Venous Collaterals Research Articles

Management of Deep Vein Thrombosis of the Upper Extremity

Case 1: A 34-year-old previously healthy male office manager was admitted with acute onset of heaviness, pain, and functional impairment of his right arm. The arm was cyanotic and massively swollen (Figure 1). For the past weeks, he reported transient paresthesia of his right arm during overhead activities and was unable to perform repetitive or strenuous arm exercise. He had a fracture of the right clavicle after a ski accident 5 years previously. The fracture was managed conservatively. There was no personal or family history of thrombosis. Conventional phlebography confirmed axillary and subclavian vein thrombosis (Figure 2, top), and treatment with intravenous unfractionated heparin was started. Figure 1. Clinical presentation of case 1 with massive swelling and cyanosis of the right arm (left). One day after pharmacomechanical thrombolysis, signs of thrombosis have markedly improved (right). Figure 2. Baseline digital subtraction venogram from case 1 with extensive filling defects in the axillary subclavian veins (top). Control venogram after 15 hours of pharmacomechanical thrombectomy confirmed resolution of filling defects and restored venous flow (middle). Positional venography obtained during abduction of the right arm confirmed the venous thoracic outlet syndrome with residual stenosis of the subclavian vein at the costoclavicular junction (white arrow, bottom). Case 2: A 55-year-old man with lung cancer presented with swelling, heaviness, and pain in his left arm 1 week after completion of chemotherapy administered via a left-sided indwelling central venous catheter. Axillary and subclavian vein thrombosis was confirmed by ultrasonography. Low-molecular-weight heparin (LMWH) was initiated, and the catheter was removed 3 days later because it was no longer functional. At 1 week, pain and functional impairment had not improved, and the circumference of the left upper arm had increased by 2 cm. Case 3: A 65-year-old woman with metastatic ovarian cancer presented with swelling of the face and both arms, headache, …

Technical considerations for radical resection of a primary leiomyosarcoma of the vena cava

BackgroundRadical resection provides the best hope for cure in leiomyosarcoma of the inferior vena cava (IVC). Multi-visceral resection is often indicated by extensive tumour involvement. This report describes the technical challenges encountered during resection of a retrohepatic IVC leiomyosarcoma. MethodsComputed tomography showed an IVC leiomyosarcoma measuring 7.8 × 10.0 × 19.3cm in a 41-year-old patient. The tumour reached the confluence of the hepatic veins, displacing the caudate lobe anteriorly and extending towards the IVC bifurcation inferiorly. En bloc resection of the IVC tumour with a right hepatic and caudate lobectomy, and a right nephrectomy was performed. ResultsSubsequent to a Cattel manoeuvre, the operative procedures carried out can be broadly categorized in four major steps: (i) mobilization of the infrahepatic IVC and tumour; (ii) mobilization of the suprahepatic IVC from diaphragmatic attachments; (iii) right hepatectomy with complete caudate lobe resection, and (iv) en bloc resection of the IVC tumour. This approach allowed the entire length of tumour-bearing IVC to be freed from the retroperitoneum and avoided the risk for iatrogenic tumour rupture during dissection at the retrohepatic IVC. Reconstruction of the IVC was not performed in the presence of venous collaterals. ConclusionsExperience in liver resection and transplantation, and appreciation of the hepatocaval anatomy facilitate the safe and radical resection of retrohepatic IVC leiomyosarcoma.

EComment. The challenges of surgical management of lung pathologies with an anomalous pulmonary vein

