS was 11.53 months. The 1, 3 and 5-year DFS rates were 46%, 18% and 18%, respectively. Graft thrombosis occurred in 3 patients (20%) during follow-up. Six patients were prescribed follow-up anticoagulation. Conclusion: IVC resection, though a technically demanding procedure, can be safely performed to achieve complete tumor resection with relative survival improvement and acceptable mortality and morbidity rates in selected patients.

Tromboflebite Séptica da Veia Porta como Complicação de Apendicite Aguda

A pileflebite é uma tromboflebite da veia porta, ou suas tributárias, secundária a um processo infeccioso intra-abdominal. Apresentamos o caso de um homem de 40 anos que recorre ao serviço de urgência com dor abdominal nos quadrantes inferiores, vómitos biliares com oito dias de evolução. Analiticamente: leucocitose de 17 000 uL, proteína C reativa elevada. Ecografia abdominal compatível com apendicite aguda. Realizou apendicectomia de McBurney. Ficou internado no Serviço de Cirurgia. Ao dia 2 de internamento iniciou febre e distensão abdominal. Na tomografia computorizada abdominal constata-se veia porta com trombo endoluminal não completamente obstrutivo, que se estende à veia mesentérica superior (ocluída nos ramos proximais e segmentares). Iniciou hipocoagulação e antibioterapia, ficando orientado para consulta externa, onde realizou estudo protrombótico e excluídas causas de doença hepática. Estudo de imagem aos 3 meses de hipocoagulação mostrou trombose da porta recanalizada, sem colaterização.

Formation of Collateral Veins in a Graft Pancreas After a Simultaneous Pancreas and Kidney Transplantation: A Case Report

A graft vein thrombosis is the main cause of early graft failure after pancreas transplantation. We report a case of formation of collateral veins in a graft pancreas after transplant. A 30-year-old woman underwent simultaneous pancreas and kidney transplantation. She was discharged 16 days after the operation with good pancreas and kidney function. A total occlusion of the portal vein was discovered on computed tomography (CT) performed at an outpatient clinic. She had no symptoms or signs of hyperglycemia. Venography was attempted for vein thrombectomy but failed. After 2 weeks of heparinization therapy, the edema disappeared and perfusion of the graft pancreas improved. However, the thrombotic occlusion was not resolved on CT. Arteriography of the Y-graft revealed collateral veins. She was discharged with warfarin. She is currently doing well without any symptoms or signs. This is the first reported case of collateral vein formation in a grafted pancreas after pancreas transplantation.

Novel Treatment Techniques for Recanalization of Femoral-Popliteal Deep Venous Occlusion From Chronic Thrombosis

Patients with postthrombotic syndrome due to previous femoral-popliteal deep venous thrombosis often experience lifestyle-limiting lower-extremity pain and swelling. Conservative treatment options include compression stockings and lymphedema massage, but in many cases these treatments only temporarily and partially improve symptoms. Ultrasound and venography in patients with postthrombotic syndrome often show only partial recanalization of the femoral vein with significant collateral vein formation. These abnormal veins are insufficient for adequate venous drainage from the lower extremity as evidenced by the patient's continued symptoms. Recanalization of the occluded or partially occluded femoral vein using prolonged venoplasty, with or without chemical thrombolysis, combined with optimizing anticoagulation and conservative treatment measures, results in lasting improvement in symptoms for a high percentage of patients.

Congenital agenesis of the inferior vena cava presenting with acute renal failure

Agenesis of the inferior vena cava (IVC) is a rare congenital disorder. Herein, we present a 35-year-old male case of agenesis of the IVC and disseminated pelvic venous congestion with complete extrinsic ureteral obstruction due to compression who was admitted with acute renal failure following contrast injection for a computed tomography scan. Renal functions of the patient returned to normal after hemodialysis. However, during follow-up, malabsorption occurred due to intraabdominal congestion and collateral vein formation. Subsequently, he developed malnutrition and infection and died despite, a full supportive therapy.

A different way to look at varicose veins.

The development of varicose veins is commonly attributed to vessel wall degeneration. The idea that varicose veins occur because of pathological processes, however, is challenged by certain observations. For example, their high prevalence (50% or greater) in many populations makes it statistically "normal" to have varicose veins; their well-established genetic predisposition raises the possibility that this high prevalence reflects a survival benefit. One way to explain this apparent contradiction is to theorize that varicose veins are produced by the same mechanism(s) that lead to the growth and remodeling of other types of blood vessels. If so, being "good" at forming varicose veins may also predispose to being "good" at forming various types of collateral blood vessels when necessary. A selected literature review was conducted. Works chosen for review included those suggesting that: the process of varicose vein formation may share the same basic mechanisms as the formation of collateral veins, arteries, and lymphatic vessels; and clinical outcomes may be different between subjects with and without varicose veins. Evidence suggests that subjects who are "good" at forming varicose veins may also be "good" at forming various types of collateral vessels, and they may have better overall survival (with less cardiovascular morbidity) than those without varicose veins. Varicose veins may be "the price we pay" for anenhanced ability to form collateral vessels when necessary.

