Thrombosis Of Developmental Venous Anomaly Research Articles

Developmental venous anomaly thrombosis in a patient with coronavirus disease 2019-associated hypercoagulability: illustrative case.

Spontaneous thrombosis of a developmental venous abnormality (DVA) is a rare complication associated with hypercoagulability. The objective of this case report is to describe an association between DVA thrombosis and mild coronavirus disease 2019 (COVID-19) infection in a vaccinated patient. A 28-year-old male with hypertension presented with severe headache and left-sided hemiparesis. Five weeks prior to presentation, the patient experienced mild respiratory symptoms and tested positive for COVID-19. Admission brain computed tomography (CT) showed a large right parieto-occipital intracerebral hemorrhage with surrounding edema. CT venography and catheter angiography showed a thrombosed DVA with associated venous infarction as the hemorrhage etiology. He was treated with decompressive hemicraniectomy, external ventricular drain placement, and systemic anticoagulation. The patient was functionally independent (modified Rankin Scale score, 2) at 4-month follow-up. Hypercoagulability work-up was unremarkable. Delayed DVA thrombosis after the COVID-19 infectious period may represent an association between the infection and a protracted systemic viral-induced hypercoagulable state. The severity of COVID-19 symptomatology does not appear to correlate with risk of DVA thrombosis. Young patients with a recent history of COVID-19 infection who present with venous infarction should be evaluated for an underlying thrombosed DVA.

Infratentorial Developmental Venous Abnormalities and Inflammation Increase Odds of Sporadic Cavernous Malformation

Goal: Sporadic brain cavernous malformations commonly correlate with developmental venous anomalies; however, developmental venous anomalies may exist without cavernous malformations. Infratentorial location and specific angioarchitectural features of the developmental venous anomaly increase the odds of a concomitant malformation. Animal data also suggest chronic inflammatory disease, oxidative stress, and angiogenesis promote cavernous malformation development. We sought to determine potential clinical and radiologic factors promoting development of sporadic cavernous malformations. Methods: One hundred and forty-five patients with sporadic, nonradiation-induced brain cavernous malformations (63 with radiologic-apparent and 82 with radiologic-occult developmental venous anomalies) were compared to developmental venous anomaly controls without associated malformation. Data collection included demographic information, comorbidities, medications at diagnosis, and location of the developmental venous anomaly and/or malformation. Logistic regression with likelihood ratios, odds ratios and 95% confidence intervals were calculated comparing malformation cases with controls. A similar analysis compared malformations with radiologic-apparent anomalies to controls. Results: Compared to controls, cases were more likely to have had a major infectious illness (10.3% versus 2.3%; P = .0003 and/or chronic inflammatory disease (31.7% versus 21.3%; P = .0184) prior to diagnostic magnetic resonance imaging. Infratentorial location was more common in cavernous malformation cases (31.7% versus 15.7% controls; P ≤ .0001) with similar findings in cavernous malformation with radiologic-apparent developmental venous anomalies versus controls. Conclusions: Infratentorial developmental venous anomalies location, major infectious illness, and chronic inflammatory disorders increase the odds of sporadic cavernous malformation formation. Inflammation may promote local thrombosis of developmental venous anomalies, trigger angiogenic response through increased vascular permeability, or promote cavernous malformation through Toll-like receptor 4.

Clinical manifestations and imaging findings of thrombosis of developmental venous anomalies

To determine clinical manifestations, imaging findings and outcome of patients with thrombosed developmental venous anomalies (DVAs). The radiology database was searched retrospectively for thrombosed DVAs between 01/01/2000 to 07/01/2016. Demographic variables, associated risk factors, clinical manifestations, imaging findings, treatments, and follow-up were recorded. Six patients were found (four female and two male; age range 16-45 years with mean age, 21.3 years). The most common clinical presentation was headaches followed by neurological deficits and seizures. Venous infarction, parenchymal haemorrhage, venous congestive oedema were noted as the radiological findings. Clinical outcome was favourable in all patients with complete recovery or persistence of mild neurological symptoms. Thrombosed DVAs may occur under rare circumstances, which lead to variable symptoms. Familiarity with this entity and early recognition of associated findings including venous infarction, parenchymal haemorrhage, and venous congestive oedema would help early diagnosis and prompt treatment.