I read with great interest the work of Schiavon et al. in which they re-anastomosed the posterior segmental vein of the right upper lobe draining into the lower pulmonary vein during a right lower bilobectomy for lung cancer in other to avoid performing a pneumonectomy, should the vascular element be wrongfully sectioned at the surgery [1]. They went further to state that the risk of serious complications during pulmonary resection in patients with anomalous pulmonary venous connection is high and included bleeding and postoperative oedema in the residual lung amongst other complications. It is noteworthy to state that anomalous pulmonary venous connections can also occur in Sinus venosus atrial septal defects (SV-ASD) with equal challenges during surgeries for lung pathologies in these patients. An anomalous pulmonary vein with SV-ASD is defined as an interatrial defect with the right pulmonary vein draining directly into the right atrium or from the superior vena cava (SVC) or the inferior vena cava into the right atrium [2]. Besides the enumerated complications, other complications that could present a serious challenge to the thoracic surgeon are the complete transposition of the remaining pulmonary veins converting an initial acyanotic congenital cardiac problem to cyanotic one. This can occur when a left pneumonectomy is done in a patient with uncorrected SV-ASD for conditions such as tuberculosis or traumatic shattered lung. Furthermore, pulmonary venous collaterals may subsequently form, leading to systemic desaturation in the years following this surgical option [3,4]. So, for the aforementioned reasons, it is important to be watchful when considering surgical management of pulmonary pathologies in the setting of anomalous pulmonary venous connection (with or without SV-ASD) by re-implantation or re-anastomosing of the anomalous pulmonary vein to the common pulmonary vein instead of merely transecting or ligating the vessel. Conflict of Interest: None declared

Portal vein thrombosis in a patient with Turner’s syndrome: A case report

This work aimed at reporting a case of Turner’s syndrome with portal vein thrombosis and elevated levels of factor VIII and von Willebrand factor. A 14-year-old Libyan girl was admitted for evaluation of infantilism and pallor; meanwhile, she was found to be of short stature, with webbing of the neck. Chromosomal studies showed monosomy pattern Turner’s syndrome (45XO). Abdominal ultrasound displayed a hugely enlarged spleen. Computed tomography (CT) imaging of the abdomen revealed portal vein thrombosis and dilated venous collaterals in porta hepatis. Thrombophilia screening demonstrated elevated levels of factor VIII (207IUdl–1) and von Willebrand factor (450IUdl–1). It was concluded that this was a case report on the unusual finding of portal vein thrombosis in a patient with Turner’s syndrome in whom high levels of factor VIII and von Willebrand factor were found. Detailed molecular epidemiological study is recommended to clarify this finding and its underlying factors.

The role of contrast- enhanced MRV in preoperative assessment of parasagittal meningiomas and sinusconfluence meningiomas

Objective The purpose of this study was to find whether contrast - enhanced magnetic resonance venography (CEMRV) is a good method for preoperative assessment of parasagittal meningiomas and sinus confluence meningiomas.Methods Thirty -five consecutive parasagittal meningiomas and sinus confluence meningiomas patients underwent surgery in eight months in our ward. All patients underwent CEMRV to define the degree of involvement of the sagittal sinus and depict collateral veins,and some patients also underwent TOFMRV or DSA.Results The CEMRV and DSA showed that sagittal sinus and sinus confluence were completely or partially patent in 25 patients and occluded in 10 patients,which were confirmed by the operations.The images of collateral venous and dural sinus were clearer in CEMRV and DSA than in TOF MRV. The numbers of collateral venous were more accurate in CEMRV than in TOFMRV.Conclusion CEMRV can well define the degree of involvement of the sagittal sinus and depict collateral veins,which make it a good choice for preoperative assessment of parasagittal meningiomas and sinus confluence meningiomas. Key words: Contrast- enhanced magnetic resonance venography; Sagittal sinus; Sinus confluence ; Meningioma ; Preoperative evaluation

Superior mesenteric artery syndrome: spectrum of CT findings with multiplanar reconstructions and 3-D imaging

This article reviews the causes, clinical presentation, and CT diagnosis of superior mesenteric artery (SMA) syndrome. In conjunction with an appropriate clinical history, several CT findings can suggest the diagnosis of SMA syndrome. These findings include narrowing of the aortomesenteric angle and distance, distension of the stomach and duodenum, and dilatation of the left renal vein with left-sided venous collaterals.

Portal biliopathy

Biliary ductal changes are a common radiological finding in patients with portal hypertension, however only a small percentage of patients (5%-30%) develop symptomatic bile duct obstruction. The exact pathogenesis is not clear, but an involvement of factors such as bile duct compression by venous collaterals, ischemia, and infection is accepted by most authors. Although endoscopic retrograde cholangiopancreatography was used to define and diagnose this condition, magnetic resonance cholangiopancreatography is currently the investigation of choice for diagnosing this condition. Treatment is indicated only for symptomatic cases. Portosystemic shunts are the treatment of choice for symptomatic portal biliopathy. In the majority of patients, the changes caused by biliopathy resolve after shunt surgery, however, 15%-20% patients require a subsequent bilio-enteric bypass or endoscopic management for persistent biliopathy. There is a role for endoscopic therapy in patients with bile duct stones, cholangitis or when portosystemic shunt surgery is not feasible.

