Endovascular correction of an infantile intracranial venous outflow obstruction

2013 ◽  
Vol 12 (6) ◽  
pp. 660-663 ◽  
Author(s):  
Maryam Soltanolkotabi ◽  
Shahram Rahimi ◽  
Michael C. Hurley ◽  
Robin M. Bowman ◽  
Eric J. Russell ◽  
...  
Keyword(s):  
Visual Acuity ◽  
Venous Pressure ◽  
Transverse Sinus ◽  
Venous Hypertension ◽  
Sigmoid Sinus ◽  
Dural Sinus ◽  
Stent Insertion ◽  
Outflow Obstruction ◽  
Venous Outflow ◽  
Venous Outflow Obstruction

The authors report on the case of a 7-year-old boy who presented with a reduced level of activity, macrocephaly, prominent scalp veins, and decreased left-sided visual acuity. Imaging workup demonstrated generalized cerebral volume loss, bilateral chronic subdural hematomas, absent left sigmoid sinus, hypoplastic left transverse sinus, and severe focal weblike stenosis of the right sigmoid sinus. Right sigmoid sinus angioplasty and stent insertion was performed, with an immediate reduction in the transduced intracranial venous pressure gradient across the stenosis (from 22 to 3 mm Hg). Postprocedural diminution of prominent scalp and forehead veins and spinal venous collateral vessels was followed by a progressive improvement in visual acuity and physical activity over a 1-year follow-up period, supporting the efficacy of angioplasty and stent insertion in intracranial venous outflow obstruction. There are multiple potential causes of intracranial venous hypertension in children. Development of dural sinus stenosis in infancy may be one such cause, mimicking the clinical presentation of other causes such as vein of Galen malformations. This condition can be ameliorated by early endovascular revascularization.

Combined transvenous and transarterial embolization of a tentorial—incisural dural arteriovenous malformation followed by primary stent placement in the associated stenotic straight sinus

2003 ◽  
Vol 99 (3) ◽  
pp. 579-583 ◽  
Author(s):  
Neil A. Troffkin ◽  
Cole Blease Graham ◽  
Turgut Berkmen ◽  
Ajay K. Wakhloo
Keyword(s):  
Stent Placement ◽  
Clinical Course ◽  
Transarterial Embolization ◽  
Dural Sinus ◽  
Outflow Obstruction ◽  
Venous Outflow ◽  
Straight Sinus ◽  
Venous Outflow Obstruction ◽  
Aggressive Clinical Course ◽  
Dural Avm

✓ Dural arteriovenous malformations (AVMs) involving the tentoria—incisura are associated with an aggressive clinical course characterized by subarachnoid and intracranial hemorrhage (ICH). In these lesions, venous outflow obstruction precipitates leptomeningeal venous drainage, resulting in the arterialization of pial veins and the formation of venous aneurysms, both of which are prone to hemorrhage. Stenotic lesions of the dural sinuses also contribute to the development of retrograde leptomeningeal drainage, which is responsible for the aggressive clinical course of the dural AVM. Endovascular approaches are successful in the treatment of these lesions and of any potential venous outflow obstruction caused by stenosis of a dural sinus. The authors report on a patient with a tentorial—incisural dural AVM and an accompanying stenotic venous sinus. A combined transvenous and transarterial embolization procedure was performed, resulting in complete obliteration of the dural AVM, followed by primary stent placement across a stenotic segment of the straight sinus and normalization of venous outflow. The authors conclude that dural AVMs can be treated safely by using a combined transarterial and transvenous approach and that an extensive search for venous outflow obstruction often reveals stenosis of a draining sinus. Consideration should be given to primary stent placement in the stenotic sinus to protect against ICH.

Intracranial Venous Hypertension and the Effects of Venous Outflow Obstruction in a Rat Model of Arteriovenous Fistula

Neurosurgery ◽  
1991 ◽  
Vol 29 (3) ◽  
pp. 341-350 ◽  
Author(s):  
Joshua B. Bederson ◽  
Otmar D. Wiestler ◽  
Oliver Brüstle ◽  
Peter Roth ◽  
Rosmarie Frick ◽  
...  
Keyword(s):  
Arteriovenous Fistula ◽  
Rat Model ◽  
Venous Hypertension ◽  
Outflow Obstruction ◽  
Venous Outflow ◽  
Venous Outflow Obstruction

scholarly journals Episcleral venous pressure level in patients with thyroid associated orbitopathy

2018 ◽  
Vol 11 (3) ◽  
pp. 21-25
Author(s):  
Vitaly V. Potemkin ◽  
Elena V. Goltsman ◽  
Maria S. Kovaleva
Keyword(s):  
Venous Pressure ◽  
Outflow Obstruction ◽  
Venous Outflow ◽  
Precise Data ◽  
Episcleral Venous Pressure ◽  
Venous Compression ◽  
Main Index ◽  
Venous Outflow Obstruction ◽  
Temporal Quadrant ◽  
Severity Of The Disease

Thyroid associated orbitopathy (TAO) occurs in patients with various diseases of the thyroid gland. The levels of episcleral venous pressure (EVP), intraocular pressure and intraorbital pressure are inter- related. There are no precise data on the change of EVP in patients with TAO. Purpose. To evaluate EVP in patients with compensated and sub-compensated TAO forms. Methods. Data of 41 eyes of 22 patients were enrolled into the study. The main index to be evaluated was the EVP. Results. EVP level was significantly higher in complete venous compression in the lower- temporal quadrant in patients with sub-compensated TAO stage (p = 0.013). Conclusion. The degree of venous outflow obstruction and the EVP level of are interrelated. Thus, the level of EVP can be used as an additional factor in assessing the severity of the disease course and the treatment efficacy.