Thrombotic Disorders

Thrombotic Disorders

Neonatal Hepatitis With Hepatofugal Portal Flow and Collateral Veins: Report of Three Cases

Neonatal hepatitis, a syndrome occurring in children, has various etiologies, such as viral infection, unidentified disorders of bile salt synthesis, and other poorly understood metabolic diseases. It is characterized by jaundice, giant cell hepatitis, and, rarely, liver failure necessitating liver transplantation. We experienced 3 cases of idiopathic neonatal hepatitis with unusual progressive fibrosis presenting with retrograde portal flow and portal-systemic shunt. Clinical manifestations were hyperammonemia, hyperbilirubinemia, and coagulopathy. Characteristic histological findings were giant cell transformation of hepatocytes and progressive severe fibrosis. Two patients underwent living donor liver transplantation. We consider that liver transplantation is indicated in cases of neonatal hepatitis with hepatofugal portal flow and collateral vein formation.

Portal vein thrombosis in liver cirrhosis

Portal vein thrombosis (PVT) is observed in 10-20% of patients with liver cirrhosis, which is responsible for 20% of all PVT cases. The main pathogenic factor of PVT in cirrhosis is the obstacle to portal flow, but acquired and inherited clotting abnormalities may play a role. The formation of collateral veins allows many patients to remain asymptomatic and prevents the onset of clinical complications also in patients with totally occlusive PVT. Gastrointestinal bleeding, thrombosis of superior mesenteric vein and refractory ascites are typical manifestations of PVT. Instrumental diagnosis can be obtained by colour-doppler ultrasonography. Future studies should verify whether asymptomatic PVT worsens liver failure, or if its life-threatening complications reduce survival in patients with cirrhosis. Moreover, randomized controlled trials should clarify the potential effectiveness of anticoagulant therapy in the treatment of PVT.

Is portal vein cavernous transformation a component of congenital hepatic fibrosis

Congenital hepatic fibrosis (CHF) is an autosomal recessive disorder that belongs to the family of fibropolycystic liver diseases. This family includes a spectrum of disorders which are usually found in combination with each other and are usually inherited. Clinically fibropolycystic diseases have three effects being present in different proportions, those of a space occupying lesion, of portal hypertension and of cholangitis. In most patients, the first manifestations of CHF are signs and symptoms related to portal hypertension such as splenomegaly and varices. Portal hypertension in these patients has been attributed to the hypoplasia or compression of the portal vein radicles in the fibrous bands. Cavernous transformation of the portal vein (CTPV) is a relatively rare condition resulting from extrahepatic portal vein obstruction with recanalization or collateral vein formation to bypass the obstruction. It has been found that patients with CHF having an accompanying CTPV have relatively large splenomegaly and suffers more frequent episodes of bleeding from esophageal varices. We believe that CTPV is a congenital component of CHF and also one of the important causative factors of portal hypertension in these patients.

Late Vascular Occlusion of Central Lines in Pediatric Malignancies

To determine whether thrombi or vascular occlusion represent a late complication persisting several years after removal of central venous lines (CVLs) in children and adolescents treated for childhood cancer. Children whose treatment for malignancy included placement of a CVL that had been removed at least 2 months previously were studied during scheduled follow-up that included contrast-enhanced computed tomography. Spiral volume acquisition was used to obtain 3-mm images from the chest apices through the right hilum, and three-dimensional reconstruction of angiograms was performed. Thrombosis/occlusion was defined as narrowing, obstruction, or filling defect of the deep venous system, with or without the formation of collateral veins. Charts were reviewed to document patient characteristics, previous CVL complications, administration of hyperalimentation, use of urokinase, and family history of venous thrombosis. Twenty-three patients treated for solid tumors and 2 treated for B-cell acute lymphocytic leukemia or lymphoma were studied. Lines had been in place from 0.2 to 36 months (median, 7.4) and were removed at 2.3 to 121.8 months (median, 32.5) before study. Nine patients received hyperalimentation for periods ranging from 2 to 38 weeks (median, 12). Four patients had required urokinase instillations, and one developed superior vena cava syndrome; 4 had a CVL-related infection (two superficial and two Candida line infections). Occlusion was seen on computed tomography angiograms in 3 of the 25 patients (12%; 95% confidence interval: 4.5-31%). One of the patients with occlusion had superior vena cava syndrome; none had a family history of thrombosis, use of a double lumen CVL, or multiple instillations of urokinase. Persistent asymptomatic vascular occlusion does occur as a late complication of CVL placement for treatment of childhood malignancies, although the frequency appears low among patients treated primarily for solid tumors. Prospective studies of large numbers of patients with a broader spectrum of diagnoses are necessary to define the incidence of and risk factors for this complication and to assess the need for prevention with anticoagulation or other therapy. Pediatricians caring for patients with a history of cancer and CVLs should be aware that these patients may have persistent vascular occlusion that could predispose them to recurrent thrombosis or postphlebitic syndrome.