Chest and Abdominal Wall Varicosities

A 40-year-old African American man with a history of sickle cell disease (SCD), deep venous thrombosis and alcohol abuse was transferred to the medical intensive care unit for worsening agitation and stridor. Physical examination revealed a symmetrically swollen neck with large palpable veins over the anterior chest wall and abdomen. Figure 1 is an axial computed tomographic image of his chest which illustrates several large superficial collateral veins (arrows). A volume rendered computed tomographic image in Figure 2 depicts the extent of his chest and abdominal wall varicosities (arrows). The presence of extensive venous collateralization suggested that the thrombosis had been present for a prolonged period of time. Although SCD is a hypercoagulable state, a compelling causal link with venous thromboembolism is not well established. 1. Austin H. Key N.S. Benson J.M. et al. Sickle cell trait and the risk of venous thromboembolism among blacks. Blood. 2007; 110: 908-912 Crossref PubMed Scopus (169) Google Scholar , 2. Stein P.D. Beemath A. Meyers F.A. et al. Deep venous thrombosis and pulmonary embolism in hospitalized patients with sickle cell disease. Am J Med. 2006; 119: 897.e7-897.e11 Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar However, a higher prevalence of pulmonary embolism and to a lesser extent deep venous thrombosis has been observed in African Americans with SCD. 2. Stein P.D. Beemath A. Meyers F.A. et al. Deep venous thrombosis and pulmonary embolism in hospitalized patients with sickle cell disease. Am J Med. 2006; 119: 897.e7-897.e11 Abstract Full Text Full Text PDF PubMed Scopus (148) Google Scholar A negative laboratory evaluation for a second hypercoagulable state suggested that SCD was the cause for the thrombosis. The patient was eventually discharged on subcutaneous enoxaparin twice daily. Figure 2 View Large Image Figure Viewer

Usefulness of the Guglielmi detachable coil for embolization of a systemic venous collateral after Fontan operation: A case report

Embolization of collateral veins is often treated with rigid coils (Gianturco and interlocking detachable coils type). However, when dealing with tortuous and dilated collateral veins, there is a high risk for technical failure and coil migration due to inflexibility of the coils. To safely and successfully solve this problem, Guglielmi detachable coils (GDC) can be used for embolization. Their flexibility allows for easy navigation in tortuous veins, low risk of unintended coil release or coil migration, and safe deployment. A 12-year-old girl with a single ventricle had severe cyanosis and a low exercise tolerance 5 years after Fontan procedure. The symptoms were caused by a tortuous and dilated collateral from the left phrenic vein into the left pulmonary vein, forming a right-to-left shunt. The collateral, which had a large diameter and high flow, and therefore a high risk of coil migration, was successfully embolized with 8 GDC. There were no complications such as coil migration or cerebral infarction. Transcatheter embolization increased her systemic oxygen saturation from 81%-84% to 94%-95%, and increased her ability to exercise. The embolization procedure using flexible GDC was low risk compared with other rigid coil embolization techniques when performing embolization of tortuous and dilated collateral veins.

Entrapment of the Left Renal Vein: A Rare Cause of Proteinuria

To the Editor: A 26-year-old man visited our institution for evaluation of proteinuria. He intermittently presented with acute urinary retention. Other urological evaluations were unremarkable. Urinalysis exhibited trace proteins without hematuria. Renal duplex and enhanced computed tomography (CT) of the abdomen and pelvis were performed. The duplex ultrasound typically demonstrated aortomesenteric anatomy with entrapment of the left renal vein (LRV) (Fig. 1). The diameters of the LRV at the hilar and aortomesenteric portions were measaured as 11 mm and 1.2 mm, respectively. The duplex ultrasound also indicated a significantly higher ratio of the peak systolic velocity (PSV) to the hilar renal vein PSV at the point of renal vein compression (> 6). This observation demonstrates the diminished volume of flow and dampened pulsatility upon spectral analysis of the left renal vein. Enhanced CT angiography revealed compression of the left renal vein between the aorta and the superior mesenteric artery (Fig. 2). The Nutcracker syndrome is defined as a rare cause of hematuria and flank pain caused by compression of the left renal vein between the aorta and the superior mesenteric artery where it passes at the point of bifurcation of the arteries [1]. The observed compression causes venous hypertension and the formation of renal venous collaterals leading to the subsequent rupture of the septum between the veins and the collecting system, and finally, resulting in hematuria and flank pain [2, 3]. In this particular patient case, although rare, the nutcracker should be included as the potential cause of proteinuria in addition to hematuria in the absence of other renal diseases. References