Surgical removal of a foreshortened right innominate vein Wallstent causing venous outflow obstruction

Vascular ◽  
2022 ◽  
pp. 170853812110689
Author(s):  
Kristin Schafer ◽  
Eric Goldschmidt ◽  
Andrew Seiwert
Keyword(s):  
Upper Extremity ◽  
Venous Hypertension ◽  
Complete Relief ◽  
Surgical Removal ◽  
Central Venous ◽  
Outflow Obstruction ◽  
Venous Outflow ◽  
Central Venous Stenosis ◽  
Venous Stenosis ◽  
Venous Outflow Obstruction

Objectives: Stenting of central venous stenosis to preserve upper extremity hemodialysis access is well-described, though upper extremity complications secondary to these stents are less frequently discussed. Methods: We present the case of a 43-year-old male with a right brachiocephalic fistula who developed symptoms of venous hypertension following placement of a Wallstent for central venous stenosis. Workup demonstrated venous outflow obstruction secondary to stent foreshortening into the right subclavian vein. Results: The Wallstent was removed in a piecemeal fashion using an open surgical technique and a HeRO graft was placed for dedicated fistula outflow with complete relief of the patient’s symptoms. Conclusion: In situations where a stent has migrated and endovascular removal is not possible, individual Wallstent fibers can be removed through a limited venotomy.

Styloidogenic Jugular Venous Compression Syndrome: Diagnosis and Treatment: Case Report

Neurosurgery ◽  
2011 ◽  
Vol 70 (3) ◽  
pp. 783-783 ◽  
Author(s):  
Shervin R. Dashti ◽  
Peter Nakaji ◽  
Yin C. Hu ◽  
Don F. Frei ◽  
Adib A. Abla ◽  
...  
Keyword(s):  
Jugular Vein ◽  
Pseudotumor Cerebri ◽  
Styloid Process ◽  
Clinical Results ◽  
Venous Hypertension ◽  
Diagnosis And Treatment ◽  
Outflow Obstruction ◽  
Venous Outflow ◽  
Jugular Veins ◽  
Venous Outflow Obstruction

Abstract Background and Importance: Intracranial venous hypertension is known to be associated with venous outflow obstruction. We discuss the diagnosis and treatment of mechanical venous outflow obstruction causing pseudotumor cerebri. Clinical Presentation: We report 2 patients presenting with central venous outflow obstruction secondary to osseous compression of the internal jugular veins at the craniocervical junction. The point of jugular compression was between the lateral tubercle of C1 and a prominent, posteriorly located styloid process. In both cases, catheter venography showed high-grade jugular stenosis at the level of C1 with an associated pressure gradient. The dominant jugular vein was decompressed after the styloid process was resected. Postoperative imaging confirmed resolution of the jugular stenosis and normalization of preoperative pressure gradients. In both cases, the symptoms of intracranial hypertension resolved. Conclusion: Intracranial venous hypertension may result from extrinsic osseous compression of the jugular veins at the skull base. Although rare, this phenomenon is important to recognize because primary stenting not only is ineffective but also may actually exacerbate the outflow obstruction. The osseous impingement of the dominant jugular vein can be relieved via a decompressive styloidectomy, and the clinical results can be excellent.

scholarly journals Dural sinus volume in children with syndromic craniosynostosis and intracranial hypertension

2020 ◽  
Vol 25 (5) ◽  
pp. 506-513
Author(s):  
Robbin de Goederen ◽  
Iris E. Cuperus ◽  
Robert C. Tasker ◽  
Bianca K. den Ottelander ◽  
Marjolein H. G. Dremmen ◽  
...  
Keyword(s):  
Intracranial Hypertension ◽  
Case Series ◽  
Dural Sinus ◽  
Outflow Obstruction ◽  
Venous Outflow ◽  
Syndromic Craniosynostosis ◽  
Cerebral Mri ◽  
Significant Difference ◽  
Venous Outflow Obstruction ◽  
Venous Volume

OBJECTIVEIntracranial hypertension is a major concern in children with syndromic craniosynostosis (sCS). Cerebral venous hypertension caused by cerebral venous outflow obstruction is believed to contribute to intracranial hypertension. The authors therefore hypothesized that cerebral venous volume would be increased in those children with sCS and intracranial hypertension.METHODSIn a case series of 105 children with sCS, of whom 32 had intracranial hypertension, cerebral MRI techniques were used to quantify the volume of the superior sagittal sinus, straight sinus (StrS), and both transverse sinuses.RESULTSLinear regression showed that total cerebral venous volume increased by 580.8 mm3 per cm increase in occipitofrontal head circumference (p < 0.001). No significant difference was found between the intracranial hypertension group and the nonintracranial hypertension group (p = 0.470). Multivariate ANOVA showed increased StrS volume (as a proportion of total volume) in the intracranial hypertension group (8.5% vs 5.1% in the nonintracranial hypertension group, p < 0.001). Multivariate logistic regression showed that a 100-mm3 increase in StrS volume is associated with increased odds of having intracranial hypertension by 60% (OR 1.60, 95% CI 1.24–2.08).CONCLUSIONSAlthough intracranial hypertension was not associated with total cerebral venous volume increase, it was associated with an isolated increase in StrS volume. Hence, it is unlikely that general cerebral venous outflow obstruction is the mechanism of intracranial hypertension in sCS. Rather, these findings indicate either a central cerebral vulnerability to intracranial hypertension or a mechanism involving venous blood redistribution.

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