The management of venous aneurysms
Peter Gloviczki, Michael C. Dalsing, Bo Eklöf, Fedor Lurie, Thomas W. Wakefield, Monika L. Gloviczki in Handbook of Venous and Lymphatic Disorders, 2017
The pathogenesis of venous aneurysms found in association with major vascular malformations is somewhat easier to understand. During embryologic development, the major vascular and lymphatic spaces coalesce and separate to form the arterial, venous, and lymphatic components of the circulatory system. Arteriovenous malformations are formed by abnormal communications between the artery and vein. Cystic hygromas occur when there is a failure of the lymph sacs to completely separate from the venous system. The failure of the jugular venolymphatic to completely mature may explain the high incidence of cervical and thoracic venous aneurysms with cystic hygromas.9 On occasion, a persistent jugular sac may be misinterpreted as a venous aneurysm.10 The etiology of a solitary peripheral venous aneurysm is the most difficult to understand. The very localized nature of these lesions suggests a specific abnormality in the vein wall. Similar to arterial aneurysms, the media of the vein wall is thinned with loss of smooth muscle.11 The reason for the frequent occurrence of venous aneurysms in the popliteal vein is unknown, but may be related to the findings of Lev and Saphir.7,8
Practice Paper 2: Answers
Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar in Get ahead! Medicine, 2016
Hereditary haemorrhagic telangiectasia (also known as Osler–Weber–Rendu syndrome) is a rare autosomal dominant disease in which the patient develops multiple telangiectasias on the skin, lips and mucosal surfaces. Arteriovenous malformations may also be found in the soft tissues, brain, liver and lungs. These lesions are friable and prone to bleeding. The most common symptom is recurrent and severe epistaxis. Patients with gastrointestinal lesions can suffer acute or chronic gastrointestinal bleeding. Problematic telangiectasias on the skin, nose and gastrointestinal tract may be treated by laser therapy. Larger arteriovenous malformations can be treated with embolization or surgery. Oral iron supplementation is often required to treat iron-deficiency anaemia that develops secondary to chronic blood loss.
Vascular
Michael Gaunt, Tjun Tang, Stewart Walsh in General Surgery Outpatient Decisions, 2018
Treatment is multidisciplinary, involving a vascular surgeon, vascular radiologist, cardiolo gist, plastic surgeon, orthopaedic surgeon and sometimes a maxillofacial surgeon. Half of all lesions can be managed satisfactorily with compression hosiery and analgesia as required. In addition, small superficial arteriovenous malformations may be cured by surgical excision. For larger lesions not suitable for conservative treatment because of site or size, or for symptoms not controlled by conservative measures, further intervention consists of embolisation or surgical treatment. High flow lesions tend to be treated by repeated bouts of arterial or direct puncture embolisation to control symptoms over many years. Those lesions thought to be suitable for surgical excision can be pre-treated with embolisation to decrease intra-operative vascularity and blood loss.Low flow lesions are treated by direct puncture sclerotherapy under imaging control and either local or general anaesthetic. This tends to control the lesion rather than cure it and may need to be reviewed at regular intervals.
Thrombosed orbital arteriovenous malformation in a patient with lymphangioleiomyomatosis
Published in Orbit, 2022
Elzbieta Mechel, Ann Q. Tran, Andrea Tooley, Michael Kazim
Arteriovenous malformations are communications between arteries and veins, which bypass capillary vasculature, presumed to be developmental anomalies caused by failure of embryonic vasculature to differentiate.7 The pathophysiology of AVM formation remains unclear; however, numerous studies have looked at VEGF associations.8–10 VEGF has been implicated in the pathophysiology of cerebral AVMs, histologically equivalent to orbital AVMs.8 Expression of VEGF receptors has been examined in orbital vascular lesions, including venous malformations, capillary hemangiomas, lymphatic malformations, and lymphaticovenous malformations.9 Despite their congenital origin, AVMs may manifest later in life under the stimulation of menarche, pregnancy, or trauma, drawing parallels to a similar phenomenon seen in LAM.10 Estrogen has been causally implicated due to its ability to stimulate VEGF production.10 Rapamycin, which can decrease cell proliferation and lymphangiogenesis, has been examined as treatment of cerebral and orbital AVMs, the same mechanisms which support its use in LAM.11,12 Although no association has been reported between AVMs and LAM to date, these two entities share behavioral similarities, in particular VEGF expression and estrogen sensitivity, warranting consideration that LAM disease may promote a microenvironment suitable for AVM growth.1,2,8–10
Neuroimaging in professional combat sports: consensus statement from the association of ringside physicians
Published in The Physician and Sportsmedicine, 2023
Nitin K Sethi, John Neidecker
The CT is extremely sensitive in detecting the stigmata of acute TBI such as bleeding and bone pathology (craniofacial fractures, fractures of the orbits). It has the added advantage of widespread availability, short scan time, and low cost. The MRI is superior to a CT for detecting the stigmata of chronic TBI [1,6]. The ability of the MRI to detect hematomas improves over time as the composition of the blood changes [1,6]. The overwhelming majority of patients with mild brain injury frequently show no parenchymal abnormality on MRI [1,6]. However, coincidental structural brain abnormalities are found in about 2–3% of all studies, including meningiomas, coincidental, and non-pathologic anomalies, and small often unruptured cerebral aneurysms [1]. Small circle of Willis cerebral aneurysms are better visualized with CT or MR angiography. Large arteriovenous malformations (AVMs) can be readily identified on CT and MRI [7]. With reference to contact sports, relevant abnormalities include hemorrhagic cortical contusions, petechiae, or foci of altered signal that represent white matter shear injury (diffuse axonal injury) [1,5,6]. When petechiae resolve, they can leave a permanent hemosiderin deposition on the MRI [1]. While the MRI is superior to a CT in the detection of axonal injury, it is insensitive in detecting acute hemorrhage (oxy-Hgb and deoxy-Hgb) within 48–72 h after injury; emphasizing the value of CT without contrast in rapid triage of patients with acute TBI.
Surgical management and outcome of adult posterior cranial fossa and spinal hemangioblastoma: a 6-case series and literature review
Published in Neurological Research, 2020
Bruno Splavski, Blazej Zbytek, Kenan I. Arnautovic
Unlike Type 1 tumors, Types 2–4 are extremely vascularized tumors that enhance on MRI scans with contrast, contain flow voids in their enhancing parts, and may contain cysts of different sizes (Types 3 and 4). Surgical management must be planned in a similar manner as management of arteriovenous malformations due to their extreme tendency for hemorrhaging. Therefore, microsurgical technique has to be planned to circumscribe the tumor and carefully dissect, coagulate, and divide arterial feeders in a systematic fashion [27]. The venous drainage coagulation and interception must be left until the very end of the surgery following elimination of all arterial feeders. For Types 2–4 tumors, preoperative preparation of blood transfusion and close communication with anesthesia are of tremendous importance. Finally, gross total resection should be the goal since leaving tumor parts may lead to significant postoperative hemorrhage and poor clinical outcomes [25–27,33,53].
Related Knowledge Centers
- Birth Defect
- Central Nervous System
- Vein
- Capillary
- Artery
- Vascular Anomaly
- Cerebral Arteriovenous Malformation
- Asymptomatic
- Neurology
- Autopsy