A Case of Exercise-Induced Hematuria Presenting as Gross Hematuria Lasting One Week

Exercise-induced hematuria is a phenomenon occurring in subjects who participate in strenuous exercise. Rapid resolution is an important feature of exercise-induced hematuria. We report here a case of exercise-induced hematuria presenting as gross hematuria lasting 1 week in a 19-year-old male patient. Gross hematuria developed after strenuous exercise about 3 years ago. Three months ago, recurrent gross hematuria was lasting 1 week, regardless of exercise intensity. Compression of the left renal vein between the aorta and superior mesenteric artery, without prominent venous collaterals, was detected by computed tomography. However, no abnormalities were detected by renal venography, arteriography or kidney biopsy. Exercise-induced hematuria occurs with a high incidence, but is self-limiting. In contrast, recurrent and gross hematuria can be associated with bladder carcinoma or vascular abnormality. This should be kept in mind, and urological evaluations such as cystoscopy and angiography are necessary in gross and recurrent hematuria. (Korean J Med 2012;82:95-99)

Caval Agenesis With a Hypoplastic Left Kidney in a Patient With Trauma on Warfarin for Deep Vein Thrombosis

Congenital anomalies of the inferior vena cava (IVC) are rare, but recognized, causing deep venous thrombosis. We present a case of a 50-year-old patient with trauma who suffered an intracranial hemorrhage secondary to a fall while on anticoagulation for deep vein thromboses. Venous return from the lower extremities was determined to be through dilated lumbar venous collaterals into the azygous and hemiazygous systems. A second interesting anatomic finding was a hypoplastic left kidney.

High Venous Pressure in the Main Renal Vein Causing Development of Peritransplant Venous Collaterals in Renal Transplant Patients

We will show the sonographic appearance of peritransplant venous collaterals in renal transplants with renal venous hypertension. Three cases of renal transplants with pericapsular vessels were identified at our institution. Two cases were related to renal vein thrombosis. The third case had pericapsular vessels secondary to venous hypertension from arterialization of the transplant renal vein by a preexisting right thigh arteriovenous graft. The development of high venous pressures in renal transplants leading to the collaterals' venous drainage has been rarely described. This finding should be recognized as a rare complication of renal transplants but does not necessarily lead to transplant failure.

Venous Access Salvage Techniques

For patients who need long-term central venous access but who have developed obstruction of the usual central veins, "salvage" access techniques offer successful alternatives. These techniques include translumbar inferior vena cava access, transhepatic inferior vena cava access, catheterization of small venous collaterals, and recanalization of occluded veins. Inferior vena cava access techniques allow a range of devices to be placed, including ports, infusion catheters, and hemodialysis catheters. Collateral vessels may be too small to allow for large-caliber devices, such as hemodialysis catheters. Success rates for these access techniques are high and complications are infrequent. These access routes are in general quite durable. Adults and children can be treated. Once placed, devices are managed and used as they would be for any routinely placed venous access device.