Hemorrhagic presentation without venous infarction caused by spontaneous thrombosis of developmental venous anomaly and angiographic change after treatment

Abstract Developmental venous anomalies (DVAs) have been known benign anatomical variations and generally do not cause symptoms. Although several cases of venous infarction caused by DVA thrombosis have been reported, it not common in itself. But only hemorrhagic presentation in DVA is extremely rare. We describe a case with large intracerebral hemorrhage (ICH) without venous infarction caused by DVA thrombosis and angiographic change of successful treatment.

Serial imaging and SWAN sequence of developmental venous anomaly thrombosis with hematoma: Diagnosis and follow-up

Developmental venous anomalies (DVAs) are usually asymptomatic. We report a case of DVA thrombosis with recurrent tiny frontal hematoma in a 24-year-old man. The contribution of T2-GRE and SWAN sequences are discussed. Follow-up attested complete recanalization after anticoagulation.

Postpartum Thrombosis of Developmental Venous Anomaly Complicated by Venous Infarct and Subarachnoid Hemorrhage (P3.276)

Postpartum Thrombosis of Developmental Venous Anomaly Complicated by Venous Infarct and Subarachnoid Hemorrhage (P3.276)

Spontaneous thrombosis of developmental venous anomaly (DVA) with venous infarct and acute cerebellar ataxia

Developmental venous anomaly (DVA), formally known as venous angioma, is a congenital anatomic variant of the venous drainage of the brain. Although they typically have a benign clinical course and a low symptomatic rate, thrombosis of a drainage vein may occur, leading to potentially debilitating complications. We report a unique case of spontaneous thrombosis of a posterior fossa developmental venous anomaly with cerebellar infarct in a 61-year-old man who presented with acute onset cerebellar ataxia. DVA thrombosis was well-depicted on CT and MR studies. Patient was put on anticoagulant therapy and complete recanalization was seen on follow-up imaging.

Thrombosis of a Developmental Venous Anomaly in Inflammatory Bowel Disease: Case Report and Radiologic Follow-up

Developmental venous anomalies (DVAs) are benign embryologic vascular variants, and before the advent of computed tomography and magnetic resonance imaging were supposed to be rare conditions. Usually, DVAs are asymptomatic and accidentally discovered during routine brain imaging studies, but sometimes they can be the cause of disabling neurologic symptoms. We describe the clinical and neuroradiologic follow-up of a 62-year-old man with a history of inflammatory bowel disease (IBD) presenting with new onset epilepsy and intracranial hemorrhage caused by thrombosis of a DVA who fully recovered after treatment with oral anticoagulant therapy. Patients with IBD have an increased risk of thrombosis because of inflammatory activity and the hypercoagulable state. Here we describe the first case of DVA thrombosis in a patient with IBD, and we show clinical and neuroradiologic follow-up after anticoagulant therapy.

008 Developmental venous anomaly thrombosis: case report and review of the literature

A 31-year-old gentleman presented with sudden onset headache and seizures requiring intubation. CT brain demonstrated a thrombosed developmental venous anomaly (DVA) and occipital infarction; intravenous heparin was commenced. Shortly afterwards...