Effort thrombosis: Role of interventional therapy

Effort thrombosis, a form of axillary-subclavian vein occlusion in young people, was identified in patients referred over a 5-year period. Eleven of 120 patients (9%) with venous occlusion from many causes had effort thrombosis. They were treated acutely with heparin and then by thrombolysis, angioplasty, surgical bypass, or a combination. Five of the 10 patients with thrombolysis or surgery had patent veins on follow-up venography, but 9 of these later developed axillary-subclavian reocclusion. By later follow-up, however, all patients were asymptomatic at the time of collateral vein formation. We conclude that effort thrombosis leads to recurrent occlusion of the axillary-subclavian vein, short-term (12-month) recurrence of symptoms with exercise, and progressive compensatory collateral vein development. Radiographic documentation of reestablished venous flow is important, and can be used to guide the completion of treatment.

Evaluation of hemodynamics and hepatic mitochondrial function on extrahepatic portal obstruction in the rat

An animal model resembling clinical cases with extrahepatic portal vein obstruction was developed. The changes in hepatic mitochondrial function and the hepatic hemodynamics including hepatic regional blood flow, portal venous pressure, and portogram were evaluated to assess the effect of portal vein obstruction in the model. Portal vein ligation in this model was a simple and easy maneuver and could produce collateral veins to the liver--cavernomatous transformation--which were obviously seen in clinical patients with extrahepatic portal obstruction. Hepatic blood flow was significantly decreased until 5 days after portal vein ligation; however, hepatic blood flow was gradually increased and reached the normal value at 3 weeks after portal vein ligation due to the formation of the collateral veins to the liver. Respiratory parameters of mitochondria were gradually decreased and reached the lowest levels at 5 days after portal vein ligation, while they recovered to normal values in accordance with increasing hepatic blood flow at 3 weeks after portal vein ligation. In extrahepatic portal obstruction, although the liver is temporarily deteriorated by portal vein obstruction such as portal vein thrombosis, hepatic blood flow and the liver functions are to be normally improved with the formation of collateral veins to the liver.

A case of multiple arteriovenous malformations and diffuse venous abnormalities with facial port-wine stain

A case of left facial port-wine stain with right hemiparesis is reported. Radiologically, two arteriovenous malformations (AVM) and diffuse venous abnormalities were observed in the left hemisphere. AVM were seen in the basal ganglia. One was fed by a perforating artery from the MCA and drained into the superior petrosal sinus, and the other was fed by a perforating artery from the basilar artery and drained through the vein of Rosenthal into an extremely dilated vein of Galen. Venous abnormalities were obstruction and a decrease in the superficial cortical veins, as well as the formation of collateral veins in both the cortex and white matter. This case resembles Sturge-Weber syndrome (SWS), but there were no signs of leptomeningeal angiomatosis or venous angioma. We have been unable to find any case reports on SWS with AVM or AVM with diffuse venous abnormalities. We discuss the differences between our case and SWS.

Superior Vena Caval System Obstruction

1) Eleven cases with superior vena caval obstruction are presented with clinical studies including venous pressures and phlebograms. We believe that the incidence of this syndrome is higher than is generally realized. 2) Since frequently there are no specific symptoms referable to the obstruction the diagnosis depends first on careful routine inspection for evidence of localized venous pressure elevation or superficial collateral vein formation. The presence of a mediastinal mass itself is indication for further study for evidence of venous abnormality. 3) The diagnosis can readily be established by the simple procedure of bilateral venous pressure determinations using especially the hand exercise technique. 4) While not necessary for the diagnosis, phlebograms often add precise information depicting the anatomical site and degree of obstruction and collateral channel formation. 5) The prognosis of superior vena caval obstruction usually depends the primary disease. If obstruction is gradual adequate collateral formation develops by-passing the obstruction. One case of complete obstruction remained asymptomatic for 50 years, with death occurring from another cause.