Duodenal Varices: A Rare Cause of Massive Gastrointestinal Hemorrhage

Purpose: Variceal bleeding is one of the leading causes of mortality in patients with portal hypertension. Although the development and bleeding from gastroesophageal varices occurs commonly in this patient population, bleeding from ectopic varices at other gastrointestinal sites is unusual. Here we present two cases of fatal gastrointestinal hemorrhage from ruptured duodenal varices, both in the setting of cirrhosis and portal hypertension. Both patients, a 27-year-old Caucasian and a 54-year-old African American male, had a history of chronic liver disease secondary to chronic hepatitis C infection and chronic alcohol abuse with previous episodes of gastrointestinal bleeding from esophageal varices. They presented to the hospital with hematemesis, hematochezia and hypovolemic shock. Continuous octreotide and pantoprazole intravenous infusions were started. After aggressive fluid resuscitation, transfusion of blood products and endotracheal intubation; an emergent esophagogastroduodenoscopy was performed revealing actively bleeding varices in the second portion of the duodenum that was controlled with band ligation. Their hospital course, however, was complicated with recurrent gastrointestinal bleeding. MELD scores were higher than 20. Though consideration was given to alternative therapeutic options such as balloon occluded retrograde transvenous obliteration (BRTO) and transjugular intrahepatic portosystemic shunt (TIPS), both patients were changed to category three (comfort care) by patient/family request and expired within a few days of their presentation. These cases illustrate the potential for massive and recurrent gastrointestinal hemorrhage from duodenal varices. These lesions are rare and a high index of suspicion is required to detect them. Ectopic varices comprise large portosystemic venous collaterals located anywhere other than the gastroesophageal region. Ectopic varices including duodenal varices account for between 1% and 5% of all variceal bleeding. The management of such ectopic varices is difficult, and although a few therapeutic options exist, there is no consensus as to the best treatment option.

A Hepatic Outflow Obstruction (Budd-Chiari Syndrome) Case due to Antithrombin III Deficiency

Purpose: Patient was referred to our Service for assesment of ascites and hepatosplenomegaly. He was complaining of abdominal dullness, nausea and fatigue over the past 4 weeks. In July 2009, he was diagnosed with septic arthritis, brucellosis and he was performed arthroscopic debridement and given brucella treatment. In control examination pulmonary thromboembolism was diagnosed, his medication was warfarin but he discontinued it. 4 weeks later he referred to our service. Computed tomography revealed hepatosplenomegaly, suspected thrombus formation in the vena cava inferior at the suprarenal and infrarenal levels, heterogenity of liver parenchyma, massive ascites (Fig. 1). Doppler ultrasonography revealed very slow flow signal, hepatic venous collaterals. Endoscopy revealed Grade I-II esophagus varices. Inferior/superior vena cavagraphy showed total occlusion of inferior vena cava and lower extremity venous drainage was flowing directly to superior vena cava via paravertebral collaterals and hemiazygous vein (Fig. 2). We have reported a very rare alliance of multiple hypercoagulable situations (decreased activitiy, decreased antigenic concentration of AT, low protein C activity, heterozygote Factor V Leiden mutation) which caused Budd-Chiari Syndrom. BCS is a rare but crucial situation and thrombofilia is a basis for BCS, and a complete search for thrombofilia is very critical.FigureFigure

Three-dimensional computed tomography analysis of venous collaterals between the middle hepatic vein tributaries and the right hepatic vein in the donor remnant right lobe: Report of a case

We report how three-dimensional computed tomography (3D-CT) showed the development of obvious venous collaterals between the middle hepatic vein (MHV) tributaries and the right hepatic vein (RHV) in the remnant right lobe of a donor liver. The donor was a healthy 34-year-old man who donated the left lobe of his liver with the MHV. The 3D-CT calculated that the total drainage of the MHV tributaries was 413 ml, corresponding to 59% of the total remnant liver. The congestion calculated by 3D-CT decreased from 286 ml on postoperative day (POD) 7 to 28 ml on POD 35, corresponding to 36% and 3% of the total remnant liver, respectively. The donor was discharged from hospital with almost normal liver function, and 3D-CT analysis on POD 35 detected obvious venous collaterals between the MHV tributaries and the RHV. These findings suggest that reconstruction of the MHV tributaries in the donor remnant right lobe may not be necessary.