Venous Angiomas

Venous angiomas are currently widely referred to as developmental venous anomalies (DVAs), reflecting the prevailing concept that they represent anomalous, but functional, venous channels within the brain parenchyma. Although DVAs are not infrequently associated with other vascular malformations that harbor hemorrhage risk or can present symptomatically, isolated DVAs themselves appear to be benign lesions with little demonstrable link to hemorrhage, seizures, or headaches. Treatments to remove or occlude DVAs are consequently unnecessary. Furthermore, obliteration of a DVA can be harmful as it can lead to impairment in regional cerebral venous drainage, with the resultant risk of venous congestion, infarction, and hemorrhagic conversion, and the potential for devastating consequences from cerebral edema and mass effect. Consequently, even in the management of associated vascular malformations, it is important to preserve the DVA. In rare cases, DVAs can produce direct compressive symptoms, leading to obstructive hydrocephalus or neurovascular compression. In such cases, cerebrospinal fluid diversion or direct microvascular decompression, respectively, without disruption of the DVA itself is appropriate. In the uncommon setting of spontaneous DVA thrombosis leading to venous infarction, anticoagulation, as recommended for dural and cortical venous thrombosis, is a reasonable consideration. Hemorrhagic presentation from a presumed isolated DVA should prompt careful evaluation for an associated vascular malformation as the true etiology of hemorrhage.

Thrombosis of a Developmental Venous Anomaly With Hemorrhagic Venous Infarction

A 17-year-old female presented with a 4-day history of severe left frontal headache, nausea, and vomiting that was worst in the morning. Neurologic examination revealed an alert, conversant teenager with a right facial droop and no other focal neurological signs. Medical history was significant only for occasional headaches and a 1-year history of oral contraceptive use. Head CT showed a small amount of hemorrhage, edema, and a probable thrombosed venous structure in the left frontal lobe (Figure 1, panel A). MRI of the brain showed flow voids in the left frontal region consistent with a developmental venous anomaly (DVA), with surrounding edema (Figure 1, panel B), scattered T2 hypointensity consistent with areas of hemorrhage, and weakly positive diffusion-weighted imaging consistent with a small hemorrhagic venous infarction. There was also significant edema and mass effect. MRA was normal. MRV showed a partially thrombosed deep vein draining the left frontal lobe. Thrombosis of the DVA and absence of other vascular malformations was confirmed by digital subtraction angiography (DSA). The partially occlusive clot within the venous collector of the DVA is well delineated on the sagittal view of the post-contrast MRI and on the lateral projections of the angiogram. (Figure 2, panels A and B). Figure 1 Axial Head CT and MRI of the Brain showing Developmental Venous Anomaly Thrombosis Figure 2 Sagittal Contrast-Enhanced MRI of the Brain and Digital Subtraction Angiography confirming DVA Thrombosis

Thrombosis of Developmental Venous Anomalies of the Brain After Liver Transplantation

Thrombosis of Developmental Venous Anomalies of the Brain After Liver Transplantation

POSTPARTUM THROMBOSIS OF A DEVELOPMENTAL VENOUS ANOMALY

Developmental venous anomaly (DVA) is a common congenital vascular abnormality that typically has a benign natural history. The lesion likely occurs after atresia or thrombosis of normal venous structures, leading to compensatory retention of embryologic medullary venules.1,2 These venules form an umbrella- shaped arrangement (caput medusae) and cluster into a large central vein that drains into the deep or superficial venous system.1,2 Spontaneous thrombosis of the central vein of a DVA can rarely occur, and lead to symptomatic nonhemorrhagic venous infarction.2–7 Most reported cases of DVA thrombosis demonstrate no underlying predisposition.2–6 One report of nonhemorrhagic venous infarction attributes thrombosis to hypercoagulability induced by puerperium, oral contraceptive use, and smoking.7 We report a case of DVA thrombosis occurring in a postpartum patient on hormonal contraception. ### Case report. A 16-year-old G1P1 woman presented after three brief simple motor seizures involving the right arm and face occurring over 3 days. She denied persistent symptoms. After the first seizure, she had presented to another hospital and was treated with phenytoin, but did not undergo any neuroimaging studies. Four years previously, she had three episodes of right face, arm, and leg shaking, lasting 2 minutes, without altered consciousness. A routine EEG revealed occipital slowing, but no epileptiform discharges. Brain MRI revealed multiple small vessels …