A very rare cause of low-back pain and sciatica: deep vein thrombosis due to absence of the inferior vena cava mimicking the clinical and radiological signs of lumbar disc herniation

The authors report a very rare cause of low-back pain and sciatica in a patient with iliac vein thrombosis attributed to absence of the infrarenal segment of the inferior vena cava (IVC) with massively dilated venous collaterals draining via a paraspinal plexus into the azygous system. This 21-year-old man presented with acute low-back pain radiating to the left ventral thigh. The initial CT scan revealed an intraspinal lesion that mimicked lumbar disc herniation. Further clarification revealed an iliac vein thrombosis, which was triggered by the absence of the infrarenal segment of the IVC, a very rare vascular anomaly. Collateral venous return was developed and led to lumbar varicosities and epidural vein engorgements. Laboratory examinations revealed factor V mutation as a predisposing factor for thrombosis. The patient's symptoms were relieved with anticoagulation and antiinflammatory therapy. Absence of the infrarenal IVC associated with iliac vein thrombosis should be regarded as a very rare cause of radicular and low-back pain, and this condition can mimic the clinical and radiological signs of lumbar disc herniation. Sciatica might be the first clinical manifestation of this rare venous anomaly.

A Transgenic Model for Conditional Induction and Rescue of Portal Hypertension Reveals a Role of VEGF-Mediated Regulation of Sinusoidal Fenestrations

Portal hypertension (PH) is a common complication and a leading cause of death in patients with chronic liver diseases. PH is underlined by structural and functional derangement of liver sinusoid vessels and its fenestrated endothelium. Because in most clinical settings PH is accompanied by parenchymal injury, it has been difficult to determine the precise role of microvascular perturbations in causing PH. Reasoning that Vascular Endothelial Growth Factor (VEGF) is required to maintain functional integrity of the hepatic microcirculation, we developed a transgenic mouse system for a liver-specific-, reversible VEGF inhibition. The system is based on conditional induction and de-induction of a VEGF decoy receptor that sequesters VEGF and preclude signaling. VEGF blockade results in sinusoidal endothelial cells (SECs) fenestrations closure and in accumulation and transformation of the normally quiescent hepatic stellate cells, i.e. provoking the two processes underlying sinusoidal capillarization. Importantly, sinusoidal capillarization was sufficient to cause PH and its typical sequela, ascites, splenomegaly and venous collateralization without inflicting parenchymal damage or fibrosis. Remarkably, these dramatic phenotypes were fully reversed within few days from lifting-off VEGF blockade and resultant re-opening of SECs' fenestrations. This study not only uncovered an indispensible role for VEGF in maintaining structure and function of mature SECs, but also highlights the vasculo-centric nature of PH pathogenesis. Unprecedented ability to rescue PH and its secondary manifestations via manipulating a single vascular factor may also be harnessed for examining the potential utility of de-capillarization treatment modalities.

Comments regarding ‘Venous Angioplasty is Safe to Perform and May Have Benefits Forin Patients with Multiple Sclerosis. Results of a Pilotcase Control Pilot Study’

This small pilot study follows on from the prospective study of 65 patients by the same group, published in the Journal of Vascular Surgery (JVS) in 2009.1 The authors do not explain what this small pilot was supposed to achieve in terms of a power calculation for a larger trial, nor do they explain the rationale for the strange methodology of submitting half the group to immediate treatment and the other half to delayed treatment at 6 months. Presumably, they felt that patients would not agree to enter the trial unless they received treatment? This is not the usual basis for planning a randomised controlled trial and one that is unlikely to be acceptable to any organisation that might fund a larger trial in the future. If the authors are serious about their conclusion that a large multicentre randomised trial is now required, then this pilot should have been designed with more attention towards the design of that trial. The authors suggest that one of the objectives of this trial of only 15 patients was to assess safety. The number was wholly inadequate to answer this objective, especially in view of their previous larger study and another much larger study of 564 endovascular procedures in 331 patients from Poland.2 Whether or not the procedure is safe, and many think that it is not, other questions remain, including the possible pathophysiological mechanisms of chronic cerebrospinal venous insufficiency (CCSVI). The authors and others claim that CCSVI is a syndrome characterized by stenosis of the internal jugular and/or azygous veins and formation of collateral venous channels. They claim that these stenoses are far more common in Multiple Sclerosis (MS) sufferers but other researchers have found no increase in the frequency of these abnormalities in MS sufferers compared to normals.3 The last and possible the most important question is whether the procedure is efficacious both technically and clinically. The authors own results are disappointing in respect of the technical question, as their one-year patency rate was only 73%. Restenosis